Abstract

Abstract Background Chronic rhinosinusitis (CRS) is one of the leading causes of olfactory. Olfactory impairments in CRS can be classified into two broad mechanisms of impairment: conductive losses from obstruction of the nasal passages, or sensorineural causes from damage to the olfactory neuroepithelium. Nestin is one type of intermediate filament protein, was a specific marker for OE stem cells. It was found that nestin is actually expressed in the axonal ends and inferior processes of OE sustentacular cells in the basal compartment of the epithelium. Nestin immunoreactivity, which is clearly present in the sustentacular cell layer of normosmic patients, was slightly reduced in the OE of subjects suffering from hyposmia. In contrast, in the OE of anosmics, nestin expression was found to be noticeably reduced. This indicates that expression of nestin protein is related to olfactory function and is down regulated with loss of olfactory function. Methods This study included 60 patients (20 chronic rhinosinusitis with polyps patients (CRSwp), 20 chronic rhinosinusitis without polyps patients (CRSsp), and 20 controls). Biopsies taken from olfactory mucosa during surgery. Immunohistochemical examination was done using nestin protein marker, a marker directly related to function in olfactory mucosa, to examine the etiology of olfactory dysfunction in CRS. Results There was a significant difference between the three study groups was found regarding olfaction. While there was a highly statistically significant difference between the three groups regarding nestin staining pattern, however, when comparing the two cases groups, the difference was not significant. Nestin staining decreased in both cases groups and patients with CRSwp have more olfactory dysfunction than patients with CRSsp. This means that while the inflammatory process is strongly present in both groups, the presence of polyps increases olfactory function loss. Conclusion Olfactory dysfunction in patients with CRS is multifactorial where both obstructive and inflammatory causes contribute in the pathogenesis.

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