1. Background and aims - We studied the Feto-placental interface (FPI), in the Gestational Diabetes Mellitus (GDM), to present his specific structural modifications and his cellular injuries. Method - 30 placentas, obtained after delivery from pregnant mothers with GDM and normal pregnancies. The samples of the two equal groups, collected by 5 sections, were specifically prepared using three types of histological stains: Hematoxylin-Eosin,(H.E.) Masson’s Trichrome (M.Tr.) and Van Gieson(V.G.). The histological study was centered upon: FPI, the trophoblast, villous stroma and fetal capillaries. The statis- tical results of the data were performed using SPSS 17.0. Results -Through optical microscopy were identified different degrees of following lesions of the FPI (Table I): hyperplasia of the syncytiotrophoblast (Fig.1), villous edema and frequent Hofbauer cells in stromal chan- nels (Fig.2), perivillous and intervillous fibrosis, in clusters of fibrinoid (Fig.3), large number of syncytial knots by trophoblast agglutination - bud, node and bridge(Fig.4), chorangiosis(Fig.5), erythroblasts, intra- and extra-capilar in terminal immature villi (Fig.6), thickened of the basement membrane of FPI. Histological Aspects of the Feto-placental Interface in the Gestational Diabetes Mellitus Rodica Ilie 1, C. Ilie 2, Florina Capitan 2, Alexandra Nyiredi 2, Ileana Enatescu 2 1 Emergency Children’s Hospital, Louis Ţurcanu, Timisoara, Romania 2 Victor Babes University of Medicine and Pharmacy, Timisoara, Romania 1 Emergency Children’s Hospital, Louis Ţurcanu, Timisoara, Romania 2 Victor Babes University of Medicine and Pharmacy, Timisoara, Romania Fig.1 - H.E., V.G., M.Tr., x20 – Discontinuities of syncitiotrophoblast layer Table 1 – Microscopical lesions of the FPI Table 1 – Microscopical lesions of the FPI Fig.2 - H.E., V.G., M.Tr., x20, 40 - Edema and Hofbauer cells in stromal channels Fig.4 - H.E., x40 - Trophoblast agglutination Fig.6 Fig.6 - H.E., M.Tr., x40,100 - Erythroblasts, intra- and extracapilar in terminal immature villi, sludge. Fig.3 - H.E., V.G., M.Tr., x20, 40 - Perivillous and intervillous fibrosis, in clusters Fig.5- V.G., x40 - Chorangiosis Conclusions - Histological changes in the FPI in GDM are factors contributing to the fetal anoxia with impact on placental vascular permeability, angiogenesis and trophoblastic syncytial changes. We believe them the causes of the placental abnormalities and complications (miscarriage, stillbirth, macrosomia, and congenital anomalies). References – (1) Desoye G, Hauguel-De Mouzon S, The Human Placenta in Gestational Diabetes Mellitus, Diabetes Care, 2007 july; 30 (suppl 2) : 120-126; (2) Kingdom J, Huppertz B, Seaward G, Kaufmann P. Development of the placental villous tree and its consequences for fetal growth. Eur J Obstet Gynecol Reprod Biol. 2000; 92 (1):35–43.