The Influence of<i>TLR4</i>,<i>CD14</i>,<i>OPG</i>, and<i>RANKL</i>Polymorphisms in Periodontitis: A Case-Control Study

Abstract

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 the TLR4 A896G (rs4986790), TLR4 C1196T (rs4986791), CD14 C-260T (rs2569190), RANKL ( TNFSF11 , rs2277438), and OPG ( TNFSF11B C163T, rs3102735) polymorphisms in periodontitis. A case-control study was conducted on patients with periodontitis (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mi>N</mml:mi><mml:mo>=</mml:mo><mml:mn>203</mml:mn></mml:math>) and controls (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mi>N</mml:mi><mml:mo>=</mml:mo><mml:mn>213</mml:mn></mml:math>) 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<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.05</mml:mn></mml:math>. Differences in TLR4 , CD14 , RANKL , and OPG genotype 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. The TLR4 896 A/G genotype was a risk factor for periodontitis in males (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M4"><mml:mtext>OR</mml:mtext><mml:mo>=</mml:mo><mml:mn>2.86</mml:mn></mml:math>), and the TLR4 1196C/C genotype was a risk factor for nonsmoking males (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M5"><mml:mtext>OR</mml:mtext><mml:mo>=</mml:mo><mml:mn>1.85</mml:mn></mml:math>) when compared to women. The RANKL A/A and the OPG T/C genotype was associated with the risk of the disease in nonsmoking men compared to nonsmoking women with the same genotype (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M6"><mml:mtext>OR</mml:mtext><mml:mo>=</mml:mo><mml:mn>1.96</mml:mn></mml:math>and<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M7"><mml:mtext>OR</mml:mtext><mml:mo>=</mml:mo><mml:mn>2.9</mml:mn></mml:math>, respectively). In conclusion, TLR4 , CD14 , RANKL , and OPG variants were not associated with periodontitis. However, TLR4 , RANKL , and OPG polymorphisms could be a risk for periodontitis in males regardless of smoking habits.