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A substantial proportion of patients with septic arthritis experience poor joint outcomes, often necessitating joint replacement surgery. Here, we show that monocyte depletion confers full protection against bone erosion in a septic arthritis mouse model. In the infected synovium, Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes exhibited increased expression of osteoclastogenesis-related molecules, including CCR2, c-Fms, and RANK.\n                    <jats:italic>S<\/jats:italic>\n                    .\n                    <jats:italic>aureus<\/jats:italic>\n                    lipoproteins induced elevated levels of RANKL, MCSF, and CCL2 in joints, with synovial fibroblasts identified as the major RANKL producer. Anti-RANKL treatment prevented bone destruction in both local and hematogenous septic arthritis murine models. Importantly, combining anti-RANKL treatment with antibiotics provided robust protection against joint damage. Our results indicate that the infiltration and transformation of monocytes into bone-destructive, osteoclast-like cells are key mechanisms in septic arthritis. Combining anti-RANKL and antibiotic therapy represents a promising therapy against this devastating disease.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.184954","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T12:00:37Z","timestamp":1741694437000},"source":"Crossref","is-referenced-by-count":3,"title":["Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis"],"prefix":"10.1172","volume":"10","author":[{"given":"Zhicheng","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."},{"name":"Center for Clinical Laboratories, the Affiliated Hospital of Guizhou Medical University, Guiyang, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Meghshree","family":"Deshmukh","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anders","family":"Jarneborn","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."},{"name":"Department of Rheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miriam","family":"Bollmann","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."},{"name":"SciLifeLab and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carmen","family":"Corciulo","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Institute of Neuroscience and Physiology, University of Gothenburg, Sweden."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pradeep Kumar","family":"Kopparapu","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abukar","family":"Ali","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mattias N. 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