PERIODONTAL POCKET.pptx.................

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1. PERIODONTAL POCKET Presented by: Dr divjot Guided by: dr aruna nautiyal

2. CONTENTS DEFINITION CLASSIFICATION POCKET CONTENTS PATHOGENESIS HISTOPATHOLOGY DIAGNOSIS AND TREATMENT

3. definition The periodontal pocket is defined as a pathologically deepened gingival sulcus around a tooth at the gingival margin. Carranza, 10 th edition

4. Classification of periodontal pockets Gingival pocket   is formed by gingival enlargement without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva AKA pseuedopocket Periodontal pocket  produces destruction of the supporting periodontal tissues , thereby leading to the loosening and exfoliation of the teeth.

5. DEEPENING OF THE GINGIVAL SULCUS BY CORONAL MOVEMENT BY APICAL MOVEMENT COMBINATION

6. PERIODONTAL POCKET ACCORDING TO THE RELATION WITH ALVEOLAR BONE

7. SUPRABONY INFRABONY Base of pocket coronal to alveolar bone Base of pocket apical to the alveolar bone Bone destructive pattern horizontal Bone destructive pattern vertical Interproximally , transseptal fibers are restored during progressive periodontal disease are arranged horizontally Transseptal fibers are oblique On facial and lingual surfaces, PDL fibers beneath the pocket follow normal horizontal oblique course between tooth and bone PDL fibers follow angular pattern off adjacent bone.

8. Classification of pockets according to involved tooth surfaces. A,  Simple pocket.  B,  Compound pocket.  C,  Complex pocket

9. CLINICAL FEATURES

10. POCKET CONTENTS

11. PATHOGENESIS

12. INITIAL PHASE

13. Advanced Lesion

14. Pristine gingiva Initial lesion Established lesion Advanced lesion

15. Pathogenesis at the histologic level Histologically, the gingival sulcus is lined by the sulcular epithelium. The sulcular epithelium is structurally different from and less permeable than the junctional epithelium This open system, which lacks a physical barrier in the form of a keratinized cell layer, allow microorganisms and their products to invade the junctional epithelium Schroeder HE, Listgarten MA. The gingival tissues: the architecture of periodontal protection. Periodontol 2000 1997: 13: 91–120.

16. THEORIES OF PATHOGENESIS SKILLEN(1922): epithelial attachment offers a weak barrier for the spread of infection downwards in the connective tissue. Pathological change occurs leading to apical migration of the epithelial cells. GOTTLIEB (1926,1927): root surfaces changes are the main cause of pocket formation rather than changes in the gingival tissues.

17. WILKINSON(1935): pocket formation is the result of proliferation and downgrowth of epithelial attachment or oral epithelium with inflammation playing secondary role. BOX(1941): pocket formation occurs due to imperfect junction between the epithelium and the cementum or too thin epithelial lining, it offers a poor defence mechanism.

18. CALCULUS INFLAMMATION

19. SUPRAGINGIVAL CALCULUS SUBGINGIVAL CALCULUS

20. Hillmann G, Vipismakul V, Donath K. Die Entstehung plaquebedingter Gingivataschen im Tiermodell . Eine histologische Studie an unentkalkten Dunnschliffen . € Dtsch Zahnarztl Z € 1990: 45: 264–266 ( i ) the epithelial cells first recede and later, as a consequence of this, biofilm can migrate apically; or (ii) bacterial products force the epithelial cells to migrate apically.

21. why does loss of cellular continuity, and thus loss of structural integrity, occur at all at this site? 1- direct effect of spread of bacteria 2- increased inflammation Potempa J, Banbula A, Travis J. Role of bacterial proteinases in matrix destruction and modulation of host responses. Periodontol 2000 2000: 24: 153–263 Bostanci N, Belibasakis GN. Porphyromonas gingivalis : an invasive and evasive opportunistic oral pathogen. FEMS Microbiol Lett 2012: 333: 1–9

22. GINGIPAINS   Gingipains are involved in adherence to and colonization of epithelial cells, hemagglutination and hemolysis of erythrocytes, disruption and manipulation of the inflammatory response, and the degradation of host proteins and tissues. Gingipains from  Porphyromonas gingivalis  – Complex domain structures confer diverse functions

23. HISTOPATHOLOGY

24. Detachment of junctional epithelium from the tooth surface and conversion into pocket epithelium. Proliferation of epithelial ridges Focal micro-ulcerations Increased permeability Increased migration of neutrophilic granulocytes Change in direction of the exudate from apico -coronal to horizontal (i.e. toward the tooth root surface) Significant reduction in height of the junctional epithelium.

25. SOFT TISSUE CHANGES

26. BACTERIAL INVASION. Bacterial penetration into the epithelium Bacterial penetration into the connective tissue due to breach into the continuity of the basal lamina.

27. Microtopography of the Gingival WalL

28.   bacterial accumulation   Area of quiescence   bacterial–leukocyte interaction intense cellular desquamation

29. SURFACE TOPOGRAPHY OF TOOTH WALL OF PERIODONTAL POCKET

30. Root Surface Wall CEMENTUM SURFACE BACTERIAL ADHESION

31. Interdental space, showing inflamed gingiva and caries on proximal tooth surfaces.

32. Periodontal Pockets as Healing Lesions Outer collagenous layer Inflamed and ulcerated inner layer

33. If the inflammatory fluid and cellular exudate predominate, the pocket wall is bluish red, soft, spongy, and friable, with a smooth, shiny surface; at the clinical level, this is generally referred to as an edematous pocket wall. If there is a relative predominance of newly formed connective tissue cells and fibers, the pocket wall is more firm and pink, clinically referred to as a fibrotic pocket wall

34. PERIODONTAL DISEASE ACTIVITY Periodontal pockets go through periods of exacerbation and quiescence. These periods of quiescence and exacerbation are also known as periods of inactivity and periods of activity. Periods of quiescence are characterized by a reduced inflammatory response and little or no loss of bone and connective tissue attachment. A buildup of unattached plaque, with its gram-negative, motile, and anaerobic bacteria, starts a period of exacerbation in which bone and connective tissue attachment are lost and the pocket deepens. Clinically, active periods show bleeding, either spontaneously or with probing, and greater amounts of gingival exudate.

35. SITE SPECIFICITY Periodontal destruction does not occur in all parts of the mouth at the same time but rather on a few teeth at a time or even only some aspects of some teeth at any given time. This is referred to as the site specificity of periodontal disease. Sites of periodontal destruction are often found next to sites with little or no destruction . Therefore the severity of periodontitis increases with the development of new disease sites and the increased breakdown of existing sites.

36. ASSESMENT AND DIAGNOSIS

37. CLINICAL EVALUATION

38. POCKET DEPTH CLINICAL ATTACHMENT LOSS Distance from free gingival margin tot the base of the sulcus Distance from the CEJ to the base of the sulcus

39. Same pocket depth with different levels of recession Different pocket depths with same clinical attachment level .

40. PREVENTION STRATEGIES

41. POCKET WATCH: A simple method to diagnose the role of AST in a pocket Components of the extracellular matrix and its dissolved products are present in GCF of destructive pocket releases sulphide ions. AST activity determined by pocket watch provides not only an index of cell death but of the extent of the destructive pockets.

42. TREATMENT MODALITIES

43. NON SUGICAL SURGICAL SCALING AND ROOT PLANNING Resective surgeries Local Drug Deliveries. Gingival curettage Photodynamic Therapy Gingivectomy Systemic antimicrobials Regenerative surgeries Re-attachment procedures New attachment procedures

44. REFEERENCES Carranza10 Periobasics , Nitin Saroach The periodontal pocket , NIKOLAOS DONOS, Perio 2000 The periodontal pocket: pathogenesis, histopathology and consequences DIETER D. BOSSHARDT , perio 2000

45. THANK YOU !