骨质疏松性骨折后全身骨量丢失的循证学依据及可能机制

Evidence and possible mechanisms of systemic bone loss after osteoporotic fracture

骨质疏松性骨折后的骨质丢失现象,其发生机制可能与骨折后失用所致的骨细胞机械刺激下降、化学信号、炎症因子以及细胞因子等因素相关。骨折后全身骨量丢失的程度会随着年龄、骨折严重程度以及骨折次数的增长而增加,同时,局部骨折发生后全身的骨折风险增加揭示了骨量丢失的全身性特征。骨折后全身骨量丢失可能会加速骨质疏松症的发展进程,急性、进行性骨质丢失可能对患者造成一系列负面影响,包括骨质疏松性骨痛、内置物或假体松动、假体周围骨折以及再次骨折风险的增加等。目前,骨折引起的骨量丢失,其机制和理论基础仍处于探索阶段,RAP和SAP理论、骨修复矿物质需求理论以及骨修复储备理论等,对于骨折后的骨量丢失提供了较为合理的解释。

The mechanism of bone loss after osteoporotic fracture may be related to factors such as decreased mechanical stimulation of osteocytes,related chemical signaling pathway proteins,inflammatory factors and related cytokines caused by disuse after fracture.The degree of systemic bone loss after fracture increases with age,fracture severity,and number of fractures,and the increased risk of systemic fracture after local fracture development reveals the systemic character of bone loss.In fact,the systemic bone loss after fracture may accelerate the progression of osteoporosis,and acute,progressive bone loss may have a range of negative effects,including osteoporotic bone pain,loosening of inserts or prostheses,periprosthetic fractures,and an increased risk of refractures.At present,the relevant mechanism and theoretical basis of bone loss caused by fracture are still in the exploration stage,and RAP and SAP theory,bone repair mineral demand theory and bone repair reserve theory provide a more reasonable explanation for bone loss after fracture.