Department of Stomatology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Diabetes Technol Ther. 2010 Jan;12(1):65-73. doi: 10.1089/dia.2009.0085.
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.
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.
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.
Under mechanical forces, diabetes prolonged duration of degradation of PDL and remodeling of PDL and resorption of alveolar bone.
糖尿病相关牙周炎导致的牙槽骨吸收引起的牙齿病理性移位，常通过正畸治疗来矫正。然而，正畸治疗的恢复往往因不明原因而延迟。本研究探讨了链脲佐菌素诱导的糖尿病对正畸牙齿移动过程中牙周韧带（PDL）和牙槽骨改建相关蛋白表达的影响。
48 只 Sprague-Dawley 大鼠随机分为两组：“正常”组和“糖尿病”组（每组 n = 24）。糖尿病通过单次链脲佐菌素（65 mg/kg）诱导。正畸诱导后 3、7 和 14 天处死动物。在压力侧，通过免疫组织化学方法测量胶原 I 型（Col-I）、基质金属蛋白酶 1 型（MMP-1）和基质金属蛋白酶组织抑制剂 1 型（TIMP-1）的表达变化。在张力侧，通过苦味酸-天狼猩红染色评估 Col-I 和胶原 III 型（Col-III）纤维。观察牙槽骨表面的破骨细胞。
糖尿病增加了 PDL 中 MMP-1 和 Col-III 的表达，降低了 Col-I 的表达。正畸诱导后，破骨细胞作用延迟，糖尿病组 Col-III/Col-I 和 MMP-1/TIMP-1 比值高于正常组。糖尿病组 MMP-1/TIMP-1 比值在第 7 天达到峰值，而正常组比值接近对照水平。糖尿病组似乎在正畸运动引起的损伤恢复方面较差。
在机械力作用下，糖尿病延长了 PDL 的降解、PDL 和牙槽骨的改建时间。
