Abstract
Fracture repair is dependent on local and systemic molecular and cellular processes. During fracture repair, mesenchymal stem cells are systemically recruited to the fracture site, and cytokines are released from the fracture site into the vascular system. In a significant minority of fractures, healing delays result from adverse clinical factors that interfere with these processes. Extrinsic factors, such as aging and smoking, adversely affect the molecular and cellular processes occurring locally in the fracture site. Fracture fixation affects healing through local changes in the biologic signaling within the fracture callus. Current biologic treatment of fractures includes the local application of osteoinductive bone morphogenetic proteins (ie, BMP-2, BMP-7) and cell-based therapies. Although clinical results with bone morphogenetic proteins have been satisfactory, they have not been as impressive as those reported in animal studies. Further understanding of the biology of fracture repair may lead to improved treatment modalities.
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