The effect of LPS receptor antibody on experimental periodontitis in mice

牙周病是一组感染，导致牙龈发炎和牙周组织破坏，在严重的情况下，伴随着牙槽骨的损失，最终牙齿脱落。牙龈卟啉单胞菌（P.gingivalis）被认为是牙周病发病机制中最重要的致病菌。我们以前的研究表明，从牙龈卟啉单胞菌脂多糖（LPS）刺激的人牙龈成纤维细胞的信号转导途径产生白细胞介素-6，这反过来激活破骨细胞在体外。本研究用牙龈卟啉单胞菌脂多糖（LPS）建立了小鼠实验性牙周炎模型，并观察了抗LPS受体抗体对该模型的影响。用牙龈卟啉单胞菌脂多糖（LPS）诱导小鼠牙槽骨丢失。用抗LPS受体抗体预处理可抑制骨吸收。这一结果提示，抗LPS受体抗体为开发牙周病治疗药物创造了新的可能性。

Periodontal diseases are group of infections that lead to inflammation of the gingiva and destruction of periodontal tissues, and in severe cases are accompanied by loss of alveolar bone with eventual exfoliation of teeth. Porphyromonas gingivalis(P.gingivalis)has been regarded more than other periodontopathogens as playing a role in the pathogenesis of periodontal disease. Our previous research showed that the signal transduction pathway from the P.gingivalis lipopolysaccharides(LPS)-stimulated human gingival fibroblasts produces interleukin-6, which in turn activates osteoclasts in vitro. We established mouse model of experimental periodontitis with P.gingivalis LPS.In this study, we have reported effect of anti-LPS receptor antibodies on the mouse model. The alveolar bone loss was expressed by P.gingivalis LPS on the mouse models. The bone resorption was inhibited by pretreatment with anti-LPS receptor antibody. This result suggest that anti-LPS receptor antibody may create new possibility for developing a remedial drug of periodontal disease.