Mitochondrial Dysfunction in Periodontitis: Oxidative Stress, Metabolism and Alveolar Bone Loss

Periodontitis is a prevalent chronic inflammatory disease worldwide, characterised by alveolar bone resorption, which is the primary cause of tooth loss in adults. Emerging evidence has consistently underscored the presence of mitochondrial dysfunction within the gingival microenvironment of patients with periodontitis. Beyond their canonical role in adenosine triphosphate (ATP) synthesis, mitochondria orchestrate diverse physiological processes, including intracellular calcium homeostasis, reactive oxygen species (ROS) generation, apoptosis and inflammatory signal transduction. Mitochondrial oxidative stress, precipitated by the disequilibrium between explosive ROS accumulation and endogenous antioxidant defences, is pivotal in driving alveolar bone resorption. This oxidative insult not only impairs the metabolic landscape of periodontal cell populations but also disrupts bone homeostasis by modulating inflammatory cascades and cell fate trajectories. A comprehensive literature review of studies published through August 2026 was conducted to evaluate the impact of mitochondrial oxidative stress on alveolar bone resorption in periodontitis. This review delineates the specific cell populations, molecular mechanisms and signalling networks by which mitochondrial oxidative stress mediates alveolar bone loss in periodontitis, and explores the interplay with periodontal pathogens. It also highlights therapeutic strategies targeting mitochondrial oxidative stress, providing a theoretical framework for precision-targeted interventions against periodontal bone resorption.