The purpcse of the present study was to clarify the mechanism of bone metabolism in diabetes mellitus. Morphological studies of fracture healing was focused mainly on bone formation and bone resorption in diabetic rats induced by the injection of streptozotocin.
196 Wistar rats of about 100 gram body weight were used.
In the diabetic group, the process of fracture healing was remarkably retarded. Microscorpically, new periosteal bone formation was disrupted. Ultrastructural findings of the osteoblasts disclosed irregularly dilated RER and other cytoplasmic organelle which were poorly developed, these contributed to the marked reduction of osteoid formation.
On the other hand, in the callus of the calcified cartilage, there was degeneration of the chondrocytes and at the same time, malformations of the cartilage matrix and disruption of the cartilage calcification. In addition, relatively many small osteoclasts were observed. The cytoplasmic organelle and the ruffled border were poorly developed and the uptake of bone crystals was minimal in the osteoclasts of diabetic rats.
These findings suggest that the retardation of fracture healing process in the diabetic rats is caused by a series of obstructions to the bone metabolism, such as obstruction of matrix formation, abnormal calcification and obstruction of bone regeneration. This observation is based on the cellular changes ultrastructurally and are thought to have a direct and indirect effect in case of diabetes mellitus.
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