Defect of Pericyte Recruitment Can Induce Villous Hydropic Change in Complete Hydatidiform Moles
K-R Kim, T-J Kwon, JS Song, S-A Kim, SJ Robboy. University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea; National Institute of Scientific Investigation, Seoul, Republic of Korea; Duke University Medical Center, Durham, NC
Background: Why villi become hydropic in complete hydatidiform mole (CHM) is poorly understood. Most stromal blood vessels in early gestational moles are immature, lacking distinct vascular lumina and hematopoietic components, similar to the angiogenic cell cords in the normal vasculogenetic stage of early placental development (gestational weeks 5-6). Although the histologic features of the immature villous stromal vessels resemble those of normally developing placenta, the villous stroma of early moles is more frequently hydropic, raising the suspicion that leakage or permeability through the immature vessel wall is increased in early moles. We thought that a defect of pericyte recruitment around the immature blood vessels can be one possible cause of the villous hydropic change in CHMs.
Design: The structure of stromal vessels in 20 early CHMs were compared to immature stromal vessels in 61 normally developing placentas (gestational weeks 4-9) using immunohistochemical pericyte markers (a-smooth muscle actin, desmin, PDGF-b), Electron-microscopic examination was performed in 5 CHMs to examine if there is any defect of pericyte recruitment around the blood vessels in CHMs.
Results: PDGF-b was normally expressed in trophoblastic layers, villous stroma, angiogenic cell cords and mature stromal vessels both in normal placentas (from late week 5) and early moles. In normal placentas, a-smooth muscle actin was expressed only in the chorionic plate at week 4, but then gradually spread through the villous branches to form a reticular network in the villous stroma during weeks 5-8, and became accentuated around the blood vessels after week 7. In contrast, a-smooth muscle actin expression in the villous stroma was significantly decreased in the early moles, and perivascular cuffing was found only in a single instance. Desmin was not expressed around the stromal vessels both in normal placenta and CHMs.Ultrastructurally, molar immature vessels consisted of endothelial cells linearly arranged without pericyte attachment.
Conclusions: Pericyte recruitment around immature stromal vessels is defective in early moles, which may induce increased vascular leakage, and thus an important cause of villous hydropic change.
Category: Gynecologic & Obstetrics
Tuesday, March 23, 2010 1:00 PM
Poster Session IV # 129, Tuesday Afternoon