骨破坏因子RANK RANKL OPG在口腔领域研究进展  

Research Advances in Stomatology on the Factor (RANK,RANKL,OPG) of Bone Destruction

作　　者：敏杰[1] 达林泰 乌兰其其格 

机构地区：[1]内蒙古医科大学,内蒙古呼和浩特010059 [2]不详

出　　处：《内蒙古医学杂志》2014年第6期690-692,共3页Inner Mongolia Medical Journal

基　　金：内蒙古自然科学基金资助项目(2009MS1125)

摘　　要：OPG/RANKL/RANK系统信号通路对调节破骨细胞分化与骨吸收过程中具有至关重要的作用。成骨细胞及骨髓基质细胞表达RANKL与破骨细胞前体细胞或破骨细胞表面上的RANK结合后,促进破骨细胞的分化与激活,并抑制破骨细胞的凋亡;另一方面成骨细胞及骨髓基质细胞则分泌表达OPG与RANKL竞争性结合,阻止RANKL与RANK的结合。作为破骨细胞形成、分化和骨吸收调节的关键调节物OPG/RANKL/RANK系统信号通路在口腔领域中乳牙的萌出及替换、正畸牙的移动、牙周炎等生理性及病理性过程中的改建发挥功能。OPG/RANKL/RANK system signaling pathways plays a vital role to regulate osteoclast differentiation and maturation and function of bone resorption. Promote the differentiation and activation of osteoclasts,osteoblasts and bone marrow stromal cells express RANK binding RANKL and osteoclast precursor cells or on the cell surface of osteoclasts,and inhibits osteoclast apoptosis,osteoblasts and bone marrow stromal cells secrete the expression of OPG and RANKL competitive binding,prevents binding of RANKL and RANK. As osteoclast formation,differentiation and bone resorption in a key regulator of OPG / RANKL / RANK system signal path in the field oral and replacement eruption of primary teeth,orthodontic tooth moves,periodontitis and other physiological and pathological process,alterations to function.

关 键 词：骨破坏 骨保护素 核因子ΚB受体活化因子配体 核因子ΚB受体活化因子 

分 类 号：R782[医药卫生—口腔医学]