Oxidative Stress and Oral microbiota in Periodontitis (Brief-Review)

International Journal of Biomedicine, Dec 2025

The investigation of periodontitis pathogenesis is critically important due to its global prevalence. It has been established that periodontitis is associated with chronic periodontal inflammation, alveolar bone loss, the development of oxidative stress, and oral microbiota dysbiosis. Oxidative stress biomarkers (e.g., malondialdehyde, 8-OHdG) and genetic factors (CXCR4, SELL, ITGAL) exacerbate tissue damage and osteoclastogenesis. The oral microbiota plays a significant role in the development and progression of periodontitis through complex interactions with host immune responses, mediated by pathogenic bacteria like Porphyromonas gingivalis and their metabolic byproducts. Emerging therapies targeting OS (e.g., resveratrol, curcumin) and microbial balance highlight the need for integrated treatment strategies. In this context, it is particularly relevant to investigate the interplay between oxidative stress and microbial dysbiosis to develop targeted therapeutic strategies for the prevention and treatment of periodontitis and its systemic complications.

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Oxidative Stress and Oral microbiota in Periodontitis (Brief-Review)

International Journal of Biomedicine 15(4) (2025) 634-638 http://dx.doi.org/10.21103/Article15(4)_RA2 REVIEW ARTICLE INTERNATIONAL JOURNAL OF BIOMEDICINE Oxidative Stress and Oral Microbiota in Periodontitis (Brief-Review) Marina A. Darenskaya1*, Ivan S. Goncharov1,2, Natalya A. Yuzvak1, Sergey I. Kolesnikov1, Natalya E. Bolshedvorskaya2, Lyubov I. Kolesnikova1 1 2 Scientific Centre for Family Health and Human Reproduction Problems, Irkutsk, Russian Federation Irkutsk State Medical University, Irkutsk, Russian Federation Abstract The investigation of periodontitis pathogenesis is critically important due to its global prevalence. It has been established that periodontitis is associated with chronic periodontal inflammation, alveolar bone loss, the development of oxidative stress, and oral microbiota dysbiosis. Oxidative stress biomarkers (e.g., malondialdehyde, 8-OHdG) and genetic factors (CXCR4, SELL, ITGAL) exacerbate tissue damage and osteoclastogenesis. The oral microbiota plays a significant role in the development and progression of periodontitis through complex interactions with host immune responses, mediated by pathogenic bacteria like Porphyromonas gingivalis and their metabolic byproducts. Emerging therapies targeting OS (e.g., resveratrol, curcumin) and microbial balance highlight the need for integrated treatment strategies. In this context, it is particularly relevant to investigate the interplay between oxidative stress and microbial dysbiosis to develop targeted therapeutic strategies for the prevention and treatment of periodontitis and its systemic complications. (International Journal of Biomedicine. 2025;15(4):634-638.) Keywords: periodontitis • pathogenesis • oxidative stress • inflammation • oral microbiome • systemic links For citation: Darenskaya MA, Goncharov IS, Yuzvak NA, Kolesnikov SI, Bolshedvorskaya NE, Kolesnikova LI. Oxidative Stress and Oral Microbiota in Periodontitis (Brief-Review). International Journal of Biomedicine. 2025;15(4):634-638. doi:10.21103/ Article15(4)_RA2 Abbreviations 8-OhdG, 8-hydroxy-2-deoxyguanosine; AH, arterial hypertension; AOD, antioxidant defense; CAT, catalase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, reduced glutathione; LPO, lipid peroxidation; NO, nitric oxide; OS, oxidative stress; ROS, reactive oxygen species; SOD, superoxide dismutase; TBARs, thiobarbituric acid reactants; WHO, World Health Organization. Relevance of Studying Periodontitis Periodontitis is one of the most common diseases, affecting between 50% and 90% of individuals in developing countries and between 4% and 76% in developed countries 1 According to the World Health Organization (WHO). intact periodontitis occurs only in 2-10% of cases, while inflammatory periodontal diseases are detected in 90-95% of the adult population.2 Periodontitis is characterized by prolonged periodontal inflammation, including the gum, periodontal ligament, and alveolar bone, with loss of the latter.3 The main cause, as a rule, is pathogenic microorganisms contained in plaque.4 The decisive predisposing factors are the fact of smoking, poor oral hygiene, genetic component, gastrointestinal disorders, etc.5 At a young age, traumatic effects, bleeding gums, partial dentition, low bone mineral density, and obesity are added.6 It was also noted that disorders in the immune system, local changes in acid-base balance, hypoxia, and other adverse factors contribute to the proliferation of pathogenic microorganisms, an increase in the activity of opportunistic infection, and the progression of inflammatory and destructive periodontal diseases.7 In recent years, it has been proven that periodontitis, as an inflammatory process, can be epidemiologically related to other chronic diseases, which include cardiovascular, neurodegenerative, autoimmune, oncological, and others.8-10 Understanding the pathology and etiology of periodontitis is crucial to developing effective approaches to periodontitis treatment. Oxidative Stress in Periodontitis Genesis Currently, more than 200 diseases associated with the involvement of free radicals are known. They are characterized by changes in the internal environment and vascular disorders, which indicate a single mechanism of development – an M. A. Darenskaya et al. / International Journal of Biomedicine 15(4) (2025) 634-638 imbalance in the “lipid peroxidation (LPO) – antioxidant defense (AOD) “LPO – AOD system. The term oxidative stress (OS) is widely used to describe this imbalance.11 LPO-AOD plays an important role in adaptive reactions, reducing the activity of inflammatory processes, pathology, and maintaining homeostasis.12 The predominant role of this type of reaction in modifying cell membrane structure, xenobiotic metabolism, regulating the immune response, cell proliferation, vascular permeability, and receptor sensitivity is well established.13 The activation of LPO reactions in the membranes of the endoplasmic reticulum, mitochondria, and lysosomes undoubtedly plays a crucial role in the functioning of normal cellular systems, presumably determining overall reactivity and resistance to pathogenic factors.14 Modern studies confirm that the insufficiency of AOD factors contributes to the uncontrolled intensification of LPO processes, which play a crucial role in the development of various pathologies, including those associated with periodontal disorders.15 Moreover, the development of OS occurs not only due to a decrease in the buffer capacity of the AOD system, but also due to a violation of its mobilization in response to an increase in the activity of prooxidant factors. Protection of cells from LPO at different stages is implemented by various systems of both enzymatic and nonenzymatic nature.16 At the same time, LPO reactions in the membranes of various cellular compartments play a crucial role in determining the overall reactivity of the body and its resistance to pathogenic influences.17 It was proven that OS plays a key role in the pathogenesis of periodontitis. Studies revealed changes in the expression of genes associated with oxidative stress (OS genes) in patients with periodontitis.18,19 In total, 74 genes were isolated in periodontitis, the expression of which changes during OS, including 65 genes with increased expression and 9 genes with reduced expression. Six key genes (CXCR4, SELL, FCGR3B, FCGR2B, PECAM1, and ITGAL) are involved in leukocyte intercellular adhesion, phagocytosis, and cellular extravasation, which highlights their role in the pathogenesis of the disease.20 CXCR4 is one of the most expressed OS genes in periodontal tissues. It plays a key role in podocyte damage, proteinuria, and glomerular sclerosis under oxidative stress. The neutralization of CXCR4 suppresses the resorption of the alveolar bone in periodontal inflammation. CXCR4 also suppresses the release of nitric oxide from macrophages and is involved in modulating mechanical sensitivity in periodontitis. (...truncated)


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Marina A. Darenskaya, Ivan S. Goncharov, Natalya A. Yuzvak, Sergey I. Kolesnikov, Natalya E. Bolshedvorskaya, Lyubov I. Kolesnikova. Oxidative Stress and Oral microbiota in Periodontitis (Brief-Review), International Journal of Biomedicine, 2025, pp. 634-638, Volume 4, DOI: 10.21103/Article15(4)_RA2