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Osteogenic Effects of Traumatic Brain Injury on Experimental Fracture-Healing

¹ Department of Orthopaedics, Boston Medical Center, Dowling 2 North, 850 Harrison Avenue, Boston, MA 02118. E-mail address for M. Boes: mattboes{at}hotmail.com. E-mail address for M. Kain: mikain{at}bmc.org. E-mail address for S. Kakar: sanjeev.kakar{at}bmc.org. E-mail address for P. Tornetta III: ptornetta{at}pol.net
² Orthopaedic Research Laboratory, Boston University School of Medicine, 715 Albany Street, R-205, Boston, MA 02118
³ Department of Orthopaedics, Boston Medical Center, 720 Harrison Avenue, Suite 808, Boston, MA 02118. E-mail address for T. Einhorn: thomas.einhorn{at}bmc.org

Investigation performed at the Department of Orthopaedics, Boston Medical Center, and the Orthopaedic Research Laboratory, Boston University School of Medicine, Boston, Massachusetts

In support of their research for or preparation of this manuscript, one or more of the authors received grants or outside funding from the Orthopaedic Trauma Association and the Orthopaedic Research and Education Foundation. None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

Methods: A standard closed femoral fracture was produced in forty-three Sprague-Dawley rats. Twenty-three of the rats were subjected to additional closed head trauma that produced diffuse axonal injury similar to that observed in patients with a traumatic brain injury. Twenty-one days after the procedure, all animals were killed and fracture-healing was assessed by measuring callus size and by mechanical testing. Sera from the animals were used in subsequent in vitro experiments to measure mitogenic effects on established cell lines of committed osteoblasts, fibroblasts, and mesenchymal stem cells.

Results: Biomechanical assessment demonstrated that the brain-injury group had increased stiffness (p = 0.02) compared with the fracture-only group. There was no significant difference in torsional strength between the two groups. Cell culture studies showed a significant increase in the proliferative response of mesenchymal stem cells after exposure to sera from the brain-injury group compared with the response after exposure to sera from the fracture-only group (p = 0.0002). This effect was not observed in fibroblasts or committed osteoblasts.

Conclusions: These results support data from previous studies that have suggested an increased osteogenic potential and an enhancement of fracture-healing secondary to traumatic brain injury. Our results further suggest that the mechanism for this enhancement is related to the presence of factors in the serum that have a mitogenic effect on undifferentiated mesenchymal stem cells.

Clinical Relevance: Fracture-healing may be enhanced by an associated traumatic brain injury. Further understanding of this systemic response could lead to important insights about systemic therapeutic strategies for the enhancement of skeletal repair.

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