Nasal Physiology

Jeremiah A. Alt, MD, PhD
Noam Cohen, MD, PhD


The physiologic function of the nose includes respiration, conditioning inspired air, vocal resonance, olfaction, nasal resistance, protection of the lower airway, and ventilation and drainage of the sinuses.

The nose is a natural pathway for breathing. During respiration the nose acts as an air conditioning unit by performing humidification, heat transfer, and filtration. The nasal mucosa can help adjust the humidity and temperature of the air before it reaches the lungs. The large surface area of the nasal mucosa helps regulate the temperature and humidity of inspired air. The nasal cycle is a rhythmic cycle of growth of venous sinusoids that alters between the left and right nasal passages. The activation of sympathetic nerve fibers (part of the autonomic, i.e. automatic, nervous system) controls blood flow to the nasal cavity and nasal mucosa. Alternating the volume of blood between the left and right nasal passages varies between individuals but on average occurs every 4 hours. Nasal secretions and mucus production is controlled by parasympathetic autonomic innervation and is also cyclical with increased secretion on the side with the greatest airflow. This diurnal nasal cycle is normal, but can be a source nasal obstruction for some patients that may require evaluation.

The nose is thought to be a resonating chamber for certain consonants in speech during exhalation. This is evident during phonation (making the sound) of M, N, and NG, as sound passes upwards through the nasopharynx and is emitted through the nose. Many nasal conditions causing obstruction of the nose affect the quality of the voice. 

Our ability to smell stems from specialized olfactory neuroepithelium found high in the nasal cavity. Impaired olfaction is commonly observed in patients with sinonasal disease with a prevalence reported up to 30-60% of this patient population and is a criterion used for the diagnosis of chronic rhinosinusitis. Olfactory dysfunction in rhinosinusitis is likely due to many different reasons, stemming from both physical obstruction and an inflammatory component that damages the olfactory neuroepithelium.

As we breathe, the nose is constantly exposed to inhaled debris and microbes (viruses, bacteria, and fungus). The respiratory system has developed several lines of defense to combat this continuous assault. Larger particles are trapped by the nasal vibrissae (hairs at the front of the nose). Smaller particles are trapped in the mucus, considered to be one of the initial defenses of the airway. Mucus is designed to trap inhaled particles (including microbes) that are subsequently cleared from the airways. Nasal secretions also contain enzymes, anti-microbial mediators, and immune cells, which kill unwanted bacteria and viruses. The vast majority of mucus is propelled into the throat where it is swallowed and destroyed by the products of the stomach. Mucus containing pathogens and debris can also be coughed up or sneezed out.

The mechanism by which mucus is propelled to the throat involves the rhythmic beating of very small cellular projections, known as cilia (which look like hair), which line the airways (Figure 1).

Figure 1: Representation of cilia in the upper respiratory system.

In order for the mucus produced in the sinuses to reach the throat, the cilia throughout the sinonasal cavity are “programmed” to beat in a very specific direction. Each sinus has an ostium (opening) that the cilia carry the mucus towards and through into defined anatomical areas within the sinonasal cavity (see sinus anatomy). The middle meatus is located lateral to the middle turbinate and accepts drainage from the frontal, maxillary, and the anterior ethmoid sinuses. Posteriorly, the superior meatus is below the superior turbinate, which accepts drainage from the posterior ethmoid sinuses. The drainage continues medially into the sphenoethmoidal recess, which also accepts drainage from the sphenoid sinus and ends up in the nasopharynx or the upper part of the throat and subsequently swallowed.

Cilia continuously beat to drive the debris-laden mucus from the airways. Ciliated cells have multiple sensors that allow the cell to respond to locally produced mediators and/or certain cues, such as changes in mucus thickness and mucus loads to make their cilia increase the speed at which they beat. By increasing the speed at which they beat, the cilia can generate more force and thus continue to clear the heavier mucus, or clear normal mucus at a faster rate. Conversely, when mucociliary clearance is inhibited or slowed there may be an increased incidence of rhinosinusitis, as seen in patients with cystic fibrosis (see cystic fibrosis).

While the ciliated cells respond to environmental cues, environmental insults can also affect cilia function in a detrimental manner. Many microbes that attack the airways produce toxins that rapidly alter cilia movement. Paralyzing the cilia stops the movement of mucus and optimizes the conditions for infection. Infection perpetuates a local inflammatory response and it is becoming clear that even the inflammatory molecules our bodies produce to fight infection also have detrimental effects on cilia function thereby worsening the insult and further hindering mucus clearance. The combination of microbes and inflammation over a relatively short period can lead to loss of cilia (Figure 2).

Figure 2: Note the extensive loss of cilia.

The upper respiratory system needs a mechanism by which it can detect and initiate an appropriate response to microbes. Bitter taste receptors (T2Rs), identified in the cilia of sinonasal epithelial cells, are an emerging receptor class that may be contributing to this mechanism via recognition and removal of microbes. For example activation of one specific T2R, T2R38, by molecules secreted by gram-negative (a particular type of) bacteria, stimulates the ciliated cells to produce nitric oxide, which in turn increases mucociliary clearance and directly diffuses into the mucus where it kills bacteria. Furthermore, genetic variability of T2R38 may explain why certain individuals are more susceptible to developing gram-negative infections and inflammation. Additional T2Rs are expressed throughout the respiratory epithelium but the role of these T2Rs have yet to be identified.

This combination of microbial and inflammatory products is often found in the upper airway of patients with chronic rhinosinusitis. The good news is that if the microbes can be removed and the inflammation controlled, the cilia can regrow and resume proper movement of mucus.

Why certain individuals can easily recover from an upper respiratory infection without developing chronic rhinosinusitis while others seem to always progress to a lengthy course is not completely understood. What we do know is this: when it comes to the development of chronic rhinosinusitis many factors including anatomic variations, microbial exposure, as well as an individual’s inflammatory response play a role. Novel approaches are being developed to help combat sinonasal infection, improve removal of mucus, accelerate sinus healing, and control the inflammation.

An understanding of the physiology of the nose is critical to understand nasal symptoms and diseases that can develop in the nose and sinuses, which are described further under the tabs conditions and treatments.

Revised 02/17/2015
©American Rhinologic Society