During the menstrual cycle, the endometrium undergoes a series of histologic and cytologic changes that culminate in menstruation if pregnancy does not result45,46 and 47 (see Fig. 95-2). The basal layer of the endometrium, nearest the myometrium, undergoes little change during the menstrual cycle and is not shed during menses. The basal layer regenerates an intermediate spongiosa layer and a superficial compact epithelial cell layer, both of which are sloughed at each menstruation. Under the influence of estrogen, with IGF-I likely acting as a paracrine mediator, the endometrial
glands in these two functional layers proliferate during the follicular phase, leading to thickening of the mucosa. During the luteal phase, the glands become coiled and secretory under the influence of progesterone, with IGF-II being the suspected paracrine mediator.48 The endometrium becomes much more edematous and vascular, largely because spiral arteries develop in the functional layers. With the decline of both E₂ and progesterone in the late luteal phase, endometrial and blood vessel necrosis occurs, and menstrual bleeding begins. The local secretion of prostaglandins appears to initiate vasospasm and consequent ischemic necrosis of the endometrium, as well as the uterine contractions that frequently occur with menstruation.49 Thus, prostaglandin synthetase inhibitors can relieve dysmenorrhea (i.e., menstrual cramping).50 Fibrinolytic activity in the endometrium also peaks during menstruation, thus explaining the noncoagulability of menstrual blood.51 Because of the characteristic histologic changes that occur during the menstrual cycle, endometrial biopsies can be used to date the stage of the menstrual cycle and to assess the tissue response to gonadal steroids.46,47 Transvaginal ultrasound is a less invasive modality that has a 76% accuracy in assessing endometrial stage as compared to biopsy.52