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目的:建立糖尿病合并牙周炎大鼠模型,观察比较近牙槽嵴区牙周膜内肿瘤坏死因子-a(TNF-a)的含量,探讨高血糖对牙周组织炎症程度的影响。方法:糖尿病大鼠(STZ组)模型采用链脲佐菌素一次性腹腔注射制备,单纯牙周炎组(N组)注射同剂量的枸橼酸钠缓冲液。成模且稳定后(4周),两组都采用大鼠牙颈部丝线结扎的方法诱导牙周炎模型,于结扎后1周,2周,3周处死大鼠,采用组织学方法,免疫组织化学结合MATLAB7.0.1图像灰度定量分析法,研究近牙槽嵴区牙周膜中TNF-a水平的变化及牙周组织炎症的进展程度。结果:N组与STZ组除0周外各时间点两组之间比较有显著性差异(P<0.001);N组内各时间点每两组之间比较有统计学差别(P<0.05);STZ组内各时间点每两组之间比较有统计学差别(P<0.05)。随时间的增加,各组大鼠的炎症程度增加,TNF-a的表达水平增加,STZ组的病变进展程度显著重于N组。结论:一次性腹腔注射STZ+牙颈部丝线结扎可成功建立实验性糖尿病大鼠的牙周炎模型。高血糖浓度使糖尿病大鼠牙槽骨TNF-a的表达水平增加,降低了机体的损伤-修复能力,牙周组织的炎症进一步加重。
OBJECTIVE: To establish a rat model of diabetes mellitus with periodontitis and observe the content of tumor necrosis factor-a (TNF-a) in the periodontal ligament of the alveolar ridge and to investigate the effect of hyperglycemia on the periodontal inflammation. Methods: The diabetic rats (STZ group) were injected intraperitoneally with streptozotocin (STZ). The rats in periodontitis group (group N) were given the same dose of sodium citrate buffer solution. The rats were sacrificed at 1, 2 and 3 weeks after ligation, and histological methods were used to immunize the rats Histochemistry combined with MATLAB7.0.1 image grayscale quantitative analysis of alveolar ridge zone periodontal membrane TNF-a levels and periodontal tissue inflammation progression. Results: There was a significant difference (P <0.001) between N group and STZ group at each time point except for 0 week. There was a significant difference between each two groups in N group (P <0.05) There was a significant difference between every two time points in STZ group (P <0.05). With the increase of time, the inflammation degree of each group increased, the expression of TNF-a increased, and the progression of STZ group was more serious than that of N group. Conclusion: A one-time intraperitoneal injection of STZ + cervical ligament ligation successfully established periodontitis model of experimental diabetic rats. Hyperglycemia can increase the expression of TNF-a in alveolar bone of diabetic rats, reduce the damage-repair ability of the body, and further aggravate the inflammation in periodontal tissues.