Rising estrogen levels provide negative feedback on pituitary FSH secretion, which begins to wane by the midpoint of the follicular phase. In addition, the growing follicles produce inhibin-B, which suppresses FSH secretion by the pituitary. Conversely, LH initially decreases in response to rising estradiol levels, but late in the follicular phase the LH level is increased dramatically (biphasic response).
4.
At the end of the follicular phase (just before ovulation), FSH-induced LH receptors are present on granulosa cells and, with LH stimulation, modulate the secretion of progesterone.
5.
After a sufficient degree of estrogenic stimulation, the pituitary LH surge is triggered, which is the proximate cause of ovulation that occurs 24 to 36 hours later.
Ovulation heralds the transition to the luteal–secretory phase.
6.
The estrogen level decreases through the early luteal phase from just before ovulation until the midluteal phase, when it begins to rise again as a result of corpus luteum secretion. Similarly, inhibin-A is secreted by the corpus luteum.
7.
Progesterone levels rise precipitously after ovulation and can be used as a presumptive sign that ovulation has occurred.
8.
Progesterone, estrogen, and inhibin-A act centrally to suppress gonadotropin secretion and new follicular growth. These hormones remain elevated through the lifespan of the corpus luteum and then wane with its demise, thereby setting the stage for the next cycle.
Cyclic Changes of the Endometrium
In 1950, Noyes, Hertig, and Rock described the cyclic histologic changes in the adult human endometrium (57) (Fig. 7.10). These changes proceed in an orderly fashion in response to cyclic hormonal production by the ovaries (Fig. 7.9). Histologic cycling of the endometrium can best be viewed in two parts: the endometrial glands and the surrounding stroma. The superficial two-thirds of the endometrium is the zone that proliferates and is ultimately shed with each cycle if pregnancy does not occur. This cycling portion of the endometrium is known as the decidua functionalis and is composed of a deeply situated intermediate zone (stratum spongiosum) and a superficial compact zone (stratum compactum). The decidua basalis is the deepest region of the endometrium. It does not undergo significant monthly proliferation but, instead, is the source of endometrial regeneration after each menses (58).
The existence of endometrial stem cells was assumed but difficult to document. Researchers found a small population of human epithelial and stromal cells that possess clonogenicity, suggesting that they represent the putative endometrial stem cells (59). Further evidence of the existence of such cells, and their source, was provided by another study that showed endometrial glandular epithelial cells obtained from endometrial biopsies of women undergoing bone marrow transplants, express the HLA type of the donor bone marrow (60). This finding suggests that endometrial stem cells exist, and that they reside in bone marrow and migrate to the basalis of the endometrium. Furthermore, the timing of the appearance of these cells following the transplant was as long as several years. This fact may prove to be of clinical importance in patients with Asherman syndrome who experienced a loss of functional endometrium; repair of the uterine anatomy may eventually result in a functioning endometrial cavity.
Figure 7.10 The number of oocytes in the ovary before and after birth and through menopause.