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Serum After Traumatic Brain Injury Increases Proliferation and Supports Expression of Osteoblast Markers in Muscle Cells
Dieter Cadosch, MD, PhDc1; Andrew M. Toffoli, MD1; Oliver P. Gautschi, MD1; Sönke P. Frey, MD1; René Zellweger, MD2; Allan P. Skirving, MD2; Luis Filgueira, MD1
1 School of Anatomy and Human Biology, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia. E-mail address for D. Cadosch: dcadosch@gmx.net
2 Department of Orthopaedic and Trauma Surgery, Royal Perth Hospital, Wellington Street, Perth, WA 6000, Australia
View Disclosures and Other Information
Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity.

Investigation performed at the University of Western Australia, Crawley, and the Royal Perth Hospital, Perth, Western Australia, Australia

Copyright ©2010 American Society for Journal of Bone and Joint Surgery, Inc.
J Bone Joint Surg Am, 2010 Mar 01;92(3):645-653. doi: 10.2106/JBJS.I.00097
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Abstract

Background: 

Traumatic brain injury is associated with an increased rate of heterotopic ossification within skeletal muscle, possibly as a result of humoral factors. In this study, we investigated whether cells from skeletal muscle adopt an osteoblastic phenotype in response to serum from patients with traumatic brain injury.

Methods: 

Serum was collected from thirteen patients with severe traumatic brain injury, fourteen patients with a long-bone fracture, and ten control subjects. Primary cultures of skeletal muscle cells isolated from patients undergoing orthopaedic surgery were performed and characterized with use of immunofluorescence microscopy, reverse transcription-polymerase chain reaction, and Western blot analysis. Proliferation and osteoblastic differentiation were assessed with use of commercial cell assays, Western blot analysis (for Osterix protein), and the Villanueva bone stain.

Results: 

All serum-treated cell populations expressed the osteoblast marker Osterix after one week in culture. Cells treated with serum from all study groups in mineralization medium had increased alkaline phosphatase activity and mineralized nodules within the mesenchymal cell subpopulation after three weeks in culture. Serum from patients with traumatic brain injury induced a significant increase (p = 0.02) in the rate of proliferation of primary skeletal muscle cells (1.87 [95% confidence interval, 1.66 to 2.09]) compared with the rate induced by serum from patients with a fracture (1.42 [95% confidence interval, 1.21 to 1.58]) or by serum from controls (1.35 [95% confidence interval, 1.15 to 1.54]).

Conclusions: 

Human serum supports the osteoblastic differentiation of cells derived from human skeletal muscle, and serum from patients with severe traumatic brain injury accelerates proliferation of these cells. These findings suggest the early presence of humoral factors following traumatic brain injury that stimulate the expansion of mesenchymal cells and osteoprogenitors within skeletal muscle.

Clinical Relevance: 

A better understanding of the pathophysiological mechanisms that lead to the formation of heterotopic ossification in patients with a traumatic brain injury may be helpful in the prevention and treatment of this complication.

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    References

    Accreditation Statement
    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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