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- Open Access
The influencing of environmental and genetics factors on bone metabolism in juvenile idiopathic arthritis children
© Kostik et al; licensee BioMed Central Ltd. 2008
- Published: 15 September 2008
- Juvenile Idiopathic Arthritis
- Total Alkaline Phosphatase
- Arthritis Activity
- Bone Mineralization Loss
- Osteocalcine Gene
Bone mineralization losses depend on not only inflammatory aggression and complication of arthritis therapy or presence of whole numbers of genetic factors, influencing on bone metabolism, inflammation, immune system's functions and the therapy effectiveness.
The aim of our study was to research bone metabolism status depending on molecular markers and inflammatory activity in JIA children.
We included 184 JIA children, 77 boys and 112 girls. Bone mineralization was detected by dual-energy X-ray absorptiometry of lumbar spine L1–L4. Bone biochemical markers were osteocalcine, C-terminal telopeptides, parathyroid hormone (PTH), Ca, Ca++, P, total alkaline phosphatase (TAP) activity. We've detected ApaI-, TagI-, BsmI-restriction length polymorphism assay of vitamin D (VDR) receptor gene, Hind III osteocalcine gene, Sp I type I collagen Iα chain (ColIαI), BclI glucocorticoid receptor gene (GCR).
Low bone mineral density (LBMD) for age was detected then Zscore < -2 SD in 36 children, 18 girls and 18 boys. Girls with LBMD had lower height and weight, earlier age of arthritis onset and higher clinical and paraclinical arthritis activity parameters, higher osteocalcine and lower PTH. Children, who received glucocorticoids had lower BMD-Zscore, Ca in boys and lower BMC, BMD, BMD-Zscore, Ca, P, TAP activity in girls. Boys with normal BMD had frequently GG genotype Bcl I GCR. We have revealed positive correlation A allele ApaI VDR and negative correlation B allele BsmI VDR with BMD.
We have detected opposite changes of bone mineralization between boys and girls, due to large numbers of environmental and genetics factors.
This article is published under license to BioMed Central Ltd.