The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

Abstract

The endoplasmic reticulum (ER) is a principal organelle for folding, post‐translational modifications and transport of secretory, luminal, and membrane proteins. ER stress is a condition induced by the accumulation of unfolded or misfolded proteins owing to a variety of physiological and pathological phenomena. To overcome the deleterious effects of ER stress, unfolded protein response (UPR) is initiated to translocate and remove the misfolded and accumulated proteins. Plenty of evidence shows the correlation between ER stress/UPR and the pathology of inflammatory disease. Periodontal disease is a chronic inflammatory disease characterized by the irreversible destruction of periodontal tissues, which associates with the onset and progress of several systemic diseases. Periodontopathic bacterium and pro‐inflammatory mediators play a pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease. As an inflammatory disorder of the periodontium, periodontal disease is highly related to ER stress. In this review, we provide an overview of the pathophysiological effect of ER stress on periodontal disease through five aspects as follow: ER stress and periodontal tissue remodeling, including both soft tissue and hard tissue; ER stress and the inflammation; ER stress and systematic effect during the periodontal disease; last but not least, ER stress and the autophagic apoptosis in cells.

Identification of Endoplasmic Reticulum Stress-Related Biomarkers of Periodontitis Based on Machine Learning: A Bioinformatics Analysis

“…Consistently, we obtained similar results in the KEGG pathway analysis, further probing that these DEGs are involved in protein processing in the ER. Moreover, our enrichment results are consistent with existing experimental studies, demonstrating the involvement of ER in the pathological pathway of periodontitis and proving the correlation between ERS and periodontitis [35].…”

“…ERAD can protect cells from the adverse effects of ERS, but excessive ERAD can be harmful 10 Disease Markers by disrupting cellular homeostasis and inducing apoptosis via UPR [42]. Moreover, when ERS induces excessive tissue apoptosis, destruction of periodontal soft tissues can occur [35]. A recent study has shown that proper expression levels of ERLEC1 are critical in osteogenic differentiation, and the occurrence of abnormal jaw development could be associated with pathogenic variants of ERLEC1 [43].…”

miR-1260b inhibits periodontal bone loss by targeting ATF6β mediated regulation of ER stress

“…This indicated an inhibitory effect of miR-1260b on ER stress. Although the association between ER stress and periodontal disease has been well accepted ( Jiang et al, 2022 ), the direct effect of ER stress on osteoclastogenesis remains unclear. Yamada et al (2015) reported that the ER stress inducer, tunicamycin, did not induce osteoclast differentiation without RANKL.…”

“…Its pathology is characterized by inflammation of the periodontium and subsequent destruction of the tooth-supporting alveolar bone, which is a major cause of tooth loss in adults ( Kajiya and Kurihara, 2021 ). Recently, studies have focused on the influence of endoplasmic reticulum (ER) stress on periodontitis ( Jiang et al, 2022 ). ER is the principal organelle that plays an essential role in the folding and structural maturation of proteins.…”

Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives

“…A surge of evidence has emerged linking the pathology of various diseases to ER stress and UPR [ 8 , 9 ]. In recent years, an increasing number of studies have concentrated on the involvement of ER stress in the pathophysiology of chronic obstructive pulmonary disease (COPD).…”