Autophagy is an evolutionarily conserved process essential for cellular homeostasis and human health. As a lysosome‐dependent degradation pathway, autophagy acts as a modulator of the pathogenesis of diverse diseases. The relationship between autophagy and oral diseases has been explored in recent years, and there is increasing interest in the role of autophagy in periodontal disease. Periodontal disease is a prevalent chronic inflammatory disorder characterized by the destruction of periodontal tissues. It is initiated through pathogenic bacterial infection and interacts with the host immune defense, leading to inflammation and alveolar bone resorption. In this review, we outline the machinery of autophagy and present an overview of work on the significance of autophagy in regulating pathogen invasion, the immune response, inflammation, and alveolar bone homeostasis of periodontal disease. Existing data provide support for the importance of autophagy as a multi‐dimensional regulator in the pathogenesis of periodontal disease and demonstrate the importance of future research on the potential roles of autophagy in periodontal disease.

The mineralization capability of cementoblasts is the foundation for repairing orthodontic treatment‐induced root resorption. It is essential to investigate the regulatory mechanism of mineralization in cementoblasts under mechanical compression to improve orthodontic therapy. Autophagy has a protective role in maintaining cell homeostasis under environmental stress and was reported to be involved in the mineralization process. Long noncoding RNAs are important regulators of biological processes, but their functions in compressed cementoblasts during orthodontic tooth movement remain unclear. In this study, we showed that compressive force downregulated the expression of mineralization‐related markers. LincRNA‐p21 was strongly enhanced by compressive force. Overexpression of lincRNA‐p21 downregulated the expression of mineralization‐related markers, while knockdown of lincRNA‐p21 reversed the compressive force‐induced decrease in mineralization. Furthermore, we found that autophagy was impeded in compressed cementoblasts. Then, overexpression of lincRNA‐p21 decreased autophagic activity, while knockdown of lincRNA‐p21 reversed the autophagic process decreased by mechanical compression. However, the autophagy inhibitor 3‐methyladenine abolished the lincRNA‐p21 knockdown‐promoted mineralization, and the autophagy activator rapamycin rescued the mineralization inhibited by lincRNA‐p21 overexpression. Mechanistically, the direct binding between lincRNA‐p21 and FoxO3 blocked the expression of autophagy‐related genes. In a mouse orthodontic tooth movement model, knockdown of lincRNA‐p21 rescued the impeded autophagic process in cementoblasts, enhanced cementogenesis, and alleviated orthodontic force‐induced root resorption. Overall, compressive force‐induced lincRNA‐p21 inhibits the mineralization capability of cementoblasts by impeding the autophagic process.

Background: Migration of cementoblasts to resorption lacunae is the foundation for repairing root resorption during orthodontic tooth movement. Previous studies reported that autophagy was activated by compression in periodontal ligament cells. The aim of this study was to investigate the migration of cementoblasts and determine whether autophagy is involved in the regulation of cementoblast migration under compressive force.Methods: Flow cytometry was employed to examine the apoptosis of murine cementoblasts (OCCM-30) at different compression times (0, 6, 12, and 24 hours) and magnitudes (0, 1.0, 1.5, and 2.0 g/cm 2 ). Cell proliferation was examined using the CCK-8 method. Wound healing migration assays and transwell migration assays were performed to compare the migration of cementoblasts. Chloroquine (CQ) and rapamycin were used to inhibit and activate autophagy, respectively. The level of autophagy was determined using western blotting and immunofluorescence staining. The expression of matrix metalloproteinases (MMPs) was assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blot analysis, and enzyme-linked immunosorbent assay (ELISA). Results: Cell apoptosis and proliferation did not significantly change in OCCM-30 cells under mechanical compression at magnitude of 1.5 g/cm 2 for 12 hours. However, the migration of cementoblasts was significantly inhibited after the application of compressive force. MMP2, MMP9, and MMP13 mRNA expression was decreased, and MMP9 and MMP13 protein expression and secretion level were also decreased. Further, autophagic activity was inhibited in cementoblasts under compressive force. Treatment with chloroquine reduced the cellular migration, and rapamycin partially relieved the inhibition of cementoblast migration induced by the compressive force. MMP9 and MMP13 mRNA expression, protein expression, and secretion levels showed a similar trend. Conclusion:Migration of OCCM-30 cells was inhibited under compressive force partially dependent on the inhibition of MMPs, which was mediated by downregulation of autophagy. The findings provide new insights into the role of e128