The effect of streptozotocin-induced experimental diabetes mellitus on calvarial defect healing and bone turnover in the rat

Tooth socket healing is delayed in diabetes mellitus due to impairment of the healing process. One reason for the poor healing may be an abnormal vascular response. The object of our experiments was to study the effect of diabetes mellitus on bone healing using a calvarial wound. Streptozotocin, injected intraperitoneally, was used to induce diabetes in rats. Both insulin-treated, streptozotocin-dosed animals and normal rats were used as controls. Bone formation was measured in the diabetic femur and tibia, and healing of bone defects by guided tissue regeneration was assessed. Cancellous bone volume and bone formation in the femur were greatly reduced in the diabetic model, indicating either a defect of mineralization or osteoid formation. The length, dry weight, ash weight and calcium content of the tibiae of diabetic rats were significantly less than those of the control groups. In a second experiment, a sterile wound was made in the calvaria of diabetic rats, and covered internally and externally with Gore-Tex(R) membrane. Exuberant formation of a primitive bone was evident, with little evidence of osteoclastic resorption of the necrosed bone ends. This was despite the impaired bone formation observed in the long bones in the first experiment.