It has been proposed that individual genetic predisposition may contribute to persistent apical periodontitis. Cytokines are associated with levels of inflammation and are involved in caries, pulpal, and periapical tissue destruction. They also play a major role in bone resorption. In this study, we hypothesized that polymorphisms in some cytokine genes may contribute to an individual's increased susceptibility to apical tissue destruction in response to deep carious lesions.
Method:
Subjects with deep carious lesions, with or without periapical lesions (≥ 3 mm) were ascertained through the University of Pittsburgh School of Dental Medicine Dental Registry and DNA Repository and at the University of Texas School of Dentistry at Houston. Genomic DNA samples of 316 patients were sorted into 2 groups: 136 cases with deep carious lesions but no periapical lesions (controls) and 180 cases with deep carious lesions and periapical lesions (cases). Nine single nucleotide polymorphisms in IL1β, IL6, TNF, RANK, RANKL and OPG, were selected for genotyping. Genotypes were generated by endpoint analysis using Taqman chemistry in a real-time polymerase chain reaction instrument. Differences in allele and genotypic frequencies between cases and controls were calculated using Fisher and Chi-square tests. P-values ≤ 0.05 indicated statistically significant differences between the groups.
Result:
A SNP in IL1β (rs1143643) showed allelic (P=0.02) and genotypic (P=0.004) association in the individuals with deep caries and periapical lesions.
Conclusion:
Variations in IL1β may be associated with periapical lesion formation in individuals with untreated deep carious lesions. Future studies could help predict host susceptibility to developing periapical lesions.