Recurrent Aphthous Stomatitis (RAS) is a frequent chronic disease of the oral cavity that affects 5–25 % of the population with a plethora of predisposing factors. Despite its equivocal etiology, immune alterations, hematologic deficiencies and oxidative stress has been reported to be significant etiologic factors. Stress and obesity are other environmental factors that have been studied to understand associations with RAS.

This study investigated the association of stress, hematologic parameters, oxidative indices and other selected salivary factors in a case control study on RAS Methods: Twenty-two participants each in both case and control groups were recruited with saliva and serum samples collected from them after a self-administered Recent Life Changing Questionnaire (RLCQ). OHI-S and salivary flow rate (SFR) were calculated with selected hematologic parameters and oxidative indices such as Total oxidant (TOS) and anti-oxidant (TAS) levels and their ratio - Oxidative Stress Index (OSI). Anti-oxidative indices of Ferric-Reducing Antioxidant Power (FRAP) and Glutathione Peroxidase Activity (GsPHx) were also estimated. Results: The RAS group had a significantly higher RLCQ scores at a median of 145 more than the control (57.5). There was no significant in their obesity indices, however there was a significant higher mean in the ESR (p< 0.0001) and Vit B12 (p = 0.0001); OHI-S was also significantly higher in the RAS group with a median of 1.65. Both the salivary and serum TOS were significantly higher in the RAS (10.0 ± 3.8, 15.4 ± 8.9) compared to the control group (7.92 ± 1.49, 9.56 ± 3.5). GsPHx activity was significantly higher in both the saliva and serum in the control group (0.08 ± 0.08, 0.19 ± 0.11) while nil significant difference was found in the FRAP activity. Regression showed most important variables to be the salivary GsPHx activity, followed by serum OSI and GsPHx activity.

The oxidative indices of TOS, TAS and GsPHx can serve as significant biomarkers in detecting RAS. This further corroborates the role of immune dysregulation in the etiology and predisposition to RAS.