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Table 2 Differences between RA and SpA [8, 37]

From: Mechanistic rationales for targeting interleukin-17A in spondyloarthritis

• Characterized primarily by symmetric polyarthritis and inflammation resulting in cartilage and bone destruction • Oligo/polyarthritis is more often asymmetrical
• Axial involvement is rare • Characterized primarily by axial disease of the sacroiliac joints and spine
• More common in women than men • More common in men than women
• ACPA and RF antibodies are common • ACPA and RF antibodies are absent
• Strong genetic association with HLA-DR • Most common genetic involvement is HLA-B27
• Central clinical feature is synovitis • Affects the axial skeleton and peripheral joints with synovial involvement, especially in entheses, bone, and bone marrow (osteitis)
• Driven by B- and/or T-cell autoreactivity • Driven by innate immune cells (e.g., macrophages, PMN cells, mast cells)
• Macrophage effectors of synovial inflammation are driven predominantly by IFNγ • Macrophage effectors of inflammation are driven predominantly by IL-17
• More pronounced hyperplasia of the synovial lining versus SpA • Increased vascularity versus RA
• Extra-articular features include rheumatoid nodules, vasculitis, pneumonitis, scleritis • Extra-articular features include IBD, psoriasis, uveitis, aortitis
• Little or no signs of tissue repair with joint damage • Joint damage is characterized by new cartilage and bone formation (remodeling)
  1. ACPA anti-citrullinated protein antibody, HLA human leukocyte antigen, IBD inflammatory bowel disease, IFN interferon, IL interleukin, PMN polymorphonuclear, RA rheumatoid arthritis, RF rheumatoid factor, SpA spondyloarthritis