Endometriosis is defined as the presence of ectopic endometrial-like tissue outside the uterus cavity. This disease, afflicting women during their reproductive age, is mainly associated with pelvic pain and infertility. Sampson's theory which supports the ability of endometrial fragments from retrograde menstruations to slough through fallopian tubes and reach peritoneal environment has been recognized as the most plausible explanation for endometriosis during many years. However, further studies provided evidence that fundamental abnormal changes may occur within the eutopic endometrium of women with endometriosis compared to that of women without endometriosis. These dysfunctions included genetic predisposition, genes aberrantly expressed such as matrix metalloproteinases, Hox genes, integrins, anti-apoptotic genes Bcl-2, but also steroid hormones, immuno-inflammatory factors and angiogenesis. This review aims at summarizing and emphasizing a non exhaustive panel of biochemical and molecular factors abnormally expressed in the eutopic endometrium and related to the pathogenesis of endometriosis.
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