The Influence of Thyroid Hormones on Protein Oxidative Modification in Case of Experimental Periodontitis

Abstract

Introduction. The inflammatory-dystrophic process in periodontium is accompanied by its hypoxia, which causes the activation of free radical oxidation processes. Tissue destruction in periodontal diseases is considered to be the result of an altered inflammatory/immune response to microbial plaque and involves massive release of neutrophils, reactive oxygen species and enzymes.
 The aim of the study – to establish the protein oxidative modification in blood and periodontium in case of periodontitis combined with hyper- and hypothyroidism in rats.
 Research Methods. Experimental studies were carry out on 48 mature male, nonliner, white rats, which were divided into the following groups: І – control animals; ІІ – animals with periodontitis; ІІІ – animals with periodontitis combined with hyperthyroidism; IV – animals with periodontitis combined with hypothyroidism. Protein oxidative modification (POM) was determined in blood serum and periodontium homogenate by the method of I.F. Meschyshyn.
 Results and Discussion. The results of our studies showed that the intensity of the processes of protein oxidative modification was significantly increased in animals of all experimental groups vs control group. The content of aldehyde- and ketone derivatives of the alkali nature changed more pronounced than the content of aldehyde and ketone derivatives of neutral nature.
 Conclusions. Thus, the experimental periodontitis is accompanied by a marked increase in the intensity of the protein oxidative modifications both in the homogenate of periodontal tissues and in the blood serum. Imbalance of thyroid hormones increases oxidative stress in experimental periodontitis, especially pronounced in hyperthyroidism.

Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review

“…Aside from effects on cellular behaviors of osteoblasts and osteoclasts, TH further modifies oxidative homeostasis, immuno-inflammatory responses and local microbiome in periodontitis tissue. Thyroid dysfunctions tend to intensify oxidative stress in periodontitis, enhancing the amplitude of both lipids peroxide oxidation and protein oxidative modifications [ 100 , 101 ]. Compared to controls with periodontitis only, rats with comorbidity of experimental periodontitis and thyroid disorders were found to have more neutrophils with decreased transmembrane potential, which further triggered cellular apoptosis of neutrophils by overproducing reactive oxygen species (ROS) and destructing the mitochondrial inner membrane.…”