High disease activity in ankylosing spondylitis is associated with increased serum sclerostin level and decreased wingless protein-3a signaling but is not linked with greater structural damage

BACKGROUND: Clinical activity of ankylosing spondylitis (AS) predicts the natural course of the disease and the response to treatment. Several molecules are involved in new bone formation resulting in structural damage in patients with AS. However, the link between the clinical and molecular phenomena has not yet been fully established. The aim of the study was to investigate the relation between markers of bone remodeling and inflammation with clinical activity and structural damage in AS. METHODS: We assessed the serum levels of sclerostin, Dickkopf-1 protein, Wingless protein-3a, bone morphogenic protein-7, matrix metalloproteinase-3, osteoprotegerin, bone alkaline phosphatase and inflammatory markers in 50 AS patients with high disease activity (BASDAI ≥ 4), 28 with low disease activity (BASDAI <4), and 23 healthy controls. Cervical and lumbar spine x-rays were performed in 46 patients to measure structural damage (mSASSS). RESULTS: Sclerostin level was significantly greater in high disease activity patients than in controls. Wingless protein-3a and Dikkopf-1 protein levels were significantly lower in high activity group compared to low activity group and controls. Negative correlation was found between sclerostin and Dikkopf-1 protein in high activity group (R = −0.28, P = 0.048). The median mSASSS values were not different between patient groups. CONCLUSIONS: Higher disease activity in AS may not be per se associated with greater new bone formation.