The clinical picture of psoriatic arthritis (PsA) is heterogeneous, potentially involving numerous organs and tissues, such as skin and joint. From a clinical point of view, discrete tissue PsA features develop and respond to treatments apparently independently. The pathogenic events occurring in the various tissues are only partially understood. Although the vast majority of known genetic predisposing factors are shared between patients with skin psoriasis (PSO) and those affected by PsA, some tissue-specific variants have been identified. Furthermore, current data suggest that the TNF pathway and IL-23/Th17 pathways may be differentially activated in distinct tissue sites. In this review, we briefly describe current knowledge on the pathogenesis of PsA in terms of genetic predisposition, environmental factors and immunology, advancing our hypothesis to explain why a common immunologic process can express itself with significant differences in various tissues.
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