Wagner Doris, Fahrleitner-Pammer Astrid
Department of Surgery, Medical University of Graz, Graz, Austria.
Wien Med Wochenschr. 2010 Sep;160(17-18):452-7. doi: 10.1007/s10354-010-0818-x. Epub 2010 Aug 16.
The coupling of bone formation and resorption is mediated through the OPG/RANK/RANKL system. OPG and RANKL are mainly produced by osteoblasts but also a variety of other tissues. The binding of RANKL to RANK, its natural receptor which is expressed by osteoclasts, accelerates bone resorption. OPG acts as decoy receptor and prevents the interaction of RANKL with RANK and therefore leads to a decrease in activity, survival and proliferation of osteoclasts. Since assays for measurements of serum OPG and RANKL have become commercially available, intense research focused on serum OPG/RANKL levels in context with underlying disease, age, co-morbidities, bone density, and fractures has derived. This review aims to provide an overview if and to which extent serum OPG and RANKL levels may reflect bone metabolism in patients with osteoporosis and metabolic bone disease.
骨形成与骨吸收的偶联是通过骨保护素/核因子κB受体活化因子/核因子κB受体活化因子配体（OPG/RANK/RANKL）系统介导的。OPG和RANKL主要由成骨细胞产生，但也可由多种其他组织产生。RANKL与其天然受体RANK（由破骨细胞表达）结合，可加速骨吸收。OPG作为诱饵受体，可阻止RANKL与RANK相互作用，从而导致破骨细胞活性、存活和增殖降低。由于检测血清OPG和RANKL的方法已商业化，因此针对潜在疾病、年龄、合并症、骨密度和骨折等情况下血清OPG/RANKL水平的深入研究已经展开。本综述旨在概述血清OPG和RANKL水平是否以及在何种程度上可反映骨质疏松症和代谢性骨病患者的骨代谢情况。
