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24 results

Page 1 of 2

  • 8 - Trophoblast invasion and uterine artery remodelling in primates

  • Edited by Graham J. Burton, David J. P. Barker, Ashley Moffett, Kent Thornburg
  • Book:
    The Placenta and Human Developmental Programming
    Published online:
    04 February 2011
    Print publication:
    16 December 2010, pp 92-101

  • Summary

    This chapter tries to identify some trends of placental evolution in primates by comparing placental organization between those with haemochorial placentas, with special attention to the great apes. Due to the possible relevance to placental pathologies and pregnancy complications, it particularly focuses on trophoblast invasion and uterine spiral artery remodelling. In Old World monkeys, a cytotrophoblastic shell is formed but remains intact throughout pregnancy, showing a clear demarcation from the underlying decidua where there is little interstitial invasion by extravillous trophoblast. Endovascular invasion starts much earlier in rhesus monkeys than in the human. Decidualization in the human is more extensive than in rhesus monkeys and baboons, and has been related to the deeper trophoblast invasion in our own species. A few cases of pre-eclampsia have been described in chimpanzees and gorillas, but no information is available about a possibly impaired invasion depth or defects in spiral artery remodelling.

Placental Bed Disorders
  • Basic Science and its Translation to Obstetrics
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Published online:
    06 July 2010
    Print publication:
    03 June 2010
  • 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.

  • Chapter 4 - What is defective:

  • from Section 2: - Placental bed vascular disorders
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 22-28

  • Summary

    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 11 - Deep trophoblast invasion and spiral artery remodeling

  • from Section 4: - Deep placentation
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 97-108

  • Summary

    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.

  • Section 6: - Genetics

  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 165-194

  • Summary

    This chapter presents a partial history of ideas about the maternal-fetal boundary of the gravid human uterus. It discusses the modern theoretical understanding of parent-offspring relations and how this predicts a complex interplay of cooperation and conflict. The chapter also considers how this interplay is expressed in relations between the endometrium and early human embryos. Prior to the late 1890s, the human embryo was not generally perceived as invading maternal tissues. Decidual reactions occur only in mammals with invasive placentation. Genetic variants that enhance fetal fitness and maternal residual fitness will be favored by natural selection regardless of whether they are expressed in the mother or the fetus. The evolutionary relations between a mother and a fetus are fundamentally similar to the relations between the same two genetic individuals after the birth of the fetus.

  • Section 8: - Translation to obstetrics

  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 243-289

  • Summary

    This chapter addresses the clinical evidence that complications in the second half of gestation are manifestations of dysfunctional formation of the placenta in early pregnancy. The major ultrasonic measure of fetal growth in early pregnancy is the crown-rump length (CRL), which is conceptually self-explanatory and technically described. A number of studies have addressed ultrasonic assessment of the placenta in the first trimester and the two main approaches have been three-dimensional ultrasound to estimate placental volume and Doppler flow velocimetry to assess resistance in the uterine circulation. First trimester maternal serum levels of pregnancy-associated plasma protein A (PAPP-A) have been widely studied in the assessment of Down's syndrome risk. A number of studies have directly compared the screening performance of combining ultrasonic and biochemical measurements. Understanding the nature of the common determinants of pregnancy complications and cardiovascular disease may reveal insights into the pathophysiology and prevention of both.

  • Section 7: - Risk factors, predictors, and future management

  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 195-242

  • Summary

    This review of epidemiological aspects of preeclampsia focuses on family data, with particular emphasis on the recurrence of preeclampsia within sibships and between generations. Preeclampsia has been a major cause of stillbirth and infant mortality. The great improvement related to stillbirth is clearly the result of induced early delivery of the most severe cases of preeclampsia. Usually, recurrence of preeclampsia is studied using data from two successive pregnancies, preferably the first and second pregnancy. Preeclampsia is related to increased risk of a perinatal death, and it is well documented that fertility subsequent to a perinatal death is increased. First birth and high maternal age are well known risk factors for preeclampsia. The relation between preeclampsia and fetal growth restriction is well established. In recent years the proportion of preeclampsia with preterm delivery has increased due to early induction of pregnancy.

  • Section 2: - Placental bed vascular disorders

  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 11-28

  • Summary

    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 1 - The placental bed in a historical perspective

  • from Section 1: - Introducing the placental bed
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 1-4

  • Summary

    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.

  • Section 1: - Introducing the placental bed

  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 1-10

  • Summary

    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 13 - Animal models of deep trophoblast invasion

  • from Section 5: - Comparative anatomy and research models
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 127-139

  • Summary

    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.

  • Section 3: - Uterine vascular environment

  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 29-74

  • Summary

    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.

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