1. PERIODONTAL POCKET

2. DEFINITION A periodontal pocket is defined as pathologically deepened gingival sulcus. It is one of the most important clinical features of periodontal diseases.

3. CLASSIFICATION Gingival pocket Periodontal Pocket Suprabony(supracrestal/supraalveolar) Intrabony(infrabony/subcrestal/intraalveolar)

4. CLINICAL FEATURES Bluish red,thickend marginal gingiva Bluish red vertical zone(GM AM) Gingival bleeding Suppuration Tooth mobility Diastema formation Symptoms-localised pain/pain deep in the bone

5. PATHOGENESIS Inflammatory changes in CT of GS Cellular&fluid inflm. exudate causes degeneration of CT&gingival fibers Just apical to JE collagen fibers destroyed Area is occupied by inflammatory cells & edema

6. PATHOGENESIS Contd.. Two mechanism of collagen loss Collagenases+Enzymes secreated by fibroblasts,PMNs&Macrophages- MMPs became extracellular &destroyes collegen fibroblast phagocytise collagen fibers by extending cytoplasmic process to the ligamentum-cementum interface&degrade collagen fibrils&fibrils of cementum matrix

7. PATHOGENESIS Contd.. As a result of the loss of collagen the apical cells of JE proliferate along the root,extending finger like projections 2/3cells in thickness. PMNs invade the coronal end of JE in no. PMNs not joined to one another/to epithelial cells by desmosomes

8. PATHOGENESIS Contd.. 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)

9. PATHOGENESIS Contd… 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(NUG-ulcer and not pocket formation)

10. HISTOPATHOLOGY C.T. - Edematous&densely infilterated plasma(80%),lymphocytes,PMNs -various degree of degeneration -single/multiple necrotic foci -proliferation of endothelial cells -newly formed capillaries,fibroblast, colagen fibres

11. HISTOPATHOLOGY Contd J.E. -at base of pocket is much shorter than sulcus -coronoapical length 50-100µm -variation in length,width &condition of epithelial cells

12. HISTOPATHOLOGY Contd Epithelial of lateral wall of pocket shows proliferative&degenerative changes Epithelial buds/interlacing cords of epithelial cells from lateral wall adjacent inflamed c.t. Apically than JE Epithelial projections+remainder of lateral epithelium infiltrated with leucocytes &edema

13. HISTOPATHOLOGY Contd Cells under go vascular degeneration &rupture to form vesicles Progressive degeneration&necrosis of epithelium ulceration of lateral wall Exposure of underlying CT &suppuration

14. BACTERIAL INVASION Filaments,rods&coccoid organism with gm-ve cell walls found in intercellular spaces(CP) P.gingivalis&P.intermedia&AA in Gingiva (AP) Bacteria invade intercellular spaces &accumulate on BL Some cross BL &invade CT (Bacterial invasion/translocation)

15. MICROTOPOGRAPHY OF THE GINGIVAL WALL OF THE POCKET Several irregular&oval/elongated areas(pocket wall) with adjacent distance 50-200µm(SEM) Following areas 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

16. PERIODONTAL POCKET AS HEALING LESIONS PP are ch infl lesion constantly repair Distructive & constructive changes Edematous pocket Fibrotic pocket

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

18. SIGNIFICANCE OF PUS FORMATION Pus is common feature of periodontal diseases Secondary sign Reflects nature of inflammatory changes in pocket wall Not indicated severity of the supporting tissue

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

20. ROOT SURFACE WALL Contd.. Penetration of growth of bacteria leads to fragmentation&breakdown of the cementum Results in areas of necrotic cementum,seprated from the tooth by masses of bacteria Endotoxin also detected in the cemental wall of periodontal pocket

21. DECALCIFICATION&REMINERALI ZATION OF CEMENTUM se mineralization an exchange,on exposure to the oral cavity of minerals&organic components at cementum saliva interface se in disease root surface,Ca,Mg,P,&F Microhardnes remains unchanged Hypermineralised zone 10-20µm thick& up to 50µm

22. AREAS OF DEMINERALIZATION Commonly related to root caries Exposure to oral fluid&bacterial plaque results proteolysis of sharpey’s fibers 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

23. SURFACE MORPHOLOGY OF THE TOOTH WALL OF PP 1-cementum covered by calculus 2-attached plaque 3-the zone unattached plaque 4-the zone where JE is attached to the tooth 5-zone of semidestroyed CT fibres 3,4,5-plaque free zones -it is remember that plaque free zone refers to attached plaque -unattached plaque contains gm+ve cocci,rods,filaments,fusiforms&spirochetes -most apical zone contains gm-ve rods&cocci

24. PERIODONTAL DISEASE ACTIVITY PP go through periods of excervation&quiescence Period of quiescence: *reduced inflammatory response *little/no bone&CT attachment loss *unattached plaque with gm-ve motile&anaerobic bacteria

25. PERIODONTAL DISEASE ACTIVITY Contd.. Period of excervation: *bone & CT attachment loss *pocket deepens *this period may lost for days/months&is followed by period of remission/quiescence These periods of quiescence& excervation are also known as period of activity&period of inactivity

26. SITE SPECIFICITY Periodontal destruction does not occur in all parts of the mouth but rather on a few teeth at a time or even only some aspect of some teeth at any given time Severity of periodontal diseases increases by the development of new disease site, the increased breakdown of existing sites

27. PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKETS Spread of infection from PP may cause pathologic changes in the pulp Such changes give rise to painful symptoms Involvement of pulp in the periodontal diseases through apical foramen/lateral canals

28. RELATION OF CAL&BONE LOSS TO POCKET DEPTH Severity of attachment loss is generally not correlated with pocket depth Degree of attachment loss depends on the location of the base of the pocket on the root surface Where as pocket depth is the distance between the base of the pocket &crest of the gingival margin

29. AREA BETWEEN THE BASE OF POCKET&ALVEOLAR BONE Distance between apical end of JE &alv bone is constant Distance between apical end of calculus &alv bone is constant in human PP=1.97mm±33.16% Distance between attached plaque to bone is never less than0.5mm&never more than2.7mm

30. PERIODONTAL ABSCESS It is a localized purulent inflammation in the periodontal tissues. Also known as lateral/parietal abscess Abscess localized in gingiva(gingival abs) Microscopically: -localized accumulation of viable&non viable PMNs pus(center) -acute inflammatory reaction surrounds the purulent area &overlying epithelium -acute abscess chronic abcess

31. PERIODONTAL CYST Uncommon lesion that produces localized destruction of periodontal tissue along a lateral root surface,most often in mandibular canine premolar area Microscopically : The cystic lining may be -loosely arranged,nonkeratinized,thickend, proliferating epithelium -thin nonkertinized epithlium -an odantogenic keratocyst

32. MCQ-1 How much probing pocket depth of a clinically normal gingival sulcus in humans (a)1-2mm (b)2-3mm (c )3-4mm (d)4-5mm

33. MCQ-2 The pocket is formed by gingival enlargement without underlying periodontal destruction is called (a)Pseudo pocket (b)True pocket (c )subcrestal pocket (d)Infrabony pocket

34. MCQ-3 Which type of pocket is most common in furcation areas (a)Simple pocket (b)Compound pocket (c )spiral pocket (d)Supracrestal pocket

35. MCQ-4 A patient has a chief complain of pain in upper right first molar. On examination a purulent inflammation with 8mm of pocket depth was observed on facial aspect of 16.What is the confirmatory diagnosis of that lesion? (a)Periodontal cyst (b)Periodontal abscess ( c)Periapical cyst ( d)Gingival abscess

36. MCQ-5 One of the following lesions have a reduced inflammatory response and little or no loss of connective tissue and bone. A buildup of unattached plaque, with its gram-negative, motile and anaerobic bacteria. (a)period of specificity (b)period of quiescence (c)period of exacerbation (d)period of inactivity

37. MCQ-6 The severity of periodontal diseases is depends on (a)probing pocket depth (b)loss of attachment (c)periodntal abscess (d)gingival abscess

38. MCQ-7 Which of the following factor is responsible for flaccidity in the gingival wall of the periodontal pocket (a)circulatory stagnation (b)destruction of gingival fibers (c)atrophy of the epithelium (d)edema and degeneration