硬化蛋白和RANKL/RANK/OPG信号通路在慢性牙周炎中的作用

Background: Chronic periodontitis are associated with the resorption of alveolar bone. Sclerostin participates in the process of bone resorption through the RANKL/RANK/OPG pathway. However, the mechanism of bone resorption and sclerostin expression in chronic periodontitis is unclear. In this study, the purpose was to evaluate the mechanism of action of sclerostin in human chronic periodontitis. Methods: Saliva and gingival crevicular fluid were collected from systemically healthy non-periodontitis (n=30) and chronic periodontitis subjects (n=30). The protein levels of sclerostin, RANKL and OPG in saliva and gingival crevicular fluid were detected by enzyme linked immunosorbent assay (ELISA). Results: Sclerostin levels in saliva and gingival crevicular fluid were significantly higher in the chronic periodontitis group than the non-periodontitis group (P < 0.05). The level of OPG is significantly lower but the RANKL level and the ratio of RANKL/OPG was significantly higher than that in the non-periodontitis group in saliva and gingival crevicular fluid (P < 0.05). Sclerostin levels in saliva and gingival crevicular fluid were significantly positively correlated with PD, CAL and BOP (P < 0.05). Conclusions: The results showed that sclerostin may affect bone tissue damage of chronic periodontitis through RANKL/RANK/OPG pathway. It will provide a new insight into the diagnosis and treatment of periodontitis patients.