Table 2.

Differences between RA and SpA [8, 37]

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