The effect of exenatide and metformin on the healing of periapical lesions. Animal experiment study

Aim: The aim of this study is to evaluate the effects of metformin and exenatide drugs used in the treatment of type-2 diabetes mellitus on bone formation in the defect areas with the help of micro computed tomography and histological analysis. Materials and Methods: In this study, 27 female Albino Wistar rats were used. One-sided, 3 mm diameter and 2 mm deep circular craniotomy defect was created in the parietal bones of the animals with low speed rotary instrument and trephan bur. Animals were randomly divided into three groups (n=9). The metformin group received 100 mg/kg/day metformin intraoral route; exenatide was administered intraperitoneally to the exenatide group at a dose of 3 μg/kg/day. No medication was administered to the control group. At the end of the tenth day, all animals were sacrificed using high dose anesthetic and the bones containing the defect site were separated. Bones were screened by microcomputed tomography; density and volume values were calculated. The samples were then subjected to histological analysis. The presence of osteoblast and osteoclast cells was evaluated for the presence of fibrous tissue and complete implantation of the damaged area into intact bone tissue. Results were analyzed by Kruskal-Wallis analysis of variance and Conover test. p<0.05 was considered statistically significant. Results: There was no significant difference between the groups in terms of the resulting bone volume (p=0.317), bone density (p=0.496), presence of fibrous connective tissue (p=0.072), and complete implantation of the damaged area into the original bone tissue (p=0.386). There was a significant difference in metformin and exenatide groups in terms of osteoblast (p=0.007) and osteoclast (p=0.007) cells compared to control groups. Conclusion: Exenatide and metformin drugs showed similar effect with respect to bone volume and density in the control group. However, they accelerated bone healing by increasing osteoblastic and osteoclastic cell formation.