摘要
目的:建立低位咬合动物模型,揭示在低位咬合下咬肌疼痛的神经生物学机制,为临床颞下颌关节紊乱病(TMD)的预防和诊治提供依据.方法:将48只SD大鼠随机分为实验磨全牙列组(A组)、磨后牙组(B组)、磨前牙组(C组)和对照组,每组12只.采用人工磨低大鼠不同牙列段牙齿的方法建立低位咬合动物模型,于干预后1,2,4wk后将各组分别处死大鼠4只.取咬肌浅层制作石蜡切片行SP免疫组织化学染色(SABC法),观察咬合降低后大鼠咬肌中SP表达的变化.结果:免疫组织化学结果显示,在实验1,2,4wk各实验组大鼠咬肌中P物质阳性表达均较对照组高,差异具有统计学意义(P<0.05);而在各实验组组间A组高于C组也高于B组,但差异不显著;各实验组大鼠咬肌中P物质阳性表达随实验时间的增长而增加,但差异无显著性.结论:SP神经源性的作用与咀嚼肌损伤的关系密切,SP参与了低位咬合引起的咀嚼肌损伤的病理变化过程.
AIM:To establish an animal model of infraocclusion,probe deeply into the neurobiologic mechanism of infraocclusion of masseter muscle and provide a new method for prevention and treatment of TMD.METHODS:Fourty-eight rats were divided into 3 experimental groups and 1 control group randomly.Their different part of denture were ground artificially to establish an animal model of infraocclusion.They were group A,ground all denture group,group B,ground posterior denture group,group C,ground anterior denture group,and the control group.The rats of the 4 groups were executed 1 week,2 weeks and 4 weeks late(n=4/group each time).The superficial layer of masseter muscle was harvested to have substance P SABC immunohistochemistry staining,thus to observe the changes of substance P reaction.RESULTS:Substance P SABC immunohistochemistry staining showed,the reaction of substance P in experimental groups was higher than those in control group at every experimental stage(P〈0.05),while group A was higher than group C,group C was higher than group B,and in each group,the reation of substance P increasedwith the extension of the duration of the experiment.CONCLUSION:Substance P had a close relationship with masseter muscle injuries,and substance P may be a partner in the pathological changes of masseter muscle injuries.
出处
《第四军医大学学报》
CAS
北大核心
2009年第22期2565-2567,共3页
Journal of the Fourth Military Medical University
基金
陕西省科学技术研究发展计划(2008K14-06)