For more than 70 years, various theories have been promulgated to explain the pathogenesis of endometriosis. These theories included the induction theory, the celomic metaplasia theory, the embryonic rests theory. Although some of these theories have not been completely abandoned, at present, retrograde menstruation is considered the primum movens responsible for the development of the disease, at least in its form of peritoneal implants. Therefore, there is a general consensus concerning the genesis of peritoneal lesions that would be attributed to the survival, adhesion, proliferation, invasion and vascularization of endometrial tissue regurgitated through the fallopian tubes during menstruation, an idea referred to as “implantation theory”. Conversely, the pathogenesis of ovarian endometriosis and of specific forms of deep endometriosis is still controversial. Thus, presently, one of the main source of debate is whether or not the different forms of the disease have a unique common etiology or, conversely, represent three separate entities with different pathogeneses. Aalthough epidemiological, surgical, and pathological data tend to suggest that peritoneal, ovarian, and the so-called “deep” lesions constitute different expressions of a single disease with a unique pathogenetic mechanism, i.e. retrograde menstruation, this model is not able to explain the various aspects of endometriosis fully and at present cannot be recognized as the sole ultimately valid explanatory model.