{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T23:36:16Z","timestamp":1787009776518,"version":"build-2736575974"},"reference-count":77,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:00:00Z","timestamp":1779235200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:00:00Z","timestamp":1779235200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2026,5,31]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Chronic periodontitis (CP) and postmenopausal osteoporosis (PMOP) are prevalent chronic inflammatory diseases characterized by bone resorption; however, the shared molecular mechanisms between them remain unclear. Hub genes associated with CP and PMOP were identified through bioinformatics analysis. Lipopolysaccharide (LPS)\u2010stimulated MC3T3\u2010E1 osteoblasts were used to establish an in\u00a0vitro model, followed by lentiviral\u2010mediated matrix metalloproteinase 14 (MMP14) knockdown. Cell viability and apoptosis were assessed using the Cell Counting Kit\u20108 assay and flow cytometry, respectively. Levels of inflammatory cytokines and oxidative stress markers were measured by enzyme\u2010linked immunosorbent assay. Intracellular ROS were detected using 2\u2032,7\u2032\u2010dichlorodihydrofluorescein diacetate fluorescence staining. Western blot analysis was performed to assess the expression of osteoclast\u2010related markers. The involvement of the JAK2\/STAT3 pathway was assessed using the JAK2 agonist RO8191 and inhibitor AG490. PDGFRB, MMP14, VWF, PECAM1, FLT1, and CXCR4 were identified as hub genes and were all upregulated in LPS\u2010stimulated MC3T3\u2010E1 osteoblasts. Silencing MMP14 improved cell viability and reduced apoptosis, inflammatory cytokine release (TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106), oxidative stress markers (MDA and ROS), and osteoclast\u2010associated markers (CTX\u2010I, TRAP, and Cathepsin K), while restoring SOD activity. Mechanistically, MMP14 silencing decreased the phosphorylation levels of JAK2 and STAT3. The protective phenotype caused by MMP14 silencing was significantly abolished by RO8191 but mimicked by treatment with AG490. MMP14 may represent a potential molecular link between CP\u2010associated bone loss and PMOP. Modulation of the MMP14\u2013JAK2\/STAT3 signaling axis may represent a promising research direction for inflammation\u2010related bone loss.<\/jats:p>","DOI":"10.1096\/fj.202600092rr","type":"journal-article","created":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T12:47:48Z","timestamp":1779281268000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["<scp>MMP14<\/scp>\n                    Silencing Alleviates Inflammation\u2010Associated Bone Loss in Chronic Periodontitis and Postmenopausal Osteoporosis in Association With Reduced\n                    <scp>JAK2<\/scp>\n                    \/\n                    <scp>STAT3<\/scp>\n                    Signaling"],"prefix":"10.1096","volume":"40","author":[{"given":"Xiliang","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of Stomatology Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China  Chengdu 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