Pathophysiology and etiologic factors of chronic rhinosinusitis

Our current understanding of chronic rhinosinusitis (CRS) is that its etiology is multifactorial. One example of a distinct disease process leading to CRS is aspirin sensitivity, in which a dysregulation of eicasanoid metabolism leads to upper and lower airway inflammation. Genetic conditions involving impairment of ciliary function, such as primary ciliary dyskinesia and cystic fibrosis, are also relatively well understood. However, the majority of CRS cases do not have a clear pathophysiology. There continues to be controversy regarding the roles of allergic rhinitis and exposure to environmental inhalants such as cigarette smoke. The importance of microbial pathogens is under scrutiny, with fungi, viruses, and bacteria (including their biofilms and superantigens) likely playing a contributory role rather than acting as the sole cause of CRS as was once thought. Finally, techniques in molecular and cell biology have elucidated several inflammatory markers and cell mediators that are dysregulated in CRS. This has led to the distinction between CRS with and without polyps, which are regarded as having overlapping but distinct cellular pathways. In conclusion, a better understanding of the pathophysiology of CRS is crucial to developing effective therapies.