Vasculogenesis in complete and partial hydatidiform mole pregnancies studied with CD34 immunohistochemistry.

BACKGROUND

Defective chorionic villous vascularization is present in pregnancies complicated by absent or abnormal embryonic development. The aim of this study was to investigate the embryonic and/or maternal genomic influence on vasculogenesis in diploid complete hydatidiform mole (CHM) and in triploid partial hydatidiform mole (PHM) in comparison with normal development.

METHODS

Mean villous stromal area and functional vascular area, vessels with a lumen and haemangiogenetic cords, peripherally or centrally located were measured and counted in chorionic villi of 12 CHM, 12 normal pregnancies (termination of pregnancy, TOP) and 15 PHM of which nine were without an embryo (PHM-E) and six were with an embryo (PHM + E), using quantitative CD34 immunohistochemistry.

RESULTS

TOP showed significantly more vessels per chorionic villus, centrally and peripherally located (median, range), than CHM, PHM-E and PHM + E (4.0, 0-9 versus 0.0, 0-11, 0.0, 0-18 and 1.0, 0-21). CHM showed significantly more centrally located cords than PHM-E, PHM + E and TOP (1.5, 0-22 versus 1.0, 0-15, 0.5, 0-8 and 1.0, 0-2).

CONCLUSIONS

Initiation of chorionic villous vasculogenesis is independent of the maternal genome (CHM). The development of an embryo, however, is obligatory for the modulation of normal vascularization resulting in a well developed vasculosyncytial membrane.