OBJECTIVE: To determine the serum Dickkopf-related protein 1 (Dkk-1) and sclerostin levels, and their relationship to structural damage and disease activity in patients with ankylosing spondylitis (AS), as well as to compare the serum Dkk-1 and sclerostin levels in patients receiving and not receiving anti-TNF-a treatment. MATERIALS AND METHOds: This cross-sectional study included 44 AS patients and 41 healthy age- and gender- -matched controls. Demographic data, disease activity parameters, and Bath Ankylosing Spondylitis Radiologic Index (BASRI) scores were recorded. Serum Dkk-1 and sclerostin levels were measured using commercially available ELISA. RESULTS: Serum Dkk-1 levels were lower (P > 0.05) and sclerostin levels were significantly lower (P < 0.05) in the AS patients than in the controls. Dkk-1 and sclerostin levels were similar in the patients that did and didn't receive anti-TNF-a treatment, and in the patients with active and inactive disease (P > 0.05). There wasn’t a correlation between serum Dkk-1 or sclerostin levels, and disease activity indices (P > 0.05). BASRI scores did not correlate with serum Dkk-1 or sclerostin levels (P > 0.05). DISCUSSIOn: Sclerostin expression is impaired in AS, but this is not the case for Dkk-1. The lack of an association between Dkk-1 or sclerostin levels, and anti-TNF-a treatment, disease activity indices, and radiological damage might indicate that neither the Dkk-1 nor sclerostin level induce inflammation and radiological damage in AS patients. Pathologic bone formation in AS might be due to molecular dysfunction of sclerostin and Dkk-1 at the cellular level.
OBJECTIVE: To determine the serum Dickkopf-related protein 1 (Dkk-1) and sclerostin levels, and their relationship to structural damage and disease activity in patients with ankylosing spondylitis (AS), as well as to compare the serum Dkk-1 and sclerostin levels in patients receiving and not receiving anti-TNF-a treatment. MATERIALS AND METHOds: This cross-sectional study included 44 AS patients and 41 healthy age- and gender- -matched controls. Demographic data, disease activity parameters, and Bath Ankylosing Spondylitis Radiologic Index (BASRI) scores were recorded. Serum Dkk-1 and sclerostin levels were measured using commercially available ELISA. RESULTS: Serum Dkk-1 levels were lower (P > 0.05) and sclerostin levels were significantly lower (P < 0.05) in the AS patients than in the controls. Dkk-1 and sclerostin levels were similar in the patients that did and didn't receive anti-TNF-a treatment, and in the patients with active and inactive disease (P > 0.05). There wasn’t a correlation between serum Dkk-1 or sclerostin levels, and disease activity indices (P > 0.05). BASRI scores did not correlate with serum Dkk-1 or sclerostin levels (P > 0.05). DISCUSSIOn: Sclerostin expression is impaired in AS, but this is not the case for Dkk-1. The lack of an association between Dkk-1 or sclerostin levels, and anti-TNF-a treatment, disease activity indices, and radiological damage might indicate that neither the Dkk-1 nor sclerostin level induce inflammation and radiological damage in AS patients. Pathologic bone formation in AS might be due to molecular dysfunction of sclerostin and Dkk-1 at the cellular level.
Authors: Inês P Perpétuo; Rita Raposeiro; Joana Caetano-Lopes; Elsa Vieira-Sousa; Raquel Campanilho-Marques; Cristina Ponte; Helena Canhão; Mari Ainola; João E Fonseca Journal: PLoS One Date: 2015-12-16 Impact factor: 3.240