Periodontal pocket

Periodontal pocket/histopathology/pathogenesis/clinical features

1. PERIODONTAL POCKET

2. CONTENTS Definition Classification  Clinical features  Pathogenesis  Histopathology  Periodontal disease activity  Site specificity  Pulp changes associated with periodontal pockets Relationship of attachment loss and bone loss to pocket depth Area between base of pocket and alveolar bone relationship of pocket to bone Periodontal abscess Periodontal cyst Conclusion Reference

3. INTRODUCTION Gingival sulcus is the space between the neck of the tooth and the circumferential gingival tissue. Sulcus , when it deepens { as in periodontal disease } due to the apical migration of junctional epithelium, accompanied by attachment loss, it is referred to as periodontal pocket. Probing depth of clinically normal gingival sulcus = 2-3mm

4. DEFINITION The Periodontal pocket is defined as a pathologically deepened gingival sulcus . - CARRANZA 1OTH edition  It is one of the most important clinical features of periodontal disease.

5. CLASSIFICATION Deepening of the gingival sulcus may occur by Coronal movement of the gingival margin (gingival enlargement) Apical displacement of the gingival attachment A combination of the two processes

6. 1.ACCORDING TO MORPHOLOGY Gingival pocket (pseudo pocket )- This type of 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 . B. Periodontal pocket -  This type of pocket occurs with destruction of the supporting periodontal tissues. Progressive pocket deepening leads to the destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth.

7. Gingival Suprabony Intrabony pocket pocket pocket

8. DIFFERENCES BETWEEN SUPRABONY & INTRABONY POCKETS   SUPRABONY POCKET   Supracrestal  or supra alveolar.  Base of the pocket is coronal to the level of alveolar bone .  Lateral wall consist of the soft tissue alone. INTRABONY POCKET   Infrabony , subcrestal , intraalveolar .  Base of the pocket is apical to crest of alveolar bone.  Lateral wall consist of the soft tissue and bone.

9.     Suprabony pocket Horizontal pattern of bone destruction . Transpetal fibers are arranged horizontally. PDL fibers [facial & lingual] follow normal horizontal-oblique course       Intrabony pocket  Vertical (angular) pattern of bone loss . Transeptal fibers are arranged obliquely. PDL fibers follow angular patern of adjacent bone

10. ACCORDING TO THE NUMBER OF SURFACES INVOLVED Simple Compound Complex SIMPLE POCKET - It involves only one tooth surface. COMPOUND POCKET-  It involves two or more tooth surface. COMPLEX POCKET - Where the base of the pocket is not in direct communication with the gingival margin. It is also known as a  spiral pocket.

11. CLINICAL FEATURES SIGNS-- Enlarged , bluish – red thickened marginal gingiva with a 'rolled' edge. A bluish red vertical zone from the gingival margin to alveolar mucosa. Gingival bleeding and suppuration. Tooth mobility. Loss of stippling. Diastema formation. Gingival bleeding Gingival suppuration

12. SYMPTOMS Localized pain or  "pain deep in the bone". Usually painless but may give rise to localized /radiating pain or sensation of pressure after eating which gradually reduces. A foul taste in localized areas. Sensitivity to hot and cold. Toothache in the absence of caries is also sometimes present. A tendency to stuck material inter proximally. Urge to dig a pointed instrument in the gums. Feeling of loose teeth.

13. CORRELATION OF CLINICAL AND HISTOPATHOLOGIC FEATURES OF THE PERIODONTAL POCKET    CLINICAL FEATURES HISTOPATHOLOGICAL FEATURES Gingival wall of pocket presents- Bluish red discoloration Flaccidity A smooth, shiny surface Pitting on pressure C irculatory stagnation . D estruction of gingival fibers & surrounding tissues. A trophy of epithelium. Edema and degeneration. Gingival wall may be pink and firm Fibrotic changes Bleeding is elicited by gently probing soft tissue wall of pocket Increased vascularity, thinning and degeneration of epithelium, & proximity of engorged vessels to inner surface. On probing, inner aspect of pocket is generally painful Pus may be expressed by applying digital pressure. Pain on tactile stimulation is caused by ulceration of inner aspect of pocket wall. Pus occurs in pockets with suppurative inflammation of inner wall.

14. PATHOGENESIS Inflammatory changes in the C.T. OF gingival sulcus Collagenases and MMPs Activate fibroblasts for phagocytizing collagen Gingival collagen fiber destruction Proliferation of apical cells of J.E. along the root

15. PMNs volume reach 60% or more Detachment of the coronal portion of J.E. from the root Pocket formation

16. Two mechanisms of collagen loss Collagenases & other enzymes secreted by various cells such as fibroblasts, PMNs leukocytes & macrophages, becomes extracellular & destroy collagen; these enzymes that degrade collagen and other macromolecules into small peptides are called MATRIX METALLOPROTEINASES Fibroblast phagocytize collagen fibers by extending cytoplasmic process to the ligament- cementum interface & degrade the inserted collagen fibrils & the fibrils of the cementum matrix.

17. The transformation of a gingival sulcus into periodontal pocket creates an area where plaque removal becomes impossible , & the following mechanism, is followed

18. HISTOPATHOLOGY SOFT TISSUE WALL   Connective tissue Edematous and densely infiltrated with plasma cells (approx. 80%), lymphocytes and a scattering of PMNs. Blood vessels - increased in number, dilated and engorged. Exhibits varying degrees of degeneration. Shows proliferation of endothelial cells with newly formed capillaries, fibroblast and collagen fibers. ii. Junctional epithelium: At the base of the pocket is usually much shorter Coronoapical length is reduced to only 50-100  μm .

19. iii. Lateral wall: Most severe degenerative changes. Epithelial buds or interlacing cords of epithelial cells project from the lateral wall into the adjacent inflamed C.T. & apically than the J.E. Densely infiltrated by leukocytes & edema from the inflamed C.T. Cells : vacuolar degeneration and form vesicles. Ulceration and suppuration .

20. 2. BACTERIAL  INVASION Studies have shown that bacterial invasion occurs in the apical & lateral areas of the pocket wall. Intercellular spaces of the epithelium - Filaments, rods and coccoid organism with predominant gram-negative cells Porphyromonas gingivalis Prevotella intermedia ,   Aggregatibacter   actinomycetemcomitans

21. MICROTOPGRAPHY OF GINGIVAL WALL AREAS OF RELATIVE QUIESCENCE- showing flatten surface with minor depression and mounds and occasional shedding of cells. AREAS OF BACTERIAL ACCUMULATION- presenting as  epithelial  surface depressions, with abundant debris and bacteria clumps penetrating into the enlarged intercellular spaces. These bacteria are usually cocci , rods, and filament with few spirochetes.

22. AREAS OF EMERGENCE  OF LEUKOCYTES- where leukocytes appear in the pocket wall through holes located in the intercellular spaces. AREAS OF LEUKOCYTE- BACTERIA INTERACTION- where numerous leukocytes are present & covered with bacteria in an apparent process of phagocytosis. Bacterial plaque associated with epithelium is seen either as an  organised matrix covered by a fibrin-like material in contact with the surface of cells or as bacteria penetrating into the intercellular spaces

23. 5. AREAS OF INTENSE EPITHELIAL DESQUAMATION- which consist of semi – attached and folded epithelial squames  , sometimes partially covered with bacteria. 6. AREAS OF ULCERATION- with exposed connective tissue. 7. AREAS OF HEMORRHAGE- with numerous erythrocytes. Areas of haemorrhage Areas of ulceration

24. PERIODONTAL POCKET AS HEALING LESIONS Periodontal pockets are chronic inflammatory lesions which undergo repair . The condition of the soft tissue wall of the periodontal pocket result from the interplay of the destructive and constructive tissue changes . Their balance determine clinical features of the pocket wall . Constructive tissue changes Formation of C.T. cells, collagen fibers, appear more firm & pink Destructive tissue changes Fluid & cellular inflammatory exudate , pocket wall is bluish red ,soft, spongy & friable with smooth, shiny surface FIBROTIC POCKET EDEMATOUS POCKET

25. POCKET CONTENTS Debris – microorganism and products ( enzymes, endotoxins, and other metabolic products) Gingival fluid Food remnants Salivary mucin Desquamated epithelial cells Leukocytes Plaque-covered calculus         

26. SIGNIFICANCE OF PUS FORMATION Secondary sign. Nature of the inflammatory changes.      Not an indication of depth of pocket/ severity of destruction.

27. ROOT SURFACE WALL Cause pain Recurrence of infection Complicate periodontal treatment . CHANGES IN ROOT

28. STRUCTURAL CHANGES

29. PATHOGENIC GRANULES Represents areas of collagen degeneration or areas where collagen fibrils have not been fully mineralized initially. AREAS OF INCREASED MINERALIZATION highly mineralized superficial layer increase the tooth resistance to decay   associated with increased perfection of the crystal structure. AREAS OF DEMINERALISATION-   Commonly related to root caries , dominant organism is A. viscosus

30. CHEMICAL CHANGES The mineral content of the exposed cementum is increased.   Exposed cementum may absorb calcium, phosphorous & fluoride from its environment.           Development of highly calcified layer that is resistant to decay. The ability to absorb substance may be harmful, because absorb material may be toxic.

31. CYTOTOXIC CHANGES Endotoxins found in the cementum of periodontally involved teeth. Endotoxins limits the proliferation and attachment of fibroblasts to the diseased root surfaces.

32. Surface morphology of tooth wall with periodontal pocket

33. PERIODONTAL DISEASE ACTIVITY Periodontal pockets go through periods of exacerbation  and quiescence resulting from episodic bursts of activity followed by periods of remission.                            PERIODS OF REMISSION OR QUIESCENCE/INACTIVITY PERIODS OF EXACERBATION/ACTIVITY Gram positive bacteria proliferates Reduced inflammatory response Little or no born and connective tissue attachment loss . Build up of unattached log with its gram negative, motile, and anaerobic bacteria Bone and connective tissue attachment loss pocket deepens.

34. SITE SPECIFICITY

35. Pulp changes associated with periodontal pocket Spread of infection from periodontal pockets causes pathological changes in the pulp leading to painfull symptoms Involvement of the pulp occurs through either the apical foramen or the lateral canals in the root.

36. RELATIONSHIP OF ATTACHMENT LOSS & BONE LOSS TO POCKET DEPTH Pocket formation causes loss of attachment of the gingiva and denudation of the root surface. The severity of the attachment loss is generally, but not always, correlated with the depth of the pocket. This is because the degree of attachment lost depends on the location of the base of the pocket on the root surface, whereas the pocket depth is the distance between the base of the pocket and the Crest of the gingival margin.

37. AREA BETWEEN BASE OF POCKET AND ALVEOLAR BONE Normally, the distance between the apical end of the junctional epithelium and the Alveolar bone is relatively constant. The distance between the apical extend of the calculus and the alveolar Crest in human periodontal pockets is most constant, having a mean length of 1.97 mm. Wade , assessed the relation between pocket base, epithelial attachment and alveolar process and found that the distance from attached plaque is never less than 0.5 mm and never more than 2.7 mm.

38. Periodontal abscess A localised purulent inflammation in the periodontal tissues. Also known as - lateral or parietal  abscess. Abcesses localised in the gingiva, due to injury to the outer surface of the gingiva, and not involving the supporting structures are called Gingival Abscesses.

39. MICROSCOPICALLY localised accumulation of viable and non viable PMNs within the periodontal pocket wall . PMNs liberate enzymes digest tissue & cells pus (present in center of the Abscess) overlying epithelium exhibits intracellular and extracellular edema invasion of leukocytes. Chronic abscess when its purulent content drains into a fistula into the outer gingival surface

40. - PERIODONTAL ABSCESS FORMATION MAY OCCUR IN THE FOLLOWING WAYS-

41. PERIODONTAL CYST Uncommon Lesion that produces localised destruction of the periodontal tissues along a lateral root surface Most often in the mandibular canine-premolar area.

42. The following possible etiologies have been suggested: Odontogenic cyst Lateral dentigerous cyst Primordial cyst of supernumerary tooth germ. Stimulation of epithelial rests of the periodontal ligament by infection from a periodontal Abscess or the pulp through an accessory root canal.

43. 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.

44. REFERENCE CARRANZA 10 th AND 13 th EDITION SHALU BATHLA textbook of PERIODONTICS