Kerachian Mohammad Amin, Harvey Edward J, Cournoyer Denis, Chow Terry Y K, Séguin Chantal
Department of Human Genetics, McGill University, Montreal, Quebec, Canada.
Endothelium. 2006 Jul-Aug;13(4):237-44. doi: 10.1080/10623320600904211.
Vascular hypotheses provide compelling pathogenic mechanisms for the etiology of avascular necrosis of the femoral head (ANFH). A decrease in local blood flow of the femoral head has been postulated to be the cause of the disease. Several studies in human and animal models of ANFH have shown microvascular thrombosis. Endothelial cell damage could be followed by abnormal blood coagulation and thrombus formation with any resulting degeneration distal to the site of vascular occlusion. Other studies suggest that thrombophilia, particularly impaired fibrinolysis, plays a potential role in thrombus formation in ANFH. Reduction in shear stress due to decreased blood flow could lead to apoptosis of endothelial cells, which can ultimately contribute to plaque erosion and thrombus formation. Dysregulation of endothelial cell activating factors and stimulators of angiogenesis or repair processes could also affect the progression and outcome of ANFH. Likewise, regional endothelium dysfunction (RED), referred to as a potential defect in endothelial cells located in the feeding vessels of the femoral head itself, may also have a crucial role in the pathogenesis of ANFH. Molecular gene analysis of regional endothelial cells could also help to determine potential pathways important in the pathogenesis of ANFH.
血管假说为股骨头缺血性坏死（ANFH）的病因提供了令人信服的致病机制。股骨头局部血流减少被认为是该疾病的病因。在人类和动物ANFH模型中的多项研究已显示微血管血栓形成。内皮细胞损伤之后可能会出现异常凝血和血栓形成，继而导致血管闭塞部位远端的任何变性。其他研究表明，血栓形成倾向，尤其是纤维蛋白溶解受损，在ANFH的血栓形成中起潜在作用。由于血流减少导致的剪切应力降低可能会导致内皮细胞凋亡，最终可能导致斑块侵蚀和血栓形成。内皮细胞激活因子以及血管生成或修复过程刺激因子的失调也可能影响ANFH的进展和结局。同样，局部内皮功能障碍（RED），即位于股骨头自身供血血管中的内皮细胞潜在缺陷，在ANFH的发病机制中也可能起关键作用。对局部内皮细胞进行分子基因分析也有助于确定在ANFH发病机制中重要的潜在途径。
