[The peritoneal environment: physiopathogenesis of endometriosis]

In this report an hypothetical model of the pathophysiology of endometriosis is reviewed based on recent literature, focusing a variety of factors within the specific environment confined by peritoneum, whose alteration has repercussion among endometriotic and immune response cells relationships. At this point vasoactive substances, cytokines (interleukines and growth factors), and menstrual cycle hormones may act as soluble mediators that are able to induce several effects over cellular proliferation, growth and differentiation; and expression of new antigenic epitopes and cell adhesion molecules. This interactions are evident through inflammatory and immune responses, wound repair, fibrosis and pelvic adhesion formation, producing an adequate peritoneal environment for the initiation, maintenance, and progression of endometriotic implants. These finally leads to endometriosis-associated symptoms as pelvic pain, dysmenorrhea, dyspareunia and infertility.