Related Experiment Video
Updated: Oct 2, 2026
Scanning Skeletal Remains for Bone Mineral Density in Forensic Contexts
Published on: January 29, 2018
Changes in markers of bone metabolism during dexamethasone treatment for chronic lung disease in preterm infants
P C Ng1, C W K Lam, G W K Wong
1Department of Paediatrics, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong. pakcheungng@cuhk.edu.hk
Insights
Systemic corticosteroids significantly lower bone formation markers (BALP, osteocalcin) and bone resorption markers (Dpd) in preterm infants. This indicates corticosteroids primarily inhibit bone growth by reducing bone formation.
Area of Science:
- Neonatal research
- Pediatric endocrinology
- Bone metabolism
Background:
- Preterm infants are susceptible to bone metabolism disturbances.
- Systemic corticosteroids are used in preterm infants but their impact on bone is not fully understood.
Purpose of the Study:
- To characterize changes in serum and urinary bone markers in early postnatal life.
- To assess the effect of systemic corticosteroids on bone metabolism in preterm infants.
Main Methods:
- Measured serum bone-specific alkaline phosphatase (BALP) and osteocalcin for bone formation.
- Monitored urinary deoxypyridinoline (Dpd) for bone resorption.
- Collected samples from corticosteroid-treated and untreated preterm infants at various time points.
Main Results:
- Serum BALP and osteocalcin were significantly lower in corticosteroid-treated infants compared to controls.
- Urinary Dpd was also significantly lower in treated infants, though less pronounced.
- Linear bone growth rate was higher in the untreated group.
Conclusions:
- Systemic corticosteroids suppress bone formation markers (BALP, osteocalcin) and to a lesser extent resorption markers (Dpd).
- Corticosteroid-induced inhibition of bone growth appears to be primarily mediated by decreased bone formation.
Aim:
To characterise the change in serum and urinary bone markers in the early postnatal period, and to assess the effect of systemic corticosteroid on bone metabolism in preterm infants.
Methods:
Bone formation was quantified by measurement of serum concentrations of bone specific alkaline phosphatase (BALP) and osteocalcin. Bone resorption was measured by monitoring creatinine adjusted urinary deoxypyridinoline (Dpd) concentration. Blood and urinary samples were collected from corticosteroid treated infants (n = 19) immediately before the start (T(d-pre)), three weeks after the start (T(d-end)), and two (T(d-post2)) and four weeks (T(d-post4)) after the end of the dexamethasone course. Untreated patients (n = 30) had specimens taken at week 3 (T(wk-3)), 6 (T(wk-6)), 8 (T(wk-8)), and 10 (T(wk-10)) of postnatal age.
Results:
Serum concentrations of BALP and osteocalcin at T(d-end) were significantly lower than pretreatment levels and the levels at the corresponding time point (T(wk-6)) of the non-treatment group. In contrast, urinary Dpd concentration at T(d-end) was not significantly decreased compared with the pretreatment level. However, it was significantly lower than the urinary Dpd concentration at T(wk-6) of the non-treatment group. The rate of increase in lower leg length was significantly higher in the non-treatment group between weeks 3 and 6 than in the corresponding period during dexamethasone treatment in the corticosteroid group.
Conclusion:
Systemic corticosteroid causes appreciable suppression of serum BALP and osteocalcin and, to a lesser extent, urinary Dpd. The results suggest that corticosteroid inhibits bone growth mainly by decreasing bone formation.