Endometriosis: a review on its pathogenesis.

Although peritoneal endometriosis was recognized in 1860, its pathogenesis still remains unclear. Several theories attempt to explain the pathogenesis of this condition. From these, the implantation theory maintains that peritoneal endometriosis is the result of implantation and subsequent growth of retrogradely shed viable endometrial cells. Based on a second theory, the peritoneal mesothelium transforms to an endometrium-like tissue under the influence of products of regurgitated endometrium (induction). Cell adhesion molecules could be functionally involved in the binding of the endometrial cells to the peritoneal lining. In peritoneal endometriosis, a delicate equilibrium seems to exist between attacking forces (retrograde menstruation) and the defense mechanisms. On one hand, the amount and the nature of the regurgitated menstrual debris seems important to the development of the disease. On the other hand, the active intra-abdominal milieu may be involved. This milieu probably converts the regurgitated endometrial tissue into single cells via loss of functional cell adhesion properties. Endometriosis may result form the impairment of the function of the peritoneal milieu in disposing of the regurgitated cells. Alternatively, the endometriosis may occur if the number of regurgitated cells is too large. An intact peritoneal lining may be an important additional line of defense in preventing the binding of the endometrial cells. Endometriosis is likely to develop if such defense mechanisms fail. Here, the scientific basis of the endometriosis theories is discussed.