Document Type : Original Article
Authors
1
Dept. of Oral and Maxillofacial Pathology and Microbiology, Post Graduate Institute of Dental Sciences, Pandit BD Sharma University of Health Sciences, Rohtak, Haryana-124001, India.
2
Post Graduate Student, Dept. of Oral and Maxillofacial Pathology and Microbiology, Post Graduate Institute of Dental Sciences, Pandit BD Sharma University of Health Sciences, Rohtak, Haryana-124001, India.
3
Dept. of Microbiology, Post Graduate Institute of Medical Sciences, Pandit BD Sharma University of Health Sciences, Rohtak, Haryana-124001, India.
10.30476/dentjods.2026.111335.3031
Abstract
Background: Tobacco use is a major etiological factor in oral potentially malignant disorders (OPMDs) and oral cancer. Cotinine, a stable metabolite of nicotine, serves as a reliable biomarker of tobacco exposure and can be non-invasively detected in saliva. Leptin, an adipokine involved in immune and inflammatory pathways, demonstrates altered expression in neoplastic conditions and is reported to be reduced in smokers. In this context, evaluating salivary cotinine and leptin may provide valuable insights into tobacco exposure and oral carcinogenesis.
Purpose: This study aimed to quantify, compare, and correlate salivary cotinine and leptin levels among tobacco smokers (TS), oral leukoplakia (OL), and oral squamous cell carcinoma groups (OSCC).
Materials and Method: This observational analytical cross-sectional study comprised 63 male participants categorized into three groups: TS, OL, and OSCC, with 21 participants in each group. Unstimulated fasting saliva samples were collected and salivary cotinine and leptin levels were quantified using enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed using the Mann-Whitney U test, Kruskal-Wallis test, one-way ANOVA and Spearman’s rank correlation test, with p Value < 0.05 considered statistically significant.
Results: Mean salivary leptin and cotinine levels were lowest in the OSCC group, followed by TS and highest in the OL group, with a statistically significant difference observed for leptin (p= 0.001). Mean cotinine levels among active smokers were significantly different within the OSCC, OL and TS groups (p= 0.007, 0.014 and < 0.001, respectively). A significant positive correlation was observed between salivary leptin levels and body mass index (BMI) in OL group (p = 0.008).
Conclusion: Salivary leptin shows promise as a non-invasive biomarker in oral carcinogenesis, with elevated levels in OL and reduced levels in OSCC, along with a significant association with BMI. In contrast, salivary cotinine primarily reflects tobacco exposure and lacks discriminatory potential, indicating independent roles of these biomarkers.
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