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首页> 外文期刊>Diabetes technology & therapeutics >Periodontal ligament remodeling and alveolar bone resorption during orthodontic tooth movement in rats with diabetes.
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Periodontal ligament remodeling and alveolar bone resorption during orthodontic tooth movement in rats with diabetes.

机译:糖尿病大鼠正畸牙齿移动过程中的牙周膜重塑和牙槽骨吸收。

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BACKGROUND: Pathological displacement of teeth caused by periodontitis-related bone loss in patients with diabetes is often corrected with orthodontic treatments. However, recovery from orthodontic therapy is often delayed for unclear reasons. This study explored effects of streptozotocin-induced diabetes in rats on protein expression involved in remodeling of the periodontal ligament (PDL) and alveolar bone during orthodontic tooth movement. METHODS: Forty-eight Sprague-Dawley rats were randomly divided into two experimental groups: "normal" and "diabetes" (n = 24 each). Diabetes was induced by a single dose of streptozotocin (65 mg/kg). Animals were euthanized at 3, 7, and 14 days after orthodontic induction. Changes in expression of collagen type I (Col-I), matrix metalloproteinase type 1 (MMP-1), and tissue inhibitor of MMP-1 (TIMP-1) were measured immunohistochemically in the pressure side. Col-I and collagen type III (Col-III) fibers were assessed by picrosirius red staining in the tension side. Osteoclasts were observed on the surface of the alveolar bone. RESULTS: Diabetes increased expression of MMP-1 and Col-III and decreased expression of Col-I in PDL. After the orthodontic induction, osteoclast action was delayed, and higher Col-III/Col-I and MMP-1/TIMP-1 ratios persisted in the diabetes group compared with the normal group. The ratio of MMP-1/TIMP-1 in the diabetes group reached a peak on Day 7, whereas the ratio remained at near control levels in the normal group. The diabetes group appeared to have worse recovery from damage caused by orthodontic movement. CONCLUSIONS: Under mechanical forces, diabetes prolonged duration of degradation of PDL and remodeling of PDL and resorption of alveolar bone.
机译:背景:在糖尿病患者中,由牙周炎相关的骨质流失引起的牙齿病理性移位通常可以通过正畸治疗得到纠正。但是,由于不清楚的原因,正畸治疗的恢复通常会延迟。这项研究探讨了链脲佐菌素诱发的糖尿病大鼠对正畸牙移动过程中牙周膜(PDL)和牙槽骨重塑相关蛋白表达的影响。方法:将48只Sprague-Dawley大鼠随机分为两个实验组:“正常”和“糖尿病”(每组24只)。单剂量链脲佐菌素(65 mg / kg)可诱发糖尿病。正畸诱导后第3、7和14天对动物实施安乐死。免疫组织化学法在压力侧测量I型胶原蛋白(Col-1),1型基质金属蛋白酶(MMP-1)和MMP-1组织抑制剂(TIMP-1)的表达变化。 Col-I和III型胶原(Col-III)纤维通过在张紧侧的picrosirius红色染色进行评估。在牙槽骨表面观察到破骨细胞。结果:糖尿病患者PDL中MMP-1和Col-III的表达增加而Col-I的表达减少。正畸诱导后,破骨细胞作用被延迟,与正常组相比,糖尿病组的Col-III / Col-I和MMP-1 / TIMP-1比率持续较高。糖尿病组中MMP-1 / TIMP-1的比例在第7天达到峰值,而正常组中该比例保持在接近对照水平。糖尿病组似乎从正畸运动引起的损伤中恢复较差。结论:在机械作用下,糖尿病延长了PDL的降解,PDL的重塑和牙槽骨的吸收。

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