Carranza 2015, 12th edition, Chapter 20, The Periodontal Pocket

Carranza's Clinical Periodontology, 12th edition, Chapter 20, The Periodontal Pocket
The periodontal pocket, which is defined as a pathologically deepened gingival sulcus, is one of the most important clinical features of periodontal disease. ....

1. The periodontal pocket Carranza’s Clinical Periodontology, 12 th Edition Chapter 20 Mostafa Montazeri , Resident of Periodontics, IAU Tehran

2. Periodontal Pocket: pathologically deepened gingival sulcus one of the most important clinical features of periodontal disease

3. Classification Gingival pocket: gingival enlargement without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva Periodontal pocket: Destruction of the suppo rting periodontal tissues  Lo osening and exfoliat ion of the teeth

4. Classification Two types of periodontal pockets exist : Suprabony ( supracrestal or supraalveolar ): The bottom of the pocket is coronal to the underlying alveolar bone Intrabony ( infrabony, subcrestal, or intraalveolar ): The bottom of the pocket is apical to the level of the adjacent alveolar bone. the lateral pocket wall lies between the tooth surface and the alveolar bone

5. Classification Pockets can also be spiral (i.e., originating on one tooth surface and twisting around the tooth to involve one or more additional surfaces ) most common in furcation areas

6. Clinical Features B luish-red thickened marginal gingiva; a bluish-red vertical zone from the gingival margin to the alveolar mucosa; gingival bleeding and suppuration ; tooth mobility ; diastema formation Symptoms : localized pain or pain “deep in the bone .” The only reliable method of locating periodontal pockets and determining their extent is careful probing of the gingival margin along each tooth surface

7. Pathogenesis The initial lesion: the inflammation of the gingiva Changes involved in the transition from the normal gingival sulcus to the pathologic periodontal pocket are associated with different proportions of bacterial cells in dental plaque . Healthy gingiva: mostly coccoid cells and straight rods . Diseased gingiva: Increased numbers of spirochetes and motile rods

8. Pathogenesis

9. Pathogenesis The two mechanisms associated with collagen loss (1) collagenases and other enzymes secreted by various cells in healthy and inflamed tissue; Fibroblasts , PMNs , and macrophages ( 2 ) fibroblasts phagocytize collagen fibers by extending cytoplasmic processes to the ligament–cementum interface and degrading the inserted collagen fibrils and the fibrils of the cementum matrix

10. Pathogenesis As a consequence of the loss of collagen, the apical cells of the junctional epithelium proliferate along the root and extend fingerlike projections that are two or three cells in thickness

11. Pathogenesis As a result of inflammation, PMN s invade the coronal end of the junctional epithelium in increasing numbers. The PMNs are not joined to one another or to the epithelial cells by desmosomes.  T he coronal portion of the junctional epithelium detaches from the root as the apical portion migrates  apical shift When the relative volume of PMNs reaches approximately 60% or more of the junctional epithelium, the tissue loses cohesiveness and detaches from the tooth surface.

12. pathogenesis Extension of the junctional epithelium along the root requires the presence of healthy epithelial cells . Marked degeneration or necrosis of the junctional epithelium impairs rather than accelerates pocket formation (NUG) Degenerative changes seen in the junctional epithelium at the base of periodontal pockets are usually less severe than those in the epithelium of the lateral pocket wall

13. pathogenesis The degree of leukocyte infiltration of the junctional epithelium is independent of the volume of inflamed connective tissue  T his process may occur in gingiva with only slight signs of clinical inflammation

14. Histopathology The connective tissue is edematous and densely infiltrated with plasma cells (approximately 80% ), lymphocytes , and a scattering of PMNs . The blood vessels are increased in number, dilated , and engorged Varying degrees of degeneration Single or multiple necrotic foci are occasionally present . In addition, proliferation of the endothelial cells, with newly formed capillaries, fibroblasts , and collagen fibers

15. Histopathology The junctional epithelium at the base of the pocket is usually much shorter than that of a normal sulcus. the coronoapical length of the junctional epithelium is reduced to only 50 - 100 Micron The most severe degenerative changes in the periodontal pocket occur along the lateral wall ; proliferative and degenerative changes

16. Histopathology The severity of the degenerative changes is not necessarily related to pocket depth . Ulceration of the lateral wall may occur in shallow pockets , and deep pockets are occasionally observed in which the lateral epithelium is relatively intact or shows only slight degeneration. The epithelium at the gingival crest of a periodontal pocket is generally intact and thickened , with prominent rete pegs

17. Histopathology; Bacterial invasion Filaments , rods , and coccoid organisms with predominant gram-negative cell walls have been found in intercellular spaces of the epithelium The presence of Porphyromonas gingivalis and Prevotella intermedia in the gingiva of aggressive periodontitis cases. A.actinomycetemcomitans has also been found in the tissues

18. Histopathology; Mechanisms of tissue destruction T he host’s cells (e.g., neutrophils, macrophages, fibroblasts, epithelial cells) produce proteinases , cytokines , and prostaglandins that can damage or destroy the tissues

19. Microtopograpghy of the gingival wall SEM; several areas in the soft-tissue (gingival) wall of the periodontal pocket in which different types of activity take place. These areas are irregularly oval or elongated and adjacent to one another measure about 50 to 200 μicron  T he pocket wall is constantly changing as a result of the interaction between the host and the bacteria

20. Microtopograpghy of the gingival wall 1. Areas of relative quiescence 2 . Areas of bacterial accumulation ; mainly cocci , rods , and filaments , with a few spirochetes 3. Areas of emergence of leukocytes 4 . Areas of leukocyte–bacteria interaction 5 . Areas of intense epithelial desquamation 6. Areas of ulceration , with exposed connective tissue 7 . Areas of hemorrhage

21. Periodontal pockets as healing lesions The condition of the soft-tissue wall of the periodontal pocket results from the interplay of the destructive and constructive tissue changes . Edematous pocket wall ; 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 Fibrotic pocket wall ; If there is a relative predominance of newly formed connective tissue cells and fibers , the pocket wall is more firm and pink

22. Pocket contents Periodontal pockets contain debris that consists principally of microorganisms and their products (enzymes, endotoxins, and other metabolic products), gingival fluid , food remnants , salivary mucin , desquamated epithelial cells , and leukocytes .

23. Pocket contents Pus is a common feature of periodontal disease, but it is only a secondary sign It is not an indication of the depth of the pocket or the severity of the destruction of the supporting tissues. Extensive pus formation  S hallow pockets , whereas deep pockets may exhibit little or no pus

24. Root surface walls As the pocket deepens, collagen fibers embedded in the cementum are destroyed, and cementum becomes exposed to the oral environment. Collagenous remnants of Sharpey fibers in the cementum undergo degeneration, thereby creating an environment favorable to the penetration of bacteria. Viable bacteria have been found in the roots of 87% of periodontally diseased noncarious teeth.

25. Root surface walls Bacterial penetration into the cementum can be found as deep as the CDJ and it may also enter the dentinal tubules . Penetration and the growth of bacteria leads to fragmentation and breakdown of the cementum surface and results in areas of necrotic cementum that are separated from the tooth by masses of bacteria

26. Decalcification and Remineralization of Cementum Areas of increased mineralization; Probably a result of an exchange of minerals and organic components at the cementum– saliva interface after exposure to the oral cavity. The mineral content of exposed cementum increases Increased minerals in diseased root surfaces: Calcium , Magnesium , Phosphorus and Fluoride Microhardness remains unchanged increased tooth’s resistance to decay

27. Decalcification and Remineralization of Cementum Areas of demineralization are often related to root caries Unlike enamel caries, root surface caries tend to progress around rather than into the tooth. Active root caries lesions  W ell-defined yellowish or light-brown areas; Frequently covered by plaque , and they have a softened or leathery consistency on probing Inactive lesions  W ell-defined darker lesions with a smooth surface and a harder consistency on probing

28. Decalcification and Remineralization of Cementum The dominant microorganism in root surface caries is Actinomyces viscosus when plaque levels and pocket depths decrease after periodontal therapy (both nonsurgical and surgical ), a shift in oral bacteria occurs  R eduction in periodontal pathogens, an increase in S. mutans , and the development of root caries

29. Decalcification and Remineralization of Cementum Areas of cellular resorption of cementum and dentin are common in roots that are unexposed by periodontal disease. No particular significance; symptom free , L ikely to undergo repair However , if the root is exposed by progressive pocket formation before repair occurs, these areas appear as isolated cavitations that penetrate into the dentin

30. Surface Morphology of Tooth Wall The following zones can be found in the bottom of a periodontal pocket 1 . Cementum covered by calculus 2 . Attached plaque (typically 100 to 500 μicron ) 3. The zone of unattached plaque 4. The zone of attachment of the junctional epithelium to the tooth. The extension of this zone, which in normal sulci is more than 500 μm , is usually reduced in periodontal pockets to less than 100 μ m . 5. A zone of semi destroyed connective tissue fibers

31. Surface Morphology of Tooth Wall Zones 3 , 4 , and 5 make up the “ plaque-free zone ” The total width of the plaque-free zone varies according to the type of tooth ( molars> incisors ) and the depth of the pocket (it is narrower in deeper pockets )

32. Periodontal disease activity periodontal pockets go through periods of exacerbation and quiescence. Periods of quiescence; R educed inflammatory response and little or no loss of bone and connective tissue attachment. period of exacerbation A buildup of unattached plaque, with its gram-negative , motile , and anaerobic bacteria during which bone and connective tissue attachment are lost and the pocket deepens

33. Periodontal disease activity Clinically, active periods show: Bleeding , either spontaneously or with probing, and greater amounts of gingival exudate. Histologically , the pocket epithelium appears thin and ulcerated, and an infiltrate composed predominantly of plasma cells and PMNs.

34. Relationship of Attachmen t Loss and Bone Loss to Pocket Depth The severity of the attachment loss in pocket formation is generally but not always correlated with the depth of the pocket. Pockets of the same depth may be associated with different degrees of attachment loss and pockets of different depths may be associated with the same amount of attachment loss

35. Relationship of Attachmen t Loss and Bone Loss to Pocket Depth The severity of bone loss is generally but not always correlated with pocket depth

36. Area Between Base of Pocket and Alveolar Bone The distance between the apical end of the junctional epithelium and the alveolar bone is relatively constant. The distance between the apical extent of calculus and the alveolar crest in human periodontal pockets is most constant , having a mean length of 1.97 mm (±33.16 %) The distance from attached plaque to bone is never less than 0.5 mm and never more than 2.7 mm

37. Relationship of pocket to bone In infrabony pockets , the base of the pocket is apical to the crest of the alveolar bone, and the pocket wall lies between the tooth and the bone. The bone loss is in most cases vertical . in suprabony pockets , the base is coronal to the crest of the alveolar bone , and the pocket wall lies coronal to the bone. The type of bone loss is always horizontal

38. Periodontal Abscess A periodontal abscess  L ocalized purulent inflammation in the periodontal tissues It is also known as a lateral abscess or a parietal abscess Periodontal abscess formation may occur in the following ways:

39. Periodontal Abscess Extension of infection from a periodontal pocket deeply into the supporting periodontal tissues Lateral extension of inflammation from the inner surface of a periodontal pocket into the connective tissue of the pocket wall. Formation in a pocket with a tortuous course around the root. Incomplete removal of calculus during treatment of a periodontal pocket. After trauma to the tooth or with perforation of the lateral wall of the root in endodontic therapy

40. Lateral periodontal cyst most often in the mandibular canine–premolar area. It is considered to be derived from the rests of Malassez or other proliferating odontogenic rests. A periodontal cyst is usually asymptomatic , without grossly detectable changes, but it may present as a localized, tender swelling Radiographically, an interproximal periodontal cyst appears on the side of the root as a radiolucent area bordered by a radiopaque line

41. THE END