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Spiral arteries in the placental basal plate: (A) normal spiral artery with complete vessel transformation in the decidua basalis adherent to the placenta (H&E: A1, 13; A2, 403); (B) partial vessel transformation (H&E: B1, 53; B2, 403); (C) muscularised unremodelled decidual spiral artery (H&E: C1, 53; C2, 403; Immunohistochemical reaction with a-smooth muscle actins antibody: C3, 403).
Source publication
Modification of the spiral arteries with loss of the muscular vascular wall, invaded by the trophoblasts, represents the goal of the physiological vascular adaptation during human implantation. When physiological vascular changes do not occur, an unfavourable evolution of gestation may develop as suggested by uterine biopsies studies.
To evaluate t...
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Citations
... Most of them are observed in pregnancies of 32 weeks and above (Tikkanen et al., 2011). The etiology is a chronic process that leads to decidual necrosis, placental infection, and bleeding by vascular disruption, largely due to abnormalities in the development of spiral arteries Avagliano et al., 2011). A small portion of the ablation placenta is caused by mechanical trauma and sudden uterine decompression (such as the birth of twins, premature rupture of membranes in polyhydramnios, etc.) (Melamed et al., 2012). ...
... In addition, maternal factors such as obesity, hypertension, and autoimmune diseases increase the risk of developing HDP. Furthermore, the degree of inflammation of maternal blood vessels before pregnancy may contribute to the onset of HDP [136][137][138]. In recent years, it has been reported that autophagy is involved in placental hypoxia and that autophagy failure is associated with the onset of PE [139,140]. ...
In humans, the placenta provides the only fetomaternal connection and is essential for establishing a pregnancy as well as fetal well-being. Additionally, it allows maternal physiological adaptation and embryonic immunological acceptance, support, and nutrition. The placenta is derived from extra-embryonic tissues that develop rapidly and dynamically in the first weeks of pregnancy. It is primarily composed of trophoblasts that differentiate into villi, stromal cells, macrophages, and fetal endothelial cells (FEC). Placental differentiation may be closely related to perinatal diseases, including fetal growth retardation (FGR) and hypertensive disorders of pregnancy (HDP), and miscarriage. There are limited findings regarding human chorionic villous differentiation and placental development because conducting in vivo studies is extremely difficult. Placental tissue varies widely among species. Thus, experimental animal findings are difficult to apply to humans. Early villous differentiation is difficult to study due to the small tissue size; however, a detailed analysis can potentially elucidate perinatal disease causes or help develop novel therapies. Artificial induction of early villous differentiation using human embryonic stem (ES) cells/induced pluripotent stem (iPS) cells was attempted, producing normally differentiated villi that can be used for interventional/invasive research. Here, we summarized and correlated early villous differentiation findings and discussed clinical diseases.
... The pulsatile flow with higher pressure generates ischemia-reperfusion injury and placental stress [4]. Maternal obesity and chronic vascular inflammation were also shown to be independent risk factors of poor spiral artery remodeling [40]. The syncytiotrophoblast is the first layer exposed to the injury, but the villi are entirely damaged as well. ...
Placental syndromes include pregnancy loss, fetal growth restriction, preeclampsia, preterm delivery, premature rupture of membranes, placental abruption and intrauterine fetal demise. This paper discusses the common etiopathogenesis of those syndromes and the role of angiogenic biomark-ers in their development. Pregnancy implantation, placental development and maternal adaptation are complex processes in which fetal and maternal cells interact. The syncytiotrophoblast, trophoblast, uterine natural killer cells and regulatory T cells interfere and interact in all the above-mentioned processes. The proper angioneogenesis and vasculogenesis of the placenta, as well as maternal circulatory adaptation, are dependent on angiogenic factor expression. Insufficient maternal immuno-tolerance, dysregulation in uterine natural killer or regulatory T cell function, syncytiotrophoblast and trophoblast ischemia and hypoxia or impaired balance in angiogenic factors are all related to the occurrence of placental syndromes. Differences in the time of impairment onset and its intensity and correlation with other dysfunctions result in the development of a specific syndrome. The clinical manifestations in the form of a combination of specific symptoms determine the diagnosis. However, they are just symptoms of an underlying complex trophoblast disorder.
... These changes were absent to deficient in eight cases, which is an expected finding in PIH. 8,[14][15][16] However, in remaining three cases we could not comment on these changes as the sections were not taken from the representative placental bed. It is difficult to identify the placental bed in postpartum uteri. ...
Background The uterus shows tremendous increase in size during pregnancy to nurture the fetus within it. It may show a spectrum of physiological changes or pathological lesions that may affect the pregnancy favorably or adversely. The main purpose of our study was to analyze the physiological changes in the uterus during pregnancy and the postpartum period, thereby gaining deeper knowledge.
Materials and Methods We studied a total of 152 uterine specimens obtained from obstetric hysterectomies and maternal autopsies for the presence or absence of normal physiological changes. As a control group, an equal number of surgical uterine specimens received for abnormal uterine bleeding were studied.
Results Decidual change was observed from 6 weeks of gestation to 16 days postpartum. It was partially deficient to absent in four cases of placenta accreta. Myometrial hypertrophy was seen in 150 cases (98.68%) from 8 weeks of gestation till 30 days postpartum period. Vascular remodeling was partially deficient to absent in eight cases of pregnancy-induced hypertension. Preischemia of myometrial fibers was an unexpected finding noticed from 20 weeks of gestation to 16 days postpartum in 131 cases (86.18%). Cervical wall hemorrhages were seen in 84.84% cases of vaginal delivery and in only 17.64% cases of lower segment cesarean section.
Conclusion Ours is the first study to describe the duration of the routine physiological uterine changes during pregnancy. The relationship between cervical wall hemorrhages and vaginal delivery as well as between myometrial preischemia and gestational age, both being normal physiologic findings, was found to be statistically significant.
... The dense networks of blood vessels within the placenta are responsible for exchanging gases, nutrients, and waste between mother and fetus throughout pregnancy, which is essential for proper fetal growth [1]. Abnormal development of the placental vasculature may lead to placental insufficiency, which is characterized by a poor uterine condition and results in various pregnancy complications for both the mother and fetus, including preeclampsia (PE) [2], fetal growth restriction (FGR) [3], stillbirth [4], or miscarriage [5]. ...
Background:
Preeclampsia (PE) is associated with insufficient placental perfusion attributed to maldevelopment of the placental vasculature. Reactive oxygen species (ROS) are implicated in angiogenesis, but their regulatory effects and mechanisms in placental vascular development remain unclear.
Methods:
Placental oxidative stress was determined throughout gestation by measuring 4-hydroxynonenal (4HNE) and malondialdehyde (MDA). The antioxidant MitoQ was administered to pregnant mice from GDs 7.5 to 11.5; placental morphology and angiogenesis pathways were examined on GDs 11.5 and 18.5. Moreover, we established a mouse mFlt-1-induced PE model and assessed blood pressure, urine protein levels, and placental vascular development on GDs 11.5 and 18.5. Human umbilical vein endothelial cells (HUVECs) were treated with various H2O2 concentrations to evaluate cell viability, intracellular ROS levels, and tube formation capability. MitoQ, an AKT inhibitor and an ERK1/2 inhibitor were applied to validate the ROS-mediated mechanism regulating placental angiogenesis.
Results:
First-trimester placentas presented significantly higher MDA and 4HNE levels. MitoQ significantly reduced the blood vessel density and angiogenesis pathway activity in the placenta on GDs 11.5 and 18.5. Serum sFlt-1 levels were elevated, and we observed poor placental angiogenesis and PE-like symptoms in cases with mFlt-1 overexpression. Moderate H2O2 treatment promoted HUVEC proliferation and angiogenesis, whereas these improvements were abolished by MitoQ, AKT inhibitor, or ERK1/2 inhibitor treatment.
Conclusions:
Moderate ROS levels are essential for placental angiogenesis; diminishing ROS with potent antioxidants during placentation decreases placental angiogenesis and increases PE risk. Therefore, antioxidant therapy should be considered carefully for normal pregnant women during early gestation.
... Las manifestaciones clínicas se producen a lo largo del tiempo e incluyen ligeras hemorragias intermitentes, oligohidramnios y restricción del crecimiento fetal asociada a la redistribución del flujo sanguíneo cerebral (disminución del índice de pulsatilidad de la arteria cerebral media). [7][8][9] Papel de la trombina. La trombina desempeña un papel clave en las consecuencias clínicas del desprendimiento de la placenta y puede ser importante también en su patogénesis. ...
... It occurs before placental trophoblast invasion (10)(11)(12). Defective decidualization has been associated with impaired spiral artery remodeling and preeclampsia (13)(14)(15). In preeclamptic women, low plasma levels of insulin growth factor-binding protein-1 (IGFBP1), a decidualization marker, have been reported (14). ...
Atrial natriuretic peptide (ANP) is an important hormone in cardiovascular biology. It is activated by the protease corin. In pregnancy, ANP and corin promote uterine spiral artery remodeling, but the underlying mechanism remains unknown. Here we report an ANP function in uterine decidualization and TNF-related apoptosis-induced ligand (TRAIL)-dependent death in spiral arterial smooth muscle cells (SMCs) and endothelial cells (ECs). In ANP- or corin-deficient mice, uterine decidualization markers and TRAIL expression were decreased, whereas in cultured human endometrial stromal cells (HESCs), ANP increased decidualization and TRAIL expression. In uterine spiral arteries from pregnant wild-type mice, SMC and EC loss occurred sequentially before trophoblast invasion. In culture, TRAIL from decidualized HESCs induced apoptosis in uterine SMCs, but not in ECs with low TRAIL receptor expression. Subsequently, cyclophilin B was identified from apoptotic SMCs that up-regulated endothelial TRAIL receptor and caused apoptosis in ECs. These results indicate that ANP promotes decidualization and TRAIL expression in endometrial stromal cells, contributing to sequential events in remodeling spiral arteries, including SMC death and cyclophilin B release, which in turn induces TRAIL receptor expression and apoptosis in ECs.
... The underlying reason why advanced maternal age increases the risk of placental abruption is speculative. Most abruptions appear to be related to a chronic placental disease process, wherein, abnormalities in the early development of the spiral arteries, which could be affected by maternal age, can lead to decidual necrosis, placental inflammation, and possibly infarction, ultimately resulting in vascular disruption and bleeding [23][24][25]. ...
Objective
Placental abruption is a significant obstetric complication that affects both maternal and neonatal mortality and morbidity. The present study examined the effect of maternal age on the incidence of placental abruption.
Methods
We used data of singleton pregnancies from the Japan Environment and Children’s Study, which was a prospective birth cohort study conducted between January 2011 and March 2014 across 15 regional centers in Japan. A multiple regression model was used to identify whether maternal age (<20 years, 20–24 years, 25–29 years, 30–34 years, and ≥35 years) is a risk factor for placental abruption. The analyses were conducted while considering the history of placental abruption, assisted reproductive technology, number of previous deliveries, smoking during pregnancy, body mass index before pregnancy, and chronic hypertension.
Results
A total of 94,410 Japanese women (93,994 without placental abruption and 416 with placental abruption) were recruited. Herein, 764, 8421, 25915, 33517, and 25793 women were aged <20 years, 20–24 years, 25–29 years, 30–34 years, and ≥35 years, respectively. Besides advanced maternal age (≥35 years; adjusted odds ratio: 1.7, 95% confidence interval: 1.1–2.5), teenage pregnancy was also a risk factor for placental abruption (adjusted odds ratio: 2.8, 95% confidence interval: 1.2–6.5) when the maternal age of 20–24 years was set as a reference.
Conclusions
In the Japanese general population, besides advanced maternal age, teenage pregnancy was associated with placental abruption. Recently, the mean maternal age has been changing in Japan. Therefore, it is important for obstetric care providers to provide proper counseling to young women based on up-to-date evidence.
... Findings on the physiological properties of blood flow in relation to abnormal placentation show that the inflow of maternal blood into the intervillous space (IVS) is indeed turbulent [11], and velocity is increased by a factor 10-20 compared to that of normal placentation [12]. The maternal high-velocity turbulent jets creating vortices of inflow in the intervillous space are the main contributors to the endothelial shear-stress injuries related to placental lesions and subsequent manifestation of FGR [12][13][14]. This micro-rheological change in the IVS cannot currently be identified clinically. ...
... In this perspective, the predictive performance of the biosensor should be assessed as a potential future method embracing several current challenges. Firstly, use of the biosensor addresses an aspect of placental dysfunction inaccessible for clinical examination until now-a direct marker of rheological change understood to link insufficient remodeling of the spiral arteries to arterial turbulence and FGR [11][12][13][14]. Secondly, it is not limited by expert handling as is the use of obstetric ultrasound, and thirdly, the technological advances of the biosensor integrate physiological data ready for various objective and artificial intelligent interpretation models allowing for monitoring irrespective of setting. ...
One strategy for improving detection of fetal growth restriction (FGR) is developing biosensors identifying placental dysfunction as a leading pathogenesis for FGR. The aim of this pilot study was to investigate the performance of a biosensor specified to detect placental dysfunction by means of maternal arterial turbulence acoustics in a low-resource setting. A cohort of 147 singleton pregnant women were prospectively followed with double-blinded biosensor tests, sonographic estimation of fetal weight (EFW) and Doppler flow at 26–28, 32–34 and 37–39 weeks of pregnancy. Full term live births with recorded birth weights (BWs) and without major congenital malformations were included. Outcomes were defined as (A) a solitary biometric measure (BW < 3rd centile) and as (B) a biometric measure and contributory functional measure (BW < 10th centile and antenatally detected umbilical artery pulsatility index > 95th centile). Data from 118 women and 262 antenatal examinations were included. Mean length of pregnancy was 40 weeks (SD ± 8 days), mean BW was 3008 g (SD ± 410 g). Outcome (A) was identified in seven (6%) pregnancies, whereas outcome (B) was identified in one (0.8%) pregnancy. The biosensor tested positive in five (4%) pregnancies. The predictive performance for outcome (A) was sensitivity = 0.29, specificity = 0.97, p = 0.02, positive predictive value (PPV) was 0.40 and negative predictive value (NPV) was 0.96. The predictive performance was higher for outcome (B) with sensitivity = 1.00, specificity = 0.97, p = 0.04, PPV = 0.20 and NPV = 1.00. Conclusively, these pilot-study results show future potential for biosensors as screening modality for FGR in a low-resource setting.
... On the other hand, this work revealed that 10(50%) of placental sections in obese group showed features of villous hypovascularity. These findings are in accordance with those of other workers 26,31,32 .It has been reported that there is an increase in the frequency of abnormal modifications of the spiral arteries which lead to an alteration in the placental vascular function. On the other hand, hyperplasia of the tunica muscularis was shown in the main stem vessels of the villous tree that leads to the reduction of the blood flow in cases of obese mother 33 . ...
Background: Obesity becomes one of the most universal medical problems that affects women at reproductive period. It has a complicated drawback on mother and child health. Aims: To evaluate the placental histological changes of obese mothers in comparison to pregnant women with normal body mass index. Methods: This work is a prospective case-control study in which the placentae were obtained from 40 singleton pregnant women who delivered at Al-Khansaa Maternity Teaching Hospital, Mosul, Northern of Iraq, starting from December 2019 to February 2020. The women were classified into two groups: Group 1 which includes 20 women with BMI ranged between 18-24.9 kg/m
