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Chronic Periodontitis

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Chronic Periodontitis

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  1. 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 Localized Generalized

  2. Learning Outcomes • Describe the development of a periodontal pocket. • Relate clinical characteristics to the histopathologic changes for chronic periodontitis. • Compare the gingival pocket with the periodontal pocket. • Determine the severity of PD activity using clinical data.

  3. 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

  4. 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

  5. Clinical Characteristics • Deep red to bluish-red tissues • Thickened marginal gingiva • Blunted/cratered papilla • Bleeding and/or suppuration • Plaque/calculus deposits

  6. Clinical Characteristics • Variable pocket depths • Horizontal/vertical bone loss • Tooth mobility

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

  8. 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

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

  10. 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

  11. Development of Periodontal Pocket

  12. Continuous Cycle! • Plaque  gingival inflammation  pocket formation  more plaque

  13. 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

  14. 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

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

  16. Clinical: 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

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

  18. 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

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

  20. 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

  21. Periodontal Pocket • Suprabony pocket

  22. 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

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

  24. 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

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

  26. Stages of Periodontal Disease

  27. Periodontal Pathogens • Gram negative organisms dominate • P.g., P.i., A.a. may infiltrate: • Intercellular spaces of the epithelium • Between deeper epithelial cells • Basement lamina

  28. Periodontal Pathogens • Pathogens include: • Nonmotile rods: • Facultative: • A.a., E.c. • Anaerobic: • P. g., P. i., B.f., F.n. • Motile rods: • Facultative: • C.r. • Spirochetes: • Anaerobic, motile: • Treponema denticola

  29. Periodontal Disease Activity • Bursts of activity followed by periodsof quiescence characterized by: • Reduced inflammatory response • Little to no bone loss & CT loss • Accumulation of Gram negative organisms leads to: • Bone & attachment loss • Bleeding, exudate • May last days, weeks, months

  30. 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

  31. Overall Prognosis • Dependent on: • Client compliance • Systemic involvement • Severity of condition • # of remaining teeth

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

  33. Subclassification of Chronic Periodontitis

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