Non-steroidal, anti-inflammatory drugs and statins are two widely prescribed drug classes that affect bone formation. The aim of this study was to elucidate the effect of diclofenac and simvastatin in artificial bone defect healing. One hundred and forty-four male Wistar rats were used, and the specimens were divided into groups, with respect to the route of drug administration and the type of defect healing (with or without collagen membrane), and subgroups, with respect to the study duration (2, 4 or 8 weeks). Diclofenac was intramuscularly administered while simvastatin was administered both systemically and locally. Animals were euthanized and specimens were histomorphometrically analyzed to evaluate the percentage of new bone formation (%). Bone healing that occurred without any intervention developed more steadily than that of all other groups. Diclofenac exerted a clear, direct inhibitory effect on bone healing and its systemic administration should be avoided. The systemic administration of simvastatin was related to severe myopathy, while the solvent for the local administration of simvastatin seemed to play significant role in bone growth, as simvastatin, when it is administered intraperitoneally in a DMSO solution, appeared to promote bone healing. Local administration may have a significant impact on bone healing and it should be further investigated with the type of solvent or carrier that is used, which both may play a significant role in bone repair induction.

Purpose: In this study, we aimed to explore the effects of sitagliptin on diabetic nephropathy using an experimental animal model while referring to various aspects of the Dipeptidyl peptidase- IV inhibitors literature findings. Methods: 27 male BKS.Cg- + Leprdb/+ Lepr/+ OlaHsd mice, 8 weeks old, were evenly separated into three groups. For 12 weeks, group D and L received a high (200 mg/Kgr/day) and low (10 mg/kg/day) dosage of sitagliptin, respectively, while group N did not receive any treatment. Biochemical tests on urinary and blood samples of each animal as well as histopathological examination for specific lesions of the kidneys were performed at the end of the experimental study. Results: Both high (D) and low (L) sitagliptin dosage were found to significantly reduce serum glucose, microalbumin, and albumin to creatinine ratio (ACR) when compared with the control group, while high sitagliptin dose, additionally, showed a significant reduction of urinary creatinine (P < 0.01). Moreover, sitagliptin had a positive effect on histopathology findings; sitagliptin significantly reduced moderate/severe mesangial matrix expansion (P < 0.001 for both groups), thickening of the basal membrane, vascular pole hyalinosis capsule cell hyperplasia, and thickening of the Bowman’s capsule compared with control group. Conclusion: Sitagliptin appears to improve the biochemical parameters regarding kidney function and acts beneficially by reducing the extent of renal histopathological damage caused by DM.