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AMD3100, a stem cell mobilizer, aids fracture healing in mice



DOI:10.1038/bonekey.2013.220

AMD3100, an inhibitor of chemokine receptor 4 (CXCR4), is already approved as an agent for mobilizing hematopoietic stem cells into the peripheral blood of bone marrow transplant patients. In this study, Toupadakis et al. investigated its impact on fracture healing in a mouse model.

C57BL/6 mice with a transverse femoral fracture were treated with AMD3100 by injection for 3 days after surgery, or with saline. Treated and control mice were assessed by flow cytometry, cell culture and automated hematology at the 24-h point. Fracture healing was assessed on day 84.

As expected, mice treated with AMD3100 showed significantly higher levels of circulating endothelial progenitor cells, mesenchymal stromal cells and hematopoietic stem cells. Callus volume was significantly larger (P<0.0001) on day 21, and by day 84 the mice had signs of faster bone remodeling with a significantly smaller total callus volume and mineralized bone volume. Their callus was stronger with higher bone mineral density.

Editor’s comment: The positive effects of AMD3100 treatment on cranial bone defects and intramembranous bone formation after bone marrow ablation have been demonstrated previously. Importantly, this study shows that AMD3100 positively modulates endochondral fracture repair, with effects apparent in the early and late stages of fracture healing. Mobilizing progenitors to influence fracture repair is an attractive concept, but further studies in challenged models are now needed.


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