伴放线放线杆菌在高血糖大鼠牙周炎致病作用的实验研究

The mechanisms of cell apoptosis in alveolar bone destroy and repair in diabetic periodontitis

目的探讨伴放线放线杆菌(Aggregatibacter actinomycetemcomitans,Aa)增强牙周组织炎症反应及促进细胞凋亡的内在联系。方法制备高血糖大鼠动物模型,并以血糖正常大鼠作为对照,口内接种Aa,并以抗生素及caspase-3抑制药治疗,通过检测牙龈Aa抗体、牙龈组织凋亡、静脉血炎细胞变化分析Aa在牙周病,尤其是高血糖环境下发病过程的作用。结果 Aa接种于高血糖或正常血糖大鼠口内后,均可以引起宿主局部炎症反应,牙龈Aa抗体均升高,高血糖组明显高于血糖正常组(P<0.01),牙龈凋亡水平也具有同样的表现。从静脉血观察炎细胞改变发现两组间无显著差异(P>0.05),仅粒细胞百分比升高(P<0.05)。此外,通过应用抗生素及caspas-3抑制药可以缓解牙周炎症及凋亡水平。结论高血糖大鼠接种Aa后牙周炎症明显加重,其机制与宿主局部炎症反应增强,以及细胞凋亡增多相关。另外抗生素治疗能够显著改善高血糖大鼠牙周炎症反应,但不能有效减少凋亡。

Objective We planned to discuss the possible mechanisms of cell apoptosis in diabetic periodontitis. Method We reduced the diabetics periodontitis in rats by Streptozocin and steel wire and analyzed apoptosis in this animal model. Result Diabetes increased the intensity and duration of the inflammatory infiltrate （P〈0.01）. The formation of osteoclasts and percent eroded bone in the diabetic group were significantly higher than the control group （P〉0.05） Diabetes also increased apoptosis and reduced the number of osteoblasts, and periodontal ligament fibroblasts （P〈0.05）. Conclusion An induced periodontal destruction in rats by significantly increasing the inflammatory response, and enhancing cell apoptosis through a caspase-3- dependent mechanism. Antibiotics had more effect on hyperglycemia than in normoglycemic rats.