Our purpose was to examine the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), either singly (10μg/kg) or with 17β-estradiol (E 2 , 100μg/kg), on the growth of endometriosis in a mouse endometriosis model by employing histo-morphometrical analysis as well as expression of arylhydrocarbon receptor (AhR) and estrogen receptor (ER). Epithelial height, stromal thickness, and proliferative activity of the endometriotic lesions were significantly increased by E 2 in ovariectomized mice, whereas co-administered TCDD significantly reduced these effects. TCDD alone did not affect the proliferative activity but rather reduced the epithelial height and stromal thickness. ER expression in the luminal epithelium was decreased by E 2 compared with ovariectomy alone, while TCDD significantly increased it. On the other hand, stromal ER expression was significantly increased by ovariectomy and decreased by E 2 , though TCDD did not further enhance this expression. These results indicate that a short-term exposure to TCDD failed to increase the growth of endometriotic lesion and the direct effect of TCDD probably depends on a cell-specific interaction with ovarian steroids mediated by their own receptors. These initial findings in intact tissue of mouse endometriosis may suggest critical roles of steroid hormones in the pathogenesis of endometriosis in relation to endocrine disruptors.