Abstract
Psoriatic arthritis (PsA) is an inflammatory form of arthritis that belongs to the family of spondyloarthritis (SpA) and is related to skin psoriasis. The incidence and prevalence of the disease vary considerably between countries. PsA is classified into axial PsA and peripheral PsA, with a wide range of other extra-articular manifestations. Although the aetiology of the disease is unknown, genetic, environmental, and immunologic factors appear to affect its appearance. In recent years, the role of the immune system in the pathogenesis of PsA has been increasingly investigated. Specific cytokines such as tumour necrosis factor (TNF), interleukin (IL-) 17 and IL-23, play an essential role affecting joint structures. This observation led to the emergence of tumour necrosis factor inhibitors (TNFi) that offer considerable therapeutic benefit to PsA patients. However, chronic inflammation causes bone loss, while new bone formation may also occur in both peripheral and axial skeleton. The molecular mechanisms underlying these processes have not yet been fully understood. So far, the role of the Wnt/β-catenin pathway and its inhibitors (Dickkopf and sclerostin) has been evaluated in ankylosing spondylitis (AS), but in PsA has not been studied sufficiently. The present study aims to investigate the epidemiological characteristics and clinical features (articular and extra-articular manifestations) as well as the treatment of PsA patients in the region of northwestern (NW) Greece. It also aims to evaluate the role of specific cytokines and sclerostin in patients with PsA, giving evidence to possible future biomarkers or even therapeutic targets for the disease.
Highlights
Psoriatic arthritis (PsA) is a form of spondyloarthritis (SpA) that typically presents in people with skin psoriasis
There are many different treatment options available for PsA patients: non-steroidal anti-inflammatory drugs, corticosteroids, disease-modifying drugs such as methotrexate (MTX) or leflunomide, cyclosporine, sulfasalazine, and other agents such as apremilast, Janus kinase (JAK) inhibitors, and biological agents.22Apremilast is an orally-active small molecule that inhibits phosphodiesterase-4 (PDE4) and regulates inflammatory mediators. It is efficacious in the treatment of moderate-to-severe plaque psoriasis and has a favourable safety profile and efficacy across a broad range of the clinical features of PsA.[23]
JAK inhibitors are a promising therapeutic option for PsA, and the selective JAK1/3 inhibitor tofacitinib is approved for the treatment of active PsA, where it is indicated in combination with MTX for patients who have had an inadequate response or who have been intolerant to prior therapy with a DMARD.[24]
Summary
Serological and Immunological Characteristics in Greek Patients with Psoriatic Arthritis: The Role of IL-17, IL-23, and Sclerostin.
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