mechanism of alteration of the pharyngoglottal closure reflex by cigarette smoking

Prolonged cigarette smoking has long been known to produce a variety of respiratory tract diseases smokers are more predisposed to the development of chronic bronchitis, emphysema and bronchogenic carcinoma. Recent studies claimed that cigarette smoking in addition altered the elicitation of the pharyngoglottal closure reflex [PGCR] protecting the laryngeal inlet. Therefore, this led to the development of aspiration related respiratory complications in smokers. These studies although proving the adverse effect of smoking on the PGCR, defined that the mechanism underlying this effect was still unknown. The aim of the present study was to try to find an explanation of this mechanism through examining the ultra structural changes produced by smoking in the epiglottis which has a fundamental role in the proceeding of this reflex. Biopsies from the lingual surface of the epiglottis of 36 prolonged smoker men were examined by the scanning electron microscope. They were divided into 3 groups [12 each]; light, moderate and heavy smokers; in respect to the number of cigarettes smoked per day. Control specimens were obtained from corresponding area in 8 male cadavers. Epithelial changes in the form of cellular atypism, necrosis, hyperplasia and keratosis were observed. Obvious manifestations of inflammation were detected as disorganization and thickening of the subepithelial connective tissue fibers. The subepithelial nerve fibers were thinned out in most of the specimens and were hardly visible in some. All these changes progressed successively in light, moderate and severe smokers specimens. It could be concluded that cigarette smoking may altered the sensitivity of the epiglottis either through the epithelial damage or through the inflammatory process or through a direct negative effect on its nerves. The affection of the sensory function of the epiglottis consequently could contribute to and could greatly explain the mechanism of the alteration of the PGCR in smokers