The Skin-Bone Axis in Psoriasis: An Emerging Osteoimmunological Perspective

Psoriasis is a chronic inflammatory skin disease accompanied by systemic comorbidities such as metabolic syndrome and cardiovascular disease. Bone homeostasis is tightly regulated by immune cells through the receptor activator of nuclear factor-κB ligand (RANKL)-RANK-osteoprotegerin (OPG) axis and inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin (IL)-17. Although bone destruction has been extensively characterized in psoriatic arthritis (PsA), whether the skeleton is affected in psoriasis without clinically apparent arthritis remains unsettled: population-based data suggest a modest, inconsistently replicated excess of fractures, yet pooled analyses show no corresponding reduction in areal bone mineral density. This review integrates evidence from osteoimmunology, the bone marrow immune niche, microbiome research, and clinical studies to propose the skin-bone axis as a conceptual framework linking chronic cutaneous inflammation to systemic skeletal remodeling beyond joint involvement. Because the strength of the supporting evidence varies widely across these domains, we grade each component of the proposed axis explicitly as established, extrapolated, or hypothetical, identifying bone marrow niche remodeling, trained immunity, and microbiome-mediated skeletal regulation as hypothesis-generating rather than demonstrated, and we appraise the confounding introduced by lifestyle, comorbidity, and cumulative corticosteroid exposure. We conclude by defining the knowledge gaps and study designs required to determine whether bone health should be incorporated into psoriasis management.