山羊激素性股骨头坏死组织的病理学及钙、磷实验研究

目的：建立山羊激素性股骨头缺血坏死（SANFH）的动物模型。探讨其发病病因及机制。方法：12只山羊随机分为3组，A组正常对照组；B组采用内毒素LPS加激素MP联合造模；C组为内毒素LPS加激素MP联合造模后，从第5周开始，追加激素DXM；各组分别于第0、2、4、6、8、10、12周行钙、磷及钙磷乘积指标测定，12周处死动物并进行组织病理学观察。结果：与正常组相比，B、C组钙、磷及钙磷乘积明显较A组低（P〈0．01），C组较B组钙、磷及钙磷乘积更低，两组相比有差异性（P〈0．05）。病理学观察显示：与A组相比，B、C组山羊出现较为典型的激素性股骨头坏死动物模型表现。但B、C组间比较差异有统计学意义。结论：①采用内毒素加激素MP、5周后加地塞米松DXM能够诱导出接近临床典型的SANFH动物模型；②钙磷异常可能是激素性股骨头坏死的重要发病机制之一。

Research on Pathology and Values of Calcium and Phosphonium in Steriod-induced Avascular Necrosis and Femoral Head in Goats

Objective：To establish a steroid-induced avascular necrosis of femoral head （SANFH） model in goats and to explore the cause and mechanisms. Methods.. Twelve goats were randomly divided into three groups. Group A was normal control. Goats in group B and group C were treated with lipopoly saccharide （LPS） and methyl prednisolone （MP） in order to cause SANFH. Then group C was treated with dexamethasone （DXM） after 5 weeks. Calcium, phosphonium, calciumphosphorus product were tested in every group at 0, 2, 4, 6, 8, 10 and 12 weeks, respectively. Histopathology was observed by the microscope at the 12th week. Results： Compared with normal group, the serum values （including calcium, phosphnium, calcium-phosphorus product） of group B and C were significantly lower （P〈0.01）. Moreover, the above values in group C were remarkably lower than group B. There was significant difference between the two groups （P〈0. 05）. Compared with normal group, the model groups showed more typical clinical manifestations of SANFH. There was significant difference in the degree of SANFH between group t3 and group C. Conclusion： The SANFH model could be induced by LPS, MP and DXM after 5 weeks, and it was much more similar to typical clinical SANFH. Calcium-phosphonium abnormalities may be one of the important mechanisms of SANFH.