İmmunohistochemical and ultratructural examination between inflammatory and angiogenetic relation at the umblical cord-placenta junction in severe and non-severe preeclampsia patients

Aim: Aim of this study was to investigate relationship between inflammation, apoptosis and angiogenetic relation on umblical cord-placenta junction of placentas of severe and non-severe preeclamptic patients. Materials and Methods: Experimental group of 20 severe and 20 non-severe preeclamptic and 20 normotensive patients' placentas were dissected for paraffin-wax processing. Histochemically, Hematoxylin-Eosin and Masson trichrome staining; immunohistochemically TNF, Endothelin-1 and Bax immunostaining were performed. Tissues were ultrastructurally analyzed by electron microscopy and micrographed. Results: Due to preeclampsia, an increase in fibrin accumulation in chorionic villi, enlargement in syncytial nodes, edema and hyalinized structures in the connective tissue area around stem villi, hypertrophy in decidual cells in the congestion areas, degeneration and apoptotic changes in decidual cells in severe preeclampsia were observed. With respect to severity of preeclampsia, ET-1 expression in the vascular endothelial cells of the maternal surface and vessels in chorion villi showed a positive reaction. In severe preeclampsia, TNF-α levels were increased in the inflammatory cells around the vessels in maternal-fetal interface and in decidual macrophages. With respect to severity of preeclampsia, increased Bax expression was found in the decidua cells in maternal side and trophoblast cells with stem villus. In ultrastructurally severe preeclampsia, pyknotic decidual cell nuclei and diffused chromatin distribution, excessive expansion of endoplasmic reticulum cisterns and degenerative mitochondria were seen. Conclusion: Depending on the severity of preeclampsia; as hypoxia increases, changes in inflammatory, trophoblast, decidual and endothelial cells were thought to affect the maternal and fetal development by increasing placental dysfunction and cell death.