IL‐1α (− 889) promoter polymorphism is a risk factor for osteomyelitis

Abstract

As osteomyelitis (OM) induces the synthesis of inflammatory cytokines and IL‐1 mediates bone resorption by osteoclasts we determined if there is an association between certain common polymorphisms of the genes encoding proinflammatory cytokines (IL‐1α and β, IL‐6, TNF‐α) and OM in adults. The IL‐1α (− 889) TT genotype was significantly more frequent among 52 OM patients than in 109 healthy controls (13/52, [25.0%] vs. 9/109, [8.3%], P = 0.0081, χ² = 7.01, OR = 3.7, 95% CI, 1.35–10.34). Patients who were homozygous for the T allele were younger than the rest of the OM patients (mean age 35.7 ± 11.5 vs. 58.1 ± 18.6 years, P = 0.001). IL‐1β TT (+ 3953) polymorphism was also more frequent in OM patients (P = 0.014, χ² = 5.12, OR = 5.1, 95% CI, 1.21–52.14), but IL‐1β is in linkage disequilibrium with the IL‐1α *T (P < 0.001). Route of infection, chronicity of the infection, type of microorganism isolated, and frequency of relapses were similar in patients with and without the IL‐1α TT genotype. There were no associations between OM and polymorphisms of other cytokines genes. IL‐1α serum levels were significantly increased in all the OM patients independently of their IL‐1 genotype compared to the controls (P = 0.021). Although IL‐1α serum levels were not significantly higher in patients with the IL‐1α (− 889) polymorphism, this does not exclude a difference in production of IL‐1α by osteoclasts or other inflammatory cells at the site of infection.