OPG/RANKL对骨改建的调控作用  

RANKL and OPG regulation on bone remodeling

作　　者：赵熠[1] 蔡育[2] 王贻宁[1] 

机构地区：[1]武汉大学口腔医学院修复科,湖北武汉430079 [2]武汉大学口腔医学院口腔颌面外科,湖北武汉430079

出　　处：《上海口腔医学》2010年第4期443-446,共4页Shanghai Journal of Stomatology

摘　　要：通过破骨细胞对旧骨的吸收和成骨细胞的新骨形成,骨组织发生空间形态的改变,这种新骨替代旧骨的过程称为骨改建。绝经后的骨质疏松症和许多病变中骨改建率增加,但新骨形成不足,骨量减少,骨折几率增加。骨吸收依赖于被称为RANKL的细胞因子,而OPG与RANKL结合后,可阻止其单一同源受体RANK的活化。大量的体内和体外实验表明,RANKL与OPG的比例是影响骨吸收和骨改建的重要决定因素之一。Bone remodeling is a spatially coordinated lifelong process whereby old bone is absorbed by osteoclasts and replaced by bone-forming osteoblasts.Postmenopausal osteoporosis and other conditions are associated with an increased rate of bone remodeling,which leads to accelerated bone loss and increased risk of fracture.Bone resorption is dependent on a cytokine known as RANKL（receptor activator of NF-κB ligand）.The catabolic effects of RANKL are prevented by osteoprotegerin（OPG） that binds RANKL and thereby prevents activation of its single cognate receptor called RANK.Evidence in numerous disease models and settings suggests that the ratio of RANKL：OPG represents an important role on bone resorption and remodeling.

关 键 词：骨吸收 骨改建 骨保护素 核因子κ-B受体活化因子配体 

分 类 号：R580[医药卫生—内分泌]