Abstract

The effects of low-level laser therapy (LLLT) on a bone defect model in streptozotocin-induced diabetic (STZ-D) rats was examined. LLLT accelerates bone fracture repair in healthy animals, but its effect in diabetic animals is unclear. Twenty-eight rats were divided into five groups: 1 (diabetes, no LLLT), 2 (diabetes, LLLT high dose), 3 (diabetes, LLLT low dose), 4 (no diabetes, no LLLT), and 5 (no diabetes, LLLT low dose) Diabetes was induced by a single injection of STZ in rats of groups 1, 2, and 3. A bone defect was made in the right tibia of rats in all groups. The defect in groups 2, 3, and 5 was treated with LLLT (890 nm, 70 W, 3000 Hz, circular beam shape, and 1 cm(2) spot size). Doses of 23.3 J/cm(2) (530 s) for group 2 and 11.6 J/cm(2) (265 s) for groups 3 and 5 were applied three times a week. The right tibias were collected 42 days after surgery and subjected to three-point bending test on a material testing machine (MTM) until fracture occurred. Data was automatically recorded on the MTM formed the load-deformation curve. Mann-Whitney test showed that LLLT with 11.6 J/cm(2) significantly increased bending stiffness and maximum force in diabetic rats compared with group 1 (both p = 0.041). LLLT in an experimental diabetic model enhanced bone repair with a higher bending stiffness and maximum force compared to the control group.

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