Li Na, Chen Qi, Feng Yi, Wang Yin
Silk Crossing Clinic, Affiliated Hospital of North Sichuan Medical College, Nanchong, People's Republic of China.
School of Stomatology, North Sichuan Medical College, Nanchong, People's Republic of China.
J Inflamm Res. 2025 Jun 13;18:7781-7794. doi: 10.2147/JIR.S533791. eCollection 2025.
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.
糖尿病与牙周炎之间存在双向关系。对于糖尿病患者，高血糖可通过引发炎症反应、增强氧化应激和促进牙槽骨吸收来加剧牙周组织破坏。同时，作为一种慢性炎症性疾病，牙周炎涉及牙周病原体及其分泌的毒力因子，可引发全身炎症反应。因此，这会加剧胰岛素抵抗并升高血糖水平，从而形成恶性循环。尽管对糖尿病与牙周炎之间的关联进行了广泛研究，但这种联系背后的确切机制仍是一个持续争论的话题。自噬是一种负责维持细胞稳态的关键防御机制，在这种关系中起着至关重要的作用。新出现的证据表明，自噬通过调节病原体清除、调节炎症和免疫反应、维持骨代谢以及微调自噬活性来影响牙周组织炎症和血糖水平。因此，靶向调节自噬是治疗糖尿病性牙周炎的一种有前景的治疗策略。在本文中，我们将综述自噬在糖尿病与牙周炎双向关系中的机制。阐明这些机制将加深对糖尿病与牙周炎复杂关系的理解，通过调节自噬途径为糖尿病性牙周炎的联合治疗提供新的治疗策略，并为开发有效干预措施奠定理论基础。
