Tumor necrosis factor inhibitor therapy and risk of serious postoperative orthopedic infection in rheumatoid arthritis

Introduction Postoperative infections, such as periprosthetic septic arthritis, postoperative osteomyelitis, and deep-wound infection, are a particularly devastating complication of orthopedic surgery. They incur significant morbidity in terms of patient suffering and disability, prolonged hospitalization, frequent need for additional surgical procedures, and delay in rehabilitation. Moreover, there is a 3-fold increase in mortality in orthopedic procedures complicated by joint sepsis or osteomyelitis (1). The use of aggressive aseptic operating conditions, including laminar flow and perioperative antibiotic administration, has decreased the overall incidence of postoperative orthopedic infections to 1–2% (2). Despite these advances, rheumatoid arthritis (RA) remains an independent risk factor for postoperative orthopedic infection, with infection rates 2–4 times higher than those reported in patients without RA (3,4). The recent development of tumor necrosis factor (TNF ) inhibitors has revolutionized the care of patients with RA. TNF , a highly inflammatory macrophage-derived cytokine, plays a critical role in the joint destruction of patients with RA (5). Treatment of patients with RA using TNF inhibitors provides symptomatic and functional improvement and slows radiographic progression of disease (6). However, TNF inhibitors also enhance the risk of infection with mycobacteria and other opportunistic microorganisms in humans (7). Less is known about the effect of TNF inhibitors on susceptibility to common bacterial infections, in particular those associated with postoperative infections. To address this clinically important issue, we investigated the association of TNF-inhibitor therapy with serious postoperative infection in patients with RA who underwent orthopedic surgery.