CHRONIC PERIODONTITIS

DR. VATSALA SINGH

 Introduction

• Adult periodontitis/ Chronic adult periodontitis (obsolete

terms)

• 1999 classification- Chronic periodontitis, it can occur

in children & adolescents in response to chronic plaque &
calculus formation

• Most prevalent form

• Slowly progressing, systemic/environmental factors-

aggressive
 Definition
• “An infectious disease resulting in inflammation within
supporting tissues of the teeth, progressive attachment
loss and bone loss”

( Fleming TF, 1999)

• Major clinical & etiologic characteristic of the disease:

1. Microbial plaque formation

2. Periodontal inflammation

3. Loss of attachment & alveolar bone

 Sequelae

Periodontal Gingival
Pocket Recession
(PD: shallow or deep,
ongoing AL BL )

Tooth mobility
 Clinical features
1. Supra & subgingival plaque formation associated with calculus
formation

2. Gingival inflammation (pale red Magenta, colour, contour,

consistency, margins, surface texture, flattened or cratered papillae

3. Pocket formation (variable)

4. Loss of periodontal attachment

5. Loss of alveolar bone

6. Suppuration or exudation

7. Spontaneous bleeding or bleeding in response to probing

8. Tooth mobility (advanced cases)

• Regular home care measures: not visible

• Long standing, low grade inflammation: thickened

fibrotic marginal tissue obscuring underlying
inflammation.
 Radiographic features

• Evidence of bone loss: horizontal/vertical

• Crest of interdental bone fuzzy, density reduced (>2mm)

• Lamina dura ill defined

• Furcation areas: radiolucency

 Disease distribution
• Site specificity: e.g proximal surfaces involved facial
spared

• May be

Localised : < 30% sites involved, show AL & BL

Generalised: > = 30% sites involved

• Pattern of bone loss:

Horizontal: suprabony pockets

Vertical: infrabony pockets

 Disease severity
• Function of time

• Increase in age AL & BL Increase in destruction

• For entire mouth/sextant/quadrant/individual tooth:

A. Slight (mild): no more than 1-2mm of clinical AL

B. Moderate: 3-4mm of clinical AL

C. Severe: 5mm or more clinical AL

 Symptoms
• Patient may become aware....

• Painless

1. Bleeding from gums

2. Spaces between teeth as a result of tooth movement

3. Teeth have become loose

4. Areas of localised dull pain, sometimes radiating deep into jaw

5. Pain present in absence of caries caused by exposed

roots(sensitivity)

6. Food impaction

7. Gingival tenderness/itchiness
 Disease progression
• Slow, modified by systemic, environmental, behavioural or
genetic factors

• Onset: anytime, adolescence, clinically significant in later

• Does not progress at an equals rate in all affected sites

• More frequently: INTERPROXIMAL AREAS

In accessibility to plaque control measures (e.g

overhanging margins of restorations, maloposed teeth, areas
of food impaction
 Models of disease
progression (AL)
Random/episodic Asynchronous/multipl
Continuous burst e burst
• Slow & continuous • Short bursts of • Destruction occurs
destruction followed around affected teeth
• Constant progressive by periods of no during defined periods of
rate through out destruction. life.
duration of disease. • Interspersed with periods
• Random in respect of inactivity.
to tooth & • Chronology of bursts is
chronology asynchronous
• Attachment loss of 2mm or more/year indicator of
accentuated disease progression.

• Patients should be treated quickly to change

bacterial milieu by reduction in probing depth &
improved oral hygiene.

• Bone loss initiated by specific group of pathogenic

organism
 Prevalence
• Increased in prevalence & severity with age

• Affects both genders equally

AGE ASSOCIATED AGE

RELATED
 Risk factors
Prior history of periodontal
disease

• Not a risk factor, risk predictor

• Positive: greater risk for

developing AL & BL

• Successfully treated patients if

allowed to accumulate plaque will
develop disease
1. Local factors

• Plaque accumulation: primary initiating agent in ethology

• AL &BL associated with increased proportion of gram negative

organism e.g Pg, Tf, Td (Red complex)

Specific plaque hypothesis

“ implies that although there occurs increase in

proportion of gram-ve microorganism, it is presence of
increased proportions of members of red complex that
precipitates attachment and bone loss”
• Plaque retentive factors retain plaque in proximity to periodontal tissues
providing ecological niche for plaque growth and maturation.e.g calculus,
carious lesions, margins, crowded/malaligned teeth, root concavities etc.
2. Systemic factors

Diabetes: synergistic effect of plaque accumulation &

modulation of effective host response (diabetes) can result in a
more severe extensive periodontal disease

3. Environmental & Behavioural factors:

Smoking:extent severity increased, more supra & less

subgingival calculus, less bleeding on probing

Emotional stress:associated with necrotising ulcerative

diseases, effect on immune statement

Socio-economic status:poor oral hygiene

4. Genetic factors

• Multifactorial disease in which normal balance between

microbial plaque and host response is disrupted.

• Can occur changes in plaque deposition or host response.

• Periodontal destruction is seen among family members &

across different generation suggesting genetic basis for
susceptibility to disease.
• Increased susceptibility to disease because of genetic
profile that accentuates IL-1 production.

• IL-1 genotype-increased risk of tooth loss by 2.7 times

• Smoker-2.9times, Smoker + IL-1 genotype-7.7

times
 Diagnosis

• Dental history

• Systemic/medical history

• Radiographic examination

• Clinical examination
Differential diagnosis
 Treatment

• Based on severity and extent

• Patient education: informed about relationship between

deposits and periodontal destruction, maintenance of oral
hygiene, brushing techniques etc.

• Patient motivation

• Non surgical periodontal therapy: scaling & root planing,

antibiotics, LDD, HMT, PDT etc.