Endometriosis: Etiology and Pathophysiology of Infertility

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This review examines the pathogenesis of endometriosis via retrograde menstruation and pelvic contamination, highlighting the immune system's role and the unclear mechanisms linking the disease to infertility.

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Abstract

The risk for developing endometriosis begins at puberty and extends to menopause in women of all races. The major pathway in the pathogenesis of this disease is the transplantation of endometrial cells to the pelvis and other abdominal organs via retrograde menstruation. Although retrograde menstruation appears to be a near universal occurrence, those women who are at particular risk for developing the disease have menstrual characteristics that increase the amount and duration of menstrual contamination of the pelvis. The ability of the body's immune system to remove this debris may play a significant independent role. In spite of the apparent association of infertility and endometriosis, there is a paucity of evidence to identify a clear cause-and-effect relationship or to clarify the specific mechanism(s) of infertility due to this enigmatic disease. Areas that warrant additional attention include the effect of endometriosis on ovulation, the impact of the immune system on the development of endometriosis, and the effect of peritoneal inflammation on reproduction. A better understanding of these areas will lead to more efficacious and specific therapies for endometriosis-associated infertility.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Infertility, Female Pelvic Neoplasms Endometriosis Female Humans Infertility, Female Infertility, Female Menstruation Disturbances Menstruation Disturbances Pelvic Neoplasms

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

Cited by (18)

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License: CC0 · commercial use OK