Detecting structural and functional mitochondrial abnormalities in periodontal tissues using an experimental periodontitis model

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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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作者简介

Albina Abdullaeva

Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency

编辑信件的主要联系方式.
Email: albi.95@mail.ru
ORCID iD: 0009-0002-0538-7454
SPIN 代码: 4355-9186

MD

俄罗斯联邦, Moscow

Valentina Olesova

Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency

Email: olesova@implantat.ru
ORCID iD: 0000-0002-3461-9317
SPIN 代码: 6851-5618

MD, Dr. Sci. (Medicine), Professor

俄罗斯联邦, Moscow

David Akopov

Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency

Email: akopov.85@bk.ru
ORCID iD: 0009-0000-0603-9406

MD

俄罗斯联邦, Moscow

Serazhutdin Abdullaev

Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency

Email: saabdullaev@gmail.com
ORCID iD: 0000-0002-1396-0743
SPIN 代码: 3485-8990

Dr. Sci. (Biology)

俄罗斯联邦, Moscow

参考

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2. Fig. 1. Modeling of periodontitis in laboratory animals of the experimental group: a — application of a ligature by sewing a polyfilament non-absorbable thread into the gum in the area of the lower jaw incisors; b — soft tissues of the periodontium of the studied group of animals on the 14th day of the experiment after application of ligatures; staining with fuchsin and picric acid; ×100.

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3. Fig. 2. Analysis of nuclear and mitochondrial DNA damage and repair. Amplification of long nDNA (8.7 kilobase pairs) and mDNA (10.9 kilobase pairs) fragments by long-distance quantitative polymerase chain reaction. The results are standardized by measured short nDNA (110 base pairs) and mDNA (117 base pairs) fragments from the same DNA samples. EIPD, experimentally induced periodontal disease; C, control; nDNA, nuclear DNA; mDNA, mitochondrial DNA; PCR, polymerase chain reaction. The data are presented as percentages relative to the control group of rats; * the significance level is p <0.05.

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4. Fig. 3. Analysis of total (a) and mutant (b) mitochondrial DNA copies in periodontal tissues. EIPD, experimentally induced periodontal disease group; C, control group; mDNA, mitochondrial DNA. The data are presented as percentages relative to the control group of rats; * the significance level is p <0.05.

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5. Fig. 4. Expression of mDNA genes involved in oxidative phosphorylation (ATP6, ND2, CytB) in soft periodontal tissues of rats with experimentally induced periodontal disease (EIPD). The data are presented as percentages relative to the control group of rats (C); * the significance level is p <0.05.

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6. Fig. 5. Changes in H2О2, malondialdehyde (MDA), and glutathione concentrations in soft periodontal tissues of rats with experimentally induced periodontal disease (EIPD). The data are presented as percentages relative to the control group of rats (C); * the significance level is p < 0.05.

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СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
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