引导骨再生技术对血管化组织工程骨修复兔股骨缺损过程中骨形态发生蛋白-2成骨及表达的影响

Effect of guided bone regeneration on expression level of bone morphogenetic protein-2 in repair of femoral defects with vascularized engineered-bone in rabbits

目的 探讨引导骨再生（GBR）技术对血管化组织工程骨修复兔股骨缺损过程中局部骨形态发生蛋白-2（BMP-2）的成骨量及表达的影响,以明确GBR技术在血管化组织工程骨应用中的作用. 方法 将兔自体骨髓基质干细胞经诱导后与β-磷酸三钙材料复合,植入制备的兔股骨缺损处并在材料侧槽中植入股动静脉束,其中实验组9例,血管化组织工程骨用可吸收性GBR屏障膜包裹 对照组9例,单纯植入血管化组织工程骨,分别于术后4、8、12周通过形态学检测新生骨量,ELISA法检测骨缺损局部BMP-2的表达量. 结果 随着时间进展各组成骨量逐渐增加（实验组4、8、12周时新生骨的相对面积比分别为7.31%±0.55%,35.23%±3.07%,76.09%±3.71%,对照组4、8、12周时新生骨的相对面积比分别为17.26%±1.17%,54.50%±4.26%,82.57%±4.11%,差异均有统计学意义（P〈0.05） 且同一时间点实验组成骨量低于对照组,差异有统计学意义（P〈0.05） 术后4、8、12周时实验组骨缺损局部BMP-2 OD值分别为0.334±0.012,0.245±0.008,0.172±0.009,对照组骨缺损局部BMP-2 OD值分别为0.389±0.008,0.289±0.008,0.189±0.009 术后4周时两组骨缺损内BMP-2表达量均达峰值,此后即开始出现不同程度的下降 术后4、8、12周时骨缺损局部BMP-2表达量实验组均低于对照组,差异均有统计学意义（P〈0.05）. 结论 GBR屏障膜会降低血管化组织工程骨修复兔股骨缺损局部的成骨量,并减少骨缺损过程中局部BMP-2的表达量.

Objective To evaluate the effect of guided bone regeneration （GBR） on expression level of bone morphogenetic protein-2 （BMP-2） and bone formation in repair of femoral defects with vascularized engineered-bone in rabbits. Methods Eighteen healthy New Zealand rabbits were randomized into 2 e-qual groups. A segmental bone defect of 150 mm in length was made at the right femur in each rabbit and fixed with a plate. The gaps in the experiment group were plugged with the engineered bones and femoral vascular bundle, which were wrapped by GBR membrane. The vascularized engineered-bone plugged in the gaps in the control group, however, was not wrapped by GBR membrane. The expression levels of BMP-2 of the implants were examined by ELISA kits 4, 8, 12 weeks after implantation. Results The new bone formation was significantly higher in the control group at the end of 4, 8, 12 weeks （P 〈 0.05）. The expression levels of BMP-2 in the control group were also siguificantly higher than in the experimental group at all time points after operation （P〈0.05）. The expression of BMP-2 peaked at 4 weeks. Conclusion GBR will down-regulate BMP-2 release in models of femoral defect in rabbits.