{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,15]],"date-time":"2026-03-15T15:56:21Z","timestamp":1773590181318,"version":"3.50.1"},"reference-count":36,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2023,9,12]],"date-time":"2023-09-12T00:00:00Z","timestamp":1694476800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2023,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Temporomandibular joint (TMJ) osteoarthritis (OA) is a common type of TMJ disorders causing pain and dysfunction in the jaw and surrounding tissues. The causes for TMJ OA are unknown and the underlying mechanism remains to be identified. In this study, we generated genetically\u2010modified mice deficient of two homologous microRNAs,<jats:italic>miR\u2010204<\/jats:italic>and<jats:italic>miR\u2010211<\/jats:italic>, both of which were confirmed by in situ hybridization to be expressed in multiple TMJ tissues, including condylar cartilage, articular eminence, and TMJ disc. Importantly, the loss\u2010of\u2010function of<jats:italic>miR\u2010204<\/jats:italic>and<jats:italic>miR\u2010211<\/jats:italic>caused an age\u2010dependent progressive OA\u2010like phenotype, including cartilage degradation and abnormal subchondral bone remodeling. Mechanistically, the TMJ joint deficient of the two microRNAs demonstrated a significant accumulation of RUNX2, a protein directly targeted by<jats:italic>miR\u2010204\/\u2010211<\/jats:italic>, and upregulations of \u03b2\u2010catenin, suggesting a disrupted balance between osteogenesis and chondrogenesis in the TMJ, which may underlie TMJ OA. Moreover, the TMJ with<jats:italic>miR\u2010204\/\u2010211<\/jats:italic>loss\u2010of\u2010function displayed an aberrant alteration in both collagen component and cartilage\u2010degrading enzymes and exhibited exacerbated orofacial allodynia, corroborating the degenerative and painful nature of TMJ OA. Together, our results establish a key role of<jats:italic>miR\u2010204<\/jats:italic>\/<jats:italic>\u2010211<\/jats:italic>in maintaining the osteochondral homeostasis of the TMJ and counteracting OA pathogenesis through repressing the pro\u2010osteogenic factors including RUNX2 and \u03b2\u2010catenin.<\/jats:p>","DOI":"10.1002\/jcp.31120","type":"journal-article","created":{"date-parts":[[2023,9,12]],"date-time":"2023-09-12T08:38:48Z","timestamp":1694507928000},"page":"2668-2678","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Loss of<i>miR\u2010204<\/i>and<i>miR\u2010211<\/i>shifts osteochondral balance and causes temporomandibular joint osteoarthritis"],"prefix":"10.1002","volume":"238","author":[{"given":"Jian","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois 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