Association of HIF-1α and TNFα single nucleotide polymorphisms with periodontal disease in diabetic patients

Objective: Periodontal disease is a prevalent chronic inflammatory condition affecting the supporting structures of teeth and is considered one of the chronic complications of Type 2 diabetes mellitus (T2DM). Both diabetes and periodontal diseases are complex, multifactorial diseases to which genetic factors play a crucial role in susceptibility. The TNF-α/HIF-1 pathway might have a regulatory function in periodontal tissues. Several case-control studies have examined the association between TNF-α G308A or HIF-1α C1772T polymorphisms and diabetes complications, but the results have been inconsistent. We aimed to investigate the association between two specific genetic variants -HIF-1α C1772T and TNF-α G308A- and periodontal disease in patients with type 2 diabetes. Methods: A total of 109 individuals were enrolled in the study including 24 chronic periodontitis with T2DM (group 1), 35 gingivitis with T2DM (group 2), 26 non-diabetic individuals with chronic periodontitis (group 3) and 24 periodontally healthy non-diabetic individuals (group 4). The normal allelic and genotype distribution of these variants was analyzed in healthy Turkish adults (n: 120), independent of the study cohort. Allele and genotype distribution of group 4 and healthy Turkish adults were similar. Allelic and genotypic comparisons between group 4 and other groups were evaluated by PCR-RFLP. Allelic, dominant, and recessive genetic models were calculated to assess the strength of the association. Results: We found a significant association between the A allele at TNF-α G308A and the risk of gingivitis in T2DM (OR=3.75, CI:1.015–13.860, p=0.048). There was no association detected between HIF-1α C1772T polymorphisms and risk for periodontal diseases with T2DM. Conclusion: These results suggest that TNF G308A polymorphism may be involved in the pathogenesis of periodontal disease in diabetics. Future studies may contribute to the investigation of the potential polygenic predisposition of the diseases and reinforce our findings.