Journal of voice : official journal of the Voice Foundation · 2017
Laryngopharyngeal Reflux and Voice Disorders: A Multifactorial Model of Etiology and Pathophysiology.
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Lechien Jerome R, Saussez Sven, Harmegnies Bernard, Finck Camille, Burns James A
Аннотация
OBJECTIVE: The aim of this paper is to shed light on the pathogenesis and pathophysiological mechanisms underlying the development of hoarseness related to laryngopharyngeal reflux disease (LPRD).
MATERIAL AND METHODS: PubMed, Embase, and The Cochrane Library were searched for the terms reflux, laryngopharyngeal, laryngitis, voice, and hoarseness. Experimental and clinical studies providing substantial information about the occurrence of voice disorders, laryngeal histologic changes, or any pathophysiological processes related to LPRD were included by two independent investigators.
RESULTS: Of the 104 studies reviewed, 47 studies that met our inclusion criteria were analyzed. LPRD leads to significant macroscopic and microscopic histopathologic changes in the mucosa of the vibratory margin of the vocal folds. More and more studies suspect that epithelial cell dehiscence, microtraumas, inflammatory infiltrates, Reinke space dryness, mucosal drying, and epithelial thickening are probably responsible for the hoarseness related to reflux and the impairment of the subjective and objective voice quality evaluations.
CONCLUSION: Future clinical studies examining the pathophysiology of hoarseness related to LPRD should take into consideration all potential mechanisms involved in the development of hoarseness.
MATERIAL AND METHODS: PubMed, Embase, and The Cochrane Library were searched for the terms reflux, laryngopharyngeal, laryngitis, voice, and hoarseness. Experimental and clinical studies providing substantial information about the occurrence of voice disorders, laryngeal histologic changes, or any pathophysiological processes related to LPRD were included by two independent investigators.
RESULTS: Of the 104 studies reviewed, 47 studies that met our inclusion criteria were analyzed. LPRD leads to significant macroscopic and microscopic histopathologic changes in the mucosa of the vibratory margin of the vocal folds. More and more studies suspect that epithelial cell dehiscence, microtraumas, inflammatory infiltrates, Reinke space dryness, mucosal drying, and epithelial thickening are probably responsible for the hoarseness related to reflux and the impairment of the subjective and objective voice quality evaluations.
CONCLUSION: Future clinical studies examining the pathophysiology of hoarseness related to LPRD should take into consideration all potential mechanisms involved in the development of hoarseness.