The Role of Autophagy in the Regulation of Bidirectional Relationships in Diabetic Periodontitis.

Abstract

A bidirectional relationship exists between diabetes and periodontitis. For individuals with diabetes, hyperglycemia can exacerbate periodontal tissue destruction by triggering inflammatory responses, enhancing oxidative stress, and promoting alveolar bone resorption. Meanwhile, as a chronic inflammatory disease, periodontitis involves periodontal pathogens and their secreted virulence factors, which can elicit systemic inflammatory responses. Consequently, this intensifies insulin resistance and elevates blood glucose levels, establishing a vicious cycle. Despite extensive research on the association between diabetes and periodontitis, the precise mechanisms underlying this connection remain a topic of ongoing debate. Autophagy, a crucial defensive mechanism responsible for maintaining cellular homeostasis, plays a vital role in this relationship. Emerging evidence indicates that autophagy influences inflammation in periodontal tissue and blood glucose levels by regulating pathogen clearance, modulating inflammatory and immune responses, maintaining bone metabolism, and fine-tuning autophagic activity. As such, targeting modulation of autophagy represents a promising therapeutic strategy for managing diabetic periodontitis. In this paper, we will provide a review of the mechanisms of autophagy in the bidirectional relationship between diabetes and periodontitis. Elucidating these mechanisms will enhance a more profound comprehension of the intricate relationship between diabetes and periodontitis, provide novel therapeutic strategies for the combined treatment of diabetic periodontitis by regulating the autophagy pathway, and establish a theoretical foundation for the development of effective interventions.