Abstract
Juvenile spondyloarthritis (JSpA) refers to a diverse spectrum of immune-mediated inflammatory arthritides whose onset occurs in late childhood and adolescence. Like its adult counterpart, JSpA is typified by a strong association with human leukocyte antigen-B27 (HLA-B27) and potential axial involvement, while lacking rheumatoid factor (RF) and distinguishing autoantibodies. A characteristic manifestation of JSpA is enthesitis (inflammation of insertion sites of tendons, ligaments, joint capsules or fascia to bone), which is commonly accompanied by bone resorption and new bone formation at affected sites. In this Review, advances in the role of HLA-B27, enthesitis and its associated osteoproliferation in JSpA pathophysiology and treatment options will be discussed. A deeper appreciation of how these elements contribute to the JSpA disease mechanism will better inform diagnosis, prognosis and therapy, which in turn translates to an improved quality of life for patients.
Highlights
Juvenile spondyloarthritis (JSpA) is a heterogeneous group of inflammatory arthritides whose onset occurs before the age of 16
JSpA includes children meeting the criteria for juvenile idiopathic arthritis (JIA) categories of enthesitis related arthritis (ERA), juvenile psoriatic arthritis (JPsA), and juvenile ankylosing spondylitis (JAS), reactive arthritis and inflammatory bowel disease (IBD)-associated arthritis
The preferential alleviation of spinal inflammation and ankylosis with IL-17A blockade in AS patients convincingly suggests that IL-17, not IL-23, is the major cytokine directing disease pathogenesis at least in axial SpA and that it is likely to be generated in an IL-23-independent manner
Summary
Juvenile spondyloarthritis (JSpA) refers to a diverse spectrum of immune-mediated inflammatory arthritides whose onset occurs in late childhood and adolescence. JSpA is typified by a strong association with human leukocyte antigenB27 (HLA-B27) and potential axial involvement, while lacking rheumatoid factor (RF) and distinguishing autoantibodies. A characteristic manifestation of JSpA is enthesitis (inflammation of insertion sites of tendons, ligaments, joint capsules or fascia to bone), which is commonly accompanied by bone resorption and new bone formation at affected sites. In this Review, advances in the role of HLA-B27, enthesitis and its associated osteoproliferation in JSpA pathophysiology and treatment options will be discussed.
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