{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T05:48:35Z","timestamp":1777614515806,"version":"3.51.4"},"reference-count":53,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2021,4,12]],"date-time":"2021-04-12T00:00:00Z","timestamp":1618185600000},"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":["Molecular Oral Microbiology"],"published-print":{"date-parts":[[2021,6]]},"abstract":"<jats:p>\n                    The dysregulation of immune system plays a crucial function in periodontitis development. Pro\u2010inflammatory cytokines are thought to be critical for the generation and development of periodontitis. The enhanced activity of osteoclasts contributes to periodontitis pathogenesis. Nuclear factor\u2010\u03baB (NF\u2010\u03baB) signaling pathway directly enhances osteoclast differentiation and maturation. 2\u2010[(aminocarbonyl)amino]\u20105\u2010(4\u2010fluorophenyl)\u20103\u2010thiophenecarboxamide (TPCA\u20101) is a I\u03baB kinases (IKK) inhibitor. This research aimed to investigate whether TPCA\u20101 had influence on the pathogenesis of chronic periodontitis. Mouse chronic periodontitis was induced by an in vivo ligature\u2010induced periodontitis model. TPCA\u20101 was intravenously injected into mice after chronic periodontitis induction. Bone marrow\u2010derived macrophages were cultured in macrophage colony\u2010stimulating factor (M\u2010CSF)\u2010conditioned media with receptor activator of nuclear factor\u2010kappa B ligand (RANKL) induce in vitro osteoclast differentiation. Western blot was used to analyze protein levels and mRNA levels were analyzed through qRT\u2010PCR. TPCA\u20101 promoted osteoclastogenesis and osteoclast\u2010related gene expression in vitro. The production of pro\u2010inflammatory cytokines in osteoclasts induced by lipopolysaccharides was inhibited by TPCA\u20101 in vitro. In vitro TPCA\u20101 treatment inhibited\n                    <jats:italic>Aggregatibacter actinomycetemcomitans<\/jats:italic>\n                    (A.a)\u2010induced expression of pro\u2010inflammatory cytokines and NF\u2010\u03baB signal activation in osteoclasts. The induction of chronic periodontitis was inhibited by the absence of IKKb in mice. This research demonstrates that the treatment of TPCA\u20101 negatively regulates inflammation response and inhibits the osteoclastogenesis through the inactivation of NF\u2010\u03baB pathway in mouse chronic periodontitis model.\n                  <\/jats:p>","DOI":"10.1111\/omi.12335","type":"journal-article","created":{"date-parts":[[2021,3,25]],"date-time":"2021-03-25T20:55:48Z","timestamp":1616705748000},"page":"192-201","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["TPCA\u20101 negatively regulates inflammation mediated by NF\u2010\u03baB pathway in mouse chronic periodontitis model"],"prefix":"10.1111","volume":"36","author":[{"given":"Bo","family":"Wang","sequence":"first","affiliation":[{"name":"School of Public Health Xi\u2019an Jiaotong University Health Science Center Xi\u2019an Shaanxi China"},{"name":"Department of Stomatology Xi'an People's Hospital Xi\u2019an Shaanxi 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