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The pathogenesis of periodontitis involves a complex interaction between the microbial challenge and the host immune response. The individual immunoinflammatory response has a great contribution in the pathogenesis of the disease and becomes a trigger in the process of bone remodeling which is a characteristic of the disease. Thus, the aim of this study was to evaluate the influence of theTLR4A896G (rs4986790),TLR4C1196T (rs4986791),CD14C-260T (rs2569190),RANKL(TNFSF11, rs2277438), andOPG(TNFSF11BC163T, rs3102735) polymorphisms in periodontitis. A case-control study was conducted on patients with periodontitis ( N=203 ) and controls ( N=213 ) over 30 years of age, without diabetes mellitus, acute infections, and osteoarthritis, and patients without aggressive periodontitis, i.e., stage IV and C degree of periodontitis, and any periodontal treatment performed in the last 6 months. Genotypes were determined by the PCR-RFLP and sequencing method. The frequency comparisons between case and controls were performed using the chi-square test and logistic regression (OpenEpi and SNPStats software). The risk (OR) was evaluated for values of P<0.05 . Differences inTLR4,CD14,RANKL, andOPGgenotype and allele frequency distributions were not observed between patients and controls. However, some variants were a risk factor for the development of periodontitis when considering gender and smoking habits. TheTLR4896 A/G genotype was a risk factor for periodontitis in males ( OR=2.86 ), and theTLR41196C/C genotype was a risk factor for nonsmoking males ( OR=1.85 ) when compared to women. TheRANKLA/A and theOPGT/C genotype was associated with the risk of the disease in nonsmoking men compared to nonsmoking women with the same genotype ( OR=1.96 and OR=2.9 , respectively). In conclusion,TLR4,CD14,RANKL, andOPGvariants were not associated with periodontitis. However,TLR4,RANKL, andOPGpolymorphisms could be a risk for periodontitis in males regardless of smoking habits.
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Zacarias et al. (2019) studied this question.
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