Microvascular density in conditions of endometrial atrophy

Irregular menstrual bleeding in users of hormonal contraception represents the single major reason for discontinuation of these contraceptive methods. The mechanisms which underlie these bleeding disturbances are poorly understood, but appear to be associated with changes in the endometrial microvasculature following abnormal patterns of sex steroid exposure. Endometrial microvascular density is known to be increased in users of the low-dose levonorgestrel contraceptive implant, Norplant. This study explores microvascular density in other conditions of spontaneous (post-menopausal) and induced (danazol and goserelin) endometrial atrophy. Endometrial biopsies were fixed, paraffin-embedded and sections were immunostained using anti-CD34 antibody to identify vascular endothelial cells. The mean microvascular density (+/-SEM) for control samples was 186 +/- 8 vessels/mm2. There were no statistically significant changes in vascular density observed across the menstrual cycle. Mean microvascular density in spontaneous and induced endometrial atrophy did not differ significantly from that observed in the control population. The mean microvascular density was 230 +/- 17 vessels/mm2 in 31 postmenopausal women, 269 +/- 67 vessels/mm2 in 25 subjects treated with danazol was and 191 +/- 45 vessels/mm2 in nine subjects treated with goserelin. These findings suggest that the mechanisms controlling microvascular density in conditions of endometrial atrophy may vary according to the nature of the atrophic stimulus.