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However, the physiological effects of BMP signaling on mandibles are largely unknown, as\u00a0the mandible has distinct functions and characteristics from other bones. In this study, we investigated the roles of BMP signaling in bone homeostasis of the mandibles by deleting BMP type I receptor <jats:italic>Acvr1<\/jats:italic> in osteoblast lineage cells with <jats:italic>Osterix<\/jats:italic>\u2010Cre. We found mandibular bone loss in conditional knockout mice at the ages of postnatal day 21 and 42 in an age\u2010dependent manner. The decreased bone mass was related to compromised osteoblast differentiation together with enhanced osteoclastogenesis, which was secondary to the changes in osteoblasts in vivo. In vitro study revealed that deletion of <jats:italic>Acvr1<\/jats:italic> in the mandibular bone marrow stromal cells (BMSCs) significantly compromised osteoblast differentiation. When wild type bone marrow macrophages were cocultured with BMSCs lacking <jats:italic>Acvr1<\/jats:italic> both directly and indirectly, both proliferation and differentiation of osteoclasts were induced as evidenced by an increase of multinucleated cells, compared with\u00a0cocultured with control BMSCs. Furthermore, we demonstrated that the increased osteoclastogenesis in vitro was at least partially due to the secretion of soluble receptor activator of nuclear factor\u2010\u03baB ligand (sRANKL), which is probably the reason for the mandibular bone loss in vivo. Overall, our results proposed that ACVR1 played essential roles in maintaining mandibular bone homeostasis through osteoblast differentiation and osteoblast\u2010osteoclast communication via sRANKL.<\/jats:p>","DOI":"10.1002\/jcp.30183","type":"journal-article","created":{"date-parts":[[2020,11,30]],"date-time":"2020-11-30T04:40:46Z","timestamp":1606711246000},"page":"4580-4591","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["<i>Acvr1<\/i> deletion in osteoblasts impaired mandibular bone mass through compromised osteoblast differentiation and enhanced sRANKL\u2010induced osteoclastogenesis"],"prefix":"10.1002","volume":"236","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5634-8063","authenticated-orcid":false,"given":"Yue","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Oral Pathology,\u00a0Hospital of Stomatology Jilin University Changchun China"},{"name":"Key Laboratory of Tooth 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