PSORIASIS BEYOND THE SKIN: FROM CUTANEOUS INFLAMMATION TO OSTEOARTICULAR DAMAGE

Abstract

Psoriasis is an immune-mediated inflammatory disease that extends beyond the skin, behaving as a systemic condition capable of affecting joints, entheses and periarticular structures. The IL-23/Th17 axis, through production of interleukin (IL)-17, IL-22 and tumor necrosis factor alpha (TNF-α), sustains both cutaneous inflammation and the musculoskeletal damage observed in psoriatic arthritis (PsA), which affects up to 30% of psoriasis patients during their lifetime. This article aims to narratively review the mechanisms linking cutaneous inflammation to osteoarticular involvement in psoriatic disease, addressing systemic pathophysiology, peripheral arthritis, enthesitis, dactylitis and axial involvement, bone remodeling mechanisms (simultaneous erosion and new bone formation), risk factors for articular progression, the role of the nail as an early marker, and screening tools available to dermatologists. Results indicate that enthesitis constitutes a central anatomical and immunological link between skin, nail and joint, through the synovio-entheseal complex, and that the same IL-23/IL-17/TNF-α pathway that activates keratinocytes in the skin acts on osteoclasts and osteoblasts in the joint, explaining the peculiar coexistence of bone erosion and new bone formation in PsA. Factors such as severe psoriasis, nail and scalp involvement, obesity, family history and non-specific arthralgia increase the risk of transition to PsA, and tools such as the Psoriasis Epidemiology Screening Tool (PEST) allow dermatologists to identify patients with suspected PsA early and refer them for diagnostic confirmation. Recognizing psoriasis as a systemic, rather than purely cutaneous, disease is essential for early PsA diagnosis and prevention of irreversible joint damage.