早期创伤性股骨头缺血性坏死兔模型早期治疗分子机制探讨

Molecular Mechanism in Early Treatment of Early Stage Traumatic Avascular Necrosis of Femoral Head in a Rabbit Model

目的探讨早期创伤性股骨头缺血性坏死的分子机制。方法建立早期创伤性股骨头缺血性坏死兔模型,应用免疫组化方法观察股骨头缺血性坏死发生发展过程。结果股骨头缺血性坏死早期血管生成抑制,股骨头内重要组织损伤伴细胞凋亡,同时可见Ⅰ型胶原和Ⅲ型胶原介导的纤维化修复和血管性血友病因子诱生的新生血管。结论早期创伤性股骨头缺血性坏死存在短期的自我恢复,这可能为早期创伤性股骨头缺血性坏死提供一个最佳治疗时机。

Objective To study the molecular mechanism of the early stage traumatic avascular necro- sis of femoral head. Methods We established a rabbit early stage traumatic avascular necrosis of femoral head model. The process of avascular necrosis of femoral head was observed by immunohistochemical stai- ning. Results In early stage traumatic avascular necrosis of femoral head, the suppression of angiogene- sis, significant tissue damage within the femoral head and accompanied cell apoptosis were observed in os- teonecrosis of femoral head. We also observed the repairative fibrosis mediated by type I collagen and type III collagen and neovascularization induced by von Willebrand factor. Conclusion Such a short-term res- toration may provide an optimal timing for therapy of early stage traumatic osteonecrosis of femoral head in clinic application.