Immunohistochemical analysis of proliferative activity and steroid receptor expression in peritoneal and ovarian endometriosis

Objective: To assess the proliferative activity of eutopic and ectopic endometrium throughout the menstrual cycle and its correlation to steroid receptor content. Design: The immunohistochemical use of Ki 67 was applied to investigate the proliferation index. A recently advanced stereographic computer technology was used to investigate steroid receptors. Setting: University hospital department of gynecology. Patient(s): Biopsies of eutopic endometrium, black and red peritoneal endometriotic lesions, and ovarian endometriomas were taken from infertile patients and classified according to the phase of the cycle. Result(s): In normal endometrium, the glandular proliferation index was highest during the proliferative phase and was statistically significantly reduced during the secretory phase. No proliferative activity was observed in the late secretory phase. No statistically significant differences were found between ectopic endometrium and eutopic endometrium except during the late secretory phase, when proliferative activity was still present in endometriotic tissue. The stromal proliferation index was similar in red lesions, ovarian endometriomas, and eutopic endometrium during the secretory phase. In normal endometrium, the highest concentrations of estrogen receptors (ERs) and P receptors (PRs) occurred in the epithelial and stromal cells during the late proliferative phase of the menstrual cycle. Estrogen receptor and PR content declined throughout the secretory phase. In ectopic endometrium, PR persisted in the glandular epithelium during the late secretory phase. Estrogen receptors persisted in the glandular epithelium and stroma of red peritoneal lesions and ovarian endometriomas during the late secretory phase. Conclusion(s): The high proliferative activity and the persistence of ERs and PRs in the stroma of red lesions and ovarian endometriomas emphasize the primordial role of the stroma in the development of endometriosis and suggest different mechanisms of proliferation control from those observed in eutopic endometrium. (C) 1997 by American Society for Reproductive Medicine.