Placental Morphology Research Articles

Ultrasound Placental Remodeling Patterns and Pathology Characteristics in Patients with History of Mild SARS-CoV-2 Infection during Pregnancy

Introduction: This research aims to describe a progressive pattern of ultrasound placental remodeling in patients with a history of SARS-CoV-2 infection during pregnancy. Materials and Methods: This was a longitudinal, cohort study which enrolled 23 pregnant women with a history of former mild SARS-CoV-2 infection during the current pregnancy. Four obstetricians analyzed placental ultrasound images from different gestational ages following COVID infection and identified the presence and degree of remodeling. We assessed the inter-rater agreement and the interclass correlation coefficients. Pathology workup included placental biometry, macroscopic and microscopic examination. Results: Serial ultrasound evaluation of the placental morphology revealed a progressive pattern of placental remodeling starting from 30-32 weeks of gestation towards term, occurring approximately 8-10 weeks after the SARS-CoV-2 infection. Placental changes-the "starry sky" appearance and the "white line" along the basal plate-were identified in all cases. Most placentas presented normal subchorionic perivillous fibrin depositions and focal stem villi perivillous fibrin deposits. Focal calcifications were described in only 13% of the cases. Conclusions: We identified two ultrasound signs of placental remodeling as potential markers of placental viral shedding following mild SARS-CoV-2. The most likely pathology correspondence for the imaging aspect is perivillous and, respectively, massive subchorionic fibrin deposits identified in most cases.

Ovarian Stimulation in Mice Resulted in Abnormal Placentation through Its Effects on Proliferation and Cytokine Production of Uterine NK Cells.

Ovarian stimulation is associated with an increased incidence of abnormal placentation. Uterine natural killer (uNK) cells are the major subpopulation of decidual immune cells, which are crucial for placentation. In a previous study, we found that ovarian stimulation impairs uNK cell density on gestation day (GD) 8.5 in mice. However, it was not clear how ovarian stimulation led to a reduction in the density of uNK cells. In this study, we constructed two mouse models, an in vitro mouse embryo transfer model and an estrogen-stimulated mouse model. We used HE and PAS glycogen staining, immunohistochemical techniques, q-PCR, Western blot, and flow cytometry to analyze the mouse decidua and placenta, and the results showed that SO resulted in a fetal weight reduction, abnormal placental morphology, decreased placental vascular density, and abnormal density and function of uNK cells. Our results suggest that ovarian stimulation resulted in aberrant estrogen signaling and may contribute to the disorder of uNK cells caused by ovarian stimulation. Together, these results provide new insights into the mechanisms of aberrant maternal endocrine environments and abnormal placentation.

Don't sugar coat it: The independent and synergistic impacts of obesity and gestational diabetes on placental parameters.

Don't sugar coat it: The independent and synergistic impacts of obesity and gestational diabetes on placental parameters.

A high-fat diet changes placental morphology but does not change biochemical parameters, placental oxidative stress or cytokine levels

IntroductionThe placenta is an organ that forms the bridge between mother and fetus during pregnancy. Changes in the intrauterine environment directly impact the fetus’ health, with maternal nutrition determining its development. This study analyzed the effects of different diets and probiotic supplementation during pregnancy on the biochemical parameters of maternal serum and placental morphology, oxidative stress, and cytokine levels in mice. MethodsFemale mice were fed standard (CONT), restrictive (RD), or high-fat (HFD) diets before and during pregnancy. During pregnancy, the CONT and HFD groups were divided into two groups that received the Lactobacillus rhamnosus LB1.5 three times per week (CONT + PROB and HFD + PROB). The RD, CONT, or HFD groups received vehicle control. Maternal serum biochemical parameters (glucose, cholesterol, and triglycerides) were evaluated. The morphology, redox profile (thiobarbituric acid reactive substances, sulfhydryls, catalase, and superoxide dismutase enzyme activity), and inflammatory cytokines (interleukins 1α, 1β, IL-6, and tumor necrosis factor-alpha) were evaluated in the placenta. ResultsThe serum biochemical parameters presented no differences between the groups. Regarding placental morphology, the HFD group showed an increased thickness of the labyrinth zone compared to the CONT + PROB group. However, no significant difference was found in the analysis of the placental redox profile and cytokine levels. DiscussionRD and HFD, for 16 weeks before and during pregnancy, as well as probiotic supplementation during pregnancy, caused no change in serum biochemical parameters nor the gestational viability rate, placental redox state, and cytokine levels. However, HFD increased the thickness of the placental labyrinth zone.

Placental leukocyte infiltration accompanies gestational changes induced by hyperthyroidism.

The endocrine and immunological disruption induced by hyperthyroidism could alter gestation, placenta, and fetal development. This study suggests an immunological role of thyroid hormones in gestation. Thyroid dysfunctions lead to metabolic, angiogenic, and developmental alterations at the maternal-fetal interface that cause reproductive complications. Thyroid hormones (THs) act through their nuclear receptors that interact with other steroid hormone receptors. Currently, immunological regulation by thyroid status has been characterized to a far less extent. It is well known that THs exert regulatory function on immune cells and modulate cytokine expression, but how hyperthyroidism (hyper) modulates placental immunological aspects leading to placental alterations is unknown. This work aims to throw light on how hyper modulates immunological and morphological placental aspects. Control and hyper (induced by a daily s.c. injection of T4 0.25 mg/kg) Wistar rats were mated 8 days after starting T4 treatment and euthanized on days 19 (G19) and 20 (G20) of pregnancy. We removed the placenta to perform qPCR, flow cytometry, immunohistochemistry, Western blot and histological analysis, and amniotic fluid and serum to evaluate hormone levels. We observed that hyper increases the fetal number, fetal weight, and placental weight on G19. Moreover, hyper induced an endocrine imbalance with higher serum corticosterone and changed placental morphology, specifically the basal zone and decidua. These changes were accompanied by an increased mRNA expression of glucocorticoid receptor and monocyte chemoattractant protein-1, an increased mRNA and protein expression of prolactin receptor, and an increase in CD45+ infiltration. Finally, by in vitro assays, we evidenced that TH induced immune cell activation. In summary, we demonstrated that hyper modulates immunological and morphological placental aspects and induces fetal phenotypic changes, which could be related to preterm labor observed in hyper.

The Relation between Prepregnancy Body Mass Index and Abnormal Placental Morphology and Birth Weight

Background: Birth is enormously important, and the care that a woman receives during laboraffects women`s health physically and emotionally in the short and long-term periods. The placentaplays a pivotal role during pregnancy by being intimately connected to the mother and fetus. Aim ofthe current study is to examine the relation between prepregnancy body mass index and abnormalplacental morphology and birth weight. Methods: A descriptive correlational research design wasused for this study to achieve the study aim. Sample: A purposive of 150 laboring women wereenrolled in the study. Setting: the study was conducted at the delivery unit at Al kaser AliniUniversity Hospital, Cairo University, Egypt.Tools: Three tools were used to collect the data; 1)Structured Interviewing Questionnaire, 2) Maternal Assessment Tool, And 3) Neonatal AssessmentTool. Results: The mean age of the study sample was 29.77 ± 5.47 years old. The meanprepregnancy body mass index (BMI) was 26.22 ±3.20 and there is a positively correlated with itand newborn birth weight (r=0.18; p=0.02), placental weight (r=0.16; p =0.04), and placentalthickness (r=0.21; p=0.03). Conclusions: The study findings concluded that prepregnancy bodymass index parameters which are known to influence birth weight and determinants of abnormalplacental morphology. Recommendations: Authoritive personnel should encourage protocols anddevelop guides/checklists for placental examination in health care facilities

Obesity and gestational diabetes independently and collectively induce specific effects on placental structure, inflammation and endocrine function in a cohort of South African women.

Maternal obesity and gestational diabetes mellitus (GDM) are associated with insulin resistance and health risks for mother and offspring. Obesity is also characterized by low-grade inflammation, which in turn, impacts insulin sensitivity. The placenta secretes inflammatory cytokines and hormones that influence maternal glucose and insulin handling. However, little is known about the effect of maternal obesity, GDM and their interaction, on placental morphology, hormones and inflammatory cytokines. In a South African cohort of non-obese and obese pregnant women with and without GDM, this study examined placental morphology using stereology, placental hormone and cytokine expression using real-time PCR, western blotting and immunohistochemistry, and circulating TNFα and IL-6 concentrations using ELISA. Placental expression of endocrine and growth factor genes was not altered by obesity or GDM. However, LEPTIN gene expression was diminished, syncytiotrophoblast TNFα immunostaining elevated and stromal and fetal vessel IL-6 staining reduced in the placenta of obese women in a manner that was partly influenced by GDM status. Placental TNFα protein abundance and maternal circulating TNFα concentrations were reduced in GDM. Both maternal obesity and, to a lesser extent, GDM were accompanied by specific changes in placental morphometry. Maternal blood pressure and weight gain and infant ponderal index were also modified by obesity and/or GDM. Thus, obesity and GDM have specific impacts on placental morphology and endocrine and inflammatory states that may relate to pregnancy outcomes. These findings may contribute to developing placenta-targeted treatments that improve mother and offspring outcomes, which is particularly relevant given increasing rates of obesity and GDM worldwide. KEY POINTS: Rates of maternal obesity and gestational diabetes (GDM) are increasing worldwide, including in low-middle income countries (LMIC). Despite this, much of the work in the field is conducted in higher-income countries. In a well-characterised cohort of South African women, this study shows that obesity and GDM have specific impacts on placental structure, hormone production and inflammatory profile. Moreover, such placental changes were associated with pregnancy and neonatal outcomes in women who were obese and/or with GDM. The identification of specific changes in the placenta may help in the design of diagnostic and therapeutic approaches to improve pregnancy and neonatal outcomes with particular significant benefit in LMICs.

Placental perfusion using intravoxel incoherent motion MRI combined with Doppler findings in differentiating between very low birth weight infants and small for gestational age infants

IntroductionAbnormalities in placental morphology and function can lead to small for gestational age infants (SGA) and very low birth weight infants (VLBWI). In this study, we explored the value of intravoxel incoherent motion (IVIM) histogram parameters, MRI morphological parameters, and Doppler findings of the placenta in differentiating between VLBWI and SGA. MethodsThirty-three pregnant women who were diagnosed with SGA and met the inclusion criteria were enrolled in this retrospective study and divided into two groups: 22 with non-VLBWI and 11 with VLBWI. The IVIM histogram parameters (perfusion fraction (f), true diffusion coefficient (D), and pseudo-diffusion coefficient (D*)), MRI morphological parameters, and Doppler findings were compared between groups. The diagnostic efficiency was compared by receiver operating characteristic (ROC) curve analysis. ResultsThe Dmean, D90th, D*90th, fmax, and placental area of the VLBWI group were significantly lower than those of the non-VLBWI group (p < 0.05). The values of umbilical artery pulsatility index, resistance index (RI), and peak systolic velocity/end-diastolic velocity were significantly higher in the VLBWI group than in the non-VLBWI group (p < 0.05). D90th, placental area, and umbilical artery RI had the highest areas under the curve (AUCs) of the ROC curves, at 0.787, 0.785, and 0.762, respectively. A combined predictive model (D90th, placental area, and umbilical artery RI) improved the performance in differentiating between VLBWI and SGA compared with the single model (AUC = 0.942). DiscussionIVIM histogram (D90th) and MRI morphological (placental area) parameters and a Doppler finding (umbilical artery RI) may be sensitive indicators for differentiating between VLBWI and SGA.

Placentation in the Mexican scincid lizard Plestiodon brevirostris (Squamata: Scincidae).

Viviparity is the reproductive pattern in which females gestate eggs within their reproductive tract to complete their development and give birth to live offspring. Within extant sauropsids, only the Squamata (e.g., snakes, lizards, and amphisbaenians) evolved viviparity, representing 20% of the existing species. The genus Plestiodon is represented by 43 species and is one of the most widely distributed genera of the Scincidae in Mexico. The goal of this research has been to determine the placental morphology and ontogeny during gestation in the lizard Plestiodon brevirostris. Specimens were dissected to obtain the embryonic chambers and the embryos were categorized to carry out the correlation between the development stage and the placenta development. The embryonic chambers were processed using the conventional histological technique for light microscopy. The identified embryonic stages were 4, 29, 34, 36, and 39. A thin eggshell surrounds the egg in early developmental stages; however, this structure is already absent in the embryonic hemisphere during the developmental stage 29. The results revealed that P. brevirostris is a lecithotrophic species, but a close maternal-fetal relationship is established by tissue apposition. Ontogenically, the placental types that form in the embryonic hemisphere are the chorioplacenta, choriovitelline placenta, and chorioallantoic placenta; whereas the omphaloplacenta is formed in the abembryonic hemisphere. The structure of the chorioallantoic placenta in P. brevirostris suggests that it may play a role during gas exchange between the mother and the embryo, due to the characteristics of the epithelia that comprise it. The structure of embryonic and maternal epithelia of the omphaloplacenta suggests a role in the absorption of the eggshell during gestation and possibly in the transport or diffusion of some nutrients. In general, it is evident that ontogeny and placental characteristics of P. brevirostris match those of other species of viviparous lecithotrophic scincids.

Impaired placental hemodynamics and function in a non-human primate model of gestational protein restriction

Maternal malnutrition increases fetal and neonatal morbidity, partly by affecting placental function and morphology, but its impact on placental hemodynamics are unknown. Our objective was to define the impact of maternal malnutrition on placental oxygen reserve and perfusion in vivo in a rhesus macaque model of protein restriction (PR) using advanced imaging. Animals were fed control (CON, 26% protein), 33% PR diet (17% protein), or a 50% PR diet (13% protein, n = 8/group) preconception and throughout pregnancy. Animals underwent Doppler ultrasound and fetal biometry followed by MRI at gestational days 85 (G85) and 135 (G135; term is G168). Pregnancy loss rates were 0/8 in CON, 1/8 in 33% PR, and 3/8 in 50% PR animals. Fetuses of animals fed a 50% PR diet had a smaller abdominal circumference (G135, p < 0.01). On MRI, placental blood flow was decreased at G135 (p < 0.05) and placental oxygen reserve was reduced (G85, p = 0.05; G135, p = 0.01) in animals fed a 50% PR diet vs. CON. These data demonstrate that a 50% PR diet reduces maternal placental perfusion, decreases fetal oxygen availability, and increases fetal mortality. These alterations in placental hemodynamics may partly explain human growth restriction and stillbirth seen with severe PR diets in the developing world.

Effects of Gestational Intermittent Hypoxia on Placental Morphology and Fetal Development in a Murine Model of Sleep Apnea.

Obstructive sleep apnea (OSA) during pregnancy is characterized by episodes of intermittent hypoxia (IH) during sleep, resulting in adverse health outcomes for mother and offspring. Despite a prevalence of 8-20% in pregnant women, this disorder is often underdiagnosed.We have developed a murine model of gestational OSA to study IH effects on pregnant mothers, placentas, fetuses, and offspring. One group of pregnant rats was exposed to IH during the last 2weeks of gestation (GIH). One day before the delivery date, a cesarean section was performed. Other group of pregnant rats was allowed to give birth at term to study offspring's evolution.Preliminary results showed no significant weight differences in mothers and fetuses. However, the weight of GIH male offspring was significantly lower than the controls at 14days (p<0.01). The morphological study of the placentas showed an increase in fetal capillary branching, expansion of maternal blood spaces, and number of cells of the external trophectoderm in the tissues from GIH-exposed mothers. Additionally, the placentas from the experimental males were enlarged (p<0.05). Further studies are needed to follow the long-term evolution of these changes to relate the histological findings of the placentas with functional development of the offspring in adulthood.

Twin pregnancy: Live fetus with complete hydatidiform molar—A case report

Gestational trophoblastic disease encompasses a range of lesions, each culminating in varied clinical manifestations. Among these, the simultaneous occurrence of molar changes within the placenta and a viable fetus remains a particularly elusive and challenging presentation, posing intricate dilemmas for obstetricians. In this article, we delineate a distinct case involving a 21-year-old woman with a history of consanguineous marriage. She was referred from Médecins Sans Frontières to the Rafic Hariri University Hospital during her 19th week of gestation. With an unremarkable medical history and uncomplicated previous pregnancies, her presentation to the Rafic Hariri University Hospital was punctuated by symptoms of premature labor. Clinical evaluations revealed ruptured membranes, a fetus-positioned breech, and discernible complications tied to the placental morphology. Given these clinical findings, a decision was made in favor of a Cesarean delivery. Prior to this, the patient had been administered corticosteroids and tocolytics. Subsequent delivery produced a live male infant at 34 + 5 gestational days, and further assessment unveiled a complete molar pregnancy. The coexistence of a viable fetus alongside a complete molar pregnancy is an infrequently documented phenomenon, underlining the clinical significance of this case. A comprehensive literature survey reinforced the exceptional nature of our findings. Postpartum, both the mother and neonate were monitored for a month, ensuring their well-being. This case accentuates the paramountcy of prompt and precise diagnostic interventions when faced with atypical presentations. It further underscores the imperative for obstetricians to possess nuanced expertise in confronting the intricate challenges posed by gestational trophoblastic disease, ensuring optimal maternal and neonatal outcomes.

Paternal obesity induces epigenetic aberrations and gene expression changes in placenta and fetus.

Paternal epigenome regulates placental and fetal growth. However, the effect of paternal obesity on placenta and its subsequent effect on the fetus via sperm remains unknown. We previously discovered abnormal methylation of imprinted genes involved in placental and fetal development in the spermatozoa of obese rats. In the present study, elaborate epigenetic characterization of sperm, placenta, and fetus was performed. For 16 weeks, male rats were fed either control or a high-fat diet. Following mating studies, sperm, placenta, and fetal tissue were collected. Significant changes were observed in placental weights, morphology, and cell populations. Methylation status of imprinted genes-Igf2, Peg3, Cdkn1c, and Gnas in spermatozoa, correlated with their expression in the placenta and fetus. Placental DNA methylating enzymes and 5-methylCytosine levels increased. Furthermore, in spermatozoa, DNA methylation of a few genes involved in pathways associated with placental endocrine function-gonadotropin-releasing hormone, prolactin, estrogen, and vascular endothelial growth factor, correlated with their expression in placenta and fetus. Changes in histone-modifying enzymes were also observed in the placenta. Histone marks H3K4me3, H3K9me3, and H4ac were downregulated, while H3K27me3 and H3ac were upregulated in placentas derived from obese male rats. This study shows that obesity-related changes in sperm methylome translate into abnormal expression in the F1-placenta fathered by the obese male, presumably affecting placental and fetal development.

MORPHOLOGICAL AND IMMUNOHISTOCHEMICAL FEATURES OF PLACENTA AND PLACENTAL FACTOR IN WOMEN WITH ISOLATED CONGENITAL HEART DEFECTS IN NEWBORN

Introduction. Congenital heart defects (CHD) in fetus can affect the course of pregnancy, cause changes in the functioning of the pregnant woman's systems and metabolic and hemodynamic disorders. The relevance of the problems CHD is primarily due to their high frequency in newborns (5-9 per 1,000 live births) depending on geographical differences and the significant share among multiple congenital malformations and the need for surgical treatment in the neonatal period. Placenta, as one of the least studied human organs, plays not only a crucial role in the process of organogenesis, but also in the "programming" of human health after fetal and newborn periods. For today, it’s important to determine the association between the CHD and placental abnormalities, the nature and consequences of which need further study.Objective. To study morphological and immunohistochemical features of placental structures in parturients with isolated congenital heart defects in the newborn.Material and methods. Over the period 2020-2021, 90 pregnant women aged 17 to 39 years (mean age 28.36±5.08) who gave birth at 37-41 weeks, and their placents, of which 30 had different forms of CHD in the newborn, were examined on a hospital-based sample. Patients were divided into two groups: the study - women with CHD in the newborn, and control - somatically healthy motherswith healthy children. Given the different etiologies of cardiovascular defects in fetus, as well as the presence of different risk factorsfor their occurrence, in order to minimize their impact on the emergence of isolated CHD, considered appropriate selection criteria for pregnant women with non-syndromic forms of cardiovascular defects, as the presence of genetic syndrome can affect intrauterine fetaldevelopment, which makes it impossible to determine a single effect of CHD development. The selection criteria in this study included:somatically healthy woman, unburdened pregnancy, natural insemination (without using of reproductive technologies), the presence of isolated heart disease in the fetus, confirmed by a cardiologist using echocardiography. Organometric, macroscopic, general histological and immunohistochemical methods were used to study placental morphology and placental factors.Results. Analyzing the data on the morphological features of placentas from women with CHD in the newborn, we should note the presence of circulatory disorders in 60% of cases, namely multiple infarcts, complete or partial obliteration of arteries and arterioles with perivascular fibrosis (in the stem villi – 15%, intermediate – 10%, terminal - 10%), reduced number of fetal vessels in the terminal villiand syncytiocapillary membranes, abrupt vasodilation of intermediate villi. Complete or partial replacement of villous epithelium by fibrinoid masses in 20% was also detected. Immunohistochemical study of placental growth factor showed less pronounced expression in syncytia, decidual sheath and stromal cells (1-2 points) compared with control (2-3 points).Conclusions. The revealed morphological and immunohistochemical changes in the placental barrier at different levels refer to the damage of maternal and fetal placenta structures of parturients with isolated neonatal heart disease, which lead to impaired stromalvascular processes with reduced perfusion. This confirms the world data on the presence of placental-cardiac axis and can be a predictor of CHD at the early stages of placental structure study, as well as in further prediction of the child's health.

Interactions between maternal health and placental morphology on neonate body composition

BackgroundWe aimed to examine maternal metabolic correlates of neonate body composition, and the potential mediating effect of the placenta. MethodsData were collected throughout pregnancy and at delivery. An oral glucose tolerance test (OGTT) was conducted in order to diagnose or rule out gestational diabetes mellitus (GDM). Maternal weight and blood pressure were taken and hypertension and gestational weight gain (GWG) were defined. Gestational age, birth weight (BW) and weight to length ration (WLR) were recorded. Photographs were taken of the placenta, and the widths and lengths were measured digitally. Body composition was analysed via air displacement plethysmography or dual-energy x-ray absorptiometry. Mediation models were conducted to determine the mediation effect of the placental variables on the relationships between maternal health variables and neonate outcomes. Next, interaction terms were added to models to determine how maternal and placental variables interacted in their effect on neonate outcomes. ResultsA total of n = 280 women were included in the analysis. Majority were overweight or obese. Fourteen percent of women developed GDM during pregnancy, 5% had hypertension during pregnancy, 32% were HIV positive, and 32% had anemia. For the birth weight outcome, coefficients of BMI were attenuated by the addition of placental variables (Model 1 ß=18.66 vs Model 2 ß=16.40). Similar patterns were evident for GWG and hypertension, and for the WLR outcome. In all cases the addition of the placental variables attenuated associations between maternal exposures and neonatal outcomes, yet the level of significance did not change. Inclusion of interaction terms reversed the direction of the relationships between hypertension and BW and WLR, and between GWG and WLR. ConclusionThe placenta buffers some harmful effects of obesity, GWG, and hypertension on neonate size, and placental efficiency interacted with most maternal risk factors to either counteract, or attenuate relationships with neonate size at birth. However the placenta was unable to completely counteract the negative effect of excess nutrient supply on in utero growth.

Placental Morphology and Morphometry: Is It a Prerequisite for Future Pathological Investigations?

Successful pregnancy is dependent on implantation, nutrient and gas exchange, as well as fetal protection from the immunologic attack. Placental pathologies and preterm delivery closely correlate with the size and shape of the placenta. Additionally, normal vaginal microbiota is disturbed during viral insults such as SARS-CoV-2 and HIV, with consequent placental anomalies. This chapter focuses on placental development, morphology, and pathology while also investigating placental bed structure and function. Placental anomalies with regard to HIV-1 and SARS-CoV-2 infection and placental morphometric image analysis and its relevance for verification of placental pathology are explored. Since image analysis remains optional for routine diagnostic purposes, authentication of placental appraisal warrants the use of measurable predefined definitions. Immunohistochemical analyses of placental morphology and angiogenic, epithelial, and apoptotic mechanisms facilitate research into etiopathogenetic pathways involved in placental anomalies with a focus on discovering novel diagnostic foci. Thus, image analyses as an adjunct to complement pathological investigations are recommended.

Effects of Diabetes and Hypertension on Placenta

Placental insufficiency is the failure of the placenta to supply nutrients to the fetus and remove toxic wastes; it is a common cause of intra uterine growth restriction (IUGR), fetal distress peri and postnatal mortality. Specifically gestational diabetes and hypertension during pregnancy alters placental architecture which contributes to insufficiency of the placenta. Placenta is the most accurate record of infant’s prenatal experiences. Clinical condition such as hypertension and diabetes that complicate pregnancy leads to significant structural changes in placenta, these histological changes and morphological alterations in placenta lead to insufficiency, resulting in IUGR and fetal distress. In the present study morphology of placentas collected from diabetic and hypertensive pregnancy will be observed, the histo-pathological findings will be recorded and correlated to birth weight, APGAR scores and congenital anomalies of babies and will be compared to the findings in normal placentas also. This study will be beneficial for obstetrician and pediatrician in gathering knowledge about patho genesis of placental insufficiency; it will add to the knowledge on placental morphology and will high light the abnormalities in placental anatomy.

Contribution of Second Trimester Sonographic Placental Morphology to Uterine Artery Doppler in the Prediction of Placenta-Mediated Pregnancy Complications.

Second-trimester uterine artery Doppler is a well-established tool for the prediction of preeclampsia and fetal growth restriction. At delivery, placentas from affected pregnancies may have gross pathologic findings. Some of these features are detectable by ultrasound, but the relative importance of placental morphologic assessment and uterine artery Doppler in mid-pregnancy is presently unclear. To characterize the association of second-trimester sonographic placental morphology markers with placenta-mediated complications and determine whether these markers are predictive of placental dysfunction independent of uterine artery Doppler. This was a retrospective cohort study of patients with a singleton pregnancy at high risk of placental complications who underwent a sonographic placental study at mid-gestation (160/7-246/7 weeks' gestation) in a single tertiary referral center between 2016-2019. The sonographic placental study included assessment of placental dimensions (length, width, and thickness), placental texture appearance, umbilical cord anatomy, and uterine artery Doppler (mean pulsatility index and early diastolic notching). Placental area and volume were calculated based on placental length, width, and thickness. Continuous placental markers were converted to multiples on medians (MoM). The primary outcome was a composite of early-onset preeclampsia and birthweight &lt; 3rd centile. A total of 429 eligible patients were identified during the study period, of whom 45 (10.5%) experienced the primary outcome. The rate of the primary outcome increased progressively with decreasing placental length, width, and area, and increased progressively with increasing mean uterine artery pulsatility index (PI). By contrast, placental thickness followed a U-shaped relationship with the primary outcome. Placental length, width, and area, mean uterine artery PI and bilateral uterine artery notching were all associated with the primary outcome. However, in the adjusted analysis, the association persisted only for placenta area (adjusted odds ratio [aOR] 0.21, 95%-confidence interval [CI] 0.06-0.73) and mean uterine artery PI (aOR 11.71, 95%-CI 3.84-35.72). The area under the ROC curve was highest for mean uterine artery PI (0.80, 95%-CI 0.71-0.89) and was significantly higher than that of placental area (0.67, 95%-CI 0.57-0.76, p = 0.44). A model that included both mean uterine artery PI and placental area did not significantly increase the area under the curve (0.82, 95%-CI 0.74-0.90, p = 0.255), and was associated with a relatively minor increase in specificity for the primary outcome compared with mean uterine artery PI alone (63% [95%-CI 58-68%] vs. 52% [95%-CI 47-57%]). Placental area is independently associated with the risk of placenta-mediated complications yet, when combined with uterine artery Doppler, did not further improve the prediction of such complications compared with uterine artery Doppler alone.

Relationship between placental hemodynamics and placental histological analysis in third trimester.

To investigate whether vascularization index (VI), flow index (FI), and vascularization flow index (VFI) correlate with the pathological structure of the placenta and whether there were any differences in VI, FI, VFI, and placental pathological structure between the normal and preeclampsia (PE) groups. Fifty-five pregnant women (normal group, n=27; PE group, n=28) underwent VI, FI, and VFI at four locations in the placenta during the second and third trimesters. Two hematoxylin and eosin (HE)-stained specimens of the postpartum placenta were prepared. We randomly selected two of these locations and used ImageJ, an open-source image package, to quantify intervillous blood vessels (IBV), intervillous spaces (IS), and intervillous blood vessels + intervillous spaces (IBV + IS) per unit placenta and analyzed their correlation with VI, FI, and VFI. There was no positive correlation between VI, FI, VFI, IBV, IS, and IBV + IS. There were no significant differences in VI, FI, and VFI between the normal and PE groups; however, there were significant differences in IBV, IS, and IBV + IS in the PE group compared to those in the normal group. Placental hemodynamics measured by VI, FI, and VFI were not positively correlated with placental morphology in the third trimester. There were no differences in the VI, FI, and VFI in the third trimester between the normal and PE groups, suggesting that these may reflect placental circulatory insufficiency.

Association of placental morphology and fetal birth weight

Background: The placenta plays a crucial role in sustaining pregnancy and supporting healthy foetal growth and function. Placental morphology predicts illness patterns in adults and foetal development. Birth weight is a significant predictor of a child's survival, healthy development, and growth. The connection between birth weight and perinatal outcome has long been understood in obstetrics. As is generally known, low birth weight is a known risk factor for the child's long-term health. The aim of the study was to find any association between birth weight, gender and placental morphology. Methods: An analytical cross sectional study was conducted in the anatomy department of Anatomy, Bhaarath Medical college and Hospital, Chennai. Placentae of 200 were collected. Morphological analysis including placental weight, number of cotyledons, site of umbilical cord insertion and fetal and maternal surface area, were measured in normal and low birth weight babies. Results: Birth weight showed a positive connection with gestational age. Birth weight and greater values in men were positively and significantly correlated with placental parameters (p 0.001). Regression models employing the newborn's sex and placental morphometry were used to estimate the birth weight; weight (R2=0.461), surface area (R2=0.411), and volume (R2=0.456) were calculated.