Shcherba V. V., Korda M. M.

PHAGOCYTIC AND METABOLIC ACTIVITY OF BLOOD NEUROFILS IN RATS WITH PERIODONTITIS ON THE BACKGROUND OF HYPER- AND HYPOTHYROIDISM


About the author:

Shcherba V. V., Korda M. M.

Heading:

DENTISTRY

Type of article:

Scentific article

Annotation:

In recent years, periodontal disease has become of the global medical and social problem due to their widespread and adverse effects on the overall health of the population. Inflammatory periodontal disease are considered not only as a local inflammation of the tissues surrounding the tooth, caused by the microflora of the plaque, but also as the body’s response to bacterial infection. The aim of our study was to investigate the phagocytic and metabolic activity of blood neutrophils in rats with periodontitis without concomitant pathology and combined with hyperthyroidism and hypothyroidism. The study was conducted on 48 white male rats, which were divided into the following groups: I – control animals; ІІ – animals with the model of periodontitis; III – rats with periodontitis and hyperthyroidism; IV – rats with periodontitis and hypothyroidism. As indices of phagocytosis, phagocytic activity, phagocytic index and phagocytic number were determined. Oxygen dependent bactericidal activity of blood neutrophils was studied using nitrosin tetrazolium test (NST-test). The increase of phagocytic activity of blood neutrophils (by 25.3%; p<0.001) and decrease by 1.4 times (p<0.001) of their absorption capacity in animals with simulated periodontitis was found. The number of diphorosa-positive cells in the spontaneous NST-test in animals with simulated periodontitis significantly increased by 32.8% and in the activated group by 40.1% relative to the control group. When calculating the metabolic activation factor, its reliable increase was set by 41.0%. In rats with periodontitis, against the hypothyroidism, the phagocytic activity of blood neutrophils relative to control has not significantly changed, but it was by 23.9% (p<0.001) lower relative to animals with simulated periodontitis without concomitant pathology and by 16.1% (p<0.001) lower in comparison with rats with periodontitis and hyperthyroidism. The number of dyroxant-positive cells in the activated NST-test in this group of animals did not significantly change with respect to control, but was by 24.9% lower for animals with simulated periodontitis without concomitant pathology and by 31.7% lower compared to rats with periodontitis and hyperthyroidism. At the same time, the reserve indicator was by 14.9% significantly lower in relation to control, and by 20.8% less in relation to animals with simulated periodontitis without concomitant pathology and did not significantly change compared with rats with periodontitis and hyperthyroidism. The metabolic activation coefficient in rats with periodontitis and hypothyroidism was by 25.6% (p<0.001) lower in animals with simulated periodontitis without concomitant pathology and by 32.2% (p<0.001) less in comparison with rats with periodontitis and hyperthyroidism. Thus, inflammation, subject to experimental periodontitis, runs on the background of altered phagocytosis, whose dysfunction is accompanied by an increase in the phagocytic activity of neutrophils and a simultaneous decrease in their absorbing capacity. The increase in the parameters of the spontaneous and activated NST-test under the condition of the experimental periodontitis indicates activation of oxygens-dependent mechanisms of phagocyte killing and their bactericidal property. The imbalance of thyroid hormones in the condition of experimental periodontitis significantly affects the functional and metabolic activity of phagocytes, especially in hypothyroidism, which indicates the depletion of metabolic reserves of these cells and the violation of the process of phagocytosis.

Tags:

periodontitis, hyperthyroidism, hypothyroidism, neutrophils

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Publication of the article:

«Bulletin of problems biology and medicine» Issue 1 Part 2 (143), 2018 year, 373-378 pages, index UDK 616.314.17-008.1-06:616.441-008.61/64-06:616.155.34]-092.9

DOI: