糖皮质激素诱导股骨头坏死发病机制的研究进展  

Pathogenesis of glucocorticoid-induced osteonecrosis of the femeral head

作　　者：汪亮 刘耀升 刘蜀彬 

机构地区：[1]解放军第三O七医院骨科,北京100071

出　　处：《中华损伤与修复杂志（电子版）》2015年第5期60-66,共7页Chinese Journal of Injury Repair and Wound Healing(Electronic Edition)

基　　金：北京市科委首都临床特色应用研究(Z121107001012093)

摘　　要：非创伤性股骨头坏死(ONFH)的病理生理比创伤性ONFH更为复杂,因糖皮质激素在多系统路径中的多重效应,故其诱导的ONFH呈现出巨大的挑战。这些途径包括糖皮质激素在成骨细胞分化、成骨细胞和破骨细胞凋亡、脂质代谢、凝血途径和钙代谢中的影响,它们彼此间相互联系,因而更加难以明晰其发病机制。宿主因素和基础疾病已被证实在ONFH发生风险方面起着重要的作用。遗传变异的识别在防治ONFH方面也有助于对患者提供个体化的方案。The pathophysiology of non-traumatic osteonecrosis of the femoral head is more complex than that of traumatic osteonecrosis, and corticosteroid-induced osteonecrosis presents a huge challenge because of the multiple effects of corticostcroids on multi-system pathways. These pathways include the effects of corticosteroids on osteoblast differentiation, osteoblast and osteoclast apoptosis, lipid metabolism, coagulation pathways, and calcium metabolism. These pathways are frequently interrelated with each other, which makes the pathogenesis even more difficult to understand. Host factors and underlying disease have been shown to play a significant role in the risk of developing osteonecrosis. Identification of genetic variants that convey additional risk will also help to personalize the way we care, both in the prevention and treatment of osteonecrosis.

关 键 词：糖皮质激素类 股骨头坏死 治疗学 发病机制 

分 类 号：R681.8[医药卫生—骨科学]