Abstract：
BACKGROUND: To evaluate the presence of myofibroblasts (MFs) in the development of lip carcinogenesis, through the correlation of clinical, histomorphometric and immunohistochemical parameters, in actinic cheilitis (ACs) and lower lip squamous cell carcinomas (LLSCCs).
METHODS: Samples of ACs, LLSCCs, and control group (CG) were prepared by tissue microarray (TMA) for immunohistochemical TGF-β, α-SMA, and Ki-67 and histochemical hematoxylin and eosin, picrosirius red, and verhoeff van gieson reactions. Clinical and microscopic data were associated using the Mann-Whitney, Kruskal-Wallis/Dunn, and Spearman correlation tests (SPSS, p < 0.05).
RESULTS: ACs showed higher number of α-SMA+ MFs when compared to CG (p = 0.034), and these cells were associated with the vertical expansion of solar elastosis (SE) itself (p = 0.027). Areas of SE had lower deposits of collagen (p < 0.001), immunostaining for TGF-β (p < 0.001), and higher density of elastic fibers (p < 0.05) when compared to areas without SE. A positive correlation was observed between high-risk epithelial dysplasia (ED) and the proximity of SE to the dysplastic epithelium (p = 0.027). LLSCCs showed a higher number of α-SMA+ MFs about CG (p = 0.034), as well as a reduction in the deposition of total collagen (p = 0.009) in relation to ACs and CG. There was also a negative correlation between the amount of α-SMA+ cells and the accumulation of total collagen (p = 0.041). Collagen and elastic density loss was higher in larger tumors (p = 0.045) with nodal invasion (p = 0.047).
CONCLUSIONS: Our findings show the possible role of MFs, collagen fibers, and elastosis areas in the lip carcinogenesis process.
METHODS: Samples of ACs, LLSCCs, and control group (CG) were prepared by tissue microarray (TMA) for immunohistochemical TGF-β, α-SMA, and Ki-67 and histochemical hematoxylin and eosin, picrosirius red, and verhoeff van gieson reactions. Clinical and microscopic data were associated using the Mann-Whitney, Kruskal-Wallis/Dunn, and Spearman correlation tests (SPSS, p < 0.05).
RESULTS: ACs showed higher number of α-SMA+ MFs when compared to CG (p = 0.034), and these cells were associated with the vertical expansion of solar elastosis (SE) itself (p = 0.027). Areas of SE had lower deposits of collagen (p < 0.001), immunostaining for TGF-β (p < 0.001), and higher density of elastic fibers (p < 0.05) when compared to areas without SE. A positive correlation was observed between high-risk epithelial dysplasia (ED) and the proximity of SE to the dysplastic epithelium (p = 0.027). LLSCCs showed a higher number of α-SMA+ MFs about CG (p = 0.034), as well as a reduction in the deposition of total collagen (p = 0.009) in relation to ACs and CG. There was also a negative correlation between the amount of α-SMA+ cells and the accumulation of total collagen (p = 0.041). Collagen and elastic density loss was higher in larger tumors (p = 0.045) with nodal invasion (p = 0.047).
CONCLUSIONS: Our findings show the possible role of MFs, collagen fibers, and elastosis areas in the lip carcinogenesis process.
摘要：
背景：为了评估在唇癌发生发展过程中肌成纤维细胞（MFs）的存在，通过临床的相关性，组织形态学和免疫组织化学参数，在光化性唇炎（AC）和下唇鳞状细胞癌（LLSCCs）中。
方法：AC样品，LLSCCs,对照组(CG)采用组织芯片(TMA)制备TGF-β免疫组织化学,α-SMA,Ki-67和组织化学苏木精和伊红，黄连红,和Verhoeffvangieson的反应.使用Mann-Whitney将临床和微观数据相关联，Kruskal-Wallis/Dunn,和Spearman相关性检验(SPSS，p<0.05)。
结果：与CG相比，AC显示出更多的α-SMAMF（p=0.034），这些细胞与太阳弹性蛋白（SE）本身的垂直扩张有关（p=0.027）。SE区域胶原沉积较低(p<0.001)，TGF-β的免疫染色（p<0.001），与没有SE的区域相比，弹性纤维的密度更高（p<0.05）。在高危上皮发育不良（ED）与SE与发育不良上皮的接近度之间观察到正相关（p=0.027）。LLSCCs显示相对于CG的α-SMA+MF数量较高(p=0.034)，以及与AC和CG相关的总胶原沉积减少(p=0.009)。α-SMA+细胞的数量与总胶原的积累之间也存在负相关(p=0.041)。在较大的肿瘤（p=0.045）伴结节浸润（p=0.047）中，胶原和弹性密度损失更高。
结论：我们的发现表明了MFs的可能作用，胶原纤维，和嘴唇癌变过程中的弹性沉着区。
方法：AC样品，LLSCCs,对照组(CG)采用组织芯片(TMA)制备TGF-β免疫组织化学,α-SMA,Ki-67和组织化学苏木精和伊红，黄连红,和Verhoeffvangieson的反应.使用Mann-Whitney将临床和微观数据相关联，Kruskal-Wallis/Dunn,和Spearman相关性检验(SPSS，p<0.05)。
结果：与CG相比，AC显示出更多的α-SMAMF（p=0.034），这些细胞与太阳弹性蛋白（SE）本身的垂直扩张有关（p=0.027）。SE区域胶原沉积较低(p<0.001)，TGF-β的免疫染色（p<0.001），与没有SE的区域相比，弹性纤维的密度更高（p<0.05）。在高危上皮发育不良（ED）与SE与发育不良上皮的接近度之间观察到正相关（p=0.027）。LLSCCs显示相对于CG的α-SMA+MF数量较高(p=0.034)，以及与AC和CG相关的总胶原沉积减少(p=0.009)。α-SMA+细胞的数量与总胶原的积累之间也存在负相关(p=0.041)。在较大的肿瘤（p=0.045）伴结节浸润（p=0.047）中，胶原和弹性密度损失更高。
结论：我们的发现表明了MFs的可能作用，胶原纤维，和嘴唇癌变过程中的弹性沉着区。
