Although much has been elucidated in the past 170 years concerning the precise mechanism of ciliary function in the healthy or diseased human respiratory system, significant questions remain. The first description of ciliary action is credited to Sharpey in 1835. However, the importance of mucosal function was not apparent until Hilding's investigations of the postsurgical canine sinus demonstrated scar formation and disruption of mucociliary clearance. Subsequently, several techniques for mucosal coverage of exposed bone, most notably by Sewall and Boyden, were reported. The underlying physiology explaining the importance of the mucosa and the concept of mucosal preservation became apparent with the description of the sinonasal mucociliary flow patterns by Messerklinger; and thus the restoration of natural sinus physiology, ie, mucociliary clearance, became the goal of both medical and surgical treatment of sinonasal inflammatory disease. Clearance of benign and pathological substances in the mucus is governed by the propulsive force of the beating cilia and the physical characteristics of the overlying mucus. The respiratory cilia continually beat in a coordinated fashion, and in times of stress (eg, exercise, infection, or fever) ciliary beat frequency increases to accelerate mucus clearance. Thus, upper airway ciliary motility is under dynamic modulation. Multiple investigations incontrovertibly demonstrate a marked decrease in sinonasal mucociliary clearance in patients with chronic rhinosinusitis. Possible explanations for this finding are 1) a reduced basal ciliary beat frequency, 2) an alteration of the viscoelastic properties of airway secretions, and/or 3) a blunted dynamic response of sinonasal cilia to environmental stimuli. Studies of the first two explanations yield conflicting results, and to date, the third possibility remains uninvestigated. A review of the current understanding of the cellular regulation of respiratory ciliary activity and its contribution to chronic rhinosinusitis is presented.