The effect of LPS receptor antibody on experimental periodontitis in mice

牙周病是一组感染，会导致牙周炎和牙周组织的破坏，在严重的情况下，会伴随着牙槽骨丢失，最终导致牙齿脱落。牙龈卟啉单胞菌(P.gigivalis)在牙周病的发病机制中所起的作用比其他牙周病原体更多。我们先前的研究表明，牙龈假单胞菌脂多糖(LPS)刺激的人牙龈成纤维细胞的信号转导途径产生IL-6，进而在体外激活破骨细胞。我们建立了实验性牙周炎小鼠模型。在本研究中，我们报道了抗脂多糖受体抗体对小鼠牙周炎模型的影响。用牙周炎杆菌脂多糖诱导小鼠牙槽骨丢失。抗脂多糖受体抗体可抑制骨吸收。这一结果提示，抗脂多糖受体抗体可能为开发牙周病的治疗药物创造新的可能性。

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.