Does smoking influence tryptophan metabolism in periodontal inflammation? A cross‐sectional study

Abstract

ObjectivesThe aim of this study was to identify the effects of smoking and periodontal inflammation on tryptophan‐kynurenine metabolism as well as the correlation between these findings and clinical periodontal parameters.BackgroundIt has been shown that the tryptophan amino acid's primary catabolic pathway, the kynurenine pathway (KP), may serve as a key biomarker for periodontal disease. Although there are studies investigating the effect of smoking on KYN‐TRP metabolism, the effect of smoking on periodontal disease through KP has not been revealed so far.MethodsThe salivary and serum samples were gathered from 24 nonsmoker (NS‐P) stage III, grade B generalized periodontitis and 22 smoker (S‐P) stage III, grade C generalized periodontitis patients, in addition to 24 nonsmoker (NS‐C) and 24 smoker (S‐C) periodontally healthy control individuals. Saliva and serum IL‐6, kynurenine (KYN), and tryptophan (TRP) values, and KYN/TRP ratio were analyzed by liquid chromatography‐mass spectrometry. Clinical periodontal measurements were recorded.ResultsSalivary TRP values were significantly higher in both periodontitis groups than control groups (p < .05). Salivary KYN values were highest in NS‐P group (p < .05). Salivary KYN values did not differ significantly between periodontitis groups (p = .84). Salivary KYN/TRP ratio was significantly lower in NS‐P group compared to other groups (p < .001). Serum TRP value is higher in S‐P group than other groups; however, significant difference was found in S‐C group (p < .05). Serum KYN values were significantly lower in smokers than nonsmokers. Serum KYN/TRP ratio is higher in NS‐P group. NS‐P group has the highest salivary IL‐6 levels, NS‐C group has the lowest values (p < .05).ConclusionsOur results point out that smoking exacerbates inflammation in the periodontium and increases TRP destruction and decreases IDO activity by suppressing KP in serum. As a result, kynurenine and its metabolites may be significant biomarkers in the link between smoking and periodontal disease.