Chronic Periodontitis This presentation will probably involve audience discussion, which will create action items. Use PowerPoint to keep track of these action items during your presentation In Slide Show, click on the right mouse button Select “Meeting Minder” Select the “Action Items” tab Type in action items as they come up Click OK to dismiss this box This will automatically create an Action Item slide at the end of your presentation with your points entered. Chronic Periodontitis Algonquin College

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

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

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

Clinical Characteristics Gingiva moderately swollen Deep red to bluish-red tissues Blunted and rolled gingival margin Cratered papilla Bleeding and/or suppuration

Clinical Characteristics Plaque/calculus deposits Variable pocket depths Loss of periodontal attachment Horizontal/vertical bone loss Tooth mobility

CLASSIFICATION 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 Periodontitis Severity Pocket Depths CAL Bone Loss Furcation Early 4-5 mm 1-2 mm Slight horizontal Moderate 5-7 mm 3-4 mm Sl – mod Involved Advanced > 7 mm  5 mm Mod-severe vertical

DISEASE DISTRIBUTION : It is a site-specific disease CLINICAL SIGNS - - Inflammation ,pocket formation ,attachment 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. - E.g..-proximal surface with plaque may have C.A.L. - And plaque free surface –FACIAL surface of same tooth may be without disease.

SYMPTOMS Patient notices - gum bleed space appear between teeth due to tooth movement May be painless (sleeping disease )goes unnoticed Some time pain due to caries , root hypersensitivity To cold /hot or both PAIN-may be-- dull—deep radiating in the jaw Area of food impaction can cause more discomfort 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

Periodontal Pathogens Contn… Pathogens include: Nonmotile rods: Facultative: Actinobacillus a. E.c Anaerobic: P. g., P. i., T.f., F.n. Motile rods: C.r. Spirochetes: Anaerobic, motile: Treponema denticola

Pathogenesis – Pocket Formation Bacterial challenge initiates initial lesion of gingivitis With disease progression & change in microorganisms  development of periodontitis

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

Pocket Formation Continued extension of JE requires healthy epithelial cells! Necrotic JE slows down pocket formation Pocket base degeneration less severe than lateral

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

Development of Periodontal Pocket

Continuous Cycle! Plaque  gingival inflammation  pocket formation  more plaque

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

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.

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

Clinical & Histopathologic Features Pocket wall bluish-red Smooth, shiny surface Pitting on pressure Histopathology: Vasodilation & vasostagnation Epithelial proliferation, edema Edema & degeneration of epithelium

Clinical & Histopathologic Features Contn… Pocket wall may be pink & firm Bleeding with probing Pain with instrumentation Histopathology: Fibrotic changes dominate  blood flow, degenerated, thin epithelium Ulceration of pocket epithelium

Clinical & Histopathologic Features Contn… Histopathology: Accumulation of inflammatory products Destruction of gingival fibers Clinical : Exudate Flaccid tissues

Stages of Periodontal Disease

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

Root Surface Wall Contn… Necrotic areas of cementum form; clinically soft Act as reservoir for bacteria Root planing may remove necrotic areas  firmer surface

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

Inflammatory Pathway Contn… Interproximal: Loose CT  periodontal ligament  bone  infrabony pockets & vertical bone loss  transseptal fibers transverse in oblique direction

Inflammatory Pathway Contn… 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

Inflammatory Pathway Contn… Facial & Lingual: Loose CT  periodontal ligament  destruction of periodontal ligament fibers  infrabony pockets & vertical or angular bone loss

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

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

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 Accumulation Oral Hygiene Tooth Malposition Restoration Preserve & Quantity of certain bacteria Host defenses Subgingival Restoration Environment Calculus, smoking Connective Tissue destruction Genetic influence Inflammation Periodontopathic bacteria Smoking, Calculus Loss of Attachment M O D I F Y N G A C T R S

3) SYSTEMIC FACTORS: Type II or Non – Insulin dependent Diabetes mellitus (NIIDDM) 4) ENVIRONMENTAL & BEHAVIORAL FACTORS: Smoking Emotional Stress 5) GENETIC FACTORS: Frequent among family members and across different generations.

MANAGEMENT The treatment consists of – Non-surgical procedures Scaling Root planing Curettage 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

Prognosis of Individual Teeth Dependent on: Attachment levels, bone height Status of adjacent teeth Type of pockets: suprabony, infrabony Furcation involvement Root resorption

MCQs on Chronic Periodontitis 1.Bacteria considered to be pathogenic in chronic periodontitis is/are: a) P. gingivalis b) P. intermedia c) A. actinomycetemcomitans d) Both (a) and (b)

MCQs on Chronic Periodontitis 2. The clinical attachment loss in Moderate periodontitis is a) 1 to 2 mm b) 2 to 3 mm c) 3 to 4 mm d) 5 mm or more

MCQs on Chronic Periodontitis 3.Following histopathological changes occur in periodontium while pocket formation except: a) Cellular & fluid inflammatory exudate degenerates connective tissue. b) Apical migration of junctional epithelium along root. c) Apical portion of JE detaches. d) None of the above.

MCQs on Chronic Periodontitis 4. Risk factors for chronic periodontitis include: 1. Prior history of periodontitis. 2. Plaque accumulation on tooth and gingival surfaces. 3. Type 2 diabetes. 4. All of the above.

MCQs on Chronic Periodontitis 5.The treatment possibilities of chronic periodontitis include a) Nonsurgical periodontal therapy. b) Pocket reduction surgery. c) Correction of morphological / anatomic defects. d) All of the above.