We propose a multivariate theory for the pathogenesis of nasal polyps.
Turbulent flow of air in the lateral wall of the nose or viral-bacter
ial-host interactions produce an inflammatory change in the mucosa of
the lateral wall of the nose. Ulceration and prolapse of the submucosa
with reepithelialization and new gland formation may then follow. The
structural cells of the nasal polyp, including epithelial cells and f
ibroblasts, have the ability to produce messenger RNA for granulocyte-
monocyte colony-stimulating factor and other cytokines. Stimulation of
such an effector capability by structural cell-derived cytokines woul
d undoubtedly represent a major amplification pathway of the inflammat
ory response in nasal polyps. Allergy may be one mechanism for the dev
elopment of this cascade of events, This microenvironmental structural
inflammatory response in the nasal polyp, in turn, can affect the bio
electric integrity of the Na+ and Cl- channels at the luminal surface
of the respiratory epithelial cell. The change in the Na+ absorption,
which has been demonstrated in our studies, may result in an increased
movement of water into the cell and into the interstitial fluid, The
resultant edema can lead to growth and enlargement of the nasal polyp,
Finally, the rapid recurrence of nasal polyps despite adequate surger
y may reflect some intrinsic phenotypic characteristic of nasal epithe
lial cells in the lateral wall of the nose, which is likely to be unde
r genetic control.