Chronic inflammatory lesions of the placenta are characterized by the infiltration of the organ by lymphocytes, plasma cells and/or macrophages, and may result from infections (viral, bacterial, parasitic) or be of immune origin (maternal anti-fetal rejection). The three major lesions are villitis (when the inflammatory process affects the villous tree), chronic chorioamnionitis (which affects the chorioamniotic membranes), and chronic deciduitis (which involves the decidua basalis). Maternal cellular invasion is a common feature of the lesions.
Villitis of unknown etiology (VUE) is a destructive villous inflammatory lesion characterized by the infiltration of maternal T cells (CD8+ cytotoxic T cells) into chorionic villi. Migration of maternal T cells into the villi is driven by the production of T cell chemokines in the affected villi. Activation of macrophages in the villi has been implicated in the destruction of the villous architecture. VUE has been reported in association with preterm and term fetal growth restriction, preeclampsia, fetal death and preterm labor. Infants whose placentas have VUE are at risk for death and abnormal neurodevelopmental outcome at the age of 2.
Chronic chorioamnionitis is the most common lesion in late spontaneous preterm birth and is characterized by the infiltration of maternal CD8+ T cells into the chorioamniotic membranes. These cytotoxic T cells can induce trophoblast apoptosis and damage the fetal membranes. The lesion is frequently accompanied by villitis of unknown etiology and evidence of maternal anti-fetal antibodies and deposition of complement in the umbilical vein. Chronic deciduitis consists of the presence of lymphocytes or plasma cells in the basal plate of the placenta. This lesion is more common in pregnancies resulting from egg donation and has been reported in a subset of patients with premature labor. Chronic placental inflammatory lesions are now considered to represent maternal anti-fetal rejection and this process can be associated with the development of a novel form of fetal systemic inflammatory response syndrome characterized by an elevation of the fetal plasma T cell chemokine (CXCL10).
The evidence that maternal anti-fetal rejection may underlie the pathogenesis of many chronic inflammatory lesions of the placenta is reviewed. This article includes figures and histologic examples of all chronic inflammatory lesions of the placenta.