Allen Jacqui
Centre for Voice and Swallowing, University of California, Davis, Sacramento, California 95817, USA.
Curr Opin Otolaryngol Head Neck Surg. 2010 Dec;18(6):475-80. doi: 10.1097/MOO.0b013e32833fecd1.
The prolonged debilitation, loss of income, and decrement in quality of life caused by vocal fold scar is exacerbated by our inability to successfully treat this difficult problem. As technology focuses on developing innovative treatments, we need to fully appreciate and understand the mechanisms giving rise to glottal scar, on both a macroscopic and microscopic level. This review examines recent literature pertaining to the gross and molecular mechanisms which give rise to vocal fold scar.
Mechanisms of vocal fold scar production have been examined in both macroscopic and microscopic detail. Trauma and injury involving any aspect of the lamina propria, particularly the deeper layers, may result in epithelial tethering and scar formation. At the molecular level, early inflammatory cytokines activate and recruit fibroblasts which then drive the fibrotic cascade. Transforming growth factor-β enhances fibrosis and is balanced by tissue matrix metalloproteinases and hepatocyte growth factor activity. Molecular signaling offers novel opportunities to intervene in scar formation.
New work investigating the cause of vocal fold scar identifies complex molecular processes leading to fibrosis in the lamina propria. Improved mechanistic understanding offers insight into prevention strategies and possible targets for antifibrotic therapies that may help prevent or treat this debilitating condition.
声带瘢痕导致的长期虚弱、收入损失和生活质量下降,因我们无法成功治疗这一难题而加剧。随着技术聚焦于开发创新疗法,我们需要在宏观和微观层面充分认识和理解导致声门瘢痕的机制。本综述探讨了近期有关引发声带瘢痕的大体和分子机制的文献。
已从宏观和微观细节对声带瘢痕形成机制进行了研究。涉及固有层任何方面,尤其是深层的创伤和损伤,可能导致上皮束缚和瘢痕形成。在分子水平,早期炎性细胞因子激活并募集成纤维细胞,进而驱动纤维化级联反应。转化生长因子-β增强纤维化,而组织基质金属蛋白酶和肝细胞生长因子活性对其起平衡作用。分子信号传导为干预瘢痕形成提供了新机会。
研究声带瘢痕成因的新工作确定了导致固有层纤维化的复杂分子过程。对机制的深入理解为预防策略和抗纤维化治疗的可能靶点提供了思路,这可能有助于预防或治疗这种使人衰弱的病症。