Kamath Ramya Ravindra, Basavanthappa Prahlada Nayaka, Bindu B J, Murthy C Narayana, Rajeev Gouri Priya, Raisa S
Apollo Hospitals Bangalore: Apollo Hospitals Bannerghatta, Bengaluru, India.
Department of ENT-Head & Neck Surgery, Basaveshwara Medical College & Hospital, Chitradurga, 577501 Karnataka India.
Indian J Otolaryngol Head Neck Surg. 2024 Oct;76(5):4064-4073. doi: 10.1007/s12070-024-04784-8. Epub 2024 Jun 11.
Primary acquired Cholesteatoma is a complex issue for otolaryngologists, with its development mechanisms still unclear due to the intricate anatomy of this region. It's aetiopathogenesis remains poorly understood and this aggressive clinical condition often leads to various complications. Recent research explores myofibroblast and fibronectin's potential roles in pathomechanisms of Cholesteatoma.
To determine and analyze the role of myofibroblast and fibronectin in the aetiopathogenesis of Cholesteatoma.
In a cross-sectional study at a tertiary care hospital, 30 patients with chronic suppurative otitis media with cholesteatoma were surgically treated, and intraoperative biopsy specimens were collected. These specimens were processed and subjected to histopathological examination, including immunohistochemical staining with Alpha-smooth muscle actin and anti-fibronectin antibody to identify myofibroblast and fibronectin presence. The data were then analyzed to investigate the aetiopathogenesis of cholesteatoma in this cohort.
On immunostaining, 25 blocks (83.33%) were positively stained for Alpha-SMA (-0.0007), whereas 29 blocks (96.67%) were positively stained for fibronectin ( < 0.0001), suggesting a statistically significant association between the presence of both myofibroblast and fibronectin with cholesteatoma perimatrix. Additionally, a statistically significant association was noted between complications and positive staining for myofibroblast ( - 0.0415) and positive staining for fibronectin (-0.0254).
Our study indicates that Cholesteatoma retraction and progression are driven by myofibroblast and fibronectin mechanisms, and also links them to disease severity. This understanding opens avenues for innovative diagnostics and treatments targeting these biomarkers.
原发性获得性胆脂瘤对耳鼻喉科医生来说是一个复杂的问题,由于该区域解剖结构复杂,其发病机制仍不清楚。其病因发病机制仍知之甚少,这种侵袭性临床病症常导致各种并发症。最近的研究探讨了肌成纤维细胞和纤连蛋白在胆脂瘤发病机制中的潜在作用。
确定并分析肌成纤维细胞和纤连蛋白在胆脂瘤病因发病机制中的作用。
在一家三级护理医院进行的一项横断面研究中,对30例患有胆脂瘤的慢性化脓性中耳炎患者进行了手术治疗,并收集了术中活检标本。对这些标本进行处理并进行组织病理学检查,包括用α-平滑肌肌动蛋白和抗纤连蛋白抗体进行免疫组织化学染色,以确定肌成纤维细胞和纤连蛋白的存在。然后对数据进行分析,以研究该队列中胆脂瘤的病因发病机制。
免疫染色显示,25个切片(83.33%)α-SMA呈阳性染色(-0.0007),而29个切片(96.67%)纤连蛋白呈阳性染色(<0.0001),这表明肌成纤维细胞和纤连蛋白的存在与胆脂瘤基质周围均存在统计学上的显著关联。此外,并发症与肌成纤维细胞阳性染色(-0.0415)和纤连蛋白阳性染色(-0.0254)之间存在统计学上的显著关联。
我们的研究表明,胆脂瘤的回缩和进展是由肌成纤维细胞和纤连蛋白机制驱动的,并且还将它们与疾病严重程度联系起来。这种认识为针对这些生物标志物的创新诊断和治疗开辟了道路。