The Role of Inflammatory Biomarkers of Crevicular Fluid Involved in Modulating of Immune Protection Mechanisms in Chronic Periodontitis

Abstract

INTRODUCTION: Chronic periodontal inflammation is provoked by persistence of subgingival bacterial flora and is mediated through the production of proinflammatory cytokines that induce the innate immune reactions. АIM: To establish the interrelation of secretion of interleukin 1 and immune component of soluble CD14 co-receptor with the main periodontopathogenic microorganisms in patients with chronic generalized periodontitis. MATERIALS AND METHODS: A clinical and laboratory examination of patients with chronic generalized periodontitis (n = 100) and individuals with the intact parodontium (n = 63) was conducted. Molecular genetic studies (isolation of periodontal pathogens by polymerase chain reaction in real time), immune enzyme assay (isolation of interleukin 1 and soluble CD14 co-receptor) and statistical analysis of the data obtained were performed. RESULTS: The frequency of isolation of periodontopathogenic bacteria in patients with the diagnosis of chronic periodontitis was 96.4% (T. forsythia 81%, р 0.001; P. gingivalis 69%, р 0.001; Tr. denticola 63%, р = 0.054). In 25% of cases, C. Albicans (р 0.001), in 37% Pr. intermedia (р 0.001) and in 30% A. actinomycetemcomitans (р 0.001) were isolated. The average concentrations of soluble CD14 co-receptor were 2.13 [1.89; 2.76] pg/ml in the control group and 20.3 [17.3; 22.5] ng/ml in the group of patients with chronic periodontitis (р 0.001). Concentrations of interleukin 1 were 3.187 [2.356; 4.633] pg/ml in the control group and 33.68 [17.255; 56.915] pg/ml in the group of patients with chronic periodontitis (р 0.001). CONCLUSION: Inflammation of periodontal tissues is supported by the factors of aggression and toxins not only of known periodontal pathogens, but also by their associations, which leads to enhancement of virulence factors and increase in secretion of interleukin 1 and soluble CD14 co-receptor, which, in turn, causes destruction of alveolar bone.