MANUAL

FOR
DENTAL HYGIENIST

DEPT OF DENTAL SURGERY

ARMED FORCES MEDICAL COLLEGE
PUNE-40
 PATRON
LT GEN SB SEHAJPAL AVSM, VSM, PHDS
DGDS & COL COMDT

EDITOR – IN – CHIEF
BRIG NK SAHOO

EDITORS

Oral & Maxillofacial Periodontics

Surgery
Col PK Chattopadhyay Col SK Rath

Prosthodontics Orthodontics
Col M Viswambaran Col Rajat Mitra
Lt Col Manjit Kumar Col SS Chopra
 CONTRIBUTORS

MAJ PARUL LOHRA

MAJ SATISHA TS
SURG LT CDR K KAMALPATHEY
SURG LT CDR SAUGAT RAY
MAJ PRASANTH
MAJ TARUN DABRA
MAJ YUVRAJ ISSAR

MAJ VIJAYLAXMI MALALI

MAJ NITIN GUPTA
MAJ AZAD KHAN CHOUDHURY
MAJ V GOPALKRISHNA
MAJ VIJAY KUMAR
SQN LDR NAVEEN KS
SURG LT CDR OOMEN NAINAN
MAJ ASHISH KAMBOJ

MAJ HARSHVARDHAN
MAJ REENESH MACHERRY
MAJ ABIJIT KADU
MAJ MOHAN RANGAN
SURG LT CDR KAPIL TOMAR
MAJ SUDERAM
CAPT THIRUVALLAN
CAPT GANGANDEEP KOCHAR
 LT GEN SB SEHAJPAL, AVSM, VSM, PHDS
DIRECTOR GENERAL DENTAL SERVICES AND COL COMDT

FOREWORD

It is the ongoing education which motivates you to do things differently, to achieve results
different from the conventional average. It does not take extra time to do things perfect, it is only
a question of attitude which can change the will. It seems not so long ago when the first Dental
hygienist training course in the country was instituted at Department of Dental Surgery, AFMC.
We have come a long way in pioneering this change with different levels of continuing this
education at various levels, with frequent updates of our training curriculum and dental hygienist
training manuals.

But times and attitude do change. The past few years have brought significant developments in
dental education. This manual is the product of the great emphasis AFMC places on training
professionals, which shoulder the onerous responsibility of providing health care to the nation’s
Armed Forces.

Everyday’s achievement reposes confidence in you, insights you to go towards excellence. It is

the continuity of education which comes as a savior, motivates introspection, takes you back to
the basics and ensures corrective measures. At this juncture, this manual becomes an important
medium to stimulate newer thoughts, brings you newer techniques, informs you of the newer
materials and becomes your companion in an endeavor to achieve excellence. It has been an
attempt to incorporate the ongoing recent advances in Dentistry in a systematic way that a Dental
Hygienist is supposed to know.

I feel proud to have such a dedicated team in the corps who have put in tremendous efforts and
time in compiling this book. I hope it would serve the purpose for which it is written. To
conclude we must remember and incorporate the following words into our lives and work-

Search for excellence is the only search that never ends.

The more you achieve the more you desire.

(S B SEHAJPAL)
LT GEN
 ABOUT THE BOOK BY PROFESSOR & HOD, DEPT OF DENTAL SURGERY, AFMC, PUNE

Department of Dental Surgery. AFMC, provides education and practical training to scores of dental
hygienists every year at various levels. The requirement of updating the guides and manuals for
such courses is an ongoing task for faculty and trainees of this institution. As the knowledge of
the etiology and classification of periodontal disease and its therapy rapidly advances, the
demand for periodontal care course grows. Dental hygienists are an important clog in the
machinery of our corps in providing comprehensive oral health care to the Armed Forces.
Consequently, dental hygienists are routinely challenged to keep informed of the latest treatment
modalities and theoretical advances.

Gingivitis and periodontitis, the two major forms of diseases affecting gums and attachment
apparatus’ of the teeth, both require appropriate assessment and diagnosis in order to provide
timely, client centered therapy. The rapid advancements in dental hygiene theory and
periodontics have provided an impetus for change in professional terminology and practice. The
purpose of this manual remains to give the dental hygienist an up to date, concise, factual
reference work describing the basics of dental hygiene. In many instances, concepts are
illustrated with photographs, line drawings and tables where applicable. There is extensive use of
these aids to help the student understand more clearly and to clarify complex idea. The content is
sufficiently detailed to satisfy the requirements of the course.

The manual is designed to provide the reader with basics of health sciences, current
recommendations for non surgical periodontal care and maintenance therapy in a realistic and
practical manner. It is hoped that this effort of our institution will go a long way in providing
education and further paving the way for newer updates.

(N K SAHOO)
BRIG
 HERITAGE OF THE ARMY DENTAL CORPS
One of the criteria to get entry as a foot soldier in the East India Company was to
have a sound set of teeth as the greased paper covering the explosives and cartridges
had to be bitten open prior to firing the muskets and pistols. This could be termed as
the first known dental standards in the Indian military.
Awakening on dental fitness emerged only during Boer War when many troops
became incapable of active military duty in the war fronts due to various dental
diseases, could not chew food and had to be evacuated. The realization of a ‘biting fit’
army for ‘fighting fit’ came. The British Army tried to solve this problem by authorizing
some general practioners to come from England at their own expense and work in the
base camps.
Trained dentists from UK were not available to British Army in India. British
troops in India received basic dental treatment by medical officers. Dental treatment
was restricted mainly to maxillofacial injuries and emergencies. Indian troops had no
dental services of their own till Feb 1941. Civilian dental surgeons were employed in
each command. "Indian of Good Character" were given the privilege of denture
rehabilitation only if their duties were considered necessary. In 1915, it was decided that
recruits need not be rejected on account of decaying or missing teeth provided they
could be made fit. In 1920, 21 Dental Officers of the British Army formed the nucleus of
Army Dental Corps (British) to look after British troops in India. During the second
Great War, their number increased to 28. Wherever no Army Dental Corps (British)
officer was available, the British soldiers were treated by civilian dental surgeons. Prior
to 1939, no British soldier was sent on duty to India unless he was 'dentally fit' which
meant a clean mouth in which carious teeth had been filled and serious deficiencies, if
any, had been made good by fitting artificial dentures. The Indian troops in the same
time could only get treatment in the form of extractions of loose and painful teeth by a
Vice Roy Commissioned Officer of the Indian Medical Department (IMD). Dental
treatment required by Indian soldiers was administered by the personnel of Indian
Medical Services in the MI rooms for which only basic equipment was provided. Only
those soldiers requiring specialized treatment, whose dental disabilities occurred
during field service, were referred to IADC (BT).
There was persistent lobbying and discussions in the Indian Parliament from
1936 onwards for establishing a dental service for Indian troops. Eventually, in June
1940, the Govt agreed to establish a dental branch of the IMS (Indian Medical Services)
and designated it as IMS (D). In Aug 1940, the first selection board was held at GHQ
India. As per Army Headquarters, India Letter No Z-20769/DMS dt 17 January, first
batch of 7 officers were granted Emergency King's commission and the 'Indian
gentlemen' were ordered to join various establishments on 1st of Feb 1941.
These doctors were given 4 weeks basic military training and then sent to the
British Army Dental Centres at Dehra Dun, Rawalpindi, Poona and Quetta. Eligibility
for the IMS (D) was restricted to British subjects of Indian domicile or subjects of Indian
states who were under 45 yrs of age and had adequate dental qualifications. They
joined as lieutenants and were on probation for 3 months. The dental teams served in
different theaters of war in World War II like Burma, Siam, Singapore and Hong Kong
in Far East, in Persia and Iraq in the Middle East; Tripoli, El Alamein, Greece, Italy and
France in Europe. In 1946, King George VI granted the 'Royal' prefix to the Army Dental
Corps (British) for the exceptional performance in World War II and the Corps had a
new badge. The IMS(D) got its own badge- a laurel wreath, surmounted by a crown,
with the inscription 'IADC'. The officers were promoted to captain (the highest rank
open to them) after 1 year service and were employed for the duration of the war or as
long as their services were required. Subsequently, various army dental centres for
Indian troops were established at Indian Military Hospitals, most of them with one
chair, but a few larger ones had few chairs apart from the dental officer. Each centre
was authorised a clerk, a sweeper and a ward boy of the Indian Hospital Corps.
Dentures were fitted at the nearest dental mechanical unit set up for British troops.
There was a shortage of equipment and the dentists had to work in shifts. The work of
the first dental officers of Indian troops was highly appreciated despite constraints and
soon their strength was raised to 23 in order to keep pace with wartime mobilization.
Mobile dental units were formed to provide dental cover to forces in the field and
generally one was allotted to each group of two Indian general hospitals. Their
equipment, packed in wicker and cane panniers and wooden boxes, were bulky and
heavy to carry and proved quite unsuitable in a hot and humid climate. Indian firms
failed to produce quality products; so the units remained dependent in on imported
equipments.

Personnel of the Air force and Navy also began to receive regular dental
treatment during the Second World War. One Dental officer was posted to Calcutta for
the Air Force in 1941 and when this was found inadequate, a second followed in 1948.
Secondment of Dental officers and men of the IADC to the Air Force was commenced.
Orders were issued in November 1944 for raising five dental units for the RIAF which
started functioning in April 1945, located at Kanpur, Secunderabad, Lahore (later
moved to Hakimpet), Ambala and Jalahalli (near Bangalore), but were disbanded at the
end of the war. By 1945, 84 dental units had been raised in India, 51 of them Indian and
33 British along with 29 dental laboratory units.
The first dental officer appointed for the Indian Navy was posted to Bombay in
April 1943. Prior to this, treatment had been provided by a civilian dentist. After some
makeshift arrangements, one IADC officer, and later two officers were seconded to the
navy.
When the war came to an end, many of the dental units raised for the duration of
hostilities were disbanded, but the necessity of retaining the corps as a permanent
measure was fully accepted. A register listing 31 officers desirous of continuing in the
service was drawn out of which 26 were selected for regular commission in the Indian
Army Dental Corps. In 1947, as a result of partition, some of them went to Pakistan and
the Indian personnel of all Army Dental Centres, whether for British or Indian troops,
were united to form Military Dental Centres. A new badge was designed which had a
laurel wreath surmounted by a five pointed star, crossed elephant tusks with a lotus
flower at the base and a scroll containing the words 'ARMY DENTAL CORPS'. In 1950,
Ashoka lions replaced the star and the authorized colour was changed to dull cherry. In
1953, by the order of the President of India a new name - A D Corps was sanctioned to
be effective from 26 Jan 1950. In the late fifties, the Indian Air Force established its
own dental centres and witnessed a great evolution thereafter in terms of number of
dental centres and dental treatment facilities. The First Indian Dental officer to be
posted on the staff of General Headquarters (India), in 1947, held the rank of captain, ie,
Staff Captain. As the British officers left after independence, Indian officers took over
the administrative posts, in the rank of Major, as Deputy Assistant Director Dental
Services (DADDS) at Army Headquarters and Command Dental Advisors at the
various commands.
In December 1949, the appointment of DADDS was upgraded to ADDS
(Lieutenant Colonel). A further upgradation to Deputy Director Dental Services (DDDS)
(Colonel) took place in May 1956 and, by May 1961; the post was raised to the rank of
Brigadier, with Command Dental Advisors in the rank of Colonel, while the ranks of
Command Dental Advisors in the Western Command and Air Force were upgraded to
Brigadier and Group Captain, respectively. The Director of Dental Services functioned
as the dental advisor to the DGAFMS and also to the Directors of Medical Services of
the Army, Navy and Air Force.
The dental wing at AFMC in Poona had been disbanded in May 1947 when the
Command Dental Centres were formed and they took over the professional training of
officers and other ranks. As the service expanded, more specialized facilities were
required and in 1955 the Dental Wing at AFMC was reopened with an Assistant
Professor (in the rank of Lieutenant Colonel) and one Reader. Refresher courses in Oral
Surgery and Prosthetics were added the following year, as well as courses for junior
officers and for short service regular commission (SSRC) officers in 1957. Advanced
specialists' courses of one year duration were also established for Oral and Maxillofacial
surgery and Prosthetics in 1959; for Periodontics in 1961; and for Orthodontics in 1966.
Students from Indonesia, Sudan, Afganistan and Bangladesh also attended special
courses at the dental wing of the AFMC.
Specialist dental cover was provided by the establishment of a pool of 06 officers
in 1953 which gradually rose to strength of 36 by 1980. The training and experience of
the pool of specialists proved invaluable during the hostilities against China (1962) and
Pakistan (1965), especially in the management of casualties involving the oro-facial
region. Study leave was readily granted for courses conducted in India, and a select few
dental officers received specialist training in England, Australia and Japan.
By 1980, there were five Command Dental Centres in addition to six three-chair
centres and 42 one-chair centres in the army. The Armed Forces Dental Clinic was
opened in May 1973 to provide dental care to all personnel of the Headquarters of the
three services in Delhi. This had begun as a one-chair centre in 1951 and in 1996, it was
expanded to a nine-chair centre and presently functioning as seventeen chair centre.
Almost all the field dental units had been disbanded after the war, but when hostility
broke out in Jammu and Kashmir in 1947, dental units were raised again and fitted with
wartime equipment. As more field units were required and duly raised, a Corps Dental
Unit was authorised for each Corps in 1958, capable of providing specialized treatment.
More fields units were added in 1961 and again in 1963 and the dental units in each
division were merged as companies of field ambulances (mountain) and mobile field
hospitals were established.
The top selection post was raised to the rank of Maj General in 1967. Maj Gen
Kartar Singh, PVSM was the first Additional Director General of the Dental Services. In
keeping with the organisation and responsibilities in having a set up of nearly 400
Dental officers and allied paradental personnel, the President of India approved
restructuring of the HQ of Armed Forces Dental Services into the office of Additional
Directorate General of Dental Services wef 06 Jan 1997. The post of Command Dental
Advisor, Central Command was upgraded to the rank of Major General in Aug 1999.
In the same year, a state of the art unit – Army Dental Centre( Research &
Referral ) was raised within the hospital building of Army Hospital (R & R). This unit
will be the second such center after Armed Forces Dental Clinic, New Delhi to be a
multispeciality dental centre of the A D Corps. The Army Dental Centre( Research &
Referral ) is being housed in a state-of-art building with latest equipment for specialist
services as well as research.
A red letter day dawned in the histroy of Army Dental Corps in the year 2001,
where on the 4th of December, the office of Additional Directorate General of Dental
Services was upgraded to Directorate General of Dental Services to be headed by a
Lieutenant General. Lt Gen J L Sharma, AVSM, VSM had the privilege of being the first
Lieutenant General of the Army Dental Corps of the Indian Armed Forces and was the
first Lieutenant General to head the Dental Corps of any standing Armed Forces in the
world.
Another feather in the cap of this elite corps, was the designation of the Director
General of the Dental Services as the Colonel Commandant of the Army Dental Corps
in the year 2006. Lt Gen Paramjit Singh, PVSM, AVSM, VSM**, President’s Honorary
Dental Surgeon, the Director General of Dental Services, was bestowed with the honor
of being appointed as the first Colonel Commandant of the Army Dental Corps.
 CONTENTS

SECTION – 1 ANATOMY

SL NO. CHAPTER PAGE NUMBER

1 DIFFERENT TISSUES OF THE HUMAN BODY 1
2 ORAL CAVITY 7
3 ANATOMY OF JAWS 12
4 MUSCLES OF FACIAL EXPRESSION 18
5 SURROUNDING STRUCTURES OF TEETH 22
6 DENTITION 23
7 OCCLUSION 30
8 BLOOD AND NERVE SUPPLY OF TEETH AND ADJACENT STRUCTURES 32
9 DEVELOPMENT AND GROWTH OF TEETH 39
10 TEMPORO-MANDIBULAR JOINT 47
11 MUSCLES OF MASTICATION 54
12 SALIVARY GLANDS 59
13 HISTOLOGY OF HARD AND SOFT DENTAL TISSUES 63
14 NOTATION OF TEETH 73

SECTION – 2 PHYSIOLOGY

SL NO. CHAPTER PAGE NUMBER

1 SALIVA 75
2 BLOOD 82
3 MASTICATION 86
4 DEGLUTTITION 87
PHONATION 89

SECTION -3 PATHOLOGY AND MICROBIOLOGY

SL NO. CHAPTER PAGE NUMBER

1 INFLAMMATION 90
2 DEGENERATION 95
3 NECROSIS 96
4 STAINING AND DISCOULARATION OF TEETH 99
5 ANAMOLIES OF ORAL STRUCTURES 101
6 FLUROSIS OF TEETH 107
7 WASTING DISEASES OF TEETH 108
8 ORAL MANIFESTATION OF SYSTEMIC DISEASES 111
9 BLOOD DYSCRASIAS 117
10 HIV AND AIDS 119
11 HEPATITIS 125
12 ORAL IMMUNOLOGY 128
13 ORAL CANCER 133
14 DENTAL CARIES 137
15 WHITE LESIONS OF ORAL CAVITY 140
16 BACTERIOLOGY OF ORAL CAVITY 142
17 STERILIZATION AND DISINFECTION 144
18 ANTISEPTIC AND DISINFECTANTS 150
19 WASTE DISPOSAL 151
20 INFECTION CONTROL PROTOCOL IN DENTISTRY 153
SECTION – 4 PHARMACOLOGY

SL NO. CHAPTER PAGE NUMBER

1 GENERAL ANESTHESIA 155
2 LOCAL ANESTHESIA 161
3 ANTIBIOTICS IN DENTISTRY 166
4 HAEMOSTATIC 173
5 VASODILATORS AND VASOCONSTRICTIOR 178
6 COUNTERIRRITANTS 182
7 DENTRIFICES AND MOUTHWASHES 184
8 ANALGESICS 192
9 HYPNOTICS 196
10 OBTUNDANTS AND CAUSTUCS 200
11 DISCLOSING AGENTS 205

SECTION – 5 RADIOLOGY

SL NO. CHAPTER PAGE NUMBER

1 DENTAL RADIOLOGY 206
2 HAZARDS OF RADIATION 211
3 DENTAL FILMS 212

SECTION - 6 PERIODONTOLOGY

SL NO. CHAPTER PAGE NUMBER

1 PERIODONTAL ANATOMY 218
2 CLASSIFICATION OF GINGIVAL AND PERIODONTAL DISEASES 253
3 ACUTE AND CHRONIC GINGIVITIS 256
4 GINGIVAL ENLARGEMENT 264
5 ANUG 279
6 HERPITIC GINGIVITIS AND PERICORONITIS 285
7 ROLE OF PLAQUE AND CALCULUS IN PERIODONTAL PATHOLOGY 289
8 PERIODONTAL POCKET 297
9 CHRONIC PERIODONTITIS 301
10 AGGRESSIVE PERIODONTITIS 304
11 TRAUMA FORM OCCLUSION 307
12 HALITOSIS 313
13 PERIODONTAL MEDICINE 315
14 CLINICAL DIAGNOSIS 319
15 INTRODUCTION TO DENTAL IMPLANTS 343
SECTION – 7 PERIODONTAL INSTRUMENTATION

SL NO. CHAPTER PAGE NUMBER

1 CLASSIFICATION OF INSTRUMENTS 346
2 SHARPENING OF INSTRUMENTS 363
3 SONIC AND ULTRASONIC INSTRUMENTS 369
4 GENERAL PRINCIPLES OF INSTRUMENTATION 374
5 PERIODONTAL MICROSURGERY 385

SECTION – 8 PUBLIC HEATH DENTISTRY

SL NO. CHAPTER PAGE NUMBER

1 DENTAL ASPECTS OF PUBLIC HEALTH 389
2 ROLE OF DENTAL HYGIENISTS IN DENTAL HEALTH EDUCATION 392

SECTION – 9 ORAL AND MAXILLOFACIAL SURGERY

SL NO. CHAPTER PAGE NUMBER

1 BASIC PRINCIPLES OF ORAL SURGERY 396
2 FIRST AID TREATMENT OF MAXILLOFACIAL INJURIES 397
3 FRACTURES OF MAXILLA AND MANDIBLE 400
4 PATIENT CARE AFTER EXTRACTION AND SURGERY 404
5 NUTRITION, FEEDING AND CARRIAGE OF MAXILLOFACIAL TRAUMA 407
PATIENTS
6 FACIAL SPORTS INJURIES 411
MANAGEMENT OF MEDICAL EMERGENCIES IN DENTAL SETUP 415

SECTION – 10 SPECIAL CARE

SL NO. CHAPTER PAGE NUMBER

1 SUPPORT OF PREGNANT WOMEN 419
2 ORAL CARE FOR DENTAL IMPLANT PATIENT 424
3 CARE OF DENTAL APPLIANCES 426
4 CARE FOR THE ORAL CANCER PATIENT 428
5 ORAL CARE FOR THE PATIENT WITH HIV 431
6 CARE FOR THE SCHOOL GOING CHILDERN 433
SECTION - 1

ANATOMY
 1

INTRODUCTION

The human body is made of many tissues and organs each having its own particular
function to perform. The cells are adapted to perform the special functions of the organ
or tissue they are in. Some cells e.g. nervous system and muscle are specialized. As a
general rule the highly specialized cells are least able to withstand damage and also are
the most difficult to repair or replace.

CELL

Cell is defined as the structural and functional unit of the living body.

Fig 1.1The structure of the cell

The structure of the cell contains: (Fig.1.1)

a) Cell membrane

b) Nucleus

c) Cytoplasm containing different organelles.

 2

THE ELEMENTARY TISSUES OF THE BODY

These are
1. EPITHELIAL tissue
2. MUSCULAR tissue
3. NERVOUS tissues
4. CONNECTIVE tissue.

EPITHELIAL TISSUE:
An epithelium consists of cells which cover surfaces of the body, e.g. skin, or line hollow
organs, tubes or cavities, e.g. Blood vessels and the air cells. All epithelial cells lie on
and are held together by a homogeneous substance called a BASEMENT
MEMBRANE. Types of epithelium are:

SIMPLE EPITHELIUM:
This class consists of a single layer of cells.

COMPOUND EPITHELIUM:
Consists of more than one layer of cells

FUNCTIONS OF EPITHELIAL TISSUE

1. Protective:. It prevents injury to the underlying connective tissue, prevents

the loss of fluids from these tissues and also prevents the passage of fluid into
the structures which are covered by skin. Micro-organism cannot pass
through healthy skin but they do pass through abraded skin.

2. Secretory: Secreting glands and their ducts are composed of columnar

epithelium. Very often the epithelium lining the glands and its duct is
continuous with that of the surface in which the glands lie.

GLANDS

A gland is a secretory organ which may exist as a separate organ such as the liver,
pancreas, and spleen. All glands have a rich blood supply. They take the nutrients from
the blood circulation and use it for the production of their secretions like bile, pancreatic
juice, saliva etc. The different types are

a) Paracrine glands :Glands which pour their secretion directly on to the surface
including the sweat glands, sebaceous glands and the gastric and intestinal glands.

b) Exocrine glands: Glands which pour their secretion indirectly by means of

duct to the surface include the salivary glands, pancreas and liver.
 3

c) Endocrine organs: Those are the glands of internal secretion. A great deal of
the well being of the body depends on these glands, which through their
secretions exert an important chemical control on the functions of the body.

MEMBRANE

Layers of specialized cells which line the cavities of the body are described as membrane.
All these membrane secrete a fluid to lubricate or moisten the cavity they line. The three
principal membranes are:

1. Mucous membrane
2. Synovial membrane
3. Serous membrane

1. MUCOUS MEMBRANE is found lining the elementary tract, the respiratory

tract, and parts of the genito-urinary tract. Some of them become distended with
mucous secretion and are then called GOBLET CELLS. The cells become more
and more distended and finally ruptures and discharges its secretion on to the
surface. MUCUS is the secretion of the membrane and consists of water, salts
and protein, mucin, which gives the sticky or viscoid character to the secretion.

2. SEROUS MEMBRANES are found in the chest and abdomen, covering the
organs contained therein and lining these cavities.

The PLEURA covers the lungs and lines the thorax

The PERICARDIUM covers the heart as a double layer
The PERITONIUM covers the abdominal organs and lines the abdomen.

The characteristics which are common to all three serous membranes are that each
consists of a double layer of membrane having an intervening potential cavity which
receives the fluid secreted by the membrane. This SEROUS FLUID is very similar to
blood serum or lymph. It acts as a lubricant, and in addition it contains protective
substances and removes harmful products, passing these on to the lymphatic system.

3. SYNOVIAL MEMBRANE lines the synovial joint cavities. The commonest

examples are the synovial joints of long bones, TMJ etc. Its secretion is known as
synovial fluid which gives a protective action on the articulating surfaces of the
bone.

MUSCULAR TISSUE:

Muscle is a tissue which is specialized for contraction, and by means of this, movements
are performed. It is composed of cylindrical fibers which correspond to the cells of other
tissues.
 4

There are three types of muscle.

1. STRIPED (striated, skeletal or voluntary muscle). The individual muscle fibres

are transversely striated by alternate light and dark markings. Each fibre is
enclosed in a fine membrane – the SACROLEMMA. (muscle sheath). A number
of fibres are massed together by connective tissue to form large and small
muscles. When a muscle contracts it shortens, and each individual fibre takes part
in the movement by contracting. This type of muscle only contracts when
stimulated to do so by the nervous system.

2. UNSTRIPED (Unstriated, smooth or involuntary muscle). This type will

contract without nervous stimulation although in most parts of the body its
activity is under the control of the autonomic (involuntary) nervous system. With
the exception of cardiac muscle this variety is composed of elongated spindle-
shaped muscle cells which retain the appearance of a cell.

Involuntary muscle is found in the wall of blood and lymphatic vessels, in the walls of
the digestive tract and the hollow viscera, trachea, and bronchi, the iris, ciliary muscle of
the eye and in the involuntary muscles in the skin.
A SPHINCTER MUSCLE is composed of a circular band of muscle fibres situated at
the internal or external openings of a canal or at the mouth of an orifice, tightly closing it
when contracted. Examples include the cardiac and pyloric sphincters at the openings of
the stomach, the internal and external sphincters of the anus and urethra.

3. CARDIAC MUSCLE possesses the special property of automatic rhythmical

contraction independent of its nerve supply. This function is described as
MYOGENIC as distinct from neurogenic. Normally the action of the heart is
controlled by its nerve supply. This is found only in the muscle of the heart.

NERVOUS TISSUE:
The nervous tissue consists of three kinds of matter
(a) GREY matter forming the nerve cells
(b) WHITE matter, the nerve fibres
(c) NEUROLOGICAL, a special kind of supporting cell found only in the nervous
system, which holds together and supports nerve cells (fig.1.2)and fibres.

Fig 1.2 Structure of neuron

 5

CONNECTIVE TISSUE:

Connective tissue provides the frame-work of the body.

There are several varieties of connective tissue.

AREOLAR TISSUE: These consist of loosely woven tissue which is distributed widely
through out the body. It is placed immediately beneath the skin and mucous surfaces
forming the subcutaneous and sub mucous tissue, and it also forms the sheaths of fascia
which support, bind and connect together muscles, nerves, blood vessels and other
organs.

RATIFORM: (reticular) lymphoid or adenoid tissue is similar to areolar, but a particular

kind of cell, the lymphocyte, is present in very large numbers and forms the bulk of the
tissue. The lymphocytes are held together by fine connective tissue fibres called reticular
fibres. These are like immature collagen fibres.

MUCOID TISSUE: is found in the umbilical cord, at birth in the jelly of Wharton. It is
also found in the adult in the vitreous humour of the eye.

ADIPOSE TISSUE: Adipose or fatty tissue is deposited in most parts of the body. It is
associated with areolar tissue by the deposition of fat cells and is present in all
subcutaneous tissue except that of the eyelids and inside the cranial cavity.

ELASTIC TISSUE: This form of connective tissue contains a large proportion of elastic
fibres. It is found in the walls of arteries and in the air tubes of the respiratory tract and
assists in keeping these vessels and passages open.

FIBROUS TISSUE: is often spoken of as a white fibrous tissue because it is composed

mainly of white collagen fibres arranged in definite lines. This arrangement gives great
strength and fibrous tissue is found where resistance is required. Fibrous tissue is tough
and strong. It forms ligaments except the elastic ones and tendons. The dura mater lining
the skull and neural canal, periosteum covering bone, the strongest layers of fascia
separating muscular sheath, periodontal ligament holding the tooth are examples of
fibrous tissue.

CARTILAGE or gristle is a dense, clear blue-white substance, very firm but less firm
than bone. It is found principally at joints and between bones. The bones of the embryo
are first cartilage, then the growing centers persist as cartilage and when adult age is
reached cartilage is found covering the bone ends. Cartilage does not contain blood
vessels but is covered by a membrane, the PERICHONDRIUM, from which it derives its
blood supply.
 6

THE STRUCTURE OF BONE.

Bone forms one of the hardest connective tissues of the body.Composition:

Water - 50%

Solids :

Calcium salts - 67%

Cellular elements - 33%

Types :

COMPACT BONE TISSUE is hard and dense, it is found in flat bones and in the
shafts of the long bones, and as a thin covering over all bones.

CANCELLOUS BONE is spongy in structure. It is found principally in the ends of the

long bones, in the short bones, and as a layer in between two layers of compact tissue in
the flat bones.

PERIOSTEUM. Periosteum is a fibrous membrane covering bone. It is rich in blood

vessels, and invests the bone closely, the blood vessels from the periosteum supply in the
bone substance, and in this way help to supply the bone with blood.

ENDOSTEUM: Cavities in the spongy bone lined with delicate membrane of fibrous
tissue. In a long bone the medullary cavity is lined by endosteum which is connected
with periosteum by a fibrous lining of Tunnels.

FUNCTIONS OF BONES

1. To support soft tissues surrounding them

2. To form protective cage for viscera chest, skull, backbone
3. For attachment of muscles
4. To store, R.B.C. in Bone marrow & calcium salts.
 7

ORAL CAVITY
The entrance of the Digestive System is mouth or oral cavity. It is divided into:

Fig. 1.3: Sagittal section through the mouth

a) The vestibule which is the outer and smaller portion. It is bounded externally
by the lips and cheeks and internally by the teeth and gums.

b) The oral cavity proper which is the inner larger part (fig.1.3).

ORAL VESTIBULE

It is a cleft like space except when inflated with air. The parotid ducts and the ducts of
the mucous glands of the lips and cheeks open into it. Boundaries:
Superiorly & inferiorly – It is bound by the reflection of the mucous membrane from
the lips and cheeks or to maxillae and mandible.
Anteriorly – It opens on the face by means of the oral fissure.
Posteriorly – It communicates on each side, with the cavity of the mouth proper through
the interval between the last molar tooth and the ramus of the mandible. Through this
opening fluids may be introduced into the mouth proper

LIPS
There are four layers in each lip (1) Cutaneous (2) Muscular (3) Sub Mucous (4)
Mucous. The skin and mucous membrane is reflected from the lip on the jaw and is
raised in the median line in the form of a fold called labial frenum.The muscular layer–
constitutes the chief bulk of the lips. It is formed by the orbicularis oris and the various
muscles which converge upon the oral fissure.The sub mucous layer consists of areolar
layer and it contains numerous mucous labial glands and binds to the muscular layer.
 8

CHEEKS
There are six layers in the cheek (1) skin (2) a fatty layer which is transversed by
some of the muscles of the facial expression and by the facial artery and anterior facial
vein (3) the bucco- pharyngeal fascia (4) Buccinator muscle (5) Sub mucous areolar
tissue, in which the numerous buccal glands similar in character to the labial glands (6)
The mucous membrane. Four to five mucous glands of larger size termed the molar
glands occupy a more superficial position. The buccal pad of fat lies in the deepest part
of the fatty layer. The Parotid duct pierces the pad and the minor four layers of the cheek
and opens into the vestibule of the mouth opposite the upper second molar tooth.

GUMS AND TEETH

Gum/gingiva is composed of dense fibrous tissue covered with a smooth vascular mucous
membrane which is attached to the alveolar margin of the jaws and the necks of the teeth.

CAVITY PROPER OF THE MOUTH

The mouth proper is bounded in front and at the sides by the gums and teeth.
Posteriorly, it communicates with pharynx by means of the isthmus of the fauces. The
floor is formed by the tongue and by the mucous membrane which connects the tongue
with the inner surface of the mandible.The roof is vaulted and is formed by the hard and
soft palate. It is into the mouth proper that the sub-mandibular ducts and ducts of the
sublingual glands open.

FLOOR OF THE MOUTH

The mucous membrane is reflected from the inner side of the mandible to the side of the
tongue, but in the anterior part of the mouth the tongue lies more or less free in the oral
cavity and there, the mucous membrane stretches across the floor from one half of the
mandible to the other. Further, if the tongue is pulled upward, a median fold of mucous
membrane will be seen which connect its under surface to the floor.t is the lingual frenum.
At the side of the frenum the submandibular duct opens on the summit of the sublingual
papilla. The papilla is close to the frenum, on the anterior end of the sublingual fold.
The sublingual ducts open by minute apertures on the summit of the fold.

ROOF OF THE MOUTH

The hard and soft palates form the continuous concave vault roof of the mouth. The post
margin of the soft palate is free. The uvula hangs down from its middle and rests on the
dorsum of the tongue. A slight medium raphe runs from the uvula and ends anteriorly,
below the incisive fossa in a slight elevation termed the incisive papilla (papilla palatine).
In the anterior part of the hard palate the mucous membrane on each side of the raphe, is
thrown into three or four hard transverse corrugation or ridges called the Rugae. By
carefully palpating the post-lateral angle of the hard palate one can feel the pterygoid
hamulus.
 9

TONGUE
It is a muscular organ situated in the floor of the mouth. It is associated with the
functions of

1. Taste
2. Speech
3. Mastication
4. Deglutition
5. Cleansing

It has an oral part that lies in the mouth, and a pharyngeal part that lies in the pharynx.
The oral and pharyngeal parts are separated by a V-shaped sulcus, the sulcus terminalis.

The underside of the tongue (fig.1.6) is connected with the floor of the mouth by a
sickle shaped fold called lingual frenum. The dorsal surface (fig.1.5) is divided into an
anterior horizontal and a posterior vertical part. The first part is in contact with the palate
and the second faces the pharynx. The first is designated as palatine surface and the
second as pharyngeal surface of the tongue. The palatine surface is situated in front of
the terminal sulcus and carries lingual papillae (fili form and fungi form. Filiform
papillae are densely arranged and irregularly between the fungi form papillae).
Immediately in front of the terminal sulcus are the circumvallate papillae arranged in a
“V” shaped line with the largest papillae near or in the midline and decreasing in size
laterally and anteriorly. They are mushroom shaped structures surrounded by a deeply
cut circular trough or furrow. The wall of these troughs contains taste buds. Taste buds
are also seen on the slope of fungi form papillae. The posterior part of the lateral border
of the tongue contains the foliate papillae. They are sharp low folds. They are also the
site of the numerous taste buds.

Fig. 1.5: The dorsum of the tongue

 10

The muscles of the tongue consist of extrinsic and intrinsic muscles. The
extrinsic muscles originate from the skeleton and spread into the body of the tongue. The
later are confined to the tongue itself.

The extrinsic muscles are:-

1) Styloglossus
2) Hyoglossus
3) Genioglossus
4) Palatoglossus

STYLOGLOSUS MUSCLE – arises from the anterior surface of the styloid process,
some time with a few bundles from the stylomandibular ligament. They enter the tongue
at about the base of the palatoglossal arch.
Nerve supply is by the hypoglossal nerve
Action – Retraction of the tongue

HYOGLOSSUS MUSCLE – originates from the upper border of the greater horn of the
hyoid bone and adjacent part of the body.

Nerve supply is by hypoglossal nerve

Action is Protraction of the tongue.

GENIOGLOSSUS MUSCLE – arises from the mental tubercle or spine on the inner
surface of the chin. Nerve supply is by hypoglossal nerve
Action is Protraction

Fig. 1.6: The muscles of the tongue

 11

Intrinsic muscles are divided into longitudinal, transversal and vertical muscles.
The longitudinal muscles are divided into an upper and lower group. They are situated
close to the upper and lower borders of the styloglosus muscle. The transverse group
arises from the lingual septum. The vertical group may exist close to the lateral borders
of the body of the tongue where they stretch between the upper and lower surfaces. The
action of the intrinsic muscles is to change the shape of the tongue. Their function
combined with that of the extrinsic muscles is responsible for the great mobility
which is the versatility of the tongue.
 12

ANATOMY OF JAWS
Introduction
The human body has two jaws an upper and a lower jaw. They are called Maxilla
and Mandible respectively. The jaws form the oral cavity which is at the entrance of the
digestive canal. The masticating mechanism is formed by the teeth of upper and lower
jaws, TMJ, the muscles of mastication and the muscles of cheeks, lips and tongue.

MAXILLA

It contributes a large share in the formation of middle third of the facial skeleton.
Maxilla is a spongy bone which is well adapted to sustain, the stresses of mastication. It
is two in numbers. It consists of a central Pyramidal body which is hollowed by
maxillary sinus.
The anterior surface of the body of Maxilla presents (a) Nasal notch medially,(b)
anterior nasal spine, (c) Infra orbital foramen, 1 cm below the infra orbital margin
transmitting infra orbital nerve and vessels, (d) incisive fossa above the incisor teeth, and
(e) Canine fossa lateral to the canine eminence.

Fig 1.7 Maxillary bone

In addition to this, four processes of Maxilla are also seen.

1. Frontal process: Is directed upwards and articulates anteriorly with nasal bone,
posteriorly with lacrimal bone.
2. Zygomatic process: This process of maxilla is short but stout and articulates with
the Zygomatic bone.
3. Palatine process: This is a horizontal plate at the junction between the body and
the alveolar process. Posteriorly the Palatine process unites with the horizontal
plate of palatine bone. The posterior part of hard plate is continuous with soft
plate.
4. Alveolar process: This process of maxilla bears sockets for the upper teeth. The
posterior end of the alveolar process is the maxillary tuberosity. The existence of
alveolar bone depends upon the presence of teeth.
 13

The superior surface of maxilla forms floor of the bony socket of orbit and medial
surface of the body forms the lateral boundary of the nasal cavity.

Attachments:

a) Orbital part of orbicularis oculi

b) Medial palpebral ligament

c) Levator Labii superioris alaeque nasi

d) Levator labii superioris

e) Levator anguli Oris.

f) Nasalis and Depressor Septi.

g) Incisive muscle arises

Nerve and blood supply Infra Orbital, Greater palatine the incisive br of
trigeminal nerve, while the blood supply is from branches of maxillary artery.

MANDIBLE

It is the largest and strongest bone of the face. It has got two major parts.

1) Body: Containing alveolar process holding teeth.

2) Ramus: Containing condylar process and coronoid process.

Body:
The horizontal “U” shaped body has a dense basilar portion that contains the
neuro vascular bundle and provides for muscle attachments. The body has two
surfaces and two borders.

1. Outer surfaces (fig.1.8)

It presents symphysis menti, a median part, ridge in the upper part indicating the
linear fusion of the two halves. Mental protuberances or chin is a median triangular
projection in the lower part with mental tubercles at the inferolateral angles. Mental
foramen lies below the interval between the premolar teeth. It transmits mental nerve and
vessel which are directed backwards and upwards.
 14

An oblique line is the continuation of the sharp anterior border of the ramus of the
mandible which is directed downwards and forward towards the mental tubercle. It gives
origin to buccinator muscle as far forwards as the anterior of the first molar tooth. In
front of this depressor labi inferioris and depressor anguli oris arise from the line below
the mental foramen. Incisive fossa between the two incisor teeth gives origin to mentalis
and mental slips of orbicularis oris muscle. Above the line of the muscle origin the
surface is covered by mucous membrane of the vestibule.

Fig. 1.8: inner surface of the mandible

II. Inner surface (fig.1.9)

It presents mylohyoid line, a prominent oblique ridge, running obliquely down
wards below the third molar tooth to the median area below the Genial tubercle. It gives
origin to mylohyoid muscle, superior constriction muscle of the pharynx from above the
posterior end of mylohyoid line. Lingual nerve is related directly to the above two
muscle. Pterygomandibular raphe is attached immediately behind the third molar. Below
the mylohyoid line the surface is slightly hallowed out to form the submandibular fossa,
which lodges submandibular salivary glands. Above the mylohyoid line anteriorly, there
is sublingual fossa which lodges sublingual salivary glands. The posterior surface of
symphysis menti, above the mylohyoid line is marked by genital tubercle. The upper
genial tubercle gives origin to Genioglossus and the lower genial tubercle to geniohyoid.
The mylohyoid groove of the ramus extends to the body below the posterior end of
mylohyoid line. Digastric fossa is an oval depression which is situated bilaterally near
the midline below the mylohyoid line, which gives origin to the digastric muscle. To the
whole length of the lower border the investing layer of deep cervical fascia is attached,
but it is interrupted at the anterior border of masseter by the facial vessels and mandibular
branch of facial nerve. Still superficially near the outer surface, platysma is inserted into
the lower border.
 15

Fig. 1.9:outer surface of the mandible

B) Alveolar process

It forms the upper border of the body of the mandible. It bears 16 sockets for
permanent teeth. Periodontal membrane is attached to the cavity of the socket. After loss
of a tooth during life the alveolar bone atrophies and bottom of the socket, fills up with
new bone. Presence of deep socket in the macerated bone indicates loss of a tooth after
death.

Ramus
It is quadrilateral in shape and has two surfaces and four borders.

I. Two surfaces: Lateral surface and Medial surface

Lateral surface: It is flat and obliquely ridged. Whole of this surface except the
posterosuperior part, where it is covered by parotid glands, provides insertion to masseter
muscle.

Medial surface: It presents mandibular foramen a little above its center at the level of
occlusal surface of teeth. It leads to mandibular canal and admits the inferior alveolar
nerve and vessels. Mandibular canal open out at the mental foramen. A sharp projection
is situated at the anterior margin of the mandibular canal. It provides attachment of
spheno-mandibular ligament. The mylohyoid groove begins from the lower part of
mandibular foramen, runs downwards and forwards and gradually lost in the
submandibular fossa. The groove lodges mylohyoid nerve and vessels. Medial pterygoid
muscle is inserted on the roughened area below and behind the mylohyoid groove. The
area above and behind the mandibular foramen is related to inferior alveolar nerve and
vessels, maxillary artery and lateral pterygoid muscle.
 16

II. Four borders

- Upper
- Lower
- Anterior
- Posterior
-
Upper border of the ramus is thin and curved to form the mandibular notch which is
crossed by masseteric nerve and vessels. Lower border is backward continuation of the
base of mandible; it ends behind at the angle of the mandible. Anterior border is thin.
This border and adjoining medial surface provide insertion to the lower fibres of
temporalis muscle and tendon. Posterior border is thick; it is related to parotid gland.

D) Condylar and coronoid processes

Condylar process is a strong upward projection from the posterosuperior part of

the ramus itself. The upper end is expanded from side to side to form the head. It is
covered by fibro cartilage and articulates with temporal bone to form the TM Joint. The
constriction below the head is the neck
Coronoid process is a flattened triangular upwards projection from the antero
superior part of the ramus. Its anterior border is continuous with the anterior border of
ramus, and the posterior border bounds the mandibular notch. The lateral surface is
covered by masseter. The medial surface, upper and anterior margins provide insertion to
temporalis.

Blood supply
The external aspect of the mandible is supplied by three main arteries. Inferiorly,
the facial artery provides sublingual and sub mental branches. The lingual artery
provides medial branches and the ramus region is supplied by the masseteric and
mylohyoid branches of the maxillary artery. The inner aspect of the mandible is supplied
mostly by the inferior alveolar branch of the maxillary artery.

Ossification
Mandible is the second bone (next to clavicle) to ossify in the body. Its great part is
ossified in membrane. The parts ossifying in cartilage include the incisive part below the
incisor teeth, coronoid and condylar processes and upper half of the ramus above the
level of mandibular foramen.
 17

AGE CHANGES IN THE MANDIBLE

A) In infants and children:

The two small halves of the mandible fuse during the first year of life. The
mental foramen, at birth, opens below the sockets for the two deciduous molar teeth near
the lower border because the bone is made up of only the alveolar part with teeth sockets.
Mandibular canal runs near the lower border. The foramen and canal gradually shift
upwards. The angle is obtuse (140 degree or more) because the head is in line with the
body. The coronoid process is large and angle projects upwards above the level of the
condyle (fig.1.10).

B) In adults

The mental foramen opens midway and angle reduces to 110 degrees because the ramus
becomes almost vertical

Child

Adult

Old

Fig. 1.10 : – Age changes in mandible

C) In old age

Teeth fall out and alveolar bone is resorbed. The height of the body is reduced. The
mental foramen and mandibular canal are close to alveolar ridge. The angle becomes
again obtuse (140 degree) because ramus is oblique. Coronoid process is at higher level
than condylar process.
 18

MUSCLES OF FACIAL EXPRESSION

Facial muscles, or the muscles of facial expression, made up of thin and pale
fibres. They work under a fine control to bring about different facial expressions.
Embryologically, they develop from mesoderm of the second brachial arch, and are
therefore supplied by the facial nerve.

All of them are inserted into the skin (fig.1.11).The muscles are grouped in the following
six heads:

A. Muscle of scalp
Occipitofrontalis

B.. Muscles of auricle (around the ear)

Auricularis anterior
Auricularis superior
Auricularis posterior

C. Muscles of eyelids (around the eye)

Orbicularis oculi
Corrugators supercilli
Levator palpebrae superioris(an extraocular muscle, supplied by 3rd cranial)

D. Muscles of nose
Procerus
Compressor naris
Dilator naris
Depressor septi

E. Muscles around the mouth

Orbicularis oris
Levator labii superiors alaequae nasi
Levator labii superiors
Levator anguli oris
Zygomaticus minor
Zygomaticus major
Depressor anguli oris
Depressor labill inferioris
Mentalis
Risorius
Buccinator

F. Muscle of the neck

Platysma
 19

Functionally, most of these muscles may be regarded primarily as regulators of the three
openings situated on the face, namely the palpebral fissures of the eyes, the nostrils of the
nose, and the oral fissure or mouth. Each opening has a single, though composite,
sphincter, and a variable number of the dilators. Sphincters are naturally circular and the
dilators radial in their arrangement. The muscles are better developed around the eyes
and mouth than around the nose.

TABLE 2: FUNCTIONAL GROUPS OF FACIAL MUSCLES

Opening Sphincter Dilators

A. Palpebral fissure Orbicularis oculi 1.Levator palpebrae superioris
2.Occipitofrontalis (frontalis)
B. Oral fissure Orbicularis oris All the muscles around the mouth, except
for the Orb. Oris (sphincter), and the
Mentalis (does not mingle with Orb.
Oris)
C. Nostrils Compressor naris 1.Dilator naris
2.Depressor septi
3.Medial slip of Lev. Lab. Sup. Al. nasi

Fig. 1.11:-Facial muscles

 20

Biologically, the primary function of the facial muscles is to regulate the facial openings,
and the various facial expressions are secondary effects of their contraction.

A few of the common facial expressions and the muscles producing them are given
below:

1. Smiling the laughing : Zygomaticus major

2. Sadness : Levator tabii superioris and Levator anguli oris
3. Grief : Depressor anguli oris
4. Anger : Dilator naris and Depressor septii
5. Frowning : Corrugators supercilli and Procerus
6. Horror, terror and fright : Platysma
7. Surprise : Frontalis
8. Doubt : Mentalis
9. Grinning : Risorius
10. Contempt : Zygomaticus minor

THE RELEVANT FACIAL MUSCLES

Muscle Origin Insertion Action

1. Corrugator Medical end of Skin of mideyebrow Vertical wrinkling
supercilii superciliary arch of forehead :
frowning
2.Orbicularis Medial part of medial Concentric rings Closes lids tightly:
Oculi papebral ligament and return to the point Winking;protects
a)Orbital part, on adjoining bone of origin. eye from bright
and around the Lateral part of medial Lateral palpebral light
orbital margin papebral lig. raphe Closes lids gently,
b)Palpebral part, Lacrimal facia and Upper and lower blinking.
in the lids lacrimal bone tarsi Dilates lacrimal sac
c)Lacrimal part, directs lac, supports
lateral and deep lower lid.
to lacrimal sec
3.Orbicularis Oris Superior incisivus, Fibromuscular Closes and purses
a.Intrinsic part, from maxilla, inferior modiolus at the the mouth;
deepest stratum, incisivus, from angle of mouth numerous extrinsic
very thin sheet mandible. Lips and the muscles make it
b. Extrinsic part, Thickest middle modiolus most versatile for
two strata, stratum, derived from various types of
formed by Buccinator, thick grimaces
converging superficial stratum,
muscles derived from elevators
and depressors of lips
and angles
 21

4. Buccinator, the 1.Upper fibres, from 1.Upper fibres, Flattens cheek

muscle of cheek maxilla, opposite straight to upper lip; against gums and
molar teeth. 2.Lower fibres, teeth; prevents
2.Lower fibres, from straight to lower lip; accumulation of
mandible, opposite 3. Middle fibres food in the
molar teeth; decussate before vestibule.
3.Middle fibres, from passing to the lips.
pterygomandibular Blowing action
raphe.
5. Platysma Upper parts of Anterior fibres, to Releases pressure of
pectoral and deltoid the base of skin on the
faciae. Fibres run mandible; posterior subjacent veins;
upwards and medially. fibres, to the skin of depresses mandible;
lower face and lip, pulls the angle of
and may be mouth down wards
continuous with as in horror or
risorius. surprise

Applied Anatomy

In the infranuclear lesions of the facial nerve, for example the Bell’s palsy, the
whole of the face is paralysed. Face becomes asymmetrical and is drawn up to the
normal side. The affected side is motionless; wrinkles disappear from the forehead; eye
cannot be closed; any attempt on smiling causes drawing of the mouth to the normal side;
during mastication, food accumulates in the cheek; and articulation of the labials is
impaired.
In the supranuclear lesions of the facial nerve (usually a part of hemiplegia), only lower
part of the face is paralysed, and the upper part (Frontalis and part of Orbicularis Oculi)
escapes due to its bilateral representation in the cerebral cortex.
 22

SURROUNDING STRUCTURES OF TEETH

The surrounding structures of teeth are:

1. GINGIVA
2. PERIODONTAL LIGAMENT
3. ALVEOLAR PROCESS
4. CEMENTUM

Fig. 1.15:surrounding structure of tooth

GINGIVA

The gingival is the part of the oral mucosa that covers the alveolar processes of the jaws
and surrounds the neck of the teeth.

PERIODONTAL LIGAMENT

It is the connective tissue that surrounds the root and connects it with the bone.

ALVEOLAR PROCESS

The alveolar process is the portion of the maxilla and mandible that forms and supports
the tooth sockets. The alveolar process consists of:

CEMENTUM:
This Ccovers the Anatomic Root of the tooth
 23

DENTITION
Man has two generation of teeth (Dyphyodont), the deciduous and the permanent
dentitions. A tooth in man consists of three hard tissues, the enamel, dentin and
cementum, surrounding a soft tissue – the pulp. The dentin forms the bulk of the tooth
but it is not exposed outside. A part of the tooth is covered by enamel and the rest is
covered by cementum. The part covered by enamel is called crown and the part covered
by cementum is called root. The line of junction between enamel and cementum is called
the Cemento-enamel junction of the cervical line. The part of the root immediately
adjacent to the crown is called the neck of the tooth. The pulp cavity in the crown area is
called the pulp chamber and in the root portion it is known as root canal. There are 20
teeth in the complete deciduous dentition; ten in each jaw and in complete permanent
dentition, there are 32 teeth, sixteen in each jaw.

The numbering of teeth is done according to the quadrant they are present in.

1= Upper right quadrant

2=Upper left quadrant
3=Lower left quadrant Permanent dentition
4=Lower right quadrant

5=Upper right quadrant

6=Upper left quadrant
7=Lower left quadrant Deciduous dentition
8=Lower right quadrant

According to this system, the upper right second permanent molar is symbolized as 17.

TERMINOLOGY

LABIAL SURFACE – Is the outer surface of the anterior teeth which faces forwards
towards the lips.

BUCCAL SURFACE – surface of posterior teeth facing the cheeks (Buccinator

muscles)

LINGUAL SURFACE - The inner surface of all the teeth in the lower jaw face the
tongue and are called lingual surfaces. The corresponding surface of the upper teeth are
called palatal surface.

PROXIMAL SURFACES – Vertical surface of two adjacent teeth is called incisal edge.

OCCLUSAL SURFACE – The chewing surface of the premolars and molars.

LINE ANGLE – is formed by the junction of two surfaces e.g. mesiolabial line angle of
anterior teeth.
 24

POINT ANGLE – is formed by the junction of three surfaces e.g. mesiolabioincisal

point angle of anterior teeth

CUSP – It is a pronounced elevation on the occlusal surface of posterior teeth

TUBERCLE – is a small elevation on the crown which may not be typical.

RIDGE – is any linear elevation on the surface of the tooth.

CINGULUM – is a bulbous convexity near the cervical region of a tooth.

MARGINAL RIDGE – are ridges at the mesial and distal edges of the occlusal surfaces
of posterior teeth.

FISSURE – It is along cleft between cusps or ridges

A FOSSA – is a rounded depression

AXIAL WALL – is any wall of the pulp chamber which is parallel to the long axis of the
tooth.

HUMAN DENTITION : (PRIMARY & PERMANENT)

Two different sets of teeth erupt during the course of a human’s life i.e.

1) Primary dentition and

2) The secondary or permanent dentition

The Primary teeth:

This is the first set of teeth in the human beings, which must function until these
teeth are replaced by secondary teeth or permanent teeth. Other names are milk teeth,
temporary teeth or deciduous teeth because they are shed and replaced by other teeth later
in life. These teeth start eruption between 6 to 8 months of life and are shed by 11 to 12
years when they are replaced by permanent teeth. They are 20 in number.
Incisors – 8, Canines – 4 and molars – 8

Central incisors eruption 7 months, shedding 6-7 years

Lateral incisors eruption 8 months, shedding 7-8 years
Canines eruption 17 months, shedding 10-12 years
1st molars eruption 14 months, shedding 10-12 years
II molars eruption 21 months, shedding 10-12 years
 25

The secondary teeth or permanent teeth

They begin to erupt at the 6 years and they are meant to function throughout the
individual’s life. These teeth have no successors except these provided as substitutes
artificially. They are 32 in number.

Incisors – 8, Canines – 4, Premolars – 8 and Molars – 12

Eruption timing Central incisors – 8yrs

Lateral incisors – 7-9 yrs
Canine - 10-12yrs
I Premolars – 10 to 12 yrs
II Premolars – 10-12 yrs
I Molars – 6yrs
II Molars – 12yrs
III Molars – 17-21 yrs

Functions of teeth:

General functions of teeth are

(1) Mastication
(2) Aesthetics
(3) Phonetics

Incisors: derived from Latin word incidere which means to cut into. they are used for
shearing of food and these are forced between the posterior teeth by tongue and cheek
muscles.

Canines or cuspid: The word cusp refers to the spear shaped crown of these teeth. They
are much thicker because of a strong ridge of enamel on the labial and on the lingual
surfaces. This ridge of enamel extends from the tip of the cusp to the cervical line or
neck of tooth and therefore makes it a strong tooth. It has also good support in the bone
because it has the longest root. It is a corner tooth at the angle of the mouth which helps
it to tear the food e.g. carnivorous animals to tear the flesh of their prey and man tears
sugarcane.

Bicuspids or Premolars : Bi – two cuspids Pre-preceding the molars

They pulverize the food which has been cut into pieces by incisors and canines.

Molars – Derived from Latin – MolarisThey are the largest teeth in the mouth because of
the size of their crown and because of well developed 2 or 3 roots. Upper molars have 3
roots and lower 2 roots. The last molars are the smallest, and least functional.

Maxillary incisors are larger than mandibular teeth. The lateral incisors are more
rounded and smaller than the central incisors, which are stronger than their distal
neighbors. Lower lateral is a slightly larger than the lower central incisor.
 26

The cuspids – Maxillary canine is longest tooth in both the arches. It is bigger than
mandibular canine. The cingulum or maxillary cuspid is more prominent.

Upper 1st premolar has two roots – other all premolars have one root. Lower 1st premolar
is smallest of all permanent teeth. IInd premolars are more developed for grinding of
food. Maxillary 1st molar is largest of all the molars and has 3 well developed roots and
is most useful teeth. 3rd molars are smallest and are called wisdom teeth.

Occlusion

The biting surface of the teeth is called occlusal surfaces of teeth. Occlusion of the teeth
means functional relationship of upper and lower teeth when the jaws are closed and teeth
meet in contact with each other. Every tooth has two antagonists with the exception of
lower central incisors and upper 3rd molars. The study of surface anatomy of the teeth is
important in rendering any treatment of the teeth such as dental prophylaxis and dental
restoration. The form of the teeth is inter-relation to the functions that they are required
to perform. The crown of an incisor tooth has an incisal edge and crowns of canines,
premolars and molars have cusps. These incisal edges and cusps form the cutting
surfaces of tooth crowns.

Maintenance of tooth position

The factors which keep the teeth in position are:

i) Occlusal contact –2 antagonists except lower central incisor upper 3rd molar
ii) Intercuspal relation – interlocking of cusps – prevent drifting
iii) Muscles of face & tongue – Keep the teeth in natural zone
iv) Mesial & distal contacts – prevent their movement mesially & distally and protect
gingiva and bone.

Teeth are sustained by their own functional anatomy. Form and function go hand
in hand. They help to sustain themselves in the dental arch by assisting in the
development and protection of the tissues that support them. The following anatomic
features help in this.

1) Contours or curves of surfaces of teeth protect food impaction on gums.

2) Contact and embrasure form provide spillways for dispersion of food during
mastication. Normal contact and embrasure form is required for health of tissues.
3) Occlusal form. Mesial & distal edges have elevations of enamel called the marginal
ridges. These ridges convey the food in the proper direction.

Occlusal wear gradually decreases crown length of the teeth with edge, and teeth
tend to erupt more in the oral cavity to compensate for this loss. They become wider and
its results in overloading of the supporting structures.
 27

RESORPTON OF TEETH

Resorption of the roots of the teeth is of two types:

1) External resorption
2) internal resorption

External resorption:

1. Physiological resorption occurs in deciduous teeth; there is a gradual resorption of

their roots resulting in loss of attachment of their periodontal ligament. The
developing permanent successor tooth creates sufficient pressure by its increase in
size to produce resorption of the primary tooth root and of the bone surrounding
the root. As the root resorbs, the tooth loosens. Eventually all periodontal
ligament attachment is lost and the rootless crown of the primary tooth literally
falls off from the jaw and the process is called shedding of teeth.

If the permanent tooth does not cause pressure on the primary tooth root, the
resorption process may be delayed and continue to function for many year but quite a few
times the primary teeth are lost.

b) Other causes of external resorption are:

1. Low grade periapical chronic inflammation
2. Pressure from cysts and tumors and impacted teeth
3. Orthodontic treatment excessive pressure
4. Traumatic occlusion (excessive pressure of occlusal forces)
5. Replantation or transplantation of teeth
6. Resorption from unknown causes

Internal resorption

Idiopathic resorption – Mouth is the gate way of the body and the teeth are the sentinels
to protect it. The periodical visits are required to ensure the oral health. It can be
arranged by either carrying out periodical dental inspections by carrying out periodical
recalls for dental treatment.
 28

AVERAGE DATES OF MINERALIZATION AND ERUPTION OF THE HUMAN

DENTITION

TOOTH MINERALISATION AMOUNT ENAMEL ROOT ERUPTION

OF COMPLETED COMPLETED
ENAMEL
FORMED
AT
BIRTH
DECIDUOUS DENTITION
Upper
First 4 mths in utero Five-sixths 1 ½ mths 1 ½ yrs 7 ½ mths
molar

Second 4 ½ mths in utero Two thirds 2 ½ mths 2 yrs 9 mths

incisor

Canine 5 mths in utero One third 9 mths 3 ¼ yrs 18 mths

First 5 mths in utero Cusps united 6 mths 2 ½ yrs 14 mths

molar

Second 6 mths in utero Cusp tips still 11 mths 3 yrs 24 mths

molar isolated

Lower
First 4 ½ mths in utero Three fifths 2 ½ mths 1 ½ yrs 6 mths
incisor

Second 4 ½ mths in utero Three fifths 3 mths 1 ¾ yrs 7 mths

incisor

Canine 5 mths in utero One third 9 mths 3 ¼ yrs 16 mths

First 5 mths in utero Cusps united 5 ½ mths 2 ¼ yrs 12 mths

molar

Second 6 mths in utero Cusp tips still 10 mths 3 yrs 20 mths

molar isolated
 29

PERMANENT DENTITION

Upper
First incisor 3-4 mths - 4-5 yrs 10 yrs 78 yrs
Second incisor 10-12 mths - 4-5 yrs 11 yrs 8-9 yrs
Canine 4-5 mths - 6-7 yrs 13-15 yrs 11-12 yrs
First premolar 1 ½ -1 ¾ yrs - 5-6 yrs 12-13 yrs 10-11 yrs
Second 2-2 ¼ yrs - 6-7 yrs 12-14 yrs 10-12 yrs
premolar
First molar At birth Sometimes a 2 ½-3 yrs 9-10 yrs 6-7 yrs
trace
Second molar 2 ½-3 yrs - 7-8 yrs 14-16 yrs 12-13 yrs
Third molar 7-9 yrs - 12-16 yrs 18-25 yrs 17-21 yrs
Lower
First incisor 3-4 mths - 4-6 yrs 9-10 yrs 6-7 yrs
Second incisor 3-4 mths - 4-5 yrs 10 yrs 7-8 yrs
Canine 4-5 mths - 6-7 yrs 12-14 yrs 9-10 yrs
First premolar 1 ¾-2 yrs - 5-6 yrs 12-13 yrs 10-12 yrs
Second 2 ¼-2 ¾ yrs - 6-7 yrs 13-14 yrs 11-12 yrs
premolar
First molar At birth Sometimes a 2 ½-3 yrs 9-10 yrs 6-7 yrs
trace
Second molar 2 ½-3yrs - 7-8 yrs 14-15 yrs 11-13 yrs
 30

OCCLUSION
The subject of occlusion deals with the relationships between all the components
of the masticatory system in function, dysfunction and Para function. It includes the
morphological and functional features of contacting surfaces of opposing teeth and
restorations, occlusal trauma and dysfunction, neuromuscular physiology,
temperomandibular joint and muscle function, swallowing and mastication, psycho
physiological status, and the diagnosis, prevention, and treatment of functional
disturbances of the masticatory system.

IDEAL OCCLUSION
It is a state of occlusion in which there is no need for neuromuscular adaptation and in
which there is completely harmonious relationship in the masticatory system for
mastication as well as for swallowing, speech and esthetics.

FUNCTIONAL OCCLUSION
An occlusion in which the anatomical features of the contacting surfaces of opposing
teeth or restorations are considered to be conducive to the optimal functioning of the
masticatory system.

BALANCED OCCLUSION
An occlusion in which there is posterior and anterior tooth contact without interference in
any lateral or protrusive movement. It is a concept of occlusion in which contacts in
lateral or protrusive movements are all counter balanced appropriately to distribute
occlusal forces equally.

CENTRIC OCCLUSION
It is the position of the teeth with the jaws closed and the teeth are at maximum
intercuspation with mandible in its centric relation. There is most even and balanced
contract of upper and lower dental arches.

CENTRIC RELATION
It is the relationship of the mandible to the maxilla when the condyles are in their
rearmost and uppermost position.

In 1895 EH Angles classified malocclusion. In normal occlusion the position of

mesiobuccal and mesiolingual cusps of the maxillary first molar is as mentioned below:

a) The mesiobuccal cusp of the maxillary first molar occludes in the buccal groove
of the mandibular first molar.

b) The mesiolingual cusp of the maxillary first molar occludes in the central fossa of
the mandibular first molar.
 31

A. CLASS I MALOCCLISION: The molar teeth are in normal occlusion and the
mesiobuccal cusp of maxillary first molar fits into the buccal groove of the mandibular
first molar.

B. CLASS II MALOCCLISION: The mandibular molars are one cusp distal to their
normal position. The mesiobuccal cusp of the maxillary first molar fits in the
interproximal spaces between the mandibular second bicuspid and first molar.

a) Division 1 Labioversion of the maxillary incisors, deep overbite, mouth

Sub division unilateral distoclusion

b) Division II Retruding or bunched maxillary incisors, deep overbite

Sub division unilateral distoclusion

C. CLASS III MALOCCLISION: The mandibular molars are one cusp mesial to
their position. The mesiobuccal cusp of the maxillary first molar fits into the
interproximal space between the first and second mandibular molars.

Division Bilateral
Sub-division Unilateral

a) Type I Teeth in both arches are in good alignment, but the incisors in edge to
edge bite
b) Type II Mandibular incisors lingual to the maxillary incisors, but crowded
c) Type III Mandibular incisors labial to the maxillary incisors

CLASS IV – The teeth are in mesioclusion on one side and distoclusion on the opposite
side.

OVERJET AND OVERBITE

Over jet describes the horizontal projection of the maxillary central incisors over the
mandibular incisors. Overbite describes the vertical overlapping of the maxillary central
incisors over the mandibular incisors.
 32

BLOOD SUPPLY AND NERVE SUPPLY OF THE

TEETH AND ASSOCIATED STRUCTURES
External carotid artery gives off lingual, facial and maxillary and several other
branches.
1. The lingual artery supplies the tongue, the floor of the mouth and the
sublingual salivary gland.
2. The facial artery supplies tonsils, sub-mandibular salivary gland, muscles of
face and lips.
3. The maxillary artery supplies a major portion of the mouth.

Maxillary artery : terminal branch of the external carotid artery and begins opposite
the neck of the mandible (fig.1.17). It crosses the inferior dental nerve, passes between
two heads of lateral pterygoid muscle and enters pterygoid muscle and enters pterygo
palatine fossa where it divides into terminal branches. During its course, it gives off
inferior dental (alveolar), posterior superior dental, infraorbital, buccal and muscular
branches.

Fig. 1.17: Branches of external carotid artery

 33

Branches of external carotid artery:

1. Superior thyroid
2. Lingual
3. Facial
4. Ascending pharyngeal
5. Posterior auricular
6. Occipital
7. Maxillary
8. Superficial temporal

Blood supply of the lower teeth

Inferior alveolar artery arises from the first part of the maxillary artery (fig.1.18)in
the infratemporal fossa and descends on the medial aspect of the ramus of the mandible
to the mandibular foramen. It enters the mandibular canal in company with the inferior
alveolar nerve and at the level of the first premolar tooth bifurcates into incisive and
mental branch. It passes between the sphenomandibular ligament and the ramus and lies
posterior to the inferior alveolar nerve. It gives off a mylohyoid branch and a lingual
branch before it enters the mandibular canal. The gingival of molars are also supplied by
buccal artery.

Fig. 1.18:. Branches of maxillary artery

 34

Blood supply to upper teeth

Branches of maxillary artery supplies the upper teeth. These three arteries form a
plexus before they supply the respective teeth. They are:

1. Posterior superior alveolar artery. Supply molars

2. Middle superior alveolar artery. Supply premolars
3. Anterior superior alveolar artery. Supply incisors and canine

Blood supply of the muscles of mastication

The muscles of mastication are supplied by the masseteric artery; medial and
lateral pterygoid arteries and anterior deep temporal arteries. All these arteries are
branches of the maxillary artery.

Blood supply of the palate

Hard palate is supplied by the greater palatine artery, a branch of maxillary artery.
It accompanies the greater palatine nerve through greater palatine canal to the roof of the
mouth. In the anterior region, it ascends through the incisive canal and anastomoses with
sphenopalatine artery in the floor of the nasal cavity.

Soft palate is supplied by the lesser palatine arteries, branches of maxillary artery.
They accompany lesser palatine nerve through lesser palatine foramina and anastomoses
with the ascending palatine artery.

Blood supply of the supporting structures of teeth.

The alveolar artery gives off the following branches:

a) Dental artery: It enters through the apical foramen and supplies the pulp.
Before entering the apical foramen, it divides into branches that supply periodontium.

b) Interdental artery: It runs along the alveolar septae and gives off numerous
perforating branches that supply periodontium and anastomoses with branches of dental
artery. This terminates by supplying papillary gingiva. These perforating branches give
the alveolar bone a sieve-like appearance which accounts for the name cribriform bone.

c) Interradicular artery: It runs through the interradicular septa and gives off
perforating branches and ends up in the periodontium at the bifurcation of the roots.
 35

In the periodontal ligament, the branches of three arteries, dental, interdental and
interradicular, form anastomosis.

Venous return from the teeth and the Jaws

The veins draining the teeth and jaws are the inferior alveolar vein, posterior
superior dental vein, infraorbital vein, and palatine vein. They drain to the pterygoid
plexus of veins which in turn drains to external jugular vein via deep facial vein.

NERVE SUPPLY OF THE UPPER JAW

The upper teeth and gingival are supplied by maxillary division of trigeminal
nerve. It is purely sensory nerve arising from trigeminal ganglion.

Nerve supply for the Upper Teeth

Molars: Posterior superior dental branches of maxillary nerve supply the molar teeth, and
buccal gingival and the maxillary sinus.

Premolars: Middle superior dental nerve is a branch of infraorbital nerve. It supplies

maxillary sinus, two premolars, first molar and buccal gingival of these teeth. Thus first
molar is supplied by both posterior superior and middle superior dental nerves. Both
these nerves form plexus before supplying the teeth.

Canines and Incisors: Anterior superior dental nerve is a branch of infraorbital nerve. It
supplies canine and incisor teeth and their buccal gingival and maxillary sinus. It forms a
plexus and anastomoses with the nerves from the opposite side and with the middle
superior dental nerve. The palatal gingival of the incisors are supplied by long
sphenopalatine (nasopalatine) nerve.

Nerve supply of the palate:

Hard Plate: (a) Greater palatine nerve (anterior palatine) from sphenopalatine
ganglion emerges through greater palatine foramen and supplies palatal mucosa and
palatal gingival of the molars and canine teeth (b) Long sphenopalatine (Nasopalatine)
nerve from the sphenopalatine ganglion descends from incisive canal, form a plexus with
the nerve from the opposite side and supplies the mucous membrane and gingival behind
the incisor teeth.

Soft palate: Lesser palatine nerve (posterior palatine) from sphenopalatine

ganglion comes out through lesser palatine canal and supplies soft palate. The middle
palatine nerve from the same ganglion supplies outer area of soft palate and tonsil.
 36

Nerve supply of the lower teeth:

Lower teeth are supplied by inferior dental nerve, branch of mandibular nerve.
The branches from this nerve form plexus before entering the apical foramen. The canine
and incisors are supplied by incisive nerve, a terminal branch of inferior dental nerve.
These nerves also supply the buccal gingival of anterior teeth. The nerve in periodontal
ligament relays touch and deep pressure and those in the pulp relays only pain.

Nerve supply to Gingiva and Mucosa

Lingual gingival and floor of mouth is supplied by lingual nerve. Mucosa of

cheek and gingival buccal to molar teeth are supplied by the plexus formed by long
buccal branch of mandibular and short buccal branch of facial nerve. Labial gingival of
canine and incisors are supplied by incisive branch of Inferior alveolar nerve.

Trigeminal Nerve (Vth Cranial Nerve):

FIG 1.19: Sensory nerve supply of face

It is the largest cranial nerve. It is mixed nerve carrying both sensory and motor
fibers. It contains sensory fibers from the head region and motor fibers for muscles of
mastication. Three large nerve trunks arise from the trigeminal ganglion (semi lunar
ganglion):
(a) the Ophthalmic,
(b) the Maxillary,
(c) the Mandibular.
 37

The motor root passes beneath the ganglion and is incorporated wholly within the
mandibular division and supply muscles of mastication. A summary of the branches and
their distribution is given below:

1. OPHTHALMIC

Lacrimal (to lacrimal gland, skin of lateral part of (Sensory) upper eyelid,
conjunctiva)

Frontal Supraorbital (to forehead, scalp as far as Vertex, upper eyelid,

frontal sinus) Supratrochlear (to skin of medial part of Forehead
and medial part of upper eyelid)

Nasociliary Afferent to ciliary ganglion two long ciliary nerves (sympathetic

fibres to dilator papillae muscle, afferent fibres to iris and ciliary
body), To sphenoid and ethmoid sinus, internal nasal Branches,
Anterior part of nasal cavity, External nasal branches (skin of
lower half And tip of nose)

2. MAXILLARY

Meningeal (to dura mater-(Sensory)

Two ganglionic branches (proceed through the sphenopalatine ganglion)
Pharyngeal (mucosa of root of pharynx and Sphenoidal sinus)
Three palatine - palatine (mucosa of nerves soft Palate, inferior nasal concha),
lesser palatine (soft palate tonsil),
Middle palatine (outer soft palate and Tonsil)
Long sphenopalatine (nasopalatine) – mucosa of hard palate near
incisors, roof and septum of nose).
Short sphenopalatine (mucosa of superior and middle concha,
posterior part of nasal septum).

Orbital (orbit, lacrimal gland).

Zygomatic Zygomatico-facial (skin over zygomatic bone)

Zygomatico-temporal (skin over anterior part of temple)

Infraorbital -Posterior superior dental (gingival, cheek and molar teeth,

Maxillary sinus),
-Middle superior dental (absent in 60%) (Premolar teeth and their Buccal
gingival)
-Anterior superior dental (incisors and canine teeth and their buccal
Gingival. Mucosa of anterior part of lateral wall of inferior meatus).
-Palpebral (lower eyelid)
-Nasal (side of nose)-Labial (cheek and upper lip)
38
 39

DEVELOPMENT AND GROWTH OF THE TEETH

Each tooth develops from a tooth bud that forms deep beneath the surface in the
area of the primitive mouth that will become the jaws. A tooth bud consists of three
parts:

1. A DENTAL ORGAN (ENAMEL ORGAN) which is derived from the oral

ectoderm
2. A DENTAL PAPILLA, which is derived from the mesenchyme and
3. A DENTAL SAC, which is also derived from the mesenchyme.

The dental organ produces the tooth enamel, the dental papilla produces the tooth
pulp and the dentin, and the dental sac produces not only the cementum but also the
periodontal ligament.

When the embryo is 5 or 6 weeks old, the first sign of tooth development is seen.
In the oral ectoderm, which will of course give rise to the oral epithelium, certain areas of
basal cells begin to proliferate at a more rapid rate than cells in adjacent areas. The result
is the formation of a band, an ectodermal thickening in the region of the future dental
arches extending along a line that represents the margin of the jaws. The band of
thickened ectoderm is the DENTAL LAMINA.

Dental lamina serves as the primordium for the deciduous teeth. Later during the
development of the jaws, the permanent molars arise directly from a distal extension of
the dental lamina. The successors of the deciduous teeth develop from a lingual
extension of the free end of the dental lamina. It is known as successional lamina which
gives rise to permanent incisors, canines and premolars.

At certain points on the dental lamina, each representing the location of one of the
ten mandibular and ten maxillary deciduous teeth, the ectodermal cells of the dental
lamina multiply still more rapidly and form little knob that presses slightly into the
underlying mesenchyme. Each of these little down growths on the dental lamina
represents the beginning of the dental, organ of the tooth bud of a deciduous tooth. Not
all of these dental organs start to develop at the same time. The first to appear are in the
anterior mandibular region.

As cell proliferation continues, each dental organ increases in size and changes in
shape. As it develops, it takes on a shape that somewhat resembles a cap, with the
outside of the cap directed towards the oral surface. Inside the cap (i.e. inside the
depression of the dental organ) the mesenchymal cells increase in number, and the tissue
have appears more dense than the surrounding mesenchyme. With this proliferation, the
area of mesenchyme becomes the dental papilla.
Now surrounding the deeper side of this structure (i.e. the combined dental organ
and dental papilla), the lower part of the tooth bud forms. The mesenchyme in this area
becomes somewhat fibrous in appearance; the fibres encircle the deep side of the papilla
and the dental organ. These encircling fibres are the dental sac.
 40

During and after these developments, the shape of the dental organ continues to
change. The depression occupied by the dental papilla deepens until the dental bud
becomes a shape which has been resembling that of a bell and as these developments take
place the dental lamina which has thus far connected the dental organ to the oral
epithelium breaks up and the tooth bud loses its connection with the epithelium of the
primitive oral cavity.

Developmental stages

Despite the obvious fact that tooth development (as the development of any other
organ) is a continuous process, it is not only traditional but also didactically necessary to
divide the developmental history of a tooth into several “stages”. They are named from
the shape of the epithelial part of the tooth germ. Since the odontogenic epithelium not
only produces enamel but also is indispensable for the initiation of dentin formation, the
terms enamel organ and outer and the inner enamel epithelium are best replaced by the
terms DENTAL ORGAN and DENTAL EPITHELIUM.

Dental Lamina and Bud stage

FIG.1.27: Stages
 41

Dental Lamina: The first sign of human tooth development is seen during the sixth
week of embryonic life (11 mm embryo). At this stage the oral epithelium consists of
basal layer of high cells and surface layer of flattened cells. The glycogen droplets in
their cytoplasm are lost in routine preparations, giving them an empty appearance. The
epithelium is separated from the connective tissue by a basement membrane. Certain
cells in the basal layer of the oral epithelium begin to proliferate at a more rapid rate than
the adjacent cells. An epithelial thickening arises in the region of the future dental
arch and extends along the entire free margin of the jaws. It is the primordium of the
ectodermal portion of the teeth known as the dental lamina. Mitotic figures are seen not
only in the epithelium but also in the adjacent mesoderm

Tooth buds (primordial of teeth).

Simultaneous with the differentiation of the dental lamina there arise from it in
each jaw round or ovoid swellings at ten different points, corresponding to the future
position of the deciduous teeth, the primordial of the dental organs, the tooth buds. Thus
the development of the tooth germ is initiated and the cells continue to proliferate faster
than the adjacent cells. The dental lamina is shallow and microscopic section of that
show the tooth buds close to the oral epithelium.

Cap stage:

As the tooth bud continues to proliferate, it does not expand uniformly into a
larger sphere. Unequal growth in the different parts of the bud leads to formation of the
cap stage, which is characterized by a shallow invagination of the deep surface of the
bud.
 42

Outer and Inner dental epithelium

The peripheral cells of the cap stage form the outer dental epithelium as its
convexity, consisting of a single row of cuboidal cells, and the inner dental epithelium at
the concavity consisting of a layer of tall columnar cells.

Stellate reticulum (enamel pulp)

The cells in the center of the epithelial dental organ, situated between the outer
and inner epithelia, begin to separate by an increase of the intercellular fluid and arrange
themselves in a network called the stellate reticulum. The cells assume a branched
reticular form. The spaces in this reticular network are filled with a mucoid fluid rich in
albumin, giving the stellate reticulum a cushion like consistency that later support and
protects the delicate enamel forming cells.
The cells in the center of the dental organ are densely packed and form the enamel
knot. This knot projects in part toward the underlying dental papilla, so that the center of
the epithelial invaginaton shows a slightly knoblike enlargement that is bordered by the
labial and lingual enamel grooves. At the same time these arise in the increasingly high
dental organ a vertical extension of the enamel knot, called the enamel cord. Both are
temporary structures that disappears before enamel formation begins.

DENTAL PAPILLA

Under the organizing influence of the proliferating epithelium of the dental organ,
the mesenchyme, partially enclosed by the invaginated portion of the inner dental
epithelium, proliferates. It condenses to form the dental papilla which is the formative
organ of the dentin and the primordium of the pulp.

DENTAL SAC

Concomitant with the development of the dental organ and the dental papilla,
there is a marginal condensation in the mesenchyme surrounding the dental organ and
dental papilla. In this zone, gradually a denser and more fibrous layer develops, which is
the primitive dental sac. The epithelial dental organ, the dental papilla and the dental sac
are the formative tissues for an entire tooth and its periodontal ligament.

BELL STAGE

As the invagination of the epithelium deepens and its margins continue to grow,
the enamel organ assumes a bell shape.
 43

FIG .1.28:Labio-lingual section of tooth bud showing different parts

INNER DENTAL EPITHELIUM

The inner dental epithelium consists of a single layer of cells that differentiate
prior to amelogenesis into tall columnar cells, the ameloblasts. They are 4 to 5 microns
in diameter and about 40 microns high. In cross section they assume a hexagonal shape
similar to that seen later in transverse sections of the enamel rods. They are the enamel
forming cells. The cells of the inner dental epithelium exert an organizing influence upon
the underlying mesenchymal cells, which differentiate into odontoblasts.

STRATUM INTERMEDIUM
Several layers of squamous cells called stratum intermedium appear between the inner
dental epithelium and stellate reticulum. This layer seems to be essential to enamel
formation. It is absent in the part of the tooth germ that outlines the root portions of the
tooth but does not form enamel.

STELLATE RETICULUM
The stellate reticulum expands further, mainly by increase of the intercellular
fluid. The cells are star shaped, with long processes that anastomoses with those of
adjacent cells. Before enamel formation begins, the stellate reticulum shrinks by loss of
the intercellular fluid. Its cells then are hardly distinguishable from those of the stratum
intermedium. This change begins at the height of the cusp or the incisal edge and
progresses cervically.

OUTER DENTAL EPITHELIUM

The cells of the outer dental epithelium flatten to a low cuboidal form. At the end
of the bell stage, preparatory to and during the formation of enamel, the formerly smooth
 44

surface of the outer dental epithelium is laid in folds. Between the folds the adjacent
mesenchyme of the dental sac forms papillae that contain capillary loops and thus
provide a rich nutritional supply for the intense metabolic activity of the vascular enamel
organ.

DENTAL LAMINA
In all teeth except the permanent molars, the dental lamina proliferates at its deep
end to give rise to the dental organ of the permanent tooth. While it disintegrates in the
region between the dental organ and the oral epithelium. The dental organ is gradually
separated from the dental lamina at about the time when the first dentin is formed.

DENTAL PAPILLA
The dental papilla is enclosed in the invaginated portion of the dental organ.
Before the inner dental epithelium begins to produce enamel, the peripheral cells of the
mesenchymal dental papilla differentiate into odontoblasts under the organizing influence
of the epithelium. They assume a cuboidal and later a columnar form and acquire the
specific potentiality to produce dentin.

DENTAL SAC
Before formation of dental tissue begins, the dental sac shows a circular
arrangement of its fibres and resembles a capsular structure. With the development of the
root, the fibres of the dental sac differentiate into the periodontal fibres that become
embedded in the cementum and alveolar bone.

ADVANCED BELL STAGE

During the advanced bell stage, the boundary between inner dental epithelium and
odontoblasts outlines the future dentinoenamel junction. In addition, the junction of the
inner and outer dental epithelia at the basal margin of the epithelial organ, in the region of
the cervical line, will give rise to the epithelial root sheath of Hertwig.

FIG 1.29:Advanced bell stage showing root sheath at Epithelial diaphragm.

 45

FUNCTION OF THE DENTAL LAMINA

The functional activity of the dental lamina and its chronology may be considered
in three phases. The first phase is concerned with the initiation of the entire deciduous
dentition that occurs during the second month in utero. The second phase deals with the
initiation of the successors of the deciduous teeth. It is preceded by the growth of the free
and of the dental lamina (successional lamina), lingual to the dental organ of each
deciduous tooth, and occurs from about the fifth month in utero for the permanent central
incisors to 10 months of age for the second premolar. The third phase is preceded by the
extension of the dental lamina distal to the dental organ of the second deciduous molar,
which begins in the 140 mm embryo. The permanent molars arise directly from the distal
extension of the dental lamina. The time of initiation is about 4 months of fetal life (in
the 160 mm embryo) for the first permanent molar, the first year for the second
permanent molar, and the fourth to fifth year for the third permanent molar.

It is thus evident that the total activity of the dental lamina extends over a period
of about five years. Any particular portion of its functions for a much briefer period,
since only relatively short time elapses after initiation, before the dental lamina begins to
disintegrate at that particular location. However, the dental lamina still be active in the
third molar region after it has disappeared elsewhere except for occasional epithelial
remnants. The distal proliferation of the dental lamina is responsible for the peculiar
location of the germs of the permanent molars. They develop in the ramus of the
mandible and in the tuberosity of the maxilla.

FATE OF THE DENTAL LAMINA

During the cap stage the dental lamina maintains a broad connection with the dental
organ, but in the bull stage it begins to break up by mesenchymal invasion, which first
penetrates its central portion and divides it into the lateral lamina and the dental lamina
proper. The mesenchymal invasion is at first incomplete and does not perforate the
dental lamina. The dental lamina proper proliferates only at its deeper margin, which
becomes a free and situated lingually to the dental organ and forms the primordium of the
permanent tooth. The epithelial connection of the dental organ with the oral epithelium is
served by the proliferating mesoderm. Remnants of the dental lamina may persist as
epithelial pears or islands within the jaw as well as in the gingival.

VESTIBULAR LAMINA
Labial and buccal to the dental lamina, another epithelial thickening develops
independently and somewhat later. It is the vestibular lamina, also termed lip-furrow
band. It subsequently follows out and forms the oral vestibule between the alveolar
portion of the jaws and the lips and cheeks.
 46

STAGES IN TOOTH GROWTH

Morphologic stages Physiologic processes

Dental Lamina Initiation

Bud stage
Cap stage (early)
Cap stage (advanced) Proliferation

Bell stage (early) Histodifferentiation

Bell stage (advanced) Morphodifferentiation

Formation and enamel Apposition

and dentin matrix
 47

TEMPOROMANDIBULAR JOINT

The temperomandibular joint is a unique joint. It is unique in its anatomy,

histology and function. Though anatomically there are two joints, a right and a left, yet
functionally the joints act as one unit. It is like atlanto-occipital joint which is bilateral
anatomically but acts as one unit functionally. Therefore, the right and the left joints are
really two halves of one joint, the cranio-mandibular joint (Sicher). Though it is one joint
yet paradoxically there are two compartments - an upper and a lower.

No other joint has created so much controversy amongst scientists and investigators
regarding its movements during function. The controversy exists because most of the
movements are tried on dried skull with no articular cartilage in between. In life, during
occlusion, cranial bones and condyle never come in contact and therefore the movements
in dried skull become un-natural.

Evolution

Temperomandibular joint is found only in mammals. The jaw joint of mammals

is entirely different than that of non-mammals. In mammals the mandibular condyle is
convex and there is the presence of intra-articular disc in non-mammals, the condyle is
concave and the disk is absent. In reptiles, the mandible consists of several bones,
namely, dentary, quadrate, and articulare. Of these three bones, only dentary is retained
in the human mandible. The other two bones, quadrate and articulare which are derived
from Merkel’s cartilage have been incorporated as bones of middle ear (malleus and
incus). The joint between malleus and incus in man is homologous to jaw joint in
reptiles. In mammals the jaw joint occurs between squamous portions of temporal and
dentary

.
Anatomy

The temperomandibular joint is a bilateral ginglymo-arthrodial or sliding – hinge

joint. The compound synovial joint is formed by mandibular fossa and articular
eminence of temporal bone and mandibular condyle with the articular disk interposed in
between (fig.1.23). The mandible forms joints on both sides of the skull. However, one
condyle cannot be moved without moving the other. The complete intra-articular disk
divides the joint cavity into an upper larger cavity and a lower smaller cavity.
 48

FIG 1.23: Anatomy of TMJ

The cranial component of the joint is formed by the squamous portion of

temporal bone. It consists of a concave fossa posteriorly known as glenoid fossa or
mandibular fossa and a convex anterior articular eminence. The articular eminence has
a flat anterior slope and is continuous with infratemporal surface of temporal bone. The
portion of temporal bone connected with spine of sphenoid. The posterior wall is formed
by post glenoid process of the temporal bone which lies between mandibular fossa and
tympanic bone. The articular fossa is separated from the tympanic bone by the squamo-
tympanic fissure laterally. Medially this fissure divides into fissures, an anterior petro-
squamosal fissure and a posterior petro-tympanic fissure
The articular fossa is not a functional part of the joint. The fossa comes in
contact with only posterior part of articular disk. The condyle rests on the posterior slope
of the articular eminence. The fossa is not subjected to any pressure or friction.
However, it is the most vulnerable part of the joint during injury. The post glenoid
process is not significant functionally. The condyle never braces it in life as is seen to do
in dried skull.
 49

The condyle of the mandible measures 2 cms medio-laterally and 0.5 cms antero-
posteriorly. The distance between the centers of two condyles is 10 cms. The long axis
of the condyle is at right angles to the plane of the ramus. The condyle is convex both
antero-posteriorly and medio-laterally and runs in the same direction as that of articular
eminence. The articular surface of the condyle points antero-superiorly. When viewed
from lateral aspect, the condyle seems to bend anteriorly. The long axis of condyle is at
right angles to the plane of the ramus and therefore deviates about 13 degree from the
frontal plane. The two axis, if extended, form an angle of 150 degree. If extended
medially and posteriorly, the axis would cross at the anterior margin of foramen magnum;
this angulation on two sides may be different axis. The condyle projects to the medial
side of the ramus. The sharp border of sigmoid notch leads to lateral tip of condyle and
thus three-forths of condyle lies medial to the ramus and is supported by a triangular
buttress.
The capsule is loose, funnel-shaped and surrounds the joint. Its cranial attachment is
along anterior border of articular eminence and laterally follows the articular margins.
Posteriorly, it is attached to the broad area of the post
glenoid process. Medially, it is attached to the base of angular spint of the sphenoid
bone. The mandibular attachment is on lateral and medial aspects of the neck below the
points of attachment of the disk. Anteriorly it is attached to the sharp ridge which bounds
the articular surface of condyle. The lateral surface of the capsule is thickened and forms
temporo-mandibular ligament.
 50

The temporomandibular ligament is triangular in shape, the base being towards

the cranial side at the zygomatic process of temporal bone and the apex is at the neck of
the mandible just below the lateral condylar pole. The capsule is weak anteriorly and
condylar dislocation is not uncommon at this site. The medial aspect of the condyle is
strengthened by spheno-mandibular ligament. The capsule is attached anteriorly to a
muscle, the lateral pterygoid, which pulls the disk forward and downward. Posteriorly, it
is attached to the articular fossa, the disk and the condyle .

The intra-articular disk lies between the condyle and the articular eminence.
The upper surface of the disk is saddle-shaped, concave antero-posteriorly and convex
medio-laterally. The lower surface is concave in both directions.
Each compartment of the joint cavity has its own synovial membrane, which lines
the fibrous capsule and covers the loose retrodiscal pad and is inserted on the neck of the
mandible. Therefore, a portion of the neck of the mandible is intracapsular. The synovial
membrane is absent over all the four articulating surfaces. The disk is thin at the center.
It is attached to the medial and lateral poles of the condyle and therefore is carried
forward with the condyle during mandibular movement.
The lateral pterygoid muscle is attached to the disk, the capsule and the neck of
the mandible. During the forward movement of the condyle the disk also moves forward.
This forward movement of the disk is not due to the pull of the muscle but by virtue of its
attachment to both sides of the condyle. The muscle merely stabilizes the disk during
mastication.
Anteriorly, the disk blends with the joint capsule and posteriorly, it is attached to the
capsule via a highly vascular loose connective tissue known as the retrodiscal pad. When
the disk moves anteriorly along with the condyle, the loose connective tissue allows this
mobility. The fibrous connective tissue covering the mandibular and temporal surfaces
and the central area of the disk in a vascular. The avascularity helps in adaptation of the
tissue to resist pressure.

The extra-capsular ligaments of the joint are:

1. The spheno-mandibular ligament, extending from the spine of the sphenoid
bone to lingual of mandibular foramen. This ligament is a part of remnant of Meckel’s
cartilage. It supports medial fibres of the capsule.
2. The stylo-mandibular ligament, extending from the styloid process to posterior
border of ramus above the angle of the mandible. It separates the submandibular gland
from the parotid gland.

Blood supply
Arterial supply from branches of maxillary artery branch of external carotid
artery. Veins of the joint drain to superficial temporal veins, pterygoid plexus and
maxillary veins.
Lymphatic vessels from lateral surface and anterior surface drain into
preauricular and parotid nodes. Posterior and medial surface drain into submandibular
nodes.
 51

Nerve supply

The articular nerves consist of protective, proprioceptive and tropic

(nourishment) components. The articular branches are derived from Vth cranial from
both its anterior and posterior division. The anterior surface is innervated by branches of
masseteric nerve from anterior division and the posterior part is supplied by branches of
the auriculo-temporal nerve from the posterior division. The nerves supply the capsule,
synovial tissue and periphery of the disk. The articular cartilage and central portion of
the disk do not have any nerve supply (and blood supply).

MOVEMENTS OF TMJ
Depression (as in opening movements)
This is a very complicated movement occurring in both upper and the lower
factions of the temperomandibular joints. In the lower compartment the head of the
mandible takes a hinge movement and in the upper compartment the head of the
mandible along with the disk takes a gliding movement forwards. In the initial phase,
only hinge movement operates and in the later phase, the gliding movement operates.
The muscles concerned in this movement are digastric, lateral pterygoid and other
suprahyoid muscles. There is combined forward pull of the two lateral pterygoid muscles
and backward-downward pull of the two anterior bellies of digastric and other suprahyoid
muscles. Mandible will rotate around a movable axis which passes through bellies of
digastric retract the mandible; the pull of suprahyoid muscles will cause a retarded
opening movement provided hyoid is stabilized by infrahyoid muscles. Along with
contraction of lateral pterygoid there is relaxation of temporalis, masseter and medial
pterygoid muscles.

Elevation (as in closing)

This movement is caused by the masseters, two medial pterygoids and two
temporal muscles (anterior fibres). During closure with protrusion, the lateral and medial
pterygoids contract. The condylar heads remain forward on the articular eminences.
During closure with retraction, posterior temporal muscles and masseters contract and the
pterygoids relax and the condyles return to glenoid fossa.

Protrusion
The combined pull of the lateral pterygoids move mandible forward. The posterior
horizontal fibres of temporalis relax. The masseters, medial pterygoids and anterior
vertical fibres of temporalis remain in tonic contraction and prevent separation of the
teeth. The condyles of the mandible with the articular disks move downward and
forward by the contraction of lateral pterygoids.
 52

Retrusion
The head of condyle with the articular disks are carried back into the glenoid fossae. The
posterior fibres of the temporal muscles of both sides contract along with relaxation of
lateral pterygoids. The teeth remain in contact by other muscles.

Lateral Movement
Lateral movements are produced by the combined action of the elevators and retruders on
the working side and protruders of the non-working side. The condyle of the side
towards which the jaw is moving is carried back into the glenoid fossa by the posterior
fibres of the temporalis of that side and held there by the tonic contraction of all the
muscles of that side. The other condyle and articular disk is pulled forward and inward
by the lateral pterygoids so that the jaw rotates around a vertical axis passing through the
fixed condyle.

Structure

The temperomandibular joint has the following components:

1. Mandibular condyle
2. Mandibular fossa and articular tubercle
3. Articular disc
4. Articular capsule

Mandibular condyle

It is semi cylindrical structure, the long axis lying at right angle to the ramus. It is
convex both antero-posteriorly and medio-laterally. The articular surface is covered by a
layer of fibrous tissue consisting of dense collagen and fibroblasts running parallel to
articular surface. Lying under this tissue is a plate of hyaline cartilage. Under the
cartilage is a layer of calcified cartilage. Under this is a zone of cartilage destruction and
under it is the bone. This transition from bone to fibrous tissue is gradual. The growth of
condyle occur in fibrous tissue covering which is transformed into cartilage and then to
bone.

Articular disc

It is an oval structure attached to the capsule anteriorly, medially and laterally. Its
posterior border is thick and is connected with a loose vascular tissue which is attached to
the capsule. It consists of dense collagen bundles running in various directions. Elastic
fibres are few. The fibroblasts are flat, elongated and has cytoplasmic processes. As age
advances, some of these fibroblasts change to cartilage cells. Islands of hyaline cartilage
may be seen. Most areas of the disk do not have blood supply except for the posterior
part.
 53

Synovial Cavities

The superior and inferior synovial cavities are lined by synovial membrane
consisting of thin loose vascular connective tissue thrown into villi. The cavity surface is
lined by endothelial cells. They contain clear synovial fluid which lubricates the joint.

Mandibular Fossa

It is concave and is situated in the temporal bone. It is covered by dense

connective tissue which is thickest in the anterior part. The deepest layer may be
calcified.

Articular Capsule

It consists of dense collagen fibres. It is thick on lateral aspect of the joint and is
called the temperomandibular ligament.
 54

MUSCLES OF MASTICATION

Introduction:

The four muscles of mastication which move the mandible during mastication and speech
are masseter, temporalis, lateral pterygoid and medial pterygoid. They are derived from
one muscle mass and are arranged in that order from superficial to the deep plane. Since
they develop from the mesoderm of the first bronchial arch, they are supplied by the
nerve of that arch, the mandibular nerve. Besides these four major muscles of
mastication, there are suprahyoid group of muscles also, which helps in mastication.
These are geniohyoid, mylohyoid and anterior belly of digastric muscle.

MASSETER MUSCLE
It is quadrilateral shaped muscle which covers lateral surface of ramus of mandible and it
has three layers.

ORIGIN
a) Superficial layer (largest): Originates from anterior 2/3 of lower border of zygomatic
arch and adjoining zygomatic process of maxilla.

b) Middle layer: Originates from anterior 2/3 of deep surface and posterior 1/3 of lower
border of zygomatic arch.

Deep layer: From deep surface of zygomatic arch.

 55

FIBRES
Superficial fibres pass downwards and back at 45 degrees. Middle and deep
fibres pass vertically downwards. These layers are separated posteriorly by an artery and
nerve.

INSERTION
Superficial layer inserts into lower part of lateral surface of ramus of mandible.
Middle layer into middle part of ramus and deep layer inserts into upper part of ramus
and coronoid process (fig.1.12).

NERVE AND BLOOD SUPPLY

Masseteric nerve a branch of anterior division of mandibular nerve innervates the
muscle. The massenteric artery which is branch of maxillary artery supplies the muscle.

ACTION: Elevates mandible to close mouth and to bite.

Fig. 1.12:Masseter muscle

TEMPORALIS MUSCLE
It is a fan shaped muscle

ORIGIN:
a) Temporal fossa, excluding zygomatic bone
b) Temporal fossa

FIBRES: The fibres converge and pass through the gap deep to zygomatic arch. The
fibres are divided into three groups. These are anterior, middle and posterior fibres.

INSERTION
The fibres inserts at the margins and deep surface of the coronoid process and
anterior border of ramus of mandible (fig.1.13).
 56

NERVE & BLOOD SUPPLY

Two deep temporal branches from anterior division of mandibular nerve innervate
the muscle. The blood supply is by middle and deep temporal arteries. Middle temporal
artery is a branch superficial temporal artery while deep temporal is a branch of maxillary
artery.

ACTION Anterior fibres elevate the mandible while posterior fibres retract the protruded
mandible. The muscle helps in-side to side grinding movement.

Fig. 1.13: Temporalis muscle

LATERAL PTERYGOID MUSCLE

It is short conical muscle and has upper and lower heads.

ORIGIN
a) Upper head (small) originates from infratemporal surface and crest of greater
wing of sphenoid.
b) Lower head (Larger) originates from lateral surface of lateral pterygoid plate.
FIBRES
The fibres run backwards and laterally and converge for insertion (fig.1.14).

INSERTION
The muscle inserts at pterygoid fovea on the anterior surface of neck of mandible
and also anterior margin of articular disc and capsule of temporo mandibular joint.
 57

NERVE AND BLOOD SUPPLY

Nerve supply is a branch from anterior division of mandibular nerve and blood is
supplied by a branch from maxillary artery.

ACTION
a) Superficial head (small): Originates from tuberosity of maxilla and adjoining bone.
b) Deep head (large): Originates from medial surface of lateral pterygoid plate and
adjoining process of palatine bone.

Fig. 1.14:Lateral and medial pterygoid muscles

MEDIAL PTERYOID MUSCLE

This muscle is quadrilateral in shape and has a small superficial and larger deep head.

ORIGIN
a) Superficial head (small): Originates from tuberosity of maxilla and adjoining bone.
b) Deep head (large): Originates from medial surface of lateral pterygoid plate and
adjoining process of palatine bone.

FIBRES
The fibres run downwards backwards and laterally (fig.1.14).

INSERTION
The muscle inserts on a roughened area on the medial surface of angle, below and
behind the mandibular foramen and mylohyoid groove.

NERVE AND BLOOD SUPPLY

Nerve supply is by medial pterygoid branch from the main trunk of mandibular
nerve. Blood is supplied by a branch from maxillary artery.

ACTIONS
It elevates mandible and also helps to protrude the mandible. With the lateral
pterygoid the muscle brings about side to side grinding (chewing movements)
 58

.Apart from these four major muscles the suprahyoid group of geniohyoid,
mylohyoid and anterior belly of digastric muscles, have the common features of
mandibular depressor action. These muscles originate on the hyoid bone and insert on
anterior part of the mandible. They are assisted in their action by the stylohyoid muscle,
which tends to fix the hyoid bone in position so that the other suprahyoid muscles may
open the mouth forcefully.

MUSCLES OF MASTICATION- SUMMARY

Muscle Action
1. Masseter Elevation of mandible while closure of
the mouth
2. Temporalis a) Elevation of mandible
b Retraction of mandible by posterior
fibres
c) Side to side grinding movement
3. Lateral pterygoid a) Depression of mandible while opening
the mouth
b) Protrusion of mandible
c) Side to side movement
4. Medial pterygoid a)Elevation of mandible
b)Side to side movement
 59

SALIVARY GLANDS
These glands are meant for the production of saliva. The different salivary glands present
in humans are:

I. Major salivary glands (fig.1.4)

a) Parotid glands
b) Sub-mandibular gland (sub-maxillary gland)
c) Sub-lingual glands

II. Minor salivary glands

a) Lingual serous glands
b) Lingual mucus glands
c) Buccal glands
d) Labial glands
e) Palatal glands

Fig. 1.4:Major salivary glands

A Gland is a unit of structure and function, involved in the manufacture and discharge of
a secretion.
 60

CLASSIFICATION OF GLANDS

Glands may be classified in many ways

1. According to number of cells involved:

a) Unicellular e.g. goblet cells, multicellular e.g. salivary gland

2. According to size:
a) Major e.g. Parotid
b) Minor, e.g., mucous glands of cheek

3. According to morphology
a) Alveolar (acinar)
b) Tubular
c) Tubulo-acinar

4. According to branching of the duct:

a) Simple (non-branching)
b) Compound (branching)

5. According to presence of ducts:

a) Exocrine (ducts are present) e.g. salivary gland
b) Endocrine (ductless) e.g. pituitary

6. According to type of secretion

a) Serous (albuminous) e.g. parotid
b) Mucous e.g. minor salivary glands of cheek
c) Mixed (sero-mucous), e.g. submandibular

7. According to damage of secretory cells at discharge

a) Merocrine (no damage) e.g. salivary gland
b) Apocrine (cells contribute part of their protoplasmic substance to their secretion)
e.g. some sweat glands
c) Holocrine (there is extreme damage of the cell, secretion consists of altered cells
of the gland itself) e.g. sebaceous gland

In using a nomenclature, combination of various classifications are used.

 61

Other Classification of Salivary glands

Salivary glands are multicellular, merocrine, exocrine glands. They may be
classified according to size, location or type of secretion.

1. According to size:

a) Major (extrinsic). There are three pairs of major glands – parotid, submandibular
and sublingual, flow of saliva is continuous
b) Minor (intrinsic). Flow of saliva is intermittent. e.g. buccal glands. There are 400-
500 minor glands in oral cavity (not seen in gingival and anterior part of hard
palate).

2. According to location

I. Glands whose ducts open in the vestibule

A. Lip : 1. Superior labial

2. Inferior labial
B. Cheek : 1. Parotid
2. Buccal

II. Glands whose ducts open in oral cavity proper

A. Floor of mouth 1. Submandibular

2. Sublingual (major)
3. Sublingual (minor)
4. Gloss palatine
B. Tongue 1. Body: Anterior lingual (of Blandin and Nuhn)
2. Base: Posterior lingual
a) Von Ebner (around vallate Papilla)
b) Tonsil, Lingual
C. Palate Palatine

3. According to secretion

I. Serous 1. Parotid
2. Von Ebner (Posterior lingual near vallate papilla)

II. Mucous 1. Palatine

2. Posterior lingual-tonsillar
3. Gloss palatine
 62

III.. Mixed 1. Submandibular (Predominantly serous)

2. Sublingual (Predominantly mucous)
3. Blandin-Nuhn (anterior lingual) predominantly mucous
4. Buccal (predominantly mucous)
5. Labial (superior and inferior) predominantly mucous

Structural Pattern of the salivary gland

Basically a salivary gland consists of parenchymatous secretory cells and stromal

connective tissue . A capsule may be present. Capsule consists mostly of collagenous
tissue with few elastic and reticular fibres.

Trabeculae

Connective tissue strands from capsule traverse the glands and divide them into
lobules. These septae carry blood vessels, nerves and excretory ducts. The septal
connective tissue consists of mesenchymal cells, fibroblasts, plasma cells, lymphocytes
and fat cells. The connective tissue of the septae spreads into the lobules forming stroma
for the secretory units.

Secretory Cells

The secretory cells are either serous or mucous. They are organized to form acini.
The cell morphology varies according to cycle of activity. During the resting phase there
is organization of the cytoplasmic organelles and the nucleus. In the elaborative phase,
there is actual synthesis of the secretory product. There is accumulation of the product
and the shape of the cell is altered. During the secretory phase there is actual liberation
of the secretory product.

Fig. 1.25: Structure of salivary gland duct system

 63

HISTOLOGY OF SOFT AND HARD DENTAL TISSUES

The hard dental tissues include

(1) Enamel
(2) Dentin
(3) Cementum
(4) Alveolar bone.

The soft tissues includes

(1) Pulp
(2) Periodontal ligament
(3) Gingiva.

ENAMEL

FIG .1.30 Structure of enamel showing rod, rod sheath at rod substances

Histologically enamel, the outermost covering of tooth which lies adjacent to the
dentin contains the following:
(1) Enamel Rods
(2) Rod sheath
(3) Cementing inter-rod substances
 64

Enamel rods:

They arise from dentino-enamel junction and proceeds uninterruptedly to the

external surface of tooth. In general rods are perpendicular to the dentino-enamel
junction. In cervical region and in the cusps they are wavy. They appear round or oval in
cross section. . In permanent teeth, the rods in cervical areas are directed apically and at
acute angle with dentino-enamel junction. In deciduous teeth, rods are oriented
perpendicular to D.E. junction.

Rod sheath:

This is present peripheral to the rods. It is les calcified, contains more organic
substance.

Inter Rod substance:

This substance is in between the enamel rods and acts as a cementing substance.

HUNTER SCHREGER BANDS

When a longitudinally ground section of tooth is seen in reflected light, a series

of dark and light bands are seen in enamel, known as Hunter Schreger bands. These are
due to differences in degree of mineralization.

INCREMENTAL LINES OF RETZIUS

On a ground section of a tooth, when seen under light microscope, concentric

brown lines are seen in the enamel that is incremental line of Retzius. They terminate at
the enamel surface. These are due to rhythm of mineralization or variations in organic
structure. The Neonatal line is the line which separates postnatally produced enamel from
that produced before birth. It is nothing but an accentuated incremental line.
 65

CEMENTO ENAMEL JUNCTION

FIG .1.31:Cemento enamel junction

Cementum may overlap enamel in 65%; meet at edge to edge in 25% and no
meeting in 10%.
ENAMEL TUFTS:
Unbraided projections seen arising from D.E. junction into enamel are the
enameltufts,which are like a tuft of grass.
ENAMEL SPINDLES:
Odentoblastic processes of dentin projecting into enamel are enamel spindles.

THE DENTINO-ENAMEL JUNCTION:

The dentin at D.E. junction is pitted, into these pits the rounded projection of enamel
are fitted.

ENAMEL CUTICLE: The crown of a newly erupted tooth is covered by a delicate

membrane known as enamel cuticle. It gives a protective coating to enamel and a
polished surface.

PRIMARY CUTICLE – It is formed by ameloblasts, which is a final secretory product.

SECONDARY CUTICLE – It is the cellular layer that has become keratinized.

CHEMICAL COMPOSITION
Inorganic substance 95%
Organic substance 5%
Water 4.5%
 66

Inorganic substance–Mainly calcium hydroxyapatite crystals. Majority of

inorganic elements are calcium and phosphorus. Others are fluorides, silver, aluminum,
barium, copper, magnesium.

Organic substances – Protein in the form of keratin, carbohydrates, lipids, citrates etc.

DENTIN
It forms the largest portion of tooth and gives the basic shape to it.

CHEMICAL COMPOSITION

(1) Inorganic ((70%)

(2) Organic (17%)
(3) Water (13%)

Hydroxyapatite 52% Collagen 15%

Calcium 35% Citric acid 1%
Phosphorus 17%

In traces sodium, potassium, proteins, lipids, magnesium, lead,

Fluorine, others ½ %
 67

HISTOLOGY

Dentin is composed of 2 constituents

(1) Dentinal tubules containing the protoplasmic processes of odontoblasts
(2) Dentinal Matrix

FIG .1.32:Structure of Dentine

Dentinal tubules – They arise from odontoblastic process extend through the body of
dentin, may extend to enamel as enamel spindles. They contain odontoblasts processes
which are protoplasmic extensions from odontoblasts. The length of odontoblastic
process is 2 to 3 mm. Diameter is 1 to 1.5. They are wider at pulp at end and narrows
outwardly. They give lateral branches which anastomoses with the branches of adjacent
odontoblastic processes. The dental tubules run as a curved “S” shaped course, starting at
perpendicular to the pulp surface. They are straight in the root and under the cusps.

Dentin Matrix – There are a calcified collagenous fibrils in the dentin, which is more
calcified than adjacent dentin, which is traversed by dentinal tubules. It is divided into:

1. Peritubular dentin – Immediately around the odontoblastic process, which is

more calcified than adjacent dentin

2. Intertubular dentin – which is present in between the dentinal tubules, less calcified.

This forms the main mass of dentin, containing collagenous. Material, amorphous
organic ground substance, and smaller amount of apatite crystals.

Other forms of dentin are:

1) Mantle Dentin – This is the first formed dentin, which is the most peripheral part
of dentin, consisting of (1) Korff (X) fibre and (2) B – fibre.

2) Pre Dentine: It is the newly formed dentine which is located adjacent to the pulp
tissue. It is not mineralized.
3) Circumpulpal Dentine: It forms the remaining part of dentine other than Mantle
dentine. It represents the dentine formed before root completion.
 68

Various histological features of Dentin

1. Incremental lines of Von-Ebner

These lines mark the sites of transition between alternating periods of accelerated
and retarded growth

2. Neonatal line:
These are the hypo calcified bands seen in dentin separating the prenatal and
postnatal dentin. These are seen only in deciduous teeth and permanent 1st molar.

3. Interlobular dentin:
These are the irregular areas of hypo calcified matrix formed due to failure of
union of inorganic calcospherite granules.
4. Dental junctions

a) Dentino Enamel junction

b) Dentino predentin junction – interface between calcified and
Uncalcified dentin
c) Predentin pulp junction

TYPES OF DENTIN

1) Primary Dentin – Dentin that is formed during the various periods of tooth
development, to the time when tooth takes its anatomic position in the oral cavity. It
represents the dentine which forms before root completion.

2) Secondary Dentin (Regular dentin): This is seen as a regular, uniform layer around the
pulp cavity which forms after root completion.

3) Secondary Reparative & irregular dentin. This is localized deposit of dentin on the
wall of pulp cavity as a result of erosion, attrition, caries etc.

4. Sclerotic Dentin. This is formed due to change in structure of primary dentin, as a

response to aging, erosion, abrasion. It is commonly seen in roots.

5. Dead tract. These are seen as dark lines, formed due to groups of dead,
degenerated dentinal tubule.
 69

CEMENTUM
HISTOLOGY OF CEMENTUM
Cementum covers the dentin of the anatomical root of teeth

CHEMICAL COMPOSITION

1) Inorganic (45% - 50%)

Hydroxyapatite (Calcium phosphate)
Copper, Fluorine, Iron, lead
Potassium, silica, sodium, zinc

2) Organic matter (50 – 55%)

Collagen fibre
Interfibrinallar substance
(Mucopolysaccharides)

Histology: 2 types of cementum

1. Acellular cementum covers the cervical 3rd of root. It does not contain cells.
Sharpey’s fibres make up most of the structure of acellular cementum. They are inserted
at right angles into the root surfaces and penetrate deep into the cementum. Acellular
cementum also contains other collagen fibrils that are calcified and irregularly arranged.

2) Cellular cementum: They contain cells (cementocytes) in individual spaces (Lacunae

that communicate with each other through a system of anastomosing canaliculi. This is
less calcified.

FIG .1.33:Cellular and Acellular cementum

1. Acellular cementum (primary)

2. Cellular cementum (secondary
 70

ALVEOLAR BONE

FIG .1.34:Structure of alveolar bone

It consists of:
1) An external plate of cortical bone formed by Haversion bone and compacted
bone lamellae.

2) Inner socket wall of thin, compact bone called the Alveolar Bone proper
(Cribriform plate/lamina Dura)

3) Cancellous trabeculae between these 2 compact layer.

Cells and intercellular Matrix

Cells are osteocytes, enclosed within lacunae. The processes extend into
canaliculi that radiate from lacunae. When there is bone resorption, appearance of eroded
bone surfaces known as Howships is there. Lacunae are seen with multinucleated cells
known as osteoclasts.

Socket wall
It consists of dense, lamellated bone arranged in Haversian system and Bundle
bones. Bundle bone lies adjacent to the periodontal ligament containing large number of
Sharpe’s fibre. The cancellous portion, which found in inter radicular and interdental
spaces contains trabeculae, which encloses irregularly shaped marrow spaces lined with
flattened endosteal cells.
The periosteum – This covers the outer surface of the bone, compared of cells that can
change into osteoblasts and fibroblasts. The endosteum – This is the tissue lining the
internal bone surface. This is composed of a single layer of osteoprogenitor cells and
connective tissue.
 71

Other fibres
Elastic and oxytalan fibres are also seen.

Interstitial tissue – The blood vessels, lymphatics and nerves of periodontal ligament are
contained in spaces between the principal fibre bundles.

THE DENTAL PULP

The pulp is a specialized loose connective tissue
It consists of cells, fibres and a ground substance
In addition, defence cells, odontoblasts are a part of dental pulp

CELLS

a) Fibroblasts and fibres

Amongst the fibres some are of collagenous in nature. The Korff’s fibres
originate from among the pulp cells as thin fibres, thickened at the periphery of the pulp
to form relatively thick bundles that pass between the odontoblasts.

b) Odontoblasts

They give rise to odontoblastic process. Their body is columnar in shape with an
oral nucleae.Each cell extends cytoplasmic process into a tubule in the dentin

In the crown of the pulp, a cell-free layer can be found just inside the layer of
odontoblasts. This layer is known as “Zone of Weil) or Sub-odontoblastic layer, which
contains a network of nerve fibre i.e. sub odontoblastic plexus.
 72

Defence cells – Histiocytes, undifferentiated mesenchymal cells which are present close
to the capillary walls – pericytes

Intercellular substance – They consist of the

(i) ground substance

(ii) fibres

The ground substance is gelatinous and is called the cement substance the
fibres are of two types:
a) Pre collagenous or Reticular or Korff’s fibre
b) Collagenous fibres

Within the ground substance, the blood vessels, and lymph vessels are distributed.
 73

NOMENCLATURE OF DENTITION
1. Universal system:

Starts from right side upper third molar and finish at right side 3rd lower molar.

Permanent dentition:

Deciduous dentition:

ABCDE FGHIJ
TSRQP 0NMLK

if we want to say lower left first molar then 19.

Zsimondy and palmer system

Dentition is divided in four quadrants each has 1-8 teeth

12345678 9 10 11 12 1314 15 16
32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17

Permanent dentition:

87654321 12345678
87654321 12345678

Deciduous dentition

EDCBA ABCDE
EDCBA ABCDE
 74

Example : if permanent lower right first molar to be shown

FDI system :

Most followed

Mouth is divided in four quadrants

Upper right - 1 Upper left -2

Lower right -4 Lower left -3

No. from 1-8 in each quadrants

8-1 1-8
8-1 1-8

It is denoted by 2 no.

First no. denotes – quadrant

Second no. denotes teeth

Eg.- 46 means 4th quadrant and 6 th teeth i.e lower right first molar

It is called four six not fortysix

Deciduous dentition:

Quadrants 6
5
8 7

Teeth each quadrant 1-5

So 55 means upper right second deciduous molar.

SECTION - 2

PHYSIOLOGY
 75

SALIVA

Saliva is the fluid released into the oral cavity by salivary glands and is the result of both
secretion and excretion.

Functions of saliva

1. Helps formation of bolus by moistening solid food

2. Moistens epithelium and teeth and protects them
3. Flushes and clean oral cavity
4. Helps in speech by moistening epithelial surface
5. Helps digestion via ptyalin and maltose by hydrolyzing starch
6. Helps in perception of taste by dispersing and dissolving food
7. Excretes body metabolites (electrolytes water and protein)
8. Has bacteriolytic action via lysozymes and mutines
9. Decreases blood clotting time. Oral tissues bleed less than
rest of the body.
10. Regulation of body temperature – In dogs and cattle

Chemical Composition

 The composition varies from man to man, from one gland to another, from
food to food and in stimulated and resting saliva, average composition is
as follows:
 Water 99%, Solid 0.5%, inorganic 0.2%, organic 0.3%
 Inorganic constituents are bicarbonates, chlorides and phosphates of
calcium, magnesium, potassium and sodium.
 There are also thiocyanate, bromide, iodide, fluoride, and copper, oxygen
and carbon dioxide.
 Organic constituents are proteins (glycoprotein intrinsic salivary proteins,
serum proteins, like albumin and globulin, mucin, enzymes-ptyalin,
lysozyme, lipase, phosphates, vitamins – pantothenic acid, riboflavin,
nicotinic acid, and vitamin K, carbohydrate galactose, mannose, fructose,
glucose, desquamated epithelial cells, salivary corpuscles (resemble
leucocytes, derived from gingival sulcus)

Quantity of secretion

 The amount of saliva secreted varies from person to person, depending on

type of food taken, age, degree of mechanical stimulation, emotional
condition, etc.
 On an average, 1500 ml is secreted per day under normal condition.
Salivary flow is continuous.
 It varies from 3 to 110 cc per hour (average 20.6 cc) 25% contributed by
parotid, 70% submandibular and 5% sublingual gland.
 76

 The pH of Saliva varies from 5.6 to 7.6 (average is 6.8). the factors
influence pH are, type of diet, time of day, rate of flow, emotional state,
etc.

Control of Salivation

 Salivation is controlled exclusively by nervous system.

 The salivary glands are richly supplied with both sympathetic and
parasympathetic nerves.
 The parasympathetic supply to submandibular and sublingual glands
comes via the corda tympani nerve.
 These fibres arise in the superior salivatory nucleus in medulla oblongata.
The fibres pass through the geniculate ganglion of the facial nerve and
descend with this nerve, cross to chorda tympani and proceed along with
lingual nerve.
 It forms synapse with post ganglionic fibres from sub maxillary ganglion.
 The post-ganglionic neurons supply the secretory cells.
 The fibres leave the brain stem along with gloss pharyngeal nerve (IX),
join small superficial petrosal nerve and synapse in the otic ganglion. Post
ganglionic nerves supply the gland via auriculotemporal nerve.
 The postganglionic sympathetic supply for all the three glands
originates in the superior cervical ganglion. They course along with
external carotid artery and its branches.
 It is believed that there is independent innervation of the serous and
mucous cells. Stimulation of parasympathetic fibres produces highly
mucous saliva and a sympathetic stimulation produces a serous flow.
 Saliva is produced by an active process.
 It is thought that after an impulse arrives at the neuroglandular junction, a
substance is released which alters the permeability of the cells and the cell
content is emptied.
 Most probably, the fibres of different threshold innervate various types of
secretory cellos.
 That is why, with increasing stimulation, not only the concentration and
volume is augmented, but also the composition is altered.
 Unconditional reflex response is evoked by the presence of food in mouth
or movements of the jaws and tongue.
 The amount and composition of saliva depends on the nature of the
stimulation.
 Palatable food brings a large amount of saliva.
 Meet produces viscid, mucinous saliva and dry bread produces copious
saliva with high ptyalin content.
 Acids also act as a salivary stimulant.
 Conditioned reflex response may be provided by smell, sight or even
though of food.
 77

FACTORS AFFECTING SALIVARY FLOW

 The secretion of saliva is controlled exclusively by nerves.

 No hormone has been discovered which controls the rate of flow.
 It has been estimated that the total volume of saliva amounts to between
1.0 and 1.5 liters a day.

The Resting Flow

 The resting flow of saliva can be studied some hour after a meal, either by
means of Lashley cannula, or by allowing saliva o drain directly into a
breaker from the open mouth with the head bent forward to a horizontal
position.
 The average rate has been found to be 26 ml per hour and the range of
variation being 2.5 to 110 ml per hour.

Psychic Flow

 The experiments of Pavlov have proved the existence of conditioned

reflexes in the control of the salivary flow.
 It has been observed that by experience, stimulation primarily connected
with food may cause a secretion of saliva in animals.
 Lashley found that mention of food, even to a hungry individual, had no
effect on parotid flow, but the sight of food gave a positive response.

Unconditioned Reflexes

1. Presence of food in the mouth is powerful stimulus to salivation and experiments

show that this effect is made up of three main components.
2. The Taste forms one group of stimuli and there is evidence that different tastes vary
in their effectiveness.
3. Mechanical stimulation of the oral mucosa by the food
4. Masticatory movements which normally follow the taking of food also stimulate
human parotid. Mastication is accompanied by many sensory impulses, such as
mechanical irritation of the oral mucosa, pressure on the teeth, and kinesthetic impulses
from the masticatory muscle
5. Salivation is inhibited during muscular exercise and during the application of sensory
stimuli to the skin.
6. Mental work increases the secretion rate.
7. The acts of swallowing and yawning are followed by a transient increase in rates of
flow from the period and then usually a compensatory pause.
8. Chemical stimuli vary greatly in their effectiveness as salivary stimuli. Chemical
irritation of the lining of the stomach or any other stimulus leading to nausea is also a
powerful stimulus to salivation.
 78

9. Since nausea is usually a lead to vomiting, the value of saliva in diluting and
washing away the irritant is obvious.
10. Animal experiments have shown that the presence of food in the stomach causes a
flow of saliva known as the gastro salivary reflexes.
11. This is difficult to investigate in man.
12. Chronic irritation of the esophagus, resulting from disease e.g. Carcinoma of the
esophagus is often accompanied by excessive salivation.

SALIVA IN THE HEALTH & DISEASE, FACTOR AFFECTING ITS FLOW

 Saliva is a true secretion due to vital activity of cells of the three pairs of salivary
glands and the numerous buccal glands.
 The passage of various blood elements into the mouth is not well understood.
 The total amount of saliva secreted has been estimated as 1 to 1.5 liters per day.
 Its amount and compositions varies in the same individual depending upon
various factors.
 Saliva plays a dual role against the health of an individual.
 Based upon its constituents it performs various useful functions in maintaining the
oral and general health.
 On the other hand, it also contributes in giving rise to various pathological
conditions in the oral cavity.

SALIVA IN HEALTH

1. Physical and Mechanical functions

Lubrication: The mucin and water contents of saliva act as lubricant during
mastication, formation of bolus of food and swallowing.
Taste: Saliva converts the food materials into solution which is essential for the
sensation of taste.
2. Digestive functions
 The only important digestive enzyme present in the saliva is Ptyalin or salivary
amylase.
 The amylase contents vary considerably with age, with an average of 25 years, the
amount varies between 10-15 units of amylase per ml.
 The enzyme digests cooked starch only.
 It is the alpha type of amylase and breaks down the starch molecules
simultaneously in many place into large number of dextrin molecule which are
then more slowly attacked forming molecules.
 The action of amylase is inhibited by acids and the optimal pH for its activity is
6.8, therefore the main action of amylase remain in the mouth and in the stomach
before secretion of gastric hydrochloric acid.

3. Antibacterial function
A. Mechanical removal of bacteria: A large number of micro-organism are present
in the Saliva which contributes to its antibacterial effect.
 79

1. Leucotoxin and opsonin:

These substances are responsible for the presence and phagocyte activity of leucocytes in
saliva. It has been shown that saliva increases capillary permeability and poses
chemotactic activity towards leucocytes.The attraction of leucocytes is governed by
leucotoxin, polypeptide in the saliva.Opsonin is the substance which is responsible for
phagocytes by the leucocytes.It has been seen that in the absence of opsonin the
leucocytes do not show phagocytosis.

Lysozyme: Discovered by Fleming (1922). This enzyme breaks down the

polysaccharides hence its action is limited only on those bacteria which contains
polysaccharides.
Inhibin – Reported by Dold (1934). This substance inhibits the growth of lactobacillus
and diphtheria bacilli.
Mutinase – These are the substances in the saliva which render pathogenic organism into
non-pathogenic by mutation.

Gamma globulin
 The concentration of gamma globulin is more in the gingival sulcus sensitive of
the route of entrance for blood elements in the oral cavity.
 Their action against the bacteria is of two types.

a) Certain gamma globulin known as immunoglobulin possess antibody
properties.
b) The globulin attaches itself to lactobacilli and can both inhibit their growth
and cause their lysis.

B. Bacterial antagonism
 There is evidence that some organisms can not survive in the mouth in the
presence of certain other organisms.
 The action is based upon their metabolic products.
 It can be demonstrated that washing of blood agar culture of strepto cocci
colonies, produced inhibition effect on the other organisms.

4. Saliva and blood coagulation

 When freshly shed blood is diluted with saliva its clotting time is reduced.
 Saliva has been found to possess coagulation effects on the blood owing to the
presence of factor VII, IX, X PTA and Hageman factor.

5. Buffering power of saliva

 It is the capability of the saliva to resist against the change in pH.
 Bicarbonate is the strongest buffer in saliva and the phosphate also plays some
role, when proteins are chief buffers of plaque.
 Buffers work by converting highly ionized substance acid or alkali in the more
weakly ionized substance.
 80

 Unstimulated saliva which has lower bicarbonate content is a less powerful buffer
near naturality.

6. Water balance
 As shown by Cannoh (1934) the ‘dry mouth reflex’ stimulates the secretion of
saliva, which prevents drying of the pharynx and thirst is avoided.
 But if the body tissues are short of water, the reflex does not occur and the thirst is
satisfied by intake of water.

7. Excretion
 Saliva is a route of excretion also, by which certain substances are excreted.
 It can be effective only for those substances that are either destroyed or rendered
insoluble in the gut after swallowing.
 Mercury & lead are excreted through saliva in poisoning cases but are re-observed
by the intestine, and cannot be considered as true excretion.
 On the other hand excreted glucose in diabetic cases is destroyed in the mouth and
excretion of viruses in viral infection is also destroyed in the G.I.T, which can be
taken as true excretion.

SALIVA IN DISEASE
Precipitation of calculus
 Calculus is believed to be an important factor in causing periodontal disease.
Histological studies indicate that all the constituents of calculus are derived from
saliva such as mucin, inorganic salts and micro-organisms.
 Saliva is a saturated solution of calcium phosphate.
 Some of the insoluble calcium phosphate is present in colloidal form and some is
bound to salivary proteins.
 Various views have been put up regarding the precipitation and formation of
calculus.
 Presence of CO2 in saliva is important in keeping the calcium in solution form.
 The loss of CO2 from saliva resulting in precipitation of calcium salts is the most
widely accepted view.
 Enzyme phosphates releases phosphate ions from organic phosphates in saliva
and thus by mass action causing precipitation, has also been reported.

Dental plaque:

 Dental plaque is a thin yellowish film found on the surface of teeth which are
inaccessible to brushing.
 Mucin and micro organism from saliva are the main factors responsible for the
formation of plaque, which leads to caries and calculus formation.
 It is firmly held on the tooth surface and can not be removed by rinsing and
stream of water.
 The microscopic studies show that the plaque consists of closely matted
organisms of filamentous type embedded in a matrix of uncertain origin.
 81

 It also contains various type of bacterial, epithelial cells and food debris.
 The factors concerned in the formation of plaque are not well understood.
 It is believed that bacteria growing on the tooth surface, by acid production, cause
the precipitation of mucin which would entangle bacteria and provide a medium
for further growth and repetition of cycle.

Dental caries

 The pH of saliva plays an important role in the incidence of caries.

 Calcium phosphate is insoluble at neutrality but if the saliva becomes acidic of
particular pH will be reached at which the solubility of calcium phosphate
becomes so high that the concentration of ions in the solution failto saturates it.
 Below this critical pH the inorganic material of the tooth will be dissolved in
saliva. This pH is usually between 5.5 and 6.5 resulting in caries.

Role of salivary enzymes:

 The enzyme of saliva is potential etiologic factors in gingival and periodontal

diseases.
 The enzymes normally contained in saliva are derived from glands, bacteria,
tissues and leucocytes.
 Certain enzymes which increase in saliva during gingivitis and periodontal
disease are: Hyaluronidase, lipase, B-glucuronidase, chondroltin sulfatase, amino
acid decarboxylases, catalase, peroxidase and collagenase.
 Many components of gingival and connective tissues are good substrates for the
activity of these enzymes.
 The acid mucopolysaccharides, hyaluronic acid and chonroitin sulfate in the inter-
cellular substance of the gingival epithelium and connective tissue are destroyed.
These enzymes producing a break in the continuity of the oral epithelium.
 This break in continuity causes invasion of bacteria and their toxins into the
tissues giving rise to the pathological conditions.
 82

BLOOD

 Blood is a connective tissue in fluid form.

 It is also known as fluid of growth because it carries nutritive substances from the
digestive system.
 It can also be called the fluid of health since it protects the body against the
diseases and get rid of waste products.

Properties:
1. Colour: Red in colour. Arterial blood is scarlet red and venous blood is purple red.
2. Volume: 5 liters in normal adult.
3, Reaction and pH: Slightly alkaline and its pH is 7.4 in normal conditions.
4. Specific gravity. 1.052 – 1.061.
5. Viscosity: Five times more viscous than water.

COMPOSITION

 Blood contains the blood cells which are called formed elements and the liquid
portion is known as plasma.

BLOOD CELLS (45% OF TOTAL VOLUME OF BLOOD)

They are three types:
a) Red blood cells or erythrocytes
b) White blood cells or Leukocytes
c) Platelets or thrombocytes

PLASMA

 55% of total volume of blood is plasma.

 It is a straw coloured clear liquid. It contains 91-92% water and 8-9% solids.
 The solids are organic and inorganic substances.

Organic substances are:

a) Protein: albumin, globulin, fibrinogen

b) Carbohydrates: glucose
c) Fats: neutral fats, phospholipids and cholesterol
d) Amino acid
e) Non proteins nitrogenous substances: ammonia, creatine, creatinine, urea, uric
acid f) External secretions: hormones
g) Enzymes: Amylase, alkaline phosphatase, acid phosphatase, lipase, protease,
esterase etc.
h) Antibiotics: immunoglobulin.
 83

Inorganic substances are:

Sodium, calcium, potassium, magnesium, chloride, iron, iodide, copper,
phosphates.
Gases present in plasma
Oxygen, carbon dioxide

FIG .2.2: RBC and Different types of WBC

FUNCTIONS OF BLOOD:

1. Nutrient function:
 Substance like glucose, amino acid, lipids and vitamins derived from the
digested food absorbed from the gastrointestinal tract and carried to
different parts of the body.

2. Respiratory function
 Transport of gases is done by the blood.

3. Excretory Function:
 Waste products formed in the body are removed by blood and carried to
the excretory organs like kidney, skin, liver etc.
 84

4. Transport of Hormones and Enzymes:

 Hormones are transported from the source organ to different parts of the
body.

5. Regulation of water balance

6. Regulation of acid base balance. Plasma protein and hemoglobin acts as buffers and
help in regulation of acid base balance.
7. Regulation of body temperature.

8. Storage function
 Water, protein, glucose, sodium, potassium are very important
requirements of the body tissue.
 Blood act as a readymade reservoir for those substances.
 During starvation, fluid loss, electrolyte loss, these substances are taken
from the blood by the body tissues.

9. Defensive function:
 White blood cells are responsible for these functions.
 Neutrophills and monocytes engulf the bacteria by a process known as
phagocytosis. Lymphocytes are involved in the production of antibodies.
 Eosinophils are responsible for detoxification disintegration and removal of
foreign proteins.

Normal values:

RBC
Adult male 4.5 – 6.5 millions per cubic mm of blood
(Mean 5.5 X10 12 / L)
Adult female 3.8 – 5.8 million per cubic mm
(Average – 4.8 X10 12L)
Life 120 days

WBC
Adult – 4000 – 11000 (1 cu. Mm of blood
Poly morphs – 50-75% (3000 – 6000)
Eosinophils 2-4% (150-450)
Basophils 0 –1% (0 – 100)
Monocytes 2-6% (200-600)
Lymphocytes 20-30% (1500-2700)

Life span of WBC

N 2-5 days
E 7-12 days
B 12-15 days
M 2-5 days
L ½ - 1 day
 85

Platelets
Adult – 1500000 – 400000/cumm of blood
Life span 6-10 days

Hemoglobin (Hb)
Adult male 13-18.0 gm/dl
Adult Female 11.5 – 16.5 gm/dl.

Bleeding time
Ivy’s method 2-7 minutes
Template method 2.5 – 9.5 min

Clotting time
Lee & White method - 4-9 min at 67 Degree C.
 86

MASTICATION

 It is the process of cutting and breaking down the large food particles into
small particles and grinding them into a soft bolus.

Significance of mastication

 It is the first mechanical process to which food is subjected.

 The following are the significances:

a) Breaking down into smaller particles

b) Mixing of saliva with food substances thoroughly
c) Lubrication and moistening of dry food by saliva so that bolus can be easily
swallowed.
d) Appreciation of the taste of the food.
e) Increases the surface area of the food for the digestive enzyme to act.

Nervous control of mastication

 It is mostly a reflex process.

 It is the result of a highly complex neuromuscular activity.
 It can be carried out voluntarily also.
 The center of the mastication is situated in medulla and cerebral cortex.
 The muscles of mastication are supplied by Vth cranial nerve, trigeminal nerve.
 Teeth, temperomandibular joint and muscles of mastication are responsible for the
process of mastication.
 Tooth contacts occur during most of the chewing strokes.
 The maximum load on natural teeth during chewing is 8-15 kg.
 The tongue directs the food between the teeth and exerts a crushing effect by
pressing the substance against the hard palate.
 The cheeks and lips keep the food from escaping between the teeth.
 Once the bolus formation is ready it pushes back to oropharynx for deglutition.
 87

DEGLUTITION
The swallowing is the food is known as deglutition.

It occurs in three stages:

 Oral stage, when food from the mouth enters the pharynx.
 Pharyngeal stage when food enters the esophagus from pharynx
 Esophageal stage when food enters stomach from esophagus.

Oral stage (First stage)

 It starts after mastication.

 Once the bolus is formed it is placed over posterodorsal surface of the tongue.
 This is called preparatory stage.
 Then the front part of the tongue is retracted and depressed, posterior part is
elevated. This makes the bolus to move backward.
 Then tongue presses against hard palate which helps the food bolus to move
backwards.

Pharyngeal stage (Second stage)

 It is an involuntary stage.
 Food passes from pharynx to esophagus at this stage.
 The various movements are co-coordinated so that the bolus enter only into the
esophagus and prevent the entry into nasopharynx, back to mouth & larynx.
 The entry of food to nasopharynx is prevented by an extension of soft palate
known as uvula.
 The entry of food into larynx is prevented by epiglottis and back entry to oral
cavity is prevented by position of the tongue against hard palate mainly.
 All the above mentioned factors act together so that the bolus moves easily into
esophagus.
 The whole process takes place with in 1-2 seconds and this process is purely
involuntary.

Esophageal stage or third stage

 This is also an involuntary stage.

 Function is the transportation of food from esophagus to stomach.
 The movements of esophagus are specifically organized for this function and the
movements are called peristaltic curves.
 By this movement food is always propelled down along the GI tract, away from
the mouth.
 88

Two types of peristaltic contractions are produced by esophagus.

a) Primary peristaltic contraction: When bolus reaches the upper part of

esophagus.
a) Secondary peristaltic contraction. This arises in esophagus locally due to the
distention of upper esophagus by the bolus

Deglutition reflux

 Though the beginning of swallowing is a voluntary act, later it becomes

involuntary and is carried out by a reflex action called deglutition reflex.
 The center if deglutition is located t the floor of the fourth ventricle in medulla
oblongata of brain.
 89

PHONATION

 Speech is an expression of thought by production of articulate sounds bearing a

definite meaning.
 It is brought about by co-ordinate activity of different parts of brain, particularly
the motor, sensory areas

Mechanism of speech

 It is by the coordinated activities of central speech apparatus and peripheral

speech apparatus.
 The central apparatus consist of higher centers i.e. cortical and sub cortical centers
in brain.
 Peripheral apparatus includes larynx or sound box, pharynx, mouth, nasal cavities,
tongue and lips.

Development of speech

First stage

 In first stage in the development of speech is the association of certain

words with visuals, tactile, auditory and other sensations aroused by
objects in the external world.

Second stage

 New neuronal circuits are established during the development of speech in

this stage.

Nervous control of speech

 Speech is an integrated and well co-coordinated motor phenomenon.

 So many parts of the CNS are involved in this mechanism.
 In about 95% of human being, the left cerebral hemisphere is functionally
dominant in those persons who are right handed.

Applied physiology

The following are the disorders of speech:

1. Aphasia: Inability to speak words

2. Anarthria or Dysarthria: Inability or difficulty to speak
3. Agnosia: Inability to understand the words
 SECTION - 3

PATHOLOGY &
MICROBIOLOGY
 90

INFLAMMATION
DEFINITION

Inflammation is defined as the local response of living mammalian tissues to injury due
to any agent. It is a body defense reaction in order to eliminate or limit the spread of
injurious agent as well as to remove the consequent necrosed cells & tissues.

The agents causing inflammation may be as under :-

1. Physical agents. Heat, Cold, Radiation, Mechanical trauma .

2. Chemical agents. Organic & Inorganic poison.

3. Infective agents. Bacteria, Viruses & their toxins.

4. Immunologic agents. Cell mediated and Antigen. Antibody reactions.

SIGNS OF INFLAMATION.

The Roman writer Celsus in 1st centaury AD named the famous four cardinal
signs of inflammation as

(a) RUBOR (Redness)

(b) TUMOR (Swelling)

(c) CALOR(Heat)

(d) DOLAR(Pain)

To these, fifth sign “ FUNCTIO LAESIA” (loss of functions was later added by
Virchow).

Types of Inflammation :-

Depending upon the defense capacity of the heart and the duration of response.
Inflammation can be classified as acute and chronic.

1. Acute Inflammation : is of short duration and represents the early body reaction
and is usually followed by repair.

2. Chronic Inflammation : is of longer duration and occurs either after the

causative agents of acute inflammation persists for a long time or the stimulus is such that
if induces chronic inflammation from the beginning.
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ACUTE INFLAMMATION.The changes in acute inflammation can be conveniently

described unde 2 headings :-

1. Vascular events.

2. Cellular events. VASCULAR EVENTS

Transient Vasoconstriction of arterioles

Persistent Progressive Vasodilatation

Increase in local hydrostatic Pressure

Slowing /Stasis of Microcirculation

Leucocytic Margination

Altered Vascular Permeability

CELLULAR EVENTS

Exudation of leucocytes Phasocytosis

Changes in fermed elements of blood Recognition and attachment

stage

Rolling and adhesion Engulfment stage

Emigration Degranulation stage

Chemotoxis Killing of degradation

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Chemical Mediators of inflammation :-

These are a large and increasing number of endosenous compounds, which can
enhance vascular permeability. The substances acting as chemical mediator of
inflammation may be released from the cells, the plasma or damaged tissue itself. They
are broadly classified into 2 groups :

Mediators released from cells

Mediators originating from plasma

Cell derived mediators:

Vasoactive amines : histamine and serotouin

Arachidonic acid metabolites (eicosanoids)

Lysosomal components

Platelet activating factor

Cytokines

Nitric oxide and oxygen metabolites

Plasma derived mediators

These include the various products derived from active and interaction of 4 interlinked
systems : kinin. dotting fibrinolytic and complement.

The inflammatory cells:

derived from 2 sources with common morphology, function and origin.

Blood monocytes – 4-8 % of circulating leucocytes.

Tissue macrophages

Macrophages in inflammation

Histiocytes, macrophages preseur in CT

Kupffer cells ,macrophages of liver

A lveolar macro phages in lungs

Macrophages of bone marrow

 93

Systemic effects of acute inflammation

Fever

Leucocytosis

Lymphangitis – lymphadenitis

Shock

Fate of Acute inflammation

Resolution

Healing by scarring

Suppuration

Chronic inflammation.

CHRONIC INFLAMMATION

Chronic inflammation can be caused by one of the following 3 ways

Chronic inflammation following acute inflammation

Recurrent attaches of acute inflammation

Chronic inflammation starting demove

General features of chronic inflammation

Mononuclear cell infiltrate

Tissue destruction / necrosis

Proliferative changes

Systemic effects of Chronic Inflammation

Fever

Anaemia

Leucocytosis
 94

ESR erythrocyte sedimentation increases

Amyloidosis.

Types of Chronic Inflammation – 2 types

Chronic non-specific inflammation

Chronic qranulomatour inflammation.

 95

DEGENERATION
Cell Injury : Cell injury is defined as a variety of stresses a cell encounters as a result of
changes in its internal and external environment.

All cells of the body have in built mechanism to deal with changes in environment to
some extent. The cellular response to stress varies and depends upon:

The type of cell and tissue involved

On extent and type of cell injury

Normal Cell

Increased functional Mild to moderate Severe Persistent

demand stress stress

Adaptations Reversible Cell Irreversible

injury Cell injury

Atropy, hypertro Degenerations

phyhyperplascs Subcellular alterations Cell death
Metaplasic Dysplasics intercellular
accumulations

Stress removed Stress removed

Normal cell Repair and

restored Healing
 96

NECROSIS
Definition: Necrosis is defined as focal death along with degeneration of tissue by
hydrolytic enzymes liberated by cells. It is invariably accompanied by inflammatory
reaction.

Necrosis can be caused by various agents such as: hypoxia, chemical & physical
agents, microbial agents and immunological injury.

WOUND HEALING

Healing is the body response to injury in an attempt to restore normal structure and
function. The process of heating involves 2 distinct processes:-

Regeneration – when healing takes place by parenchyma cells and usually results in
complete restoration of the original tisssues

Repair – when the healing takes place by proliferation of connecting tissve elements
resulting in fibrous & scarring

Wound healing:- Healing of skin wounds provides a classical example of combination

of regeneration and repair described above.

This can be accomplished in the following two ways

Healing by primary intention

Healing by secondary intention

HEALING BY PRIMARY INTENTION :-

This is defined as healing of a wound which has the following characteristres

Clean & uninfected

Surgically incised

Without much loss of cells and tissues and

Edges of wound are approximated by surgicalsutures

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SEQUENCE OF EVENTS:-

Initial hacmorrhage :- Immediately after injury, the space between the

approximated surfaces of incised wound is filled with blood which then clots and
seals the wound against dehydration and infection.

Acute inflammatory response :- This occurs within 24 hrs with appearance of

polymorphs

Epithelial changes:- The basal cells of the epidermis from both the cut margins start
proliferating and migrating towards incisional space in the form of epithelial spurs.

Organization :- By 3rd day fibroblasts also invade the wound area. By 5th day new
collagen fibrils start forming. In 4 weeks, the scar tissue with scanty cellular and
vascular elements, a few inflammatory cells and epithelialised surface is formed.

Suture tracks :- Each suture track is a separate wound and incites the same
phenomena as in healing of the primary wound.

HEALING BY SECONDARY INTENTION:-

This is defined as healing of a wound having the following

characteristics:-

Open with large tissue defect, at times infected

Having extensive loss of cells and tissues and

The wound is not approximated by surgical sutures but left open.

Sequence of events:-

Initial haemorrhage

Inflammatory phase

Epithelial changes

Granulation tissue - The main bulk of secondary healing is by granulations.

Granulation tissue is formed by proliferation of fibroblasts and neovascularisation
from adjoining viable elements.

Wound contraction – contraction of the wound is an important feature of secondary

healing not seen in primary healing.

Presence of infection – Bacterial contamination of an open wound delays the process

of heating due to release of bacterial toxing that provoke necrosis & thrombosis.
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Complication of wound Healing

1. Infection

2. Implantation

3. Pigmentation

4. Deficient scar formation

5. Incision hernia

6. Hypertrophied scars & keloid formation.

7 Neoplasia
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STAINING OR DISCOLOURATION OF TEETH

The normal colour of Primary teeth’s bluish white. The color of permanent teeth is
grayish yellow. Grayish white or yellowish white. The color of teeth is determined by
the translucency and the thickness of the enamel, the thickness and color of the
underlying dentin, and the color of the pulp. Alterations in the color may be physiologic
or Pathologic and endogenous or exogenous in nature.

Classification of tooth Discoloration/Staining

Tooth discoloration can be classified as either extrinsic or intrinsic.

Extrinsic discoloration.

Extrinsic discolorations are found in the outer surface of the teeth are usually local
origin such as tobacco stains. Some extrinsic discoloration, such as the green
discoloration associated with the Nasmyths membrane in children , and tea and tobacco
stains are almost impossible to eliminate without grinding because the stains penetrative
surface of the crowns and are impossible to remove by chemical means above.

Intrinsic discoloration.

Intrinsic discolorations are stains within the enamel and dentin caused by the
deposition or incorporation of substances within their structures, such as tetracycline
stains. If incorporated into dentin, they become visible because of the translucency of
enamel. They can be related to phases of tooth development.

Causes of tooth discoloration

The principal causes of teeth discoloration are :-

Percompositions of pulp tissue.

Excess hemorrhage after pulp removal.

Trauma

Medicaments

Filling Materials
 100

In addition to these causes, teeth may be discolored because of general systemic

conditions.

e.g. Red/Purple discoloration - Congenital Porphyria.

Violaceous- hereditary opalescent dentin.

Mottled brown - Endemic Fluorosis
Grayish brown - Erythroblastosis fetalis
Brown - Jaundice
Yellow /gray brown - Tetracyclines

Discoloration from systemic causes occurs only during developmental stages of the
teeth.
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ANOMALIES/DEVELOPMENTAL DISTURBANCES OF
ORAL STRUCTURES

JAWS

Agnathia - extremely rare congenital defect characterised by absence of maxilla or

mandible.
Micrognathia. Means a small jaw either maxilla or mandible may be affected.

LIPS AND PALATE

Double Lip- Is an anomaly characterised by a fold of excess tissue on the inner mucosal
aspect of the lip.
Cleft Lip – Results due to defect in development or maturation of embryonic processes.
Heredity is an important etiologic factor.
Types - Unilateral partial cleft lip.

Unilateral complete cleft lip.

Bilateral partial cleft lip
Bilateral complete cleft lip
Midline cleft/Hair line lip.
May or may not be associated with cleft /palate.

ORAL MUCOSA
Fordyce’s Granules. This is not a disease of the oral mucosa, but rather a
developmental anomaly characterised by collections of sebaceous glands are various
sites in the oral cavity.

GINGIVA

Fibromatosis Gingiva– Diffuse fibrous orvergrowth of gingival tissues.

TONGUE

Micro glossia- is a rare congenital anomaly manifested by the presence of a small or

rudimentary tongue.
Macroglossia – enlarged tongue.
Ankyloglossia – Occurs as a result of fusion between tongue and floor of the mouth.
Also called “Tongue tie.
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Cleft Tongue – Rare condition due to lack of fusion of lateral lingual swellings.
Fissured tongue- is a malformation manifested clinically by numerous small furrows or
grooves on the dental surface.
Hairy tongue- Characterised by hypertrophy of the filiform papillae of tongue.
Benign Migrating Glossitis. Charactersied by multiple areas of desquamations of the
inform papillae of the tongue in an irregular pattern.
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ANOMALIES OF THE TEETH

Anomaly is derived from ‘Anomalia’ a Greek word meaning developmental

disturbance.Teeth are of importance for aesthetics, speech, mastication and development
of occlusion. These anomalies have effect on functions of teeth.

Hypoplasia has effect on aesthetics and causes psychological inferiority complex.

Position, size and number of teeth have adverse effect on quality of speech. It has effect
on mastication especially anodontia. Premature loss or retention of primary teeth results
in malocclusion. Social stigma e.g. Hutchinson’s teeth has powerful effects.

Causes:

Some of these factors are:

(1) Hereditary
(2) Systemic disease
(3) Intake of drugs e.g. tonic containing metallic Ions and antibiotics
(4) Excessive fluoride content or water
(5) trauma
(6) X-ray radiation
(7) Infections
(8) Nutritional deficiencies.

Anomalies will occur if these factors come into play during formation of enamel,
dentin and cementum.

The Anomalies can be considered under the following headings: Size, number, form,
structure and eruption.

Size:

a) Microdontia – the teeth are smaller in size than normal teeth. The disturbance may be
localized in areas 2/2 or 8/8. the lateral incisors may be peg or cone shaped. Rarely, the
condition may be generalized.

b) Macrodontia: Teeth are larger in size. The disturbance may be localized or

generalized. Roots are abnormally long. This is rarely seen.
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Form:

a) Dilaceration: This refers to a bend in the root or crown of a forming tooth. Due to
trauma crown or root may form at an angle and this presents problem at the time of
extraction.

b) Fusion: fusion of two teeth results from union of two normally formed teeth from
separate tooth germs. This fusion may be partial or complete.

c) Concrescence: Fusion in this case occurs after root formation has been completed.
The roots are united by cementum.

d) Gemination: This can occur in temporary as well as permanent dentitions. In this two
teeth are produced from single bud. The result is a tooth with two crowns common pulp
chamber and single root.

e) Dens in Dente: This odontoma is though to arise from invagination of developing

crown before calcification. It varies in extent from an exaggerated lingual pit to the
appearance or a complete tooth within a tooth.

Number:
a) Anodontia: there may be complete absence of both dentitions in one or both jaws. It
is very rare. In other cases, many teeth may be congenitally missing. Commonly
affected teeth are 8/8, 4/4, 2/2, 8/8, 4/4

b) Supernumerary teeth: Very rarely, at birth, one or two teeth are found in the incisal
region. This requires extraction. These teeth are called ‘Predeciduous Dentition’.
Sometimes teeth are found embedded under tooth of permanent dentition and these are
called ‘Post permanent Dentition’. Mesiodens are found in the midline between 1/1.
These may be impacted, palatally or labially placed. Another is in 4/4 region. To
prevent malocclusion and for reasons of aesthetics, extraction of teeth is indicated.

Structure:
a) Enamel Hypoplasia: In this, enamel formation of deciduous and permanent dentition
is defective or absent. Thin brown stained enamel chips off easily. There may be small
grooves pits or fissures on the enamel surface. The disturbance is result of malnutrition
or endemic fever at time of crown development. Teeth usually affected are 1/1 and 6/6.
1/1 6/6

b) Amelogenesis Imperfects: This is a rare idiopathic condition in which there is

generalized defective enamel formation, before the matrix undergoes calcification.

c) Dentinogenesis Imperfecta: This also is a rare idiopathic condition in which there is

defective dentin laying down.
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Eruption
a) Premature eruption: Some teeth of deciduous or permanent dentition erupt into the oral
cavity prior to dates of eruption accepted as normal.

b) Delayed eruption: Some teeth especially deciduous and permanent may appear much
later than when they should have erupted.

c) Impacted teeth: Some teeth may be prevented by mechanical obstruction of bone or

fibrous tissue from erupting into the oral cavity. 8/8 is invariably impacted.
8/8

d) Ankylosed teeth: A few teeth, which are not exfoliated, get fused to bone and may
remain submerged.

FIG. Dilaceration of lateral incisor. FIG. Molar showing Taurodontism.

FIG. Dentinogenesis Imperfecta Type I. FIG. Anterior teeth showing Enamel

hypoplasia
 106

FIG. Amelogenesis Imperfecta. FIG. Peg shaped lateral incisors.

 107

FLUOROSIS OF TEETH
Etiology

Fluorosis of teeth is due to presence of excess fluorine in drinking water. It is

specially affected by ingestion of fluoride containing drinking water during the time of
tooth formation.
Normally, water contains fluorine, at a level of 0.8 to 1 PPM. If it is more than 1
PPM, it may lead to fluorosis.

Histopathology

It is a type of hypoplasia due to disturbance of ameloblasts during the formative

stage of tooth development. The cell product, the enamel matrix is defective and
deficient. The higher level of fluoride also interferes with calcification process of matrix.

Clinical features
Depending upon the level of fluoride in the water supply. There is a wide range of
severity in the appearance of mottled teeth varying from

1. Occasionally white flecking and spotting of enamel

2. Mild changes manifested by white opaque areas involving more of tooth
surface areas
3. Corroded appearance of tooth.
This fluorosis may affect the most of the tooth surfaces. Teeth moderately or severely,
affected may have a tendency for wear and even fracture of enamel. All these features
are known as Mottling of enamel.

Severe mottling in Fluorosis

Treatment

1. Mottled enamel is frequently stained an unsightly brown colours. For

cosmetic reasons, it has become the practice to go for bleaching the
affected teeth.
2. For decreasing the intake of fluorine, De-fluoridation of water can be taken
up.
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WASTING DISEASES OF TEETH

Attrition
Defined as the physiologic wearing away of a tooth as result of tooth-to-tooth
contact, as in mastication. This occurs only on the occlusal, incisal, proximal surfaces of
tooth. It is associated with aging process.
It may be seen in the deciduous dentition as well as permanent, but severe
attrition is seldom seen in deciduous, as they are not retained normally for any great
period of time. However, children suffering from dentinogenesis imperfects or
amelogenesis imperfecta may show pronounced attrition from ordinary masticatory
forces.

Clinical manifestations
1, Appearance of small polished facet on a cusp tip or ridge.
2. Flattening of incisal edge.
3. Because of slight mobility of teeth in their sockets, a manifestation of the resiliency of
the periodontal ligament, similar facets appear at the contact points on the proximal
surface of the teeth.
4. As the person becomes older there is gradual reduction in cusp height and consequent
flattening of the occlusal inclined places.

Variations
1. Men exhibit more severe attrition than women of the same age group.
2. May also be a result of differences in the coarseness of the diet or of habits such as
chewing tobacco or bruxism, either of which would predispose to more rapid attrition.
3. Certain occupation, in which the worker is exposed to an atmosphere of abrasive dust
and cannot avoid getting the material into his mouth, also are important in the etiology of
severe attrition.

Fate
1. Advance attrition in which enamel has been completely worn away in one or more
areas, sometimes results in an extrinsic yellow or brown staining of the exposed dentin
from food or tobacco.
2. Loss of cuspal interdigitation
3. Exposure of dentinal tubules and the subsequent irritation of odontoblastic process
result in formation of secondary dentin.
4. Pulp horns may be exposed.

ABRASION
Abrasion is the pathologic wearing away of tooth substance through some
abnormal mechanical process. Abrasion usually occurs on the exposed root surfaces of
teeth, but it may also be seen on incisal or proximal surfaces.
 109

Causes
1. Injudicious use of toothbrush – in such cases abrasion manifests itself as a ‘V’
shaped or wedge shaped ditch on the root side of the cemento-enamel junction in teeth
with some gingival recession. The exposed dentin appears highly polished. The angle
formed at the depth of the lesion, as well as that at enamel edge is rather a sharp one.

2. Occupation or habit of the patient:

A) The habitual opening of bobby pins with the teeth may result in notching of
the incisal edge of maxillary central incisor
B) Similar notching may be noted in carpenters, shoemakers or tailors who hold
nail, tacksor pins between the teeth
C) Pipe smokers

3. Improper use of dental floss and toothpicks may produce lesions on the proximal
surface (exposed root), which also should be considered a form of abrasion.

Fate
The exposure of dentinal tubules and the consequent irritation of the odontoblastic
process stimulate the formation of secondary dentin.

EROSION

Erosion is defined as loss of tooth substance by a chemical process that does not
involve known bacterial action.

The smooth lesions, which exhibit no chalkiness, occur most frequently on the
labial and buccal surfaces of teeth. Shallow, broad, smooth, manifests the loss of tooth
substance highly polished, scooped out depression on the enamel surface adjacent to the
cemento-enamel junction. The lesion usually involves several teeth.

Etiology:

Unknown, but it may be due to

1. Citrate content of saliva
2. Local acidosis in the periodontal tissues resulting from damage dueto
. traumatogenic occlusion
3. Chronic vomiting cases – Loss of enam
el through dissolution by gastric
hydrochloric acid.
4. Consumption of large quantities of highly acidic carbonated beverages or
lemon juice.
5. Industrial workers – working in industries involving the use of acids.
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Treatment

1. Attrition: treatment of psychological. Restoration is given to protect dentin and

pulp. Dentures and occlusal splints restore vertical height and lost tooth.

2. Abrasion: faulty habits must be corrected. Enamel and dentin margins to be

restored by conservative treatment.

3. Erosion: A change of profession is suggested. Alkaline toothpastes are

prescribed. Conservative treatment is done to preserve pulp and restore aesthetics.
 111

ORAL MANIFESTATION OF SYSTEMIC DISEASE

Certain bacteria, viruses and fungi produce diseases, which are manifested in or
about the oral cavity. The microbial specificity or non specificity is characteristic of
infectious diseases wherever they may occur in the body.

SYPHILIS

It is also known as lues disease and is caused by spirochete, Treponema pallidum.

It may be either acquired or congenital (mother). The organism can infect the person
through mucous membrane or abraded skin or through sexual intercourse with a syphilitic
person. It may also result from kissing. Cases have been reported where dentist got
syphilis in the nail bed through saliva.

The clinical course of syphilis is divided into three stages, i.e. primary, secondary
and tertiary. The oral manifestations of these stages are mentioned below.

Primary Stage:

After incubation period of about one month, the Syphilitic chancre develops at the site of
infection. Extra genital chancre is found on the lips, tongue and palate. These chancre
may appear as small abrasions or resemble the penile chancre. These usual primary
lesions are elevated, ulcerated nodule showing local indurations and producing regional
lymphadenitis. Such a lesion on the lip may have a brownish, crusted appearance.

The intraoral chancre is an ulcerated lesion covered by a grayish white membrane, which
may be painful because of secondary infection. These chancre contain highly contagious
spirochetes, which are clearly visible by darkfield examination. An enlarged lymph node
is always found along the lymphatics draining the area of the chancre.

Secondary Stage:

Also called metastatic stage, which commences about six weeks after the primary
lesion. In this stage there are diffuse eruptions on the skin and mucous membrane. On the skin,
macules or papules may be there. The oral lesions, called “Mucous pathes” are usually
multiple, painless, grayish white plaques overlying an ulcerated surface. They occur
mostly on the tongue, gingival or buccal mucosa. They are often ovoid or irregular in
shape and are surrounded by an erythematous zone. The patches coalesce to form so
called ‘Snail track ulcer’. The patches are highly contagious and the serological reaction
is always positive.

Tertiary Stage

These lesion usually do not appear for several years and involve chiefly
cardiovascular system, the central nervous system and certain other tissue and organs.
 112

The gumma is the chief localized tertiary lesion and occurs mostly on the skin, mucous
membrane, liver, testes and bone. The lesion varies from a millimeter to several
centimeters in diameter. The tonsils, soft palate, hard palate and tongue may be affected.
It is initially yellow, homogeneous mass of rubber like consistency, which undergoes
degeneration and produce ulceration. These ulcers have soft edge with depressed base
and discharge yellow fluid. Bone of hard palate and nose may be affected leading to
necrosis and perforation of hard palate and collapse of nasal bridge. Tongue may be
involved either by small gummas and coalescing to form large gumma. The most
frequent lesion, on the tongue is development of chronic superficial glossitis in which it
is divided into many lobules by fissures. There may be leukoplakia due to involvement
of skin, which become edematous.

CONGENITAL SYPHILIS

It is transmitted to the offspring only by infected mother and is not inherited.

There are a number of stillbirths due to congenital syphilis.
Person with this disease manifest a variety of lesions including high palatal arch,
saddle nose, relative protuberance of mandible, rhagades and saber skin.
In the classical disease the Hutchinson’s triad, hypoplasia of the incisor and molar
teeth, eighth nerve deafness and interstitial keratitis is present.

DIABETES

This disease is due to disturbances of Insulin, secretion by pancreas. It is

characterized by loss of weight, fatigue, marked thirst, marked hunger and polyuria.

Oral features are dryness of mouth (Xerostomia) and sweet taste in mouth.
Tongue is red and painful with marginal indentations and coating on the dorsal surface.
There is diffuse erythema of oral mucosa. In these individuals there is tendency o
formation of supragingival calculus with gingival which are spongy, purplish and bleed
easily. There is pocket formation and more incidences of gingival and periodontal
abscess resulting in loss of tooth

TUBERCULOSIS

Oral lesions in tuberculosis are rare. Oral tuberculosis however is always a

secondary lesion and occurs in patient affected with advanced pulmonary tuberculosis.

An increased incidence of gingivitis and chronic destructive periodontal disease as

well as alveolar bone changes, characterized by enlargement of the cancellous spaces
have been reported in some cases but are not confirmatory. The sites most frequently
involved with ulcers are pharynx, tonsils, tongue, and hard and soft palate. They may
occur on the buccal mucosa and at the commissures of the lips.
 113

VITAMIN DEFICIENCIES

Vitamin ‘A’

Source – Fish liver oil, Milk, egg yolk and butter

Dosage – Adult 5000 I.U/day, 4-6 yrs 2500 IU, pregnancy 6000 IU.

Lactation 8000 IU in deficiency 5000 to 10000 IU

Oral manifestation due to deficiency

It is believed that deficiency may cause atrophy of enamel forming cells to a non-
specified stratified epithelium which results in enamel hypoplasia and poor
mineralization of dentine.

There is keratin zed metaphase of epithelium and thus increased susceptibility to

infection. There are disturbances in bone growth shape and texture. Gingival shows
epithelial hyperplasia and hyperkeratinization with proliferation of the epithelial
attachment. Subgingival calculus formation is also there. It is believed that pocket
formation does not occur in vitamin ‘A’ deficiency if local deposits are not there but
when local irritants are present, pockets are deeper than in non deficient animals and
present associated hyperkeratosis.

Vitamin ‘B’ complex:

Deficiency signs may be due to the deficiency of one of the following

components which make vitamin ‘B’ complex i.e. Thiamin (B1), Riboflavin (B2),
Nicotinamide, Pyridoxin (B6), Pantothemic acid and Cyanocobalamin (B12).

Thiamine Deficiency

Source – Outside bran coats of grain and rice and yeast, others are ripe peas and beans
etc.
Requirement Adult 500-700 IU (94.42 – 2.0 mg)
Infants 100-200 IU (0.3 – 0.6 mg) in deficiency
Adults 10-25 mg. Massive dose 25-100 mg

The following oral disturbances have been related to thiamine deficiency.

Hypersensitivity of oral mucosa

Minute vesicles on buccal mucosa, under the tongue or the palate
Erosion of oral mucosa

It has been postulated that the activity of the oral flora is diminished in thiamine
deficiency.
 114

Riboflavin B2

Source - Yeast and liver of vertebrates

Requirement – Adult 2.3 mg

Deficiency symptoms include – glossitis and cheilosis. Glossitis is characterized

by magenta discoloration and atrophy of papillae Disappearance of the papillae of tongue
varies and depends upon the severity of deficiency and the dorsum presents patchy
atrophy. Cheilosis is one of the most frequent changes. It begins as a tiny, raw, painful
area at the commissure of the lips, at the mucogingival junction. In severe cases multiple
fissures develop. The lesion tends to spread to lower lip causing fissuring but
characteristically spares the upper lip.

Nicotonic Acid

Source - Yeast, whole cereals, liver, eggs

Requirements - 15-25 mg in deficiency 100-500 mg can be given.

The oral changes include glossitis, which is the earliest clinical sign. In acute
form there is hyperemia, enlargement of papillae and indentation of the margin, following
by atrophic changes and resultant glazed surface. The tongue in acute stage is ‘beefy
red’, painful with burning. In chronic cases there is fissuring of the tongue.

Pantothenic Acid

Source – In animals liver and kidney and in plants the storage organs such as rice husks.
Requirements – 50-200 mg/day
Deficiency signs have been notice in animals but not in human beings.
These include angular cheilosis, hyperkeratosis with ulceration and necrosis of the
gingival and oral mucosa, proliferation of the basal cell layer of oral epithelium and
resorption of the crest of alveolar bone.

Pyridoxin (B6)

Sources – Yeast and rice polishing, also seeds and the grams and covering of cereals such
as wheat and maize.

Requirement – Little is known. In few cases daily doses of 10 mg – 100 mg have been
given. In deficiency edematous magenta tongue has been noted.
 115

Folic Acid

Source Occurs widely in animals and green vegetables.

Requirement 5-20 mg

In deficiency there is soreness and burning sensation of the tongue accompanied

by the atrophy of the filiform papillae. Necrotic changes in gingival, periodontal
ligament and alveolar bone without an inflammatory response attributed to
granulocytopenia associated with deficiency.

Vitamin B12

Source – Liver, egg, fish and meal

The deficiency results in pernicious anemia and these patients have glossopyrosis
(burning of tongue_ with a sore, red tongue and baldness of the dorsum due to atrophy of
lingual papillae. In severe cases there may be atrophic changes of the oral mucosa.

Vitamin C

Source – All living plants are excellent sources but it is abundant in citrus fruits, berries,
apple, pears etc. Considerable amount is present in human milk but is less in cow’s milk.

Requirement – 50-100 mg/day

In extreme deficiency ‘Scurvy’ results in which there are hemorrhage tendencies and
retardation of wounds healing. There is failure of formation and maintenances of
intercellular substances in tissues of mesenchymal origin, osteoporosis, increased
capillary permeability, susceptibility to traumatic hemorrhages and sluggishness of blood
flow.

Gingiva is hemorrhagic, bluish red, enlarged and friable. Alveolar bone loss results from
ascorbic acid deficiency. There may be chances of hemorrhages in the periodontal
ligament.

Vitamin D

Source Liver oil of fish, egg yolk and butter

Requirement For babies, children and adolescents is 400 IU. Adults require little less.
 116

Its deficiency will cause disturbances in calcification of bones and teeth. There is
osteoporosis of alveolar bone and reduction in the width of periodontal ligament. The
rate of cementum formation is normal but calcification is defective. Resorption of
cementum has been noted in ricketic individu
 117

BLOOD DYSCRASIAS

The various elements of the blood as well as its liquid portion i.e. serum, play
extraordinary role in many physiologic mechanisms and processes in the human body.
The oral lesions of these diseases are similar to the other lesions of oral cavity, which
occur due to irritation of infection. However, thee lesions vary in severity as per the
disease.

1. Microcytic Anaemia

It is also called pernicious anemia and is due to lack of “intrinsic factor” from the
gastric mucosa resulting in failure of absorption of Vitamin B12.
The patient complaints of painful, burning tongue which is beefy red in colour In
some cases shallow ulcer resembling apthous ulcer occur on the tongue. Along with
glossodynia, glossopyrosis, there is gradual atrophy of papillae causing bald tongue
called as Hunter’s glossitis.
The fiery red appearance of tongue may subside but again may recur. Sometimes,
the inflammation may extend to involve the entire oral mucosa but often the rest of oral
mucosa exhibit pale yellowish tinge.

2. Polycythemia

In this disorder there is abnormal increase in the number of red blood cells. The
oral mucous membrane appears deep purplish red, the gingival and tongue being most
prominently affected. The cyanosis is due to excess of reduced haemoglobin. The
gingival are often engorged and swollen and bleed upon slightest provocation.
Submucosal petechiae are also common, as well as echymosis and hematoma.

3. Leukemia

The disease is characterized by overproduction of white blood cells, which appear

in the blood in immature form.
It may be myeloid involving granulocyte series or lymphoid – involving
lymphocyte series or monocyte involving monocyte series.
The clinical oral manifestation includes gingivitis, gingival hyperplasia,
hemorrhage petechiae and ulceration of mucosa. The gingival hyperplasia except in
edentulous patient is usually generalized and varies in severity. In severe cases the teeth
may be almost completely hidden.
The gingival are boggy edematous and deep red. They bleed easily. The gingival
swelling is due to the leukemic infiltration in areas of mild chronic irritation. The
gingival hemorrhage is due to ulceration of the sulcus epithelium and necrosis of the
underlying tissues. Rapid loosening of teeth due to necrosis of the periodontal
ligament has been reported and is some cases destruction of the alveolar bone also
occurs.
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4. Purpura

It is defined, as a purplish discoloration of the skin and mucous membrane due to

the spontaneous extravasations of blood and in itself is a symptom rather than a disease
entity. It may be thrombocytopenic purpura or non-thrombocytopenic purpura.

In majority of cases that is severe and often profuse gingival hemorrhage which may
be spontaneous and usually arises in the absence of skin lesions. Petechiae also occur on
the oral mucosa, commonly on the palate and appear as numerous tiny, grouped clusters
of reddish spots only a millimeter or less in diameter. Ecchymosed lesions may enlarge
to form such mucosal haematomas, which present as large dark tumors.

5. Hemophilia, Christmas disease, pseudohemophilia

Deficiency of antithemophilic globulin (AHG) leads to hemophilia, deficiency of

Christmas factor leads to Christmas disease (Hemophilia viii) and deficiency of plasma
thromboplastin antecedent (PTA) leads to pseudohemophilia (also called Von
Willebrand’s disease). These disease present similar clinical features except hemophilia
is sex linked and occur only in males.

Oral manifestations are spontaneous bleeding or persistent bleeding following

minor trauma. The most important difference between purpura and hemophilia is:

In Purpura: bleeding time is increased but clotting time is normal

In Hemophilia: Clotting time is increased but bleeding time is normal.
 119

AIDS

What AIDS?

1. AIDS stands for Acquired Immune Deficiency Syndrome, and represents the clinical
consequence of being infected by HIV (Human immunodeficiency virus)

2. HIV is primarily a blood borne virus.

Transmission

1. Transmission occurs via blood and semen

2. Transmission probably requires repeated blood – blood or blood mucosa contract
3. In the general population transmission is related to promiscuity and mainly occurs
during (anal) sexual intercourse usually in promiscuous homosexuals or bisexuals.

4. Transmission also occurs

a) Via transfusion with contaminated blood products

b) Antenatally from mother to child
c) By use/sharing of dirty needles

5. There is no evidence of transmission by bedding, clothing, and food or by aerosol.

6. The main hazard to dental workers arises from needle stick injuries.

High risk groups:

1. Homosexual/bisexual men, especially who change their partners frequently.

2. Intravenous drug abusers who share injection equipment
3. Hemophiliacs and other recipients of unscreened blood
4. Infants born to infected mothers.

Sign and symptoms:

1. Usually symptom less

2. Sometimes, glandular fever like symptoms lasting from 3-14 days

3. Sign may include:

- Bilateral lymphadenopathy
- hepatospleenomegaly
- Rashes or candidiasis (oral thrush)
 120

Oral Manifestations:

a) Candidiasis (thrush) – can be angular, oral and/or oesophageal is the commonest oral
lesion – rubbing off leaves a raw bleeding surface.

b) Oral viral Leukoplakia (OVL) – hairy, corrugated or fatty smooth leukoplakia occurs
mainly on the tongue, uni or bilaterally, and unable to rub off.

c) Kaposi Sarcoma – a rare vascular tumor seen as a localized red or purple the flat or
raised lesion on the hard palate or skin Mostly seen in homosexuals and is the first
presenting symptom.

d) Herpes Simplex Virus (HSV) “Cold Sores” occurs intraorally and naso labial can
occur in other organs also. They are troublesome, recurrent and spread with disastrous
results.

e) Squamous cell carcinoma (SCC) – occurs in younger people without predisposing

cases of smoking, alcoholism and poor nutrition.

f) Lymphoma – Limited to the brain and non Hodgkins type. Untoward lesions in the
mouth require biopsy.

g) Papiloma – human papiloma viruses produce oral lesions on the gingival as are
Condylotoma acuminata. These can be excised and should be examined
histopathologically.

h) Xerostomia and recurrent oral ulceration – increase with poor general health, lack of
oral hygiene and with mouth breathing.

j) Recurrent apthous ulceration

k) Erythema multiformae – common in sick patients as in destructive

- Major weight loss
- Unexplained diarrhoea
- Fever and Severe thrush

Incubation time between HIV infection and AIDS varies from 15 months to 14 years.

Maximal precautions against patient positive with hepatitis b and

suspected/diagnosed with aids
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Advance preparation
1. Use hand pieces, contrangles and water syringes that can be sterilized.
2. Treat the patient in a separate enclosed room, and keep all materials needed for
surgery ready to prevent contamination with traffic.
3. Use disposable materials wherever possible
4. Disinfect and drape all surfaces, that is:
a) Entire dental chair
b) Control switches
c) Instrument tray, support for hand pieces, suction and air water syringe
d) Halogen light/lamp handle, X-ray head and controls
5. The patient should be seen preferably at the end of the day to allow time for
preparation and clean up.

Protection of the dental Personnel

1. Wear a disposable paper gown or cloth gown that can be sterilized.
2. Cover the hair with the cap
3. Wear safety glasses with a side shied that can be disinfected
4. Wear two pairs of surgical gloves
5. Wear two surgical ties – on masks

Patient preparation
1. Cover hair with disposable cap
2. Use a disposable drape over clothing
3. Provide protective glasses

Protection during treatment

1. Touch only draped or covered areas
2. Avoid procedures that have a high risk of injury to hands
3. Avoid high – aerolisation procedures
4. Use a disposable radiographic holder
5. Submerge the exposed plastic film in iodine scrub diluted with alcohol (1 for
30 minutes), rinse and dry before processing.

Post treatment procedures

1. Place all instruments and reusable linen in the sterilizer, after sterilisation
clean and sterilize a second time.
2. Keep all disposable covers and materials in a bag for direct incineration.
Sterilize first.
3. SOAK - prosthetic appliances
- Rubber base impressions
- other appliances

In iodine surgical scrub diluted 1: 1 in alcohol for 30 minutes. Alginate

impressions should be handled with gloves.
 122

4. Disinfect all surfaces which have been touched but not draped, with iodine
surgical scrub diluted 1: 1 with alcohol, OR 0.5% hypochlorite and kept WET minutes.
Then wash with alcohol or water

Oral hairy leucoplakia

Kaposi’s sarcoma
 123

POST EXPOSURE PROPHYLAXIS (PEP)

On exposure to a needle stick injury, the individual should report to MO i/c MI

Room or DMO. He will send the patient for HIV testing and start 2 drug PEP regimens.
When HIV status is not known, the first dose of ART to be started immediately and if the
serum report is negative the PEP can be discontinued.

Exposure Status of Exposure

1) Percutaneous 1) Low risk – asymptomatic HIV

(a) Not severe – solid needle viral load < 1500 c/ml
Superficial scratch 2) High risk – symptomatic HIV
(b) Severe – large bore needle, needle high viral load, AIDS patients
in artery and vein, deep injury

2) Mucosa & non intact skin exposure 3) Unknown – consider the case as
a) Small volume – droplets risky and 2PEP should be started
b) Large volume – major blood splash

Percutaneous injuries
Exposure Source
Low risk High risk Unknown
Not severe 2 PEP 3 PEP 2 PEP
Severe 3 PEP 3 PEP 2 PEP

Mucous Membrane & non-intact skin exposure

Exposure Source
Low risk High risk Unknown
Small Volume 2 PEP 2 PEP No PEP / 2 PEP
(drops)
Large Volume 2 PEP 3 PEP No PEP/2 PEP
(Blood splash)

Recommended regimens
Category
3 drug PEO/Basic regimen
3 drug PEP/Expanded regimen
Drug regimen
Zidovudine/ AZT 300 mg BD &
Lamivudine 150 mg BD for 28 days
Zidovudine + Lamivudine as above plus
Indinavir 800 mg TID/Nelfinavir 750 mg TDS for
28 days
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 Start PEP immediately

 Advice individual to practice safe sex or avoid sex, avoid breast feeding
And avoid donation of blood, body fluids or organs until serology is
Negative for 6 months post exposure
 Greatest risk is at 6-12 wks after the exposure
 Single serology is not confirmatory. Repeat at 6 wks, 3 mths & 6 mths
 125

HEPATITIS
There are presently 3 viral forms of hepatitis. They are:

a) Hepatitis A (Infectious)
b) Hepatitis B (Serum)
c) Hepatitis non A/non B

Of these Hepatitis B virus infection (HBV) is considered an occupational risk for dental
professional and other health care workers. It is a risk that includes the possibility of
dental personnel getting HBV from an infected patient and the potential transmission of
HBV to susceptible patients from infected dental personnel.

Infectious Hepatitis (Type A)

1. Hepatitis a is transmitted through contaminated blood and water and as a result of poor
hygiene.

2. The virus multiplies in the intestinal tract and then invades the blood stream
subsequently localizing in the liver.

3. Laboratory tests are available to detect hepatitis A. These specific tests include the
detection of IgM antibodies to hepatitis A, which indicate active disease and IgG
antibodies to hepatitis A, which indicates convalescence or immunity.

4. Although hepatitis a is not considered a major health hazard for dental personnel, a
consultation with physician is indicated for all dental patients with a history of hepatitis.

Serum Hepatitis (Type B)

The prevalence of Hepatitis B is particularly high amongst people whose
occupation, illness bring them into contact with infected blood, blood products, saliva
and semen. They include: Dentists, Surgeons, Gynecologists, Anesthetist, Pathologists,
Hygienists, DORAs and Ots.Humans are only reservoir, and infected carriers are the
means of spread in the community.

1. Hepatitis B is commonly thought to be transmitted through instruments

contaminated with blood. However, the virus is found in all body fluids, including saliva
of an infected individual. Thus it can be transmitted by anything with saliva, including
hand pieces spray.
2. The incubation period is from 2 to 3 months. In some patients there is no clinical
illness, but only abnormalities in the chemistry of liver function.

3. In others, the symptoms may include anorexia, nausea, vomiting, jaundice, fever,
weakness, malaise, and abdominal discomfort in the upper right quadrant, joint pain and
uticaria. The average minimum length of disability with the disease is 7 weeks.
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4. If the dental surgeon suspects that a patient has hepatitis B, or is a carrier, he may
order a hepatitis blood profile to be performed before treating the patient. These include
tests for hepatitis A and HbsAg and anti-HbsAg tests to detect hepatitis B.

5. HBAsAg is the surface antigen coating of the hepatitis b virus. A positive HbsAg
test implies that the whole virus as well as virus surface antigen particles are being
formed in the person’s infected liver and that the person’s blood can transmit the disease.
Thus, a patient with a positive HbsAg test is considered a potential carrier.

6. A test can also be performed for anti HbsAg, the antibody to the surface antigen
of Hepatitis B. anti HbsAg is protective against infection and a positive test indicates that
the person is immune to hepatitis b infection.

7. Hepatavax B engerix is a vaccine recommended for all dentists, auxillaries dental

technicians. One dose is given initially, a second dose a month later and final dose 6
months after the first. A booster is recommended after 5 years.

8. The hepatitis B vaccine will protect only against hepatitis B. Protection is about
80% at one month, 77% after two, 87% at three months and 95% after the third dose. If
an individual is exposed during this period to an infectious carrier, receiving immune
globulin will not interfere with the effectiveness of safety of the Heptavx B vaccine.

Prior to immunization, personnel may be tested to determine if they already have

been infected with the hepatitis B virus. An HbsAg positive test indicates that the person
is already immune. Anyone who tests as being already immune does not need the
Heptavax B vaccine.

Hepatitis Non A / non B

Hepatitis non A / non B is diagnosed by means of exclusion, since commercial

laboratory testing is not presently available. Hepatitis non A/non B is similar to Hepatitis
B as to mode of transmission and the presence of a carrier state.

Special precautions when treating hepatitis patients

Because of the serious threat posed by Hepatitis B, special precautions must be

taken to protect both personnel and other patients from the spread of the disease.

1. Wear disposable gloves even when taking radiographs. Wipe saliva from film
packets and place them on a paper towel. Open packets and process films. Keep all
debris on the paper towel and throw away. Remove gloves and throw them away.

2. Wear safety glasses, a mask and gloves during all procedures.

3. While still wearing gloves, remove soiled instruments by picking them up on a paper
towel.
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4. Sterilize instruments before scrubbing them, wrap instruments in the towel label
“Hepatitis” and autoclave.

5. After the instruments have been autoclaved, scrub them (wearing heavy
household gloves). Repackage and autoclave again/

6. Toss all disposables into a lined trash can (so they will not be handled again)

7. Disinfect everything touched during treatment.

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IMMUNITY
Immunity is the response of the body to microorganisms and foreign materials.

Type of Immunity

Immunity may be innate, i.e. inborn, or acquired, i.e. developed after birth.

Innate

Humans are immune to many diseases which affect other animals. For example,
humans are not affected by he disease of rabbits, myxomatosis, and conversely, the more
virulent human diseases, such as syphilis, affect few other animals. This innate immunity
is a feature of the species to which humans or other animals belong and does not depend
upon any defense mechanism being set up after birth.

Acquired

Acquired immunity is developed during life and may be either active, resulting from
antibodies formed by the body, or passive resulting from antibodies donated from another
animal. It may also be either naturally or artificially acquired.

1. Active natural immunity follows a natural infection. In some cases, such as

chickenpox and measles, it lasts for life and in others, like influenza and the
common cold; the period of immunity is much faster.

2. Active artificial immunity is acquired by vaccination, which is a simulated

infection. Although the vaccine injected is either killed or harmless, the
immunity produced is effective against the natural infection. The body’s
response with both types of active immunity is usually termed the immune
response.
3. Passive natural immunity is found in newborn babies. Antibodies from the
mother’s serum cross the placenta and enter the fetal circulation, conferring a
degree of immunity for the first 3-6 months of life.
4. Passive artificial immunity involves the injection of antibodies into the blood
stream of an individual who has come in contact with an infection to which he
or she has no immunity. In the past the injected antibodies were usually
obtained from animals, often horses, but modern techniques of genetic
engineering may soon permit the production of antibodies in the laboratory
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The immune response

The acquired immune system is able to recognize and react specifically to foreign
material (usually called an antigen), but does not normally react to the body’s own
component. Antigens are substances, which have a large molecular size, usually proteins,
and defense actions. Bacteria entering the tissues, for example, may be killed, but if
toxins are produced, these will require to be neutralized. Thus different responses will
occur depending upon the type of antigen/

Two main types of immunological defense reactions can be triggered by antigens

entering the body: the humoral and the cell-mediated. Both responses are usually
involved simultaneously but it is simpler to consider them separately.

Humoral immune response

In this type of reaction, the antigen is attacked by specific proteins released from
immune cells. The immunoglobulins are types of serum globulins called
gammaglobulins, and each one is specific to the antigen which triggered its formation.

The antigen is phagocytosed by macrophages which process the antigen and

instruct a lymphocyte (the B lymphocyte in this case). The B lymphocyte, once
stimulated by the antigen, changes into a plasma cell and produces immunoglobulins
which react with the antigen. This type of response is referred to as humoral because the
immunoglobulins can be released some distance from the site of infection and are carried
in the blood to the area.

Cell-mediated immune response

In this response the T lymphocyte is activated to produce local factors – the

lymphokines. The T cell is attracted to the site of the antigen and interacts directly to
destroy it. The lymphokines have a whole range of effects, one of which is damage to
cell membranes. Although this may destroy foreign microbes, the potential also exists for
damaging the body’s own cells. The lymphokines also initiate and increase the body’s
inflammatory responses. A factor which activates osteoclasts to resorb bone, osteoclast-
activating factor, has been identified and is thought to be formed by activated
lymphocytes.

Components of the immune response

It can be seen that the immune response consists of certain cell, proteins and
tissues which function together to provide protection from foreign material entering the
body. The commonest sources of danger are the millions of organism, both commensal
and pathogenic, which exist in our environment, but a splinter of wood embedded in the
skin will provoke the same defences.
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The cells – The lymphocyte is the most important cell in the immune response.
There are two types of lymphocyte – the B cell, which arises initially in the collections of
lymphoid glands (bursa) surrounding the gut, and the T cell, which arises from the
thymus. The origins of these cells are not really of significance to the dental hygienist,
but they explain the choice of the letters B and T. Once produced, the B and T
lymphocytes colonize the lymphoid tissue scattered throughout the body and produce
clones of cells with similar defensive abilities.

Other cells are also important. Neutrophil polymorphs act to phagocytose the antigens
and damaged tissue. Large macrophages found throughout the body also phagocytose
antigens, process them and instruct the B and t cells, so initiating the immune response.
The mast cell is also important.
These are found attached to the walls of small blood vessels, and in certain
immunological reactions they release histamines and other similar substances, which
cause many of the vascular changes seen in hay fever and other allergic conditions.

The proteins involved in immune reactions are very complex and only an outline
of their functions will be discussed.

Compliment is a series of proteins and enzymes present in the blood, which is

activated by the combination of immunoglobulins and antigens. Its main function is to
assist in the destruction of organisms or to promote their phagocytosis. In addition,
complement factors trigger the inflammatory response.

Immunoglobulins (antibodies) are produced by plasma cells and released into the blood
stream. Their functions range from helping polymorphs to phagocytose bacteria, to
neutralizing toxins. Once the body has been stimulated to produce immunoglobulins,
long-lived memory cells remain in the circulation, which can be triggered to initiate the
production of large amounts of plasma cells and hence immunoglobulins, should be
antigen be encountered again. This is why, once some diseases have been suffered, we
obtain lifelong immunity (but not, regrettably, to caries or periodontal disease).

The immunoglobulins are given alphabetical letters – G, M, A and E to

distinguish them. Immunoglobulin G is the commonest antibody in serum and can cross
the placenta and protect the fetus and baby in the early months of life. Immunoglobulin
M is a very large protein which is mainly in body secretions such as saliva, milk and
tears. It defends mucosal surfaces, such as in the oral cavity, from bacterial invasion.
Immunoglobulin e is found in serum and on the surface of mast cells. It is responsible for
many of the features of allergic reactions.

The lymphokines are produced by activated T cells when simulated by contact.

They perform various functions, including attracting other lymphocytes, attracting and
activating macrophages and damaging bacterial cell walls. However, they also cause
local damage and this is believed to be one of the sources of tissue damage in periodontal
disease.
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The tissues of the immune system produce the various cells. The main ones are
the bone marrow and the lymph nodes scattered throughout the body.

Pathogenicity of organisms
As stated at the beginning of this chapter, micro-organism may be divided into
pathogenic and commensal types. Pathogenic micro-organisms are capable of producing
agents called toxins, which are harmful to the tissues. These are of two types: exotoxins
and endotoxins.
Exotoxins are given off by the organism and circulate freely throughout the body.
They are extremely potent, causing a great deal of damage in small quantities. A typical
feature of diseases caused by exotoxins is that the micro-organisms remain localized in
one area which exotoxins cause widespread damage, as happens in diphtheria and
tetanus.

Endotoxins are produced within the organism and are only released when it dies
and breaks up. They are less potent than exotoxins and, if they produce generalized
symptoms, it is because of the invasiveness of the organism. In other words, the micro-
organisms themselves disperse throughout the body. Tuberculosis and syphilis are
examples of such diseases.

Endotoxins may also be produced as a result of the breakdown of the cell of

necrotic commensal organisms. Commensal organism do not produce potent toxins but
are capable of producing low-grade damage as in, for example, periodontal disease. The
commensal organism colonizing the tooth surface irritate the gingival and provoke the
inflammatory and immune responses in a number of ways. The main methods are by the
presence of enzymes, endotoxins and other antigens in the plaque bacteria.

Enzymes help to damage the crevicular epithelium and make it more permeable to
the infiltration of other microbial byproducts such as endotoxins. They are also proteins
and as such are antigenic and therefore provoke the immune response. The endotoxins
are produced when cell wall components are released from plaque organism after they are
lysed. These infiltrate through the junctional epithelium and are very potent initiators of
both the inflammatory and immune responses. The organism, their enzymes and
endotoxins ca, therefore, all be seen to be powerful inducers of the immune response, of
both cell-mediated and humoral type.

Role of the immune response in periodontal disease.

Initially the immune response appears to play a protective role, preventing plaque
micro-organism from penetrating the gingival tissues. However, whilst being a defensive
mechanism for the whole body, the immune response is capable of being locally harmful.
This is illustrated by the intense local reaction which may result from injecting certain
antigens subcutaneously. This reaction may prevent spread of the antigen, but is locally
damaging.
 132

With continued, low-grade, long-term stimulation of the humoral and cell-

mediated responses, plaque products will initiate and cause the progression of periodontal
disease, with the body’s own mechanism being responsible for most of the breakdown of
the periodontal tissues.

Abnormalities of the immune response

Hypersensitivity

Hypersensitivity is the technical term for allergy and can be defined as an immune
reaction which produces tissue damage in the host. The immunological reactions which
result in tissue damage are identical with those which destroy micro-organism. As
already noted, the immune response, whilst being a defensive mechanism, can under
certain circumstances cause tissue damage.

Hypersensitivity does not imply an exaggerated immune response, but merely a

response which happens to cause tissue damage to the host.

Examples of hypersensitivity are asthma, hay fever and allergic reactions to

certain drugs, including penicillin. In relation to drugs, the hypersensitivity reaction to
the first exposure to the drug may produce relatively mild symptoms, such as nausea,
pyrexia or skin rashes. However, the secondary exposure to the same drug is likely to
have a much more severe systemic effect, known as anaphylaxis. Such a reaction can, of
course, even result in death.

Autoimmunity

Autoimmunity means the production of an immune response to the host’s own

tissues. There is a failure of the immune system to recognize ‘self’ proteins. This is
usually due to these proteins becoming slightly altered by relatively simple compounds or
elements being attached to them. An example of this is the contact dermatitis which
occasionally results from substances such as iodine coming in contact with the skin. The
same effect can result from antigens coming in contact with tissue cells and attaching
themselves to the cell membrane. There is, as a result, an immune reaction against the
intact tissue cell, which has the antigen as an integral part of it.

It is this type of reaction which causes rheumatic fever. An exotoxin secreted by

bacteria lodged in the throat circulates in the blood and becomes attached to the synovial
membrane of joints and valves of the heart. The resulting immune response causes an
inflammatory reaction in these tissues. Autoimmunity is also associated with certain
relatively uncommon oral conditions, such as pemphigus.
 133

ORAL CANCER

Tumor – By definition Tumor is simply a swelling of the tissue. In the strict sense, the
word does not imply a neoplastic process.

Neoplasm – A neoplasm is often considered as an independent, uncoordinated new

growth of tissue which is potentially capable of unlimited proliferation and which does
not regress after removal of the stimulus which produced the lesion

Type Benign
Malignant

Benign tumor – It remain compact, localized and increase in size slowly. Benign tumor
are encapsulated, which forms a clear boundary between them and the surrounding
healthy tissue. It only harms the patient by its bulk and its position which may obstruct
an important structure.

Malignant tumor – This type of tumor on the other hand, are non capsulated. They are
invasive in nature and the tumor grows at the expense of tissue in which it lies. There is
ulceration. It is very painful and causes death of the patient. There is evidence of spread
by metastasis. Normally the basement membrane is broken. It spreads into surrounding
tissues and the boundary is indefinite. It appears as a diffuse swelling. It is fixed to the
surrounding tissues due to deep infiltration. Lymph node are enlarged due to secondary
growth. The patient becomes anemic and debilitated.

Malignant tumors can be broadly categorized into two types.

1. Carcinoma (Cancer)
2. Sarcoma

Carcinoma – It is a malignant tumor of epithelial origin

Sarcoma – It is malignant tumor of connective tissue origin

Difference between carcinoma and Sarcoma

Carcinoma
1. Epithelial origin
2. Stroma formed by host cells
3. Common after 40 yrs of age
4. Skin ulcerates due to growth
involvement
5. Metastasis by lymphatics
Sarcoma
1.Connective tissue origin
2. Formed by tumor cells
3. Common in young
4. Ulcerates due to pressure
5. Metastasis by blood stream
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ORAL CANCER

This type of tumor arises from the oral epithelium. The most common location for oral
cancer is tongue followed by lip and the least common location is palate. The
male/female ratio I 2: 1.

Etiology
The cause of oral cancer is not known at the present time. Little evidence has
been found for a genetic role. However, several factors have been found to be associated
with the development of oral cancer. These are called predisposing factors. There is
increasing evidence that human papilloma virus, herpes simplex virus play role in the
etiology of oral cancer.

Predisposing factors in oral cancer

1. Age of the patient

2. Tobacco use (Cigarettes, pipes, cigar, smokeless tobacco)
3. Excessive alcohol intake
4. Nutritional deficiencies (iron, vitamin a, Zinc, copper
5. Syphilis - Tertiary syphilis
- Arsenic compounds used to treat syphilis
6. Poor oral Hygiene
7. Chronic physical and Thermal Trauma
8. Defective immune system (Congenital, acquired).
9. Viruses – Papilloma virus, Herpes simplex virus, EB virus Cytomegalo virus &
HIV

Classification of oral carcinomas

1. Squamous cell carcinoma

a) Carcinoma in situ
b) Well differentiated
c) Moderately differentiated
d) Poorly differentiated
e) Undifferentiated

2. Verrucous carcinoma
3. Glandular epithelial tumors
4. Unclassified carcinoma
 135

Clinical presentation

Signs

1. Sq. cell carcinoma may appear as a white and/or red patch

2. An exophystic mass/ulceration
3. A granular raised lesion or combination of thee
4. Ulcerated lesions often will have raised margins that are indurated on palpation
5. White lesions with areas of erythematous to have a higher incidence of being
cancerous than do homogenous white lesions
6. In case of tongue involvement, if it involves the deeper structure and involve the
hypoglossal nerve, if the patient is asked to protrude the tongue, will deviate towards the
involved side. Carcinoma of palate can involve the glossopharyngeal and/or vagus
nerves, resulting in unilateral paralysis of the soft palate and loss of the gag reflex on the
involved side. This can be associated with hidden head and neck tumors in the
nasopharynx and pharynx.

Symptoms

1. Tend to develop late in the course of the disease

2. In advanced lesion pain may become significant
3. Large lesion in the posterior portion of the oral cavity may interfere with the passage
of food and air, the patient may complain of weight loss and difficulty in breathing.
4. Other symptoms include pain, hoarseness, dysphagia, intractable ulcers, bleeding,
numbness, loosening of teeth and change in the fit of a denture.

Laboratory findings

The diagnosis of oral cancer is dependent on a microscopic examination by an

oral or general pathologist. Tissue is taken from the involved site and is given for
histopathological examination.

The system of classification and staging of oral carcinomas

T Size of primary tumor

TIS – Carcinoma in Situ
T1 – Lesion less than 2 cm in diameter
T2 – Lesion 2-4 cm in diameter
T3 – Lesion greater than 4 cm in diameter
T4 – Massive lesion with deep invasion

N –Regional Lymph node involvement

No – No palpable nodes
N1 – Single node, Homolateral, 3 to 6 cm or multiple nodes
Homolateral, None over 6 cm
N2 – Single/Multiple homolateral nodes, one greater than 6 cm in diameter,
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Or Bilateral nodes or contralateral nodes

M Metastasis

Mo – Not known distant metastasis

M1 – Distant metastasis – PUL, OSS (Osseous_
HEP (Hepatic) BRA (Brain)

Staging of oral cancer

Stage Classification

I T1 No Mo

II T2 No Mo

III T3 No Mo
T1 T2 or T3 N1 Mo

IV T4 No N1 Mo
Any T any N M1

Management of oral cancer

1. Surgical
2. Medical
a) Radiation
b) Chemotherapy

Oral cancer
 137

DENTAL CARIES

Dental caries or tooth decay is a disease of the calcified tissues of the teeth,
characterized by demineralization of the inorganic portion and destruction of the organic
substance of the tooth.

It is one of the most common diseases in the world and there are few people who
have not suffered from it at some stage. It usually begins soon after the teeth erupt into
the oral cavity. It affects persons of both sexes in all races, all socioeconomic strata and
every age group.

Etiology
Cariogenesis – There is no universally accepted opinion about the etiology of dental
caries. Over the years, three principal theories of cariogenesis have been suggested.

a) Proteolytic theory

According to this theory, the organic portion of enamel or dentine is first

destroyed by proteolytic enzymes produced by plaque bacteria. Thereafter the
unprotected calcified portion is destroyed, possibly by acids. This theory seems more
rational in caries of cementum or dentine where the organic portion is moderately high.
This theory is not relevant in enamel caries, where the mineralized portion makes up
some 96% of the total teeth matter.

b) Proteolysis – Chelation theory

Chelation is a chemical process where metallic ions are lost from complex
molecules because they are attracted to other complex molecules. This process does not
depend upon acidity and can take place at neutral or even alkaline pH. According to the
proteolysis – chelation theory, the protein element of the tooth is first broken down by the
proteolytic enzymes of plaque into amino acids. The aminoacid then chelate with
calcium ions of the calcium hydroxyapatite, gradually decalcifying the tooth substance.

c) Acidogenic theory
In 1882 WD Miller culminated a hypothesis in which he stated, “Dental decay is a
chemico-parasitic process consisting of two stages, decalcification of enamel, which
results in total destruction and decalcification of dentine followed by dissolution of the
softened residue.
The sugar of diet is converted into acids by the action of the plaque bacteria and
the acids subsequently destroy the calcified materials of the tooth.

Bacteria: Various bacterial strains are capable of converting sugar into acids.
There are streptococcus mutans, lactobacillus acidophilus, streptococcus sanguis and
streptococcus salivarius.
 138

Sugar – Refined pure carbohydrates are more caries producing than complex
ones. The sucrose is worst in relation to causing caries. Polysaccharides are less easily
fermented by plaque bacterias than monosaccharides and disaccharides.

Acids – Dental plaque has a resting pH which is fractionally on the acidic side of
neutral (pH approx 6.8) and roughly 10 minutes after exposure to sugar, it reaches its
lowest pH in the region of 5 before slowly returning to normal over a period of 30-60
min. A number of acids are produced by the action of plaque bacteria on sugar and the
most significant is lactic acid. It is seen that calcium hydroxyapatite will begin to
dissolve when pH is 5.5 or less and this is referred to as the critical pH.

Secondary factory – Secondary etiological factors are those which are not directly
involved in causing a disease but influence the disease to a greater or lesser extent. These
factors are numerous as follows:

a) Poor oral hygiene:

It is an obvious feature that caries tends to be more prevalent in dirty mouth than
clean one. More the plaque is allowed to accumulate on teeth; the more is the acid build
up and attack on the tooth surface. Tooth brushing will remove foodstuff lodged between
teeth, thus preventing release of sugar into saliva over a long period.

b) Diet:
The diet has been shown to affect the caries rate in various ways.

1) Composition – The quantity of sugar consumed has less effect than type of
sugar. Sucrose is particularly harmful. The consumption of fluorides can halve the caries
rate.

2) Consistency – Soft sticky foodstuff will cling to the teeth and remain in the
mouth for longer periods than others. They are then able to release sugars into the plaque
over a long period. The fibrous food does not remove plaque to any significant extent
from the teeth and although they may be preferable to sweet sticky foods, they are no
substitute for normal tooth brushing. On the contrary the apples neither clean the teeth
but have an adverse effect on plaque pH.

3) Frequency – More frequently the sugar is consumed, the greater is the period
during which acid is available to attack the tooth.
c) Saliva

More the viscosity of saliva there is greater difficulty with oral hygiene and more
chances of caries. The rate of salivary flow varies throughout the day and is minimal
during sleep. This is the reason for stressing the importance of cleaning the teeth before
going to bed. In patients with xerostomia there is a risk of increased caries rate.
 139

d) Pregnancy

In relation to dental caries there was a proverb – A tooth for a baby. But this is
not acceptable because in no way calcium from enamel can be resorbed into the blood
stream once the tooth has erupted.

e) Teeth: The teeth themselves can influence the caries rate in several ways.

1) Form – Teeth with deep developmental pits and fissures are more likely to be
prone to caries. The fissure of teeth narrow to an extent where they cannot be made
plaque free by tooth brushing.

2) Position – Crowding and malalignment make oral hygiene much more difficult.
This will tend to cause an increase in both periodontal disease and caries.

3) Structure – Areas of hypocalcification may be more prone to caries and of

course teeth with reasonable fluoride content are much less susceptible to caries. The
critical pH of calcium hydroxyapatite is 5.5 and that of calcium fluorapatite is near 4.5.

f) Iatrogenic factors
Iatrogenic means are caused by humans. Even well designed dentures and
orthodontic appliances are at risk because of trapping dental plaque. The margin of best
restoration are liable to secondary caries.

Clinical picture:

Caries attack the enamel, cementum and dentine gradually eating into and
destroying the tooth. The clinical picture varies with the site and the extent of the lesion.
Following types of caries are found:

1) Smooth surface caries – It is found most commonly at the interproximal

contact points but it can occur on any smooth surface of the tooth. It appears as a chalky
white area which gradually becomes roughened due to breakdown of the enamel.
Eventually an open cavity is formed. As dentine is softer than enamel the caries destroys
it more quickly undermining the enamel. The caries is visible through translucent enamel
as bluish white area. In the next stage the caries spreads in the dentine and it leaves a
progressively larger area of enamel unsupported and eventually the enamel collapses
leaving an open carious cavity. The caries at the base may be either soft and creak
coloured or hard and dark. With the continuing spread of the lesion, the pulp eventually
becomes involved and infected producing pulpal inflammation known as pulpitis. The
extension of pulpitis through the apical foramen into the periodontal ligament is known
as apical abscess.
 140

WHITE LESIONS

Leukoplakia
Lichen Planus

Oral sub mucous fibrosis

Disease Clinical features Cause

1 LEUKODERMA Most commonly seen on buccal mucosa Unknown
along posterior occlusal plane, bilaterally.
Clinically resembles Leukoplakia
2 LEUKOPLAKIA Asymptomatic white patch which cannot Unknown. May be
be wiped off. Males are more affected. related to Tobacco and
Common sites involved are buccal alcohol use
mucosa, floor of mouth, tongue, lips
3 HAIRY Filiform to flat patch on lateral tongue, Opportunistic E.B. virus
LEUKOPLAKIA often bilateral, occasionally on buccal infection
mucosa, asymptomatic
4 WHITE SPONGE Asymptomatic, bilateral, dense, shaggy, Hereditary, autosomal
NEVUS white or gray, generalized opacification dominant
of buccal mucosa affected but other
membranes may be involved
5 FOCAL Asymptomatic white patch, commonly on Chronic irritation from
(FRICTIONAL) edentulous ridge, buccal mucosa and snuff or chewing tobacco.
HYPERKERATOSIS tongue. Does not rub off. Common
 141

6 MUCOSAL BURNS Painful white fibrin exudates covering Chemicals (Asprin). Heat
superficial ulcer with erythematous ring. & Electrical burns
Common
7 GEOGRAPHIC White annular lesions with atrophic red Unknown
TONGUE centers, pattern migrates over dorsum of
tongue, varies in intensity and may
spontaneously disappear. Occasionally
painful
8 LICHEN PLANUS Bilateral white striae (Wickhams) Unknown. May be
asymptomatic except when erosions are precipitated by stress,
present. Seen in middle ages. Buccal hyperimmune condition
mucosa most commonly affected, with
9 CANDIDIASIS Painful elevated plaques can be wiped off Opportunistic fungus
leaving eroded, bleeding surface. candida albicans
Associated with poor oral hygiene,
systemic antibiotics, systemic diseases,
debilitation, Decreased immune response,
chronic infections may result in
erythematous mucosa without obvious
white colonies. Common
10 ORAL SUB Areas of opacification with loss of
MUCOUS elasticity. Any oral lesion affected esp.
FIBROSIS buccal mucosa, tongue. Associated
 142

BACTERIOLOGY OF ORAL CAVITY

Group of microorganisms that reside at particular surfaces of the body are referred
to as the normal or commensal flora (i.e. living in co-operation with the host).

The interaction between the commensal normal flora and its host is considered an
Ecosystem. As in all ecosystems, this relationship is often fragile and can be disturbed
by minor shifts in the balance of a variety of factors. In humans, a normal ecological
balance is necessary for maintenance of health.

The topographical arrangement of the oral cavity with its varied terrain of teeth,
gingival crevices or pockets, buccal and lingual sulci, lips and tongue has great influence
on the physical parameters of bacterial colonization.
Microflora of oral cavity consists of various bacteria (rods, cocci, aerobic,
anaerobic).

Gram Positive Cocci:

Streptococci – About 90% of streptococci have been found in plaque and isolated.

Streptococcus mutans – is the principal etiological agent of human dental caries. These
produce both soluble and insoluble extracellular glucose polymers (glucans/mutans) from
sucrose and levans (polymers of fructose) which form the matrix of dental plaque.

Streptococcus Sanguis is also capable of producing extracellular glucans from sucrose.

These streptococci are common in dental plaque and often the predominant plaque
streptoccal species.

Streptococcus salivarius – produces extracellular fructans (levans) from sucrose.

Streptococcus mitior (mitis) include a-hemolytic streptococci common to the oral
cavity.
Streptococcus milleri is particularly numerous in gingival crevice.
Staphylococcus and Micrococcus are catalase +ve, Gram +ve cocci which are
frequently isolated from the oral cavity.
Staphylococcus salivarious is a commensal of dorsum of tongue.
Peptostreptococcus and Peptococcus are anaerobic Gram +ve cocci which are
commonly isolated from the oral cavity.

Gram Negative Cocci

Neisseria species are common isolates in the mouth and are characteristically
aerobic or facultative, oxidase positive, Gram –ve proportion of the organisms which
initially colonize clean tooth surfaces probably due to presence of an extracellular slime
or capsular material.
 143

Anaerobic counterpart of Neisseria, Veillonella species are also common in

mouth, often in relatively high in numbers.

Gram Positive Rods and filaments

Actinomyces species comprise a large proportion of Gram +ve Rods isolated from oral
cavity and include A Israeli, A. naeslundii, A. viscosus and A. odontolyticus.

The Gram +ve Rod, Lactobacillus is associated with unrestored carious lesions.

Other anaerobic rods and filaments that have been isolated from the mouth
include Leptotrichia buccalis, Arachnia, Proprioni bacterium, Eubacterium species.

Gram negative rods & filaments

Haemophilus species are G-ve aerobic and facultative rods that have been shown
to be frequently present in saliva and on oral mussel surfaces and may be present in
dental plaque.

Fusobacterium and Bacteroids species are anaerobic G-ve filaments and rods,
which are commonly isolated from dental plaque, especially in subgingival region.

Capnocytophaga is the predominant G-ve facultative rod in the gingival sulcus of

the aged.

Other Microorganisms:
Spirochetes are common inhabitants of the gingival crevice. 3 distinct species, which
may be present, are – Treponema denticola, Treponema macrodentium, and T. oralis.

Yeasts particularly candida albicans, are also common oral isolates from healthy
individuals.

Protozoa including Entamoeba gingivalis, Trichomonas, Selenomonas species

are often seen.

Most viruses are considered as transients; however, Herpes virus hominis (HSV)
is carried by many people. Likewise, Epstein-Barr and Varicella-Zoster viruses are
often considered as normal oral flora and Hepatitis B virus and Cytomegalo virus may
be found in oral cavity in the carries state.

Actinobacillus actinomycetemcomitans, P. gingivalis and B. forsythus have been

found to be major periodontopathogens
 144

STERILIZATION AND DISINFECTION IN DENTAL

PRACTICE
INTRODUCTION

There has never been a greater need for infection control-not just in hospitals or general
medical and dental surgeries, but in other work environments such as veterinary
practices, chiropody, professional beauty clinics, tattoo artistry, acupuncture,
hairdressing, laboratories in the food and water industries, schools, and colleges.

Visual or verbal identification that patient or client is free from infection should
not be relied upon. They may be reluctant to advise you or they may not even know that
they are infected. Visually they may appear perfectly normal, however, many blood-
borne viruses like Hepatitis b and HIV, for example, may not display any outward signs
or symptoms. Infection control procedures should be practiced wherever and whenever
there is the potential for exposure to viruses or bacteria.

HOW IS AN INFECTION TRANSMITTED?

There are a number of ways by which infection or disease can be transmitted

from one individual to another:

. Contaminated instruments
. Aerosol or airborne
. Personal contact
. Contaminated food and water

Many bacteria are harmless or may cause only minor discomfort. However,
some bacteria can cause serious ailments, which could ultimately be fatal. The
introduction of an infection control policy and procedures can be designed to give
maximum protection against transmission by any or all of the above routes.

WHAT IS INFECTION CONTROL?

Infection control is the total discipline that provides for a safer working
environment for both practitioner and patient. It can include:

- The wearing of suitable protective clothing, for example gloves, masks,

eyewear

- Maintaining a clean and tidy treatment area, ensuring only essential

equipment is kept in the area.
 145

- Ensuing equipment and work surfaces are regularly cleaned and

disinfected between patients

- Immunization of staff Identification of high risk patients enabling

appropriate infection control procedures to be implemented in
preparation for their treatment
- Sterilization of all instruments that are used in the course of treatment
immediately after use and for some procedures immediately before use.

Regular training of all staff in infection control techniques, including emergency

procedures when cross infection is suspected (i.e. needle stick injury)

The adoption of an effective control policy is of paramount importance. Advice

should be sought from your local Health authority or infection control officer on policy
and procedure recommendations for your particular professional discipline.

DO I STERILIZE OR DISINFECT?

The short answer is “If it can be sterilized, sterilize it”

Sterilization is the complete destruction of all micro organisms, including the

most resistant bacterial spores”.

Disinfection is “the killing of pathogenic organisms, but not usually of bacterial

spores”

Chemical disinfection may not destroy the agents responsible for harmful or life
threatening disease such as Hepatitis B or HIV. In practical terms, disinfectants are used
on such items as work surfaces, treatment room furniture and equipment. For
instruments used in the course of treatment, especially those, which may come into
contact with, blood or mucous, sterilization should be the standard required within your
infection control policy. Particular attention should be paid to hollow instruments or
those made up from components, such as dental headpieces, where in the course of
treatment, blood and mucous can migrate inside the instrument. Unless proper and
effective sterilization is carried out between patients, contaminated blood and mucous
can be transferred to the next patient. Remember, sterilization provides the greatest of
safety.

HOW CAN I STERILIZE MY INSTRUMENTS

There are a number of ways to sterilize instruments some more advantageous than
others. In the first instances, you should establish with the manufacturer their
recommendations on suitable methods for sterilization of each particular item.

For instruments other than ‘sharps’, cleaning should be carried out after use to remove
solid debris, blood, and other matter. Failure to clean could result in contaminated
material being ‘backed’ onto the instrument. Particular attention should be paid to the
 146

cleaning of hollow instruments, such as dental hand pieces, where contaminated

materials may be out of sight. Instrument with sharp edges, particularly from high-risk
patients, should be sterilized prior to the cleaning process to avoid danger during
handling, and then re-sterilized for use.

In any sterilization process, the most important features the equipment should exhibit
are:

1. Controlled cycle, where the physical conditions required to achieve

sterilization are present and controlled automatically, thus removing potential
for user error,

2. Lid lock, where access to the items during a sterilization cycle is prohibited
by means of locking system, thus preventing items being added or removed
before the cycle has been completed.

METHODS OF STERILIZING

By autoclave
An autoclave uses steam under pressure for a specific period of time (see Table
1) to sterilize. Autoclaving is the preferred method of sterilization by healthcare
professionals worldwide, including the World Health Organization (WHO) and the
centers for diseases control (CDC), because it is a rapid, simple and effective process.
Also, as it does not use chemical, it is safer and more environmentally friendly.
Autoclaving is also more cost effective than other methods, and with fully automatic
equipment can give the most reliable and reproducible in practice sterilization process.

There are three types of autoclaving process:

For unwrapped instruments and utensils

These may be portable or transportable which do not require connection to mains

steam, water, or drainage. They also run on standard mains electricity supply. They
should be fully automatic in operation and achieve one (or more) of the temperature/time
standard listed in Table 1. Autoclave for unwrapped instruments is not suitable for the
sterilization of wrapped or porous loads.

Sterilization is effected by moist heat, the condensation of steam onto surfaces of

the instrument releases latent heat. Instruments should therefore be loaded in the
autoclave so that all their surfaces are exposed to steam.

NB: Non-electric steam sterilizers work on the same principle as the unwrapped
instrument autoclave.
 147

TABLE I
RECOMMENDED STERILIZATION TEMPERATURES AND TIMES FOR
AUTOCLAVES

134oC for 3 minutes 134oC 3

126oC for 10 minutes o
136 C 10
121oC for 15 minutes o
121 C 15
But rely on an independent heat source (gas or liquid fuel burner) are used where is no
mains electricity available.

For porous loads

These autoclave have pre-vacuum and post-drying cycles. When sterilizing wrapped
instruments or surgical packs (cloth), it is necessary first to remove all the air from
the chamber and packs by means of a vacuum pump and steam purge stage. This
ensures that there are no air pockets, which could prevent steam penetration and
therefore sterilization. Secondly, the load must be dried in the chamber at the end of
the cycle to ensure that there are no microbes retained in the pack, which could
compromise the sterility of the pack when stored.
For fluids

These autoclaves may have variable cycle parameters (temperature and time) for
the different conditions suitable for sterilizing liquids and media. In addition, many have
a post sterilization cooling stage and pressure ballasting with sterile air to reduce the
cycle time and prevent bottles or bags exploding in the chamber or during unloading.
Other methods of sterilization are:

By Cold chemicals
This method involves the immersion of the instrument in a chemical sporicidal
solution.
Depending on the type or strength of the chemicals used and the instrument(s) to
be sterilized, sterilizing time can range from 7 to 12 hours. While this system may be of
value in sterilizing unwrapped instruments not suited to those methods involving
autoclaving temperatures, it is generally not a preferred method because of the potential
hazards in using and disposing of the toxic chemicals. It cannot be used to sterilize
textiles or liquids. After removal from the solutions, instruments must be rinsed using
sterile water and therefore cannot be stored sterile. Many systems do not have lid locks
or controlled cycles, which can lead to user error and ineffective treatment.

By chemical vapour
This uses a chemical sporicidal solution, which is vaporized, within the sealed
chamber of the equipment. Again a useful system for sterilizing delicate instruments but
it can be more expensive than other methods due to the cost of special chemicals, and
instruments are dried before starting a cycle. There are also potential hazards in using
and disposing of the chemicals used. This cannot be used for sterilizing cloth or liquids.
 148

By Gas
This method uses toxic gases, e.g. ethylene oxide or formaldehyde with low
temperature steam as the sterilizing agent. Whilst the method can be effective,
particularly for very delicate instruments, the process requires very specialized
equipment, installation, and handling of the toxic used. It is therefore not a system
suited to general practice applications.

By Dry Heat
Involves the application of very high temperatures for long periods (see table 2),
which makes the method unsuitable for many instruments, particularly those for which a
rapid turnaround is required. Hot air cannot be used for plastics, rubber or textiles.
Modern dry heat sterilizers have door-interlocking devices, controlled cycles and chart
recorders that have greatly increased their cost.

By steel ball/glass bead

A simple process, which involves heating, steel balls or glass beads in a chamber
into which the instrument is inserted. Temperatures required are similar to that for dry
heat sterilizers. However, the method is only suitable for very small instruments, and
only those parts in contact with the balls or beads are sterilized. This method is not
suitable for hollow instruments.

UNACCEPTABLE METHODS OF STERILIZATION

Water boilers
Immersion of instruments in boiling water does not achieve sterilization as many
bacterial spores can withstand boiling. As a method of disinfection only, it can be useful,
however, the lack of lid locks or controlled cycles on most types of this equipment can
lead to ineffective disinfection. Cross infection from contaminated water (containing
bacterial spore not killed by boiling).

TABLE – 2

RECOMMENDED STERILIZATION TEMPERATURES AND TIMES FOR DRY

HEAT

175o C FOR 20 Minute 175o C 20

165o C for 40 minutes 165o C 40
155o C for 120 minutes 155o C 120

Domestic pressure cookers

Although pressure cookers operate on a similar principle to autoclaves, they are
designed for cooking, not sterilizing. There is no guarantee that a domestic pressure
cooker will reach a high enough temperature or, without a controlled cycle, maintain
temperature for the required length of time to achieve sterilization. Domestic pressure
cookers should not be used for sterilization.
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STERILIZATION INDICATORS
There are three types of indicators, which are widely used:

1. Biological indicators
These are the only direct methods of validating sterilization as they show
destruction of microbiological life. Unfortunately, they do not provide an instant result
as following the sterilization process. They must be incubated or processed to determine
‘pass’ or ‘fail’ their reliability depends on strict quality control during manufacture and
decrease during storage. Manufactures instructions for use must be followed at all times.
Biological indicators are available for all forms of sterilization.
2. Chemical indicators:
These do not verify sterilization, but confirm the item has been exposed to the
physical conditions required to effect sterilization. They can monitor the conditions of
time, temperature, moisture or gas depending on the sterilization method being used.
When used with gaseous processes, they will indicate quantitatively the presence of the
sterilant but must be located throughout the chamber and load to measure penetration.
Chemical indicators will give an instant result.

3. Mechanical indicators
These include temperature-measuring devices with gauges or LED displays (time
and temperature) and chart recorders/printers. They indicate that required parameters
have been reached during the cycle. Should any one of the parameters fall to reach the
minimum within the cycle requirements, it should be assumed that the items are not
sterile. The use of chart recorders or printers allows data to be kept with practice records
or the sterilizer service history.

MAINTENANCE

All equipments should be maintained in accordance with the manufactures’

instructions and the recommendations contained within Health Authority publications on
the use of sterilizers in practice. Full records should be kept of the service history.
 150

ANTISEPTICS AND DISINFECTANTS

The term antiseptic, germicide and disinfectant are often confused and sometimes
used synonymously.

Antiseptic - It is the drug, which inhibits or arrests the growth of microorganisms but
does not necessarily destroy them. These are used on living tissue.

Germicide - An agent capable of destroying microorganisms

Disinfectant – It is a substance, which kills pathogenic microorganism. These are used

on nonliving substances instruments etc.

Mechanism of Action - The action ranges from simple precipitation of proteins by

Ag No, or other heavy metals to complex actions interfering with enzymatic processes,
which are essential for multiplication and survival of microorganisms. The phenol
coefficient is used as a test for the evaluation of effectively, but it has its limitations.
Some of these drugs may prove highly irritant on the skin or oral mucosa, or may be
corrosive on metal instruments.

Desirable properties:
1. The essential property is that the drug should destroy microorganisms rapidly and
completely without being toxic to hot cells. So efficacy as germicide must be balanced
against injury to tissues.
2. The drug must penetrate well. To achieve this, the drugs are formulated so as to
have low surface tension, which allows spreading.

3. The drug must be active in presence of organic material and not be inhibited by
it.
4. It should have a pleasant odour, taste and should not stain.
5. It must be stable so that it should not be prepared again and again each time.

In dentistry the antiseptics and disinfectants have two general uses:

a) Disinfection of instruments

b) Treatment of accessible infections.

Most of the drugs and methods used fall short in one or more of the desirable
properties mentioned above, hence there are numerous drugs in use and the selection of a
suitable one is often difficult.

The killing effect of dry heat is due to protein denaturation, oxidative damage
and toxic effect of elevated levels of electrolytes. The lethal effect of moist heat is due to
denaturation and coagulation of protein.
 151

WASTE DISPOSAL
MANAGEMENT OF BIOMEDICAL WASTE

BIOMEDICAL WASTE has been defined in GOI Gazette as “any waste, which is
generated during the diagnosis, treatment or immunization of human beings or animals,
or in research activities, or in production or testing off biologicals”

HAZARDS
Biomedical/waste can adversely affect human health by 3 methods: -

1. Hazards for patients attending health care.

2. Hazards for health care workers
3. Hazards for community at large.

In health care settings: -

- 85% of generated waste – Non Hazardous
- 15% of generated waste – 10% - Infectious hazardous waste
5% - Non-infectious hazardous waste

STEPS IN WASTE MANAGEMENT

1. Waste Survey
- Differentiate the type of waste
- Quantify the waste generation
- Determine the point of generation & disinfection

2. Categorization of waste – Tissue waste, chemical, instrument, sharps, liquids,

medicines

3. Segregation and safe storage – sharps/non-sharps, chemical/cytotoxic

4. Choice of bins and receptacles – plastic, metal bins

5. Handling & treating
- Labeling of bins & waste
- Disposable items have to be shredded/mutilated
- Extreme care while handling sharps
- Disposable items should be dipped in disinfectant
- Liquid waste should be treated with chemical disinfectant
- Mercury, amalgam should be kept in sulphide solution
- Needle tips to be put in disinfectant & shredded or burnt
 152
WASTE CATEGPRY, COLOUR CODING & IT’S DISPOSAL
Category Type of waste Type of Colour Treatment & Disposal
container
1 Human anatomic Plastic bags Yellow Incineration/deep
waste (human burial
tissues e.g. teeth,
gingival,
mucosa)
4 Waste sharps Plastic Blue/White Disinfectant/autoclave
(Needles, bags/Puncture transparent microwave/shredding
syringes, scalpel, proof
blades, glass- containers
capable of
causing cuts)
5 Discarded Plastic bags Black Incineration/
medicines & Disposal in land fills
cytotoxic drugs
(Outdated,
contaminated
drugs, medicines)
6&7 Soiled wastes Disinfected Red or Incineration/
(Blood, fluid, container & Blue Autoclave/microwave/
soiled dressings, Plastic bag shredding
cotton, plaster,
linen,
bedding/tubing,
catheters, IV
sets)
8 & 10 Liquid waste & - - Disinfectant/Discharge
chemical waste Plastic bag Black In drain/landfills
 153

INFECTION CONTROL IN DENTISTRY

 An aggressive approach called standard precautions that treat all human
blood and body fluids as potentially infectious for HIV, Hepatitis and other
blood borne pathogens is routinely followed.

 Dental instruments are categorized into three categories:

Critical - Instruments that invade sterile tissues or enter vascular system

example forceps, scalers, chisels, surgical burs, probe etc.

Semi critical - Instruments which come in contact with mucous membranes

but do not invade tissues-dental mirror, restorative instruments, hand piece,
impression trays etc.

Non critical - Instruments are those which contact intact skin only example
medicament jars, glass slabs etc

 Critical materials are autoclaved / heat sterilized. Semi critical materials are
preferably autoclaved/heat sterilized or if heat sensitive treated with a high
level sterilization for 10 hrs with 2% Glutaraldehyde, 0.5% sodium
hypochlorite or as recommended by the manufacturer. Non-critical materials
can be disinfected with an intermediate to low-level disinfectant.

 All dental health care personnel should be immunized against Hepatitis B

virus and tetanus.

 History taking is specific to identify HIV, Hepatitis B and TB patients. This

includes non-dietary weight loss of 10 lbs in 6 months and sores in mouth
that may be recurring.
 Protective barriers like surgical and utility gloves are used consistently, and
to be replaced after each patient.
 Masks to protect face, oral and nasal mucosa are used and changed after each
patient or after 20-60 min.
 Regular eyewear with side shields to protect against splatter and spray should
be used.
 Protective clothing like aprons, lab coats, gowns, head covers, and shoe
covers/slippers are used.
 Pre-procedural mouth rinse with 0.2% chlorhexidine is done for each case
except in routine examination cases.

 Aerosol is minimized using high volume suction. Sudden jerky movement of

chair and talking to patient when his mouth is open is discouraged.
 154

 Sharps are handled using needle recapper or one handed scooping technique
or with one handed technique.
 Hand washing with 4% chlorhexidine or 3% parachlorometaxylenol (PCMX)
with scrubbing for 15 seconds is followed.
 Used instruments pass through a procedure of pre-cleaning, corrosion control,
drying, lubrication, packaging, sterilization, drying and cooling, storage and
distribution before being used again if of a critical/semi critical category.
 Sterilization monitoring is done daily with chemical strips and weekly with
biological monitoring.
 Surface and equipment asepsis is done by surface covers (especially of light
handles, chair switches, X-ray machine switch etc) or by precleaning and
disinfection (spray-wipe-spray technique).
 Any prosthesis or impression taken out of the oral cavity is disinfected with
2% glutaraldehyde or 0.5% hypochlorite for 10 min before use.
 Gloves, plexiglass shields, eyewear and air suction >200 ft/min is used in the
laboratory while handling infective material
 Surface covers or 10 min of 2% glutaraldehyde immersion and washing
maintains radiographic asepsis.
 Anti retraction valves and water line flushing for 10 sec is done after each
patient.
 Aspirators are flushed with a disinfectant cleaner. Suction bottles have 30 ml
of 2% glutaraldehyde or 60 ml of 2% hypochlorite.
 Bacterial waterline filters are maintained on unit waterlines. Dental unit
water reservoirs are kept dry at the end of the day and disinfectant cleaner
filled and kept overnight once a week.
 Heat labile instruments are autoclaved at 121 degree C, 151 lbs/Psi for 15-30
mins or alternatively 136 degree C, and 30 lbs/Psi for 3-5 minutes except
surgical carbide burs and dental mirrors, which are preferably heat sterilized
in a hot air oven at 160o C for one hour. Glass bead sterilization
is done for endodontic instruments at 210-230o C for 30 sec. Hand pieces are
autoclaved after alcohol wiping, lubrication and packing. Hand pieces are
lubricated with two separately labeled oilcans for pre-sterilization and post-
sterilization.
 Manufacturer’s recommendations are followed closely in disinfecting or
sterilizing instrument/equipment.
 SECTION - 4

PHARMACOLOGY
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GENERAL ANAESTHESIA

 General Anesthesia for dental care in children and adult is sometimes necessary
in order to provide safe, efficient and effective care.

 Depending on the patient it can be administered in an ambulatory or hospitalized

case.

 The safety of the patient and practitioner should be of paramount importance

regardless of the method used.

Preoperative procedure
 Although General Anesthesia can be given in the dental office in presence of a
qualified anesthetist and essential equipments, the safest place to administer is
the hospital.

 Parental or guardian written consent must be taken before administering it.

 Documentation regarding dental treatment needs, unmanageability in dental

clinic, and the associated medical problems must be included in the patient’s
hospital record.

 With the consulting anesthetist the dental surgeon should plan the dental
procedures in a rigid time schedule.

Anesthetic Procedure
 Facilities for artificial ventilation and for the administration of oxygen and
aspirating equipment for cleaning mouth, pharynx and trachea should always be
available.

 Nasotracheal intubation is preferred to ensure good access to the oral cavity.

 The patient’s eyes should be covered with damp gauze for protection against
dental and material debris.

 Great care should be taken to prevent blood or any type of debris from entering
the patient’s throat.

 A mouth prop should be used to keep the mouth open.

 The pharyngopalatine area is sealed off with a strip of moist 3-inch sterile gauze
approximately18 inches long.

 This throat pack is tightly packed around the tube.

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 This pack prevents the gases to escape and does not allow debris to enter the
throat.

 A rubber dam may be used when carrying restorations for a dry field and better
visibility.

The following monitoring equipments are usually available:

(1) Stethoscope

(2) Automatic sphygmomanometer

(3) Electrocardiograph leads

(4) A temperature-monitoring device

(5) A pulse oximeter and a capnography device.

Indications for GA
1. Patients with certain physical, mental or medically compromised patients.

2. Patients in whom LA is ineffective because of acute infection, allergy or

anatomic variations.

3. Extremely uncooperative, fearful, anxious or uncommunicative child

Contra indications:

1. Healthy and cooperative patients

2. When GA cannot be given on medical ground

AGENTS USED

1. NITROUS OXIDE (N2O)

 It is a colourless, non-irritating gas with sweet taste.

 It is also called laughing gas as it produces excitement and delirium.

 It is used with oxygen and ether and the technique is called “gas oxygen
ether (G-O-E) technique”.
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 It is the safest of the anesthetic agent with rapid induction, recovery and a
better analgesic action in subanaesthetic concentration. Nausea, vomiting
and irritation is uncommon with N2O

2. ETHER

 Anesthetic ether contains 96-98% diethyl ether.

 It is highly inflammable, colourless, volatile, liquid with pungent smell.

 It is usually used along with oxygen and nitrous oxide.

 It is also a safest anesthetic agent with excellent analgesia, therefore

provides excellent pain relief under light anaesthesia.

 The induction with ether is slow and laryngeal spasm may occur because
of pungent smell.

 Nausea and vomiting appear during recovery and the recovery is slow.

 Alcoholics are tolerant to ether, it is economical.

3. HALOTHANE (Fluothane):

 It is a heavy colourless liquid with sweet odour supplied in amber

coloured bottles.

 It has a fruity odour and readily attacks all metals like stainless steel,
brass, copper and rubber elements.

 A special apparatus is required to achieve precise control of

concentration. 2 – 3% halothane in oxygen produces loss of
consciousness and the maintenance dosage is 1-2%.

 It is non inflammable and does not irritate respiratory passage.

 Induction of anaesthesia is quick and pleasant without laryngo spasm.

 It provides a bloodless field and is preferred for plastic surgery.

 As it posseses poor analgesic properties, sedative and narcotics may be

used for premedication.

 Halothane is expensive also.

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4. THIOPENTONE

 It is a thiobarbiturate and is used as thiopentone sodium.

 These are used intravenously to produce anaesthesia.

 The induction is very quick and pleasant with ease in administration.

 The incidence of vomiting and excitement is less.

 There is speedy recovery after small doses without post anaesthetic complication.
Thiopentone sodium 0.5 to 1 gm is used as a freshly prepared and 2.5% solution
for intravenous anaesthesia.

 This agent is used for operation of short duration.

 This anaesthesia is contraindicated in presence of hepatic/renal damage in

shock, in airway obstruction, in bronchial asthma, and porphyria. When it is used
pre-medication with atropine is a must.

5. ETHYL CHLORIDE

 Ethyl chloride is a non irritating, highly volatile and inflammable liquid

with a boiling point of 12o C.

 The vapour has a characteristic but not unpleasant odour.

 It induces general anaesthesia within 2-3 minutes.

 Because of its quick induction property it is mainly used for induction of general
anaesthesia.

 When sprayed on the skin it rapidly evaporates and thus cools the skin thereby
producing transient paralysis of cutaneous sensory nerve endings.

 The local anaesthesia effect last from a few seconds to a minute and so incision
of an abscess can be carried out within this time.

 If ethyl chloride spray is used as local anaesthetic the skin should be prepared
with petrolatum to prevent sloughing.

 The spray may produce local oedema with decreased resistance to infection and
delayed wound healing.
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6. KETAMINE

 It is a new non barbiturate general anaesthetic agent.

 It is effective in both intramuscular and intravenous routes.

 Following a single dose (1-2 mg/kg for IV) it induces a state of dissociative
anaesthesia characterized by complete analgesia combined with amnesia.

 Analgesia lasts for about 40 minutes while anaesthesia lasts for about 15 minutes
only.

 The drug increases the blood pressure and can be used in presence of shock.

 Other general anaesthetic agents are tri-chloroethylene, Methoxyflurane,

cyclopropane, propanidid, methohexital etc.

1. PROPOFOL

 Newer group,Action not very well understood.Duration : 3-5 minutes

 Dosage : Adults (upto 55 yrs age) 2-2.5 mg/kg

 Adverse Involuntary movements,Burning, stinging at site of injection,

 Abdominal cramps

PREANAESTHETIC MEDICATION
Refer to use of drugs before anesthesia to make it more pleasant and safe

Aims are:-

1. Relief of anxiety and apprehension preoperatively for smooth

induction

2. Amnesia pre and postoperative events

3. Supplement analgesic action of anesthetics and potentiate so that

less anesthetic is needed.

4. Decreses sectetions and vagal stimulations caused by anesthetics

5. Antiemetic effect extended to postoperative period.

6. Decrese acidity and volume of gastric juices so that less

damaging if aspirated.
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One or more drugs may be used to achieve this

Benzodizepams- diazepam 5-10 mg oral

Anticholinergics- atropine 0.6 mg (i.m. or i.v.)

Antiemetic- metroclopramide 10-20 mg i.m.

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LOCAL ANESTHESIA

Local anaesthesia is loss of sensation, especially pain in a localized area without loss of
consciousness.

Loss of sensation in a part of body can be achieved by:

a. Refrigeration i.e. application of ice

b. Making tissue anemic

c. Use of drugs

 The mode of action of local anaesthetics is to block nerve conduction,

probably by preventing normal passage of ions through the nerve
membrane.

 All sensation i.e. pain, temperature, pressure and motor functions are
affected by the local anaesthetic agent.

 The type of local anaesthesia used in dentistry are:

a) Topical or surface anaesthesia

b) Local infiltration

c) Field block

d) Nerve block

a) Topical or surface anaesthesia

 Free nerve endings in accessible areas are rendered incapable of sensation by the
application of a suitable local anesthetic drug i.e. 5% xylocaine jelly.

 Mucous membrane abraded skin and the cornea of the eye respond well to topical
application of a local anaesthetic agent.

b) Local infiltration

 The terminal nerve endings in the area of surgery are flooded with the local
anaesthetic solution making them incapable of transmitting an impulse.

 The surgery is performed in the area in which the anaesthetic solution has been
deposited.
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c) Field block

 The local anaesthetic agent is deposited in the proximity of a large terminal nerve
trunks.

 All areas beyond this nerve trunk are anaesthetized.

d) Nerve block

 The main nerve trunk is blocked by the anaesthetic solution and hence the area
beyond the blocked region anaesthetized e.g. Inferior alveolar nerve block

Indications for use of LA

a) Cavity preparation in painful teeth

b) Pulpotomy, pulpectomy and root canal therapy

c) Extraction of teeth

Minor oral surgerySurgical extraction

i) Apicoectomy

ii) Gingivectomy, flap procedures

iii) Removal of cyst

iv) Alveolectomy and alveoloplasty

v) Excision of small growth

vi) Biopsy

CONTRAINDICATION
a. Refusal by patient

b. In presence of infection, the LA does not act because of acidic pH

c. Allergy to local anaesthesia

d. In children because of lack of cooperation LA may not be used

e. In mentally retarded people

f. In patients suffering from bleeding disorders like hemophilia, Christmas

g. disease or Von Willebrand’s disease

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METHOD OF USE
a) Nerve block – may be obtained either by intra oral or extra oral routes

b) Field block and local infiltration

i) Subucosal injection

ii) Paraperiosteal injections

iii) Intra osseous injections

iv) Interseptal injections

v) Intraligamentary injections

COMPLICATIONS

A) DUE TO LA SOLUTION
a) Toxicity

b) Allergy

c) Anaphylaxios

d) Infections

e) Local irritations

B) DUE TO NEEDLE INSERTION

a) Syncope

b) Pain

c) Needle tract infection

d) Broken needle

e) Haematoma

f) Prolonged anaesthesia
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LOCAL ANAESTHETIC DRUGS

Lignocaine hydrochloride

 It is the most commonly used drug and is stable and can be stored at room
temperature for a long time.

 It is used as a topical anaesthetic agent in concentration of 2-5%.

 A 2% solution is used together with the small amount of adrenaline (1:80000).

 The adrenaline increases the duration of anaesthesia by inducing vasoconstriction

in the area and thus confining the anaesthetic to the site of infection,

 It has also the advantage of improving visibility by reducing bleeding.

 This 2% solution is used for nerve block, field block and local infiltration.

Use of adrenaline containing local anaesthetic is contraindicated in patients with

Ischaemic coronary disease, hypertension, taking tricyclic anti-depressants or
hypotensive drugs such as Beta-blocker.

Prilocaine :

 3% of prilocaine with felypressin as a vasoconstrictor can be safely used on

patients with coronary disease.

 3% prilocaine is available in the brand name of citanest with octapressin as

vasoconstrictor

EQUIPMENT:

 The local anaesthetic is provided in a glass, 2 ml cartridge which has thin plastic
seal at one end and a rubber bung at the other.

 When it is placed in syringe the double end needle pierces the plastic seal and
solution is injected when the plunger at the other end pushes down the rubber
bung.

 To reduce cross infection the plastic end of cartridge or needle should not be
touched. A pair of fine haemostat should be kept nearby to remove the broken
needle while giving anaesthesia.
 165

 Now-a-days the aspirating syringe can be used safely to avoid injecting the
solution into blood vessels.

 In a normal individual 20 ml is the maximum amount of local anaesthetic with a

vasoconstrictor which can be safely administrated.

 4mg/kg – Maximum recommended dose.

 166

ANTIBIOTICS IN DENTAL PRACTICE

Introduction
 Discovery of Sulphonamide and antibiotics ushered in a new era in history of
medical sciences.

 Subsequent new discoveries have revolutionized drug therapy.

 Their ever increasing use indicates their indispensability.

 In order to assess their usefulness, we must understand basic principles of

antibiotic therapy, nature and functions of drugs and their toxic effects.

Historical events:

 Ever since disease was attributed to microbial activity, medical research has been
directed towards discovery of newer agents which could kill or eliminate the
pathogens without any damage to the host tissue.

 The first chemotherapeutic synthesized was Salvarsan an arsenical compound

used in treatment of syphilis.

 For next 20 years progress was not significant.

 In 1935, Domark demonstrated that a Dye ‘Prontosil’ – rubrum’ could suppress

streptococcal infection in mice.

 This paved the way for development of sulphonamides.

 In 1929 Fleming discovered penicillin but it was in 1940 that it came into use.

 With development of antibiotics, sulphonamides have come to a thing of the past.

 The National Formulary 1955 advised that “Sulphonamides should not be

administered to ambulant patients”.

Mode of action
 Action of sulphonamide is “Bacteriostatic”.

 It blocks the bacterial enzyme system concerned with production of PABA

essential for growth and multiplication.

 Penicillin is “Bacteriostatic” and :Bactericidal”.

 167

 Drug strength is maintained in pus, except “Penicillinase” producing bacteria

which destroy antibiotics.

 Aureomycin, Terramycin and Chloromycetin are ‘Bacteriostatic’.

 The action of antibiotics is directed towards bacteria and not their toxins,
therefore in disease where toxins are to be neutralized.

 E.g. tetanus, gangrene diphtheria – antitoxin therapy is of prime importance.

 Antibiotic do not promote healing or tissue growth.

 Therefore cardinal principles of surgery must still be followed.

 The defence mechanism of the body may take several days to destroy the
organisms, so antibiotics must be continued for adequately long duration.

 It is a natural process of solution by which one creature destroys another in order

to survive and drugs which show the ‘phenomenon are called ‘Antibiotics’.

PENICILLINS

Bactericidal

Effective against Gram +ve – aerobic and anaerobic.

Insensitive to it are:

Enterococcus, Gram –ve cocci, fungi, viruses, Rickettsiae

Bacteriostatic – low concentration Bacterioidal – high conc

Destroyed by HCl and penicillinase

Penicillin –G(Benzyl Penicillin):

Narrow spectrum antibiotic

Activity limited to gram positive bacteria and few others:

Cocci – streptococci, staphalococcus

Bacilli- B. anthracis, Corynebactrium deptheriae, all clostridia,Listeria,Spirochetes

Dose: Procaine pencillin G 0.5-1 MU i.m. 12 hr

Benzathine Pencillin G : 0.6 -2.4 MU i.m. every 2-4 wks

 168

Semisynthetic pencillin:

1. Acid resistant alternative to pencillin G- phenoxymethy pencillin ( pencillin

V)

2. Penicillinase resistant pencillins: Oxacillin, Cloxacillin

3. Extended spectrum pencillins

a) Aminopencillins : ampicillin , amoxicillin

b) Carboxypencillin :carbenicillin

c) Ureidopencillin : Mezolocillin, Piperacillin

d) Mecillinam : (amdinocillin)

B-lactamase inhibitors: Clavulanic acid , Sulbactam

Cloxacillin:

 Highly pencillinase as well as acid resistant

 less active against pencillin G sensitive organisms

 it is more active than Methicillin against pencillinase producing Staph.

 Dose : 0.25 – 0.5 gram orally 6 hourly

Ampicillin:

 Active against all organisms sensitive to PnG,in addition many garm negative
bacilli eg.- H. influenza, E. coli,Proteus ,Salmonella and Shigella are inhibited.

 Dose : 0.5-2gm oral/i.m./i.v. every 6 hourly

Amoxicillin:

Smilar to ampicillin in all respect except:

Oral absorption is better

Incidence of diarrhea is less.

Less active against shigella and H. infuenzae

Dose : 0.25-1 gm TDS oral

 169

Agumentin

 (Amoxicillin 500mg + Clavuanic acid 125mg)

 Addition of clavuanic acid reestablishes the activity of amoxicillin

against B-lactamase producing resistant Staph. aureus , H. influenza, N.
gonorrhea,E.coli, Proteus,Klebsiella,Salmonella, Shigella and Bact.
Fragilis.

CEPHALOSPORINS

 Semisynthetic antibiotics

 Derived from ‘cephalosporin –C’ obtained from fungus

Cephalosporium.

 Chemically related to pencillin the nucleus consist of of B-lactum ring

 All ceplalosporins are Bactericidal—inhibition of bacterial cell wall

synthesis

First generation –

1) Cephalothin

2) Cefazolin

3) Cephaloridine

4) Cephalexin

5) Cephadine

6) Cefadroxil

Second generation -

1) Cefuoxime

2) Cefoxitin

3) Cefaclor

4) Cefuroxime
 170

Third generation -
1) cefotaxime

2) Ceftizoxime

3) Ceftriaxone

4) Ceftazidime

5) Cefoperazone

6) Cefixime

Fourth generation -

1) Cefepime

2) Cefpirome

DOXYCYCLINE

 Belongs to Tetracycline group, Bacteriostatic

 Effective against Gram positive, Gram negative, Ricketssiae, Spirochetes,

Mycoplasma

 Adverse effects - Permanent staining of teeth, Superinfection

 Contraindicated in Pregnancy, children < 12 yrs

 Dosage - Adult – 250 – 500 mg 8 hrly

ERYTHROMYCIN
 Belongs to macrolide group

 Primarily bacteriostatic

 Used in patients allergic to Penicillin

 Used in Acne vulgaris

 Adverse reactions like Hepatotoxicity, ototoxicity & Renal failure

 Dosage - 1 g daily b.i.d /q.i.d (Adult)

 30-50 mg/kg/day in 3 -4 divided doses (child)

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GENTAMICIN
 Active against aerobic, Gram negative and some Gram positive organisms2.
Domestic pressure cookers

 Used in neonatal infections, burns, Skin infection

 Adverse – Nephrotoxicity

 Dose - 1mg/kg 8 hrly IM in severe infections

METRONIDAZOLE
 Belongs to nitro imidazole group

 Effective against anaerobic bacteria

Adverse reactions include

 Peripheral neuropathy

 Superinfection

 Metallic taste

 Alcohol intake during Metronidazole therapy can lead to a Disulfiram

like reaction

 Dose- Adult 400 mg b.i.d

CIPROFLOXACIN
 Fluoroquinolone Antimicrobial

 Bactericidal especially for gram negative bacteria

 Used in UTI, LRTI, Gynaecological infections and surgical prophylaxis

 Adverse - Contraindicated in children since it can cause tendenitis,

ruptured tendon

 Dose - 500 mg 1 b.i.d.

AMOXYCILLIN
Semisynthetic Penicillin

Bactericidal

Gram positive, Gram negative bacteria

 172

Adverse - Rash, Diarrhoea , Superinfection

 Dose - 260 – 500 mg t.i.d. (Adult) & 125 mg t.i.d (child)

NEWER ANTIBIOTICS

AZITHROMYCIN
- Belongs to macrolide group

- Spectrum similar to Erythromycin

- Also effective against Gram negative organisms

- High concentration achieved in macrophages and polymorphonuclear

leukocytes

- Dosage - 500 mg OD (Adults)

- For Children :

- 15-25 kg – 200 mg OD x 3 xday

- 26-35 kg – 300 mg OD x 3 days

- 36 – 45 kg – 400 mg OD x 3 days

CLARITHROMYCIN
- Macrolide group

- Active against atypical mycobacteria

- Dosage

- Adult – 250-500 mg b.i.d

- Child 7.5 mg/kg 12 hrly

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HAEMOSTATICS
Introduction
- Haemostatics are the agents which arrest bleeding.

- When these agents are acting locally then they are called
styptics.

- Bleeding can be from gums, tooth socket, ruptured vein or

arteriole, blood vessels of a fractured bone or from adjacent soft
tisues.

- Haemostasis can be achieved by different methods.

They are divided as:

1. Haemostasis achieved by physical method:

a) Pressure application

b) Tourniquet

c) Cold

d) Use of cautery

e) Ligation

2. Haemostasis achieved by using Haemostatic agent:

a) Agents acting locally

i) Tannic acid/Alum/Turpentine

ii) Thrombin

iii) Thromboplastin

iv) Fibrin

v) Gelfoam

vi) Oxidised cellulose

vii) Russel viper venom

viii) Bone wax

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ix) Adrenaline

b) Agents acting systematically

i) Fibrinogen

ii) Antihaemophilic globulin

iii) Plasma or blood

iv) Calcium

v) Vitamin and rutin

vi) Certain snake venoms

vii) Vitamin K

viii) EACA (Epsilon Amino Caproic Acid)

ix) Sclerosing agents

PHYSICAL METHOD
a) Pressure

Bleeding can be controlled by pressure from swabs and this is undoubtedly the most
effective method for almost all intra oral wounds. A dry gauze swab is packed into the
wound over the bleeding area and digital pressure is maintained over the swab for a
minimum of two and half minutes and pressure should be more than clotting time.

b) Cold

Cold compress produce Vasoconstriction thus produce haemostasis

c) Use of cautery

It produces haemostasis by thermal coagulation

d) Tourniquet

Reduces the venous drainage thus producing haemostasis

 175

Locally acting agents:

Tannic acid :

Tannic acid or turpentine applied on gauze packs or cotton wool to stop bleeding.

It is dangerous and can cause second degree burns at the angle of the mouth and on the
lips if it is applied in a bleeding socket.

Thrombin :

It is obtained from bovine plasma

1. It is stable as a dry powder stored between 2 to 8o C is however, inactive below pH 5.

2. Thrombin therapy is restricted to local application in oozing of blood.

Thromboplastin :

1. It is extracted from brain on lung tissue of freshly killed rabbits.

2. It is used for determination of prothrombin time and as a local haemostatic in surgery.

Fibrin :

1. It is obtained from human plasma and is used in the dehydrated form as sheets from
which segments of any desired size may be cut for use on bleeding surfaces. When used
in combination with a thrombin solution, it also acts as a mechanical barrier and holds
thrombin in position over the bleeding area.

Gelfoam :

1. It is a porous, pressed form of gelatin sponge used in conjunction with thrombin to

control oozing of blood from surface wounds.
2. Gel foam is usually moistened with sterile, isotonic saline before use.
3. It is completely absorbed within 4 to 6 weeks, and hence may be left in place after
suturing of an operative wound.
4. Gel foam is available as cones, packs, sponges and powder.

Oxidised cellulose (oxycel) :

1. Oxycel is surgical gauze treated with nitrogen dioxide, and it produces clotting by a
reaction between haemoglobin and cellulosic acid, oxycel, when wet with tissue fluid,
becomes sticky and gummy and exerts its haemostatic effect by mechanical blockage.
2. Oxycel is usually absorbed completely within 2 to 10 days.
3. It interferes with bone regeneration.
 176

Venom

Russel viper venom will certainly precipitate clot formation when applied on a pledget of
cotton wool.

Bone wax

A purely mechanically acting haemostatic agent is bone wax which consists of bees wax
7 parts by weight, olive oil 2 parts, phenol 1 part,. This substance is racked into bleeding
bone ends to control the haemorrhage. It forms wax granules.

Adrenalin

It is used with the help of a gauze or wool pack. Dilution is 1 : 1000.

It is absorbed from skin or mucous membrane and causes vasoconstriction.

Agents acting systematically:

Fibrinogen :

It is sterile fraction of human plasma, is used for restoring normal fibrinogen levels in
haemorrhagic conditions.

Anti haemophilic globulin

Antihaemophilic globulin or concentrate of factor VIII (AHG) is highly effective in the

treatment of classical haemophilia. igh potency of human AHG is prepared from pooled
normal human plasma. It is given IV, in the dose of 15-16 units/kg/day.

Plasma or blood

Fresh frozen plasma is suitable for the treatment of most coagulation disorders since it
contains all the coagulation factor. Whole blood is not the choice as large volumes are
required

Calcium

Calcium therapy, particularly by parenteral route, is restored to control of bleeding.

Except in the presence of calcium deficiency such treatment is not useful.

Vitamin C

Vit C can control bleeding only in the presence of scurvy. The oral dose is 50-100 mg
of Vit C, repeated 3-4 times a day.
 177

Snake venom :

Especially Russel viper and copper head snake venoms enhance coagulation by
stimulating thrombo kinase.

Vitamin K :

It is fat soluble vitamin but is not single entity but occurs naturally in the form of at least
two distinct substances - vitamin K1 and K2. Both are derivatives of napthoquinone. Vit
K is essential for the biosynthesis of prothrombin and factors VII, IX and X. Apart from
the action on blood coagulation vit K do not possess any other Pharmacological actions.

EACA

Continuous uncontrolled haemorrhage associated with excessive fibrinolytic activity has

been considered on indication for EACA therapy. The drug has been used to control
haemorrhage in abruptic placentae, post partum haemorrhage and haemorrhage after
some surgical proceedings. Dose is 100 mg/kg, or orally 4 times a day.

Sclerosing agents :

Sclerosing agents are irritating substances employed to obliterate varicose veins.

They have also been employed for fibrosing uncomplicated haemorrhoids.
 178

VASOCONSTRICTORS AND VASODILATORS

Drugs which constrict blood vessels are called Vasoconstrictors.

1. ADRENALINE

- It is sympathetic neurohormonal transmitter of the adrenal medulla.

- It causes vasoconstriction of the blood vessels when applied locally or

given as a I/V injection.

- For haemostatic effect gauze is soaked in adrenaline and applied on

mucous membrane or packed into socket.

- It may be injected subcutaneously and action lasts for ½ to one hour.

- Strong solution produces sloughing and very large amounts may result
in dry socket. Intravenous injection – It increases the rate and the
cardiac output of the heart.

- There is a rise of blood pressure due to vasoconstriction but the vessels

of skeletal muscles are dilated. It also produces a thick viscous
secretion from salivary glands.

- Dose – Control of haemorrhage

- Topical – 1: 1000 to 1:20000 Bleeding from arterioles & capillaries

- Use with local anaesthdtics : 1 : 800000 to 1 : 200000

- Intracardiac – 0.2 to 0.3 ml of 1 : 1000

- Ventricular Fibrillation – .5 to 1 mg (5 – 10 ml of 1 : 10000 every 5

minutes)

NOR ADRENALINE
- A catecholamine secreted from adrenal medulla mainly used for
elevating the blood pressure in shock.

ISO PRENALINE (ISOPROTERENOL)

- Isoprenaline is the most powerful synthetic, beta receptor stimulant

drug
 179

- Dose - 5 to 20 mg sublingually

- Inhalation - 5 ml of 1 : 200 solution

- Isoprenaline is sometimes being advocated as a cardiac stimulant in the

treatment of bacteremic shock.

EPHEDRINE
- It is alkaloid obtained from plants of genus ephedra.

- Increases blood pressure both by peripheral vasoconstriction and by

increasing the cardiac output.

- It relaxes the bronchial smooth muscle.

- It increases the metabolic rate and oxygen consumption

- DoseOral 15-60 mg t.i.d ,I/M or SC - 15 to 45 mg

- Nasal drops 1% is used

Used for 1. Bronchial asthma

2. Nasal Decongestion

3. Hypotension

AMPHETAMINE
- It increases the systolic and diastolic blood pressure.

- It does not elevate cardiac output significantly.

- Dose – 5 to 10 mg given in the morning and at mid-day

Uses: 1. Narcolepsy – 30 to 40 mg per day

2. Obesity

3. In certain cases of epilepsy

METARAMINOL (ARAMINE)

- Resembles nor adrenaline raises blood pressure by vasoconstriction.

- Rise in blood pressure accompanied by bradycardia.

- It increases the cardiac output; cardiac metabolism and force of

ventricular contraction
 180

Dose – I/M 2-10 mg, I/V 0.5 to 10 mg

METHEDRINE
- Action of these drugs is like amphetamine but more prolonged.

- Dose – 5 to 10 mg. Useful for obesity

ERGOT
- Powder or crystal are readily soluble in water.

- It has a vasoconstricting effect on arterioles. Effect lasts for 4-6 hrs.

Used in control of uterine bleeding and causes powerful uterine
contraction.

- Accumulative effect results in poisoning, nausea, vomiting, tingling

sensation at finger tips and toes and may result in gangrene.

FELYPRESSIN (OCTAPRESSIN)

- Synthetic polypetide resembles vasopressin, the naturally occurring

posterior pituitary hormone combined with local anaesthetic agent.
Dose - 0.03 per ml (5.4 mg per ml)

- 3% prilocaine + Felypressin – (Citanest)

- Advantage : It can be given to patients with cardiovascular disease.

VASODILATORS

AMYL NITRATE:

- When inhaled from broken capsule it dilates arterioles and causes fall
of blood pressure.

- There is sweating, palpitation, fainting attacks, giddiness, throbbing of

head and flushed face.

- It dilates coronary artery and relieves pain of angina.

- Dose – 0.5 to 1 mg sublingually

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PRISCOL

- It is a peripheral vasodilator.

- It antagonizes the action of adrenaline. Used in the treatment of

Raynauds disease.

POTASSIUM, THIOCYANATE –

- regulated doses decreases blood pressure. Side effects are nausea,

vomiting, diarrhoea, Acute poisoning can occur.

PHENTOLAMINE :

- They produce dilatation of the peripheral blood vessels, particularly the

arterioles and capillaries of the skin, increases the mobility of the gut
and the secretion of hydrochloric acid.

- The salivary, lacrimal, respiratory and pancreatic secretions are also

augmented

PRAZOSIN –

- This drug acts by blocking alpha receptors.

- It dilates both arteries and veins, causing reduction in venous return

and cardiac output.

- It is used to treat essential hypertension

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COUNTER IRRITANT AGENTS

HEAT

 It is applied in the form of hot water bottle on the skin.

 In oral cavity it is used as a mouth wash.

 Application of heat gives relief from dry socket.

 Hot mouth washes relieve pain from abscess and ulcers.

POULTICE

 A kaolin poultice consists of kaolin 52.

 7% with boric acid Methylsalicylate and Thymol made into a paste with
glycerine.
 Action is by heat.

LINSEED-MUSTARD

 It has irritant properties.

 It is added to linseed poultice. (2 parts mustard + 28 parts linseed).

 Mustard leaf can be cut and applied too.

IODINE

 Useful mild counter irritant for the oral mucosa & gingival.

 Used as 10% solution in glycerine.

TINCTURE ACONITE

 Produce tingling sensation, followed by numbness.

 Used for deep pocket.

 50% of this solution can be used for pain against neuralgias.

CAMPHOR

 When rubbed ino the skin it acts as a counter irritant to relieve neuralgia.

MENTHOL

 Used as 15% in cones, ointments and 20% in liniments along with clove oil.
 183

COUNTER IRRITANTS

This term is applied to a group of irritant drugs which, when applied over skin or mucous
membrane produces by sensory stimulation, a local inflammatory reaction of redness
with sensations of heat and tingling followed by a moderate degree of local anaesthesia
from subsequent paralysis of sensory endings. According to intensity of reaction, these
drugs are divided into 3 groups.

1. RUBEFACIENTS

 Mild irritant acting on the skin or mucous membrane stimulate sensory

nerve ending and produce irritation resulting in inflammation, redness,
due to increased flow of blood.

 This increased flow of blood bring more phagocytes to the area so that
the bacterial, chemical irritants are combated.

 The initial stimulation follows fatigue of depression of the nerve so that

superficial anaesthesia results and local or referred pain is relieved.

The drugs are also capable of producing.

a) Acceleration of the heart

b) Rise in blood pressure

c) Shallow rapid respiration

2.VASICANTS

 These are moderate counter irritant.

 In the hyoperaemic area, plasma exudates collect in the stratum corneum and the
epidermis is raised to form blisters.

 Blisters are very painful and undergo resolution after few days.

3. PUSTULANTS

 These are severe irritants and cause rapid painful inflammation and blister
formation.

 Leucocytes are killed by the bacteria and irritants, thus pus is formed in the
blisters. The blisters burst and the healing is caused by scar formation.
 184

DENTIFRICES AND MOUTHWASHES

 Tooth powders or toothpastes are mechanical aids to cleansing and polishing of
teeth with brush.

 They consist of the following ingredients:

1. An abrasive

2. Detergent or cleansing agent

3. An antiseptic and fluorides

4. Flavouring agent

5. Colouring agent

6. Sweetening agent

7. Humectant

8. Thickening agent

ABRASIVE –

- These are fine powders which help mechanically the action of a

toothbrush.

- To remove gritty particles it is passed through 60 mesh powder sieve.

Dibasic calcium phosphate has least abrasive action.

- Calcium carbonate and chalk are used.

 Abrasive agents commonly used are:

 Calcium carbonate – a white fine antacid powder

 Chalk – a white amorphous, antacid powder

 Calcium phosphate – a white amorphous powder

 Other agents are:

o Milk of magnesia, Kaolin, aluminium oxide, silicon oxide

o Precipitated chalk is frequently combined with magnesium carbonate or

oxide or magnesium hydroxide in proportion 1: 4.
 185

 Staumic oxide 5-10% may be added if a very high polish is required.

 PH of saliva is 6.6 but varies.

 Slight acidity of dentrifice stimulates flow of saliva; on the other hand, alkaline
dentrifice neutralizes acids of formation, and also dissolves mucin.

 Sodium benzoate 5% dissolves calcium in a Kaolin base.

DETERGENT OR CLEANSING AGENT

These act a) by lowering surface tension e.g. soap

b) dissolving proteins e.g. soluble alkalis

c) by evolving O2 e.g. peroxides

 The most commonly used is hard soap.

 Hard soap acts as emollient and cleansing agent by dissolving fatty material and
mucin plaques.

 It lowers surface tension and loosens debris adherent to teeth and is added from 5-
25% to providers or pastes.

 It acts as a lubricant and foams on teeth.

 Others used are sodium lauryl sulfate and sodium lauryl sarcosinate.

 Sodium Ricinoleate is a valuable soap for treating gingival infections.

 Soluble alkalis – Potassium hydroxide, sodium bicarbonate dissolves protein

debris. Sodium, calcium magnesium perborates and magnesium peroxide liberate
O2 and help to detach debris and exfoliated epithelium.

 These also act as deodorants.

ANTISEPTIC –

These are included in dentifrices but their value in bacterial growth restriction is limited.

Phenol, thymol, menthal - .25% - 1%

Euginol - 1%

Clove oil, Cinnamon - 1-3%

Potassium chlorate - 2-3%

Boric acid - 2-5%

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Camphor, borax - 5-10%

FLAVOURING AGENT

 Mostly these are volatile oils e.g. thymol, clove, wintergreen, cinnamon, rose.

 These also act as antiseptics.

SWEETING AGENT

 Lactose upto 10% is used. It does not ferment.

 Saccharin sodium is best.

 It is 200 times sweeter than sugar and does not ferment and 0.1% is added.

COLOURING AGENTS

 Added to toothpastes, which contain toxic antiseptics.

 Patients are attracted to pleasing colours.

 Chlorophyll green is in demand at present.

 Liquor carmini 2% is also used.

o Methylene blue - .001 % blue

o Megenta - .5%

HUMECTANTS

 It binds all ingredients together and keeps dentifrice moist. E.g., glycerin and
sorbitol.

THICKENING AGENT

 These are carboxymethyl cellulose alginate and amylase.

TOOTHPASTES

 Tooth powders are converted into pastes by use of syrup, honey, glycerin. 0.1 –
0.2% Tragacanth may be added to improve consistency.

 1% liquid paraffin may be added so that it can be removed from a tube with ease.

 For desensitizing and anticariogenic action, sodium fluoride,stannous fluoride,

sodium monofluorophosphate has been added.
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 Sensodyne toothpaste contains 10% strontium chloride.

 Emoform, having 10% formaldehyde acts on hypersensitive dentin.

 Colgate total, a newly marketed dentifrice contains triclosan, fluoride and gantrez
for added protection.

 Deodorants – These eliminate halitosis and leave behind freshness and tingling
sensation

MEDICATED DENTRIFICES

A) Anti plaque and anti gingivitis Dentrifices

1. Chlorhexidine (1%)

2. Trioclosan (in combination with zinc citrate)

B) Anti calculus Dentrifices

1. 2% zinc chloride

2. 1.25% - 5% Pyrophosphate salts

3. Triclosan (0.2%)

C) Anti Caries Dentrifice

Fluorides :

a) Sodium Fluoride

b) Sodium Monofluorophosphate

c) Stannous Fluoride

d) Potassium Fluoride

e) Aluminium Fluoride

Maximum permissible concentration of Fluoride: Adults- 1500 ppm,

Child (< yrs) - 250 ppm

MOUTH WASHES

 It is used as an aid to physiotherapy.

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 Simple rinsing of the mouth with plain water will remove mechanically any
detachable or soluble debris.

 It removes bacteria and their products by its irrigation power.

 The mechanical action is increased if used with compressed air and carbondioxide
sprays.

 This method is useful for treatment in bed patients.

 Various chemicals have been now incorporated based on rational to make them –

a) Ant caries

b) Ant calculus

c) Desensitizing

d) Preventive and therapeutic

 Mouthwashes have no classification and are considered as cosmetics.

 According to mode of action they may be:

1) Oxidizing

2) Acid and alkalis

3) Coaltar agents

4) Desensitizing

5) Physical agent

6) Therapeutic for diseases

Oxidizing

 This action is due to Nascent oxygen and effervescence.

 The mechanical action helps in cleaning deposits.

 The antiseptic action may be effected by free radicals and bleaching agents are
also added.

Drugs added are Hydrogen peroxide – 3% ,Potassium permanganate 1/5000 to

1/1/1000. These produces stains. Potassium chlorate 2% may also be used.
Perborate was marketed as Amosan.
 189

Acids and alkalis -

 This makes a soothing and bland mouthwash.

 It withdraws water from bacteria.

 Detergent action neutralizes acids of fermentation.

 Sodium bicarbonate is used 2% strength.

 Chelating agents have a capacity to remove calcium salts from mineral structure.

 Thus it prevents incorporation of Ca in the soft matrid. 5 – 10% soln in water is

used.

 It has a good smell and a cooling effect.

Astringents

 Act by precipitating the proteins on the surface to produce a protective layer

against bacterial invasion.

 Alum, tannic acid 5 gr in one fluid ounce is useful for tender swollen gums and
helps heal ulcerations.

 Other drugs are zinc chloride, zinc acetate, acetic and citric acids.

Coaltar derivatives

 Phenol has a caustic or corrosive action.

 In small concentrations it is an anodyne antiseptic useful for aphthous ulcer and

dry sockets.

Physical agents

 It acts by mechanical rinsing action and high osmotic pressure.

 Normal saline is used as a cleaning mouth wash.

 Hypertonic saline has cleansing and protein solvent action used after prophylaxis
and gingivitis.

Anaesthetic mouthwash

 produces and acts as surface anaesthetic.

 Useful in painful oral ulcers and ANUG.

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 Must be used 30 mts prior to meals or must be used in between meals.

 These are anodyne mouthwashes.

Properietary group (Amosan)

 Sodium Peroxyborate monohydrate.

 This yields 65% more oxygen than Sodium perborate.

 Cases show better healing

Ascoxal

 It has been tried and compared with Hydrogen peroxide in management of

ANUG.

 It reduces the viscosity of saliva.

 It has demucopoly saccharide antimicrobial effect.

 There is marked inhibiting of calculus formation.

 It is pleasant in taste.

 Available in tablet and contains Vit C 100 mg. Sodium bicarbonate 75 mg,
Copper sulfate as a catalyst only in traces

Bocasin

 1 tab is put in a glass of water.

 It is effective in ANUG which shows 73% improvement in 48 hrs.

 It is buffered with sodium bitarterate.

Dettolin

 Contains Chloroxylenol 1.02% w/v, menthol .12% w/v and absolute alcohol
60.8% w/v.

Listerine

 is an essential oil mouthwash which coagulate organic matter.

 It reduces secretion of saliva and washes away the mucin.

 191

 It acts as a deodorant and removes halitosis.

Chlorhexidine

 has pronounced antiseptic properties.

 10 ml of 2% or 15 ml of .12% aqueous solution of CHX mouthwash done twice

inhibits development of dental plaque.

 Its side effect is brown staining of teeth, tongue and resin restorations.

 Antiseptics used in mouth rinses:

1. Triclosan

o Broad spectrum of activity

o Effective against Gram positive and gram negative. bacteria

o Anti plaque efficacy

o Used in combination with Zinc citrate.

2. Metal Ions

o Stannous Fluoride (reduce acid formation in plaque)

o Anti Gingivitis effect

o Reduce halitosis by eliminating volatile sulfur – containing compounds

(VSC)

3. Chlorhexidine

o 0.12% ideal

o Antiplaque effect

o Gets adsorbed to surfaces and increased duration of action

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ANALGESICS
Analgesics are drugs which relieve pain without producing unconsciousness.

As the treatment of pain is one of the prime functions of dental practitioner, it is

important that he should not only be familiar with the various technical procedures, but
that he should also be conversant with the types of classes of drugs necessary to relieve
or control this symptom in his patients. Analgesics may act centrally (selective
depressant effect on the central nervous system) or may act peripherally due to a direct
effect on pain receptors.

Can be classified as:

 Opoid analgesics

 Non steroidal anti-inflammatory drugs (NSAIDS)

OPOID ANALGESICS
Properties - More potent

- Useful in severe visceral pain

- High abuse potential

- Euphoric feeling after intake

- Can cause respiratory depression

Drugs - Morphine, Pethidine, Pentazocine

a) MORPHINE – Dosage : Adult – 10-50 mg 4 hrs

(Severe pain) Child – 5-10 mg

B) PETHIDINE - Dosage : 25 – 100 mg SC/IM

or

25 – 50 mg IV 3 hrly

C) PENTAZOCINE - Dosage Adult 25-100 mg q.i.d

Child 25 mg q.i.d
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NEWER OPOID

Tramadol - Excellent analgesic

- Respiratory depression lesser

- No dependence

- Post operative pain

Dosage Adults – 100 mg SC/IM/IV, Child - 1-1.5 mg / kg

NON STEROIDAL ANTI INFLAMMATORY DRUGS (NSAIDS)

Properties - Commonly used

- Cannot be used for severe pain

- Safer analgesics

- Anti-inflammatory

- Anti-pyretic

NSAIDS further classified as:

Non selective COX-2 inhibitors

Selective COX-2 inhibitors

(COX – Cyclooxygenase)

1. Non-selective COX-2 inhibitors

Includes: Aspirin, Paracetamol, Piroxicam

Ibuprofen, Diclofenac, Indomethacin

ASPIRIN

Relief is provided when pain is of aching type, as in headache, TMJ dysfunction and dry
socket.

Adverse reactions:

1. Gastro-intestinal disturbances may lead to gastrointestinal bleeding

2. Prevents platelet aggregation. Therefore cannot be given in bleeding disorders.

Dose – 300 mg 8 hrsAspirin, Phenacetin 250 mg, codeine phosphate – 8 mg

 194

PARACETAMOL

This mild analgesic is the principal metabolite formed in the liver from phenacetin and
acetanilide used in patients who are sensitive to Aspirin, have history of peptic ulcer or
suffer from Haemophilia or other bleeding disorders.

Dose –500 mg 8 hrly

IBUPROFEN

This is a mild analgesic commonly used in dentistry.

It has minimal side effects.

It has got excellent anti-inflammatory properties generally used in soft tissue

inflammation and post extraction.

INDOMETHACIN

It has moderate analgesic properties along with anti-inflammatory property.

It causes severe gastric irritation and bone marrow depressio

Dose – 50 mg 2-3 times a day.

PIROXICAM

Dosage 20-40 mg OD

DICLOFENAC

Potent anti-inflammatory, analgesic and antipyretic

Available as Sodium and Potassium salts

Dose – 50 mg b.i.d (Adult)

1-3 mg/kg/day (Child)

NEWER NSAIDS

Ketoprofen :

Propionic acid derivative

 195

Dose – 50 mg bd/t.i.d ,300 mg in severe cases.

Ketorolac:

 Belongs to NSAID

 More potent analgesic

 Dosage10-20 mg initially followed by 10 m 6 hrly

2. Selective COX-2 inhibitors

Drugs Nimesulide Celecoxib

Meloxicam

NIMESULIDE

Potent anti-inflammatory.

Inhibits Histamine release

Dose: 100 mg b.i.d (Adult)

5 mg/kg/day in divided doses (Child)

MELOXICAM

- New NSAID of Oxicam group

- Selective action on COX-2

Dose: 7.5 – 15 mg OD

CELECOXIB

Anti-Rheumatoid drug,

Dose - 200 mg/daily

 196

HYPNOTICS
Introduction
A hypnotic drug is one which produces sleep resembling natural sleep.

A sedative, on the other hand, is a drug that reduces excitement.

Hypnotics and sedatives both induce depression of central nervous system, the
difference being mainly quantitative.

Classification of Hypnotics:

I. Urea derivatives

a) Diureides - Barbiturates

b) Related ureides – Glutethimide, Methyprylone

II. Benzodiazepines

III. Alcohols – Chloral hydrate

IV. Aldehydes - paraldehyde

V. Acetylated carbilols – Ethinamate

VI. Miscellaneous : Methaqualone ,Antihistaminics and Scopolamine

VII. Inorganic ions – Bromide

 Drugs like Morphine and Pethidine, besides its analgesic properly, also posses
hypnotic property.

 Hence, they are grouped as Anodyne hypnotic.

 It must be emphasized, that they should not be used as hypnotics in the absence
of severe pain.

UREA DERIVATIVES
Barbiturates:

It is a derivative of Barbituric acid and in the past the most commonly employed
hypnotics. It is colourless, odourless, crystalline solids with a bitter taste and are
sparingly soluble in water. They dissolve rapidly in the organic solvents like chloroform
and ether
 197

.Conventionally, the barbiturates are divided according to their duration of action as:

a) Long acting (8 hour or more)

e.g. Phenobarbitone

b) Intermediate acting (4 to 8 hrs)

e.g. Amylobarbitone

Butobarbitone

Pentobarbitone

c) Short acting (less than 4 hrs)

e.g. Secobarbitone

Hexobarbitone

d) Ultrashort acting (IV)

e.g. Thiopentone

Methohexitone

Pharmacological Action
Barbiturates cause reversible depression of the activity of all excitable tissue, the
CNS being exquisitely sensitive.

However, hypnotic drugs produce very little effects on cardiac, smooth or skeletal
muscles.

CNS – Barbiturates can achieve various depth of depression of CNS

1.Sedation and hypnosis – The long and intermediate acting barbiturates are used for
this purpose. Thus Phenobarbitone is given in the dose of 15 mg 3 to 4 times daily.

2.Anaesthetic effect – The short acting Thiobarbiturates administered IV produce basal

or general anaesthesia dose – Thiopentone sodium i.e. 0.5 to 1.0 g powder. It is used as a
freshly prepared 2.5% solution for IV anaesthesia, as basal or for induction.

3.Anticonvulsant effect – All the barbiturates administered anaesthetic doses are

capable of inhibiting or abolishing drug induced convulsions.

4.Analgesic effect – Barbiturates cannot reduce pain without producing a loss of

consciousness.
 198

5.Spinal cord – Reflexes of spinal cord are depressed by barbiturates

6.Eyes – Hypnotic doses has no effect on the eyes but moderate increase in the dose
elicit Nystagmus.

CVS – Therapeutic doses may cause slight fall in blood pressure and decrease in heart
rate

GIT – Sedative doses of barbiturate has no effect on GIT. Toxic doses of barbiturate
retard peristalsis.

Kidney – IV barbiturates results in reduction in urinary output.

Liver – No significant effect

Absorption rate and excretion

Barbiturates and their salts are readily absorbed orally and intramuscularly. They
are weak acids and the maximum absorption occurs from the stomach where the
barbiturates exist in an unionized form.

Therapeutic uses of Barbiturate:

a) As sedative and hypnotic

b) As anti-convulsant

c) Preanaesthetic medication

d) General anaesthetics

e) As antipsychotic drugs

Adverse Reaction
a) Intolerance – Urticaria, Angioneurotic oedema etc

b) Prolonged therapy may produce Megaloblastic anaemia

c) May depress Foetal respiration

d) Drug interaction – Barbiturates when combined with other CNS

depression drugs such as alcohol, benzodiazepine may cause severe

depression.

e) Drug dependence – Repeated administration of barbiturates causes drug

dependence. Manifestation of chronic barbiturate intoxications are thick

 199

slurred speech, ataxia, impaired superficial and deep reflexes, hypotonia,

nystagmus and difficulty in accommodation.

g) Acute Barbiturate poisoning – results from ingestion of an over dose either

accidentally or with suicidal intent. It is characterized by depression of the
CNS particularly the respiration and peripheral circulatory collapse.

Benzodiazepines Derivatives:

These are mainly used in anxiety states and neurosis.

These drugs are sometimes called as minor tranquilizers because they have claiming
effect in anxiety states associated with neurotic personality, situational crisis and
physical disease.

All Benzodiazepines have a hypnotic action.Diazepam (5-10 mg), Flurazepam (15-30

mg) and Nitrazepam (5-10 mg) have proved highly effective hypnotics.

These drugs cause sedation, hypnosis, decreased anxiety, muscle relaxation and some of
them also posses anticonvulsant activity.

The benzodiazepines are adequately absorbed when given orally.

Alcohol:

a) Ethanol – Taken at bed time, ethyl alcohol may act as a mild sedative.
However, it can not be recommended as a hypnotic as in small doses it may produce
excitement. In addition, there is the danger of drug dependence

b) Chloral Hydrate – It is a white crystalline substance, readily soluble in water.

Doses – As a mixture 0.5 to 2.0 gm

Children syrup 125 mg/year to max 375 mg

Infants syrup 50-75 mg per dose

Aldehydes:

Paraldehyde – It is colourless, transparent and inflammable liquid with a

characteristic odour. Paraldehyde is given by rectal or intramuscular route to produce
hypnosis.

Dose – Inj 5-10 ml – Intramuscularly

Inj 15 – 30 Rectally.
 200

OBTUNDENTS AND CAUSTICS

Obtundents are drugs used to dull or abolish the sensation or sensitiveness of

dentin to allow its painless excavation.

Their action is by:

(a) Paralyzing the nerve fibril e.g. local anodynes

(b) Precipitating proteins and killing nerve tissue e.g. Caustics.

A good obtundent should act painlessly, penetrate dentin rapidly, but not too
deeply as it may cause inflammation or necrosis of pulp and that it should not stain
enamel or Dentin.

Drugs used are:

1. Phenol

It is a protoplasmic poison. It causes tingling and then numbness.

It acts rapidly but does not penetrate deeply, because it is not soluble in saline or
albuminous fluids. It does not stain healthy dentin but darkness infected dentin. 80%
phenol is used, and is vapourized with hot air syringe to promote penetration.

It is neutralized with alcohol, glycerine or all.

2. Creosote

Acts as an anodyne on exposed pulp.

At first irritates and paralyses sensory nerve endings causing numbness and analgesia.
Penetration is deeper than phenol. It is vapourised with hot air syringe.

3. Clove oil

It paralyses nerve fibrils.

It penetrates slowly so requires to be sealed into the cavity for few days.

It stains dentin yellow.

It is a common ingredient of antiseptic pastes or temporary filing for sensitive dentin.

 201

4. Camphor, Thymol, Menthol

These volatile oils act like clove oil. Spirit of camphor, alcoholic solution of menthol
dried with hot air syringe are good obtundents.

Thymol crystals are sealed in cavities. Thymol 2, phenol 2, camphor 1 applied to

sensitive dentin is useful.

5. Dentalone

It is a saturated solution of chlorbatol.

It is a mixture of oil of cloves, cassia and wintergreen.

It is nontoxic, obtundent for exposed pulp and sensitive dentin.

6. Alcohol

It dehydrates and precipitates proteins and is used in 70-95% strength, in a dry cavity.

It is painless, does not stain and is nontoxic to the pulp.

7. Zinc chloride

It is an astringent caustic.

It precipitates proteins.

On application there is brief acute pain and then desensitization.

It does not penetrate deeply, does not stain and is a safe drug. Its 5-10% solution is
used.

8. Silver Nitrate

a safe caustic, is less painful than zinc chloride.

It acts rapidly and is precipitated as phosphate or chloride.

It does not penetrate deeply.

It stains dentin black and used as 10% solution.

9. Paraformaldehyde

from this drug formaldehyde is liberated which precipitates proteins.

Obtundent action is slow and painless. It does not stain. It penetrates deeply.
 202

Paraformaldehyde + Zinc oxide :

made into a paste with clove oil can be sealed into cavities for 6-7 days

10. Arsenic trioxide

It is toxic on living cells.

It penetrates deeply and rapidly.

In deep cavities it is not to be used due to chances of necrosis.

It is very painful and toxic.

11. Liquor soda Ethylate

18% solution of sodium ethylate in 95% alcohol.

It turns brown on standing and must be freshly prepared.

In presence of water it decomposes into alcohol and sodium hydroxide.

It causes slight pain, rapid obtundent effect and does not penetrate deeply nor stains.

CAUSTICS
Caustics : Drugs that cause necrosis or tissue death and dissolution of tissues.

1. Acids -Nitric, Trichloroacetic, lactic and chromic

2. Alkalis -Sodium and potassium hydroxide

3. Metallic salts -Silver nitrate, zinc sulphate and chloride, copper sulphate

4. Protoplasmic poisons -Phenol and arsenic trioxide

Nitric Acid:

It is a useful caustic.

It acts superficially as it does not dissolve the protein precipitates.

It is painful, stains yellow and erodes enamel and dentin. 10% solution is used to
devitalize pulp. It is neutralized with Sodium bicarbonate.

Trichloracetic Acid :

It is an antiseptic and rapid caustic.

 203

It is less painful ad more suitable for mucous membranes. 50% solution cauterizes
gums, polyp etc. 5-20% solutions is used on aphthous ulcers, Vincent’s infection,
gingival pockets.

Dilute solutions remove tobacco stains.

Lactic Acid:

It is very useful caustic for oral use due to low toxicity.

It can be applied in cases of leukoplakia and aphthous ulcers.

It is used for removing diphtheroid membrane.

Chromic Acid :

10-20% is used on acute ulcerative gingivitis and cancrum oris.

It is an antiseptic, caustic, oxidizing and antibacterial agent.

All acids are toxic to cells and have following properties:

a) Withdraw water

b) Neutralize alkalinity

c) Precipitate proteins and dissolve acid albumins

Alkalis are caustic and have following properties:

a) Withdraw water from cells

b) Form alkaline albumins with proteins and soaps with fats

c) They are less painful and deep penetrating. They gelatinize tissues

Sodium and Potassium Hydroxide

These are unsuitable for dental treatment.

Syringe with water to neutralize and prevent deep penetration

Metallic Salts

They are caustic due to toxic metallic ions.

They precipitate proteins.

They do not penetrate deeply and so have to be applied repeatedly.

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They are painful.

Silver nitrate 10%, Zinc sulphate, Zinc chloride 10% solution are used on aphthous
ulcers, and for desensitizing dentin.

Copper sulphate is a very painful caustic.

Phenol precipitates proteins. It penetrates deeply.

Arsenic Trioxide is a protoplasmic poison and causes necrosis of tissue cells, nerve
fibrils, lymph and blood vessels. It is toxic and causes acute pain.
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DISCLOSING AGENTS

Definition:

These are tablets, solutions and wafers capable of staining bacterial deposits on
the surfaces of teeth, tongue and gingival. They are excellent oral hygiene aids because
they provide the patient with a self educational and self motivational tool to improve the
efficiency of plaque control

Disclosing solutions:

1) Basic fuchsin – 6 gms

Ethyl alcohol – 100 ml

Add : 2 drops water in a dappen dish

2) Potassium iodide 1.6 gms

Iodine crystal 1.6 gms

Water 13.4 ml

Glycerin 30 ml

Wafers:

FD red (Erythrosine) 15 mg

Sodium chloride 0.747 %

Sodium sucaryl 0.747%

Calcium stearate 0.995%

Soluble saccharin 0.186%

White oil 0.124%

Flavoring agent 2.239%

Sorbital 7 gm

Disclosing solutions are applied to teeth surface with cotton swab diluted in water. They
produce heavy staining of plaque and soft tissues. It is an acceptable method for
plaque control. Disclosing wafers are crushed between teeth and swished around the
mouth for 30 seconds without swallowing.
SECTION - 5

DENTAL
RADIOLOGY
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DENTAL RADIOGRAPHY
Radiographs are the pictures produced by X-rays coming in contact with an
appropriate film, in a similar manner to the production of photographs by light
rays. They are sometimes referred to as roentgenographs.

Dental radiographs are taken by passing X-rays through the teeth and jaws and
recording the resultant shadow on an X-ray film.

 Where a photographic camera is pointed at a scene and the shutter release

pressed, light enters through the lens and is recorded on the film as an
image.

 If, by some misfortune, your hand happens to be in front of the lens at the
time of shooting, a shadowy image of this appears on the film.

 If instead of your hand you held a more transparent object in front of the
lens, such as a glass rod, the shadow would not be so dark.

 In a similar way, X-rays emitted from an X-ray machine and directed at

an X-ray film will record the shadow of anything in the path of the rays.

 X-rays are useful because they can penetrate many objects without leaving
a shadow, but the denser a substance is, the more likelihood there is of it
casting a shadow on the film.

 The more dense an object is, the more complete will be the shadow:

 The enamel of a tooth will produce a more marked shadow than will
dentine and an amalgam restoration will have an even more marked
shadow than enamel.

A large number of terms used in radiography have the prefix ‘radio’: such as radio-
opaque, which describes an object through which X-rays cannot pass and which therefore
casts a shadow on the film, and radiolucent, which describes an object through which X-
rays can pass and which therefore does not cast a shadow on the film.
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Production of X-rays

 Primary rays are produced in the X-ray machine when a stream of electron
strike a target area made of Tungsten.

 The electrons are produced somewhat in the same way as the action inside
a television set, with a very high voltage occurring through conversion
from the normal house current.

 The electrons are emitted from a glass tube, which is usually suspended in
oil for heat absorption.

 The primary rays are highly penetrating and these produce the required
image on the film.

 However, some rays are reflected from more solid objects which they
cannot penetrate and may be scattered in different directions.

 These rays are called secondary rays and are an undesirable feature of an
X-ray examination.

Precautions

 X-rays are a boon to mankind if used carefully and sensibly.

 Repeated and excessive exposure of the same regions of the body to the
X-rays will eventually bring about changes which are cumulative (i.e. they
add up) and may thus do a great deal of damage.

 The X-rays themselves do not ‘add up’ in the body but the slight changes
that excessive exposure produces in the affected cells remain, and
eventually the cells may be irreversibly altered.

 The taking of dental radiographs is relatively safe, since the amount

radiation used in dental radiographs is much less than that used in most
medical views.

 It is the operator who is principally at risk, rather than the patient, since
the operator may be repeatedly exposed to small levels of radiation over a
long period of time.

 Therefore, sensible precautions should be taken to ensure that there are no

unwanted side effects.
 208

The precautions that need to be taken when using radiographs are governed by the
Ionizing Radiations Regulations 1985 and there is an approved code to practice
published by the Health and Safety Commission.Dental hygienists should be familiar
with the advice given in these documents which are listed, together with other relevant
material, at the end of this chapter.These documents provide detailed advice and the main
points include the following:

1. Primary considerations:

a) Radiograph a patient only if clinically necessary

b) The radiation protection supervisor (RPS) shall ensure that all staff understand and
observe the local rules.

c) Only a trained and competent operator should use the X-ray equipment

2. Equipment:

a) Ensure that the equipment is of adequate tube rating – not lower than 50 kV and
preferably about 70 kV.

b) The beam diameter should not exceed 60 mm measured at the patient end of the cone.

c) Ensure correct beam filtration: equivalent to at least 1.5 mm of aluminium for X-ray
tube voltages up to and including 70 kV and 2.5 mm of aluminium (of which 1.5 mm is
permanent) for X-ray tube voltages above 70 kV.

d) Ensure that the equipment is regularly checked and properly maintained.

e) If a fault in the equipment occurs, it should be disconnected and the RPS notified.

3. Films and film holders:

a) Use the minimum number of films consistent with adequate diagnosis.

b) Use the fastest film available consistent with good film quality. Intensifying screens
must be used for extraoral and vertex occlusal views.

c) A film holder should be used if possible. The operator should never hold the film, the
patient or the tube housing during exposure.

4. Operating technique:

a) Persons whose presence is unnecessary for the examination should be excluded from
the X-ray room.
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b) The operator must stand outside the controlled area. This will be achieved by being at
least 2.0 m from the tube and the patient, and being outside the primary beam.

c) Ensure that the exposure is correctly set and a minimum exposure time is used.

d) Ensure that the exposure is properly terminated – observe the warning signals.

e) Where it is likely that a fetus will be irradiated by the primary beam a protective apron
should be used.

f) Personal monitoring of staff should be carried out if their individual workload exceeds
150 intraoral or 50 panoral films per week.

g) Disconnect X-ray unit from the main supply after use in order to de-designate the
controlled area and to eliminate the possibility of an inadvertent exposure.

h) All films should be correctly processed.

i) Routine checks should be made to detect if any deterioration in the quality of

radiographs occurs

j) In cases of accidental overexposure the recommended procedures must be followed.

5. X-ray room and environment:

a) Room size should be large enough to provide safe accommodation for those persons
who have to be in the room during exposure. This will be achieved if there is sufficient
space to allow the operator to be 2.0 m or further from the tube and patient and well
outside the primary beam.

b) Additional protective panels: These may be required if the work load exceeds 150
mA/mm per week for panoramic films or 30 mA/mm per week for intraoral films. This
is roughly equivalent to 50 panoramic or 300 intraoral films.

c) A dental surgery or any other room should not be used for other work (or as a
passageway) whilst radiography is in progress.

d) Radiation warning sign: If the room door opens directly into an area where the
instantaneous dose rate is greater than 7.5 µSv/h a radiation warning sign should be
displayed.

e) Automatic warning signal: If the controlled area extends to the room entrance an
automatic warning signal indicting emission of radiation is required to warn against
entry.

f) Persons in all occupied areas outside the X-ray room should be adequately protected
 210

6. Routine dental radiography:

a) Training and competence: A person clinically or physically directing an exposure shall

have received adequate training (‘Clinically directing’ means having a clinical
responsibility for the decision to affect an exposure. ‘Physically directing’ means
affecting the exposure).

b) Where it is necessary to support a small child or handicapped patient the advice of a

Radiological Protection authority (RPA) must be sought.

c) Where a film holder cannot be used and the patient is unable to hold the film, a person
assisting must observe adequate protective measures in accordance with the advice of a
RPA.

d) Exposure values should be checked before using the X-ray machine, particularly if
changing between long and short cone techniques.

e) Attenuation of beam: Since the beam is not fully absorbed by the patient it should be
considered as extending beyond the patient until it has been attenuated by distance or
intercepted by shielding such as a brick wall.

7. Panoramic radiography

a) Automatic warning signal: Where the controlled area extends to the entrance of the X-
ray room an automatic warning signal indicating when the equipment is in the ready state
and radiation is being emitted should be provided at the room entrance.

b) Rotation faults: The irradiation switch should be released immediately if the rotational
movements fails to start or stops before the full arc is covered.

8. Cephalometry:

a) Cephalometry should not be carried out without prior consultation with a RPA.

b) Ordinary dental X-ray equipment operating at less than 60 kV should never be used for
cephalometry. Equipment operating at or above 60 kV may be suitable if used with
specially designed auxillary equipment.
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HAZARDS OF RADIATION

ORAL TISSUES

1. Atrophy of oral mucosa – Prolonged exposure

2. Mucosites

3. Candidiasis

4. Loss of taste

5. Dryness of mouth

6. Retardation of teeth growth

7. Radiation caries

8. Osteoradionecrosis

WHOLE BODY
1. Damage to blood cells

- Anemia

- Infection

- Hemorrhage

2. Gastrointestinal effects

3. Developmental anomalies

4. Cancer

5. Leukemia

6. Gene mutation
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DENTAL FILMS AND THEIR USES

1. Dental films are supplied as film packets of various sizes.

2. Each packet is in fact a light sealed envelope of a soft paper material

containing a film, a sheet of black paper protecting against light leakage,
and a sheet of lead foil.

3. Any rays striking the lead foil have already passed through the subject and
the film and are therefore no longer useful.

4. Thus the lead foil performs the function of absorbing these excess primary
rays as well as preventing secondary rays being reflected back by
scattering on to the film.

5. Care must be taken that films are not sharply bent or the outer packets
torn.

6. A sharp bend will often show up on the developed film as a black line or
crescent shaped mark.

7. A torn packet will let in light which will affect the film in a similar
manner to X-rays. It may be necessary to bend the film, however, for it to
be accommodated by the shape of the mouth, but the bend should be no
more than a gentle curve.

There are several sizes and types of dental films.

PERIAPICAL FILMS

The most usual size, called standard, is 3.2 x 4.1 cm (1.1/4 x 1.5/8 in). There is a smaller
size, 2.2 x 3.5 cm (7/8 x 1.1/4 in), often called child size, but this is frequently used for
taking radiographs of adult anterior teeth.

The periapical film shows the entire tooth, and usually the lengths of 3-4 teeth are
accommodated on a standard film. They are useful for detecting:

1. The state of the alveolar bone supporting the teeth. Periapical views are
particularly important in the assessment of the severity of chronic periodontal
disease.

2. Changes around the apex of a tooth.This may denote the presence of a chronic
abscess and abnormality.
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3. The length of a root canal in endodontics and the position of a root canal
filling in relation to the apex.

4. Fractures of the roots and retained root tips.

5. Missing or unerrupted teeth.

6. Supernumerary teeth

7. Impacted teeth

8. Malformation of the roots which may make an intended extraction more

complicated.

BITEWING FILMS

These may be the same as periapical films with the addition of a tab placed
centrally on the face, towards the tube, so that the patient holds this between the teeth
(hence bitewing) and the X-ray beam is directed along the axis of the tab.

There is a longer film (no.3 bitewing), 5.4 x 2.7 cm (2 x 1 in). this covers all the
posterior teeth, but distortion is possible.

Bitewings show only the crowns and cervical portion of the roots of the teeth, but
have the advantage of showing both upper and lower teeth at the same time. This means
that, if the radiographs are being taken to examine the crowns (e.g. for interproximal
caries), one bitewing will show the same area as two periapicals, that is only half the
amount of exposure to X-ray is needed. Bitewings, therefore, are mainly used for full-
mouth surveys to check for caries or early periodontal disease.

OCCLUSAL FILMS

These are somewhat larger, 5.7 x 7.6 cm (2.1/2 x 3 in), and are placed between
the teeth in the occlusal plane. Their purpose is to show all or a large part of the
mandibular arch or the maxilla in one film. They may be used to detect abnormalities
such as salivary duct calculi in the floor of the mouth, or to localize a tooth or an object in
another plane of the jaw. They are often taken to record the position of buried teeth, such
as upper canines or lower third molars. It is possible to discover and identify the shape
and extent of cysts, fracture lines in the jaws and other abnormalities of the bones such as
tumors, both benign and malignant.
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ORTHOPANTOMOGRAPHS (OPG)

These are the most common extraoral radiographs with which the dental hygienist
will come in contact.They are larger films, measuring 30x15 cm, placed in a curved
cassette and designed to give a panoral picture of the entire dentition on the one film.
The film is placed on one side of the head and the X-ray source is set on the other side.
The source moves around in an arc, exposing a thin line of the film as it does so.In this
way a flattened-out view of the entire dentition and the surrounding structures is
produced.These films are extremely useful in making an overall assessment of the
patient’s dentition, but they have the disadvantage of lacking the clarity of detail found in
periapical views.

The radiation dosage involved in taking an orthopantomograph is only 80% of

that involved in a full-mount periapical survey.

OTHER EXTRAORAL FILMS

There are many other extraoral films used in dentistry, especially in oral surgery
and orthodontics. However, the dental hygienist probably will not be very involved with
any of these views. It is unlikely that the hygienist would be required to take such views
and they are unlikely to contain the sort of information which the dental hygienist would
wish to have. If further information is required about these views, the student is referred
to standard texts on dental radiography.

Exposing the film

Little is to be gained by detailed written descriptions of the techniques of using

dental X-ray machines. Practical skills are best taught by demonstration and practice
under supervision.

However, it is necessary to know the factors which influence the density of the
image on the film and to understand the principles behind the two basic techniques for
taking periapical radiographs.

The density of the image

This means the darkness of the pictures on the film. This is influenced by the
following factors:

1. Kilovoltage : The greater the kilovoltage, the denser the image

2. Current : The greater the current, the denser the image.

3. Time: The longer the exposure, the denser the image.

 215

4. Film: The faster the film, the denser the image.

5. Distance: The nearer the film to the source, the denser the image.

BASIC TECHNIQUES FOR PERIAPICAL FILMS

Periapical films may be exposed by either the Bisecting angle technique (short
cone technique), or the Paralleling technique (long cone technique).

Bisecting angle technique

This uses a near approximation to obtain an image on the film, which is as little
distorted as possible. Because the film, when placed in the mouth, does not ordinarily lie
parallel to the long axis of the tooth, the most accurate image will be obtained by
directing the central ray of the X-ray beam perpendicular to the bisection of the angle
between the long axis of the tooth and the film.

Paralleling technique
If the film is, in fact, placed parallel to the long axis of the tooth, either by
interposing a cotton wool roll between them, or by using special paralleling device
holders, the central ray of the beam can be directed perpendicularly to both film and
tooth, producing a more accurate picture. Since the film and tooth are further apart, the
source must be placed further away from the film, hence the long cone.

Angulation
It is not possible in this text to detail all the angulations and film positions for the
numerous different views. Some excellent illustrations and directions for the technique
of film placement can be obtained from the X-ray supply companies, especially Kodak
and (for long cone) Rinn.

HELPFUL HINTS:

1. A few patients gag badly when the film is placed in the mouth, especially on the
posterior part of the palate. To overcome this, some operators apply topical anaesthetic
to the mucosa of the palate for a few minutes. (No topical anaesthetic is of value unless it
is given time – at least 2 minutes – to work!). But the best method by far is to spray the
side of the film which is placed against the tissues with ethyl chloride. The thin film may
then be placed in position with no reaction.

2. When placing the film in the patient’s mouth, make sure that the embossed dot on the
edge of the film is placed occlusally. Then, when the film is being clipped to a hanger for
processing, it can be clipped near the embossed dot with the knowledge that no important
part of the radiograph is being damaged. Alternatively, some dentists like the film to be
placed with the dot always at the lower edge. In this way, there is never any doubt about
whether the film is of upper or lower teeth, which lets the inexperienced orientate the film
without the help of anatomical landmarks.
 216

3. When a periapical film is being taken for a lower molar tooth, patients often have some
difficulty holding the film packet in place. If the occlusal edge of the film is clamped by
artery forceps, these can be held by the patient so that the film is in the correct position,
either with the hand, or by closing the teeth gently on to the handle. Special flanged
forceps can be obtained for this purpose.

Processing the film

Once again, it is not the purpose of this text to detail the stages involved in
processing a film. These can be learned adequately only by practice. However, the
hygienist should have grasped the theory of developing and processing prior to practicing
the techniques.

Developing:

Once the film has been exposed to the X-rays it contains an invisible, latent
image, which is covered into a visible one by the developing solution. The emulsion of
the film contains silver salts and the developer acts on those which have exposed to the
X-rays, precipitating the silver. The density of the image is affected by the following:

1. Temperature – The warmer the solution, the darker or denser the image.

2. Time – The longer the film is in the developer, the darker it gets.

3. Concentration – The stronger the development solution, the darker the image it
produces.

4. Age of the solution – The developer will eventually become ‘worked out’ if used for
too long and the image will be pale and weak.

The various manufacturers of developer give tables of recommended times and

temperatures for using their products. The solution should be mixed according to the
instructions and the times and temperatures carefully adhered to.

Fixing

The fixing solution serves two purposes – it dissolves off the unused emulsion,
thus clearing the film, and it fixes the image permanently on the film, so that it is no
longer affected by exposure to light.
 217

The time and temperature of fixing are not as critical as they are for developing.
Once the film has been cleared it can be viewed briefly in the daylight, without harm, but
it should be kept in the fixed for the full recommended time before being finally washed
and dried. Firms can be left in the fixer for longer than recommended time, but should
not be left longer than 1 hour, or the density of the image may be reduced.

Washing

Thorough washing after processing is essential to remove all chemicals from the
film, because if they are left they will cause staining. This can only be done adequately
in running water.
 SECTION - 6

PERIODONTOLOGY
 218

ANATOMY OF PERIODONTAL TISSUES

Periodontal tissues are those tissues that surounds and hold the tooth in its socket.
PERIODONTAL TISSUES INCLUDE
1. GINGIVA
2. CEMENTUM
3. PERIODONTAL LIGAMENT
4. ALVEOLAR BONE

CLASSIFICATION OF ORAL EPITHELIUM

All the soft tissues of the mouth are collectively known as the oral mucosa.
 219

They are divided into three different types as follows:

1. Masticatory mucosa / is tissue that is firmly attached to the underlying bone

keratinized mucosa
2. Lining mucosa
3. Specialized mucosa
and covered with parakeratinized or keratinized
epithelium. The gingiva and the tissue covering the
hard palate are examples of masticatory mucosa.
is composed of oral tissues that are loosely attached
to their underlying structures and covered with
nonkeratinized epithelium. The mucosa covering the
lips, cheek, floor of the mouth, inferior surface of the
tongue, soft palate, uvula, and alveolar mucosa are
examples of lining mucosa.
covers the dorsal surface of the tongue and is adapted
to accommodate for the sensation of taste.

GINGIVA

Gingiva is that part of the oral mucosa that covers the alveolar process of the jaw and
surrounds the neck of the teeth.
The gingival can be divided into three areas
1. Marginal gingiva (FG) (free or unattached gingiva)
2. Attached gingiva (AG) (firmly attached to underlying tooth and bone)
3. Interdental gingiva (located between adjacent teeth

Divisions of the gingiva: marginal gingiva, attached gingiva, interdental gingiva, and
alveolar mucosa
 220

.
FG : FREE GINGIVA, AG : ATTACHED GINGIVAL, MGJ : MUCO GINGIVAL JUNCTION

MARGINAL GINGIVA
The marginal gingiva is the most coronally positioned portion of the gingiva. It is
not attached to the tooth, and it creates the soft tissue wall of the gingival sulcus (the
shallow space between the marginal gingival and the tooth. In health the marginal
gingiva is knife-edged in contour, firm in consistency, and smooth in texture. It extends
apically to the free gingival groove, the shallow depression in the gingival surface
approximately 1 mm wide that corresponds to the most coronal aspect of the gingival
attachment to the tooth. In some patient the free gingival groove is pronounced, while in
others it is absent.

HEALTHY GINGIVAL TISSUES.: Note tapered contours, pointed interdental

gingiva, free gingival groove (GG), stippled texture alveolar mucosa (AM) and
mucogingival junction
 221

ATTACHED GINGIVA

1. It is Just apical to the marginal gingiva and the free gingival groove.
2. It is firmly bound to the underlying tooth and alveolar bone.
3. The attached gingiva is tapered in contour, stippled in texture, and firm in
consistency
4. Stippling refers to the irregular surface of the gingiva, which resembles the surface
of an orange.)
5. The attached gingiva varies in width from one area of the mouth to another and can
range from less than 1 mm to 9 mm.
6. The width depends principally on the teeth involved, their buccolingual position in
the arch, and the location of frenum or muscle attachments.
7. In general the attached gingiva is widest on the incisor teeth, ranging from 3.5 to
4.5 mm in the maxilla and 3.3 to 3.9 mm in the mandible.
8. It provides gingival tissue that can withstand the mechanical forces of tooth
brushing and prevents movement of the marginal gingiva when tension is placed on
the alveolar mucosa. In the past a minimal width of attached gingiva was
considered necessary for gingival health, but recent studies have shown that
gingival health and attachment levels can be maintained in the absence of attached
gingiva.
9. The attached gingiva is bound coronally by the free gingival groove and apically
by the mucogingival junction. Keratinized gingiva is covered with keratinized or
parakeratinized stratified squamous epithelium. This includes the free or marginal
gingiva as well as the attached gingiva and is different from the non-keratinized
epithelium that forms the soft tissue wall of healthy sulcus or pocket.

WIDTH OF ATTACHED GINGIVA

Width of attached gingiva is the distance between the mucogingival junction and the
projection on the external surface of the bottom of the gingival sulcus or periodontal
pocket.
 222

Maxilla greater than Mandible

Anterior greater than Posterior

FACIAL INCISOR REGION FACIAL ASPECT OF PREMOLARS

Maxilla: - 3.5 to 4.5 mm Maxilla: - 1.9 mm
Mandible: - 3.3 to 3.9 mm Mandible: - 1.8 mm

INTERDENTAL GINGIVA
1. The interdental gingiva in the interproximal space created by adjacent teeth in
contact.
2. In the mesiodistal dimension the shape of the interdental gingiva, while generally
triangular,depends on the proximal contours of the teeth creating the interproximal space.
If the contours are flat with broad interproximal contacts, the gingiva will be narrow and
short.
3. If the proximal contours are more convex with a small coronally positioned contact
area, the interdental gingiva will be broad and high. When teeth overlap, the interdental
space is small or absent, resulting in bulbous gingiva.
4. In the buccolingual dimension the interdental gingiva terminates coronally with
separate buccal and lingual peaks of tissue joined by a depression known as the gingival
col. If thegingival tissue has receded to the point that it no longer touches the
interproximal contact area or if diastema is prevalent, no col will be seen. The col is
present only when the gingiva surrounds the gingival surface of the interproximal contact
area

Shows interdental col present clinically and histological section

 223

GINGIVAL SULCUS, SULCULAR AND JUNCTIONAL

EPITHELIUM

The gingival sulcus is the shallow space between the marginal gingiva and the tooth.
Histologically the sulcus is lined with nonkeratinized sulcular epithelium and extends
from the crest of the marginal gingival to the most coronal level of the junctional
epithelium.
The average depth is 1.8 mm with variation upto 0-6 mm.

The healthy gingival sulcus depth as determined clinically with periodontal probe
(Probing depth) is slightly deeper (2 to 3 mm) than the histologically measured depth
because the probe often penetrates the delicate epithelial lining of the gingival sulcus.

At the base of the crevice the gingiva is attached to the tooth by means of a 1 mm wide
layer of epithelial cells attached to the cementum surface in the same way as they are
attached to each other. This band is known as the junctional epithelium.

It establishes the histological gingival attachment level and is formed by a uniting of the
oral epithelium and the reduced enamel epithelium during tooth eruption The junctional
epithelium gives way to a band of connective tissue, 1 mm beyond the gingival crevice.
This connective tissue is approximately 1 mm wide and contains collagen fibres arranged
in group

Biological width

The gingival crevice, junctional epithelium and connective tissue attachment, make up
the biological width of the gingiva. It will always reestablish itself after any damage to
the gingiva and must not be violated beyond the gingival crevice by instrumentation.

Biological
Width
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Epithelium
The gingival tissues are made up of fibrous connective tissue covered by stratified
squamous epithelium. The epithelium that covers the oral surface of the attached and
marginal gingiva is either parakeratinized or keratinized, while the sulcular epithelium
and the junctional epithelium are nonkeratinized. The sulcular epithelium is thinner,
which makes it easier for the products of dental plaque to penetrate into the connective
tissue of the gingiva and stimulate inflammation and tissue destruction. The epithelium
that covers the alveolar mucosa is thin and nonkeratinized.

OUTER EPITHELIUM
1. The outer epithelium that is keratinized or parakeratinized is composed of four layers
of cells. 2. The deeper cells are cuboidal in shape (basal cells) and form the stratum
basale.
3. The second layer of cells, called the stratum spinosum, is composed of polygonal
cells. The next layer is composed of cells that are flattened in shape with prominent
basophilic keratohyaline granules in the cytoplasm. This layer is known as the stratum
granulosum.
4. The most superficial layer, the stratum corneum, is a cornified layer that they be
keratinized (no nuclei), parakeratinized (retained nuclei), or both. The epithelial cells are
formed as basal cells and gradually change to the characteristics of each of the cell layers
as they migrate toward the surface. This process is known as keratinization.
5. The cells are ultimately sloughed from the keratinized surface layer. The cell
turnover rate in experimental animals is about 10 to 12 days for the oral epithelium and
1 to 6 days for the junctional epithelium.
6. The thickness of gingival epithelium is formed by balance between basal epithelium
cell formation and sloughing of older cells at surface. The epithelial cells are joined
together by structures known as desmosomes, tight junctions, and intercellular ground
substance. The basal cells are attached to the basement membrane by hemidesmosomes.
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Histological view of oral epithelium and underlying connective tissue

The junction between keratinized gingival oral epithelium and its underlying
connective tissue is usually wavy in shape. The projections of epithelial cells into the
connective tissue are known as rete pegs. The intervening projections of connective
tissue are known as connective tissue papillae. The alternating pattern of connective
tissue papillae and epithelial rete pegs are thought to be related to the stippled (Orange
peel like) surface texture of attached gingiva.

Different cell types in various layers of oral

keratinized epithelium

2. SULCULAR EPITHELIUM
A balance between new basal cell formation and the sloughing of older cells at the
surface maintain the thickness of the gingival epithelium.
The crevicular and the junctional epithelium are not as thick as the oral epithelium. And
in health have no rete pegs and are not keratinized. The epithelium in this area is
composed principally of the stratum basale and the stratum spinsosum.
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3. JUNCTIONAL EPITHELIUM
The basal cells in the junctional epithelium are joined to the tooth by hemidesmosomes
and a basal lamina. This attachment is similar to that between epithelium and fibrous
connective tissue. The basal lamina is composed of a lamina densa adjacent to the tooth
surface and a lamina lucida to which the hemidesmosomes of the epithelial cells are
attached.
Keratinisation are of the following types :
Types of keratinisation-
1. Orthokeratinization
2. Parakeratinization
3. Non-keratinization

Keratinisation type Features

1 Orthokeratinization is a homogenous layer of keratin present in the
superficial part of the epithelium which does not contain
any nuclear remnants. Only some areas of gingival
epithelium are orthokeratinized.

2 Parakeratinization consists of keratin layer consisting of nuclear remnants

and keratohyalin

3 Non-keratinization has neither stratum granulosum nor coreum and

superficial cells have visible nuclei.

GINGIVAL CONNECTIVE TISSUE

The connective tissue of the gingiva is known as the lamina propria. It is divided into
two layers:
The papillary layer, adjacent to the epithelium, and
The reticular layer, contiguous with the periosteum on the alveolar bone.
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The lamina propria consists primarily of the following:

Collagen fibers
Intercellular ground substance
Cells
Blood Cells
Nerves

BLOOD SUPPLY OF GINGIVA

Blood supply comes from the

1. supra periosteal arteries
2. vessels of periodontal ligament
3. arterioles which come out form
crest of interdental septum

NERVE SUPPLY

The gingival component of the periodontium is innervated by terminal branches

of periodontal nerve fibers and by branches of the infra orbital and palatine or lingual,
mental and buccal nerves.

GINGIVAL FIBERS

The collagen fibers help to hold the marginal gingiva tightly against the tooth and
provide a firm junction of the attached gingiva to the underlying tooth, root and alveolar
bone.
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Dentogingival group These are the most numerous fibers, extending from cervical
cementum to lamina propria of both the free and the attached
gingiva

Alveologingival group These fibers radiate from the bone of the alveolar crest and
extend into the lamina propria of the free and attached gingiva

Circular group This small group of fibers forms a band around the neck of the
tooth, interlacing with other groups of fibers in the free gingiva
and helping to bind the free gingiva to the tooth.

Dentoperiosteal group
Running apically from the cementum over the periosteum of the
outer cortical plates of the alveolar process, these fibers insert
into either the alveolar process or the vestibular muscle and
floor of the mouth. (They run interdentally from the cementum
of one tooth, over the alveolar crest, to the cementum of the
adjacent tooth known as transseptal fibers, they constitute the
transseptal ligament).

Transseptal Group
These fibers run interdentally from the cementum just apical to
the base of the junctional epithelium of one tooth over the
alveolar crest and insert into a comparable region of the
cementum of the adjacent tooth. Together these fibers constitute
the transseptal fiber system, collectively forming an interdental
ligament connecting all the teeth of the arch.

The Supracrestal fibers – in particular, the transseptal fiber system – have been
implicated as a major cause of post retention relapse of orthodontally positioned teeth. It
is the inability of the transseptal fiber system to undergo physiologic rearrangement that
has led to this conclusion. Although the rate of turnover is not as rapid as in the PDL,
recent studies have shown that the transseptal fiber system is capable of turnover and or
remodeling under normal physiologic conditions, as well as during therapeutic tooth
movement.
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Gingival fibers
. Collagen fibers are strong ropelike cords that bind and hold tissues together in a
functioning unit. Their structure consists of three polypeptide chains wound together to
form a basic collagen molecule. The molecules aggregate side by side to form collagen
filaments, which in turn are accumulated to form the collagen fibril. The collagen fibers
found in the gingival fibers are composed of many collagen fibrils held together by
proteoglycans. The viscous intercellular ground substance consists principally of
mucopolysaccharides and glycoproteins. These substances help to regulate the
distribution of water, electrolytes, and metabolites in the tissues.
In contrast to the dense mass of firmly bound collagen fibers found in the gingiva, the
connective tissue of the alveolar mucosa is composed of more loosely arranged collagen
fibers interspersed with elastic and muscle fibers. They are not firmly attached to the
underlying bone, and therefore, this tissue can be moved easily to adapt to the changing
shapes and sizes of the muscles during function.

Following are the most prominent cells found in the gingival connective tissue:
Plasma cells
fibroblasts
Mast cells
lymphocytes

CLINCIAL DISCREPTION OF NORMAL GINGIVA

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COLOUR OF GINGIVA The colour of healthy gingival is uniformly coral pink from the attach
ed gingiva through to the crest of the marginal gingiva..However, co
nsiderable variation exists depending on the amount of melanin in the
tissues, the thickness of the epithelium, the degree of keratinization, a
nd the vascularity of the connective tissue. Dark-skinned people often
exhibit a dark blue or brown colour. Red
to bluish-red changes are often characteristic of gingival inflammatio
n.
GINGIVALCONTOUR The marginal and attached gingiva are usually tapered in contour, end
ing coronally in knife-edged margins. The interdental gingiva is gene
rally pointed. However, the contours of the gingiva vary depending
upon the shape of the teeth, the buccolingual position of the teeth in th
e arch, and the size of the interproximal embrasure space. In gingival
disease the contours are often rounded and enlarged because of vascul
ar stagnation and increased formation of collagen fibers.

GINGIVALCONSISTENCY . In health the gingiva is usually resilient and firm because of the dens
e collagenous nature of the gingival connective tissue. In gingival dis
ease the consistency may be soft and boggy, because of vascular stagn
ation and a decrease in the amount of gingival collagen fibers, or extre
mely firm,because of excessive formation of collagen (fibrosis).
GINGIVALSURFACETEXTURE The surface texture of the gingiva is described as being stippled like a

n orange peel or smooth and shiny. The attached gingival and the cen
tral portions of the interdental gingival are stippled and the marginal g
ingival is smooth. The degree of stippling varies considerably among
patients and in different parts of the same mouth.. A reduction or lack
of stippling is frequently seen in inflamed gingiva.

GINGIVALPOSITION The level on the tooth at which the gingiva is attached is known as the
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gingival position. When teeth first erupt into the oral cavity the gingiva
l attachments are close to the tips of the crown, however, they
gradually shift to cervico-enamel junction

NORMAL AND STIPPLING OF GINGIVA

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PERIODONTAL LIGAMENT

The periodontal ligament is the connective tissue that surrounds the root and connects it
with the bone. It is continuous with the connective tissue of gingiva and communicates
with the marrow spaces through vascular channels of the bone.

Periodontal fibers:
The most important elements of the periodontal ligament are the principal fibers, which
are collagenous, are arranged in bundles, and follow wavy course when viewed in
longitudinal sections. Terminal portions of the principle fibers that insert into cementum
and bone are termed as Sharpey’s fibers. The principal fiber bundles consist of individual
fibers that form a continuous anastomosing network between tooth and bone.
The collagen biosynthesis occurs inside fibroblasts to form tropocollagen molecules.
These aggregate to into microfibrils that are packed together to form fibrils. These fibrils
associate to form fibers to form bundles.

COLLAGEN FIBRES AND BUNDLES

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In histological sections the following distinct groups of principal fibers are noted:

1. DENTOGINGIVAL,
2. ALVEOLAR CREST,
3. TRANSSEPTAL,
4. INTERRADICULAR,
5. HORIZONTAL,
6. OBLIQUE
7. APICAL FIBER
BUNDLES.

oblique fibers, They occupying nearly two thirds of the ligament, are inserted into
bone coronal to their insertion into cementum. This geometric
arrangement of the oblique fibers is ideally suited to absorb intrusive
forces generated during mastication. In order to attach the tooth in its
alveolus, the fibers must be embedded in mineralized bone and
cementum
The transseptal They extends interproximally over the alveolar crest and is embedded
group in the cementum of adjacent teeth. They are remarkably constant
finding and are reconstructed even after destruction of alveolar bone
has occurred in periodontal disease.
Alveolar crest They extend obliquely from cementum just beneath the junctional
fibers epithelium to the alveolar crest. They prevent the extrusion of the
tooth and resist lateral tooth movements. Their incision does not
significantly increase tooth mobility
Horizontal These fibers extend at right angles to long axis of tooth from
group cementum to alveolar bone.
Apical group These fibers radiate from the cementum to the bone at the fundus of
the socket. They do occur on incompletely formed roots.

Interradicular They fan out from the cementum to the bone in the furcation areas of
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fibers multi rooted teeth.

Other well-formed fiber bundles interdigitate at right angles or splay around and between
regularly arranged fiber bundles. Less regularly arranged collagen fibers are found in the
interstitial connective tissue between the principal fiber groups; this tissue contains the
blood vessels, lymphatics, and nerves.
Although the periodontal ligament does not contain mature elastin two immature forms
are 1. OXYTALAN,
2. ELUANIN.

The so-called oxytalan fibers run parallel to the root surface in a vertical direction and
bend to attach to cementum in the cervical third of the root. They are thought to regulate
vascular flow. An elastic meshwork has been described in the periodontal ligament as
being composed of many elastin lamellae with peripheral oxytalan fibers and eluanin
fibers. Oxytalan fibers have been shown to develop de novo in the regenerated
periodontal ligament.
The principal fibers are remodeled by the periodontal ligament cells to adapt to
physiologic needs and in response to different stimuli.
In addition to these fiber types, small collagen fibers associated with the larger principal
collagen fibers have been described. These fibers run in all directions, forming a plexus
called the indifferent fiber plexus.

CELLULAR COMPONENTS
Four types of cells have been identified in the periodontal Ligament: connective tissue
cells, epithelial rest cells, immune system cells, and cells associated with neurovascular
elements.
Connective tissue cells include
1. fibroblasts,
2. cementoblasts,
3. osteoblasts.
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Fibroblasts are the most common cells in the periodontal ligament and appear as ovoid or
elongated cells oriented along the principal fibers and exhibiting pseudopodia like
processes. These cells synthesize collagen and also possess the capacity to phagocytose
"old" collagen fibers and degrade them by enzyme hydrolysis. Thus collagen turnover
appears to be regulated by fibroblasts in a process of intracellular degradation of collagen
not involving the action of collagenase. Osteoblasts and cementoblasts, as well as
osteoclasts and odontoblasts, also are seen in the cemental and osseous surfaces of the
periodontal ligament.
The defense cells include neutrophils, lymphocytes, macrophages, mast cells, and
eosinophils. These, as well as those cells associated with neurovascular elements, are
similar to those in other connective tissues.

Fibroblasts are the most abundant cells in the periodontal ligament, and are responsible
for metabolism of extracellular matrix components. The periodontal ligament is known to
have heterogeneous population of fibroblasts. A subpopulation of osteoblast-like
fibroblasts, rich in alkaline phosphatase, has been identified in the periodontal ligament
These cells have the capacity to give rise to bone cells and cementoblasts. They are also
responsible for the production of acellular extrinsic fiber cementum in the mature
periodontal ligament. Periodontal ligament fibroblasts are also needed to maintain the
normal width of the periodontal ligament by preventing the encroachment of bone and
cementum into the periodontal ligament space. The factors responsible for this activity
have yet to be identified.

GROUND SUBSTANCE

The periodontal ligament also contains a large proportion of ground substance filling the
spaces between fibers and cells. It consists of two main components:
1. glycosaminoglycans, such as hyluronic acid and proteoglycans
2. glycoproteins such as fibronectin and laminin.
3. It has high water content (70%).
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The periodontal ligament also contains calcified masses called cementicles, which are
adherent or detached from root surfaces. Cementicles may develop from calcified
epithelial cell rests; around spicules of cementum or bone traumatically displace into
periodontal ligament; from calcified sharpey’s fibers; thrombosed vessels in periodontal
ligament.

FUNCTIONS OF PERIODONTAL LIGAMENT:

Physical Function
Formative
Nutrition
Proprioception

The physical functions of the periodontal ligament entail the following:

1. Provision of a soft tissue "casing" to protect injury from mechanical forces

2. Transmission of occlusal forces to the bone
3. Attachment of the teeth to the bone
4. Maintenance of the gingival tissues in their proper relationship to the teeth
5. Resistance to the impact of occlusal forces (shock absorption)
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RESISTANCE TO THE IMPACT OF OCCLUSAL FORCES (SHOCK

ABSORPTION).

Two theories relative to the mechanism of tooth support have been considered: the
tensional and viscoelastic system theories.
tensional theory . The of tooth support ascribes to the principal fibers of the
periodontal ligament the major responsibility in supporting the
tooth and transmitting forces to the bone. When a force is applied
to the crown, the principal fibers first unfold and straighten and
then transmit forces to the alveolar bone, causing an elastic
deformation of the bony socket. Finally, when the alveolar bone
has reached its limit, the load is transmitted to the basal bone.
Many investigators find this theory insufficient to explain available
experimental evidence.

viscoelastic system The considers the displacement of the tooth to be largely controlled
theory by fluid movements, with fibers having only a secondary role.
When forces are transmitted to the tooth, the extracellular fluid
passes from the periodontal ligament into the marrow spaces of
bone through foramina in the cribriform plate. These perforations
of the cribriform plate link the periodontal ligament with the
cancellous portion of the alveolar bone and are more abundant in
the cervical third than in the middle and apical thirds.After
depletion of tissue fluids, the fiber bundles absorb the slack and
tighten. This leads to blood vessel stenosis. Arterial back pressure
causes ballooning of the vessels, and passage of blood ultrafiltrates
into "the tissues, thereby replenishing the tissue fluids.
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ALVEOLAR BONE

Bone is both an organ and a tissue. It is one of the hardest tissues of a human body and is
biologically, a highly plastic tissue.
Bone is a specialized mineralized connective tissue consisting by a
1. 33% organic matrix
2. 67% inorganic material.

The organic matrix (33%) consists of

1. 28% of type I collagen or osteoid collagen and
2. 5% non collagenous proteins, including osteonectin, osteocalcin, bone
morphogenetic proteins, bone proteoglycans and bone sialoprotein

The inorganic ions present are predominantly

1. calcium and phosphorus.
2. Magnesium,
3. carbonate,
4. hydroxyl,
5. chloride,
6. fluoride,
7. citrate,
8. sodium
9. potassium

Most of the calcium, phosphate and hydroxyl ions are in the form of needle shaped
crystals that are given the name Hydroxyapatite (Ca10 (PO4)6 OH2). The organic matrix
is permeated by hydroxyapatite and makes up the 67% of the bone. The ca ions bind to
osteonectin and osteocalcin (which are in large quantity) which in turn play a key role in
mineralizing of bone.
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In living bone 20% of its weight is made up by water. About 85%of total salts present in
bone are in the form of Ca2PO4 and about 10% in the form of calcium carbonate. 97% of
total calcium in the body is located in bone.
The calcium salts present in bone are not ‘fixed’. i.e., there is considerable interchange
between calcium stored in bone and that in circulation. When calcium level in blood rises
calcium is deposited in bone and when the level of calcium in blood falls, calcium is
withdrawn from bones to bring blood levels back to normal. These exchanges take place
under the influence of hormones like parathormone produced by parathyroid gland,
calcitonin produced by thyroid gland, oestrogen, glucocorticoids, Vit. D.
Bones have been classified as long or flat on their gross appearance. Long bones include
the bone of the axial skeletal (e.g., tibia, femur, radius, ulna and humerus). Flat bones
include all the skull bones plus the sternum, scapula and pelvis.
At the bone ends, the marrow is red in colour. Apart from blood vessels this red marrow
contains numerous masses of blood forming cells (haemopoetic tissue). In the shaft of the
bone of an adult the marrow is yellow. This yellow marrow is made up predominantly of
fat cells. Some islets of haemotopoetic tissue may be seen here also. In bones of a feotus,
or of a young child, the entire bone marrow is red. The marrow in the shaft is gradually
replaced by yellow marrow with increasing age.

GROSS BONE HISTOLOGY:

Characteristic of all bones are a dense outer sheet of compact bone with a uniform
smooth texture and without any obvious spaces in it, and a central medullary or marrow
cavity. In living bone the cavity is filled with either red or yellow bone marrow. The
marrow cavity is interrupted, particularly at the ends of long bones by a network of bone
trabeculae of tiny rods or plates of bone and contains numerous spaces which resembles a
‘sponge’ in appearance. This is spongy or calcellous bone. Adult bones whether compact
of trabecular consist of microscopic layers or lamellae. 3 distinct types of layering are
recognized
1. Circumferential,
2. Concentric and
3. Interstitial.
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Circumferential lamella encloses the entire adult bone, forming its outer perimeter.
Concentric lamellae make up the bulk of the compact bone and form the basic metabolic
unit of the bone, the ‘osteon’. The osteon is a cylinder of bone. Generally oriented
parallel to the long axis of the bone. The centre of each is a canal, the Haversian canal,
which is lined by a single layer of bone cells that cover the bone surface. Each of these
canals houses a capillary. Adjacent Haversian canals are interconnected by Volkmann
canals, which are channels like Haversian canals and containing blood vessels, thus
creating a rich vascular network through out the compact bone. The interstitial lamellae
are interspersed between adjacent concentric lamella and fill the spaces between them.
They are actually fragments of preexisting concentric lamella and can take a multitude of
shapes.
Surrounding every bone is an osteogenic (bone cell forming) connective tissue
membrane, the periosteum which consists of 2 layers. The inner layer next to the bone
surface consists of bone cells, their precursors and a rich microvascular supply. The outer
layer is more fibrous. Both of the internal surfaces of the compact and cancellous bone
surfaces are covered by a single layer of bone cells, the endosteum, which physically
separates the bone surface with from the bone marrow within.

BONE CELLS:
In bone, separate cells are primarily responsible for the formation,
resorption and maintenances of osteo architecture. Classically 3types of bone cells are
described, each with specific function;
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1. Osteoblasts - which form bone,

2. Osteocytes - inactive osteoblasts or lining cells maintaining bone.
3. Osteoclast – which resorb bone.

Osteoclast is likely aided in the resorption process by wandering macrophages and

cytokines emitted by neighbouring osteoblast.
As the osteocyte is derived from the osteoblasts it is more correct to consider bone cells
as coming form 2 groups only, the 1st concerned with formation and maintenance and 2nd
with removal.

OSTEOBLASTS:
Osteoblasts are the uninucleated cells that synthesis both collagenous
and non collagenous bone proteins (the organic matrix, ‘osteoid’). They are responsible
for mineralization and are derived form a multipotent mesenchymal cell. The osteoblasts
are considered to differentiate through a precursor cell, the preosteoblast. They are found
lining in the growing surfaces of bone, sometimes giving an epithelium like appearances.
Osteoblasts are of varied shapes (oval, triangular, cuboidal etc.) and there are numerous
gaps between adjacent cells and forming gap junctions. The nucleus of an osteoblast is
ovoid and euchromatic and cytoplasm is basophilic. The inactive osteoblast or lining cell
manages bone maintenances through controlling ion fluxes into and out of bone and by
secreting additional phosphoproteins and glycoproteins. The bone matrix that is laid
down by osteoblasts is not mineralised and is referred to as osteoid. While new osteoid is
being deposited, the older osteoid located below the surface becomes mineralised as the
mineralization front advances.

OSTEOCYTES:
These are the cells of the mature bone. As osteoblast secrete bone matrix, some of them
become entrapped in lacunae and are then called Osteocytes. The number of osteoblast
becoming Osteocytes varies depending on the rapidity of bone formation. The more rapid
the formation, the more Osteocytes is present per unit volume. Embryonic or woven born
(absences of lamellar structure, collagen fiber bundles run randomly in different direction
interlacing with each other) and repair bone have more osteocyte than lamellar bone.
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After their formation, osteocyte gradually lose most of their matrix synthesizing
machinery and become reduced in size. The space in the matrix occupied by an osteocyte
is called is called the osteocytic lacunae. Narrow extensions of this lacunae form enclosed
channels or canaliculi arefrom radiating osteocytic processes.
Thus osteocyte maintains contact with adjacent osteocyte and with the osteoblasts or
lining cells on the bone surfaces – the endosteum, periosteum and Haversian canals.
Failure of any part if this interconnecting system results in hypermineralisation (sclerosis)
and death of the bone.

FUNCTIONS OF OSTEOCYTES

1. Helps to maintain the integrity of the lacunae and canaliculi and thus keep open
the channels for diffusion of nutrition through bone.
2. They play a role in removal or deposition of matrix and of calcium when
required. Osteocytes have eosnophilic or slightly basophilic cytoplasm.

OSTEOCLASTS:
These are bone removing cells. They are found in relation to surfaces
where bone removal is taking place. At such locations the cells occupy pits called
resorption bays or Howship’s lacunae. Osteoclast are multinucleated (20 or more) large
cells (20-100µm in diameter). At sites of bone resorption the surface of osteoclasts show
many faults which are described as a ruffled membrane. Removal of bone by osteoclasts
involves demineralisation and to removal of matrix. Recent studies have shown those
osteoclasts are derived from monocytes of blood.

OSTEO PROGENITOR CELLS:

These are stem cells of mesenchymal origin that can proliferate and convert themselves
into osteoblasts whenever there is need for bone formation. It resembles fibroblasts and
they are numerous in the feotus. In adults the y are present over periosteal and endosteal
aspects of bone surface.
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BONE LINING CELLS:

These cells form a continuous epithelium like layer on bony surfaces where active bone
deposition or removal is not taking place. These cells are flattened. They are also seen on
periosteal and endosteal surfaces and line spaces and canals within bone. These cells can
change to osteoblast when bone formation is needed.

BONE DEVELOPMENT:
Although histologically not different from other, bone formation occurs by 3
mechanisms,
1. ENDOCHONDRAL,
2. INTRAMEMBRANOUS
3. SUTURAL.

Endochondral bone takes places when cartilage is replaced by bone. This occurs at
formation the ends of long bones, vertebra, ribs, at the head of the mandible
and base of the skull.
Intramembranous occurs directly within the mesenchyme in this type, the bone
bone formation develops directly within the soft connective tissue rather than on
a cartilaginous model. The mesenchymal cells proliferate and
condense. As vascularity increase at the sites of condensed
mesenchyme, osteoblast differentiates and begins to produce
bone matrix. This process occurs in the multiple sites within
each bone of the cranial vault, maxilla, and body of the mandible
and mid shaft of long bone. Once begun, intramembranous bone
formation proceeds at an extremely rapid rate.
Sutural bone growth plays an important role in the growing face and skull. Found
exclusively in skull, they are the fibrous joint between bones.
Their function is to permit the skull and face to accommodate
growing organs such as the eyes and brain.
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BONE TURN OVER:

During both embryonic bone development bone is being formed very
rapidly, primarily (but not exclusively) on the periosteal surface, simultaneously, bone is
being destroyed along the endosteal surface at focal points along the periosteal surface
(bone remodeling) and within the osteon of compact bones. During bone growth, bone
formation is occurring at a greater rate than resorption. This replacement of old bone by
new is called is called bone turn over. Bone turn over rates of 30%- 100% per year is
common in rapidly growing children. Most of the bone present today in a child will not
be present at a year from now.
Bone turn over does not stop when adulthood is reached, but the rate
slows. The rate of cortical bone turn over is approximately 5% per year, whereas turn
over of trabecular bone and endosteal surface of cortical bone can approach 15% per
year. Primary osteons of fetal bone are resorbed by osteoclasts to make room for
expanding marrow cavity or undergo turn over by replacing it.
As the osteoclast move through bone the leading edge of resorption is
termed the cutting cone which is characterized as an array of Howships’s lacunae, each
housing an osteoclast. Behind this cutting cone there is a migration of uninucleated cells
on to the roughened cylinder. As these cells differentiate into osteoblasts, they produce a
coating termed a cement or reversal line, which is a thin layer of several phosphoproteins
that act as a mineralised adhesive and bind the old bone to new bone to be secreted. On
the top of the reversal line they begin to lay down new bone matrix, mineralizing from
the outside in. This entire area of the osteon where active formation occurs is termed the
filling cone.The repeated deposition and resorption of bone tissue accommodates the
growth of the bone without losing function or its relationship to neighbouring structures
during the remodeling phase.

ALVEOLAR PROCESS (Pars alveolaris)

DEVELOPMENT:
The development of the roots begins after enamel and dentin formation
has reached the future cementoenamel junction. The enamel organ plays an important
role in root development by forming Hertwig’s epithelial root sheath, which moulds the
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shape of the roots. Hertwig’s root sheath consists of outer and inner enamel epithelia
only. When these cells have induced the differentiation of radicular cells into
odontoblasts and the 1st layer of radicular dentin has been laid down, the Hertwig’s
epithelia root sheath loses its structural continuity and closeness to the surface of the root.
Before the primary cementum can form, the epithelial root sheath must
fragment to form isolated epithelial fragments called epithelial rest of malassez. Through
the spaces in between these epithelial fragments the follicular cells reach the new formed
root. In this location the follicular cells differentiate into cementoblast which produces
acellular cementum or primary cementum.
As the root and its covering of primary cementum form, new bone is
deposited against the crypt wall. The deposition of this wall gradually reduces the space
between the crypt wall and the tooth to the dimensions of the periodontal ligaments.
Collagen fiber bundles also form coincidence with the bone and extend from it a short
way into the follicle to form a fibrous fringe. This new bone is formed by the cells
originating from the dental follicle.
According to Orban an alveolar process in strict sense of the word
develops only during the eruption of the teeth. The growth part of the alveolar process is
gradually incorporated in to the maxillary and mandibular body, while its 3 borders have
got a rapid growth rate. During the period of rapid growth a tissue may develop at the
alveolar crest that combines the characteristic of both cartilage and bone and is called
chondroite bone. The alveolar process forms with the development and eruption of teeth
and conversely, it gradually diminishes in height after teeth loss.

ALVEOLAR BONE:
The alveolar process is that part if the maxilla or mandible that forms,
supports and carrying the teeth. Otherwise, this is the bone which contains sockets or
alveoli for the teeth. As a result of the functional adaptation 2 parts of the alveolar
process may be distinguished:
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1. ALVEOLAR BONE PROPER

2. THE SUPPORTING BONE.

The alveolar bone proper consists of a thin lamella of cortical or compact bone
surrounding the root. Fibers of the periodontal ligament are embedded in this bone. So
it’s also referred to as bundle bone. Alveolar bone proper is perforated by many foramina
which transit nerves and vessels. So it is sometimes referred to as cribriform plate
(lamina cribriformis). In roentgenograms, the alveolar bone proper appears as an oblique
line called the lamina dura. This apparent radio opacity is due to the thick bone without
trabeculations that X-rays must penetrate and not due to any increased mineral content.
The supporting bone surrounds the alveolar bone proper and provides
additional functional support. Supporting bone consist of outer plate of compact or
cortical bone formed by Haversian bone and compacted bone lamellae which is on the
vestibular (lingual) and oral (buccal) surfaces of the alveolar process (outer cortical
plate). The cancellous trabecular or spongy bone sandwiched between these cortical
plates and alveolar bone proper (inner cortical plate) is another sort of supporting bone.
The alveolar process is divisible into separate areas on anatomic basis,
but it functions as a unit with all parts interrelated in the support of the teeth. Occlusal
forces that are transmitted from the periodontal ligament to the inner wall of the alveolus
are supported by the cancellous trabeculae, which in turn are buttressed by labial and
lingual cortical plates. The inner cortical plate or alveolar bone proper contains sharpey’s
fibers of the periodontal ligament fibers and the outer cortical plate is covered by a
fibrous and cellular periosteum. The shape of the alveolar crest under normal conditions
depends on the
a. Contour of the enamel of adjacent teeth.
b. The relative position of the adjacent cementoenamel junction
c. The degree of eruption of the teeth.
d. Vertical positioning of the teeth
e. The oro vestibular width of the teeth.
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The cortical plates are continuations of the compact bone of the principal mass or the
body of maxilla and mandible. The thickness of the cortical plate varies significantly
throughout the arch. The labial and buccal cortical plate is generally thicker than the
lingual plate in the mandible, except in the incisor region, whereas the palatal cortical
plate usually thicker than the facial plate in the maxilla. In the maxilla, numerous
Volkmann’s canals have been described near the vestibular osseous canals; through this
canals course the vascular, nervous and lymphatic elements into the substance of the
bone. Volkmann’s canals of the mandibular alveolar bone are fewer in number than in the
maxilla but larger in diameter. In both jaws, the Volkmann canal serve the additional
function o0f supplying the periodontal ligaments, via hundreds of pores that are present
in the alveolar bone proper. The size and orientation of the trabeculae which is between
the cortical plate and alveolar bone proper are correlated with the intensity of the
functional stimuli. The magnitude of this layer, i.e., the spongiosum in the mandible is
less than the intermaxilla. In some location, spongiosum may be entirely absent, with
fusion of cortical plate and cribriform plate. The pattern of trabecular organization
between the cribriform and cortical plates is structurally and functionally related to the
specific stresses to which various segments of dental arch are subjected. Each root of all
multirooted teeth has its own alveolus. The alveoli of multirooted teeth are separated by
osseous inter radicular septa, which are composed of only 2 components, spongiosum and
alveolar bone (cribriform plate). The trabecula within the interradicular septa course
mainly horizontally vis-à-vis the occlusal plane of the arch.
Because of the inserting sharpey’s fibers the alveolar bone reveals a
double fibrillar orientation. Sharpey’s fibers run perpendicular to the bone surface. There
collagen is produced by periodontal ligament fibroblast. No cell is entrapped in these
fibers. At their insertion in bone, they become mineralised, with their periphery being
hypermineralised and their core hypomineralised. This specific type of bone, i.e., the
bundle bone covers the whole socket, as the cementum surrounds the root. As a result, the
periodontal ligament is never in anatomical or functional relationship with the supporting
bone. The layer of functional bundle bone is thin; it ranges between 100-200 µm in
humans. The bundle bone may appear thicker on one side of socket (the apposition one),
but its outer layer is likely functional, as suggested by the regularly spaces cement lines.
These cement lines act like boundaries between the bones formed on sides, interrupting
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or modifying the course of extrinsic fibers, this results in the formation of successive
functional layers. (Bundle bone is not unique to the jaws; it occurs throughout the skeletal
system wherever ligaments and muscle are attached).
The plasticity of bundle bone is reflected in varying forms of sharpey’s
fiber attachment. During tooth eruption, cemental fibers appear 1st, followed by sharpey’s
fibers from bone. Sharpey’s fibers are more widely spaced than fibers from cementum.
Alveolar fibers later extend into the middle zone to join the lengthening cemental fibers.
Individual fibers rather than being continuous consisted of 2 separate parts spliced
together midway between cementum and bone in a zone called intermediate plexus

BONE MARROW:
In the embryo and new bone, the cavities of all bones are occupied by
red haemopoetic marrow. The red marrow gradually undergoes a physiologic fatty or
yellow inactive type of marrow. In the adult the marrow of the jaw is normally of yellow
or inactive type. However, foci of red bone marrow are occasionally seen in jaws, often
accompanied by resorption of bony trabeculae. Common locations are the maxillary
tuberosity and maxillary and mandibular molar and premolar areas which may be visible
radiographically as zones of radiolucency.

PERIOSTEUM AND ENDOSTEUM:

The periosteum consists of an inner layer composed of cells that have
the potential to differentiate into osteoblast and outer layer that is rich in blood vessels
and nerves and is composed of collagen fibers and fibroblast. Bundles of periosteal
collagen fibers penetrate the bone binding the periosteum to the bone. The endosteum is
composed of single layer of osteoprogenitor cells and small amount of connective tissue.

INTERDENTAL SEPTUM:
The interdental septum consists of cancellous supporting bone enclosed
within a compact border which separates the adjacent alveoli. It’s bordered by the socket
walls of approximating teeth and the facial and lingual cortical plates.
The interdental septa at the cervical region are thinner and here the
inner cortical plates are fused and cancellous bone is frequently missing. Apically, the
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septa are thicker and generally contain intervening cancellous bone and sometimes
Haversian bone. In 85% of cases the space between mandibular 1st molar and 2nd
premolars consists of both lamina dura and cancellous bone. But in about 15% of cases
only the lamina dura is seen. If roots are too close, an irregular window can appear in the
bone between adjacent roots. Thus, between maxillary molars the septum consists of both
lamina dura and cancellous bone in 66.6% of cases and only lamina dura in 20.8% and
has a fenestration in 12.5% cases.

OSSEOUS TOPOGRAPHY:
The bone contour confirms to the prominences of the roots, intervening
vertical depressions that taper towards the margin. The height and thickness of facial and
lingual bony plates are affected by the alignment of the teeth, by the angulation of root to
the bone and by occlusal forces.
On teeth in labial version, the margin of the labial bone is located
farther apically than on tooth in proper alignment. The bone margin is thin to a knife edge
and presents an accentuated arc in the direction of the apex. All teeth in lingual version,
the facial bony plate is thicker than normal. The margin is blunt, rounded and horizontal.
Effect of root to bone angulation on the height of alveolar bone is most noticeable on the
palatal roots of maxillary molars. The bone margin is located farther apically on the roots,
which form relatively acute angles with the palatal bone. The cervical portion of the
alveolar plate is sometimes considerably thickened on the facial surface apparently as
reinforcement against occlusal forces.

FENESTRATIONS AND DEHISCENCE’S: Isolated areas in which the root is

denuded of bone and the root surface is covered by periosteum and overlying gingiva are
termed fenestrations. In these instances marginal bone is intact. When the denuded areas
extend through the marginal bone the defect is called dehiscence.
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Such defects occur on approximately 20% of the teeth. They occur

more on the facial bone than on the lingual and are more common on anterior teeth than
on posterior teeth and are frequently bilateral. There is microscopic evidence of lacuna
resorption at margins. The cause of these defects is not clear. Prominent root contours,
malpositions and labial protrusions of the root combined with a thin bony plate are
predisposing factors. Fenestration and dehiscences are important, because they may
complicate the outcome of the surgery and may predispose to gingival recession.

REMODELING OF ALVEOLAR BONE:

In contrast to its apparent rigidity, alveolar bone is the least stable of
the periodontal tissue because its structure is in a constant state of flux. This dynamic
nature is in response to the functional demands. A considerable amount of internal
remodeling takes place by means of resorption and formation, which are regulated by
local and systemic influences. Local influences include functional requirements on the
tooth as well as age related changes in bone cells and systemic influence is hormonal.
Remodeling affects its height, contour and density and is manifested in 3 areas:
a. adjacent to the periodontal ligament,
b. in relation to the periosteum of the facial and lingual plates,
c. Along the endosteal surface of the marrow spaces.

Initiation of remodeling sequence involves the recruitment of osteoclast progenitor cells

to the remodeling site. These cells fuse and differentiate into the mature osteoclast. Here
the osteoblastic lineage is believed to play the role in the regulation and modulation of
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osteoclastic functions, including bone resorption as well as osteoclast recruitment and

differentiation. Such interactions between osteogenic and osteoclastic cells may provide
the physiological and anatomic basis for the coupling of bone formation and resorption.

PHYSIOLOGIC MIGRATION OF THE TEETH:

Teeth have got a tendency to migrate mesially in humans and primates.

Tooth movement does not end when active eruption is completed and tooth is in
functional occlusion. With time and wear, the proximal contact areas of the teeth are
flattened and the teeth tend to move mesially. This is referred to as physiologic mesial
migration. By the age of 40, it results in a reduction of about 0.5cm in length of the dental
arch from the midline to the 3rd molars. Alveolar bone is reconstructed in compliance
with the physiologic mesial migration of the teeth.
On the osseous surfaces subjected to compressive forces (mesial wall of
an alveolus), osteoclastic activity and bone resorption are observed. Such bony surfaces
are characterized by a moth-eaten appearance. Due to the resorptive activities of
osteoclastic cells that are normally observed within Howship’s lacunae on the surface of
the bone undergoing resorption. Osseous surfaces subjected to tensional forces (such as
and is a wall of an alveolus) exhibit the formation of and accumulation of bundle bone,
which exhibits a laminar appearances and contains no trabecular components, no osteons
and no fatty marrow spaces. With time, bundle bone may reconsolidate and assume the
appearance of alveolar bone. . The role of forces generated during mastication and the
general direction of the occlusal wear are the other mechanical factors governing tooth
movements also, in contrast, an anterior component of occlusal forces or forces from
cheek and tongue and angulations of the roots do not influence the tooth movements. The
remodeling bone always preserve the periodontal ligament width.
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CEMENTUM

Cementum is the calcified avascular mesenchymal tissue that forms the outer covering of
the anatomic root.
It begins at the cervical portion of the teeth, at the cemento-enamel junction and
continues to the apex. It furnishes a medium for the attachment of the collagen fibres that
bind the tooth to the surrounding structures.
A. By location
a) Radicular cementum : found on root surface.
b) Coronal cementum : cementum that forms on enamel covering the
crown

B Cellularity.

a. Cellular cementum : cementum containing cementocytes in lacunae in matrix

b. Acellular cementum : cementum without any cells in matrix

Sharpey’s fibres that are continuous with the principal fibers of periodontal ligament.
Since the fibers were originally produced by periodontal ligament fibroblasts, they are
considered “extrinsic” to cementum
The thickness of radicular cementum increases with age. It is thicker apically than
cervically thickness may range from 0.05 to 0.6mm

SHARPEYS
FIBERS

Sharpey’s fibers insertion in to the cementum

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CLASSIFICATION OF PERIODONTAL DISEASES

1. GINGIVAL DISEASES
a) Plaque induced gingival diseases
b) Non-plaque induced gingival diseases
2. CHRONIC PERIODONTITIS
a) Localized
b) Generalized
3. AGGRESSIVE PERIODONTITIS
a) Localized
b) Generalized
4. PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASE

5. NECROTIZING PERIODONTAL DISEASES

a) Necrotizing ulcerative gingivitis (NUG)
b) Necrotizing Ulcerative periodontitis (NUP)
6. ABSCESSES OF THE PERIODONTIUM
a) Gingival abscess
b) Periodontal abscess
c) Pericoronal abscess
7. PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS
a) Endodontic periodontal lesion
b) Periodontal endodontic lesion
c) Combined lesion
8. DEVELOPMENTAL OR ACQUIRED DEFORMITIES AND CONDITIONS
a) Localized tooth related factors that predispose to plaque induced gingival diseases
b) Mucogingival deformities
c)Occlusal trauma
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CLASSIFICATION OF GINGIVAL DISEASES

DENTAL PLAQUE INDUCED GINGIVAL LESIONS
Gingivitis associated with dental plaque only with and without contributing factors
1. Gingivitis modified by systemic factors.
a) Endocrine conditions e.g. puberty, pregnancy, diabetes mellitus
b) Associated with blood dyscreasoas e.g. Leukemia
2. Gingival diseases modified by medications e.g. oral contraceptives, phenytoin etc
3. Gingival diseases modified by malnutrition

NON PLAQUE INDUCED GINGIVAL LESIONS

1. Gingival diseases of specific bacterial origin e.g. streptococcal

2. Gingival diseases of viral origin e.g. Herpes virus infection
3. Gingival diseases of fungal origin e.g. candida
4. Gingival diseases of genetic origin e.g. Hereditary gingival fibromatosis
5. Gingival manifestation of systemic conditions
a) Mucocutaneous e.g. lichen planes, pemphigus, vulgaris
b) Allergic reaction e.g. Mercury, acrylic
6. Traumatic lesions chemical, physical, thermal
7. Foreign body reaction
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GINGIVITIS

Gingivitis (inflammation of gingiva) is the most common type of gingival disease.

The role of inflammation in gingival diseases varies in 3 ways:

1. Inflammation may be primary due to bacterial plaque.

2. Inflammation may be secondary, superimposed on systemically caused gingival

disease. E.g. inflammation commonly complicates gingival hyperplasia

3. Inflammation may be precipitating factor responsible for clinical changes in

patients with systemic conditions that of themselves do not produce clinically
detectable gingival disease e.g. Gingivitis in Pregnancy

PLAQUE INDUCED GINGIVITIS

PLAQUE CAN BE SEEN USING DISCLOSING AGENTS
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Course of gingivitis

1. Gingivitis can occur with sudden onset and short duratrion –Acute Gingivitis

2. Recurrent gingivitis can occur after treatment

3. Chronic gingivitis is slow in onset and of long duration.

DESCRIPTION OF GINGIVAL IN GINGIVITIS :

Gingivitis can be
1. Localised : involving only one site

2. Generalised : involving full mouth

Based on extent gingivitis can be

bleeding on probing
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1. Margin : - Marginal gingivits

2. Extending to papilla : papillary gingivits

3. Extending to attached gingiva : Diffuse Gingivitis

Indicators of gingivitis

1. Increased production of GCF

2. Bleeding on probing

Gingival bleeding varies in extent severity and duration.

Absence of bleeding on probing following treatment is an excellent predictor of arrest of
the disease.
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Clinical features seen in gingivitis

Gingiva in health and disease

CLINICAL DESCRIPTION OF GINGIVITIS

STAGES OF GINGIVITIS

THE INITIAL GINGIVAL LESION (STAGE I GINGIVITIS):

Inflammation quickly develops as plaque is deposited on the tooth. Within 24 hours

marked changes are dilation of capillaries and increased blood flow. Clinically, this
initial response of gingiva to bacterial plaque (Subclinical gingivitis) is not apparent.
The initial lesion is localized to the region of the gingival sulcus. The tissues affected
include a portion of Junctional epithelium, oral sulcular epithelium and the most
coronal portion of the connective tissue. As the lesion enlarges, the GCF flow
increases, Bacteria and their products may thus be flushed from the sulcus. In 2 – 4
days of plaque build up the cellular response is well established. Leukocytes move
through the connective tissue and majority seems to accumulate in the Junctional
epithelium and gingival sulcus region and this can be correlated with the increase in
flow of GCF into sulcus.
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Microscopically, changes in blood vessel morphologic features and adherence of

neutrophils to vessel walls (margination) occur within 1 week and sometimes as early
as 2 days after plaque has been allowed to accumulate They can be seen in increased
quantities in the connective tissue, Junctional epithelium and gingival sulcus.
Exudation of fluid from the sulcus and extra vascular proteins are present.

STAGE – I GINGIVITIS

EARLY GINGIVAL LESION (STAGE II GINGIVITIS):

The early lesion overlaps and evolves from the initial lesion with no clear cut dividing
line. The early lesion occurs after approximately 7 days of plaque accumulation. The
vessels below the Junctional epithelium remain dilated, but their numbers increase
due to the opening up of previously inactive capillary beds. Thus the clinical signs of
erythema may appear, mainly owing to the proliferation of capillaries and increased
formation of capillary loops between retepegs. Bleeding on probing may be evident.
There is an increase in the amount of collagen destruction; 70% of the collagen is
destroyed around the cellular infiltrate. The main fiber groups affected are the circular
and dentogingival fiber groups. Lymphocytes and neutrophils are the predominant
infiltrating leukocytes at this stage and very few plasma cells are noted within the
lesion. PMNs that have left the blood vessels in response to chemotactic stimuli from
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plaque components travel to the epithelium, cross the basement lamina and are found
in epithelium and are emerging in the pocke6t area. PMNs engulf the bacteria in the
process of phagocytosis and release lysosomes. The basal cells of Junctional and
sulcular epithelium have now proliferated and represent an attempt by the body to
enhance the innate barrier to plaque.

Microscopic examination reveals leukocyte infiltration in the connective tissue

beneath the Junctional epithelium, consisting of mainly lymphocytes but also
composed of migrating neutrophils, as well as macrophages, plasma cells and mast
cells. The Junctional epithelium becomes densely infiltrated with neutrophils, as does
the gingival sulcus and the Junctional epithelium may begin to show development of
retepegs.

ESTABLISHED GINGIVAL LESION (STAGE III GINGIVITIS):

In chronic gingivitis (Stage III), the blood vessels become engorged and congested;
venous return is impaired and blood flow become sluggish. The result is localized
gingival anoxemia, which superimposes a somewhat bluish hue on the reddened
gingiva. Extravasation of RBCs into the connective tissue and break down of
hemoglobin into its component pigments can also deepen the colour of the
chronically inflamed gingiva. The distinguishing feature of the established lesion is
predominance of b-lymphocytes and of plasma cells. Increases in the proportions of
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plasma cells were evident with long standing gingivitis, but the time for the
development of the classic “established lesion” may exceed 6 months.

Collagenolytic activity is increased in inflamed gingival tissues by enzyme

collagenase. Collagenase is normally present in gingival tissues and is produced by
some oral bacteria and by PMNs. In comparison with the Junctional epithelium,
pocket epithelium is more permeable to the passage of substances into and out of the
underlying connective tissues and may be temporarily ulcerated.

Established lesions do seem to be reversible after successful periodontal therapy and

most lesion as such do not seem to progress. In histologic section, an intensive,
chronic inflammatory reaction is observed

STAGE – III GINGIVITIS

THE ADVANCED LESION (STAGE IV GINGIVITIS; STAGE OF

PERODONTAL BREAKDOWN)

Extension of the lesion into alveolar bone characterizes a 4th stage known as the
advanced lesion, which represents frank and overt periodontitis.
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As the pocket deepens, probably due to the epithelium spreading apically in response
to plaque irritation and destructive episodes, plaque continues its apical down growth
and flourishes an aerobic ecologic niche. The inflammatory cell infiltrate extends
laterally and further apically into the connective tissues. This lesion also features
surface ulceration, suppuration, and fibrosis of gingiva, destruction of alveolar bone
and periodontal ligament, tooth mobility, drifting, tooth exfoliation other than
periodontal pockets. Plasma cells predominate in the lesion, although lymphocytes
and macrophages are also present. the highly organized fiber bundles of the marginal
gingiva lose their characteristic orientation and architecture completely Within the
hypercellular infiltrated tissue portion, collagen fibres are practically absent, although
dense fibrosis may be apparent in the surrounding area. Bone destruction by
osteoclastic resorption begins along the crest of the alveolar bone, usually in the
interdental septum around the communicating blood vessels. As the marrow spaces
are opened, both red and white marrow become hypercellular, undergo fibrosis and
become transformed into scar-like connective tissue. There are also periods of acute
exacerbation and quiescence as the disease progresses.

STAGE – IV GINGIVITIS
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GINGIVAL ENLARGEMENT

Increase in the size of the gingival is a common feature of the gingival disease.

Classification of gingival enlargement

CLASSIFICATION:

The many types of gingival enlargement can be classified according to etiologic

factors and pathologic changes as follows:

I. Inflammatory enlargement
A. Chronic
B. Acute
II. Drug-induced enlargement

III. Enlargements associated with systemic diseases

A. Conditioned enlargement
1. Pregnancy
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2. Puberty
3. Vitamin C deficiency
4. Plasma cell gingivitis
5. Nonspecific conditioned enlargement (
B. Systemic diseases causing gingival enlargement
1. Leukemia
2. Granulomatous diseases (Wegener’s granulomatosis,
sarcoidosis,)

IV. Neoplastic enlargement (gingival tumors)

A. Benign tumors
B. Malignant tumors

V. False enlargement

Using the criteria of location and distribution, gingival enlargement is designated

as follows:
Localized: Limited to the gingiva adjacent to a single tooth or group of teeth

Generalized: Involving the gingiva throughout the mouth

Marginal: Confined to the marginal gingiva

Papillary: Confined to the interdental papilla

Diffuse: Involving the marginal and attached gingivae and papillae

Discrete: An isolated sessile or pedunculated tumor like enlargement

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The degree of gingival enlargement can be scored as follows:

Grade 0: No signs of gingival enlargement

Grade I: Enlargement confined to interdental papilla
Grade II: Enlargement involves papilla and marginal gingiva
Grade III: Enlargement covers three quarters or more of the crown

INFLAMMATORY ENLARGEMENT

Gingival enlargement may result from chronic or acute inflammatory changes..

inflammatory enlargements commonly are a secondary complication to any of the other
types of enlargement, creating a combined gingival enlargement. In these cases it is
important to understand the double etiology and treat them adequately.

Chronic Inflammatory Enlargement

Clinical Features: Chronic inflammatory gingival enlargement originates as a

slight ballooning of the interdental papilla and/or the marginal gingiva. In the early stages
it produces a life preserver-shaped bulge around the involved teeth. This bulge can
increase in size until it covers part of the crowns. The enlargement may be localized or
generalized and progresses slowly and painlessly, unless it is complicated by acute
infection or trauma.
Occasionally, chronic inflammatory gingival enlargement occurs as a discrete
sessile or pedunculated mass resembling a tumor. It may be interproximal or on the
marginal or attached gingiva. The lesions are slow growing and usually painless. They
may undergo spontaneous reduction in size, followed by exacerbation and continued
enlargement. Painful ulceration sometimes occurs in the fold between the mass and the
adjacent gingiva.
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Etiology: Chronic inflammatory gingival enlargement is caused by prolonged

exposure to dental plaque. Factors that favor plaque accumulation and retention include
poor oral hygiene, as well as irritation by anatomic abnormalities and improper
restorative and orthodontic appliances.

Gingival Changes Associated with Mouth Breathing: Gingivitis and gingival

enlargement are often seen in mouth breathers.The gingiva appears red and edematous
with a diffuse surface shininess of the exposed area. The maxillary anterior region is the
common site of such involvement. In many cases the altered gingiva is clearly
demarcated from the adjacent unexposed normal gingival

Acute Inflammatory Enlargement

Gingival Abscess: A gingival abscess is a localized, painful, rapidly expanding lesion
that is usually of sudden onset. It is generally limited to the marginal gingiva or
interdental papilla. In its early stages it appears as a red swelling with a smooth, shiny
surface. Within 24 to 48 hours, the lesion usually becomes fluctuant and pointed with a
surface orifice from which a purulent exudate may be expressed. The adjacent teeth are
often sensitive to percussion. If permitted to progress, the lesion generally ruptures
spontaneously.
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Etiology, Acute inflammatory gingival enlargement results from bacteria carried deep
into the tissues when foreign substances such as a toothbrush bristle, a piece of apple
core, or a lobster shell fragment is forcefully embedded into the gingiva. The lesion is
confined to the gingiva and should not be confused with periodontal or lateral abscesses.

Periodontal (Lateral) Abscess: Periodontal abscesses generally produce enlargement of

the gingiva, but they also involve the supporting periodontal tissues.
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DRUG INDUCED GINGIVAL ENLARGEMENT:

Gingival enlargement is a well-known consequence of the administration of some

anticonvulsants, immunosuppressant, and calcium channel blockers and may create
speech, mastication, tooth eruption, and aesthetic problems.
Clinical Features: The growth starts as a painless beadlike enlargement of the
interdental papilla and extends to the facial and lingual gingival margins. As the
condition progresses, the marginal and papillary enlargements unite; they may develop
into a massive tissue fold covering a considerable portion of the crowns, and they may
interfere with occlusion.
The enlargement is chronic and slowly increases in size. When surgically
removed, it recurs. Spontaneous disappearance occurs within a few months after discon-
tinuation of the drug.

Anticonvulsants
The first drug-induced gingival enlargements reported were those produced by
phenytoin (Dilantin). Other drugs known to induce gingival enlargement are emotoin,
and mephenytoin. Other anticonvulsants that have the same side effect are the
succinimides (ethosuximide, methsuxmimide, and valproic acid.)
Gingival enlargement occurs in about 50% of patients receiving the drug,
Systemic administration of phenytoin accelerates the healing of gingival wounds in
nonepileptic humans and increases the tensile strength of healing abdominal wounds in
rats.

Immunosuppressants
Cyclosporine is a potent immunosuppressive agent used to prevent organ transplant
rejection and to treat several diseases of autoimmune origin. Cyclosporine-induced
gingival enlargement is more vascularized than the phenytoin enlargement, occurs in
approximately 30% of patients receiving the drug, is
more frequent in children, and its agnitude appears to
be related more to the plasma.
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Calcium Channel Blockers

Calcium channel blockers are drugs developed for the treatment of cardiovascular
conditions such as hypertension, angina pectoris, coronary artery spasms, and cardiac
arrythmias.

Idiopathic Gingival Enlargement

Idiopathic gingival fibromatosis is a rare condition of undetermined cause. It has
been designated by such terms as gingivomatosis, elephantiasis, idiopathic fibromatosis,
hereditary gingival hyperplasia, and congenital familial fibromatosis.

Clinical Features: The enlargement affects the attached gingiva, as well as the
gingival margin and interdental papillae, in contrast to phenytoin-induced overgrowth,
which is often limited to the gingival margin and interdental papillae. The facial and
lingual surfaces of the mandible and maxilla are generally affected, but the involvement
may be limited to either jaw. The enlarged gingiva is pink, firm, and almost leathery in
consistency and has a characteristic minutely pebbled surface. In severe cases the teeth
are almost completely covered, and the enlargement projects into the oral vestibule. The
jaws appear distorted because of the bulbous enlargement of the gingiva. Secondary
inflammatory changes are common at the gingival margin.
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Normal gingiva Fibromatosis

ENLARGEMENTS ASSOCIATED WITH SYSTEMIC DISEASES

Many systemic diseases can develop oral manifestations that may include gingival
enlargement. These diseases and/or conditions can affect the periodontium by two
different mechanisms:

1. Magnification of an existing inflammation initiated by dental plaque.

o Conditioned Enlargements/ includes hormonal conditions (e.g.,
pregnancy and puberty), Nutritional diseases such as vitamin C
deficiency, and
o Nonspecific conditioned enlargement; in which the systemic influ-
ence is not identified.
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2. Manifestation of the systemic disease independently of the inflammatory status of the

gingiva.

 Systemic Diseases Causing Gingival Enlargement

 Neoplastic Enlargement (Gingival Tumors)

Conditioned Enlargement
Conditioned enlargement occurs when the systemic condition of the patient exaggerates
or distorts the usual gingival response to dental plaque. The specific manner in which the
clinical picture of conditioned gingival enlargement differs from that of chronic gingivitis
depends on the nature of the modifying systemic influence. Bacterial plaque is necessary
for the initiation of this type of enlargement. However, plaque is not the sole determinant
of the nature of the clinical features.
The three types of conditioned gingival enlargement are hormonal (pregnancy, puberty),
nutritional (associated with vitamin C deficiency), and allergic. Nonspecific conditioned
enlargement is also seen.

Enlargement in Pregnancy: Pregnancy gingival enlargement may be marginal and

generalized or may occur as single or multiple tumor-like masses. During pregnancy
there is an increase in levels of both progesterone and estrogen, which, by the end of the
third trimester, reach levels 10 and 30 times the levels during the menstrual cycle,
respectively.These hormonal changes induce changes in vascular permeability leading to
gingival edema and an increased inflammatory response to dental plaque.

MARGINAL ENLARGEMENT: Marginal gingival enlargement during pregnancy

results from the aggravation of previous inflammation, and its incidence has been
reported as 10% and 70%. The gingival enlargement does not occur without the presence
of bacterial plaque.
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TUMORLIKE GINGIVAL ENLARGEMENT: The so-called pregnancy tumor is not a

neoplasm; it is an inflammatory response to bacterial plaque and is modified by the
patient's condition. It usually appears after the third month of pregnancy but may occur
earlier.
Clinical Features: The lesion appears as a discrete, mushroomlike, flattened spherical
mass that protrudes from the gingival margin or more commonly from the interproximal
space and is attached by a sessile or pedunculated base. It tends to expand laterally, and
pressure from the tongue and the cheek perpetuates its flattened appearance. Generally
dusky red or magenta, it has a smooth, glistening surface that often exhibits numerous
deep red, pinpoint markings. It is a superficial lesion and ordinarily does not invade the
underlying bone.

Enlargement in Puberty: Enlargement of the gingiva is sometimes seen during puberty.

It occurs in both male and female adolescents and appears in areas of plaque
accumulation.

Enlargement in Vitamin C Deficiency: Enlargement of the gingiva is generally

included in classic descriptions of scurvy. It is important to recognize that such
enlargement is essentially a conditioned response to bacterial plaque. Acute vitamin C
deficiency does not of itself cause gingival inflammation, but it does cause hemorrhage,
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collagen degeneration, and edema of the gingival connective tissue. These changes
modify the response of the gingiva to plaque to the extent that the normal defensive
delimiting reaction is inhibited, and the extent of the inflammation is exaggerated
(Glickman 1948). The combined effect of acute vitamin C deficiency and inflammation
produces the massive gingival enlargement in scurvy.

CLINICAL FEATURES: Gingival enlargement in vitamin C deficiency is marginal; the

gingiva is bluish red, soft, and friable and has a smooth, shiny surface. Hemorrhage,
occurring either spontaneously or on slight provocation, and surface necrosis with
pseudomembrane formation are common features.

Plasma Cell Gingivitis: Plasma cell gingivitis is also referred to as atypical gingivitis
and plasma cell gingivostomatitis and often consists of a mild marginal gingival
enlargement that extends to the attached gingiva.

Nonspecific Conditioned Enlargement: Pyogenic granuloma is a tumorlike gingival

enlargement that is considered an exaggerated conditioned response to minor trauma. The
exact nature of the systemic conditioning factor has not been identified.

CLINICAL FEATURES: The lesion varies from a discrete spherical, tumorlike

mass with a pedunculated attachment to a flattened, keloid like enlargement with a broad
base. It is bright red or purple and cither friable or firm, depending on its duration; in the
majority of cases it presents with surface ulceration and purulent exudation. The lesion
tends to involute spontaneously to become a fibroepithelial papilloma or persists
relatively unchanged for years.
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Systemic Diseases Causing Gingival Enlargement

Several systemic diseases may, by different mechanisms, result in gingival
enlargement. These are uncommon cases and will be only briefly discussed.

Leukemia
CLINICAL FEATURES: Leukemic enlargement may be diffuse or marginal,
localized or generalized. It may appear as a diffuse enlargement of the gingival mucosa,
an oversized extension of the marginal gingiva, or a discrete tumorlike inter-proximal
mass. In leukemic enlargement the gingiva is generally bluish red and has a shiny
surface. The consistency is moderately firm, but there is a tendency toward friability
and hemorrhage, occurring either spontaneously or on slight irritation.
Granulomatous Diseases

WEGENER'S GRANULOMATOSIS: Wegener's granulomatosis is a rare disease

characterized by acute granulomatous necrotizing lesions of the respiratory tract,
including nasal and oral defects.
Sarcoidosis: Sarcoidosis is a granulomatous disease of unknown etiology. It
starts in individuals in their twenties or thirties, affects predominantly blacks and can
involve almost any organ, including the gingiva, where a red, smooth, painless
enlargement may appear.

NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)

Benign Tumors of the Gingiva

Epulis is a generic term used clinically to designate all discrete tumors and
tumorlike masses of the gingiva serves to locate the tumor but not to
describe it. Most lesions referred to as epulis are inflammatory
rather than neoplastic.
Fibroma Fibromas of the gingiva arise from the gingival connective tissue or
from the periodontal ligament. They are slow-growing, spherical
 276

tumors that tend to be firm and nodular but may be soft and
vascular. Fibromas are usually pedunculated. Hard fibromas of the
gingiva are rare; most of the lesions diagnosed clinically as fibromas
are inflammatory enlargements
Papilloma Papillomas are benign proliferations of surface epithelium
associated with the human papilloma virus (HPV). Gingival
papillomas appear as solitary, wartlike or "cauliflower"-like
protuberances and may be small and discrete or broad, hard
elevations with minutely irregular surfaces.

Malignant Tumors of the Gingiva

Carcinoma: Oral cancer accounts for less than 3% of all malignant tumors in the body
but is the sixth most common cancer in males and the twelfth in females. The gingiva is
not a frequent site of oral malignancy (6% of oral cancers).
Squamous cell carcinoma is the most common malignant tumor of the gingiva. It
may be exophytic, presenting as an irregular outgrowth, or ulcerative, which appear as
flat, erosive lesions. It is often symptom free, often going unnoticed until complicated by
inflammatory changes that may mask the neoplasm but cause pain; sometimes it becomes
evident after tooth extraction. They are locally invasive, involving the underlying bone
and periodontal ligament of adjoining teeth and the adjacent mucosa. Metastasis is
usually confined to the region above the clavicle; however, more extensive involvement
may include the lung, liver, or bone.

Malignant Melanoma: Malignant melanoma is a rare oral tumor that tends to occur in
the hard palate and maxillary gingiva of older persons. It is usually darkly pigmented and
is often preceded by the occurrence of localized pigmentation. It may be flat or nodular
and is characterized by rapid growth and early metastasis. It arises from melanoblasts in
the gingiva, cheek, or palate. Infiltration into the underlying bone and metastasis to
cervical and axillary lymph nodes are common.
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SARCOMA: Fibrosarcoma, lymphosarcoma, and reticulum cell sarcoma of the gingiva

are rare; only isolated cases have been described in the literature. Kaposi's sarcoma often
occurs in the oral cavity of patients with acquired immunodeficiency syndrome (AIDS),
particularly in the palate and the gingiva.

METASTASIS: Tumor metastasis to the gingiva is not common. Such metastasis has
been reported with various tumors, including adenocarcinoma of the colon, lung
carcinoma, primary hepatocellular carcinoma, renal cell carcinoma, hypernephroma,
chondrosarcoma, and testicular tumor.

FALSE ENLARGEMENT
False enlargements are not true enlargements of the gingival tissues but may appear as
such as a result of increases in size of the underlying osseous or dental tissues. The
gingiva usually presents with no abnormal clinical features except the massive increase in
size of the area.
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Underlying Osseous Lesions

Enlargement of the bone subjacent to the gingival area occurs most commonly in tori and
exostoses, but it can also occur in Paget's disease, fibrous dysplasia, cherubism, central
giant cell granuloma, ameloblastoma, osteoma, and osteosarcoma. One example of this
type of enlargement is shown in. The gingival tissue can appear normal or may have
unrelated inflammatory changes.

Underlying Dental Tissues

During the various stages of eruption, particularly of the primary dentition, the labial
gingiva may show a bulbous marginal distortion caused by superimposition of the bulk of
the gingiva on the normal prominence of the enamel in the gingival half of the crown.
This enlargement has been termed developmental enlargement.
 279

ACUTE GINGIVAL LESIONS

Acute lesions are by definition of sudden onset limited duration and with well defined
clinical features, by contrast with chronic gingivitis which frequently not painful, Acute
gingival lesions are usually easier to diagnose

ACUTE NECROTISING ULCERATIVE GINGIVITIS

Necrotizing ulcerative gingivitis is inflammatory destructive of the gingiva, which
presents characteristic signs and symptoms.

SYNONYMS
- ulcero membranous gingivitis
- ANUG.
- Vincent’s gingivitis
- Vincent’s gingivo stomatitis.
- Necrotising gingivostomatitis.
- Trench Mouth

Vincent first described the mixed fusospirochetal microbiota of the so called ‘Vincent’s
Angina’ characterized by Necrotic Areas in the gingiva
Acute Necrotising ulcerative gingivitis is a distinct and specific disease. However with
the increasing incidence of severe immune deficiency states such as AIDS the lesion has
become more well recognized and often encountered in developed countries. In
developing countries ANUG remains a commonly diagnosed clinical lesions. This is
because of the existing poor nutritional status; stressful living conditions, poor oral
hygiene. In recent years there has been increasing recognition for the need to further
study ANUG; particularly in a view of its contribution to the incidence of cancrum oris –
which has been described as a “neglected third world disease” children in Africa.
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Pathogenic potential of microorganism:-

1. Spirochetes can invade the vital connective tissue . The pathogenic potential is
further substantiated by the fact that both fuso bacteria and spirochetes can
liberate endotoxins. This may be by Direct or Indirect effect. Indirectly –
endotoxcins can contribute to tissue.

Etiology:-
NUG is caused by specific Bacteria, namely a fusiform Bacillus and spirochaetal
organism. Constant flora is composed of provotella intermedia, in addition to fuso
bacteria, treponemas and selenomonas species. The variable flora consists of
heterogeneous ray of Bacterial types.
ii) Local predisposing factors:-
- Pre-existing gingivitis:-
- Deep periodontal pockets and pericoronal flaps are
- Areas of gingiva traumatized by opposing teeth in malocclusion
- 98% of the patients with NUG were smokers

Debilitaling Disease:-
This may predispose the development of NUG. These disease include chronic diseases
such as syphilis and cancer, severe GIT disturbances like ulcerative colitis. and Blood
dyscrasias Nutritional deficiency resulting from debilitating disease may be an additional
predisposing factor.
Mechanism:-
Psychosomatic factors:
stress
examinations
emotional events in life

FEATURES: - It often occurs as an acute episode; it under goes a diminution in severity

leading to sub Acute stage with milder clinical symptoms.
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- Disease may subside spontaneously without treatment. Such patients generally

have history of repeated remissions and exacerbations. Recurrence in this is
frequent.
Oral Signs:-
- lesions are punched out crater like depression at the crest of the interdental
papillae, subsequently extending into marginal gingival and rarely to
attached gingiva and oral mucosa.
- Surface of gingival craters in covered by a gray pseudomembranous
slough, demarcated from the remainder of the gingiva by a pronounced
linear erythema
- In some instance, the lesions are demarcated of the surface
pseudomembrane, exposing the gingival margin, which is red, shiny and
haemorrhagic.
- Spontaneous gingival hemorrhage or pronounced bleeding on the slightest
stimulation.
- Fetid odor
- Increased Salivation.
Symptoms:-
- Lesions are sensitive to touch.
- Constant radiating, gnawing pain which is intensified by eating spicy or
hot foods and chewing.
- Metallic foul taste,
- Pasty saliva.
-
Extraoral and systemic signs and symptoms:-
- Local lymphadenopathy.
- Slight elevation in temperature.
- Marked systemic complications like high fever, increased pulse rate,
leucocytosis, loss of appetite and general lassitude.
- Insomnia.
- Constipation
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- GIT disorders.
- Headache
- Mental depression.
- In rare cases, severe sequel such noma or gangrenous stomatitis have been
described
-
CLINICAL COURSE:-
If untreated, NUG may lead to NUP with a progressive destruction of the periodontium
and denudation of the roots.

A) Pindborg et al 1966 have described the following stages in progress of NUG.

i. only the tip of the interdental papilla affected.
ii. lesion extends to marginal gingiva and causes punched out papilla
iii. Attached gingiva is affected
iv. Bone is exposed.

B) Horning and cohen et al 1995 extended the staging of these oral necrotizing disease as
follows.
Stage 1 – Necrosis of tip of the interdental papilla 93%
Stage 2 – Necrosis of the entire papilla (19%)
Stage 3 – Necrosis extending to gingival Margin (21%)
Stage 4 – Necrosis extending also to the attached gingiva (1%)
Stage 5 – Necrosis extending into buccal or labial mucosa (6%)
Stage 6 – Necrosis exposing alveolar Bone (1%)
Stage 7 – Necrosis perforating skin of check (0%)

Stage 1 is NUG
Stage 2 may be either NUG or NUP because attachments loss have occurred.
Stage 3 & 4 are NUP
Stage 5 & 6 are necrotizing stomatitis.
Stage 7 is Noma.
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- .

Treatment:
Day 1

a. Local treatment limited to gently removing the necrotic pseudomembrane

with a pellet of cotton saturated with hydrogen peroxide [H2O2.]
b. Advised bed rest and rinse the mouth every 2 hours with a diluted 3%
hydrogen peroxide [H2O2.]
c. Systemic antibiotics like penicillin or metronidazole can be prescribed

Day 2
a. If condition is improved, proceed to the treatment described for ambulatory
patients. If there is no improvement at the end of the 24 hours, a bedside visit
should be made. The treatment include again gently swab the area with hydrogen
peroxide, instructions of the previous day are repeated.

Sub gingival scaling and curettage are contraindicated at this time because of possibility
of extending the infection to deeper tissues.

Instruction to the patient:

1. Avoid smoking, alcohol.
2. Rinse with 3% hydrogen peroxide and warm water for every two hours.
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3. Confine tooth brushing to the removal of surface debris with a bland

dentifrice, use of interdental aids and chlorhexidine mouth rinse are
recommended

2nd Visit
Scalers and curettes are added to the instrumentarium, shrinkage of the gingiva
may expose previously covered calculus which is gently removed. Same instructions are
reinforced.
3rd Visit
Scaling and root planing are repeated, plaque control instructions are given.
Hydrogen peroxide rinses are discontinued.
4th Visit
Oral hygiene instructions are reinforced and thorough scaling and root planing are
performed.
5th Visit
Appointments are fixed for treatment of chronic gingivitis, periodontal pockets
and pericoronal flaps and for the elimination of all local irritants.
Patient is placed on maintenance programme.

Supportive systemic treatment:-

- copious fluid consumption
- Analgesics
- Bed rest.
Nutritional supplements:-
- Vitamin B Complex and Vit C.
 285

PRIMARY HERPETIC GINGIVO STOMATITIS.

It is a viral infection of the oral cavity caused by the herpes simplex virus type 1
(HSV 1). It occurs most often in infants and children younger than 6 years of age) but it
is also seen in adolescents and adults. It occurs with equal frequency in male and female
patients.

Oral signs:-
- It appears as a diffuse, shiny erythematous involvement of the gingiva and the
adjacent oral mucosa with varying degrees of edema and gingival Bleeding.
- In its initial stage it may appear as discrete, spherical gray vesicles dispersed in
different areas. E.g. labial and Buccal Mucosa, soft palate, pharynx and tongue.
After approximately 24 hours the vesicles rupture and form painful small ulcers
with a red, elevated halo like margin and a depressed yellow, and grayish white
central portion.
- Diffuse, edematous, erythematous enlargement of the gingiva with a tendency
towards bleeding is seen.
- Course of the disease is 7-10 days. The diffuse gingival erythema and edema that
appear early in me disease persist for several days after ulcerative lesions have
healed. Scarring does not occur in the areas of healed ulceration.

Oral symptoms:-
- Generalized soreness of the oral cavity which interferes with eating and drinking.
- The ruptured vesicles are sensitive to touch, thermal changes and foods.

Extra Oral and systemic signs and symptoms:-

- Involvement of the lips, face (herpes labialis, cold sore) with vesicles and surface
scale formation may accompany the intra oral disease.
- Cervical Adenitis, fever as high as 101 – 105 F and generalized malaise are
common.
 286

History:-
The condition frequently occurs after a episode of febrile disease such as
pneumonia, meningitis, influenza and typhoid. It also tends to occur during periods of
anxiety, strain or exhaustion.
Location of the virus is in the gasserian ganglion. The virus may descend to the lip
through the trigeminal nerve, which may explain why the location of the blister on the lip
is usually seen.
Diagnosis:-
- Patients history and clinical findings. Laboratory diagnosis include
a. Direct smear:- Material is obtained from the base of the lesions and smeared and
stained. Presence of multi nuclear giant cells, containing intra nuclear
eosinophilic inclusion Bodies. However this cannot distinguish from other
infections like CMV, varicella zooster virus.
b. Innoculation of the virus from a suspected site, to tissue culture.
c. Virus can be determined by an election microscopic examination and specific
HSV Antigens can be detected in cells from the lesions by Immuno florescence.

Treatment Various medications have been used in the treatment of this condition
including;
Palliative treatment – makes the patient comfortable until the disease runs its course (7-
10 days). Plaque food debris and superficial calculus are removed to reduce gingival
inflammation.
Supportive treatment: Copious fluid intake and systemic antibiotic therapy for
management of toxic systemic complications. For relief of pain, systemically
administered aspirin is usually sufficient.
Local application of ‘Acyclovir’ ointment
Plaque, food debris, and superficial calculus to be removed
 287

HERPITIC GINGIVOSTOMATITIS

PERICORONITIS

Definition: It is an acute infection which refers to inflammation of gingiva and

surrounding soft tissues of an incompletely erupted tooth. It occurs most frequently in
the mandibular third molar area.
Types- Acute, sub acute or chronic.

Clinical features:
Signs and symptoms: Include markedly red, edematous suppurating lesion that is
extremely tender with radiating pain to the ear, the throat and floor of the mouth. The
patient is extremely uncomfortable because of the foul taste and inability to close the
jaws. In addition to the pain, swelling of the cheek in the region of the angle of the jaw is
seen.
Acute pericoronitis: It is identified by varying degrees of involvement of pericoronal flap
as well as with systemic complications. An influx of inflammatory fluid and cellular
exudates results in an increase in bulk of the flap which interferes with complete closure
of the jaws. The flap is traumatized by contact with the opposing jaw and inflammatory
involvement is aggravated.
Lymphadenitis is a common finding; the patient may also have toxic systemic
complications such as fever, leukocytosis and malaise.
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Complications
 The involvement may become localized, in the form of pericoronal abscess.
 If it occurs in a partly erupted vital tooth it may give rise to cyst formation.
 It may spread posteriorly into the oropharyngeal area and medially into the base
of the tongue, making it difficult for the patient to swallow.
 Depending on the severity there is involvement of the submaxillary, cervical,
deep cervical and retropharygeal lymph node.
 Peritonsillar abscess formation, cellulitis and Ludwig’s angina are infrequent but
nevertheless potential sequelae of acute pericoronitis.

Treatment: The treatment of pericoronitis depends on:

 Severity of the inflammation.
 The systemic complications and,
 The advisability of, retaining the involved tooth.
First visit
1. The area is gently flushed with warm water to remove superficial debris and
exudate followed by application of topical anesthetic agent.
2. The flap is reflected with a scaler and the underlying debris is also removed and
the area is flushed with warm water.
3. Instructions to the patient include hourly rinses with a solution of a tea spoonful
of salt in a glass of warm water, rest, copious fluid intake and administration of
systemic antibiotics, if toxic symptoms are present.If the gingival flap is swollen
and fluctuant an anteroposterior incision to establish drainage is made In the
next visit, determination is made as to whether the tooth is to be retained or
extracted. This decision is governed by the likelihood of further eruption into a
good functional position. If it is decided to retain the tooth, the necessary
surgical procedures are performed using a periodontal knife or electro surgery.
Under anesthesia, a wedge shaped incision
is made to section a tissue that includes the
gingival flap with the tissue distal to the
involved tooth as well.
 289

ROLE OF PLAQUE AND CALCULUS IN PERIODONTAL

PATHOLOGY

The disease association of dental deposits make them of common interest to clinicians
and investigators in all branches of dentistry and the contributions from the clinical and
basic sciences have led to availability of a broad spectrum of information, while major
discrepancies and missing links in our knowledge of dental deposits continue to exist and
there are numerous unsolved problems, the general nature of these substances, their
source, and their relationship to disease are beginning to become apparent.

Dental Deposits can be classified as

Soft Deposits Hard deposits Pigmented deposits stain

1) Food debris 1) Calculus 1) Intrinsic

2) Material alba 2) Extrinsic

3) Acquired pellicle 3) Internalized

4)Plaque and/or Bio-film.

Material alba - material alba or white material is a white curde of matter composed of
aggregates of micro-organisms, leukocytes and dead exfoliated epithelial cells,
randomly organized and loosely adherent that frequently occurs on top of bacterial
plaque with few or no food particles & lakhs the regular internal pattern observed in
plaque.
 290

Antony van Leeuwenhoek in 1663 first described oral bacteria. In his letter to the royal
society in London he said he could see more living organisms in his oral cavity than
human beings in his home country Netherlands.It took almost two hundred years until
mankind realized relationship between bacteria and disease. Since then research has been
performed extensively regarding the development and microbiology of dental plaque and
calculus.
DEFINITION
Dental plaque – can be defined as the soft deposits that form the biofilm adhering
to the tooth surface or other hard surface of the oral cavity includes removable and fixed
restorations.
PATHOGENESIS
Non – specific plaque hypothesis-
Maintains that periodontal disease results from the elaboration of noxious
products by the entire plaque flora. This thinking suggests that only large amount of
plaque would produce greater amount of noxious products which would overwhelm the
host defense.

Specific plaque hypothesis-

States that only certain plaque is pathogenic and its pathogenicity depends on the
presence of or increases in specific microorganisms. Only specific organisms produce
substances that modulate the destruction of host tissue.Acceptence of specific plaque
hypothesis spurred by the recognition of Actinobacillus actinomycetamcomitans as a
pathogen in localized aggressive periodontitis

Composition of Dental plaque-.

One gram of plaque contains 2×10 bacteria. 500 distinct microbial species are found in a
plaque. Analysis by ribosomal DNA sequence suggests 30%of microorganisms
associated with gingivitis represent previously uncultivated thus there is more to be
identified. Intercellular matrix amounts for 20 to 30% of plaque mass.
 291

Organic constituents→
- Glycoprotein – from saliva is an important component of pellicle.
- Polysaccharide – produced by bacteria of which dextran is the predominant form.
- Albumin – originating from the crevicular fluid.
- Lipid – from the membranes of disrupted bacteria and host cells.

Inorganic constituent-
- predominantly calcium and phosphorus
- other minerals are NA, PH, and fluoride

STRUCTURE
Recent microscopic technique suggests plaque is actually heterogeneous in
structure with clear evidence of open fluid filled channels running through the plaque
mass. These channels may provide for circulation within the plaque to facilitate
movement of soluble molecules. The matrix confers specialized environment for the
bacteria thus the substance produced by the bacteria remains within the plaque and
becomes concentrated.

FORMATION OF DENTAL PLAQUE

It is highly ordered and predictable ecologic succession. The process is divided
into three phases.
1. Formation of the dental pellicle.
2. Initial colonization of the tooth surface.
3. Secondary colonization and plaque maturation.
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FORMATION OF THE DENTAL PLAQUE

MICROBIAL COMPOSITION OF DENTAL PLAQUE

Supragingival plaque-
- tooth surface- gram+ve cocci and rods
- outer surface- gram-ve rods and filaments
Subgingival plaque-
Host inflammatory cells and mediators have considerable influence.
- tooth surface- gram-ve rods and cocci
- tissue surface- gram-ve rods and cocci as well as large number of filament,
flagellated rods and spirochetes.

Host inflammatory cells and mediators have a considerable influence on growth and
development of the bacteria. The apical border of the plaque mass is separated from
the junctional epithelium by a layer of host leukocytes.
 293

Significance of the Biofilm Environment

- Allows considerable bacterial interaction. Eg; F. nucleatum has the ability to
coaggregate with facultative and anaerobic species. Also reduces oxidation-
reduction potential.
- Helps in formation of a complex.
- Early colonizers- independent or purple complex
- Secondary colonizers-
Green complex- AA, Capnocytophaga
Orange complex- Fusobacterium, Prevortella
Red Complex- associated with bleeding on probing
- Resistance of the bacteria to the antimicrobial agents is significantly increased in the
biofilm environment.
 294

CALCULUS
Calculus consists of mineralized bacterial plaque that forms on the surface of natural
teeth and dental prosthesis.According to the relation to the gingival margin they are
classified as:
- Supragingival
- Subgingival

Supragingival Calculus
- white or whitish yellow
- claylike consistency
- easily detached
- rapidly reoccur
- color influenced by food and tobacco.
- Seen associated with buccal surface of maxillary molars and lingual surface of
mandibular anterior teeth.
-
Subgingival Calculus
- Explorer is used for detection.
- Typically hard and dense
- Dark brown or greenish white
- Firmly attached to the tooth surface
- Usually extend nearly to the base of the pocket.
- Reduction in inflammation and pocket depth is seen with removal of subgingival
calculus.
Prevalence
- supragingival calculus starts early in life shortly after the tooth eruption.
- Maximum calculus seen in round 20 – 30 years.
- Facial surface will have less calculus
- Accumulation appeared symmetric
- Subgingival calculus appeared either independently or with supragingival calculus
interproximally.
 295

Contents of calculus :

Organic content Inorganic content

- protein polysaccharide complexes - Ca- 39%
- Desquamated epithelial cells - Phosphorus- 19%
- Leukocyte - Cu- 1.9%
- Various type of microorganism. - Mg- .8%
Trace amount of Na, Zn, Strontium, Cu,
Mg, Tungsten, Gold, Aluminum, silicon,
Iron and fluorine.

Four Main crystal forms-

Crystal structure of calculus
- Hydroxyapatite – 58%
- Mg whitelockite- 21%
- Octacalcium phosphate- 12%
- Brushite- 9%

Calcium to phosphorus is higher subgingivally and Na increases with depth of

periodontal pocket.

Attachment to the Tooth Surface

1. By Organic pellicle
2. Mechanical locking into surface irregularity
3. Close adaptation of calculus undersurface of unaltered cementum surface
4. Penetration of calculus onto the cementum( Calculocementum)
 296

FORMATION OF CALCULUS.

Precipitation of mineral salts starts between 1st and 14th days but calcification can
occur as early as 4 to 8 hours Calcifying plaque may become 50% in 2 days and 60-90%
in 12 days. Inorganic material increases as plaque develops into calculus Microorganisms
are not always essential in calculus formation. Saliva and gingival crevicular fluid are the
source of minerals for the sub and supragingival calculus respectively. Plaque has the
ability to concentrate the minerals 2 to 20 times than saliva .Separate foci of calcification
increase in size and coalese to form calculus and is formed in layers. Rate of calculus
accumulation vary from person to person thus classified as heavy, moderate and slight
calculus formers. Time required to reach maximum level is 10 weeks to 6 months.

Theories regarding the mineralization of Calculus.

1. Mineral precipitation results from a local rise in the degree of saturation of Ca and
Ph ions. A rise in the pH of the saliva causes precipitation of calcium phosphate salts
by lowering the precipitation constant. Colloidal proteins in the saliva bind Ca and
Ph ions and maintains a supersaturated solution.
2. Seeding agents induce small foci of calcification that enlarge and coalesce to form a
calcified mass This concept has given rise to the belief of heterogeneous nucleation.
Carbohydrate-protein complex may initiate calcification by removing Ca from the
saliva and binding with it to form a nuclei.

Role of microorganisms in the mineralization of Calculus

Mineralization starts extracellularly around both gram+ve and –ve bacteria. Some
organisms also have the ability to form intracellular apatite crystals. Calculus formation
spreads until the matrix and bacteria calcifies.
 297

PERIODONTAL POCKET
Definition
The periodontal pocket is defined as a pathologically deepened gingival sulcus. It is one
of the most important clinical features of periodontal disease.

Classification of periodontal pocket.

Based on the morphology and their relationship with adjacent structures.

1. Gingival Pocket (pseudo pocket)- this type of pocket is formed by gingival

enlargement without destruction of the underlying periodontal tissues. The
gingival sulcus is deepened because of increased bulk of gingiva.

2. Periodontal pocket. This type of pocket occurs with destruction of the

supporting periodontal tissues.
a. Suprabony pocket- (supracrestal or supra alveolar)-the bottom of the
pocket is coronal to the crest of the alveolar bone.
b. Intrabony (infrabony, subcrestal or supraalveolar) in which the bottom of
the pocket is apical to the level of the adjacent alveolar bone. The lateral
pocket wall lies between the tooth surface and the alveolar bone.

II. According to the surfaces involved of the tooth.

1. Simple pocket- only 1 of the 4 surfaces of the tooth involved.

2. Compound pocket-two or more surfaces involved but all communicate
with the oral cavity.
3. Complex pocket- two or more surfaces involved, but only 1 communicates
with the oral cavity.
Pockets can also be spiral (originating on one tooth surface and twisting around the tooth)
to involve one or more surfaces. Mostly seen in furcation areas. (Cul de Sac)
 298

Pathogenesis of periodontal pocket

Inflammatory gingivitis and periodontitis are associated with the accumulation of
microbial plaque. In addition, several atrophic and degenerative diseases, such as occlusal
traumatism, alveolar atrophy, and desquamative gingivitis, affect the supporting struc-
tures.

Early Concepts of Pathogenesis

One of the earliest concepts of the pathogenesis of periodontitis has been proliferation
and apical migration of the cells of the epithelial attachment with pocket formation.

Stages in the Pathogenesis

The natural history of inflammatory gingival and periodontal disease is not understood
completely, and important aspects of its pathogenesis remain obscure.

The Initial Lesion

The Early Lesion

The Established Lesion

The Advanced Lesion

Pocket Morphology
The features of periodontitis in humans include the presence of gingival and periodontal
pockets, inflammation, formation of a pocket epithelium, and bone resorption. The
interdental bone is affected more often than is bone on the buccal and lingual surfaces or
bone in the deeper, interradicular region.The first and then the second molars and incisors
are the teeth most frequently and severely affected, whereas the canines, and to a lesser
extent the premolars, are involved far less frequently and severely.
The pattern of distribution is symmetric; the same teeth are affected on the right and left
sides and in the maxillary and mandibular arches. Indeed, this distribution occurs,
although to a lesser extent, in individual patients with adult and rapidly progressive
periodontitis. Bone destruction may be horizontal without forming craters or may
excavate deep angular bone craters with one, two, or three walls. The greatest symmetry
 299

is seen with juvenile periodontitis, which characteristically affects only the first
permanent molars and/or the incisors .Symmetry is lost, however, when other systemic
diseases predispose the patient to periodontitis

Histopathology of the periodontal pocket

Once a pocket is formed several microscopic features are present in the following
sections.
1. Soft tissue wall
2. Root surface wall.

Pocket Contents

Periodontal pockets contain debris consisting principally of microorganisms and their

products (enzymes, endotoxins, and other metabolic products), gingival fluid, food
remnants, salivary mucin, desquamated epithelial cells, and leukocytes. Plaque-covered
calculus usually projects from the tooth surface. Purulent exudate, if present, consists of
living, degenerated, and necrotic leukocytes; living and dead bacteria, serum, and a scant
amount of fibrin. The contents of periodontal pockets filtered free of organisms and
debris have been demonstrated to be toxic when injected subcutaneously into
experimental animals.

CLINICAL EXAMINATION OF PERIODONTAL POCKET

Examination for periodontal pocket must include consideration of the following
1. Presence and distribution on each tooth surface
2. Pocket depth
3. Level of attachment on the root
4. Type of pocket

Signs and symptoms

Although probing is the only reliable method of detecting pockets certain clinical signs
may suggest their presence.
1. Bluish red marginal gingiva
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2. Bluish red vertical zone extending from the gingival margin to the attached
gingiva.
3. A rolled edge separating the gingival margin from the tooth.
4. An enlarged edematous gingiva
5. Bleeding on probing or spontaneously
6. Presence of suppuration
7. Loose teeth
8. Migration of teeth.

Symptoms
1. Localized or sometimes radiating pain
2. Sensation of pressure after eating
3. Food impaction
4. Foul taste in localized areas
5.Sensitivity to hot or cold food
6.Toothache in absence of caries
7.Diastema formation.

Detection of pockets
The only accurate method of detecting and measuring periodontal pocket is careful
exploration with a periodontal probe.
Gutta percha points or calibrated silver points can be used with the radiograph to assist in
determining the level of attachment of periodontal pockets.

Pocket probing
The two different pocket depths are
1. Biologic or histologic depth
2. Clinical or probing depth
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CHRONIC PERIODONTITIS

Chronic Periodontitis – The transition from gingivitis to periodontitis is

characterized by clinical evidence of crestal bone loss. The gingiva clinically
becomes bluish red, soft oedematous there is loss of stepping, bleeding while
brushing. As a result of crestal bone loss there is presence of periodontal
pockets.

Following characteristics are common in patients with chronic periodontitis:

1. Prevalent in adults but can occur in children.
2. Amount of destruction consistent with local factors.
3. Associated with a variable microbial pattern.
4. Subgingival calculus frequently found.
5. Slow to moderate rate of progression with periods of rapid progression.
6. Possibly modified by or associated with (a) Systemic diseases such as
diabetes mellitus and HIV infection (b) Local factors (c) Environmental factor
such as cigarette smoking and emotional stress.

Chronic Periodontitis is localized when <30% of sites involoved.

Chronic Periodontitis is Generalized when >30% of sites involved.

ACCORDING TO SEVERITY
Slight: 1-2mm of clinical attachment loss.
Moderate: 3-4mm of clinical attachment loss.

Severe: > 5mm of clinical attachment loss.

ACCORDING TO EXTENT
Low: 1 – 10 sites
Medium: 11- 20 sites
High: >20 sites
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In chronic perodontitis, bacteria most often cultivated at high levels include

perodontitis gingivalis, B forsytus, P intermedia, C rectus, Eikenella corrodens, F
nucleatum, A actinomycetemeomitans, Trephonema etc. In periodontally active
sites (with recent attachment loss) C rectus, P gingivalis, P intermedia, F
nucleatum and B forsythus were found to be elevated. The red complex consists
of P gingival, B forsythus and T denticals. It is an important clinical parameter of
destructive periodontal diseases.

Clinical Features of Chronic Perodontitis.

1. Gingival inflammation (Colour Pale red to magenta and texture loss of

stipping alteration).
2. Bleeding on probing from pocket area.
3. Loss of clinical attachment
4. Loss of alucolar bone both horizontal and vertical.
5. Reduced resistance of periodontal tissue to probing (periodontal pockets)
6. Variable features enlargement / recession of gingiva, root furcation exposure,
tooth mobility, drifting and eventually expoliation of teeth.
Symptoms
Usually painless, occasionally pain present, sensitivity to heat, cold or both. Area
of localized dull pain, radiating deep into jaw. Presence of areas of food
impactions. Gingivals tenderness or itchiness.

ETIOLOGY
bacterial plaque is the etiologic factor responsible for inducing host inflammatory
process. In healthy host, small but variable amounts of bacterial plaque are
controlled by body defense mechanism with no net destruction. The host
response to bacterial plaque is influenced by individual’s genotype, or genetic
make up and by environmental influences.
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fibroblast inflammation, the chronic cellular infiltrate consisting mainly of plasma

cells lymphocytes and macrophages. Clusters of plasma cells were found
between the remains of collagen fibre bundles and around blood vessels.

Periodontal Therapy

Chronic periodontitis can be trated successfully by intensive initial non surgical

therapy and this outcome can be maintained over time with supportive
periodontal therapy. The basic treatment of periodontitis evolves the removal of
both sub and supragingival plaque.

MILD PERIODONTITIS MODERATEPERIODONTITS SEVERE PERIODONTITIS

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AGGRESSIVE PERIODONTITIS

INTRODUCTION

 Familial background

 Lack of relationship between local etiologic factors and presence of

deep periodontal pockets.

 Distinctive radiographic pattern of alveolar bone loss.

 Rate of progression.

 Lack of involvement of primary teeth.

CLASSIFICATION
In the absence of an etiologic classification, aggressive forms of periodontal disease have
b een defined based on the following

 Non-contributory medical history

 Rapid attachment loss and bone destruction.

 Familial aggregation of cases

Secondary features that are considered to be generally but not universally present
are:

 Amounts of microbial deposits inconsistent with the severity of periodontal

tissue destruction

 Elevated proportions of Actinobacillus actinomycetemcomitans and, in

some Far East populations, Porphyromonas gingivalis

 Phagocyte abnormalities. Hyper responsive macrophage phenotype,

including elevated production of PGE2 and IL-1 in response to bacterial
endotoxins

 Progression of attachment loss and bone loss may be self-arresting.

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Localized aggressive periodontitis (LAP)

 Circumpubertal onset

 Localized first molar/incisor presentation with interproximal attachment

loss on at least two permanent teeth, one of which is a first molar, and
Involving no more than two teeth other than first molars and incisors

 Robust serum antibody response to infecting agents.

 Microorganism involved is mainly A.a

Generalized aggressive Periodontitis (GAP)

 Usually affecting persons under 30 years of age, but patients may be

older.

 Generalized interproximal attachment loss affecting at least three

permanent teeth other than first molars and incisors.

 Pronounced episodic nature of the destruction of attachment and alveolar

bone.

 Poor serum antibody response to infecting agents.

 Microorganism involved is mainly P.gingivalis.

2. Aggressive Periodontitis following characteristics
1. All common otherwise clinically healthy patient.
2. Rapid attachment loss and bone destruction.
3. Amount of microbial deposits inconsistent with disease severity.
4. Familial aggregation of diseased individuals.

Following are common but not universal

1. Diseased sites infected with A actintomycetencomitans.
2. Abnormalities in phagocyte function.
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TRAUMA FROM OCCLUSION

Trauma from occlusion (TFO) can be defined as periodontal tissue injury caused
by excessive occlusal forces, beyond the adaptive capacity of the periodontium. The
occlusion that produces such injury is called traumatic occlusion. This traumatic
occlusion may also cause painful spasms, injure the temporomandibular joint and
produce excessive tooth wear.

Periodontal ligament and the alveolar bone require mechanical stimulus from
occlusal forces in order to remain structurally sound. When occlusal forces are
insufficient then periodontal tissues show atrophy but when occlusal forces exceed the
physiologic limit, the injury is produced in periodontal tissues and is known as trauma
from occlusion.

It must be understood that malocclusion does not necessarily produce trauma. On

other hand otherwise, anatomically and esthetically acceptable dentition there may
produce injury to the periodontium.

The occlusion that produces periodontal injury is called traumatic occlusion

or occlusal disharmony or functional imbalance or occlusal dystrophy. An increased
occlusal force is not traumatic if the periodontal tissue can accommodate it.

Trauma from occlusion may be of following types:

1. Acute trauma from occlusion

2. Chronic trauma from occlusion
3. Primary trauma from occlusion
4. Secondary trauma from occlusion

1. Acute Trauma from occlusion – A sudden change in occlusal forces caused by

restorations or prosthetic appliances may alter the direction of occlusal forces on
teeth. This causes tooth pain, increased mobility and sensitivity to percussion. If
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forces are removed by finishing restoration/appliance then it may subside. Some

times the tooth/teeth shift from the forces, causing self-correction of forces.
Otherwise periodontal abscess, necrosis or cemental tear may be produced. In
few cases symptom free chronic condition may persist.

2. Chronic trauma from occlusion – It is more common than the acute one and is
caused by gradual changes in the occlusion produced by tooth wear, drifting
and extrusion of teeth combined with parafunctional habits such as bruxism
and clenching. There is loosening of teeth, widening of periodontal ligament and
angular defects in alveolar bone without pocket. In the initial phase of tooth
mobility there is alveolar bone resorption, reduction of periodontal ligament with
increase in the width of periodontal ligament. In the second phase of tooth
mobility, traumatic lesions heal with permanent widening of the periodontal
ligament space along with adaptation to the increased forces.

3. Primary trauma from occlusion – In previously healthy periodontium if there

is alteration in the occlusal forces, it may cause primary trauma from occlusion.
The alteration in the occlusal forces may be due to:

a) Insertion of a high filling

b) A prosthesis creating excessive force on abutment and antagonist teeth
c) The drifting of teeth or extrusion into the space of missing teeth
d) Orthodontic movement of teeth into functionally unacceptable positions

The forces do not initiate pocket formation because supragingival crestal fibres
are not affected and so there is no apical migration of the junctional epithelium.

4. Secondary trauma from occlusion – When there is reduced capacity of the

periodontium to withstand occlusal forces then the previously well-tolerated
occlusal force become traumatic. This type of tissue injury due to impairment of
adaptive capacity of periodontium is known as secondary trauma from occlusion.
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Bone loss due to marginal inflammation reduces the periodontal attachment area
resulting in increased burden on remaining tissue. Moreover systemic disorders may
inhibit anabolic activity or induce degenerative changes in the periodontium.

Changes produced by TFO alone – In absence of local factors i.e. plaque calculus etc.
the trauma from occlusion may cause following:

a) Widening of periodontal ligament

b) Angular defects in the alveolar bone without pocket formation
c) Loosening of teeth

TRAUMA FROM OCCLUSION

Other changes – Based upon clinical impression rather than substantial evidence the
following clinical changes may be associated with trauma from occlusion.
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a) Food impaction
b) Abnormal habits
c) Recession
d) Gingival bleeding, hyperplasia of gingiva
e) Cheek biting
f) Obscure facial pain
g) Pulpal hyperemia resulting in hypersensitivity to cold, pulpitis, pulp
necrosis and pulp stone
h) Pericementitis
i) Limited excursion of mandible
j) Unlimited excursion of mandible
k) Blanching of gingiva on application of occlusal forces

pathological migration of teeth due to TFO

Recession of the gingiva, which may be asymmetrical, associated with resorption of the
alveolar crest.
McCall’s cleft – Indentation in the gingival margin, generally on one side of the tooth.
Two clefts frequently occur on the same tooth. Intermittent compression of the
periodontal ligament followed by abnormal flushing of the gingival capillaries and
enlargement and engorging of gingival vessels were considered to be responsible for
clefting.
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Absence of stippling – interpreted as evidence of edema secondary to trauma.

Distended veins in the oral mucosa

Sharply demarcated linear depressions – In the alveolar mucosa, parallel to long axis
of root and overlying the septal bone.

PATHOLOGICAL MIGRATION OF TEETH

RADIOGRAPHIC SIGNS
1. Widening of the periodontal space often with thickening of the lamina dura along
the lateral aspect of the root in the apical region and in bifurcation areas.
2. Vertical rather than horizontal destruction of interdental septum with formation of
intrabony defects.
3. Root resorption
4. Radiolucence and condensation of alveolar bone.

Physiological adaptive capacity of the periodontium to occlusal forces

Periodontal tissue can adapt to increased occlusal forces by thickening and

strengthening of the periodontal ligament and increase in the density of alveolar bone.
When adaptive capacity is exceeded destructive changes follow in the periodontal
ligament, alveolar bone and in the tooth surface. The adaptive capacity varies in different
persons and in the same person at different times. The effect of occlusal forces upon the
periodontium is influenced by:

a) Direction of occlusal forces

b) Duration of occlusal forces
c) Magnitude of occlusal forces
d) Frequency of occlusal forces
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The principal fibers of periodontal ligament are so arranged that they can best
accommodate occlusal forces directed in the long axis of the tooth. Constant pressure
on the bone causes resorption, whereas intermittent force favours bone formation.
Lateral or horizontal forces are accommodated by bone resorption in area of pressure
and bone forming in area of tension. Torques or rotational forces cause both tension
and pressure and usually injure the periodontium.

Effects of insufficient occlusal forces

a) Degeneration of periodontium
b) Atrophy of periodontal fibers
c) Osteoporosis of alveolar bone
d) Reduction of bone height
Hypo function results from an open bite relationship, absence of junctional
antagonists or unilateral chewing habits that neglect one side of the mouth.
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HALITOSIS
Halitosis or Foeter oris is defined as foul, offensive or bad breath. Bad breath is
due to some physiological changes and some pathological causes. Pathologically, it may
be due to local causes or, systemic causes. Physiologically the change in breath is due
to the following conditions.

1. Change with age

In young children odour is sweet and pleasant. As the age advances, it becomes
disagreeable. This is due to local changes in mouth and also changes in metabolism.
2. Changes during the day
Usually morning breath in all persons after getting from sleep is pungent and unpleasant.
It is due to putrification of epithelial and food debris and saliva, which lay accumulated
during sleep.

3. Menstrual breath
It appears with onset of periods. The odour is unpleasant due to pathological
conditions; it may be local or systemic.

Local causes
a) Retention of food around the teeth – Food particles retained in cervical areas,
interdental spaces, and deep pockets and on the tongue may get decomposed by bacteria
causing halitosis.
b) Putrification of Saliva – Saliva due to stagnation and putrification by bacteria
causes halitosis.
c) Gingivitis and Periodontitis – Blood and pus formation due to bacterial action
in these diseases produce halitosis.
d) Dental caries – Multiple caries are a common cause of halitosis. The food
particles and saliva sustained in large cavities and the necrosed dentin and pulp cause
halitosis.
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e) Coated tongue – Accumulated food particle and desquamated epithelial cells

on the rough surface of tongue cause halitosis. This is seen in gastrointestinal
disturbances.
f) Mouth Breathing – Unpleasant breath is due to reduced salivary flow,
gingivitis of anterior teeth and change in bacterial flora.
g) Dehydration – Salivary secretion is reduced encouraging greater bacterial
activity and causing foul breath.
h) Artificial dentures – Deposits of plaque, food, debris, accumulate on denture
surfaces. Purification of food debris and stagnation of saliva deposits cause halitosis.
j) Smokers Breath – It is due to nicotine deposits in the mouth

Systemic causes
a) Halitosis from nasopharynx – Chronic sinusitis, tonsillar infections,
laryngitis, and pharyngitis are the common causes of halitosis.
b) Aromatic food consumption – e.g. Onion, garlic, after absorption in the
blood, the lungs exhale the aroma of the foodstuff.
c) Impaired digestion of fats.
d) Metabolic diseases – like Diabetes causes typical foul breath of acetone.
Leukemia results in ammonia odour.
e) Lung disease – chronic bronchitis, lung gangrene produce foul odours.
Pulmonary TB, empyema, and other infected conditions are associated with halitosis.

MANAGEMENT

a) Oral prophylaxis
b) Restorations/Extractions of carious teeth
c) Periodontal surgery to eliminate pockets
d) Proper brushing and mouthwash after meals. Mouth breathing can also be
corrected by oral screens
e) Dentures should be kept clean. They should not be worn at night
f) Smoking should be reduced and stopped
g) All pathological conditions should be treated
h) Avoid aromatic food substances
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PERIODONTAL MEDICINE

Advances in science and technology over the last century have greatly expanded our
knowledge of pathogenesis of periodontal disease. Periodontal disease is an infectious
disease. However, environmental, physical, social and host stresses may modify and
affect disease expression. Certain systemic diseases may modify the initiation and
progression of periodontitis and gingivitis.
Evidence emerging in the last decade has shed light on the converse side of relationship
between systemic health and oral health that is potential effects of periodontal disease on
a wide range of organ systems like
Cardiovascular/cerebrovascular system
Atherosclerosis
Coronary heart disease
Angina, MI and cerebrovascular accident (stroke)
Endocrine system
Diabetes mellitus
Reproductive system
Preterm low birth weight babies
Respiratory system
Chronic destructive pulmonary disease
Acute bacterial pneumonia

FOCAL INFECTION THEORY

In 1900, William Hunter, a British physician, first developed the idea that oral
microorganisms were responsible for wide range of systemic diseases. He claimed that
restoration of carious teeth rather than extraction lead to trapping of infection. In
addition to caries and pulpal necrosis he identified gingivitis and periodontitis as foci of
infection. This theory fell into disrepute in 1940s and 1950s when widespread infections
failed to reduce or eliminate systemic conditions.
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Mechanism of focal infection

There are two generally accepted mechanisms in the possible production of focal
infection.
1. There may be a metastasis of microorganisms from an infected focus by either
hematogenous or lymphogenous spread.
2. The toxin or toxic products may be carried through the blood stream or
lymphatic channel, from a focus to a distance site where they cause a hypersensitive
reaction in the tissues.
The spread of microorganisms through vascular or lymphatic channel is a
recognized phenomenon, as is their localization in tissues. This localization preference is
probably an environmental phenomenon rather than inherent or developed feature of the
microorganism
The production of toxins by microorganisms and their dissemination by vascular
channels are also recognized occurrences. One of the most dramatic examples is of
scarlet fever, the remarkable cutaneous features of the disease being due to the
erythrogenic toxin liberated by the infecting streptococci.

ORAL SEPSIS AND ITS EFFECTS ON GENERAL HEALTH

Oral sepsis has been related to general health since the very inception of the theory of
focal infection early in the twentieth century. This theory originating during the infancy
of microbiology as a science was based chiefly upon clinical observation but with little
scientific foundation.Focus of infection refers to a circumscribed area of tissue, which is
infected with exogenous pathogenic microorganisms and is usually located near mucous
or cutaneous surface.

Oral foci of infection and its spread

A variety of situations exist in the oral cavity, which are source of infection and which
may set up distant metastasis. These include:
1. Infected periapical lesions such as periapical granuloma, cyst and abscess
2. Teeth with infected root canal
3. Periodontal diseases with special reference to tooth extraction or manipulation
 317

Subgingival environment as a reservoir of bacteria:

The sub gingival micro biota in patients with periodontitis provides a significant
and persistent gram-negative bacterial challenge to the host. These organisms and their
products such as lippolysaccharides (LPS) have ready access to circulation through
sulcular epithelium, which is ulcerated. Hence, bacteremia is common with mechanical
trauma while eating, brushing, flossing, and scaling. This leads to an immuno-
inflammatory response by host producing variety of systemic disorders.
Significance of oral foci of infection
There have been a vast number of reports based chiefly on clinical evidence to
show that oral foci of infection either cause or aggravate many systemic conditions like:
Arthritis
Arthritis of the rheumatoid type is a disease of unknown etiology and the patient
has a high antibody titer to a group of haemolytic streptococci. Because of the
occurrence of streptococcal infection in the mouth it may precede the initial or recurrent
attacks.
Sub Acute Bacterial Endocarditis
It can without doubt be related to oral infection, since
a) There is close similarity in most instances between the etiologic agent of the disease
and the microorganism of the oral cavity, in the dental pulp and in periapical lesions.
b) Symptoms of sub acute bacterial endocarditis have been observed in some instances
shortly after tooth extraction and
c) Transient bacteremia follows tooth extraction
The causative organism of SABE is streptococcal viridans. Numerous studies indicated
that tooth extraction is often followed by streptococcal bacterimia that may cause SABE.
Gastro intestinal diseases These diseases have been periodically related to oral foci of
infection. Gastric and duodenal ulcers have reportedly been produced experimentally by
the injection of streptococci. But the low pH of the gastric secretion is an adequate
defense against such infection.
Ocular diseases Ocular diseases have been attributed in the ophthalmologic literature to
primary foci of infection such as those associated with the teeth, tonsils, sinuses etc.
Skin diseases Skin diseases such as acne, tinea, eczema, scabies, urticaria, psoriasis etc.
may be related to oral foci or infection.
 318

Renal diseases Streptococcus haemolyticus may be the causative organism but the
chance of renal diseases due to oral foci of infection is very less.

DISTANT SPREAD OF ODONTOGENIC INFECTION

The spread of odontogenic infection through some potential space, may lead to
mediastinitis, mediastinal abscess, pleural effusion, empyema, pericarditis, cellulitis of
face and Ludwig’s angina. Sometimes a number of neurological complications may
accompany odontogenic infections. These complications may be fatal. They include
cavernous sinus thrombosis, brain abscess and meningitis. The mask area of the face is
the dangerous area from which the infections can enter the brain.

PERIODONTAL DISEASE AND CHD

Periodontal disease has been related to coronary heart disease/atherosclerosis and
myocardial infarction. Patients with periodontitis have 25% more risk for CHD
compared to periodontally healthy individuals. Since CHD is a major cause of death, so,
it is important to identify this relationship amongst our patients in day-to-day practice.
The level of oral hygiene is also associated with CHD. Patients with poor oral hygiene
have two fold increased risk for CHD.

PERIODONTAL DISEASE AND DIABETES MELLITUS (DM)

The relationship between diabetes mellitus and periodontal disease has been extensively
examined and found that DM increases risk for periodontitis. Periodontitis has been
labeled as sixth complication of DM apart from retinopathy, nephropathy, neuropathy etc.
and control of periodontitis has beneficial effect on glycemic control of diabetic patient.
Mechanical therapy wit systemic antibiotics (Doxycycline) is useful.

PERIODONTAL DISEASE AND PREGNANCY OUTCOME

Low birth weight infant (less than 2500 gm) and premature delivery (before 37
weeks) has been related to periodontitis in mother. Research has examined a relationship
between preterm labour and maternal periodontal infection, which can be prevented by
motivating potential mothers and pregnant women for good oral hygiene maintenance
and carrying out prophylaxis at an early stage.
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CLINICAL DIAGNOSIS

Diagnosi s: It is defined as t he use o f scient ific and skilled t echnique t o

est ablish t he cause and nat ure of pat ient illness.
Proper diagnosis is essent ial for int elligent treat ment . Per iodont al
d iag no sis should first det er mine
 Whet her disease is present ?
 Ident ify t he t ype, ext ent , dist r ibut io n and sever it y
 Fina lly provide an underst anding o f t he under lying pat ho logic
processes and t heir cause.
Per iodont al diagnosis inc ludes
 Taking and recording pat ient s hist or y
 Examinat io n
 Evaluat ion o f sign and s ympt oms as well as t he result s o f var iou s
t est s
Number of vi sits
Usually t wo vis it s are required, since t he examinat io n procedures
are t ime consuming.
Fi rst visit
 Overall appr aisal o f t he pat ient
 Medical hist or y
 Dent al hist or y
 Radiogr aphic sur vey
 Cast s
 Phot ographs
 Review of init ia l examinat ion
Second visit
 Oral examinat io n
 Examinat io n o f t eet h
 Examinat io n o f per iodo nt ium
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App raisal of patient

Clin icians should at t empt overall apprais al. T his includes pat ient ment a l
and emot io nal st at us, t emperament , at t it ude and physio logic age. The
pat ient s at t it ude t owards dent al t reat ment can be assessed. General
feat ures, pallor, skin r ashes obesit y should be assessed.

Vital statistics
This inc ludes
 Name
 Age
 Sex
 Address
 Phone number
 Mar it al st at us
 Occupat ion
Phys ician or dent ist s who reffer ed t he pat ient should be recorded.

Chief comp laint

The chief co mplaint should be recorded in t he pat ient s own words.
The p at ient usually co mpla ins o f bleeding gums, loose t eet h, spreading o f
t eet h wit h appear ance o f spares, foul t ast e in gu ms, it chy feeling in t he
gu ms.
Pain o f var ied t ypes and durat ion inc luding const ant dull,
gnawing pain, dull pain aft er eat ing, deep radiat ing pain in jaws,
sensit ivit y when chewing, bur ning sensat ion of gums.

Denta l history
The dental history should address the following areas:-
1. Visit t o t he dent ist , frequency, dat e of most recent vis it . Oral
prophylaxis by dent ist and dat e of most recent cleaning.
2. Toot h brushing
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- t ype of brush
- frequency o f use
- met hod
- int er val o f replacing brush
- dent r ifice used
- addit io nal cleansing aids – dent al floss, mout h washes
3. Ort hodont ic t reat ment
- Durat ion
- Dat e of t er minat io n
- Habbit correct io n
4. Pain in t eet h or gums – nat ure, durat ion provoking fact ors and
relieving fact ors.
5. Bleeding gums – when first not ed, spont aneous on br ushing o r
eat ing at night or wit h regular per iodic it y manner in which it is
st opped.
6. Bad t ast e in mout h and areas of food impact io n.
7. Mobilit y o f t eet h
8. Hist ory o f previous per iodont al proble m – nat ure o f t he cond it io n,
if previously t reat ed t he t ype of t reat ment
9. Not e miss ing t eet h and ask t he reason for reason for remo val o f
t eet h.

Medical hi story
A healt hy quest ionnair e is useful. Medical hist ory will aid clinic ia n
in Diagnosis o f oral manifest at ion o f syst emic disease
The det ect io n of syst emic co ndit io ns t hat ma y be affect ing t he
per io dont al t issues
The medical history should address the following areas:
1. General healt h and appearance
2. Medical exa minat io n
3. Major illnesses, hospit a lizat io ns, surger ies
 322

4. Medicat ions prescr ibed by physic ian-

Is the patient under the care of a physician? The name, address and
telephone number of the physician should be recorded because direct
communication may be necessary.
All the possible effects of these medications should be carefully analyzed
to determine their effect, if any on the oral tissues and to avoid administering
medications that would cause adverse drug interactions. Special inquiry should be
made regarding the dosage and duration of therapy with anticoagulants and
corticosteroids.
5. Age fact ors
6. Height and weight
7. Self- medicat io n
8. Family medical hist ory
9. Daily diet
10. Alco ho l co nsumpt io n
11. Allergies
Any history of allergy should be recorded, including sensitivity to drugs
(e.g. aspirin, codeine, barbiturates, antibiotics or dental materials.
12. Art hr it is
13. Blood disorder
14. Bleeding
Abnormal bleeding tendencies should be noted, such as
nosebleeds, prolonged bleeding from minor cuts, spontaneous ecchymoses
and excessive menstrual bleeding.
15. Cancer
16. Cardiocascular diseases
a. Congenit al heart disease; rheumat ic heart disease
b. Hypert ensio n
c. Angina pect oris
d. Heart diseases
e. Surgically correct ed cardio vascu lar lesio ns
f. Cerebrovascular accident (st roke)
 323

17. Co mmunicable diseases

a. Hepat it is B
b. Tuber culo sis
c. Sexually t ransmit t ed diseases (STDs)
d. Herpes
e. HIV infect ion, AIDS
18. Diabet es Mellit us
19. Ears
20. Endocr ine
21. Epilepsy

Personal hi story
i. Ora l hygien e p ractice
Tooth b rushing
 T ype o f brush
 Frequency o f use
 Technique o f brushing
 Text ure of filament s
 Frequency o f changing brush

Dent ri fice
 Powder or past e

Additional clean sing devices

 Dent al flo ss
 Wat er irr igat ion
 I mplant care
 Mout hr inses – frequenc y, purpose

ii. Daily diet

 Vit amin supplement s
 Appet it e
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 Regular it y o f meals
 Veget ar ian or non- veg et ar ian

iii. Allergy
Allergic t o
 Lat ex
 Anest het ics
 Penicillin
 Medicament s
 Food
 Iodine

Habits
 Clenching, bruxisms
 Mout h breat hing
 Bit ing object s – finger na ils
 Cheek or lip bit ing
 Awareness of habit s
 Mast icat or y musc le t iredness
Substance abu se
Tobacco
For m o f t obacco , amount used and frequency

Alcohol con su mption

Frequency and amount

Fa mi ly history
Family medical hist or y – predisposit io n to cert ain disease (e.g.)
d iabet es, hypert ensio n
Family dent al hist or y – parent al t oot h loss or maint enance
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Intraoral radiographic survey

It requires full mout h int ra-oral radiographic ser ies – 14 per iapica l
films; 4 bit e wings.

Panoramic radio graphs are a simple and convenient view o f t he

dent al arch and surrounding st ruct ures. They are helpful in det ect ing
develo pment al ano ma lies, pat ho logic lesion of t eet h and jaws, fr act ures
and dent al screening examinat io n of large groups.

They pro vide infor mat io n o f overall radiographic pict ure o f t he

d ist r ibut io n and sever it y o f bo ne dest ructio n in per iodont al disease but a
co mplet e int raoral ser ies in required for per iodont al d isease diagnosis and
t reat ment planning.

Casts
Casts indicate the position of the gingival margins and the position and
inclination of the teeth, proximal contact relationships and food impaction areas. Casts
are important records of the dentition before it is altered by treatment. Casts also serve as
visual aids in discussions with the patient.

Clini cal photograph

Co lor phot ographs are useful for r ecording t he appearance o f t he
t issue before and aft er t reat ment . Photographs cannot always be relied o n
fo r co mpar ing subt le co lor changes in t he gingiva, but t hey do depict
g ing ival morpho logic changes. . With the advent of digital clinical photography,
record keeping for mucogingival problems has become important (e.g. areas of gingival
recession, frenum involvement, papilla loss).
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SECOND VISIT
General examination
Post ure, gait
Height , weight
General healt h st at us
Hair, scalp
Voice, cough, horsenness
Anemia, jaund ice, cyanosis
Vital signs
1. Body temperatu re
Normal 37 0 C (98.6 0 F)
Range 35.5 0 to 37.5 0 C
(Oral) – 9.6 0 to 99.5
2. Pulse rat e
Normal r ange 60 – 100/ min
3. Blood pressu re
Systolic mmHg Diastoli c mm Hg
No rmal < 130 < 85
Hig h nor mal 130 – 139 85 – 89
Hypert ensio n
St age 1 140 – 159 90 – 99
St age 2 160 – 179 100 – 109
St age 3 180 – 209 110 – 119

4. Respi ration
Normal 14 – 20 / minut e

Clini cal examination

Ext ra oral
1. Face
 Expressio n – evidence o f fear or apprehensio n
 Shape t wit ching, paralys is
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 Jaw mo vement s dur ing speech

 Injur ies and symmet r y
2. Skin
Co lor, t ext ure, blemishes, t raumat ic lesio n, erupt ions, swelling
3. Eyes
S ize of pupil
Co lour of scler a
E yeglasses
Prot ruding eye balls
4. Lymph node
Palpable
Enlarged
Tender
Fixed
Palpat e t he pre, post crevicular subment al, submandibu lar lymp h
nodes
5. Lips
 Obser ve clo sed and open- co mpet enc y (puker ing)
 Co lour, t ext ure, size
 Angular chelosis
 Mout h breat hing

6. TMJ
 Obser ve full range o f mo vement s o f mandible
 Pat h of mandible when opening and clo sing
 Int er incisal opening
 Auscult at ion and palpat ion o f each T MJ
 Tender ness, sensit ivit y
 Noises – clicking, propping, grat ing
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Ora l examination
Ora l hygiene
Cleanliness o f oral cavit y is appraised in t erms of accumulat ed foo d
debr is, plaque, mat er ia alba, st ains. Dis closing agent s used for plaque
det ect io n. OHI-S can be used
Halito si s
Fet or exore or fet or oris is foul or o ffensive odo ur emanat ing fro m
o ral cavit y.
Ori gin
Ora l
 Ret ent io n o f odor iferous food part icles
 Coat ed tongue
 ANUG
 Dehydrat io n
 Car ies
 Art ificia l dent ures
 S mo kers breat h
 Healing surgical wound
Ext ra-oral
 Respirat ory t ract infect ion

- Bronchit is
- Pneumo nia
- Bronchiect asis
 Alco ho lic br eat h
 Uremic breat h wit h kidney dys funct io n
 Acet one odour of diabet es

Chronic per iodont it is w it h pocket for mat io n can also cause

unp leasant mout h odour fro m accumulat ed debr is and increased rat e o f
put refact io n of t he saliva.
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Int ra oral examination

Soft tissues
 Labia l and buccal mucosa
 Tongue
 Floor of mout h
 Saliva- The quality and quantity of saliva
 Hard palat e, so ft palat e
 Tonsillar regio n, t hroat
Examination of Lymph nodes: Because periodontal, periapical and other diseases
may result in lymph node changes, the diagnostician should routinely examine and
evaluate head and neck lymph nodes. Lymph nodes can become enlarged and indurated
as a result of an infectious episode, malignant metastases.
Primary herpetic gingivostomatitis, necrotizing ulcerative gingivitis (NUG), and
acute periodontal abscesses may produce lymph node enlargement. After successful
therapy, lymph nodes return to normal in days or weeks.
Examination of the teeth
 Erosion
 Abrasion
 Attrition:
 Abfraction:
 Dental stains
Hypersensitivity
Root surfaces exposed by gingival recession may be hypersensitive to thermal
changes or tactile stimulation. These may be located by gentle exploration with a probe
or cold air.

Proximal contact relationships

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Slightly open contacts permit food impaction. The dentist should check the
tightness of contact using clinical observation and dental floss. Abnormal contact
relationships may also initiate occlusal changes

Cla ssi fication of emb rasu res

The space apical t o t he cont act area forms t he ging ival embr asure,
p yra mid shaped space filled wit h gingival papilla.
Class- I Int erdent al papilla fills spaced bet ween adjacent t eet h
in co nt act .

Class- II Int erdent al papilla is part ially receded result ing in

small opening under cont act .

Class- III Int erdent al papilla has co mplet ely receded leaving
t riangular opening under co nt act .

Progeressio n is Class I  Class II  Class III 

Tooth mobi lity

All teeth have a slight degree of physiologic mobility, which varies for different
teeth and at different times of the day. Mobility is greatest on arising in the morning and
progressively decreases. When awake, mobility is reduced by chewing and swallowing
forces, which intrude the teeth in the sockets.
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Single-rooted teeth have more mobility than multi-rooted teeth; incisors have the
most mobility. Mobility is principally in a horizontal direction.

Tooth mobility occurs in the following two stages:-

1) In the initial stage the tooth moves within the confines of the periodontal ligament
(PDL). This is associated with viscoelastic distortion of the PDL and redistribution of the
periodontal fluids, interbundle content, and fiberes. This initial movement occurs with
forces of about 100g and is about 0.05 to 0.10mm (50-100µm).
2) The secondary stage occurs gradually and entails elastic deformation of the
alveolar bone in response to increased horizontal forces.
When a force such as that applied to teeth in occlusion is discontinued, the teeth
return to their original position.

Causes of mobi lity

Mobility beyond the physiologic range is termed abnormal or pathologic.

Increased mobility is caused by one or more of the following factors:-
1) Loss of tooth support (bone loss) can result in mobility. A tooth with short,
tapered roots is more likely to loosen than one with normal size or bulbous roots having
same amount of bone loss.
2) Trauma from occlusion, or injury produced by excessive occlusal forces or
incurred because of abnormal occlusal habits (e.g. bruxism, clenching), is a common
cause of tooth mobility.
3) Extension of inflammation from the gingival or from the periapex into the PDL
results in changes that increase mobility.
4) Periodontal surgery temporarily increases tooth mobility for a short period.
5) Tooth mobility is increased in pregnancy.
6) Pathologic processes of the jaws that destroy the alveolar bone or the roots of the
teeth can also result in mobility.
Eva luation of mobi lity
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Toot h is he ld fir mly bet ween t he handles of t wo met allic

inst ru ment s or wit h met allic inst rument and finger and an effort is mad e
to mo ve it in all direct ions abnor mal mo bilit y most oft en occur s
facio lingually. Mobilit y ( implant s) evaluat ed wit h elect ronic device –
per io t est .

Miller (1950) graded mobi lity

Grade I - slight ly more t han nor mal
Grade II - moderat ely mor e t han nor mal
Grade III - sever e mo bilit y facio lingually
and/o r mesiodist ally,
combined wit h vert ical displacement .

Deg rees of mobi lity

 Minut e or no movement
- class 0 mo bilit y
 Movement in arc <1mm
- Class I mobilit y
  1mm < 2mm
- Class II mobilit y
  2mm depressio n
- Class III mo bilit y

Sensitivity to percu ssion

 Feat ure of acut e infla mmat io n of per iodont al ligament
 Percussio n at different angles t o long axis o f t oot h oft en aids in
lo calizing t he sit e of infla mmat ory invo lvement .

Occlusi on
 Int ercuspal posit io n
 Ant er ior cont act
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Fremitu s
Fremit us means t he palpable vibrat io n or movement , in dent ist r y it
refer s t o t he vibrat ory pat t erns of t he t eet h.
Pro cedu re
Seat t he pat ient up r ight and head st abiliz ed against head rest index
fing er is fir mly placed over t he cer vical t hird each maxillar y t oot h in
successio n st art ing wit h most post erior toot h on one side and mo vin g
aro und t he arch pat ient is request ed to click t he post er ior t oot h.

Record by t oot h number where vibr at ion is fe lt and t he t eet h where

act ual mo vement is not ed

N = nor mal ( no vibr at ion)

+ = one degree fremit us
Only slight vibr at ion can be felt
++ = t wo degree fremit us
Toot h is clear ly palpable but mo vement is barely vis ible.
+++ = T hree degr ee fr emit us
Movement is clear ly obser ved visually

Significance
Toot h wit h fremit us has excess cont act , premat ure cont act .
1. Well dist r ibut ed post er ior cont act
2. Coupled cont act s bet ween opposing t eet h
3. S moot h excursive mo vement wit hout int er ference.
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Exa mination of the gingi val clinical markers

Appearan ce in Health
Co lo r Unifor mly pale pink or coral pink
Var iat ions in pigment at ion relat ed t o complexio n,
race

S ize Not enlarged

Fit s snug ly around t he t oot h

Shape (cont our) Margina l gingiva:

Knife-edged, flat fo llows a cur ved line
about t he t oot h
Papilla:
1. nor mal co nt act : papilla is po int ed and
pyra midal; fills t he int erproxima l area
2. space (diast ema) bet ween t eet h; ging iva is
flat or saddle shaped

Co ns ist ency Fir m

At t ached gingiva fir mly bound down

Free gingiva: smoot h

At t ached gingiva: st ippled

Po sit ion o f gingiva l Fully erupt ed t oot h: margin is 1 – 2mm above

marg in cement oename l junct ion, at or slight ly below t he
enamel co nt our

Po sit ion o f Dur ing erupt io n alo ng t he enamel sur face. Full y
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ju nct ional erupt ed toot h: t he junct ional epit helium is at t he

ep it helium cement o-ename l junct ion.

Muco gingival Make c lear demar cat io n bet ween t he pink,

ju nct ions st ippled, at t ached gingiva and t he darker alveo lar
mucosa wit h smoot h shiny sur face

Exa mination of periodontiu m

It is import ant to det ect t he ear liest signs of g ingival and
per io dont al disease.

Peri odontal pocket s

Examinat io n inc ludes
 Presence and dist r ibut io n on each t oot h sur face
 Pocket dept h
 Level o f at t achment on root
 T ype o f pocket (infr abony or suprabony)

Detection of pocket s
The only accurat e met hod of det ect ing and measur ing per iodont a l
po cket s is careful explor at ion wit h a per iodo nt al probe. Pocket s are no t
det ect ed by radiographs.
Gut t a percha po int s or calibrat ed silver point s can be used wit h
rad io graph t o assist in det er mining t he le vel o f at t achment o f per iodo nt al
po cket s.

Pocket probing
There ar e t wo differ ent pocket dept h
Biologi c depth:
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The dist ance bet ween gingival mar gin and t he base o f t he pocket
(co ro nal end o f junct io nal epit helium).
Probing depth:
This is t he d ist ance t o which an ad hoc inst rument penet rat es int o
t he po cket . The dept h of penet rat io n of pr obe in a pocket depends on
 S ize of probe
 Force wit h which it is int roduced
 Direct ion o f penet rat ion
 Res ist ance o f t issues
 Convexit y o f t he crown
Probing force
0.75N of probing force has been found to be well t oler at ed and
accurat e.
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Three walled

Two walled

One walled

Probing technique
The probe is insert ed parallel t o vert ical axis o f t oot h and ‘walked ’
cir cu mferent ially around each sur face o f each t oot h to det ect t he areas o f
deepest penet rat ion.
To det ect int erdent al crat er t he probe should be placed obliquel y
fro m facia l and lingual sur faces t o explore t he deepest point of t he pocket
lo cat ed beneat h t he cont act point .
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Level of attach ment

Clini cal attach ment level – t he level of at t achment is t he dist ance

bet ween t he base o f t he pocket and t he cement o -ena mel junct io n.

Determining the level of attach ment

a. When gingiva l margin is locat ed on t he anat omic crown, t he leve l
of at t achment is det er mined by subt ract ing fro m dept h o f t he pocket
t he dist ance fro m ging ival margin t o t he cement o-ename l junct ion.
I f bot h are same lo ss o f at t achment is 0.
b. When t he gingiva l marg in co incides wit h t he cement o -ename l
junct ion, t he lo ss o f at t achment equals t he pocket dept h.

When gingiva l margin is lo cat ed apical t o t he cement o -ename l junct io n,

t he lo ss of at t achment will be great er t hen pocket dept h, t herefore t he
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d ist ance fro m cement o-ena mel junct io n t o gingiva l margin should be
added t o t he pocket dept h.
Determination of disease activity
Active lesion s
 Bleed on probing
 Large amount of fluid and exudat es
 Bact er ia – spirochet es and mot ile bact er ia

Inactive lesion s
 Lit t le or no bleeding o n probing
 Minimal amount of gingival fluid
Micro scopy – cocco id cells
In pat ient wit h aggressive per io dont it is progressive and no n
pro gressing sit es ma y show no differ ences in bleeding on probing.
Fu rcation involvement
Furcat ions are t he co mmo n sit e for recur rence o f act ive bone loss
wit h p er iodont it is. Dist al furcat io ns o f ma xillar y mo lars are most co mmo n
sit e o f recurrent per iodont it is. Explore t he furcat io n wit h Nab er’s p rob e,
Hamp probe.
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By Glickman (1953)
Grade I – incipient bo ne loss which ma y or may not be vis ible o n
radiograph.
Grade II – culde sac
Grade III – t unnel; or ifice furcat ion opening is occluded b y
gingiva.
Grade IV – ging iva does not cover t he or ifice of furcat io n.

Amount of attached gingiva

This is t he dist ance fro m t he pro ject ion on t he ext ernal sur face o f
t he bott om o f gingiva l sulcus or pocket t o t he mucoging ival junct io n.
Kerat inized gingiva includes marginal gingiva.

Assessing width of attached gingiva

 Det er mined by subt ract ing t he sulcus pocket dept h fro m t he t ot al
widt h of ging ival (gingiva l margin t o mucogingival line)

Recession (Denuded root s)

Miller (1985) classified recessio n as
Cla ss I
Includes marginal t issue recessio n t hat does not ext end t o t he
mu co g ingical junct io n. There is no loss of bo ne or soft t issue in t he
int er ndent al area. This can be narrow or wide (groups 1 and 2 in Sullivan
Alk ins classified).

Cla ss II
Cons ist s o f margina l t issue recessio n t hat ext ends beyo nd t he
mu co g ingiva l junct ion. T here is no lo ss of bone or so ft t issue in t he
int erdent al area. T his can be subclassified as narrow or wide (group 3 and
4 Su llivan and Alkins classificat io n)
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Cla ss III
The marginal t issue r ecess io n t hat ext ends t o or beyo nd t he
mu co g ingiva l junct ion beyo nd in addit io n t here is bone and/or soft t issu e
lo ss int erdent ally or malposit io ning o f t he toot h.

Cla ss IV
This marginal t issue recessio n t hat ext ends t o or beyo nd t he
mu co g ingiva l junct io n wit h severe bone loss and so ft t issue loss
int erdent ally and/or sever e toot h malposit io n.

CLASS I CLASS II

CLASS III CLASS IV

Alv eo lar bon e loss

The alveo lar bone levels are evaluat ed by clinical and radiographic
examinat io n.
Tran sgingival p robing (soundin g) helps t o provide infor mat io n o f bone
archit ect ure. Area is anaest he it ized t he probe should be walked alo ng t he
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toot h-t issue int er face so t hat t he operator can feel t he bony t opography.
The probe can also be passed hor izo nt ally t hrough t issue t o provide mor e
t hree dimensio nal infor mat io n (t hickness, height , shape).
Radiographi c evaluation
Access
 Bone co ndit io n
 Toot h condit io n
 Root anat omy
Palpation
Palpating the oral mucosa in the lateral and apical areas of the tooth may help
locate the origin of radiating pain that the patient cannot localize infection deep in the
periodontal tissues and the early stages of a periodontal abscess may also be detected by
palpation.
Suppuration
The presence of an abundant number of neutrophils in the gingival fluid
transforms it into purulent exudates.
Clinically, the presence of pus in a periodontal pocket is determined by placing
the ball of the index finger along the lateral aspect of the marginal gingival and applying
pressure in a rolling motion toward the crown. The purulent exudate is formed in the
inner pocket wall, and therefore the external appearance may give no indication of its
presence. Pus formation does not occur in all periodontal pockets.
PROGNOSIS
Is t he pr ed ict io n o f dur at ion, course and t er minat io n o f t he disease and
it s respo nse t o t reat ment . It can be o f
 Excellent
 Good
 Fai r
 Poo r
 Questiona lb le
 Hopeles
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INTRODUCTION TO DENTAL IMPLANTS
Implant: A graft or insert set firmly or deeply into or onto the alveolar process that may
be prepared for its insertion.

Dental implant:

A substances that is placed into the jaw to support a crown or fixed or removal denture.

Indication:

1. For completely edentulous pt. with advanced residual ridge resorption.

2. For partially edentulous arches where removable partial dentures may
weaken the abutment teeth.
3. Single tooth replacement where FPD cannot be placed.
4. Pt’s desire.

Advantage:

1) Preserve bone
2) Improved function
3) Aesthetics
4) Stability retention
5) Comfort

Requirements:

1. Adequate dense healthy jaw bone to support an implant.

2. Disease free healthy gingiva.
3. Pt must keep implants clean a visit the dentist regularly for checkup.

Contraindications:

1. Uncontrolled or crippling ds eg. Leukemia, uncontrolled DM pt on

chemotherapy / Radiation
2. Poorly motivated pt.
3. Pregnancy
4. Lack of muscular coordinator
5. Insufficient bone

Biomaterials used:
 344

I. Metals and metal alloys:

Titanium & tantalum
Alloys : Titanium Aluminium Vanodium
Cobalt Chromium Molybedenum
Iron Chromium Nickel
II. Ceramic & carbons:
a) Aluminium oxide ceramic
b) Carbon & carbon – silicon compounds
c) Hydroxyappatite as solid material & surface coating
III. Polymers & composites:
Cross linked polymers such as
a) Polymethyl methacrlate
b) Silicon rubber
c) Polyethylene

Types of implants:

1. Endosseous
2. Subperiosteal
3. Transosseous

1) Endosseous:Placed within bone

3 types:
B- blade
C- cylinder
S- screw

2) Subperiosteal
Consists of metal framework attached on top of alveolar bone but beneath the
gingiva and Indicated in severly atrophied jaw

3) Tranosseous
Consist of metal post or ‘U’ shaped frame that passes through the bone and
gingival.
Usedi n mandibular anterior region

Implant bone interface

Two basic means
a) Fibroosseous integration:
 345

Defined as tissue to implant contact, inter position of healthy collagenous

tissue between implant and bone

b) Osseointegration
Proposed by Branmark, Schroeder.
They called it fuctional ankylosis
- Contact establibhed between normal remodelled bone and implant surface
- No interpositioning of connective tissue
- Refers to as direct contact between bone and implant at light microscopic
level
- Electron microscopicly of bone – Titanium interface however shows
presence of connective tissue between and bone.
Biointegration:

Achieved with bioactive materials such as hyroxyappatite or bio glass which bond directy
to bone similar to ankylosis
 SECTION - 7

INSTRUMENTATION
 346

PERIODONTAL INSTRUMENTS AND INSTRUMENTATION

Periodontal instruments are designed for specific purposes, such as removing calculus,

planning root surfaces, curetting the gingiva, and removing diseases tissues. On first

investigation, the variety of instruments available for similar purposes appears confusing

with experience; however, clinicians select a relatively small set that fulfills all

requirements.

APPLICATION:

The instrument application refers to the toot surfaces as areas of the mouth on which

instrument can be used. Each instrument is limited to one of the following application.

Classification of Periodontal Instruments:

According to use: Examination I Diagnostic instruments and Treatment instruments

According to purpose: (Glickman)
a. Periodontal probes
b. Explorer.
c. Scaling, Root planing and Curettage instruments.
d. Cleansing and polishing instruments.
e. Surgical instruments. .
Classification of Surgical Instrument
Instruments to
1. Incise

2. Elevating mucoperiosteum

3. Controlling hemorrhage.

4. Removing bone.

5. Grasp tissues

6. The renewal of soft tissues from

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7. Removal of soft tissues from bony defect.

8. Providing suction.

9. Transfer sterile instruments.

10. Irrigation.

11. Suturing mucosa: Needle holder, Needles, Suture material and Suture Scissors.

PART OF INSTRUMENTS

The parts of each instrument are referred to as the working end, shank and handle.

Working Ends:

Parts are:

1. Face: Shaded surface

2. Back: surface opp to face

3. Lateral surface: Shaded surface on either side of face

4. Cutting edge: Line formed where face and lateral surface meet

DIAGNOSTIC INSTRUMENTS

DENTAL MIRROR (odontoscope)

Hand instrument with follows:

1. Indirect vision

2. Retraction of cheek, tongue hidden by them

3. Indirect illumination: Reflects light in dark area

4. Transillumination: Reflects light through out teeth

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Periodontal Probes:

Tapered, rod like instrument with a blund rounded or rectangular tip.

Calibrated probe – In mm for measurement.

Furcation probe – evaluate bone support information of sulcus, pocket depth, clinical

attachment level, width of attached gingiva, assess for bleeding/exudate and size of oral

lesions.

Probing: Walking the tip with in sulcus / pocket for purpose of determining disease

activity.

Technique:

(a) Adaptation: Tip is placed in contact with tooth surface with the length of probe

parallel as possible. St. is called at Col. Regrow to reach under contact.

(b) Stroke Technique: Strokes must be close to each other (1mm step) to access entire

oral cavity.

(c) Probing pressure should be 10-20 gms.

A guidance system to ensure proper angulation:

 Complete sterilization of all portious entering the mouth

 No biohazard from material / electric shock

 Direct electronic reading and digital output.

Classification of Probes:

I. Conventional /1st generation:

Margins color coded (Calibration at 3mm section)

Unc – 15 probe (Caliberation at 1mm, colour cod at 5-10-15)

University of michigan ‘O’ probe with Williams mark (Calibration at

1,2,3,5,7,8,9,10mm) 6miss.
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Michigan ‘O’ probe (Calibration at 3,6,8mm)

WHO probe /PSn screening (Calibration 3.5, 8.5, 11.5)

Colour coding from 3.5-5.5, 0.5mm ball at tips

Naber probe – detect furcation

II. Pressure Sensitive probes /2nd Generation

TPS (True pressure sensitive probe)

Yeapple probe

III. Computerized probes /3rd Generation

Florida probe

Toronta automated probe

Foster miller

EXPLORERS:

Explores are used to locate subgingival deposits and carious areas and to check the

smoothness of the root surfaces after root planing. Explores are designed with different

shapes and angels. With various uses, as well as limitation. The periodontal probe can be

useful in the detection of subgingival deposits.

Tactile Sensitivity: During subgingival instrumentation, the clinician relies on his or her

sense of touch to locate calculus deposits hidden beneath the gingival margin. Tactile

sensitivity is the ability to detect tooth irregularities by feeling vibrations transferred.

Shepherded hook and straight explorer design:

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The shepherded hook is an impaired explorer; one working end can be used throughout

the dentition. This explorer has two design limitations. The short lower shank restricts it

to use on the crown of the tooth. The second design limitation is the sharp, pointed tip

luben used subgingivally, the sharp point of the explorer is directed towards the

junctional epithelium and could cause trauma to the base of the sulcus.

Shepherded hook explorer are used for detection of dental caries and examination of

occlusal surface and restoration. Examples of shepherded hook explorer include 23 and

54 explorer.

STRAIGHT EXPLORER:

Straight explorer is an unpaired explorer one working end can be used throughout the

dentition. The explorer type has the design limitation of a short lower shank and a pointed

tip. They are used to detect dental caries and examination of occlusal surface and the

surface of restoration e.g. 6,6A, 6L and the 6xL explorer.

SCALING AND CURETTING INSTRUMENTS

Sickle scalers (Supra gingival scalers): A sickle scaler is a debridement instrument with a

pointed back and two cutting edges that meet in a point. Sickle scales are confined to

supragingival use and should not be used on root surface. Sickle scalers are either

available in either anterior or posterior design. Sickle scalers are used with a pull stroke.
 351

Anterior scalers are limited to use on anterior treatment sextants often they are single

ended instrument since only one working end is needed to instrument the crown of

anterior teeth.

Posterior scalers are designed for use on posterior sentants, but they also may be used an

anterior teeth. Usually two posterior sickles are paired on double ended instruments.

The basic design can be obtained with different blade size and shank type to adapt to

specific uses. The U15/30, ball and Indiana university sickle scalers are large. The

jaguette sickle scalers #1, 2 and 3 have medium size blades. The curved 204 sickle

scalers are available with large, medium or small blades.

Design highlight of sickle scalers:

Pointed back

Pointed tip

Triangular in cross section

Two cutting edges per working end

Face is perpendicular to the lower shank

Example of sickle scalers:

Anterior sickle scalers: CD-1, Jacquettle-30, Jacquettle 33, whiteside-2, USC-128,

Towner-U 15, Goldman-46, and Goldman-47 posterior sickle scalers. Jacquette 34/35,

Jacquette 14/15, Jacquette 31/32, Ball 2/3, Mecca 11/12, and the catatonia 107/108.

Use of sicle scaler

Note: instrument grasp and adaptation
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CURETTES

The curette is the instrument of choice for removing deep subgingival calculus, root

planning, altered cementum and removing the soft tissue lining the periodontal pocket.

Each working end has a cutting edge on both sides of the blade and a rounded toe. The

curette is finer than the sickle scaler and does not have any sharp point or corners other

than the cutting edge of the blade.

Therefore, curette can be adapted and provide good access to deep pocket with a conven

basic. Both single and double end curettes. Both single and double ended curettes can be

obtained, deending on the preference of the operation.

There are two basic type of curettes:

1) Universal curet

2) Area specific curet

Universal curette:

This type of curette is called universal because it can be applied to all tooth surface in

both anterior and posterior sextants of mouth. Universal curette are used on crown and

root surfaces (subgingivally and subgingivally).

Design Highlights of universal curettes:

 Rounded back

 Rounded toe

 Semicircular in cross section

 2 cutting edges per working end

 Face is perpendicular to the lower shank

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Example of universe curette:

Columbia curettes #13-14, 2R/2L and 4L/4L Barnhart 1/2, Barnhart 5/6, younger good

7/8; mallery 1/2, Larger ½; Larger 5/6, and Langi 17/18.

Area specific curettes:

GRACY curettes: Gracy curettes are representative of the area specific curettes, a set of

several instruments designed and angled to adapt to specific anatomic area of the

dentition.

Double ended Gracy curette:

Gracy #1-2 and 3-4 anterior teeth
Gracy # 5-6 – Anterior teeth and premolar
Gracy # 7-8 and 9-10 posterior teeth facial and lingual
Gracy # 11-12 – posterior teeth mesial
Gracy # 13-14 – posterior teeth distal.

Although some clinicians prefers the enhanced tactile sensitivity that the flexible shak of

the finishing gray provides. Recent additional to the Gracy curette set have been the

gracy #15-16 and 17-18.

The Gracy #15-16 is a modification of the standard #11-12. It consists of a gracy #11-12

blade combined with the more acutely angled #13-14 shank. The new shank angulation of

gracy #15-16 allows better adaptation to the posterior, mesial surfaces from a front

position with intra-oral rests.

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The gracy #17-18 is a modification of #13, 14. It has a terminal shank elongated by 3mm

and a more accentuated angulation of the shank to provide complete occlusal clearance

and better access to all posterior distal surfaces.

Single ended gracy curette can also obtained, for these curette a set comprises 14

instruments.

Comparison of specific (GRACY and Universal curette):

Gracy
Area of use Set of money curette
designed for specific area
and surfaces
Cutting edge use One cutting edge used;
work with outer edge only
curvature Curved in two plane blade
curves up and to the side
BLADE ANGLE Offset blade face of blade
beveled at 600 to shank
Universal
One curette design for all
areas and surfaces
Both cutting edge used
work with either outer and
inner edge
Curved in 1 plane blade
curved up, not to side
Not offset face of blade
beveled at 900 to the shank

GRACY curettes are available with either a “rigid or a “finishing” type of shank. The

rigid gracy has a larger, stronger and less flexible shank and blade than the standard

finishing gracy. The rigid shank makes it possible to remove moderate to heavy

Columbus without using a separate set to heavy scalers such as sickles and toes.

\
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EXTENDED SHANK CURETTES:

Extended shank curettes such as the Hu-friendly after five curettes are modified of the

standard Gracy curette design. The terminal shank is 3mm longer allowing extension into

deeper periodontal pocket of 5mm or more other features include a thinned blade for

smoother subgingival insertion and reduced tissue distension and a larger diameter,

tapered shank. All standard Gracy numbers erupt for #9-10 (i.e. 1-2, 3-1, 5-6, 7-8, 11-12,

13-14) are available in the after five series. The after five curette are available in finishing

and rigid designs.

Mini bladed curettes: Mini-bladed curette such as Hu-friendly mini five curette are

modification of the after five curette. They feature blades that are half the length of the

after five or standard gracy curettes. The shorter blade allows easy insertion and

adaptation in deep, narrow pockets, furction, developmental grooves, line angles and

deep, tight facial lingual or pocket pockets. Mini five curettes are available in both

finishing and rigid design as with after five, the mini fives are available in all the standard

gracy number except for the #9-10.

The Gracy Curettes: The Gracy curettes are another set of four mini-bladed curettes sub

and H 1-2 are used for anterior and premolars, the H 11-12 is used for posterior, mesial

surface and #13-14 is used for postal distal surface. The blade has been curved slightly

upward this curettes allows the Gracy curette to adapt more closely to the tooth surface

than any. Other curettes especially on the anterior teeth and on line angles. However the

curettes also carrier the potential for gouging and “grooving” into the root surface.
 356

GRACEYS AREA SPECIFIC CURVETTE S

FILES

Files have a series of blade on a base. The primary function is to fracture or crush

tenacious calculus. Files can easily gauge and roughen root surface when used

improperly, therefore they are not suitable for five scaling and root planing. The curette

edge of file are multiple, at a 90-105 to lower shank. The shank is short and rigid

functional shank.

Anterior – simple design

Posterior – complex design

Files are sometimes used for removing overhanging margin of dental restoration eg.

Orban 10/11, orban 12/13.

Chisel Scalers: These are designers for the proximal surface of teeth too closely spaced

to permit the use of other scales, is usually used in the anterior part of the mouth. It is a
 357

double ended instrument with a curved shank at one end and a straight shank at the other;

the blades are slightly curved and have a straight cutting edge beveled at 45 degrees. The

instrument is activated with a push motion while the side of the blade is held firmly

against the root.

HOE scalers: Hoe scalers are used for scaling of ledge or rings of calculus. The blade is

bent at 99 degree angle; the cutting edge is beveled at 45 degree. The blades are slightly

bound so that it can maintain contact at 2 point on a convex surface. The back of the

blade is rounded, and the blade has been reduced to minimum thickness to permit access

to the roots.

Mc calls Hoe scalers # 3,4,5,6,7 and 8 are a set of 6 hoe scalers.

CLEANSING AND POLISHING INSTRUMENTS:

Rubber cups: Rubber cup consist of a rubber shell with or without webbed configuration

in the hallow interior. They are used in the hand piece with a special prophylaxis angle. A

good cleansing and polishing paste that contains fluoride should be used and kept moist

to minimize frictional heat as the cup revolves.

Bristle brushes: Bristle brushes are available in wheel and cup shapes. The brushes is

used in the hand piece with a polishing paste.

Dental tape: Dental tape with polishing paste is used for polishing proximal surface that

are unaccessible to other polishing instrument.

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Air powder polishing:

In early 1980’s, specially designed hand piece was introduced that deliver an air powder

slurry of warm water and sodium bicarbonate, the instrument is called prophy-I. This

system is effective for the removal of intrinsic stain and soft deposits by mechanical

abrasion and provides warm water for rinsing and lavage.

Patient with medical histories of respiratory illnesses, hypertension, hamodralysis,

sodium – restricted diets and those on medication affecting the electrolyte balance is not

candidate for the use of the air-powder polishing device.

THE DENTAL ENDOSCOPE:

The dental endscope has been introduced recently for use subgingivally in the diagnosis

and treatment of periodontal disease called perioscopy system.

It is consisting of 0.99 diameter reusable fiber optic endoscopic over which is fitted a

disposable sterile sheath the fiber optic endoscopic files onto periodontal probes and

ultrasonic instruments that have been designed to accept it. The sheath delivers water

irrigation that flushes the pocket while the endoscopic is in use and keeps the field clear.

The fiber optic endoscopic attach to the medical grade charged coupling device (CCD)

video camera and light source that provides an image on a flat panel video monitor for

viewing during subgingival exploration and instrumentation. It enables the operator to

detect the presence and location of subgingival deposits and guides the operator in their

through removal.
 359

Magnification ranges from 24 x to 46 x enabling visualizing of even minute deposits of

plaque and calculus. The perioscopy system can also be used to evaluate for caries,

defective restoration (sub gingival, root fracture and resorption).

The EVA system:

Probably the most efficient and least traumatic instruments for correcting overhanging or

over contoured proximal alloy and resin restoration are the motor driven diamond files of

the EVA prophylaxis instrument. These files which come in symmetric pairs, are made of

aluminium in the shape of a wedge protruding from a shaft, one side of the wedge is

diamond coated, the other side is smooth.

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SURGICAL INSTRUMENTS

Periodontal surgery is accomplished with numerous instruments periodontal surgical

instrument are classified:

1) Excisional incisioanl instrument

2) Surgical curettes and sickles

3) Periodontal elevators

4) Surgical chisel

5) Surgical files

6) Scissors

7) Hemostats and tissue forceps

15/ 30 HUFRIEDY UNIVERSAL SCALER

Excisional & Incisional Instrument:

1) Periodontal knives (Gingivectomy knives): The Kirkland knife is representative of

knives typically used for gingivectomy these knives can be obtained as either

double ended or single instrument.

2) Interdental knives: The orban knife #1-2, 3 and 4 are examples of knives used for

interdental areas. These spear shaped knives have cutting edges on both sides of the

blade and are designed with either double ended or single ended blades.

3) Surgical blades: Scalpel blades of different shapes and sizes are used in periodontal

surgery. The most common blades are #12D, 15 and 15C. The #12D blade is beak-
 361

shape blade with cutting edges on both sides. The 15H blade is used for thinning

flaps and general purpose. The #15C blade, a narrower version of the # 15blade, is

useful for making the initial, scalloping type incision.

4 Surgical curettes and sickles:

Larger and leaver curettes and sickle are often needed during surgery for the

removal of granulation tissue, fibrous interdental tissues, and tenacious sub

gingival deposits.

Eg. Prichard deposits

Kirkland deposits

5 Periosteal elevators:

The periosteal elevator are needed to reflect and move flap after the incision has

been made for flap surgery. The Woodson and Prichord elevator are well designed.

6 Surgical Chisels:

The back-action chisel is used with a pull motion, whereas the straight chisel (eg.

heield sterdt, Ochsenbein #1,2) is used with a push motion.

7 Tissue forceps:

Is used to hold the flap during suturing. It is also used to position and displace flap

is reflected.

8 Scissors and nippers:

Used to remove tabs of tissue during gingivectomy, turn the margin of flaps, and

enlarge incision in periodontal abscess and to remove muscle attachment.

9. Needle holder:
 362

Are used to suture the flap at the desired position after the surgical process has

completed. Eg. Castroviejo needle holder for delicate, precise technique.

GRADUATED MARKINGS ON WILLIAMS

PERIODONTAL PROBE
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SHARPENING OF PERIODONTAL INSTRUMENTS

It is impossible to carry out periodontal procedures efficiently with dull instruments. A

sharp instrument cuts more precisely and quickly than a dull instrument. The dull

instrument reduces tactile sensitivity and hinders control, as it requires more pressure

when used. Therefore, to avoid wasting time and operating haphazardly, clinicians must

be thoroughly familiar with the principals of sharpening and able to apply then to produce

a keen cutting edge on the instruments they are using.

SHARPNESS AND HOW TO EVALUATE?

The cutting edge of an instrument is formed by the angular junction of two surface of its

blade. When the instrument is sharp, this junction is a finish line running the length of the

cutting edge. As the instrument is used, metal is warm away at the cutting edge, and the

junction of the face and lateral surface becomes rounded or dull. The cutting edge

becomes a rounded surface rather than an acute angle.

Sharpness can be evaluated by light and touch in one of the following

ways:

1) When a dull instrument is held under a light, the rounded surface of its cutting edge

reflects light back to the observer. It appears as a bright line running the length of

the cutting edge. The actively angled cutting edge of a sharp instrument, on the other

hand has no surface area to reflect light. When a sharp instrument is held under a

light, no bright line can be observed.

 364

2) Tactile evaluation of sharpness is performed by drawing the instrument lightly

across an acrylic rod known as a sharpening "test stick". A dull instrument will slide

smoothly, without 'biting' into the surface and raising a light shaving as a sharp

instrument would.

OBJECTIVE OF SHARPENING

The objective of sharpening is to restore the file, then linear cutting edge of the

instrument. This is done by grinding the surfaces of the blade until their junction is once

again sharply angular rather than rounded.

It is important to restore the cutting edges without distorting the original angles of the

instruments. When these angles have been altered, the instrument does not function as it

is designed to function, which limits its effectiveness.

SHARPENING STONES

Sharpening stones may be quarried from natural mineral deposits or produced artificially.

In either case, the surface of the stone is made up of abrasive crystals that are harder than

the metal of the instrument to be sharpened. Coarse stones have larger particles and cut

more rapidly, they are used on instruments that are dull. Finer stones with smaller crystals

cut more slowly and are reserved for final sharpening to produce and finer edge and for

sharpening instruments that are only slightly dull. E.g. Indian & Arkansas stones natural

abrasive stones

Carborandum, ruby, ceramic stones ~ synthetically produced.

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Sharpening stones can also be categorized by their method of use:

a) Mounted rotary stones: These stones are mounts on a metal mandrel and used in a

motor drive hand-piece. They may be cylindrical, conical or disc shaped. These stones

are generally not recommended for routine use blc

1) Difficult to control precisely and thus can seen the shape of the instrument.

2) Tend to wear down the instrument quickly.

3) They can generate quite a bit of frictional heat, which may affect the temper of the

instrument.

b) Unmounted stones:

They come in variety of sizes and shapes. Some are rectangular with flat or groomed

surface, whereas others are cylindrical or cone shaped.

Unmounted stones may be used in two ways:

The instrument may be stabilized and held stationary while the stone is drawn across it. -

Or the stone may be stabilized and held stationary while the instrument is drawn across it.

PRINCIPLES OF SHARPENING

1) Choose a stone suitable for the instrument to be sharpened, one that is of an

appropriate shape and abrasiveness.

2) Use a sterilized sharpening stone of the instrument to be sharpened will not be

resterilized before it is used on a patient.

3) Maintain a stable, firm grasp of both the instrument and the sharpening stone. This

ensures that the proper angulation is maintained throughout the controlled

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sharpening stone. In this manner, the entire surface of the instrument can be reduced

evenly, and the cutting edge is not improperly beveled.

4) Establish a proper angle between the sharpening stone and the surface of the

instrument on the basis of the understanding of its design.

5) Avoid excessive pressure. Heavy pressure will cause the stone to grind the surface

of the instrument more quickly and may shorten the instruments life unnecessarily.

6) Avoid the formation of "wire edge" characterized by minute filamentous projections

of metal extending as a roughened edge from the sharpened cutting edge. When the

instrument is used on root surfaces, these projections will provide a grooved surface

rather than a smooth surface. A wire edge is produced when the direction of the

sharpening stroke is produced when the direction of the sharpening stroke is away

from, rather than into or towards the cutting edges. When back and forth or up and

down sharpening strokes are used, formation of a curve edge can be avoided by

finishing with a down stroke towards cutting edge.

7) Lubricate the stone during sharpening. This minimizes clogging of the abrasive

surface of the sharpening stone with metal particles removed Itom the instruments. It

also reduces heat produced by triction. Oil should be used for natural stones and

water for synthetic.

8) Sharpen instruments at the first site of dullness. A grossly dull instrument is

inefficient and requires more pressure when used, which hinders control.

Furthermore, sharpening such an instrument requires the removal of a great deal of

metal to produce a sharp cutting edge. This shortens the effective life of the

instrument.
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SHARPENING INDIVIDUAL INSTRUMENTS

a) UNIVERSAL CURETTES

Sharpening the lateral surface: When a flat, hand held stone is correctly applied to the

lateral surface of the curette to maintain 70-80 degree angle (Apply the sharpening stone

to the lateral surface of the curette so that the angle between) the face of the blade and the

stone is 100-110 degrees.

Beginning at the shank and the cutting edge and then working towards the toe activate the

stone with short up and down strokes. Use, consistent light pressure and keep the stone

continuously in contact with the blade. Make sure that the 110-11 Odegree angle is

constantly maintained.

As the stone is moved, along the cutting edge, finish each section with a down stroke into

or towards the cutting edge. This will minimize the formation of wire edge.

Sharpening of the blade: this may be done by moving a hand held cylinder or cone

shaped stone back and forth across the surface of the blade.

AREA SPECIFIC:

Hold the curette so that the face of the blade is parallel with the floor. Because the blade

is offset, the shank ofthe instrument will not be perpendicular to the floor.

Identity the end to be sharpened. Apply the stone to the lateral wall so that the angle

between the blade and the stone is 110-110 degree.

Activate short up and down strokes, working from the shank end of the blade to the

curved toe. Finish with a down stroke.

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SICKLE SCALER:

A large flat stone may be used to sharpen. The stone is stabilized on the table or cabinet

with the left hand with a modified pen grasp and applied to the stone so that the angle

between the face of the blade and the stone is 100-110 degree. The right hand then pushes

and pulls the sickle across the surface of the stone.

CHISEL AND HOE:

to sharpen the chisel, stabilize a flat sharpening stone on the flat surface. Grasp the

instrument with the modified pen grasp. A 45-degree angle between the beveled surface

and the face of the blade should be maintained.Hoe scalers are sharpened in the same way

except that a pull stroke is used rather than push stroke.

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ULTRASONIC AND SONIC INSTRUMENTS

Ultrasonic instruments may be used for scaling, curving and removing stains. Their

action is derived from physical vibrations of particles of matter, similar to sound waves,

at frequencies ranging from 20,000 hertz to many million cycles per second, above the

range of human hearing.

There are two common types of ultrasonic units

a) Piezo electric

b) Magnetostrictive

Both types of units are composed of following:

1) An electric power generator that deriyes energy in the form of high frequency

vibrations to a handpiece

2) A handpiece

3) Electric and water outlets

4) A foot control.

Ultrasonic vibrations at the tip of instruments range from 20,000 to 45,000 cycles per

second, depending on the manufacturer.

In Magnetostrictive unit, the pattern of vibrations of the tip is elliptical, which means that

all sides of the tip are active and will work when adapted to the tooth. In Piez'o electric

units, the patter of the vibration of the tip is linear or back and forth which means only 2

sides of the tip are active and will work when adapted to the tooth.
 370

The Piezo electric is less common but tend to provide safety for use on patients

with cardiac pacemaker devices. With a magnetostrictor handpiec:e, energy is carried

from the power generator through strips that encircle the handpiece. The insert is

composed by many Magnetostrictive that convert the electricaL energy in the handpiece

to mechanical energy in the form of rapid vibrations. The vibrations may vary from

20,000 to 29,000 cycles/second. These cycles cause the tip of the insert to altematingly

increase or decrease, thus the tip moves approximately 1/1000 of an inch in a back and

forth, circular or figure-eight motion. It is the tip motion that disrupts the calculus

deposit.

Sonic units consist of a handpiece that attaches to a compressed airline and uses a variety

of specially designed tips. Vibration is 2000-6500 cycles/sec. Less power for calculus

removal.

USES:

1) They are mainly employed for the gross removal of calculus supragingivally and in

shallow, accessible pockets.

2) Sometimes they can also be used to plane root surfaces.

3) Used for debriding after periodontal surgery.

4) Remove overhanging margins on amalgam restorations.

DISADVANTAGES:

1) The water spray helpful in some ways in the ultrasonic units tends to impede

visibility. 2) Also the bluntness of the instrument tip also tends to limit tactile

sensitivity.
 371

3) The vibrations have been shown to disrupt tissue by lifting up epithelium and

dismembering collagen bundles in young, growing tissues.

CLINICAL APPLICATION: In general, the lowest power consistent with effectiveness

should be used. After the instrument is prepared for use the tip should seen between the

fingers to guard against excessive vibrations and heat production. All tips are designed to

operate in a wet field and have attached water outlets. The spray is directed at the end of

the tip to dissipate the heat generated by the ultrasonic vibrations. Within the water

droplets of this spray mist are tiny vacuum bubbles that quickly collapse releasing energy

in the process known as cavitation. The cavitating water spray also serves to flush

calculus, plaque and debris dislodged by the vibrating tip from the pocket. Sonic units do

not release heat way ultrasonic do, but they still have water for cooling and flushing away

debris.

The hand piece and the tip should be applied with very light but firm pressure - a feather

touch and brush stroke. The time of application should be kept as short as practical. The

tip should be kept in motion at all time as the instrument being used. A periodontal

explorer should be used during ultrasonic instrumentation to check the root surface. The

water spray should be ample, particularly in areas where the flow of the tip may be

blocked (subgingivally). It is important not to use the tip that has rough surfaces or spurs,

as they would scratch the tooth surfaces.

Influence on hard and soft tissue: The effect of ultrasonic instruments on the tooth

surface may range from little or no change to a characteristic, fine, stippled or granular
 372

pattern of varying depth. The main effect on the soft tissue is a fragmentation and

washing away of the sulcular lining and adjacent tissue (gingival curettage). Coagulation

has also been reported.

The depth and degree of these tissue effects are governed by the quantity of ultrasonic

energy applied. This quantity is determined by the following factors.

1) Power setting (amplitude of tip motion

2) Applied pressure

3) Relative sharpness of the tip

4) Angle of application

5) Tune of exposure per unit area.

The healing of the wounds produced by ultrasonic instrumentation appears to be similar

to that of wound produced by hand instrumentation. Both the time required for
epithelization and the reappearance of an inflammatory infiltrate in the adjacent
connective tissue during have been studied and are reported to be similar to that for hand
scaling (Schaffer, E.M., and Stende).

INDICATIONS:

1) Ultrasonic curettage is particularly useful in the early phases of treatment and when
tissues are hemorrhagic.
2) The washed field also moves the instruments convenient for calculus removal.
during periodontal surgery.
3) In addition, the instrumentation with lavage is helpful in the treatment of acute
ANUG It enhat:1ces resolution of the acute phase of this disease.
4) Gingival healing is reported to occur more rapidly after ultrasonic and curettage.
This may be the review of the lavage.
5) The instrumentation is useful in patients with heavy supragingival calculus. 6) Many
patients experience less pain during instrumentation.
[But some patients have reported tooth sensitivity after repeated use].
 373

Caution is called for in the presence of baked porcelain inlays or jacket crowns. Root

surfaces treated with an ultrasonic scaler should be finished with curettes.

CONTRADICTIONS:

1) Individuals with infections disease

2) Individuals with strong gap reflex

3) Young children

4) Individuals who experience pain on use

5) Individuals with cardiac pacemakers

6) Patients having asthma

UTILIZATION:

1) Use short, rapid, vertical or oblique strokes.

2) Use light pressure with a feather like touch.
3) Tip or lateral surface of the instrument must be contact with the deposit for it to be
dislodged.
4) Tip should be kept in constant motion and never remain stationary in one area too
long.
5) Instrument tip should be blunt, not sharp and pointed, to avoid damaging the root
surface.
6) Proper instrument tip should be used-for maximum efficiency in removal of
deposits.
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GENERAL PRINCIPLES OF INSTRUMENTATION

1) Accessibility (positioning of patient and operator)

2) Visibility, illumination, and retraction.
3) Condition of instruments (Sharpness)
4) Maintaining a clean field
5) Instrument stabilization
6) Instrument activation

INDIRECT VISION RETRACTION OF RETRACTION OF

AND INDIRECT CHEEK FOR TONGUE FOR
ILLUMINATION BETTER VISION BETTER VISION

I. ACCESSIBILITY:

Accessibility (positioning of patient and operator) facilitates throughness of

instrumentation. The position of the patient and operator should provide maximum

accessibility to the area of operation. Inadequate accessibility impedes through

instrumentation prematurely tires the operator and diminishes his or her effectiveness.

Clinical chair: your thigh should be parallel to the floor and you should be able to reset

your heels on the floor.

When working from clock position 9-120C your legs and the stool base should form’s a

tripod, some what like legs of 3-legged stool.

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VISIBILITY ILLUMINATION AND RETRACTION:

Whenever possible, direct vision with direct illumination from the dental light is most

desirable if this is not possible, indirect vision may be obtained by using the mouth mirror

and indirect illumination may be obtained by using the mirror to reflect light to where it

is needed. Indirect vision and indirect illumination are often used simultaneously.

Retraction: Provides visibility, accessibility and illumination depending on the location of

the area of operation, the fingers and for the mirror are used for retraction of the cheeks

or the tongue, the index fingers is used for retraction of the lips or cheeks when retraction

care should be taken to avoid irritation to the angles of the mouth. If the lips and the skin

are dry, softening the lips with petroleum jelly before instrumentation is begum is a

helpful prevention against cracking and bleeding careful retraction is especially important

for patient with a history of recurrent herpes labiates.

Condition of instruments (sharpness):

Before any instrumentation, all instruments should be inspected to make sure that they

are clean, sterile, and in good condition. The working ends of pointed or bladed

instruments must be sharp to be effective. Sharp instruments enhance tactile sensitivity

and allow the clinician to work more precisely and efficiently.

Maintaining a clean field:

Despite good visibility, illumination and retraction, instrumentation can be hampered if

the operation field is obscured by saliva, blood and debris. The pooling of the saliva

interferes with visibility during instrumentation and impedes control because a firm

finger rest cannot be established on wet, slippery tooth surfaces. Adequate suction is
 376

essential and can be achieved with a saliva ejector or if working with an assistant, an

aspirator.

Instrument Stabilization:

Stability of the instrument and the hand is the primary requisite for controlled

instrumentation stability and control are essential for effective instrumentation and

avoidance of injury to the patient or clinician.

Instrument Grasp:

A proper is essential for precise control of movements made during periodontal

instrumentation.

The most effective and stable grasp for all periodontal instrument is the modified pen

grasp. Although other grasps are possible this modification of the standard pen grasp

ensures the greatest control in performing intro oral procedures.

The thumb, index finger and middle finger are used to hold the instrument as a pen is

held, but the middle finger is positioned so that the side of the pad next to fingernail is

resting on the instrument shank. The Indian finger is bent at the second joint from the

finger tip and is positioned well above the middle finger as the same side of the handle.

The pad of the thumb is placed midway between the middle and Index fingers on the

opposite side of the handle. This creates a triangle of force or tripod effect that enhances

control because it counter acts the tendency of the instrument to turn uncontrollably.
 377

The modified pen grasp also enhance tactile sensitivity because slightly irregularities on

the tooth surface are best perceived when the tactile sensitive pad of the middle finger is

placed on the shank.

The palm and thumb grasp is useful for stabilizing instrument during sharpening and

for manipulating air and water syringe but it is not recommended for periodontal

instrumentation.

MODIFIED PEN GRASP PALM AND THUMB GRASP

Finger Rest: The finger rest serves to stabilize the hand and the instrument by producing

a firm fulcrums as movement are made to activate the instrument.

The fourth finger is prepared by most clinicians for the finger rest. Although it is possible

to use the third finger for finger this is not recommended, because it restricts the are of

movement during activation of strokes.

Finger rest may be generally classified as:

Intra-oral finger rest

Extra-oral fulcrums

The following examples illustrate the different variations the intra oral finger rest.
 378

1) Conventional: The finger rest is established on tooth surface immediately adjacent

to the working area.

2) Cross Arch: The finger rest is established on the tooth surface on the other side of

some arch.

3) Opposite arch: The finger rest is established on the tooth surface on the surface

arch (eg. mandibular arch finger rest is established on the index finger or thumb

of non-operating.

Conventional finger rest Opposite arch finger rest Opposite arch finger rest
Extra oral fulcrum:

5. finger on finger rest : this is done to reinforce the rest for better grip and safe

instrument activation

Are essential for effective instrumentation of some aspect of the maxillary posterior

teeth. Extra oral fulcrum are not finger rest in the literal sense, because the tips or

pads of the fingers are not used for extra oral fulcrum as they are for intra-oral finger

rests.

Finger on finger rest

 379

Palm up: The palm up fulcrum is established by resting the backs of the middle and

fourth finger on the skin overlying the lateral surface of the mandible on the right side of

face.

Palm down: The palm down fulcrum is establish by resting the front surfaces of the

middle and fourth fingers on the skin overlying the lateral aspect of the mandible on the

left side of the face.

EXTRA ORAL PALM UP EXTRAORAL PALM DOWN

Instrument Activities:

Adaptation refers to the manner in which the working end of the periodontal instrument is

placed against the surface of a tooth.

The objective of adaptation is to make the working end of the instrument conform to the

countour of the tooth surface, precise adaptation must be maintained to avoid trauma to

soft tissue and root surface and to ensure maximum effectiveness of instrumentation.

The cutting edge has 3 imaginary sections:

1) Leading third

2) Middle third
 380

3) Lower third

The leading third is the section of the cutting edge that is used most often during

instrumentation.

Angulations:

Refers to the angle between the face of the bladed instrument and the tooth surface. It

may also be called tooth blade relationship during scaling and root planing, optimal

angulation is between 45 and 900.

During scaling strokes on heavy, tenuous calculus, angulation should be just less than 900

so that the cutting edge “bites into the calculus with angulation of less than 45 degree the

cutting edge will not bite into the or engage the calculus properly instead it will slide over

the calculus, smoothing or “burnishing” it. If angulation is more than 90 degrees, the

lateral surface of the blade rather than cutting edges will be against the tooth.

Lateral pressure:

Refers to the pressure created when force is applied against the surface of a tooth with the

cutting edge of a bladed instrument. The exact amount of pressure applied must be varied

according to the nature of the calculus.

Blade angulation:

(A) 0 degrees correct angulation for blade insertion

(B) 45 to 90 degrees correct angulation for scaling and root planing

(C) Less than 45 degrees incorrect angulation for scaling and root planing
 381

(D) More than 90 degrees incorrect angulation for scaling and root planing, correct

angulation for gingival curettage.

Blade adaptation:

The curettage on the left is properly adapted to the root surface. The curette on the right

side incorrectly adapted the toe pits out. Lacerating the soft tissue.

INSTRUMENTATION IN MAXILLARY ARCH

 382

INSTRUMENTATION IN MANDIBULAR ARCH

PMT SET
 383

LA SYRINGE

PERIOSTEAL ELEVATOR

NABERS PROBE

BP HANDLE

ORBANS INTERDENTSAL KNIFE

WILLIAMS PERIODONTAL

CASTRO VIEGO SCISSORS

 384

GOLDMAN FOX SCISSOR

BONE SPOON ECCAVATOR

TISSUE NIPPER

PERIODONTAL MICROSURGERY
NEEDLE HOLDER
 385

PERIODONTAL MICROSURGERY
Microsurgery is defined as refinement in surgical technique by which visual acuity is
increased using a microscope at magnification exceeding 10x.

- It increase clinical accuracy.

- Important for diagnosis.
- Important for non surgical procedure in periodontology
Magnification system

1. Magnifying loupes
2. Simple loupes
3. Compound loupes
4. Prism telescopic loupes
Microscope

Periodontal microsurgery introduces the potential for less invasive surgical approach in
periodontics. This is ex emplified by decreased need for vertical releasing incisions and
greater use of smaller surgical sites.

Advantage:

- Reduced incision size

- Reduced surgical retraction
- Decreased postoperative pain
- Rapid healing
Under magnification periodental surgeon can visualise gross crushing & teasing of
delicate tissue which otherwise appear as gentle surgery under unaided aye.

Now periodontist can most accurate and atraumatic handling of tissue to enhance wound
healing.
 386

Microsurgical instruments:
 387

Conclusion:

Microsurgery offers new opportunities for periodontal surgery that can enhance the
therapeutic result for the variety of procedure.

It improves

1. Cosmetics
2. Rapid healing
3. Minimal discomfort
4. Enhance pt acceptance
 388

INSTRUMENT LAY OUT FOR PERIODONTAL SURGERY

 SECTION - 8

PUBLIC HEALTH
DENTISTRY
 389

PUBLIC HEALTH ASPECT OF DENTISTRY

Public health aspect of dentistry deals with dental health education of the public
in order to achieve the following goals:

1. Prevention of onset of dental diseases

2. Prevention of mutilating effects of dental diseases by

a) Early detection

b) Early treatment of diseases

3. Prevention of recurrence of the diseases by recall visits after thorough

treatment

PREVENTIVE DENTISTRY

 The main aim of public health is to reduce the diseases of the hard and soft tissues
and reduce the time required to treat these diseases.

 This is carried through the following methods:

1. Dental Health Education:

 Our AD Corps gives emphasis on the importance of oral hygiene lectures

and annual dental inspections.

 Dental health education is carried out through:

a) Lectures - with audio visual aids

b) Posters - used as a motivating force

c) Dental health education with models and charts

d) Films and slides

e) Radio and TV programmes

 390

1. Periodic check up:

 By annual dental inspection.

 This is done every 6 months to observe following things:

a) Oral hygiene status

b) Condition of teeth and surrounding investing tissues

3. Oral physiotherapy and home care with help of following means:

a) Proper tooth brushing and gingival massage

b) Interdental cleaning and massage

c) Dental floss and dental tape

d) Oral rinsing with water

e) Fibrous diet for better cleaning aids

4. Preventive treatment:

Oral prophylaxis to remove following

a) Materia Alba is soft deposit on the gingival third of crowns Consisting of

mucous, soft food debris, epithelial cells, and bacterial masses.

b) Mucinous films and plaque commonly seen on the interproximal surfaces,

consisting of colloidal materials and bacterial

c) Calculus deposit

Oral prophylaxis consists of

1. Scaling by hand instruments or ultrasonic scalers by using pumice

and hydrogen peroxide

2. Polishing and removal of stains.

3. Removal of occlusal irregularities

4. Prophylactic restoration

5. Prophylactic orthodontic treatment

 391

6. Elimination of abnormal habits

7. Fluoridation for dental caries prevention.

 Fluoride ions reach the enamel matrix and form calcium

fluroapatite crystals in place of hydroxyapatite, which is
more caries resistant.

 Fluorides can be administered:

I. During enamel development –

 By systemic administration through fluoride in the table salt or adding fluoride

into water to make the concentration of fluoride 1 ppm.

II. After the development of teeth is completed topical fluoride administration– a) a)

Use of fluoride toothpaste

b) Topical fluoride application in the form of

- 2% Sodium fluoride

- Stannous fluoride

- Acidulated fluoride gel

5. Diet and Nutrition

During pregnancy balance diet to be taken along with fluorides

a) Non-sticky food containing proteins to be given

b) Infancy-Breast feeding emphasized upon

6. Dental Health Surveys

a) Dental surgeons for educating the children and their parents about dental
health

b) Dental clinics in public sector

c) Dental clinics along with all the hospitals

 392

ROLE OF DENTAL HYGIENIST IN DENTAL HEALTH

EDUCATION

Responsibilities of the Dental Hygienist in patient education are:

a) To build confidence in the patient that the dental services are the best for the
individual.

b) Dental caries is a continuous process, regular dental appointments should be

c) The patient to be motivated to carry out his or her part of dental care through
tooth brushing and practicing other methods of home care.

AIMS AND OBJECTIVES OF DENTAL HEALTH EDUCATION

Definition of Health

 Health is defined as a state of complete physical, mental and social well-being,

not merely the absence of disease or infirmity (WHO)

Definition of dental health

 It is defined as the adoption and maintenance of sound oral health practices and
the use of oral health services judiciously, which result in improvement of the oral
health status of both the individual and the community.

THE PRIMARY OBJECTIVES OF HEALTH EDUCATION (WHO, 1969)

To persuade people

1. To adopt and sustain health practice

2. To use judiciously and wisely health services available to them

3. To take their own decisions both individually and collectively to

improve their health status and environment

The prevention and control of dental ill health fits this framework.

i) Dental disease can be controlled if individuals would adopt and sustain the
healthy life practices of controlling sugar intake and effective plaque removal.
 393

ii) The correct use of the available dental services can aid in the early diagnosis
and treatment of disease.

iii) The health of the mouth can be improved by the community taking steps to
alter the environment by implementing fluoridation of public water supplies.

Dental ill health is greatly influenced by individual behaviour therefore health

education by modifying habits detrimental to dental well-being should be an important
preventive health measure.

In order to improve the effectiveness and scope of dental health education a sound
theoretical dental health education message has been published Health education council,
(1979), the dental profession can ensure consisting in both surgery based and public
preventive programs.

DENTAL HEALTH AND CHILDREN

 The three most important factors related to health of children are

1). Adequate diet

2). Good oral hygiene

3). Regular and adequate dental care

 One of the most important factors is a balanced die, low in easily fermentable
carbohydrates.

 In addition to diet control, one of the parents should be educated in brushing the
primary teeth regularly as soon as they erupt.

 The brushing should be continued until the child is old enough to be instructed in
the proper and systematic use of the toothbrush.

 Periodic and continuous visits beginning by at least two years of age should be
made to dentist.

 Carious teeth should be restored as soon as the lesions become evident clinically
or radiographically.

 Topical applications of fluoride should be made at least once a year.

 Every effort should be made to preserve the primary teeth, until the time of their
normal exfoliation and the eruption of the permanent teeth.

 In addition to the importance of diet control, the parents should be impressed

upon the significance of the child’s first permanent molar.
 394

 These teeth are most frequently neglected than many other teeth, since many
parents mistake them for the primary teeth.

 Thumb sucking is considered by many to be normal in a child 2 ½ to 3 years of

age.

 If the habit persists beyond this age, it is desirable to discourage the habit at an
early age, before it becomes deep seated

PUBLIC HEALTH
 Public health is concerned with and is directed towards the improvement
and protection of the health of a group, community, state or of a
population in aggregate (Knutson)

Definition

The science and art of preventing disease, prolonging life and promoting
physical health and efficiency through organized community efforts
(Winslow).

Historical background

 Winslow’s definition of public health, which was given in 1920, is

considered too broad and created on umbrella under which almost
everything could be gathered and falls to meet the criteria of modern
public health.

 The concept of public health is different today to what it was fifty years
ago.

 From the control of physical environment and communicable diseases,

public health has moved to the preventive, therapeutic, and rehabilitative
aspects of chronic diseases and behavioral disorders, which are currently
the major health problems in the developed countries.

 The current emphasis in the field of health is also on the application of

modern management techniques for improving the efficiency of health
care delivery systems.

 An operational definition of public health therefore must change with the

times.
 395

A recent definition of public health that meets the criteria of modern public health
is as follows:

“Public health is the planning, carrying out and evaluation of health

measures and system services so that both maintain and improve the health of a
population group and prevent and control diseases within that population group”.
 SECTION - 9

ORAL AND
MAXILLOFACIAL
SURGERY
 396

BASIC PRINCIPLES OF ORAL SURGERY

Approach to oral surgery must be psychological, biological and scientific.

Knowledge of surgical bacteriology is necessary. No mouth is sterile. Due to large
number of bacteria always present, every extraction wound is a potentially infected
wound. The knowledge of various oral pathogens their normal behavior and various
diseases they cause and their sensitivity to particular antibiotics are knowledge on which
diagnosis and treatment is based.

REQUISITES FOR SURGERY

1. Surgical pathology

2. Physiology, e.g., physiology of shock, haemorrage, fever, vomiting, and diahorrea

blood circulation, lymphatic channels.
3. Nutritional status of the patient

4. Debilitating diseases, effects of vitamin deficiency e.g., vit A, D, E, K, C,

5. Sterilization and asepsis.

ART OF SURGERY

ESSENTIALS ARE

1. Control of pain by anesthesia

2. Methods to obviate infections
3. Maintain haemostasis – a method to control haemorrage.
4. Restoration of function and aesthetics

SURGERY NEEDS

1. Preparation of the surgeon

2. Preparation of the patient
3. Preparation of dressing and instrument
4. Team work and spirit between interdiscipline
5. Thorough professional knowledge and ethical principles.
 397

FIRST AID TREATMENT OF MAXILLOFACIAL

INJURIES

Injuries of the face and jaw are frequently associated with other injuries. One
should be aware that the care of injuries of the maxillofacial region is a part of the total
treatment plan. Cooperation with surgeons, neurosurgeons, ENT and Eye specialists is
often necessary. Many a time first id treatment is administered by lay personnel as well
as by trained aides (Ambulance driver) and emergency physicians (surgeons or
anesthesiologists). The most important measures are maintenance of patent airway,
temporary cessation of hemorrhage and provision of blood/fluid replacement to support
circulation.

AT THE ACCIDENT SITD AND DURING TRANSPORT AIRWAY

MAINTENANCE

a. Oral cavity be cleaned of coagulated blood, or vomitus, bacteria/loose tooth to be

removed.

b. Place the patient in such a position where blood seepage and vomitus can flow out
and is achieved through lateral positioning of the patient. ( left lateral position of
the patient). Supine position is contraindicated during transportation of the patient
to the maxillofacial unit.

c. Patient airway to be maintained in bilateral mandibular fractures as the presence

of the vomitus, haematoma or severe lingual swelling can lead to compression of
the passage of air.

d. In case of crushing injuries of the mandible, enodtracheal intubation or emergency

tracheostomy to be performed.

e. Transportation of the patient in sitting position with head bent down is

indicated for less severe injuries of the maxillofacial injuries.
 398

CONTROL OF THE BLEEDING

Temporary homeostasis includes simple measures by

1. Placing external bandages.

2. Place chin sling and or barrel bandage
3. Placement of gauze pads
4. Immobilization of the mandible with chin sling dressing
5. Pressure bandages are generally insufficient to control haemmorage from large
arteries. The intermittent pressure should be exerted on the carotid artery if
possible
6. Digital pressure should be provided until definitive haemostasis is achieved
7. Blood replacement by provision of fluid and necessary when shock symptoms are
present or threatened

HOSPITAL TREATMENT

Immediate surgery

1. Control of bleeding difficult and unsatisfactory

2. Tracheostomy
3. Soft tissue injuries to be attended on the same day of the injury
4. If GA is to be administered aspiration of the contents of stomach is required

MANAGEMENT OF SHOCK

1. Assessment of blood loss

2. Monitoring the response with adjustments in the rate of transfusion

SIGNS OF SHOCK

1. cold skin extremities

2. increased respiratory rate
3. tachycardia
4. hypotension
5. dilation of the pupils

Good rule to assess the blood loss is to measure the blood pressure if the systolic
blood pressure is less than 100mm Hg then a considerable amount of blood loss has
taken place.
 399

MANAGEMENT

1. Establish IV access.
2. If systolic blood pressure is less than 100 mmhg immediately crystalloids are
to be started, like plasma itself or dextran while awaiting for fresh blood
3. Monitor central venous pressure
4. Measure the urine output
5. Heamoglobin level and acid base level to be monitored
 400

FRACTURES OF MAXILLA AND MANDIBLE

MAXILLARY FRACTURES

Maxillary fractures may occur unilaterally or bilaterally. It may occur by itself or

may be associated with fractures of Zygomatic bone, nasal bones, and mandible or with
other cranial bones.

Anatomical consideration

1. Chance of infection if fracture involve the maxillary sinus

2. Fracture line follows Zig-Zag fashion
3. Muscles don’t produce displacement
4. Maxilla is usually displaced downwards and backwards

Classification

1. Dento alveolar fractures

2. Subzygomatic
a) Le Fort I (low level)
b) Le Fort II (Pyramidal)

3. Suprazygomatic
a) Le Fort III (High level)

CLINICAL FEATURES

1. DENTO-ALVEOLAR FRACTURES

1. There may bed fracture of crowns of teeth or the alveolar bone.

2. Inner surface of the upper lip shows laceration, edema and ecchymoses.
3. There may be disturbance in occlusion.
4. Gums may be lacerated and there may be deformity of alveolus.

2. LE FORT I FRACTURES

1. There may be swelling of upper lip;

2. Dentoalveolar portion of maxilla is mobile.
3. There is malocclusion with anterior open bite.
4. Midpalatine split may be seen with diastema between the central incisors.
 401

3. LE FORT II & III FRACTURES

1. Bilateral ecchymoses, gross bilateral edema causing the ballooning of the face
2. Lengthening of the mid face is seen
3. Bilateral circumorbital ecchymoses (panda facies),
4. Posterior gaging of teeth
5. Nares are filled with blood and mouth breathing is noted.
6. Anesthesia or parsthesia over the distribution of infra orbital nerve is noted
7. Presence of facial nerve palsy due to neuroproxia.

MANDIBULAR FRACTURES

Fracture of mandible occurs more frequently than any other fracture of the facial
skeleton. Fracture of the mandible may broadly be divided into two main groups.

1. Fracture with no gross comminution of the bone and without significant loss of hard
Or soft tissue.

2. Fracture with gross comminution of the bone and with extensive loss of both hard and
soft tissue. The majority of the fractures fall in the first category. Those in the
second group either result from missile injuries in war situation, industrial injuries or
major road accident.

CLASSIFICATION

There are no completely satisfactory classifications of mandibular fractures. The

main classification is under following head:

a) Type of fracture
b) Site of fracture
c) Cause of fracture

Simple These encompass closed linear fracture of the condyle, coronoid, ramus
and edentulous body of the mandible.
Green stick This type of fracture is a rare variant of the simple fracture and is found
exclusively in children.
Compound Fractures of the tooth bearing portions of the mandible are nearly
always compound into the mouth via the periodontal membrane and
some severe injuries are compound through the overlying skin
Comminuted Direct violence to the mandible from penetrating sharp objects and
missiles may cause limited or extensive comminution.
Pathological When the fracture occurs by a pathological condition e.g. osteomyelitis
or neoplasm.
 402

2. Site of fracture
a) Dento alveolar
b) Condyle
c) Coronoid, Ramus, Angle, Body (Molar/premolar areas)
d) Symphysis
e) Parasymphysis

From the point of view of treatment the pattern of the mandibular fracture is
extremely important and can be considered under the following heading:

a) Unilateral
b) Bilateral
c) Multiple
d) Comminuted

CLINICAL FEATURES

Before carrying out a careful clinical examination of the mandibular fracture, the
face should b gently cleaned with warm water or swab to remove clotted blood, road dirt
so as to enable an accurate evaluation to be made of any soft tissue lacerations and
associated ecchymoses. Similarly, the mouth should be examined for loose or broken
teeth or dentures.

a) Dentoalveolar fractures

Dentoalveolar fracture consists of avulsion, sublaxation or fracture of the teeth

with or without an associated alveolar fracture and they may occur alone or in
conjunction with any other type of mandibular fracture. Gross comminution of the
alveolar occurs following severe trauma, but more after the alveolar fracture consists of
one or two distinct fragments containing teeth.

b) Condylar fracture

This is most common fracture of the mandible and it may easily fail to be detected
on casual examination. It can be classified as intracapsular or extracapsular and
unilateral/bilateral fracture. The extracapsular fracture may exist with or without
dislocation of the condylar head. If there is unilateral fracture it is shifted towards the
fractured side. If there is bilateral condylar fracture there may be presence of anterior
open bite. Sometimes the hematomas surrounding a fractured condyle may track
downwards and backwards below the external auditory canal. This gives rise to
ecchymoses of the skin just below the mastoid process on the same side.
 403

c) Fracture of the coronoid process

This is a rare fracture but sometimes there may be fracture due to the muscular
pull and if the tip of coronoid process is detached the fragment is pulled upwards toward
the Infratemporal fossa. On examination there may be ecchymoses in the area and
tenderness on palpation over the region of the coronoid process. There may be pain and
limitation of mandibular movements especially on protrusion of the mandible.

d) Fracture of the ramus

Fracture confined to the ramus is rare and there are two main types:
1) Single fracture – This may also be regarded as a very low extracapsular
condylar fracture with both the coronoid process and condylar neck and head on the
upper fragment.
2) On extra oral and intra oral inspection there may be some swelling and
ecchymoses. Palpation produces tenderness, over the ramus both extra and intra orally
and mandibular movements produce pain over the area.

e) Fracture of the angle

There may be swelling at the angle and obvious deformity and step deformity.
Intra orally there is step deformity behind the last molar tooth. Some time there may be
hematoma formation intra orally. Anesthesia or paraesthesia may be present. There may
be presence of tenderness at the angle movements and crepitus may be present at the
fracture site. There is pain on attempted movement of the mandible and reflex spasm of
the muscles of mastication.

f) Fracture of the body (molar/premolars region)

The physical signs and symptoms are similar to those of fractures of the angle in
most cases. When teeth are present fracture causes disturbance of the occlusion
premature contact occurs on the distal segment because of the displacing action of the
attached muscle. Sometimes there is presence of gingival tears. In case of gross
displacement, the inferior dental artery may be torn and this can give rise to severe
hemorrhage.

g) Fracture of Symphysis and Parasymphysis

It may be associated with unilateral or bilateral condylar fracture. Mostly these
fractures are undisplaced. The presence of bone tenderness and a small lingual
hematoma may be the only physical signs. Severe trauma to the Symphysis can lead to
considerable disruption of the anatomy. The fracture line is oblique which results in over
riding of the fragment. If there is Bilateral Parasymphysis fracture then there may be fall
of the tongue, followed by respiratory obstruction. A fracture of the Symphysis is not
accompanied by anesthesia of the skin of the mental region unless the mental nerves are
injured after emergence from the foramina.
 404

CARE OF THE MOUTH AFTER EXTRACTIONS AND

MINOR SURGICAL OPERATIONS
1. Do not disturb the pad given in your mouth for one hour.

2. Do not wash your mouth vigorously for 24 hrs after the extraction, as you will
wash the blood clot out of the socket and cause yourself pain.

3. Next day, you may start to wash out your mouth as it is important to keep the
mouth clean so that the wound heals quickly.

4. Fill an ordinary tumbler with hot water. Dissolve a level teaspoonful of common
salt in it. Allow the hot water to cool until you can use it in your mouth without burning
yourself. Take a mouthful, hold it over the wound and keep it there. When the heat
begins to go out of it, spit it out and take another mouthful and hold it in the same way.
Keep doing this until you have used all the salt water. Repeat this at least four times a
day until your next appointment. You should use your toothbrush in the normal way for
the rest of the mouth.

5. Do not touch the operated area with finger, tip of the tongue or any other foreign body
as that delays healing.

6. Should bleeding occur, rinse out with cold water and use a pad made of clean
cotton wool or gauze and bite hard on it for half an hour. Pressure is best applied by
biting on the pad and should be kept for at least half an hour.

7. Slight swelling and discomfort may be expected for a few days. If you have pain,
take one or two of the tablets given to you. Do not take more than two of these tablets.

8. You should however, report to your MI room immediately if you have:

a) Persistent bleeding
b) An increase in swelling or pain
 405

Tooth extraction

1) Avoiding the creation of suction in the mouth, as when drinking through a straw
2) Avoiding rinsing mouth vigorously when drinking
3) Avoid drinking hot liquids or alcohol (which dilate blood vessel and may cause
bleeding)
4) Eating liquid or soft diet that requires minimal chewing

PERIODICAL ATTENDANCE FOR DENTAL TREATMENT

The mouth is the gate way of the body. A poor dental and oral health adversely
affects the general health in a number of ways. It can affect by the local spread or
worsening of the orodental diseases or by the systemic or general effect on the health of
the patient. This general spread can be through gastrointestinal tracts, the blood stream or
lymphatic system.

Examples are:
1. Periodical attendance for maxillofacial injury cases. This includes

Irrigation of the part by

a) Normal saline – 0.9% most commonly used

b) H2O2 – 1.4% gives out nascent oxygen
c) Soda bicarb mouth washes. It is good because like H2O2 it also dissolves
mucous and blood and washes away debris.
2) Periodical attendance for postoperative check up and surgical extraction e.g. after
apicectomy and after fitting of fixed and removal appliances for post insertion
observations and treatment.

3) Periodical attendance for review of fixed appliances in orthodontics, for

maxillofacial injury cases.

4) The screws and hooks should be checked and tightened. If necessary check the
splints, check for electrolytic ulcers and extra oral pin fixation.

5) Periodical attendance for the progress of the treatment of the dental diseases like
leukoplakia, sub mucous fibrosis, syphilitic ulcers.

6) Periodical attendance for control of caries and periodontal diseases

a) topical fluoride application at 3 years, 7 years, 9 yrs, and 11 years and
b) Oral prophylaxis at regular intervals.
 406

The method of controlling infection

a) Irrigation
1. By Hudson’s water syringe or an antiseptic solution .
2. The patient is encouraged to use a mouthwash as frequently as possible
Especially after a meal using normal saline or hypertonic saline solution.
3. 4% Soda bicarbonate solution when used dissolves the blood clot and the
Mucous. The solution used must be warm. When the irrigation is being carried
Out, a kidney tray is held below the oral cavity. The patient’s head should bed
pointing towards the ground to prevent choking and to allow escape of fluids
Out of the mouth.
4.5% normal saline or hydrogen peroxide solution may be used in the same way
for irrigation.

After syringing, the oral tissues are swabbed and made dry using cotton in a tweezer.
The swab of cotton removes debris left sticking to tissues or teeth. It will also separate
the slough. Use the syringe once or twice more to finally clean the oral cavity. Lastly,
weak antiseptic liquid for e.g. tincture iodine is applied over soft tissue. The patient may
be encouraged to use a tooth brush.

Maintenance of fixation appliances

a) Check and report any broken or loose wires. A tie wire, a rubber elastic, eyelet or
circumferential wire may be broken or loose. This requires immediate tightening or
replacement.

b) Some wires or hooks may be hurting the lips or cheek or tongue. These are bend
away from tissues or gutta-percha is placed on them.

c) The splint may have become loose, and requires, reseating and cementing.
Splints may become loose due to disintegration of cementum in oral saliva.

d) Check and treat electrolyte ulcers. These occur due to dissimilar metals in the
presence of saliva.

e) Dry crusts of serum around pins fixed into bone or from soft tissues must be
removed carefully.

f) Chin hair around pins must be shaved and waterproof elastoplast is fixed around
the pins over a dry ribbon gauze dressing.

g) All universal joints must be checked and tightened periodically if found loose to
ensure rigid fixation. Vaseline can be applied on rods and joints to prevent routing.

h) All metal hooks of acrylic plates must be polished with pumice and glycerin and a
hand brush, but the fixation must not be disturbed.
 407

.
NUTRITION, FEEDING AND TRANSPORTATION OF MAXILLOFACIAL
INJURY CASES

NUTRITION

The nutritional requirements associated with injury or surgery are related to the extent of
the injury, the greater the injury, the greater the nutritional requirements. Injuries can be
divided into three categories, minor, moderate and severe/massive tissue injury. Minor
tissue injury involves only transient starvation and minimal blood and fluid loss. The
majority cases fit in this category are simple fractures, tooth extraction or minor oral
surgical procedure. Moderate injury involves a major mass of tissue and transient loss of
blood volume. This type of injury includes the majority of effective soft tissue operation
without infection, major fractures, jaw fractures or single jaw orthognathic surgery.

Massive tissue injury includes massive burns, severe hemorrhage, gunshot wounds and
extensive automobile accident injuries. Oral and maxillofacial surgery patient in this
category include those having a mandibular resection for cancer, receiving a broken jaw
as a result of gunshot or undergoing multiple orthognathic procedures.

Energy requirement – Surgery increases the BMR and thus the energy requirement.
Energy stores are mobilized during surgery and immediately after, when oral intake is
stopped.

1. Protein requirement – Proteins and essential amino acids are needed in adequate
quantities to heal wounds and fight infections. Proteins help in fibroblast proliferation
and collagen formation.

2. Carbohydrate requirement – Carbohydrate is a major energy source and adequate

amounts of carbohydrate and fat are necessary to prevent excessive oxidation of amino
acids for caloric needs.

3. Fat requirements – fat provides an energy source and spares dietary and body
protein.

4. Vitamin requirements

Vit C- It helps in synthesis of bone matrix, also influences

Resistance to infection
Vit B- Complex Helps in wound healing
Vit A Growth and maintenance of epithelial tissues, bone matrix
Formation, wound healing and immunologic response
Vit K Its requirement is for the synthesis of prothrombin and clotting
Factors IV, VII, IX and X.

5. Minor requirement
Zinc, Iron, copper, Magnesium and other trace elements
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Nutritional assessment

A complete nutritional assessment includes an evaluation of the usual dietary intake,

anthropometric measurements and clinical and biochemical data.

Planning nutritional care in oral and maxillofacial surgery

1. Preoperative recommendations

A decision of active nutritional assessment support before oral and maxillofacial

surgery should be based on the nutritional assessment of the patient, including the dietary
history, biochemical and clinical data, and the clinical situation.

2. Post operative recommendations for specific conditions

The nutritional therapy and requirements of the patient having oral and maxillofacial
surgery are determined by the nutritional status of the individual, the nature and severity
of the pathologic abnormality, the amount and type of nutrients lost from the body during
surgery and the duration of injury and disease. The requirements are also influenced by
the type of surgical procedure, the time of recovery and the limitations to ingestion of
food.

Infection

If the patient is septic and dehydrated, hospitalization may be required to replaced body
fluids and electrolytes. Infection increases nutrient requirements for protein, folic acid,
pyridoxine and pantothenic acid. A soft regular diet may be resumed once the infection
has subsided.

Resection of cyst/benign tumor

A liquid diet is generally recommended for 2-3 days to eliminate the possibility of debris
setting in the wound and increasing bacterial growth and chances for infection. The diet
may be advance from liquid to soft consistency in 2-7 days.

Resection of malignant lesion

Surgical resection after cancer of oral cavity is influenced by the requirement of protein
and sufficient amount of Vit A and C and zinc. After surgical resection it may be
necessary to use nasogastric feeding if the patient is unable to swallow. A liquid or
blended diet should be used initially until the wound has healed, then a soft diet can be
given.
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Bone grafting

The nutritional requirements are increased after bone grafting. There are two surgical
wounds to repair in the oral or facial region and other at the donor site. Adequate
amounts of protein, calories, ascorbic acid, vitamin A, Vit D and calcium are needed for
bone as well as soft tissue regeneration.

Jaw immobilization

This situation is a major handicap, interfering with eating, chewing, drinking and
maintaining good oral hygiene. The patient in maxillomandibular fixation required full
liquid food, a commercial liquid supplements or a blended diet may be taken by drinking
from a cup or sucking through a straw.

Feeding

1. Oral feeding

If the patient is conscious and can take diet through the oral cavity then the following
diets are recommended. The clear liquid diet included only clear juices, beverages,
gelatin and broth. If a patient can swallow and tolerate liquids, a full liquid diet is
recommended since it is more nutritionally adequate. A full liquid diet can include fruit
and vegetable juices cooked cereals, eggs in the form of eggnog or custards and milk.
Vitamin and mineral supplement are recommended for patients who have been subjected
to moderate or severe stress. Patient can switch over to blended diet or soft diet
depending upon the state of recovery.

2. Nasogastric tube feeding

Nasogastric tube feeding is necessary for a comatose patient or a patient with an

orocutaneous fistula. Patient tolerance of nasogastric tube feeding is influenced by
osmolarity, the rate of flow and general condition of the patient. The flow should be
approximately 10 ml/minute, a faster rate can cause gastrointestinal cramping and
diarrhea. For intermittent feeding small amounts of formula followed by water (50 ml
formula plus 50 ml water) given every two hours decrease the possibilities of intolerance.
Feeding can be gradually increased to tolerance, usually 200 to 350 ml/feeding.

Parenteral nutrition

It is an alternative route for providing adequate nutrients when the external route
is not sufficient. Indications for using parenteral nutrition are after severe trauma when
nutrient needs are very high for abnormalities of the GIT such as vomiting, before and
after surgery in the nutritionally depleted patient and as a supplement to oral feeding.
Central venous parental nutrition is necessary when the GIT can not be used. For the
central venous route a catheter is inserted through the subclavian vein into the superior
vena cava. This allows rapid dilution of hypertonic solution by the large volume of blood
circulating through the heart.
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TRANSPORTATION

If a patient of maxillofacial injury can walk he must be made to do so with shoulder

support from his colleagues or ambulance assistants. If he can sit up he should be
transported as sitting case. He should bend his face forward; place it in between his
knees. If 0wever, he has to be carried on a stretcher, his forehead is supported by a
bandage. The patient always should be placed in a stable, left sided lateral position. This
ensures blood and secretions to drain out and prevents falling back of the tongue. If
necessary a tongue forceps or suture is passed through the tongue. Blood transfusion and
IV drip if started must be continued. Patient must be always be accompanied by a
vigilant nursing staff who checks constantly for respiration.

OT PROTOCOL
The operating room is merely a clean environment in which we do surgery. It is not
sterile. The ceiling, walls and floors are regularly disinfected, especially following a
contaminate case. The air may be filtered or flow past and UV radiation device to reduce
bacterial counts. The operating rooms are set away from the hospital by two sets of
doors. People are required to remove their street clothes and wear scrub suits before
entering the operating rooms. Masks, gowns, gloves and special shoes or shoe covers are
worn during the operation.

The scrub suit consists of a pair of pants and a skirt or blouse, which should be tucked
inside. A cap is placed over the hair. If the surgeon has long hair, surgical hoods are
available and should be used. A mask is then tied in place over the surgeon’s nose and
mouth. Conductive shoes should be worn.
These shoes will prevent the buildup of static electricity, which could cause a spark and
subsequent explosion involving the volatile inflammable gases. The shoes also lessen the
chance of patient electrocution. Today the many electrical devices surrounding and
attached to the patient in the operating room are potential sources of electric shock. By
wearing of conductive shoes the surgeon becomes an alternate pathway for aberrant
currents. If conductive shoes are not available the surgeon must use conductive shoe
covers. These have a conductive string that runs along the bottom of the shoe cover and
exits at the heel.
After entering the OT and before gowning, personnel should take precautions to
avoid contaminating open packs of draping material or instruments. Contact should not
be made with any person who is scrubbed and gowned. Once the patient is prepared ad
draped, only those who are scrubbed, gowned and gloved may work in the surgical site.
The backs of those gowned are considered nonsterile, as are areas below waist.
Therefore one must be careful to keep the arms above the waist when resting and not to
back into any sterile areas. Also, one must remember that the mask and surgical cap are
not sterile, and these can contaminate any sterile object they touch. Some hospitals have
sterilizable handles that may be attached to the light so the surgeon may adjust it, but
when these are not available, the light must be adjusted by the operating room assistant
not scrubbed for the case.
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FACIAL SPORTS INJURIES

Sports are good exercise and enjoyed too, the down side is that it can result in a variety of
injuries to the face. Many injuries are preventable by wearing the proper protective gear,
and attitude toward safety can make a big difference. However, even the most careful
person can get hurt. When an accident happens, it is your response that can make the
difference between a temporary inconvenience and permanent injury.

When someone gets hurt:

Ask, “Are you all right?” Determine whether the injured person is breathing and
knows who and where they are. Be certain the person can see, hear and maintain
balance. Watch for subtle changes in behavior or speech, such as slurring or stuttering.
Any abnormal response requires medical attention. Note weakness or loss of movement
in the forehead, eyelids, cheeks and mouth. Look at the eyes to make sure they move in
the same direction and that both pupils are the same size. If any doubts exist, seek
immediate medical attention.

When medical attention is required, what can you do?

- Call for medical assistance

- Do not move the victim, ore remove helmets or protective gear
- Do not give food, drink or medication until the extent of the injury
has been determined.
- Be very careful while handling body fluids. In an emergency
protect hands with plastic bags.
- Apply pressure to bleeding wounds with a clean cloth or pad,
unless the eye or eyelid is affected or a loose bone can be felt in a
head injury. In these cases, do not apply pressure but gently cover
the wound with a clean cloth. Apply ice or a cold pack to areas
that have suffered a blow (such as a bump on the head) to help
control swelling and pain.

Facial Fractures

Sports injuries can cause potentially serious broken bones or fractures of the face.
Common symptoms of facial fractures include:

- Swelling and bruising, such as a black eye

- Pain or numbness in the face, cheeks or lips
- Double or blurred vision
- Nosebleeds
- Changes in teeth structure or ability to close mouth properly.
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If any of these symptoms occur, be sure to visit the emergency room where X-rays may
be taken to determine if there is a fracture.

Upper face

When hit in the upper face (by a ball for example) it can fracture the delicate bones
around the sinuses, eye sockets, and bridge of the nose or cheek bones. A direct blow to
the eye may cause a fracture, as well as blurred or double vision. All eye injuries should
be examined by an eye specialist.

Lower face

When jaw or lower face is injured, it may change the way teeth fit together. To restore a
normal bite, surgeries often can be performed from inside the mouth to prevent visible
scarring of the face, and broken jaws often can be repaired without being wired shut for
long periods.

Fracture of teeth:

Contact sports can lead to fracture or avulsion of teeth, especially in the anterior region.
When tooth is avulsed then it should be washed with clean water, no attempt should be
made to scrub the tooth. The avulsed tooth should be carried in the patient’s mouth or
milk. Immediate assistance of a dental surgeon should be sought for possible
reimplantation of tooth.

Soft tissue injuries:

Bruises cuts and scrapes often result from high speed or contact sports, such as
boxing, football, soccer, ice hockey, bicycling skiing etc. Most can be treated at home,
but some require medical attention. Get immediate medical care when there are:

- Deep skin cuts

- Obvious deformity or fracture
- Loss of facial movement
- Persistent bleeding
- Change in vision
- Problems in breathing and/or swallowing
- Alterations in consciousness or facial movement

Bruises
Also called contusions, bruises result from bleeding underneath the skin. Applying
pressure, elevating the bruised area above the heart and using an ice pack for the first 24
to 48 hours minimizes discoloration and swelling. After two days, a heat pack or hot
 413

water bottle may help more. Most of the swelling and bruising should disappear in 1-2
weeks.

Cuts and scrapes

The external bleeding that results from cuts and scrapes can be stopped by immediately
applying pressure with gauge or a clean cloth. When the bleeding is uncontrollable go to
the emergency room.
Scrape should be washed with soap and water to remove any foreign material that could
cause infection and discolouration of the skin. Scrapes or abrasions can be treated at
home by cleaning with 3% hydrogen peroxide and covering with an antibiotic ointment
until the skin is healed. Cuts or lacerations, unless very small, should be examined by a
physician. Stitches may be necessary, and deeper wounds may have serious effects.
Following stitches cut should be kept clean and free of scabs with hydrogen peroxide nad
antibiotic ointment, bandages may be necessary to protect the area from pressure or
irritation from clothes.

Nasal Injuries

The nose is one of the most injured areas on the face. Early treatment of a nose injury
consists of applying a cold compress and keeping the head higher than the rest of the
body. Seek medical attention in the case of:
- Breathing difficulties
- Deformity of the nose
- Persistent bleeding
- Cuts

Bleeding

Nosebleeds are common and usually short-lived. Often they can be controlled by
squeezing the nose with constant pressure for 5 to 10 minutes. If bleeding persists, seek
medical attention. Bleeding also can occur underneath the surface of the nose. An
otolaryngologist/plastic surgeon will examine the nose to determine if there is a clot or
collection of blood beneath the mucus membrane of the septum (a septal hematoma) or
any fracture. Hematomas should be drained so the pressure does not cause nose damage
or infection.

Fractures

Some otolaryngologist set fractured bones right away before swelling develops, while
others prefer to wait until the swelling is gone. These fractures can be repaired under
local or general anesthesia, even weeks later.Ultimately, treatment decisions will be made
to restore proper function of the nasal air passages and normal appearance and structural
support of the nose. Swelling and bruising of the nose may last for 10 days or more.
 414

Neck injuries

Minor or severe, all neck injuries should be thoroughly evaluated surgeon. Injuries may
involve specific structures within the neck, such as the larynx (voice box), esophagus
(food passage) or major blood vessels and nerves.

Prevention of Facial Sports Injuries

The best way to treat facial sports injuries is to prevent them. To ensure a safe
athletic environment, the following guidelines are suggested:

- Be sure the playing areas are large enough that players will not run
into walls or other obstructions.
- Cover unrecoverable goal posts and other structures with thick,
protective padding.
- Carefully check equipment to be sure it is functioning properly.
- Require protective equipment – such as helmets and padding for
football, bicycling and rollerblading, facemasks, head and mouth
guards for baseball, ear protectors for wrestlers, and eyeglass
guards or goggles for racquetball and snowmobiling are just a few.
- Prepare athletes with warm-up exercises before engaging in intense
team activity.
- In the case of sports involving fast-moving vehicles, for example–
check the path of travel, making sure there is no obstructing
fences, wires or other obstacles.
- Enlist adequate adult supervision for all children’s competitive
sports.
 415

MANAGEMENT OF MEDICAL EMERGENCIES IN DENTISTRY

Medical emergencies in the dental office setting are an unavoidable occurrence among
patients as well as persons who accompany them and also among the dental professionals
and hence the understanding of such conditions becomes necessary for patient triage,
treatment, disposition and documentation of the emergency incidence in both treatment
and non-treatment locations. It is the responsibility of dental health care providers to be
familiar with the medical emergency protocol. In addition, efforts to seek and maintain
advanced emergency training through continuing education courses e.g. Advanced
Cardiac Life Support (ACLS), Pediatric Advanced Life Support (PALS), and Advanced
Trauma Life Support (ATLS)

Prevention of Emergencies

All patients who request admission to the dental center are required to provide complete
medical history to be included in their dental patient records. It is the responsibility of
the faculty/health care provider to review and update the medical history prior to
initiation of treatment. In addition, vital signs (temperature, blood pressure pulse,
respiration) must be taken and recorded.

- On initial visit and annual medical history review

- Before any procedure where local anaesthesia or any other
systemic medication is to be administered
- At each visit if the patient has a history of hypertension,
cardiovascular disease, or diabetes mellitus
- For non-cooperative children/adults only a pulse is required prior
to oral conscious sedation.

What to do in case of emergency

- Conscious, vital signs (blood pressure, pulse and respiratory rate)

are to be taken
- Immediately and the dental chair positioned according to patient
symptoms
- An oxygen tank is to be brought to the scene and when
appropriate, oxygen is to be administered.
- If the patient is unconscious, CPR is to be initiated immediately.
- A chronological recording of the emergency event is to be initiated
as soon as sufficient personnel are available
- It is expected that the first person on the scene will initiate
emergency treatment as outlined above until a faculty member
arrives.
 416

Emergency equipment monitoring

A. Oxygen equipment

Emergency oxygen tanks and equipment located in dental surgery be checked weekly.
Written inspection records will be kept with the equipment detailing date and inspector.

B. Departmental emergency equipment

Any departmentally maintained emergency drugs and equipment must be on record.

Such equipment is to be checked weekly by a member of that department.

CPR (Cardio pulmonary resuscitation)

This procedure is indicated in case of cardiac arrest which is a condition in which

circulation ceases or stops and vital organs are deprived of oxygen. In a dental center it is
commonly seen with the following situations:

- Cardiac disease
- Respiratory obstruction
- Massive blood loss
- Hypoglycemia
- Syncope/fainting
- Effect of drugs e.g. Allergy to drugs

AIM of CPR

Maintain oxygenation of the brain, lung and heart by rescue breathing and cardiac
compression.

STEPS

A- AIRWAY
B – BREATHING
C – CIRCULATION

a) Airway:

Open the mouth and clear the airway, tilt the head and lift the chin, clear the mouth of
foreign bodies like vomitus, loose dentures etc.
 417

b) Breathing:

Ascertain presence or absence of breathing by looking at the chest movements,

placing the ear near the victim’s nose and auscultation of the chest. If breathing is absent
then it can be supported in the following ways:

- Mouth to mouth
- Mouth to nose
- Mouth to airway

c) Circulation:

Check for carotid pulse along with other pulses, if absent or week/irregular
external cardiac compression should be started to establish circulation, which can be done
as follows:

- Position the patient supine on firm surface

- Locate the lower margin of the victim's rib cage
- Locate the lower part of the sternum (central part of rib cage)
- Place hand on top of the first, with long axis of the rescuers hand
perpendicular to the long axis of the sternum.
- Fingers are interlocked
- Rescuers elbow locked so that the arms are straight.
- Start compression to depress the chest by ½ to 1 ½ inches
- Feel for carotid pulse, optimal compression would generate a carotid pulse

When two rescuers are available the compression ventilation ratio should be 5: 1
and when a single rescuer is available then the ratio should be 15: 1.

LIST OF PRIMARY INJECTABLE EMERGENCY DRUGS

S.No Category Name of drug Quantity Dosage

1 Allergy Inj. Adrenaline 1 preloaded 1:1000/ml Im/sc
syringe & 3-4 1:10000/ml/iv
1ml amp
2 Antihistamine Inj 3-4 1ml amp 25-30 mg im/iv
Chlorphenaramine
3 Anticonvulsant Inj. Diazepam 10 ml vial 5 ml iv/im
4 Analgesic Inj Morphine sulfate 2-3 1ml amp 10mg/ml

LIST OF SECONDARY INJECTABLE EMERGENCY DRUGS

S.No Category Name of drug Quantity Dosage

1 Vasopressor Inj 2-3 1ml amp 20 mg/ml
Methoxamine
2 Corticosteroid Inj 12ml vial 50 mg/ml
 418

Hydrocortisone
3 Antihypoglycemic 5% Dextrose 1 50 ml vial 500 mg/ml
4 Narcotic Inj Nalaxone 2-3 1 ml amp 0.4 mg/ml
Antagonist

LIST OP PRIMARY NONINJECTABLE EMERGENCY DRUGS

S.No Category Name of Drug Quantity Dosage

1 Oxygen Oxygen 1 cylinder
2 Vasodilator Nitroglycerine 1 bottle/25 tab .3mg

LIST OF SECONDARY NONINJECTABLE EMERGENCY DRUGS

S.No Category Name of drug Quantity Dosage

1 Respiratory stimulant Aromatic 6-12 .3 ml
ammonia vaporoles
2 Antihypoglycemics Carbohydrate Any form -
3 Bronchodilator Metaproterenol Inhaler 1-2
inhalations/hr
SECTION – 10

SPECIAL CARE
DENTISTRY
 419

SUPPORTIVE CARE FOR PREGNANT WOMEN

Gums that are free of disease are important to having a healthy mouth and a healthy body. This
becomes even more important for expecting mothers.Special precautions are needed to be taken
before attempting any procedure in the treatment of pregnant women.

General precautions:

For all female patients in reproductive age menstrual history/history of pregnancy should be
elicited in the presence of an attendant / relative.
Elective dental procedures can be delayed until after delivery, however most common dental
procedures can be safely performed during pregnancy

1. Emergency dental treatment can and should be provided any time during the
pregnancy regardless of trimester.
2. The best time to address active dental disease (cavities, etc.) during pregnancy is
during the second trimester and early part of the third trimester.
3. When treating a pregnant patient it is important to make sure that appointments
are kept short and that the patient is in a comfortable position to avoid possible
supine hypotension and syncope.
4. Always protect the patient and fetus by using a lead apron when making
radiographs.
5. Avoid prescribing medications that are considered teratogenic by the FDA such
as: tetracycline,doxycycline, streptomycin, benzodiazepines, and erythromycin
estolate.
6. When local anesthetics are used, a local anesthetic that has a vasoconstrictor is
advisable.
7. Avoid nitrous oxide during the first trimester. Consult with an obstetrician before
using after the first trimester.
8. It is acceptable to use Chlorhexidine throughout pregnancy.
9. Systemic fluoride is not advised during the course of pregnancy. There are not
safety concerns, but rather prenatal fluoride is not considered to be beneficial.

All health care professionals should advise women that the following actions will
improve their health:

• Brush teeth twice daily with a fluoride toothpaste and floss daily.
• Limit foods containing sugar to mealtimes only.
• Choose water or low-fat milk as a beverage. Avoid carbonated beverages during
pregnancy.
 420

• Choose fruit rather than fruit juice to meet the recommended daily fruit intake.
• Obtain necessary dental treatment before delivery.

RECOMMENDATIONS FOR PRENATAL CARE PROVIDERS

• Assess problems with teeth and gums and make appropriate referral to an oral health
care provider.
• Encourage all women at the first prenatal visit to schedule an oral health examination if
one has not been performed in the last six months, or if a new condition has occurred.
• Encourage all women to adhere to the oral health professional’s recommendations
regarding appropriate follow-up.
• Document in the prenatal care plan whether the woman is already under the care of an
oral health professional or a referral is made.
• Facilitate treatment by providing written consultation for the oral health referral.
• Develop a list of oral health referral sources that will provide services to pregnant
women.
• Share appropriate clinical information with oral health professionals.
• Respond to any questions that the oral health professional may ask.
Prenatal care providers may suggest the following to reduce tooth decay in pregnant
women experiencing frequent nausea and vomiting:
• Eat small amounts of nutritious foods throughout the day.
• Use a teaspoon of baking soda (sodium bicarbonate) in a cup of water as a rinse after
vomiting to neutralize acid.
• Chew sugarless or xylitol-containing gum after eating.
• Use gentle tooth brushing and fluoride toothpaste to prevent damage to demineralized
tooth surfaces.

RECOMMENDATIONS FOR ORAL HEALTH PROFESSIONALS

Oral health professionals should render all needed services to pregnant women because:

• Pregnancy by itself is not a reason to defer routine dental care and necessary treatment
for oral health problems.
• First trimester diagnosis and treatment, including needed dental x-rays, can be
undertaken safely to diagnose disease processes that need immediate treatment.
• Needed treatment can be provided throughout the remainder of the pregnancy; however,
the time period between the 14th and 20th week is ideal.
Oral health professionals are encouraged to take the following actions for pregnant
women:

Plan definitive treatment based on customary oral health considerations including:

• Chief complaint and medical history

• History of tobacco, alcohol and other substance use
• Clinical evaluation
• Radiographs when needed
 421

• Develop and discuss a comprehensive treatment plan that includes preventive,

restorative and maintenance care.
• Provide emergency care at any time during pregnancy as indicated by oral condition.
• Provide dental prophylaxis and treatment during pregnancy, preferably during early
second trimester but definitely prior to delivery.

Position Pregnant Women Appropriately During Treatment

 Keep the head at a higher level than the feet.

 Place a small pillow under the right hip, or have women turn slightly to the left to
avoid dizziness or nausea.

MANAGEMENT OF ORAL HEALTH PROBLEMS IN PREGNANT WOMEN

The oral health professional is encouraged to:

1. Implement best practices in the assessment of caries risk and management

2. Perform a comprehensive gingival and periodontal examination
3. Consider the following as strategies to decreasecariogenic bacterial load:
4. Suggest fluoride toothpaste along with fluoride mouth rinses
5. Restore untreated caries.
6. Recommend chlorhexidene mouth rinses and fluoride varnish as appropriate.
7. Recommend the use of xylitol-containing chewing gum.

Use the following when clinically indicated

• Local anesthetic with epinephrine

• Analgesics and antibiotics
• Radiographs with thyroid collar and abdominal apron
• Non-steroidal anti-inflammatory drugs for 48 to 72 hours.
• Avoid aspirin, aspirin-containing products, erythromycin estolate and tetracycline.
• Discuss the benefits, risks and alternatives to treatments prior to fourteen weeks
• Complete restorations with permanent materials, if possible, during pregnancy.
• Complete all necessary dental procedures prior to delivery.

Consult with the prenatal care provider when considering:

• Deferring treatment because of pregnancy

•Co-morbid conditions that may affect management of dental problems such as
diabetes,hypertension or heparin treated thrombophilia
• An anesthesia other than a local block such as intravenous sedation or general
anesthesia tocomplete the dental procedure
 Postpartum
422
For the Mother
 Maintain good oral health.
 Limit foods containing sugar to mealtimes only.
 Avoid saliva-sharing behavior, including:
• Sharing spoons or other utensils.
• Cleaning a dropped pacifier or toy by putting it in your mouth.

For the Infant

 After the first tooth erupts, wipe your baby’s teeth after feeding with a soft cloth
or soft-bristled toothbrush.
 Avoid putting your baby to bed with a bottle or sippy cup containing anything
other than water.
 Ask your baby’s health professional about your baby’s oral health status.
 Schedule your baby’s first dental visit for between ages 6 and 12 months.

Pregnancy gingivitis is a common form of gum disease known to develop in almost half of all
pregnant women likely due to the change in hormones. When kept at-bay, pregnancy gingivitis
generally ends shortly after the birth of the child

The following guidelines were developed by the AAP in response to the growing concern
surrounding oral health during pregnancy:
1. Health Education - Counseling and early intervention by healthcare providers such as
physicians, nurses, and dentists to provide expectant mothers with the tools and resources
necessary to understand the importance of oral health care during pregnancy.
1. Oral Hygiene - Removing the bacterial plaque which researchers have connected to
preterm birth and low birth-weight babies, is essential. Using the correct brushing and flossing
methods greatly increase the amount of plaque that is removed from the teeth and gums.
2. Fluoride - The American Dental Association recommends the use of toothpaste with
fluoride by persons over the age of six. Echoing their sentiment, the AAP oral health guidelines
advise the continued use of fluoridated toothpaste during pregnancy, and recommends the use of
anover-the-counter alcohol-free fluoride rinse to help reduce the amount of plaque in the mouth.
3. Nutrition - Educating expectant mothers about proper diet and nutrition during
pregnancy will limit unnecessary sugar intake and in turn, prevent plaque build up.
4. Treating Existing Tooth Decay - Expectant mothers are encouraged to have existing
tooth decay treated during their pregnancy, which experts believe is a completely safe practice
during pregnancy. Restoring decayed teeth will help achieve oral health by removing the bacteria
associated with tooth decay.
 423

5. Transmission of Bacteria- Expectant mothers are discouraged from sharing food and
utensils in order to prevent the transmission of the bacteria known to cause tooth decay.
6. Use of Xylitol Gum- Expectant mothers are encouraged to chew xylitol gum (four
times a day) as research suggests that chewing this gum may decrease the rate of tooth decay in
children.
 424

ORAL CARE FOR DENTAL IMPLANT PATIENT

A comprehensive knowledge of implant dentistry allows the dental hygienist to function in many
of the stages of dental implant therapy and help the therapist perform a great service to the client
who requires prosthodontic treatment.

In the first year

Following restoration of the implant, frequent recalls are needed.
1. The client should be assessed every three months. Recall for the implant client after those
initial 12 months should be dictated by the client’s individual needs. These factors include stability
of the implant tissues, periodontal health of the surrounding teeth, systemic health, and the
effectiveness of home-care procedures.

2. Maintenance visits include periimplant evaluations, prosthetic evaluations, deposit removal,

home-care reinforcement and modifications, and radiographs when indicated.A comparison of
findings to baseline data can indicate impending problems with the
implant.

The evaluation of the health of the periimplant tissue should include:

Implant mobility can be a sign of significant problems. Stability of the implant should be assessed
at each recare appointment. Mobility can occur at the abutment prostheses connection and requires
repair. Mobility of the implant body is more serious, as it implies a loss of integration.

Clinical inspection for signs of inflammation.

The dental hygienist should also note the nature of deposits on the implant abutment. The presence
or absence of debris, plaque, and supragingival or subgingival calculus should be noted

Removal of deposits should be accomplished only with instruments that are incapable of damaging
the implant surface. A variety of instruments
 425

Similar to curets and scalers are available in plastic, nylon, or graphite. Gold-tipped instruments
can be used but must be examined before use for exposure of the underlying metal and should
never be sharpened.

If a client is performing an effective home-care regimen, subgingival calculus should be light.

Calculus is not firmly attached to the implant because of the nonporous titanium surface and
should be easily removable.

The dental hygienist should scale with short working strokes and light pressure to prevent trauma
to the delicate periimplant sulcus. Upon insertion of the instrument, the blade should be closed
against the abutment and then opened past the deposit. The deposit should be engaged apically
with the stroke extending coronally. A horizontal, oblique, or vertical stroke should be used,
depending on the location
Prostheses can sometimes limit access of the scaler, and an ultrasonic or sonic scaler can facilitate
removal of deposits.When using the sonic or ultrasonic
Device to scale the implant abutment, the metal instruments must be covered with plastic tips.

The airpowered abrasive unit is contraindicated by some investigators.A review of several studies
examining several types of instruments and their effects on the implant surfaces reveals the air-
abrasive unit to be safe and effective in removing
deposits. A rubber cup can be used to polish the implant surface with a nonabrasive paste or tin
oxide.

As home-care factors greatly into health of the implant, the dental hygienist should motivate the
client to continue the regimen. If home care has not been
Effective, the dental hygienist should question the client and attempt to resolve those issues. If the
employed auxiliary aids are not effective, it may be necessary to modify or change the client’s
techniques or change the type of aid.

The dentist should be immediately be informed of any problems or concerns. Changes in implant
health must be addressed immediately, as should problems related to occlusion, prosthetics, and
mobility.

Periimplant mucositis is similar to gingivitis around a tooth in its bacterial etiology and its
reversibility. This bacterial infection is marked by inflammatory changes with bleeding on
probing, edema, and tenderness. Its unchecked progression can lead to periimplantitis, which
affects the surrounding bone. Increased pocket depth, presence of exudate, and bone loss
accompany the inflammation in the periimplant soft tissue
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CARE & CLEANING OF DENTAL APPLIANCES

Dental prostheses, appliances, and items used in their fabrication (e.g., impressions,
occlusal rims, and bite registrations) are potential sources for crosscontamination and should be
handled in a manner that prevents exposure of Dental hygienist, patients, or the office environment
to infectious agents

1. Appliances and prostheses delivered to the patient should be free of

contamination.Communication between the laboratory and the dental practice is also key at this
stage to determine which one is responsible for the final disinfection process.

2. Dental prostheses, impressions, orthodontic appliances, and other prosthodontic

materials (e.g., occlusal rims, temporary prostheses, bite registrations, or extracted teeth) should be
thoroughly cleaned (i.e., blood and bioburden removed), disinfected with a hospital isinfectant
with a tuberculocidal claim, and thoroughly rinsed before being handled in the in-office laboratory
or sent to an off-site laboratory

3. The best time to clean and disinfect impressions, prostheses, or appliances is as

soon as possible after removal from the patient’s mouth before drying of blood or other bioburden
can occur.

4. In the laboratory, a separate receiving and disinfecting area should be established

to reduce contamination in the production area. are used on contaminated or potentially
contaminated appliances, prostheses, or other material, they should be heat-sterilized, disinfected
between patients, or discarded (i.e.,disposable items should be used)
5. Heat-tolerant items used in the mouth (e.g., metal impression tray or face bow
fork) should be heat-sterilized before being used on another patient

6. Items that do not normally contact the patient, prosthetic device, or appliance but
frequently become contaminated and cannot withstand heat-sterilization (e.g., articulators, case
pans, or lathes) should be cleaned and disinfected between patients and according to the
manufacturer’s instructions. Pressure pots and water baths are particularly susceptible to
contamination with microorganisms and should be cleaned and disinfected between patients

7. Environmental surfaces should be barrier-protected or cleaned and disinfected in

the same manner as in the dental treatment area.
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8. Unless waste generated in the dental laboratory (e.g., disposable trays or

impression materials) falls under the category of regulated medical waste, it can be discarded with
general waste.

9. Personnel should dispose of sharp items (e.g., burs, disposable blades, and
orthodontic wires) in puncture-resistant containers.

Patient care for appliances

1. Fixed appliances
It is essential for dental bridge wearers to floss the bridges using superfloss because
the spongy portion can remove plaque from the under surfaces of the bridges. Flossing
seems difficult for people wearing fixed orthodontic appliances. In that case, a floss
threader or superfloss can be used to guide the floss to facilitate the removal of plaque
from the adjacent tooth surfaces.
2. Removable partial denture
Dental plaque also adheres onto the surfaces of dentures and removable orthodontic
appliances. Wearers of these appliances should use the following steps to clean them:
a. Remove the appliance from the mouth.
b. Brush the appliance with toothbrush and liquid soap thoroughly .
c. After clean the appliance, immerse it in a cup of water overnight.
d. Wheneverthe appliance is not in use, clean it and immerse it in water.

The dental hygienist should:

1. Point out the areas where patient omits in cleaning and advise him on the
effective ways to do so. If the plaque-removal technique is adequate, he will give him assurance to
continue in your ways.
2. Help patient to improve your oral hygiene techniques and introduce appropriate
cleaning tools so as to protect his teeth and tooth supporting tissues from the damage of plaque.
3. Identify and correct the factors causing plaque accumulation such as dental
calculus and rough surfaces of dental fillings in order to reduce plaque accumulation.
 428

ORAL CARE CONSIDERATIONS FOR CANCER

PATIENTS

Patients who undergo cancer treatment sometimes are unaware that it can affect the
teeth, gums, salivary glands and other oral tissues. In some cases, patients delay or stop their
cancer treatment because they experience painful side effects in their mouths.

Chemotherapy and radiation treatments can cause several oral side effects:
1. inflammation and ulceration of the mucous membranes;
2. painful mouth and gums;
3. an increase in the risk of developing oral and systemic infections;
4. xerostomia (commonly called “dry mouth”), a condition in which saliva is thickened,
reduced or absent;
5. Rampant tooth decay;
6. burning, peeling or swelling tongue;
7. stiffness in the jaw;
8. impaired ability to eat, speak or swallow;
9. change in ability to taste;
10. poor diet because of problems with eating.

Before and after care

1. When possible, schedule a thorough dental checkup at least two weeks before treatment
begins. At this visit, update medical history record and provide the telephone number for the
physician who is handling the cancer therapy.
2. During cancer treatment, continue to gently brush teeth twice a day unless the dentist
recommends otherwise.
3. Should use fluoridetoothpaste Patients who receive cancer treatment of the head and neck
sometimes discover that they cannot tolerate the flavor of their regular toothpaste.
If this happens try another flavor that will not irritate mouth tissues.
4. Continue to gently floss once a day. If the gums are sore or bleeding in places avoid those
areas but continue to floss other teeth until the condition improves.
5. Dentist may recommend a mouthrinse in addition to daily brushing. May be advised to
use fluoride gel at home to help reduce the likelihood of tooth decay.
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6. Rinse mouth several times a day with a solution of baking soda and salt, followed by a
plain water rinse. Use one-quarter teaspoon of baking soda and one-eighth teaspoon of salt in one
cup of warm water. This is particularly helpful for vomiting after cancer treatment.
7. If xerostomia develops, dentist may recommend a saliva replacement, available at
pharmacies. Taking frequent sips of water, sucking on ice chips or sugar-free candy, or chewing
sugarfree gum may provide relief.
8. Eat a balanced diet. Soft, moist foods such as cooked cereals, mashed potatoes and
scrambled eggs may be suitable if mouth is sore.
9. Avoid using tobacco and alcohol and schedule regular dental checkups.

How should cancer patients care for their mouths?

Patients who have cancer should continue a regular oral hygiene program, including brushing
teeth and gums with a soft bristle brush two to three times per day. If the bristles are too hard,
either patient can rinse the toothbrush in hot water for 15 seconds to soften them or use an ultra-
soft toothbrush. Use a mildtasting toothpaste because flavored pastes might irritate patient’s
mouth. If toothpaste does irritate, you can rinse with a solution of salt and water. Patient also can
use an antibacterial mouth rinse for gum disease, but avoid mouth rinses that
contain alcohol. Gently floss your teeth at least once per day.

What can patients do about dry mouth?

Cancer patients who experience dry mouth should clean their mouths and teeth at least four times
per day and floss at least once per day. But if there are areas of bleeding or soreness on
the gums, floss gently or avoid flossing those areas altogether. Cancer patients need to use a
fluoride toothpaste when brushing their teeth and apply a fluoride gel as recommended
by their dentist. Patients also can rinse their mouths several times per day with a solution of
baking soda and salt in warm water, followed by rinsing with water. Dentist also may
recommend a mouth rinse you can use in addition to regular brushing and flossing.

What should a cancer patient eat?

Because of the changes in the ability to taste, patients who are undergoing cancer treatment may
find it more difficult to eat the foods they are used to eating. Cancer patients should eat
a balanced diet, including soft, moist foods like cooked cereal, mashed potatoes, and scrambled
eggs, or as recommended by their physician. It is important for patients undergoing cancer
treatment to get the right amount of nutrients and calories. If needed, patients can take vitamin
supplements that provide healthy minerals and calories. Avoid using tobacco and drinking
alcohol during treatment. Acidic foods, such as grapefruit, orange juice, and tomato sauce, may
cause irritation. Patients also should avoid acidic, high-sugar beverages like soda and energy
drinks

Oral mucositis, also called stomatitis, is a common, debilitating complication of cancer

chemotherapy and radiotherapy, occurring in about 40% of patients. It results from the systemic
effects of cytotoxic chemotherapy agents and from the local effects of
radiation to the oral mucosa. Oral mucositis is inflammation of the mucosa of the mouth which
ranges from redness to severe ulceration. Symptoms of mucositis vary from pain and discomfort
to an inability to tolerate food or fluids. Mucositis may also limit the patient’s ability to tolerate
either chemotherapy or radiotherapy. Mucositis may be so severe as to delay treatment and so
 430

limit the effectiveness of cancer therapy. Patients with damaged oral mucosa and reduced
immunity resulting from chemotherapy and radiotherapy are also prone to
opportunistic infections in the mouth. The mucositis may affect patients' gum and dental
condition, speech and self esteem are reduced, further compromising patients’ response to
treatment and/or palliative care.
.
Treatment regimens typically include dental work to eliminate caries and existing gum disease
before beginning cancer treatment, followed by thorough and frequent cleaning of the
oral cavity with a variety of products, some form of pain relief, anti-inflammatory treatment as
required and aggressive antimicrobial treatment for any new mouth infections

Recommendations - Oral Care Protocol

All patients at risk of developing mucositis should receive a standardised oral care regime as an
ongoing component of their care. The aim of this regimen is to achieve and maintain a clean
mouth and to limit opportunistic infection via the damaged mucosa. This information is based on
Level IV evidence (expert opinion).
1) Mucositis Assessment
Assess condition of the patient’s mouth daily. While there is no evidence to suggest any one
assessment tool is better than others, below is the World Health Organisation grading of
mucositis as an example of a typical tool.
Grade Signs And Symptoms
0 No symptoms
1 Sore mouth, no ulcers
2 Sore mouth with ulcers, but able to eat normally
3 Liquid diet only
4 Unable to eat or drink
2) Before Commencement Of Therapy
Interventions that may be beneficial prior to the commencement of treatment include:
 treatment of caries and dental disease; and
 education regarding the importance of orodental hygiene, how to maintain oral hygiene
and to develop adaily routine of oral care.
3) Post Therapy
Interventions that may be beneficial following treatment include:
 clean teeth and gums after meals and before sleep with tooth brush or swab as tolerated;
 rinse the mouth regularly;
 if dentures are worn, remove and clean them daily and leave out while at rest;
 avoid painful stimuli such as hot food and drinks, spicy food, alcohol and smoking;
 regular inspection of mouth by the patient and health professionals;
 report any redness, tenderness or sores on the lips or in mouth;
 provide comfort measures such as lubrication of the lips, topical anaesthesia and
analgesics;
 prompt treatment of mucositis symptoms and oral infections.
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ORAL CARE GUIDELINES FOR HIV PATIENTS

1. A widely used treatment for the Linear Gingival Erythema and/or NUP lesion in
HIV+ individuals involves gross scaling to remove visible plaque and calculus deposits and
debridement of necrotic tissue when present.

2. Access for both debridement and for topical antimicrobial therapy is aided by the
fact that pocket depths are often minimal in the NUP lesion. During debridement, povidone-
iodine irrigation has been used for its antiseptic and anesthetic effects.

3. Antibiotics should be used with caution due to the increased risk of overgrowth
of Candida albicans, and other microflora associated with HIV infection. To prevent overgrowth
of opportunistic microorganisms the use of a concurrent antifungal agent has been
recommended. Narrow spectrum antibiotics such as metronidazole which leave much of the
aerobic Gram positive flora unperturbed has also been recommended to prevent Candida
overgrowth in the management of LGE and NUP lesions.

4. Following initial debridement, follow-up visits are necessary in order to

thoroughly remove plaque, calculus, and other deposits and to provide strict plaque control
instruction. Home use of an antimicrobial mouthrinse such as chlorhexidine has been shown to
be an effective therapeutic aid in reducing the acute symptoms of LGE and NUP in HIV+
patients and in preventing the recurrence of these lesions.

5. The response to therapeutic intervention may, however, depend upon the patient's
current HIV stage, intake of systemic medication to treat the HIV infection itself (e.g.,
zidovudine [AZT]), intake of antibiotics, and oral habits (e.g., tobacco smoking).
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OTHER PERIODONTAL CONSIDERATIONS

1. The NUP and LGE lesions seen in HIV+ subjects are often superimposed on
conventional periodontitis.HIV+ patients with pre-existing periodontitis have a greater
rate of attachment loss over time when compared with matched HIV-negative controls. In
HIV+ subjects, the prevalence and severity of common forms of periodontal diseases
such as chronic inflammatory periodontal disease (adult periodontitis) may vary between
risk groups due to other factors such as oral hygiene levels, smoking habits, medications,
etc.

2. With HIV+ patients, in addition to linear gingival erythema and necrotizing ulcerative
periodontitis, several other lesions may localize in the periodontium. The gingiva is the
second most common site for intraoral Kaposi's sarcoma.

3. Gingival papillary wart-like lesions similar in appearance to venereal warts (gingival

condyloma accuminata) have also been reported.

4. Lymphomas and other tumors associated with HIV can appear as distinct
gingivalmucosal enlargements and on radiographs as discrete radiolucencies in the
alveolar bone.

There are several general considerations in the periodontal management of the HIV-infected
patient with or without periodontal disease. To date there have been no reported clinical studies
on alterations in healing following periodontal surgical procedures in HIV+ patients. In studies
on other intraoral surgical procedures, there were no differences in the incidence of dry socket
following extraction or in the incidence of post scaling bacteremias between HIV-infected and
non-infected individuals. However, HIVinfected patients have shown delayed healing after
other forms of surgery.
During any procedure, the current principles of strict infection control as recommended by
OSHA should be carefully followed, not only for patients with known HIV infection, but for all
patients in order to insure the maximum safety for both health care provider and the patient.
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DENTAL CARE FOR SCHOOL GOING CHILDREN

Foods with sugars can cause harm to teeth. Show these types of foods through flip charts and
models of the following:

• Sweets/candies

• Cakes

• Chocolates

• Ice-cream

• Fizzy/ carbonated drinks

Children aged 6 years and below, do not have the manual dexterity to perform adequate tooth brushing
for proper plaque removal. Their parents or carer should supervise the brushing and complete the
process by brushing the child’s teeth. This supervision should continue until the child has mastered the
proper technique. Children should be taught to systematically clean every tooth surface that is. the
outer, inner and biting surfaces of upper and lower teeth to ensure effective brushing.

School going children can follow some simple rules for a great smile.
These are:

A. Good Home Care

1. Parents should supervise the child's brushing and flossing. One-third of parents allow their children
to brush and floss unsupervised.

2. The best time to brush is after breakfast and before bed.

3. Encourage your child to floss at least once a day.

4. Supervise your child's flossing until age 10.

5. Snack in moderation. Cheese, vegetables and yogurt are all nutritious snacks.
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B. Fluorides
1. Fluoride not only helps prevent tooth decay, but can also cure cavities in their early stages. A healed
cavity is stronger than the original surface.

2. A pediatric dentist can advise parents about sources of fluoride supplements, fluoride treatments,
fluoridated toothpaste and fluoride mouth rinses.

3 A pea-size amount of toothpaste on the brush is plenty for fluoride protection. Children should spit
out, not swallow, the toothpaste after brushing.

C. Sealants
1. Most cavities occur in places that sealants could have protected. Four out of five cavities in children
under age 12 occur on the biting surfaces of the back teeth.

2. Children with just a single application of sealants on their back teeth had 50% less tooth decay and
tooth restoration after 15 years that children with sealants.

3. The teeth most at risk of decay and therefore most in need of sealants are the six-year and twelve-
year molars.

D.Regular Dental Visits

1. Teeth cleanings remove plaque build-up on the teeth. Plaque irritates the gums and causes decay.

2. It is essential to get an on-going assessment of changes in a child's oral health by a pediatric dentist.
For example, a child may need additional fluoride, dietary changes, sealants, or preventive
orthodontics for ideal dental health.
This updated handbook has been primarily written
For the dental hygienists of the armed forces . The syllabus
Prescribed by the DENTAL COUNCIL OF INDIA has been
Carefully followed as a guideline. This Is a comphresive
Illustrated coverage available with focused guidance on
basic Subject. The objective is to generate interest in the
budding Dental Hygienists to become important members
in the oral Health care delivery system.