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Objective: To test the hypothesis that the expression of the different isoforms of the estrogen receptor alpha (ER-α) and beta (ER-β) and the progesterone receptor A (PR-A) and B (PR-B) would be differentially modulated in uteri with adenomyosis compared with controls and that modulation would be related to the menstrual cycle., Design: Case control, blinded comparison., Setting: University department., Patient(s): 54 premenopausal women with and 35 without uterine adenomyosis as the sole pathology., Intervention(s): Multiple samples studied using immunohistochemistry for estrogen and progesterone receptors., Main Outcome Measure(s): Histomorphometric analysis of receptor expression., Result(s): The ER-α expression in the adenomyotic endometrium was different from that of the normal endometrium and the foci in the midsecretory phase of the cycle, but expression of ER-α in the inner and outer myometrium was not statistically significantly different. The ER-β expression was statistically significantly elevated in the adenomyotic functionalis gland during the proliferative phase and throughout the myometrium across the entire menstrual cycle. Expression of PR-A was similar to that of PR-B, with reduced expression in the basalis stroma, and inner and outer myometrium in the adenomyotic samples. The pattern of ER-β, PR-A, and PR-B expression was similar in the endometrial basalis and adenomyotic foci., Conclusion(s): These data suggest ER-β expression and the lack of PR expression are related to the development and/or progression of adenomyosis and might explain the poor response of adenomyosis-associated menstrual symptoms to progestational agents., (Copyright © 2011 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.)

The mRNAs encoding several Wnt ligands, Frizzled receptors, and Wnt antagonists were detected in human endometrium, including SFRP1; the levels of SFRP1 mRNA were higher in the proliferative phase of the menstrual cycle and increased in endometriotic tissue compared with control eutopic endometrium, and they were detected in both glandular and stromal cells but were more abundant in the stroma. Our results suggest that Wnt signaling could function in normal endometrial physiology and the the Wnt signalling inhibitor SFRP1 might play a role in endometrial growth and endometriosis development.