本文選題：牽引 + 顳下頜關節(jié)��； 參考：《鄭州大學》2017年碩士論文

【摘要】：滑膜是顳下頜關節(jié)囊內軟組織的重要組成成分,在維持關節(jié)的各種功能方面有重要作用。當有外界應力作用時,應力使口頜系統(tǒng)肌鏈的穩(wěn)定狀態(tài)發(fā)生改變,引起顳下頜關節(jié)周圍肌肉的不平衡,使滑膜細胞在接受外界刺激信號后,直接或間接產生一些細胞因子,這些因子會引起自身和關節(jié)其他組織的適應、改建和破壞。IL-1β和VEGF是滑膜組織中常見的細胞因子,其超生理量的表達會介導一系列的化學反應,引起相應靶細胞的免疫反應。IL-1β是重要的促炎細胞因子之一,可直接和細胞膜上的受體結合,刺激各種膠原酶的生成,產生局部破壞作用,加重局部炎癥反應;也可以通過誘導其他細胞因子的生成間接地參與關節(jié)的破壞機制。VEGF屬于血小板生長因子家族,能特異性作用于血管內皮細胞,促使內皮細胞游走、增殖,在炎癥部位形成新的血管,維持關節(jié)的炎癥狀態(tài),使炎癥部位發(fā)生增生、充血;也可以誘導和活化各種酶,改變血管通透性,促進多種炎癥因子的釋放等。目的:單側Ⅱ類牽引改變了口頜系統(tǒng)肌鏈的穩(wěn)定狀態(tài),引起顳下頜關節(jié)及其周圍組織發(fā)生改變,通過觀察和分析滑膜的組織學改變及IL-1β、VEGF表達的改變,來探討單側Ⅱ類牽引對成年大鼠牽引側顳下頜關節(jié)滑膜的影響,進而為臨床應用提供部分參考。方法:180只8周齡的SD(Sprague-Dawley)雄性大鼠,隨機分為三組:實驗組(A組),假手術組(B組),空白組(C組),每組60只。A組,在大鼠的右下第一磨牙和右上切牙之間固定Ni-Ti拉簧,加力20ɡ,建立單側Ⅱ類牽引模型;B組,同A組固定拉簧,功能位加力0ɡ;C組,不固定拉簧。每組再按時間點(1d、3d、7d、14d、21d、28d)隨機分為6個亞組,每亞組10只。按各亞組的時間點處死各組大鼠,取其右側顳下頜關節(jié)雙板區(qū)的滑膜組織進行HE、免疫組織化學染色,觀察滑膜的組織學變化,檢測IL-1β、VEGF的表達。結果:A組的病理分值和B組、C組比較有統(tǒng)計學意義(P0.001);A組的IL-1β、VEGF平均光密度值和B組、C組比較有統(tǒng)計學意義(P0.001)。病理分值與IL-1β、VEGF的MOD表達之間有顯著正相關性(r1=0.912,r2=0.930;P0.001)。結論:單側Ⅱ類牽引可引起牽引側顳下頜關節(jié)滑膜組織發(fā)生組織學改變,這種改變與滑膜組織IL-1β、VEGF的表達有正相關性。
[Abstract]:Synovium is an important component of soft tissue in temporomandibular joint capsule and plays an important role in maintaining joint function. When there is external stress, the stress changes the stable state of the muscle chain of the oral and mandibular system, causes the imbalance of the muscles around the temporomandibular joint, and makes the synovial cells produce some cytokines directly or indirectly after receiving the external stimulation signal. These factors cause adaptation to themselves and other articular tissues. Remodeling and destroying. IL-1 尾 and VEGF are common cytokines in synovial tissue, and their superphysiological expression mediates a series of chemical reactions. IL-1 尾 is one of the important pro-inflammatory cytokines, which can directly bind to the receptors on the cell membrane, stimulate the production of various collagenase, produce local destruction and aggravate the local inflammatory reaction. VEGF belongs to the platelet growth factor family, which can specifically act on vascular endothelial cells, promote endothelial cell migration and proliferation, also can indirectly participate in the destruction mechanism of joint by inducing the formation of other cytokines. New blood vessels are formed in the inflammatory site to maintain the inflammatory state of the joint and make the inflammatory site proliferate and hyperemia. It can also induce and activate various enzymes change vascular permeability and promote the release of a variety of inflammatory factors. Objective: unilateral class 鈪，

本文編號：2108816