Metabolic bone disease of prematurity
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Updated: Nov 4, 2026
Murine Hind Limb Long Bone Dissection and Bone Marrow Isolation
Published on: April 14, 2016
M C Backström1, A L Kuusela, R Mäki
1Tampere University Hospital, Department of Pediatrics, Tampere University Medical School, Finland.
Insights
Metabolic bone disease is common in premature infants, often due to low phosphorus. Optimal mineral and vitamin D needs require further study for better infant care.
Area of Science:
- Neonatalogy
- Pediatric Endocrinology
- Nutritional Science
Background:
- Metabolic bone disease (MBD) is increasingly diagnosed in very-low-birth-weight infants.
- Radiological rickets observed in 55% of infants <1000g and 23% of infants <1500g.
- Fractures occur in 24% of infants <1500g.
Purpose of the Study:
- To review the etiology, pathogenesis, diagnosis, and future management of MBD in premature infants.
- To highlight the need for establishing optimal mineral and vitamin D requirements.
- To discuss current recommendations and potential adjustments.
Main Methods:
- Review of existing literature on MBD in premature infants.
- Analysis of etiological factors including mineral deficiencies and drug effects.
- Discussion of diagnostic challenges and current recommendations.
Main Results:
- Insufficient phosphorus supplementation is a primary etiological factor.
- Multifactorial causes include calcium, vitamin D deficiency, drugs, aluminum, and immobilization.
- Bone mineral density measurement is key for subclinical disease, but no single perfect diagnostic method exists.
Conclusions:
- Optimal mineral and vitamin D intake for premature infants needs precise definition.
- Current European vitamin D recommendations (800-1000 IU/day) may be excessive with mineral supplementation.
- Extended mineral supplementation duration, potentially until 3.5kg body weight, may be necessary.
Abstract:
Metabolic bone disease is recognized with increasing frequency in very-low-birth-weight infants. Radiological changes characteristic of rickets have been found in 55% of infants with a birth weight of less than 1000 g and in 23% of infants weighing less than 1500 g at birth. Twenty-four per cent of infants with a birth weight of less than 1500 g have fractures. The main aetiological factor is insufficient phosphorus supplementation. The aetiology is, however, multifactorial and also includes calcium deficiency, vitamin D deficiency, certain drugs, aluminium loading and immobilisation. The method of choice in detecting subclinical mineral bone disease of prematurity is measurement of bone mineral density, but there is as yet no single good diagnostic method available for premature infants. The optimal mineral and vitamin D requirement of the premature infant must be established so that proper recommendations can be given. The current recommended vitamin D dose in Europe (ESPGAN 800-1000 IU/day) is probably too high when extra minerals are supplied. Moreover, the duration of mineral supplementation may need to be continued until the infant has reached a body weight of 3.5 kg. This article deals with the aetiology, pathogenesis, diagnosis and future prospects of metabolic bone disease of prematurity.
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