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Bone mineralization and bone mineral metabolism in children with juvenile rheumatoid arthritis
P H Pepmueller1, J T Cassidy, S H Allen
1Harry S Truman Veterans Administration Hospital, Columbia, Missouri, USA.
Insights
Juvenile rheumatoid arthritis (JRA) in children is linked to lower bone density due to reduced bone formation, not resorption. Disease severity directly impacts bone mass, suggesting treatments to boost bone formation are needed.
Area of Science:
- Pediatric Rheumatology
- Bone Metabolism
- Osteoporosis Research
Background:
- Juvenile rheumatoid arthritis (JRA) can lead to osteopenia, affecting bone health in children.
- Understanding the mechanisms behind bone loss in JRA is crucial for effective management.
Purpose of the Study:
- To investigate the mechanisms of osteopenia in JRA by assessing bone mineralization, content, and density (BMC and BMD).
- To correlate bone health parameters with disease severity markers in pediatric patients.
Main Methods:
- Dual x-ray absorptiometry (DXA) was used to measure BMC and BMD in 41 children with JRA and 62 healthy controls.
- Serum and urine analyses were performed to evaluate mineral levels, vitamin D, hormones, and bone turnover markers (osteocalcin, BAP, TRAP).
Main Results:
- Children with JRA exhibited decreased BMD across all measured sites, particularly at cortical bone.
- Low levels of osteocalcin and bone-specific alkaline phosphatase (BAP) indicated reduced bone formation, while low tartrate-resistant acid phosphatase (TRAP) suggested decreased resorption.
- Disease severity, assessed by clinical and laboratory markers, negatively correlated with bone mass and was strongly associated with reduced bone formation markers.
Conclusions:
- Decreased bone mineralization in JRA is associated with impaired bone formation, linked to disease severity.
- Clinical strategies to stimulate bone formation should be considered for prepubertal children with active JRA.
Objective:
To identify mechanisms of the osteopenia associated with juvenile rheumatoid arthritis (JRA) by determining parameters of bone mineralization, and bone mineral content and density (BMC and BMD), in children with JRA.
Methods:
BMC and BMD were measured by dual x-ray absorptiometry in 41 children with JRA and 62 healthy children. Serum samples were analyzed for concentrations of minerals, vitamin D, parathyroid hormone, osteocalcin, bone-specific alkaline phosphatase (BAP), procollagen I carboxy-terminal propeptide, and tartrate-resistant acid phosphatase (TRAP), and urinary excretion of deoxypyridinoline crosslinks and calcium.
Results:
BMD was decreased in all sites in JRA patients. BMD, corrected for age, height, weight, and bone area, was decreased at cortical bone sites (1/3 radius, upper and lower extremities, and whole body). Low concentrations of osteocalcin and BAP suggested reduced bone formation, and low TRAP levels suggested decreased resorption. Clinical scales of disease severity were negatively correlated with measures of bone mass. Laboratory markers of disease severity were highly correlated with decreases in markers of bone formation, but not with those of resorption. Although laboratory findings were similar for children with oligoarticular and polyarticular disease, differences in bone mass were greater in children with polyarticular disease.
Conclusion:
These data suggest an association between decreased bone mineralization in JRA and low bone formation that is related to disease severity. Efforts to stimulate bone formation, therefore, need to be considered clinically in prepubertal children with active JRA.