Table 1_Immune–metabolic convergence in skeletal remodeling disorders: shared osteoimmune, senescent and lipid mechanisms across aging-related and immune-mediated bone disease.docx

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’s 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-κB ligand (RANKL)–osteoprotegerin (OPG) axis, the interleukin-17/tumor necrosis factor-α/interleukin-6 network, senescence-associated secretory phenotype (SASP) amplification, phospholipid peroxidation and ferroptosis, and Wnt–sclerostin–Dickkopf-1 (DKK-1) balance.