title: Axial spondyloarthritis.
abstract: The term axial spondyloarthritis covers both non-radiographic disease and radiographic disease (also known as ankylosing spondylitis). Some studies have been performed to investigate the prevalence of axial spondyloarthritis, although most are limited to patients with radiographic disease. A strong genetic association has been shown between axial spondyloarthritis and human leukocyte antigen-B27 (HLA-B27), but the pathogenetic role of HLA-B27 has not yet been clarified. Tumour necrosis factor (TNF), IL-17, IL-23 and downstream pathways also seem to be important - based on the good results of therapies directed against these molecules - but their exact role in the inflammatory process is also not yet clear. Elucidating the interaction between osteoproliferation and inflammation will be crucial for the prevention of long-term structural damage of the bone. The development of new criteria for classification, diagnosis and screening of patients with axial spondyloarthritis will enable earlier intervention for this chronic inflammatory disease. MRI has become an important tool for the early detection of axial spondyloarthritis. NSAIDs and TNF blockers are effective therapies, including in the early non-radiographic stage. Therapeutic blockade of IL-17 or IL-23 seems to be a promising new treatment option. Tools for measuring quality of life in axial spondyloarthritis have become relevant to assess the impact that the disease has on patients. These diagnostic and therapeutic advances will continue to change the management of axial spondyloarthritis, and new insights into the disease pathogenesis will hopefully accelerate this process. For an illustrated summary of this Primer, visit: http://go.nature.com/51b1af.
authors.affiliation: Rheumatology, Charité, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany.
authors.forename: Joachim
authors.initials: J
authors.lastname: Sieper
authors.affiliation: Rheumazentrum Ruhrgebiet, Herne, Germany.
authors.forename: Jürgen
authors.initials: J
authors.lastname: Braun
authors.affiliation: Faculty of Medicine, Paris Descartes University, Department of Rheumatology, Hôpital Cochin, Assistance Publique, Hôpitaux de Paris, INSERM (U1153), Clinical Epidemiology and Biostatistics, PRES Sorbonne Paris-Cité, Paris, France.
authors.forename: Maxime
authors.initials: M
authors.lastname: Dougados
authors.affiliation: Clinical Immunology and Rheumatology and Amsterdam Rheumatology and Immunology Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Dominique
authors.initials: D
authors.lastname: Baeten
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D001368:Axis, Cervical Vertebra / Q000000981:diagnostic imaging; D015796:HLA-B27 Antigen / Q000235:genetics; D006801:Humans; D020381:Interleukin-17 / Q000235:genetics; D053759:Interleukin-23 / Q000235:genetics; D008279:Magnetic Resonance Imaging; D025241:Spondylarthritis / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000235:genetics; D013167:Spondylitis, Ankylosing / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000235:genetics
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015796:HLA-B27 Antigen; D020381:Interleukin-17; D053759:Interleukin-23; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha