Chatzopoulos K, Kourtis A, Tantsis A, Agorastos T

4th Department of Obstetrics and Gynecology, Aristotelian University of Thessaliniki, Medical School, Hippokrateio hospital, Thessaloniki, Greece
 

Correspondence: Agorastos Theodoros, Hippokrateio hospital, 49 Konstantinoupoleos St, GR-54642 Thessaloniki, Greece. Ε-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.

 


 

Abstract

The etiopathogenesis of endometriosis is complex. During menstruation, endometrial cells reflux backwards to the peritoneal cavity. In cases of endometriosis these cells have reduced apoptotic response due to activation of oncogenes and deregulation of normal apoptotic mechanisms. By entering the peritoneal cavity, they contact an environment rich in estrogens and growth factors that favors their survival. The activation of metalloproteinases 2 and 9 and the failure of the primary immunological reaction allow the attachment of the cells to the peritoneal surface where the action of VEGF results in angiogenesis. Complex immunological defects result in failure of eradication of the ectopic cells, whereas activation of positive feedback circuits of inflammatory mediators and induction of mechanisms enhance the survival potential of the ectopic cells. This is mainly due to the prostaglandin E2-induced estrogen expression, the overexpression of aromatase and the resistance in the action of progesterone. Finally, the genetic basis of the hormonal overexpression lies in the insufficient methyliosis of the promoters of critical, normally inactive, genes.
 

Key words: endometriosis; etiopathogenesis; molecular mechanisms