CS4-8)The Periodontal Pocket-Prof.Dr.Tolga Tözüm.pdf

Prof. Dr. TOLGA TOZUM YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Learning outcomes: 1-Will be able to define periodontal pocket, explain the importance of periodontal pocket in periodontal diseases, list the types of periodontal pockets. 2- Will be able to define how to measure periodontal pocke...

Prof. Dr. TOLGA TOZUM YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Learning outcomes: 1-Will be able to define periodontal pocket, explain the importance of periodontal pocket in periodontal diseases, list the types of periodontal pockets. 2- Will be able to define how to measure periodontal pocket and distinguish between periodontal and gingival pockets clinically. 3-Will be able to list the histopathology of the periodontal pocket and describe its association with the clinic, explain the pathogenesis of the periodontal pocket. 4-Will be able to define and clinically distinguish attachment loss. 5- Will be able to define periodontal disease activity and distinguish it clinically. 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. All different types of periodontitis,changes in the periodontal pocket, mechanisms of tissue destruction, and healing mechanisms. However, they differ with regard to their etiology, natural history, progression, and response to therapy. Classification Deepening of the gingival sulcus may occur as a result of coronal movement of the gingival margin, apical displacement of the gingival attachment, or a combination of the two processes. Pockets can be classified as follows: Gingival 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 Periodontal pocket produces destruction of the supporting periodontal tissues, thereby leading to the loosening and exfoliation of the teeth. The remainder of this chapter refers to this type of pocket. Two types of periodontal pockets exist, as follows: Suprabony (supracrestal or supraalveolar) occurs when the bottom of the pocket is coronal to the underlying alveolar bone. Intrabony (infrabony, subcrestal, or intraalveolar) occurs when the bottom of the pocket is apical to the level of the adjacent alveolar bone. With this second type, the lateral pocket wall lies between the tooth surface and the alveolar bone Pockets can involve one, two, or more tooth surfaces, and they can be of different depths and types on different surfaces of the same tooth and on approximal surfaces of the same interdental space. Pockets can also be spiral (i.e., originating on one tooth surface and twisting around the tooth to involve one or more additional surfaces)These types of pockets are most common in furcation areas. Clinical Features Clinical signs that suggest the presence of periodontal pockets include a bluish-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; and symptoms such as 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. 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. Diseased gingiva is associated with increased numbers of spirochetes and motile rods. However, the microbiota of diseased sites cannot be used as a predictor of future attachment or bone loss, because their presence alone is not sufficient for disease to start or progress. Bacterial Invasion Bacterial invasion of the apical and lateral areas of the pocket wall has been described in human chronic periodontitis. Filaments, rods, and coccoid organisms with predominant gram-negative cell walls have been found in intercellular spaces of the epithelium. Hillmann and colleagues have reported the presence of Porphyromonas gingivalis and Prevotella intermedia in the gingiva of aggressive periodontitis cases. Actinobacillus actinomycetemcomitans 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 as well as accumulating on the basement lamina. Some bacteria traverse the basement lamina and invade the subepithelial connective tissue. Mechanisms of Tissue Destruction The inflammatory response triggered by bacterial plaque unleashes a complex cascade of events aimed at destroying and removing bacteria, necrotic cells, and deleterious agents. However, this process is nonspecific; in an attempt to restore health, the host’s cells (e.g., neutrophils, macrophages, fibroblasts, epithelial cells) produce proteinases, cytokines, and prostaglandins that can damage or destroy the tissues. Microtopography of the Gingival Wall Scanning electron microscopy has permitted the description of 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, and they 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. The following areas have been noted: 1. Areas of relative quiescence, showing a relatively flat surface with minor depressions and mounds and occasional shedding of cells. 2. Areas of bacterial accumulation, which appear as depressions on the epithelial surface, with abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. These bacteria are mainly cocci, rods, and filaments, with a few spirochetes.. 3. Areas of emergence of leukocytes, in which leukocytes appear in the pocket wall through holes located in the intercellular spaces. 4. Areas of leukocyte–bacteria interaction, in which numerous leukocytes are present and covered with bacteria in an apparent process of phagocytosis. Bacterial plaque associated with the epithelium is seen either as an organized matrix covered by a fibrinlike material in contact with the surface of cells or as bacteria penetrating into the intercellular spaces 5. Areas of intense epithelial desquamation, which consist of semiattached and folded epithelial squames, which are sometimes partially covered with bacteria 6. Areas of ulceration, with exposed connective tissue 7. Areas of hemorrhage, with numerous erythrocytes. The transition from one area to another could result from bacteria accumulating in previously quiescent areas and triggering the emergence of leukocytes and the leukocyte–bacteria interaction. Periodontal Pockets as Healing Lesions Periodontal pockets are chronic inflammatory lesions and thus are constantly undergoing repair. Complete healing does not occur because of the persistence of the bacterial attack, which continues to stimulate an inflammatory response, thereby causing degeneration of the new tissue elements formed during 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, this is generally referred to as an 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 referred to as a fibrotic pocket wall. 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 the subgingival plaque. In some cases, inflammation and ulceration on the 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. 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. Plaque covered calculus usually projects from the tooth surface.Purulent exudate, if present in the patient, consists of living, degenerated, and necrotic leukocytes; living and dead bacteria; serum; and a scant amount of fibrin. The contents of periodontal pockets, when filtered free of organisms and debris, have been demonstrated to be toxic when injected subcutaneously into experimental animals.Pus is a common feature of periodontal disease, but it is only a secondary sign. The presence of pus or the ease with which it can be expressed from the pocket merely reflects the nature of the inflammatory changes in the pocket wall. Root Surface Walls 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.Pathologic granules have been observed with light and electron microscopy, and they may represent areas of collagen degeneration or areas in which collagen fibrils have not been fully mineralized initially. In addition, bacterial products (e.g., endotoxins) have also been detected in the cementum wall of periodontal pockets. When root fragments from teeth with periodontal disease are placed in tissue culture, they induce irreversible morphologic changes in the cells of the culture. Such changes are not produced by normal roots. Diseased root fragments also prevent the in vitro attachment of human gingival fibroblasts, whereas normal root surfaces allow the cells to attach freely. When placed in the oral mucosa of the patient, diseased root fragments induce an inflammatory response, even if they have been autoclaved. Decalcification and Remineralization of Cementum Areas of increased mineralization65 are 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, and the minerals that are increased in diseased root surfaces include calcium, magnesium, phosphorus, and fluoride. Areas of demineralization are often related to root caries. Exposure to oral fluid and bacterial plaque results in proteolysis of the embedded remnants of Sharpey fibers; the cementum may be softened, and it may undergo fragmentation and cavitation. Unlike enamel caries, root surface caries tend to progress around rather than into the tooth. Active root caries lesions appear as welldefined yellowish or light-brown areas; they are frequently covered by plaque, and they 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. Surface Morphology of Tooth Wall. The following zones can be found in the bottom of a periodontal pocket : 1. Cementum covered by calculus, in which all of the changes described in the preceding paragraphs can be found. 2. Attached plaque, which covers calculus and which extends api- cally from it to a variable degree (typically 100 to 500 μm). 3. The zone of unattached plaque that surrounds attached plaque and extends apically to it. 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 μm. 5. A zone of semidestroyed connective tissue fibers may be apical to the junctional epithelium60 Periodontal Disease Activity For many years the loss of attachment produced by periodontal disease was thought to be a slow but continuously progressive phenomenon. More recently, as a result of studies of 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 as a result of 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. A buildup of unattached plaque, with its gram-negative, motile, and anaerobic bacteria, starts a period of exacerbation during which bone and connective tissue attachment are lost and the pocket deepens. Site Specificity Periodontal destruction does not occur in all parts of the mouth at the same time; rather, it occurs on a few teeth at a time or even only on some aspects of some teeth at any given time. This is referred to as the site specificity of periodontal disease. Sites of periodontal destruction are often found next to sites with little or no destruction. Therefore, the severity of periodontitis increases with 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 they may 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 pulp canals after pocket infection reaches them. Atrophic and inflammatory pulpal changes occur in such cases (see Chapters 52 and 63). Relationship of Attachment 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. This is because the degree of attachment loss depends on the location of the base of the pocket on the root surface, whereas 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. The 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. 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 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. These findings suggest that the bone-resorbing activity induced by the bacteria is exerted within these distances. However, the finding of isolated bacteria or clumps of bacteria in the connective tissue and on the bone surface may modify these considerations. 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. Alternatively,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. This creates some microscopic differences that have some therapeutic importance. They 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. In suprabony pockets, the alveolar crest gradually attains a more apical position in relation to the tooth, but it retains its general morphology and architecture. The interdental fibers that run over the bone from one tooth to the other maintain their usual horizontal direction. In infrabony pockets, the morphology of the alveolar crest changes completely, with the formation of an angular bony defect. The interdental fibers in this case run over the bone in an oblique direction between the two teeth of the interdental space. Periodontal Abscess A periodontal abscess is a localized purulent inflammation in the periodontal tissues. It is also known as a lateral abscess or a parietal abscess. Abscesses that are localized in the gingiva, that are caused by injury to the outer surface of the gingiva, and that do not involve the supporting structures are called gingival abscesses. Gingival abscesses may occur in the presence or absence of a periodontal pocket Periodontal abscess formation may occur in the following ways: 1. 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. Formation of the abscess results when drainage into the pocket space is impaired. 3. Formation in a pocket 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. 4. Incomplete removal of calculus during treatment of a periodontal pocket. The gingival wall shrinks, thereby occluding the pocket orifice, and a periodontal abscess occurs in the sealed-off portion of the pocket. 5. After trauma to the tooth or with perforation of the lateral wall of the root in endodontic therapy. In these situations, a periodontal abscess may occur in the absence of periodontal disease. Periodontal abscesses are classified according to location as follows: 1. Abscess in the supporting periodontal tissues along the lateral aspect of the root. With 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. The bacterial invasion of tissues has been reported 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. Lateral Periodontal Cyst The periodontal cyst, which is also called lateral periodontal cyst, 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. 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. Its radiographic appearance cannot be differentiated from that of a periodontal abscess. 1-Newman M, Takei H, Klokkevold P, Carranza F. Newman and Carranza (2019); Clinical Periodontology, 13th Ed., Elsevier.