Abstract
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.
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.