Introduction. Our analysis of scientific data has showed that the problem of studying the etiopathogenesis of chronic inflammatory periodontal diseases with comorbidity of the gastrointestinal tract pathology in the course of tobacco smoking requires more specificity and further research.
Objective. To evaluate the levels of biochemical oral fluid markers of smokers with inflammatory periodontal diseases in the course of chronic hyperacid gastritis.
Materials and methods. We examined 90 patients (men and women) aged 25 to 44 years, who were divided into 3 groups. The first group (main group) consisted of 48 smoking patients with chronic generalized periodontitis of the initial-I, I stage in the course of chronic hyperacid gastritis. Smoking experience in the main group was more than 10 years, the number of cigarettes smoked from 15 to 25 per day. The second group (comparison group) consisted of 22 patients with chronic generalized periodontitis of the initial stage-I, I stage in the course of chronic hyperacid gastritis without a bad habit. The control group consisted of 20 healthy individuals. To evaluate lipid peroxidation processes, the levels of malondialdehyde and diene conjugates were determined. The state of antioxidant protection was studied by catalase and superoxide dismutase activity levels. The antioxidant-prooxidant index was calculated by catalase activity and the malondialdehyde concentration. The activity of the urease enzyme was determined as a marker of the oral cavity microbial contamination. The level of nonspecific immunity was assessed by lysozyme activity. The degree of dysbiosis was calculated by urease and lysozyme activity. The activity of the elastase enzyme was determined as an indicator of inflammation and destruction of the periodontal tissues.
Results. The study revealed that the values of all oral fluid biochemical markers in patients of the main group were significantly different from those in the comparison group and control group: the activity of catalase, lysozyme and the value of the antioxidant-prooxidant index were significantly lower, the concentration of malondialdehyde, diene conjugates, superoxide dismutase, the activity of urease and elastase, the degree of dysbiosis is much higher, which indicates more pronounced violations of oral homeostasis.
Conclusion. Our research discovered that the more severe changes of the oral homeostasis of the main group patients compared with the comparison group are due to the course of comorbid pathology (chronic generalized periodontitis, chronic hyperacid gastritis and tobacco smoking for 10 years), which worsened the course of the pathological process both in the oral cavity and in the gastrointestinal tract.