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Gingivitis is the initial manifestation of periodontal disease, characterized by bacteria and inflammatory mediators, such as IL-32. This study aimed to determine whether the rs45499297 genetic variant of the IL32 gene and its serum and salivary levels are associated with gingivitis. In addition, we investigated whether transcription factors bind differentially in the presence of this genetic variant.
The study was conducted with 147 subjects. The rs45499297 variant was analyzed using the PCR-RFLP technique, while cytokine levels were measured using the ELISA assay. The affinity of the transcription factors in the presence of the gene variant was analyzed using bioinformatics methods.
The results suggest that schooling, salivary flow, lipids, and salivary IL-32 levels were associated with gingivitis. Furthermore, the TC genotype, in the presence of obesity, conferred an increased risk of gingivitis, which was associated with lower serum IL-32 levels. Bioinformatics analysis revealed that the transcriptional factor LRH1 binds with a higher affinity to the C allele than to the T allele of the studied genetic variant.
The findings of this study demonstrate the multifactorial nature of gingivitis, wherein the interplay between genetics and obesity serves as a regulatory factor in inflammation and periodontal risk. The preferential binding of LRH1 to the C allele suggests a molecular link between the genetic variant, inflammatory dysregulation, and the altered metabolic environment in obesity.
Our data show that the rs45499297 gene variant is only associated with gingivitis in the presence of obesity and affects serum cytokine levels. Additionally, we identified the potential involvement of LRH1 in regulating the IL 32 gene expression.
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