title: Structural bone changes in spondyloarthritis: mechanisms, clinical impact and therapeutic considerations.
abstract: Spondyloarthritis (SpA) is an inflammatory disease of the spine, the peripheral joints and the entheses and shares some clinical features with rheumatoid arthritis (RA). Chronic inflammation of musculoskeletal structures leads to disease symptoms such as pain and stiffness and structural changes in the bone tissue. Furthermore, therapies for SpA are based on those for RA, which attempt to inhibit synovial inflammation that leads to retardation or even arrest of structural damage. However, in SpA, the bone tissue directly exposed to inflammation (osteitis) is the trabecular bone of the vertebrae, but not the cortical bone surface as in RA (synovitis). Therefore, the success of treatment strategies for structural changes in RA may not be appropriate for SpA. In this article, the authors discuss the pathophysiology of structural damage in SpA and concepts for the preservation of the physiologic bone architecture in patients with SpA.
authors.affiliation: Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany. georg.schett@uk-erlangen.de
authors.forename: Georg
authors.initials: G
authors.lastname: Schett
mesh_terms: D019485:Bone Morphogenetic Proteins / Q000502:physiology; D001842:Bone and Bones / Q000473:pathology* / Q000503:physiopathology*; D015232:Dinoprostone / Q000502:physiology; D006801:Humans; D008214:Lymphocytes / Q000473:pathology; D010000:Osteitis / Q000473:pathology / Q000503:physiopathology; D010010:Osteoclasts / Q000473:pathology; D025241:Spondylarthritis / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D051153:Wnt Proteins / Q000502:physiology
chemical_list: D019485:Bone Morphogenetic Proteins; D014409:Tumor Necrosis Factor-alpha; D051153:Wnt Proteins; D015232:Dinoprostone