Chronic Deciduitis Research Articles

Chronic Inflammatory Placental Lesions Correlate With Bronchopulmonary Dysplasia Severity in Extremely Preterm Infants.

Correlation of BPD with placental pathology is important for clarification of the multifactorial pathogenesis of BPD; however, previous reports have yielded varying results. We report placental findings in no/mild BPD compared to moderate/severe BPD, and with and without pulmonary hypertension (PH). Eligible infants were 230/7-276/7 weeks gestational age. BPD was defined by the need for oxygen at ≥28 days with severity based on need for respiratory support at ≥36 weeks. Acute and chronic inflammatory placental lesions and lesions of maternal and fetal vascular malperfusion were examined. Of 246 eligible infants, 146 (59%) developed moderate/severe BPD. Thirty-four (23%) infants developed PH, all but 1 being in the moderate/severe BPD group. Chronic deciduitis (32% vs 16%, P = .003), chronic chorioamnionitis (23% vs 12%, P = .014), and ≥ 2 chronic inflammatory lesions (13% vs 3%, P = .007) were more frequent in the moderate/severe BPD group. Development of PH was associated with placental villous lesions of maternal vascular malperfusion (30% vs 15%, P = .047). The association of chronic inflammatory placental lesions with BPD severity has not been previously reported. This supports the injury responsible for BPD as beginning before birth in some neonates, possibly related to cytokines associated with these chronic inflammatory lesions.

Placenta histopathology in SARS-CoV-2 infection: analysis of a consecutive series and comparison with control cohorts

Infection by SARS-CoV-2 has been shown to involve a wide range of organs and tissues, leading to a kaleidoscope of clinical conditions. Within this spectrum, an involvement of the fetal-maternal unit could be expected, but, so far, the histopathological evaluation of placentas delivered by women with SARS-CoV-2 infection did not show distinct hallmarks. A consecutive series of 11 placentas, delivered by 10 women with COVID-19 admitted to our Obstetrics and Gynecology clinic have been investigated and compared to a control cohort of 58 pre-COVID-19 placentas and 28 placentas delivered by women who had a previous cesarean section. Four out of eleven placentas showed changes consistent with chronic villitis/villitis of unknown etiology (VUE), while in one case, chronic histiocytic intervillositis was diagnosed. Thrombo-hemorrhagic alterations were observed in a subset of cases. Compared to the control cohort, chronic villitis/VUE (p < 0.001), chronic deciduitis (p = 0.023), microvascular thrombosis (p = 0.003), presence of infarction areas (p = 0.047) and of accelerated villous maturation (p = 0.005) showed higher frequencies in placentas delivered by women with COVID-19. Chronic villitis/VUE (p = 0.003) and accelerated villous maturation (p = 0.019) remained statistically significant by restricting the analysis to placentas delivered after a previous cesarean section. The observed differences in terms of pathological findings could be consistent with SARS-CoV-2 pathogenesis, but just a subset of alterations remained statistically significant after adjusting for a previous cesarean section. A careful consideration of potential confounders is warranted in future studies exploring the relationship between COVID-19 and pregnancy.

470 Pregnancy outcomes and placental-histopathology in pregnancies complicated by preeclampsia in different maternal BMI groups

We aimed to investigate pregnancy outcomes in correlation with placental histopathology in pregnancies complicated by preeclampsia - stratified by three different maternal body mass index (BMI) groups. Medical records and placental pathological reports of all pregnancies complicated by preeclampsia between 2008-2019 in a single tertiary center were reviewed. Preeclampsia was diagnosed according to the current ACOG guidelines. The study population was divided into 3 groups according to maternal pre-gestational BMI: Underweight group (UWG) - BMI < 22 kg/m2 Normal weight group (NWG) – 22 kg/m2 ≤ BMI ≤ 28 kg/m2 Over-weight group (OWG) - BMI > 28kg/m2 Data regarding maternal characteristics, neonatal outcomes, and placental histopathological lesions were compared between the groups. Adverse neonatal outcome was defined as ≥ 1 early neonatal complication. Placental pathology was classified by the current "Amsterdam" criteria. Maternal age was more advanced in the NWG (n=98) and OWG (n=98) compared to the UWG (n=99). The rates of diabetes (8% vs. 12% vs. 31%) as well as chronic hypertension (8% vs. 14% vs. 23%), and Cesarean deliveries (64% vs. 75% vs. 78%) increased with the increase of BMI, while concurrent fetal growth restriction < 10th percentile decreased with the increase of BMI (24% vs. 17% vs. 12%). In placental pathology- placental weight < 10th centile decreased with the increase of BMI (36% vs 29% vs. 20%). Both Maternal vascular malperfusion (MVM) lesion and chronic deciduitis (CD) were more prevalent in both the UWG and OWG, compared to the NWG (76% vs. 74% vs. 56%, and 4% vs. 6% vs. 0%, respectively). The groups did not differ in the rates of severe features, gestational age at delivery, and neonatal outcomes. In pregnancies complicated by preeclampsia, BMI correlated with background morbidities and the rate of Cesarean deliveries. Interestingly - in placental pathology, both the UWG and the OWG were associated with higher rates of both MVM and CD, compared to the NWG suggesting that in both BMI extremes placental pathology is more pronounced.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Maternal-Fetal Inflammation in the Placenta and the Developmental Origins of Health and Disease.

Events in fetal life impact long-term health outcomes. The placenta is the first organ to form and is the site of juxtaposition between the maternal and fetal circulations. Most diseases of pregnancy are caused by, impact, or are reflected in the placenta. The purpose of this review is to describe the main inflammatory processes in the placenta, discuss their immunology, and relate their short- and long-term disease associations. Acute placental inflammation (API), including maternal and fetal inflammatory responses corresponds to the clinical diagnosis of chorioamnionitis and is associated with respiratory and neurodevelopmental diseases. The chronic placental inflammatory pathologies (CPI), include chronic villitis of unknown etiology, chronic deciduitis, chronic chorionitis, eosinophilic T-cell vasculitis, and chronic histiocytic intervillositis. These diseases are less-well studied, but have complex immunology and show mechanistic impacts on the fetal immune system. Overall, much work remains to be done in describing the long-term impacts of placental inflammation on offspring health.

Brief Report: Chronic Placental Inflammation Among Women Living With HIV in Uganda.

HIV-exposed, uninfected (HEU) children have poorer early-life outcomes than HIV-unexposed children. The determinants of adverse health outcomes among HEU children are poorly understood but may result from chronic placental inflammation (CPI). We enrolled 176 pregnant women living with HIV (WLWH) taking antiretroviral therapy in southwestern Uganda and 176 HIV-uninfected women to compare CPI prevalence by maternal HIV serostatus. Placentas were evaluated histologically by an expert pathologist for presence of CPI, defined as chronic chorioamnionitis, plasma cell deciduitis, villitis of unknown etiology, or chronic histiocytic intervillositis. Placentas with CPI were additionally immunostained with CD3 (T cell), CD20 (B cell), and CD68 (macrophage) markers to characterize inflammatory cell profiles. WLWH and HIV-uninfected women had similar age, parity, and gestational age. Among WLWH, the mean CD4 count was 480 cells/µL, and 74% had an undetectable HIV viral load. We detected CPI in 16 (9%) placentas from WLWH and 24 (14%) from HIV-uninfected women (P = 0.18). Among WLWH, CPI was not associated with the CD4 count or HIV viral load. Villitis of unknown etiology was twice as common among HIV-uninfected women than WLWH (10 vs. 5%, P = 0.04). Among placentas with CPI, more villous inflammatory cells stained for CD3 or CD68 among HIV-uninfected women than WLWH (79% vs. 46%, P = 0.07). CPI prevalence did not differ by HIV serostatus. T-cell (CD3) and macrophage (CD68) markers were more prevalent in placental inflammatory cells from HIV-uninfected women. Our results do not support CPI as a leading mechanism for poor outcomes among HEU children in the antiretroviral therapy era.

Relationship of chronic endometritis with chronic deciduitis in cases of miscarriage

BackgroundThe presence of chronic deciduitis (CD) was determined in patients diagnosed with or without chronic endometritis (CE) before pregnancy.ObjectiveTo study the effect of CE on decidua in cases of miscarriage.MethodsDecidual tissue was obtained from the patients who miscarried at the first pregnancy within a year after the diagnosis of the presence or absence of CE. The number and distribution pattern of plasma cells stained with CD138 in decidual tissue in 10 high-power fields (HPFs) was examined. The prevalence of CD diagnosed with four different grade; grade 0, no plasma cell in 10 HPFs, thus Non-CD;grade 1, rare single plasma cells; grade 2, rare clusters or more than 5 single cells total; and grade 3, many plasma cells with more than 5 clusters, were examined and compared between Non-CE and CE.ResultsThe incidence rate of CD of grade2 + 3 was significantly higher in CE than Non-CE (53.8%; 7/13 vs. 0%; 0/13, P < 0.01). Presence of clusters or a number of plasma cells in 10 HPFs of decidua showed a sensitivity of 53.8%, a specificity of 100%, a positive predictive value of 100%, and a negative predictive value of 68.4% for the diagnosis of CE.ConclusionPresence of clusters of plasma cells or five or more of plasma cells in decidua was found in more than half of CE, but not found in Non-CE. When CD with cluster or five or more of plasma cells is confirmed histologically in miscarriage decidual tissue, the presence of CE before the pregnancy should be suspected.

Placentas From Women of Advanced Maternal Age.

The percentage of pregnant women with advanced maternal age (AMA) has increased during the past several decades due to various socioeconomic factors and advances in assisted reproduction. These pregnancies are associated with adverse maternal and fetal outcomes. However, the underlying placental pathology has not been well described. To investigate the placental histopathology associated with AMA pregnancies. Placental pathology from 168 AMA women 35 years or older at delivery was reviewed. The cases were subdivided into 2 age subgroups, ages 35 to 39 and 40 or older, as well as a "pure AMA" subgroup where the only indication for placental examination was AMA. A group of 60 consecutive non-AMA placentas was also identified and used as comparison. The spectrum of histologic features in each case was catalogued. Of the overall AMA cases, meconium deposition was seen in 55% (93 of 168), chorangiosis in 40% (68 of 168), and acute chorioamnionitis in 36% (60 of 168). Fetal vascular malperfusion was also seen with high frequency (30%; 50 of 168). Two histologic alterations found to be significantly different between the 35 to 39 and greater than 40 age subgroups were fetal vascular malperfusion (11% [7 of 65] versus 42% [43 of 103]; P = .001) and delayed villous maturation (1.5% [1 of 65] versus 13% [13 of 103]; P = .02). The pure AMA subgroup showed no statistically significant differences compared with the overall AMA group. Chronic deciduitis was the only statistically significant difference between the overall AMA group and the non-AMA comparison group (14% [23 of 168] versus 30% [18 of 60]; P = .02). Our findings, particularly the high frequency of fetal vascular malperfusion, suggest that AMA should be an independent indication for placental pathologic examination.

Villitis of unknown etiology and chronic deciduitis are not associated with human papilloma virus and enterovirus infection.

Villitis of unknown etiology (VUE) and chronic deciduitis with plasma cells (CD) are supposed to be non infectious placental lesions caused by a pathologic immune reaction similar to a host versus graft mechanism. In some investigations, infection of human trophoblastic cells with human papilloma virus (HPV) has been described, and a relationship with miscarriage, preeclampsia, and chronic inflammatory placental lesions has been suspected. Infection with enterovirus, especially Coxsackievirus, has been observed in cases with spontaneous abortion and adverse perinatal outcome, respectively. We investigated 20 cases with VUE and 30 cases with chronic deciduitis with plasma cells. The placenta specimens were analyzed for expression of HPV capsid protein by immunohistochemistry, for presence of HPV DNA via polymerase chain reaction (PCR), and for presence of enterovirus mRNA using RT-PCR, respectively. VUE was associated with maternal diseases: atopic lesions in 21%, other autoimmune diseases in 15.5%, and obesity in 31.5%, respectively. Birth weight below the 10th percentile was detected in 63% of the cases with VUE. Chronic deciduitis was associated with preterm labor and preterm premature rupture of membranes (26%). Intrauterine fetal demise occurred in 5 cases with CD (18.5%). HPV DNA, HPV capsid protein, and enterovirus mRNA were not detected in all investigated VUE or CD cases. Our investigations show that a causal role for enterovirus and human papilloma virus in the development of VUE and CD is unlikely. Therefore, HPV vaccination is unlikely to reduce the incidence of VUE and CD in the future.

The histologic evolution of revealed, acute abruptions

There is considerable interest in using pathology to confirm acute abruptions. It has been suggested that pathologic findings can help to determine the timing of abruptions. Because of the dearth of evidence in the literature supporting this claim and its medicolegal implications, we undertook this study to explore further the possibility of timing abruptions by histopathology. We sought to correlate bleeding interval (duration from maternal presentation with vaginal bleeding [revealed abruption] to placental delivery) with placental histopathologic findings. We performed a retrospective review of clinical data and placental pathology from all cases of clinically diagnosed, acute, revealed abruptions at a single, large institution in New England between 2000 and 2015. Cases were identified based on clinical diagnoses, bleeding intervals were calculated from clinical notes, and histologic evaluations were performed by 2 pathologists blinded to the bleeding intervals. A total of 177 cases were analyzed. Of these, 103 (58%) had histologic findings corroborating the clinical diagnosis of abruption. The most frequent finding was maternal surface indentation (51 cases) followed by intravillous hemorrhage (50 cases). The former was also the earliest finding, with a minimum bleeding interval of 4 minutes. In multivariate modeling, plasma cell deciduitis was significantly associated with a longer bleeding interval (median 63 hours). If there were 2 pathologic findings, there was a trend toward a longer bleeding interval. There was modest sensitivity for the pathologic diagnosis of acute revealed abruption. Although there was not a clear, stepwise progression of histologic lesions; the presence of 2 or more findings tended to be seen with longer bleeding intervals. Our results suggest that histologic findings cannot be used to time acute revealed abruptions reliably, and any interpretation of such should be made with caution.

Placental Lesions in Meconium Aspiration Syndrome

BackgroundMeconium aspiration syndrome (MAS) is defined by respiratory distress requiring supplemental oxygen in a meconium-stained neonate. MAS is clinically subclassified as mild, moderate, and severe according to the oxygen requirement. The aims of this study were to compare the histological findings in the placentas of MAS neonates with those of meconium-stained but non-MAS neonates and to analyze the correlation between the severity of MAS and the grade of its histological parameters.MethodsWe collected 160 singleton term placentas from neonates with meconium staining at birth from a tertiary medical center, Seoul, Republic of Korea. We reviewed hematoxylin and eosin sections of tissue samples (full-thickness placental disc, chorioamniotic membranes, and umbilical cord).ResultsFunisitis was present more frequently in MAS than in non-MAS (p < .01), of which the stage was correlated with the severity of MAS (p < .001). The histological findings consistent with maternal underperfusion and chronic deciduitis were more frequent in MAS than in non-MAS (p < .05). There was a correlation between the degree of chorionic vascular muscle necrosis and the severity of MAS (p < .05).ConclusionsOur results suggest that fetal inflammatory response evidenced by funisitis occurs prenatally in MAS and that the stage of funisitis and of chorionic vascular muscle necrosis may be a predictive marker of the severity of MAS.

Placental Pathologic Associations With Morbidly Adherent Placenta: Potential Insights Into Pathogenesis.

Background The pathology that underlies morbidly adherent placenta (MAP) is poorly understood. The objective of this study was to describe the placental pathology, especially implantation site pathology, associated with MAP. Methods This was a single institution, retrospective case-control study design examining placentas of patients who delivered between January 2008 and September 2013. MAP cases were defined by the need for clinical intervention at delivery beyond spontaneous placental delivery or simple manual extraction of the placenta. Controls consisted of patients with placentas sent for examination due to a history of maternal malignancy with no clinical suspicion of accreta. Placental pathologic findings of maternal vascular underperfusion (MVU), acute inflammation, chronic inflammation, fetal vascular obstruction, and hemorrhage were recorded and compared using bivariable and multivariable analyses. Results Three categories of pathologic changes were seen more commonly in MAP placentas (N = 101) than control placentas (N = 110): chronic basal inflammation, villous changes of MVU, and retromembranous and subchorionic/intervillous hemorrhage. In multivariable analyses adjusted for confounders, basal chronic villitis (aOR 5.6, 1.73-18.18), plasma cell deciduitis (aOR 2.63, 1.08-6.39), increased syncytial knots (aOR 3.92, 1.57-9.75), villous agglutination (aOR 24.85, 2.78-221.75), increased perivillous fibrin (aOR 5.08, 1.49-17.34), and the presence of subchorionic/intervillous thrombi (aOR 4.01, 1.63-9.86) remained associated with MAP. Conclusions MAP is highly associated with evidence of intraparenchymal placental hemorrhage, villous changes of MVU, and a lymphoplasmacytic infiltrate at the implantation site. The contribution of this basal chronic inflammatory infiltrate to MAP requires further investigation.

Chorionic Histiocytic Hyperplasia is Associated With Chronic Inflammatory Lesions in the Placenta.

Background Chorionic histiocytic hyperplasia (CHH) is a cellular proliferation at the base of the chorion that was identified by the authors in examining placentas for chronic chorioamnionitis (CC). This study is a retrospective review of cases diagnosed with CHH, describing its incidence alone and with associated lesions, and the immunophenotype of lesional cells. Design In this retrospective study, a laboratory information system search over a 34-month period using the key phrase "chorionic stromal" was performed. Cases identified were reviewed for presence of the following: CC, chronic villitis (CV), chronic deciduitis (CD), maternal (MIR), and fetal (FIR) acute inflammatory responses, meconium deposition; and whether CD3 immunostaining was performed. Incidences were tabulated and compared with known prevalences in our population. Select cases were stained with various immunostains to identify cell lineage and X and Y fluorescent probes to identify fetal or maternal cell origin in cases with male infants. Results Eighty cases of CHH were identified during the study period. Incidences of inflammatory lesions associated with CHH were: CV (54/80, 68%), CD (32/80, 40%), CC (25/80, 31%), MIR (39/80, 49%), and FIR (9/80, 11%). Only chronic inflammatory lesions had a significant correlation with the co-incidence of CHH. CC was identified alongside CHH in 12 of 22 cases in which a CD3 immunostain was performed. The cell population in CHH was vimentin+, CD68+, CD3-, CD45-, CD56-, hPL-, SMA-, OCT 3/4- and, in some cases, variably mixed with CD3+ lymphocytes. The cells had a male genotype by fluorescent in situ hybridization analysis. Conclusion The association of CHH with acute and chronic inflammatory conditions and its immunophenotype suggest that it may be a reactive process. CD3 immunostaining is helpful to identify concurrent CC.

Decidual arteriolopathy with or without associated hypertension modifies the underlying histomorphology in placentas from diabetic mothers.

The aim of this study was to retrospectively document the impact of hypertensive conditions in pregnancy and decidual arteriolopathy on the patterns of placental injury in maternal diabetes mellitus (MDM). Among all 5248 > 20 weeks' placentas, the frequencies of 19 selected clinical and 24 placental phenotypes were compared between 287 MDM placentas and 4961 remaining placentas (control group [CG]) before and after further exclusion of 85 and 611 patients with hypertensive conditions (gestational hypertension, pre-eclampsia, chronic hypertension). Cesarean section rate, heavy placentas, decidual arteriolopathy, microscopic chorionic pseudocysts, and chorangiosis were more common in MDM than in the CG both before and after exclusion of hypertensive conditions. The frequencies of preuterine patterns of chronic hypoxic placental injury and plasma cell deciduitis became statistically significant only after exclusion of hypertensive conditions. Hypertensive conditions of pregnancy may obscure the underlying preuterine placental hypoxic pattern in MDM placentas. Even in normotensive patients, decidual arteriolopathy, and shallow placental implantation significantly impact placental histomorphology in MDM.

Placental histological lesions in fetal and neonatal alloimmune thrombocytopenia: A retrospective cohort study of 21 cases

BackgroundAlloimmunization against human platelet antigens (HPAs) can occur prenatally and induce fetal/neonatal alloimmune thrombocytopenia (FNAIT). The aim of this study was to identify placental histological features associated with platelet alloimmunization and their clinical significance. MethodsThis study examined 21 placentas from FNAIT-affected pregnancies and 42 age-matched control cases, all collected from pathology departments in the Rhône-Alpes region. Clinical and laboratory findings were collected for each FNAIT case. Two pathologists reviewed the placental slides of each FNAIT and control case. Histological features, with special emphasis on chronic inflammatory lesions, were evaluated. Differences between the two groups were calculated with odds ratios (ORs) and assessed with Wald's chi-square. ResultsFNAIT was associated with a significantly higher frequency of chronic chorioamnionitis (CC) (OR 14, 95%CI 1.7–113.8), basal chronic villitis (BCV) (OR 17, 95%CI 2–145.6) and chronic intervillositis (CIV). Chronic villitis (CV) (OR 3.7, 95%CI 0.9–15.2) and chronic deciduitis (CD) (OR 4.7, 95%CI 0.79–28.2) were also more frequent in the FNAIT than the control group, but these differences were not statistically significant. ConclusionsFNAIT is significantly associated with CC, BCV, and CIV. This chronic inflammatory reaction is preferentially localized on the maternofetal interface. Anti-HPA alloimmunization may trigger an immunological conflict similar to graft-versus-host disease.

Placental Pathologic Associations with Morbidly Adherent Placenta: Potential insights into Pathogenesis

The pathology that underlies morbidly adherent placenta (MAP) is poorly understood. The objective of this study was to describe the placental pathology, especially implantation site pathology, associated with MAP. This was a single institution, retrospective case-control study design examining placentas of patients who delivered between January 2008 and September 2013. MAP cases were defined by the need for clinical intervention at delivery beyond spontaneous placental delivery or simple manual extraction of the placenta. Controls consisted of patients with placentas sent for examination due to a history of maternal malignancy with no clinical suspicion of accreta. Placental pathologic findings of maternal vascular underperfusion (MVU), acute inflammation, chronic inflammation, fetal vascular obstruction and hemorrhage were recorded and compared using bivariable and multivariable analyses. Three categories of pathologic changes were seen more commonly in MAP placentas (N=101) than control placentas (N=110): chronic basal inflammation, villous changes of MVU and retromembranous and retromembranous/intervillous hemorrhage. In multivariable analyses adjusted for confounders, chronic basal villitis (aOR 5.6, 1.73-18.18), plasma cell deciduitis (aOR 2.63, 1.08-6.39), increased syncytial knots (aOR 3.92, 1.57-9.75), villous agglutination (aOR 24.85, 2.78-221.75), increased perivillous fibrin (aOR 5.08, 1.49-17.34), and the presence of subchorionic/intervillous thrombi (aOR 4.01, 1.63-9.86) remained associated with MAP. MAP is highly associated with evidence of intraparenchymal placental hemorrhage villous changes of MVU, and a lymphoplasmacytic infiltrate at the implantation site. The contribution of this basal chronic inflammatory infiltrate to MAP requires further investigation.

Pathoanatomical and clinical aspects of the placenta in preterm birth

Prematurely born children show a clearly elevated risk for perinatal morbidity, long-term pediatric morbidities and development of chronic diseases in adulthood compared to babies born at term. The pathoanatomical investigation of placentas from preterm births is useful for assessing the etiology, the risk of recurrence and the prognosis for the child. The focus is on presenting the clinical and pathoanatomical characteristics of acute chorioamnionitis as a frequent cause of preterm induction of labor and pregnancy-induced hypertension, in particular preeclampsia as a frequent reason for elective cesarean section. Other lesions, sometimes of unclear etiology associated with preterm birth and substantially elevated risk of recurrence are reviewed. The clinical correlations and therapeutic options of the various diseases are discussed taking the risk of recurrence into consideration. Examination of placentas, association with the clinical course and a literature search. Acute chorioamnionitis and omphalovasculitis can be histologically subdivided into different stages which correlate with the clinical severity and the prognosis for the newborn child. Chronic deciduitis, chronic chorioamnionitis, villitis of unknown etiology, massive perivillous fibrin deposition and chronic histiocytic intervillositis are entities of unclear etiology associated with recurrent abortion and preterm birth. Autoimmune diseases and thrombophilia are occasionally associated with these pathologically defined lesions. Pregnancy-associated hypertensive disease and particularly preeclampsia as the cause of intrauterine developmental delay and elective cesarean section often show characteristic pathoanatomical placental lesions, which can give indications for the severity and duration of the disease and the prognosis for the child. Early onset (<34 weeks of gestation) and late onset preeclampsia show clinical and morphological differences. Subsequent pregnancies are classified as being at risk and screening for preeclampsia should be clinically performed.

Chronic Placental Inflammation in Twin Pregnancies.

Background:Chronic placental inflammation, such as villitis of unknown etiology (VUE) and chronic chorioamnionitis (CCA), is considered a placental manifestation of maternal anti-fetal rejection. The aim of this study is to investigate its frequency in twin pregnancies compared to singleton pregnancies.Methods:Three hundred twin placentas and 1,270 singleton placentas were consecutively collected at a tertiary medical center in Seoul, Republic of Korea from 2009 to 2012. Hematoxylin and eosin sections of tissue samples (full-thickness placental disc and chorioamniotic membranes) were reviewed.Results:Non-basal VUE was more frequent in twin placentas than in singleton placentas (6.0% vs 3.2%, p < .05). In preterm birth, CCA was found less frequently in twin placentas than in singleton placentas (9.6% vs 14.8%, p < .05), reaching its peak at an earlier gestational age in twin placentas (29–32 weeks) than in singleton placentas (33–36 weeks). CCA was more frequent in twin pregnancies with babies of a different sex than with those with the same sex (13.8% vs 6.9%, p=.052). Separate dichorionic diamniotic twin placentas were affected by chronic deciduitis more frequently than singleton placentas (16.9% vs 9.7%, p<.05).Conclusions:The higher frequency of non-basal VUE in twin placentas and of CCA in twin placentas with different fetal sex supports the hypothesis that the underlying pathophysiological mechanism is maternal anti-fetal rejection related to increased fetal antigens in twin pregnancies. The peak of CCA at an earlier gestational age in twin placentas than in singleton placentas suggests that CCA is influenced by placental maturation.

Overlap Chronic Placental Inflammation Is Associated with a Unique Gene Expression Pattern.

Breakdown of the balance between maternal pro- and anti-inflammatory pathways is thought to allow an anti-fetal maternal immune response that underlies development of chronic placental inflammation. Chronic placental inflammation is manifested by the influx of maternal inflammatory cells, including lymphocytes, histiocytes, and plasma cells, into the placental membranes, villi, and decidua. These infiltrates are recognized pathologically as chronic chorioamnionitis, chronic villitis of unknown etiology, and chronic deciduitis. Each of these histological entities is associated with adverse fetal outcomes including intrauterine growth restriction and preterm birth. Studying the gene expression patterns in chronically inflamed placenta, particularly when overlapping histologies are present, may lead to a better understanding of the underlying mechanism(s). Therefore, this study compared tissue with and without chronic placental inflammation, manifested as overlapping chronic chorioamnionitis, chronic villitis of unknown etiology, and chronic deciduitis. RNA expression profiling was conducted on formalin fixed, paraffin embedded placental tissue using Illumina microarrays. IGJ was the most significant differentially expressed gene identified and had increased expression in the inflamed tissue. In addition, IGLL1, CXCL13, CD27, CXCL9, ICOS, and KLRC1 had increased expression in the inflamed placental samples. These differentially expressed genes are associated with T follicular helper cells, natural killer cells, and B cells. Furthermore, these genes differ from those typically associated with the individual components of chronic placental inflammation, such as chronic villitis, suggesting that the inflammatory infiltrate associated with overlapping chronic chorioamnionitis, chronic villitis of unknown etiology, and chronic deciduitis differs is unique. To further explore and validate gene expression findings, we conducted immunohistochemical assessment of protein level expression and demonstrate that IgJ expression was largely attributable to the presence of plasma cells as part of chronic deciduitis and that IgA positive plasma cells are associated with chronic deciduitis occurring in combination with chronic chorioamnionitis and chronic villitis of unknown etiology but not with isolated chronic deciduitis.

Chronic deciduitis is underdiagnosed in the setting of acute chorioamnionitis: results of a departmental audit in a tertiary obstetric hospital

The poorly understood entity of chronic deciduitis is regarded as uncommon, and little literature exists regarding its significance or incidence. We determined to examine the incidence of chronic deciduitis, based on the agreed definition of decidual plasma cells, in the setting of acute chorioamnionitis in a series of placental specimens: and to determine the inter-observer reliability between pathologists and trainees at all levels of training in the diagnosis of chronic deciduitis. Ninety placentas with acute chorioamnionitis were reviewed by three pathologists and three registrars for the presence of chronic deciduitis. The criteria for analysis of deciduitis included the presence and pattern of distribution of plasma cells within the decidua basalis and decidua parietalis. Our preliminary results show a much higher rate of chronic deciduitis than initially reported, particularly involving the decidua basalis, detected by both pathologists and registrars. Chronic deciduitis is underdiagnosed at our institution. The lack of recognition of chronic deciduitis impairs attempts to determine its clinical significance in the setting of co-existing acute chorioamnionitis.

Chronic inflammatory lesions of the placenta

The chronic inflammatory lesions of the placenta often run in the shadows of the better-known acute inflammatory processes of the placenta, such as acute chorioamnionitis and acute funisitis. A heterogeneous population of T-cell lymphocytes, plasma cells, and macrophages is the primary player in chronic villitis, chronic chorioamnionitis, chronic deciduitis, and chronic intervillositis, and eosinophils are an added component of eosinophilic/T-cell chorionic vasculitis. The histologic appearance, sites of occurrence in the placenta, and pathogeneses of these entities are reviewed.