{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T13:00:38Z","timestamp":1790341238241,"version":"4.1.0"},"reference-count":160,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:00:00Z","timestamp":1790294400000},"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>\n                    Bone and joint disorders of the aging musculoskeletal system are conventionally treated as separate clinical entities. This disease-centered view aids diagnosis but obscures the immune, inflammatory, senescent and metabolic programs they share. This Review compares five of them, grouped by etiology rather than by age: two aging-driven remodeling disorders, osteoporosis (OP) and osteoarthritis (OA); two immune-mediated arthritides in which aging modifies rather than causes the skeletal outcome, rheumatoid arthritis (RA) and psoriatic arthritis (PsA); and one focal, largely monogenic disorder included as a boundary case, Paget\u2019s disease of bone (PDB). RA and PsA are not treated as age-related diseases; they are included because they show most directly that immune activation alone can redirect skeletal remodeling. The review is narrative and mechanism-oriented, based on a structured, auditable search (Section 2); we compare evidence across diseases rather than claim exhaustive synthesis. Skeletal aging, immunosenescence, inflammaging and lipid dysregulation converge on five nodes: the receptor activator of nuclear factor-\u03baB ligand (RANKL)\u2013osteoprotegerin (OPG) axis, the interleukin-17\/tumor necrosis factor-\u03b1\/interleukin-6 network, senescence-associated secretory phenotype (SASP) amplification, phospholipid peroxidation and ferroptosis, and Wnt\u2013sclerostin\u2013Dickkopf-1 (DKK-1) balance. Across diseases these nodes generate different skeletal outputs: systemic bone loss in OP; cartilage degeneration with subchondral remodeling in OA; erosion with impaired repair in RA; erosion combined with ectopic bone formation in PsA; and focal high-turnover remodeling in PDB. Disease identity, we argue, is set by the sign and relative weighting of node activity rather than by which nodes are engaged; the opposing direction of DKK-1 regulation in RA and PsA is the clearest example. Ferroptotic injury is resolved by cell type rather than treated as uniformly harmful, and PDB is retained as a comparator showing that shared-node activation is permissive rather than deterministic. Candidate biomarkers and pathway-directed therapies are summarized with their translational gaps. Every disease \u00d7 mechanism combination is graded on a four-level evidence scheme (E1, established human evidence, to E4, indirect or\n                    <jats:italic>in vitro<\/jats:italic>\n                    only) defined in Section 2.\u00a0A cross-disease, mechanism-informed approach may improve risk stratification, identify treatable endotypes, and guide future trials in immune-metabolic skeletal disease.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1949165","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:18:28Z","timestamp":1790338708000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Immune\u2013metabolic convergence in skeletal remodeling disorders: shared osteoimmune, senescent and lipid mechanisms across aging-related and immune-mediated bone disease"],"prefix":"10.3389","volume":"17","author":[{"given":"Ting-ting","family":"Guo","sequence":"first","affiliation":[{"name":"Liaoning University of Traditional Chinese Medicine","place":["Shenyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong-Xin","family":"Zheng","sequence":"additional","affiliation":[{"name":"Liaoning University of Traditional Chinese Medicine","place":["Shenyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing-dan","family":"Jiang","sequence":"additional","affiliation":[{"name":"Liaoning University of Traditional Chinese Medicine","place":["Shenyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,25]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/s2665-9913(23)00163-7","article-title":"Global, regional, and national burden of osteoarthritis, 1990\u20132020 and projections to 2050: a systematic 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