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Prolonged pregnancy describes a pregnancy that progresses beyond 42 weeks (294 days). The aetiology of prolonged pregnancy is incompletely understood, although factors such as advanced maternal age and obesity increase the risk of prolonged pregnancy. Prolonged pregnancy is associated with an increased incidence of perinatal mortality; in particular, the incidence of stillbirth increases from 39 weeks onwards, with a significant increase beyond 41 weeks’ gestation. The biological explanation for this has yet to be confirmed. Placental ageing has been proposed as a possible mechanism. As the placenta is responsible for the nutrient and energy demands of the fetus, which are considerable in late pregnancy, a decrease in its ability to function may provide an explanation for the increasing perinatal mortality rate seen in prolonged pregnancy.

Here we review evidence for ageing processes occurring in the placenta. A number of biomarkers of ageing are seen within the placenta as gestation progresses. These include evidence of increased apoptosis, senescence, autophagy, and oxidative stress in trophoblast, the primary functional cell in the placenta, in prolonged pregnancy. As these processes play a key role in the ageing process of other tissues, the accumulation of these markers here is consistent with placental ageing. In addition, there are morphological changes in trophoblast in prolonged pregnancy which suggest impaired mitochondrial and placental function. The findings summarised in this review illustrate the growing evidence of both structural and biochemical features of ageing shown in placentas of prolonged pregnancy, providing insight into underlying mechanisms which may initially be adaptation to in utero stress, but later develop to become pathological. Future work is needed to determine whether these changes impact upon placental function and whether placental biomarkers could be used as a surveillance tool in prolonged pregnancy.