Alterations of endochondral ossification in rats with acute experimental diabetes.
The alterations in bone metabolism is a common observation among the long-term complications encountered in diabetic patients, even in patients treated with insulin. Type 1 diabetes is associated with osteopenia. However, little is known regarding the early responses of bone metabolism to sustained hyperglycemia. The aim of this study was to study histological and histomorphometrically the tibiaes of rats in an experimental model of acute diabetes. Twenty four Wistar male rats weighing 220-260 gr were used. They were divided into 3 groups: I) control, II) experimental diabetes, and III) experimental diabetes treated with insulin. Diabetes was induced in groups II and III with a single i.p. injection of 60 mg/kg of streptozotocin; animals in the control group received an equivalent volume of the vehicle. At 24 hours of induction, glycemia was quantitatively measured. In the corresponding group, human NPH insulin was administered daily from the day 2. In the ninth day of experiment, all animals were sacrified and the tibiaes were resected, which were processed to obtain longitudinal histologic sections. The sections were stained with hematoxylin and eosin, photographed and histomorphometrically evaluated. The results show that the full width of the cartilage is lower in diabetic animals (359.9 ± 74.7 μm) and in diabetic animals treated with insulin (479.31 ± 62.93 μm) compared to controls (738.11 Μ ± 47.53 μm), with statistically significant differences (p <0.05). It was also noted a significant decrease in the volume of subcondral bone in diabetic rats, with the presence of a adipose bone marrow. This situation was not completely reversed in the group treated with insulin. Previous studies conducted in our laboratory showed that the alveolar bone does not significantly alter its activity or its volume short-term after the establishment of diabetes. The results shown in this study reflect that diabetes early alters endochondral ossification, bone remodeling and the activity of bone marrow. Grants: UBACyT O013 and CONICET PIP 6010. Keywords: diabetes, insulin, endochondral ossification.