Adult-onset Still's disease (AOSD) is an autoimmune inflammatory arthritis that typically affects adolescents and adults ranging from age 16-40 years. Major etiological mechanisms behind cause a dysfunction of the innate and cellular immunity (limited) leading to activation of effector cells of the disease. Although the pathogenesis of adult-onset Still's disease is largely knwon to be idiopathic. Triggers of AOSD lead to activation of toll-like receptors (TLR) and activation of immune system. Pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) play an important role in the etiopathogenesis of AOSD. They lead to release of various cytokines in the body such as interleukin-1 beta (IL-1), interleukin-6 (IL-6), interleukin-17, interleukin-18, interferon-alpha (IFN-alpha) and tumor necrosis factor (TNF-alpha). These cytokines play major roles in modifying the normal working of the body and produce the typical clinical pictiure associated with AOSD. Some distinct HLA alleles have been shown to be associated with AOSD such as HLA-DR4, HLA-Bw35 (associated with good prognosis), HLA-DRB1, HLA-DRw6 (joint root involvement), HLA-B17, HLA-B35 and HLA-DR2. On gross examination, the involved joints may exhibit soft tissue swelling, cartilage loss, joint erosions and carpal ankylosis (late during the disease process). On microscopic examination of the joint fluid, typical features associated with inflammatory joint disease may be observed.
Adult-onset Still's disease pathophysiology
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