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Definition

Chronic Periodontitis can be defined as “an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.”

- Previously known as adult periodontitis or slowly progressive periodontitis.

- Occur as a result of extension of inflammation from the gingiva into deeper periodontal tissue.

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Common Characteristics

Onset - any age; most common in adults

Plaque initiates condition Subgingival calculus common finding Slow-mod progression; periods of

rapid progression possible Modified by local factors/systemic

factors/stress/smoking

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Extent & Severity

Extent: Localized: <30% of sites affected Generalized: > 30% of sites affected

Severity: entire dentition or individual teeth/site Slight = 1-2 mm CAL Moderate = 3-4 mm CAL Severe = 5 mm CAL

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Clinical Characteristics Gingiva

moderately swollen

Deep red to bluish-red tissues

Blunted and rolled gingival margin

Cratered papilla Bleeding and/or

suppuration

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Clinical Characteristics Plaque/calculus

deposits Variable pocket

depths Loss of

periodontal attachment

Horizontal/vertical bone loss

Tooth mobility

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CLASSIFICATION

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A) Based on Disease Distribution:

Localized:Periodontitis is considered localized when <30% of the sites assessed in mouth demonstrate attachment loss and bone loss.

Generalized:Periodontitis is considered generalized when >30% of the sites assessed demonstrate attachment loss and bone loss.The pattern of bone loss in chronic periodontitis can be vertical or horizontal.

Sub classification of Chronic PeriodontitisSeverity Pocket

DepthsCAL Bone

Loss

Furcation

Early 4-5 mm 1-2 mm Slight

horizontal

Moderate 5-7 mm 3-4 mm Sl – mod

horizontal

Advanced > 7 mm 5 mm Mod-severe

horizontal

vertical

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DISEASE DISTRIBUTION : It is a site-specific disease

CLINICAL SIGNS -

- Inflammation ,pocket formation ,attacment loss ,bone loss - All caused by site specific effects of a sub-gingival plaque accumulation

- That is why the effect are on one side only –other surface may maintain normal attachment level.

- Eg.-proximal surface with plaque may have C.A.L.

- And plaque free surface –FACIALsurface of same tooth may be without disease.

SYMPTOMS

Patient notices--

1. gum bleed

2. space appear between teeth due to tooth movement

3. May be painless (sleeping disease )goes unnoticed

4. Some time pain due to caries , root hypersensitivity

5. To cold /hot or both

6. PAIN-may be-- dull—deep radiating in the jaw

7. Area of food impaction can cause more discomfort

8. May be gingival tenderness or itchiness found

Periodontal Pathogens

• Gram negative organism dominate• P.g., P.i., A.a. may infiltrate:

• - Intercellular spaces of the epithelium• - Between deeper epithelial cells• - Basement lamina

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Periodontal Pathogens Contn. Pathogens include:

Nonmotile rods: Facultative:

Actinobacillus a. E.c. Anaerobic:

P. g., P. i., B.f., F.n.

Motile rods: Facultative:

C.r.

Spirochetes: Anaerobic, motile:

Treponema denticola

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Pathogenesis – Pocket Formation Bacterial

challenge initiates initial lesion of gingivitis

With disease progression & change in microorganisms development of periodontitis

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Pocket Formation

Cellular & fluid inflammatory exudate degenerates CT

Gingival fibers destroyed Collagen fibers apical to JE destroyed

infiltration of inflammatory cells & edema

Apical migration of junctional epithelium along root

Coronal portion of JE detaches

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Pocket Formation

Continued extension of JE requires healthy epithelial cells!

Necrotic JE slows down pocket formation

Pocket base degeneration less severe than lateral

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Pocket Formation

Continue inflammation: Coronal extension of gingival margin JE migrates apically & separates from

root Lateral pocket wall proliferates &

extends into CT Leukocytes & edema

Infiltrate lining epithelium Varying degrees of degeneration &

necrosis

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Development of Periodontal Pocket

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Continuous Cycle!

Plaque gingival inflammation pocket formation more plaque

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Classification of Pockets Gingival:

Coronal migration of gingival margin Periodontal:

Apical migration of epithelial attachment Suprabony:

Base of pocket coronal to height of alveolar crest

Infrabony: Base of pocket apical to height of alveolar

crest Characterized by angular bony defects

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Histopathology

Connective Tissue: Edematous Dense infiltrate:

Plasma cells (80%) Lymphocytes, PMNs

Blood vessels proliferate, dilate & are engorged.

Varying degrees of degeneration in addition to newly formed capillaries, fibroblasts, collagen fibers in some areas.

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Histopathology

Periodontal pocket: Lateral wall shows most severe

degeneration Epithelial proliferation & degeneration Rete pegs protrude deep within CT Dense infiltrate of leukocytes & fluid

found in rete pegs & epithelium Degeneration & necrosis of epithelium

leads to ulceration of lateral wall, exposure of CT, suppuration

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Clinical & Histopathologic Features Clinical :1. Pocket wall bluish-

red2. Smooth, shiny

surface3. Pitting on

pressure

Histopathology:1. Vasodilation &

vasostagnation2. Epithelial

proliferation, edema

3. Edema & degeneration of epithelium

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Clinical & Histopathologic FeaturesContn… Clinical:1. Pocket wall may

be pink & firm2. Bleeding with

probing3. Pain with

instrumentation

Histopathology:1. Fibrotic changes

dominate2. blood flow,

degenerated, thin epithelium

3. Ulceration of pocket epithelium

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Clinical & Histopathologic FeaturesContn… Clinical :1. Exudate2. Flaccid tissues

Histopathology:1. Accumulation of

inflammatory products

2. Destruction of gingival fibers

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Stages of Periodontal Disease

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Root Surface Wall

Periodontal disease affects root surface: Perpetuates disease Decay, sensitivity Complicates treatment

Embedded collagen fibers degenerate cementum exposed to environment

Bacteria penetrate unprotected root

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Root Surface Wall Contn…

Necrotic areas of cementum form; clinically soft

Act as reservoir for bacteria Root planing may remove necrotic

areas firmer surface

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Inflammatory Pathway

Stages I-III – inflammation degrades gingival fibers

Spreads via blood vessels: Interproximal:

Loose CT transseptal fibers marrow spaces of cancellous bone periodontal ligament suprabony pockets & horizontal bone loss transseptal fibers transverse horizontally

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Inflammatory Pathway

Interproximal: Loose CT periodontal ligament

bone infrabony pockets & vertical bone loss transseptal fibers transverse in oblique direction

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Inflammatory Pathway

Facial & Lingual: Loose CT along periosteum marrow

spaces of cancellous bone supporting bone destroyed first alvoelar bone proper periodontal ligament suprabony pocket & horizontal bone loss

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Inflammatory Pathway

Facial & Lingual: Loose CT periodontal ligament

destruction of periodontal ligament fibers infrabony pockets & vertical or angular bone loss

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Periodontal Disease Activity Bursts of activity followed by periods of

quiescence characterized by: Reduced inflammatory response Little to no bone loss & CT loss

Accumulation of Gram negative organisms leads to: Bone & attachment loss Bleeding, exudates May last days, weeks, months

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Periodontal Disease Activity Period of activity followed by period

of remission: Accumulation of Gram positive bacteria Condition somewhat stabilized

Periodontal destruction is site specific

PD affects few teeth at one time, or some surfaces of given teeth

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Prevalence:

Chronic Periodontitis increases in prevalence & severity with age.

Affect both the sexes equally.

It is an age-associated, not age related disease.

RISK FACTORS FOR DISEASE:1) PRIOR HISTORY OF PERIODONTITIS—predictor-more risk for developing damage to periodontium.2) LOCAL FACTORS:

Plaque AccumulationOral HygieneTooth MalpositionRestoration

Preserve & Quantity of certain bacteriaHost defencesSubgingival RestorationEnvironmentCalculus, smoking

Connective Tissue destructionGenetic influenceInflammationPeriodontopathic bacteriaSmoking, Calculus

Loss of Attachment

MODIFYING

FACTORS

3) SYSTEMIC FACTORS: Type II or Non – Insulin dependent Diabetes Mellitus (NIIDDM)

4) ENVIRONMENTAL & BEHAVIORAL FACTORS: Smoking Emotional Stress5) GENETIC FACTORS: Frequent among family members and across different generations.

GENERAL CONCEPT FOR ETIOLOGY OF CHRONIC PERIODONTITISPlaque accumulation

Maturation of Plaque

Quality & Quantity of periodontopathic Plaque accumulation

Maturation of Plaque

Quality & Quantity of periodontopathic bacteria

InflammationPlaque accumulation

Maturation of Plaque

Quality & Quantity of periodontopathic bacteria

Inflammation

Connective tissue destruction.

Connective tissue destruction.bacteriaInflammation

Connective tissue destruction.

Host status and defences

Plaque accumulationPlaque accumulationMaturation of PlaqueMaturation of PlaqueQuality & Quantity of Quality & Quantity of periodontopathic bacteriaperiodontopathic bacteria

InflammationInflammation

connective tissue connective tissue destruction.destruction.

MANAGEMENT The treatment consists of –1. Non-surgical procedures

Scaling Root planing Curettage

2. Surgical procedure Pocket reduction surgery

Resective Regenerative

Correction of morphological / anatomic defects

Overall Prognosis

Dependent on: Client compliance Systemic involvement Severity of condition # of remaining teeth

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Prognosis of Individual Teeth Dependent on:

Attachment levels, bone height Status of adjacent teeth Type of pockets: suprabony, infrabony Furcation involvement Root resorption

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