Cell biology of laryngeal epithelial defenses in health and disease: Further studies

David Bulmer, Peter E. Ross, Sophie E. Axford, Nikki Johnston, Gulnaz A. Gill, Jeffrey P. Pearson, Peter W. Dettmar, Marguerite Panetti, Massimo Pignatelli, James A. Koufman

Research output: Contribution to journalArticlepeer-review

147 Citations (Scopus)


This is the second annual report of an international collaborative research group that is examining the cellular impact of laryngopharyngeal reflux (LPR) on laryngeal epithelium. The results of clinical and experimental studies are presented. Carbonic anhydrase (CA), E-cadherin, and MUC gene expression were analyzed in patients with LPR, in controls, and in an in vitro model. In patients with LPR, we found decreased levels of CAIII in vocal fold epithelium and increased levels in posterior commissure epithelium. The experimental studies confirm that laryngeal CAIII is depleted in response to reflux. Also, cell damage does occur well above pH 4.0. In addition, E-cadherin (transmembrane cell surface molecules, which have a key function in epithelial cell adhesion) was not present in 37% of the LPR laryngeal specimens. In conclusion, the laryngeal epithelium lacks defenses comparable to those in esophageal epithelium, and these differences may contribute to the increased susceptibility of laryngeal epithelium to reflux-related injury.

Original languageEnglish
Pages (from-to)481-491
Number of pages11
JournalAnnals of Otology, Rhinology and Laryngology
Issue number6
Publication statusPublished - Jun 1 2003


  • Carbonic anhydrase
  • Cell biology
  • Cellular defenses
  • E-cadherin
  • Extraesophageal reflux
  • Gastroesophageal reflux
  • Laryngopharyngeal reflux
  • Mucin
  • Mucus
  • Reflux
  • Vocal fold

ASJC Scopus subject areas

  • Otorhinolaryngology

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