Chapter # 03

Anatomy, Structure and function of periodontium

Oral mucosa: “Moist lining of the oral cavity” that can be divided into 03 zones:

1. Masticatory mucosa: Gingiva, covering of the hard palate

2. Specialized mucosa: Dorsum of the tongue
3. Lining mucosa:Line the reminder of the oral cavity (buccal, labial and soft palate)

Periodontium

“The normal periodontium provides the support necessary to maintain teeth in function. It consists of four principal components:
1. Gingiva
2. Periodontal ligament
3. Cementum
4. Alveolar bone”

1. Gingiva
“In an adult, normal gingiva covers the alveolar bone and tooth root to a level just coronal to cemento-enamel junction”.
Classification of gingiva:
The gingiva is divided anatomically into:

1. Marginal gingiva
2. Attached gingiva
3. Interdental gingiva

Marginal gingiva: “Marginal or unattached gingiva is the terminal edge or border of the gingiva that surrounds the teeth in collar-like fashion and
demarcated from the adjacent attached gingiva by a shallow linear depression called the free gingival groove. (About 1mm wide)

Attached gingiva: The attached gingiva is continuous with the marginal gingiva. It is firm, resilient and tightly bound to the underlying periosteum of alveolar
bone and is demarcated from the relatively loose and moveable alveolar mucosa by the mucogingival junction
The width of the attached gingiva on the facial aspect differs in different areas of the mouth. It is generally greatest in the incisor region (3.5 to 4.5mm in the
maxilla, 3.3 to 3.9mm in the mandible) and narrower in the posterior segment (1.9mm in the maxillary first premolars and 1.8mm in the mandibular first
premolars)
Mucogingival junction remains stationary throughout adult life.

Interdental gingiva: “The interdental gingiva occupies the gingival embrasure, which is the interproximal space beneath the area of tooth contact. The
interdental gingiva can be “pyramidal” or it can have a “col” shape.”
Gingival sulcus: “The gingival sulcus is V-shaped shallow crevice or space around the tooth bounded by the surface of the tooth on one side and the epithelium
lining the free margin of the gingiva on the other side.”

Microscopic features of gingiva

Gingiva is composed of the overlying stratified squamous epithelium and the underlying central core of connective tissue. Although the epithelium is
predominantly cellular in nature, the connective tissue is less cellular and composed primarily of collagen fibers and ground substance.

A. Gingival Epithelium - stratified squamous epithelium being composed of 02 types of cells:

1. Keratinocytes – principal cell type
2. Non-keratinocytes
 Melanocytes - dendritic cells located in the basal and spinous layers of the gingival epithelium.
 Langerhans cells - dendritic cells located among keratinocytes at all suprabasal levels. They belong to the mononuclear phagocyte system.
 Merkel cells - located in the deeper layers of the epithelium; they harbor nerve endings and they are connected to adjacent cells by desmosomes.
They have been identified as tactile preceptors.

Layers of stratified squamous epithelium:

1. Stratum basale
2. Stratum spinosum
3. Stratum granulosum
4. Stratum corneum

Functions of gingival epithelium

• The epithelial compartment was thought to provide only a physical barrier to infection and the underlying gingival attachment.
 • The main function of the gingival epithelium is to protect the deep structures while allowing for a selective interchange with the oral epithelium.
This is achieved via the proliferation and differentiation of the keratinocytes.

• Mechanical, chemical, water and microbial barrier

• Signaling function
Divisions of gingival epithelium: Gingival epithelium is divided into following 03 types:

1. Oral /outer epithelium: “Keratinized mostly parakeratinized stratified squamous epithelium covering the crest and outer surface of the marginal
gingiva and the surface of the attached gingiva ranging in Thickness from 0.2 to 0.3mm.”
It is composed of 4 layers;
a. Stratum basale
b. Stratum spinosum
c. Stratum granulosum
d. Stratum corneum
2. Sulcular epithelium: “Thin, non-keratinized stratified squamous epithelium without rete pegs lining the gingival sulcus and it extends from the coronal
limit of the junctional epithelium to the crest of the gingival margin.”
3. Junctional epithelium: “A collar-like band of stratified squamous non-keratinizing epithelium being 3 to 4 layers thick in early life, but that number
increases with age to 10 or even 20 layers and formed by the confluence of oral epithelium and reduced enamel epithelium.”
Renewal of gingival epithelium: The oral epithelium undergoes continuous renewal. Its thickness is maintained by a balance between new cell formation in
the basal and spinous layers and the shedding of odd cells at the surface. The mitotic activity exhibits a 24-hour periodicity, with the highest and lowest rates
occurring in the morning and evening respectively

B. Gingival connective tissue – The connective tissue of the gingiva is also known as lamina propria. It consists of two layers:
1. Papillary layer – consists of papillary projections between the epithelial rete pegs.
2. Reticular layer – contiguous with the periosteum of the alveolar bone.
Components of the gingival connective tissue: Gingival connective tissue has 02 components;

1. Cellular component – fibroblasts, fixed macrophages, histiocytes, adipose cells and eosinophils
2. Extracellular matrix
a) Ground substance – fills the space between fibers and cells being composed of:
  High water content
 Proteoglycans
 Glycoproteins
b) Fibers
 Collagen fibers – Type-I forms “GINGIVAL FIBERS”.
 Elastic fibers – composed of oxytalan, elaunin and elastin fibers.
 Reticular fibers – fine mature connective tissue fibers.
Gingival fibers:
“Connective tissue of the marginal gingiva is densely collagenous and it contains a prominent system of collagen fiber bundles called gingival fibers”.

These fibers consist of type I collagen.

05 groups of fiber bundles compose this system of gingival fibers.

1. Dentogingival group: These are most numerous fibers. Extending from cervical cementum to the
propria of the free and attached gingiva.
2. Alveologingival group: These radiate from the bone of alveolar crest and extend into lamina propria
of the free and attached gingiva.
3. Circular group: This small group of fibers forms a band around the free gingiva neck of the
tooth, interlacing with other groups of fibers in free gingiva and helping to bind
gingiva to the tooth.
4. Dentoperiosteal group: Running apically from the cementum over periosteum of the outer cortical
plates of the alveolar process.
5. Transseptal fiber system: These fibers run interdentally from the cementum of one tooth over the alveolar Crest and insert into a comparable region of
the cementum of adjacent tooth.
Functions of gingival fibers:

• Brace the marginal gingiva firmly against the tooth

• To provide rigidity, necessary to withstand the forces of mastication.
• To unite the free gingiva with cementum of the root and adjacent attached gingiva.
Repair of Gingival connective tissue: Because of the high turnover rate, the connective tissue of the gingiva has remarkably good healing and regenerative
capacity. However the reparative capacity of gingival connective tissue is not as great as that of the periodontal ligament or the epithelial tissue.
Blood supply, lymphatics and nerves

03 sources of blood supply to the gingiva is as follows:

1. Supraperiosteal arterioles
2. Vessels of the periodontal ligament
3. Arterioles which emerge from the crest of the interdental septa
The lymphatic drainage of the gingiva brings in the lymphatics of the connective tissue papillae.
Gingival innervation is derived from fibers that arise from nerves in the periodontal ligament and from the labial, buccal and palatal nerves. Following nerve
structures are present in CT:

 Free nerve endings

 Meissner type tactile corpuscles
 Krause type end bulbs – temperature receptors
 Encapsulated spindles

Correlation of clinical and microscopic features of the gingiva

Color:
The color of the attached and marginal gingiva is generally described as “coral pink”, it is produced by the vascular supply, the thickness and degree of
keratinization of the epithelium and the presence of pigment-containing cells.

• Lighter in blond individuals with fair complexions than in swarthy, dark haired individuals.
The alveolar mucosa is red, smooth and shiny rather than pink and stippled.
Physiologic pigmentation (Melanin)
Melanin is a non-hemoglobin derived brown pigment with the following characteristics:

• Melanin is responsible for normal pigmentation of the skin, the gingiva and the reminder of the oral mucous membrane.
• Melanin is present in all normal individuals but it is absent or severely diminished in albinos.
 • It is prominent in black individuals.
• Ascorbic acid directly down regulates melanin pigmentation in gingival tissues.
Distribution of oral pigmentation in black individuals: Gingiva 60%, hard palate
61%, mucous membrane 22%, tongue 15% Size:
The size of the gingiva corresponds with the sum total of the bulk of cellular and intracellular elements and their vascular supply.
Contour:

• The marginal gingiva envelops the teeth in collar like fashion and follows a scalloped outline on the facial and lingual surfaces.
• It forms a straight line along teeth with relatively flat surfaces.
• On teeth in labial version, the normal arcuate contour is accentuated and the gingiva is located farther apically.
• On teeth in lingual version, the gingiva is horizontal and thickened

Shape:
When the proximal surfaces of the crowns are relatively flat fasciolingually, the interdental gingiva is narrow mesiodistally. Conversely, with proximal surfaces
that flare away from the area of contact, the mesiodistal diameter of the interdental gingiva is broad.
Thus in anterior region of the dentition, the interdental papilla is pyramidal in form, whereas the papilla is more flattened in a buccolingual direction in the
molar region.
Consistency:
The gingiva is firm and resilient and with the exception of the movable free margin, tightly bound to the underlying bone. The gingival fibers contribute to the
firmness of the gingival margin.
Surface Texture:
The gingiva presents a textured surface similar to that of an orange peel and is referred to as stippled. Stippling is best viewed by drying the gingiva.

• The attached gingiva is stippled, the marginal gingiva is not

• Stippling is less prominent on lingual than facial surfaces
• Stippling varies with age. It is absent during infancy, it appears in some children at about 5 years of age, it increases until adulthood and it frequently
begins to disappear during old age.
Position:
The position of the gingiva is the level at which the gingival margin is attached to the tooth. When the tooth erupts into the oral cavity, the margin and sulcus
are at the tip of the crown; as eruption progresses, they are seen closer to the root.

2. Periodontal ligament
“The periodontal ligament is a complex vascular and highly cellular connective tissue that surrounds the tooth root and connects it to the inner wall of the
alveolar bone.”
Average width of periodontal ligament is 0.2 mm.

 Diminished in hypofunction and unerupted teeth

 Increased in hyperfunction

Composition:

Cellular elements: Four types of cells have been identified in the PDL:

1. Connective tissue cells – fibroblasts, cementoblasts and osteoblasts

2. Epithelial rest cells
3. Immune system cells/Defense cells
4. Cells associated with neurovascular elements
Extracellular matrix: It consists of:
1. Ground substance: Fills the space between fibers and cells consisting of following components:
 High water content – 70%
 Glycoproteins – fibronectin, laminin
 Glycosaminoglycans – hyaluronic acid, proteoglycans
2. Fibers: collagen fibers, oxytalan and elaunin fibers
Types of collagen in PDL:

 Type I (Principal fibres)

  Type III (Reticular fibers)
 Type IV (Basal lamina)
 Type XII (Alignment and organization of periodontal fibers during tooth development)
 Type VI (Immunolocalized in the PDL and the gingiva)
Importance Of Collagen: Flexibility and strength to the tissues

Principal fiber Groups:

The principal fibers of the periodontal ligament are arranged in six groups that develop sequentially in the developing root:

Principal fibers Origin Insertion

Transseptal fiber system
Alveolar crest group
Horizontal group
Oblique group
(most numerous)
Apical group
Inter-radicular group
(only in multirooted teeth)
Run interdentally from cementum of one tooth over the Insert into a comparable region of the cementum of adjacent
alveolar crest. tooth.
Attached to cementum just below CEJ Into rim of the alveolus
Just apical to alveolar crest group Just below the alveolar crest
Running from the cementum Into bone coronally
From cementum around apex of the tooth root To the bone (form the base of the socket)
Running from cementum Into the bone (forming the crest of Interradicular septum)
Functions of PDL: Following are important functions of PDL:

1. Physical functions:
 Provision of a soft tissue ‘casing’ to protect the vessels and nerves from injury by mechanical forces
 Transmission of occlusal forces to the bone
 Attachment of the teeth to the bone
 Maintenance of the gingival tissues in their proper relationship to the teeth
 Resistance to the impact of occlusal forces i.e., shock absorption

Two theories are considered regarding shock absorption

The Tensional Theory – The principal fibers of the PDL are the major factor in supporting the tooth and transmitting forces to the bone.
The Visco-elastic System Theory – The displacement of the tooth is largely controlled by fluid movements with fibres having only a secondary role.
2. Formative and remodeling function – Cells of the PDL participate in the formation and resorption of cementum and bone which occur during physiological
movement, during accommodation of periodontium to occlusal forces and during repair of injuries.

3. Nutritional function – PDL is highly vascularized and supplies nutrients to the cementum, bone and gingiva by the way of blood vessels and it also provides
lymphatic drainage.
4. Sensory function – PDL is abundantly supplied with sensory nerve fibers that are capable of transmitting tactile, pressure and pain sensations via trigeminal
pathways. Four types of neural terminations are as follows:

 Free endings: Treelike configuration and carry pain sensation

 Ruffini like mechanoreceptor: Located in the apical area
 Coiled Meissner corpuscles: Located in the mid root region
 Spindle like pressure and vibration endings: Surrounded by a fibrous capsule, Located in the apex
 3. Cementum
“Cementum is avascular, mineralized connective tissue that forms the outer covering of the anatomic root.”
Physical characteristics:

 Hardness < Dentin

 Light yellow in color
 Permeability of cellular cementum is greater than Acellular cementum and this permeability diminishes with age.
 Thinnest on the coronal half of the root i.e. 16 to 60 μm.
 Thickest in the apical 3rd and in the furcation area i.e. ≤ 150 to 200 µm.
 Thicker in distal surfaces than in mesial surfaces because of mesial drift.

Functions of cementum: Following are the functions of cementum.

1. Anchorage: Provides a medium for the attachment of collagen fibers that bind tooth to the alveolar bone
2. Adaptation: In response to tooth wear and movement.
3. Repair: Associated with repair of periodontal tissues and damage to roots such as fractures and resorptions
Patterns of CEJ:

1. TYPE – 1: In about 60% - 65% cases cementum overlaps the enamel.

2. TYPE – 2: In about 30% cases edge-to-edge butt joint exists.
3. TYPE – 3: In about 5% - 10% cases cementum and enamel fails to meet which cause
accentuated sensitivity because of exposed dentin.
Composition of cementum:

Cementum

Cells Extracellular Matrix

Organic Matrix Inorganic

Cementoblasts Matrix

Fibers
Cementocytes Ground Substance Non- Hydroxyapatite Crystals
Collagenous
Collagenous Proteins
Proteins

Cementoclasts
Collagen type – Proteoglycans
I (90%)

Collagen type – Glycoproteins

III (5%)

Phosphoproteins
Extrinsic fibers

Alkaline phosphtase
Intrinsic fibers
Classification of cementum
Cementum can be classified on the basis of:
1. Presence or absence of cells 3. Location
a) Acellular cementum a) Coronal cementum
b) Cellular cementum b) Radicular cementum
2. Origin of fibers 4. Presence or absence of collagen fibrils in the matrix
a) Extrinsic fiber cementum a) Fibrillar cementum
b) Intrinsic fiber cementum b) Afibrillar cementum

Features Acellular cementum Cellular cementum

Formation Forms before tooth reaches occlusal plane - first Forms after tooth reaches occlusal plane i.e. secondary
formed cementum / primary cementum cementum

Cells Absent Present (Cementocytes)

Location Cervical 3rd or half of the root Apical portion of the root and in the furcation area
i.e. coronal portion of the root

Rate of formation Slower Faster

Calcification More calcified Less calcified

Arrangement of collagen fibers Regularly arranged Irregularly arranged

Incremental lines More i.e. closer together Sparse i.e. wide apart

Sharpey’s fibers and their More and completely calcified Less and completely or partially calcified
calcification

Thickness Thin cementum i.e. 30 to 230 µm Thick cementum i.e.100 to 1000 µm

Function Anchorage Adaptation and Repair

SCHROEDER’S CLASSIFICATION
On the basis of presence or absence of cells and collagen fibers in matrix, location and origin of fibers, SCHROEDER classified cementum into 05 different
types.
1. Acellular afibrillar cementum
2. Acellular extrinsic fiber cementum
3. Cellular mixed stratified cementum
4. Cellular intrinsic fiber cementum
5. Intermediate cementum

Features Acellular Afibrillar Acellular Extrinsic Fiber Cellular Mixed Stratified Cellular Intrinsic Intermediate
Cementum Cementum Cementum Fiber Cementum Cementum
(AAC) (AEFC) (AMSC) (AIFC)

Fibers Absent Densely packed bundles Extrinsic and intrinsic fibers Intrinsic fibers from the
of Sharpey’s fibers cementum matrix

Cells Absent Absent Present Present Cellular remnants of

HERS

Formed by Cementoblasts Fibroblasts and Fibroblasts and Cementoblasts

cementoblasts cementoblasts

Location Coronal cementum i.e. Cervical 3rd of the root Apical 3rd of the root and in Resorption lacunae Cemento-dentinal
CEJ and may extend farther furcation area junction (CDJ)
apically

Thickness 1 – 15 µm 30 – 230 µm 100 – 1000 µm

 4. Alveolar process
“Alveolar process is the portion of the maxilla and mandible that forms and supports the tooth sockets (alveoli) which forms when tooth erupt to provide the
osseous attachment to the forming periodontal ligament; it disappears gradually after the tooth is lost.”

 Alveolar processes are the tooth-dependent bony structures.

 Alveolar bone is formed by intra-membranous ossification.
Parts of alveolar process: Alveolar process consists of the following 03 parts:

1. An external plate of cortical bone is formed by haversian bone and compacted bone lamellae.
2. The inner socket wall of thin, compact bone called the alveolar bone proper is seen as lamina dura in radiographs.
3. Cancellous trabeculae between two compact layers act as supporting alveolar bone.
Composition: Alveolar bone consists of following 02 components:
a) Inorganic matrix – 2/3rd being composed of :
 Minerals – calcium and phosphate along with hydroxyl, carbonate, citrate
 Mineral salts – Hydroxyapatite crystals
 Traces of other ions – sodium, magnesium and fluorine
b) Organic matrix – 1/3rd being composed of:
 Collagenous proteins – Type-I 90%
 Non-Collagenous proteins – osteonectin, osteopontin, osteocalcin, phosphoproteins, bone morphogenetic protein, proteoglycans
 Paracrine factors – cytokines, chemokines and growth factors
Sequence of events in the resorptive process:
1. Attachment of osteoclasts to the mineralized surface of bone.
2. Creation of sealed acidic environment through the action of proton pump, which demineralizes bone and exposes the organic matrix.
3. Degradation of exposed organic matrix to its constituent amino acids via the action of released enzymes (acid phosphatase, cathepsin)
4. Sequestering of mineral ions and amino acids within the osteoclast.

Socket wall:
 The socket wall consists of dense, lamellated bone, some of which is arranged in haversian systems and bundle bone.
  Bundle bone is the term given to bone adjacent to the periodontal ligament that contains a great number of sharpey fibers. It is localized within the
alveolar bone proper.
 The cancellous portion of alveolar bone consists of trabeculae that enclose irregularly shaped marrow spaces lined with a layer of thin, flattened
endosteal cells.
 Cancellous bone is found predominantly in the Inter-radicular and interdental spaces. In an adult human, more cancellous bone exists in the maxilla than
in the mandible.

Bone marrow:
 In the embryo and the newborn, the cavities of all bones are occupied by red hematopoietic marrow. The red marrow gradually undergoes a physiologic
change to the fatty or yellow inactive type of marrow.
 In the adult, the marrow of the jaw is normally of the latter type, and red marrow is found only in the ribs, sternum, vertebrae, skull, and humerus.
However, foci of the red bone marrow are occasionally seen in the jaws, often accompanied by the resorption of bony trabeculae.
 Common locations are the maxillary tuberosity, the maxillary and mandibular molar and premolar areas, and the mandibular symphysis and ramus
angle, which may be visible radio graphically as zones of radiolucency.
 Chapter # 04
Aging and periodontium
Age changes in gingival epithelium
 Thinning and decreased keratinization of gingival epithelium
 Increased epithelial permeability to pathogens
 Decreased resistance to functional trauma
 Flattening of rete pegs
 Altered cellular density
Age changes in gingival connective tissue
 Coarse and denser gingival CT
 Reduction in organic matrix production
 Reduction in vascularization
 Increase in number of fibers – elastic, collagen
 Qualitative and quantitative changes to collagen include:
Increased rate of conversion of soluble to insoluble collagen
Increased mechanical strength
Increased denaturing temperature
Increased collagen content
Increased collagen stabilization

Age changes in periodontal ligament

 Decrease number of fibroblasts and a more irregular structure
 Decreased organic matrix production
 Decreased epithelial cell rests
 Increased amount of elastic fibers
 Width of PDL will increased if tooth is wit excessive occlusal loading and will decreased if tooth is unopposed i.e. hypofunction
  Decreased cellular proliferation/mitotic activity
 Impairment of repair potential

Age changes in cementum

 Increase in Cemental width which is greater apically and lingually, increase may be 5 to 10 times wider
 Greater irregularity in the surface facing PDL

Age changes in alveolar bone

 Increased osteoporosis
 Decreased vascularity
 Greater irregularity in the surfaces of alveolar bone facing PDL
 Less regular insertion of collagen fibers
 Healing rate of bone in extraction sockets appears to be unaffected

Age changes in bacterial plaque

 Dentogingival plaque accumulation increases with age because of:
Increase in hard tissue surface area resulting from gingival recession
Surface characteristics of exposed root surface as a substrate for plaque accumulation as compared with enamel
 Chapter # 16
Defense Mechanisms of Gingiva

Defense
Mechanisms

Non -Sspecific Specific

Host -
Tissue Adaptive
Microbial
resistance immunity
symbiosis

Local
Anatomical Mucous Epithelial
inflammatory
factors barriers Barriers
response

Gingival
Attached crevicular fluid Junctional PMNs -
Stippling Gingival fibers Saliva
gingiva epithelium Leukocytes
(GCF)
1. Saliva
“Saliva is a viscous, clear, watery fluid secreted by the salivary glands that begins digestion of food.”

Composition of saliva: Saliva is composed of:

1. Water – 99.5 %
2. Solids – 0.5 %
a. Organic substances
 Antibacterial factors – lysozyme, lactoferrin, defendins, lactoperoxidase, peptides, agglutinins, myeloperoxidase.
 Salivary antibodies – IgA, IgG, IgM
 Enzymes – parotid amylase, maltase, lipase, glycoprotein, proteolytic enzymes
 Salivary buffers – bicarbonate-carbonic acid system
 Coagulation factors – factor VIII, IX, X, XII, plasma thromboplastin and active fibrinolytic enzyme
 Nitrogenous substances – urea, uric acid, creatinine
 Leukocytes – PMNs
 Desquamated epithelial cells
b. Inorganic substances
 Ions – sodium, potassium, calcium, fluoride, chloride, bromide, bicarbonate, phosphate
 Gases – oxygen, nitrogen and carbon dioxide

Role of saliva in oral health

Functions Salivary component Probable mechanism
1. Lubrication and physical protection Glycoproteins Coating similar to gastric mucin
Mucoids
2. Cleansing Physical flow Clearance of debris and bacteria
3. Buffering Bicarbonate Antacids
Phosphate
4. Tooth integrity and maintenance Minerals – Fluoride Maturation
Re-mineralization
Glycoprotein pellicle Mechanical protection
5. Antibacterial action IgA Control of bacterial colonization
 Lysozyme Breaking of bacterial cell wall
Lactoperoxidase Oxidation of susceptible bacteria
Clinical importance of saliva
 Systemic and local disease markers are available through saliva.
 It is considered a main biological fluid for diagnosis of human health and disease.
 Low saliva is a risk factor for caries and periodontal diseases.
 Low saliva delays wound healing in oral cavity.
Xerostomia: “It is defined as dry mouth resulting from reduced or absent saliva flow.”
Etiology: Following are causes of xerostomia:
 Removal of salivary glands
 Decreased production of saliva
 Medications side effects
 Radiotherapy
 Chemotherapy
 Autoimmune diseases
 Sjogren syndrome

Treatment:
 Fluoride rinses and dentrifices
 Frequent water intake
 Artificial salivary substitutes
 Reduced consumption of alcohol, spicy and acidic foods
2. Gingival Crevicular Fluid (GCF)
“GCF is an inflammatory exudate rather than a continuous transudate consisting of a vast array of biochemical factors, components of connective tissue,
epithelium, inflammatory cells, serum and microbial flora that inhabit the gingival margin or sulcus (pocket).”

Methods of collection: GCF is collected by following 04 methods:

 Absorbing paper strip
  Placement of twisted threads around and into the sulcus
 Micro-pipettes
 Intra-Crevicular washings

Methods of GCF measurement: The amount of GCF collected can be measured by following 02 methods:
 Ninhydrin-staining method
 Electronic method

Composition of GCF: It is composed of:

 Cellular elements – bacteria, desquamated epithelial cells, leukocytes (neutrophils, lymphocytes, monocytes, macrophages)
 Inorganic compounds – electrolytes such as sodium, potassium and calcium.
 Organic compounds
Carbohydrates – glucose hexosamine and hexuronic acid.
Proteins
Enzymes – collagenases and phospholipases (lysosomal and cytoplasmic enzymes)
Antibodies – IgG, IgM and complement
Metabolic and bacterial products – lactic acid, urea, endotoxins, cytotoxic substances, hydrogen sulpfide, hydroxyproline and antibacterial
factors

Clinical significance: GCF is a biological fluid that has potential in diagnostic and disease management. Factors that influence the amount of GCF are:
 Circadian periodicity – Gradual increase in amount of GCF from 6am to 10pm and a decrease thereafter.
 Sex hormones – Female sex hormones, pregnancy, ovulation and hormonal contraceptives all increase GCF production.
 Mechanical stimulation – Chewing, vigorous gingival brushing, gingival massage, and intrasulcular placement of paper strips increases the production
of GCF.
 Smoking – Produces an immediate transient but marked increase in GCF flow but, in long term, a decrease of salivary and GCF flow.
 Periodontal therapy – An increase in GCF production during the healing period after periodontal surgery.

Drugs in GCF: Drugs that are excreted through the GCF are following:
 Tetracycline
 Metronidazole – flagyl
Functions of GCF: The gingival fluid is believed to do following functions:
 Cleanse material from the sulcus
 Contain plasma proteins that may improve adhesion of the epithelium to the tooth
 Possess antimicrobial properties
 Exert antibody activity to defend the gingiva
3. Junctional epithelium
“It is collar like band of stratified squamous non-keratinizing epithelium formed by confluence of the oral epithelium and reduced enamel epithelium during
tooth eruption.”

The ability of JE to resist penetration of bacterial toxins depends upon the following:

 Degree of keratinization
 Thickness
 Degree of attachment to tooth surface
 Turn-over rate
 Chapter # 05
Classification of diseases and conditions affecting the periodontium
Gingival Diseases
Plaque induced gingivitis
1. Gingivitis associated with plaque only
 With local contributing factors such as plaque and calculus
 Without local contributing factors
2. Gingival diseases modified by following factors:
 Systemic factors
Associated with blood dyscrasia – leukemia
Associated with endocrine system – puberty, menstrual cycle, pregnancy and diabetes mellitus
 Medications
Drugs influenced gingival enlargement – immunosuppressant (cyclosporine), Ca +2 channels blockers (nifedipine), anticonvulsant
(phenytoin), oral contraceptives.
Drugs influenced gingivitis – oral contraceptives
 Malnutrition
Vitamin C deficiency gingivitis
Long chain omega 3 fatty acids gingivitis

Non – plaque induced gingivitis

1. Gingival diseases of following origins
Bacterial origin – streptococcus species, treponema pallidum, neisseria gonorrhea
Viral origin – Varicella zoster virus
Fungal origin – Candida species, histoplasmosis
Hereditary origin – Hereditary gingival fibromatosis
2. Gingival diseases modified by systemic factors
Mucocutaneous lesions – lichen planus, phemphigoid, phemphigus vulgaris, lupus erythematosus, drug induced.
Allergic reactions – dental restorative materials (Hg, Ni, acrylic) and reactions attributable to tooth pastes, dentifrices, rinses, mouthwashes,
chewing gums and food additives
 3. Foreign body reactions – amalgam
4. Traumatic lesions
Self inflicted
Iatrogenic
Factitious
Accidental

Periodontitis
“An inflammatory disease of supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive
destruction of the periodontal ligament and alveolar bone with increased probing depth formation, recession, or both.”

Clinical Features

 Detectable attachment loss as a result of inflammatory destruction of PDL and alveolar bone
 Periodontal pocket formation
 Changes in the density and height of subjacent alveolar bone
 Recession of marginal gingiva

Clinical signs of inflammation

 Changes in color, contour and consistency

 Continue bleeding with probing during sequential visits

Classification of Periodontitis

According to AAP world workshop in clinical periodontitis,1989

A. Adult onset Periodontitis
 Age of onset >35 years
 Slow rate of diseased progression
 No defects in host defenses
 Less aggressive
B. Early onset Periodontitis
 Age of onset < 35 years
 Rapid rate of diseased progression
 Defects in host defenses
 More aggressive
C. Periodontitis associated with systemic diseases
 Diabetes
 Down syndrome
 HIV infection
 Papillon – Lefevre syndrome
D. Necrotizing ulcerative periodontitis
Similar to acute NUG but with associated clinical attachment loss
E. Refractory Periodontitis
Recurrent periodontitis that doesn’t respond to treatment
According to AAP international workshop for classification of periodontal diseases,1999

A. Chronic periodontitis
On the basis of extent of disease
 Localized form
 Generalized form

On the basis of severity of disease (clinical attachment loss)

 Mild form: 1 – 2mm CAL

 Moderate form: 3 – 4mm CAL
 Severe form: > 5mm CAL
B. Aggressive periodontitis
 Localized form
 Generalized form
C. Periodontitis as a manifestation of systemic diseases

1. Necrotizing periodontal diseases

 Necrotizing ulcerative gingivitis
 Necrotizing ulcerative periodontitis
2. Abscesses of periodontium
“A periodontal abscess is a localized purulent infection of periodontal tissues” and it is classified by its tissue of origin such as:
 Gingival abscess
 Periodontal abscess
 Pericoronal abscess
3. Periodontitis associated with endodontic lesion
The classification of lesions that affect the periodontium and the pulp is based on the sequence of disease process:
 Endodontic – periodontal lesion
 Periodontal – endodontic lesion
 Combined lesion
4. Periodontitis as a manifestation of hematologic disorders
 Acquired neutropenia
 Leukemia
 Other
5. Periodontitis as a manifestation of genetic disorders
 Down syndrome
 Papillon – Lefevre syndrome
 Leukocyte adhesion deficiency syndromes
 Glycogen storage diseases
 Cohen syndrome
 Characteristics Chronic periodontitis Aggressive periodontitis
Prevalent rates Prevalent in adults but also can occur in children Prevlent in children
Amount of destruction Associated with local factors such as accumulation of plaque Associated with a positive family history of aggresive disease
and calculus
Rate of progresion Slow to moderate rate of progression i.e. slow attachment loss Moderate to severe rate of progression i.e.rapid attachment loss
and bone destruction and bone destruction
Defects in host defenses No defect sin host defenses Defects in host defenses
Aggressiveness Less aggresive More aggresive
Microbial pattern Associated with a variable microbial pattern Amount of microbial deposits inconsistent with disease severity
Localized form < 30% of teeth involved First molar or incisor disease with proximal attachment

Generalized form > 30% of teeth involved Proximal attachment loss affecting at least 3 teeth other than
first molars and incisors
Radiographic features:
 Widening of PDL space
 Vertical bone loss
 Indistinct lamina dura

Treatment:
 Daily brushing and flossing
 Antimicrobial agents and mouthwashes
 Antibiotics
 Removal of infected tissue
 Surgery
 Chapter # 18
Clinical features of gingivitis
Classification of gingivitis: Gingivitis can be classified on the basis of:
1. Course and duration
a) Acute gingivitis: Sudden onset, short duration, painful
b) Chronic gingivitis: Slowly onset, long duration, painless
c) Recurrent gingivitis: Reappear after eliminated by treatment
2. Distribution/diagnosis
a) Localized gingivitis: Confined to the gingiva of a single tooth or group of teeth
b) Generalized gingivitis: Involves the entire mouth
c) Marginal gingivitis: Involves the gingival margin
d) Papillary gingivitis: Involves the inter-dental papillae
e) Diffuse gingivitis: Affects the gingival margin, the attached gingiva, and the inter-dental papillae.

Hallmarks of gingivitis

Feature Healthy gingiva Gingivitis

Color Coral pink Red
Contour Knife- edged and scalloped Rolled with bulbous papillae
Consistency Firm and resilient Edematous
Texture Stippling of attached gingiva Loss of stippling
Gingival bleeding on probing
The 02 earliest signs of gingival inflammation that precedes established gingivitis – stage 3, are:

 Increased GCF production

 Bleeding from gingival sulcus on gentle probing

Gingival bleeding on probing can be associated with:

1. Local factors
2. Systemic changes
 3. Medications
A. Gingival bleeding associated with local factors

 Caries  Partial dentures

 Frenum pull  Lack of attached gingiva – loss of stippling
 Iatrogenic factors  Gingival recession
 Malpositioned teeth  Faulty brushing techniques
 Overhanging restorations  Orthodontic treatment
 Mouth breathing  Fixed retainers

B. Gingival bleeding associated with systemic changes

 Vascular abnormalities – vitamin C deficiency, allergy  Hormonal replacement therapy

 Platelet disorders – thrombocytopenic purpura  Oral contraceptives
 Hypoprothrombinemia – vitamin K deficiency  Pregnancy
 Coagulation defects – hemophilia, leukemia  Menstrual cycle
 Deficient platelet thromboplastic factor  Diabetes

C. Gingival bleeding associated with medications

 Antiplatelet medications – aspirin

 Anticoagulant – warfarin
 Anticonvulsants – phenytoin
 Antihypertensive calcium channel blockers – nifedipine, verapamil and sodium valporate
 Immunosuppressive drugs – cyclosporine
 Oral contraceptives

Color changes in gingiva

Color changes in gingiva can be due to:
1. Gingivitis
2. Metallic pigmentation
 3. Systemic factors
A. Gingivitis: Gingivitis can be
a) Acute gingivitis – gingiva becomes red in color because of the followings:
 Increased vascularization
 Reduced degree of epithelialization

Gingiva becomes pale in color because of followings:

 Reduced vascularization in association with fibrosis of corium

 Increased epithelial keratinization
b) Chronic gingivitis – gingiva becomes red or bluish red because of followings:
 Vascular proliferation
 Reduction of keratinization
 Venous stasis
c) Acute necrotizing ulcerative gingivitis – gingiva becomes dull, whitish gray
B. Metallic pigmentation: Increased permeability of irritated blood vessels permits the seepage of heavy metals such as bismuth, arsenic, mercury, lead, silver,
into the surrounding tissue which discolor gingiva. Metals typically produce a black or bluish line in the gingiva that follows the contour of margin. The
pigmentation may also appear as isolated black blotches involving the inter-dental, marginal and attached gingiva.
C. Systemic factors: These factors can be:
a) Endogenous factor
 Melanin
 Bilirubin
 Iron
 Blood dyscrasia
 Endocrine disturbances
 Metabolic disturbances
b) Exogenous factors
 Atmospheric irritant – coal, metal, dust
 Coloring agents in food and lozenges
 Tobacco
  Amalgam implants

Changes in gingival consistency

Changes in gingival consistency can be due to:
1. Gingivitis
2. Calcified masses in gingiva
3. Tooth-brushing

Changes in gingival surface texture

The surface of normal gingiva usually exhibits numerous small depressions and elevations that give the tissue an orange peel appearance and referred to as
stippling which is restricted attached gingiva.

 In patients with chronic inflammation, the gingival surface is smooth and shiny if the changes are exudative or firm and nodular if the changes are
fibrotic.
 In patients with atrophic gingivitis, the gingival surface is smooth produced by epithelial atrophy.
 In patients with chronic Desquamative gingivitis, peeling of the gingival surface occurs.
 In patients with hyperkeratosis, the leathery texture of gingival surface occurs.
 In patients with drug-induced gingival over-growth, nodular gingival surface occurs.

Changes in gingival position

These changes can be due to:
1. Traumatic lesions
2. Gingival recession
A. Traumatic Lesions and their sources can be:
a) Chemical injuries – aspirin, H2O2, silver nitrate, phenol, endodontic materials
b) Physical injuries – lip, oral and tongue piercing
c) Thermal injuries – hot drinks and food
B. Gingival recession is clinically defined as “the exposure of the root surface by an apical shift in the position of gingiva.” It can be classified as:
a) Localized gingival recession – limited to one tooth or group of teeth.
 b) Generalized gingival recession – present throughout the mouth.
Causes of gingival recession:-

 Faulty or abrasive tooth brushing techniques  Deep overbite leading to excessive incisal overlaps resulting in
 Tooth malposition leading to calculus deposition traumatic injury to gingiva
 Friction from soft tissues resulting gingival ablation  Self- inflicted damage to gingiva due to parafunctional habits
 Gingival inflammation  Periodontitis
 Abnormal frenum attachment  Pressure from a poorly designed partial denture
 Iatrogenic dentistry  Overhanging dental restorations
 Use of toothpick  Root-bone angle
 Trauma from occlusion
 Standard oral hygiene procedures – tooth brushing and flossing

Treatment of gingival recession:-

1. Surgical treatment
2. Non-surgical treatment
 Correction of tooth brushing techniques
 Removal of parafunctional habits
 Correction of malocclusion by braces
 Use of dental floss
 Use of desensitizing agents for the treatment of dentinal sensitivity

Clinical significance of gingival recession:-

 Exposed root surfaces are susceptible to caries.

 Abrasion or erosion of the cementum exposed by recession leaves an underlying dentinal surface that can be sensitive.
 Excessive exposure of root surface can result in hyperemia of the pulp and associated symptoms.
 Inter-proximal recession creates oral hygiene problems results in plaque accumulation.

Changes in gingival contour

Changes in gingival contour can be due to:
1. Gingival enlargement
 2. Gingivitis
Indentations of gingival margin can be:
Stillman clefts – a specific type of gingival recession that consists of a narrow, triangular-shaped gingival recession.
McCall festoon – a rolled, thickened band of gingiva that is usually seen adjacent to cuspids when recession approaches to the mucogingival junction

Chapter # 17
Gingival inflammation
“Gingivitis is defined as an inflammation of gingival tissues associated with a tooth without previous attachment loss or a tooth that has previously undergone
attachment and bone loss ( with reduced periodontal support) but is not currently losing attachment even though gingival inflammation is present.”

Classification of gingivitis: Gingivitis can be classified on the basis of:

3. Course and duration
d) Acute gingivitis: Sudden onset, short duration, painful
e) Chronic gingivitis: Slowly onset, long duration, painless
f) Recurrent gingivitis: Reappear after eliminated by treatment
4. Distribution/diagnosis
f) Localized gingivitis: Confined to the gingiva of a single tooth or group of teeth
g) Generalized gingivitis: Involves the entire mouth
h) Marginal gingivitis: Involves the gingival margin
i) Papillary gingivitis: Involves the inter-dental papillae
j) Diffuse gingivitis: Affects the gingival margin, the attached gingiva, and the inter-dental papillae.

Stages of gingival inflammation

Depending upon the time duration following are the 4 stages of gingival inflammation:
1. Stage–I gingival inflammation: The initial lesion
2. Stage– II gingival inflammation: The early lesion
3. Stage– III gingival inflammation: The established lesion
4. Stage– IV gingival inflammation: The advanced lesion
Stage Time (days) Blood Vessels Junctional and Predominant Collagen Fibers Clinical
Sulcular Epithelia Immune Cells Findings
Initial lesion 2 to 4 days after Vascular dilation Infiltration by PMNs PMNs – leukocytes Perivascular loss Increased
Sub clinical beginning of plaque Vasculitis gingival fluid
gingivitis accumulation flow into the
sulcus due to
increased
migration and
accumulation of
leukocytes with
gingival sulcus
Early lesion 4 to 7 days (1 week) Vascular Infiltration by PMNs T – lymphocytes 70 % increased Erythema and
Early gingivitis after beginning of proliferation Development of rete loss of circular BOP due to
Clinical gingivitis plaque accumulation Angiogenesis pegs or ridges and dentogingival proliferation and
Atrophic areas fibers around the angiogenesis of
cellular infiltrate capillaries
Increased
gingival fluid
flow
Established 14 to 21 days (2 to 3 Vascular Same as early lesion Plasma cells Continued loss of Changes in
lesion weeks) after beginning proliferation but more advanced B – lymphocytes of collagen fibers of colour, size,
Chronic of plaque accumulation Angiogenesis with rete pegs that G1 and G2 subclasses gingiva texture and so on
gingivitis Blood stasis protrude the Gingival pocket
Sluggish and slow underlying CT formation
blood flow Basal lamina is
Increased blood destroyed in some
viscosity areas
Advanced lesion 28 days (4 weeks) Same as early and Same as early and Plasma cells Destruction of Same as early
Phase of established lesion established lesion but B – lymphocytes PDL collagen and established
periodontal Vascular more destruction Increased IL-1B fibers lesion
breakdown proliferation Decreased IL-8 Periodontal
Angiogenesis pocket formation
 Blood stasis Clinical
Sluggish and slow attachment loss
blood flow Gum recession
Increased blood Alveolar bone
viscosity breakdown

Chapter # 20
Acute gingival infections
1. Necrotizing ulcerative gingivitis
“A microbial disease of gingiva that most often occurs in an impaired host, manifests with the characteristic clinical signs of necrosis and sloughing of gingival
tissues and may be accompanied by systemic symptoms.”

Clinical features:
Oral signs

 Punched out lesions

 Crater-like depressions at the crest of inter-dental papillae that extend to marginal gingiva
 Surface of gingival crater is covered by a gray, pseudo membranous slough that is demarcate from the reminder of gingival mucosa by a pronounced
linear Erythema
 Spontaneous gingival hemorrhage and pronounced bleeding after the slightest stimulation
 Fetid odor
 Increased salivation

Oral symptoms

 Lesions are extremely sensitive to touch

 Constant radiating, gnawing pain that is intensified by eating spicy or hot foods and chewing
 Metallic foul taste
 Excessive amount of pasty saliva

Extraoral signs and symptoms

In mild and moderate stages

 Local lymphadenopathy
 Slight elevation in temperature

In severe cases

 High fever
 Increased pulse rate
 Leukocytosis
 Loss of appetite
 General lassitude
 Insomnia
 Constipation
 GIT disorders
 Headache
 Mental depression

In rare cases

 Gangrenous stomatitis
 Noma (orofacial gangerene )

Etiology:
 Role of bacteria
 Impaired host response
 Local predisposing factors
Preexisting gingivitis
Injury to gingiva
Smoking
Preexisting chronic gingival diseases and periodontal pockets
Malocclusion trauma
 Systemic predisposing factors - Immunodeficiency
Relationship of bacteria and NUG:
Light microscopy shows that the exudate on the surface of necrotic lesions contains micro-organisms that morphologically resemble cocci, fusiform bacilliand
spirochetes.

Differential diagnosis:
NUG must be differentiated from the conditions that resemble it in some aspects such as:

 Herpetic gingivostomatitis
 Gonococcal gingivostomatitis
 Streptococcal gingivostomatitis
 Aphthous stomatitis
 Desquamative gingivitis
 Chronic Periodontitis
 Candidiasis
 Dermatosis
 Agrnulocytosis
 Diphtheritic lesions
 Syphilitic lesions

Differentiation of NUG, Chronic Desquamative Gingivitis and Chronic Periodontal Disease

Characteristics NUG Desquamative gingivitis Chronic periodontal disease

Bacterial smear Bacterial smear shows fuso-spirochetal Bacterial smear reveals numerous epithelial Bacterial smear vary
complex cells and few bacterial forms
Involvement Marginal gingiva affected Diffuse involvement of marginal and Marginal gingiva affected
attached gingiva and other areas of oral
mucosa
History Acute history Chronic history Chronic history
Pain Painful May or may not be painful Painless if uncomplicated
Surface appearance Pseudo membrane Patchy desquamation of gingival Usually no desquamation, but purulent
epithelium material may appear from pockets
Necrosis Papillary and marginal necrotic lesions Papillae don’t undergo necrosis Papillae don’t undergo noticeable necrosis
Gender Affects adults of both genders and Affects adults, most often women Usually found in adults, occasionally
occasionally affects children found in children
 Odor Characteristic fetid odor No odor Some odor but not strikingly fetid

Treatment:
 Oral hygiene instructions
 Antiseptic Mouthwashes
 Antibiotics
 Superficial scaling
 Surgical correction of gingival contour

2. Pericoronitis
“Pericoronitis is defined as inflammation of gingiva in relation to the crown of an incompletely erupted tooth.”
Pericoronitis can be:

 Acute
 Sub acute
 Chronic

Etiology:
 Infection in soft tissue surrounding a partially erupted wisdom tooth
 Poor oral hygiene
 Trauma
 Foreign body trapped beneath the tissue flap
 Excessive tooth gum

Clinical features:
 Partially erupted or impacted mandibular 3rd molar is most common site
 Red, swollen, suppurating lesion that is exquisitely tender
 Radiating pains to ears, throat and floor of mouth
  Foul taste
 Trismus
 Inability to close jaws
 Swelling of neck in region of angle of jaw
 Lymphadenitis
 Bacterial growth and impaction of food debris in operculum – space between crown and gingival flaps

Treatment:
 Saline water gargles
 Oral antiseptics – topical applications, mouth washes
 Antibiotics
 Excision of operculum
 Extraction of tooth

Complications:-
 Localized pericoronal abscess
 Difficulty in swallowing when it extends posteriorly into oropharyngeal area and medially to base of tongue
 Depending on severity and extent of infection, there may be involvement of following lymph nodes:
Submaxillary lymph nodes
Posterior cervical lymph nodes
Deep cervical lymph nodes
Retropharyngeal lymph nodes
 Peritonsillar abscess
 Cellulitis
 Ludwig angina
 Chapter # 08
Biofilm and Periodontal Microbiology
“The term biofilm describes relatively un-definable microbial community associated with a tooth surface or any other hard non-shedding material.”
Composition of biofilm: Biofilms are composed of microbial cells encased within matrix of extracellular polymeric substances such as polysaccharides,
proteins and nucleic acids. The intercellular matrix consists of following materials derived from saliva, GCF and bacterial products:

 Organic material – include polysaccharides produced by bacteria, proteins i.e. albumin originates from GCF, glycoproteins derived from saliva, lipid
material from food debris and DNA.
 Inorganic material – predominantly are calcium and phosphorous and trace amounts of other minerals such as sodium, potassium and fluoride.

Major ecosystems of oral cavity

On the basis of physical and morphologic criteria, the oral cavity can be divided into 06 major ecosystems /niches, each with the following distinct ecological
determinants:

1. The intraoral and supra-gingival hard surfaces – teeth, implants, restorations and prostheses
2. Sub-gingival regions adjacent to a hard surface – periodontal and peri-implant pocket
3. The Buccal palatal epithelium and the epithelium of the floor of the mouth
4. The dorsum of the tongue
5. The tonsils
6. The saliva

Tooth deposits
Tooth deposits are divided into 03 categories:

1. Material alba
2. Dental plaque
3. Calculus
 Difference between tooth deposits

Material alba Dental plaque Calculus

Appearance White, cheese like accumulation
Composition Soft accumulation of salivary proteins,
some bacteria, many desquamated
epithelial cells, and occasional
disintegrating food debris
Structure Lacks an organized structure and is
therefore not as complex as dental plaque
Effect of rinsing Easily displaced with a water spray
Method of removal No treatment is required
Resilient clear to yellow-grayish
substance
Primarily composed of bacteria in a
matrix of salivary glycoproteins and
extracellular polysaccharides
Definite, regular structure considered to
be a biofilm
Does not dislodge by rinsing or with use
of sprays
Proper brushing
Use of antiseptic mouthwashes
Hard deposits that forms via the
mineralization of dental plaque
Generally covered by a layer of
unmineralized dental plaque
Hard, mineralized structure
Does not dislodge by rinsing or with use
of sprays
Scaling and root planning

Dental plaque
“Dental plaque is clinically defined as structured, resilient, yellow-grayish soft deposits that form the biofilm adhering to the tooth surface or hard other hard
surfaces in the oral cavity, including removable and fixed restorations.”
Classification of dental plaque

1. Supragingival plaque/Marginal plaque – found at or over the gingival margin

2. Subgingival plaque – found below the marginal gingiva, between the tooth and the gingival Sulcular tissue.
a) Tooth associated cervical plaque
b) Tissue associated plaque
Composition of dental plaque
Dental plaque is mainly composed of followings:
  Micro-organisms – 1g of plaque contains approximately 1011 bacteria
 Host cells – epithelial cells, macrophages and leukocytes
 Organic compounds – include polysaccharides produced by bacteria, proteins i.e. albumin originates from GCF, glycoproteins derived from saliva,
lipid material from food debris and DNA.
 Inorganic compounds – predominantly are calcium and phosphorous and trace amounts of other minerals such as sodium, potassium and fluoride.

Formation of dental plaque

The dental plaque formation is divided into 03 phases

1. Formation of pellicle
2. Initial adhesion/attachment of microorganisms
3. Secondary colonization and maturation of plaque
Formation of pellicle: Hydrophobic macromolecules begin to adsorb on the tooth surface to form a conditioning film called as acquired pellicle. The pellicle is
composed of a variety of salivary glycoproteins that are derived from saliva, GCF, bacterial and host tissue cells. The pellicle alters the charge and free energy
of the tooth surface, with in turn increases the efficiency of bacterial adhesion.
Initial adhesion/attachment of microorganisms: The initial steps in colonization of teeth by bacteria occur in 03 phases:
Phase – I: Transport of microbes to the pellicle surface
Phase – II: Initial reversible adhesion
Phase – III: Strong attachment
Secondary colonization and maturation of plaque:
Control and removal of dental plaque

 Scaling and root planning

 Mechanical intervention – tooth brushing and flossing
 Chemical intervention – antiplaque agent
 Chapter # 23
The Periodontal Pocket
“Pathologically deepened gingival sulcus bordered on one side by tooth surface and on the other side by ulcerated Sulcular epithelium and has junctional
epithelium at its base.”
Classification of periodontal pocket
A. On the basis of morphology

1. Gingival/Free pocket
2. Periodontal/True pocket
a) Suprabony/Supracrestal/Supralveolar pocket
b) Infrabony/Subcrestal/Infralveolar pocket
B. On the basis of number of surfaces involved

1. Simple pocket
2. Compound pocket
3. complex pocket
Contents of periodontal pocket

 Debris consisting of microorganisms and their products

Enzymes
Endotoxins – lipopolysaccharides
Metabolic products
 Gingival Crevicular fluid
 Food remnants
 Salivary mucin
 Desquamated epithelial cells
 Leukocytes
  Plaque-covered calculus
 Purulent exudate consisting of:
Living, necrotizing and degenerated leukocytes
Living and dead bacteria
Serum
Scant amount of fibrin
Clinical signs and symptoms
Signs

 Bluish red thickened gingival margin

 Gingival bleeding and suppuration from gingival margin
 Shiny, discolored and puffy gingiva associated with exposed root surfaces
 Tooth mobility, diastema and migration of teeth

Symptoms

 Toothache – localized pain

 Radiating pain in deep bone
 Foul taste/smell in localized areas
 Sensation of pressure after eating, which gradually diminishes

Histopathology
Areas in soft tissue gingival wall of periodontal pocket are:

1. Areas of relative quiescence: Flat surface, minor depressions

2. Areas of bacterial accumulation: Depressions on epithelial surfaces leading to abundant bacterial debris and clumps
3. Areas of leukocytes emergence: Entry of leukocytes through holes located in the intercellular spaces
4. Areas of leukocyte-bacteria accumulation: Leukocytes are covered with bacteria resulting in phagocytosis
5. Areas of intense epithelial desquamation: Semi-attached and folded epithelium squames are covered with bacteria
6. Areas of ulceration: With exposed CT
7. Areas of hemorrhage: With numerous erythrocytes
Pathogenesis

Correlation of clinical and histological features of periodontal pocket

Clinical features Histopatholgical features
Color Bluish red discoloration Circulatory stagnation
Surface texture Smooth and shiny surface Atrophy of the epithelium and edema
Pitting on pressure Edema and degeneration
Consistency Flaccidity Destruction of gingival fibers and surrounding tissues
Fibrotic changes predominate over exudation and degeneration
Less frequently, the gingival wall may be pink and firm and often ulcerated
Bleeding Bleeding on probing Increased vascularity
Thinning and degeneration of epithelium
Proximity of engorged vessels to the inner surface
Pain When explored with probe, the inner aspect of the pocket is Ulceration of the inner aspect of the pocket wall
generally painful
Pus In many cases, pus may be expressed with the application of Suppurative inflammation of the inner wall
digital pressure

Treatment of periodontal pocket

1. Non-surgical treatment
 Topical or oral antibiotics to control infection
 Scaling and root planning
 Maintenance of oral hygiene
2. Surgical treatment
 Respective surgeries
  Regenerative surgeries
 Laser

Complications of periodontal pocket

1. Gingivitis
2. Periodontitis
3. Periodontal abscess
4. Gingival recession
5. Tooth mobility
6. Root/Cemental caries
 Chapter # 03

NUTRITION IN HEALTH AND DISEASE

Nutrition
“Nutrition is defined as the science of food and its relationship to health that is concerned primarily with the part played by the nutrients in body growth,
development and maintenance.”

Nutrients
“Nutrients are the organic and inorganic complexes contained in food.”

Classification of nutrients
Nutrients are divided into following categories:

1. Macronutrients: Form the main bulk of food and contain:

 Carbohydrates
 Fats
 Proteins.
2. Micronutrients: Required in small amounts and contain followings:
 Minerals: calcium, phosphorous and magnesium
 Vitamins: water soluble vitamins (vitamins of B group and C) , fat soluble vitamins ( vitamin A, D, E and K)
 Trace elements: WHO recognized 14 trace elements which should be present in human nutrition? These are iron, iodine, copper, cobalt,
chromium, fluorine, zinc, manganese, molybdenum, tin, nickel, silicon, selenium and vanadium.

Oral manifestations associated with malnutrition

The clinical evaluation of a patient may show specific pathologic changes in oral tissues caused by malnutrition.
Lips
The changes in lips are usually observed on exposed mucosa and angles of mouth. Riboflavin, niacin and iron deficiencies are associated with these lesions.
The most common lesions are:
Cheilosis – Chapping and fissuring of lips
Angular lesions
Teeth
The conditions seen in teeth are:
Mottled enamel
Linear enamel Hypoplasia
Melanodontia – Black teeth
Malposition
Gums
The conditions seen in gums are:
Scorbutic type gums – A symptom of scurvy in which there is triangle shaped areas between teeth show redness of gums which occurs due to vitamin C
deficiency
Gingivitis – Due to poor oral hygiene
Hypertrophic gingivitis – due to vitamin C deficiency
Tongue
The conditions seen in gums are:
Filiform and fugiform papillary atrophy
Papillary hypertrophy or heperemia
Magenta tongue
Scarlet red Glossitis
Beefy red Glossitis
 Sources Average Daily Functions Deficiency
Animal Plant Requirement
sources sources
(vegetables
and plants)
Proteins Milk, meat, Pulses, 75 gm 1. Body building 1. Kwashiorkor
eggs, cheese, cereals, 2. Repair and maintenance of body 2. Delayed eruption and Hypoplasia of
fish beans, nuts tissue deciduous teeth
3. Maintenance of osmotic 3. Cementum deposition is retarded
pressure 4. Resorption of alveolar bone
4. Synthesis of certain substances
like:
 Antibodies
 Plasma proteins
 Hemoglobin
 Enzymes
 Hormones
 Coagulation factors
Fats Milk, fat of Ground nut, 55 gm 1. High energy foods thus provide Excessive intake of fats causes:
meat and fish, mustard, energy  Obesity
eggs, cheese, sesame, 2. Serve as vehicles for fat soluble  Coronary heart diseases
ghee and coconut vitamins  Increased risk of colon cancer and
butter 3. Fats in body support viscera breast cancer
such as heart, kidney and
intestine
4. Essential fatty acids are needed
by body for:
 Growth
 Structural integrity of cell
membrane
 Decreased platelet
adhesiveness
Carbohydrates Starch: cereals, roots and 400 gm 1. Essential for:
 tubers  Oxidation of fats
Sugars: monosaccharides,  Synthesis of certain essential
disaccharides amino acids
Dietary fibers: vegetables,
fruits and grains
Calcium Ca: milk, milk products, Ca: 400 to 500 gm 1. Provide rigidity and strength to 1. Altered calcification
eggs, fish bone and teeth 2. Increased dental caries
Phosphorous P: vegetables P: 1.5 mg 2. Make up most of the skeletal 3. Reduction in alveolar bone formation
structures
Magnesium Vegetables 200 to 300 gm 1. Constituent of bones and present 1. Irritability
in all body cells 2. Tetany
2. Essential for normal metabolism 3. Hyper-reflexia
of calcium and potassium 4. Reduction in alveolar bone formation
5. Gingival hyperplasia
6. Widening of PDL
Vitamin A Fish liver oil, Spinach, 5000IU 1. Indispensible for normal vision 1. Night blindness
liver, eggs, papaya, 2. Necessary for maintaining the 2. Bitot’s spots
cheese, mango, integrity and normal functioning 3. Corneal xerosis
butter, whole carrots of glandular and epithelial 4. Keratomalacia
milk, fish and tissues 5. Hyperkeratosis and hyperplasia of
meat 3. Supports skeletal growth gingival tissue
especially 6. Atrophy of odontoblasts
7. Atrophy of salivary glands
8. Reduced salivary flow
9. Increase in caries susceptibility
10. Enamel Hypoplasia
Vitamin D Sunlight Adults: 100 IU Helps in absorption of calcium Rickets
Foods: liver, egg yolk, butter, Infants and children: Used in maintenance of calcium Osteoporosis
cheese, milk, fish fat 200 IU homeostasis Osteomalacia
Pregnancy and Maintenance of skeletal integrity
lactation: 400 IU
Vitamin E Vegetables oils, cotton seeds, 10 gm Antioxidants 1. Haemoytic anemia
sunflower seeds, egg yolk and 2. Hyppoplastic anemia
butter 3. Degenerative lesions in skeletal
muscles and heart
4. Anatomic changes in nervous system:
 Ataxia

Vitamin K Vitamin K1: fresh green
vegetables, cow’s milk
Vitamin K2 : synthesized by
intestinal bacteria
Vitamin C Fresh fruits, green leafy
vegetables, germinating
pulses, amla and guava
Thiamine B1 Whole grain cereals, wheat,
gram, yeast, pulses, oil seeds,
nuts
Meat, fish, eggs, vegetables
and fruits contain smaller
amounts
Riboflavin B2 Milk, eggs, liver, kidney,
green leafy vegetables
Meat and fish contain small
amounts
Niacin B3 Liver, kidney, meat, poultry,
fish, legumes and ground nuts
Pyridoxine B6 Milk, liver, meat, egg yolk,
fish, whole grain cereals,
legumes and vegetables
 Dysarthria
 Loss of pain sensation
 Depressed tendon reflexes
Stimulate the production and release 1. Bleeding
of certain coagulation factor 2. Delayed healing of wounds
3. Prothrombin content of blood is
markedly decreased
4. Blood clotting time is prolonged
Adults: 40 mg 1. Tissue oxidation 1. Scurvy
Children: 40 mg 2. Needed for the formation of 2. Bleeding from gums
Infants: 20 mg collagen 3. Gingival hyperplasia
Lactation: 80 mg 4. Swelling of tongue
5. ANUG
6. Lack of periodontal support making
teeth loose to the point of exfoliation
1.5mg 1. Essential for utilization of 1. Beriberi
carbohydrates 2. Burning tongue
2. Involved in direct oxidative 3. Hyperesthesia of oral mucosa
pathway for glucose 4. Wernick’s encephalopathy
1.5 mg 1. Fundamental role in cellular 1. Angular stomatitis
oxidation 2. Cheilosis
2. Cofactor involved with energy 3. Glossitis
metabolism 4. Seborrhoeic dermatitis around
nasolabial fold
18 mg 1. Metabolism of carbohydrates, 1. Pellagra
fats and proteins 2. Glossitis
2. Essential for normal functioning 3. Stomatitis
of skin, intestine and nervous 4. Diarrhea
system 5. Dermatitis
6. Dementia
Adults: 2mg Metabolism of carbohydrates, Peripheral neuritis
Pregnancy and amino acids and fats
lactation: 2.5 mg
 Folic acid B9 Liver, meat, dairy products, Adults: 100µg 1. Synthesis of nucleic acid 1. Megaloblastic anemia
eggs, milk, fruits and cereals Pregnancy: 300µg 2. Needed for normal development 2. Glossitis
Lactation: 150µg of blood cells in the marrow 3. Cheilosis
Children: 100µg 4. GIT disturbances

Vitamin B12 Liver, kidney, meat, fish,
eggs, milk and cheese
Also synthesized by bacteria
in colon
Adults: 1µg 1. Biochemical role in synthesis of 1. Megaloblastic anemia
Pregnancy and fatty acids in myelin 2. Pernicious anemia
lactation: 1.5µg 2. Co-operates with folic acid in 3. Demyelinating
Infants and children: synthesis of DNA neurological lesions in the spinal cord
0.2µg 4. Infertility

Trace elements in dental caries

Trace elements in human dental enamel are derived from the environment during mineralization and during and after maturation of tooth. Navia (1972)
summarized the cariogenic effect of many of the minerals in a list complied to indicate relative cariogenicity.
Cariostatic elements: F, P
Mildly cariostatis elements: Mo, V, Cu, Sr, B, Li, Au
Caries inert elements: Ba, Al, Ni, Fe, Pd, Ti
Caries promoting elements: Se, Mg, Cd, Pt, Pb, Si
 Chapter: 01 HEALTH, DISEASE AND INFECTION
HEALTH
DEFINITIONS OF HEALTH
The oldest definition is:
“Health is the absence of disease.”
According to WEBSTER:
“Health is the condition of being sound in body, mind or spirit, especially freedom from physical disease or pain.”
According to WHO:
“Health is a state of complete physical, social and mental well-being and not merely an absence of disease or infirmity.”

CHANGING CONCEPTS OF HEALTH

a) Biomedical concept: According to this concept:
“Health is absence of disease and if one is free of disease than the person is considered to be healthy.”
b) Ecological concept: According to this concept:
“Health is a dynamic equilibrium between man and his environment.”
And
“Disease is maladjustment of the human organism to environment.”
c) Psychosocial concept: According to this concept:
“Health is influenced by social, psychological, cultural, economic and political factors which are considered while defining and measuring health.”

d) Holistic concept: According to this concept:

 “All sectors of society have an effect on health, in particular agriculture, food, industry, education and other sectors.”
“Health implies a sound mind, in a sound body, in a sound family, in a sound environment.”

DIMENSIONS OF HEALTH
Health is multi-dimensional. WHO envisages 03 specific dimensions namely:
1. Physical dimension: “Perfect functioning of the body.”
2. Mental dimension: “A state of balance between the individual and the surrounding world, a state of harmony between oneself and others, a
coexistence between the realities of the self and that of other people and that of the environment.”
3. Social dimension: “Quantity and quality of an individual’s interpersonal ties and the extent of involvement with the community.”
4. Other dimensions of health are:-
 Spiritual dimension
 Emotional dimension
 Vocational dimension
 Political dimension
 Philosophical dimension
 Environmental dimension
 Educational dimension
 Nutritional dimension
 Preventive dimension
 Cultural dimension
 Socioeconomic dimension

INDICATORS OF HEALTH
“Indicators measure the health status of a community and compare the health status of one country with that of another for:
 Assessment of health care needs
 Allocation of scarce resources
 Monitoring and evaluation of health services, activities and programs.”
Characteristics of indicators: An ideal indicator should be:
1. Valid
2. Feasible
3. Reliable
4. Relevant
 5. Sensitive
6. Specific
Classification of indicators : The indicators of health can be classified as:
1. Mortality indicators
 Crude death rate – “number of deaths per 1000 population per year in a given community”
 Expectation of life – “average number of years that will be lived by those born alive in a population”
 Infant mortality rate – “ratio of deaths under 1 year of age in a given year to the total number of live births in the same year, usually expressed
as a rate per 1000 live births”
 Child mortality rate – “number of deaths at age 1-4 years in a given year per 1000 children in that age group at the midpoint of the year
concerned”
 Maternal mortality rate
2. Morbidity indicators – The following morbidity indicators used for assessing ill health in community.
 Incidence and prevalence
 Notification rates
 Attendance rates at OPD, health centers, etc.
 Admission, readmission and discharge rates
 Duration of stay in hospitals
3. Disability rates – falls into 2 groups:
 Event-type indicators
 Person-type indicators
Sullivan’s index = life expectancy – (probable period of bed disability + inability to perform major activities)
4. Nutritional status indicators
 Anthropometric measurements of pre-school children
 Heights of children at school entry
 Prevalence of low birth weight
5. Health care delivery indicators
 Doctor-population ratio
 Doctor-nurse ratio
 Population-bed ratio
6. Utilization rates
7. Indicators of social and mental health
8. Environmental indicators – Reflect the quality of physical and biological environment in which diseases occur and in which the people live.
9. Socioeconomic indicators
10. Health policy indicators
 11. Indicators of quality of life
12. Other indicators

DISEASE
DEFINITIONS OF DISEASE
Simplest definition is:
“Disease is any deviation from normal functioning or state of complete physical or mental well-being.”
According to WEBSTER:
“Disease is a condition in which body’s health is impaired, a departure from a state of health, an alteration of the human body interrupting the performance of
vital functions.”

CONCEPTS OF CAUSATION OF DISEASE

Following are the 04 concepts of causation of a disease:
1.
Germ theory of disease
2.
Epidemiological triad
3.
Multifactorial causation
4.
Web of causation
1. Germ theory of disease: According to this concept:
“Disease is generally referred to as one-to-one relationship between the causal agent and disease.”
Or
“A specific agent is responsible for one disease only.”
The disease model is as follows:

Disease agent Man Disease

Epidemiological triad: According to this concept:

“Disease is the result of an interaction between agent, host and environment which are collectively called epidemiological triad.”
a) Agent factors
 “An agent is a substance, living or non-living, or a force, the excessive presence or relative lack of which may initiate a disease process.”
Disease agents are classified as:
Biological agents: Viruses, bacteria, fungi, protozoa and metazoa.
Physical agents: Excessive heat, cold, humidity, pressure, radiation, electricity and sound.
Chemical agents: These agents can be:
o Exogenous agents: Metals, allergens, fumes,
o Endogenous agents: Urea, uric acid, ketones, etc.
Nutritional agents: Excess or deficiency of fats, carbohydrates, water, minerals, etc.
Social agents: Smoking, poverty, abuse of drugs and alcohol, unhealthy lifestyles, social isolations, etc.
Mechanical agents: Chronic friction and mechanical forces.
b) Host factors
“A host is a person or other animals that get diseased to an infectious agent under natural conditions.”
Host factors can be classified as:
1. Demographic characteristics: Age, sex.
2. Biological characteristics: Genetic factors.
3. Social and economic characteristics: Education, occupation, and marital status
4. Lifestyle factors: Personality traits, living habits, and physical exercises.
c) Environmental factors
“An environment is man’s external surroundings.”
It is divides into three components:
i. Physical environment: This is universe of non- living things with which man is in constant interaction such as Air, water, soil, climate, heat, light,
noise, debris and radiation.
ii. Biological environment: This is universe of living things, which surrounds man, including man himself.
iii. Psychosocial environment: This is the universe of those factors which are affecting the personal health, health care and community well-being, that
stem from the psychosocial make up of an individual and the structure and functions of social groups.
2. Multifactorial causation: According to this concept:
“A disease is a result of many factors such as social, economic, cultural, genetic, and psychological.”
Diseases such as coronary heart diseases and lung cancers are due to multiple factors i.e.
 Excess of fat intake
 Smoking
 Lack of physical exercise
Obesity, etc.
3. Web of causation: According to this concept:
“Disease is a result of complex interaction of all predisposing or risk factors.”
Removal or elimination of just one link is sufficient to control disease.

NATURAL HISTORY OF DISEASE

“It describes the way in which a disease evolves over time from the earliest stage of its pre-pathogenesis phase to its termination as recovery, disability or death,
in the absence of treatment or prevention.”
Each disease has its own unique natural history, which is not necessarily the same in all individuals.
Phases of natural history of a disease
1. Pre-pathogenesis phase
2. Pathogenesis phase
3. Recovery phase
Pre-pathogenesis phase: This phase refers to the period during which disease agent has not yet entered man, but the factors which favour its interaction with
human host already exist in the environment.
Potentially, we all are in the pre-pathogenesis phase of many diseases
Pathogenesis phase: This phase refers to the period which begins with the entry of disease agent in the susceptible human host. The pathogenesis phase may be
modified by intervention measures such as immunization and chemotherapy.
a) Early pathogenesis phase: This phase in chronic disease is referred to as Pre-symptomatic Phase.
b) Late pathogenesis phase: By the time, Signs and Symptoms appears the disease is already advanced into the late pathogenesis phase – symptomatic
phase.
Recovery phase: The final outcome of the disease may be recovery, disability or death.

RISK FACTORS
“The term risk factor means an attribute or exposure that is significantly associated with the development of a disease.” Risk factors are:
 May be truly causative
 May be merely contributory
 Can be modified
  Cannot be modified
Identification of risk factors: To identify risk factors and estimate the degree of risk epidemiological methods are needed which are:
 Case control studies
 Cohort studies
Significance of risk factors: The detection of risk factors will help in the prevention and intervention of diseases.

SPECTRUM OF DISEASE
“The term spectrum of disease is a graphic representation of variations in the manifestations of disease.”
 At the one end of disease, spectrum is subclinical infections which are not ordinarily identified.
 In the middle of the spectrum, lie illness ranging in severity from mild to severe.
 At the other end of disease, spectrum are fatal illness.

ICEBERG OF DISEASE
According to this concept, disease in a community may be compared with an iceberg.
Parts of iceberg: An iceberg consists of 3 parts:

1. Floating Tip: Represents what the physician sees in the community. It includes:
 Apparent cases
 Symptomatic cases
 Clinical cases
 Diagnosed cases
“Diagnostic tests are done for tip of iceberg.”
2. Submerged portion: Represents what the physician does not see in the community i.e. the hidden portion of the disease. It includes:
 Latent cases
 In apparent cases
 Pre-symptomatic cases
 Undiagnosed cases
 Carriers
“Screening tests are done for hidden portion of iceberg.”
3. Waterline: Represents the demarcation between apparent and in apparent disease or symptomatic disease and pre-symptomatic disease.
Iceberg phenomena shown by:
 Hypertension
 Diabetes
 Anemia
 Malnutrition
 Obesity
 Mental illness
Iceberg phenomena not shown by:
 Measles
 Rabies
 Tetanus
Significance of iceberg phenomena: The hidden part of the iceberg constitutes an important, undiagnosed reservoir of infection or disease in the
community, and its detection and control is a challenge to modern techniques in preventive medicine.

DISEASE PREVENTION AND CONTROL

“It is the establishment of a state of equilibrium between the disease agent, host and environment components of the disease process.”
It includes:
1. Disease Control
2. Disease Elimination
3. Disease Eradication
DISEASE CONTROL: It describes the measures aimed at reducing:
1. The incidence of disease
2. The duration of disease and consequently risk of transmission
3. The effects of infections both physical and psychosocial complications
4. The financial burden to the community
 DISEASE ELIMINATION DISEASE ERADICATION
Definition “Interruption of transmission of disease.” Literally means to “tear out by roots”
“Termination of all the transmission of infection by extermination of the
infectious agents.”
Limited to Geographical regions or areas Worldwide
Examples Elimination of measles in Sri Lanka Worldwide eradication of smallpox
Elimination of polio and diphtheria from large geographic areas
SCREENING FOR DISEASES
“The search for unrecognized disease or defect by means of rapidly applied tests, examinations or other procedures in apparently healthy individuals.”
A screening test is not intended to be a diagnostic test. Followings are few differences between screening and diagnostic tests.

Screening tests Diagnostic tests

Done to those who are apparently healthy or asymptomatic. Done to those with suggestive signs or symptoms.
Applied to a group of individuals. Applied to a single person.
Results are not conclusive. Results are conclusive and final.
Less accurate More accurate
Less expensive More expensive
Not a basis for treatment Basis for treatment
It is initial examination. It is referred to the physician if the screening test results are positive.
Basic purpose is to sort out from a large group of apparently healthy Basic purpose is to establish the presence or absence of disease i.e. confirms a
persons those likely to have the disease or at the increased risk of disease diagnosis.
under study i.e. early detection of disease or risk factors

CRITERIA FOR SCREENING

The criteria for screening are based on two considerations:
1. Disease to be screened
2. Test to be applied

Criteria or characteristics of disease:

The disease to be screened should fulfill the following criteria before it is suitable for screening:
 The condition should be important health problem – prevalence should be high
 There should be recognizable latent or early asymptomatic stage.
  The natural history of the condition should be adequately understood
 There is a test that can detect the disease prior to the onset of signs and symptoms.
 Facilities should be available for confirmation of diagnosis.
 There is an effective treatment.
 There is good evidence that early detection and treatment reduces morbidity and mortality.
 The expected benefits exceed the risks and costs.

Criteria or characteristics of screening test:

The test must satisfy the criteria of followings:
 Acceptability – “test should be acceptable to the people at whom it is aimed being painless, comfortable and un-embarrassing.”
 Repeatable – “the test must give consistent results when repeated more than once on the same individual or material, under same conditions.” It
depends upon 3 major factors:
Observer variation
Biological variation
Errors related to technical methods
 Validity – “it expresses the ability of a test to separate or distinguish those who have the disease from those who do not.” It has 2 components:
 Sensitivity: “The ability of a test to identify correctly all those who have the disease that is true positive.” A 90% sensitivity means that 90%
of the diseased people screened by the test will give a “true positive” result and the remaining 10% a “false negative” result.
Sensitivity = a / (a + c) x 100

 Specificity: “The ability of a test to identify correctly all those who do not have the disease that is true negative.” A 90% specificity means
that 90% of the non-diseased people screened by the test will give a “true negative” result and the remaining 10% a “false positive” result.
Specificity = b / (b + d) x 100

Screening test result by diagnosis

Screening Test Diagnosis Total
Results Diseased Non-Diseased
Positive a (true positive) b (false positive) a+b
Negative c (false negative) d (true negative) c+d
Total a+c b+d a+b+c+d

 Yield
 Simplicity
 Safety rapidity
  Ease of administration
 Ease of cost
Uses of screening:
1. Case detection
2. Control of disease
3. Research purpose
4. Educational opportunities

INFECTION
DEFINITION OF INFECTION
“The entry and development or multiplication of an infectious agent in the body of a man or animal.”
DYNAMICS OF DISEASE TRANSMISSION
Communicable diseases are transmitted from the reservoir or source of infection to susceptible host. Basically there are 3 links in the chain of transmission:
1. Reservoir / Source of infection
a) Human reservoir
b) Animal reservoir
c) Reservoir in non-living things
2. Modes of transmission
a) Direct transmission
i. Direct contact
ii. Droplet infection
iii. Contact with soil
iv. Inoculation into skin or mucosa
v. Trans-placental(vertical)

b) Indirect transmission
i. Vehicle-borne
ii. Vector-borne
Mechanical
Biological
iii. Air-borne
Droplet nuclei
 Dust
iv. Fomite-borne
v. Unclean hands and fingers
3. Susceptible host
Reservoir / source of infection: The starting point for the occurrence of a communicable disease is the existence of a reservoir or source of infection.
Source of infection Reservoir
“The person, animal, object or substance from which an infectious agent passes “Any person, animal, arthropod, plant or substance or combination of
or is disseminated to the host is called source of infection.” these in which an infectious agent lives and multiplies, on which it
depends primarily for survival, and where it reproduces itself in such
manner that it can be transmitted to a susceptible host is called reservoir.”
The reservoir may be of 3 types:
a) Human reservoir – 2 types of human reservoir exists:
Cases: “A person in the population or study group identified as having particular disease, health disorder or condition under investigation.”
Carriers: “An infected person or animal that harbors a specific infectious agent in the absence of discernible clinical disease and serves as a
potential source of infection for others.”
b) Animal reservoir – the diseases and infections that are transmissible to man from vertebrates are called ZOONOSES. Zoonotic diseases (over
100) include:
 Rabies (bats, dogs and other mammals)
 Yellow fever (Aedes mosquito)
 Influenza (influenza virus)
 Anthrax (sheep)
c) Reservoir in non-living things – soil and inanimate matter can also act as reservoirs of infection. For example soil may harbor agents that cause
tetanus, anthrax, and mycetoma.
Modes of transmission: Depending upon the infectious agent, portal of entry and local ecological conditions, communicable diseases can be transmitted
in different ways.

Modes of transmission Portal of entry Infectious diseases

1) Direct transmission
a) Direct contact Skin to skin STD, AIDS, leprosy, skin and eye infections
Mucosa to mucosa
Mucosa to skin
b) Droplet infection Spray of droplets of saliva and nasopharyngeal secretions Respiratory infections, eruptive fevers, many infections
during: of nervous system, common cold, diphtheria, whooping
Coughing cough, TB, meningococcal meningitis.
 Sneezing
Speaking
Spitting
Talking into the surrounding

c) Contact with soil Through soil, compost or decaying vegetable matter Hookworm larvae, tetanus, mycosis
d) Inoculation into skin or mucosa Skin Rabies virus by dog bite, hepatitis B virus through
Mucosa contaminated needles and syringes.
e) Trans-placental Through placenta TORCH agents – Toxoplasma gondii, Rubella virus
Cytomegalovirus and Herpes virus
2) Indirect Transmission
a) Vehicle-borne Water Infections of alimentary tract:
Food  Acute diarrhea
Ice  Typhoid fever
Blood  Cholera
Serum
Plasma
Biological products such a tissues and organs
b) Vector-borne Arthropod or a living carrier:
Anopheles mosquito Malaria
Housefly Dysentery
Tse -Tse fly African sleeping sickness
Aedes mosquito Dengue fever
c) Air-borne
d) Droplet nuclei Tiny particles that represent the dried residues of droplet TB, influenza, chickenpox, measles
i.e. smog Pneumonia, psittacosis
e) Dust Larger droplets may be:
Expelled during:
 Talking
 Coughing
 Sneezing
Settle down by their sheer weight on the:
 Floors
 Carpets
 Furniture
 Cloths
  Bedding
 Linen and other objects in the immediate
environment
Particles blown from the soil by wind
including fungal spores
f) Fomite-borne Fomites – belongings of host, include soiled: Diphtheria, typhoid fever, bacillary dysentery, hepatitis
 Clothes A, eye and skin infections
 Towels
 Handkerchiefs
 Cups
g) Unclean hands and fingers Directly – hand to mouth Respiratory infections such as:
Indirectly  Influenza
 Colds
 COVID – 19

Susceptible Host: “An infectious agent seeks a susceptible host aiming successful parasitism.”
Stages of parasitism: Following 4 stages have been described in successful parasitism:
First stage: The infectious agent must find a portal of entry by which it may enter the host.
Second stage: On gaining entry into the host, the organisms must reach the appropriate tissue site of election in the body of host where it may find optimum
conditions for its multiplication and survival.
Third stage: The disease agent must find a way out of the body i.e. portal of exit in order that it may reach new host and propagate its species.
Fourth stage: After leaving the human body, the organism must survive in the external environment for sufficient period till a new host is found and does not
cause the death of the host but produce only a low grade immunity so that host is vulnerable gain and again to the same infection.
 Sussceptible Infectious
host agent

Portal of
Reservior
entery

Mode of
Portal of exit
transmission

Stages of an infectious disease: All infectious diseases pass through 5 stages.

1st stage – incubation period or infected stage: The time interval between invasion by an infectious agent and appearance of the first sign or symptom
of disease in question.
2nd stage – the onset or prodromal or infective stage: This starts when the first symptoms appear and continue until the condition is well developed.
3rd stage – the period of advance or fastigium or potentially symptomatic stage: All the symptoms are now increasing in severity until a
climax is reached.
4th stage – period of defervescence or stage of decline: All the symptoms are now decreasing in severity.
5th stage – period of convalescence or recovery or decline stage: The patient has overcome completely the invaders or toxins.
 Chapter: 05
HEALTH EDUCATION
DEFINITIONS OF HEALTH EDUCATION
“Health education is the profession of educating people about health.”
“Health education can be defined as the principle by which individuals and groups of people learn to behave in a manner conducive to the promotion,
maintenance, or restoration of health.”
WHO defines health education as:
“Any combination of learning opportunities and teaching activities designed to facilitate voluntary adaptations of behaviors that are conducive to health.”

CHANGING CONCEPTS OF HEALTH EDUCATION

Followings are the changing concepts of health education:
 Prevention of disease to promotion of healthy lifestyles.
 Modification of individual behavior to modification of social environment in which the individual lives.
 Community participation to community involvement.

OBJECTIVES OF HEALTH EDUCATION

The 3 main objectives of health education are:
1. Informing the people
2. Motivating people
3. Guiding into action
Informing the people: The primary objective of the health education is to inform the people or provide scientific knowledge about prevention of disease and
promotion of health.
Motivating people: Informing people about health is not merely enough.
 They must be motivated to change their habits and the ways of living which are detrimental to health, like pollution of water, cigarette smoking,
physical activity, etc.
 The accent should be motivating the “consumer” to make his own decision and choices about health matters, i.e. what kind of health actions to be taken,
and when and under what conditions to take them.
Guiding into action: Informing and motivating the people is not merely enough.
  People need help to adopt and maintain healthy practices and lifestyles, which may be totally new to them. So, governments have a major responsibility
to provide the necessary infrastructure of health services.
 People need to be encouraged “to use judiciously and wisely the health services available to them.”

APPROACH TO HEALTH EDUCATION

There are basically 4 well-known approaches to health education. They are:
1. Regulatory approach
2. Service approach
3. Educational approach
4. Primary health care approach

Approaches Aims Disadvantages

1. Regulatory or legal approach The regulatory or legal approach seeks to protect the health of It requires vast administrative machinery to enforce
public through the enforcement of laws and regulations, e.g. laws and also involves considerable expenditure.
food adulteration act, epidemic diseases act, etc.
2. Service approach This approach aims at providing all the health facilities needed It was not based on the “felt needs” of the people.
by the community in the hope that people would use them to
improve their own health.
3. Educational approach It involves motivation, communication and decision making. The results are slow.
The results are permanent and enduring.
4. Primary health care approach This is a new approach starting from the people with their full No.
participation and active involvement. The underlying objective
is to help individuals to become self reliant in matter of health
which in turn make the capable in identifying their health
problems and finding workable solutions.

Health education and Propaganda: Health education and propaganda are not the same. They differ in number of characteristics. Followings are few
differences between health education and propaganda:

Health education Propaganda

Knowledge and skills are actively acquired by people. Knowledge is installed in the mind of people.
 Initiates people to think for themselves. Discourages thinking because of readymade slogans.
Makes people to use judgment before action i.e develops reflective Results in reflexive behavior where people tend to take impulsive actions.
behavior.
Primitive desires are disciplined in this process. It arouses and stimulates the primitive desires.
Appeals to reasoning. Appeals to emotions.
Person tries to acquire knowledge through self-reliant activity. Person receives knowledge passively and it is spoon-fed.
End results are aimed at developing favorable attitude, habits and skills. End results bring no change in attitude or behavior.
PRINCIPLES OF HEALTH EDUCATION
The main principles of health education on the principles of learning include:
1. Good human relations – health educator must be kind and sympathetic.
2. Social leader – we learn best from the people whom we respect and regard. So, in health education we try to penetrate the community through the
leaders i.e. village headman, school teacher or political worker. The attributes of the leader are:
Understands the needs and demands of the community
Provides proper guidance
Takes the initiative
Easily accessible to the people
Respective to views and suggestions of the people
Selfless, honest, impartial, considerate and sincere
3. Motivation – “wakening of desire to learn.” There are 2 types:
Primary: “These are inborn desires which initiate people to take action” e.g. hunger, survival.
Secondary: “These desires are created by external forces or incentives” e.g. praise, reward.
4. Participation – people should be encouraged to be a part of health education.
5. Credibility – the degree to which the message to be communicated is perceived as trustworthy by the receiver.
6. Interest – health education must be related to interest of people i.e. based on “felt needs”.
7. Comprehension – teaching should be within the mental capacity of the audience.
8. Known to unknown – health educator must start where the people are and with what they understand and then proceed to new knowledge.
9. Learning by doing – the Chinese proverb “if I hear, I forget; if I see, I remember; if I do, I know” illustrates the importance of learning by doing.
10. Reinforcement – constant repetition like a booster dose that leaves a stronger impression on mind and helps to understand and accept new principles.
11. Feedback – the health educator can modify the elements of the system in the light of feedback from his audience.
12. Setting an example – health educator should set a good example in the things he is teaching which will help the people to look upon him and lead a
healthy lifestyle.
13. Soil, seed, and sower – soil refers to “people to whom education is given”, seed refers to “the heath facts to be given to the people”, and sower refers to
“the transmitting media.”

COMMUNICATION IN HEALTH EDUCATION

 “Communication can be regarded as a two way process of exchanging or shaping ideas, feelings and information.”
It forms the basis for exchange of ideas or information and plays a significant role in human daily life.
Key elements in communication
Communication is generally made up of 4 key elements which are the followings:
1. Communicator
2. Audience
3. Message
4. Channels of communication
1. Communicator: “He is the originator of the message who knows the objectives, understands the needs of audience, identifies the interests of the people and
knows the proper medium for communication to be used.”
2. Audience: “They are the consumers of the message who should have patience to listen to the communicator and should also clarify their doubts which they
have not understood.”
3. Message: It is the information a communicator wishes his audience to receive, understand, accept, and act upon. A message should have the following
properties:
Based or related to interests of people
Clear and easily understandable
Specific
In conjunction with the objectives of the programme
4. Channels of communication: “It is the medium of communication and an attempt to keep the teaching process interesting and entertaining.”
Types of Communication: There are different types of communication:
1. One-way communication (didactic method)
2. Two-way communication (Socratic method)
3. Verbal communication
4. Non-verbal communication
5. Formal communication
6. Informal communication
7. Visual communication
Barriers of Communication: Barriers in communication can be classified as:
 Physiological barriers – difficulties in hearing, expression.
  Psychological barriers – emotional disturbances and neurosis.
 Environmental barriers – noise, invisibility, congestion.
 Cultural barriers – levels of knowledge and understanding, customs, beliefs, attitudes.

EDUCATIONAL AIDS IN HEALTH EDUCATION

Health educators make use various aids in the process of health education. They can be classified mainly into 3 categories:
1. Audio aids
2. Visual aids
 Requiring projection
 Not-requiring projection
3. Combined audio visual (AV) aids
1. Audio aids: Based on principle of sound and electricity. These include the following:
Tape recorder
Microphones
Amplifiers
Radio
Gramophones
2. Visual aids: These can be:
a. Requiring projection: Including
Slides
Film strip
Bioscope
Projectors
b. Not-Requiring projection: Including
Models
Black boards
Charts
Leaflets
Posters
Exhibitions
3. Combined AV aids: These include the following:
TV
 Sound films (cinema)
Slide-tape combination
Multimedia computers

METHODS IN HEALTH COMMUNICATION

The methods in health education may be grouped into 3 main types depending upon the objectives to be achieved, the behavior to be influenced and available
funds.
1. Individual approach
 Personal contact
 Home visit
 Personal letters
2. Group approach
 Chalk and talk (lectures)
Flip charts
Flannel graph
Exhibits
 Demonstration
 Group discussion
 Panel discussion
 Symposium
 Workshop
 Pole playing (socio drama)
 Conferences and seminars
 Colloquy
3. Mass approach – Education of the general public
 Television
 Radio
 Newspaper
 Printed material
 Direct mailing
 Posters
 Folk methods
 Internet
 Films
 Bill boards and signs
  Health museums and exhibitions

Approaches Size of Aims Disadvantages

population
Individual approach  It may be given in personal interviews in the  The numbers of people we reach are small.
consultation room of the doctor or in health  Health education is given only to those who come in
center or in homes of people. The people contact with us.
involved are public health nurses, health visitors
and health inspectors.
 In this approach we can discuss, argue and
persuade the individual to change his behavior.
 It provides opportunities to ask questions in terms
of specific interests.
Group approach
1. Chalk and talk  Oral presentation of facts, organized thoughts and  Students are involved to a minimum extent.
– lecture ideas by a qualified person.  Learning is passive.
 Information is transferred to a large group in a  Don’t stimulate thinking or problem solving capacity.
short period.
 Talk should not exceed more than 20 minutes.
 The lecture method can be more effective by
combining with suitable audio-visual aids as:
Flip charts
Flannel graphs
Exhibits

2. Demonstratio  Planned presentation to show how to perform a

n skill or procedure.
 Performed step by step in front of audience
making them understandable and involve in
discussion.
 Upholds the principle of “seeing is believing” and
“learning by doing”
 Has high motivational value.

 Aggregation of people seated in a circle and

interacting in face to face situations.  Unequal participation of members.
3. Group  Some participate may deviate from the subject.
 discussion  Permits to learn by freely exchanging their ideas,
knowledge and opinions.
 There should be a group leader who initiates,
avoids side conservations, encourages everyone
to participate and sums up the discussion in the
end.
Rules of group discussion:
Listen to others and don’t interrupt
Express ideas clearly and concisely
Accept criticism
Help to reach conclusions

 Two-way discussion in which qualified persons  No specific agenda

talk about a topic and discuss the given problem  No order of speaking
4. Panel in front of a large group or audience.  No sets of speech
discussion  The discussion should be spontaneous and
natural.
 After speaker’s discussion, the audience is invited
to take part.

 It is a series of speeches on selected subjects.  There is no discussion among symposium members.

 Each expert presents an aspect of the subject
briefly.
5. Symposium
 Audience may raise questions.
 At the end, chairman makes a comprehensive
summary.

 It is a series of meetings usually 4 or more with  Needs a lot of baseline ground work.
emphasis on individual work, within the group,
with the help of consultants and resource
6. Workshop personnel.
 It provides opportunities to improve his
effectiveness as a professional worker.

 Social drama
 Based on assumptions that many values in
situation cannot be expressed in words so, it is
 7. Role-playing dramatized by the group.
 Used to discuss social problems.
 Useful educational tool for school children.

 Usually held on a regional, state, or national

level.
 Range from half a day to a week length.
8. Conferences
and seminars  Audience gets the opportunity for direct
participation.
9. Colloquy
Mass approach Usually These are one way communication approach which  This approach used when alone is insufficient in
millions are based on local needs and are useful in changing human behavior, and has to be used in
transmitting messages to the people even in remotest conjunction with other methods for it to be effective.
places. This is the approach that can give high returns  Distorted information
for the time and money involved. These includes:
 Television
 Radio
 Health magazines
 News papers
 Printed materials
 Direct mailing
 Posters, bill boards and signs
 Health museums and exhibitions
 Films
The mass media are only instruments. As such they
are neither good nor bad; what matters is the message
they carry and the way the message is delivered.

Chapter: 09
 INFECTION CONTROL AND STERLIZATION
DEFINITION OF INFECTION
“The entry and development or multiplication of an infectious agent in the body of a man or animal results in infection.”

THE INFECTIOUS PROCESS

A chain of events is required for the spread of an infectious agent. These are:
1. Essential features for disease transmission
 An infectious agent
 Reservoir
 Portal of exit
 Mode of transmission
 Portal of entry
 A susceptible host
2. Factors that influence the development of infection
3. Factors that alter normal infection
 Abnormal physical conditions
 Systemic diseases
 Drug therapy
 Prostheses and transplants

Sterilization
“Sterilization is the process by which all the forms of life are destroyed.”

Methods of sterilization

The various approved methods of sterilization are:

1. Moist heat
2. Dry heat
3. Chemical vapor
4. Ethylene oxide

Principles of action Advantages Disadvantages

Moist heat – steam 1. Sterilization is achieved by action of heat  All microorganisms, spores and  May corrode carbon steel
under pressure and moisture; pressure serves only to attain viruses are destroyed quickly instruments, if precautions are
high temperature. and efficiently. not taken.
“Destruction of
2. Air must be excluded; otherwise steam  Most economical method of  Unsuitable for oils or powders
microorganisms by penetration and heat transfer are prevented. sterilization. that are impervious to heat.
moist heat takes 3. Space between objects is essential to ensure
place as a result of access for the steam.
inactivation of 4. Materials must be thoroughly cleaned and
essential cellular air-dried.
5. Air discharge occurs in a downward
proteins or enzymes
direction; load must be arranged for free
which causes passage of steam towards the bottom of
coagulation of autoclave.
proteins.” 6. Temperature must remain at 121oC at 15
pounds pressure for 15 minutes after the
meter shows that proper pressure and
temperature have been reached.
7. Use 30 minutes for heavy loads to ensure
penetration.
Dry heat 1. Sterilization is achieved by the action of  Useful for materials that cannot  Long exposure time required;
“The action of dry heat that is conducted from the exterior be subjected to steam under penetration slow and uneven.
surface to the interior of object. pressure.  High temperature is critical to
heat is oxidation.”
2. Time required to penetrate heat varies  When maintained at correct certain materials.
among materials. temperature it is well suited for
3. A temperature of 160o maintained for 2 sharp instruments.
hours; 170o for 1 hour.  No corrosion as compared with
4. Timing must start after the desired steam under pressure.
temperature has been reached.
5. Temperature above 160o may destroy the
sharp edges of cutting instruments.
Chemical vapor 1. A complication of alcohols, formaldehyde,  Corrosion – rust-free operation  Cannot be used for materials or
sterilizer ketone, water + acetone heated under for carbon steel instruments. objects that can be altered by
pressure produces a gas that is effective as a  Ability to sterilize in a relatively chemicals that make the vapor or
strigling agent. short total cycle. that cannot withstand the high
2. Microbial and viral destruction results from  Use of operation and care of the temperature.
the permeation of the heated formaldehyde equipment.  Adequate ventilation is needed;
and alcohol. cannot use in a small room.
3. Heavy, tightly wrapped or sealed packages  Slight odor, which is rarely
would not permit the penetration of the objectionable.
vapours.
4. Minimum of 20 minutes with temperature
from 127oC to 132oC with 20 to 40 pounds
pressure in accord with manufacturer’s
directions.

Chapter # 10
 INTRODUCTION TO DENTAL PUBLIC HEALTH

Dental public health

“Dental public health is the science and art of preventing and controlling oral diseases, promoting oral health and improving quality of life through organized
community efforts.”

Tools of dental public health

Followings are 05 tools of dental public health:
1. Epidemiology
2. Biostatics
3. Social sciences
4. Principles of administration
5. Preventive dentistry

Personal versus community health care

Similarities Differences

Personal health care Community health care Personal health care Community health care
1. Examination 1. Survey 1. Deal with one patient at a time. 1. Deals with groups of people.
2. Diagnosis 2. Analysis 2. Higher take home pay with less 2. Salaried employee with fringe
3. Treatment planning 3. Programme planning fringe benefits. benefits such as pension, sick
4. Treatment 4. Programme operation leave, paid leaves, etc.
5. Payment for service 5. Finance 3. Goals are coincidentally related. 3. Goals are socially determined.
6. Evaluation 6. Appraisal 4. The patient comes to dental 4. The public health worker goes
practitioner. to the community.
5. One’s own decision. 5. Decisions are made over a
considerable period of time and
with several groups.
6. Independent health care 6. Their work is visible and
Chapter # 13
provider. publically accountable.

PLANNING, SURVEY AND EVALUATION

 Planning
Definition “The systemic approach to define the
problem, setting priorities, developing
specific goals and objectives, determining
alternative strategies and a method of
implementation is called planning.”
Objectives/Purposes 1. To match the limited resources with
many problems.
2. To eliminate wasteful expenditure or
duplication of expenditure.
3. To develop the best course of action to
accomplish a defined objective.
Types 1. Problem solving planning
2. School based programme planning
3. Coordination of efforts and activities
planning
4. Planning for allocation of resources
Steps 1. Needs assessment
2. Setting priorities
3. Development of goals, objectives and
activities
4. Identification of resources and
constrains
5. Alternative strategies
6. Implementation
7. Evaluation and revision
Pathfinder survey
“It is a practical, economical survey sampling methodology which aims to
include the most important population subgroups likely to have different
disease levels and to cover a standard number of subjects in specific index age
Survey Evaluation
“A non-experimental investigation in “The collection and analysis of
which information is systemically information to determine the programme
collected, analyzed and evaluated to performance is called evaluation.”
determine the amount of disease
problems in a community is called
survey.”
1. Initially, to provide a full picture of 1. To find out how well the programme
the oral health status and needs of a works – to measure its success.
population. 2. To provide information for decision
2. Subsequently, to monitor changes in making.
disease levels or patterns. 3. To measure the effect.
4. If there is lack of success then
modifications are done to improve the
programme.
1. Descriptive survey 1. Formative evaluation
 Cross-sectional 2. Summative evaluation
 Longitudinal
2. Analytic/Explanatory survey
 Cross-sectional
 Longitudinal
1. Establishing the objective 1. Determine what is to be determined
2. Designing the investigation 2. Establishment of standard and criteria
3. Selecting the sample 3. Planning the methodology
4. Conducting the examinations 4. Gathering information
5. Analyzing the data 5. Analysis of results
6. Drawing the conclusions 6. Taking decisions
7. Publishing the reports 7. Revaluation
 Chapter # 14

DENTAL AUXILIARIES
“A dental auxiliary or ancillary is a person who is given responsibility by a dentist so that he or she can help the dentist render dental care, but who is not
himself or herself qualified with a dental degree.”

WHO classification of Dental Auxiliaries

A. Non-operating auxiliaries
a) Clinical: A person who assists the professional in his clinical work but does not carry out any independent procedures in the oral cavity.
1) Dental surgery assistant
2) Dental secretary /receptionist
3) Dental health educator
b) Laboratory: A person who assists the professional by carrying out certain technical laboratory procedure.
1) Dental laboratory technician
B. Operating auxiliaries: A person who, not being a professional is permitted to carry out certain treatment procedures in the mouth under the direction
and supervision of a professional.
1) School dental nurse
2) Dental therapist
3) Dental hygienist
4) Expanded function dental ancillaries - EFDA

Duties of Dental Auxiliaries

1) Dental secretary / Receptionist
This is a person who assists the dentist with his secretarial work and patient reception duties.
2) Dental health educator
This is a person who instructs in prevention of dental diseases and who may also be permitted to apply preventive agents intra-orally, however, not
allowed undertaking any intraoral procedure.
3) Dental laboratory technician
This is a person who fulfills the prescriptions provided by dentists regarding the extra-oral construction and repair of oral appliances and bridge
work. The duties of dental technician include:
1. Casting of models from impression made by dentist
2. Fabrication of dentures, splints, orthodontic appliances, inlays, crowns and special trays
4) Dental therapist
This is a person who is permitted to carry out to the prescription of a supervising dentist, certain specified preventive and treatment measures
including:
1. Preparation of cavities
2. Restoration of teeth
3. Administration of local analgesia
4. Clinical caries diagnosis
5. Vital pulpotomies under rubber dam in deciduous teeth
6. Extraction of deciduous teeth under local anesthesia
7. Interception of X-rays
5) Dental school nurse
This is a person who is permitted to diagnose dental disease and to plan and carry out certain specified preventive and treatment measure without
the supervising dentist. The duties of school dental nurse include:
1. Oral examination.
2. Prophylaxis
3. Topical fluoride application.
4. Advice on dietary fluoride supplements.
5. Administration of local anesthesia.
6. Cavity preparation
7. Placement of amalgam filling in primary and permanent teeth.
8. Pulp capping.
9. Extraction of primary teeth.
10. Individual patient instruction in tooth brushing and oral hygiene.
11. Classroom and parent-teacher dental health education.
12. Referral of patient to private practitioners for more complex services such as:
 Extraction of permanent teeth
 Restoration of fractured permanent incisors
 Orthodontic treatment
6) Dental hygienist
This is a person who is licensed and registered to practice dental hygiene under the laws of appropriate state, province, territory or nation under the
supervision of dentists. The duties of dental hygienist include:
1. Cleaning of mouths and teeth with particular attention to calculus and stains.
2. Topical application of fluorides, sealants, and other prophylactic solutions.
3. Screening of patients as individuals or in group so that they me be referred to dentists for treatment.
4. Instruction in oral hygiene.
5. Resource work in the field of dental health.
7) Dental surgery assistant
The duties of dental surgery assistant include:
1. Reception of the patient.
2. Preparation of the patient for any treatment he or she may need.
3. Preparation and provision of all necessary facilities such as mouthwashes and napkins.
4. Sterilization care and preparation of instruments.
5. Preparation and mixing of restorative materials including both fillings and impression materials.
6. Care of the patient after treatment until he or she may leaves.
7. Clearing away of materials and preparation of instruments for reuse.
8. Preparation of surgery for next patient.
9. Assistance with X-rays work and processing and mounting of X-rays.
10. Instruction of patients, where necessary, in correct use of the tooth brush.
 Chapter # 20

PRIMARY PREVENTIVE SERVICES

Plaque control
Plaque control is the removal of microbial plaque and the prevention of its accumulation on the teeth and adjacent gingival surfaces. It is an effective way of
treating and preventing gingivitis and prevention of periodontal diseases.

Classification of plaque control

A. Mechanical plaque control
1. Tooth brushes
a) Mechanical tooth brushes
b) Electric tooth brushes
2. Interdental oral hygiene aids
a) Dental floss
b) Dental floss holder
c) Dental floss threader
d) Pipe cleaner
e) Tongue cleaner
f) Gauze strip
g) Interdental tip stimulator
h) Interdental brush
i) Wedge stimulator
j) Tooth pick
k) Tooth pick holder
3. Dentrifices
 B. Chemical plaque control  Nuclease
1. Antibiotics  Dextranase
 Penicillin  Mutanase
 Vancomycin 6. Metallic salts
 Kanamycin  Zinc sulphate
 Erythromycin  Zinc citrate
2. Phenols 7. Oral irrigation devices
 Listerine 8. Fluoride
 Thymol  Sodium fluoride
 Eucalyptol  Sodium mono-fluoro-phosphate
3. Quaternary ammonium compounds  Stannous fluoride
 Cetylpridinium chloride 9. Oxygenating agents
 Benzalconium chloride  Peroxide
4. Bisbiguanides 10. Natural products
 Chlorhexidine  Sanguinarine
 Alexidine 11. Other antiseptics
 Octenidine  Iodine
5. Enzymes  Povidone-iodine
 Protease  Chloramine T
 Lipase

MECHANICAL PLAQUE CONTROL

A. Tooth brushes
1) Manual tooth brush: A manual tooth brush is made up of 3 parts:
a) Handle – divided into:
Toe: This is the extreme end of head
Heel: This is closest to handle
b) Head
c) Bristles – when bristles are bunched together they are termed as tufts.
 There is a constriction between handle and the head termed as shank. Toothbrushes can be classified as:
a) On the basis of sizes: Large, medium and small
b) On the basis hardness or stiffness: Hard, medium and soft

2) Electric tooth brush: The head of electric tooth brush is smaller than the manual tooth brush and is removable for replacements.
The 03 basic patterns that the head follows when the motor is started are:

a) Reciprocating: A back and forth movement

b) Arcuate: Up and down movement
c) Elliptical: A combination of reciprocating and arcuate
Special uses of electric tooth brush:

 Parental brushing of children’s teeth

 For patients who are physically handicapped
 Mentally retarded patients
 Aged patients
 Patients with poor dexterity

B. Interdental oral hygiene aids: Uses of interdental oral hygiene aids are:
 These aids are used to remove plaque and debris that are adherent to the teeth, restorations, orthodontic appliances, and gingiva in the inter-proximal
embrasures.
 It polishes the surfaces as it removes the debris.
 They are used for massaging the interdental papillae and to reduce gingival bleeding.
 They contribute to general oral sensation and the control of halitosis.

C. Dentifrices: A substance used with a tooth brush for the purpose of cleaning the accessible surfaces of the teeth. They are available in different
forms:

 Tooth powders
 Tooth pastes
 Liquids
 Gels
 Dentrifices are classified into 02 categories:
1. Cosmetic dentifrices: Clean and polish the teeth.
2. Therapeutic dentifrices: Reduce some disease process in mouth such as caries incidence, gingivitis, calculus formation, tooth sensitivity.
Dentifrice ingredients / Composition
1. Abrasives – 20 to 40%: Used in the removal of heavy plaque, adhered stains, and calculus deposits. They include:
 Calcium pyrophosphate
 Di-calcium phosphate
 Calcium carbonate
 Sodium bicarbonate
 Hydrated silica
2. Humectants – 20 to 40%: Used to stabilize the composition and reduce water loss by evaporation. They include:
 Glycerin
 Sorbitol
3. Foaming agents / Soaps and detergents – 1 to 2%: Help to remove debris from the teeth and dissolve other ingredients. They include:
 Sodium lauryl sulphate
 Sodium N-lauryl-sarcosinate
4. Binding agents – 2%: Used to prevent separation of the components in the tube during storage. They include:
 Sodium alginate
 Methylcellulose
5. Flavouring agents – 2%: Provide an immediate taste sensation and have a relatively long-lasting flavour.
6. Sweetening agents – 2%: They include:
 Sorbitol
 Glycerin
 Mannitol
7. Therapeutic agents – 2%: Stannous fluoride
8. Preservatives – 1%: Benzoic acid is used to inhibit bacterial growth on binding agent.
 Disclosing agents
“A disclosing agent is a preparation in liquid, tablet, or lozenge form that contains a dye or other coloring agent which are used to identify bacterial plaque
deposits for instruction, evaluation and research.”

Purpose of disclosing agents

 Personalized patient instruction in the location of soft deposits and the techniques for removal.
 Self evaluation by the patient on daily basis.
 Counting evaluation of effectiveness to determine the need for revisions of the plaque control procedures.
 Preparation of plaque indices.
 To gain new information about the incidence and formation of deposits on the teeth.

Ideal properties of disclosing agents

1. Intensity of color: The color should contrast with normal colors of oral cavity.
2. Duration of intensity: The color should not rinse off immediately with ordinary rinsing methods.
3. Taste: The taste should be pleasant and encourage cooperation of patient.
4. Irritation to the mucous membrane: It should produce no irritation or allergic reaction.
5. Diffusibility: It should be thin enough so it can be applied readily to the exposed surfaces of the teeth.

Classification of disclosing agents

1. Iodine solution preparation

a) Skinners solution
b) Diluted tincture of iodine
2. Bismarck browns (Easlick’s disclosing solution)
3. Merbromin
4. Erythrosin
a) Rinse application
b) Topical application
c) Tablet form
5. Fast green
6. Fluorescein
7. Two-tone
 8. Mercurochrome preparation
a) Mercurochrome solution 5%
b) Flavoured mercurochrome solution

Method of application

1. Dry the teeth with compressed air

2. Retract cheek or tongue
3. Use swab or small cotton pellet with cotton pliers to carry the solution to the teeth
4. Apply solution to the crowns of the teeth only
5. Direct the patient to spread the agent over all surfaces of the teeth with the tongue

Caries Activity Test

“Caries activity tests are the tests that estimate the actual state of disease activity progression or regression.”
1) Lactobacilli colony count test
2) Snyder’s test
3) Alban’s test (Modified Snyder Test)
4) Salivary buffer test
5) Salivary reductase test
6) Enamel solubility test
7) Streptococcus mutants level in saliva
Lactobacilli colony count test

saliva is collected by chewing 1gm of parraffin

sample is vigrously shaken

1ml aliquote from dilution is placed in petri-dishes containing 10ml of

Ragosa's lactobacilli selective medium

incubate for 4 days

no of lactobacilli colonies that are developed are counted.

Results
No of organisms Degree of caries activity
1 – 1000 Little or no
1000 – 10000 Slight
10000 – 100000 Moderate
100000 – more Marked
Snyder’s test

It is based on the assumption that the amount of acid produced in a medium is proportionate to the number of lactobacilli in the
inoculums. The medium used for the test has a pH of approximately 5.0 which is optimum for lactobacilli to grow.
STEP – I: Preparation of medium

61gm of Snyder's agar powder , 1L boiled water and glacial acetic acid are added to prepare medium

approximately 5ml of sterile test tubes are collected

and stored in refrigerator untill needed.

The classical formula of Snyder’s agar per liter of purified water is:
Dextrose – 20gm
Agar – 16gm
Pancreatic digest of casein – 13.5gm
Yeast extract – 6.5gm
Sodium chloride – 5gm
Bromocresol green – 0.029gm
STEP – II: Test procedure

5ml test tube from refrigerator is taken

liquify at 100oC

add 0.1ml of saliva stimulated with 1gm of parraffin

cool test tube at 45oC

shake test tube vigrously

incubate for 72 hours at 37oC

STEP – III: Results

At the end of 24 hours and again at 48 and 72 hours, the color of the medium is recorded as 1 to 4 on the basis of whether the color remains same or
changes to light green, a light yellow, or a definite yellow.
The medium is blue at Ph 5.0, green at Ph 4.6, yellowish at Ph 4.2 and yellow at pH 3.8.

Alban’s test (Modified Snyder’s test)

At the time of the test, a 5ml tube of semi-solid agar is removed from the refrigerator but it is not heated. The patient is asked to spit unstimulated saliva directly
into the tube until there is thin layer of saliva covering the surface of green agar. The tube is then incubated for 4 days. The color changes are scored from 0 to
4, with the score being based on the amount of color changes occurring from top to bottom in the tube.

Results
Color No color change Color change to yellow in Color change to yellow in Color change to yellow in Color change to yellow
change the top of ¼ of tube the ½ mark of tube the ¾ mark of tube along entire length of tube
Score 0 1 2 3 4
+ ++ +++ ++++
 Pits and Fissure Sealants
Definition
Pits and fissure sealants are defined as “a cement or a resin which is introduced into unprepared occlusal pits and fissures of caries susceptible teeth forming a
mechanical and physical protective layer against the action of acid producing bacteria and their substrates.”
Indications
A deep occlusal fissure
A deep fossa
A deep lingual pit
Contraindications
Open occlusal carious lesions
Caries exist on other surfaces of the same tooth
A large occlusal restoration is already present
Types of pits and fissure sealants
Three different kinds of plastics have been used as occlusal sealants:
1. Polyurethanes
2. Cynoacrylates
3. Bisphenol A-glycidylmethylacrylate (BIS-GMA) – sealant of choice
Polymerizing of the sealant
When the liquid paste – monomer is acted upon by the catalyst, repeating chemical bond begin to form, increasing in number and complexity as the hardening
process – polymerization proceeds. Finally the resultant hard product is known as polymer. Two methods have been employed to catalyze polymerization:
1. Light cured polymerization by use of either UV light or visible blue light
2. Self cured polymerization by addition of initiator usually benzoyl peroxide.
Requisites for sealant retention

 The tooth surface should have a maximum surface area.

 The tooth should have deep, irregular pits and fissures.
  The tooth should be cleaned.
 The tooth should be absolutely dried at the time of sealant placement.
 The tooth surface should be uncontaminated with saliva residues.

Procedure of pits and fissure application

1. Surface cleanliness of the tooth by use of pumice and water slurry
2. Dryness of the tooth surface by compressed air and dry field can be maintained by the use of rubber dam, applying cotton rolls over the opening of
parotid duct.
3. Preparing the tooth for sealant application by use of 36% to 40% orthophosphoric acid – etching agent for 10 seconds followed by water flush and tooth
surface is dried for 10 seconds.
4. Application of sealant
 Assignment
Submitted to: Dr. Ayesha
Submitted by: Safura Ijaz
Subject: Operative Dentistry
Department: AHS-DT Final year
Roll No.: 04

Difference between infected dentin, affected dentin and sclerotic dentin

Infected dentin Affected dentin Sclerotic dentin
Definition: Primarily characterized by Primarily characterized by demineralization of Primarily characterized by
bacterial contamination. intertubular dentin and of initial formation of hypermineralization of dentinal tubules
intratubular fine crystals at advancing front of resulting in narrowing or complete closure
caries lesion. of dentinal tubules that run through dentin.
Mineral content: Low Partially demineralized High
Collagen : Irreversibly denatured collagen Collagen cross-linking remains intact Denatured collagen
Color : Dark brown or black Light yellow or brown Dark brown or black
Consistency: soft Softer than normal dentin Hard and brittle
Bacteria: Present May be present Absent
Sensitivity: Most Mild/moderate Least
Permeability: Increased permeability Variable permeability Greatly reduced permeability
Remineralization Not possible Possible Not possible
:
Histologic Necrotic and contaminated zone Demineralized zone Hypermineralized zone
appearance:
Treatment: Can be easily excavated with Resistant to hand excavation and can only be Usually require no treatment
hand and rotatory instrumentation removed by exerting pressure  Total etch technique
 Air abrasion

Difference between pulpotomy and pulpectomy

Pulpotomy Pulpectomy – RCT
Definition: Removal of coronal pulp Removal of whole pulp i.e. cornal pulp and radicular pulp
Indications: Vital teeth  Non-vital teeth
 Abscess
 Irreversible pulpitis
Performed on/Type of Specific to baby teeth Specific to permanent teeth
teeth:
Goal/Purpose: Allows baby teeth to function until natural exfoliation Aims to preserve the permanent tooth indefinitely

Difference between direct pulp capping and indirect pulp capping

Features Direct pulp capping Indirect pulp capping
Pulp exposure: Visible Not exposed
Dentin layer: Removed Thin layer left behind
Procedure: A calcium hydroxide lining material is placed on A calcium hydroxide lining material is placed to
the exposed pulpal tissue and a small amount of cover the remaining demineralized dentin. A GIC
surrounding dentin. A sealing liner or a sealing restoration is then placed followed by a sealing
restoration is then placed to seal out bacteria and restoration to seal out bacteria and their by
their by products. products.