Rescue by birth: defective placental maturation and late fetal mortality

Stallmach, Thomas; Hebisch, Gundula; Meier, Karin; Dudenhausen, Joachim W.; Vogel, Martin

doi:10.1016/s0029-7844(00)01208-4

Cited by 85 publications

(100 citation statements)

References 17 publications

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“…Areas denuded of epithelial cells also appear within the maternal epithelial lining of the crypts. Placental maturation results in a reduction of the distance between the foetal and maternal blood supplies to meet the growing nutritional demands of the foetus in the last months of pregnancy (Bjö rkman 1954, Bjö rkman & Sollen 1960, Woicke et al 1986, Williams et al 1987, Schoon 1989, Stallmach et al 2001.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of bovine peripartal placentomes: detection of molecular pathways potentially involved in the release of foetal membranes

Streyl¹,

Kenngott²,

Herbach³

et al. 2012

Reproduction

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The mechanisms underlying detachment of foetal membranes after birth in cows are still unclear. To address this problem in a systematic manner, we performed the first holistic transcriptome study of bovine placentomes antepartum (AP; nZ4 cows) and intrapartum (IP; nZ4 cows) using Affymetrix GeneChip Bovine Genome Arrays. Three placentomes were extracted from each cow, and tissue samples from the contact zones of the placentomes (foeto-maternal units) were recovered by systematic random sampling and processed for RNA extraction and for stereological quantification of cellular composition. Statistical analysis of microarray data (false discovery rate 1%) revealed 759 mRNAs with at least twofold higher levels in the samples of the AP group, whereas 514 mRNAs showed higher levels in the IP group. The differentially expressed genes were classified according to biological processes and molecular functions using the Functional Annotation Clustering tool of the DAVID Bioinformatics Resources. Genes with higher mRNA levels in the AP group were nearly completely related to mitotic cell cycle and tissue differentiation. During parturition, a complete shift occurred because the genes with higher mRNA levels in IP were nearly all related to three different physiological processes/complexes: i) apoptosis, ii) degradation of extra cellular matrix and iii) innate immune response, which play a fundamental role in placental detachment. These results are an excellent basis for future studies investigating the molecular basis of retained foetal membranes.

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Section: Introductionmentioning

confidence: 99%

Gene expression profiling of bovine peripartal placentomes: detection of molecular pathways potentially involved in the release of foetal membranes

Streyl¹,

Kenngott²,

Herbach³

et al. 2012

Reproduction

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“…68 Villous hypomaturity is responsible for 22.5% of intrauterine deaths 69 and has a 70-fold increased risk of associated fetal death, with a 10-fold risk for recurrence, compared with baseline. 70 The fetuses die because of hypoxia, 1 but they can be rescued by earlier delivery. 70 There is an association between maternal diabetes mellitus 71 and fetal anomalies 72 and maturation defect placentas, but vasculosyncytial membranes are also decreased in umbilical cord hypercoiling.…”

mentioning

confidence: 99%

“…70 The fetuses die because of hypoxia, 1 but they can be rescued by earlier delivery. 70 There is an association between maternal diabetes mellitus 71 and fetal anomalies 72 and maturation defect placentas, but vasculosyncytial membranes are also decreased in umbilical cord hypercoiling. 73 Diabetes mellitus is a state of chronic oxidative stress, 74 and glycemia appears to have an affect on the capillary, but not the stromal component, of chorionic villi.…”

mentioning

confidence: 99%

Hypoxic Patterns of Placental Injury: A Review

Stanek

2013

Archives of Pathology &Amp; Laboratory Medicine

125

126

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Context.—In utero hypoxia is an important cause of perinatal morbidity and mortality and can be evaluated retrospectively to explain perinatal outcomes, to assess recurrence risk in subsequent pregnancies, and to investigate for medicolegal purposes by identification of many hypoxic placental lesions. Definitions of some placental hypoxic lesions have been applied relatively liberally, and many of them are frequently underreported. Objectives.—To present a comprehensive assessment of the criteria for diagnosing acute and chronic histologic features, patterns, and lesions of placental and fetal hypoxia and to discuss clinicopathologic associations and limitations of the use thereof. The significance of lesions that have been described relatively recently and are not yet widely used, such as laminar necrosis; excessive, extravillous trophoblasts; decidual multinucleate extravillous trophoblasts; and, most important, the patterns of diffuse chronic hypoxic preuterine, uterine, and postuterine placental injury and placental maturation defect, will be discussed. Data Sources.—Literature review. Conclusions.—The placenta does not respond in a single way to hypoxia, and various placental hypoxic features should be explained within a clinical context. Because the placenta has a large reserve capacity, hypoxic lesions may not result in poor fetal condition or outcome. On the other hand, very acute, in utero, hypoxic events, followed by prompt delivery, may not be associated with placental pathology, and many poor perinatal outcomes can be explained by an etiology other than hypoxia. Nevertheless, assessment of placental hypoxic lesions is helpful for retrospective explanations of complications in pregnancy and in medicolegal investigation.

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“…The most common cause is placental dysmaturity or placental maturation defect [24]. Such placentas are of normal size or even large, but with a pale cut surface.…”

Section: Intrauterine Death Near Termmentioning

confidence: 99%

“…About 5% of unselected placentas examined without indication reveal this pattern, and, up to now, there is no clue as to its cause. Although only 2% of fetuses with a dysmature placenta will actually die, this risk is 70-fold that of a fetus with a normal placenta [24]. A mother who has lost a child due to placental dysmaturity has a tenfold higher risk of recurrence compared with baseline.…”

Section: Intrauterine Death Near Termmentioning

confidence: 99%

Placental pathology: its impact on explaining prenatal and perinatal death

Stallmach

Hebisch

2003

Virchows Archiv

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This review considers six main situations in which pathologists are expected to report and interpret placental messages for obstetricians, neonatologists and, indirectly, parents: (1) abortion is the body's corrective response to the embryonic defect suggested by malformed chorionic villi; (2) infection causing chorionic villous inflammation is specific and haematogenous; pathogen identification is mandatory, in contrast to chorioamnionitis caused by increased local immunosuppression allowing indiscriminate bacterial entry; (3) prematurity and (4) intrauterine growth restriction are often associated with pregnancy-specific disease (pre-eclampsia) or preexisting maternal conditions (systemic lupus); parental studies may improve outcome in subsequent pregnancies; (5) intrauterine death near term is often due to placental dysmaturity featuring a severely reduced number of syncytiocapillary membranes; it accounts for the death in utero of 3 in 1000 pregnancies; detection helps to minimise recurrence in subsequent pregnancies; (6) twins are best confirmed as monozygous by the absence of chorionic tissue in the dividing membranes; most monochorionic twins have vascular connections whose detailed analysis is requested only if there are inter-twin differences in growth and colour. From a formal point of view, many more bits of pathology than discussed in this review can be found in placentas and, with the advances in ultrasonography, might even be seen prior to birth. The extent of such a disturbance might ultimately affect fetal growth, which is amenable to prenatal detection offering the chances for an appropriate management. In contrast, dysmaturity is a great challenge as no predictive tests are as yet available.

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Rescue by birth: defective placental maturation and late fetal mortality

Abstract: Placental maturation defect can be a cause of fetal hypoxia. Although the risk of stillbirth is 70-fold that of a normal placenta, few affected fetuses actually die. The risk of recurrent stillbirth is tenfold above baseline and occurs mostly after 35 weeks' gestation.

Cited by 85 publications

References 17 publications

Gene expression profiling of bovine peripartal placentomes: detection of molecular pathways potentially involved in the release of foetal membranes

Gene expression profiling of bovine peripartal placentomes: detection of molecular pathways potentially involved in the release of foetal membranes

Hypoxic Patterns of Placental Injury: A Review

Placental pathology: its impact on explaining prenatal and perinatal death

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