Periodontal pocket

PERIODONTAL POCKET

1. PERIODONTAL POCKET MOHAMED HARIS. P.M . READER MALABAR DENTAL COLLEGE

2. Contents Introduction Definition Classification Clinical features Pathogenesis Histopathology Microtopography of gingival wall Periodontal pockets as healing lesions Root surface wall Pocket contents Periodontal disease activity

3. Relation of attachment loss and bone loss to pocket depth Periodontal abscess Periodontal cyst Detection of pocket Conclusion References

4. Introduction Chronic periodontitis is defined as plaque induced inflammation of periodontal tissue which has resulted in destruction of periodontal ligament,loss of crestal alveolar bone,and apical migration of epithelial attachment ( junctional epithelium). These process are usually collectively known as loss of attachment. Periodontitis is characterized by the presence of inflammation at the marginal gingiva,together with loss of attachment, which normally results in the formation of periodontal pocket and often reffered to as destructive periodontal disease. It is always preceeded by gingivitis,but not all gingivitis progresses to periodontitis . If the sulcus depth extends beyond 3mm it is known as pocket. It is one of the most important clinical feature in periodontal diseases

5. Periodontal pocket is defined as pathologically deepened gingival sulcus . Deepening of gingival sulcus may occur by coronal movement of the gingival margin,apical displacement of gingival attachment or combination of both . It is bordered by the tooth on one side,by ulcerated epithelium on the other and has the junctional epithelium at its base

6. CLASSIFICATION Depending upon i ts morphologic characteristics: Gingival pocket (pseudo pocket ) : formed by gingival enlargement without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva Periodontal pocket(absolute/true pocket ): This type of pocket occurs with destruction of the supporting periodontal tissues. Progressive pocket deepening leads to destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth.

7. Depending upon its relationship to crestal bone periodontal pocket classified as: Suprabony / Supracrestal /Supra-alveolar pocket Infrabony / intrabony / subcrestal /intra-alveolar pocket Gingival pocket Suprabony pocket Infrabony pocket

8. Compound pocket - Two or more tooth surfaces were involved. - Base of the pocket in direct communication with the gingival margin along each of the involved surfaces . Depending upon the number of surfaces involved Simple pocket - It involves only one tooth surface

9. Complex pocket - Spiral pocket that orginates on one tooth surface and twists around the tooth to involve one or more additional surfaces. - Their only communication with the gingival margin is at the surface where pocket originates. - More commonly observed in furcation areas Depending upon nature of soft tissue wall of pocket - Edematous pocket - Fibrotic pocket Depending upon the disease activity - Active pocket - Inactive pocket -

10. DIFFERENCES BETWEEN SUPRABONY & INFRABONY POCKETS Suprabony Base of the pocket is coronal to the crest of alveolar bone Pattern of bone destruction is Horizontal Inter proximally the transseptal fibers are restored horizontally during progressive periodontal disease in the space between the base of the pocket and crest of the alveolar bone Infrabony Base of the pocket is apical to the crest of the alveolar bone so that the bone is adjacent to soft tissue wall Pattern of bone destruction is angular/vertical Inter proximally the transseptal fibers are restored obliquely and they extend from the cementum below the base of the pocket along alveolar bone over the crest of the cementum of the adjacent tooth

11. On the facial and lingual surfaces the principal fibers beneath the pocket follow their normal horizontal oblique course between the tooth and the bone On the facial and lingual surfaces the principal fibers beneath the pocket follow angular pattern of the adjacent bone

12. CLINICAL FEATURES Signs - Enlarged bluish red marginal gingiva with a rolled edge separated from the tooth - Reddish blue vertical zone extending from the marginal gingiva to attached gingiva and sometimes into alveolar mucosa - Break in the faciolingual continuity of the interdental gingiva - Shiny, discolored, and puffy gingiva - Gingival bleeding - Purulent exudate of the marginal gingiva in response to digital pressure - Mobility, extrusion, and migration of teeth - Development of diastema

13. Symptoms - Periodontal pockets are generally painless but may give rise to the following symptoms - Localized pain or sensation of pressure after eating which gradually diminishes - Foul taste in localized areas - Tendency to suck material in the interproximal spaces - Radiating pain deep in the bone - A gnawing feeling or feeling of itchiness in the gums and urge to dig pointed instrument into gums and relief obtained from resultant bleeding - F ood stick between teeth or teeth feel loose or preference to eat on the other side - Sensitivity to heat and cold - Toothache in the absence of caries

14. CORRELATION OF CLINICAL AND HISTOLOGIC FEATURES OF PERIODONTAL POCKET The gingival wall of periodontal pocket presents: Varying degrees of bluish red discoloration Flaccidity Smooth , shiny surface Pitting on pressure Circulatory stagnation Destruction of gingival fibers and surrounding tissues Atrophy of epithelium and edema Edema and degeneration of connective tissue

15. Gingival wall may be pink and firm Bleeding is elicited by gently probing the soft tissue wall of pocket When explored with a probe inner aspect of pp generally painful Fibrotic changes predominate over exudation and degeneration particulatly in relation to outer surface of the pocket wall. Increased vascularity Thinning and degeneration of epithelium Proximity of engorged vessels to inner surface Pain upon tactile stimulation due to Ulceration of the inner aspect of the pocket wall

16. Pus may be expressed by applying digital pressure Pockets with suppurative inflammation of the inner wall

17. Theories of the pathogenesis of periodontal pockets Destruction of the gingival fibers is a prerequisite for the initiation of pocket formation. (Fish) The initial change in pocket formation occurs in the cementum . (Gottlieb) Stimulation of the epithelial attachment by inflammation rather than destruction of gingival fibers is a prerequisite for the formation of periodontal pocket.( Aisenberg ) 4 ) Pathologic destruction of epithelial attachment due to infection or trauma is the initial histologic change in pocket formation.( Skillen ) 5) The periodontal pocket is initiated by invasion of bacteria at the base of the sulcus or the absorption of bacterial toxins through the epithelial lining of the sulcus .(Box)

18. 6) Pocket formation initiated with defect in the sulcus wall.(Becks) Proliferation of the epithelium of the lateral wall, rather than epithelium at the base of the sulcus , is the initial change in the formation of periodontal pocket.(Wilkinson) Two – stage pocket formation (James and Counsell ) - Proliferation of the subgingival epithelium (epithelial attachment) - Loss of superficial layers of proliferated epithelium which produces space or pocket. Inflammation is the initial change in the formation of periodontal pocket.(J. Nuckolls) Pathologic epithelial proliferation occurs secondary to non inflammatory degenerative changes in the periodontal membranes.

19. Most accepted recent concept is that the apical migration of apical cells of junctional epithelium and deattachment of coronal portion of junctional epithelium leads to intraepithelial cleft and pocket formation and deepening.

20. Pathogenesis The initial lesion in the development of periodontitis is the inflammation of the gingiva in response to a bacterial challenge. 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 is associated with few microorganisms, mostly coccoid cells and straight rods. Pathologic changes that leads to the deepening of the gingival sulcus may occur by: - Movement of gingival margin in the direction of crown(produces gingival pocket). - Migration of junctional epithelium apically and its seperation from the tooth surface. - Combination of above processes. Diseased gingiva is associated with increased numbers of spirochetes and motile rods.

21. Pocket formation starts as an inflammatory change in the connective tissue wall of the gingival sulcus . The cellular and fluid inflammatory exudate causes degeneration of the surrounding connective tissue, including the gingival fibers. Just apical to the junctional epithelium, collagen fibers are destroyed and the area becomes occupied by inflammatory cells and edema. Immediately apical to this is a zone of destruction and an area of normal attachment. Earlier concept assumed that after the initial bacterial attack ,periodontal tissue destruction continued to be linked to bacterial action. Recently it was established that host immunoinflammatory response to the initial and persistant bacterial attack unleashes mechanism that lead to collagen and bone destruction. These mechanism are related to various cytokines,some produced normally by cells in noninflammed tissue and others by cells involved in the inflammatory process such as polymorphonuclear leukocytes (PMNs), monocytes and other cells leading to collagen and bone destruction.

22. The two mechanism associated with collagen loss are: (1) Collagenases and other enzymes secreted by various cells in healthy and inflamed tissue such as fibroblasts , polymorphonuclear leukocytes, and macrophages become extra cellular and destroy collagen(these enzymes that degrade collagen and other matrix macromolecules into small peptides are called matrix metalloproteinases ) and (2) Fibroblasts phagocytize collagen fibers by extending cytoplasmic processes to the ligament- cementum interface and degrade the inserted collagen fibrils and the fibrils of the cementum matrix . As a consequence of the loss of collagen, the apical cells of the junctional epithelium proliferate along the root, extending fingerlike projections 2-3 cells in thickness. As a result of inflammation, polymorphonuclear neutrophils (PMNs) invade the coronal end of the junctional epithelium in increasing numbers. 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.

23. Thus the coronal portion of the junctional epithelium detaches from the root as the apical portion migrates sulcus bottom shifts apically, and the oral sulcular epithelium occupies a gradually increasing portion of the sulcular (pocket) lining. Extension of the junctional epithelium along the root requires the presence of healthy epithelial cells. Marked degeneration or necrosis of the junctional epithelium retards rather than accelerates pocket formation. 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. Because migration of the junctional epithelium requires healthy, viable cells, it is reasonable to assume that the degenerative changes seen in this area occur after the junctional epithelium reaches its position on the cementum .

24. With continued inflammation, the gingiva increases in bulk, crest of the gingival margin extends coronally and the junctional epithelium continues to migrate apically along the root and seperates from it. The transformation of a gingival sulcus into a periodontal pocket creates an area where plaque removal becomes impossible. The rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation.

25. Histopathology Soft Tissue Wall The connective tissue is edematous and densely infiltrated with plasma cells (approximately80%),lymphocytes, and a scattering of PMNs. The blood vessels are increased in number, dilated, and engorged, particularly in the sub epithelial connective tissue layer. It exhibits varying degrees of degeneration. Single or multiple necrotic foci are occasionally present. Connective tissue also shows proliferation of the endothelial cells with newly formed capillaries,fibroblasts and collagen fibers. The junctional epithelium at the base of the pocket is usually much shorter than that of a normal sulcus . Marked reduction in the length width and condition of epithelial cells, usually the coronoapical length of the junctional epithelium is reduced to only 50 to 100μm.

26. The most severe degenerative changes in the periodontal pocket occur along the lateral wall and the epithelium of the lateral wall of pocket presents striking proliferative and degenerative changes. Progressive degeneration and necrosis of the epithelium lead to ulceration of the lateral wall, exposure of the underlying inflamed connective tissue, and suppuration. Ulceration of lateral wall may occur in shallow pockets and deep pockets are occasionally observed in lateral epithelium is relatively intact or shows only slight degeneration. Epithelium at the gingival crest of periodontal pocket is generally intact and thickened with prominent rete pegs.

27. Bacterial invasion Filaments, rods, and coccoid organisms with predominant gram-negative cell walls have been found in intercellular spaces of the epithelium. Presence of P gingivalis and Prevotella intermedia in the gingiva of aggressive periodontitis cases and A a has also been found in the tissues. Bacteria may invade the intercellular space under exfoliating epithelial cells, but they are also found between deeper epithelial cells and accumulating on the basement lamina. Some bacteria may traverse the basement lamina and invade the subepithelial connective tissue. The presence of bacteria in the gingival tissues has been interpreted by different investigators as bacterial invasion or as passive translocation of plaque bacteria. It has significant clinicopathologic implications and has not yet been clarified.

28. Microtopography of the Gingival Wall of the Pocket These areas are irregularly oval or elongated and adjacent to one another and measure about 50 to 200 µm . These findings suggest that the pocket wall is constantly changing as a result of the interaction between the host and the bacteria. Following areas are: Areas of relative quiescence , showing a relatively flat surface with minor depressions and mounds and occasional shedding of cells. Areas of bacterial accumulation, These bacteria are mainly cocci , rods, and filaments, with a few spirochetes. 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 and covered with bacteria in an apparent process of phagocytosis . -Bacterial plaque associated with epithelium is seen either as an organized matrix covered by a fibrinlike material in contact with surface of cells or as bacteria penetarting into the intercelleular spaces.

29. Areas of intense epithelial desquamation ,shows semi attached and folded epithelial squames with one end attached to the pocket wall surface and other other end free towards the pocket space Area of ulceration , occasionally seen surrounded by areas of hemorrhage.Bottom of ulcer shows exposed collagen fibers and various connective tissue cells. Areas of hemorrhage , with numerous erythrocytes seen.

30. A= Area of quiescence B= Area of bacterial accumulation C= Areas of leukocyte – bacteria interaction D=Areas of intense epithelial desquamation

31. The transition from one area to another could be postulated as follows: - B acteria accumulate in previously quiescent areas, triggering the emergence of leukocytes and the leukocyte-bacteria interaction. - This would lead to intense epithelial desquamation and finally to ulceration and hemorrhage

32. Mechanism of tissue destruction Inflammatory response triggered by bacterial plaque unleashes a complex cascade of events aimed at destroying and removing bacteria,necrotic cells and deletorious agents. This process is non specific and in the attempt to restore health,hosts cell,such as neutrophils,macrophages,fibroblats,epithelial cells and produce proteinases,cytokines and prostoglandins that can damage or destroy the tissues.

33. Periodontal Pockets as Healing Lesions Periodontal pockets are chronic inflammatory lesions and as are constantly undergoing repair. Complete healing does not occur because of the persistence of the bacterial attack, which continues to stimulate an inflammatory response, causing degeneration of the new tissue elements formed in the continuous effort at repair. The condition of the soft tissue wall of the periodontal pocket results from the interplay of the destructive and constructive tissue changes. Their balance determines clinical features such as color, consistency, and surface texture of the 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 known as 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 and clinically known fibrotic pocket wall

34. Edematous and fibrotic pockets represent opposite extremes of the same pathologic process, not different disease entities. They are subject to constant modification, depending on the relative predominance of exudative and constructive changes. Fibrotic pocket walls may be misleading because they do not necessarily reflect what is taking place throughout the pocket wall. The most severe degenerative changes in periodontal tissues occur adjacent to the tooth surface and subgingival plaque. In some cases, inflammation and ulceration inside of the pocket are walled off by fibrous tissue on the outer aspect. Externally the pocket appears pink and fibrotic, despite the inflammatory changes occurring internally.

35. Root Surface Wall The root surface wall of periodontal pockets often undergoes changes that are significant because they may perpetuate the periodontal infection, cause pain, and complicate periodontal treatment. As the pocket deepens, collagen fibers embedded in the cementum are destroyed creating an environment favorable to the penetration of bacteria. Viable bacteria have been found in the roots of 87% of periodontally diseased noncarious teeth. Bacterial penetration into the cementum can be found as deep as the cementodentinal junction and may also enter the dentinal tubules. Penetration and growth of bacteria leads to fragmentation and breakdown of cementum surface and results in areas of necrotic cementum , seperated from the tooth by masses of bacteria. Bacterial products such as endotoxins,have been detected in the cementum wall of periodontal pockets.

36. These changes are manifested clinically by softening of the cementum surface, which is usually asymptomatic but painful when a probe or explorer penetrates the area. They also constitute a possible reservoir for reinfection of the area after treatment. During the treatment, these necrotic areas are removed by root planning until a hard smooth surface is reached.

37. Root cementum suffers Structural Chemical and Cytotoxic changes Structural changes – Presence of pathologic granules: may represent areas of collagen degeneration or areas where collagen fibrils have not been fully mineralized initially. Decalcification and Remineralization of Cementum . - Areas of increased mineralization - Areas of demineralization - Areas of cellular resorption and dentin

38. Areas of increased mineralization are probably a result of an exchange, on exposure to the oral cavity,of minerals and organic components at the cementum saliva interface. Chemical changes:The mineral content of exposed cementum increases . Minerals are increased in diseased root surfaces: calcium," magnesium phosphorus, and fluoride . Microhardness , remains unchanged. The development of a highly mineralized superficial layer may increase the tooth resistance to decay. Absorption property of cementum could be harmful if absorbed materials are toxic to the surrounding tissues

39. The hypermineralized zones are detectable by electron microscopy and are associated with increased perfection of the crystal structure and organic changes suggestive of a subsurface cuticle . No decrease in mineralization was found in deeper areas, indicating that increased mineralization does not come from adjacent areas. A loss of, or reduction in, the cross-banding of collagen near the cementum surface and a subsurface condensation of organic material of exogenous origin are seen

40. Areas of demineralization are commonly related to root caries. Exposure to oral fluid and bacterial plaque results in proteolysis of the embedded remnants of Sharpey's fibers; the cementum may be softened and may undergo fragmentation and cavitation . Active root caries lesions appear as well-defined yellowish or light-brown areas, are frequently covered by plaque, and have a softened or leathery consistency on probing. Inactive lesions are well-defined darker lesions with a smooth surface and a harder consistency on probing. The dominant microorganism in root surface caries is Actinomyces viscosus , although its specific responsibility in the development of the lesion has not been established and other bacteria such as Actinomyces naeslundii , Streptococcus mutans , Streptococcus salivarius , Streptococcus sanguis , and Bacillus cereus have been found to produce root caries in animal models.

41. Quirynen et aI (1999) reported that when plaque levels and pocket depths fall after periodontal therapy (both conservative and surgical), a shift in oral bacteria occurs, leading to a reduction in periodontal pathogens and an increase in S. mutans and the development of root caries. Katz RV (1984) conducted an prevalence rate study of root caries in 20- to 64-year-old individuals and revealed that 42% had one or more root caries lesions and that these lesions tended to increase with age

42. The tooth may not be painful, but exploration of the root surface reveals the presence of a defect, and penetration of the involved area with a probe causes pain. Caries of the root, may lead to pulpitis , sensitivity to sweets and thermal changes, or severe pain. Pathologic exposure of the pulp occurs in severe cases. Root caries may be the cause of toothache in patients with periodontal disease and no evidence of coronal decay. Caries of the cementum requires special attention when the pocket is treated. The necrotic cementum must be removed by scaling and root planing until firm tooth surface is reached, even if this entails extension into the dentin. Bacterial endotoxins may penetrate deep into the cementum of untreated periodontally involved teeth. Endotoxins limits the proliferation and attachment of fibroblasts to the diseased root surfaces. Thus this cementum may act to perpetuate the destructive effects of periodontal disease,by acting as a reservoir for potentially destructive products.

43. Areas of cellular resorption of cementum and dentin are common in roots unexposed by periodontal disease . These areas are of no particular significance because they are asymptomatic and as long as the root is covered by the periodontal ligament, they are apt to undergo repair. If the root is exposed by progressive pocket formation before repair of such areas occurs, these appear as isolated cavitations that penetrate into the dentin. These areas can be differentiated from caries of the cementum by their clear-cut outline and hard surface. They may be sources of considerable pain, requiring the placement of a restoration.

44. Surface morphology of tooth wall Following zones are: 1. Cementum covered by calculus 2. Attached plaque , which covers calculus and extends apically from it to a variable degree, probably 100 to 500 µm. 3. The zone of unattached plaque that surrounds attached plaque and extends apically to it. 4. The zone where the junctional epithelium is attached 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 µm. 5. Apical to the junctional epithelium, there may be a zone of semidestroyed connective tissue fibers.

45. Areas 3, 4, and 5 compose the so-called plaque-free zone seen in extracted teeth. The total width of the plaque-free zone varies according to the type of tooth (it is wider in molars than in incisors) and the depth of the pocket (it is narrower in deeper pockets). It is important to remember that the term plaque-free zone refers only to attached plaque because unattached plaque contains a variety of gram-positive cocci and various gram-negative morphotypes including cocci , rods, filaments, fusiforms , and spirochetes. The most apical zone contain predominantly gram-negative rods and cocci

46. Pocket Contents Periodontal pockets contain debris consisting principally of microorganisms and their products (enzymes, endotoxins , and other metabolic products), gingival fluid, food remnants, salivary mucin , desquamated epithelial cells, and leukocytes. Plaque-covered calculus usually projects from the tooth surface. Purulent exudate , if present, consists of living, degenerated, and necrotic leukocytes; living and dead bacteria; serum; and a scant amount of fibrin. The contents of periodontal pockets filtered free of organisms and debris have been demonstrated to be toxic when injected subcutaneously into experimental animals

47. Pus is a common feature of periodontal disease, but it is only a secondary sign. It merely reflects the nature of the inflammatory changes in the pocket wall. It is not an indication of the depth of the pocket or the severity of the destruction of the supporting tissues. Extensive pus formation may occur in shallow pockets, whereas deep pockets may exhibit little or no pus.

48. Periodontal disease activity More recently, as a result of studies on the specificity of plaque bacteria, the concept of periodontal disease activity has evolved. According to this concept, periodontal pockets go through periods of exacerbation and quiescence, resulting from episodic bursts of activity followed by periods of remission. Periods of quiescence are characterized by a reduced inflammatory response and little or no loss of bone and connective tissue attachment. 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. This period may last for days, weeks, or months and is eventually followed by a period of remission or quiescence in which gram-positive bacteria proliferate and a more stable condition is established . These periods of quiescence and exacerbation are also known as periods of inactivity and periods of activity

49. 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,polymorphonuclear leukocytes,or both are seen. Bacterial samples from the pocket lumen, analyzed with darkfield microscopy, show high proportions of motile organisms and spirochetes. Over time, bone loss detected radiographically .

50. Episodic pattern of chronic periodontitis Socransky et al (1984) had conducted a longitudinal clinical study and recorded clinical attachment loss at individual sites in different subjects over time periods ranging from 2-5 years. They have revealed that despite the presence of inflammation,most sites showed no progression during the study period. Instead,attachment loss occurred at only a few sites and even at these sites was interspersed with long periods of stability or quiscence . This type of episodic,site specific attachment loss has given rise to burst theory of chronic periodontitis . It has further proposed that these bursts might occur randomly through out an individuals life( random burst) or there may be periods when bursts of periodontal breakdown in many sites are more likely (asynchronous multiple burst).

51. Implications of burst theories are: Gingival inflammation at a site may not indicate that further periodontal breakdown is occuring or that it will occur at a later date. Periodontal disease is site-specific and may affect different teeth in the same mouth at different rates. Full-mouth periodontal charting on a regular basis is necessary to identify sites with attachment loss,to determine the pattern and rate of progression and to determine the patients susceptibility. Individual serial radiograph based on findings in periodontal charting may be needed to confirm disease progression but radiographs must not be repeated without a sound cause and therefore must be based on clinical evidence. Each tooth must be considered seperately for treatment. In these studies ,only large changes ≥ 3mm of clinical attachment level could be reliably measured and smaller changes could not be detected. These studies show clearly that site specific,episodic disease progression does occur they do not preclude other patterns of progression including slow regular progression also occuring . Episodic progression would predominate in susceptible patients with more rapid rates of progression

52. 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. It is most commonly found on the sites of periodontal destruction next to sites with little or no destruction. Severity of periodontitis increases by the development of new disease sites and with the increased breakdown of existing sites. Pulp changes associated with periodontal pockets The spread of infection from periodontal pockets may cause pathologic changes in the pulp. Such changes may give rise to painful symptoms or adversely affect the response of the pulp to restorative procedures. Involvement of the pulp in periodontal disease occurs through either the apical foramen or the lateral canals in the root after infection spreads from the pocket through the periodontal ligament. Atrophic and inflammatory pulpal changes occur in such cases Servere breakdown of pulp is seen only when periodontal pocket extends to the pocket.

53. Relation of attachment loss and 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 loss 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. 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. Severity of bone loss is generally, but not always, correlated with pocket depth. Extensive attachment and bone loss may be associated with shallow pockets if the attachment loss is accompanied by recession of the gingival margin, and slight bone loss can occur with deep pockets.

54. Area between the base of the pocket and the 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 extent of calculus and the alveolar crest in human periodontal pockets is most constant, having a mean length of 1.97 mm ± 33.16%. Distance from attached plaque to bone is never less than 0.5 mm and not more than 2.7 mm. These findings suggest that the bone- resorbing activity induced by the bacteria is exerted within these distances. Finding of isolated bacteria, clumps of bacteria, or both in the connective tissue and on the bone surface may modify these considerations

55. Relationship of the periodontal pocket to bone The inflammatory, proliferative,and degenerative changes in intrabony and suprabony pockets are the same, and both lead to destruction of the supporting periodontal tissues. The principal differences between intrabony and suprabony pockets are the relationship of the soft tissue wall of the pocket to the alveolar bone, the pattern of bone destruction, and the direction of the transseptal fibers of the periodontal ligament.

56. PERIODONTAL ABSCESS A periodontal abscess is a localized purulent inflammation in the periodontal tissues . It is also known as a lateral or parietal abscess. Abscesses localized in the gingiva, caused by injury to the outer surface of the gingiva, and not involving the supporting structures are called gingival abscesses. They may occur in the presence or absence of a periodontal pocket. Periodontal abscess formation may occur in the following ways: Extension of infection from a periodontal pocket deeply into the supporting periodontal tissues and localization of the suppurative inflammatory process along the lateral aspect of the root. 2. Lateral extension of inflammation from the inner surface of a periodontal pocket into the connective tissue of the pocket wall. Localization of the abscess results when drainage into the pocket space is impaired.

57. 3. Formation of pocket that with a tortuous course around the root, a periodontal abscess may form in the cul -de- sac, the deep end of which is shut off from the surface. Incomplete removal of calculus during treatment of a periodontal pocket. Gingival wall shrinks, occluding the pocket orifice, and a periodontal abscess occurs in the sealed-off portion of the pocket. 5. A periodontal abscess may occur in the absence of periodontal disease after trauma to the tooth or perforation of the lateral wall of the root in endodontic therapy.

58. Periodontal abscesses are classified according to location as follows: 1. Abscess in the supporting periodontal tissues along the lateral aspect of the root. In this condition, a sinus generally occurs in the bone that extends laterally from the abscess to the external surface. 2. Abscess in the soft tissue wall of a deep periodontal pocket Bacterial invasion of tissues seen in abscesses; the invading organisms were identified as gram negative cocci , diplococci , fusiforms , and spirochetes. Invasive fungi were also found and were interpreted as being opportunistic invaders. Microorganisms that colonize the periodontal abscess have been reported to be primarily gram-negative anaerobic rods. Based on the nature/or duration : Acute & Chronic

59. MICROSCOPIC FEATURES An abscess is a localized accumulation of viable & nonviable PMNs within the periodontal pocket wall. The PMNs liberate enzymes that digest the cells and other tissue structures, forming the liquid product known as pus, which constitutes the center of the abscess. An acute inflammatory reaction surrounds the purulent area, and the overlying epithelium exhibits intracellular and extracellular edema and invasion of leukocytes. The localized acute abscess becomes a chronic abscess when its purulent content drains through a fistula into the outer gingival surface or into the periodontal pocket and the infection causing the abscess is not resolved.

60. ACUTE PERIODONTAL ABSCESS SIGNS: An ovoid elevation of the gingiva along the lateral aspect of the root . Red & edematous gingiva with a smooth, shiny surface . Varied shape & consistency- dome like and relatively firm, or pointed and soft . In most cases pus may be expressed from the gingival margin with gentle digital pressure. SYMPTOMS: Throbbing, radiating pain Exquisite tenderness of the gingiva to palpation Sensitivity of the tooth to palpation Tooth mobility Lymphadenitis Less frequently systemic effects such as- fever, leukocytosis , malaise.

61. CHRONIC PERIODONTAL ABSCESS SIGNS: A sinus opening onto the gingival mucosa seen along the length of the root. The orifice of the sinus may appear as a difficult-to-detect pinpoint opening, which, when probed, reveals a sinus tract deep in the Periodontium . The sinus may be covered by a small, pink, bead like mass of granulation tissue. SYMPTOMS: Usually asymptomatic. May have a history of intermittent exudation. Patient may report episodes of- dull, gnawing pain, slight elevation of the tooth, a desire to bite down on and grind the tooth. Chronic periodontal abscess often undergoes acute exacerbations with all the associated symptoms.

62. Diagnosis: of the periodontal abscess requires correlation of the history and clinical and radiographic findings. The suspected area should be probed carefully along the gingival margin in relation to each tooth surface to detect a channel from the marginal area to the deeper periodontal tissues. Continuity of the lesion with the gingival margin is clinical evidence that the abscess is periodontal. The abscess is not necessarily located on the same surface of the root as the pocket from which it is formed. Pocket at the facial surface may give rise to a periodontal abscess interproximally . It is common for a periodontal abscess to be located at a root surface other than that along which the pocket originated, because drainage is more likely to be impaired when a pocket follows a tortuous course

63. PERIODONTAL CYST It is an uncommon lesion that produces localized destruction of the periodontal tissues along a lateral root surface, most often in the mandibular canine premolar area . The following possible etiologies have been suggested: 1.Odontogenic cyst caused by proliferation of the epithelial rests of Malassez;the stimulus initiating the cellular activity is not known. 2. Lateral dentigerous cyst retained in the jaw after tooth eruption. 3. Primordial cyst of supernumerary tooth germ. 4. Stimulation of epithelial rests of the periodontal ligament by infection from a periodontal abscess or the pulp through an accessory root canal. A periodontal cyst is usually asymptomatic and 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. Its radiographic appearance cannot be differentiated from that of a periodontal abscess

64. DETECTION OF POCKETS The only accurate method of detecting and measuring periodontal pockets is careful exploration with a periodontal probe. They are are not detected by radiographic examination. Periodontal pocket is a soft tissue change. Radiographs indicate areas of bone loss where pockets may be suspected; they do not show pocket presence or depth, and consequently they show no difference before or after pocket elimination unless bone has been modified. Gutta percha points or calibrated silver points can be used with the radiograph to assist in determining the level of attachment of periodontal pockets. They may be used effectively for individual pockets or in clinical research, but their routine use throughout the mouth would be difficult to manage. Clinical examination and probing are more direct and efficient

65. POCKET PROBING The two different pocket depths are (1) biologic or histologic depth and (2) clinical or probing depth. The biologic depth is the distance between the gingival margin and the base of the pocket (the coronal end of the junctional epithelium). This can be measured only in carefully prepared and adequately oriented histologic sections. The probing depth is the distance to which an instrument (probe) penetrates into the pocket. The depth of penetration of a probe in a pocket depends on factors such as size of the probe,force with which it is introduced, direction of penetration, resistance of the tissues, and convexity of the crown. Probe penetration can vary depending on the degree of tissue inflammation.

66. In humans, the probe tip penetrates to the most coronal intact fibers of the connective tissue attachment . The depth of penetration of the probe in the connective tissue apical to the junctional epithelium in a periodontal pocket is about 0.3 mm. This is important in evaluating differences in probing depth before and after treatment, as the reduction in probe penetration may be a result of reduced inflammatory response rather than gain in attachment . The probing forces have been explored by several investigators forces of 0.75 N have been found to be well tolerated and accurate. Interexaminer error (depth discrepancies between examiners) was reported to be as much as 2.1 mm, with an average of 1.5 mm, in the same areas.

67. PROBING TECHNIQUE The probe should be inserted parallel to the vertical axis of the tooth and "walked" circumferentially around each surface of each tooth to detect the areas of deepest penetration. special attention should be directed to detecting the presence of interdental craters and furcation involvements. To detect an interdental crater, the probe should be placed obliquely from both the facial and lingual surfaces so as to explore the deepest point of the pocket located beneath the contact point. In multirooted teeth the possibility of furcation involvement should be carefully explored. The use of specially designed probes (e.g., Nabers probe) allows an easier and more accurate exploration of the horizontal component of furcation lesions.

68. Level of attachment versus pocket depth. Pocket depth is the distance between the base of the pocket and the gingival margin. It may change from time to time even in untreated periodontal disease owing to changes in the position of the gingival margin, and therefore it may be unrelated to the existing attachment of the tooth. The level of attachment is the distance between the base of the pocket and a fixed point on the crown, such as the cementoenamel junction. Changes in the level of attachment can be due only to gain or loss of attachment and afford a better indication of the degree of periodontal destruction. Shallow pockets attached at the level of the apical third of the root connote more severe destruction than deep pockets attached at the coronol third of the roots

69. Determining the level of attachment When the gingival margin is located on the anatomic crown, the level of attachment is determined by subtracting from the depth of the pocket the distance from the gingival margin to the cementoenamel junction. If both are the same, the loss of attachment is zero. When the gingival margin coincides with the cementoenamel junction, the loss of attachment equals the pocket depth. When the gingival margin is located apical to the cementoenamel junction, the loss of attachment is greater than the pocket depth, and therefore the distance between the cementoenamel junction and the gingival margin should be added to the pocket depth.

70. BLEEDING ON PROBING. The insertion of a probe to the bottom of the pocket elicits bleeding if the gingiva is inflamed and the pocket epithelium is atrophic or ulcerated. Noninflamed sites rarely bleed. In most cases, bleeding on probing is an earlier sign of inflammation than gingival color changes" Depending on the severity of inflammation, bleeding can vary from a tenuous red line along the gingival sulcus to profuse bleeding. After successful treatment, bleeding on probing ceases. To test for bleeding after probing, the probe is carefully introduced to the bottom of the pocket and gently moved laterally along the pocket wall. Sometimes bleeding appears immediately after removal of the probe; other times it may be delayed a few seconds. Therefore the clinician should recheck for bleeding 30 to 60 seconds after probing.

71. As a single test, bleeding on probing is not a good predictor of progressive attachment loss; however its absence is an excellent predictor of periodontal stability.' When present in multiple sites of advanced disease, bleeding on probing is a good indicator of progressive attachment loss.'" Armitage (1996), performed a meta-analysis of the various studies and concluded that the presence of bleeding on probing in a "treated and maintained patient population" is an important risk predictor for increased loss of attachment.

72. WHEN TO PROBE: Probing of pockets is done at various times for diagnosis, and for monitoring the course of treatment and maintenance. The initial probing of moderate or advanced cases is usually hampered by the presence of heavy inflammation and abundant calculus and cannot be done very accurately. The purpose of this initial probing, together with the clinical and radiographic examination is done, however, with the main purpose of determining whether the tooth can be saved or should be extracted. After the patient has performed an adequate plaque control for some time and calculus has been removed, the major inflammatory changes disappears, and a more accurate probing of the pockets can be performed. This second probing is for the purpose of accurately establishing the level of attachment and degree of involvement of roots and furcations.Data obtained from this probing provides valuable information for treatment decisions. Periodontal treatment probings are done to determine changes in pocket depth and to ascertain healing progress after different procedures

73. PROBING AROUND IMPLANTS Since periimplantitis can create pockets around implants, probing around them becomes part of examination and diagnosis. To prevent scratching of the implant surface, plastic periodontal probes should be used instead of the usual steel probes used for the natural dentition.

74. Matuliene G et al (2008) conducted a retrospective cohort study , 172 patients were examined after Active periodontol therapy and supportive periodontal therapy (SPT) for 3-27 years (mean 11.3 years ) and investigated the influence of residual PPD >or=5 mm and bleeding on probing (BOP) after active periodontal therapy on the progression of periodontitis and tooth loss. Results showed that the number of residual PPD increased during SPT. Compared with PPD<or=3 mm, PPD=5 mm represented a risk factor for tooth loss. At patient level, heavy smoking, initial diagnosis, duration of SPT and PPD>or=6 mm were risk factors for disease progression, while PPD>or=6 mm and BOP>or=30% represented a risk for tooth loss. They concluded that residual PPD>or=6 mm represent an incomplete periodontal treatment outcome and require further therapy.

75. Armitage et al (1977) evaluated the penetration of probe in healthy beagle,dogs specimen using a standardized force of 25gms. They concluded that probe penetrated the epithelium to about 2/3 rd of its length in healthy specimens, it stopped 0.1 mm short of its apical end in gingivitis specimens and in periodontitis specimens probs tips went past the most apical cells of the junctional epithelium. Thus penetration varies depending on the force of introduction and degree of tissue inflammation.

76. Glauser WM et al (1982) conducted a study on block biopsies comprising dental and gingival tissues taken from the buccal side of 8 beagle dogs between the age of 1-4 years following the application of cotton floss ligatures for periods of 4 to 21 days or upto 5 months. The tissues were processed for light and electromicroscopic examination. The observation revealed that the pocket epithelium : 1.does not attach to the tooth 2.forms irregular ridges and over connective tissue paipllae,thin covering which occasionally ulcerate 3.consisits of cells only some of which show a tendency to differentiate 4.presents a basal lamina complex which discontinuities and multiplications 5.infiltrated mainly by T and B lymphocytes and plasma cells and is transmigrated by neutrophilic granulocytes.

77. Methods of pocket therapy The methods for pocket therapy can be classified under three main headings: New attachment techniques offer the ideal result because they eliminate pocket depth by reuniting the gingiva to the tooth at a position coronal to the bottom of the preexisting pocket. - New attachment is usually associated with filling in of bone and regeneration of periodontal ligament and cementum . 2. Removal of the pocket wall is the most common method. The wall of the pocket consists of soft tissue and may also include bone in the case of intrabony pockets. It can be removed by the following: • Retraction or shrinkage, in which scaling and root planing procedures resolve the inflammatory process and the gingiva therefore shrinks, reducing the pocket depth.

78. Surgical removal performed by the gingivectomy technique or by means of an undisplaced flap. • Apical displacement with an apically displaced flap . 3. Removal of the tooth side of the pocket , which is accomplished by tooth extraction or by partial tooth extraction ( hemisection or root resection)

79. Conclusion Periodontal pocket is an area that is inaccessible for plaque removal resulting in the establishment of following feedback mechanism for further plaque buildup: Plaque gingival inflammation periodontal inflammation periodontal pocket formation more plaque build up. Bacterial factors which might result in disease progression include an increase in total no of bacteria,the presence or overgrowth of specific pathogenic bacteria in the flora or direct invasion of the tissues by bacteria. The rationale of treatment of a pocket ( reduction or elimination) is to establish a periodontal environment where bacterial plaque can be easily removed and free form plaque.

80. References Clinical Periodontology ( Carranza 8th,10 th and 11th edition.) Pathology of periodontal diseases.David.M.Williams . Periodontics.Grant , Stern & Everett .5 th edition Contemporary periodontics.Genco,Goldman and Cohen Outline of periodontics.JD M anson and BM Eley.5 th Edition Armitage GC,Svanberg GK,Loe H.Microscopic evaluation of clinical measurements and connective tissue attachment levels.J Clin Periodontol 1977;4:173.

81. Glauser WM,Schroeder HE.The Pocket Epithelium.A Light and Electronmicroscopic Study.J Periodontol 1982;53:133. Matuliene G,Pjetursson BE,Schmidlin K, Bragger U,Zwahlen M,Lang NP.Influence of residual pockets on progression of periodontitis and tooth loss:Results after 11 years of maintenance.J Clin Periodontol 2008;35:685-695.

82. Thank you