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Pathophysiology of placental-derived fetal growth restriction.
Am J Obstet Gynecol. 2018 02; 218(2S):S745-S761.AJ

Abstract

Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited.

Authors+Show Affiliations

Center for Trophoblast Research, Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge, United Kingdom. Electronic address: gjb2@cam.ac.uk.EGA Institute for Women's Health, Faculty of Population Health Sciences, University College London, London, United Kingdom.

Pub Type(s)

Journal Article
Review
Video-Audio Media

Language

eng

PubMed ID

29422210

Citation

Burton, Graham J., and Eric Jauniaux. "Pathophysiology of Placental-derived Fetal Growth Restriction." American Journal of Obstetrics and Gynecology, vol. 218, no. 2S, 2018, pp. S745-S761.
Burton GJ, Jauniaux E. Pathophysiology of placental-derived fetal growth restriction. Am J Obstet Gynecol. 2018;218(2S):S745-S761.
Burton, G. J., & Jauniaux, E. (2018). Pathophysiology of placental-derived fetal growth restriction. American Journal of Obstetrics and Gynecology, 218(2S), S745-S761. https://doi.org/10.1016/j.ajog.2017.11.577
Burton GJ, Jauniaux E. Pathophysiology of Placental-derived Fetal Growth Restriction. Am J Obstet Gynecol. 2018;218(2S):S745-S761. PubMed PMID: 29422210.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathophysiology of placental-derived fetal growth restriction. AU - Burton,Graham J, AU - Jauniaux,Eric, PY - 2017/09/18/received PY - 2017/11/13/revised PY - 2017/11/13/accepted PY - 2018/2/10/entrez PY - 2018/2/10/pubmed PY - 2019/5/21/medline KW - AKT/mTOR KW - apoptosis KW - atherosis KW - chorion laeve KW - electron transport chain KW - extravillous trophoblast KW - failure of physiologic transformation KW - fetal growth restriction KW - fetoplacental weight ratio KW - hemochorial placentation KW - interstitial trophoblast KW - intervillous space KW - intraplacental oxygen concentration KW - mitochondria KW - oxidative stress KW - perivillous fibrin deposition KW - placenta KW - placental infarct KW - placental inflammation KW - placental location KW - reactive oxygen species KW - spiral arteries KW - ultrasound imaging KW - unfolded protein response KW - villi regression KW - villous hypoplasia SP - S745 EP - S761 JF - American journal of obstetrics and gynecology JO - Am. J. Obstet. Gynecol. VL - 218 IS - 2S N2 - Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited. SN - 1097-6868 UR - https://www.unboundmedicine.com/medline/citation/29422210/Pathophysiology_of_placental_derived_fetal_growth_restriction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0002-9378(17)32344-X DB - PRIME DP - Unbound Medicine ER -