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The Role of Mesenchymal Stem Cells in the Functions and Pathologies of the Human Placenta
Published in Ornella Parolini, Antonietta Silini, Placenta, 2016
Gina Diamanta Kusuma, Padma Murthi, Bill Kalionis
The presence of a vascularized allogeneic placenta, the developing fetus, and its membranes in the maternal uterus poses significant challenges for the maternal and fetal immune systems. Pathologies associated with immune response or inflammatory lesions include chorioamnionitis, chronic intervillositis, and chronic deciduitis. The term chorioamnionitis refers to acute inflammation of the placental membranes (amnion and chorion) and is a leading cause of maternal and fetal complications, including preterm birth and neonatal infection (Romero et al. 2002; Ogunyemi et al. 2003). The inflammatory process is generally regarded as a continuum. During the early stage, the neutrophils involved in this inflammatory response are usually maternal (migrating from intervillous sac, decidual vessels, or both) in origin. During later stages, fetal neutrophils (migrating from fetal surface vessels of the chorionic plate or umbilical cord) are involved. Chronic intervillositis is characterized by an intervillous infiltrate of mononuclear cells (monocytes, lymphocytes, and histiocytes) of maternal origin, and the infiltration is frequently associated with either villous or intervillous fibrinoid deposition (Contro et al. 2010). Chronic deciduitis is characterized by abundant lymphocyte infiltration within the decidua (Khong et al. 2000).
Association of Placental Pathologic Findings with the Severity of Necrotizing Enterocolitis in Preterm infants – A Matched Case-Control Study
Published in Fetal and Pediatric Pathology, 2023
Parvesh Mohan Garg, Jaslyn L. Paschal, Md Abu Yusuf Ansari, Lauren Billington, Jennifer Ware, Kristin Adams, Youssef Al Hamda, Adebamike Oshunbade, Charles R. Rosenfeld, Imran N. Mir
Based on the Amsterdam Placental Workshop Group Consensus Statement recommendations, the histopathologic abnormalities assessed were divided into the following subcategories [12]. Acute histologic chorioamnionitis with or without fetal inflammatory response [14].Chronic villitis with or without obliterative fetal vasculopathy.Maternal vascular malperfusion (MVM) including maternal vascular lesions (decidual arteriopathy, mural hypertrophy, incomplete transformation of spiral arteries, and decidual necrosis), infarcts, hemorrhage or hematoma, thrombi, villous changes (chorangiosis, syncytial knots, distal villous hypoplasia, and accelerated villous maturation), and placental hypoplasia [15–17].Fetal vascular malperfusion (FVM).Other inflammatory lesions (chronic deciduitis with plasma cells, massive chronic intervillositis, perivillous fibrin, and histiocystic intervillositis), delayed villous maturation, and villous edema [18].
Combined Placental Maternal Floor Infarction and Cytomegalovirus Placentitis: A Case Report
Published in Fetal and Pediatric Pathology, 2022
Mana Taweevisit, Montakarn Tansatit, Piriya Sutthiruangwong, Noppachai Siranart, Paul Scott Thorner
The placenta had a 3-vessel umbilical cord and weighed 150 g (10th–25th percentile). The maternal surface showed a firm, yellow-white zone with focal extension into the placental substance (Fig. 1A). Histologic examination showed the features of MFI with eosinophilic fibrinoid material obliterating the intervillous space and encasing chorionic villi (Fig. 1B). Extravillous trophoblasts were occasionally seen within the fibrinoid material. Villous capillaries showed involution, with persistence of villous stromal cells and hemosiderin deposition. There was also chronic deciduitis and an extensive proliferative villitis with necrosis (Fig. 1C). Isolated CMV-infected cells were identified within villi (Fig. 1D). The inflammatory infiltrate consisted of T-lymphocytes and histiocytes with occasional B-lymphocytes, as identified by CD3, CD68 and CD20 immunostaining, respectively. CD4 and CD8 immunostaining showed an overwhelming predominance of CD8-positive T cells, although the most common inflammatory cells were macrophages (Fig. 2). Plasma cells were not identified by light microscopy nor by immunostaining for CD138.
Histopathology of Third Trimester Placenta from SARS-CoV-2-Positive Women
Published in Fetal and Pediatric Pathology, 2022
Mai He, Priya Skaria, Kasey Kreutz, Ling Chen, Ian S. Hagemann, Ebony B. Carter, Indira U. Mysorekar, D. Michael Nelson, John Pfeifer, Louis P. Dehner
Placentas from SARS-CoV-2-positive women did not demonstrate specific pathology or pathological pattern. There were no significant differences in individual or group histopathological features between the study and control groups. In the study group, ten of 21 placentas (47.6%) had features of maternal vascular malperfusion (MVM) which was not significantly different from the four of 20 placentas (20%) with MVM in the control group. Between the study and control groups, there were ten of 21 (47.6%) placentas in the study group with any features of fetal vascular malperfusion (FVM), not significantly different from the eight of 20 control placentas (40%) with FVM features. There were two of 21 study group and three of 20 control placentas with a maternal inflammatory response, and two of 21 study group, and four of 20 control placentas with a fetal inflammatory response. Each of the two groups had one placenta with villitis of unknown etiology (VUE) and four placentas with chronic deciduitis with plasma cells. A single placenta, in the study group, exhibited T/eosinophilic vasculitis. None of these pathologies were found to be more frequent in our group of COVID-19 test-positive patients. There were no differences in abnormal cord insertion or cord coiling between the two groups, nor any differences in chorioamnion pathology.