Repair of osteopenia in children with juvenile rheumatoid arthritis.

To test the hypothesis that the presence of osteopenia in juvenile rheumatoid arthritis is directly correlated with clinical disease activity and therefore reversible, we prospectively studied cortical bone mineral density (BMD) serially in 27 children. Twenty-four (89%) had BMD > or = 2 SD below age-related normal values (disease duration 49.3 +/- 7.7 months) at the beginning of the study. Of 27 children who had clinical disease improvement measured by a disease activity score during our study period, 17 (63%) had significant improvement or significant normalization, or both, of their BMD (0.34 +/- 0.13 gm/cm2 at initiation and 0.41 +/- 0.17 gm/cm2 at completion, p < 0.05; disease activity score of 3.4 +/- 0.2 at initiation and 1.4 +/- 0.2 at completion, p < 0.005). The increase in BMD was associated with a similar directional change in serum osteocalcin concentrations (4.6 +/- 1 ng/ml at initiation vs 9.1 +/- 1.1 ng/ml). The 10 patients whose disease became or remained active had a decreased or unchanged low serum osteocalcin level and BMD (BMD 0.37 +/- 0.17 gm/cm2 at initiation and 0.37 +/- 0.16 gm/cm2 at completion; disease activity score of 3.1 +/- 0.3 at initiation and 3.4 +/- 0.2 at study completion). We conclude that children with JRA who have improvement in their disease activity have an improvement in BMD heralded by an increase in serum osteocalcin values.

Abnormalities in serum osteocalcin values in children with chronic rheumatic diseases.

We studied bone mineral metabolism prospectively in 113 children with chronic rheumatic diseases (juvenile arthritis, systemic lupus erythematosus, and juvenile dermatomyositis) to determine the relationship of serum levels of osteocalcin to rheumatic disease activity and corticosteroid usage, and to determine, in part, the cause of osteopenia in this population. Disease activity was quantitated by historical, clinical, and serologic means and an activity score derived. The 113 children were divided according to the expression of their disease, which was active (group 1: mean score 3.42, mean erythrocyte sedimentation rate 28 mm/hr) or inactive (group 2: score 1.7, erythrocyte sedimentation rate 15 mm/hr) (p less than 0.02 group 1 vs group 2 for each value), or which remitted during the study (group 3). We found that serum levels of osteocalcin, but not those of ionized calcium, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone, were reduced in group 1 children even before corticosteroid therapy was employed. Children in both group 2 and group 3 had normal osteocalcin levels despite the use of corticosteroids. The reduced levels of osteocalcin were predictive of a reduction in bone mass measured by photon absorptiometry in 16 of 19 children so studied. We conclude that skeletal abnormalities that result in a reduced bone mass occur in the clinical course of the majority of children with active chronic rheumatic diseases, are associated with reduced osteocalcin levels, and are not related to the use of corticosteroids. Serum osteocalcin levels may be a sensitive marker for reduced osteoblast activity and bone formation in children with chronic rheumatic diseases.