Type 2 diabetes mellitus impairs tooth supraeruption by disrupting periapical alveolar bone remodeling

The mechanisms by which type II diabetes mellitus (T2DM) impairs tooth supraeruption following tooth loss remain incompletely understood, with evidence suggesting disruption of alveolar bone remodeling. This study aimed to investigate the effects of T2DM on apical alveolar bone remodeling during tooth supraeruption in a mouse model.

A T2DM mouse model with unopposed mandibular molars was established, including a control group (n = 70) and an experimental T2DM group (n = 70). We systematically analyzed periapical alveolar bone volume, periodontal ligament morphology, supraeruption distance, and histomorphometric counts of osteoblasts and osteoclasts. mRNA expression levels of osteogenesis-related factors were assessed by real-time quantitative polymerase chain reaction (RT-qPCR). Protein expression was evaluated by immunohistochemistry. Data were analyzed using Student’s t-test, with significance set at P < 0.05.

T2DM significantly altered the alveolar bone remodeling microenvironment. The diabetic group exhibited reduced osteoblast numbers and decreased mRNA expression of transforming growth factor-β (Tgf-β), insulin-like growth factor-1 (Igf-1) and periostin (Postn), as well as reduced protein expression of TGF-β, IGF-1, and POSTN (P < 0.05). Conversely, osteoclast numbers were increased, accompanied by elevated Runx2 mRNA and RUNX2 protein expression (P < 0.05). This bone imbalance resulted in reduced periapical bone volume and disorganized periodontal tissue structure. Consequently, the degree of tooth supraeruption was significantly reduced in T2DM mice compared to controls (P < 0.05).

T2DM impairs tooth supraeruption by downregulating osteoblast-related factors, increasing osteoclast numbers and activity, and disrupting alveolar bone remodeling capacity. This study provides a theoretical foundation for future clinical research on the mechanism by which type 2 diabetes mellitus affects tooth supraeruption.