Periodontal pockets

pockets

1. PERIODONTAL POCKET

2. Content Introduction Classification Clinical features Theories of pathogenesis Pathogenesis Histopathology Periodontal Disease Activity Site Specificity Relation of Attachment Loss to Pocket Depth Conclusion References

3. Introduction Pathologically deepened gingival sulcus

4. Classification Gingival pocket (pseudo pocket) Periodontal pocket

5. Classification Suprabony / Supracrestal / Supraalveolar Intrabony/ Infrabony / Subcrestal / Intraalveolar

6. Classification Suprabony Pocket Intrabony Pocket Base of pocket Pattern of destruction

7. Classification Suprabony Pocket Intrabony Pocket Transseptal fibers PDL fibres (Facial & Lingual)

8. Classification Simple Compound Complex

9. Clinical Features Extrusion & migration Diastema Enlarged, bluish-red marginal gingiva “Rolled” edge Reddish-blue vertical zone Shiny & puffy gingiva Gingival bleeding Purulent exudate

10. Clinical Features

11. Theories of Pathogenesis Two stage pocket formation (James & Counsell , 1927) Proliferation of subgingival epithelium Loss of superficial layers of proliferated epithelium Space or pocket

12. Theories of Pathogenesis Pocket formation : Initiated in a defect in sulcus wall (Becks,1929) Between oral & enamel epithelium Degeneration of enamel epithelium Not covered by oral epithelium “ locus minoris resistentiae ” Portal of entry for bacteria Inflammation Oral epithelium proliferation Shuts off nutrition from enamel epithelium Degradation & ↑ pocket depth

13. Theories of Pathogenesis Pocket formation : Initiated in a defect in sulcus wall (Becks,1929) Between oral & enamel epithelium

14. Theories of Pathogenesis Pathologic destruction of epithelial attachment due to infection or trauma : Initial histologic change in pocket formation ( Skillen , 1930) Epithelial attachment : Area of low resistance Infection / Trauma Pathologic dissolution of epithelial attachment Pocket formation Accumulation of debris in pocket

15. Theories of Pathogenesis Proliferation of the epithelium of lateral wall is the initial change in formation of the periodontal pocket (Wilkinson, 1935) Proliferation & down growth of oral epithelium Thickening of epithelial lining of sulcus Cells along inner aspect of sulcus deprived of nutrition Degeneration & necrosis Calcification of necrotic cells Separation of calcified masses from adjacent normal epithelium Pocket or trough

16. Theories of Pathogenesis Periodontal pocket is initiated by invasion of bacteria at base of the sulcus or absorption of bacterial toxins through epithelial lining of sulcus (Box,1941) Initial invasion of bacteria at base of sulcus Inflammation in underlying CT Ulceration at base Sloughing of epithelium Loss of attachment to cementum Progressive loss of CT & penetration of pocket into deeper tissues

17. Theories of Pathogenesis Orban & Weinmann,1942 Subgingival bacterial growth : Secondary to pocket

18. Theories of Pathogenesis The initial change in pocket formation occurs in the cementum. (Gottlieb 1926, 1946) Continuous eruption of teeth : Down growth of epithelial attachment Continues deposition of new cementum : Prevents accelerated migration of epithelial attachment Normal deposition of cementum impaired : Dissolution of organic connection between cementum & gingiva

19. Theories of Pathogenesis Destruction of gingival fibers : Pre-requisite for initiation of pocket formation (Fish, 1948) Top most fibers digested & absorbed Epithelium proliferates until healthy fiber is reached

20. Theories of Pathogenesis Simulation of the epithelial attachment by inflammation : Prerequisite for initiation of the periodontal pocket ( Aisenberg & Aisenberg , 1948) Inflammation Epithelium migrates along root Epithelial cells burrow between intact gingival fibers Enmesh connective tissue fibers in epithelial network Secondary fiber degeneration

21. Theories of Pathogenesis Inflammation is the initial change in the formation of the periodontal pocket ( Nuckolls & Dienstein , Bell & Rule, 1950) Inflammation in connective tissue ↑ Mitotic activity ↑ Keratin Cellular desquamation

22. Theories of Pathogenesis Basal epithelial cells at bottom of sulcus : Proliferate into connective tissue Open lesion Repair of lesion : Periodontal pocket

23. Theories of Pathogenesis Waerhaug, 1976 Bacteria spreading subgingivally Pocket formation

24. Theories of Pathogenesis Pathologic epithelial proliferation occurs secondary to non inflammatory degenerative changes in the periodontal membrane “ Periodontosis ” Non-inflammatory degeneration of collagen fibers Migration of epithelial attachment along the root

25. Theories of Pathogenesis Schroeder and Attstrom (1980) Microbial invasion of subgingival dentogingival junction Destroy coronal epithelial attachment Pathological pockets

26. Theories of Pathogenesis Takata & Donath (1988) Early & established lesion Degenerative changes in most coronal part of JE Intraepithelial cleavage Degeneration of cells lining the cleavage Deep crevice formation

27. Theories of Pathogenesis Advanced lesions Deep pocket epithelium Toxic bacterial products Mechanical irritation of calculus Thin and ulcerated Typical periodontal pocket

28. Pathogenesis Initial lesion : Inflammation of gingiva Not a predictor of future attachment & bone loss Hillman 1998

29. Pathogenesis Cellular & inflammatory exudate : Degeneration of CT & fibers Apical Cells of JE : Fingerlike projections Coronal portion : Detaches from the root 60% PMNs : Loss of tissue cohesiveness Sulcus shifts apically Matrix Metalloproteinases Taichman 1968, Takada 1988 Phagocytosis Deporter 1980

30. Pathogenesis Gingival sulcus Periodontal pocket Plaque removal impossible Rationale for pocket reduction : Eliminate areas of plaque accumulation

31. Histopathology Soft tissue wall Connective tissue

32. Histopathology Junctional epithelium 50-100 µm Cells : Well formed & in good condition Slight to marked degeneration

33. Histopathology Lateral wall Most severe degenerative changes Epithelial buds or interlacing cords of epithelial cells Dense infiltration Cells : Vacuolar degeneration & form vesicles Ulceration & suppuration

34. Histopathology Severity of degenerative changes : Not related to pocket depth Epithelium of gingival crest : Intact with prominent retepegs Predominant gram-negative filaments, rods & cocci ? Bacterial invasion ? Passive translocation of plaque bacteria

35. Histopathology Microtopograghy Irregular oval/elongated areas : 50 - 200 microns Saglie et al 1975 Relative quiescence Bacterial accumulation Emergence of leucocytes Leucocytes bacterial interaction Intense epithelial desquamation Ulceration Haemorrhage

36. Histopathology

37. Histopathology Periodontal pocket as a healing lesion Chronic inflammatory lesions Persistence bacterial attack Repair Degeneration of new tissue elements

38. Histopathology Edematous pocket Fibrotic pocket

39. Histopathology Pocket contents Debris Microorganisms & products Gingival fluid Food remnants Salivary mucin Desquamated epithelial cells Leukocytes Plaque-covered calculus Purulent exudate

40. Histopathology Significance of Pus Formation Secondary sign Nature of the inflammatory changes Not an indication of depth of pocket / severity of destruction

41. Histopathology Root surface wall

42. Histopathology Structural Changes Pathologic granules Areas of increased mineralization Areas of demineralization

43. Histopathology Pathologic granules : Collagen degeneration / Incompletely mineralized collagen fibrils Bass 1951 Areas of increased mineralization : Exchange of minerals & organic components at cementum-saliva interface Selvig 1969 Perfection of crystal Subsurface cuticle 10-20µm thick

44. Histopathology Areas of demineralization : Root carries Herting 1967

45. Histopathology Active root caries lesions Inactive root caries lesions

46. Histopathology Severe Cases Actinomyces viscosus Caries Pulpitis

47. Histopathology Necrotic cementum : Removed by scaling & root planing Areas of cellular resorption of cementum & dentin : Roots unexposed by periodontal disease

48. Histopathology Chemical Changes Mineral content increased Calcium, Magnesium, Phosphorus, Fluoride Microhardness : Unchanged Exposed cementum : Resistant to decay Selvig 1966

49. Histopathology Cytotoxic Changes Bacterial penetration : Cemento -dentinal Junction Endotoxins Diseased root fragments : Prevents in-vitro attachment of human gingival fibroblasts

50. Histopathology Surface Morphology of Tooth Wall

51. Periodontal Disease Activity Models of Disease Progression Continuous Random / Episodic burst Asynchronous multiple burst Synchronous burst Epidemiologic Brownian motion / Stochastic Fractural

52. Periodontal Disease Activity Bone loss in untreated periodontal disease occurs in episodic manner McHenry 1981

53. Periodontal Disease Activity Periods of quiescence Period of exacerbation Reduced inflammatory response Little or no bone & CT attachment loss Build-up of unattached plaque Bone & connective tissue attachment lost Pocket deepens Bleeding & Gingival exudate Epithelium thin & ulcerated Inflammatory infiltrate Motile organisms & spirochetes

54. Site Specificity Some aspects of some teeth at any given time New site : Increased severity

55. Relation of Attachment loss to Pocket Depth

56. Conclusion Understanding the etiopathogenesis, histopathology and progression of periodontal pockets is essential to provide the patient with the successful treatment outcomes and monitoring the response to therapy.