牙龈蛋白及其对破骨和成骨细胞功能的影响
Effect of gingipains on osteoclasts and osteoblasts
作者：侯玉帛1 刘歆婵2 于海燕1 崔磊华3 于维先4
Author：Hou Yubo1, Liu Xinchan2, Yu Haiyan1, Cui Leihua3, Yu Weixian4
收稿日期：2015-12-07 年卷（期）页码：2016,43(5):609-613
期刊名称：国际口腔医学杂志
Journal Name：International Journal of Stomatology
关键字：牙龈卟啉单胞菌,牙周炎,牙龈蛋白,成骨细胞,破骨细胞,
Key words：Porphyromonas gingivalis,periodontitis,gingipains,osteoclasts,osteoblasts,
基金项目：吉林省卫生厅资助项目（20102045）；吉林省发改委资助项目（2013C022-4）；吉林省科技厅资助项目（20150101076JC）
中文摘要
牙龈卟啉单胞菌分泌的牙龈蛋白作为牙周病的一种重要的毒力因子，一方面通过降解骨保护蛋白（OPG）及促进核因子-κB（NF-κB）受体活化因子配体（RANKL）的释放激活OPG/RANKL/NF-κB受体活化因子信号转导通路，进而诱导破骨细胞前体细胞向破骨细胞分化，增强破骨细胞功能；另一方面，牙龈蛋白可通过线粒体依赖性内在程序性细胞死亡通路和肿瘤坏死因子受体家族介导的外在程序性细胞死亡通路诱导成骨细胞程序性细胞死亡，抑制成骨细胞功能，最终导致牙槽骨丧失。本文就近年来牙龈蛋白及其对破骨和成骨细胞功能的影响相关研究进展作一综述。
英文摘要
Gingipains are cysteine proteases produced by Porphyromonas gingivalis, one of the major virulent agents of periodontal diseases. On the one hand, gingipains promote the differentiation of osteoclasts to enhance osteoclast function by activating the osteoprotegerin(OPG)/receptor activator of nuclear factor-κB(NF-κB) ligand(RANKL)/receptor activator of the NF-κB signaling pathways through degradation of OPG and induction of RANKL. On the other hand, gingipains inhibit osteoblast function by inducing osteoblast apoptosis through the external pathway mediated by the tumor necrosis factor receptor family and the mitochondrial pathway. These effects eventually lead to alveolar bone loss. This paper presents recent progress on gingipains and their effects on the functions of osteoclasts and osteoblasts.
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