Endometriosis results from the dislocation of basal endometrium

TLDR

The study tests the hypothesis that adenomyotic and endometriotic lesions originate from basal endometrium using samples from normal and adenomyotic uteri, excised lesions, and menstrual blood. Immunohistochemical analysis of ER, PR, PR(B), and P450A in endometrial tissues revealed distinct cyclical expression patterns between basalis and functionalis layers. Lesions exhibited basalis‑like cyclical receptor expression, a higher prevalence of shed basalis fragments in menstrual blood, and stem‑cell–like properties, supporting that ectopic endometrial tissue arises from dislocated basal endometrium.

Abstract

The hypothesis is tested that both adenomyotic and endometriotic lesions are derived from basal endometrium.Normal uteri and uteri with adenomyosis obtained by hysterectomy, excised endometriotic lesions and menstrual blood of women with and without endometriosis were used. Estrogen receptor (ER), progesterone receptor (PR), progesterone receptor B isoform (PR(B)) and P450 aromatase (P450A) immunohistochemistry was performed with the use of specific monoclonal antibodies.With respect to the parameters studied there was a fundamental difference between the cyclical patterns of the basalis and the functionalis of the eutopic endometrium. The endometrium of endometriotic and adenomyotic lesions mimicked the cyclical pattern of the basalis. The peristromal muscular tissue of endometriotic and adenomyotic lesions displayed the same cyclical pattern of ER and PR expression as the archimyometrium. There was a significantly higher prevalence of fragments of shed basalis in menstrual blood of women with endometriosis than in healthy controls.These data suggest that ectopic endometrial lesions result from dislocation of basal endometrium. Dislocated basal endometrium has stem cell character resulting in the ectopic formation of all archimetrial components such as epithelial and stromal endometrium as well as peristromal muscular tissue.