目的:探究内源性甲状旁腺激素(parathyroid hormone,PTH)缺失是否通过降低血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达,导致骨折愈合过程中血管再生减弱,延迟骨折愈合。方法:构建PTH基因敲除(PTHKO)小鼠的骨折模型,摄X线片观察骨折愈合情况,用免疫组化方式检测骨合成代谢以及血管形成指标。结果:PTHKO小鼠VEGF表达量下降,血小板内皮细胞黏附分子(platelet endothelial cell adhension molecule,PEGAM)免疫组化阳性减少,骨钙蛋白(osteocalcin,OCN)活性下降,骨折愈合延迟。结论:内源性PTH缺失可能通过减少间充质干细胞或成骨细胞释放VEGF,导致骨折端血管减少,成骨活性受到抑制,从而影响软骨内成骨,最终导致骨折愈合延迟。
Objective:To explore whether the lack of endogenous PTH causes angiogenesis weakness by reducing the expression of VEGF during fracture healing and delays fracture healing. Methods:We constructed PTH knockouted mice fracture model,and observed fracture healing from X-ray film and detected bone anabolism and angiogenesis using immunohistochemistry. Results:VEGF expression was decreased in PTHKO mice. Immunohistochemical analysis showed that positive PEGAM was reduced. OCN activity was decreased and fracture healing was delayd. Conclusion:Lack of endogenous PTH may release VEGF by reducing mesenchymal stem cells or osteoblasts,reduce vascular fracture,inhibit osteoblastic activity, surpress endochondral ossification and lead to fracture healing delay eventually.