The cause of ankylosing spondylitis is not fully understood, but the disease seems related to the immune system. The largest single genetic contribution is from the gene for human leukocyte antigen (HLA)-B27, and several elements including interactions in the context of a genetic background between the gut microbiome, innate-like lymphoid cells are important in the pathogenesis of the entheses along the axial skeleton. At the sites of pathology, the major mediators are tumor necrosis factor (TNF)-alpha and interleukin (IL)-17A.

AS is characterized by involvement of the spine and sacroiliac (SI) joints, peripheral joints, entheses, and digits, although extra-skeletal organs may also be affected. Spinal and SI involvement typically results in inflammatory back pain. The spinal involvement is more extensive in ankylosing spondylitis (AS) and may result in complications, including fracture and neurologic compromise in a very small number of patients. The major musculoskeletal features include SI joints and spinal involvement, hip and shoulder involvement, peripheral arthritis (in joints other than the hip and shoulder), costovertebral, manubriosternal, sternoclavicular, and costochondral inflammation, inflammation of extraspinal entheses, dactylitis. Systemic manifestations include other extra-articular manifestations such as uveitis, intestinal involvement, skin changes and osteoporosis.

The primary goals of management are to optimize short- and long-term health-related quality of life through relief of symptoms, maintenance of function, prevention of spinal complications, minimization of extraspinal and extraarticular manifestations and comorbidities, and maintenance of effective psychosocial functioning. In most patients with symptomatic AS, nonsteroidal anti-inflammatory drug (NSAID) can be used as initial therapy, and in patients who inadequate response to initial therapy with at least two NSAIDs consecutively, tumor necrosis factor (TNF)-alpha inhibitor should be used rather than treating with NSAIDs alone.