Objectives: The 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.Background: It 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.Methods: The 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.Results: Salivary 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).Conclusions: Our 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.

Human beta-defensins are host defense peptides with broad antimicrobial and inflammatory functions. In the oral cavity, these peptides are produced mainly by the keratinocytes of the epithelium; however, fibroblasts, monocytes, and macrophages also contribute to oral human beta-defensin expressions. The resident and immune cells of the oral cavity come into contact with various microbe-associated molecular patterns continuously and simultaneously. The overall antimicrobial cellular response is highly influenced by local and environmental factors. Recent studies have produced evidence showing that not only systemic chronic diseases but also systemic factors like hyperglycemia, pregnancy, the long-term use of certain vitamins, and aging can modulate oral cellular antimicrobial responses against microbial challenges. Therefore, the aim of this narrative review is to discuss the role of systemic factors on oral human beta-defensin expressions.

Objective: Annexin-1 (ANXA1), a member of the annexin family, plays a role in the resolution of inflammation and the regulation of anti-inflammatory responses, while annexin-2 (ANXA2) is involved in the initiation of the inflammatory responses. The aim of this study was to determine the effects of annexin family (ANXA1 and ANXA2) in periodontal disease. Methods: Healthy participants (n:25) and stage III, grade B periodontitis (n:25) patients enrolled for this study. Clinical periodontal parameters and the periodontal inflamed surface area (PISA) levels were noted. Serum, saliva, and gingival crevicular fluid (GCF) samples were collected to measure the ANXA1, ANXA2 and IL-1β levels. Results: Salivary and serum concentrations of ANXA1 was significantly lower in the periodontitis group than in the control group (respectively, p = 0.0177 and p = < 0.0001). Periodontitis patients demonstrated higher serum ANXA2 and IL-1β concentrations compared to controls (respectively, p = 0.0002 and p = 0.0017). As an inflammatory index; saliva, serum and GCF ANXA1/ANXA2 ratio were significantly lower in the periodontitis group compared to healthy controls. Conclusions: The data suggest that periodontitis is associated with a disruption of the balance between pro-inflammatory mechanisms (ANXA2 and IL-1beta) and inflammation resolution (ANXA1), in parallel with PISA levels. Clinical Trial Registration: ClinicalTrials.gov NCT06554756 (15/08/2024).