摘要
目的:将自行构建的质粒载体pcDNA3.1-hOPG,通过体内转染,评价OPG直接基因转染疗法对大鼠实验性牙周炎牙槽骨吸收的影响,为牙周炎以及种植体周炎的生物治疗提供实验依据。方法:将30只SD大鼠随机分为3组,即Ⅰ组生理盐水组(n=10,100μg/只)、Ⅱ组pcDNA3.1(-)组(n=10,100μg/只)、Ⅲ组pcDNA3.1-hOPG组(n=10,100μg/只)。通过丝线结扎、接种牙周炎可疑致病菌、喂高糖软食诱发实验性牙周炎。结扎28d后处死,通过大体标本、组织学等观察牙槽骨吸收、OPG及破骨细胞变化。结果:Ⅲ组结扎侧OPG表达强度增加,牙槽骨吸收量减少(P<0.05),活化破骨细胞数降低(P<0.05)。结论:OPG重组质粒转染,减少破骨细胞数量,有效减缓实验性牙周炎引起的牙槽骨吸收破坏。
Objective:Through recombinant plasmid pcDNA3.1-hOPG transformation in in vivo,this study is undertaken to determine the effect of OPG gene therapy on alveolar bone resorption caused by experimental periodontitis in rats,and supply an experimental foundation for further clinical application of OPG gene therapy in the treatment of periodontitis and peri-implantitis.Methods:Thirty female healthy SD rats were randomly divided into three groups:group Ⅰ(n=10):100μg physiological saline injected;group Ⅱ(n=10):100μg pcDNA3.1(-)plasmid injected;group Ⅲ(n=10):100μg pcDNA3.1-hOPG plasmid injected.Silk ligatures,drinking water containing 10%glucose,and mixed periodontopathic bacteria were used to create periodontitis.Four weeks after ligature,all specimens were evaluated through morphological observation.Results:In experimental periodontitis models,compared with groupⅠand groupⅡ,OPG IOD and OPG/RANKL in group Ⅲwere enhanced(P<0.05),alveolar bone resorption and active osteoclasts decreased respectively(P<0.05).Conclusions:OPG overexpression mediated by recombinant plasmid in vivo suppressed osteoclastogenesis and osteoclast activity,and helped to prevent alveolar bone height reduction caused by experimental periodontitis.
出处
《中国口腔种植学杂志》
2009年第2期125-125,共1页
Chinese Journal of Oral Implantology