{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T07:01:00Z","timestamp":1789542060690,"version":"build-2803163510"},"reference-count":51,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2023,10,30]],"date-time":"2023-10-30T00:00:00Z","timestamp":1698624000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Oral Microbiology"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Macrophage colony\u2010stimulating factor (M\u2010CSF) and interleukin\u201034 (IL\u201034) are ligands for the colony\u2010stimulating factor\u20101 \u00a0receptor (CSF\u20101r) expressed on the surface of monocyte\/macrophage lineage cells. The importance of coordinated signaling between M\u2010CSF\/receptor activator of the nuclear factor kappa\u2010\u0392 ligand (RANKL) in physiological and pathological bone remodeling and alveolar bone loss in response to oral bacterial colonization is well established. However, our knowledge about the IL\u201034\/RANKL signaling in periodontal bone loss remains limited. Recently published cohort studies have demonstrated that the expression patterns of IL\u201034 are dramatically elevated in gingival crevicular fluid collected from patients with periodontitis. Therefore, the present study aims to evaluate the effects of IL\u201034 on osteoclastogenesis in vitro and in experimental ligature\u2010mediated model of periodontitis using male mice. Our initial in vitro study demonstrated increased RANKL\u2010induced osteoclastogenesis of IL\u201034\u2010primed osteoclast precursors (OCPs) compared to M\u2010CSF\u2010primed OCPs. Using an experimental model of ligature\u2010mediated periodontitis, we further demonstrated elevated expression of IL\u201034 in periodontal lesions. In contrast, M\u2010CSF levels were dramatically reduced in these periodontal lesions. Furthermore, local injections of mouse recombinant IL\u201034 protein significantly elevated cathepsin K activity, increased the number of tartrate\u2010resistant acid phosphatase (TRAP)\u2010positive osteoclasts and promoted alveolar bone loss in periodontitis lesions. In contrast, anti\u2010IL\u201034 neutralizing monoclonal antibody significantly reduced the level of alveolar bone loss and the number of TRAP\u2010positive osteoclasts in periodontitis lesions. No beneficial effects of locally injected anti\u2010M\u2010CSF neutralizing antibody were observed in periodontal lesions. This study illustrates the role of IL\u201034 in promoting alveolar bone loss in periodontal lesions and proposes the potential of anti\u2010IL34 monoclonal antibody (mAb)\u2010based therapeutic regimens to suppress alveolar bone loss in periodontitis lesions.<\/jats:p>","DOI":"10.1111\/omi.12437","type":"journal-article","created":{"date-parts":[[2023,10,30]],"date-time":"2023-10-30T07:32:01Z","timestamp":1698651121000},"page":"93-102","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Effects of IL\u201034 and anti\u2010IL\u201034 neutralizing mAb on alveolar bone loss in a ligature\u2010induced model of periodontitis"],"prefix":"10.1111","volume":"39","author":[{"given":"Carolina","family":"Duarte","sequence":"first","affiliation":[{"name":"Department of Oral Sciences and Translational Research College of Dental Medicine Nova Southeastern University  Davie Florida USA"},{"name":"Hussman Institute for Autism Miller 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