What is the pathophysiology of nasal polyps?

Updated: Oct 25, 2019
  • Author: John E McClay, MD; Chief Editor: Ravindhra G Elluru, MD, PhD  more...
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The pathogenesis of nasal polyposis is unknown. Polyp development has been linked to chronic inflammation, autonomic nervous system dysfunction, and genetic predisposition. Most theories consider polyps to be the ultimate manifestation of chronic inflammation; therefore, conditions leading to chronic inflammation in the nasal cavity can lead to nasal polyps.

The following conditions are associated with multiple benign polyps:

  • Bronchial asthma - In 20-50% of patients with polyps
  • CF - Polyps in 6-44% of patients with CF [1]
  • Allergic rhinitis
  • AFS - Polyps in 85% of patients with AFS
  • Chronic rhinosinusitis
  • Aspirin intolerance - In 8-26% of patients with polyps
  • Alcohol intolerance - In 50% of patients with nasal polyps
  • Churg-Strauss syndrome - Nasal polyps in 50% of patients with Churg-Strauss syndrome
  • Young syndrome (ie, chronic sinusitis, nasal polyposis, azoospermia)
  • Nonallergic rhinitis with eosinophilia syndrome (NARES) - Nasal polyps in 20% of patients with NARES

Most studies suggest that polyps are associated more strongly with nonallergic disease than with allergic disease. Statistically, nasal polyps are more common in patients with nonallergic asthma (13%) than with allergic asthma (5%), and only 0.5% of 3000 atopic individuals have nasal polyps.

Several theories have been postulated to explain the pathogenesis of nasal polyps, though none seems to account fully for all the known facts. Some researchers believe that polyps are an exvagination of the normal nasal or sinus mucosa that fills with edematous stroma; others believe that polyps are a distinct entity arising from the mucosa. On the basis of a review of the literature and several intricate studies of the bioelectric properties of polyps, Bernstein derived a convincing theory regarding the pathogenesis of nasal polyps, building on other theories and information from Tos et al. [2, 3]

In Bernstein's theory, inflammatory changes first occur in the lateral nasal wall or sinus mucosa as the result of viral-bacterial host interactions or secondary to turbulent airflow. In most cases, polyps originate from contact areas of the middle meatus, especially the narrow clefts in the anterior ethmoid region that create turbulent airflow, and particularly when narrowed by mucosal inflammation. Ulceration or prolapse of the submucosa can occur, with reepithelialization and new gland formation.

During this process, a polyp can form from the mucosa because the heightened inflammatory process from epithelial cells, vascular endothelial cells, and fibroblasts affects the bioelectric integrity of the sodium channels at the luminal surface of the respiratory epithelial cell in that section of the nasal mucosa. This response increases sodium absorption, leading to water retention and polyp formation.

Other theories involve vasomotor imbalance or epithelial rupture. The vasomotor imbalance theory postulates that increased vascular permeability and impaired vascular regulation cause detoxification of mast-cell products (eg, histamine). The prolonged effects of these products within the polyp stroma result in marked edema (especially in the polyp pedicle) that is worsened by venous drainage obstruction. This theory is based on the cell-poor stroma of the polyps, which is poorly vascularized and lacks vasoconstrictor innervation.

The epithelial rupture theory suggests that rupture of the epithelium of the nasal mucosa is caused by increased tissue turgor in illness (eg, allergies, infections). This rupture leads to prolapse of the lamina propria mucosa, forming polyps. The defects are possibly enlarged by gravitational effects or venous drainage obstruction, causing the polyps. This theory, though similar to Bernstein's, provides a less convincing explanation for polyp enlargement than the sodium flux theory supported by Bernstein's data. Neither theory completely defines the inflammatory trigger.

Patients with CF have a defective small chloride conductance channel, regulated by cyclic adenosine monophosphate (cAMP), which causes abnormal chloride transport across the apical cell membrane of epithelial cells. The pathogenesis of nasal polyposis in patients with CF could be associated with this defect.

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