Assessment of Oxidant-Antioxidant Status and Stress Factor in Recurrent Aphthous Stomatitis Patients: Case Control Study.

Abstract

Despite its vast occurrence, the aetiology of Recurrent Aphthous Stomatitis (RAS) still remains unknown and its aetiology is multifactorial. The factors believed to be associated with the aetiology of RAS, may disturb the equilibrium of oxidant-antioxidant status of the organism and may accelerate the formation of free radicals, resulting in Oxidative Stress (OS). Psychological stress is believed to act as a triggering factor or modifying factor for RAS. To find whether oxidant-antioxidant status and psychosocial stress play a role in the pathogenesis of RAS. The study was conducted on 60 subjects over a period of one year (August 2014-August 2015) equally divided into two groups-patients with RAS and healthy controls. Psychosocial stress was analyzed by using Recent Life Changes Questionnaire (RLCQ). Saliva was analyzed to evaluate Superoxide Dismutase (SOD) and Glutathione Peroxidase (GSHPx) activities, Malondialdehyde (MDA) and Uric Acid (UA) levels in both the study and the control groups, using UV spectrophotometry. The mean value of salivary SOD and MDA was increased while the activity of GSHPx and UA decreased in the study group when compared to the controls; the difference being statistically significant (p<0.005). The mean RLCQ stress score was also found to be increased in the RAS group, which showed elevated levels of mental stresses when compared to physical stresses. No significant association was observed between SOD, MDA, GSHPx and UA with high levels of stress score (p>0.05). In the study group, no correlation was observed between the study variables and gender, the number of ulcer episodes in one year, the number of ulcers per episode or the duration of ulcers. This study shows that salivary antioxidant levels show a significant difference in response to OS in RAS patients. An increase in levels of psychosocial stress is seen associated with patients with RAS indicating its role as a modifying or triggering factor in the initiation of RAS.