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Th17細(xì)胞在人慢性根尖周炎中的定位研究

發(fā)布時間:2018-03-12 14:03

  本文選題:根尖肉芽腫 切入點:根尖囊腫 出處:《安徽醫(yī)科大學(xué)》2014年碩士論文 論文類型:學(xué)位論文


【摘要】:目的通過檢測Th17細(xì)胞的特異性標(biāo)記維甲酸相關(guān)孤核受體(Retinoic acid-relatedorphan nuclear receptor, ROR)-γT和白細(xì)胞介素(interleukin, IL)-17在人根尖肉芽腫和根尖囊腫中的表達(dá),來闡明Th17細(xì)胞在根尖周病變中的存在情況及作用。方法收集安徽醫(yī)科大學(xué)附屬口腔醫(yī)院口腔頜面外科2011年11月至2013年7月經(jīng)根尖手術(shù)切除的根尖周炎病損組織,將其進(jìn)行病理鑒定選取根尖肉芽腫和根尖囊腫組織作為實驗組,同時進(jìn)行炎癥分級。收集埋伏阻生智齒拔除時需鑿骨患者的健康牙槽骨5例,作為正常對照組。免疫組織化學(xué)分析所有樣本中RORγT和IL-17的表達(dá)情況。采用Image Pro Plus6.0對所有樣本中RORγT和IL-17的蛋白表達(dá)量進(jìn)行檢測。 結(jié)果共有根尖囊腫18例,根尖肉芽腫22例,其中,輕度炎癥浸潤5例,中度炎癥浸潤11例,重度炎癥浸潤24例。RORγT表達(dá)于所有的根尖周炎病損組織中并顯著高于正常對照組(P<0.05)和陰性對照組(P<0.05),正常對照組和陰性對照組中沒有檢測到RORγT的表達(dá),但其在根尖肉芽腫和根尖囊腫中的表達(dá)無顯著差異(P=0.967);RORγT在輕度、中度和重度炎癥細(xì)胞浸潤中的表達(dá)水平均顯著高于正常對照組和陰性對照組(P<0.05),但三組間并無統(tǒng)計學(xué)差異;與對照組相比,IL-17在根尖周炎病損組織中的的蛋白表達(dá)水平均顯著增高。RORγT和IL-17的蛋白表達(dá)水平在根尖肉芽腫和根尖囊腫中均呈正相關(guān),分別為r=0.935,P<0.05和r=0.803,P<0.05。 結(jié)論 1.本實驗通過免疫組織化學(xué)的方法,借助Th17細(xì)胞的特異性標(biāo)記RORγT和IL-17,初步證明了Th17細(xì)胞存在于人根尖肉芽腫和根尖囊腫的病損組織中。 2. RORγT和IL-17在正常根尖周組織中沒有表達(dá),提示Th17細(xì)胞可能參與了根尖周病的發(fā)病過程。 3. RORγT和IL-17在不同炎癥浸潤程度之間的差異并無統(tǒng)計學(xué)意義,提示Th17細(xì)胞可能對根尖周病變的炎癥進(jìn)展作用不大。
[Abstract]:Objective to detect the expression of Retinoic acid-relatedorphan nuclear receptor, ROR- 緯 T and interleukin, IL)-17 in human apical granuloma and apical cyst by the specific labeling of retinoic acid acid-relatedorphan nuclear receptor in Th17 cells. To elucidate the existence and role of Th17 cells in periapical lesions. Methods the lesions of periapical periodontitis were collected from November 2011 to 2013 in oral and maxillofacial surgery, affiliated stomatology hospital of Anhui Medical University. The apical granuloma and apical cyst tissue were selected as experimental group and inflammatory grading was performed. 5 cases of healthy alveolar bone were collected from patients with impacted impacted wisdom teeth. The expression of ROR 緯 T and IL-17 in all samples was analyzed by immunohistochemistry as a normal control. Image Pro Plus6.0 was used to detect the protein expression of ROR 緯 T and IL-17 in all samples. Results there were 18 cases of apical cyst and 22 cases of apical granuloma. The expression of .ROR 緯 T in 24 patients with severe inflammatory infiltration was significantly higher than that in normal control group (P < 0.05) and negative control group (P < 0.05), but no expression of ROR 緯 T was detected in normal control group and negative control group. However, there was no significant difference in the expression of ROR 緯 T between apical granuloma and apical cyst. The expression of ROR 緯 T in mild, moderate and severe inflammatory cell infiltration was significantly higher than that in normal control group and negative control group (P < 0.05), but there was no significant difference among the three groups. Compared with the control group, the expression of IL-17 protein in periapical lesions was significantly higher. ROR 緯 T and IL-17 protein expression levels were positively correlated with those in apical granuloma and apical cysts, which were respectively 0. 05 and 0. 803 (r = 0. 05) and 0. 803 (P < 0. 05), respectively. Conclusion. 1. In this study, the presence of Th17 cells in the diseased tissues of human apical granuloma and apical cyst was preliminarily demonstrated by the immunohistochemical method and the specific labeling of ROR 緯 T and IL-17 by Th17 cells. 2. ROR 緯 T and IL-17 were not expressed in normal periapical tissues, suggesting that Th17 cells may be involved in the pathogenesis of periapical disease. 3. There was no significant difference between ROR 緯 T and IL-17 in different degree of inflammatory infiltration, suggesting that Th17 cells may have little effect on inflammatory progression of periapical lesions.
【學(xué)位授予單位】:安徽醫(yī)科大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2014
【分類號】:R781.3

【參考文獻(xiàn)】

相關(guān)期刊論文 前2條

1 衛(wèi)書盛;川島伸之;鈴木規(guī)元;許婧;須田英明;;Th17相關(guān)細(xì)胞因子在大鼠實驗性根尖周炎表達(dá)的研究[J];北京口腔醫(yī)學(xué);2010年01期

2 周艷;徐艷;;慢性牙周炎病人基礎(chǔ)治療前后Th17型細(xì)胞因子及RORC的表達(dá)變化[J];牙體牙髓牙周病學(xué)雜志;2012年02期



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