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Updated: Apr 27, 2026
Establishment of a Segmental Femoral Critical-size Defect Model in Mice Stabilized by Plate Osteosynthesis
Published on: October 12, 2016
Establishment of a bilateral femoral large segmental bone defect mouse model potentially applicable to basic research
Junchao Xing1, Huiyong Jin2, Tianyong Hou1
1National 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.
Background:
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.
Materials And Methods:
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.
Results:
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.
Conclusions:
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.
