激素性股骨头坏死模型兔骨组织病理及功能变化

背景：目前对激素性股骨头坏死的研究均未涉及成骨细胞、破骨细胞变化所引起的细胞功能改变。目的：观察激素性股骨头坏死模型兔骨代谢指标及骨组织病理学变化。方法：将32只新西兰大白兔随机等分为正常组和模型组。模型组臀肌注射醋酸氢化可的松注射液8.0 mg/kg,每周2次,持续8周,建立激素性股骨头坏死兔模型;正常组注射等量的生理盐水。结果与结论：与正常组比较,模型组从第2周开始血清钙、磷显著降低(P < 0.05),而抗酒石酸酸性磷酸酶活性显著升高 (P < 0.05);从第4周开始,模型组骨特异性碱性磷酸酶水平升高,骨钙素水平降低(P < 0.05);模型组骨特异性碱性磷酸酶水平至第8周有所下降。与正常组比较,模型组股骨转子骨密度从第2周开始降低(P < 0.05),股骨头骨密度从第4周开始降低(P < 0.05);成骨细胞数从第4周开始明显降低,破骨细胞数从第4周开始明显升高(P < 0.05)。提示激素可通过损伤骨组织细胞引起骨塑形及骨重建的破坏,造成骨矿物盐的丢失,引起激素性股骨头坏死的发生。

Bone tissue function and pathological changes of hormone-induced avascular necrosis of the femoral head in rabbits

BACKGROUND:So far, research on hormone-induced avascular necrosis of the femoral head does not involve cell function change induced by the alteration of osteoblast and osteoclast.OBJECTIVE:To investigate bone metabolism and bone tissue pathological changes of hormone-induced avascular necrosis of the femoral head in rabbits.METHODS:A number of 32 New Zealand white rabbits were randomly divided into two groups, control group and model group. The model rabbits were injected with 8.0 mg/kg hydrocortisone acetate twice a week for 8 weeks to produce avascular necrosis model of the femoral head. The control rabbits were injected with equivalent physiological saline.RESULTS AND CONCLUSION:Compared with the control group, the serum calcium and phosphate level of model group dropped significantly since the 2nd week (P < 0.05), while the enzymatic activity of tartrate-resistant acid phosphatase rised significantly (P < 0.05). Bone specific alkaline phosphatase level of model group increased while bone gla protein level decreased at the start of the 4th week (P < 0.05). Bone specific alkaline phosphatase level of model group declined by the 8th week. Compared with the contrl group, the femoral intertrochanter bone mineral density of model group dropped since the 2nd week (P < 0.05), and the bone mineral density of femoral head dropped since the 4th week (P < 0.05). From the 4th week, the amount of osteoblast decreased significantly, while the osteoclast amount increased significantly (P < 0.05). These results suggest that hormone can damage bone shaping and bone remodeling by damaging bone cells, reduce the content of mineral salt used for bone formation, and lead to hormone-induced avascular necrosis of the femoral head.