Myogenic progenitors contribute to open but not closed fracture repair

BMC Musculoskeletal Disorders

Research Article

Oliver Birke¹  Alyson Morse¹  Lauren Peacock¹  Kathy Mikulec¹  Aaron Schindeler²  David G Little²  Renjing Liu² 

[1] Orthopaedic Research & Biotechnology Unit, The Children's Hospital at Westmead, Sydney, Australia;Orthopaedic Research & Biotechnology Unit, The Children's Hospital at Westmead, Sydney, Australia;Discipline of Paediatrics and Child Health, Faculty of Medicine, University of Sydney, Sydney, Australia;

关键词: Open Fracture;    Tibial Fracture;    Bone Repair;    Myogenic Cell;    Fracture Repair;   

DOI  :  10.1186/1471-2474-12-288

 received in 2011-06-27, accepted in 2011-12-22,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundBone repair is dependent on the presence of osteocompetent progenitors that are able to differentiate and generate new bone. Muscle is found in close association with orthopaedic injury, however its capacity to make a cellular contribution to bone repair remains ambiguous. We hypothesized that myogenic cells of the MyoD-lineage are able to contribute to bone repair.MethodsWe employed a MyoD-Cre+:Z/AP+ conditional reporter mouse in which all cells of the MyoD-lineage are permanently labeled with a human alkaline phosphatase (hAP) reporter. We tracked the contribution of MyoD-lineage cells in mouse models of tibial bone healing.ResultsIn the absence of musculoskeletal trauma, MyoD-expressing cells are limited to skeletal muscle and the presence of reporter-positive cells in non-muscle tissues is negligible. In a closed tibial fracture model, there was no significant contribution of hAP+ cells to the healing callus. In contrast, open tibial fractures featuring periosteal stripping and muscle fenestration had up to 50% of hAP+ cells detected in the open fracture callus. At early stages of repair, many hAP+ cells exhibited a chondrocyte morphology, with lesser numbers of osteoblast-like hAP+ cells present at the later stages. Serial sections stained for hAP and type II and type I collagen showed that MyoD-lineage cells were surrounded by cartilaginous or bony matrix, suggestive of a functional role in the repair process. To exclude the prospect that osteoprogenitors spontaneously express MyoD during bone repair, we created a metaphyseal drill hole defect in the tibia. No hAP+ staining was observed in this model suggesting that the expression of MyoD is not a normal event for endogenous osteoprogenitors.ConclusionsThese data document for the first time that muscle cells can play a significant secondary role in bone repair and this knowledge may lead to important translational applications in orthopaedic surgery.Please see related article: http://www.biomedcentral.com/1741-7015/9/136

【 授权许可】

Unknown   
© Liu et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.