Abstract
Background: Recent research indicates that mitochondrial dysfunction plays a significant role in the development and progression of oral inflammation, such as periodontitis and pulpitis. Aim: To assess structural and functional mitochondrial abnormalities in periodontal tissues using an experimental periodontitis model in rats. Materials and methods: The study used male Wistar rats aged 4 months, with a body weight of 221.0±7.5 g. Simple randomization was used to divide the animals into two groups (n=10 each). Group 1 (control) consisted of intact animals, while Group 2 consisted of animals with experimentally induced periodontitis. A ligature-induced periodontitis model was used, with a non-absorbable polyfilament thread sutured into the gum near the mandibular incisors. Histological examinations were used to validate the experimental periodontitis model. The following molecular genetic and biochemical parameters were assessed: nuclear DNA and mitochondrial DNA (mtDNA) damage, abundance and heteroplasmy of mtDNA, mitochondrial gene expression, and levels of hydrogen peroxide (H2O2), malondialdehyde, and reduced glutathione. Results: The resulting experimental periodontitis model revealed histological changes in periodontal tissues, indicating periodontitis in the animals. On day 14 after ligation, histological findings showed that Group 2 had more significant mtDNA damage and heteroplasmy in periodontal tissues than Group 1 (control). Moreover, Group 2 showed a decrease in the expression of mtDNA genes involved in adenosine triphosphate synthesis. This group also had lower glutathione levels and higher H2O2 and malondialdehyde levels than the control group. Conclusion: The experimental periodontitis model in rats revealed structural and functional mitochondrial abnormalities in periodontal tissues. New approaches to assessing mitochondrial function in periodontitis may facilitate the diagnosis and treatment of the disease and its complications.
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