Orthopaedic MD

Ankylosing spondylitis (AS) is a chronic, progressive inflammatory rheumatic disease involving primarily the sacroiliac joints and the axial skeleton. The main clinical features are back pain and progressive stiffness of the spine. Oligoarthritis of the hips and shoulders, enthesopathy, and anterior uveitis are common, and involvement of the heart and lungs is rare. The current understanding of the pathogenesis of this disorder is limited. Despite the strong association between human leukocyte antigen B27 (HLA-B27) and susceptibility to AS reported over the past 30 years, the exact pathogenic role of HLA-B27 in AS and other spondyloarthropathies has yet to be determined. The authors present a review of the literature pertaining to the pathogenesis of AS over the past several decades.
Elias Dakwar, M.D.; Jaypal Reddy, M.D, M.Ch., D.N.B.; Fernando L. Vale, M.D.; Juan S. Uribe, M.D. Neurosurg Focus. 2008;24(1):E2.

hip joint:
- is affected in upto 50 % of patients with AS, and when it occurs it is often bilateral;
- protrusio and hip flexion contractures are common;
- heterotopic ossification may follow THR;
- total hip replacement:
- hetertopic ossification;
- occurs in 20-40 % of hip replacements and is more common w/ trochanteric osteotomy;
- to avoid heterotopic ossification consider insertion of a cemented acetabular component followed by 750 rads around the component;
Wheeless' Textbook of Orthopaedics

Biomarkers may provide information that promotes understanding of prognosis, disease activity, and pathogenesis in ankylosing spondylitis. Biomarkers reflecting disease activity (metallo- proteinase-3) and inflammatory lesions on magnetic resonance imaging predict new bone formation and are ameliorated by anti- tumor necrosis factor therapy, yet this treatment may not prevent new bone formation. Moreover, elevated levels of biomarkers reflecting tissue repair (bone-specific alkaline phosphatase) post- treatment together with magnetic resonance imaging indicates such treatment may even promote repair through new bone formation. Tumor necrosis factor regulation of Dickkopf-1 may con- stitute a molecular brake that controls osteoblastogenesis through wingless and bone morphogenetic proteins in an established inflammatory lesion in ankylosing spondylitis.
Editorial Walter P Maksymowych Arthritis Research & Therapy 2009, 11:101 (full text)