The placenta's healthy growth and functioning, which keeps the mother and foetus linked for the exchange of waste, nutrients and blood gases are essential for normal embryonic development and long-term survival [Weissgerber, et al., 2006, Red-Horse et al., 2004, Baschat, et al., 2004]. Preeclampsia is a medical condition, caused by abnormal placental formation. The cause of this common prenatal sickness, which affects 9%–12% of pregnancies, is still a mystery. It is a major contributor to mother and foetal mortality as well as morbidity [Livingston, et al., 2000, Errera, et al., 2013, Huppertz, et al., 2011, Smith, et al., 2015].

Like other epithelia, the villous placenta is constantly renewed, and the syncytiotrophoblast is kept in place by fusing with the cytotrophoblasts beneath it. In conditions like preeclampsia, fewer arterioles are broken by invasive cytotrophoblasts because of anomalies in adhesive molecule changing, demonstrating that this subgroup of trophoblast cell populations failed to mature normally. In these situations, the outermost decidua is the only area where cytotrophoblast penetration occurs [Huppertz, et al., 2010, Han, et al., 2006, Zhou, et al., 1993].

Twenty pregnancies (study group) were found to have severe intrauterine growth retardation (IUGR) using a set of prenatal criteria. Reduced amniotic fluid volume and estimated foetal weight that is below the 10th percentile (defined as three centimetres or less being the highest vertical depth of amniotic fluid devoid of cords) Preeclampsia, which was defined as having blood pressure that exceeded 140/100 mmHg on a minimum of two occasions, followed by an increase in the diastolic blood pressure that exceeded 25 mmHg, occurred after 20 weeks of gestation throughout each pregnancy in the study group. A positive finding of +3 on dipstick testing or a protein excretion of 0.3 g/24 hours were further signs of proteinuria. The research group's entire membership was born by scheduled caesarean surgery.

All newborns exhibited IUGR symptoms. The control group included a singleton pregnancy that produced live births, structurally healthy neonates, and fetuses with normal growth rates (and a comparable mean gestational age) as the study group. The middle portion's full thickness was sampled, and processing was done as previously mentioned. Regular paraffin embedding procedures were followed, and samples were sliced at 5m to 7m and hematoxylin and eosin stained. Digital SEM was used for scanning electron microscopic (SEM) research. The specimen pieces were fixed in 2.5% glutaraldehyde at 4 °C for 2 hours after being post-fixed in 2% osmium tetroxide and rinsed with a cacodylate buffer solution. The samples were dried in various ethanol concentrations solutions. A portion of every specimen was laid out on a stub as well as marked using gold (3 nm) for SEM analysis. Toluidine blue semithin segments were sliced and formed, and the leftover pieces of these samples were inserted in epoxy glue.

Age and gestational age at birth was similar in preeclamptic women and controls. Nevertheless, birth, mean arterial pressure, Preeclamptic women's weight, placental weight, and other characteristics were substantially different as compared to normal patients (P <0.01). Control placentas exhibited a distinct appearance, showing trophoblastic cell types arranged in thin layers surrounding a central connective tissue core. Each villous was densely packed with foetal capillaries. Also, intervillous gaps containing maternal blood separated the villi from one another.

Preeclamptic placentas showed specific histological modifications. The nuclei of the syncytiotrophoblasts had a distinct distribution and a propensity to cluster, especially in regions where the syncytial layers protrude through the intervillous spaces. The villous tree has a pseudo-labyrinthine look because of the long, slender syncytial threads that span the intervillous intervals linking one villus to another. Sectioned syncytial strands or sprouts can be recognized as there is no villous core.

High levels of cellularity and fibrillar content can be seen in the connective tissue villous stoma, which causes the entire villous core to have a strong affinity for collagen staining. In most villi, fetal capillaries have typically vanished, yet on occasion they have still been discernible. Red blood cells have only been shown to be present inside the lumina of a tiny number of preserved capillaries.

The central core of connective tissue, which grew inside the ends of the villi, entirely took the role of the embryonic blood sinusoids. Despite the lack of any sort of capillary wall structure, certain fetal nucleated red blood cells could be perceived in a few uncommon villi. These cells appeared to dwell directly in the connective tissue stroma. Atheromatous progression and endothelial wall deterioration were present at all phases in each branch of the main umbilical arteries. In the basal decidual arterioles, endothelial deterioration, escalating fibrosis, and destruction were seen. Such terminal villous structures could be identified by their profusion of small, many buds that resemble villi and their sinusoidal-shaped projections, which were identical in shape and dimensions to the apical dilatations of the capillaries loops. Capillary loops appeared more numerous and deeper in comparison to the ones in the control group. The majority of capillary loops lack coiling, while preeclamptic cases of extended loops had considerably fewer branches. Compared to controls, there were substantially fewer terminal villi, which looked like long drainpipes. In preeclamptic cases, there were huge plaques of a fibrin-like material that commonly extended across multiple villi over the superficial surfaces of the villous tissues. The villi's outside surface exhibits noticeable folds and wrinkles, as though the trophoblast were stacked up.

Table 1

This study concluded by demonstrating that ischemia damage to placental tissue and maldeveloped terminal villi occur in preeclampsia-complicated placentas. These findings are consistent with an increase in fetoplacental vascular resistance when there was none in the umbilical artery before delivery. The disorder's poor gas and nutrient transfer is explained by these findings.