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Updated: Feb 16, 2026

Human Placental and Decidual Organ Cultures to Study Infections at the Maternal-fetal Interface
Published on: July 21, 2016
Placental Dysfunction as a Key Element in the Pathogenesis of Preeclampsia
1Department of Obstetrics and Gynaecology, Inselspital, Bern University Hospital, Bern, Switzerland, Institute of Biochemistry and Molecular Medicine, University of Bern, Bern, Switzerland.
Abstract:
Placental pathology is associated with major pregnancy disorders and the concept of the Great Placental Syndromes encompasses disorders of placentation, such as preeclampsia with and without fetal growth restriction, preterm labor, preterm premature rupture of membranes, late spontaneous abortion, and placental abruption. Preeclampsia is divided between the early and late onset variety and placental dysfunction is a central feature in the pathogenesis of both. In the early onset type, syncytiotrophoblastic stress seems to be related to an inherent defect of the trophoblast. Vascular protection of early placental development is replaced by vascular dysfunction. In late onset preeclampsia, maternal factors, such as genotypic predisposition to endothelial disease, and an impairment of antioxidant defence with a limited capacity of the maternal clearing system to cope with the increasing charge of apoptotic cell debris, are at the center of pathogenesis. Syncytiotrophoblastic stress in late pregnancy has been related to molecular senescence and late onset preeclampsia may be viewed as an exaggeration of normal placental ageing.
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