Objectives. Periodontitis is an inflammatory disease characterized by connective tissue loss and alveolar bone destruction. Interleukin-8 (IL8) is important in the regulation of the immune response. The aim of this study was to analyze four polymorphisms in the IL8 gene in relation to chronic (CP) and aggressive (AgP) periodontitis. Methods. A total of 492 unrelated subjects were included in this case-control association study. Genomic DNA of 278 patients with CP, 58 patients with AgP, and 156 controls were genotyped, using the 5′ nuclease TaqMan assay, for IL8 (rs4073, rs2227307, rs2227306, and rs2227532) gene polymorphisms. Subgingival bacterial colonization was investigated by the DNA-microarray detection kit in a subgroup of subjects . Results. Allele and genotype frequencies of all investigated IL8 polymorphisms were not significantly different between the subjects with CP and/or AgP and controls ( ). Nevertheless, the A(？251)/T(+396)/T(+781) and T(？251)/G(+396)/C(+781) haplotypes were significantly less frequent in patients with CP (2.0% versus 5.1%, , OR？=？0.34, 95% CI: 0.15–0.78, resp., 2.0% versus 4.5%, , OR？=？0.41, 95% CI: 0.18–0.97) than in controls. Conclusions. Although none of the investigated SNPs in the IL8 gene was individually associated with periodontitis, some haplotypes can be protective against CP in the Czech population. 1. Introduction Periodontitis is an inflammatory disease which is initiated and maintained by the gram-negative bacteria of the subgingival biofilm [1]. Specific pathogen associated molecular patterns (PAMPs) and bacterial virulence factors stimulate an inflammatory host response that finally results in destruction of periodontal tissue and tooth loss [2]. Chronic periodontitis (CP) and generalized aggressive forms of periodontitis (AgP) appear to be associated with certain pathogens, including Porphyromonas gingivalis, Campylobacter rectus, Tannerella forsythia, Peptostreptococcus micro, and Treponema species [3, 4]. Treponema denticola, P. gingivalis, and T. forsythia, characterized as the “red complex,” were strongly associated with the clinical progression of chronic periodontitis [1–5]. In contrast, AgP was more often diagnosed in patients positive for Aggregatibacter actinomycetemcomitans, but there were many individuals with AgP who did not harbor this microorganism [6]. In addition to the microbial challenge, other factors, such as genetics, environment, and host factors, play a role in the pathogenesis of these diseases [7–9]. Various compounds, such as cytokines, representing an important pathway of
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