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This review explores how DGC functions may extend to skeletal pathophysiology by appraising the known roles of its major ECM ligands, and likely associated DGC signalling pathways, in regulating cartilage and bone cell behaviour and emergent skeletal phenotypes. These considerations will be contextualised by highlighting the potential of studies into the role of the DGC in isolated chondrocytes, osteoblasts and osteoclasts, and by fuller deliberation of skeletal phenotypes that may emerge in very young mice lacking vital, yet diverse core elements of the DGC. Our review points to roles for individual DGC components\u2014including the glycosylation of dystroglycan itself\u2014beyond the establishment of membrane stability which clearly accounts for severe muscle phenotypes in muscular dystrophy. It implies that the short stature, low bone mineral density, poor bone health and greater fracture risk in these patients, which has been attributed due to primary deficiencies in muscle\u2010evoked skeletal loading, may instead arise due to primary roles for the DGC in controlling skeletal tissue (re)modelling.<\/jats:p>","DOI":"10.1111\/iep.12525","type":"journal-article","created":{"date-parts":[[2025,2,11]],"date-time":"2025-02-11T04:59:57Z","timestamp":1739249997000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Extracellular matrix: Dystroglycan interactions\u2014Roles for the dystrophin\u2010associated glycoprotein complex in skeletal tissue dynamics"],"prefix":"10.1111","volume":"106","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9508-8652","authenticated-orcid":false,"given":"Mark","family":"Hopkinson","sequence":"first","affiliation":[{"name":"Skeletal Biology Group, Comparative Biomedical Sciences 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