IUGR involves the poor growth of the foetus, stillbirth, miscarriage, and premature delivery.

Roughly 80% of the VUE cases are in term placentas (greater than 37 weeks of pregnancy).

In the third trimester, syncytial knots (nucleated clusters formed in the syncytiotrophoblast) break off [4] and are shed from the foetal placental villi.

The barrier could breakdown either by upstream foetal thrombosis or ischemic damage from maternal infarction.

The necrosis of syncytiotrophoblasts could arise as a result of the activation of coagulation components, complement system or platelets by antibodies or antiphospholipids.

[6] Maternal lymphocytes can enter the foetal stroma by passing the villous trophoblastic barrier via the anchoring villi.

The trafficking of maternal lymphocytes responding to an antigen in the chronic deciduitis could activate and enter via the decidua.

[11] Foetal macrophages in VUE proliferate and are activated as a result of the up-regulation of MHC class 2 antigen expression.

[12][13][14] Examination of a male placenta with VUE demonstrated that 11.2% of the intravillous CD3+ lymphocytes were foetal, and 88.8% were maternal.

[1] The composition of inflammatory infiltrate in VUE on a cellular level is primarily macrophages and lymphocytes.

Class 2 major histocompatibility complex (MHC) antigens on macrophages are up-regulated at sites of VUE.

Infectious villitis involves a greater part of the placenta (umbilical cord, chorionic plate, membranes) compared to VUE (terminal and stem villi).

[1] There are no known prevention methods for VUE, but it is predicted that it could be due to infection by Treponema pallidum, Toxoplasma gondi, and cytomegalovirus.

Obese women are more likely to develop VUE; this could be due to obese women having larger placentas, thus having a greater number of villous macrophages which could increase the efficiency of antigen presentation resulting in VUE.