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While DC-STAMP gene expression is upregulated in the gingival tissue with periodontitis, its pathophysiological roles in periodontitis remain unclear. To evaluate the effects of DC-STAMP in periodontitis, anti-DC-STAMP\u2013monoclonal antibody (mAb) was tested in a mouse model of ligature-induced periodontitis ( n = 6\u20137\/group) where Pasteurella pneumotropica ( Pp)-reactive immune response activated T cells to produce receptor activator of nuclear factor kappa-B ligand (RANKL), which, in turn, promotes the periodontal bone loss via upregulation of osteoclastogenesis. DC-STAMP was expressed on the cell surface of mature multinuclear OCs, as well as immature mononuclear OCs, in primary cultures of RANKL-stimulated bone marrow cells. Anti-DC-STAMP-mAb suppressed the emergence of large, but not small, multinuclear OCs, suggesting that DC-STAMP is engaged in the late stage of cell fusion. Anti-DC-STAMP-mAb also inhibited pit formation caused by RANKL-stimulated bone marrow cells. Attachment of ligature to a second maxillary molar induced DC-STAMP messenger RNA and protein, along with elevated tartrate-resistant acid phosphatase\u2013positive (TRAP+) OCs and alveolar bone loss. As we expected, systemic administration of anti-DC-STAMP-mAb downregulated the ligature-induced alveolar bone loss. Importantly, local injection of anti-DC-STAMP-mAb also suppressed alveolar bone loss and reduced the total number of multinucleated TRAP+ cells in mice that received ligature attachment. Attachment of ligature induced significantly elevated tumor necrosis factor\u2013\u03b1, interleukin-1\u03b2, and RANKL in the gingival tissue compared with the control site without ligature ( P &lt; 0.05), which was unaffected by local injection with either anti-DC-STAMP-mAb or control-mAb. Neither in vivo anti- Pp IgG antibody nor in vitro anti- Pp T-cell response and resultant production of RANKL was affected by anti-DC-STAMP-mAb. This study illustrated the roles of DC-STAMP in promoting local OC cell fusion without affecting adaptive immune responses to oral bacteria. Therefore, it is plausible that a novel therapeutic regimen targeting DC-STAMP could suppress periodontal bone loss.<\/jats:p>","DOI":"10.1177\/0022034517690490","type":"journal-article","created":{"date-parts":[[2017,2,15]],"date-time":"2017-02-15T14:34:24Z","timestamp":1487169264000},"page":"685-693","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":32,"title":["DC-STAMP Is an Osteoclast Fusogen Engaged in Periodontal Bone Resorption"],"prefix":"10.1177","volume":"96","author":[{"given":"W.","family":"Wisitrasameewong","sequence":"first","affiliation":[{"name":"Department of Periodontology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand"},{"name":"Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA"},{"name":"Harvard School of Dental Medicine, Boston, MA, 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