Rousseau Bernard, Kojima Tsuyoshi, Novaleski Carolyn K, Kimball Emily E, Valenzuela Carla V, Mizuta Masanobu, Daniero James J, Garrett C Gaelyn, Sivasankar M Preeti
Department of Otolaryngology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Cells Tissues Organs. 2017;204(2):93-104. doi: 10.1159/000472251. Epub 2017 Jun 24.
We investigated the timeline of tissue repair of vocal fold epithelium after acute vibration exposure using an in vivo rabbit model. Sixty-five New Zealand white breeder rabbits were randomized to 120 min of modal- or raised-intensity phonation. After the larynges were harvested at 0, 4, 8, and 24 h, and at 3 and 7 days, the vocal fold tissue was evaluated using electron microscopy and quantitative real-time polymerase chain reaction. There was an immediate decrease in the microprojection depth and height following raised-intensity phonation, paired with upregulation of cyclooxygenase-2. This initial 24-h period was also characterized by the significant downregulation of junction proteins. Interleukin 1β and transforming growth factor β1 were upregulated for 3 and 7 days, respectively, followed by an increase in epithelial cell surface depth at 3 and 7 days. These data appear to demonstrate a shift from inflammatory response to the initiation of a restorative process in the vocal fold epithelium between 24 h and 3 days. Despite the initial damage from raised-intensity phonation, the vocal fold epithelium demonstrates a remarkable capacity for the expeditious recovery of structural changes from transient episodes of acute phonotrauma. While structurally intact, the return of functional barrier integrity may be delayed by repeated episodes of phonotrauma and may also play an important role in the pathophysiology of vocal fold lesions.
我们使用体内兔模型研究了急性振动暴露后声带上皮组织修复的时间线。65只新西兰白色种兔被随机分为两组，分别进行120分钟的正常强度或增强强度发声。在0、4、8和24小时以及3天和7天后采集喉部，使用电子显微镜和定量实时聚合酶链反应对声带组织进行评估。增强强度发声后，微突起深度和高度立即降低，同时环氧合酶-2上调。最初的24小时还表现为连接蛋白的显著下调。白细胞介素1β和转化生长因子β1分别在3天和7天上调，随后在3天和7天时上皮细胞表面深度增加。这些数据似乎表明，在24小时至3天之间，声带上皮从炎症反应向修复过程的启动发生了转变。尽管增强强度发声造成了初始损伤，但声带上皮显示出从急性发声创伤短暂发作中迅速恢复结构变化的显著能力。虽然结构完整，但功能屏障完整性的恢复可能会因反复的发声创伤而延迟，并且可能在声带病变的病理生理学中也起重要作用。
