Metformin modulates alveolar bone parameters and gene expression in streptozotocin-induced type 2 diabetic rats

Diabetes mellitus (DM) is linked with defective bone healing and metabolic disturbances that increase fracture risk. Although metformin (MET) is used traditionally as first-line treatment for type 2 diabetes (T2DM), its effectiveness in completely reversing diabetic bone homeostasis is uncertain. The present study was conducted to assess the short-term effect of MET on alveolar bone histological structure and osteoblastic gene expression in rats with streptozotocin (STZ)-induced type 2 diabetes mellitus (T2DM).

Eighteen adult male Wistar rats were divided equally into three groups (n = 6/group): control group (non-diabetic) was injected with saline, STZ group (diabetic) received 10% fructose solution for 2 weeks followed by an injection of a single dose of STZ (40 mg/kg), and MET group (diabetic with MET-treatment) received 100 mg/kg/day MET for 30 days. Alveolar bone was assessed by histological and histomorphometric analysis, cone beam computed tomography (CBCT), and reverse transcription-polymerase chain reaction (RT-PCR) analysis of bone-related gene expression.

The STZ group showed pronounced decreases in total bone area, osteoblast area, and bone-related gene expression (RunX2, osteocalcin, COL1A1) compared to the control group. MET significantly improved these parameters compared to the STZ group.

Metformin significantly increased total bone area and osteoblastic gene expression (Runx2, osteocalcin, and COL1A1) compared to untreated diabetic rats but did not fully restore them to control (non-diabetic) levels. These results suggest a partial protective effect of metformin in alveolar bone in this short-term T2DM rat model.