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Little is known about the early response of bone metabolism to hyperglycemia, or transient hyperglycemia, caused by poor compliance with treatment or inadequate control of diabetes in patients with type 1 diabetes. There are no studies comparing early diabetes-related alterations in endochondral ossification with those occurring through time. In order to histomorphometrically evaluate the growth cartilage and subchondral bone of male Wistar rat tibia shortly after experimentally inducing type 1 diabetes, thirty-five male Wistar rats were divided into 5 groups: Group A: control; Group B: induction of diabetes; euthanasia at one week; Group C: induction of diabetes plus insulin treatment; euthanasia at one week; Group D: induction of diabetes; euthanasia at six weeks; Group E: induction of diabetes plus insulin treatment; euthanasia at six weeks. Diabetes was induced by single intraperitoneal injection of 60mg/kg body weight of streptozotocin dissolved in citrate buffer pH 4.0. Two days after inducing diabetes, treatment with subcutaneously injected human insulin was initiated, according to protocol. The following parameters were evaluated: Tibial subchondral bone volume; trabecular area; bone surface; trabecular number; trabecular thickness. Tibial subchondral bone volume and epiphyseal cartilage width were significantly lower in both experimental groups as compared to controls. Insulin treatment resulted in values similar to controls. As shown by the microarchitecture of subchondral trabecular bone, all parameters were lower in diabetic animals, except for trabecular width which was similar to that observed in controls. The alteration in bone metabolism manifests in long bones very early in the course of diabetes, suggesting it would be advisable to analyze bone response as soon as possible following diagnosis of the disease, in order to prescribe treatments aimed at preventing further alterations in bone architecture.

Epiphyseal Cartilage and Subchondral Bone of Rat Tibia as Early Targets of Diabetes Type I