**4. Placenta as a casualty and not the cause**

*Prediction of Maternal and Fetal Syndrome of Preeclampsia*

tangential sectioning of highly branched fetal villi.

cleavage of syncytial cytoskeleton may be defective [17, 18].

**3.3 Wavelike apoptotic shedding**

**3.4 Arrested apoptotic shedding**

**3.5 Aponecrotic shedding**

**3.6 Necrotic shedding**

eclampsia [17, 18].

and plasma membrane had local defects.

totic shedding and pathological necrotic shedding.

identified [17, 18].

bridges between the neighboring villi that look like drumstick or mushroomlike projections containing normally structured nuclei. These are artifacts caused by

In cases of placentas of fetal growth restricted with absent diastolic flow, there is a large decrease in the number of cytotrophoblastic cells, and the thickness of syncytiotrophoblast is also less [19]. The nuclei in syncytiotrophoblast accumulate like a ring around the vertical axis of villi. The underlying pathology is yet to be

Apoptotic syncytial nuclei accumulate in knot-like structures but do not get extruded into the intervillous space. This is also seen in the cases of fetal growth restriction with absent diastolic flow. At some places the sites with nuclei are even larger than the cross section of villi from which they arise. It is seen that a large number of these giant knots form all over the placenta. In these cases the apoptotic

Aponecrosis is a term used when signs of apoptotic trophoblast turnover and shedding are associated with signs of syncytial necrosis. Apoptosis continues with damaged plasma membranes, water influx and secondary hydropic changes of cellular structures, and release of cytoplasmic contents. This process is also called as secondary necrosis. Since apoptosis is a programmed cell death depending on cell energy, lack of cell energy reserves could be the cause of aponecrosis. These villous explants contain cell-free DNA, cell-free actin, and membrane-wrapped nuclei. In some studies in preeclampsia, the villous explants that had the packaged nuclei showed early signs of chromatin condensation, but the cytoplasm was edematous

In pure necrotic shedding, the villous explants contain edematous nuclei in a hydropic cytoplasm with membrane defects. Placentas from severe preeclampsia and severe Rh incompatibility have shown features of necrotic shedding. The complete absence of chromatin condensation showed that the apoptotic pathway was blocked by inhibitory proteins and never restarted. In an experiment on pregnant guinea pigs, complete blockage of energy metabolism of trophoblast was done by monoiodine acetate or sodium fluoride (inhibitors of glycolysis). Continuous release of necrotic villous explants leads to the features of pre-

If cytotrophoblast keeps growing and accumulating as syncytiotrophoblast and does not shed, it will lead to intrasyncytial accumulation of old and aged trophoblastic components which finally necrose. Cytoplasmic blebbing of syncytium with nuclear and cytoplasmic edema is a hallmark feature of necrotic shedding. Though there are phenotypic similarities among different types of villous explants, there are differences in modes of nuclear chromatin aggregation, nuclear or cytosolic edema. Cracks in the plasma membrane help to differentiate between physiological apop-

**12**
