Molecular pathways and genetic factors in the pathogenesis of laryngopharyngeal reflux

Abstract

The prevalence of laryngopharyngeal reflux (LPR) has been constantly rising in the western world and affects today an alarmingly high percentage of the general population. Even though LPR and gastroesophageal reflux disease (GERD) are both the product of gastroesophageal reflux and seem to be sibling disorders, they constitute largely different pathological entities. While GERD has been for a long time identified as a source of esophageal disease, LPR has only recently been associated with head and neck disorders. Despite the high incidence of LPR and its great impact on patients' quality of life, little is known regarding its pathogenesis. On the other hand, studying the molecular and genetic basis of a disease is of fundamental importance in medicine as it offers better insight into the pathogenesis and opens new, disease-specific therapeutic trends. The aim of this study is to enlighten any known or suspected molecular mechanisms that contribute to the pathogenesis of LPR, and to suggest new trends for future research.

Double probe pH-monitoring findings in patients with benign lesions of the true vocal folds: comparison with typical GERD and the effect of smoking

“…Both LPR and GERD are thought to be the result of GER, although they constitute largely different pathological entities [15]. It is estimated that up to 10% of patients visiting ENT specialists have a clinical condition attributed to GERD [16].…”

Expression of claudin-3 in the esophagus and larynx of rat reflux model

“…LPR results in symptoms in the pharynx, larynx, paranasal sinuses and even the middle ear [1][2][3]. LPR and gastroesophageal reflux disease (GERD) are related disorders.…”

The management of periprosthetic leakage in the presence of supra-oesophageal reflux after prosthetic voice rehabilitation

“…Since the effects of proteolytic enzymes, which are components of gastric juice, can persist for several hours, autolysis or delayed wound healing can occur, especially in the presence of local injuries that can be caused when a prosthesis is cleaned or replaced. In these cases, damage can be a direct result of acid-induced or pepsin-induced autolysis of the mucosa or can occur as a result of alterations in intercellular junctional complexes at the molecular level or as a result of abnormalities and abacterial inflammatory reactions at the immunological level [3,9,12,17,32,34,39,43,45].…”