咬合創(chuàng)傷對大鼠顳下頜關節(jié)中鈣黏蛋白-11表達的影響
發(fā)布時間：2018-09-04 08:49
【摘要】：研究背景與目的:臨床上常見由牙齒異常接觸、咀嚼功能紊亂和醫(yī)源性因素等導致的咬合干擾產(chǎn)生的咬合創(chuàng)傷。咬合創(chuàng)傷能夠對顳下頌關節(jié)產(chǎn)生各種生物學影響,近年來研究發(fā)現(xiàn)鈣黏蛋白-11(cadherin-ll,Cad-ll,CDH-ll)與顳下頜關節(jié)發(fā)生、發(fā)育及顳下頌關節(jié)紊亂病等密切相關。本研究通過建立大鼠咬合創(chuàng)傷模型,觀察咬合創(chuàng)傷前后顳下頌關節(jié)的組織形態(tài)學變化及IL-6、TNF-α、Cad-11在顳下頜關節(jié)中的分布表達情況等,探討咬合創(chuàng)傷影響顳下頜關節(jié)的機制,以及Cad-11在此過程中的相關作用,為顳下頌關節(jié)紊亂病的病因機制、臨床診斷與治療等研究提供新的靶點和思路。實驗方法:本實驗將45只8周齡雄性Wistar大鼠(體重約180-220g)隨機分為實驗組一(Experiment group Ⅰ,EG Ⅰ)、實驗組二(Experiment groupⅡ,EGⅡ)和對照組(Control group,CG)三大組。EG Ⅰ中,通過在大鼠下頜右側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為EGⅠ各組基礎上分別去除咬合創(chuàng)傷2周,即1w+2w、2w+2w及4w+2w組,每組各5只大鼠;對照組為無咬合創(chuàng)傷的大鼠,每組各3只大鼠。所有大鼠于相應時間點處死并取材,標本經(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。通過蘇木精一伊紅染色(hematoxylin-eosin staining,HE染色)進行顳下頌關節(jié)的組織形態(tài)學觀察;通過免疫組織化學染色(immunohistochemical staining,IHC 染色)檢測 IL-6、TNF-α、Cad-11的表達情況,并用ImagePro-Plus6.2軟件行相應的平均光密度值計算,通過Graphpad Prism6.x.C統(tǒng)計軟件進行相應的數(shù)據(jù)統(tǒng)計分析。實驗結果:第一部分大鼠咬合創(chuàng)傷模型的建立本實驗及課題組前期實驗均已驗證,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Wistar大鼠牙周組織造成了明顯的病理損傷,成功建立了咬合創(chuàng)傷模型。第二部分咬合創(chuàng)傷大鼠顳下頜關節(jié)的組織形態(tài)學觀察咬合創(chuàng)傷大鼠的顳下頌關節(jié)HE染色組織形態(tài)學分析顯示:EG Ⅰ中1w組大鼠的顳下頜關節(jié)出現(xiàn)明顯炎癥反應,主要表現(xiàn)為吞噬小泡增多、關節(jié)軟骨細胞腫大;2w及4w組炎癥情況減輕,但出現(xiàn)軟骨細胞簇狀增生、軟骨基質粘液樣改變等病理變化;EGⅡ中大鼠的顳下頌關節(jié)與對照組正常組織無明顯差異。第三部分咬合創(chuàng)傷大鼠顳下頜關節(jié)中IL-6、TNF-α和Cad-11的表達變化咬合創(chuàng)傷大鼠的顳下頌關節(jié)免疫組織化學染色結果顯示:CG中IL-6、TNF-α和Cad-11呈弱陽性表達,主要分布于髁突肥大細胞層、肥大細胞層與增殖層交界處;EG Ⅰ中1w組大鼠顳下頌關節(jié)的肥大細胞層、肥大細胞層與增殖層交界處可見 IL-6、TNF-α 和 Cad-11 呈強陽性表達(P0.05);2w 組及 4w 組的 IL-6、TNF-α和Cad-11與1w組相比表達強度均減弱(P0.05);EGⅡ中1w+2w組的髁突組織內IL-6、TNF-α和Cad-11的表達量高于各自對照組(P0.05),但2w+2w和4w+2w組內IL-6、TNF-α和Cad-11的表達與各自的對照組無統(tǒng)計學差異(P0.05)。結論:通過粘接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)傷相關研究。在咬合創(chuàng)傷早期,大鼠顳下頌關節(jié)炎癥反應明顯,隨后炎癥反應減弱,造成顳下頌關節(jié)病理性損傷;去除咬合創(chuàng)傷后炎癥反應減弱,有利于顳下頜關節(jié)的組織愈合。Cad-11在炎癥反應早期可能協(xié)同IL-6、TNF-α等經(jīng)典促炎癥因子共同促進咬合創(chuàng)傷促發(fā)的顳下頜關節(jié)的炎癥反應;另外,Cad-11還可能在咬合創(chuàng)傷所致的顳下頜關節(jié)退行性變等過程中發(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.
【學位授予單位】：山東大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R782.6
本文編號：2221597
[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.
【學位授予單位】：山東大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R782.6
【參考文獻】
相關期刊論文 前5條
1 甘春蘭;陳婉;蔡捷;趙文青;吳煜;;Cadherin-11與大鼠牙齒發(fā)育關系的初步研究[J];廣西醫(yī)科大學學報;2015年01期
2 黑偉紅;劉志堅;白丁;鄭澤彬;賀紅;;大鼠牙移動性根吸收組織內鈣黏蛋白-11的表達[J];武漢大學學報(醫(yī)學版);2012年03期
3 李延武,陳力,馬肅;成年鼠髁突增齡性變化的組織學和組織化學研究[J];口腔醫(yī)學研究;2004年06期
4 馬緒臣,張震康;顳下頜關節(jié)紊亂綜合征的命名和診斷分類[J];中華口腔醫(yī)學雜志;1998年04期
5 傅開元,馬緒臣,張震康,孫開華,王晶,朱曉濱;創(chuàng)傷致家兔顳下頜關節(jié)滑膜和軟骨超微結構的改變[J];中華口腔醫(yī)學雜志;1998年01期
相關碩士學位論文 前1條
1 甘春蘭;Cadherin-11對大鼠牙髓細胞遷移、黏附和分化的影響[D];廣西醫(yī)科大學;2015年
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