{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:03:21Z","timestamp":1787015001066,"version":"build-2736575974"},"reference-count":25,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,7,9]],"date-time":"2008-07-09T00:00:00Z","timestamp":1215561600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European J Oral Sciences"],"published-print":{"date-parts":[[2008,8]]},"abstract":"<jats:p>The biological mechanisms that maintain the position of teeth in their sockets establish a dynamic equilibrium between bone resorption and apposition. In order to reveal some of the dynamics involved in the tissue responses towards occlusal forces on periodontal ligament (PDL) and alveolar bone homeostasis, we developed the first mouse model of hyperocclusion. Swiss\u2013Webster mice were kept in hyperocclusion for 0, 3, 6, and 9\u2003d. Morphological and histological changes in the periodontium were assessed using micro\u2010computed tomography (micro\u2010CT) and ground sections with fluorescent detection of vital dye labels. Sections were stained for tartrate\u2010resistant acid phosphatase, and the expression of receptor activator of nuclear factor\u2010\u03baB ligand (RANKL) and osteopontin (OPN) was analyzed by immunohistochemistry and real\u2010time polymerase chain reaction (PCR). Traumatic occlusion resulted in enamel surface abrasion, inhibition of alveolar bone apposition, significant formation of osteoclasts at 3, 6 and 9\u2003d, and upregulation of OPN and RANKL. Data from this study suggest that both OPN and RANKL contribute to the stimulation of bone resorption in the hyperocclusive state. In addition, we propose that the inhibition of alveolar bone apposition by occlusal forces is an important mechanism for the control of occlusal height that might work in synergy with RANKL\u2010induced bone resorption to maintain normal occlusion.<\/jats:p>","DOI":"10.1111\/j.1600-0722.2008.00545.x","type":"journal-article","created":{"date-parts":[[2008,7,9]],"date-time":"2008-07-09T11:24:45Z","timestamp":1215602685000},"page":"312-318","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":61,"title":["RANKL, osteopontin, and osteoclast homeostasis in a hyperocclusion mouse model"],"prefix":"10.1111","volume":"116","author":[{"given":"Cameron G.","family":"Walker","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihiro","family":"Ito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Smit","family":"Dangaria","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianghong","family":"Luan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas G. 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