ReviewFrontiers in oral health2026
Oxidative stress and antioxidant pathways in the pathogenesis of periodontitis and peri-implantitis: mechanistic insights and therapeutic potentials.
Review in Frontiers in oral health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
11 authors.
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Abstract
Background: Periodontitis and peri-implantitis are chronic, immune-mediated inflammatory diseases characterized by progressive destruction of tooth- and implant-supporting tissues. Although microbial dysbiosis initiates these conditions, accumulating evidence indicates that host-derived oxidative stress plays a central role in amplifying inflammation, impairing tissue repair, and driving irreversible bone loss. Excessive production of reactive oxygen species (ROS) disrupts redox homeostasis, induces molecular damage, and activates redox-sensitive signaling pathways that perpetuate tissue destruction. Objective: This narrative review synthesizes current mechanistic, clinical, and translational evidence on the role of oxidative stress and antioxidant defense systems in the pathogenesis of periodontitis and peri-implantitis. It further aims to critically evaluate redox-regulated molecular pathways, emerging diagnostic biomarkers, and antioxidant-based therapeutic strategies. Methods: A structured literature search was conducted using PubMed, Scopus, and Web of Science, focusing on recent experimental, clinical, and translational studies. Articles were selected based on relevance, methodological rigor, and translational applicability, with emphasis on studies addressing oxidative stress mechanisms, biomarker validity, and therapeutic interventions. Results: Evidence indicates that excessive ROS generation activates key redox-sensitive signaling pathways, including NF-κB, MAPKs, and AP-1, leading to sustained cytokine production, matrix metalloproteinase activation, mitochondrial dysfunction, and enhanced osteoclastogenesis. Concurrent impairment of endogenous antioxidant systems further exacerbates tissue vulnerability. Oxidative stress biomarkers-such as malondialdehyde, 8-hydroxy-2'-deoxyguanosine, and protein carbonyls-demonstrate associations with disease severity and treatment response; however, their clinical utility is limited by methodological heterogeneity and lack of standardization. Antioxidant-based interventions, including systemic supplementation, local delivery systems, nano-formulations, and antioxidant-enriched biomaterials, show promising adjunctive effects, although clinical outcomes remain variable due to differences in bioavailability, dosage, and patient-specific factors. Conclusion: Oxidative stress represents a central, disease-modifying axis in periodontitis and peri-implantitis. Targeting redox imbalance offers a biologically grounded framework for improving diagnostics, risk stratification, and host-modulatory therapy. However, translation into clinical practice requires standardized biomarker validation and rigorously designed, biomarker-guided clinical trials. Future strategies integrating redox biology with advanced delivery systems and precision medicine approaches may significantly enhance periodontal and peri-implant care.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.