牙周炎細胞性免疫反應與OPG/RANKL/RANK系統之關係

於最近15年來，吾人透過分子生物學之基礎，已更進一步了解於骨生物學中造骨細胞確實能調控破骨細胞之形成、分化與抑制，甚至副甲狀腺素也必須藉由造骨細胞表面之受體，來刺激破骨細胞之分化與活化，造成骨吸收。造骨細胞可藉由其表面之RANKL與破骨細胞表面之RANK結合，誘使破骨細胞成熟與活化；另一方面，造骨細胞也可分泌OPG，與RANKL結合，終止骨質之吸收作用。於牙周病之機轉中，細菌所分泌之外毒素或內毒素也可於牙周細胞性免疫中，活化CD4+T細胞與B細胞。此兩種細胞皆能表現OPGL（RANKL），促使破骨細胞分化與活動。B細胞又會分泌macrophage inflammatory protein-1α與Pmonocyte chemotactic protein-3，吸引破骨細胞之遷移與聚集，促進骨吸收。而牙周之CD8+T細胞與牙齦纖維母細胞則會表現OPG以抑制骨前細胞分化為破骨細胞，形成自我防禦。因此近幾年之骨生物學之迅速進展，可以提供我們更了解OPG/RANKL/RANK系統與牙周齒槽骨吸收之關聯，也提供吾等未來臨床之研究與治療一個新視野。

關鍵字

造骨細胞；破骨細胞； T-細胞；牙周炎

並列摘要

A new era in the field of bone biology has been explored during the last decade. The identification and characterization of OPG/RANKLIRANK system have also played an important role in the landscape of bone biology. Osteoblasts may express RANKL on cell surface and regulate the differentiation and activation of osteoclasts through cell receptor RANK by cell to cell contact. On the other hand, osteoblasts may also express OPG to bind RANKL in an autocrine modulation and hinder osteoclastogenesis. In the study of functional human T-cell immunity and RANKL controlled bone resorption, it implies that the induction of alveolar bone resorption in periodontitis is triggered by exotoxin or endotoxin of microorganism through the RANKL expression on CD4+ T cells and the consequent activation of osteoclasts. On the contrary, the CD8+T cells and gingival fibroblast may express OPG to conjugate RANKL and inhibit osteoclastogenesis. The explosion in the field of unraveling OPG/RANKL/RANK system will high-light a complete understanding of the relation between osteoc1astogenesis and periodontal destruction. In addition to providing fundamental insight in bone biology, the detailed characterization of OPG/RANKL/RANK system will open up entirely new areas for clinical research and therapeutic approach in periodontology.

並列關鍵字

osteoblast ； osteoclast ； OPG ； RANKL ； RANK ； T-cells ； periodontitis

國際替代計量

牙周炎細胞性免疫反應與OPG/RANKL/RANK系統之關係

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