糖皮质激素诱导微血管内皮细胞损伤及凋亡与股骨头坏死的关系

Relationship between glucocorticoid-induced microvascular endothelial cell injury and apoptosis with femoral head necrosis

长期大剂量糖皮质激素(GC)的使用是造成非创伤性股骨头坏死(ONFH)最常见的原因,其确切发病机制至今仍不明确。近期研究认为GC引起的ONFH与骨微血管内皮细胞(BMECs)损伤密切相关,骨内微循环功能障碍是ONFH的病理基础已得到共识,血液高凝状态、血液瘀滞和内皮细胞损伤是导致骨内微循环功能障碍的病理过程。股骨头长期暴露于GC导致局部内皮功能障碍,BMECs的损伤及凋亡在ONFH进展中发挥着重要作用。该文就GC损伤BMECs的机制、BMECs损伤与凝血功能障碍及成骨作用之间的关系进行综述。

The use of long-term large-dose glucocorticoid(GC) is the most common cause of nontraumatic osteonecrosis of the femoral head(ONFH),its exact pathogenesis remains unclear.The recent studies consider that GC induced ONFH is closely related to bone microvascular endothelial cells(BMECs) damage.It has been recognized that the dysfunction of intra-bone microcirculation is the pathological basis of ONFH,and the blood hypercoagulable state, blood stasis and endothelial cell injury are the pathological processes leading to microcirculation disturbance in bone.The femoral head long-term exposure to GC leads to local endothelial dysfunction, and the damage and apoptosis of BMECs play an important role in the progression of ONFH.This paper reviews the mechanism of BMECs injury and the relationship between BMECs injury with coagulation dysfunction and osteogenesis.