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This article is part of the supplement: 15th Paediatric Rheumatology European Society (PreS) Congress

Open Access Poster presentation

The influencing of environmental and genetics factors on bone metabolism in juvenile idiopathic arthritis children

MM Kostik1*, PB Glazkov1, MV Moskalenko2, DN Baranov1, MA Pachomova1, AA Kozyreva3, LA Scheplyagina4 and VI Larionova1

  • * Corresponding author: MM Kostik

Author Affiliations

1 State Pediatric Medical Academy, Saint-Petersburg, Russian Federation

2 Scientific and Research Institute of Hematology and Transfusiology, Saint-Petersburg, Russian Federation

3 Federal Center of Heart, Blood and Endocrinology, named by V.A. Almazov, Saint-Petersburg, Russian Federation

4 Federal Scientific and Clinical Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russian Federation

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Pediatric Rheumatology 2008, 6(Suppl 1):P3 doi:10.1186/1546-0096-6-S1-P3


The electronic version of this article is the complete one and can be found online at: http://www.ped-rheum.com/content/6/S1/P3


Published:15 September 2008

© 2008 Kostik et al; licensee BioMed Central Ltd.

Background

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.

Materials and methods

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).

Results

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.

Conclusion

We have detected opposite changes of bone mineralization between boys and girls, due to large numbers of environmental and genetics factors.