Purpose of review
To summarize the current knowledge of cellular and molecular mechanisms of nasal epithelial repair and remodeling during physical and pathophysiological conditions.
Nasal epithelial repair and remodeling is a highly organized and well coordinated process, involving inflammation, proliferation, differentiation, matrix deposition, and remodeling, and is regulated by a wide variety of growth factors and cytokines. From the in-vivo and in-vitro studies conducted in both human and animal models, undifferentiated basal cells (progenitors) are able to migrate from adjacent epithelium, spread over the denuded basement membrane, and proliferate in injured regions (self-renewal) in necessary (homeostasis) or excessive (hyperplasia) degree. Progenitor cells reorient to an apical–basal polarity, and progressively differentiate into ciliated and nonciliated columnar cells and goblet cells, reconstituting a functional respiratory epithelium after several weeks. This recovery process can be observed during various types and severity of injury, and also in common nasal diseases, including acute viral, allergic, and nonallergic rhinitis, as well as chronic rhinosinusitis with and without nasal polyps.
Although nearly 10 000 articles about nasal epithelium have been published in the last decade, the mechanisms underlying the nasal epithelial repair are still understood at only a superficial descriptive level. In order to advance rhinology to the next level of a comprehensive knowledge of the orchestrated genetic and molecular processes acting during epithelial repair, combined clinical and experimental studies using sophisticated investigational plans to elucidate the functions of both the protein-coding and regulatory portions of the human genome are required.