Table 2.
RA | SpA |
---|---|
• 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) |
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