Background It is well established that rheumatoid arthritis is associated with severe alterations of bone metabolism. In seronegative spondylarthropathies (SSPs), however, data on bone turnover are scarce and conflicting.
Methods We studied biochemical markers of bone resorption (urinary deoxy-pyridinoline (D-Pyr) and cross-linked telopeptide of collagen-1 (ICTP)), bone formation markers (osteocalcin (OC) and bone specific isoenzyme of alkaline phosphatase (BAP)) as well as serum levels of osteoprotegerin (OPG, a glycoprotein which prevents the differentiation and activation of osteoclasts) in 30 patients with ankylosing spondylitis (AS), 23 patients with psoriatic arthritis (PsoA), 10 patients with reactive arthritis (ReA) and sex- and age matched healthy controls (HC).
Results Markers of bone resorption were significantly increased in AS, PsoA and ReA patients (Table 1). In contrast, bone formation markers were found to be heterogeneous: OC was increased in AS, but not in PsoA or ReA and the levels of BAP were elevated only in patients suffering from PsoA (Table 1). Serum levels of OPG were significantly increased in the AS and PsoA-group (Table 1). Furthermore, dual energy x-ray absorptiometry (DXA) measurements of the lumbar spine and the femoral neck, performed in a subgroup of patients, showed clearly decreased T-scores (lumbar spine -0.99 ± 1.33, femoral neck -1.95 ± 1.33) in patients suffering from AS. In PsoA bone mineral density was within the normal range. * = p < 0.05. ** = p < 0.001.
Conclusion Our results suggest significant alterations of bone metabolism in patients with SSPs. It is tempting to speculate that the increased OPG levels in AS and PsoA may represent a compensatory mechanism following enhanced bone resorption.
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