{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T21:09:20Z","timestamp":1793912960429,"version":"4.8.0"},"reference-count":116,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T00:00:00Z","timestamp":1784073600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Aging-related bone diseases are increasingly recognized as disorders in which uncoupled bone remodeling remains central but is substantially modified by immune-skeletal interactions. This review consolidates current evidence for osteoimmune senescence, a framework that links senescent skeletal cells, aging immune compartments, chronic SASP signaling, impaired immune clearance, and marrow-niche deterioration to reduced bone strength and repair. Osteoporosis, rheumatoid arthritis-associated erosion, osteoarthritis, periodontal bone loss, and delayed fracture healing are clinically distinct diseases, but they may share overlapping senescence-associated osteoimmune mechanisms while retaining disease-specific endotypes. Senescent osteocytes, osteoblast-lineage cells, and bone marrow stromal cells can increase RANKL\/OPG imbalance, suppress osteogenesis, and reshape immune recruitment, whereas remodeled T cells, macrophages, neutrophils, and NK-cell surveillance pathways modify osteoclastogenesis and repair resolution. We also discuss gut-derived metabolites and imaging phenotypes as clinically important but non-specific readouts of this biology. DXA, HR-pQCT, MRI, CBCT, and molecular imaging cannot identify senescent cells directly, but they can anchor molecular hypotheses to tissue-level deterioration. Therapeutic translation will depend on matching senolytics, senomorphics, immune-recalibrating approaches, microbiota-derived metabolites, and bone-targeted delivery systems to disease stage, dominant cell population, and measurable skeletal endpoints.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1892334","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T04:46:00Z","timestamp":1784090760000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["Osteoimmune senescence in aging-related bone diseases"],"prefix":"10.3389","volume":"17","author":[{"given":"Huali","family":"Li","sequence":"first","affiliation":[{"name":"Department of Radiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingli","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Women\u2019s Hospital, School of Medicine Zhejiang University","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huanle","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Radiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,15]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"292","DOI":"10.1038\/nri2062","article-title":"Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems","volume":"7","author":"Takayanagi","year":"2007","journal-title":"Nat Rev Immunol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/46303","article-title":"Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin 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