Xing Junchao, Jin Huiyong, Hou Tianyong, Chang Zhengqi, Luo Fei, Wang Pinpin, Li Zhiqiang, Xie Zhao, Xu Jianzhong
National and Local United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, the Third Military Medical University, Chongqing, China; Laboratory of Tissue Engineering in Chongqing City, Chongqing, 400038, China; Center of Regenerative and Reconstructive Engineering Technology in Chongqing City, Chongqing, 400038, China.
National and Local United Engineering Laboratory of Tissue Engineering, Department of Orthopedics, Southwest Hospital, the Third Military Medical University, Chongqing, China; Laboratory of Tissue Engineering in Chongqing City, Chongqing, 400038, China; Center of Regenerative and Reconstructive Engineering Technology in Chongqing City, Chongqing, 400038, China; Department of Orthopaedics, No. 519 Hospital of PLA, Xichang, 615000, China.
J Surg Res. 2014 Dec;192(2):454-63. doi: 10.1016/j.jss.2014.05.037. Epub 2014 May 27.
To understand the cellular mechanism underlying bone defect healing in the context of tissue engineering, a reliable, reproducible, and standardized load-bearing large segmental bone defect model in small animals is indispensable. The aim of this study was to establish and evaluate a bilateral femoral defect model in mice.
Donor mouse bone marrow mesenchymal stem cells (mBMSCs) were obtained from six mice (FVB/N) and incorporated into partially demineralized bone matrix scaffolds to construct tissue-engineered bones. In total, 36 GFP(+) mice were used for modeling. Titanium fixation plates with locking steel wires were attached to the femurs for stabilization, and 2-mm-long segmental bone defects were created in the bilateral femoral midshafts. The defects in the left and right femurs were transplanted with tissue-engineered bones and control scaffolds, respectively. The healing process was monitored by x-ray radiography, microcomputed tomography, and histology. The capacity of the transplanted mBMSCs to recruit host CD31(+) cells was investigated by immunofluorescence and real-time polymerase chain reaction.
Postoperatively, no complication was observed, except that two mice died of unknown causes. Stable fixation of femurs and implants with full load bearing was achieved in all animals. The process of bone defect repair was significantly accelerated due to the introduction of mBMSCs. Moreover, the transplanted mBMSCs attracted more host CD31(+) endothelial progenitors into the grafts.
The present study established a feasible, reproducible, and clinically relevant bilateral femoral large segmental bone defect mouse model. This model is potentially suitable for basic research in the field of bone tissue engineering.
为了在组织工程背景下理解骨缺损愈合的细胞机制，在小动物中建立一个可靠、可重复且标准化的负重大型节段性骨缺损模型是必不可少的。本研究的目的是建立并评估小鼠双侧股骨缺损模型。
从6只小鼠（FVB/N）中获取供体小鼠骨髓间充质干细胞（mBMSC），并将其整合到部分脱矿骨基质支架中以构建组织工程骨。总共使用36只绿色荧光蛋白（GFP）阳性小鼠进行建模。将带有锁定钢丝的钛固定板附着于股骨以实现稳定，在双侧股骨干中部制造2毫米长的节段性骨缺损。左、右股骨的缺损分别移植组织工程骨和对照支架。通过X线摄影、微型计算机断层扫描和组织学监测愈合过程。通过免疫荧光和实时聚合酶链反应研究移植的mBMSC募集宿主CD31阳性细胞的能力。
术后，除两只小鼠不明原因死亡外，未观察到并发症。所有动物均实现了股骨和植入物的稳定固定及完全负重。由于引入了mBMSC，骨缺损修复过程明显加速。此外，移植的mBMSC吸引了更多宿主CD31阳性内皮祖细胞进入移植物。
本研究建立了一种可行、可重复且与临床相关的小鼠双侧股骨大型节段性骨缺损模型。该模型可能适用于骨组织工程领域的基础研究。
