内源性甲状旁腺激素促进小鼠骨折愈合

Endogenous parathyroid hormone promotes fracture healing in mice

目的:探讨甲状旁腺激素(parathyroid hormone,PTH)在小鼠骨折愈合过程中的作用。方法 :选择8周龄野生型和PTH基因敲除雄性小鼠各15只,制备右侧股骨开放性骨折模型,并于骨折后7、14、21 d处死,运用小动物显微CT及其相关软件测量骨痂区骨密度;运用组织学、免疫组织化学、X线、CT三维重建比较分析两组小鼠的术后骨折愈合情况。结果:术后14 d和21 d PTH基因敲除小鼠的骨折端骨密度显著低于PTH野生型组(P<0.05)。X线和显微CT显示PTH基因敲除小鼠骨折愈合、骨痂的塑形和PTH野生型小鼠相比均延迟。结论:内源性PTH促进小鼠骨折愈合。

Objective：To determine the role of the parathyroid hormone （PTH） in fracture healing of mice. Methods：A total of 30 male mice at 8 weeks old （including 15 wild-type mice and 15 PTH gent knockout mice） were selected to establish right femur fracture model. At 7,14 and 21 days after the operation,the mice were sacrificed for measurement of bone mineral density （BMD） of the callus by micro-CT. To determine the role of PTH in fracture healing,the fracture models were assessed by histology, immunohistochemistry,X ray and micro-CT. Results：At 14 and 21 days after the operation,BMD in PTH gene knockout mice was significantly reduced compared to that in PTH wild-type mice （P 〈 0.05）. X ray and micro-CT scanning showed that the fracture healing and the callus transformation and remodeling in PTH gene knockout mice were both delayed compared to those in wild-type mice. Conclusion：This study suggests that endogenous PTH promotes the fracture healing in mice.