ABSTRACT
BACKGROUND:Increasing attention has been paid on the role of advanced glycation end products in bone tissue. Glucose metabolic disorder is one of the main reasons for the increase of advanced glycation end products. OBJECTIVE:To observe the change of advanced glycation end products expressed in type 2 diabetes rats, and to investigate the relationship between impaired fracture healing and change of advanced glycation end products expression in vivo. METHODS:Thirty Sprague-Dawley rats were randomly and equal y divided into two groups:control group (normal feeding) and experimental group (high fat and sucrosum diet feeding to establish type 2 diabetes model). After diabetes models were established, the model of distraction osteogenesis in the left tibiae of al the rats was produced. Distraction was given 0.3 mm per day and continued for 14 days. RESULTS AND CONCLUSION:After the traction was complete, cal us formation in distraction gap was obviously reduced in experimental group compared with control group by X-ray examination. The array of microcolumn formation was disordered and the area of primary matrix front was catachromasis by histology examination. The enzyme-linked immunosorbent assay results showed that, the level of advanced glycation end products was obviously elevated (P<0.01) while osteocalcin was obviously reduced (P<0.01) in experimental group in comparison with control group. The formation of distraction cal us was impaired in the process of fracture healing and blood of type 2 diabetes rats. The increase of advanced glycation end products may be one of the reasons that cause impaired fracture healing in diabetic rats.