مرکز منطقه ای اطلاع رساني علوم و فناوري

Abstract :

Periodontitis is an infectious disease characterized by inflammation in gingiva and rezorption of alveolar bone. Bacterial factors and immune system of the host- mediated proinflammatory molecules- are involed in this inflammatory process. Because of involving both immunology and bone metabolism, the etiology of periodontitis is being examined in a new interdisciplinary field called “osteoimmunology”. Recently investigated molecules that are thought to be responsible for bone loss, are OPG, RANKL, RANK. RANKL, its receptor RANK–stimulating osteoclast maturation- and decoy receptor OPG –inhibiting RANKL to induce osteoclastogenesis- are key molecules that regulate osteoclast recruitment and function. The axis of these three molecules are critical for pathologic lesions in chronic inflammation, bone and vascular pathologies. RANKL levels in gingival tissue and gingival crevicular fluid of the patients with periodontitis are higher than those of periodontally healthy people. Therefore destruction of the periodontal tissues can be improved by blocking RANKL expression and function. Biologic approaches targeting RANKRANKL- OPG axis seem to be a new concept over the pathogenesis of periodontal lesions and future therapeutic options.