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背景:糖皮质激素(Glucocorticoid,GC)是目前治疗自身免疫性、结缔组织性疾病的主要方法之一,但治疗后部分患者常发生骨坏死,对其病理机制的深入研究对该病的预防很有必要。目的:探讨糖皮质激素诱发骨丢失的机制。设计:随机对照实验研究。地点和对象:实验在解放军总医院骨科完成,研究对象为成年新西兰白兔31只,雌雄不限,体质量3.0～4.0kg,购于解放军总医院实验动物中心。本院确诊为激素性骨坏死并行髓芯减压或全髋关节置换术患者的病理标本21例,年龄(48.30±6.09)岁。干预:①复制Yamamoto氏骨坏死模型,通过病理学、骨丢失检测和免疫组化染色观察骨保护素(OPG)/破骨细胞生成抑制因子(OCIF)表达改变与破骨细胞分化、骨丢失的关系。②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,免疫组化染色了解激素性骨坏死股骨头局部OPG/OCIF蛋白的表达改变。主要观察指标:各实验组骨密度,激素性骨坏死股骨头局部OPG/OCIF蛋白的表达。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:动物模型和临床资料均表明:糖皮质激素抑制骨骼局部的OPG表达,使破骨细胞?
BACKGROUND: Glucocorticoid (GC) is one of the main methods for the treatment of autoimmune and connective tissue diseases. However, some patients often have osteonecrosis after the treatment, and further studies on its pathological mechanism are of great value in the prevention of the disease Is necessary. Objective: To investigate the mechanism of glucocorticoid-induced bone loss. Design: Randomized controlled trial. Location and Subjects: The experiment was performed in the orthopedics department of General Hospital of People’s Liberation Army. Subjects were 31 adult New Zealand white rabbits, both male and female. The body weight was 3.0-4.0 kg and purchased from the Laboratory Animal Center of Chinese PLA General Hospital. Our hospital diagnosed as hormone osteonecrosis and core decompression or total hip arthroplasty in patients with pathological specimens of 21 cases, age (48.30 ± 6.09) years of age. Intervention: (1) Yamamoto’s osteonecrosis model was duplicated. The changes of osteoprotegerin (OPG) / osteoclastogenesis inhibitory factor (OCIF) expression and osteoclast differentiation and bone loss were observed by pathology, bone loss detection and immunohistochemical staining relationship. ② Twenty-one pathological specimens of patients with steroid-induced osteonecrosis were collected and compared with femoral specimens without osteo-metabolic disease. Immunohistochemical staining was used to detect the expression of OPG / OCIF protein in the femoral head of osteonecrosis of the hormones. MAIN OUTCOME MEASURES: BMD of experimental group and expression of OPG / OCIF protein in femoral head of steroid-induced osteonecrosis in each experimental group. Results: After the administration of glucocorticoid, secondary bone loss occurred gradually (P <0.01) and osteoclast abnormality (P <0.05) after secondary administration of OPG. Compared with the normal control group, the patients with steroid-induced osteonecrosis The femoral head local OPG expression was significantly reduced (P <0.05). Conclusion: Both animal model and clinical data indicate that glucocorticoids can inhibit the expression of OPG in bone and make osteoclast?