In the absence of implantation, glandular secretion ceases and an irregular breakdown of the decidua functionalis occurs. The resultant shedding of this layer of the endometrium is termed menses. The destruction of the corpus luteum and its production of estrogen and progesterone is the presumed cause of the shedding. With withdrawal of sex steroids, there is a profound spiral artery vascular spasm that ultimately leads to endometrial ischemia. Simultaneously, there is a breakdown of lysosomes and a release of proteolytic enzymes, which further promote local tissue destruction. This layer of endometrium is then shed, leaving the decidua basalis as the source of subsequent endometrial growth. Prostaglandins are produced throughout the menstrual cycle and are at their highest concentration during menses (60). Prostaglandin F2α (PGF2α) is a potent vasoconstrictor, causing further arteriolar vasospasm and endometrial ischemia. PGF2α produces myometrial contractions that decrease local uterine wall blood ﬂow and may serve to expel physically the sloughing endometrial tissue from the uterus.
Dating the Endometrium
The changes seen in secretory endometrium relative to the LH surge were thought to allow the assessment of the “normalcy” of endometrial development. Since 1950, it was felt that by knowing when a patient ovulated, it was possible to obtain a sample of endometrium by endometrial biopsy and determine whether the state of the endometrium corresponds to the appropriate time of the cycle. Traditional thinking held that any discrepancy of more than 2 days between chronologic and histologic date indicated a pathologic condition termed luteal phase defect; this abnormality was linked to both infertility (via implantation failure) and early pregnancy loss (63).
Evidence suggests a lack of utility for the endometrial biopsy as a diagnostic test for either infertility or early pregnancy loss (56). In a randomized, observational study of regularly cycling, fertile women, it was found that endometrial dating is far less accurate and precise than originally claimed and does not provide a valid method for the diagnosis of luteal phase defect (64). Furthermore, a large prospective, multicenter trial sponsored by the National Institutes of Health showed that histologic dating of the endometrium does not discriminate between fertile and infertile women (65). Thus, after half a century of using this test in the evaluation of the subfertile couple, it became clear that the endometrial biopsy has no role in the routine evaluation of infertility or early pregnancy loss.
The number of oocytes peaks in the fetus at 6 to 7 million by 20 weeks of gestation (66) (Fig. 7.10). Simultaneously (and peaking at the 5th month of gestation), atresia of the oogonia occurs, rapidly followed by follicular atresia. At birth, only 1 to 2 million oocytes remain in the ovaries, and at puberty, only 300,000 of the original 6 to 7 million oocytes are available for ovulation (66,67). Of these, only 400 to 500 will ultimately be released during ovulation. By the time of menopause, the ovary will be composed primarily of dense stromal tissue with only rare interspersed oocytes remaining.