Ankylosing spondylitis (AS) is histopathologically characterized by subchondral bone marrow inflammation in sacroiliac and peripheral joints. It preferentially involves fibrocartilaginous tissues rich with aggrecan and type II collagen. Among many HLA and non-HLA genes, HLA-B27 plays a major role in its etiopathogenesis. Suggested hypotheses for HLA-B27’s role in the pathogenesis of AS can be summarized as presentation of arthritogenic peptides to cytotoxic T cells, those peptides presented to T cells which are derived from HLA-B27 itself being arthritogenic, and inflammation due to specific biological characteristics of the HLA-B27 molecule. Furthermore, chronic intestinal inflammation caused by intestinal bacteria and cytokines contributes to the pathogenesis. Because AS is a chronic and disabling rheumatic disease, it is important to document the disease process and outcome, to assess treatment efficacy and to establish these goals in an objective and standard fashion. Although inflammation markers such as erythrocyte sedimentation rate and C reactive protein might be valuable in diagnosis and follow-up, they are frequently insufficient in describing disease status and severity while destructive changes develop in the spine and peripheral joints. Therefore, in addition to clinical measures such as modified Schober, chest expansion, and occiput-to-wall distance, patient centered assessment tools for pain, disease activity, functional impairment and quality of life have been developed and become available for wide clinical use. Direct radiography is still being widely used for diagnosis and follow-up. Also, magnetic resonance imaging has started to appear in diagnostic algorithms for its superior sensitivity to detect subchondral inflammation in early disease process.