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目的 :研究转化生长因子 (TGFα)在中耳胆脂瘤中的表达 ,探讨TGFα在胆脂瘤上皮细胞增生中的可能作用。方法 :31例胆脂瘤上皮标本及 10例正常外耳道皮肤组织标本制成石蜡切片 ,应用免疫组化 (S P)染色法检测上述两种标本中TGFα的表达情况 ,并采用多媒体彩色图文分析系统 ,对染色结果进行定量分析。结果 :TGFα阳性表达定位于胞浆 ,胆脂瘤上皮组织均呈中等阳性或强阳性反应 ,2 1例标本呈现从基底层向角质层染色逐渐增强的趋势 ,皮下结缔组织中可见散在的阳性细胞 ,主要为成纤维细胞、单核 巨噬细胞、浆细胞 ,少数为淋巴细胞 ;外耳道皮肤组织的阳性反应集中在表皮层 ,其中 8例标本表现为表皮全层稀疏均一的弱阳性表达。胆脂瘤上皮和正常外耳道表皮的TGFα积分吸光度分别为 2 .4 31± 0 .5 87及 1.4 6 3± 0 .14 7,两者差异有显著性意义(t’ =1.95 ,P <0 .0 5 )。结论 :胆脂瘤组织中TGFα的含量较正常皮肤组织显著增高 ,TGFα可能以自分泌和旁分泌机制参与胆脂瘤上皮增生的调节 ,局部炎症反应可能构成特殊微环境 ,诱发并维持胆脂瘤上皮的高度增生
Objective: To investigate the expression of transforming growth factor (TGFα) in cholesteatoma and to explore the possible role of TGFα in the proliferation of cholesteatoma epithelial cells. Methods: 31 cases of cholesteatoma epithelial specimens and 10 cases of normal external auditory canal skin specimens were made paraffin sections, immunohistochemical (SP) staining was used to detect TGFα expression in the above two specimens, and the use of multimedia color graphic analysis system , Quantitative analysis of staining results. Results: The positive expression of TGFα was located in the cytoplasm. The epithelial tissues of cholesteatoma showed a moderate or strong positive reaction. The staining of 21 cases showed a gradual increase from the basal layer to the stratum corneum. Scattered positive cells were seen in the subcutaneous connective tissue , Mainly fibroblasts, mononuclear macrophages, plasma cells, a small number of lymphocytes; external auditory meatal skin tissue positive reactions concentrated in the epidermis, of which 8 cases of specimens showed the full thickness of the epidermis sparse uniform weak positive expression. The TGFα integral absorbance of cholesteatoma epithelium and normal external auditory canal epidermis were respectively 2.31 ± 0.87 and 1.4 6 3 ± 0.14 7, the difference was significant (t ’= 1.95, P <0. 0 5). Conclusion: The content of TGFα in cholesteatoma tissue is significantly higher than normal skin tissue. TGFα may participate in the regulation of epithelial hyperplasia of cholesteatoma with autocrine and paracrine mechanism. Local inflammatory reaction may constitute special microenvironment to induce and maintain cholesteatoma Epithelial hyperplasia