Mineral and bone physiology in the foetus, preterm and full-term neonates

Area of Science:

• Mineral metabolism
• Fetal and neonatal physiology
• Skeletal development

Background:

• The mother is the primary source of minerals for the fetus, with the placenta actively transporting them against gradients.
• Fetal serum mineral concentrations are higher than maternal levels, aiding bone accretion and preparing for postnatal calcium drops.
• Parathyroid hormone-related peptide (PTHrP) and parathyroid hormone (PTH) are key regulators of fetal mineral homeostasis and skeletal mineralization.

Purpose of the Study:

• To elucidate the roles of maternal-placental transport and key hormones in fetal mineral accretion.
• To describe the physiological changes in mineral balance and hormonal regulation at birth.
• To identify factors predisposing preterm infants to osteopenia of prematurity.

Main Methods:

• Review of existing literature on fetal and neonatal mineral physiology.
• Analysis of hormonal roles (PTHrP, PTH, calcitriol) in mineral homeostasis.
• Examination of the transition from placental to enteral mineral supply at birth.

Main Results:

• Placental active transport maintains higher fetal mineral levels, supporting bone growth.
• Postnatal calcium levels transiently fall due to loss of placental transport and hormonal shifts.
• Maturation of PTH and calcitriol levels, along with gut and kidney function, restores calcium homeostasis.

Conclusions:

• Maternal-fetal mineral transfer and hormonal regulation are critical for skeletal development.
• The transition at birth presents challenges for mineral homeostasis, particularly in preterm neonates.
• Delayed intestinal maturation and increased mineral demands in preterm infants increase their risk for osteopenia of prematurity.