Abstract
Background: It is known that mitochondrial dysfunction is involved in the pathogenesis and progression of periodontitis, affecting oxidative stress and regulating inflammatory reactions. Therefore, in recent years, research on mitochondria-directed therapeutic approach to periodontal tissue diseases has been rapidly growing. AIM: Evaluate the effect of the drugs Metrogyl and Aicar on structural and functional disorders in the mitochondria of periodontal tissues in an experimental model of periodontitis in laboratory rats. Materials and methods: Male white Wistar rats weighing 221 ± 7.5 g at the age of 4 months were used in this work. The animals were divided by simple randomization into four groups, 10 animals in each: Group 1 – intact (control group); Group 2 – rats with modeled periodontitis; Group 3 – rats with modeled periodontitis and the use of Metrogyl; Group 4 – rats with modeled periodontitis and combined use of Metrogyl and Aicar. Experimental periodontitis (EP) in rats was modeled by the ligature method by suturing a polyfilament non-absorbable thread into the gum in the area of the lower incisors. The following molecular genetic and biochemical parameters were used: damage to nuclear DNA (nDNA) and mitochondrial DNA (mtDNA), mtDNA copy number and the level of heteroplasmy, as well as the levels of malondialdehyde (MDA) and reduced glutathione (GSH). Results: The data from this study showed that on the 14th day after ligation, animals in the periodontal tissue have an increased level of damage and mtDNA heteroplasmy, compared to the control group. The same animals showed a decrease in the GSH level, while the MDA level was increased compared to the control animals. In other groups of rats with EP, the modulation of these damages was assessed using Metrogyl, as well as the combined use of Metrogyl and Aicar. It was shown that for all the parameters studied, the combined use of Metrogyl and Aicar led to a more effective reduction in mitochondrial disorders, compared to the group of rats that received only Metrogyl. Conclusions: The combined use of Metrogyl and Aicar drugs had a more effective effect on reducing mitochondrial dysfunction in periodontal tissue in rats with EP, in contrast to the group in which only Metrogyl was used. Thus, the use of traditional drugs in combination with mitochondria-targeted compounds that reduce oxidative stress may serve as a new therapeutic approach to various periodontal tissue diseases.
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More From: A.I. Burnasyan Federal Medical Biophysical Center Clinical Bulletin
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