【摘要】：正畸牙移動(dòng)是壓力側(cè)骨吸收伴隨張力側(cè)骨形成的骨改建過程,許多免疫介質(zhì)如炎癥因子、生長因子等都參與正畸牙移動(dòng)過程。因此牙齒移動(dòng)被認(rèn)為屬于無菌炎癥反應(yīng)過程。MT01屬免疫抑制型ODN,前期研究表明,MT01能夠抑制由TLR9激活引起的機(jī)體炎癥反應(yīng),防止組織細(xì)胞受損,并能夠促進(jìn)牙移動(dòng)過程中牙槽骨的成骨細(xì)胞分化,抑制破骨細(xì)胞增值活化。那么,TLR9是否參與引發(fā)正畸牙移動(dòng)牙槽骨炎癥反應(yīng)的過程,MT01又是否能夠通過抑制TLR9信號(hào)通路,從而抑制牙移動(dòng)過程中的炎癥反應(yīng)。根據(jù)所提出的科學(xué)問題,本實(shí)驗(yàn)將探討MT01對(duì)正畸牙移動(dòng)中牙周組織免疫反應(yīng)的調(diào)控作用及可能的機(jī)制。目的:建立大鼠正畸牙移動(dòng)模型,局部途徑給藥,通過RT-q PCR方法檢測(cè)探討TLR9、TRAF6和其下游炎癥因子IL-6在實(shí)驗(yàn)性牙移動(dòng)過程中牙周組織表達(dá)水平的變化,以及MT01對(duì)牙周組織TLR9、TRAF6和IL-6表達(dá)水平的影響,評(píng)價(jià)MT01對(duì)大鼠正畸牙移動(dòng)后牙周組織改建的影響作用。方法:72只雄性Wistar大鼠,隨機(jī)分為無藥物干預(yù)組(n=36)及藥物干預(yù)組(n=36),0.49 N力近中移動(dòng)大鼠上頜第一磨牙,于加力后第3、7、14、21天處死。其中,每組6只斷頭處死后分別獲取上頜第一磨牙近遠(yuǎn)中側(cè)牙槽骨,行實(shí)時(shí)定量熒光PCR檢測(cè)TLR9、TRAF6和IL-6m RNA的相對(duì)表達(dá)量;其余每組3只于心臟灌注處死后取上頜第一磨牙及其周圍牙周組織制作石蠟切片,經(jīng)HE染色觀察牙周組織形態(tài)變化。結(jié)果:①無MT01干預(yù)下,加力組張力側(cè)TLR9、TRAF6和IL-6m RNA各時(shí)間點(diǎn)表達(dá)量均顯著高于對(duì)照組(P0.01),壓力側(cè)加力7、14、21天時(shí)TLR9、TRAF6和IL-6m RNA表達(dá)量均顯著高于對(duì)照組(P0.01),且壓力組及張力組各個(gè)因子相對(duì)表達(dá)量于第7天達(dá)高峰;②MT01干預(yù)下,給藥組張力側(cè)加力3天時(shí)TLR9、TRAF6和IL-6相對(duì)表達(dá)量與對(duì)照組無統(tǒng)計(jì)學(xué)差異,加力14、21天時(shí)TLR9和IL-6表達(dá)量均低于對(duì)照組(P0.01),TRAF6表達(dá)量與對(duì)照組無顯著差異,壓力側(cè)加力3天時(shí)TLR9和IL-6相對(duì)表達(dá)量即顯著降低,加力21天時(shí)TLR9、TRAF6和IL-6三者表達(dá)量均顯著低于對(duì)照組(P0.01);③HE染色觀察顯示,給藥組大鼠第一磨牙壓力側(cè)牙槽骨吸收程度較對(duì)照組輕,且張力側(cè)成骨較對(duì)照組活躍;結(jié)論:實(shí)驗(yàn)性牙移動(dòng)牙周組織中TLR9、TRAF6及其下游炎癥因子IL-6的表達(dá)升高;MT01能夠抑制正畸牙移動(dòng)過程中牙周組織TLR9及下游相關(guān)因子表達(dá)。
[Abstract]:Orthodontic tooth movement is a process of bone remodeling accompanied by tension bone resorption. Many immune mediators, such as inflammatory factors and growth factors, are involved in orthodontic tooth movement. Therefore, tooth movement is considered to belong to aseptic inflammatory reaction. MT01 belongs to immunosuppressive ODN,. Previous studies show that MT01 can inhibit the inflammatory reaction caused by TLR9 activation, prevent tissue cell damage, and promote the differentiation of alveolar bone osteoblasts and inhibit the increment and activation of osteoclasts during tooth movement. Then, whether TLR9 is involved in the process of alveolar bone inflammation induced by orthodontic tooth movement, and whether MT01 can inhibit the inflammatory response in the process of tooth movement by inhibiting TLR9 signal pathway. According to the scientific questions put forward, this experiment will explore the regulatory effect of MT01 on periodontal tissue immune response in orthodontic tooth movement and its possible mechanism. Aim: to establish a rat orthodontic tooth movement model and local administration. To investigate the expression of TLR9,TRAF6 and its downstream inflammatory factor IL-6 in periodontal tissue during experimental tooth movement by RT-q PCR, and the effect of MT01 on the expression of TLR9,TRAF6 and IL-6 in periodontal tissue, and to evaluate the effect of MT01 on periodontal tissue remodeling after orthodontic tooth movement in rats. Methods: seventy-two male Wistar rats were randomly divided into two groups: no drug intervention group (n 鈮，

本文編號(hào)：2500467