The role of mitochondrial dysfunction in periodontitis: From mechanisms to therapeutic strategy

Abstract

Periodontitis is an inflammatory and destructive disease of tooth‐supporting tissue and has become the leading cause of adult tooth loss. The most central pathological features of periodontitis are tissue damage and inflammatory reaction. As the energy metabolism center of eukaryotic cells, mitochondrion plays a notable role in various processes, such as cell function and inflammatory response. When the intracellular homeostasis of mitochondrion is disrupted, it can lead to mitochondrial dysfunction and inability to generate adequate energy to maintain basic cellular biochemical reactions. Recent studies have revealed that mitochondrial dysfunction is closely related to the initiation and development of periodontitis. The excessive production of mitochondrial reactive oxygen species, imbalance of mitochondrial biogenesis and dynamics, mitophagy and mitochondrial DNA damage can all affect the development and progression of periodontitis. Thus, targeted mitochondrial therapy is potentially promising in periodontitis treatment. In this review, we summarize the above mitochondrial mechanism in the pathogenesis of periodontitis and discuss some potential approaches that can exert therapeutic effects on periodontitis by modulating mitochondrial activity. The understanding and summary of mitochondrial dysfunction in periodontitis might provide new research directions for pathological intervention or treatment of periodontitis.

Association between metal exposures and periodontitis among U.S. adults: the potential mediating role of biological aging

“…5 Overall effects of metal exposures on periodontitis in the subgroups with different smoking status. A Non-smokers (without tobacco exposure), B second-hand smokers, C smokers malfunction and induced mitochondrial DNA mutations [51], which induce excessive production of ROS [52] in mitochondria, causing oxidative phosphorylation dysfunction and cellular apoptosis through MAPK pathway [53], which exacerbate biological aging in periodontal tissues [54]. Furthermore, previous animal experiments have shown that excessive ROS is strongly associated with alveolar bone resorption in rats [55].…”

Matrix Metalloproteinases in the Periodontium—Vital in Tissue Turnover and Unfortunate in Periodontitis

“…This article will not discuss the pathogenesis of periodontitis and associated conditions, on which there are many excellent papers [ 186 , 187 , 188 , 189 , 190 , 191 , 192 , 193 , 194 , 195 , 196 , 197 , 198 , 199 ], but we must present, in short, the most significant cellular and molecular changes affecting the periodontal ECM, causing anatomical disturbances.…”

Integrated analyses revealed the potential role and immune link of mitochondrial dysfunction between periodontitis and type 2 diabetes mellitus

“…Previous research has also demonstrated that periodontitis is closely associated with MD. Multiple investigations have revealed that periodontitis patients have increased ROS production, a reduced level of adenosine triphosphate (ATP), and a reduced mitochondrial membrane potential (MMP), resulting in cell mortality in the periodontium and inhibition of tissue regeneration [12,32]. MD is caused by an unbalanced internal environment in the periodontal tissue [23].…”