Angiogenesis is essential for endometrial growth and repair, and disruption of this process may lead to common gynecological disorders, including menorrhagia and endometriosis. We have recently shown that expression of vascular endothelial growth factor (VEGF)-A and its two main receptors, VEGFR-1 and -2, is increased in idiopathic menorrhagia (IM). The aim of this study was to determine the expression of VEGFR-3 in normal and IM endometrium. Endometrial biopsies from 24 patients with IM and 18 healthy and fertile women were used for immunohistochemistry assessments and image analyses of VEGFR-3 and CD34-stained endothelial structures. We found that weak to moderate expression of VEGFR-3 was present in stroma and glands throughout the menstrual cycle without differences between patients and controls. Capillaries expressed VEGFR-3 markedly, whereas arterioles and venules stained moderately to markedly. However, we observed that vascular expression of VEGFR-3 in capillaries was 1.6-fold higher in the IM group than in controls, when assessed as the number of stained capillaries per mm(2). There was also a 2.0-fold higher number of arterioles, which were VEGFR-3 positive in the IM group. There was no difference with regard to the menstrual cycle between patients and controls. Thus, human endometrium expresses VEGFR-3, and expression of this receptor is increased in idiopathic menorrhagia. These results indicate that VEGFR-3 may play a role in the abnormal endometrial angiogenesis of IM.