Pathomorphological aspects of the placental deficiency in chlamidial And mycoplasmal infection

The peculiarities of morphogenesis of placenta lesions and pathogenesis of placental deficiency in these types of infectious pathology are studied. It is stated that the subcompensated form of the relative chronic placental deficiency in chlamidiosis can be developed, morphological vascularization indices of terminal villi being higher than normal and in mycoplasmosis such placental deficiency is connected with the partial decrease of vascularization indices. In the presence of mixed clamidia and mycoplasma infection in pregnants the dissociated type of villi lesions is observed and the placental vascularization indices (the content and state of capillaries, syncytiocapillar membranes and syncytial kidneys) ' are impaired to a greater extent resulting in chronic placental defficiency.

Changes in the immunomorphological indicators of the placenta in women with exacerbation of cytomegalovirus infection in the second trimester of pregnancy complicated by chronic placental insufficiency

Aim. To assess the change of immunomorphological parameters in the placenta in women with exacerbation of cytomegalovirus infection (CMVI) in the second trimester of pregnancy, complicated by chronic placental insufficiency.Materials and methods. The concentration of TNF-α in the homogenate of 120 placentas and the histometric parameters of chorionic villi were determined in patients who underwent latent CMVI and exacerbation of CMVI in the second trimester of gestation. Group 1 included 30 placentas from seronegative women with a physiological course of pregnancy, group 2 included 30 placentas from patients with latent CMVI and chronic compensated placental insufficiency, group 3 – 30 placentas from women with exacerbation of CMVI and chronic compensated placental insufficiency; and group 4 – 30 placentas from pregnant women with exacerbation of CMVI and chronic subcompensated placental insufficiency.Results. In the 1st group in the placenta homogenate the concentration of TNF-α was 16.8±1.86 pg/mL; the number of villi with a diameter of 30-50 microns was 25.4±2.08%, with a diameter of 60-90 microns – 64.4±2.43% and with a diameter of more than 90 microns – 10.2±0.88%; the number of terminal villi with 1-3 capillaries was 27.0±2.29%, with 4- 6 capillaries – 42.1±2.02%, with 7-10 capillaries – 23.9±1.58% and villi with more than 10 capillaries – 7.0±0.79%. In group 2, the concentration of TNF-α in the placenta homogenate was amounted to 22.1±2.06 pg/mL (p>0.05); among the villi, anatomical forms with a diameter of 30-50 μm (p<0.01) were found 1.41 times more often, and villi with a diameter of 60-90 μm (p<0.01) were 1.19 times less common; the number of villi with 4-6 capillaries decreased by 1.21 times (p<0.05) and the number of villi with 7-10 capillaries increased by 1.43 times (p<0.001). In the placentas of group 3, compared with group 2 in the homogenate, there was an increase in the concentration of TNF-α to 60.2±3.47 pg/mL (p<0.001) against the background of a decrease in the concentration of villi with a diameter of 30-50 μm to 26.4±2,61% (p<0.05), villi with 7-10 capillaries up to 20.7±1.53% (p<0.001) and an increase in the number of villi with 1-3 capillaries up to 34.8±3.05% (p<0.05). In the placental homogenate of group 4, compared with group 3, the concentration of TNF-α (p<0.05) increased 1.31 times, the number of villi with a diameter of 60-90 μm increased to 70.2±1.59%, (p<0,01) and villi with 1- 3 capillaries to 46.8±3.76% (p<0.05) with a decrease in the number of villi with a diameter of 30-50 μm to 18.9±1.69% (p<0,05), with 7-10 capillaries up to 13.3±1.36% (p<0.001) and with 10 or more capillaries – up to 3.9±0.43% (p<0.01).Conclusion. In women with exacerbation of CMVI in the second trimester of pregnancy and the development of chronic subcompensated placental insufficiency, inhibition of the growth and angiogenesis of terminal villi is observed against the background of the maximum concentration of TNF-α in the medium.

Predicting intrauterine infection risk in newborns based on morphometric parameters of placental terminal villi

Aim. To evaluate the prognostic value of micromorphometry of placental terminal villi for early diagnosis of intrauterine infections in newborns.Materials and methods. A molecular genetic and micromorphometric study of 34 placentas obtained from women whose pregnancy ended in preterm labor at 30-36 weeks and 46 placentas of persons who gave birth to full-term babies was performed. In samples of placental tissue, the polymerase chain reaction was used to identify the genome of the following pathogens of intrauterine infections: Mycoplasma hominis, Mycoplasma genitalium, Ureaplasma species (Ureaplasma urealyticum+Ureaplasma parvum), Chlamydia trachomatis, Streptococcus agalactiae, Streptococcus pyogenes, Staphylococcus aureus, Klebsiella pneumoniae, Haemophilus influenza, Listeria monocytogenes, Cytomegalovirus, Herpes simplex virus, Human herpes virus 4 type, Human herpes virus 6 type, Parvovirus B19. Morphometry was performed using an image analysis system on a Carl Zeiss microscope and Axio Imager software. An average number of capillaries in the terminal villi and the distance from the capillaries to the syncytiotrophoblast were calculated.Results. The genome of intrauterine infection pathogens was detected in 55.9% of placentas from preterm birth, including DNA of Ureaplasma species – 29.4%, Mycoplasma hominis – 23.5%, Mycoplasma genitalium – 5.9%, Streptococcus agalactiae – 11.7%, Cytomegalovirus – 5.9%, Human herpes virus 4 type – 14.8% as a part of mono- and co-infections. In full-term pregnancy, the infection of the placentas was found to be 3.4 times less – 16.3% (p<0.0002). In monoinfections, DNA of Ureaplasma species – 4.6%, Mycoplasma hominis – 6.9%, Streptococcus agalactiae – 2.3%, Human herpes virus 4 type – 2.3% were detected. An average number of capillaries (abs. value) in the terminal villi of infected placentas, both at full-term (5.35±1.07) and premature (3.97±0.19) pregnancies, proved to be significantly less than in uninfected placentas (5.74±0.05 and 4.63±0.28), respectively. An average distance from the capillaries (µm) of the terminal villi to the syncytiotrophoblast in infected placentas both at full-term (1.62±0.15) and premature pregnancies (2.20±0.2) proved to be significantly greater than in uninfected placentas (1.02±0.03 and 1.72±0.14, respectively).Conclusion. Comparison of the morphometric parameters of terminal villi in the examined placenta with an average rate of infected and uninfected placentas of full-term and premature pregnancies makes it possible to predict the risk of intrauterine infection in a newborn.

Features of violation of maturation of the chorionic tree of the placenta at immaturity of the placental bed of the uterus on the background of iron deficiency anemia in pregnant women in terms of chronic insufficiency of manure

The authors of the article investigated the quantitative parameters of the placental chorion tree during physiological pregnancy and gestation against the background of iron deficiency anemia. It has been established that iron deficiency anemia in pregnant women inhibits the development of the placental chorionic tree, which is explained by the formation of chorionic villi (through trophoblastic and free processes) and violation of the transition of terminal villi to terminal "specialized" villi. The diagnosis of chronic placental insufficiency during pregnancy on the background of iron deficiency anemia can be verified morphologically based on quantitative indicators of assessment of the structure of the placental chorionic tree - the percentage of terminal villi should be higher than 43% and the percentage of terminal "specialized" villi lower than 15%.

Isolated fetal neural tube defects associate with increased risk of placental pathology: evidence from the Collaborative Perinatal Project.

Objective: To compare placental pathology and fetal growth in pregnancies with an isolated fetal neural tube defect (NTD; cases) to those without congenital anomalies (controls). We hypothesised that cases would be at an increased risk of placental pathology and poorer anthropometric outcomes at birth compared to controls Methods: We performed a matched case-cohort study using data from the Collaborative Perinatal Project. Cases (n=74) and controls (n=148) were matched (1:2 ratio) for maternal pre-pregnancy BMI, maternal race, infant sex, gestational age at birth and study site. Primary outcomes were placental characteristics (weight and size measurements, pathology). Secondary outcomes were infant birth outcomes. Subgroup analysis was done by type of NTD (spina bifida, anencephaly or encephalocele), infant sex, and preterm/term delivery. Data were analysed using adjusted generalized linear and nominal logistic regression models. Results are presented as adjusted β or adjusted odds ratio (aOR; 95% confidence interval). Results: Cases had lower placental weight (β=-22.2 g [-37.8 - -6.6]), surface area (β=-9.6 cm2 [-18.3 - -1.0]) and birth length z-scores (β=-0.4 [-0.7 - -0.001]) compared to controls. Cases were more likely to have a single umbilical artery (vs. two; 6 [8.1%] vs. 1 [0.7%]; aOR=301 [52.6 - 1726]), overall placental hypermaturity (9 [12.2%] vs. 5 [3.4%]; aOR=6.8 [3.1 - 14.7]), and many (vs. few) Hofbauer cells (9 [12.2%] vs. 7 [4.7%]; aOR=3.02 [1.2 - 7.3]), stromal fibrosis (9 [12.2%] vs. 10 [6.8%]; aOR=3.0 [1.4 - 6.3]) and pathological edema (11 [14.9%] vs. 12 [8.1%]; aOR=3.04 [1.4 - 6.7]) in placental terminal villi compared to controls. Placental pathology varied across NTD subtypes, infant sex, and preterms vs. term pregnancies. Conclusions: Fetuses with isolated NTDs may be at increased risk of placental pathology, which could be contributing to poor fetal growth in these pregnancies and subsequent postnatal morbidities.

Placenta Pathology From Term Born Neonates With Normal or Adverse Outcome

Background The incidence of umbilical cord or placental parenchyma abnormalities associated with mortality or morbidity of term infants is lacking. Methods Placentas of 55 antepartum stillbirths (APD), 21 intrapartum stillbirths (IPD), 12 neonatal deaths (ND), and 80 admissions to a level 3 neonatal intensive care unit (NS) were studied and compared with 439 placentas from neonates from normal term pregnancies and normal outcome after vaginal delivery (NPVD) and with 105 placentas after an elective caesarian sections (NPEC). Results NPVD and NPEC placentas showed no or one abnormality in 70% and placentas from stillbirth showed two or more abnormalities in 80% of cases. APD placentas more frequently had a low weight and less formation of terminal villi. Hypercoiling was more often present in all study groups. Severe chronic villitis was almost exclusively present in APD placentas. Chorioamnionitis was significantly more frequent in APD, IPD and NS placentas and funisitis was more often observed in IPD and NS placentas. Conclusion Multiple placental abnormalities are significantly more frequent in placentas from term neonates with severe perinatal morbidity and mortality. These placental abnormalities are thought to be associated with disturbed oxygen transfer or with inflammation.

Evidence, evolution and pattern of contractile elements in villous vascular walls and stroma of human placentas of premature infants of different gestational ages. An immuno-morphologic comparative study

The contractile elements of the human placenta villous tree represent a topic of interest and many issues persist still open. Histology of the stroma and muscular wall and their evolution, in relation with the gestational age, remains to be clarified for a deeper understanding of the adaptive potential and pathogenetic mechanisms.In our study, 56 premature placentas (21-36 wks) were considered, sub-divided into four groups based on age of gestation and compared to 23 at-term placentas (37-40 wks). All cases were tested with anti-smooth muscle actin (SMA) and anti-desmin antibodies to identify the contractile elements in the stroma and in vascular walls of villi.SMA and desmin staining show evident decreased expressions during the pregnancy (temporal variation) and from proximal to distal part of the villous tree (spatial variation) being higher in the stem villi.Both pre-term and at-term placentas showed persisting, although variable, positivity for SMA and desmin staining in the stroma and in the vessel walls of the mature intermediate and terminal villi. This represents an unexpected finding and nothing alike has been previously reported in literature.Both highly premature and term placentas seem to maintain contractile components within each type of villi, represented by both myofibroblasts and mature smooth muscular cells. These components may be present in both villous vascular walls and stroma, albeit with different staining intensity.This finding allows us to imagine an active function in the regulation of the blood flow, not only in stem and intermediate immature villi but even in smaller villi.

CHARACTERISTICS OF CD68+ AND CD163+ EXPRESSION IN PLACENTA OF WOMEN WITH PREECLAMPSIA AND OBESITY

The aim: To study the peculiarities of CD68+ and CD163+ macrophage expression in the placentas of women with obesity who developed preeclampsia by applying immunohistochemical method. Materials and methods: The study included 20 placentas taken from women who delivered full-term live-birth babies. The women were divided into 4 groups of 5 individuals each: women with physiological body weight (1st group); women with class II obesity (2nd group); women with physiological body weight and preeclampsia (3rd group); women with class II obesity, who developed preeclampsia (4th group). Results: The analysis of the expression level of CD68+ and CD163+ decidual macrophages shows the predominance of CD68+ pro-inflammatory profile over CD163+ anti-inflammatory profile in women of all groups. Evaluation of CD68+ and CD163+ expression levels of Kashchenko-Hofbauer cells in the stroma of the terminal villi of the placenta shows that the expression level of CD68+ macrophages is significantly higher in women with obesity and preeclampsia than in the control, or in women with obesity or preeclampsia. There was a reverse tendency to the polarization shift in Kashchenko-Hoffbauer cells in the stroma of the terminal villi towards the predominance of CD163+ macrophages over CD68+ macrophages in all groups of women. Conclusions: The imbalance in anti-inflammatory and pro-inflammatory profile of placental macrophages with a predominance of the latter can lead to the development of preeclampsia.

HYPODYNAMIA AS A FACTOR MODIFYING FUNCTIONAL MORPHOLOGY OF HUMAN PLACENTA

The aim: Study of the functional morphology of placenta in a sedentary lifestyle of a woman during pregnancy. Materials and methods: Object of the study: placentas obtained as a result of deliveries at term from women, urban residents, aged 20–40 years old, leading a sedentary lifestyle, and patients with a sufficiently high level of physical activity, the criteria of which corresponded to WHO recommendations. Immunohistochemical and morphometric studies of the placentas were carried out, followed by statistical analysis Results: Prerequisites for reducing the efficacy of the functioning of fetoplacental complex with a sedentary lifestyle were sclerosis, the formation of intervillous fibrinoid and fibrinoid substitution of terminal villi. The inclusion of compensatory mechanisms in the form of placental hypertrophy, angiomatosis, sinusoidal transformation of the capillaries of terminal villi, thinning of the syncytiocapillary membrane associated with an increase in the content of von Willebrand factor in the villus syncytiotrophoblast, in aggregate, normalizes the exchange between maternal and fetal blood and creates certain prerequisites for the successful completion of pregnancy. However, thinning of the syncytiocapillary membrane increases the risk of rupture and direct contact of the internal media of the mother and the fetus. Conclusions: Sedentary lifestyle of a pregnant woman leads to structural and functional changes in the placenta, which can be a serious prerequisite for the development of pathological abnormalities in the function of the “mother-placenta-fetus” system. To a certain extent, these changes are leveled due to compensatory processes in the placenta, the margin of efficacy of which needs further investigation.