Pathogenesis of Bowel Endometriosis

Deep pelvic endometriosis is a specific entity defined by endometriotic lesions extending more than 5 mm under the peritoneum, including the infiltrative forms involving vital structures, such as the bowel, ureters, bladder, and rectovaginal lesions. Intestinal endometriosis is the most common extra-pelvic site and involves more frequently the rectovaginal septum, the recto-sigmoid followed by the rectum, ileum, appendix, and cecum. Several theories have been proposed for the pathogenesis of deep pelvic endometriosis: the retrograde menstruation theory, the theory of coelomic remnants metaplasia and the stem cells theory. In addition, genetic factors seem to play a role on individual’s susceptibility to endometriosis. In the last years, advances in knowledge regarding the histological definition of endometriosis occurred, introducing the profibrotic nature of the disease inside its “new” definition. In general, the natural history of endometriosis toward fibrosis resembles that characteristic of other fibrotic disease, involving myofibroblast and smooth muscle cell action, as well as the production of high levels of Transforming Growth Factor (TGF)-β, epithelial-to-mesenchymal transition, fibroblast-to-myofibroblast transdifferentiation and finally collagen deposition. In line with these concepts, histologic analyses show that in deep lesions, endometrial-like tissue represents a minor component.