Spondyloarthritis (SpA) encompasses a group of rheumatologic diseases, including axial spondyloarthritis (axSpA), psoriatic arthritis, arthritis with associated inflammatory bowel disease (i.e. Crohn’s disease and ulcerative colitis), reactive arthritis and undifferentiated SpA, which all share certain clinical, biological and genetic features. However, the pathogenesis remains largely unexplained. Recent evidence suggests an autoinflammatory component of the disease. The complement system is a cornerstone of the innate immune system. This review aims to evaluate the current knowledge of the complement system in SpA. Animal models have shown that complement activation is associated with axSpA. Complement proteins L-ficolin and H-ficolin levels are elevated in patients with axSpA, and complement factor C3 levels decrease after the initiation of tumour necrosis factor-inhibitor therapy. Associations with disease activity are inconsistent, as one study found that the serum levels of complement factors C3 and C4 did not differ in patients with different Bath Ankylosing Spondylitis Disease Activity Index scores but, in another study, were associated with baseline Ankylosing Spondylitis Disease Activity Score with C-reactive protein and Bath Ankylosing Spondylitis Disease Activity Index improvement after treatment with a tumour necrosis factor inhibitor. Future studies should focus on the complement system in various SpA entities, involvement in pathogenesis and disease progression under clinically relevant conditions.