In contrast, the spiral arterial system that supplies the decidua basalis and ultimately the placental intervillous space is altered remarkably. These spiral arterioles and arteries are invaded by trophoblasts, and during this process, the vessel walls in the basalis are destroyed. Only a shell without smooth muscle or endothelial cells remains. Importantly, as a result, these vascular conduits of maternal blood-which become the utero placental vessels-are unresponsive to vasoactive agents. Conversely, the fetal chorionic vessels, which transport blood between the placenta and the fetus, contain smooth muscle and thus do respond to vasoactive agents.
Early in pregnancy, the zona spongiosa of the decidua consists of large distended glands, often exhibiting marked hyperplasia and separated by minimal stroma. At first, the glands are lined by typical cylindrical uterine epithelium with abundant secretory activity that contributes to blastocyst nourishment. With advanced pregnancy, the glandular elements largely disappear.
he decidua basalis contributes to formation of the placental basal plate (Fig. 5-6). he spongy zone of the decidua basalis consists mainly of arteries and widely dilated veins, and by term, glands have virtually disappeared. Also, the decidua basalis is invaded by many interstitial trophoblasts and trophoblastic giant cells. Although most abundant in the decidua, the giant cells commonly penetrate the upper myometrium. Their number and invasiveness can be so extensive as to resemble choriocarcinoma.
The Nitabuch layer is a zone of fibrinoid degeneration in which invading trophoblasts meet the decidua basalis. If the decidua is defective, as in placenta accreta, the Nitabuch layer is usually absent (Chap. 41, p. 778). here is also a more supericial, but inconsistent, deposition of ibrin-Rohr stria-at the bottom of the intervillous space and surrounding the anchoring
FIGURE 5-6 Section through a junction of chorion, villi, and decidua basalis in early first-trimester pregnancy. (Used with permission from Dr. Kurt Benirschke.) villi. Decidual necrosis is a normal phenomenon in the irst and probably second trimesters (McCombs, 1964). hus, necrotic decidua obtained through curettage after spontaneous abortion in the irst trimester should not necessarily be interpreted as either a cause or an efect of the pregnancy loss.
Both decidua types contain numerous cell groups whose composition varies with gestational stage (Loke, 1995). he primary cellular components are the true decidual cells, which diferentiated from the endometrial stromal cells, and numerous maternal bone marrow-derived cells. Accumulation of lymphocytes with unique properties at the maternal-fetal interface is essential to evoke tolerance mechanisms that prevent maternal immune rejection of the fetus. These include regulatolY T cells, decidual macrophages, and decidual natural killer cells. Collectively, these cells not only provide immunotolerance but also play an important role in trophoblast invasion and vasculogenesis (PrabhuDas, 2015).
In addition to placental development, the decidua potentially provides other functions. The decidua is the source of prolactin, which is present in enormous amounts in amnionic luid (Colander, 1978; Riddick, 1979). Decidual prolactin is a product of the same gene that encodes for anterior pituitary prolactin, but the exact physiological role of decidual prolactin is unknown. Notably, decidual prolactin is not to be confused with placental lactogen (hPL), which is produced only by syncytiotrophoblast.