Publication Date

Spring 4-25-2017


School of Health Sciences


Biology: Biomedical Sciences


Ankylosing Spondylitis, Anti-inflammatory Agents, Anti-rheumatic Agents, TNFalpha Agents, HLA-B27 Antigen/genetics, Interleukin-17, Interleukin-23, BASDAI, Treatment


Analytical, Diagnostic and Therapeutic Techniques and Equipment | Biological Factors | Biological Phenomena, Cell Phenomena, and Immunity | Chemical and Pharmacologic Phenomena | Genetic Phenomena | Immune System Diseases | Medical Immunology | Medical Pathology | Other Chemicals and Drugs


Ankylosing spondylitis (AS) is a systemic autoimmune disorder that induces ankylosis of the spine (fusion of the vertebrae at their various joints) and inflammatory arthritis of peripheral joints among other symptoms. Overexpression of cytokines, the presence of genetic mutations not exclusive to the human leucocyte antigen (HLA)-B27 region, and environmental factors all have large roles in the progressive development of AS. Although a definitive pathology continues to be sought after, researchers believe the adaptive immune system in AS patients attacks fibrocartilaginous entheses (supportive connective tissue between bone and attached structures like tendon, ligament, and fascia).

AS markedly reduces proper systemic functioning in several areas of human physiology, including the musculoskeletal, cardiovascular, neurological, psychiatric, and reproductive systems in both genders. A diagnosis for this disease requires the presentation of several qualifying symptoms, namely chronic inflammatory back pain, peripheral joint arthritis, enthesitis (inflammation of the enthesis not associated with a joint), uveitis (inflammation of the uvea or inner eye layer), and positive response to non-steroidal anti-inflammatory drugs (NSAIDs), with radiological support through x-ray or magnetic resonance imaging (MRI). Upon an AS diagnosis, patients should engage in healthy lifestyle changes, non-impact exercise, and taking NSAIDs as the first pharmacological treatment. Symptoms unresolved by NSAIDs are then treated with disease modifying antirheumatic drugs (DMARDs) and/or biologic medications like a monoclonal TNFα antibody to prevent further disease progression. Continued research to understand the association between AS and interleukin (IL)-17/IL-23 is needed for development of additional biologic treatments.