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It is characterized by periodontal tissue destruction, progressively driven by the host response. In this regard, cytokines associated with tissue destruction, such as interleukin (IL)\u20136 and IL-23, use a common signaling pathway mediated by STAT3. This transcription factor is also needed for IL-17A production, a key mediator in periodontitis pathogenesis. Although several studies have reported increased activation of STAT3 in experimental periodontitis, a detailed characterization of STAT3 activation in human gingival tissues and its involvement in alveolar bone loss has yet to be explored. Using a cross-sectional study design, we detected increased proportions of pSTAT3-positive cells during periodontitis compared with health, particularly in epithelial cells and T cells. Other cell types of hematopoietic and nonhematopoietic origin also display STAT3 activation in gingival tissues. We detected increased STAT3 phosphorylation and expression of STAT3-related genes during experimental periodontitis. Next, we evaluated the role of STAT3 in alveolar bone destruction using a mouse model of STAT3 loss of function (mut- Stat3 mice). Compared with controls, mut- Stat3 mice had reduced alveolar bone loss following ligature-induced periodontitis. We also evaluated pharmacologic inhibition of STAT3 in ligature-induced periodontitis. Like mut- Stat3 mice, mice treated with STAT3 small-molecule inhibitor had reduced bone loss compared with controls. Our results demonstrate that STAT3 activation is increased in epithelial and T cells during periodontitis and indicate a pathogenic role of STAT3 in inflammatory alveolar bone loss.<\/jats:p>","DOI":"10.1177\/00220345231192381","type":"journal-article","created":{"date-parts":[[2023,9,12]],"date-time":"2023-09-12T03:38:11Z","timestamp":1694489891000},"page":"1366-1375","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":29,"title":["Increased STAT3 Activation in Periodontitis Drives Inflammatory Bone Loss"],"prefix":"10.1177","volume":"102","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9841-9405","authenticated-orcid":false,"given":"M.","family":"Arce","sequence":"first","affiliation":[{"name":"Department of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile"},{"name":"Laboratory of Oral Microbiology and Immunology, Faculty of Dentistry, University of Chile, Santiago, 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