The risk of stillbirth increases exponentially across gestation per 1000 continuing pregnancies. Stillbirth is also increased in the setting of fetal growth retardation. Data suggests that this late gestational increase in risk of stillbirth may relate to aging of the placenta and associated oxidative damage. For each tissue a balance between energy invested in tissue function and in tissue repair must be optimised. Aging related damage may occur by the expression of genes which permit damage which will only affect a small proportion of the population. In the setting of the placenta the majority of pregnancies will have delivered by 40 completed weeks (95%). Therefore if oxidative and other damage occurs to the placenta after 40 weeks only a small number of pregnancies will be affected (<5%) and genes that are associated with such aging will be retained within to species gene pool. Our data on maternal hormonal changes, placental aging pathways and using placental cell lines support this model of placental aging.

In women who have gone beyond 40 weeks of gestation we note a decline in trajectories of placental hormones. In post dates placentas we note shortening of telomers, a decline in binding of SIRT 6 to subtelomeric regions of chromosomes and an increase in lysosomal activity. In placental cell lines deprived of growth factors we observe similar changes in SIRT 6 binding. These data are consistent with the hypothesis that post dates placentas exhibit an aging phenotype that is associated with inpaired function that may contribute to the aetiology of stillbirth.