Bone Abstracts

Objectives: We evaluated role of disease activity and genetic factors in fractures predisposing among juvenile idiopathic arthritis (JIA) children.

Methods: Bone mineralization parameters were detected by dual-energy X-ray absorptiometry of lumbar spine L₁–L₄ in 197 (81 boys and 116 girls) JIA children. Bone biochemical markers included osteocalcin, C-terminal telopeptides, parathyroid hormone (PTH), Ca, Ca⁺⁺, P, total alkaline phosphatase (TAP) activity. We have detected ApaI-, TaqI-, BsmI-, Cdx2 restriction length polymorphism assay of vitamin D (VDR) receptor gene, HindIII polymorphism of osteocalcin gene, TaqI and −1997 G/T polymorphisms of I type collagen Iα chain (ColIαI), BclI polymorphism of glucocorticoid receptor gene (GCR). Disease activity was measured by clinical and laboratorial parameters and special indexes.

Results: Differently localized fractures were in 29/197 children (14.7%), 7/81 (8.6%) in boys and 22/116 (19.0%) in boys. In fracture group of JIA children we have revealed higher physician (P=0.004) and parental (P=0.01) overall disease activity by visual-analog scale (VAS), higher Steinbrocker functional class (P=0.01), indexes JADS10 (P=0.027), JADAS27, JADAS71 (P=0.02), lower BMD Z-score (P=0.027). Girls with fractures had longer disease duration (P=0.04), higher frequency of low BMD (<−2S.D, P=0.01), lower BMD Z-score (P=0.02). Boys with fractures had higher physician (P=0.02) and parental (P=0.02) overall disease activity. Also we have no differences in fracture rate due to glucocorticoids administration in JIA children. Independent predictors of osteoporotic fractures (BMD Z-score <−2.0 S.D) were: physical VAS (OR−4.52, P=0.044), DAS28 >5.3 (OR=4.99, P=0.01), Steinbrocker >I (OR=6.17, P=0.01), Steinbrocker >II (OR=18.9, P<0.00001), polyarthicular and systemic course (reference-oligoarthicular course, OR=1.68 and 6.27, respectively, P=0.03), disease duration >5years (OR=25.5, P=0.007), parental VAS >5 (OR=29, P=0.0015), number of active joints >10 (OR=5.5, P=0,007), morning stiffness >120 min (OR=4.12, P=0.03), ESR >20 mm/h (OR=3.9, P=0.037), CRP >1.2 mg/dl (OR=5.9, P=0.007). Boys with fractures had significantly frequent H allele of HindIII osteocalcin gene polymorphism (P=0.047) and TT genotype (14.3 vs 0%) of TaqI ColIαI (P=0.004).

Conclusion: we have revealed that fractures in JIA children associated with higher disease activity rather glucocorticoids administration. In JIA boys fractures were associated with presence of H allele of HindIII osteocalcine gene and TT genotype of TaqI ColIαI.