Psoriatic Disease 10 Years Later

The concept of psoriatic disease was developed and introduced 10 years ago1. It originated from a better understanding of molecular mechanisms at the basis of the pathogenesis of psoriasis and the associated musculoskeletal manifestations. In subjects susceptible through a genetic predisposition, in the presence of active environmental factors, an altered immune response induces the inflammation of both skin and musculoskeletal structures, including joints, entheses, synovial sheaths of tendons, as in dactylitis, and the axial skeleton. Tumor necrosis factor-α (TNF-α) appeared to be the prevalent molecular driver of this inflammation through the activation of epidermal keratinocytes, antigen-presenting dendritic cells, T lymphocytes, endothelial cells, and enthesosynoviocytes. Similar to that of skin and musculoskeletal structures, the microscopic involvement of the bowel described in psoriatic arthritis (PsA) was then included in the concept of psoriatic disease under the same biological propulsion sustained by TNF2. This cytokine, by stimulating the production of growth factors, adhesion molecules, and chemotactic polypeptides, contributes to the recruitment of the cellular network, which colonizes the bowel along with the skin, the joints, and the entheses1. Later, in patients with psoriasis, several studies showed an increased prevalence of metabolic syndrome with a consequential increased risk of myocardial infarction and cardiovascular mortality3. Thus, over time with the development of new lines of research, psoriatic disease increasingly appeared a systemic condition confined not only to the skin and the musculoskeletal system, but involving several different anatomical areas4,5. Along with bowel, the eye, the metabolic profile, and bone metabolism are now fields of growing attention. Regarding genetic aspects, the dominant psoriatic disease susceptibility sequences have been identified in several regions located within the MHC6. In particular, HLA-Cw0602 has been shown to be associated with cutaneous manifestations and the HLA-B*27 allele … Address correspondence to Dr. R. Scarpa, Rheumatology Unit, Department of Clinical Medicine and Surgery, University Federico II, Via S. Pansini 5, 80131 Naples, Italy. E-mail: rscarpa{at}unina.it

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