Polycystic ovary syndrome is one of the most common endocrinopathies, occurring in women in reproductive ages. Despite a long history of studies on PCOS, its etiology is still unknown and the very definition remains controversial. This paper presents the most modern concepts which explain the pathophysiology of PCOS, concentrating on a gonadotropic-ovarian and an insulin-dependent model, the roles of a inflammatory state, an endothelium injury and an oxidative stress in PCOS development, as well as postulated genetic mechanisms. The hypo-thetical model of PCOS etiopathogenesis is proposed on the base of the discussed partial concepts.