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.
Highlights
Медицинская Иммунология Medical Immunology (Russia)/Meditsinskaya Immunologiya and inflammatory/immune cells migrating to the periodont
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
Summary
Микрофлора ротовой полости формирует биопленку, индуцирующую хроническое воспаление, при котором последствия инфекции играют решающую роль в патогенезе пародонтита. Исследование уровня нейтрофилов CD64+CD16+CD14- при различных степенях тяжести пародонтита выявило статистическ и значимое увеличение количества клеток при развитии заболевания. При легкой степени тяжести ХГП выявилось существенное повышение уровня CD64+CD16+CD14- Me = 36,16% (p < 0,05) по сравнению с контрольной группой (Me = 7,7%; Q0,25 = 2,4%; Q0,75 = 12%). Исследование относительного количества моноцитов CD14+ при различных степенях тяжест и пародонтита выявило статистически значимое снижение количества клеток тяжелой степени пародонтита. Исследование уровня регуляторных T-лимфоцитов CD4+CD25+CD127low при различных степенях тяжести пародонтита выявило статистически значимое снижение количества клеток при развитии заболевания: при легкой степени тяжести ХГП (Me = 5,6%; Q0,25 = 1,8%; Q0,75 = 8%) по сравнению с контрольной группой (Me = 22,7%; Q0,25 = 12%; Q0,75 = 32%). Понимание остеоиммунных механизмов контроля ремоделирования костной ткани позволит понять патофизиологию ускоренной потери костной массы, наблюдаемой при хроническом пародонтите тяжелой степени
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