{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:30:54Z","timestamp":1791275454166,"version":"4.1.0"},"reference-count":62,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2013,7,15]],"date-time":"2013-07-15T00:00:00Z","timestamp":1373846400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,2,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Duchenne muscular dystrophy (DMD) patients exhibit skeletal muscle weakness with continuous cycles of muscle fiber degeneration\/regeneration, chronic inflammation, low bone mineral density, and increased risks of fracture. Fragility fractures and associated complications are considered as a consequence of the osteoporotic condition in these patients. Here, we aimed to establish the relationship between muscular dystrophy and fracture healing by assessing bone regeneration in mdx mice, a model of DMD with absence of osteoporosis. Our results illustrate that muscle defects in mdx mice impact the process of bone regeneration at various levels. In mdx fracture calluses, both cartilage and bone deposition were delayed followed by a delay in cartilage and bone remodeling. Vascularization of mdx fracture calluses was also decreased during the early stages of repair. Dystrophic muscles are known to contain elevated numbers of macrophages contributing to muscle degeneration. Accordingly, we observed increased macrophage recruitment in the mdx fracture calluses and abnormal macrophage accumulation throughout the process of bone regeneration. These changes in the inflammatory environment subsequently had an impact on the recruitment of osteoclasts and the remodeling phase of repair. Further damage to the mdx muscles, using a novel model of muscle trauma, amplified both the chronic inflammatory response and the delay in bone regeneration. In addition, PLX3397 treatment of mdx mice, a cFMS (colony stimulating factor receptor 1) inhibitor in monocytes, partially rescued the bone repair defect through increasing cartilage deposition and decreasing the number of macrophages. In conclusion, chronic inflammation in mdx mice contributes to the fracture healing delay and is associated with a decrease in angiogenesis and a transient delay in osteoclast recruitment. By revealing the role of dystrophic muscle in regulating the inflammatory response during bone repair, our results emphasize the implication of muscle in the normal bone repair process and may lead to improved treatment of fragility fractures in DMD patients. \u00a9 2014 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2038","type":"journal-article","created":{"date-parts":[[2013,7,15]],"date-time":"2013-07-15T13:29:07Z","timestamp":1373894947000},"page":"304-315","source":"Crossref","is-referenced-by-count":60,"title":["Delayed Bone Regeneration Is Linked to Chronic Inflammation in Murine Muscular Dystrophy"],"prefix":"10.1093","volume":"29","author":[{"given":"Rana","family":"Abou-Khalil","sequence":"first","affiliation":[{"name":"INSERM U781, Universit\u00e9 Paris Descartes-Sorbonne Paris Cit\u00e9, Institut Imagine, H\u00f4pital Necker Enfants MaladesParisFrance"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Mortreux","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shirley","family":"Lieu","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan-Yiu","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maud","family":"Wurmser","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catia","family":"Pereira","sequence":"additional","affiliation":[{"name":"INSERM U781, Universit\u00e9 Paris Descartes-Sorbonne Paris Cit\u00e9, Institut Imagine, H\u00f4pital Necker Enfants MaladesParisFrance"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fr\u00e9d\u00e9ric","family":"Relaix","sequence":"additional","affiliation":[{"name":"INSERM, UMR-S 787, UPMC Paris VI, Institut de Myologie, Facult\u00e9 de M\u00e9decine Piti\u00e9-Salp\u00e9tri\u00e8reParisFrance"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theodore","family":"Miclau","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralph S","family":"Marcucio","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic SurgeryUniversity of California at San FranciscoSan FranciscoCAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9line","family":"Colnot","sequence":"additional","affiliation":[{"name":"INSERM U781, Universit\u00e9 Paris Descartes-Sorbonne Paris Cit\u00e9, Institut Imagine, H\u00f4pital Necker Enfants MaladesParisFrance"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,7,15]]},"reference":[{"issue":"2","key":"2024020318580212700_jbmr2038-bib-0001","first-page":"59","article-title":"[Incidence of pseudarthroses in open fractures: analysis of 948 open fractures]","volume":"23","author":"Sudkamp","year":"1993","journal-title":"Aktuelle 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destruction","volume":"392","author":"Cairns","year":"2010","journal-title":"Biochem Biophys Res Commun."},{"key":"2024020318580212700_jbmr2038-bib-0005","doi-asserted-by":"crossref","first-page":"S7","DOI":"10.1097\/00003086-199810001-00003","article-title":"The cell and molecular biology of fracture healing","volume":"46","author":"Einhorn","year":"1998","journal-title":"Clin Orthop Relat Res."},{"issue":"2","key":"2024020318580212700_jbmr2038-bib-0006","doi-asserted-by":"crossref","first-page":"107","DOI":"10.1177\/154405910808700215","article-title":"Molecular mechanisms controlling bone formation during fracture healing and distraction osteogenesis","volume":"87","author":"Ai-Aql","year":"2008","journal-title":"J Dent Res."},{"issue":"8","key":"2024020318580212700_jbmr2038-bib-0007","doi-asserted-by":"crossref","first-page":"1272","DOI":"10.1002\/jbmr.5650100818","article-title":"The expression of cytokine activity by fracture callus","volume":"10","author":"Einhorn","year":"1995","journal-title":"J Bone Miner Res."},{"key":"2024020318580212700_jbmr2038-bib-0008","doi-asserted-by":"crossref","first-page":"S5","DOI":"10.1016\/j.injury.2005.07.027","article-title":"Overview of the fracture healing cascade","volume":"36","author":"Phillips","year":"2005","journal-title":"Injury."},{"key":"2024020318580212700_jbmr2038-bib-0009","doi-asserted-by":"crossref","first-page":"S11","DOI":"10.1016\/j.injury.2007.02.006","article-title":"Molecular aspects of fracture healing: which are the important molecules","volume":"38","author":"Tsiridis","year":"2007","journal-title":"Injury."},{"issue":"12","key":"2024020318580212700_jbmr2038-bib-0010","doi-asserted-by":"crossref","first-page":"1392","DOI":"10.1016\/j.injury.2005.07.019","article-title":"Current concepts of molecular aspects of bone 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