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Defined as a pathologically deepened gingival sulcus One of the most important clinical features of periodontal disease
Suprabony Pocket
CLINICAL FEATURES
The only reliable method of locating periodontal pockets and determining their extent is careful probing of the gingival margin along each tooth surface
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PATHOGENESIS
The initial lesion in the development of periodontitis is in inflammation of the gingiva in response to a bacterial challenge Pocket formation starts as an inflammatory change in the connective tissue wall of the gingival sulcus The cellular and fluid inflammatory exudates 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 Two mechanisms are considered to be associated with collagen loss:
1.
Collagenases and other enzymes secreted by various cells in healthy and inflamed tissue such as fibroblasts, polymorphonuclear leukocytes, and macrophages become extracellular and destroy collagen: these enzymes that degrade collagen and other matrix macromolecules into small peptides and are called matrix
metalloproteinases
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
Because of the loss of collagen the apical cells of the junctional epithelium proliferate along the root extending fingerlike projections two to three cells in thickness The coronal portion of the junctional epithelium detaches from the root as the apical portion migrates 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 reach approximately 60% or more of the junctional epithelium, the tissue loses cohesiveness and detaches from the tooth surface
Thus the sulcus bottom shifts apically and the oral sulcular epithelium occupies a gradually increasing portion of the sulcular (pocket) lining With continued inflammation, the gingiva increases in bulk, and the crest of the gingival margin extends coronally The junctional epithelium continues to migrate along the root and separates from it Leukocytes and edema from the inflamed connective tissue infiltrate the epithelium lining the pocket, resulting in various degrees of degeneration and necrosis Transformation of a gingival sulcus into a periodontal pocket creates an area where plaque removal becomes impossible
HISTOPATHOLOGY
Periodontal pockets are chronic inflammatory lesions and as such 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 exudates predominate, the pocket wall is bluish-red, soft, spongy, and friable, with a smooth, shiny surface If there is a relative predominance of newly formed connective tissue cells and fibers, the pocket wall is more firm and pink
Pocket Content
Contain debris consisting principally of microorganisms and their products (enzymes, endotoxins, and other metabolic products), gingival fluid, food remnants, salivary mucin, desquamated epithelium cells, and leukocytes Plaque-covered calculus usually project from the tooth surface Purulent exudates, if present, consists of living, degenerated, and necrotic leucocytes; living and dead bacteria; serum; and a scant amount of fibrin
Extracted canine. Red tissue represents the remaining attachment prior to extraction.
A build-up of unattached plaque with its gramnegative, motile, and anaerobic bacteria starts a period of exacerbation (periods of activity) 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
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
Periodontal absecess
Periodontal abscess
Gingival abscess