Molecular Changes on Maternal–Fetal Interface in Placental Abruption—A Systematic Review

Abstract

Placental abruption is the separation of the placenta from the lining of the uterus before childbirth. It is an infrequent perinatal complication with serious after-effects and a marked risk of maternal and fetal mortality. Despite the fact that numerous placental abruption risk factors are known, the pathophysiology of this issue is multifactorial and not entirely clear. The aim of this review was to examine the current state of knowledge concerning the molecular changes on the maternal–fetal interface occurring in placental abruption. Only original research articles describing studies published in English until the 15 March 2021 were considered eligible. Reviews, book chapters, case studies, conference papers and opinions were excluded. The systematic literature search of PubMed/MEDLINE and Scopus databases identified 708 articles, 22 of which were analyzed. The available evidence indicates that the disruption of the immunological processes on the maternal–fetal interface plays a crucial role in the pathophysiology of placental abruption. The features of chronic non-infectious inflammation and augmented immunological cytotoxic response were found to be present in placental abruption samples in the reviewed studies. Various molecules participate in this process, with only a few being examined. More advanced research is needed to fully explain this complicated process.

The potential value of pre-delivery hematologic index in patients with placental abruption and perinatal outcomes

“…Recently immerging data is also demonstrating the link between the in ammatory markers NLR value is higher in preeclampsia patients especially in severe preeclampsia [9]. Molecular Changes on maternal fetal Interface manifested an increased risk of abruption in cases of placental in ammatory lesions, which suggests that the pathophysiologic and etiologic basis for placental abruption is a chronic in ammatory processes [24]. Klement AH Including 11,415 patients described that NLR and PLR values were signi cantly different in the 1 st, 2nd, and 3rd trimesters in a cohort of pregnant women [25],in contrast, Liad Alfandari have demonstrated that predicting values of NLR and PLR were not signi cantly different compare the placental abruption to the control group before 20th weeks of pregnancy [26].…”

Interferon epsilon and preterm birth subtypes; a new piece of the type I interferon puzzle during pregnancy?

“…These conditions share similar biological pathways with spontaneous preterm birth, such as disruption of pro-and anti-inflammatory cytokine balance and localized changes to the function of neutrophils, macrophages, T-cells, regulatory T-cells, and Bcells at the maternal-fetal interface. [9][10][11][12] Indeed, both sterile inflammation and infectious inflammation (due to polymicrobial bacterial infection) are major contributors to preterm births. [12][13][14] However, the field lacks a complete understanding of the biological pathways that explain these observations.…”

“…[9][10][11][12] Indeed, both sterile inflammation and infectious inflammation (due to polymicrobial bacterial infection) are major contributors to preterm births. [12][13][14] However, the field lacks a complete understanding of the biological pathways that explain these observations. 3 Additionally, treatments including antibiotics, tocolytics, and progesterone supplementation have been implemented with limited success.…”

“…Preeclampsia is a leading cause of maternal mortality and affects 3%–10% of pregnancies worldwide, 6 while IUGR and placental abruption affect 8% 7 and 1% 8 of pregnancies, respectively. These conditions share similar biological pathways with spontaneous preterm birth, such as disruption of pro‐ and anti‐inflammatory cytokine balance and localized changes to the function of neutrophils, macrophages, T‐cells, regulatory T‐cells, and B‐cells at the maternal‐fetal interface 9–12 . Indeed, both sterile inflammation and infectious inflammation (due to polymicrobial bacterial infection) are major contributors to preterm births 12–14 .…”

Reproductive Immunology and Pregnancy

“…The exact etiology of placental abruption—a relatively rare, yet severe, complication of pregnancy with partial or complete placental detachment before the birth of the fetus—is unknown [ 20 ]. A systematic review of the original papers on molecular changes in the maternal–fetal interface coexisting with placental abruption was carried out by Bączkowska et al, 2021 [ 21 ]. Consistently reported chronic noninfectious inflammation and excessive cytotoxic response within the placental tissue may indicate that the disruption of the immunological processes is an important etiological factor in this obstetrical complication.…”