Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by i) persistent low back pain, ii) morning stiffness, iii) familial tendency and iv) progressed limitation on spine motion. Usually, the age of onset is around 20 years old and male: female ratio is about 3-4:1. The diagnosis of AS is based on the presence of both side sacroilitis on X ray films in company with the above-listing clinical symptoms. In some cases, syndesmophyte formation was visible along the margins of vertebral body. In more advanced cases, the ankylosis of spines can contribute to both limitation of spine motion and the worst – kyphosis formation. The inflammation of enthesis – tendon/ligament insertion site could cause widespread, migratory intermittent tender points, for example; the Achillis tendinitis and plantar facia tendinitis are two well-known enthesopathic sites. Acute anterior uveitis is the most frequent extraskeletal manifestion of AS which involved about 30 % of patients. Other extraarticular manifestions include upper pulmonary lobe fibrosis, cardiac conduction defect and aortic regurgitation. No specific laboratory finding could be used as a diagnostic marker despite the fact that around 90-95% of patients carry HLA-B27 gene. It has been 30 years since the discovery of the association of HLA-B27 with ankylosing spondylitis. Several hypotheses were proposed to explain the pathogenesis of AS including molecular mimicry theory, the arthritogenic peptide models, the modulation of intracellular bacteria survival in the presence of HLA-B27 and unfolded protein response. None of these theory is able to explain the whole spectrum of disease manifestation. Traditionally the disease is treated by NSAIDs and few disease modified antirheumatic drugs (DMARD) such as sulphasalazine and methotrexate. Recently, anti-TNF therapy was a milestone in treating severe cases. Physical therapy and exercises were useful for some patients with limited spine motion.
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