The Role of Reactive Oxygen Species and Autophagy in Periodontitis and Their Potential Linkage

Abstract

Periodontitis is a chronic inflammatory disease that causes damage to periodontal tissues, which include the gingiva, periodontal ligament, and alveolar bone. The major cause of periodontal tissue destruction is an inappropriate host response to microorganisms and their products. Specifically, a homeostatic imbalance between reactive oxygen species (ROS) and antioxidant defense systems has been implicated in the pathogenesis of periodontitis. Elevated levels of ROS acting as intracellular signal transducers result in autophagy, which plays a dual role in periodontitis by promoting cell death or blocking apoptosis in infected cells. Autophagy can also regulate ROS generation and scavenging. Investigations are ongoing to elucidate the crosstalk mechanisms between ROS and autophagy. Here, we review the physiological and pathological roles of ROS and autophagy in periodontal tissues. The redox-sensitive pathways related to autophagy, such as mTORC1, Beclin 1, and the Atg12-Atg5 complex, are explored in depth to provide a comprehensive overview of the crosstalk between ROS and autophagy. Based on the current evidence, we suggest that a potential linkage between ROS and autophagy is involved in the pathogenesis of periodontitis.

Assessment of microRNA‐144‐5p and its putative targets in inflamed gingiva from chronic periodontitis patients

“…These results may suggest its potential regulatory role in chronic periodontal inflammation. Autophagy is double‐edged sword in periodontitis by promoting cell death or blocking apoptosis . Researchers detected upregulation of microtubule‐associated protein 1 light chain 3 ( MAP1LC3 / LC3 , a key protein contributing to major steps of autophagy) and autophagosome production in periodontal ligament tissues from mild/moderate chronic periodontitis patients .…”

Dental Stem Cell-Derived Secretome/Conditioned Medium: The Future for Regenerative Therapeutic Applications

“…A delicate balance normally exists between antioxidants and oxidants in human tissues, where excessive reactive oxygen species (ROS) are effectively neutralized by antioxidants [199,200]. Low concentrations of ROS could be beneficial, aside from oxidation-reduction (redox) reactions, which may have a regulatory function, in protecting cells from apoptosis [201]. On the contrary, higher concentrations of ROS may cause direct cells' oxidation, aggravated inflammation, unregulated autophagy activity, and drives apoptosis, eventually resulting in tissue damage and dysfunction [199,200,202].…”

The role of autophagy in the pathogenesis of periodontal disease

“…The LPS of Pg induced autophagy of human gingival fibroblasts (HGFs) by promoting production of autophagy‐related proteins (ATG5, ATG12, and LC3) (Bullon et al, ; Liu, Wang, Zheng, & Luan, ) and up‐regulating the ratio of LC3‐II/LC3‐I, production of mitochondrial reactive oxygen species (mtROS), mitochondrial autophagy and autophagic cells (Liu, Li, Zhang, Cao, & Zhang, ). As an antioxidant, coenzyme Q10 (CoQ10) suppressed the above autophagy induction of LPS in Pg (Liu, Mo et al, ). The PI3K/Akt/mTOR signaling pathway was involved in the regulation of LPS from Pg on autophagy.…”

“…As an antioxidant, coenzyme Q10 (CoQ10) suppressed the above autophagy induction of LPS in Pg (Liu, Mo et al, 2017). The PI3K/ Akt/mTOR signaling pathway was involved in the regulation of LPS from Pg on autophagy.…”