ASSOCIATION OF TLR4 GENE POLYMORPHISM (rs4986790) WITH RISK OF CHRONIC PERIODONTITIS - A CASE CONTROL STUDY IN SOUTH INDIAN POPULATION
Abstract
Aim
Periodontal disease is a prevalent, enduring, multi-microbial, immuno-inflammatory condition. Toll-like receptor 4 (TLR4), which recognise pathogen-associated molecular patterns originating from diverse microorganisms, are essential components of the innate immune system. As a result, disease genes are seen as moderating disease genes in complicated disorders which recognize pathogen-associated molecular patterns originating from diverse microorganisms, are essential components of the innate immune system. This pilot study was aimed to investigate the association between the TLR4 gene polymorphism (rs4986790) and susceptibility to Chronic Periodontitis in the south Indian population.
Materials And Methods
The study was carried out at Saveetha Dental College, Chennai. After obtaining ethical approval, 50 samples were collected from patients diagnosed with chronic periodontitis (N=25) and normal healthy subjects (N=25). The PCRRFLP genotyping assay was performed using the specified forward and reverse primers flanking the locus spanning the rs4986790 polymorphic site on the TLR4 gene. The chi-square test was used to compare the genotype distribution and allele frequencies between the study groups.
Results
Statistical analysis showed that both the case and control groups were in agreement with the Hardy-Weinberg equilibrium, which is evident from the p values > than 0.05 in both the study groups. However, the genotype and allele frequency comparison between the 2 groups was found to be insignificant (p value = 0.6973).
Conclusion
The results of the present study demonstrated that the gene polymorphism rs4986790 was not significantly associated with the risk of developing chronic periodontitis in the study population. Increasing the sample size would aid us in dissecting the possible association of this polymorphism with CP. Also, investigations on other SNPs of this gene would benefit us in understanding the role of TLR4 in the development of CP.