Prevalence Of Low Bone Mineral Density In Ankylosing Spondylitis, Correlation With Disease Activity, And Serum Sclerostin Levels

Background: Ankylosing spondylitis (AS) involves pathological new bone formation in the cortical zone of vertebrae and excessive loss of trabecular bone in the center of the vertebral body causing osteoporosis (OP). OP expressed as reduced bone mineral density (BMD) is a common complication in AS. Tumor necrosis factor-alpha (TNF-alpha) causes induction of Dickkopf-1 and sclerostin, which downregulates bone formation by inhibiting wingless proteins and bone morphogenic proteins. Materials and Methods: Fifty AS patients were compared with an equal number of age- and sex-matched controls. Various biochemical and radiological parameters of disease activity were calculated. BMD was measured at antero-posterior (AP) lumbar spine, neck of femur, and lateral lumbar spine using the dual-energy X-ray absorptiometry. Serum sclerostin, TNF-alpha, interleukin-17A (IL-17A), and IL-22 levels were measured using commercial enzyme-linked immunosorbent assay kits. Results: Mean BMD at various sites was significantly lower in patients. Patients with OP and low BMD at AP and lateral spine were 38% and 72%, respectively; at neck of femur, 20% and 68% of patients had OP and low BMD, respectively. Neck of femur BMD had significant positive correlation with Bath's ankylosing spondylitis disease activity index. Serum sclerostin levels were significantly higher in patients and had significant negative correlation with modified Stoke's ankylosing spondylitis spinal score. Conclusion: Low BMD is a significant complication in AS, and more prevalent in spine as compared to femur. Neck of femur BMD varies significantly with disease activity. Low sclerostin plays a significant role in the formation of syndesmophytes.