Bone metabolism in the fetus and neonate

Abstract

During embryonic development most of the skeleton begins as a cartilaginous scaffold that is progressively resorbed and replaced by bone. Such endochondral bone development does not cease until the growth plates fuse during puberty. Growth and mineralization of the skeleton are dependent upon the adequate delivery of mineral. During fetal development, the placenta actively transports calcium, magnesium and phosphorus from the maternal circulation. After birth, the role of mineral transport is assumed by the intestines. The limited data currently available on fetal humans are largely based on cord blood samples from normal fetuses and pathological specimens from fetuses which died in utero or at birth. Consequently, much of our understanding of the regulation of fetal mineral and bone homeostasis comes from the study of animal fetuses that have been manipulated surgically, pharmacologically and genetically. Animal and human data indicate that fetal mineral homeostasis requires parathyroid hormone (PTH) and PTH-related protein-but not vitamin D/calcitriol, calcitonin or sex steroids. In the days to weeks after birth, intestinal calcium absorption becomes an active process, which necessitates that the infant depends upon vitamin D/calcitriol. However, even this postnatal function of calcitriol can be bypassed by increasing the calcium content of the diet or by administering calcium infusions.