Villegas H, González-Jiménez M A, Paredes-vivas Y, Aguilera-Suárez G, Karchmer S
Departmento de Microscopía Electrónica, Instituto National de Perinatología, México, D.F.
Ginecol Obstet Mex. 1996 Aug;64:368-76.
A villitis is a focal or multifocal inflammatory reaction of chorionic villi with infiltration of mononuclear cells and usually is associated with fibrinoid necrosis. The aetiology of villitis could be a transplacental infection of the fetus, especially with virus (VIV), in normal placentae however, the presence of villitis is referred as villitis of unknown ethiology (VED). This study was designed to characterize villitis lesions of 11 placentae, four VIV and seven VED, ultrastructural descriptive comparisons of both types of villitis are discussed. Biopsies were processed with the conventional optic and electronic microscopy techniques. Our ultrastructural observations confirmed the presence of virus in four placentae whereas no virus or bacteria were found in seven placentae. Microvilli were absent or markedly diminished, this finding was associated to the presence of fibrinoid necrosis in the stroma and clinically to intrauterine growth retardation, 4 preterm pregnancies and one obitus. Trophoblast alterations were found in both types of villitis, basal membrane thickness, is some cases associated to electrodense material similar to calcium deposites, vascuolization and the presence of edema in the stroma was observed. In some cases we noted the presence of focal fibrin deposits associated to necrosis zones in the stroma, calcium precipitates and mielinic bodies. Fetal vessels obliteration and intravascular thrombi were found in the syncitiotrophoblast placentae with viral particles CMV or rubivirus associated to an increment in Hofbauer cells and basal membrane calcifications. From our ultrastructural observations, we conclude that both types of villitis are associated to a typic immunologic reaction that induce lose of trophoblast microvilli, mononuclear infiltration and edema. This placental alterations reduce dramatically the maternofetal exchange of gases, nutrients and other active peptides and could be the cause of fetal growth retardation, inmadurity or death.