The digestive Enzyme-Based nasal dysbiosis in Empty nose Syndrome: A theory

Abstract

Empty nose syndrome (ENS) is described as an empty space in the region of the inferior and middle turbinates of patients who underwent inferior and middle turbinectomy. Patients commonly complained of dry nose, paradoxical nasal obstruction, and crust. Symptoms significantly worsen the quality of life of patients. The pathophysiology of ENS is poorly understood. Several abnormalities in the nasal airflow dynamics, air humidification and warming, mucociliary clearance, and trigeminal-related sensory function were reported but it is misunderstood why some patients with anatomical turbinate defects developed ENS, while others do not experience symptoms with similar anatomy. This paper proposes a theory associating the development of ENS with the presence of laryngopharyngeal reflux disease (LPRD). LPRD is associated with the deposit of gastroduodenal enzymes into the upper aerodigestive tract mucosa, which lead to a decrease of the defense mechanisms of mucosa (mucus hydration, bicarbonate secretion, growth factor production) and an increase of mucosa injuries. In ENS patients, the deposit of digestive enzymes into the nasal mucosa may lead to concurrent injuries of the nasal cells involved in air humidification, warming, or sensory function, and modifications of the nasal microbiome that cannot heal the injured mucosa.