中文摘要：

目的：研究S100A9蛋白在糖尿病大鼠牙周组织中的表达，探讨其在糖尿病诱发的牙周病变中可能的作用机制。方法本实验通过对SD大鼠腹腔注射链脲佐菌素（STZ）构建糖尿病大鼠模型，通过苏木精-伊红（HE）染色观察糖尿病大鼠牙周结构的变化，免疫组织化学染色观察糖尿病大鼠牙周组织中S100A9的表达与分布，同时检测其配体Toll受体4（TLR4）和核转录因子κB（NF-κB）/p-P65蛋白的表达。通过分析上述蛋白的表达规律，探讨S100A9蛋白在糖尿病诱发的牙周病变中的作用机制。结果糖尿病大鼠的牙槽骨骨小梁结构稀疏，硬骨板消失；免疫组织化学染色显示牙周膜、牙槽骨及牙龈上皮中S100A9的表达水平比对照组明显上调，TLR4在牙槽骨、牙周膜、牙龈中的表达水平相较于对照组也显著增强；p-P65在对照组中没表达，但在糖尿病组中牙周膜和牙槽骨中呈阳性表达。结论糖尿病导致大鼠牙周组织结构病变，其原因可能与S100A9介导的TLR4和NF-κB信号通路的活化有关。

英文摘要：

Objective The study seeks to investigate the expression of S100A9 and its potential role in periodontal diseases induced by diabetes.Methods A diabetic SD rat model was established through intraperitoneal injection of streptozotocin （STZ）. Hematoxylin-eosin （HE） staining was performed to study the structure of the periodontium of diabetic rats. Using immunohistochemical staining, the distribution of S100A9 expression was detected in the periodontium of diabetic rats. Ex-pressions of Toll-like receptor 4 （TLR4） （ligands of S100A9） and p-P65/nuclear factor κB （NF-κB） were also measured. Results The trabecular structure of alveolar bone was sparser, and lamina dura was disappeared in diabetic rats. Obviously higher expressions of S100A9 were observed in the periodontal ligament, alveolar bone, and gingival epithelial of diabetic rats than in the control rats. TLR4 expressions in the periodontal ligament, alveolar bone and gingival epithelial of the diabetic rats were also higher as compared to the control rats. p-P65 expression was not detected in the control rats, but was detected in the periodontal ligament and alveolar bone of the diabetic rats.Conclusion Periodontium lesions in diabetes mellitus may be induced by the activation of TLR4 and NF-κB signaling pathway meditated by S100A9.