Confined placental mosaicism and intrauterine fetal growth.

Fetal growth is a complex and dynamic process regulated by a large number of interactive factors of fetal, maternal, and placental origin. As a result, any abnormality of fetal growth has a complex multifactorial pathogenesis. It has been estimated that about 50% of intrauterine fetal growth is determined by fetal genes. Maternal disease, her nutritional intake and behaviours, such as smoking, also influence fetal growth. The placenta develops to its full size during the second trimester, to facilitate the fetal growth acceleration after 20 weeks of gestation. An abnormal pattern of placental growth earlier in gestation may result in abnormal fetal growth in the late second or third trimesters. A recently described genetic condition, confined placental mosaicism (CPM), has been shown to cause clinically significant intrauterine growth restriction (IUGR) or even intrauterine fetal death. CPM is the most common form of constitutional chromosomal mosaicism which is defined as at least two cell lines with diVerent chromosomal complements in a fetoplacental unit derived from a single zygote. In CPM only the placenta is aVected unlike in generalised chromosomal mosaicism where both the fetus and the placenta are involved. Since the first report associating CPM with idiopathic IUGR in 1983, our understanding of its prevalence and origin, as well as its specific eVect on fetal growth, has increased exponentially.