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Updated: May 12, 2026
Culturing and Measuring Fetal and Newborn Murine Long Bones
Published on: April 26, 2019
Bone metabolism in the fetus and neonate
1Faculty of Medicine, Memorial University of Newfoundland, Health Sciences Centre, 300 Prince Philip Drive, St. John's, NL, A1B 3V6, Canada, ckovacs@mun.ca.
Insights
Fetal skeletal development relies on minerals like calcium and phosphorus, transported by the placenta. Postnatal bone growth requires vitamin D (calcitriol), but fetal mineral balance is regulated by parathyroid hormone (PTH).
Area of Science:
- Skeletal Biology
- Mineral Homeostasis
- Embryonic Development
Background:
- The skeleton forms from a cartilaginous scaffold replaced by bone through endochondral ossification, continuing until puberty.
- Mineral delivery is crucial for skeletal growth and mineralization, with placental transport during fetal life and intestinal absorption after birth.
Purpose of the Study:
- To elucidate the regulatory mechanisms of fetal and neonatal mineral and bone homeostasis.
- To clarify the roles of various hormones and factors in skeletal development before and after birth.
Main Methods:
- Analysis of limited human fetal data (cord blood, pathological specimens).
- Extrapolation from animal studies involving surgical, pharmacological, and genetic manipulations.
- Review of established physiological processes in mineral transport and bone formation.
Main Results:
- Fetal mineral homeostasis depends on parathyroid hormone (PTH) and PTH-related protein, independent of vitamin D/calcitriol, calcitonin, or sex steroids.
- Postnatal skeletal development necessitates active intestinal calcium absorption, reliant on vitamin D/calcitriol.
- Neonatal calcitriol's role can be supplemented by dietary calcium or infusions.
Conclusions:
- Hormonal regulation of mineral homeostasis differs significantly between fetal and postnatal development.
- Parathyroid hormone is the primary regulator of fetal mineral balance, while vitamin D becomes essential after birth.
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.
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