Ultrastructural study on human placenta from intrauterine growth retardation cases

Abstract

A morphological study was performed on 27 human placentas from normal gestations (Group 1) and compared with those from eight cases of intrauterine growth restriction (IUGR) (Group 2). Semithin section light microscopy, transmission, and scanning electron microscopy were carried out on trophoblastic terminal villi, carefully identified under the stereomicroscope. In growth retardation cases, villi appear longer, thinner, and less vascularized, compared to the normal condition. Fibrinoid, an extracellular material of hematic origin, frequently fills villar stroma. The density of apical microvilli appears considerably reduced and occasional microvilli-free areas are observed in growth retardation cases. Moreover, the underlying basal membrane appears significantly thicker than that of normal syncytiotrophoblast. Recently, particular attention has been paid to apoptosis as a possible cell deletion mechanism in growth restriction. In our study, a majority of typical apoptotic features appear indifferently in both IUGR and normal pregnancy. Our data hints that growth retardation might be correlated with a complex of structural changes, suggestive of maternofetal traffic downregulation, but further studies are required to understand the underlying functional mechanisms.

Thrombophilic-Type Placental Pathologies and Skeletal Growth Delay Following Maternal Administration of Angiostatin4.5 in Mice

“…Similar to the findings with high doses of AS 4.5 used in this study, Battistelli et al [3] have described some thickening of subtrophoblastic basal laminae and extracellular fibrosis within the villous stroma in cases of FGR. They attributed the stromal fibrosis to excess fibrinoid, formed in part as a coagulation product.…”

“…In women with a history of FGR, approximately 60%-70% of cases are associated with some form of maternal thrombophilia, of which hyperhomocysteinemia, factor V Leiden, and acquired activated protein C resistance are the conditions most commonly diagnosed [2]. In addition to the high incidence of thrombophilic disorders, FGR is also characterized by excessive placental perivillous fibrinoid, often filling the villous stroma [3], and reduced villous growth [4], resulting in overall placental insufficiency. During normal placental development, this fibrin/fibrinoid turnover is a continuous and tightly regulated process [5] that mediates the formation of villous trees [6].…”

Chronic anaemia causes degenerative changes in trophoblast cells of the rat placenta

“…In addition, cytotrophoblastic cells showed abnormal orientation, reduction in size and density of microvilli. The decreased microvillus density observed in the current study has also been reported in other complications such as IUGR placentae [25] and preeclampsia. [17] In the rat, cytotrophoblasts continuously differentiate into ST during villous formation and development and are important in invasion of blood vessels remodeling in early stages of implantation.…”

A placental sub-proteome: The apical plasma membrane of the syncytiotrophoblast

“…Proteins of the exocyst complex have never been studied in the placenta, but may be important in maintenance of the microvilli and the apical plasma membrane of the STB. It has been reported that the STB of placentas from pregnancies complicated by intrauterine growth restriction (IUGR) have less elaborate microvilli that in normal placentas [31]. It is interesting to speculate that that expression of exocyst complex proteins may be modulated in IUGR.…”