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Myogenic progenitors contribute to open but not closed fracture repair.
BMC Musculoskelet Disord. 2011 Dec 22; 12:288.BM

Abstract

BACKGROUND

Bone 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.

METHODS

We 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.

RESULTS

In 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.

CONCLUSIONS

These 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.

Authors+Show Affiliations

Orthopaedic Research & Biotechnology Unit, The Children's Hospital at Westmead, Sydney, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22192089

Citation

Liu, Renjing, et al. "Myogenic Progenitors Contribute to Open but Not Closed Fracture Repair." BMC Musculoskeletal Disorders, vol. 12, 2011, p. 288.
Liu R, Birke O, Morse A, et al. Myogenic progenitors contribute to open but not closed fracture repair. BMC Musculoskelet Disord. 2011;12:288.
Liu, R., Birke, O., Morse, A., Peacock, L., Mikulec, K., Little, D. G., & Schindeler, A. (2011). Myogenic progenitors contribute to open but not closed fracture repair. BMC Musculoskeletal Disorders, 12, 288. https://doi.org/10.1186/1471-2474-12-288
Liu R, et al. Myogenic Progenitors Contribute to Open but Not Closed Fracture Repair. BMC Musculoskelet Disord. 2011 Dec 22;12:288. PubMed PMID: 22192089.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Myogenic progenitors contribute to open but not closed fracture repair. AU - Liu,Renjing, AU - Birke,Oliver, AU - Morse,Alyson, AU - Peacock,Lauren, AU - Mikulec,Kathy, AU - Little,David G, AU - Schindeler,Aaron, Y1 - 2011/12/22/ PY - 2011/06/27/received PY - 2011/12/22/accepted PY - 2011/12/24/entrez PY - 2011/12/24/pubmed PY - 2012/6/30/medline SP - 288 EP - 288 JF - BMC musculoskeletal disorders JO - BMC Musculoskelet Disord VL - 12 N2 - BACKGROUND: Bone 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. METHODS: We 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. RESULTS: In 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. CONCLUSIONS: These 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. SN - 1471-2474 UR - https://www.unboundmedicine.com/medline/citation/22192089/Myogenic_progenitors_contribute_to_open_but_not_closed_fracture_repair_ L2 - https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/1471-2474-12-288 DB - PRIME DP - Unbound Medicine ER -