Psoriatic arthritis occurs in a subset of psoriasis patients and is therefore commonly encountered in dermatology practice. Although its exact pathogenesis is unknown, psoriatic arthritis is thought to share common mechanisms with psoriatic skin symptoms. Innate and adaptive immune responses are abnormally activated in psoriasis and may acquire the ability to attack peripheral joints and other sites following an environmental trigger (e.g. mechanical stress, trauma, infection) in genetically susceptible patients. The increased cardiovascular risk inherent in psoriasis appears further enhanced in psoriatic arthritis, likely reflecting the overall burden of systemic inflammation contributing to atherogenic processes. Basic research and clinical trials have suggested that tumour necrosis factor is important in psoriatic arthritis pathophysiology, and accumulating evidence suggests that Th17 cells and interleukin-17A may also be important. Basic research and clinical trials inform our understanding of psoriatic arthritis pathophysiology and, in turn, help dermatologists to make better treatment decisions.