<p>Periodontitis is a highly prevalent biofilm-associated chronic inflammatory disease that is a major cause of tooth loss and is linked to increased risk of cardiovascular disease, diabetes, adverse pregnancy outcomes, and other systemic disorders. Beyond classical concepts of plaque-induced inflammation, accumulating evidence suggests that mitochondrial dysfunction and mitochondrial aging are closely associated with the inflammatory and degenerative periodontal microenvironment. Hallmarks of mitochondrial aging, including excessive mitochondria-derived reactive oxygen species, mtDNA damage and leakage, impaired NAD⁺/sirtuin signaling, disturbed mitochondrial dynamics, defective mitophagy, and metabolic reprogramming, are observed in gingival epithelial cells and fibroblasts, periodontal ligament fibroblasts (PDLCs) and stem cells (PDLSCs), osteoblasts, osteoclasts, osteocytes, and resident and infiltrating immune cells. These changes are closely linked to cellular senescence, senescence-associated secretory phenotype (SASP), NLRP3 inflammasome activation, and uncoupling of bone formation and resorption. Extracellular vesicles can mediate the transfer of damaged mitochondria and regulatory nucleic acids between immune cells and mesenchymal stem cells. Through this process, they may reshape the stem cell niche, influence periodontal bone loss, and modulate orthodontic tooth movement. This review integrates current evidence on mitochondrial aging across periodontal cell populations and delineates a mitochondrial dysfunction–cellular senescence–SASP axis in periodontal tissue breakdown. It further summarizes mitochondria-targeted interventions, including MitoQ, resveratrol, coenzyme Q10, strategies that enhance mitophagy in PDLSCs, mitochondrial transplantation, and engineered exosomes, outlining a framework in which mitochondrial imbalance contributes to periodontal inflammation and tissue breakdown and may represent a potential therapeutic target.</p>