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  • Cited by 19
  • Edited by Robert Pijnenborg, University Hospital Gasthuisberg, Leuven, Ivo Brosens, Leuven Institute for Fertility and Embryology, Roberto Romero, National Institute of Child Health and Human Development, Detroit
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Book description

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.


'… a really excellent and timely volume (especially given Robert’s retirement), scholarly, comprehensive, well presented, critical, stimulating in the presentation of new ideas and with an authoritative panel of contributors.'

Professor John Aplin - Maternal and Fetal Health Research Group, University of Manchester

'The distinctly individual writing style of the contributors keeps the reader engaged and their interpretation of published literature provides a unique insight into placental bed research and exposes the controversies that still exist … I thoroughly recommend this book to every obstetrician and basic science researcher who is interested in the field of maternal-fetal and perinatal medicine.'

Source: Acta Obstetricia et Gynecologia Scandinavica

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Page 1 of 2

  • Chapter 8 - Oxygen delivery at the deciduoplacental interface
    pp 63-74
  • View abstract


    Placental vasculature, in particular the relationship between maternal and fetal blood circulations, has been a contentious issue for a long time. In his magnificent Anatomy of the human gravid uterus William Hunter included the first drawing of spiral arteries (convoluted arteries), in what must have been the very first illustration of a human placental bed. The French anatomist Mathias Duval was probably the first to recognize the invasion of trophoblast into endometrial arteries, in this case in the rat. It it became clear that deep trophoblast invasion and associated spiral artery remodeling are essential for a healthy pregnancy. The actual depth of invasion was underrated for a long time, partly because of the increasing popularity of the decidual barrier concept. Early observations of trophoblast invasion into the spiral arteries set the stage for understanding the maternal blood supply to the placenta via the spiral arteries of the placental bed.
  • Chapter 10 - Endometrial and subendometrial blood flow and pregnancy rate of in vitro fertilization treatment
    pp 85-96
  • View abstract


    The origin of placental septa and the orifices of spiral arteries have been the subject of great controversy. The anatomy of the venous drainage has also been the subject of much discussion. The intrusive cells in the lumen as described by C. Friedlander were intensively studied by J. D. Boyd and W. J. Hamilton using their large collection of uterine specimens with the placenta in situ. The delivered placenta and fetal membranes were for many years the commonest method of obtaining material for the study of spiral artery pathology, and there were large discrepancies between the findings in this material. The method of placental bed biopsy produced useful material, but nevertheless was criticized by Hamilton and Boyd. The spiral artery anatomy as well as the vascular pathology were only revealed after studying uteri with in situ placentae pregnancy that compromise both maternal and fetal health.
  • Chapter 11 - Deep trophoblast invasion and spiral artery remodeling
    pp 97-108
  • View abstract


    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.
  • Chapter 13 - Animal models of deep trophoblast invasion
    pp 127-139
  • View abstract


    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.
  • Chapter 14 - Trophoblast–arterial interactions in vitro
    pp 140-148
  • View abstract


    The process of endometrial decidualization is a key event with direct relevance to very early pregnancy as well as subsequent pregnancy outcome. This chapter reviews the signals and pathways that control the morphological and biochemical differentiation of resident endometrial fibroblasts into secretory decidual cells. It discusses the functions of these cells at the feto-maternal interface. Decidual transformation of endometrial stromal cells can be faithfully recapitulated in culture and these in vitro studies have yielded invaluable insights into the signal pathways and downstream transcription factors that govern this differentiation process. Decidualizing stromal cells play an important role in local immunomodulation in many ways. The emergence in human beings of a cyclic decidual process has several major clinical implications; the most obvious of which is menstruation and its associated disorders. Decidualizing stromal cells and other cellular components in the superficial endometrial layer take part in menstrual shedding.
  • Chapter 16 - Fertile soil or no man’s land:
    pp 165-173
  • cooperation and conflict in the placental bed
  • View abstract


    At the site where the placenta implants there is intermingling of fetal trophoblast cells with maternal tissues. Uterine natural killer (uNK) cells are defined by the high expression of the surface marker CD56 so they are designated CD56superbright. NK cells are not a feature of the myometrium so the behavior of trophoblast in the deeper part of the uterus is independent of their influence. A further potential site where maternal immune cells can interact with endovascular trophoblast is in the spiral arteries in the decidua basalis. All uNK cells express high levels of the inhibitory receptor CD94/NKG2A whose ligand is HLA-E. HLA-G is a non-classical HLA class I molecule that was identified and found to be expressed by trophoblast cells nearly 20 years ago. The overall conclusion is that the local immunity in the human implantation site is an unusual one that is reflected in the cell types present.
  • Chapter 17 - The search for susceptibility genes
    pp 174-182
  • View abstract


    This chapter discusses placental angiogenesis, including information on placental neovascular formation as well as transformation of the vessels during gestation. By 4 weeks' gestation, the cytotrophoblasts proliferate and form the primary villi. The placenta structurally provides a very intimate relationship between the maternal blood and fetal blood. Once blood vessels are formed within the tertiary villi, they begin to remodel and adapt to the changing needs of the growing embryo and fetus. Placental angiogenesis is very complex and depends on an appropriate balance between pro-angiogenic and anti-angiogenic factors. Dysregulation of placental angiogenesis often leads to pregnancy-related diseases. Three common adverse pregnancy outcomes have been associated with defective placental vascularization: spontaneous abortion, intrauterine growth restriction (IUGR), sometimes referred to as small-for-gestational age (SGA), and preeclampsia (PE). Further characterization of angiogenesis in placental development will better inform clinicians and scientists about healthy and pathological pregnancies.

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