The bone disease of preterm birth: a biomechanical perspective

The bone disease of preterm birth has traditionally been explained by a decrease in bone formation from insufficient availability of calcium and phosphorus. However, there is emerging evidence that there is increased bone resorption in the bone disease of preterm birth, an observation that indicates some other explanation for this condition. The biomechanical model of postnatal bone formation states that, through a regulatory feedback system in the bone called the mechanostat, bone is able to respond to increased bone loading by increasing bone strength and to decreased bone loading by decreasing bone strength. It is suggested that this increased bone resorption in the markedly preterm infant compared with the term infant is secondary to decreased bone loading. Application of this model to the fetus and preterm infant suggests that intrauterine bone loading of the fetus from movement and kicking against the uterus is critical for normal fetal bone formation. The associated muscle growth from this activity also contributes to bone loading. The markedly preterm infant is deprived of much of this critical time period of intrauterine bone accretion, and bone formation occurs in the less favorable extrauterine environment, where there is significantly less bone loading.