RESUMEN

The expression and function of podoplanin (PDPN) in the normal human placenta has been debated in placental evaluation. This study emphasizes the importance of a multimodal approach of PDPN expression in normal human placentas. A complete examination is performed using immunohistochemistry, RNAscope and automated Digital Image examination (DIA) interpretation. QuPath DIA-based analysis automatically generated the stromal and histological scores of PDPN expression for immunohistochemistry and RNAscope stains. The umbilical cord's isolated fibroblasts and luminal structures expressed PDPN protein and PDPN_mRNA. RNAscope detected PDPN_mRNA upregulation in syncytial placental knots trophoblastic cells, but immunohistochemistry did not certify this at the protein level. The study found a significant correlation between the IHC and RNAscope H-Score (p = 0.033) and Allred Score (p = 0.05). A successful multimodal strategy for PDPN assessment in human placentas confirmed PDPN expression heterogeneity in the full-term human normal placenta and umbilical cord at the protein and mRNA level. In placental syncytial knots trophoblastic cells, PDPN showed mRNA overexpression, suggesting a potential role in placenta maturation.

RESUMEN

The study of the human placenta has always been appealing, given the importance of this temporal organ capable of sustaining the beginning of life and development of a new human being within the womb. Culturing placental explants has been an easy and reliable method to study some placental morphological, biochemical, and physiological features for a very long time. Besides low time consumption, requirement of few resources, and wide versatility, the placental explant in vitro culture retains cell-cell interaction in a 3D structure resembling the in vivo setting, which is why it is the option of choice for many researchers in the field. This chapter will describe a simplified method for culturing explants from human term placentas.

Asunto(s)

Placenta , Humanos , Embarazo , Femenino , Primer Trimestre del Embarazo

RESUMEN

The dissociation of whole tissue into single-cell suspensions is a critical step for techniques focused on profiling of individual cells. Here, we describe a protocol for the preparation of high-quality single-cell suspensions from human placental tissues: the basal plate (BP), placental villi (PV), and chorioamniotic membranes (CAM). This protocol also provides guidance for the cryopreservation and recovery of single-cell suspensions for later use. The methods described here have been demonstrated to be suitable for downstream single-cell applications, such as single-cell RNA-sequencing, that require viable, high-quality cell suspensions.

Asunto(s)

Criopreservación , Placenta , Embarazo , Femenino , Humanos

RESUMEN

BACKGROUND: The great obstetrical syndromes of fetal growth restriction and hypertensive disorders of pregnancy can occur individually or be interrelated. Placental pathologic findings often overlap between these conditions, regardless of whether 1 or both diagnoses are present. Quantification of placental villous structures in each of these settings may identify distinct differences in developmental pathways. OBJECTIVE: This study aimed to determine how the quantity and surface area of placental villi and vessels differ between severe, early-onset fetal growth restriction with absent or reversed umbilical artery Doppler indices and hypertensive disorders of pregnancy or the 2 conditions combined among subjects with disease severity that warrant early preterm delivery. We hypothesized that the trajectories of placental morphogenesis diverge after a common initiating insult of deep defective placentation. Specifically, we postulated that only villi are affected in pregnancy-related hypertension, whereas both villous and vascular structures are proportionally diminished in severe fetal growth restriction with no additional effect when hypertension is concomitantly present. STUDY DESIGN: In this retrospective cohort study, paraffin-embedded placental tissue was obtained from 4 groups, namely (1) patients with severe fetal growth restriction with absent or reversed umbilical artery end-diastolic velocities and hypertensive disorders of pregnancy, (2) patients with severe fetal growth restriction with absent or reversed umbilical artery Doppler indices and no hypertension, (3) gestational age-matched, appropriately grown pregnancies with hypertensive disease, and (4) gestational age-matched, appropriately grown pregnancies without hypertension. Dual immunohistochemistry for cytokeratin-7 (trophoblast) and CD34 (endothelial cells) was performed, followed by artificial intelligence-driven morphometric analyses. The number of villi, total villous area, number of fetoplacental vessels, and total vascular area across villi within a uniform region of interest were quantified. Quantitative analyses of placental structures were modeled using linear regression. RESULTS: Placentas from pregnancies complicated by hypertensive disorders of pregnancy exhibited significantly fewer stem villi (-282 stem villi; 95% confidence interval, -467 to -98; P<.01), a smaller stem villous area (-4.3 mm2; 95% confidence interval, -7.3 to -1.2; P<.01), and fewer stem villous vessels (-4967 stem villous vessels; 95% confidence interval, -8501 to -1433; P<.01) with no difference in the total vascular area. In contrast, placental abnormalities in cases with severe growth restriction were limited to terminal villi with global decreases in the number of villi (-873 terminal villi; 95% confidence interval, -1501 to -246; P<.01), the villous area (-1.5 mm2; 95% confidence interval, -2.7 to -0.4; P<.01), the number of blood vessels (-5165 terminal villous vessels; 95% confidence interval, -8201 to -2128; P<.01), and the vascular area (-0.6 mm2; 95% confidence interval, -1.1 to -0.1; P=.02). The combination of hypertension and growth restriction had no additional effect beyond the individual impact of each state. CONCLUSION: Pregnancies complicated by hypertensive disorders of pregnancy exhibited defects in the stem villi only, whereas placental abnormalities in severely growth restricted pregnancies with absent or reversed umbilical artery end-diastolic velocities were limited to the terminal villi. There were no significant statistical interactions in the combination of growth restriction and hypertension, suggesting that distinct pathophysiological pathways downstream of the initial insult of defective placentation are involved in each entity and do not synergize to lead to more severe pathologic consequences. Delineating mechanisms that underly the divergence in placental development after a common inciting event of defective deep placentation may shed light on new targets for prevention or treatment.

RESUMEN

Background and objective: Imprinted genes are important for the offspring development. To assess the relationship between obesity-related H19DMR methylation and H19 and IGF2 gene expression and offspring growth and body composition. Methods: Thirty-nine overweight/obese and 25 normal weight pregnant women were selected from the "Araraquara Cohort Study" according to their pre-pregnancy BMI. Fetal growth and body composition and newborn growth were assessed, respectively, by ultrasound and anthropometry. The methylation of H19DMR in maternal blood, cord blood, maternal decidua and placental villi tissues was evaluated by methylation-sensitive restriction endonuclease qPCR, and H19 and IGF2 expression by relative real-time PCR quantification. Multiple linear regression models explored the associations of DNA methylation and gene expression with maternal, fetal, and newborn parameters. Results: H19DMR was less methylated in maternal blood of the overweight/obese group. There were associations of H19DMR methylation in cord blood with centiles of fetal biparietal diameter (BPD) and abdominal subcutaneous fat thickness and newborn head circumference (HC); H19DMR methylation in maternal decidua with fetal occipitofrontal diameter (OFD), HC, and length; H19DMR methylation in placental villi with fetal OFD, HC and abdominal subcutaneous fat thickness and with newborn HC. H19 expression in maternal decidua was associated with fetal BPD and femur length centiles and in placental villi with fetal OFD and subcutaneous arm fat. IGF2 expression in maternal decidua was associated with fetal BPD and in placental villi with fetal OFD. Conclusion: To our knowledge, this is the first study to demonstrate associations of imprinted genes variations at the maternal-fetal interface of the placenta and in cord blood with fetal body composition, supporting the involvement of epigenetic mechanisms in offspring growth and body composition.

RESUMEN

Placental villi play a vital role in human fetal development, acting as the bridge of material exchange between the maternal and fetal. The abnormal morphology of placental villi is closely related to placental circulation disorder and pregnancy complications. Revealing placental villi three-dimensional (3D) morphology of common obstetric complications and healthy pregnancies provides a new perspective for studying the role of the placenta and its villi in the development of pregnancy diseases. In this study, we established a noninvasive, high-resolution 3D imaging platform via optical coherence tomography to reveal placental villi 3D morphological information of diseased and normal placentae. For the first time, 3D morphologies of placental villous tree structures in common obstetric complications were quantitatively revealed and corresponding 3D information could visualize the morphological characteristics of the placental villous tree from a more intuitive perspective, providing helpful information to the study of fetal development, feto-maternal material exchange, and gestational complications treatment.

RESUMEN

Intra-amniotic (IA) inflammation is associated with significant morbidities for both the mother and the fetus. Prior studies have illustrated many of the effects of IA inflammation on the uterine lining (decidua) and membranous layers of the placenta at the fetal-maternal interface. However, much less is known about the immunological response occurring within the villous placenta. Using a rhesus macaque model of lipopolysaccharide (LPS)-induced IA inflammation, we showed that pregnancy-matched choriodecidua and villi have distinct immunological profiles in rhesus pregnancies. In the choriodecidua, we show that the abundance of neutrophils, multiple populations of antigen-presenting cells, and two populations of natural killer (NK) cells changes with prenatal IA LPS exposure. In contrast, in immune cells within the villous placenta we observed alterations in the abundance of B cells, monocytes, and CD8 T cells. Prior work has illustrated that IA inflammation leads to an increase in tumor necrosis factor alpha (TNFα) at the fetal-maternal interface. In this study, pretreatment with a TNFα blockade partially reversed inflammation in the placental villi. Furthermore, we report that immune cells in the villous placenta sensed LPS during our experimental window, and subsequently activated T cells to produce proinflammatory cytokines. Moreover, this study is the first report of memory T cells in third-trimester non-human primate placental villi and provides evidence that manipulation of immune cells in the villi at the fetal-maternal interface should be considered as a potential therapeutic target for IA inflammation.

Asunto(s)

Corioamnionitis/inmunología , Vellosidades Coriónicas/inmunología , Decidua/inmunología , Leucocitos/inmunología , Activación de Linfocitos , Animales , Biomarcadores/metabolismo , Corioamnionitis/inducido químicamente , Corioamnionitis/tratamiento farmacológico , Corioamnionitis/metabolismo , Vellosidades Coriónicas/efectos de los fármacos , Vellosidades Coriónicas/metabolismo , Decidua/efectos de los fármacos , Decidua/metabolismo , Modelos Animales de Enfermedad , Femenino , Inmunofenotipificación , Leucocitos/efectos de los fármacos , Leucocitos/metabolismo , Lipopolisacáridos , Macaca mulatta , Embarazo , Transducción de Señal , Inhibidores del Factor de Necrosis Tumoral/farmacología , Factor de Necrosis Tumoral alfa/metabolismo

RESUMEN

Lower extremity venous insufficiency (VI) is a complication of pregnancy. The potential association of this venous disease with structural damage of the placenta has not been described. We analyzed the pattern of histopathologic lesions and the gene and protein expression of HIF1-α and apoptosis regulatory proteins. A prospective study was carried out on placenta samples from 43 women with pregnancy-associated VI and 24 age-matched pregnant healthy controls (HCs). Women with VI showed a significant increase in the number of villi (150.77 ± 42.55 VI versus 122.13 ± 27.74 HC) and in syncytial knots compared with those found in the placentas from HCs (67.15 ± 31.08 VI versus 42.49 ± 17.36 HC), and an increase in the number of bridges (32.40 ± 2.67 VI versus 22.73 ± 2.37 HC; P < .05). The mean number of syncytial nodes per villus is 1.37 ± 0.90 in the VI group and 0.49 ± 0.58 in the HC group (P < .001). Significant increases in the expression of Bax and caspase-3 and caspase-9 in the placentas from women with VI were observed compared with those found in HC. The expression of HIF-1α at both the messenger RNA and protein levels was also significantly increased in the placentas from women with VI. Our study demonstrates that placentas from women with pregnancy-associated VI show structural remodeling, with an increase in the number of villi and syncytial knots and enhanced apoptotic cellular death. Interestingly, this placental damage is associated with an increased expression of hypoxia-triggered molecular pathways, such as HIF-1α.

Asunto(s)

Hipoxia/metabolismo , Placenta/metabolismo , Placenta/patología , Insuficiencia Venosa/metabolismo , Adulto , Femenino , Humanos , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Preeclampsia/metabolismo , Embarazo , Estudios Prospectivos , Insuficiencia Venosa/patología

RESUMEN

INTRODUCTION: Delayed villous maturation and accelerated villous maturation diagnosed in histologic sections are morphologic manifestations of pathophysiological conditions. The inter-observer agreement among pathologists in assessing these conditions is moderate at best. We investigated whether automated image analysis of placental villi and syncytial knots could improve standardization in diagnosing these conditions. METHODS: Placentas of antepartum fetal death at or near term were diagnosed as normal, delayed or accelerated villous maturation. Histologic sections of 5 cases per group were photographed at ×10 magnification. Automated image analysis of villi and syncytial knots was performed, using ImageJ public domain software. Analysis of hundreds of histologic images was carried out within minutes on a personal computer, using macro commands. RESULTS: Compared to normal placentas, villi from delayed maturation were larger and fewer, with fewer and smaller syncytial knots. Villi from accelerated maturation were smaller. The data were further analyzed according to horizontal placental zones and groups of villous size. DISCUSSION: Normal placentas can be discriminated from placentas of delayed or accelerated villous maturation using automated image analysis. Automated image analysis of villi and syncytial knots is not equivalent to interpretation by the human eye. Each method has advantages and disadvantages in assessing the 2-dimensional histologic sections representing the complex, 3-dimensional villous tree. Image analysis of placentas provides quantitative data that might help in standardizing and grading of placentas for diagnostic and research purposes.

Asunto(s)

Vellosidades Coriónicas/diagnóstico por imagen , Interpretación de Imagen Asistida por Computador , Enfermedades Placentarias/diagnóstico por imagen , Estudios de Factibilidad , Femenino , Humanos , Proyectos Piloto , Embarazo

RESUMEN

Placental barrier regulates maternal-fetal interchange protecting the baby from damage caused by substances found in the uterine environment or circulating in the vascular system. Organophosphate (OP) pesticides are a paramount group of environmental pollutants used in intensive agriculture for protection against diseases and pests. While many studies have reported an increased risk of pregnancy alterations in pregnant women exposed to OPs, few have analyzed the effects caused by these pesticides in the placenta. Herein, we evaluated the effects of chlorpyrifos (CPF), one of the most widely used OP insecticides, on human placenta using in vitro and ex vivo exposure models. Villous cytotrophoblast cells isolated from normal human term placentas maintained their cell viability, differentiated into syncytiotrophoblast-like structures, and increased the expression of ß-hCG, ABCG2, and P-gp in the presence of CPF at concentrations of 10 to 100µM. The same doses of CPF induced marked changes in chorionic villi samples. Indeed, CPF exposure increased stroma cell apoptosis, altered villi matrix composition, basement membrane thickness, and trophoblastic layer integrity. Histomorphological and ultrastructural alterations are compatible with those found in placentas where maternal-placenta injury is chronic and able to impair the placental barrier function and nutrient transport from mother to the fetus. Our study shows that placental ex vivo exposure to CPF produces tissue alterations and suggest that human placenta is a potential target of CPF toxicity. In addition, it highlights the importance of using different models to assess the effects of a toxic on human placenta.

Asunto(s)

Cloropirifos/toxicidad , Inhibidores de la Colinesterasa/toxicidad , Vellosidades Coriónicas/efectos de los fármacos , Insecticidas/toxicidad , Trofoblastos/efectos de los fármacos , Subfamilia B de Transportador de Casetes de Unión a ATP/metabolismo , Transportador de Casetes de Unión a ATP, Subfamilia G, Miembro 2/metabolismo , Apoptosis/efectos de los fármacos , Membrana Basal/efectos de los fármacos , Membrana Basal/ultraestructura , Bioensayo , Diferenciación Celular/efectos de los fármacos , Células Cultivadas , Gonadotropina Coriónica Humana de Subunidad beta/metabolismo , Vellosidades Coriónicas/metabolismo , Vellosidades Coriónicas/ultraestructura , Relación Dosis-Respuesta a Droga , Femenino , Humanos , Proteínas de Neoplasias/metabolismo , Embarazo , Reproducibilidad de los Resultados , Medición de Riesgo , Células del Estroma/efectos de los fármacos , Células del Estroma/ultraestructura , Factores de Tiempo , Técnicas de Cultivo de Tejidos , Pruebas de Toxicidad/métodos , Trofoblastos/metabolismo , Trofoblastos/ultraestructura

RESUMEN

PURPOSE: Early pregnancy loss (EPL) affects 50-70% pregnant women in first trimester. The precise molecular mechanisms underlying EPL are far from being fully understood. Therefore, we aim to identify the molecular signaling pathways relating to EPL. EXPERIMENTAL DESIGN: We performed proteomics and bioinformatics analysis of the placental villi in women who have undergone EPL and in normal pregnant women. The proteomics data were validated by Western blot analysis. RESULTS: We identified a total of 5952 proteins in placental villi, of which 588 proteins were differentially expressed in the EPL women. Bioinformatics analysis revealed that these differentially expressed proteins participated in a variety of signaling pathways, including the focal adhesion pathway and ribosome pathway. Moreover, results of the Western blot confirmed that Desmin, Lamin A/C, MMP-9, and histone H4 were upregulated in EPL and the Lamin C/ Lamin A ratio decreased obviously in EPL. These proteins could be associated with the pathophysiology of EPL. The data have been deposited to the ProteomeXchange with identifier PXD002391. CONCLUSION AND CLINICAL RELEVANCE: Our study demonstrated that the focal adhesion pathway and ribosome pathway are involved in EPL, and these findings might contribute to unveil the pathophysiology of EPL.

Asunto(s)

Aborto Espontáneo/diagnóstico , Aborto Espontáneo/genética , Adhesiones Focales/genética , Regulación de la Expresión Génica , Ribosomas/genética , Aborto Espontáneo/metabolismo , Aborto Espontáneo/patología , Adulto , Biomarcadores/metabolismo , Estudios de Casos y Controles , Vellosidades Coriónicas/metabolismo , Vellosidades Coriónicas/patología , Desmina/genética , Desmina/metabolismo , Femenino , Adhesiones Focales/metabolismo , Adhesiones Focales/patología , Perfilación de la Expresión Génica , Histonas/genética , Histonas/metabolismo , Humanos , Lamina Tipo A/genética , Lamina Tipo A/metabolismo , Metaloproteinasa 9 de la Matriz/genética , Metaloproteinasa 9 de la Matriz/metabolismo , Embarazo , Primer Trimestre del Embarazo , Proteómica/métodos , Ribosomas/metabolismo , Ribosomas/patología , Transducción de Señal

RESUMEN

INTRODUCTION: Villitis of unknown etiology (VUE) is associated with fetal growth restriction. However, the underlying mechanisms of villous injury in placentas with VUE are still largely unknown. We aimed to verify whether apoptosis-related factors are increased in VUE placentas. Furthermore, we determined apoptosis of villous cells. METHODS: Six placentas with VUE and 3 control placentas were stained using immunohistochemistry with antibodies for CD3, CD4, CD8, CD68, CD163, perforin, granzyme B, granzyme K, and C5b-9. TUNEL assay analysis was also performed with these placentas. The percentage of cells that stained positive, CD163/CD68 ratio, percentage of C5b-9 positive area, and apoptosis index were quantified and compared between the inflammatory lesions of the VUE placentas, non-VUE inflammatory lesions of the VUE placentas, and control placentas. RESULTS: The percentages of CD3, CD4, CD8 CD68, CD163, perforin, and granzyme B positive cells were significantly higher in the inflammatory lesions of the VUE placentas (p < 0.05). The intravillous CD163/CD68 ratio was higher in the inflammatory lesions compared with the non-inflammatory lesion of the VUE placentas (p < 0.05). The percentage of granzyme K-positive cells was not significantly different between the groups. C5b-9 deposition was higher in the inflammatory lesions of the VUE placentas (p < 0.05). TUNEL-positive cells were significantly higher in the inflammatory lesions of the VUE placentas (p < 0.05). DISCUSSION: To the best of our knowledge, this is the first report to assess villous injury, especially from a viewpoint of villous apoptosis in VUE placentas. An activated perforin/granzyme pathway and C5b-9 are suggested as possible mechanisms of apoptosis.

Asunto(s)

Complejo de Ataque a Membrana del Sistema Complemento/metabolismo , Granzimas/metabolismo , Perforina/metabolismo , Enfermedades Placentarias/metabolismo , Placenta/metabolismo , Adulto , Apoptosis , Estudios de Casos y Controles , Femenino , Humanos , Etiquetado Corte-Fin in Situ , Placenta/patología , Enfermedades Placentarias/patología , Embarazo

RESUMEN

BACKGROUND: Glycosylation is the most common and structurally diverse of all the post-translational modifications of proteins. Lipids and extracellular matrices are also often glycosylated. The mammalian uterus is highly enriched in glycoconjugates that are associated with the apical surfaces of epithelial cells and the secretions released by both epithelial and stromal cells. These glycoconjugates interact primarily with sperm, the implanting embryo, the fetus, and any pathogen that happens to gain entry into the uterus. Secretions of the endometrial glands increase substantially during the luteal phase of the menstrual cycle. These secretions are highly enriched in glycoproteins and mucins that promote specific uterine functions. FINDINGS: Lectins and antibodies have been employed in the majority of the studies focused on uterine glycosylation have employed to define the expression of carbohydrate sequences. However, while these studies provide insight about potential glycosylation, precise information about glycan structure is lacking. Direct sequencing studies that employ biochemical or mass spectrometric methods are far more definitive, but have rarely been employed with uterine glycoproteins. Both lectin/antibody binding and direct carbohydrate sequencing studies that have been focused on the mammalian uterus are reviewed. The primary functional role of the eutherian uterus is to facilitate fertilization and nurture the developing embryo/fetus. Trophoblasts are the primary cells that mediate the binding of the embryo and placenta to the uterine lining. In mammals that utilize hemochorial placentation, they invade the decidua, the specialized endometrial lining that forms during pregnancy. Trophoblasts have also been analyzed for their lectin/antibody binding as a complement to the analysis of the uterine cells and tissues. They will also be reviewed here. CONCLUSIONS: The functional roles of the glycans linked to uterine and trophoblast glycoconjugates remain enigmatic. Another major question in the human is whether defects in placental or uterine glycosylation play a role in the development the Great Obstetrical Syndromes. More recent findings indicate that changes in glycosylation occur in trophoblasts obtained from patients that develop preeclampsia and preterm birth. The functional significance of these changes remain to be defined. Whether such shifts happen during the development of other types of obstetrical syndromes remains to be determined.

RESUMEN

BACKGROUND: Cytogenetic evaluation of products of conception (POC) for chromosomal abnormalities is central to determining the cause of pregnancy loss. We compared the test success rates in various specimen types and the frequencies of chromosomal abnormalities detected by G-banding analysis with those found by Oligo-SNP chromosomal microarray analysis (CMA). We evaluated the benefit of CMA testing in cases of failed culture growth. METHODS: Conventional cytogenetic results of 5457 consecutive POC specimens were reviewed and categorized as placental villi, fetal parts, and unspecified POC tissue. The CMA was performed on 268 cases. Of those, 32 cases had concurrent G-banding results. The remaining 236 cases included 107 cases with culture failure and 129 cases evaluated by CMA alone. RESULTS: The overall POC culture success rate was 75%, with the lowest for fetal parts (37.4%) and the highest for placental villi (81%). The abnormality rate was 58% for placental villi, but only 25% for fetal parts. Of the abnormalities detected, the most common were aneuploidies, including trisomy 16, triploidy, monosomy X, trisomy 22, trisomy 21 and trisomy 15, while the least encountered aneuploidies were trisomy 1, trisomy 19 and monosomies (except monosomy 21). Overall, POC specimens studied by CMA were successful in 89.6% of cases and yielded a 44.6% abnormality rate. CONCLUSIONS: Placental villi yielded higher rates of culture success and a higher percentage of abnormal karyotypes than did other specimen types. The Oligo-SNP CMA method has demonstrated a viable alternative to the G-banding method in view of its advantages in detection of submicroscopic genomic aberrations, shorter turnaround time due to elimination of time required for culture and a higher test success rate.

RESUMEN

Villitis of unknown etiology (VUE) represents a common placental inflammatory lesion, primarily, but not exclusively, identifiable T lymphocytes at term. Despite considerable evidence to contest that this simply represents a benign pathological finding, VUE remains a significantly undervalued diagnosis. Given its association with adverse pregnancy outcomes; including fetal growth restriction, preterm birth, and recurrent pregnancy loss, an increased awareness amongst clinician obstetricians is certainly warranted. The underlying immunopathogenesis of VUE remains uncertain. Despite initial theories that this represents an infectious placental lesion of undiagnosed pathogenic source, a more complex sequence of events involving the "breakdown" of maternal-fetal tolerance is emerging. Characterization of a unique inflammatory phenomenon in which both maternal and fetal T lymphocytes and Höfbauer cells interact has captivated particular research interest and has generated analogies to both the problems of allograft rejection and graft-versus-host disease (GvHD). Within the context of VUE, this review evaluates how disruption of the multidimensional immunological mechanisms underlying feto-maternal tolerance may permit abnormal lymphocyte infiltration into placental villi. We shall review the existing evidence for these events in VUE and outline areas of certain future interest.

Asunto(s)

Vellosidades Coriónicas/inmunología , Enfermedades Placentarias/inmunología , Embarazo/inmunología , Linfocitos T/inmunología , Aborto Habitual/inmunología , Vellosidades Coriónicas/patología , Femenino , Retardo del Crecimiento Fetal/patología , Feto/inmunología , Humanos , Tolerancia Inmunológica/inmunología , Intercambio Materno-Fetal/inmunología , Enfermedades Placentarias/patología , Resultado del Embarazo , Nacimiento Prematuro/inmunología , Linfocitos T/patología

RESUMEN

Para evaluar el desarrollo de la vellosidad de anclaje, en desórdenes hipertensivos del embarazo, asociados con desprendimiento prematuro grave de placenta normoinserta (DPGPN), en el laboratorio de microscopía electrónica de la Facultad de Ciencias de la Salud. Universidad de Carabobo se examinaron 20 placentas, 17 con desórdenes hipertensivos y tres de embarazos normales, en el tercer trimestre, aplicándose protocolo con las variables que determinan tipos de vellosidades según su desarrollo y cambios degenerativos encontrados con microscopía de luz. Se encontró 91% de vellosidad troncal, 92% de intermedia madura, 28% de intermedia inmadura, 47% de terminales, 92% con membrana vásculosincitial periférica y 44% de membrana vásculosincitial central y notables cambios degenerativos como cambios fibrinoides en el 100%, igual la necrosis del trofoblasto, 96% de fibrosis estromal, 88% de edema y 74% de hemorragia; además 92% de trombosis, congestión vascular y cambios de la pared del vaso y más de seis vasos en las vellosidades en 52%. El espacio íntervelloso tiene importantes cambios como los depósitos de fibrina en 84%, la trombosis íntervellosa en 76% y los infartos en 56%, estos cambios degenerativos son estadísticamente significativos. Conclusión: un acelerado crecimiento de la vellosidad empotrada en la placa basal o cercana a ella se evidencia en los resultados con simultáneos procesos indicativos de degeneración y desarrollo anormal en un ambiente de daño velloso hipóxico extenso.

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To evaluate the development of placental anchoring villi of the basal plate in hypertensive disorders of pregnancy associated with abruption placentae severe. Twenty placentas were examined. Seventeen patients with hypertensive disorders and three of normal pregnancy during the third trimester of gestation applying a protocol in order to determine types of villi according to their development and degenerative changes found with light microscopy. We found 91% of stem villi, 92% of intermediate mature villi, 28% of intermediate immature villi, 47% of terminal villi, 92% with peripheral and 44% vascular sincitial membrane and 44% central vascular sincitial membrane also remarkable degenerative changes, as fibrinoide deposits and trophoblastic necrosis in 100%, fibrous stroma 96%, edema 88% and hemorrhage 74%; moreover 92% off thrombosis, vascular congestion and changes vessel wall and mayor six vessel in 52%. Intervellous space have important changes as fibrin deposits in 84%, intervellous thrombosis 76% and intervellous attach 56%. All degenerative changes are statistically significant. Conclusion: An accelerated development of placental anchor villi or of other villous types near to basal plate were seen with simultaneous processes indicative of degeneration as extensive hypoxic villous damage and abnormal development.