The current dogma surrounding endometrial regeneration following menses includes a critical need for estrogen primed proliferation. Whilst some evidence suggests that estrogen may not be required for the initial re-epithelialisation of the uterine surface, it is widely believed that it is essential for successful stromal renewal. This study aimed to identify proliferating cell types during endometrial repair and to examine whether estrogen is required for successful repair using a previously developed mouse model. In the model, decidualisation is artificially induced, and progesterone support withdrawn; the endometrial tissue progressively breaks down by 24 h after progesterone withdrawal and by 48 h has usually undergone complete repair. Although the mice are ovariectomised, restoration of both the stromal and epithelial components proceeds rapidly following breakdown and results in what appears to be a normal endometrium. However, potential estrogenic influences from extra-ovarian sources (particularly the diet and fat) remain. In this study complete removal of extra-ovarian estrogen was achieved by maintenance of animals on a soy-free diet and administration of aromatase inhibitor letrozole. No significant differences in uterine weight or estrogen responsive genes, lactoferrin and progesterone receptor, were observed compared to control ovariectomised but otherwise untreated mice, whilst significantly higher measurements were obtained from an estrogen-added group. Importantly no significant difference in the rate of endometrial repair was observed in the complete absence of estrogen demonstrating that estrogen is not essential for complete endometrial restoration in this model.