骨保护蛋白又称破骨细胞抑制因子，可通过抑制破骨细胞分化和活性促进骨质形成并对抗因破骨细胞增强而引起的骨质疏松。医源性激素性骨坏死，目前仍无有效的治疗方法；本研究拟从分子生物学水平了解在激素性骨坏死的病变过程中，成骨细胞和骨细胞自身代谢和表型，及骨保护蛋白的表达；并考虑通过骨保护蛋白抑制破骨细胞的分化和活性来对抗激素的作用，进而阻断病程的发展达到治疗激素性骨坏死的作用。

A progressive local bone-loss appears in most patients with avascular necrosis, leading to erosion of articular cartilage and aggravated osteoarthritis. Its mechanism hasn’t been fully understood so far. According to our previous study, the bone-loss did occur in both necrotic as well as unnecrotic areas, where decreased local OPG/OCIF expression and increasing osteoclast had been noticed. In theory, the advancement of bone-loss could be halted via inhibition of osteoclast. OPG/OCIF (osteoprotegerin / osteoclastogenesis inhibitory factor) that was initially described by Simonet is a local down-regulator of osteoclast, which is a pseudo-receptor of ODF.(osteoclast differentiation factor) expressed by osteoblast. Every kind of etiological factor that induces the osteonecrosis could have an effect on bone transcription and expression of OPG/OCIF.In the present study, the therapeutic potentials of OPG/OCIF for bone-loss are tested in vivo and in vitro. In this study, a osteonecrosis modal is made to probe the relationship between the transcription and expression of OPG/OCIF and the amount and activity of osteoclasts in the bone-loss areas. Cell culture is employed to show the negative effects of rhOPG/OCIF-Fc on osteoclasts. Through these studies, it is expected to explain, at least in part, the mechanism of.bone-loss, and to provide the experimental basis for the clinical application of OPG/OCIF in treatment of avascular necrosis of the femoral head.