Bone mineral density and serum sclerostin levels in early ankylosing spondylitis: their possible correlation with a panel of disease activity and structural change parameters

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Abstract

Objective

The aim of this study was to investigate decreased bone mineral density (BMD) and serum sclerostin levels in early ankylosing spondylitis (AS) and to determine their possible correlation with a panel of disease activity parameters, functional impairment, bone turnover markers and syndesmophyte formation.

Methods

A total of 37 male patients having early AS with a disease duration of less than 10 years were included into the study and divided into two groups (group I, <5 years and group II, 5–10 years). The study also included 30 apparently healthy controls. The assessment included demographic data, clinical examination and measurement of the C-reactive protein (CRP)-based Ankylosing Spondylitis Disease Activity Score (ASDAS), the Bath Ankylosing Spondylitis Functional Index (BASFI), the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS), BMD measurement of lumbar spine and hip using dual-energy X-ray absorptiometry and determination of erythrocyte sedimentation rate (ESR), CRP levels, creatinine levels, bone alkaline phosphatase (BALP) levels, serum levels of C-telopeptides of type I collagen (sCTX) and sclerostin levels.

Results

Osteopaenia and osteoporosis of the lumbar spine were observed in 47 and 23.53% and in 35 and 15% of patients in group I and II, respectively. In the proximal femur, osteopaenia and osteoporosis were detected in 35.3 and 17.65% and in 45 and 25% of individuals in group I and II, respectively. ESR, CRP and sCTX levels were significantly higher in patients than in controls, with an insignificant difference between the patient groups. BALP levels showed an insignificant difference between the three groups. Serum sclerostin levels were significantly lower in AS patients compared with controls and in group II patients compared with those of group I. A low BMD correlated negatively with parameters of disease activity (ESR, CRP and ASDAS), BASFI scores and sCTX levels. No correlation was demonstrated between low BMDs and mSASSS and between BALP and sclerostin levels. Sclerostin showed a negative correlation with disease activity parameters (ESR, CRP and ASDAS), BASFI scores, sCTX levels, and mSASSS.

Conclusion

A low BMD is common in early AS patients; the role of inflammation seems to be pivotal in its pathogenesis. The monitoring of bone turnover markers and disease activity indices may help to predict patients at risk. Sclerostin expression is impaired in early disease and was linked to disease activity, bone turnover markers and increased structural damage, emphasizing the role of sclerostin in the pathogenesis of AS.

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