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 Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 43  |  Issue : 4  |  Page : 134-145

Light and electron microscopic study of placenta in pre-eclampsia: a trial to define underlying changes and its clinical impact


1 Department of Anatomy, Faculty of Medicine, Benha University, Benha, Egypt
2 Department of Obstetrics & Gynecology, Faculty of Medicine, Benha University, Benha, Egypt

Date of Submission14-Jul-2015
Date of Acceptance22-Jul-2015
Date of Web Publication30-Oct-2015

Correspondence Address:
Gamal E Abdel Salam
Department of Anatomy, Faculty of Medicine, Benha University, Benha, Egypt Postal code: 002013
Egypt
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DOI: 10.4103/1110-1415.168738

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  Abstract 

Objectives
The aim of this study was to evaluate histological changes of placental villi and blood vessels in pregnancy complicated by pre-eclampsia (PE) and their relation with clinical data.
Patients and methods
The study included 100 pregnant women developing PE at any time during pregnancy (PE group) and 100 pregnant women free of PE (control group). Collected data included age, gestational age, manifestations and severity of PE, neonatal birth weight (BW), and placental weight (PW). Placental tissue was obtained for light and electron microscopic examination.
Results
BW and PW showed a significant negative correlation with maternal BMI and the presence and severity of PE. Gestational age and development of PE were significant predictors for low PW, which is a significant predictor for low BW. Placentas of the PE group showed aggregation of syncytiotrophoblast cells, hyaline degeneration of connective tissue core, and endothelial lining of stem blood vessel; villous core was devoid of fetal blood vessel. Diffuse fibrous tissue formation, hypertrophic musculosa of stem blood vessel up to endarteritis obliterans and placental tissue bridges crossing intervillous spaces and villous arborization formed only of connective tissue with no cellular elements were observed. Electron microscopy confirmed these findings and showed attenuated blood vessels and excessive villous arborization covered with fibrin-like material.
Conclusion
Development of placental endarteritis obliterans with diminution of placental growth and proper invasion may underlie development of PE. Reduced PW is a reflection of this histological affection and is negatively correlated with severity of PE. Early PE is associated with more severe clinical manifestation and aggressive histological changes.

Keywords: histological placental changes, neonatal birth weight, placental weight, pre-eclampsia


How to cite this article:
Abdel Salam GE, Alam OA, Ahmed UF, Al-Sherbeny MF. Light and electron microscopic study of placenta in pre-eclampsia: a trial to define underlying changes and its clinical impact. Tanta Med J 2015;43:134-45

How to cite this URL:
Abdel Salam GE, Alam OA, Ahmed UF, Al-Sherbeny MF. Light and electron microscopic study of placenta in pre-eclampsia: a trial to define underlying changes and its clinical impact. Tanta Med J [serial online] 2015 [cited 2020 Dec 1];43:134-45. Available from: http://www.tdj.eg.net/text.asp?2015/43/4/134/168738


  Introduction Top


The placenta is a transient organ that forms during pregnancy to support the growth and development of the fetus. During human placental development, trophoblast cells differentiate through two major pathways. In the villous pathway, cytotrophoblast cells fuse to form multinucleated syncytiotrophoblast. In the extravillous pathway, cytotrophoblast cells acquire an invasive phenotype and differentiate into either interstitial extravillous trophoblasts, which invade the decidua and a portion of the myometrium, or endovascular extravillous trophoblasts, which remodel the maternal vasculature. These differentiation events are tightly controlled by the interplay of oxygen tension, transcription factors, hormones, growth factors, and other signaling molecules. More recently, microRNAs have been implicated in this regulatory process [1],[2],[3] .

The human placenta is a hemochorial placenta, which means that maternal blood is in direct contact with fetal trophoblast. The syncytiotrophoblast invades maternal venous sinuses relatively early and invades the spiral arterioles on the 17th or 18th day after conception. The lacunae, or lakes formed by maternal tissue fluid and blood, form the intervillous space; throughout the rest of pregnancy maternal blood circulates freely within the intervillous space. The placenta is divided into cotyledons, each supplied by a major branch of the umbilical artery and drained by a major tributary to the umbilical vein. These vessels enter stem villi, which branch and rebranch similar to a tree to form microscopic terminal villi suspended within the intervillous space. Each cotyledon has several anchoring villi, which extend into the decidua basalis and are anchored to it by syncytial cells and fibrin [4],[5],[6] .

Pre-eclampsia (PE) occurs in at least 5-8% of all pregnancies and is defined as new onset hypertension with proteinuria during pregnancy, and it typically occurs after 20 weeks of gestation. PE and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death, responsible for 76 000 maternal and 500 000 infant deaths each year. PE is a severe multisystem disorder, but its prevention, early diagnosis, and treatment are insufficient, as etiology and pathogenesis of the disease are still not totally understood [7],[8],[9] .

The current prospective comparative clinicoanatomical study aimed to evaluate histological changes of placental villi and their blood vessels in pregnancy complicated by PE and their relation with clinical data and pregnancy outcome.


  Patients and methods Top


Patients

The present study was conducted at the Department of Obstetrics and Gynecology, Benha University Hospital, and the Department of Anatomy, Faculty of Medicine, Benha University, from September 2012 until January 2014. After approval of the study protocol by the Local Ethical Committee and after obtaining written informed consent, all pregnant women attending the antenatal care unit were enrolled in the study to select 100 pregnant women developing PE at any time throughout their course of pregnancy as the PE group and another 100 pregnant women who completed their pregnancy free of PE manifestations as the control group. Exclusion criteria included previous history of pregnancy-related hypertension, multiple gestation, and pre-existing medical conditions such as diabetes, chronic hypertension, and renal diseases.

PE was diagnosed by the presence of gestational hypertension beginning after the 12th week of pregnancy, with an absolute systolic blood pressure of 140 mmHg or greater and/or diastolic blood pressure of 90 mmHg or greater on at least two occasions, 4 h apart, and proteinuria (one dipstick measurement ≥2+ on a voided random urine sample) [10] . Ultrasonographic examination was conducted to confirm the gestational age (GA), determine placental volume, and to exclude the presence of fetal congenital abnormalities and intrauterine growth restriction.

Antepartum data collection included the following

  1. Age : Patients were categorized as follows - group 1 included patients younger than 20 years; group 2 included patients between 20 and 29 years of age; group 3 included patients between 30 and 39 years of age; and group 4 included patients older than 39 years [11] .
  2. Gravidity and parity of enrolled pregnant women.
  3. GA : Patients were categorized as follows - group 1 included patients with GA less than 20 weeks; group 2 included patients with GA of 20-27 weeks; group 3 included patients with GA of 28-36 weeks; group 4 included patients with GA of 37-40 weeks; and group 5 included patients with GA greater than 40 weeks [12] .
  4. Blood pressure measurements and grading according to the international classification of hypertension: normotensive (degree 0), systolic arterial pressure (SAP) less than 140 mmHg and diastolic arterial pressure (DAP) less than 90 mmHg; mild hypertensive (degree 1), SAP of 140-150 mmHg or greater and DAP of 90-100 mmHg or greater; moderate hypertensive (degree 2), SAP greater than 150-160 mmHg and DAP greater than 100-109 mmHg; and severe hypertensive (degree 3), SAP greater than 160 mmHg and DAP of 110 mmHg or greater [13] .
  5. Proteinuria : The level of proteinuria was arbitrarily determined using the dipstick test and patients were categorized on the basis of the extent of protein in urine as follows - normal, free from albuminuria (score = 0); mild albuminuria (+; score = 1); moderate albuminuria (++; score = 2); and severe albuminuria (+++; scored = 3) [14].
  6. Edema evaluation clinically as present (score = 1) or absent (score = 0) [14] .
  7. Severe PE : It was defined as the presence of at-rest SAP of 160 mmHg or greater or DAP of 110 mmHg or greater on two occasions and proteinuria of 3+ or greater with the dipstick method. Other clinical manifestations such as oliguria, cerebral or visual disturbances, pulmonary edema or cyanosis, and epigastric or hypochondrial pain indicating hepatic rupture, impaired liver function of unclear pathology or intrauterine growth restriction indicate severe PE [15] .


Postpartum data collection included the following

  1. Neonatal birth weight (BW) : Low BW was defined as neonatal body weight of less than 2500 g. Newborns were categorized as normal BW if they weighed 2500 g or greater and as low BW if they weighed less than 2500 g [16] .
  2. Placental weight (PW) : After complete delivery of placenta, it was freed of the cord and membranes and was weighed. Placentas were categorized as low-weight placenta if they weighed less than 500 g and as normal-weight placenta if they weighed 500 g or greater [17] .
Placental tissue microscopic examination

  1. Fresh placentas were preserved in 10% formalin and tissue sections were obtained from different areas of the margins and center of the disk of placenta. Placental tissue specimens were processed, fixed, and stained using hematoxylin-eosin, Masson's trichrome, and Toluidine blue stains and examined using light microscopy [18] .
  2. Fresh placental tissue was preserved in glutaraldehyde combined with formaldehyde, and then were put in osmium tetraoxide and dehydrated; the dry specimens were mounted on electrically conductive double-sided adhesive tape and sputter-coated with gold or gold/palladium before examination using digital scanning electron-microscopy [19] .
Statistical analysis

Obtained data were presented as mean ± SD, ranges, numbers, and ratios. Results were analyzed using the Wilcoxon ranked test for unrelated data (Z-test), as well as the χ2 -test. Statistical analysis was conducted using SPSS (version 15, 2006; SPSS Inc., Chicago, Illinois, USA) for Windows statistical package. A P-value less than 0.05 was considered statistically significant.


  Results Top


The study included 200 pregnant women with a mean age of 27.1 ± 6.1 (range 16-46 years). Sixty-eight women were primigravida nullipara, 134 women were primipara, and 66 women were multipara. Only 48 women were overweight, whereas 152 women were obese. There was a nonsignificant (P > 0.05) difference between women who developed PE during their course of pregnancy (PE group) and women with PE-free pregnancy course (the control group) as regards age, gravidity, and parity rates. However, women in the PE group had significantly higher body weight (P = 0.041) and subsequently higher BMI (P = 0.048), despite the nonsignificantly (P > 0.05) higher frequency among BMI strata [Table 1].
Table 1 Maternal enrollment data


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The mean GA at the time of development of PE was 26.9 ± 7 (range 16-42 months). Twenty-five women developed PE at GA less than 20 weeks, 34 women developed PE at GA of 20-27 weeks, 33 women developed PE at GA of 28-36 weeks, four women developed PE at GA of 36-40 weeks, and four women developed PE at GA greater than 40 weeks. Seventy women (35%) delivered at a GA of 28-36 weeks, 103 women (51.5%) delivered at a GA of 37-40 weeks, and 27 women (13.5%) delivered at GA greater than 40 weeks. Women with PE experienced labor at significantly (P = 0.001) earlier GA compared with controls, with significantly (P < 0.001) higher frequency of pre-eclamptic women among those with earlier date of delivery [Table 2] and [Figure 1].
Figure 1: Mean gestational age (GA) at the time of delivery in both studied groups

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Table 2 Gestational age data


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All control women maintained their blood pressure measures within the normal range throughout their pregnancy course. In contrast, among PE women, 29 women were mild hypertensives with a mean SAP of 144.9 ± 3.1 and a mean DAP of 93.8 ± 2.2 mmHg. Forty-nine women were moderate hypertensives with a mean SAP of 153.7 ± 1.8 and a mean DAP of 104.8 ± 2.3 mmHg. Twenty-two women were severe hypertensives with a mean SAP of 164.8 ± 3.6 and a mean DAP of 117.8 ± 2 mmHg. The mean SAP and DAP of PE women was significantly (P < 0.001) higher compared with controls [Table 3] and [Figure 2].
Figure 2: Mean systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) of studied patients compared with controls

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Table 3 Blood pressure data of studied groups


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Fifty-seven controls had mild proteinuria, whereas the remaining 43 control women showed no proteinuria. In the PE group, 53 women had mild proteinuria, 27 women had moderate proteinuria, and 20 women had severe proteinuria. The mean proteinuria score was significantly (P < 0.001) higher in the PE group compared with the control group. Twenty-three controls and 83 PE women had edema, whereas the remaining 94 women were free of edema. The mean score for the presence of edema was significantly (P < 0.001) higher in the PE group compared with the control group. No PE woman had systemic manifestations of severity; depending on the severity of hypertension and proteinuria, 42 women had severe PE and 58 women had mild PE [Table 4].
Table 4 Patient distribution on the basis of severity of proteinuria and presence of edema with regard to pre-eclamptic severity


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Thirty-two newborns of PE women had low BW: four women had mild and 28 women had severe PE. The remaining 68 newborns of PE women had normal BW: 38 women had mild and 30 women had severe PE. Neonatal BW was significantly (P1 < 0.01) lower in PE women compared with controls. Differentially, BW of neonates of women with severe PE was significantly (P1 < 0.001) lower than that of neonates of control women and women with mild PE (P2 < 0.01). However, BW of neonates of women with mild PE was nonsignificantly (P1 > 0.05) lower than that of control women. The PE group revealed significantly (P1 < 0.01) lower PW compared with the control group. Women with severe PE showed significantly lower PW compared with both controls (P1 < 0.001) and those with mild PE (P2 < 0.01). Women with mild PE showed significantly (P1 < 0.05) lower PW compared with control women [Table 5] and [Figure 3].
Figure 3: Mean neonatal birth weight and placental weight of studied woman categorized on the basis of the presence and severity of pre-eclampsia (PE)

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Table 5 Neonatal and placental weight


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There was a significant positive correlation between neonatal BW and PW and maternal age, GA both at development of PE and delivery. However, neonatal BW showed a significant negative correlation with maternal BMI, PE diagnostic data, and severity of PE. PW showed a significant positive correlation with GA both at development of PE and delivery, whereas it showed a significant negative correlation with maternal BMI, diagnostic data, and severity of PE [Table 6].
Table 6 Spearman's correlation coefficient (r) between neonatal birth weight and placental weight and other clinical data


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Regression analysis defined GA at the time of delivery and development of PE as the persistently significant predictors for PW with positive impact for increasing PW with later development of PE, especially on approaching full term. Severity of PE, development and extent of edema, and high DAP are significant predictors in three, two, and one models, respectively, with negative impact on PW for more severe PE, presence and increased edema, and higher blood pressure especially DAP [Table 7].
Table 7 Regression analysis of clinical parameters for placental weight prediction


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Regression analysis defined PW as the persistently significant predictor for neonatal BW, followed by GA at the time of delivery, with positive impact for increasing PW with later development of PE, especially on approaching full-term on fetal weight gaining. Severity of PE and extent of edema are significant predictors in two and one models, respectively, with negative impact on neonatal BW for more severe PE and presence and increased edema [Table 8].
Table 8 Regression analysis of clinical parameters for the prediction of neonatal birth weight


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Histological examination of placental tissue

Hematoxylin and eosin-stained sections

0Normal pregnancy full-term placentas showed villi covered with syncytiotrophoblastic cells (SCs) and contained connective tissue (CT) core with normal fetal blood vessels. The intervillous spaces were filled with maternal blood [Figure 4]. Sections of mild PE full-term placentas showed villi covered with SCs and CT core enriched with fetal blood vessels [Figure 5]. Sections of severe PE full-term placentas showed aggregation of SCs, hyaline degeneration of CT core, and degeneration of endothelial lining of stem blood vessel (SBV) [Figure 6]. Other specimens of severe PE placentas showed hyaline degeneration in the wall of SBV. Villi showed side bud formation and hyaline degeneration of CT core [Figure 7]. Other specimens of full-term placenta of women with severe PE showed hyaline degeneration in the CT core of villi. Villous core was devoid of fetal blood vessel and SCs were aggregated into cell mass [Figure 8].
Figure 4: A photomicrograph of full-term placenta in normal pregnancy showing villi covered with syncytiotrophoblastic cells (SCs) and contained connective tissue core (CT) with normal fetal blood vessels (FB). The intervillous spaces (IVS) are filled with maternal blood (MB) (H and E ×250)

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Figure 5: A photomicrograph of full-term placenta in a woman with mild pre-eclampsia (PE) showing villi covered with syncytiotrophoblast (SCs) and a connective tissue core (CT) enriched with fetal blood vessels (FBV) (H and E ×250)

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Figure 6: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing aggregation of syncytiotrophoblast cells (SCs), hyaline degeneration of connective tissue core (CT), and degeneration of endothelial lining (el) of stem blood vessel (SBV) (H and E ×250)

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Figure 7: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing hyaline degeneration (HD) in the wall of stem blood vessel (SBV). Villi showing side bud (SB) formation and hyaline degeneration (HD) of connective tissue core (CT) (H and E ×250)

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Figure 8: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing hyaline degeneration (HD) in the connective tissue (CT) core of villi. Villous core is devoid of fetal blood vessel and syncytiotrophoblastic cells (SCs) aggregated into cell mass (cm) (H and E ×250)

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Masson's Trichrome stained sections of placenta

Normal pregnancy full-term placentas showed CT core of villi containing villous blood vessels and intervillous spaces rich with maternal blood [Figure 9]. Sections of severe PE full-term placentas showed diffuse fibrous tissue formation and hypertrophic musculosa of SBV up to endarteritis obliterans (EAO) [Figure 10]). Magnified pictures showed fibrous tissue formation and signs of EAO of stem artery with early stage of muscular hypertrophy and endothelial destruction [Figure 11]).
Figure 9: A photomicrograph of full-term placenta in normal pregnancy showing connective tissue core (CT) of villi containing villous blood vessels (VBV) and intervillous spaces (IVS) rich with maternal blood (MB) (Masson trichrome ×250)

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Figure 10: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing diffuse fibrous tissue formation (FT) and hypertrophic musculosa (HM) of stem blood vessel up to endarteritis obliterans (EAO) (Masson trichrome ×250)

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Figure 11: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing fibrous tissue formation (FT) and signs of endarteritis obliterans (EAO) of stem artery (arrow) with early stage of muscular hypertrophy (M) and endothelial destruction (E) (Masson trichrome ×400)

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Toluidine blue-stained sections of placenta

Normal pregnancy full-term placentas showed villi covered with syncytiotrophoblast (ST) and CT core. Intervillous spaces were filled with maternal blood [Figure 12]. Sections of severe PE full-term placentas showed ST with aggregation of nuclei in multiple nuclear masses, CT core, and intervillous spaces filled with maternal blood [Figure 13]. Other specimens showed intervillous spaces filled with maternal blood with placental bridges crossing it [Figure 14]. Higher magnification showed villous arborization formed only of CT with no cellular elements [Figure 15].
Figure 12: A photomicrograph of full-term placenta in normal pregnancy showing villi covered with syncytiotrophoblast (ST) and has a connective tissue core (CT). Intervillous spaces (IVS) filled with maternal blood (MB) (Toluidine blue ×400)

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Figure 13: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing syncytiotrophoblast (ST) with aggregation of nuclei in multiple nuclear masses (nm), connective tissue core (CT), and intervillous spaces (IVS) filled with maternal blood (MB) (Toluidine blue ×400)

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Figure 14: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing intervillous space (IVS) filled with maternal blood and placental bridges (PB) crossing the intervillous space (Toluidine blue ×100)

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Figure 15: A photomicrograph of full-term placenta in a woman with severe pre-eclampsia (PE) showing villous arborization (VA) formed only of connective tissue (CT), with no cellular elements (Toluidine blue ×400)

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Electron microscopic examination of sections of placenta

Scanning electron micrograph of full-term placenta in normal pregnancy showed normal SBV and villous arborization [Figure 16]. Higher magnification showed SBV and its branches and the villous arborization covered with red blood corpuscles [Figure 17] and [Figure 18]. Scanning electron micrograph of full-term placenta in PE patients showed attenuated blood vessels [Figure 19] and excessive villous formation [Figure 20]. Some specimens showed attenuated SBVs and excessive villous arborizations covered with fibrin-like material [Figure 21].
Figure 16: Scanning electron micrograph (EM) of full-term placenta in normal pregnancy showing normal stem blood vessel (SBV) and villous arborization (VA) (×750)

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Figure 17: Scanning electron micrograph (EM) of full-term placenta in normal pregnancy showing villous arborization (VA), stem blood vessel (SBV), and its branches (BS) (×2000)

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Figure 18: Scanning electron micrograph (EM) of full-term placenta in normal pregnancy showing villous arborization (VA) covered with red blood cells (RBCs) (×2000)

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Figure 19: Scanning electron micrograph (EM) of full-term placenta in pre-eclampsia (PE) patient showing attenuated blood vessels (arrow) (×500)

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Figure 20: Scanning electron micrograph (EM) of full-term placenta in pre-eclampsia (PE) patient showing excessive villous formation (VF) and attenuated blood vessels (arrow) (×1500)

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Figure 21: Scanning electron micrograph (EM) of full-term placenta in pre-eclampsia (PE) patient showing attenuated stem blood vessels (SBV) and excessive villous arborizations (VA) covered with fibrin-like material (×1000)

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  Discussion Top


The current study reported significantly lower PW in the PE group compared with the control group, with a significant positive correlation between PW and severity of PE and its clinical determinants. In line with these findings, Sankar et al. [20] , in gross placental morphometrical study, found that the mean PW, thickness, diameter, and surface area was significantly lower in placentas of PE patients than in that of controls. Nahar et al. [21] reported that macroscopic study of the placenta in pregnancy-induced hypertension (PIH) revealed significantly lower PW, surface area, and number of cotyledons and lower diameter of umbilical cord with more marked macroscopic infractions compared with the control group.

The study reported significantly lower neonatal BW in the PE group compared with the control group and regression analysis defined PW as a significant positive predictor for neonatal BW. These data are in agreement with those reported by Effendi et al. [22] , who found that first-trimester placental volume was significantly correlated with BW and PW and was smaller in women who delivered small-for-GA neonates, but was greater in women who delivered large-for-GA neonates.

Regression analysis of the obtained results defined severity of PE and its manifestations as significant predictors with negative impact on PW and BW. Moreover, GA at the time of development of PE was the persistently significant predictor for PW with positive impact for increasing PW with later development of PE, especially on approaching full term. These findings are in agreement with those reported by Nelson et al. [23] , who evaluated the placental pathology in women with PE occurring at varying GAs and found that placental hypoplasia was significantly associated with PE early in the third trimester; histological evidence of placental vascular lesions was significantly increased at gestations of 24-33 weeks (53%) compared with 34% at 34-36 weeks and 26% at 37 weeks.

Histological examination of placental specimens showed varied forms of placental tissue and vascular affection by PE, whereas some specimens showed aggregation of syncytiotrophoblast cells, hyaline degeneration of CT core, and degeneration of endothelial lining of SBV; villous core was devoid of fetal blood vessel. Diffuse fibrous tissue formation, hypertrophic musculosa of SBV up to EAO, and placental tissue bridges crossing the intervillous spaces and villous arborization formed only of CT with no cellular elements were evident in other specimens. Electron microscopic examination of placental specimens confirmed these findings and showed attenuated blood vessels and excessive villous arborization covered with fibrin-like material.

In line with these findings, Nahar et al. [21] reported syncytial knots in 95% and fibrinoid necrosis in 80% of PIH placentas, with more marked sclerosis, chorangiosis, and calcification. Infarction was present in 85% of PIH placentas compared with 20% in control group placentas. Sankar et al. [20] found that the histomorphometrical findings of the villous surface area and diameter were lower in PE placentas with higher density of the terminal villi than in controls due to excessive villous arborization, but the diameter and density of fetal blood vessels of PE placentas were significantly lower than those of controls. They concluded that these changes indicate a decline in all aspects of the PE placenta.

Stark et al. [24] reported multiple similar histological features in placentas of PE women, including increased syncytial knots, villous agglutination, increased intervillous fibrin, distal villous hypoplasia, acute atherosis, mural hypertrophy of membrane arterioles, muscularized basal plate arteries, increased placental site giant cells, increased immature intermediate trophoblasts, infarcts, and villitis. Moreover, Stark et al. [24] found decreased distal villous hypoplasia with increasing PW, but increased syncytial knots, increased intervillous fibrin, and increased acute atherosis with decreasing PW; early onset PE had increased syncytial knots, distal villous hypoplasia, villous agglutination, and infarcts.

Kong et al. [25] found that multifocal infarcts and villous clumps in transitional and late stages were significantly more frequent compared with the early stage. The expression of a-smooth muscle actin mRNA and protein in the basal plate of placenta were increased progressively in late, transitional, and early infarct, and it positively correlated with the number of smooth muscle cells of villous vessels and myofibroblasts of villous stroma. They concluded that these results indicated that multifocal infarct and villous clumps may affect the blood flow through the basal plate directly by blocking vessels and indirectly by making the vessels extruded by contraction of cells stained with a-smooth muscle actin.

Several recent research works tried to elucidate the relationship between placental histopathological changes and the development and severity of PE. Lockwood et al. [26] reported that deciduae from women with PE displayed significantly lower decidual natural killer cell numbers and higher chemokine levels compared with GA-matched controls. Ji et al. [3] suggested that abnormal placental development, particularly the limited invasion of trophoblast cells into the uterus with subsequent failure of the remodeling of maternal spiral arteries, is believed to cause PE and oxidative stress, including the abnormal production and/or function of signaling molecules, as well as aberrant microRNA expression may participate in the pathogenesis of PE. Choi et al. [27] documented that several miRNAs are found to be dysregulated in the placentas of PE patients and they seem to be closely associated with the early pathogenesis of PE. Stevens et al. [28] found that the total number of vessels with decidual vasculopathy correlated with higher diastolic blood pressure, higher urine protein-to-creatinine ratio, shorter GA, lower BW, 5-min Apgar score, and umbilical artery pH, as well as with increased accelerated villous maturity, infarction, and hematoma formation. There was a striking correlation of increased perinatal mortality with the number of vessels located in the decidua basalis and with vessels showing decidual vasculopathy with thrombosis. Cotechini et al. [29] , using a model of induced inflammation in pregnant rats, reported that inflammation was associated with deficient trophoblast invasion, spiral artery remodeling, altered uteroplacental hemodynamics, and placental nitrosative stress and thus resulted in fetal growth retardation. They also reported that inflammation increased maternal mean arterial pressure and was associated with renal structural alterations and proteinuria characteristic of PE.

The obtained clinical and histological results allowed concluding that development of PE could be attributed to placental vascular endangerment up to development of EAO with diminution of placental growth and proper invasion. PW, as a reflection of these histological affection, was a significant predictor of neonatal BW and is negatively correlated with severity of PE. Early development of PE is associated with more severe clinical manifestation and aggressive histological changes.

Financial support and sponsorship

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Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]


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