الفهرس 
Anatomy and PhysiologyOnly 14 pages are availabe for public view
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Abstract
The sense of smell is a primal sense for humans as well as animals. Odorants are volatile chemical compounds that are carried by inhaled air to the olfactory epithelium located in the roof of nasal cavities.
Chronic rhinosinusitis (CRS) is described as the most common cause of olfactory dysfunction, accounting for 14–30 % of cases . While olfactory impairment is a common symptom affecting 61–83 % of patients with CRS. Nevertheless, up to 25% of patients with CRS are unaware of their decreased olfactory abilities, probably because the olfactory dysfunction in CRS develops slowly and in consequence, only a few patients note this disorder (Rombaux et al.,2016).
Olfactory impairments in CRS was classified into two broad mechanisms of impairment: conductive losses from obstruction of the nasal passages, or sensorineural causes from damage to the olfactory neuroepithelium (Patel and Pinto,2014).
In our study, the study was made on 40 patients divided into 2 groups (CRSwp, CRSsp) compared to 20 control patients. We depend in this study on an immunohistochemical marker (Nestin). Nestin is a class VI intermediate filament protein that was first described as a neural stem progenitor cell marker. It is known to be expressed by various cell types during development.
It was proven in previous studies that nestin expression is directly correlating with olfactory function, i.e. it is clearly present in cells of normosmic patients, reduced in the OE of subjects suffering from hyposmia and noticeably reduced or lost in the OE of anosmics patients (Minovi A. et. al.,2010) .
Biopsies were obtained from the olfactory mucosa about 1-2 mm3 from the superior aspect of the middle turbinate or the opposed septum during functional endoscopic sinus surgery (FESS) or during septoplasty using a thu-cutting forceps
Specimens were processed for routine hematoxylin and eosin (H&E) staining and immunohistochemical staining with the nestin antibody. The slides were examined microscopically to assess the histopathological changes in the olfactory mucosa.
Our results showed that inflammatory changes and reduction of nestin expression was found in both CRSwp and CRSsp groups to be markedly significant compared to control group (P value<0.001) but with non significant difference between each other (P value 0.543) (table 11,12) and this proves that the inflammatory process is found in both groups regardless presence or absence of polyps and is responsible for the loss of function.
On the other hand it was found also that degree of olfactory dysfunction is not the same in both cases groups (CRSwp and CRSsp) and there is high significant difference in loss of function between them (P value<0.0001) (table 10). As in CRPsp was found that 75% of cases were hyposmic while in CRSwp was found that 70% of cases were anosmic.
These results led us to a new hypothesis that both obstructive and inflammatory causes share in the olfactory impairment. In cases of CRSsp only the inflammatory changes play the role causing mainly hyposmic changes while in CRSwp, the presence of obstructive agent, which is the polyps, adds on the loss of function leading to more anosmic changes.
This study is considered one of very few studies that proved multifactorial hypothesis using immunohistochemical studies with nestin protein marker.