Özdemir Çiğdem, Kuzu Selçuk, Şenol Yiğit, Yiğit Tuba, Güldün Erol, Bucak Abdulkadir, Ulu Şahin, Tokyol Çiğdem
Department of Pathology, Faculty of Medicine, Afyonkarahisar Health Sciences University, Afyonkarahisar 03030, Turkey.
Department of Otorhinolaryngology, Faculty of Medicine, Afyonkarahisar Health Sciences University, Afyonkarahisar 03030, Turkey.
Diagnostics (Basel). 2023 Jan 26;13(3):455. doi: 10.3390/diagnostics13030455.
The study aimed to evaluate the effects and relationships between mast cells in the matrix, mast cell enzymes tryptase and chymase, epithelial proliferation, microvascular density, and bone destruction in cholesteatoma. Thirty-five biopsies diagnosed with cholesteatoma and seven healthy skin tissues taken from the retro-auricular region for control were evaluated. Immunohistochemical studies were performed with CD117, CD34, Ki-67, chymase, and tryptase antibodies, in a single session for all cases and the control group. The relationship between erosion size and antibody load was determined. The mean cholesteatoma epithelium Ki-67 was higher than the control group ( < 0.001). CD117-positive mast cells, chymase-positive mast cells, tryptase-positive mast cells, and microvessel density were significantly higher in the cholesteatoma matrix compared to the control group ( < 0.002, < 0.001, < 0.005). In the group with bone erosion scores of two and above, immunohistochemical markers tended to be higher. A positive correlation was found between CD117 and chymase, tryptase, and microvessel density; between tryptase, chymase, and microvessel density; and between chymase and microvessel density. CD117-positive mast cells and chymase-positive mast cells stimulate angiogenesis, increase the epithelium's proliferative capacity in the cholesteatoma matrix, and form cholesteatoma. The increased proliferation of cholesteatoma epithelium and increased vascular density in the matrix exacerbate bone erosion.
该研究旨在评估胆脂瘤中基质肥大细胞、肥大细胞酶类胰蛋白酶和糜蛋白酶、上皮增殖、微血管密度及骨质破坏之间的影响与关系。对35例经诊断的胆脂瘤活检组织以及取自耳后区域作为对照的7例健康皮肤组织进行了评估。对所有病例及对照组均单次进行了CD117、CD34、Ki-67、糜蛋白酶和胰蛋白酶抗体的免疫组织化学研究。确定了糜烂大小与抗体负荷之间的关系。胆脂瘤上皮Ki-67的平均值高于对照组（<0.001）。与对照组相比，胆脂瘤基质中CD117阳性肥大细胞、糜蛋白酶阳性肥大细胞、胰蛋白酶阳性肥大细胞及微血管密度显著更高（<0.002、<0.001、<0.005）。在骨质侵蚀评分达到2分及以上的组中，免疫组织化学标志物往往更高。发现CD117与糜蛋白酶、胰蛋白酶及微血管密度之间；胰蛋白酶、糜蛋白酶与微血管密度之间；以及糜蛋白酶与微血管密度之间呈正相关。CD117阳性肥大细胞和糜蛋白酶阳性肥大细胞刺激血管生成，增加胆脂瘤基质中上皮的增殖能力，并形成胆脂瘤。胆脂瘤上皮增殖增加及基质中血管密度增加会加剧骨质侵蚀。
