Editorial Comments

I read with interest the papers written by Peyghambari et al (2008) and Niknafs et al (2008) on the complex issue of luteal phase support on endometrial function in mice. I would like to comment on the data generated from their studies. Luteal supplementation with either hCG or progestrone significantly improves fertilityoutcomes compared with no treatment (Pritts and Atwood, 2002) (1). Also, Walter et al (2005) reported that estrogen promotes endometrialproliferation, while progesterone is necessary for stimulating endometrial proliferation (2). Peyghambari and associates (2008) found thatuterine epithelial proliferation was optimized on 2nd day after estrogen injection. This may suggest that endometrial proliferation in response toestrogen is a common phenomenon in the uterus of ovarectomized mice. They also found that treatment of progesterone priming with estrogenmaintained the stromal proliferation, but was unsuccessful in stimulation of epithelial cells proliferation. The formation of uterine glands wasfound to be more prominent in progesterone treated mice than with estrogen+progesterone treated group. Niknafs et al (2008), on the other hand,reported that injection of progesterone alone at luteal phase did not supply an appropriate endometrial morphology for implantation. It wasshown that application of estrogen + progesterone provided an ideal endometrial state for embryo implantation. They believed that hyperstimulationof ovary may induce the morphological alterations which may decrease the endometrial receptivity during implantation. It is important to note that intheir study, Niknafs et al (2008) used superovulated mice using gonadotropins, while Payghambari et al (2008) used ovarectomized micefor their study.