98 - The Effects of Vitamin D Supplementation on Fracture Repair in Type 1 Diabetic Rats

Poster Board Number: 98
There are separate poster presentation times for odd and even posters.
Odd poster #s – first hour
Even poster #s – second hour

Abstract Body : Background and Purpose:
More than 30 million Americans have diabetes mellitus, a disease which affects multiple organ systems, including the skeleton. In the United States, 5-10% of all fractures result in delayed union or nonunion. Previous studies have demonstrated diminished bone strength and delayed fracture repair associated with diabetes. Chemical-induced rat models of type-1 diabetes requiring degradation of pancreatic beta cells using toxins such as streptozotocin or alloxan do not closely resemble the etiology of type 1 diabetes seen in humans. This study utilized spontaneously diabetic BB Wistar rats with a pathophysiology more closely aligned with the human condition.

Multiple laboratory studies have shown vitamin D3 to be a promising candidate in advancing fracture repair in healthy animal populations. This study examined the effects of vitamin D supplementation in type 1 diabetic rats. These previous studies have shown that vitamin D supplementation can increase mechanical strength in the healed fractures of healthy animal models.

We hypothesize that vitamin D3 supplementation will aid in fracture repair. This study focuses on exploring the use of vitamin D to increase the rate of fracture repair and the quality of the bone laid down at the callus site.

Materials and Methods:
Closed femoral fractures were induced in the rats. Animals then received intramuscular injections at the site of the fracture. Rats were divided into three cohorts: those receiving a high dose (HD; 1.29mg/kg) of cholecalciferol (vitamin D3), those receiving a low dose (LD; 0.129mg/kg) of D3, and those receiving vehicle only (Control).

X-rays were taken at baseline and every week for six weeks at which point the rats were euthanized and the femurs were dissected out. These bones were imaged using micro-CT with subsequent analysis using CTAn software and then tested for mechanical strength via torsional testing at 2° per second to failure. The x-rays were scored blindly for bone bridging using the Bergenstock methodology. Analysis of variance (ANOVA) with post-hoc comparison between the groups was completed with statistical significance assumed at p< 0.05.

Results:
The preliminary data, based on the evaluations of the week 6 x-rays, X-ray scores were significantly higher X-ray scores (p=0.0243) for rats receiving a high dose of cholecalciferol (5.792+/-1.719) compared to the control group (4.313+/-1.922). The treated rats produced smaller calluses than the control group, indicated by a smaller normalized maximal outside diameter (HD 184.8%+/-9.777% p=0.0317, LD 173.2%+/-15.66% p=0.0027, Control 206.6%+/-6.897%) and polar moment of inertia (HD 81.83+/-36.05 mm^4 p=0.0371, LD 64.19+/-9.807 mm^4 p=0.0113, Control 144.4+/-48.75 mm^4).

There was no significant difference between the mechanical properties of healed bones despite the treated groups having a smaller callus. This suggests the possibility of stronger bone within the callus of the rats treated with vitamin D.

Conclusion:
Vitamin D may be an inexpensive and effective treatment to aid fracture repair which may decrease non-union and infection in fractures of patients with diabetes. This could then translate to a decrease in amputations for the diabetic population. Further investigation into the use of vitamin D to aid fracture repair in diabetes could explore the effects of altering the time of treatment to determine if waiting until after the initial inflammatory phase of fracture repair has completed is more beneficial.