Abstract
The human placenta is crucial for prenatal development and good pregnancy outcome. Maternal diabetic disorder influences normal intrauterine development of individual and expresses itself in the placenta. Due to the progress in diagnostic methods and methods of metabolic compensation the macroscopic signs associated with maternal diabetes, e.g., placentomegaly, occur nowadays rarely. In the microscopic picture of placenta there are no structural differences specific for maternal diabetes. However, the application of quantitative morphological methods has revealed some differences of normal and diabetic placenta. Stereological studies have shown significantly higher total volume of peripheral villi that distorts shapes and dimensions of pores in the intervillous space, and larger surface areas of peripheral villi and villous capillaries. Methods of confocal microscopy and 3D reconstruction gave the evidence that the fetus reacts on the hypoxia in maternal diabetic environment by enhanced angiogenesis and branching of villous capillaries. The enhanced tissue volumes are conditioned by higher mitotic activity. However, it decreases the proliferative potential of cells taking part in the enlargement of key structures for maternofetal transport at the end of pregnancy. Syncytiotrophoblast produces many factors playing important roles in maternal and fetal regulation and in the placenta itself. Quantitative methods of catalytic histochemistry and immunocytochemistry pointed at the role of maternal diabetes in decreased synthesis of some of those factors (e.g., alkaline phosphatase, SP1 glycoprotein). The presented data show that the quantitative morphological methods contribute to better understanding of the influence of maternal diabetes on fetoplacental unit.