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Histological Aspects of the Feto-placental Interface in

Diabetes Mellitus

the Gestational

Rodica Ilie 1, C. Ilie 2, Florina Capitan 2, Alexandra Nyiredi 2, Ileana Enatescu 2

1 Emergency Childrens Hospital, Louis urcanu, Timisoara, Romania
2 Victor Babes University of Medicine and Pharmacy, Timisoara, Romania

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.) Massons Trichrome (M.Tr.) and Van Gieson(V.G.). The
histological study was centered upon: FPI, the trophoblast, villous stroma and fetal capillaries. The statistical 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 .

Fig.1 - H.E., V.G., M.Tr., x20 Discontinuities of syncitiotrophoblast layer

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.3 - H.E., V.G., M.Tr., x20, 40 - Perivillous and intervillous fibrosis, in clusters

Fig.6 - H.E., M.Tr., x40,100 - Erythroblasts, intra- and

extracapilar in terminal immature villi, sludge.

Fig.4 - H.E., x40 - Trophoblast agglutination

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):3543.