The influence of interleukin gene polymorphism on expression of interleukin-1 beta and tumor necrosis factor-alpha in periodontal tissue and gingivalcrevicular fluid

Background: A specific composite genotype of the polymorphic interleukin-1 (IL-1) gene cluster has recently been associated with severe periodontitis. One polymorphism of the composite periodontitis-associated genotype (PAG) has been functionally linked with expression of high levels of IL-1. The pu rpose of this study was to test whether gingival crevicular fluid (GCF) lev els of IL-1 beta and tumor necrosis factor-alpha (TNF alpha), and gingival tissue levels of IL-1 alpha, IL-1 beta, and TNF alpha correlate with PAG, a nd to examine the effect of conservative periodontal therapy on these level s. Methods: Twenty-two adults with moderate to advanced periodontal disease we re enrolled. Polymerase chain reaction amplification and restriction enzyme s were used to identify specific polymorphisms from peripheral blood sample s. GCF samples were collected at baseline and 3 weeks following conservativ e treatment and analyzed by ELISA for IL-1 beta and TNF alpha. An interprox imal gingival biopsy was collected at baseline and follow-up and analyzed f or IL-1 alpha, IL-1 beta, and TNF alpha by ELISA. Results: The genotyping identified 7 as PAG(+) and 15 as PAG(-). The 2 grou ps were comparable in terms of existing periodontitis and age. In shallow s ites (<4 mm), total IL-1 beta in GCF was 2.5 times higher for PAG(+) patien ts prior to treatment (P = 0.03), and 2.2 times higher after treatment (P = 0.04), while differences were less apparent in deeper sites. Following tre atment, a reduction in IL-1 beta concentration in GCF was seen for PAG(-) b ut not for PAG(+) patients. While not statistically significant, a trend wa s observed in mean tissue levels of IL-1 beta which were 3.6 times higher i n PAG(+) versus PAG(-) patients (P = 0.09). Conclusions: These data suggest that PAG(+) patients may demonstrate phenot ypic differences as indicated by elevated levels of IL-1 beta in GCF.