發(fā)布時(shí)間：2018-09-04 08:49

【摘要】：研究背景與目的:臨床上常見(jiàn)由牙齒異常接觸、咀嚼功能紊亂和醫(yī)源性因素等導(dǎo)致的咬合干擾產(chǎn)生的咬合創(chuàng)傷。咬合創(chuàng)傷能夠?qū)︼D下頌關(guān)節(jié)產(chǎn)生各種生物學(xué)影響,近年來(lái)研究發(fā)現(xiàn)鈣黏蛋白-11(cadherin-ll,Cad-ll,CDH-ll)與顳下頜關(guān)節(jié)發(fā)生、發(fā)育及顳下頌關(guān)節(jié)紊亂病等密切相關(guān)。本研究通過(guò)建立大鼠咬合創(chuàng)傷模型,觀察咬合創(chuàng)傷前后顳下頌關(guān)節(jié)的組織形態(tài)學(xué)變化及IL-6、TNF-α、Cad-11在顳下頜關(guān)節(jié)中的分布表達(dá)情況等,探討咬合創(chuàng)傷影響顳下頜關(guān)節(jié)的機(jī)制,以及Cad-11在此過(guò)程中的相關(guān)作用,為顳下頌關(guān)節(jié)紊亂病的病因機(jī)制、臨床診斷與治療等研究提供新的靶點(diǎn)和思路。實(shí)驗(yàn)方法:本實(shí)驗(yàn)將45只8周齡雄性Wistar大鼠(體重約180-220g)隨機(jī)分為實(shí)驗(yàn)組一(Experiment group Ⅰ,EG Ⅰ)、實(shí)驗(yàn)組二(Experiment groupⅡ,EGⅡ)和對(duì)照組(Control group,CG)三大組。EG Ⅰ中,通過(guò)在大鼠下頜右側(cè)第一磨牙粘接高出鄈平面1.0mm的3/4鈷鉻金屬冠建立咬合創(chuàng)傷模型,并分為咬合創(chuàng)傷1w、2w及4w組,每組各5只大鼠;EGⅡ?yàn)镋GⅠ各組基礎(chǔ)上分別去除咬合創(chuàng)傷2周,即1w+2w、2w+2w及4w+2w組,每組各5只大鼠;對(duì)照組為無(wú)咬合創(chuàng)傷的大鼠,每組各3只大鼠。所有大鼠于相應(yīng)時(shí)間點(diǎn)處死并取材,標(biāo)本經(jīng)固定、脫鈣、包埋等程序后,正中矢狀面制備5.0μm厚的連續(xù)切片。通過(guò)蘇木精一伊紅染色(hematoxylin-eosin staining,HE染色)進(jìn)行顳下頌關(guān)節(jié)的組織形態(tài)學(xué)觀察;通過(guò)免疫組織化學(xué)染色(immunohistochemical staining,IHC 染色)檢測(cè) IL-6、TNF-α、Cad-11的表達(dá)情況,并用ImagePro-Plus6.2軟件行相應(yīng)的平均光密度值計(jì)算,通過(guò)Graphpad Prism6.x.C統(tǒng)計(jì)軟件進(jìn)行相應(yīng)的數(shù)據(jù)統(tǒng)計(jì)分析。實(shí)驗(yàn)結(jié)果:第一部分大鼠咬合創(chuàng)傷模型的建立本實(shí)驗(yàn)及課題組前期實(shí)驗(yàn)均已驗(yàn)證,此高出鄈平面1.Omm的3/4鈷鉻金屬冠固位良好、穩(wěn)定可靠,成功對(duì)Wistar大鼠牙周組織造成了明顯的病理?yè)p傷,成功建立了咬合創(chuàng)傷模型。第二部分咬合創(chuàng)傷大鼠顳下頜關(guān)節(jié)的組織形態(tài)學(xué)觀察咬合創(chuàng)傷大鼠的顳下頌關(guān)節(jié)HE染色組織形態(tài)學(xué)分析顯示:EG Ⅰ中1w組大鼠的顳下頜關(guān)節(jié)出現(xiàn)明顯炎癥反應(yīng),主要表現(xiàn)為吞噬小泡增多、關(guān)節(jié)軟骨細(xì)胞腫大;2w及4w組炎癥情況減輕,但出現(xiàn)軟骨細(xì)胞簇狀增生、軟骨基質(zhì)粘液樣改變等病理變化;EGⅡ中大鼠的顳下頌關(guān)節(jié)與對(duì)照組正常組織無(wú)明顯差異。第三部分咬合創(chuàng)傷大鼠顳下頜關(guān)節(jié)中IL-6、TNF-α和Cad-11的表達(dá)變化咬合創(chuàng)傷大鼠的顳下頌關(guān)節(jié)免疫組織化學(xué)染色結(jié)果顯示:CG中IL-6、TNF-α和Cad-11呈弱陽(yáng)性表達(dá),主要分布于髁突肥大細(xì)胞層、肥大細(xì)胞層與增殖層交界處;EG Ⅰ中1w組大鼠顳下頌關(guān)節(jié)的肥大細(xì)胞層、肥大細(xì)胞層與增殖層交界處可見(jiàn) IL-6、TNF-α 和 Cad-11 呈強(qiáng)陽(yáng)性表達(dá)(P0.05);2w 組及 4w 組的 IL-6、TNF-α和Cad-11與1w組相比表達(dá)強(qiáng)度均減弱(P0.05);EGⅡ中1w+2w組的髁突組織內(nèi)IL-6、TNF-α和Cad-11的表達(dá)量高于各自對(duì)照組(P0.05),但2w+2w和4w+2w組內(nèi)IL-6、TNF-α和Cad-11的表達(dá)與各自的對(duì)照組無(wú)統(tǒng)計(jì)學(xué)差異(P0.05)。結(jié)論:通過(guò)粘接3/4鈷鉻金屬冠的方式建立的大鼠咬合創(chuàng)傷模型穩(wěn)定可靠,適用于咬合創(chuàng)傷相關(guān)研究。在咬合創(chuàng)傷早期,大鼠顳下頌關(guān)節(jié)炎癥反應(yīng)明顯,隨后炎癥反應(yīng)減弱,造成顳下頌關(guān)節(jié)病理性損傷;去除咬合創(chuàng)傷后炎癥反應(yīng)減弱,有利于顳下頜關(guān)節(jié)的組織愈合。Cad-11在炎癥反應(yīng)早期可能協(xié)同IL-6、TNF-α等經(jīng)典促炎癥因子共同促進(jìn)咬合創(chuàng)傷促發(fā)的顳下頜關(guān)節(jié)的炎癥反應(yīng);另外,Cad-11還可能在咬合創(chuàng)傷所致的顳下頜關(guān)節(jié)退行性變等過(guò)程中發(fā)揮重要作用。
[Abstract]:BACKGROUND AND OBJECTIVE: Occlusal trauma caused by occlusal interference caused by abnormal tooth contact, masticatory dysfunction and iatrogenic factors is common in clinic. Occlusal trauma can exert various biological effects on infratemporal song joint. In recent years, studies have found that cadherin-ll (Cad-ll, CDH-ll) and temporomandibular joint occur and develop. In this study, we established a rat model of occlusal trauma, observed the histomorphological changes of the joint before and after occlusal trauma and the distribution and expression of IL-6, TNF-a, Cad-11 in the temporomandibular joint, and explored the mechanism of occlusal trauma affecting the temporomandibular joint and the mechanism of Cad-11 in the process. Methods: Forty-five eight-week-old male Wistar rats (weighing about 180-220 g) were randomly divided into experimental group I (EG I), experimental group II (EG II) and control group (Contr I). The occlusal trauma model was established by attaching 3/4 cobalt-chromium crowns of 1.0 mm above the union plane to the right mandibular first molars of rats, and was divided into 1 w, 2 W and 4 W occlusal trauma groups with 5 rats in each group. All the rats were sacrificed at the corresponding time points, and the specimens were fixed, decalcified and embedded. The median sagittal plane was made into 5.0 micron thick serial sections. The histomorphology of the infratemporal euphoria joint was observed by hematoxylin-eosin staining (HE staining). The expression of IL-6, TNF-a and Cad-11 was detected by immunohistochemical staining (IHC staining). The average optical density was calculated by ImagePro-Plus 6.2 software. The data were analyzed by Graphpad Prism6.x.C statistical software. The model of occlusal injury in Wistar rats was established successfully. Part two: Histological observation of temporomandibular joint in occlusal trauma rats Histomorphological analysis of HE staining of the infratemporal song joint in rats with occlusal trauma showed that the temporomandibular joint of the rats in the 1st week group of EG I had obvious inflammatory reaction, mainly manifested as increased phagocytic vesicles and enlarged articular chondrocytes; the inflammation of the rats in the 2nd and 4th weeks groups was alleviated, but there were some pathological changes, such as chondrocyte cluster proliferation and cartilage matrix mucoid changes In the third part, the expression of IL-6, TNF-a and Cad-11 in TMJ of occlusal trauma rats was changed. The immunohistochemical staining results of TMJ of occlusal trauma rats showed that IL-6, TNF-a and Cad-11 in CG were weakly positive, mainly distributed in condyle. There were strong positive expressions of IL-6, TNF-a and Cad-11 in the mast cell layer and the junction between the mast cell layer and the proliferative layer in the 1st week group of EG I, and the expression of IL-6, TNF-a and Cad-11 in the 1st week group and the 4th week group were all weaker than those in the 1st week group of EG II (P 0.05). The expressions of IL-6, TNF-a and Ca-11 in condylar tissue of rats were higher than those of the control group (P 0.05), but there was no significant difference in the expressions of IL-6, TNF-a and Ca-11 between the two groups (P 0.05). In the early stage of occlusal trauma, the inflammatory reaction of rat's infratemporal song joint was obvious, and then the inflammatory reaction was weakened, which resulted in pathological injury of rat's infratemporal song joint. After removing occlusal trauma, the inflammatory reaction was weakened, which was beneficial to the tissue healing of temporomandibular joint. In addition, Cad-11 may play an important role in the process of temporomandibular joint degeneration caused by occlusal trauma.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R782.6

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