Abstract

Objective: insulin has been reported to possess anabolic effect on bone. Topical application of insulin in bone defects in diabetic rats has not been investigated. The objective of this study was to evaluate histologically the effect of topical administration of insulin for the restoration of tibial bone defects in diabetic rats. Materials and Methods: Sixteen adult male albino diabetic rats were grouped into two equal groups, group I (diabetic control) which had not received any graft, group II (experimental) which was diabetic and had received topical insulin loaded on PVP (Polyvinylpyrrolidone). Specimens were harvested on days seven and twenty eight days after surgical procedures, prepared and examined histologically by H&E (haematoxylin and eosin) stain, there were wide histological differences between the groups of this study along the different intervals of the study.Results:The histological results demonstrated that there was obvious retardation in resolving the inflammatory phase, organization of the blood clot and bone formation in the diabetic control group I than the experimental group II along the different intervals of this study. Moreover, there was great acceleration in granulation tissue formation, organization and bone formation in experimental group II which received the insulin PVP. Discussion: The enhancement in bone healing process was due to the effect of insulin which accelerates the bone regeneration by means of inflammation resolve, angiogenesis, proliferation and successive differentiation of mesenchymal cells. Conclusion: Topical applications of insulin in bone defects enhance new bone formation in diabetic rats.KEYWORDSInsulin; Bone defect; Tibia; Diabetes; Rats.

Highlights

  • Diabetes mellitus (DM) is a metabolic disorder characterized by high blood glucose level over a prolonged period.DM has led to reduced biomechanical properties of the healing fracture, reduced cellular proliferation and reduced collagen synthesis compared to non-diabetic control animals [1,2,3].Systemic insulin treatment reverses impaired bone healing in diabetic animals, possibly through enhancement of bone formation and inhibition of bone resorption [4]

  • In vitro Studies have shown that insulin has anabolic effect on bone in diabetic and non diabetic animals, insulin can influence bone growth by directly binding to its receptors presented on osteoblasts [6]

  • The group I demonstrated well organized granulation tissue at the surface of the defect characterized by tightly packed collagen bundles, osteoblasts, fibroblasts and proliferating blood vessels on the top of woven bone formation

Read more

Summary

Introduction

Diabetes mellitus (DM) is a metabolic disorder characterized by high blood glucose level over a prolonged period.DM has led to reduced biomechanical properties of the healing fracture, reduced cellular proliferation and reduced collagen synthesis compared to non-diabetic control animals [1,2,3].Systemic insulin treatment reverses impaired bone healing in diabetic animals, possibly through enhancement of bone formation and inhibition of bone resorption [4] These studies did not clarify whether this is due to direct and local effect on the fracture repair process or is a secondary effect due to systemic alterations in the metabolic state, such as by reducing hyperglycemia[5]. In order to investigate the in vivo direct effect of insulin on bone healing, insulin had been used topically through this study

Objectives
Methods
Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.