The effect of LPS receptor antibody on experimental periodontitis in mice

牙周病是一组导致牙龈炎症和牙周组织破坏的感染，在严重的情况下，伴随着牙槽骨的丧失，最终导致牙齿脱落。Porphyromonas gingivalis (P。牙周病（Gingivalis）在牙周病的发病机制中起着比其他牙周病病原体更重要的作用。我们之前的研究表明，牙龈多糖（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，而白细胞介素-6反过来激活体外破骨细胞。我们用牙龈假单胞菌LPS建立实验性牙周炎小鼠模型。在本研究中，我们报道了抗lps受体抗体对小鼠模型的影响。用牙龈卟啉脂多糖在小鼠模型上表达牙槽骨丢失。抗脂多糖受体抗体预处理可抑制骨吸收。这一结果提示抗lps受体抗体可能为开发治疗牙周病的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.