{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T18:07:04Z","timestamp":1789927624710,"version":"4.0.1"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2019,10,15]],"date-time":"2019-10-15T00:00:00Z","timestamp":1571097600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["aap.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p><jats:italic>Msx2<\/jats:italic> homeoprotein is a key transcription factor of dental and periodontal tissue formation and is involved in many molecular pathways controlling mineralized tissue homeostasis such as Wnt\/sclerostin pathway. This study evaluated the effect of <jats:italic>Msx2<\/jats:italic>\u2010null mutation during experimental periodontitis in mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Experimental periodontitis was induced for 30 days in wild\u2010type and <jats:italic>Msx2<\/jats:italic> knock\u2010in Swiss mice using <jats:italic>Porphyromonas gingivalis<\/jats:italic> infected ligatures. In knock\u2010in mice, <jats:italic>Msx2<\/jats:italic> gene was replaced by <jats:italic>n\u2010LacZ<\/jats:italic> gene encoding \u03b2\u2010galactosidase. Periodontal tissue response was assessed by histomorphometry, tartrate\u2010resistant acid phosphatase histoenzymology, \u03b2\u2010galactosidase, sclerostin immunochemistry, and terminal deoxynucleotidyl transferase\u2010mediated dUTP nickend labeling assay. Expression of <jats:italic>Msx2<\/jats:italic> gene expression was also evaluated in human gingival biopsies using RT\u2010qPCR.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>During experimental periodontitis, osteonecrosis area and osteoclast number were significantly elevated in knock\u2010in mice compared with wild\u2010type mice. Epithelial downgrowth and bone loss was similar. Sclerostin expression in osteocytes appeared to be reduced during periodontitis in knock\u2010in mice. <jats:italic>Msx2<\/jats:italic> expression was detected in healthy and inflamed human gingival tissues.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These data indicated that <jats:italic>Msx2<\/jats:italic> pathway influenced periodontal tissue response to experimental periodontitis and appeared to be a protective factor against alveolar bone osteonecrosis. As shown in other inflammatory processes such as atherothrombosis, genes initially characterized in early development could also play an important role in human periodontal pathogenesis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jper.16-0435","type":"journal-article","created":{"date-parts":[[2019,10,1]],"date-time":"2019-10-01T00:01:46Z","timestamp":1569888106000},"page":"693-704","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Experimental periodontitis in <i>Msx2<\/i> mutant mice induces alveolar bone necrosis"],"prefix":"10.1002","volume":"91","author":[{"given":"Linda","family":"Korah","sequence":"first","affiliation":[{"name":"INSERM (French National Institute of Health and Medical\u00a0Research), UMR 1109, Osteoarticular and Dental Regenerative Nanomedicine laboratory Facult\u00e9 de M\u00e9decine, FMTS (Federation of Translational Medicine Strasbourg)  Strasbourg 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