Placenta accreta is the major cause of
maternal death complicated by massive peripartum
hemorrhage. Its development is traditionally considered to be related to a decidual defect caused by previous cesarean deliveries or uterine
curettages. Usually, placental villi firmly adhere to the superficial myometrium and deeply invade, or even penetrate, the uterine wall. Abnormal uteroplacental neovascularization is another characteristic. Therefore, we hypothesized that
placenta accreta develops as a result of abnormal expressions of growth-, angiogenesis- and invasion-related factors in trophoblast populations. We have found, in pregnancies complicated by
placenta accreta: upregulated
epidermal growth factor receptor and downregulated c-erbB-2
oncoprotein in syncytiotrophoblasts; downregulated vasculoendothelial
growth factor receptor-2 expression in syncytiotrophoblasts and increased vasculoendothelial
growth factor in placental lysates; and downregulated Tie-2 expression in syncytiotrophoblasts and enhanced
angiopoietin-2 level in placental lysates. However,
matrix metalloproteinase expression was not upregulated, so the association of these invasion-related molecules with
placenta accreta is less likely. Taken together, these findings imply that complex factors, either alone or in combination, might be responsible for the development of
placenta accreta. Further studies are needed to understand the signaling pathways and possible genetic events.