Aberrant upregulation of aromatase in eutopic endometrium and implants from women with endometriosis has been reported. Aromatase induction may be mediated by increased cyclooxygenase-2 (COX-2). Recently, we demonstrated that progesterone receptor (PR)-A and PR-B serve an anti-inflammatory role in uterus by antagonizing nuclear factor B activation and COX-2 expression. PR-C, which antagonizes PR-B, is upregulated by inflammation. While estrogen receptor (ER) is implicated in endometriosis, an anti-inflammatory role of ER has been suggested. We examined stage-specific expression of aromatase, COX-2, ER and PR isoform expression in eutopic endometrium, implants, peritoneum and endometrioma samples from endometriosis patients. Endometrial and peritoneal biopsies were obtained from unaffected women and those with fibroids. Aromatase expression in eutopic endometrium from endometriosis patients was significantly increased compared to controls. Aromatase expression in endometriosis implants was markedly increased compared to eutopic endometrium. Aromatase mRNA levels were increased significantly in 'red' implants relative to 'black' implants and endometrioma cyst capsule. Moreover, COX-2 expression was increased in implants and in eutopic endometrium of women with endometriosis, as compared to control endometrium. As observed for aromatase mRNA, highest levels of COX-2 mRNA were found in red implants. The ratio of ER/ER mRNA was significantly elevated in endometriomas compared to endometriosis implants and eutopic endometrium. Expression of PR-C mRNA relative to PR-A and PR-B mRNA was significantly increased in endometriomas compared to eutopic and control endometrium. PR-A protein was barely detectable in endometriomas. Thus, whereas, PR-C may enhance disease progression, upregulation of ER may play an anti-inflammatory and opposing role.