Decidual cells prevent peri-implantational endometrical bleeding
During the menstrual cycle, the concerted effects of estradiol (E2) and progesterone induce human endometrial stromal cells (HESCs) to undergo decidualization, the collection of morphological, proliferative and biochemical changes that transforms stromal cells to decidual cells. In the luteal phase, progesterone initiates E2-primed HESCs to decidualize around blood vessels. Under continued progesterone stimulation, decidualization spreads throughout the late luteal phase and gestational endometrium. Among species with a haemochorial placenta, human trophoblasts are the most intrinsically invasive and human endometrium undergoes the most extensive decidualization reaction. Implanting blastocyst-derived syncytiotrophoblasts breach endometrial blood vessels embedded in a matrix of decidual cells. This invasive process institutes the primordial uteroplacental circulation, and provides the embryo with oxygen and nutrients. That it risks bleeding is clear from the phenomenon of chemical pregnancy, in which trophoblast-derived human chorionic gonadotrophin (hCG) appears transiently in the maternal blood followed by localized decidual bleeding. After endovascular invasion by syncytiotrophoblasts, extravillous cytotrophoblasts penetrate uterine spiral arteries and initiate the morphological changes that lead to increased intervillous blood flow. The occurrence of decidual haemorrhage during this period is associated with spontaneous abortion, abruption and preterm birth. Ectopic pregnancies are most frequently complicated by haemorrhage in primate species lacking a true decidua, thus underscoring the importance of decidual cells in preventing uterine bleeding.