{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T12:48:47Z","timestamp":1791809327382,"version":"4.3.4"},"reference-count":41,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2024,9,23]],"date-time":"2024-09-23T00:00:00Z","timestamp":1727049600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2024,9,23]],"date-time":"2024-09-23T00:00:00Z","timestamp":1727049600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["aap.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2025,6]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n B\u2010cell\u2011specific Moloney MLV insertion site\u20101(Bmi\u20101)is a crucial osteopenic target molecule. The aim of this study is to explore\u00a0the effects of Bmi\u20101 on alveolar bone resorption and\u00a0the underlying mechanisms in vitro and vivo.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n A\n Bmi\u20101<\/jats:italic>\n \u2010knockout (\n \n Bmi\u20101\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n ) mouse model was used to investigate the effect of Bmi\u20101 on alveolar bone metabolism, with micro\u2010computed tomography imaging, histology, and immunohistochemistry staining. Furthermore, we utilized a ligature\u2010induced experimental periodontitis model to examine the impact of\n Bmi\u20101<\/jats:italic>\n \u2010knockdown (\n Bmi\u20101<\/jats:italic>\n \u00b1<\/jats:sup>\n ) on inflammatory alveolar bone resorption. Finally, we stimulated human periodontal ligament stem cells (hPDLSCs) with lipopolysaccharide (LPS) to explore the potential mechanism of Bmi\u20101 overexpression in the process of osteogenesis.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Compared with wild\u2010type mice,\n Bmi\u20101<\/jats:italic>\n \u2212\/\u2212<\/jats:sup>\n mice demonstrated more alveolar bone resorption by inhibiting osteogenesis, which was characterized by decreases in Runt\u2010related transcription factor 2 and type 1 collagen formation. In addition,\n \n Bmi\u20101\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n mice had lower levels of autophagy markers such as Parkin and LC3, but higher levels of inflammation\u2010related factors such as interleukin (IL)\u20106 and IL\u20101\u03b2 in periodontal tissues. In addition,\n Bmi\u20101<\/jats:italic>\n \u2010knockdown aggravated ligature\u2010induced alveolar bone loss. Under in vitro inflammatory conditions, Bmi\u20101 overexpression stimulated osteoblast differentiation and inhibited the production of inflammatory factors, as well as the autophagy and apoptosis in hPDLSCs stimulated with LPS. When 3\u2010methyladenine (3\u2010MA), an autophagy inhibitor, was added, the osteogenic effect of Bmi\u20101 was further enhanced.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Bmi\u20101 alleviates alveolar bone resorption by regulating autophagy, indicating that it could be a potential target for periodontitis prevention and treatment.<\/jats:p>\n <\/jats:sec>\n \n Plain Language Summary<\/jats:title>\n Periodontitis is a chronic inflammatory disease, which leads to progressive destruction of periodontal tissues, manifested as periodontal pocket formation, loss of periodontal attachment and alveolar bone resorption. Currently, there is a lack of effective treatments to regenerate damaged periodontal tissues. Therefore, it is of great clinical significance to explore new mechanisms of periodontitis and effective intervention targets. B\u2010cell\u2011specific Moloney MLV insertion site\u20101 (Bmi\u20101) is involved in the regulation of the cell cycle, DNA damage repair, autophagy, bone metabolism, tumor, and other physiopathological processes. Autophagy, as an important mechanism of intracellular self\u2010regulation, plays an indispensable role in the destruction and repair of periodontal tissues. The aim of this study was to investigate the role of Bmi\u20101 on periodontal tissues and its intrinsic mechanism. The results revealed that Bmi\u20101 regulates autophagy to protect periodontal tissues, suggesting that it may be a potential target for the prevention and treatment of periodontitis.<\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/jper.23-0796","type":"journal-article","created":{"date-parts":[[2024,9,23]],"date-time":"2024-09-23T10:10:38Z","timestamp":1727086238000},"page":"694-707","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Bmi\u20101 alleviates alveolar bone resorption through the regulation of autophagy"],"prefix":"10.1002","volume":"96","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-8922-1316","authenticated-orcid":false,"given":"Yiting","family":"Chu","sequence":"first","affiliation":[{"name":"Department of Stomatology Children's Hospital of Nanjing Medical University Nanjing Jiangsu 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