The cause of ankylosing spondylitis remains unclear. Proof that this disorder is an autoimmune disease attributable to crossreactivity between bacteria and HLA-B27 is still lacking. Differences in endogenous peptide presentation by HLA-B27 subtypes might be relevant in the etiopathogenesis. Fractures of the osteoporotic spine contribute to morbidity. Spinal cord injury may occur. MR imaging enables identifying sacroiliitis earlier than plain radiography. Sweet syndrome has now been described in patients with ankylosing spondylitis and Crohn disease. Progress has been made in the assessment of ankylosing spondylitis. There are now core sets for different settings and validated instruments for functioning and disease activity that will enable demonstrating efficacy of new therapeutic interventions. The debate continues on classification of postinfectious and reactive arthritis. Bacterial antigens may be found in the inflamed joints; occasionally 16S ribosomal RNA is also demonstrated. Antibiotics seem not to be effective in postenteric reactive arthritis. More than 25 years have now elapsed since the association between ankylosing spondylitis and HLA-B27 was first described in 1973. The cause of this disease is still unknown, but a lot of progress has been made regarding the molecular structure of HLA-B27, the spectrum of disease, the clinical and radiographic assessment of ankylosing spondylitis, and its treatment. Recent advances in research on ankylosing spondylitis are reviewed here.