Objective: Vocal fold inflammation is a fundamental biological response to tissue injury or mechanical stress. Whether induced by surgical intervention or excessive vocal load, inflammation plays a dual role, facilitating tissue repair while posing a risk for maladaptive healing if prolonged. This study reviews mechanisms, recovery timelines, and clinical outcomes associated with post-surgical and phonotraumatic inflammation, emphasizing implications for rehabilitation and prevention.
Methods: A retrospective analysis is conducted of patients who underwent microflap or other phonosurgical procedures and professional voice users presenting with acute phonotrauma or post-infectious laryngitis. Clinical documentation, videostroboscopic recordings, and acoustic measures are reviewed to characterize the temporal progression of inflammation, symptom resolution, and return to baseline vibratory function. Relevant findings from recent basic science and clinical studies on inflammatory cytokine activity and extracellular matrix (ECM) remodeling were integrated to provide physiological context.
Results: Postoperative or activity-related vocal fold inflammation generally follows a predictable sequence of tissue response characterized by an initial acute phase with mucosal edema and erythema, followed by gradual cellular repair and extracellular matrix reorganization leading to restoration of pliability. The duration and severity of these stages vary depending on the nature of the injury, individual healing capacity, and adherence to vocal rest and hydration. In typical cases, perceptual and physiological improvements are observed within a few weeks, with near-complete functional recovery over time as tissue viscosity and vibratory characteristics normalize. Inflammation due to excessive vocal load or viral irritation often resolves more rapidly with conservative management, though repetitive strain or premature voice use during recovery may prolong symptoms and increase the risk of persistent edema, epithelial thickening, or scar formation.
Conclusions: Both surgical and behavioral vocal fold inflammation share overlapping biological pathways but differ in magnitude and recovery time. Early recognition and modulation of the inflammatory response are critical for preserving mucosal pliability and preventing fibrosis. Tailored recovery protocols, combining evidence-based vocal rest, hydration, and gradual reconditioning, optimize outcomes and reduce recurrence. Future studies integrating biochemical markers and imaging-based quantification of inflammation may refine therapeutic timelines and promote precision rehabilitation strategies in voice care.