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Endometriosis: a review on its pathogenesis

P J van der Linden1

  • 1Deventer Ziekenhuis, Department of Obstetrics and Gynecology, P.O. Box 5001, 7400 GC Deventer, The Netherlands. gyndev@knmg.nl

Frontiers in Bioscience : a Journal and Virtual Library
|August 1, 1997
PubMed
Summary

The exact cause of peritoneal endometriosis is unknown, but theories suggest it involves endometrial cells implanting in the abdomen or the transformation of abdominal lining cells. Defense mechanisms within the body may fail, allowing the disease to develop.

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Area of Science:

  • Gynecology
  • Pathogenesis of Endometriosis

Background:

  • Peritoneal endometriosis, recognized since 1860, lacks a clear understanding of its origins.
  • Current theories include the implantation of retrograde-menstruated endometrial cells and the transformation of peritoneal mesothelium (induction theory).

Purpose of the Study:

  • To review and discuss the scientific basis of existing theories on peritoneal endometriosis pathogenesis.
  • To explore the balance between factors promoting endometriosis and the body's defense mechanisms.

Main Methods:

  • Literature review and theoretical discussion of endometriosis pathogenesis.
  • Analysis of the roles of retrograde menstruation, peritoneal mesothelium, cell adhesion molecules, and the intra-abdominal environment.

Main Results:

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  • The implantation theory posits that viable endometrial cells implant and grow after retrograde menstruation.
  • The induction theory suggests peritoneal mesothelium transforms into endometrium-like tissue.
  • Cell adhesion molecules may facilitate endometrial cell attachment to the peritoneum.
  • The intra-abdominal environment's role in processing endometrial debris and the integrity of the peritoneal lining are critical defense factors.

Conclusions:

  • Endometriosis development may stem from an imbalance between retrograde menstruation and the body's defense mechanisms.
  • Impaired peritoneal milieu function or overwhelming numbers of regurgitated endometrial cells can contribute to disease.
  • Failure of defense mechanisms, including an intact peritoneal lining, increases the risk of endometriosis development.