Stomatological Hospital of Guang Zhou Medical College, GuangZhou, Guang-Dong Province, China.
J Periodontal Res. 2013 Apr;48(2):144-50. doi: 10.1111/j.1600-0765.2012.01512.x. Epub 2012 Jul 27.
Diabetes is a chronic hyperglycemic disorder and results in a tendency to develop osteoporosis. Furthermore, the delayed healing of tooth-extraction wounds, the activation of alveolar resorption and the suppressed formation of bone around implants are difficult for dentists to resolve. In diabetes, insulin-like growth factor I (IGF-I) appears to enhance the differentiation of osteoblasts and to activate the mineralization of bone. Hence, the aim of this study was to investigate the effects of insulin-like growth factor I on the remodeling of alveolar bone in diabetic rats.
Diabetes was induced in 40 male Sprague-Dawley rats by intravenous administration of alloxan. The teeth of the rats were extracted to investigate remodeling of alveolar bone. Insulin-like growth factor I was administered, via intraperitoneal injection, to diabetic rats following tooth extraction. The remodeling of alveolar bone was determined using radiographic data, histological analyses and tetracycline fluorescence labeling.
Compared with the control group, diabetes decreased alveolar bone formation. The height of alveolar bone and the bone-formation rate was significantly lower in the untreated diabetic group than in the control group or in the treated rats. Treatment with insulin-like growth factor I not only regulated abnormal blood glucose levels but also increased the height of the alveolar bone and increased the bone-formation rate relative to the results in diabetic animals. Furthermore, the expression of glucose transporter-1, the main transporter of glucose, was changed by hyperglycemia.
The results suggest that insulin-like growth factor I treatment increases the volume of newly formed bone following tooth extraction and normalizes the expression of glucose transporter-1 in diabetic rats, which may play an important role in bone formation and mineralization.
糖尿病是一种慢性高血糖疾病,导致骨质疏松的倾向。此外,拔牙伤口愈合延迟、牙槽骨吸收的激活和种植体周围骨形成的抑制是牙医难以解决的问题。在糖尿病中,胰岛素样生长因子 I(IGF-I)似乎增强成骨细胞的分化,并激活骨的矿化。因此,本研究旨在探讨胰岛素样生长因子 I 对糖尿病大鼠牙槽骨改建的影响。
通过静脉注射链脲佐菌素诱导 40 只雄性 Sprague-Dawley 大鼠发生糖尿病。拔牙以研究牙槽骨改建。拔牙后,通过腹腔注射给予糖尿病大鼠胰岛素样生长因子 I。使用放射学数据、组织学分析和四环素荧光标记来确定牙槽骨改建。
与对照组相比,糖尿病减少了牙槽骨形成。未经治疗的糖尿病组的牙槽骨高度和骨形成率明显低于对照组或治疗组。胰岛素样生长因子 I 的治疗不仅调节异常的血糖水平,而且增加了牙槽骨的高度,并增加了骨形成率,与糖尿病动物的结果相比。此外,高血糖改变了葡萄糖转运蛋白-1(葡萄糖的主要转运蛋白)的表达。
结果表明,胰岛素样生长因子 I 治疗可增加拔牙后新形成骨的体积,并使糖尿病大鼠的葡萄糖转运蛋白-1表达正常化,这可能在骨形成和矿化中发挥重要作用。