Introduction. The key links in the etiology and pathogenesis of periodontal tissue diseases are the quantitative and qualitative changes in the composition of the microflora of the oral cavity, with the simultaneous deterioration of oral hygiene, and reduction of local and general immunity, which occurs more often in the presence of somatic diseases. Aims. The aim of the paper was to study the features of the microbiocenosis of periodontal tissues and the production of hydrogen peroxide by gum symbionts in adolescents with catarrhal gingivitis and chronic gastroduodenitis. Methods. The condition of the microbiocenosis of the gums of 83 adolescents from 12 to 18 years, which was divided into groups depending on the diagnosed catarrhal gingivitis and chronic gastroduodenitis, was studied. Bacteriological examination was performed to isolate pure cultures of microorganisms and to identify them according to generally accepted microbiological methods. The ability of the selected cultures to produce hydrogen peroxide was studied on an indicator medium with potassium-iodine-starch system, by the iodometric method. Results. The results of microbiological studies showed significant changes in qualitative and quantitative indicators of the microbiocenosis of the gingival mucosa in the affected area of patients with gingivitis, compared with dentally and somatically healthy individuals in the control group. In the group of clinically healthy adolescents, hydrogen peroxide producers were found on the mucous membrane of the gums only in 5.0 ± 1.15% of the examinees. In catarrhal gingivitis, hydrogen peroxide producers were found in 52.4 ± 2.4 % of the examined main group subjects (p < 0.01) and in the 50.0 ± 2.5 % of the examined comparison group subjects (p < 0.01). Conclusion. Among adolescents with catarrhal gingivitis, which occurs on the background of chronic gastroduodenitis, there were more pronounced quantitative and qualitative changes in the microbiocenosis of the gums. The hydrogen peroxide produced by them can act as an additional damaging factor in the pathogenesis of the inflammatory process of the gingival area.
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