摘要
目的:探讨糖皮质激素诱发骨坏死的机制。方法:将兔复制Yamamoto氏骨坏死模型,分为对照组(4只),2,4,6和8周组,每组各5只,按照不同时间处死取材。利用双光子骨密度仪测量股骨头部的骨质密度值。收集激素性骨坏死患者的病理标本21例,以无骨代谢疾病患者的股骨标本为对照,免疫组化染色观察激素性骨坏死股骨头局部骨保护素(OPG)/破骨细胞生成抑制因子(OCIF)蛋白的表达改变。结果:糖皮质激素给药后,继发于OPG表达减低(P<0.01)和破骨细胞异常增生后,局部出现渐进性骨丢失(P<0.05);与正常对照比较,激素性骨坏死患者的股骨头局部OPG表达明显减低(P<0.05)。结论:糖皮质激素抑制骨骼局部的OPG表达,使破骨细胞异常增殖,从而出现骨丢失。
AIM:To study the mechanism of glucocorticoid(GG) induced osteonecrosis. METHODS: According to the Yamamoto's method, a model of GG induced osteonecros is was reproduced in 24 New Zealand rabbits by administration with GG.The rabbit s were divided into control group(n=4),2,4,6 and 8 weeks groups(n=5 respectively ),and they were kill for materials according to different time.The bone mineral density in femoral head was measured by using the dual photon bone densitimetry. The biopsy samples from 21 patients with glucocorticoid induced osteonecrosis an d a healthy volunteer were collected to examine the local expression level of os teoprotegerin.The changes of local osteoprotegerin(OPG) expression of osteonevro sis in femoral head and osteoclast cell inhibitive factor(OCIF) protein expressi on were observed by immunohistochemical staining. RESULTS:After the administration of GG,the local OPG expression reduced(P< 0.0 1) and the number of osteoclasts abnormally increased,followed by the aggravated bone-loss in the Yamamoto's model(P< 0.05). The local OPG expression of osteon ecrosis patients was obviously lower than that of the healthy control subject(P< 0.05). CONCLUSION:Glucocorticoid inhibits the local OPG expression of bone,and facili tates abnormal proliferation of osteoclasts which results in bone-loss.
出处
《中国临床康复》
CSCD
2004年第15期2900-2901,共2页
Chinese Journal of Clinical Rehabilitation
基金
国家自然科学基金面上资助项目(30170948).