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Our aim was to detect the role of CaMK<\/jats:styled-content>II, and its relationship with the feedback loop of Indian hedgehog (Ihh) and Parathyroid\u2010related peptide (PTHrP) in the temporomandibular joints (TMJ<\/jats:styled-content>s) OA<\/jats:styled-content>. KN<\/jats:styled-content>93, the competitive inhibitor of CaMK<\/jats:styled-content>II, was added to the culture medium in vitro and was locally injected to rats TMJ<\/jats:styled-content>s (n\u00a0=\u00a054, female) every other day for 4\u00a0weeks from the beginning of the 5th and 9th week after installing of unilateral anterior crossbite (UAC<\/jats:styled-content>), termed as 4\u00a0wk+4\u00a0wk and 8\u00a0wk+4\u00a0wk, accordingly. The RNA<\/jats:styled-content> expression of CaMK<\/jats:styled-content>II \u03b1 (1.49\u00a0\u00b1\u00a00.09), CaMK<\/jats:styled-content>II \u03b2 (3.36\u00a0\u00b1\u00a00.20), Ihh (1.88\u00a0\u00b1\u00a00.06) and PTH<\/jats:styled-content>rP (1.87\u00a0\u00b1\u00a00.12) was all enhanced, especially at 24\u00a0dyn\/cm2<\/jats:sup> in vitro (all P<\/jats:italic>\u00a0<\u00a0.05), accompanied with downregulated expression of cartilage matrix, but upregulated markers of chondrocytes differentiation (all P<\/jats:italic>\u00a0<\u00a00.05). Similarity was observed in the 4\u00a0wk+4\u00a0wk group in vivo. In the 8\u00a0wk+4\u00a0wk group, UAC<\/jats:styled-content> upregulated the RNA<\/jats:styled-content> expression of CaMK<\/jats:styled-content>II \u03b1 (1.81\u00a0\u00b1\u00a00.24), CaMK<\/jats:styled-content>II \u03b2 (1.36\u00a0\u00b1\u00a00.07) and Ihh (1.70\u00a0\u00b1\u00a00.21), however, down\u2010regulated PTH<\/jats:styled-content>rP (0.53\u00a0\u00b1\u00a00.04) (all P<\/jats:italic>\u00a0<\u00a0.05), in consonance with the protein expression. All these changes were attenuated by KN<\/jats:styled-content>93 (all P<\/jats:italic>\u00a0<\u00a0.05). In conclusion, CaMK<\/jats:styled-content>II took a role, via Ihh and PTH<\/jats:styled-content>rP pathways, in promoting biomechanically induced TMJ<\/jats:styled-content> chondrocytes differentiation, the initiation issue of UAC<\/jats:styled-content> stimulated osteoarthritic changes in rodent TMJ<\/jats:styled-content>s. Inhibiting CaMK<\/jats:styled-content>II is helpful to rescue the biomechanically stimulated cartilage degradation and prospective to be a target treatment of OA<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/joor.12629","type":"journal-article","created":{"date-parts":[[2018,3,31]],"date-time":"2018-03-31T06:00:48Z","timestamp":1522476048000},"page":"442-451","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Calcium\u2010\/calmodulin\u2010dependent protein kinase II<\/scp> in occlusion\u2010induced degenerative cartilage of rat mandibular condyle"],"prefix":"10.1111","volume":"45","author":[{"given":"Q.","family":"Liu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases and Shaanxi International Joint Research Center for Oral Diseases Department of Oral Anatomy and Physiology and TMD School of Stomatology The Fourth 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