After ovulation, the estrogen-primed endometrium responds to rising progesterone levels in a highly predictable manner. By day 17, glycogen accumulates in the basal portion of glandular epithelium, creating subnuclear vacuoles and pseudostratification. hese changes likely result from direct progesterone action through receptors expressed in glandular cells (Mote, 2000). On day 18, vacuoles move to the apical portion of the secretory non ciliated cells. By day 19, these cells begin to secrete glycoprotein and mucopolysaccharide contents into the gland lumen (Hafez, 1975). Glandular cell mitosis ceases with secretory activity due to rising progesterone levels, which antagonize the mitotic efects of estrogen. Estradiol action also diminishes because of glandular expression of the type 2 isoform of 173-hydroxysteroid dehydrogenase. his converts estradiol to the less active estrone (Casey, 1996). On cycle days 21 to 24, the stroma becomes edematous. Next, on days 22 to 25, stromal cells surrounding the spiral arterioles begin to enlarge, and stromal mitosis becomes apparent. Days 23 to 28 are characterized by pre decidual cells, which surround spiral arterioles.
Between days 22 and 25, the secretory-phase endometrium undergoes striking changes associated with predecidual transformation of the upper two thirds of the functionalis layer. The glands exhibit extensive coiling, and luminal secretions become visible. Changes within the endometrium also can mark the so-called window of implantation seen on days 20 to 24. Epithelial surface cells show fewer microvilli and cilia, but luminal protrusions appear on the apical cell surface (Nikas, 2003). hese pinopodes help prepare for blastocyst implantation. hey also coincide with changes in the surface glycocalyx that allow acceptance of a blastocyst (Aplin, 2003).
Another highlight of the secretory phase is the continuing growth and development of the spiral arteries. hese vessels arise from the radial arteries, which are myometrial branches of the arcuate and, ultimately, uterine vessels (see Fig. 5-4).
he morphological and functional properties of the spiral arter ies are unique and essential to blood flow changes seen during menstruation or implantation. During endometrial growth, spiral arteries lengthen at a rate appreciably greater than the rate of endometrial tissue thickening. his growth discordance obliges even greater coiling. Spiral artery development relects a marked induction of angiogenesis, with widespread vessel sprouting and extension. Such rapid angiogenesis is regulated, in part, through estrogen-and progesterone-regulated synthesis ofVEGF (Ancelin, 2002; Chennazhi, 2009).
The midluteal-secretory phase of the endometrial cycle is a tiation. With corpus luteum rescue and continued progesterone secretion, the endometrium is transformed into the decidua.
With luteolysis and declining luteal progesterone production, events leading to menstruation are initiated (Critchley, 2006;
Thiruchelvam, 2013).
In the late premenstrual-phase endometrium, the stroma is invaded by neutrophils to create a pseudo inflammatory appearance. These cells iniltrate primarily on the day or two immediately preceding menses onset. he endometrial stromal and epithelial cells produce interleukin-8 (IL-8), a chemotactic-activating factor for neutrophils (Arici, 1993). Similarly, monocyte chemotactic protein-1 (MCP-1) is synthesized by endometrium and promotes monocyte recruitment (Arici, 1995).