Histomorphological and morphometrical changes of placental terminal villi of normotensive and preeclamptic mothers

Abstract

Placental morphology and cellular arrangement are altered in maternal diseases such as preeclampsia (PE) in which oxygen delivery from the mother to the fetus is greatly disturbed, ultimately resulting in cellular oxidative stress. The present study was conducted at the Department of Anatomy and included 112 placentas (56 each from mothers with and without PE [controls]) collected at the Department of Obstetrics and Gynecology. A histological study was performed using hematoxylin and eosin staining. The morphology of stem and terminal villi (TV) was studied, and the surface area and diameter of TV and capillaries were measured. The gross placental morphometrical study revealed that the mean placental weight, thickness, diameter, and surface area were significantly lower in placentas with PE than in controls. The histomorphometrical findings of the villous surface area and diameter were lower in placentas with PE, whereas the TV density was higher in placentas with PE than in controls, and the differences were significant (P<0.0001). In these TV, the diameter and density of fetal blood vessels of placentas with PE were significantly lower than those of controls (P<0.05). In conclusion, the both morphological and histological changes in PE placentas are indicative of the pathogenesis of maternal and fetal morbidity and mortality in women with PE. The observed and comparative histomorphometrical changes indicate a decline in all aspects of the PE placenta, except the number of TV.

Role of ACE I/D polymorphism in pathological assessment of preeclampsia in Pakistan

“…Preceding studies also exhibited such results in which contracted vessels, PVF deposition, and obliteration of vascular lumen AP formation in stem villous was observed in PE placentas (Allaire, Ballenger, Wells, McMahon, & Lessey, 2000;Khong et al, 2016;Sankar et al, 2013). In present observations SK was more in PE patients as shown in the study conducted by Sankar et al (2013) proposing that the functional impairment of the placenta is due to structural alterations of the villous syncytiotrophoblast (Sankar et al, 2013). Thin and elongated villi were also more in PE as detected by Khong et al, 2016(Khong et al, 2016.…”

“…In present observations SK was more in PE patients as shown in the study conducted by Sankar et al () proposing that the functional impairment of the placenta is due to structural alterations of the villous syncytiotrophoblast (Sankar et al, ). Thin and elongated villi were also more in PE as detected by Khong et al, (Khong et al, ).…”

“…According to histological perspectives of placenta, abnormalities in stem villi were detected. Preceding studies also exhibited such results in which contracted vessels, PVF deposition, and obliteration of vascular lumen AP formation in stem villous was observed in PE placentas (Allaire, Ballenger, Wells, McMahon, & Lessey, ; Khong et al, ; Sankar et al, ).…”

“…The principal contributor to the pathogenesis of PE is placenta and UC, as the syndrome is resolved after delivery (Raghupathy, 2013;Surbek et al, 2001;Ukah, Magee, Payne, Hutcheon, & von Dadelszen, 2018). In hypertensive pregnancy disorder altered the architecture of the placenta and UC vessel has been observed (Barker, Thornburg, Osmond, Kajantie, & Eriksson, 2010;Ronco, Urrutia, Montenegro, & Llanos, 2009;Sankar, Bhanu, Ramalingam, Kiran, & Ramakrishna, 2013).…”

The Effects of Early-Onset Pre-Eclampsia on Placental Creatine Metabolism in the Third Trimester

“…We cannot rule out how histomorphological differences between control and PE placentae may have influenced measured AGAT and GAMT expression, as our assessments were conducted on tissue homogenates. An increase in terminal villi density, but an overall decline to villous surface area are characteristic of placental PE histology [27]. AGAT is expressed in stromal and endothelial cells of the fetal capillaries and GAMT in the syncytiotrophoblast of the fetal villi [10], so it is plausible that levels of AGAT and GAMT could be altered by changes to cell populations.…”