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    Abstract

    Periodontitis is a chronic inflammatory disease affecting nearly 50 percent of U.S. adults. It is characterized by the irreversible destruction of the alveolar bone, periodontal ligament, and gingival tissues supporting the teeth. Periodontal breakdown results from a dysbiotic relationship between the plaque bacteria and host-immune response. Initiated by the bacterial plaque biofilm, the once normal and homeostatic host defenses intended to contain the subgingival inflammation become dysregulated and hyperactive. A diagnosis of an infrabony defect, also known as intrabony, vertical, or angular defects, is made when the base of the pocket is apical to the alveolar crest. It has been documented that infrabony pockets and angular bony defects are always correlated with the apical downgrowth of subgingival plaque and the concomitant inflammation within the connective tissues. Plaque-induced inflammation results in the lysis of the connective tissue attachment and reduction in alveolar crest height, followed by subsequent proliferation of the junctional epithelium down the exposed and infected root surface.

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