Research progress on the role of mitochondrial dysfunction in the occurrence, progression and treatment of periodontitis

Periodontitis is a widespread disease worldwide, with the primary cause of tissue loss being an immune inflammatory response mediated by bacteria. Increasing evidence has revealed a significant correlation between mitochondrial dysfunction and the occurrence and progression of periodontitis. This paper provides a review of current research on the role of mitochondrial dysfunction in the occurrence and development of periodontitis and related therapies from the perspectives of oxidative stress, inflammatory responses, and the regulation of mitochondrial homeostasis. Mitochondria are the main source and target of cellular reactive oxygen species. Mitochondrial dysfunction can generate large amounts of reactive oxygen species, exacerbating local oxidative stress in periodontal tissues and causing cell toxicity and tissue damage. Mitochondria are also the center of cellular inflammatory responses, and the positive feedback loop of inflammation induced by mitochondrial dysfunction may explain the persistent and unresolved nature of periodontitis. Biomaterials loaded with pharmacological agents show potential in restoring mitochondrial function, controlling the development of periodontitis, and promoting periodontal tissue regeneration. However, the key sites of mitochondrial dysfunction in the occurrence and development of periodontitis are not yet fully understood, and the improvement of mitochondrial function in periodontal therapy is still in the experimental stage. Future research efforts should focus on the effect of mitochondrial dysfunction on periodontal cells and explore its specific mechanism in the occurrence and progression of periodontitis in order to provide new insights into the treatment of periodontitis.