perioDONTAL pocket

perioDONTAL pocket

1. Presented by: Dr. Fatima Gilani (JR-II) Moderator : Dr. Shivjot Chhina Perceptor - Dr. Kumar Saurav PERIODONTAL POCKET Seminar-6

2. 1.Definition 2.Classification of pocket 3.Pathogenesis of pocket 4.Soft tissue wall changes 5.Clinical features and their causes 6.Microtopography of gingival wall of pocket 6.Contents of pocket 7.Root surface wall of pocket 8.Diagnosis and detection of pocket 9.Treatment CONTENTS

3. A pocket is defined as a ‘pathologically deepened gingival sulcus ’. Deepening of the gingival sulcus may occur by coronal movement of the gingival margin, apical displacement of the gingival attachment , or a combination of the two processes. 1 SOURCE:- www.arestin.com DEFINITION

4. I.) Depending upon its morphology 1.) GINGIVAL/PSEUDO/RELATIVE POCKET 2.) PERIODONTAL POCKET SOURCE: Fermin A. Carranza, Newmann , Takei, Klokkevold ; Clinical Periodontology; 10 TH edition. CLASSIFICATION OF POCKET

5. B.) Types of periodontal pocket upon its relationship to crestal bone 1.) SUPRABONY POCKET 2.) INTRABONY SOURCE: Fermin A. Carranza, Newmann , Takei, Klokkevold ; Clinical Periodontology; 10 TH edition. POCKET

6. DISTINGUISHING FEATURES OF SUPRA AND INFRABONY POCKETS 1 SUPRABONY POCKET INFRABONY POCKET Also known as supracrestal or supraalveolar pocket Also known as infrabony , subcrestal and intra-alveola r pocket The base of the pocket is coronal to the level of the alveolar bone. Bottom of pocket is apical to the crest of underlying alveolar bone Lateral wall consist of soft tissue alone Lateral wall consist of soft tissue and bone Pattern of destruction of bone is horizontal Pattern of destruction of bone is vertical Interproximally transeptal fibers arrange horizontally Interproximally transeptal fibers are oblique rather than horizontal On facial and lingual surfaces periodontal ligament fibers follow horizontal- oblique course between the tooth and bone On the facial and lingual surfaces periodontal ligament fibers follow angular pattern.

7. Pockets can involve one, two, or more tooth surfaces It can be of different depths and types on different surfaces of the same tooth. TOPOGRAPHY OF HUMAN PERIODONTAL POCKET 2,3

8. C). Depending upon the number of surfaces involved 2,3 : A.) Simple pocket- involving one tooth surface B.) Compound pocket- involving two or more tooth surfaces C.) Complex pocket- where the base of the pocket is not in direct communication with gingival margin, also known as spiral pocket . SOURCE: Fermin A. Carranza, Newmann , Takei, Klokkevold ; Clinical Periodontology; 10 TH edition.

9. D.) Depending upon the nature of the soft tissue wall of the pocket A .) Edematous pocket B.) Fibrotic pocket SOURCE:-WWW..POCKETDENTISTRY.COM

10. E.) Depending upon the disease activity 4 SOURCE:- WWW.PERIOBASICS.COM

11. SOURCE:-WWW..POCKETDENTISTRY.COM CLINICAL FEATURES 1

12. SYMPTOMS

13. CLINICAL FEATURES HISTOLOGIC FEATURES 1.)Bluish red discoloration of gingival wall of pocket. Due to circulatory stagnation 2.) Flaccidity Due to destruction of gingival fibers 3.) Smooth shiny surface Due to atrophy of epithelium and edema 4.) Pitting on pressure Due to edema and degeneration 5.) Bleeding on probing Due to- 1-Increased vascularity 2-Thinning and degeneration of epithelium 3-Proximity of engorged vessel to inner surface 6. Pain on probing Due to ulceration of inner aspect of pocket wall CORELATION BETWEEN CLINICAL AND HISTOLOGIC FEATURES

14. It starts with inflammatory changes in Connective tissue of Gingival Sulcus. Cellular & fluid inflammatory exudate cause :- Degeneration of:- A.) Connective tissue B.) Gingival fibers & C.) Collagen fibers Just apical to Junctional Epithelium, collagen fibers get destroyed. ETIOPATHOGENESIS 1

15. Collagenases + Enzymes secreted by fibroblasts, PMNLs & Macrophages- MMPs became extracellular & destroyes collagen. Fibroblast phagocytise collagen fibers by extending cytoplasmic process to the ligament - cementum interface & degrade collagen fibrils & fibrils of cementum matrix. TWO MECHANISM OF COLLAGEN LOSS

16. As a result of the loss of collagen the apical cells of JE proliferate along the root ,extending finger like projections 2 or 3cells in thickness. PMNs invade the coronal end of JE in increasing numbers. PMNs not joined to one another/to epithelial cells by desmosomes Cementum denuded surface of fibers is covered by finger like extension of epithelium

17. Relative volume of PMNs reaches 60%/more of JE Tissue losses cohesiveness detach from tooth surface Coronal portion of JE detach from the root as the apical portion migrate Resulting in its apical shift & oral SE gradually occupies increased portion of the sulcus(pocket lining)

18. Extension of the JE along the root requires the presence of healthy epithelial cells. Marked degeneration/necrosis of JE impairs rather than accelerates pocket formation .

19. Connective Tissue changes - Edematous & densely infilterated plasma (80%), lymphocytes, PMNs -various degree of degeneration -single/multiple necrotic foci -proliferation of endothelial cells -newly formed capillaries, fibroblast, collagen fibres HISTOPATHOLOGY 1,5

20. Changes in Junctional Epithelium -At base of pocket is much shorter than sulcus - Corono -apical length 50-100µm -Variation in length, width & condition of epithelial cells

21. Epithelium of lateral wall of pocket shows proliferative & degenerative changes Epithelial buds/interlacing cords of epithelial cells project from lateral wall into the adjacent inflammed connective tissue and may extend apically than JE Epithelial projections + remainder of lateral epithelium are densely infiltrated with leucocytes & edema from the inflamed connective tissue.

22. Cells undergo vascular degeneration & rupture to form vesicles. Progressive degeneration & necrosis of epithelium ulceration of lateral wall and Exposure of underlying Connective Tissue & suppuration

23. Filaments, rods & coccoid organism which are gram - ve found in intercellular spaces(CP) P.gingivalis & P. intermedia & AA in Gingiva (AP)…( Hillmann et al). Bacteria invade intercellular spaces & accumulate on basement lamina. Some cross Basement Lamina & invade Connective tissue (Bacterial invasion /translocation) BACTERIAL INVASION 1,6

24. Several irregular & oval/elongated areas (pocket wall) with a width of 50-200 µm (SEM ) Following areas are seen :- 1 -Areas of relative quiescence 2-Areas of bacterial accumulation 3-Areas of emergence of leukocytes 4-Areas of leukocyte-bacteria interaction 5-Areas of intense epithelial desquamation 6-Areas of ulceration 7-Areas of hemorrhage MICROTOPOGRAPHY OF THE GINGIVAL WALL OF THE POCKET

25. 1.Areas of relative quiescence: Shows flat surface with minor depressions and mounds; occasional shedding of cells 2.Areas of bacterial accumulation: Appears as depressions on the epithelial surface with abundant debris and Bacterial clumps . Bacteria are rods , cocci , filaments, spirochetes .

26. 3.Areas of emergence of leucocytes Leucocytes appear in the pocket wall through holes located in the intercellular spaces 4.Area of leukocyte and bacterial interaction: Numerous leucocytes are present and are covered with bacteria in an apparent process of phagocytosis.

27. 5.Areas of intense epithelial desquamation: Consists of semi attached and folded epithelial remnants sometimes covered by bacteria. 6. Areas of ulceration : with exposed connective tissues 7. A reas of hemorrhage :- with numerous erythrocytes

28. Periodontal Pockets are chronic inflammatory lesion and undergo constant repair Changes can be:- Destructive changes & Constructive Edematous pocket Fibrotic pocket PERIODONTAL POCKET AS HEALING LESIONS

29. Debris consisting microorganism & products (enzymes, endotoxins & metabolic products ) Gingival fluid remnants , salivary mucin Desquamated epithelial cells & leukocyte Purulent exudate consists of living, degenerated & scant amount of fibrin POCKET CONTENTS

30. Pus is common feature of periodontal diseases It is a Secondary sign Reflects nature of inflammatory changes in pocket wall It is does not indicate the severity of the destruction of supporting tissue. SIGNIFICANCE OF PUS FORMATION

31. In deepen pocket, collagenous fibers embedded in cementum destroyed & exposed to oral environment Remnants of Sharpey’s undergo degeneration & create environment for penetration of viable bacteria Pathologic granules represent areas of collagen degeneration (optical/electron microscopy) ROOT SURFACE WALL

32. Increased mineralization as an exchange, on exposure to the oral cavity of minerals & organic components at cementum saliva interface Increase in disease root surface, Ca , Mg, P, & F Microhardness remains unchanged Hypermineralised zone 10-20µm thick& up to 50µm DECALCIFICATION & REMINERALIZATION OF CEMENTUM 1

33. Commonly related to root caries Exposure to oral fluid & bacterial plaque result proteolysis of S harpey’s fiber Cementum may be softened & undergo fragmentation & cavitation Active root caries lesions-yellowish/light brown areas, covered with plaque & soft Inactive lesions- darker with smooth surface & harder consistency Actinomyces viscosus major organism & others A. naeslundii , S. mutans , S.salivarious , S.sanguis & B.cereus AREAS OF DEMINERALIZATION

34. Various zones seen at bottom of the pocket: 1. Cementum covered by calculus . 2. Covered by attached plaque -extends apically to a variable degree upto 100-500  m 3. Zone of unattached plaque -surrounds the attached plaque and extends apically to it. 4. Zone where the junctional epithelium is attached to the tooth .The extension of this zone (in normal sulcus-500μm ) is usually reduced in periodontal pockets less than 100  m.   5. Apical to junctional epithelium . Total width of plaque free zone varies according to type of tooth-wider in molars than in incisors.

35. Various zones seen at bottom of the pocket: 1. Cementum covered by calculus . 2. Covered by attached plaque -covers the calculus and extends apically to a variable degree upto 100-500  m 3. Zone of unattached plaque -surrounds the attached plaque and extends apically to it. 1

36. Periodontal Pocket go through periods of exacerbation & quiescence Period of quiescence: Reduced inflammatory response little/no bone & CT attachment loss unattached plaque with gram- ve motile & anaerobic bacteria PERIODONTAL DISEASE ACTIVITY

37. Period of exacerbation: bone & CT attachment loss pocket deepens this period may lost for days/months & is followed by Period of remission/quiescence These periods of quiescence & exacerbation are also known as period of activity & period of inactivity