Pathogenic mechanisms in endometriosis-associated infertility

Fertil Steril. 2008 Aug;90(2):247-57. doi: 10.1016/j.fertnstert.2008.02.093.


Objective: To review the mechanisms by which endometriosis may affect reproductive function.

Design: Review of the English literature from 1986 to 2007 after searching Medline, EMBASE, Cochrane, and BIOSIS, as well as relevant meeting abstracts.

Setting: Fertility research center and obstetrics and gynecology department in a tertiary care hospital.

Result(s): There is compelling evidence in the literature that endometriosis has detrimental effects on ovarian and tubal function and uterine receptivity, resulting in female infertility. The mechanisms of infertility associated with endometriosis remain controversial and include abnormal folliculogenesis, elevated oxidative stress, altered immune function, and hormonal milieu in the follicular and peritoneal environments, and reduced endometrial receptivity. These factors lead to poor oocyte quality, impaired fertilization, and implantation.

Conclusion(s): Through unraveling the mechanisms by which endometriosis leads to infertility, researchers are sure to find a nonsurgical means to diagnose endometriosis, most likely through serum and peritoneal markers. Cytokines, interleukins, oxidative stress markers, and soluble cellular adhesion molecules all show potential to be used as a reliable marker for diagnosing endometriosis. After analyzing the pathogenic mechanisms of endometriosis, it seems that the future treatment of this entity may include cyclo-oxygenase-2 inhibitors, immunomodulators, or hormonal suppressive therapy to eliminate the need for surgical treatment of endometriosis.

Publication types

  • Review

MeSH terms

  • Cytokines / physiology
  • Embryo Implantation / physiology
  • Endometriosis / complications*
  • Endometriosis / immunology
  • Endometriosis / physiopathology
  • Female
  • Fertilization / physiology
  • Follicular Fluid / immunology
  • Granulosa Cells / physiology
  • Humans
  • Infertility, Female / etiology*
  • Male
  • Pregnancy
  • Spermatozoa / physiology


  • Cytokines