Diabetes mellitus impairs bone regeneration and biomechanics

Abstract

Background: With the rise of high-calorie diets and the aging of populations, the incidence of diabetes was increased dramatically in the world and the number of people with diabetes was predicted to rise to 600 million by 2045. Numerous studies have confirmed that several organ systems, including the skeletal system, are seriously affected by diabetes. In that study, the bone regeneration and the biomechanics of the newly regenerated bone were investigated in diabetic rats, which may provide a supplement for previous studies. Methods: A total of 40 SD rats were randomly divided into the type 2 diabetes mellitus (T2DM) group (n = 20) and the control group (n = 20). Beyond that high fat diet and streptozotocin (STZ) were jointly used in the T2DM group, there were no differences between the two groups in terms of treatment conditions. Distraction osteogenesis was used in all animals for the next experimental observation. The evaluation criterion of the regenerated bone was based on radioscopy (once a week), micro-computed tomography (CT), general morphology, biomechanics (including ultimate load, modulus of elasticity, energy to failure, and stiffness), histomorphometry (including von Kossa, Masson trichrome, Goldner trichrome, and safranin O staining), and immunohistochemistry. Results: All rats in the T2DM group with fasting glucose levels (FGL, > 16.7 mmol/L) were allowed to complete the following experiments. The results showed that rats with T2DM have a higher body weight (549.01 g ± 31.34 g) than rats in the control group (488.60 g ± 33.60 g) at the end of observation. Additionally, compared to the control group, slower bone regeneration in the distracted segments was observed in the T2DM group according to radiography, micro-CT, general morphology, and histomorphometry. Furthermore, a biomechanical test showed that there was a worse ultimate load (31.01 ± 3.39%), modulus of elasticity (34.44 ± 5.06%), energy to failure (27.42 ± 5.87%), and stiffness (34.55 ± 7.66%) than the control group (45.85 ± 7.61%, 54.38 ± 9.33%, 59.41 ± 10.96%, and 54.07 ± 9.30%, respectively). Furthermore, the decreased expressions of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) were presented in T2DM group by immunohistochemistry. Conclusion: The present study demonstrated that diabetes mellitus impairs bone regeneration and biomechanics in newly regenerated bone, a phenomenon that might be related to oxidative stress and poor angiogenesis brought on by the disease.