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

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

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)

  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