Objective. The aim of the study was to establish the dynamics of β-glucuronidase activity in subjects suffering from type 1 diabetes and chronic untreated generalized periodontitis, subjects suffering from chronic untreated generalized periodontitis only, and control subjects not suffering from generic diseases with healthy periodontal tissue. Material and Methods. The study involved 165 19–50-year-old subjects who were divided into three groups: healthy subjects (n=55), subjects with chronic untreated generalized periodontitis (n=55), and subjects with type 1 diabetes and chronic untreated generalized periodontitis (n=55). Neutrophilic leukocytes of peripheral venous blood were exposed to bacterial stimuli: opsonized zymosan, nonopsonized Staphylococcus aureus, and prodigiosan. The activity of β-glucuronidase was determined by the spectrofluorimetry method. Results. The diagnostic value of changes in β-glucuronidase activity of neutrophilic leukocytes markedly increased in all study groups after stimulation of neutrophilic leukocytes by opsonized zymosan, nonopsonized Staphylococcus aureus, and prodigiosan as compared to control media not exposed to any stimulus (P<0.001). The strongest relationship (canonical correlation coefficient eta, 0.993) between the intensity of periodontal pathology markers and the activity of β-glucuronidase of neutrophilic leukocytes in incubated media in patients with type 1 diabetes mellitus and periodontitis was found under the effect of nonopsonized Staphylococcus aureus. Conclusions. If periodontal impairment is severe, diabetes mellitus possibly causes a faster destruction of the periodontal tissue and presents a higher risk of periodontitis for patients with diabetes.

Objective. To investigate bacterial populations in subgingival and supragingival plaque samples of patients with inflammatory periodontal diseases and activities of the lysosomal enzymes – lysozyme, alkaline phosphatase, and b-glucuronidase – in peripheral venous blood, in gingival crevicular fluid, and mixed nonstimulated saliva. Methods and materials. The study included 60 patients with inflammatory periodontal diseases without any internal pathology and 24 periodontally healthy subjects. Molecular genetic assay (Micro-IDent plus, Germany) for complex identification of additional six periodontopathic bacteria was applied. The activity of lysozyme was determined turbidimetrically, the activity of alkaline phosphatase – spectrophotometrically with a “Monarch” biochemical analyzer, the activity b-glucuronidase – according to the method described by Mead et al. and modified by Strachunskii. Results. A statistically significant association between clinical and bacteriological data was found in the following cases: gingival bleeding in the presence of Eubacterium nodatum, Eikenella corrodens, Capnocytophaga spp. (P<0.01); pathological periodontal pockets in the presence of Peptostreptococcus micros (α≤0.05 and β≤0.2), Fusobacterium nucleatum (α≤0.05 and β≤0.2), Campylobacter rectus (α≤0.05 and β≤0.2), and Capnocytophaga spp. (P<0.05); and satisfactory oral hygiene in the presence of all microorganisms investigated (P<0.05). The activity of lysozyme in gingival crevicular fluid and mixed nonstimulated saliva indicates the severity of periodontal inflammation. Based on clinical data, in assessing the amount of lysozyme in mixed nonstimulated saliva, sensitivity and specificity of 100% was found. Increased activities of lysozyme, alkaline phosphatase, and b-glucuronidase were found in peripheral venous blood of patients with inflammatory periodontal disease as compared to control group. Conclusions. The main principles of the treatment of periodontal inflammatory diseases should be based on microorganism elimination, creation of individual treatment means affecting microflora in the mouth and immune system of macroorganisms.

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