Introduction. A new challenge for humanity and medicine, in particular, is the sharp increase in the use of modern systems for heating tobacco among young people. Electronic cigarettes are often marketed as a safe alternative to regular ones. However, as far as oral health is concerned, modern studies state that smoking e-cigarettes is just as harmful as smoking. Smoking is a well-known risk factor for the inflammatory diseases of the periodontal tissues. It has been proven that the probability of developing periodontal disease in a smoker is 2.5-6 times higher than in non-smokers. However, the role played by smoking in the etiology of periodontal diseases is still not fully understood. The nature and mechanism of action of harmful tobacco smoke and the changes that occur in smokers’ periodontal tissues, small salivary glands and oral fluid are of both theoretical and practical interest.The aim of the present study was to investigate the dynamics of inflammation markers in oral fluid and to determine the degree of oral dysbiosis in patients with periodontal tissue diseases, and also in patients which smoke e-cigarettes. Materials and methods. Study of inflammatory markers (urease and lysozyme activity) in oral fluid and determination of the degree of oral dysbiosis were performed for 90 patients, divided into three groups. The activity of urease was determined by the reaction with urea, with the formation of ammonia. The activity of lysozyme was determined by the bacteriolytic method. Conclusions about the degree of insemination by the microflora of the oral cavity were based on the degree of dysbiosis of the oral cavity, determined by the enzymatic method, according to Levytskyi. Results and discussion. In patients with periodontal tissue diseases who smoke e-cigarettes, a significant imbalance of the inflammatory markers in the oral fluid was noted, characterized by: a 4.5-fold increase in urease activity, a 8.3 times increase in microbial insemination, against the background of a 44.6% decrease in lysozyme activity, compared to the data in the control group, p<0.01. At the same time, in people who did not have this bad habit, the values of the above parameters, although they differed from the data in the control group, were lower – as to urease activity and the degree of oral dysbiosis, and higher, respectively – as to lysozyme activity, than in the main group, p1 <0.01, p1<0.05.Conclusions. An increase in the activity of urease and a decrease in the activity of lysozyme in the oral fluid of people with periodontal tissue diseases who smoked e-cigarettes led to an increase in the degree of oral dysbiosis. This caused the growth of the inflammatory process in the periodontal tissues and contributed to the increase in tissue permeability, which in turn produced disturbances in the periodontal components, particularly in its microcirculatory channel.
Keywords:- chronic catarrhal gingivitis
- generalized periodontitis
- lysozyme
- oral fluid
- urease