{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T20:46:28Z","timestamp":1792010788909,"version":"4.4.0"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2019,4,1]],"date-time":"2019-04-01T00:00:00Z","timestamp":1554076800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Locally produced osteoclastogenic factor RANKL plays a critical role in the development of bone resorption in periradicular periodontitis. However, because RANKL is also required for healthy bone remodeling, it is plausible that a costimulatory molecule that upregulates RANKL production in inflammatory periradicular periodontitis may be involved in the pathogenic bone loss processes. We hypothesized that macrophage migration inhibitory factor (MIF) would play a role in upregulating the RANKL-mediated osteoclastogenesis in the periradicular lesion. In response to pulp exposure, the bone loss and level of MIF mRNA increased in the periradicular periodontitis, which peaked at 14 d, in conjunction with the upregulated expressions of mRNAs for RANKL, proinflammatory cytokines (TNF-\u03b1, IL-6, and IL-1\u03b2), chemokines (MCP-1 and SDF-1), and MIF\u2019s cognate receptors CXCR4 and CD74. Furthermore, expressions of those mRNAs were found significantly higher in wild-type mice compared with that of MIF\u2212\/\u2212 mice. In contrast, bacterial LPS elicited the production of MIF from ligament fibroblasts in vitro, which, in turn, enhanced their productions of RANKL and TNF-\u03b1. rMIF significantly upregulated the number of TRAP+ osteoclasts in vitro. Finally, periapical bone loss induced in wild-type mice were significantly diminished in MIF\u2212\/\u2212 mice. Altogether, the current study demonstrated that MIF appeared to function as a key costimulatory molecule to upregulate RANKL-mediated osteoclastogenesis, leading to the pathogenically augmented bone resorption in periradicular lesions. These data also suggest that the approach to neutralize MIF activity may lead to the development of a therapeutic regimen for the prevention of pathogenic bone loss in periradicular periodontitis.<\/jats:p>","DOI":"10.4049\/jimmunol.1801161","type":"journal-article","created":{"date-parts":[[2019,2,8]],"date-time":"2019-02-08T21:21:13Z","timestamp":1549660873000},"page":"2035-2043","source":"Crossref","is-referenced-by-count":30,"title":["Elevated Expression of Macrophage Migration Inhibitory Factor Promotes Inflammatory Bone Resorption Induced in a Mouse Model of Periradicular Periodontitis"],"prefix":"10.1093","volume":"202","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6268-4941","authenticated-orcid":false,"given":"Mohammed","family":"Howait","sequence":"first","affiliation":[{"name":"School of Dental Medicine, Harvard University , Boston, MA 02115"},{"name":"Faculty of Dentistry, King Abdulaziz University , Jeddah 21589 ,","place":["Saudi Arabia"]},{"name":"The Forsyth Institute , Cambridge, MA 02142"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdullah","family":"Albassam","sequence":"additional","affiliation":[{"name":"School of Dental Medicine, Harvard University , Boston, MA 02115"},{"name":"Faculty of Dentistry, King Abdulaziz University , Jeddah 21589 ,","place":["Saudi Arabia"]},{"name":"The Forsyth Institute , Cambridge, MA 02142"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiaki","family":"Yamada","sequence":"additional","affiliation":[{"name":"College of Dental Medicine, Nova Southeastern University , Ft. Lauderdale, FL 33324"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hajime","family":"Sasaki","sequence":"additional","affiliation":[{"name":"School of Dental Medicine, Harvard University , Boston, MA 02115"},{"name":"The Forsyth Institute , Cambridge, MA 02142"},{"name":"School of Dentistry, University of Michigan , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9075-361X","authenticated-orcid":false,"given":"Laila","family":"Bahammam","sequence":"additional","affiliation":[{"name":"Faculty of Dentistry, King Abdulaziz University , Jeddah 21589 ,","place":["Saudi Arabia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariane Maffei","family":"Azuma","sequence":"additional","affiliation":[{"name":"The Forsyth Institute , Cambridge, MA 02142"},{"name":"School of Dentistry, University of Michigan , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2348-7846","authenticated-orcid":false,"given":"Luciano Tavares Angelo","family":"Cintra","sequence":"additional","affiliation":[{"name":"School of Dentistry, S\u00e3o Paulo State University , Ara\u00e7atuba, S\u00e3o Paulo 15015-050 ,","place":["Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abhay R","family":"Satoskar","sequence":"additional","affiliation":[{"name":"Department of Microbiology, The Ohio State University , Columbus, OH 43210"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoru","family":"Yamada","sequence":"additional","affiliation":[{"name":"Graduate School of Dentistry, Tohoku University , Tohoku, Sendai 980-8575 ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"White","sequence":"additional","affiliation":[{"name":"School of Dental Medicine, Harvard University , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshihisa","family":"Kawai","sequence":"additional","affiliation":[{"name":"College of Dental Medicine, Nova Southeastern University , Ft. 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