Health research has high value to society. It can provide important information about disease trends and risk factors, outcomes of treatment, functional abilities, patterns of care, and health care costs and use. The different approaches to research provide complementary insights. Clinical trials can provide important information about the efficacy and adverse effects of medical interventions by controlling the variables that could impact the results of the study, but feedback from real-world clinical experience is also crucial for comparing and improving the use of drugs, vaccines, medical devices, and diagnostics.
Below you will find links to some of the studies that have contributed to our increased understanding of spondyloarthritis.
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Diagnosing spondyloarthritis (SpA) early in young patients with inflammatory back pain and normal findings on radiographs of the sacroiliac joints (SIJ) remains a challenge in routine practice. Magnetic resonance imaging (MRI) is regarded as the most sensitive imaging modality for detecting early SpA before the radiographic appearance of structural lesions. The recently published Assessment of SpondyloArthritis International Society classification criteria for axial SpA include for the first time a positive MRI demonstrating sacroiliitis as an imaging criterion indicative of SpA together with at least 1 clinical feature of SpA. A systematic and standardized evaluation of the SIJ in patients with SpA showed that MRI has much greater diagnostic utility than documented previously and allowed a data-driven definition of a positive MRI for SpA. Single MRI lesions suggestive of inflammation can be found in the SIJ and the spine in up to one quarter of healthy controls and young patients with mechanical back pain.
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.
That gut and joint inflammation are linked in spondyloarthritis (SpA) has been recognized for almost three decades. Intriguingly, microscopic gut inflammation, which occurs frequently in patients with SpA, is an important risk factor for clinically overt Crohn’s disease and ankylosing spondylitis. This Review describes current insights into the underlying mechanisms that lead to chronic gut inflammation in patients with SpA. We propose that the development of chronic bowel inflammation in these individuals occurs through a transition phase, in which inflammation evolves from an acute into a chronic state. Our transition model implies that different cell types are involved at different stages during disease progression, with stromal cells having an important role in chronicity. In addition, deficient regulatory feedback mechanisms or genetically determined alterations in antigen presentation, endoplasmic reticulum stress, autophagy or cytokine signaling might also favor a transition from self-limiting acute inflammation to chronic inflammation. We anticipate that this transition phase might be an important window for therapeutic intervention.
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