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.
Highlights
Periodontitis is an inflammatory disease that compromises the integrity of the tooth-supporting tissues through the interplay of periodontal pathogens and the host immune response (Kinane et al, 2008; Dumitrescu, 2016)
This study reported that Jun N-terminal kinase (JNK) activation could induce the expression of genes that counter oxidative stress (Cat, Sod2, Prdx3) and apoptosis (Bcl-6) via the activation of the transcription factor forkhead box protein O1 (FoxO1) (Wang et al, 2015)
Compared with blood PMNs, thirty nuclear factor erythroid 2-related factor 2 (Nrf2) pathway-related genes were differentially expressed in oral polymorphonuclear neutrophils (oPMNs) from chronic periodontitis patients (Sima et al, 2016). These results indicated that Nrf2 and its downstream genes may be involved in the pathological process of periodontitis via their antioxidative effects
Summary
Periodontitis is an inflammatory disease that compromises the integrity of the tooth-supporting tissues through the interplay of periodontal pathogens and the host immune response (Kinane et al, 2008; Dumitrescu, 2016). Autophagy is a lysosomal degradation pathway of self-digestion (Klionsky and Emr, 2000; Yang and Klionsky, 2010; Levine and Klionsky, 2016) This process is thought to have evolved as a stress response that allows organisms to survive harsh conditions (Mizushima et al, 1998; Netea-Maier et al, 2016). Studies have clearly demonstrated that the regulation of autophagy by ROS plays both a cytoprotective and cytotoxic role in cancer development (Chen et al, 2016; Zhong et al, 2016). To contribute to the understanding of this issue, the present review focuses on redoxsensitive pathways and transcription factors related to autophagy and summarizes the physiologic and pathologic roles of oxidative stress and autophagy in periodontal tissues
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