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Local cellular immune response in chronic periodontitis

https://doi.org/10.15789/1563-0625-LCI-2377

Abstract

Microflora of the oral cavity forms a biofilm that induces response of immune system at the mucous membranes. Transition to periodontal lesion is provided by certain classes of resident mucosal immune cells and inflammatory/immune cells migrating to the periodont. In periodontal diseases, Th1, Th2, Th17, Treg are detected. T regulatory cells (Tregs) are proven to comprise the main anti-inflammatory cell population. Th17 cells and Treg cells play an important role in osteoclast differentiation. IL-17 secreted by Th17 cells affects osteoclastogenesis and may induce macrophages to enhance the local inflammatory response. In this regard, the aim of our work was to identify the local immune cells in oral cavity which are associated with severity of chronic generalized periodontitis. The oral cavity cells from 58 persons aged 38-65 years of both sexes in their mature age with a diagnosis of «chronic periodontitis» were examined by means of flow cytofluorometry. When determining levels of CD64+CD16+CD14- neutrophils in the patients with periodontitis of different severity, a statistically significant increase of this cell population was revealed upon development of this disease. In mild cases of periodontitis, a significant increase of relative CD64+CD16+CD14-  neutrophil contents was revealed (Me = 36.16%, p < 0.05) compared to the control group (Me = 7.7%, Q0.25 = 2.4%, Q0.75 = 12%). When assessing relative numbers of CD14+ monocytes in periodontitis of various severity, we revealed a significant increase in the number of these cells in severe cases. When studying levels of regulatory T lymphocytes (CD4+CD25+CD127low) in periodontitis of different severity, we revealed significantly decreased amounts of this cell population during development of the disease. In mild cases of periodontitis, a decreased level of CD4+CD25+CD127low cells (p < 0.05, Me = 1356 cells/ml) was revealed, as compared with control group (Me = 10666 cells/ml). Although the concentration of CD4+CD25+CD127low (Me = 4709 cells/ml) in the patients with moderate periodontitis was higher than the values in milder cases, the range of the main values was comparable and lower, than in control group. In severe periodontitis, a significantly decreased concentration of regulatory T lymphocytes was revealed (Me = 2637 cells/ml). These results confirm the anti-inflammatory regulatory function of Tregs. Understanding the osteo-immune mechanisms of bone remodeling control will help to understand the pathophysiology of accelerated bone loss observed in severe chronic periodontitis.

About the Authors

V. P. Mudrov
Russian Medical Academy for Postgraduate Medical Education
Russian Federation

PhD (Medicine), Assistant Professor, Department of Medical Biochemistry and Immunopathology, Academic Center of Fundamental and Translational Medicine, Russian MAPME; Doctor of Clinical Laboratory Diagnostics, Diagnostic Clinical Center No. 1, Moscow City Health Department.

Moscow


Competing Interests:

no



N. V. Davidova
N. Burdenko Main Military Clinical Hospital
Russian Federation

Doctor of Clinical Laboratory Diagnostics.

Moscow


Competing Interests:

no



T. E. Mishina
Russian Medical Academy for Postgraduate Medical Education
Russian Federation

Doctor of Clinical Laboratory Diagnostics.

Moscow


Competing Interests:

no



S. P. Kazakov
Russian Medical Academy for Postgraduate Medical Education; N. Burdenko Main Military Clinical Hospital
Russian Federation

PhD, MD (Medicine), Associate Professor, Head, Department of of Medical Biochemistry and Immunopathology, Academic Centre for Translational and Fundamental Medicine, Russian MAPME; Head, Centre of Clinical Laboratory Diagnostics, N. Burdenko Main Military CH


Competing Interests:

no



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For citations:


Mudrov V.P., Davidova N.V., Mishina T.E., Kazakov S.P. Local cellular immune response in chronic periodontitis. Medical Immunology (Russia). 2021;23(6):1389-1394. (In Russ.) https://doi.org/10.15789/1563-0625-LCI-2377

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ISSN 1563-0625 (Print)
ISSN 2313-741X (Online)