Mitochondrial Dynamics and Oxidative Stress in Periodontitis

Yibing Wang¹, Xingbo Wu¹, Yifei Shen¹, Xiayi Wang¹, Chun Hung Chu², Irene Shuping Zhao^2,3, Xueqi Gan^1,*
1 State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Department of Prosthodontics, Sichuan University, Chengdu, China
2 Faculty of Dentistry, The University of Hong Kong, Hong Kong, China
3 School of Dentistry, Shenzhen University Medical School, Shenzhen, China
* Corresponding Author: Xueqi Gan. Email: email
(This article belongs to the Special Issue: Modulation of Inflammation, Oxidative Stress, and Mitochondrial Function: Therapeutic Perspectives Across Diseases)

BIOCELL https://doi.org/10.32604/biocell.2026.079089

Received 14 January 2026; Accepted 11 March 2026; Published online 24 March 2026

Download PDF

Abstract

Periodontitis is a prevalent inflammatory disease characterized by the progressive destruction of tooth-supporting tissues. Its pathogenesis remains incompletely understood, but accumulating evidence highlights mitochondrial dynamics imbalance and oxidative stress as interconnected drivers. However, comprehensive reviews elucidating the molecular basis of this interaction are lacking. Therefore, this review aims to clarify the crosstalk between mitochondrial dynamics dysregulation and oxidative stress, and how this bidirectional interaction contributes to periodontal tissue destruction. This review first provides an overview of mitochondrial dynamics and the mechanisms of oxidative stress. We then contextualize these processes within periodontitis, detailing the dual role of reactive oxygen species (ROS), alongside imbalances in mitochondrial dynamics. Crucially, the review demonstrates how dysregulated mitochondrial dynamics, including excessive mitochondrial fission, impaired fusion, and defective mitophagy, lead to mitochondrial fragmentation and mitochondrial ROS (mtROS) overproduction, thereby amplifying inflammatory signaling. Conversely, sustained oxidative stress directly damages periodontal tissues and impairs mitochondrial quality control mechanisms, establishing a vicious cycle of mitochondrial dysfunction and ROS accumulation. Finally, we summarize emerging therapeutic strategies targeting mitochondrial dynamics and oxidative stress pathways. This review provides a deeper understanding of periodontitis pathogenesis and highlights this approach as a promising therapeutic paradigm.