Case History in periodontics

Presentation by Dr. Harshal P Patil

Guided by Dr. P.S.Rakhewar
Dr. Lisa Chacko
Dr. Manoj Thorat
 Introduction

Recording the case history of a patient is an integral part of

Periodontics. A systematically recorded case history provides great
insight to the attitude of the patient as well as the patient’s medical
and periodontal status. It helps us arrive at a diagnosis and in
framing an appropriate treatment plan.
 Demographics

Name
1. Everyone feels good when they are addressed by their name. The purpose of
asking the name of the patient is to make him feel comfortable in order to establish
a good rapport.
2. The name is also important for record purposes. It makes it easy to identify the
patient for future correspondence. It is also necessary to have complete records in
case of any medico-legal cases.
Age
1. Certain diseases are seen more commonly in certain age groups.
 Periodontal condition
Gingival disease Herpetic gingivostomatitis
Puberty associated gingivitis 11-17 years
Acute necrotizing ulcerative 15 – 30 years
gingivitis
Desquamative gingivitis
Periodontal disease Aggressive periodontitis
Chronic periodontitis
Age Reason
Children below 6 years Since the condition is contagious, adults
would be exposed to the virus in their
childhood and developed immunity.
Thus, it is seen predominantly in
children.
Hormonal changes increase:
1. Tissue response to plaque.
2. Capnocytophaga , Prevotella
intermedia and Prevotella nigrescens
which use hormones as nutrients.
Seen at any age, but most commonly
between 15-30 years. Children with
Down’s syndrome or from low
socioeconomic strata are predisposed.
40-50 years Auto-immune conditions are common in
middle aged women. An exception is
dermatitis herpetiformis which is seen in
males between 20 to 30 years.
<35 years The rate of bone loss here is 3-4 times
faster than in chronic periodontitis;
hence, the disease manifests at a
younger age.
>35 years Though the condition may begin in
adolescence, due to the slow rate of
progression it becomes clinically
significant after the age of 35.
• Prognosis of the patient depends upon the age. In two patients with the same
level of disease the older patient has a better prognosis.
• For example: If a 20 year old and a 50 year old patient have generalized 7mm
pockets, the 50 year old patient has taken much longer to lose the same amount
of attachment as to the 20 year old. The 20 year old patient would lose far more
attachment by the time she is 50. Obviously the rate of destruction is more in
the younger patient and the prognosis is obviously worse.
3. Anatomic differences:
The periodontium of children exhibits the following features:

Color of gingiva Less pale than in adults due to thinness of keratinized layer which makes the underlying vessels
more visible

Surface texture Stippling is absent up to the age of 4 years

Contour Inter-dental gingiva is broad buccolingually and narrow mesiodistally to conform to the morphology
of deciduous teeth

Sulcus depth 2.1 mm ± 0.2 mm

Lamina dura More prominent
Periodontal ligament space Wider

Marrow spaces of alveolar bone Larger

Crests of inter-dental bone Flat and within 1 to 2 mm of cementoenamel junction

The periodontium of older adults exhibits the following features:

Gingiva Thinning and decreased keratinization of epithelium leading to decreased

resistance to trauma and infection
Gingival recession due to passive eruption compensating for attrition
Increase in collagen and decrease in cell number
Periodontal ligament Decrease in fibroblasts
Increase in elastic fibers
Width of PDL space increases with occlusal loading and decreases in
hypofunction
Cementum Increase in width by 5-10 times
Alveolar bone Presents a more irregular surface
Plaque Increased accumulation due to a greater area of the tooth being exposed by
recession, no change in microflora
Host response and No change in host response but increased inflammatory response
inflammation
Response to treatment No change in response to non surgical and surgical therapy
Greater compliance with supportive periodontal therapy
 Sex
1. Some conditions have a gender bias.
Males: Chronic periodontitis, generalized aggressive periodontitis
Females: Desquamative gingivitis
2. Conditions specific to women.
• Puberty and pregnancy do not by themselves lead to gingivitis. Plaque is the cause of gingivitis and, pregnancy and puberty merely increase the
gingival response to plaque.
• Puberty, pregnancy and oral contraceptives:
In all 3 conditions there is an increase in estrogen and progesterone.
Progesterone increases vascular permeability and makes the blood vessels more tortuous.
This in turn increases the inflammation in response to bacterial plaque.
Apart from this, Prevotella intermedia use progesterone as a substitute for Vitamin K as a growth factor. These organisms are implicated in both
puberty and pregnancy associated gingivitis.
• Menopause: Deficiency of estrogen in menopause results in osteoporosis which is characterized by a reduction in bone mass. Results of some
studies indicate that osteoporotic patients might have a greater bone loss due to periodontal disease than those without osteoporosis. The
influence of systemic disease on periodontal bone loss was termed “bone factor concept” by Irving Glickman in 1950, but this term is no longer
used.
 Occupation

1. Occupational hazards.
• Abrasion: Notching on incisal edges maybe seen in carpenters and tailors who hold
bobby pins and needles between their teeth.
• Erosion: People who work in factories with acidic environments show eroded teeth.
2. Stressful jobs.
• There is an increase in the hormone cortisol in stressful conditions. Cortisol
suppresses the immune system and therefore, increases the susceptibility to
infections like periodontitis.
 Address

• Some conditions are endemic to certain geographic locations, for example

fluorosis. Fluorosis is due to increased fluoride in the water at the time of
development of the tooth and is seen to occur in the fluoride belts of the
country. It causes enamel hypoplasia and intrinsic discoloration of teeth.
Chief Complaint and History of Present Illness

• The chief complaint of the patient should always be in his/ her own words and should
include the symptoms of the patient in a chronological order.
• The history of present illness should be elicited from the patient:
1. A detailed description of the patient’s chief complaint including when the symptoms
started. In case of pain, nature of the pain as well as aggravating and relieving factors should
be included.
2. Apart from the symptoms mentioned by the patient, the dentist should try to ascertain
whether a periodontal problem exists by asking the patient if he has loose teeth, bleeding
gums, food lodgment, bad breath or pain in his gums.
Pain can be identified as that of pulpal or periodontal origin based on the following:
Pulpal pain Periodontal pain

Severe, lancinating, poorly localized pain. Dull, gnawing well localized pain or pain deep in the bone.

Increases on consuming cold/ hot food; and in the supine Increases on chewing.
position due to increased pulpal pressure.
 Past Dental History
This should include whether the patient has previously visited the dentist and the reason for the same.
1. If the patient has visited the dentist before, it shows that he/ she has a greater awareness and motivation towards
dental treatment.
2. If the patient gives a history of extractions, then it is important to find out whether the teeth extracted were carious
or mobile. Past history of periodontal disease is a risk factor for periodontal breakdown in the future.
3. If the patient has got his/ her teeth restored, the quality of these restorations should be checked. Overhanging
restorations can cause plaque accumulation and under-filled proximal restorations can lead to food impaction, both of
which are predisposing factors of periodontal disease.
Ask for history of syncope, bleeding and hypersensitivity
4. Complications seen during previous treatment.
• Syncope: Syncope is the transient loss of consciousness due to reduced blood supply to the brain. The most
common cause is anxiety towards dental treatment. There is an increase in the levels of catecholamine which
lowers peripheral resistance, causes peripheral pooling of blood and reduces cerebral blood flow. Signs and
symptoms before the onset syncope include weakness, nausea, sweating, pallor, dizziness and low pulse pressure.
• To treat syncope the patient should be made to lie down in a supine position with the legs raised to increase the
venous return to the heart and blood to the brain. When the back of the chair is reclined such that the head of the
patient is lower than his feet it is called Trendelberg position. Apart from this tight clothes should be loosened and a
patent airway maintained.
• A patient who gives a history of syncope at the previous dental visit should be well motivated for future procedures
and if necessary pre-anesthetic medications such as sedatives maybe prescribed prior to treatment.
• Drug allergies: Some patients are hypersensitive to local anesthetic agents.
It is important to find out about hypersensitivity to penicillin or local
anesthetics before initiating dental treatment
 Medical history
Ask for history of diabetes mellitus, cardiovascular problems, bleeding disorders, liver problems and
medications.
Diabetes mellitus: Periodontal disease has been described as the sixth sign of diabetes by Loe H. in 1993.
1. Periodontal findings
Hirschfeld has mentioned the following periodontal symptoms associated with diabetes:
a. Enlarged gingiva
b. Sessile or pedunculated polyps
c. Polypoid gingival proliferations
d. Abscess formation
e. Periodontitis
f. Loosened teeth
Presence of multiple periodontal abscesses is the most characteristic finding of Diabetes mellitus.
• Apart from the these findings diabetics have increased gingival bleeding, deep periodontal pockets, rapid bone
loss and tooth loss.
• Diabetics are three times as likely as non-diabetics to develop destructive periodontal disease. This is because of
the effect of diabetes on bacterial pathogens,
function of neutrophils and
altered collagen metabolism.
a. Bacterial Pathogens: Due to increased glucose in blood and gingival crevicular fluid there is an increase in mainly
the black pigmented species which includes Porphyromonas gingivalis, Prevotella intermedia and Campylobacter
rectus.
b. Neutrophil Function: Glucose metabolism is necessary for the production of ATP which is a source of energy for all
cells. Therefore, in diabetics cell function is affected and neutrophils have impaired chemotaxis, phagocytosis and
adhesion.
c. Altered Collagen Metabolism: Regular collagen turnover is necessary to maintain tissue integrity. In diabetics
Advanced Glycation End (AGE) products attach to collagen and render it less soluble and less likely to be repaired.
This damaged collagen remains in the tissues longer and breaks down easily in the presence of periodontal disease.
2. Two way relationship of diabetes and periodontitis: Infections such as periodontitis increase the tissue resistance
to insulin, reduce uptake of glucose by the cells and thus, increase the glucose concentration of blood. Therefore,
treating periodontitis will help in improving the glycemic control in diabetic patients.
Complications on the dental chair with diabetic patients-
• The most common complication on the dental chair is that of hypoglycemia or decreased blood glucose. Increased incidence is seen
in well-controlled diabetics taking insulin or sulfonylurea agents. It is important to ensure that the patient has had his meal before
the dental treatment.
• If a patient goes into hypoglycemia on the dental chair (usually at glucose levels <60mg/ dl) , then the treatment should be
discontinued and the patient should be given either juice or 4 teaspoons of sugar. Unconscious patients can be given 25ml of 50%
dextrose or 1mg glucagon intravenously.
Cardiovascular problems:
• Hypertension
• a. Time of treatment: Blood pressure is usually highest mid-morning, therefore it is better give the patient an afternoon
appointment.
• b. Use of adrenaline: Using local anesthesia without adrenaline will minimize its anesthetic action and cause the release of
endogenous adrenaline. Therefore, adrenaline should be used along with the local anesthetic agent but the concentration should not
exceed 1:100,000.
• c. Levels at which treatment is possible: All dental procedures can be performed up to a blood pressure of 160/ 100, non-surgical
techniques may be performed up to a level of 180/ 110 and after this only emergency care maybe undertaken.
• d. Drugs: Calcium channel blockers used to treat hypertension can lead to gingival enlargement. Therefore, it is essential to
document drug history in these patients.
Myocardial infarction and angina pectoris
• Patients having suffered from ischemic heart disease should avoid dental treatment for 6 months.
Anginal episodes on the dental chair should be treated by administration of nitroglycerin (sublingual)
and oxygen.
Patients with cardiac pacemakers
• Older pacemakers are unipolar and get disrupted by ultrasonic and electrosurgery units. Thus, the use
of these equipments should be avoided in these patients. However, newer pacemakers are bipolar and
unaffected by equipment generating an electromagnetic field.
Infective endocarditis
• The presence of bacteria in the blood is called bacteremia. This can trigger infective endocarditis in a
patient who gives a history of the same. Dental procedures can cause bacteremia and prophylactic
antibiotics need to be given in patients at risk for infective endocarditis.
• Usually amoxicillin is given at the dosage of 2g, 1 hour before the procedure and in patients allergic to
amoxicillin Azithromycin or Clarithromycin maybe prescribed at a dosage of 500 mg, 1 hour before the
procedure.
Bleeding disorders and liver disease
• Liver disorders are of importance as the liver is responsible for production of pro-coagulant factors and metabolism of certain
drugs. Coagulation tests such as Prothrombin time and Partial Thromboplastin time should be carried out before initiating
periodontal therapy and medications should be prescribed with caution.
Drug history
1. Drugs which directly affect the periodontium
• Examples of medications affecting the periodontium are:
• a. Drugs such as calcium channel blockers (nifidipine), anticonvulsants (phenytoin) and immunosuppressants (cyclosporine)
can lead to gingival enlargement.
• b. Oral contraceptives cause an exaggerated response to local factors.
2. Drugs which increase bleeding tendency
• Patients on salicylates (aspirin) or anticoagulants (heparin, warfarin) will have increased bleeding. It is better to take an opinion
from the physician regarding drug discontinuation during the periodontal procedure.
3. Drug interactions
• Metronidazole should be avoided in patients consuming alcohol or patients on warfarin or lithium. Similarly, ciprofloxacin
should be avoided in patients taking theophylline, caffeine or warfarin.
• Apart from these factors medical history is also important because certain drugs are contraindicated in certain conditions such
as Ibuprofen in asthmatics, Diclofenac sodium in patients with gastritis and Pencillin in patients with known hypersensitivity to
the drug.
 Family history

• Ask if family members too have periodontal problems.

• Genetic defects have been implicated in both chronic and aggressive periodontitis,
hence, it is important to know whether the patient gives a positive family history.
Polymorphisms in genes coding for Interleukin 1, TNF – α, FcgR and Vitamin D predispose
patients to periodontitis and are called genetic markers.
• Knowledge of family history becomes particularly essential in aggressive periodontitis
which is known to have familial aggregation. Thus, family members especially younger
siblings, of the patient with aggressive periodontitis should be examined for the signs of
the disease, educated about preventive measures, and monitored closely.
Personal history
Habits:
• Ask for history of smoking and alcohol consumption.
• A study by Tomar SL and Asma S in 2000 (as a part of Third National Health and Nutrition Examination
Survey or NHANES III) showed that subjects smoking greater than 30 cigarettes per day are 4 times more
likely to have periodontitis and former smokers were 1.68 times more likely. Therefore, smoking is a
known risk factor for periodontal disease. Smokeless tobacco too has been associated with localized
attachment loss and recession.
A current smoker is said to be one who has smoked atleast 100 cigarettes in his lifetime and is currently
smoking
A former smoker is one who has smoked 100 cigarettes in his lifetime but is not currently smoking.
Heavy smokers are those who smoke more than or equal to 20 cigarettes per day while those people smoking
less than 20 cigarettes per day are considered as light smokers.
• Cigarette smoke contains various injurious substances and includes a particulate and a gaseous phase.
• Particulate phase: Nicotine, Tar, Benzene, Benzopyrene.
• Gas phase: Carbon Monoxide, Ammonia, Dimethylnitrosamine, Formaldehyde, Hydrogen Cyanide,
Acrolein.
The effects that smoking has on the periodontium are:
a.Physiologic effects: Microvasculature is altered in smokers.
Nicotine stimulates the sympathetic nervous system which further leads to vasoconstriction.
This leads to decrease in bleeding on probing, gingival crevicular fluid flow, subgingival temperature and clinical signs of
inflammation.
b. Microbiologic effects: There is no change in the amount of plaque but there is a change in the bacteria present in it.
Grossi et al. in 1996 have showed that Tannerella Forsythia was 2.3 times more likely to be there in smokers than in non smokers.
Hafajjee AD and Socransky SS in 2001 have shown an increase in the Orange and Red Complexes in smokers. Increased colonization of
these periodontal pathogens is seen in shallow pockets and therefore, there is an increased prevalence of periodontal destruction.
c. Immunologic effects: The alterations in the host response causing increased periodontal breakdown are –
• Nicotine causes functional changes in neutrophil chemotaxis, phagocytosis and oxidative burst and thus, affects the innate
response.
• The humoral response is also affected by the reduced production of the IgG2 antibody.
• Concomitantly, there is increased production of tissue destructive agents such as Tumor Necrosis Factor – a, Prostaglandin E2,
elastase and collagenase.
d. Effect on calculus formation: Pindborg found a positive correlation between smoking and calculus deposition. They reported more
pipe smokers than cigarette smokers have supragingival calculus. The reasons given for this are that pH of pipe smokers is more, and
because pipe smokers circulate the smoke around the mouth.
e. Response to periodontal therapy: In smokers there is less pocket depth reduction and less gain in clinical attachment levels
following both surgical and non surgical periodontal therapy. Smokers also showed poor results in procedures such as guided tissue
regeneration and use of bone grafts. GTR membranes were exposed and less pocket reduction was achieved following placement of
Demineralized Freeze Dried Bone Allograft.
.
• The smoking history of the patient should include the following details:
a. Number of years for which the patient is smoking.
b. Number of cigarettes smoked each time.
c. Number of times in a day that the patient smokes.
d. In a former smoker it is important to know how many years he smoked for and how many years it has
been since he quit smoking.
e. In case of smokeless tobacco it is important to know the form in which it is used and which part of the
mouth it is placed in.
• Smokers should be motivated to quit smoking in the Phase I or Etiotropic phase of periodontal
therapy. The smoking cessation program has the following steps:
• Chronic alcoholism can cause cirrhosis of the liver, which can increase the bleeding tendency during
periodontal instrumentation. This is the reason for recording any history of chronic alcoholism
Oral Hygiene Habits
Frequency of tooth brushing
By finger / brush/ other
Manjan/ Tooth paste
Method – Horizontal / vertical
 Extra oral examinations
Symmetry of the face: Gross asymmetry of the face maybe observed in the
following conditions:
1. Cysts and tumors of the jaw
2. Facial fractures
3. Dentoalveolar abscess
4. Hemi-atrophy or hemi-hypertrophy
5. Bell’s Palsy
Lymph node examination
If a node is palpable, record site, size, texture,
tenderness, fixation to surrounding tissues etc

Local infections: pericoronitis,

periodontal/pericoronal/periapical abscess/lesions,
ANUG, apthous ulcers, acute herpetic
gingivostomatitis, malignancy

Systemic infections: syphilis, TB,

Bacterial/fungal/parasitic infections, malignancy,
HIV, lymphomas, leaukaemias
 TMJ examinations

• Temporomandibular joint:
Lips:
• Whether the lips are competent or not should be checked while the patient
is relaxed. If the patient is asked to close his lips, he might forcefully close it
and it becomes difficult to differentiate between potentially competent and
competent lips.
• Incompetent lips are usually associated with mouth breathing. In these
patients gingiva appears erythematous and shiny especially in the maxillary
anterior region. This change has been attributed to surface dehydration.
 Test to check mouth breathing

1. Mirror test
2. Butterfly test
3. Water holding test
 Intraoral examination
Soft tissue examinations
Parts of oral mucosa:
Buccal mucosa: Lesions of lichen Planus, leukoplakia, erthyroplakia and oral submucous fibrosis maybe seen on the
buccal mucosa.
• Physiological alterations that maybe seen include cheek bite (linea alba buccalis) and ectopic sebaceous glands
(Fordyce’s granules).
Labial mucosa: Vesicles and ulcers on the labial mucosa may be due to Herpes labialis. The scaling appointment in
these patients should be rescheduled and caution should be used during patient examination since the condition is
contagious. When it spreads to the clinician’s finger the lesion is called herpetic whitlow.
Floor of the mouth: Mucous retention cysts (Ranula) might be present in the floor of the mouth.
Tongue: The tongue has quite an irregular surface which offers ideal niches for sheltering bacteria and retaining
desquamated cells and food remnants.
Tongue coating is particularly seen in case of hairy tongue (lingua villosa) or fissurated tongue (lingua plicata). This
tongue coating is responsible for oral malodor. Tongue cleaning should be advocated in all patients to avoid halitosis.
examination
• Periodontal indices
• Oral hygiene index
• Plaque index: Silness and Loe, Quigley Hein
• Gingival index: Loe and Silness
• Periodontal Index: Russell’s index, Ramfjord’s index, CPITN index
 ORAL HYGIENE INDEX – SIMPLIFIED
( John C. Greene & Jack R. Vermillion, 1964 )
DEBRIS INDEX
SCORE CRITERIA
0 No debris or stain present
Soft debris covering not more than one-third of
1 tooth surface, or presence of extrinsic stains
without other debris regardless of surface area
covered
2 Soft debris covering more than one-third, but not
more than two thirds, of the exposed tooth
surface.
3 Soft debris covering more than two thirds of the
tooth surface.
CALCULUS INDEX
SCORE CRITERIA
0 No calculus present
1 Supragingival calculus covering not more than third of
the exposed tooth surface.
Supragingival calculus covering more than one third
but not more than two thirds of the exposed tooth
2 surface or the presence of individual flecks of
subgingival calculus around the cervical portion of the
tooth or both
Supragingival calculus covering more than two thirds
3 of the exposed tooth surface or a continous heavy
band of subgingival calculus around the cervical
portion of the tooth or both.
 INTERPRETATION OF SCORES

FOR DI/CI FOR OHI-S

GOOD 0 – 0.6 GOOD 0 – 1.2

FAIR 0.7 – 1.8 FAIR 1.3 – 3.0

POOR 1.9 – 3.0 POOR 3.1 – 6.0

 PLAQUE INDEX
( Silness P. & Loe H , 1964 )

Interpretation
SCORE CRITERIA
EXCELLENT 0

0 No plaque present

A film of plaque adhering to the free gingival margin and GOOD 0.1 – 0.9
adjacent area of the tooth. The plaque may be seen in situ
1 only after application of disclosing solution or by using
the probe on the tooth surface.
Moderate accumulation of soft deposits within the
FAIR 1.0 – 1.9
2 gingival pocket, or the tooth and gingival margin which
can be seen with the naked eye.

3 Abundance of soft matter within the gingival pocket and/or on

the tooth and gingival margin 2.0 – 3.0
POOR
 GINGIVAL INDEX
( Loe H. & Silness J , 1963

SCORE CRITERIA

0 Absence of inflammation/normal gingiva INTERPRETATION OF SCORES

1 Mild inflammation, slight change in colour, slight MILD GINGIVITIS 0.1 – 1.0
edema; no bleeding on probing.

2 Moderate inflammation; marked glazing, redness MODERATE GINGIVITIS 1.1 – 2.0

edema and hypertrophy. Bleeding on probing.

3 Severe inflammation; marked redness and SEVERE GINGIVITIS 2.1 – 3.0

hypertrophy ulceration. Tendency to spontaneous
bleeding.
 SULCUS BLEEDING INDEX (SBI)
Muhlemann H.R and Son S. in 1971

SCORE CRITERIA
0 Normal-appearing gingiva, no bleeding upon probing.
1. No colour or contour changes, but bleeding on probing.
2. Bleeding on probing, colour change(reddening),no edematous contour changes.
3. Bleeding on probing, colour change, mild inflammatory edema.
4. Bleeding on probing, colour change, severe inflammatory edema.
5. Spontaneous bleeding on probing, colour change, very severe inflammatory edema
with or without ulceration.
Gingival bleeding index (Ainamo and Bay, 1975)
The gingival bleeding index is based on recordings from all four tooth surfaces of all teeth.
Recorded as
Bleeding present +
Bleeding absent -

Gingival bleeding index is calculated as a percentage of affected sites.

USES:
It is useful for experimental studies and in practice on routine basis in individual patients.
ADVANTAGES:
Simple and easy to use.
LIMITATIONS:
Does not discriminate areas of bleeding as mesial, distal, facial, lingual surfaces .
 PERIODONTAL INDEX
(Rusell A.L, 1956)

ADDITIONAL RADIOGRAPHIC CRITERIA FOR

SCORE CRITERIA FOR FIELD STUDIES CLINICAL STUDIES
Negative. There is neither overt inflammation in the
0 investing tissues nor loss of function due to destruction of Radiographic appearance is essentially normal.
supporting tissues.
Mild gingivitis. An overt area of inflammation in the free
1 gingival does not circumscribe the tooth.
Gingivitis. Inflammation completely circumscribes the
2 tooth, but there is no apparent break in the epithelial
attachment.

4 Used only when radiographs are available There is early notch like resorption of alveolar crest.

Gingivitis with pocket formation. The epithelial attachment

has been broken and there is a pocket (not merely a There is horizontal bone loss involving the alveolar crest,
deepened gingival crevice due to swelling in the free upto half of the length of the tooth root.
6 gingiva). There is no interference with normal masticatory
function; the tooth is firm in its socket and has not drifted.
There is advanced bone loss involving more than half of
Advanced destruction with loss of masticatory function. the tooth root or a definite infrabony pocket with
8 The tooth may be loose, may have drifted, may sound dull widening of periodontal ligament. There may be root
on percussion with metallic instrument, or may be resorption or rarefaction at the apex.
depressible on its socket.
INTERPRETATION OF SCORES

Clinically normal supporting tissues 0 – 0.2

Simple gingivitis 0.3 – 0.9
Beginning destructive periodontal disease 1.0 – 1.9
Established destructive periodontal disease 2.0 – 4.9
Terminal disease 5.0 – 8.0
Gingival status
• The gingiva is the part of the oral mucosa that covers the alveolar processes of the jaws and surrounds the necks of the teeth. It is
divided into marginal, attached and interdental areas.
• Color
• The normal color of the gingiva is coral pink.
Factors which determine gingival color include:
• 1. Thickness of epithelium
• 2. Degree of keratinization
• 3. Vascular supply
• 4. Pigmentation
The changes in the color of the gingiva in inflammation are:
• Reddish pink: This is due to increased blood vessels and reduced keratinization
• Bluish red: Blue color of tissues is always associated with reduced oxygen supply; similarly gingiva turns bluish red because of
venous stasis and anoxemia
localization of these changes in color help in diagnosis:
• ANUG – marginal involvement
• Herpetic gingivostomatitis – diffuse
• Chemical irritation – patch like

Chemical burn Aspirin

Metallic pigmentation:
• Black line on gingiva-Bismuth, arsenic, mercury

Bismuth induced black line

• Lead: “Burtonian line” bluish red/deep blue

• Silver: violet marginal line
• Cause: absorbed metals are precipitated in perivascular areas as metallic sulfides into the
subepithelial connective tissue.
• Pigmentation only occurs in areas of inflammation (since increased permeability of irritated
blood vessels permit seepage of metal into surrounding tissues)
• Site: gingiva, inner surface of lips, at the level of occlusal line in cheeks, lateral border of
tongue
• Treatment: Removal of local irritating factors; discontinuity of metal containing drugs; topical
application of concentrated peroxide to oxidize dark metallic sulfides.
•
Pigmentation
Endogenous
Melanin which is increased in the following systemic
condition:
Addison’s disease (adrenal dysfunction)
Peutz Jeghers syndrome (intestinal polyposis)
Albright’s syndrome (fibrous dysplasia)
Von Recklinghausen’s disease (neurofibromatosis)
Bilirubin (Jaundice)
Iron (Hemochromatosis)
Blood dyscrasias like anemia, polycythemia, and
leukemia
Exogenous
Metallic pigmentation due to bismuth, arsenic, lead and
silver:
Pigmentation occurs when inflammation leads to
increased vascular permeability and there is precipitation
of metallic sulfides into the connective tissue. Therefore,
the treatment consists of scaling.
Tobacco
Coloring agents in food and lozenges
Amalgam tattoo or implantation of amalgam into the
gingiva
 ORAL PIGMENTATION INDEX
( Dummett, 1966 )

SCORE CRITERIA
INTERPRETATION OF SCORES

0 No clinical pigmentation ( pink tissue ) 0 No pigmentation

0.03 – 1 Mild pigmentation

1 Mild clinical pigmentation ( mild light brown
tissue ) 1.03 – 2 Moderate pigmentation

2.03 – 3 Heavy pigmentation

2 Moderate clinical pigmentation ( moderate
brown tissue )

3 Heavy clinical pigmentation ( deep brown to

black tissue )
Size
• The size of any matter depends on what it is made up of; the size of the gingiva is determined by the sum total of:
• 1. Cells
• 2. Intercellular substance
• 3. Vascular supply
Increase in the size of the gingiva is called gingival enlargement and is classified based on its etiology as:
Inflammatory Acute : Abscess
Chronic : Plaque induced gingivitis
Drug induced Antiepileptic agents: Phenytoin
Calcium channel blockers: Nifidipine
Immunosuppressants: Cyclosporine
Associated with systemic conditions Conditions in which the reaction to plaque is increased
Associated with systemic disease leading to gingival enlargement: Pregnancy, puberty,
plasma cell gingivitis, pyogenic granuloma and scurvy

Enlargement is due to the disease itself irrespective of the

plaque, for example due to leukemia, Wegener’s
granulomatosis or sarcoidosis
Neoplastic Benign: Fibroma, papilloma, giant cell granuloma
Malignant: Carcinoma, malignant melanoma
False enlargement Due to underlying bone lesion: Tori, Paget’s disease,
fibrous dysplasia, cherubism, osteoma, osteosarcoma

Cue to underlying dental tissue: prominence of enamel

during tooth eruption
• Inflammatory gingival enlargement has been graded by Bokencamp et al in
1994 as:
• Grade 0: No sign of enlargement
• Grade I: Enlargement of interdental papilla
• Grade II: Enlargement of papilla and marginal gingiva
• Grade III: Enlargement covering three quarters or more of the crown
New Clinical Index For Gingival Overgrowth [Eva Ingles 1999]
Grade 0:
• No overgrowth; firm adaptation of the attached gingiva to the underlying bone. Slight granular appearance
& a knife edged papilla present toward the occlusal surface with increase size of gingiva
Grade 1:
• Early overgrowth as evidenced by an increase in density of gingiva with marked stippling & granular
appearance.
• The tip of the papilla is rounded & probing depth is </= 3mm
Grade 2:
• Moderate overgrowth, manifested by an increase in size of papilla & rolled margins.
• The contour is still concave or straight with buccolingual dimension of up to 2mm. The papilla is retractable
Grade 3 :
• Marked overgrowth, represented by encroachment of gingiva onto the clinical crown.
• The contour is convex with buccolingual dimension of 3mm or more.
• The probing depth is > 6mm & the papilla is clearly retractable
Grade 4:
• Severe overgrowth, characterized by a profound thickening of gingiva with a large percentage of the
clinical crown covered. The papilla is retractable & the probing depth is > 6 mm & bucco lingual dimension is
approximately 3mm
 Consistency
• Normal consistency of the gingiva is firm and resilient due to:
1. Collagenous nature of the lamina propria; and
2. Contiguity with the mucoperiosteum of the alveolar bone.
It is checked with the help of blunt end of the Instrument.
• In gingivitis the consistency maybe soft and edematous due to edema, inflammatory cell infiltration and degeneration
of connective tissue elements.
• Since gingivitis is a chronic inflammatory condition the outer wall may show repair in the form of increased fibrosis
and keratinization. In these cases the gingiva appears pale pink and firm in consistency though the inner lining of the
sulcus is still atrophic or ulcerated. Here the presence of bleeding on probing helps us arrive at the diagnosis of
gingivitis irrespective of outer changes in color or consistency.
 Contour
• The contour of the gingiva is scalloped with knife edge margins.
• Gingival contour depends upon the following factors:
1. Shape of the teeth
2. Alignment of the teeth in the arch
3. Proximal contact
4. Dimension of gingival embrasure
• Contour is accentuated in labially placed teeth and the gingiva is thickened in lingually placed teeth. Besides these physiologic variations in
contour, in areas of diastema the interdental papilla is missing and the gingiva is firmly adherent to the underlying bone.
• Normal gingiva follows scalloped outline. Accentuated scalloped outline where recession is present.
• In gingivitis the knife edge is lost. The marginal gingiva is rounded and the interdental papilla is blunt.
Other inflammatory changes include:
• Stillman’s cleft is an apostrophe shaped area of recession or triangular indentation on the gingival margin.
• McCall’s festoon is a thickened band of gingiva or life preserver shaped enlargement of the gingiva most commonly in the cuspid region. These
lesions were earlier attributed to traumatic occlusion but are now known to be due to inflammation.
 Surface texture

• The attached gingiva and central portion of the interdental papilla show an
orange peel appearance called stippling. This is best visualized by drying the
gingiva. Stippling appears by 5 years of age and disappears again in old age.
• Cause of stippling: alternate rounded protuberances and depressions in the
gingival surface due to the projection of the connective tissue papilla into
the epithelium.
• Function of stippling: functional adaptation of the gingiva.
• Stippling is reduced in inflammation and increased in drug induced gingival
enlargement
 Position

• The normal position of the gingival margin is 1mm above the

cementoenamel junction.
• When the level of the gingival margin is below the CEJ it is called recession.
It is defined as the exposure of the root surface due to apical migration of
the gingival margin.
Classifications of recession:
1. Sullivan and Atkins, 1968
• Shallow, narrow
• Shallow, wide
• Deep, narrow
• Deep, wide
2. PD Miller, 1985
• Class I: Marginal tissue recession not extending beyond the mucogingival junction. There is no loss of
interdental bone or soft tissue.
• Class II: Marginal tissue recession extends to or beyond the mucogingival junction. There is no loss of
interdental bone or soft tissue.
• Class III: Marginal tissue recession extends to or beyond the mucogingival junction. There is loss of
interdental bone and soft tissue or tooth malposition
• Class IV: Marginal tissue recession extends to or beyond the mucogingival junction. There is severe
interdental bone and soft tissue loss or severe tooth malposition.
Cause of recession:
• 1. Ageing
• 2. Improper brushing habits – horizontal technique, use of toothpowder or using a hard
bristled brush
• 3. Inflammation
• 4. High frenal attachment
• 5. Labially placed teeth
• 6. Congenital defects such as thin bone margins and dehiscence.
• 7. Pressure from denture clasps
• 8. Pressure from orthodontic bands
• 9. Following periodontal surgery
• 10. Overhanging restorations
• Width of Attached gingiva
Definition: It is the distance between MGJ and the projection on the external surface of the bottom of the gingival sulcus or the periodontal pocket.

Width of keratinized gingiva= Attached gingiva + Marginal gingiva

• Width of attached gingiva=Total width of Gingiva from the margin to the MGJ - Pocket depth

Methods of determination:
• Tension test (when stretching of lip or cheek induces movement of the free gingival margin, gingiva is considered inadequate).
• Pushing adjacent mucosa coronally with a dull instrument.
• Painting mucosa with Schiller’s Potassium Iodine solution.

• In maxillary anteriors: 3.5 - 4.5 mm

• mandibular anteriors: 3.3 – 3.9 mm
• In premolars (maxillary): 1.9 mm
• In premolars (mandibular): 1.8 mm
Tension test
• Application of tension at the MGJn by retracting cheek, lip & tongue (upwards, outwards & downwards) to tighten alveolar mucosa and test for the
presence of attached gingiva.
• Area of missing attached gingiva is revealed when alveolar mucosa and frenum are connected directly to free gingiva.

PURPOSE:
• To detect adequacy of AG
• To locate frenal attachment and their proximity to free gingiva
• To identify MGJn
PROCEDURE:
• Facial: Retract cheeks and lips laterally away . Watch MGJn. Move the lips up, down and across, creating tension at MGJn.
• Lingual: Hold mouth mirror to tense mucosa of floor of mouth, gently retract side of tongue so MGJn is clearly visible.
OBSERVATIONS:
• Blanching at MGJn
• Frenal attachment
• Recession
• Movement of free gingival margin; AG
Amount of attached gingiva
• This is the distance from the projection on the external surface of the bottom of gingival sulcus or pocket to the mucogingival
junction. Keratinized gingiva includes marginal gingiva.
• Assessing width of attached gingiva
• Determined by subtracting the sulcus pocket depth from the total width of gingival (gingival margin to mucogingival line)
Tension test
• Kopczyk RA (1974); Glickman (1964)
Purpose
• To detect adequacy of width of attached gingiva
• Locate frenal attachment and their proximity to the free gingiva
• To identify promptly the mucogingival junction
• Procedure
Facial
• Retract cheeks and lips laterally by grasping the lips with thumb and index finger, watch at the mucogingival junction.
• Move the lips and cheeks up and down and across, creating tension at the mucogingival junction
Lingual
• Hold the mouth mirror to tense the mucosa of the floor of the mouth, gently retracting the side of the tongue, so that the
mucogingival junction is clearly visible.
• Request the patient to move the tongue to left, right, up to touch the palate.
Observation
• Blanching at mucogingival junction
Frenal attachments
• Areas of apparent recession where there is very little keratinized gingiva and the base of the sulcus or pocket is near the mucogingival junction
• Areas where color, size, loss of slipping, smooth shininess or other characteristic indicates need or careful probing to determine amount of
attached gingiva.
• Area where tension pulls the free gingiva from the tooth, indicating no attached gingiva.
• Frenal attachment has been described by Placek. M, Skach M, Mrklas L (1974)
• Mucosal attachment – refers to the attachment of the frenum to the mucogingival junction
• Gingival attachment – refers to the attachment of the frenum within the attached gingiva
• Papillary attachment – refers to the attachment of the frenum within the papilla
• Papilla penetrating attachment – refers to an attachment of the frenum passing through the papilla while inserting into the attached gingiva
(of the palate)
• Pull syndrome Placek et al (1974)
Detaching movement of marginal gingiva transferred from the lip by the frenum has been termed pull syndrome.
 Bleeding on probing
: Bleeding on probing is an objective sign indicating periodontal disease.
Other signs such as changes in color or consistency are subjective and might be interpreted differently by
different examiners.
The presence of bleeding on probing and exudation indicate that the disease is active.
Absence of bleeding on probing is a good prognostic indicator as it correlates with periodontal stabiltiy.
Method to check for bleeding on probing: Running the probe. It might take 30 to 60 seconds for the bleeding to
become apparent.
Reduced bleeding on probing: Smokers
Local Chronic Chronic gingivitis and periodontitis

Acute ANUG
Injuries: Mechanical, chemical and
thermal
Systemic Bleeding disorders Hemophilia, Christmas disease,
Thromocytopenia, Leukemia
Hypoprothrombinemia, Scurvy,

Hormonal changes Pregnancy, puberty, patients on oral

contraceptives, diabetes mellitus

Medications Salicylates (aspirin) and

anticoagulants (heparin, warfarin)
Exudation

• Certain changes are observed in the sulcular epithelium due to chronic inflammation. Neutrophils enter the epithelium from
the connective tissue and release hydrolytic enzymes which kill bacteria and degrade the adjacent epithelial cells as well. On
applying digital pressure on the lateral aspect of the gingival margin the pus consisting of dead and live Neutrophils, dead and
live bacteria and desquamated epithelial cells is expressed as an exudate. Therefore, this exudate does not correlate with the
pocket depth but is merely a lateral wall change which indicates that the disease is active.
Abcess
• An abscess is a localized accumulation of pus. It is different from exudation as it is well contained.
• Classifications:
• 1. Single or multiple. Multiple periodontal abscess is common in diabetics.
• 2. Occurring in the supporting tissues or occurring in the gingiva
Classification by Meng, 1999
• Gingival abscess: In previously healthy sites and caused by impaction of foreign bodies.
• Periodontal abscess: In relation to a periodontal pocket, either acute or chronic.
• Pericoronal abscess: In relation to an incompletely erupted tooth.
Differences between acute and chronic abscess
are:

Acute Chronic
Appears as an ovoid swelling and the gingiva is Presents a sinus opening
red, edematous, smooth and shiny
Accompanied by throbbing pain, tenderness Usually asymptomatic. There might be dull,
on palpation, tooth mobility, enlarged lymph gnawing pain.
nodes, fever and malaise.
Differences between gingival and periodontal
abscess
Gingival
Limited to marginal gingiva and interdental papilla
Caused by bacteria being carried deep into the tissues
when a foreign substance like a toothbrush bristles is
forcefully embedded in the gingiva
Periodontal
Usually involves attached gingiva
Caused due to the localization of inflammation because of
one of the underlying resons:
1. Extension of infection to lateral wall of pocket
2. Extension of infection deep into the supporting
periodontal tissues.
3. In the deep end of a spiral or complex pocket
4. Incomplete removal of calculus leads to shrinkage of the
gingival wall and occludes the opening of the pocket.
5. Due to perforation through the root during endodontic
therapy
Differences between periodontal and periapical
abscess

Periodontal Periapical
Periodontal pocket is present Caries is present
Tooth is vital Tooth is non-vital
Pain is usually dull and localized (easy to Pain is severe and difficult to localize (difficult to
localize due to the presence of tactile fibers in localize as pulp basically consists of only pain
the periodontal ligament) perceiving fibers)
Tender on lateral percussion Tender on vertical percussion
Usually not visible on the radiograph Appears as a periapical radiolucency
 Periodontal examination

• Periodontitis is defined as an inflammatory disease of the 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 pocket
formation, recession, or both.
• Periodontal pocket
• Definition: The periodontal pocket is defined as a pathologically deepened gingival sulcus.
• Method to check for pocket: Walking the probe. Probing should be done using a standard
force of 25 grams (Armitage et al 1977). The probing force applied is equivalent to the
capillary pressure.
 Classification:
Based on involvement of supporting periodontal tissue
Gingival (Pseudopocket) Periodontal pocket
No loss of supporting tissue, pocket is formed due to There is loss of supporting periodontal tissues
gingival enlargement and coronal migration of the
gingival margin

Based on surfaces involved

Simple Compound Complex/ Spiral

Pocket involves only one surface Pocket involves more Pocket starts on one surface, follows
than one surface a tortuous course to involve another
tooth surface

Based on relationship with bone

Suprabony (supracrestal/ supraalveolar) Infrabony (subcrestal/ intraalveolar)
Base of the pocket is coronal to the crest of the alveolar Base of the pocket is apical to the crest of the alveolar bone
bone

Horizontal bone loss Angular bone loss

Interproximally, transseptal fibers are arranged Interproximally, transseptal fibers are arranged obliquely
horizontally

Facially and lingually, periodontal ligament fibers follow Facially and lingually, periodontal ligament fibers follow an
a horizontal course angular course
• Clinical features associated with a pocket:
• 1. Bluish red marginal gingiva
• 2. Rolled edge separating gingival margin from the tooth surface
• 3. Gingival bleeding
• 4. Suppuration
• 5. Tooth mobility
• 6. Diastema formation or extruded teeth
• 7. Pain deep in the bone
Level of attachment and pocket depth:
• Pocket depth is measured from the gingival margin to the base of the
pocket whereas level of attachment is from the CEJ the base of pocket. It is
more reliable to assess level of attachment as it is from a fixed point (CEJ).
The gingival margin might move coronally due to inflammation and then
apically once the inflammation subsides.
Dimensions of the periodontal probe:
• Different shapes and sizes of periodontal probes yield different penetration depths into periodontal tissues. Periodontal probes
with a point diameter of 0.4-0.5 mm have been used successfully. Most probes are circular in cross-section. The probe should be
thin enough to reach the “true” attachment level under healthy conditions, with JE and “resistant” connective tissue, but will
penetrate the less resistant, inflamed connective tissue in diseased pockets and over-estimate loss by 0.5-1.0 mm. A thicker
periodontal probe will not reach the true attachment level. A thin blade-shaped probe will give the most accurate result, but to
access all the sites, it has to be able to be rotated 360º (Axelsson, 1982).

• Probing force
• 0.75N of probing force has been found to be well tolerated and accurate.
• Probing forces:
• The probe is inserted along the long axis of the tooth into the pocket with gentle (approximately 25 g) force until resistance is
met. 25-g of force is necessary to indent the pad of the thumb about 1-2 mm. In clinical application, what would be considered
“gentle” insertion force, do not penetrate apical termination of JE. According to some authors, forces of 0.75 N have been well
tolerated & accurate [Van der Velden, 1979]. The tip of the probe has been assumed to identify the level of the most apical cells of
the dentogingival epithelium. This, however, is not the case always (Saglie et al, 1975; Polson, 1980).

• Probe penetration depends on tissue inflammation. In health, probe tip penetrates most coronal intact fibres of connective tissue
attachment (0.3 mm) into JE [Listgarten et al, 1976]. There may be over-estimation (probe may penetrate beyond apical
termination of dentogingival epithelium due to inflammation) or under-estimation (reduction in inflammation after successful
therapy with concomitant deposition of new collagen prevents complete penetration of probe) of the true pocket.
• Probing technique

• The probe is inserted parallel to vertical axis of tooth and ‘walked’ circumferentially around each surface of each tooth to detect
the areas of deepest penetration.
• To detect interdental crater the probe should be placed obliquely from facial and lingual surfaces to explore the deepest
point of the pocket located beneath the contact point
• Probing technique:
• Probe is to be placed parallel to vertical axis of tooth and “walked” circumferentially around each surface.
• Gutta percha points or calibrated silver points with radiographs can also be used.
• In clinical practice, conventional periodontal probes are widely used to obtain two important measurements: probing
depth (PD) and clinical attachment loss (CAL).

• PD is defined as the distance from the gingival margin to the base of the probeable crevice.

• Probing depth measurements are clinically important since they provide a useful overall assessment of the depth of
periodontal pockets which are the principal habitats of periodontal pathogens.
• In addition, PD measurements can be rapidly recorded and give a good assessment of the distribution of periodontal
problems within a given patient. They are an essential component of a complete periodontal examination
• Positioning of the probe:
Manual probing is subject to measurement error because of variations in the angulation and site of insertion of the probe
and because of the difficulty in obtaining a fixed landmark as a reference point.
The probe should be kept as parallel as possible to the long axis of the root.
The tip should continuously follow the root surface, to prevent penetration of the pocket epithelium and connective tissue,
resulting in underestimation of attachment loss.
Each tooth is examined at 6 locations: MB, B, DB, DL, L, and ML. The probe may be angled approx. 10º in interproximal
areas.
Level of attachment
Clinical attachment level – the level of attachment is the distance between the base of the pocket and the cemento-enamel
junction.
Determining the level of attachment
• When gingival margin is located on the anatomic crown, the level of attachment is determined by subtracting from
depth of the pocket the distance from gingival margin to the cemento-enamel junction. If both are same loss of
attachment is 0.
• When the gingival margin coincides with the cemento-enamel junction, the loss of attachment equals the pocket depth.
• When gingival margin is located apical to the cemento-enamel junction, the loss of attachment will be greater then
pocket depth, therefore the distance from cemento-enamel junction to gingival margin should be added to the pocket
depth.
• Vertical probing attachment loss (PAL)/Clinical attachment loss (CAL):
• CAL is the distance from the cementoenamel junction to the base of the probeable crevice.

Gingival margin is located on anatomic crown: CAL= PD – (gingival margin to CEJ)

Gingival margin coincides with CEJ:CAL=PD
Gingival margin is located apical to CEJ, i.e. recession: CAL= PD + (gingival margin to CEJ)
• In single-rooted teeth, LOA occurs only vertically. In multirooted teeth, loss of attachment can
also occur horizontally, indicating furcation involvement.

• Changes in CAL can be due only to gain or loss of attachment & afford a greater/better indication
of the degree of periodontal destruction. Shallow pockets attached at the apical third of root are
more destructive than deep pockets attached at the middle third of root.

• CAL assessments are more difficult to accurately measure, but they give a better overall estimate
of the amount of damage to the periodontium than do PD measurements. In prospective studies,
CAL measurements are the most valid method of assessing treatment outcomes.

• Probing depth as well as loss of attachment (LOA) can be measured by manual probing or by more
sophisticated, automated, computer-linked, pressure-sensitive periodontal probes.
Alveolar bone loss
The alveolar bone levels are evaluated by clinical and radiographic examination.
• Transgingival probing (sounding) helps to provide information of bone architecture. Area is anaestheitized the probe
should be walked along the tooth-tissue interface so that the operator can feel the bony topography. The probe can
also be passed horizontally through tissue to provide more three dimensional information (thickness, height, shape).
Radiographic evaluation
• Access
• Bone condition
• Tooth condition
• Root anatomy

BONE SOUNDING/TRANSGINIVAL PROBING:

• In order to arrive at a correct diagnosis with respect to the alveolar bone level, presence of angular bony defects and
interdental osseous craters, etc, “sounding” may be done.
Procedure:
• Local anaesthesia
• Tip of probe is inserted into the pocket and forced through supraalveolar connective tissue to make contact with the
bone and the distance from CEJ to bone level is assessed.
 Hard Tissue examinations

• Number of teeth present

• Caries/decayed
• Missing
• Filled
• Stains/ deposits
• Wasting disease - Attrition/ erosion/ abfraction
• Occlusion
 Teeth present
• Various nomenclature systems are used as follows:

• Zsingmondy’s and palmar method: 87654321 12345678

87654321 12345678

• Universal system: 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
32 3130 29 28 27 26 25 24 23 22 21 20 19 18 17
• FDI system: two digit system :
18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28
48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38
• Stains and calculus:

• + - satins and calculus involving only cervical portions of tteth

• ++ - stains and calculus extending upto middle third of the tooth
• +++ - stains and calculus involving more than two third or involving whole of
the facial or lingual surface
Classification intrinsic and extrinsic
• Occlusion –type of angles malocclusion should be mentioned here.
• Caries/decayed ,
• missing tooth
• filled tooth
 Wasting diseases of teeth
• Wasting is defined as any gradual loss of tooth substance characterized by the
formation of smooth, polished surfaces, without regard to the possible
mechanism of this loss.
• The most systematic classification is given by Grippo, who define four
categories of wasting of tooth i.e.
• Attrision-
• Abrasion
• Erosion-Also called corrosion, erosion is a sharply defined, wedge-shaped
depression in the cervical area of the facial tooth surface."
• Abfraction
• Attrition. Attrition is occlusal wear resulting from functional contacts with
opposing teeth. Such physical wear patterns may occur on incisal, occlusal,
and approximal tooth surfaces.
• Occlusal or incisal surfaces worn by attrition are called facets.
• shiny, smooth, and curviplanar facets are usually the best indicator of
ongoing frictional activity.
• If dentin is exposed, a yellowish brown discoloration is frequently present
• Abrasion. Abrasion refers to the loss of tooth substance induced by mechanical wear other
than that of mastication.
• Abrasion results in saucer-shaped or wedge-shaped indentations with a smooth, shiny
surface. Abrasion starts on exposed cemental surfaces rather than on the enamel and
extends to involve the dentin of the root.
• A sharp “ ditching" around the cementoenamel junction appears of to the soft cemental
surface compared with the hard enamel surface.
• Toothbrushing with an abrasive dentifrice and the action of clasps are common causes of
abrasion; brushing is the much more prevalent cause'‘
• abrasion of the incisal edges results from habits such as holding objects (e.g., bobby pin,
tacks) between the teeth.
• Erosion-Also called corrosion, erosion is a sharply defined, wedge-shaped
depression in the cervical area of the facial tooth surface.
• The surfaces are smooth, hard, and polished.
• In the early stages, it may he confined to the enamel, but it generally
extends to involve the underlying dentin as well as the cementum.
• the etiology of erosion is not known. Suggested causes include
decalcification by acidic beverages' or citrus fruits and the combined effect
of acid salivary secretion and friction.
• Abfraction. A recently studied mechanism of tooth wear, abfraction results
from occlusal loading surfaces causing tooth flexure and mechanical
microfractures and tooth substance loss in the cervical area.`
Clinical pictures of attrision abrasion and
erosion
FOOD IMPACTION:
• Is the forceful wedging of food into the periodontium by occlusal forces.
It can be vertical and horizontal.
• Vertical- open contact & Contour of occlusal surface
(due to marginal ridges & grooves):
• as teeth wear down- flat surface- wedging effect of opposing cusp.
• Plunger cusp: Cusp that tend to forcibly wedge into interproximal embrasures.

• Horizontal or lateral food impaction- in caes of enlarged gingival embrasure

• lateral pressure from lips, cheeks and tongue: forces food interproximal
causing lateral food impaction.
Classification of Factors Causing Food Impaction: (Hirschfeld 1930)5
Class I: Occlusal wear
Class II: Loss of proximal contact
Class III: Extrusion beyond the occlusal plane
Class IV: Congenital morphological abnormality
Class V: Improperly constructed restorations

• Interdental bone defects: Pressure & irritation from food impaction contribute to inverted bone
architecture.
Sequelae of food impaction:
• Feeling of pressure & urge to dig
• Vague pain that radiated deep in the jaws
• Gingival inflammation
• Bleeding
• Foul taste
• Gingival recession
• Abscess formation
• Sensitivity to percussion
• Destruction of alveolar bone
• Root caries
Proximal Contacts

Normal proximal contacts do not allow any food impaction in between the teeth.
The interdental papilla fills the space up to tooth contact in normal conditions. However due to periodontal disease
there is loss of interdental soft tissue and bone levels.
Due to this, the position of interdental papilla recedes from its normal position.

Classification according to Nordland and Tarnow (1998):

Normal: The interdental papilla occupies the entire embrassure space apical to the interdental contact
point / area.
Class I: The tip of the interdental papilla is located between the interdental contact point and the level of
the CEJ on the proximal surface of the tooth.
Class II: The tip of the interdental papilla is located at or apical to the level of the CEJ on the proximal
surface of the tooth but coronal to the level of the CEJ midbuccally.
Class III: The tip of the interdental papilla is located at or apical to the level of CEJ midbuccally.
Classification of interdental embrasures, by Perry and Schmid (1996)
• Type I embrasure: The gingival papilla fills up the embrasure space
completely.
• Type II embrasure: The gingival papilla partially fills the embrasure space
due to papillary recession.
• Type III embrasure: The embrasure space is not filled. The gingival papilla
has receded extensively or it is completely lost.
Pathologic migration
• Definition: Tooth displacement that results when the balance among the factors that maintain
physiologic tooth position are disturbed by periodontal disease.
• It should be differentiated from physiologic migration or drifting. Due to proximal and occlusal
wear the tooth moves occlusally and mesially throughout life, this shortens the arch by around
0.6cm from midline to third molar by the age of 40. This is called physiologic migration.When it
occurs in the occlusal direction it is termed extrusion.
• it may be present as extrusion,facial flaring,rotation diastema and drifting of affected teeth, mostly
show combined form.

Causes:
1. Weakened periodontal support
2. Pressure from granulation tissue
3. Trauma from occlusion
4. Tongue thrusting
TRAUMA FROM OCCLUSION:
Definition: When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. The resultant injury is termed TFO.

Types: Primary and Secondary

Clinical features:

• Excessive tooth mobility; pain

• Infrabony pockets
• Pathologic migration
• Gingival recession
• Stillman’s cleft/McCall’s festoon
• Food impaction
• Wearing of teeth & appearance of facets
• Hypersensitivity of teeth
• Tenderness of TMJ & muscles of mastication
• Smudging of articulating paper
• Dull percussion note
• Vibrations from fremitus

Radiographic features:
• Widening of PDL space
• Lamina dura thickened
• Vertical/ angular bony destruction
• Radioluscence & condensation of alveolar bone
• Buttressing bone
• Root resorption
Methods of determination:
Fremitus test:
It is the measurement of the vibratory pattern of the teeth when the teeth are placed in the contacting positions and movements are made.
To measure fremitus, dampened ungloved index finger is placed along the buccal and labial surfaces of maxillary teeth (or the tooth in question) & the patient is asked to tap
the teeth together in maximum intercuspation (CO) & grind systematically in the lateral excursive movements (lateral fremitus). Vibrations are perceived. It is easier to detect
fremitus in the maxillary teeth than the mandibular teeth.

By Ingreval
Class I fremitus: Mild vibrations or movements detected
Class II fremitus: Easily palpable vibrations but no movements detected
Class III fremitus: Movements visible with naked eye

Occlusal registration strips/articulating paper

Auditory test: In centric relation, there is a distinct ringing sound during tooth contact. But in TFO, with deflection present, sound is dull and imperceptible

Fremitus
Fremitus means the palpable vibration or movement, in dentistry it refers to the vibratory patterns of the teeth.

Procedure
Seat the patient up right and head stabilized against headrest index finger is firmly placed over the cervical third each maxillary tooth in succession starting with most
posterior tooth on one side and moving around the arch patient is requested to click the posterior tooth.
Record by tooth number where vibration is felt and the teeth where actual movement is noted

N = normal (no vibration)

+ = one degree fremitus
Only slight vibration can be felt
++ = two degree fremitus
Tooth is clearly palpable but movement is barely visible.
+++ = Three degree fremitus
Movement is clearly observed visually

Significance
Tooth with fremitus has excess contact, premature contact.
Well distributed posterior contact
Coupled contacts between opposing teeth
Smooth excursive movement without interfere
TOOTH MOBILITY:
• The movement of a tooth in its socket as a result of an externally applied force. Tooth mobility is seen as one of the
measures useful in evaluatinvalue depends on the observers’s skill and experience.

Causes:
g the health of the periodontal tissues (Prichard, 1979). The most common clinical method used to examine tooth mobility is
to press the tooth in a horizontal or vertical direction with a finger, or with the handle of the blunt ends of two metal
instruments (Prichard, 1979). This method is imprecise and its Local Factors:
• Bone loss/loss of tooth support (periodontitis, TFO, endodontic problems)
• Hypofuction
• Periapical pathology, cysts or tumors
• After periodontal therapy [Nyman & Lindhe (1976), Persson (1981)]
• Orthodontic forces; heavy fuctional loads (from prosthetic appliances)
• Parafunctional habits (bruxism, clenching)
• Pathologies (tumours, cysts, osteomyelitis)
• Traumatic injuries to dentoalveolar unit
• Tooth morphology
Systemic causes:
• Age: progressively increases
• Sex & Race: females>males; Negroes more
• Menstrual cycle: Friedman (1972) observed increased horizontal tooth mobility during 4th week of menstrual cycle.
• Oral contraceptives (Dorothy, 1981)
• Stress
• Nutritional deficiency
• Pregnancy (Mobility increases from 2nd to 8th month progressively)
• Circadian rhythm (more during early morning & progressively decreases)
•
• Tooth mobility indices:
• Miller’s index (1938)
• I: first distinguishable sign of movement
• II: movt. of tooth which allows crown to deviate within 1mm of its normal position
• III: easily noticeable & allows tooth to move more than 1 mm in any direction or to be rotated
or depressed in the socket

• Modified Miller’s index

• Scores: 0, ½, 1, 1½, 2½, 3 are utilized
•
Prichard’s index (1972)
• 1: Slight mobility
• 2: Moderate mobility
• 3: Extensive mobility in a lateral or M-D direction combined with vertical displacement in
alveolus
• 4: Signs can be used for added refinement
•
Tooth mobility measuring devices:
• Periodentometer (Muhleman, 1951)
• Persson & Svenson’s devices (1980)
• Periotest (Schultz, 1987) [It helps in objective assessment of tooth mobility. The tooth is rapidly percussed 16
times (four times per second) and then the rebound attenuation patterns emanating from the tooth are
electronically recorded].
Values are calculated as:
• -8 to +9: Clinically firm teeth
• 10 to 19: Palpable mobility
• 20 to 29: Visible mobility
• 30 to 50: mobility in response to lip and tongue pressure
Periodontal pulse
• The three-dimensional physiological tooth movement synchronized with the heartbeat is called periodontal
pulsation (Diemer, 1963, 1966; Körber, 1971a,b; Igarashi et al., 1981). It is produced by changes in the calibre of
periodontal vessels due to cardiac pulsation. It has been suggested that the degree of periodontal pulsation
reflects the condition of the microcirculation and the pathophysiological properties of the periodontal tissues
(Hofmann and Diemer, 1966; Körber, 1971a). The measuring device consisted of a small magnet attached to the
tooth and an amorphous sensor that was used to detect displacement of the tooth without actually contacting
it.
Wasserman’s index (1973)
• 1: Normal
• 2: Slight mobility less than 1mm of buccolingual movement
• 3: Moderate upto 2 mm of buccolingual movement
• 4: Severe mobility more than 2 mm movement

Glickman’s index (1972)

• Normal mobility
• Pathologic mobility
Grade I: Slightly more than normal
Grade II: moderately more than normal
Grade III: severe mobility with vertical displacement

The clinical importance of increased tooth mobility is frequently overestimated. It has clearly been shown in animal experiments
that, if plaque-induced inflammation is controlled, increased tooth mobility has no effect on the level of the connective tissue
attachment (Ericson and Lindhe, 1977). Hypermobility of tooth does not necessarily mean that it has a poor prognosis, and the
mobility frequently persists after successful periodontal treatment (Lindhe and Nyman, 1975, 1984). Nevertheless, increasing
tooth mobility over time should alert the clinician to a possible deterioration of periodontal support, and such teeth require
careful evaluation for loss of clinical attachment.
• All teeth have a slight degree of physiologic mobility, which varies for different teeth and at different
times of the day. Mobility is greatest on arising in the morning and progressively decreases. During
the waking hours, mobility is reduced by chewing and swallowing forces, which intrude the teeth in
the sockets.
• Single-rooted teeth have more mobility than multi-rooted teeth; incisors have the most
mobility. Mobility is principally in a horizontal direction.
• Tooth mobility occurs in the following two stages:-
• 1) In the initial stage the tooth moves within the confines of the periodontal ligament (PDL). This
is associated with viscoelastic distortion of the PDL and redistribution of the periodontal fluids,
interbundle content, and fiberes. This initial movement occurs with forces of about 100g and is about
0.05 to 0.10mm (50-100µm).
• 2) The secondary stage occurs gradually and entails elastic deformation of the alveolar bone in
response to increased horizontal forces.
• When a force such as that applied to teeth in occlusion is discontinued, the teeth return to
their original position.
Furcation involvement
• Definition: Furcation involvement is the invasion of bifurcation and trifurcation of teeth by periodontal disease.
• Method to check for furcation involvement: A curved probe called Nabers probe is used.
Classification:
• Based on horizontal measurement of bone loss, Glickman’s classification, 1953
• Grade I: Incipient involvement which is felt as a catch with the probe.
• Grade II: There is partial loss of bone. Here the probe penetrates partially but does not pass through and
through. There maybe involvement from both sides but these are not connected since some amount of bone is
still remaining. This is called “cul de sac” which means dead end.
• Grade III: The bone loss is through and through.
• Grade IV: Along with through and through bone loss there is gingival recession leading to the furcation area
becoming clinically visible.

Based on vertical measurement of bone loss, Tarnow and Fletcher, 1984

• Subclass A: Bone loss is 0 – 3mm
• Subclass B: Bone loss is 4 – 7mm
• Subclass C: Bone loss is greater >7mm
• According to hamp et al 1975
• Degree1-horizontal loss of periodontal support not exceeding 1/3 rd
of the
width of the tooth
• Degree2 –horizontal loss of periodontal support exceeding1/3 rd
of the width of
the tooth
• Degree3- horizontal through and through destruction of periodontal tissue in
the furcation area.
Predisposing factors for furcation involvement are:
1. Short root trunk: Less attachment loss is required for furcation to be involved.
2. Trauma from occlusion: In multi-rooted teeth the axis of rotation is located in the bone
between the roots. Therefore, the bone loss in relation to increased forces on these teeth
would be in the furcation region.
3. Cervical enamel projections: These are flat ectopic extensions of enamel that extend
beyond the normal contours of the cementoenamel junction.
Development: During root formation the Hertwig’s epithelial root sheath disintegrates to
allow the dental follicle cells to come in contact with the root dentin and lay down
cementum. In areas where the root sheath has failed to disintegrate the dental follicular
cells are unable to come in contact with the dentin. The root sheath cells, which are basically
the reduced enamel epithelium, lay down enamel.
Significance: The Sharpey’s fibers of the periodontal ligament insert to cementum on one
side and to bone on the other. Therefore, in areas of cervical enamel projections there is no
attachment of the periodontal ligament fibers thereby allowing easy spread of periodontal
disease into the furcation area.
Classification by Masters and Hoskins, 1964:
Grade I: CEP extends towards the furcation entrance
Grade II: CEP approaches the furcation entrance
Grade III: CEP extends into the furcation

• 4. Enamel pearls: These are large, round deposits of enamel that can be located
anywhere on the root. They are plaque retentive areas which when present
near the furcation area can predispose the tooth to furcation involvement
• 5. Accessory pulpal canals: May extend the pulpal inflammation to the
furcation.
 EXAMINATION OF RESIDUAL RIDGE

• Seibert’s Classification:

• Class I: loss of facio- lingual width, with normal apico- coronal height

• Class II: loss of ridge height with normal width

• Class III: loss of both height & width

 STUDY MODELS

• Visual aids in discussions

• To study occlusion
• Position of the gingival margins
• Proximal contact relationships
• Splinting
• Preparation of acrylic plates
• Treatment planning
Clinical photograph
• Color photographs are useful for recording the appearance of the tissue
before and after treatment.
• Photographs cannot always be relied on for comparing subtle color changes in the
gingiva, but they do depict gingival morphologic changes.
• With the advent of digital clinical photography, record keeping for mucogingival
problems has become important (e.g. areas of gingival recession, frenum
involvement, papilla loss).
 RADIOGRAPHIC EXAMINATION

• Root length, root form, root proximity

• Estimates of remaining alveolar bone
• Osseous defects
• PDL space
• Lamina dura
• Periapical area
• Restorations, calculus
• Type and density of alveolar bone
• Anatomical landmarks
 RADIOGRAPHIC CHANGES IN
PERIODONTITIS

• Fuzziness or break in lamina dura

• Wedge shaped radioluscent areas on
crest
• Widening of periodontal ligament space
• Reduction in height of interdental septum
• Interdental craters - areas of reduced
opacity

112
• Furcation -
• radiographs at different angles
• Reduced radiodensity in
furcation Furcation involvment

• Marked bone loss adjacent to

single molar root
• Periodontal abscess –
• Radiolucency along lateral
aspect of tooth

Periodontal abscess
113
Intraoral radiographic survey
It requires full mouth intra-oral radiographic series – 14 periapical films; 4 bite wings.

Panoramic radiographs are a simple and convenient view of the dental arch and surrounding
structures. They are helpful in detecting developmental anomalies, pathologic lesion of teeth and jaws,
fractures and dental screening examination of large groups.

They provide information of overall radiographic picture of the distribution and severity of bone
destruction in periodontal disease but a complete intraoral series in required for periodontal disease
diagnosis and treatment planning.

RADIOGRAPHIC EXAMINATION:
The use of radiographic imaging as an aid in diagnosis and treatment of periodontal disease is widely
accepted.

The information supplied by radiographs includes:

Root length, root form, root proximity
Estimates of remaining alveolar bone
Osseous defects
PDL space
Lamina dura
Periapical area
Restorations, calculus
Type and density of alveolar bone
Anatomical landmarks
Types of imaging:
I] Conventional:
A] Intra-oral radiographs
• Periapical
• Bitewing
• Occlusal
Technique: Bisecting angle/ Paralleleing cone

B] Extra-oral radiographs
• Orthopantomogram and other extraoral views

II] Digital:
Specialized techniques:
Digital subtraction radiography (DSR)
• When two images of same object are registered and the image intensities of corresponding pixels are
subtracted, a uniform difference image will be obtained. If a change of follow-up image has occurred, it will
show up as a brighter area when the change represents the gain and as a darker area when the change
represents loss. Subtraction images allow detection of mineral changes of as little as 5 %.
Tuned aperture computed tomography (TACT)
• TACT is built on basic principles of tomosynthesis by shifting and combining a set of basis projections,
arbitrary slices through the object can be brought into focus. Each radiograph is taken from different angle
relative to the object and the receptor. It is shown to improve the ability of observers to detect osseous defects
around implants.
Computed Tomography (CT)
• CT provides exquisite 3-D views, however, its ability to show very small details remains limited. The application
of CT imaging for periodontal diagnosis appears to have an unfavorable cost-benefit ratio.
Computer-assisted densitometric image analysis (CADIA)
• Video camera measures the light transmitted through a radiograph, and the signals from the camera are
converted into gray-scale images. The camera is interfaced with an image processor and a computer that
allows storage and mathematical manipulation of the images
 LABORATORY INVESTIGATIONS
• Haemoglobin: Differentiate WBC count
• Males:14-18gm/dl
• Females:12-16gm/dl • polymorphs: 55 – 70% (adult)
• RBC count: • 49 – 65%
(children)
• Males: 4.6-6.2 millions/cumm
• Females: 4.2-5.4 • lymphocytes: 29 – 40% (adult)
millions/cumm • 30 – 60%
• WBC count: (children)
• 6000-11000 /cumm • Eosnophil: 1 – 6%
• Platelet Count: • Monocytes 2 – 10%
• 1,50,000-4,00,000/cumm • Basophils 0 – 1%
• ESR
• men: 4 -10 mm/hr • Glucose levels
• Women: 8 – 20 mm/hr • Fasting levels: 60-100 mg/dl
• Post prandial: <140 mg/dl
 Test Description Normal values Disease with increased
values

Bleeding Time Duke’s method and Ivy’s method. < 8 minutes Purpura, von Willebrand
Duke’s: Puncture finger tip/ ear lobe and measure the Disease
time until the bleeding stops.

Clotting Time Wright’s capillary tube method and Lee and White’s <10 minutes Deficiency of any
method. Wright’s: Puncture finger tip and collect blood procoagulant factor
in a capillary tube. At intervals break the tube and
check for a thread joining the two ends, this is the clot.

Prothrombin Time Deficiencies of extrinsic and common pathway can be < 16 seconds Deficiency of factors I, II, V,
detected VII, and X

Activated Partial Measures efficiency of intrinsic and common pathways < 40 seconds Deficiency of factors III, IX,
Thromboplastin Time and XI
Laboratory diagnosis
When the dentist detects unusual gingival or periodontal problems that cannot be explained by local causes, the possibility of contributing systemic factors must be explored. The signs and symptoms of
oral manifestations of systemic disease must be clearly understood ad analyzed and discussed with the patient’s physician.
LABORATORY INVESTIGATIONS
Haemoglobin
Males: 14-18gm/dl; Females: 12-16gm/dl
Significance: if reduced, hampers healing; risk of syncope
RBC count:
Males: 4.6-6.2 millions/cumm
Females: 4.2-5.4 millions/cumm

Decreased: anemia, dietary def., pregnancy, bone marrow failure, hodgkin’s disease, multiple myeloma, hemoglobinopathies, renal dis., collagen vascular dis.
Increased: COPD, CHD, polycythemia vera
WBC count:
6000-11000 /cumm
Decreased in: reduced defence
Increased in: infections, leukaemia

Platelet Count:
1,50,000-4,00,000/cumm
If less than 1 lakh/cumm: surgery cannot be done

Bleeding time:
Duke’s method: < 5 mins
Prolonged: thrombocytopenia, leukaemia, liver disease, drugs(NSAIDs,warfarin, streptokinase, anticoagulants), DIC, collagen vascular dis., connective tissue dis.

Clotting time:
• Capillary tube method: 1-7 min
• Kruse and Moses method: 2.5-5 mins
• Lee and White method: 5-10 mins
• Prolonged: Hemophilia, fibrinogen deficiency
Prothrombin time (PT):
• Quick Method: 10-20 s
• Deficiency of factor II, V, X
• Prolonged: Liver disease, fibrinogen deficiency, vit K def., DIC, massive transfusion
Activated partial thromboplastin time (APTT):
• 30-40 s
• Deficiency of factor II, V, VIII, IX, X, XI, XII
• Prolonged: cirrhosis, DIC, coumarin, heparin, vit K def., clotting factor deficiency
International Normalised Ratio (INR):
• It is used only to assess the control of oral anticoagulant treatment. It is the ratio of patient’s PT to a normal control based on an international reference thromboplastin which ensures standardization of
anticoagulation between different centers. INR should generally be less than 2.0. For simple surgical procedures, INR less than 2.5 is generally safe.
•
Glucose levels
• Fasting levels: 60-100 mg/dl
• Post prandial: <140 mg/dl
• Increased in Diabetes
• Significance: nutrient for bacterial growth, reduced healing

Glycated hemoglobin (HbA1c)

• 4-6%: Normal
• <7%: good diabetic control
• 7-8%: moderate diabetic control
• >8%: poor diabetic control (poor response to surgery)
BIOPSY
• It is the removal of tissue from the living organism for the purposes of microscopic examination & diagnosis.
TYPES:
• Excisional biopsy(total excision of lesion)
• Incisional biopsy (removal of small section of lesion)
• Needle aspiration (fine[FNAC]/thick bore)
• Exfoliative cytology(desquamative gingivitis, pemphigus, mucous membrane pemphigoid, lichen planus)
PUNCH BIOPSY
• 5mm disposable punches
• Cutting core of 3-4mm in depth
INCISIONAL BIOPSY
• No. 15 blade
BRUSH BIOPSY
• Special bristled instrument to retrieve cells from the spinous layer of epithelium when firmly rotated over the mucosal lesion.
• Technique
• Tissue should be perpendicularly incised with a scalpel
• Removed tissue should be handled carefully
• Lesion less than 1 cm-excisional biopsy
• Larger than 1 cm, suspicious-incisional biopsy
In clinically most suspected area
• Part of lesion and part of clinically healthy mucosa should be included in the biopsy
• In gingival biopsies, marginal and attached gingiva (effect of local irritants less likely to be present) should be included
Gingival biopsy and leukemia
• The existence of leukemia is sometimes revealed by a gingival biopsy to clarify the nature of a troublesome gingival condition and may indicate the extent of leukemic
infiltration. However, they are not sufficient to warrant routine gingival biopsy in such patients.
SUPPLEMENTAL DIAGNOSTIC TESTS
• Supplemental diagnostic tests can be used to perform two basic tasks. The first is screening, i.e., to separate diseased from non-diseased patients. The second is to detect sites
or patients undergoing the progression of periodontitis. The second task is more demanding than the first. It is also of greater importance since the clinician can easily separate
healthy from periodontitis patients based on customary clinical criteria.
 MICROBIOLOGICAL INVESTIGATION
• Bacterial culturing • Immunodiagnostic methods
• Direct microscopy • Indirect immunofluorescent assay
(IFA)
• Darkfield or Phase-contrast
microscopy • Direct immunofluorescent assay
(DIFA)
• Enzymatic methods • Membrane
• BANA test immunoassay(Evalusite)
• DNA probes • Flow cytometry /
• Restriction endonuclease Cytofluorography
analysis • ELISA

• Polymerase chain reaction • Latex agglutination

(PCR)
Presence of subgingival biofilms and high levels of specific periopathogens subgingivally:
The sole etiologic factor for periodontal disease is the microbial challenge, and a prerequisite for development of the diseased pocket and an active lesion is the presence of subgingival
periopathogens. Most of the subgingival microflora is attached to the root surface as plaque (biofilm), but the depths of the pocket also harbor many non-attaching, motile species, particularly
various sizes and forms of spirochetes.

In the biofilms, the microorganisms live in a well-organized symbiosis, supplied with nutrients via microchannels through the plaque matrix and inaccessible to phagocytozing leukocytes, chemical
plaque control agents, and antibiotics.

At 1996 World Workshop in Periodontics, it was concluded that human periodontitis is caused mainly by Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis (exogenous, transmissible
pathogens) and Bacteroides forsythus (endogenous, opportunistic pathogen). Recently, Machtei et al (1997) showed that, in deep periodontal pockets, high levels of B forsythus increase the risk for
further loss of periodontal attachment seven-fold. Other species of opportunistic endogenous periopathogens are Prevotella intermedia and Treponema denticola. The presence and levels of
subgingival periopathogens can be evaluated by subgingival sampling, with a sterile curette or paper point, and DNA probe analyses, conventional anaerobic culture techniques, or chairside tests.

Bacterial culturing
It has been frequently used as the reference method when determining the performance of a new detection method. It is the only current method capable of determining the invitro antimicrobial
susceptibility of periodontal pathogens. It can also provide a quantitative measurement of all major viable microorganisms in the specimen. It identifies only live microorganisms, therefore strict
sampling and transport conditions are essential. Some of the putative pathogens are fastidious and difficult to culture. The sensitivity of culture methods is rather low. It requires sophisticated
equipment, experienced personnel and is relatively time-consuming and expensive.

Direct microscopy
Darkfield or Phase-contrast microscopy has been suggested as an alternative to culture methods on the basis of its ability to directly and rapidly assess the morphology and motility of bacteria in
the sample. However, most of the putative periodontal pathogens (Aa, Pg, Bf, Ec) are nonmotile and therefore cannot be identified.

Immunodiagnostic methods
Immunodiagnostic methods employ antibodies that recognize specific bacterial antigens to detect target microorganism.
Advantages:
Do not require viable bacteria
Less susceptible to variation in sample processing
Less time consuming
Easier to perform (than culture)
Disdvantages:
Accuracy of immunodiagnostic tests depends greatly on the quality of the reagents used
Generally show poorer detection limits than DNA probe and PCR
Expensive
Indirect immunofluorescent assay (IFA):
It employs a secondary fluorescein-conjugated antibody that reacts with the primary antigen-antibody complex.

Direct immunofluorescent assay (DIFA):

It employs monoclonal and polyclonal antibodies conjugated to fluorescien marker that binds with bacterial antigen to form a fluorescent immunocomplex detectable under a
microscope.

Membrane immunoassay(Evalusite):
It is a commercially developed, antibody-based sandwich enzyme-linked immunosorbent assay fro detection of Aa, Pg, P intermedia. It involves linkage between the antigen and
membrane-bound antibody to form an immunocomplex that is later revealed through a colorimetric reaction. The sample wells are first coated with antibodies against antigens
specific for the target bacterial species. Antibody-antigen reactions are then detected by adding enzyme-linked antigen-specific antibodies to the sample wells, followed by the
addition of enzyme substrate.

Flow cytometry/Cytofluorography:
It is for rapid identification of oral bacteria and involves labeling bacterial cells from a patient plaque sample with both species-specific antibody and a second fluorecscein
conjugated antibody. The suspension is then introduced into the flow cytometer, which separates the bacterial cells into an almost single-cell suspension by means of a laminar
flow through a narrow tube. The sophistication and cost involved in this procedure precludes its wide usage.

ELISA:
It is similar to other radioimmunoassay in principle, but an enzymatically derived color reaction is substituted as the label in place of radioisotope. The intensity of colour depends
on the concentration of the antigen and is usually read photometrically for optimal quantification. It has been used to detect periodontopathogens.

Latex agglutination:
It is a very simple immunological assay based on the binding of protein to latex. Latex beads are coated with species-specific antibody, and when these beads come in contact
with the microbial cell surface antigens or antigen extracts, cross-linking occurs; its agglutination or clumping is visible usually in 2-5 mins. Because of their simplicity and rapidity,
these assay have great potential for chairside detection or periodontopathogens.

.
Enzymatic methods
BANA test
B forsythus, Pg, Treponema denticola and capnocytophaga species share a common enzymatic profile, since all have in common trypsin-like enzyme. The activity of this enztme can be measured
with the hydrolysis of the colour substrate N-bezoyl-dl-arginine-2-naphthylamide (BANA). When the hydrolysis takes place, it releases the chromophore, β-naphthylamide, which turns orange red
when a drop of fast granet is added to the solution.
Diagnostic kits have been developed using this reaction (e.g. Perioscan).
BANA test can serve as a marker of disease activity. Loesche et al showed that shallow pockets exhibited only 10% positive BANA reactions, while deep pockets (>7mm) exhibited 80-90% positive
BANA tests. Beck et al used BANA as a risk indicator for periodontal attachment loss.
However, it detects a very limited number of pathogens.

DNA probes:
DNA probes entail segments of single-stranded nucleic acid, labeled with an enzyme or radioisotope that can locate and bind to their complementary nucleic acid sequences with low cross-
reactivity to target organisms. The assay can rapidly test for multiple bacteria, including Aa, Pg, B intermedius, C rectus, E corrodens, F nucleatum, and T denticola.

Restriction endonuclease analysis

Restriction endonucleases recognize and cleave double-stranded DNA at specific base pair sequences. The DNA fragments are separated by electrophoresis, stained with ethidium bromide and
visualized with UV light. These DNA fragment patterns constitute a specific “fingerprint” to characterize each strain.

Polymerase chain reaction (PCR)

PCR involves a reiterate (repeated) amplification of a region of DNA flanked by a selected primer pair specific for target species. The presence of specific amplification product indicates the
presence of the target microorganism.
Advantages:
Best detection limits among nucleic acid based assays
No cross-reactivity under amplification conditions
Easy to perform
Disadvantages:
Most PCR assays use relatively small quantity of sample for the amplification process. If this quantity does not contain the targeted microorganisms, the assay will not detect it.
Subgingival plaque mat contain enzymes which may alter the amplification process.
PCR has the potential for being an ideal detection method of periodontal pathogens
• Recent increase in PD and CAL
• Recent increases in PD and CAL are highly indicative of diseased pockets, active lesions, and further attachment loss. Periodontal disease is characterized by periods of quiescence and exacerbation. This was
demonstrated by Goodson et al (1982); in untreated subjects with existing periodontal pockets, PAL was measured every month for 1 year. During this period, 83% of sites did not change significantly, 6%
exhibited significant further LOA, and 11% exhibited loss of attachment.
• In individuals who are more susceptible to periodontal disease (smokers, those with genetic IL-1 polymorphism, and type 1 diabetes) more attachment loss may be seen.
•
• Loss of compact bone from the alveolar crest
• Loss of compact bone from alveolar crest and diffused lamina dura indicates active bone resorption. It can be evaluated by periodic radiographs.
•
• BOP
• The absence of BOP is a reliable parameter of periodontal stability, provided that the assessment procedure is standardized (Lang et al, 1990). Numerous studies have shown that a 30% probability for future
attachment loss may be predicted for sites that repeatedly exhibit BOP (Claffey et al, 1990; Lang et al, 1986).
• Lang et al (1991) showed an almost linear relationship between probing force and the percentage of bleeding sites. At probing forces of greater than 0.25N (0.25g), bleeding is the result of tissue trauma, rather
than a sign of inflammation.
• Because the absence of BOP at 0.25N indicates periodontal stability, with a negative predictive value of 98-99% (Lang et al, 1990), this is the most reliable clinical variable for monitoring patients’ progress in
daily practice.
•
• Increase in periodontal pocket temperature
• One of the cardinal signs of inflammation includes calor (increase in temperature) which is related to vascular changes. Regeneration of most human periopathogens is retarded at increased temperature. Fever
is one of the nonspecific host response to local and general infections. Because body temperature has long been used to evaluate the occurrence and severity of infectious diseases, it seems logical to include
measurement of the subgingival temperature in the evaluation of periodontal pockets. This was the rationale underlying the innovation of a digital “microthermometer,” combined with a flat, thin periodontal
probe, to identify diseased periodontal pockets (Axelsson, 1982). Commercial devices have been introduced in recent years (e.g. PerioTemp System).
•
• The PerioTemp System has been described by Kung et al (1990). The device is about the size and shape of a periodontal probe and uses a small thermistor bead to determine temperature. The probe tip housed
in a casing with low thermal conductivity so that the probe itself does not alter the ambient temperature. The probe is sensitive to 0.1ºC and assesses the temperature rapidly so that the entire mouth (6 sites per
tooth, 168 sites for 28 teeth) can be evaluated quickly. The device is linked to a computer. Advanced disease is associated with a mean increase of 0.65ºC at a site.
•
• The reference temperature used is the sublingual temperature which is generally higher than the subgingival temperature. The temperature increases in deeper pockets (34.6 ºC in 4 mm pockets to 35.8 ºC in 6
mm pockets). In a study by Fedi and Killoy (1992), the temperature of the pockets more than 5 mm deep with BOP was 1-1.8 ºC higher than that of pockets less than 3 mm without bleeding. Normal temperature
is indicated by emission of a green light, slightly elevated temperature by a yellow light, and marked elevation of temperature by a red light. When the device was used to predict risk of future PAL (Haffajee et al,
1992), the most obvious difference was observed for shallow sites (less than 4 mm). It was found that 8.9% of sites with BOP and markedly elevated temperature lost 2.0 mm of PAL, compared to only 1.4% of
sites that did not bleed and were in the normal temperature range.
•
• A study of the relationship of temperature to subgingival microflora revealed that elevated subgingival temperature was associated with the presence of some putative pathogens like Prevotella intermedia and
Peptostreptococcus micros (Haffajee et al, 1992).
•
• Increase in volume of GCF
• There is strong statistical association between the volume of GCF and the extent of gingival inflammation which has led to the widespread use of measurements of GCF as an objective assessment of gingival
inflammation in clinical research studies.
•
• Presence of purulent exudate
• Conceptually, purulent exudate can be regarded as a PMNL-rich variant of GCF. Clinically, suppuration is an important sign of ongoing infection. A strong association with the risk of disease progression was
reported by Armitage et al (1994). In subjects with untreated periodontitis, the sites with suppuration at baseline (25% of total sites) were at three-fold higher risk of further bone loss during the following 6
months.
•
Increase in levels of makers of periodontal disease activity: PGE 2, MMPs, IL-1β in GCF
• Curtis (1991) clearly differentiated disease markers as
• Indicators of current disease
• Predictors of future disease progression, and
• Predictors of future disease at currently healthy sites.
• GCF has the potential to reflect both host systemic responses and local modulation of those responses arising from interaction with the bacterial burden. The
GCF is regarded as a serum transudate because most serum proteins are present in concentrations similar to those in serum itself (Cimasoni, 1983); it thus
broadly reflects the systemic immunoglobulin and complement status of the host. However, GCF is modified by the local environment associated with the
periodontal crevice or pocket.

• As the GCF migrates from the host microcirculation, through inflamed tissues, and into periodontal pocket, it acquires mediators involved in the destructive
host response and by-products of local tissue metabolism as well as PMNLs, microorganisms, and their products from the periodontal pocket. The following
four mediators in GCF have been investigated extensively for their potential application in diagnosis of active periodontal disease and prediction of further loss
of periodontal support:
• Prostaglandin E2 (PGE2)
• β-glucouronidase (βG)
• Neutrophil elastase (NE)
• Aspartate aminotransferase (AST)

Prostaglandin E2 (PGE2)
• It is a proinflammatory metabolite of arachidonic acid.
• €Released from: macrophages, PMNLs, fibroblasts
• Effects:
• Vasodilation/increased vascular permeability
• Enhanced responsiveness of receptors to painful stimuli
• Release of collagenase by inflammatory cells
• Activation of osteoclasts
• Recruitment of inflammatory cells
• Studies:
• In a study by Offenbacher et al (1986), crevicualr fluid levels of PGE 2 were three times more in subjects with aggressive periodontitis (who experience rapid
disease progression) than those with chronic periodontitis.
• In another study by Offenbacher et al (1986), GCF from sites with active periodontal disease contained a mean PGE 2 concentration of 305.6µg/ml, while inactive
sites contained about 65.7µg/ml of PGE 2.
• β-glucouronidase (βG) & neutrophil elastase
• β-glucouronidase (βG) and neutrophil elastase (serine endopeptidase) two enzymes released from the lysosomes of phagocytozing PMNLs.
• Actions of βG and NE:
• Generation of reactive oxygen metabolites (Cell damage, inactivation of protease inhibitors)
• Degradation of the connective tissue ground substance (Collagenase, elastase)
•
• βG has been correlated with the number of PMNLs in the crevice (which increase in no. during periodontal disease).
•
• Harper et al (1989) observed that the total βG activity in GCF was significantly correlated with the occurrence of subgingival periodontal pathogens
associated with the occurrence of subgingival periodontal pathogens, associated with more severe periodontal disease.
•
• Lamster et al (1988) found that the total amounts of βG level in GCF were related to the CAL over time. In another study it was found that the in
previously treated patients, persistently elevated levels of βG in GCF were associated with an increase of 6-14 times in the risk PAL during the
monitoring period [Lamster et al (1995)].
•
• NE activity is higher in patients with periodontitis than those with gingivitis; NE increases with development of experimental gingivitis (Listgarten and
Levin, 1981); and periodontal therapy tends to reduce NE activity in the fluid (Listgarten, 1992).
•
• Aspartate aminotransferase (AST)
• It is a cytoplasmic enzyme present in many body tissues. Its extracellular release is associated with cellular damage and cellular death.
•
• Crevicular AST levels are correlated with disease severity. In a 2-year study by Persson et al (1990), sites with loss of CAL by 2mm or more exhibited
significantly elevated levels of AST in GCF.
•
• IL-1
• Gamonal et al (2000) showed that the amount of crevicular IL-1β, IL-8 and IL-10 was associated with periodontal status. Engebretson et al (1999)
showed that the amount of IL-1 was 2.5 times higher in GCF and 3.5 times higher in gingival tissues before periodontal treatment in patients with
DIAGNOSIS OF VARIOUS PERIODONTAL
CONDITIONS
• Classification of periodontal disease and condition (1999 international
workshop for a classification of periodontal disease and conditions)
• The new classification (1999) is as follows:
• 1.GINGIVAL DISEASES
• a) Dental plaque induced gingival disease.
• (Can occur without attachment loss or on a periodontium with attachment
loss that is not progressing)
• 1.Gingivitis associated with dental plaque only:
• a) Without other local contributing factors
• b) With local contributing factors (See VIII A)
•
• 2.Gingival diseases modified by systemic factors
• a) Associated with the endocrine system
• 1. Puberty assoicated gingivitis
• 2. Menstrual cycle associated gigivitis
• 3. Pregnancy assoicated
• a) gingivitis
• b) pyogenic granuloma
• 1. Diabetes mellitus assoicated gingivitis
• c) assoicated with blood dyscrasias
• 1. leukemia assoicated gingivitis
• 2. Other
• 3. Gingival diseases modified by medications
d) drug influenced gingival diseases
1. drug influenced gingival enlargements
2. drug influenced gingivitis
a) oral contraceptive assoicated gingivitis
b) other
4.Gingival diseases modified by malnutrition
a) ascorbic acid deficiency gingivitis
b) other
B. Nonplaque induced Gingival lesions
1. Gingival disease of specific bacterial origin
a. Nesseria gonorrhea assoicated lesions
b. Treponema pallidum associated lesions
c. Streptococcal species assoicated lesions
d. Others
2. Gingival disease of viral origin
a) herpes virus infection
3. primary herpetic gingivostomatitis
4. recurrent oral herpes
5. varicella zoster infections
• b. other
• 1. Gingival disease of fungal origin
• a) candida species infections
• 1. generalized gingival candidiasis
• b. linear gingival erythema
• c. histoplasmosis
• d. other
• 4. Gingival lesions of genetic origin
• a. hereditary gingival fibromatosis
• b. other
• 5. Gingival manifestations of systemic conditions
• a. mucocutaneous disorders
• 1. lichen planus
• 2. pemphigoid
• 3. pemphigus vulgaris
• 4. erythema multiforme
• 5) Lupus erythematosus
• 6) Drug-induced
• 7) Other
• b. Allergic reactions
• 1) Dental restorative materials
• a) Mercury
• b) Nickel,
• c) Acrylic
• d) Other
• 2) Reactions attributable to
• a) Toothpaste’s /dentifrice’s
• b) Mouth rinses / mouth washes
• c) Chewing gum additives
• d) Foods and additives
• 3) Other
• 6) Traumatic lesions (factitious, iatrogenic, accidental)
• a) Chemical injury
• b) Physical injury
• c) Thermal injury
• 7) Foreign body reactions
• 8) Not otherwise specified (NOS)
•
• . Chronic Periodontitis
• a) Localized
• b) Generalized
• III. Aggressive Periodontitis
• a) Localized
• b) Generalized
• IV. Periodontitis as a manifestation of systemic diseases.
• A) Associated with hematological. disorders.
• 1) Acquired neutropenia
• 2) Leukemias
• 3) Other
• B) Associated with genetic disorders
• 1. Familial and cyclic Neutropenia
• 2. Down syndrome
• 3. Leukocyte adhesion deficiency syndromes
• 4. Papillon - Lefevre syndrome
• 5. Chediak – Higashi syndrome
• 6. Histiocytosis syndrome
• 7. Glycogen storage disease
• 8. Infantile genetic agranulocytosis
• 9. Cohen syndrome
• 10. Ehlers – Danlos syndrome (Types IV and VIII)
• 11. Hypophosphatasia
• 12. Other
• V. Necrotising Periodontal Diseases
• a) Necrotising ulcerative gingivitis
• b) Necrotising ulcerative periodontitis
• VI. Abscesses of the periodontium
• a) Gingival abscess
• b) Periodontal abscess
• c) Periocoronal abscess
• VII Periodontitis assoicated with endodontic lesions
• A. Combined periodontal endodontic lesions
• VIII. Developmental or Acquired Deformities and conditions
• A. Localized tooth related factors that modify or predispose to plaque induced gingival disease / periodontitis
• 1. Tooth anatomic factors
• 2. Dental restorations / appliances
• 3. Root fractures
• 4. Cervical root resorption and cemental tears
• B. Mucogingival deformities and conditions around teeth
• 1. gingival / soft tissue recession
• a. facial or lingual surfaces
• b. interproximal (papillary)
• 2. lack of keratinized gingiva
• 3. decreased vestibular depth
• 4. aberrant frenum / muscle position
• 5. gingival excess
• a. pseudopocket
• b. inconsistent gingival margin
• c. excessive gingival display
• d. gingival enlargement (see section I, parts A3 and B4)
• abnormal color
• C. Mucogingival deformities and conditions on edentulous ridges
• 1. vertictal and / or horizontal ridge deficiency
• 2. lack of gingiva / keratinized tissue
• 3. gingiva / soft tissue enlargement
• 4. aberrant frenum / muscle position
• 5. decreased vestibular depth
• 6. abnormal color

• D. Occlusal trauma
• 1. Primary occlusal trauma
• 2. Secondary occlusal trauma
 Clinically healthy gingiva

• Pale pink
• Stippled
• Thin margins
• Firm and resilient
 DIAGNOSIS OF GINGIVITIS

• Clinical signs
• Redness
• Swelling (due to increased vascular permeability; Lindhe & Rylander,
1975)
• Bleeding on probing (objective sign)
• Exudate

• Severity of gingivitis
• Löe & Silness Gingival index (1963)
 GINGIVITIS

• CLINICAL PRESENTATION
• Most common form of periodontal disease
• PD: 1-3 mm
• Clinical signs of inflammation
• Plaque usually present; calculus often seen
• Precedes periodontitis but does not always lead to periodontitis
• Reversible
• RADIOGRAPHIC PRESENTATION
• No bone loss seen
 DIAGNOSIS OF PERIODONTITIS

• Local factors
• Age of onset
• Family history
• Clinical attachment loss
• Rate/Duration of destruction/symptoms
• Radiographic evidence of destruction
• Nature and composition of microbial flora
• Alteration in host immune response
 CHRONIC PERIODONTITIS

• CLINICAL PRESENTATION:
• Pocket depth >3mm
• BOP, suppuration, other signs of active disease
• Fremitus/tooth mobility
• Furcation invasion
• RADIOGRAPHIC PRESENTATION:
• Horizontal to angular bone loss
• RADIOGRAPHIC PRESENTATION:
• Bone loss localized to the distal of the deciduous first molar
Localized form <30% of sites involved
Generalized form >30% of sites involved

Slight 1-2 mm of attachment loss

Moderate 3-4 mm of attachment loss
Severe ≥5 mm of attachment loss
 LOCALIZED AGGRESSIVE PERIODONTITIS
[PREPUBERTAL PERIODONTITIS]

• CLINICAL PRESENTATION:
• Little or no inflammation of gingiva
• Usually amenable to standard periodontal therapy with appropriate
antibiotics
• Seen after eruption of primary teeth

• RADIOGRAPHIC PRESENTATION:
• Bone loss localized to the distal of the deciduous first molar
 GENERALIZED AGGRESSIVE PERIODONTITIS
[PREPUBERTAL PERIODONTITIS]

• CLINICAL PRESENTATION:
• Extreme gingival inflammation
• Rapid bony destruction
• Often accompanied by sever functional defects of neutrophils and
monocytes
• Otitis media and URTI also found
• In some cases more sever lesions are refractory to antibiotics
•
• RADIOGRAPHIC PRESENTATION:
• Generalized bone loss
 ABSCESSES OF THE PERIODONTIUM
•
• GINGIVAL ABSCESS
• Is a localized purulent infection that involves marginal gingiva or interdental papilla.
• Confined to marginal tissues
• Previously non-diseased site
• Impaction of foreign material
• Short history of onset
•
• PERICORONAL ABSCESS
• Localized purulent infection within the tissues surrounding a partially erupted tooth.
•
• PERIODONTAL ABSCESS
• A periodontal abscess is a localized accumulation of pus within the gingival wall of a
periodontal pocket.
• History of onset, progression, previous periodontal therapy
• Continuity with gingival margin
• Vitality of tooth
• Presence/ absence of caries
• Radiographic examination
Necrotizing Ulcerative Periodontitis (NUP)

• CLINICAL PRESENTATION:
• Usually observed in individuals with HIV; immunosuppression; or
severe malnutrition
• Generalized or localized rapid soft and hard tissue destruction
• Bone sequestration, denudation
• Teeth may become mobile
• Spontaneous, usually nocturnal, gingival bleeding
• Fetid breath
• Intense, deep-seated pain
• May be preceded by necrotizing ulcerative gingivitis
Periodontitis associated with endodontic lesions

• A- Primary endodontic lesion

• B- Primary endodontic lesion with secondary periodontal
lesion
• C- Primary periodontal lesion
• D- Primary periodontal lesion with secondary endodontic
lesion
• E- True combined lesions
Periodontitis associated with endodontic lesions

• A- Primary endodontic lesion

• B- Primary endodontic lesion with secondary periodontal
lesion
• C- Primary periodontal lesion
• D- Primary periodontal lesion with secondary endodontic
lesion
• E- True combined lesions
• Good prognosis: Control of etiologic factors and adequate peri-odontal
support ensure the tooth will be easy to maintain by the patient and
clinician.
• Fair prognosis: Approximately 25% attachment loss and/or Class I
furcation involvement (location and depth allow proper maintenance with
good patient compliance).
• Poor prognosis: 50% attachment loss, Class II furcation involvement
(location and depth make maintenance possible but difficult).
• Questionable prognosis: >50% attachment loss, poor crown-to root ratio,
poor root form, Class II furcations (location and depth make access
difficult) or Class III furcation involvements; >2+ mobility; root proximity.
• Hopeless prognosis: Inadequate attachment to maintain health,comfort,
and function