Collagen breakdown in ankylosing spondylitis -: relationship to disease related parameters

Objective Patients with ankylosing spondylitis (AS) often develop osteoporosis particularly of the axis skeleton. To investigate disease-related or therapeutic influence on bone catabolism, we quantified the total excretion of the collagen crosslinks (CL) pyridinoline (Pyd) and deoxypyridinoline (Dpyd) in 91 AS patients (26 f, 65 m) in relation to disease activity or stage and therapy with NSAID. Methods CL were determined by HPLC (High Performance Liquid Chromatography). Results The AS patients show a highly significant positive correlation between Pyd and the inflammatory activity (CrP, r=0.36, p < 0.001: ESR, r = 0.379, p < 0.001). Also the quotient Pyd/Dpyd correlates positively to the inflammatory activity (CrP, r = 0.262, p < 0.001: ESR, r = 0.325, p < 0.002). In the case of increased inflammatory disease activity (CrP greater than or equal to 10 mg/l vs CrP < 10 mg/l or ESR greater than or equal to 10 30 mm vs ESR < 30 mm), Pyd excretion is raised significantly (p < 0.042 for CrP and p < 0.009 for ESR). Among those patients treated with NSAID therapy, significantly reduced levels for Dpyd (p < 0.001) and raised levels for the quotient Pyd/Dpyd (p < 0.002) appear. In the case of advanced radiological changes with evidence of syndesmophytes, Pyd (p = 0.0 14) and Dpyd (p < 0.004) were significantly raised in urine. Regarding the movement function (finger-floor distance, schober test), no significant correlation to crosslink excretion could be proven. Conclusion From our investigations, we assume that osteoporosis in AS is primarily caused by an inflammatory-mediated degradation of bone.