血管内皮细胞生长因子165及骨形态发生蛋白2促进兔骨缺损部位再血管化的研究  

Repair of long bone defects in rabbits using nano-hydroxyapatite /polyamide combined plasmids and guided bone regeneration

作　　者：邹海波[1] 周亚莉[2] 安洪[3] 蒋电明[3] 

机构地区：[1]卫生部北京中日友好医院骨科,北京100029 [2]首都医科大学附属北京天坛医院实验诊断中心 [3]重庆医科大学附属第一医院骨科

出　　处：《中华创伤骨科杂志》2007年第2期147-152,共6页Chinese Journal of Orthopaedic Trauma

基　　金：国家高科技研究发展计划（863计划）（2002AA326020）

摘　　要：目的 为大段骨缺损修复过程的血管再生探索一条可行的途径。方法 成年大耳白兔30只，随机分为五组。右前肢为实验肢体，缺损长度约15mm。第1—4组都采用胶原膜引导，结合纳米羟基磷灰石／聚酰胺骨水泥，不同的是在第1组中，复合血管内皮生长因子165（VEGF165）及骨形态发生蛋白2（BMP2）质粒；第2组复合VEGF165质粒；第3组复合BMP2质粒；第4组不复合任何质粒；第5组仅制作动物模型而不做任何处理，作为空白对照组。结果 术后2周，核素断层摄影（ECT）结果显示第1组骨缺损修复后的局部血流量高于第2、3、4组（P〈0．05）；术后4周，X线片示第1组骨缺损处的骨痂明显增多；SEM显示在正常骨与工程骨交界处可见新生的骨小梁结构以及成骨细胞的附着；ECT结果显示第1组骨缺损的局部血流量高于第2、3、4组（P〈0．01）；第2组骨缺损的局部血流量高于第3、4组（P〈0．01）；术后8周，SEM显示第1组工程骨表面成骨细胞的附着多于其它各组，ECT结果显示与术后4周相同。结论 在骨缺损的局部，联合应用表达VEGF165和BMP2质粒可以促进骨缺损局部的血液供应；附着质粒DNA的纳米羟基磷灰石／聚酰胺及引导性胶原膜在大段骨缺损局部的联合应用有助于新骨的形成。Objective To explore a feasible way for revascularization in repair of long bone defects. Methods A total of 30 healthy adult rabbits were randomly divided into 5 groups. A defect of about 15 mm was made at each right fore limb. The experimental limbs in Groups One to Four were repaired by nano-hydroxyapatite/polyamide （n-HA/PA） composite cement and medical collagen membrane guidance. Plasmids vascular endothelail growth factor 165（VEGF165） and hone morphogenetic protein（BMP2） were added in Group One; plasmids VEGF165 were added in Group Two; plasmids BMP2 were added in Group three; no plasmids were added in Group Four. Group Five served as a blank control. Results After 2 weeks, no distinct difference among groups was observed by radiography; SEM （scanning electron microscopy） showed no ostcoblasts cohered on the surface of n-HA/PA; ECT （emission computed tomography） showed increased blood flow at the bone defect site in Group One compared with other contrast groups （ P 〈 0. 05）. After 4 weeks, osteetylus filling the defect was observed by radiography in Group One. ECT showed significantly increased blood flow at the bone defect in Group One compared with other contrast groups （ P 〈 0. 01）, higher blood flow in Group Two than in Groups Three and Four （P 〈 0. 01）, but no evident difference between Group Three and Group Four. After 8 weeks, the osteetylus observed by radiography was thicker in Group One than in other groups, and no ostcotylus was observed by radiography in Group Five. The results of ECT were the same as those at the fourth week. Conclusions The angiogenesis at bone defect site can be accelerated by the plasmids, pDsVEGF165Redl-N1 and pIRES2-BMP2-EGFP. The formation of new bone can be accelerated by the combination of n-HA/PA and guided bone regeneration.

关 键 词：纳米羟基磷灰石/聚酰胺骨水泥 血管内皮细胞生长因子 骨形态发生蛋白 引导性骨再生 骨缺损 

分 类 号：R686[医药卫生—骨科学]