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It is now recognized that defective placentation in the human is a cause of many pregnancy complications, such as spontaneous abortion, preterm labor and delivery, pre-eclampsia, intrauterine growth restriction, fetal death and abruptio placenta. These clinical disorders can often have long-term consequences into adulthood, causing cardiovascular disease, obesity and diabetes for the newborn as well as an increased risk of premature death in the mother. This is the first book to be entirely focused on the placental bed, bringing together the results of basic and clinical research in cell biology, immunology, endocrinology, pathology, genetics and imaging to consolidate in a single, informative source for investigators and clinicians. Its core aim is to explore new approaches and improve current clinical practice. This is essential reading for clinicians in obstetric, cardiovascular and reproductive medicine.
This chapter reviews the features of defective physiological changes of the spiral arteries in the placental bed in association with preeclampsia and fetal growth restriction and the methodology of placental bed vascular studies. The incidence of acute atherosis ranges from 41% to 48% in a series examining placental bed biopsies, placental basal plates, and amniochorial membranes. The basal plate of a delivered placenta is highly insufficient for the study of spiral arteries as it does not even represent the whole thickness of the decidua. The total number of spiral artery openings in the placental bed for a normal pregnancy was estimated at 120 and for severe preeclampsia 72. Indeed, examination of large hysterectomy specimens with placenta in situ has shown that in severe cases of preeclampsia a small, central part of the placenta may contain spiral arteries with fully developed physiological changes.
This chapter provides a general overview of the two major components of pregnancy-associated spiral artery remodeling, the maternal (decidual) and the fetal (trophoblastic). During placentation the mother comes in close contact with semi-allogeneic fetal trophoblastic cells which play a key role in maternal-fetal physiological exchange. Focusing on spiral artery invasion, there is little direct evidence for the occurrence of intrinsic trophoblastic defects in early pregnancy. Impaired trophoblast invasion in spiral arteries may not only be due to an intrinsic defect in invasive properties, but may also be induced by maternal cells. For a long time trophoblast invasion was thought to be controlled by a restrictive action of the decidua. A stimulatory role of decidua for trophoblast invasion may also apply to the endovascular invasion of the spiral arteries. Decidua-associated vascular remodeling not only occurs in the decidua but also in the junctional zone myometrial compartment.