IFPA Meeting 2010 Workshops Report II: Placental pathology; Trophoblast invasion; Fetal sex; Parasites and the placenta; Decidua and embryonic or fetal loss; Trophoblast differentiation and syncytialisation

Abstract

Workshops are an important part of the IFPA annual meeting. At IFPA Meeting 2010 diverse topics were discussed in twelve themed workshops, six of which are summarized in this report. 1. The placental pathology workshop focused on clinical correlates of placenta accreta/percreta. 2. Mechanisms of regulation of trophoblast invasion and spiral artery remodeling were discussed in the trophoblast invasion workshop. 3. The fetal sex and intrauterine stress workshop explored recent work on placental sex differences and discussed them in the context of whether boys live dangerously in the womb.4. The workshop on parasites addressed inflammatory responses as a sign of interaction between placental tissue and parasites. 5. The decidua and embryonic/fetal loss workshop focused on key regulatory mediators in the decidua, embryo and fetus and how alterations in expression may contribute to different diseases and adverse conditions of pregnancy. 6. The trophoblast differentiation and syncytialisation workshop addressed the regulation of villous cytotrophoblast differentiation and how variations may lead to placental dysfunction and pregnancy complications

Mechanism of Congenital Chagas Disease: Effective Infection Depends on the Interplay Between Trypanosoma cruzi and the Different Tissue Compartments in the Chorionic Villi of the Human Placenta

“…Although parasite antigens can be visualized in the villous stroma, the typical amastigote nests are not present (Duaso et al, 2011b). In accordance with these results, in ex vivo infected placental explants although parasite antigens and DNA can be detected (Al Khan et al, 2011;Duaso et al, 2010;Luján et al, 2004), amastigote nests are not observed. Only few individual parasites can be detected.…”

Decreased oxidative stress may contribute to the disease process in placenta accreta

“…Placental angiogenesis and trophoblastic invasion are balanced during pregnancy. On the other hand, deterioration of the balance between angiogenic and antiangiogenic factors and also an imbalance between proinvasive and antiinvasive factors might cause abnormal uteroplacental vascularization and subsequently abnormal placental invasion (4).…”

Decreased placental and maternal serum TRAIL-R2 levels are associated with placenta accreta

“…An imbalance within these well-designed processes may cause inadequate or excessive trophoblastic invasion leading to many pregnancy associated disorders. The most common examined risk factor of abnormal placental invasion is the disturbance of the fine balance between the pro-and anti-invasive factors at the placentation site [1,2]. Previous reports indicated that the most important risk factor for placenta accreta is placenta previa in the presence of an uterine scar, and the remaining risk factors reported are multiparity, maternal age, any prior uterine surgery or curettage, uterine irradiation, endometrial ablation, Asherman syndrome or other uterine anomalies [1].…”

“…Previous reports indicated that the most important risk factor for placenta accreta is placenta previa in the presence of an uterine scar, and the remaining risk factors reported are multiparity, maternal age, any prior uterine surgery or curettage, uterine irradiation, endometrial ablation, Asherman syndrome or other uterine anomalies [1]. When all these associated risk factors are considered, it is clear that the common feature is the disruption of the fetalematernal interface by the alterations in the local microenvironment [2]. Because abnormal placental invasion is commonly located in the area of the previous hysterotomy, and because the incidence of placenta accreta appears to be increasing parallel to the increasing number of cesarean deliveries, the scarring of the uterine wall, particularly by previous cesarean deliveries, is hypothesized as the most important risk factor leading to placental hyperinvasiveness [1,2].…”

“…When all these associated risk factors are considered, it is clear that the common feature is the disruption of the fetalematernal interface by the alterations in the local microenvironment [2]. Because abnormal placental invasion is commonly located in the area of the previous hysterotomy, and because the incidence of placenta accreta appears to be increasing parallel to the increasing number of cesarean deliveries, the scarring of the uterine wall, particularly by previous cesarean deliveries, is hypothesized as the most important risk factor leading to placental hyperinvasiveness [1,2].…”