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Purpose: To investigate the effect of metformin combined with DPP-4 inhibitor on alveolar bone density in patients with type 2 diabetes mellitus and chronic periodontitis., Methods: A total of 80 patients with type 2 diabetes mellitus and chronic periodontitis were selected and randomly divided into group A and group B by random number table, with 40 patients in each group. Group A (medication alone group): oral metformin and basic periodontal treatment; Group B (combination group): DPP-4 inhibitor (sitagliptin) was taken orally in addition to group A. Before treatment (T0) and 3 months (T1) and 6 months (T2) after treatment, alveolar bone mineral density (BDM), periodontal probing depth (PD), clinical attachment loss(CAL), probing bleeding (BOP), glycated hemoglobin (HbA1c),serum phosphorus, serum calcium, adiponectin (ADP), leptin (LEP), interleukin-6 (IL-6), C-reactive protein (HS-CRP), tumor necrosis factor (TNF-α) were detected. SPSS 23.0 software package was used for data analysis., Results: Three and 6 months after treatment, PD, CAL, BOP and HbAlc in group B were significantly lower than those in group A(P＜0.05). BDM in group B was significantly higher than that in group A (P＜0.05). Compared with group A, the levels of inflammatory cytokines (IL-6, Hs-CRP, TNF-α) and leptin in group B were significantly decreased, while the level of adiponectin was significantly increased (P＜0.05)., Conclusions: Metformin combined with DPP-4 inhibitor can increase alveolar bone density in patients with type 2 diabetes mellitus and chronic periodontitis, effectively improve periodontal clinical and serum biochemical indicators, and reduce periodontal inflammation.

Adiponectin is an adipokine predominantly synthesized and secreted by adipocytes in the white adipose tissue, and it can lower the blood glucose level and increase free fatty acid oxidation. In the current study, we developed the globular domain of adiponectin (gapM1) to treat type II diabetes. In both flask and fermentor, we cultivated Pichia pastoris expressing recombinant gapM1 and established the purification procedure by using gel filtration and anion exchange chromatography. To evaluate the biological activity of recombinant gapM1, we used rat type II diabetes model fed high-fat diet in combination with low-dose STZ (Streptozocin) induction. We purified 200 mg gapM1 with purity of 96% from 10 liters of supernatant. The recombinant gapM1 significantly lowered blood glucose (34.2%), serum triglyceride (79.6%) and total cholesterol (62.1%) in type II diabetes induced rat. Therefore, the recombinant human gapM1 is successfully expressed in Pichia pastoris and effectively treated type II diabetes in rat models.