Determination of RNA/DNA Damage Associated With Oxidative Stress in Periodontitis Patients

Overview

This study looked at whether a type of gum disease called Stage III periodontitis and cigarette smoking are linked to higher levels of "oxidative stress." Oxidative stress can damage DNA and RNA, which are important parts of our cells. Two markers in saliva-8-OHdG (a sign of DNA damage) and 8-OHG (a sign of RNA damage)-were measured to understand this. Researchers included four groups of adults: smokers with periodontitis, non-smokers with periodontitis, healthy smokers, and healthy non-smokers. All participants had a dental exam, which checked things like gum inflammation, bleeding, and pocket depth. After the exam, an unstimulated saliva sample was collected from each person. The samples were tested in a laboratory using a sensitive method that measures oxidative damage. The study found that people with periodontitis had higher levels of DNA and RNA damage in their saliva than healthy people. The highest levels were seen in smokers with periodontitis. Even healthy smokers showed higher levels of oxidative stress than healthy non-smokers. In general, worse gum disease was linked to higher levels of oxidative damage. These results suggest that saliva tests for 8-OHdG and 8-OHG may help identify gum disease in a simple, non-invasive way. The findings also show that smoking adds to the body's oxidative stress, especially when gum disease is present. The study provides new information about how smoking and gum disease together may affect cell health.

Periodontitis is a chronic inflammatory disease that leads to the progressive destruction of the tooth-supporting tissues. Oxidative stress plays a central role in its pathogenesis, as excessive production of reactive oxygen species (ROS) can damage cellular structures, including lipids, proteins, and nucleic acids. Among oxidative stress-related biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-hydroxyguanosine (8-OHG) are widely recognized indicators of DNA and RNA damage, respectively. These biomarkers reflect the biochemical consequences of oxidative stress and are increasingly used to evaluate host responses in periodontal disease. Cigarette smoking is one of the strongest environmental risk factors for periodontitis and is known to enhance oxidative stress through multiple mechanisms. However, the combined effect of smoking and advanced periodontitis on salivary oxidative DNA and RNA damage has not been fully clarified. Assessing both 8-OHdG and 8-OHG simultaneously may provide deeper insight into the molecular pathways linking smoking, inflammation, and periodontal tissue destruction. This study was designed to evaluate salivary levels of oxidative nucleic acid damage in individuals with Stage III periodontitis who smoke or do not smoke, as well as in periodontally healthy controls. The study also aimed to investigate the relationship between these biomarkers and clinical periodontal measurements. By examining DNA and RNA oxidation together, the study sought to provide a multidimensional understanding of the host oxidative response in periodontitis. All participants underwent full-mouth periodontal examination performed by a calibrated clinician. Unstimulated saliva samples were collected under standardized morning conditions, processed by centrifugation to remove cellular debris, and stored at -80°C until biochemical analysis. Levels of 8-OHdG and 8-OHG were quantified using a high-sensitivity ELISA method capable of detecting multiple oxidized guanine derivatives. Biochemical findings demonstrated that oxidative DNA and RNA damage levels were higher in individuals with periodontitis compared to healthy controls, with smokers exhibiting the highest levels overall. Oxidative biomarker levels showed positive correlations with key periodontal parameters, including probing depth, clinical attachment loss, plaque accumulation, gingival inflammation, and bleeding on probing. These results suggest that the inflammatory burden of periodontitis amplifies oxidative stress at the nucleic acid level and that smoking contributes an additional biological load. In addition to biochemical assessment, buccal mucosa samples were evaluated cytologically using hematoxylin and eosin staining. All specimens showed adequate cellularity, and no significant differences in epithelial dysplasia were observed across study groups. This may be related to the predominance of superficial epithelial cells in the collected samples. Overall, this study provides an integrated biochemical and cytomorphological assessment of oxidative stress in periodontitis. The findings support the potential use of salivary 8-OHdG and 8-OHG as non-invasive biomarkers for disease monitoring and contribute novel evidence regarding the interaction between smoking, oxidative stress, and periodontal inflammation.