The bone disease of preterm birth: a biomechanical perspective
Related Experiment Video
Updated: Sep 27, 2026
Methods for In Vivo Biomechanical Testing on Brachial Plexus in Neonatal Piglets
Published on: December 19, 2019
1Department of Pediatrics, Wright State University School of Medicine, Dayton, OH 45404, U.S.A. srmmem@aol.com
Insights
Preterm infants may experience bone disease due to reduced bone loading in the extrauterine environment, leading to increased bone resorption. This challenges the traditional view of insufficient calcium and phosphorus, highlighting the importance of intrauterine mechanical stimulation for bone development.
Area of Science:
- Neonatal physiology
- Bone biology
- Biomechanics
Background:
- Traditionally, preterm infant bone disease was attributed to low calcium and phosphorus levels.
- Emerging evidence suggests increased bone resorption, indicating a need for alternative explanations.
- The mechanostat model explains bone's response to mechanical loading.
Purpose of the Study:
- To investigate the role of mechanical loading in preterm infant bone disease.
- To propose an alternative explanation for bone disease in preterm infants based on biomechanical principles.
Main Methods:
- Review and application of the biomechanical model of postnatal bone formation (the mechanostat).
- Comparison of intrauterine bone loading in fetuses versus preterm infants.
- Analysis of bone loading in extrauterine environments.
Main Results:
- Increased bone resorption, not just decreased formation, is observed in preterm infants.
- Intrauterine bone loading from fetal movement is critical for normal bone accretion.
- Preterm infants experience significantly less bone loading in the extrauterine environment.
Conclusions:
- Reduced intrauterine bone loading is a key factor contributing to bone disease in preterm infants.
- The mechanostat model provides a framework for understanding preterm bone disease related to mechanical unloading.
- Interventions promoting bone loading in preterm infants may be beneficial.
Abstract:
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.
Related Concept Videos
01:29Bone Formation by Intramembranous Ossification
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
01:29Bone Disorders
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
01:40Bone Remodeling
01:24Bone Formation by Endochondral Ossification