Potential Effect of Tobacco Consumption through Smoking and Chewing Tobacco on IL1beta Protein Expression in Chronic Periodontitis Patients: In Silico Molecular Docking Study

TLDR: The harmful effect of tobacco may increase the inflammation in periodontia by inducing the inflammatory active site of the IL1β protein in the CP patients.

Abstract: Detrimental effect of bad oral habits, such as smoking and chewing tobacco, on chronic periodontitis (CP) manifest chronic inflammation of gingival tissues which majorly results in gum bleeding, and teeth loss. A genetic association study of Interleukin 1 beta (IL1β) has been conducted in CP patients having smoking and chewing tobacco habits in regular life style. A molecular docking study has been consequently done to analyze the effect of tobacco on CP progression in depth. All statistical evaluation has been done by using SPSS v16.0. The findings of the study show the significant association of IL1β gene polymorphisms with CP increased susceptibility in combination of oral habits as mentioned earlier. The docking profile has showed the highest binding affinity of IL1β protein with the Nicotine derived Nitrosamine Ketone (NNK), one of the derivatives of nicotine which is in-taken through the habits associated with smoking and chewing tobacco. Nicotine, N-nitrosoanabasine, and N-nitrosonornicotine, the other derivatives, have also demonstrated significant impact over the IL1β protein-caused altered expression. Thus, this study concluded that the harmful effect of tobacco may increase the inflammation in periodontia by inducing the inflammatory active site of the IL1β protein in the CP patients.