{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T06:16:12Z","timestamp":1788329772026,"version":"build-2803163510"},"reference-count":43,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2024,6,21]],"date-time":"2024-06-21T00:00:00Z","timestamp":1718928000000},"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":[[2024,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>This study was designed to test the hypothesis that the leptin receptor (LepR) regulates changes in periodontal tissues and that the overexpression of the receptor for resolvin E1 (ERV1) prevents age\u2010 and diabetes\u2010associated alveolar bone loss.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>LepR\u2010deficient transgenic (TG) mice were cross\u2010bred with those overexpressing ERV1 (TG) to generate double\u2010TG mice. In total, 95 mice were divided into four experimental groups: wild type (WT), TG, LepR deficient (db\/db), and double transgenic (db\/db TG). The groups were followed from 4\u00a0weeks up to 16\u00a0weeks of age. The natural progression of periodontal disease without any additional method of periodontitis induction was assessed by macroscopic and histomorphometric analyses. Osteoclastic activity was measured by tartrate\u2010resistant acid phosphatase (TRAP) staining.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At 4\u00a0weeks, ERV1 overexpression prevented weight gain. From Week 8 onward, there was a significant increase in the weight of db\/db mice with or without ERV1 overexpression compared to the WT mice, accompanied by an increase in glucose levels. By 8\u00a0weeks of age, the percentage of bone loss in the LepR deficiency groups was significantly greater compared to WT mice. ERV1 overexpression in the db\/db TG mice prevented early alveolar bone loss; however, it did not impact the development of diabetic bone loss in aging mice after the onset of weight gain and diabetes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The findings suggest that the overexpression of ERV1 prevents LepR\u2010associated alveolar bone loss during the early phases of periodontal disease by delaying weight gain, diabetes onset, and associated inflammation; however, LepR deficiency increases susceptibility to naturally occurring inflammatory alveolar bone loss as the animal ages, associated with excess weight gain, onset of diabetes, and excess inflammation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jper.24-0060","type":"journal-article","created":{"date-parts":[[2024,6,21]],"date-time":"2024-06-21T14:48:47Z","timestamp":1718981327000},"page":"1190-1200","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Overexpression of the receptor for resolvin E1 (ERV1) prevents early alveolar bone loss in leptin receptor deficiency\u2010induced diabetes"],"prefix":"10.1002","volume":"95","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2696-3051","authenticated-orcid":false,"given":"Lina J.","family":"Su\u00e1rez","sequence":"first","affiliation":[{"name":"ADA Forsyth Institute  Cambridge Massachusetts USA"},{"name":"Universidad Nacional de Colombia  Bogot\u00e1 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