{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T21:43:46Z","timestamp":1776462226475,"version":"3.51.2"},"reference-count":34,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,3,13]],"date-time":"2013-03-13T00:00:00Z","timestamp":1363132800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J of Med Genetics Pt A"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Apert syndrome is a common craniosynostosis caused by gain\u2010of\u2010function missense mutations of fibroblast growth factor receptor 2 (FGFR2). Mice with the FGFR2 S252W mutation can elucidate the mechanism by which the human Apert syndrome phenotypes arise. However, many studies have focused on mutant skull and long bone malformation, only few studies have focused on mandible changes. Bone formation and micro\u2010architecture between 28\u2010 and 56\u2010day\u2010old mutant mice and controls were compared to investigate the changes in the mandibular micro\u2010architecture caused by the <jats:italic>Fgfr2<\/jats:italic><jats:sup>S252W\/+<\/jats:sup> mutation to provide a basis for exploring the pathogenesis and therapeutic measures of human Apert syndrome. <jats:italic>Fgfr2<\/jats:italic><jats:sup>S252W\/+<\/jats:sup> mutant mice were established, and their general characteristics, including weight, naso\u2010anal length, and calcium and phosphate content in serum and bone were tested. Calcein labeling, tartrate\u2010resistant acid phosphatase staining and toluidine blue staining were used to detect osteoblast and osteoclast activities. H&amp;E staining and micro\u2010CT detection were used to test micro\u2010architecture changes. The changes in mineral apposition rate and micro\u2010architecture of the <jats:italic>Fgfr2<\/jats:italic><jats:sup>S252W\/+<\/jats:sup> mice were statistically significant; however, the magnitude of the micro\u2010architecture became less with age. The <jats:italic>Fgfr2<\/jats:italic><jats:sup>S252W\/+<\/jats:sup> mutation may retard mandibular bone formation, decreased bone volume, and compromised skeletal architecture by regulating both osteoblastogenesis and osteoclastogenesis. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ajmg.a.35824","type":"journal-article","created":{"date-parts":[[2013,3,14]],"date-time":"2013-03-14T09:33:02Z","timestamp":1363253582000},"page":"983-992","source":"Crossref","is-referenced-by-count":11,"title":["Reduces Bone Mass as in Human Apert Syndrome"],"prefix":"10.1002","volume":"161","author":[{"given":"Xia","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Stomatology Research Institute of Surgery, Daping Hospital, The Third Military Medical University Chongqing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dongquan","family":"Pu","sequence":"additional","affiliation":[{"name":"Department of Stomatology Research Institute of Surgery, Daping Hospital, The Third Military Medical University Chongqing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ri","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Stomatology Research Institute of Surgery, Daping Hospital, The Third Military Medical University Chongqing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiangjie","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Stomatology Research Institute of Surgery, Daping Hospital, The Third Military Medical University Chongqing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiujie","family":"Wen","sequence":"additional","affiliation":[{"name":"Department of Stomatology Research Institute of Surgery, Daping Hospital, The Third Military Medical University Chongqing 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