[New insights into the pathophysiology of endometriosis]

Endometriosis is a fascinating and complex disease resulting from a dysregulation between exfoliated menstrual endometrium and the intra-abdominal environment. Increased concentrations of activated pelvic macrophages and lymphocytes and elevated levels of specific cytokines and growth factors in the peritoneal fluid support this hypothesis. The precise roles of these soluble factors are currently unknown, but we propose that a complex interplay of these locally produced cytokines, growth factors, steroids and eicosanoids modulates the growth and inflammatory behavior of ectopic endometrial implants via neovascularization. The enhanced secretion of local proangiogenic proteins by endometriosis lesions and associated immune cells (and the concomitant reduction of antiangiogenic principles) promotes the recruitment of capillaries toward the growing lesions. Ultimately, a cascade of effects on the peritoneal microenvironment results in implant proliferation and invasion. Future therapeutic strategies to target these angiogenic stimuli have the potential to block the vascular pathogenesis of endometriosis. This article gives an overview of the different factors involved in the development, growth and progression of endometriosis.