Remodeling refers to the development of specific but potentially irreversible structural changes in tissue. Caucasian eosinophilic chronic rhinosinusitis (CRS) with polyps associated or not with cystic fibrosis was discriminated by edema from CRS without nasal polyps, characterized by extensive fibrotic fields. However, changes in epithelial and extracellular matrix structures are common findings in all types of chronic inflammatory diseases of upper airways, but rarely specific and highly variable in extend. Recent studies have shown that remodeling in CRS appears to occur in parallel, rather than purely subsequent to inflammation. Furthermore, some preferential remodeling associations can be recognized. Tremendous efforts have been put in research on coagulation factors, cytokines, growth factors, and proteases supporting all phases of upper airway remodeling. The current exploration of other CRS sub-groups and of the particular link with concomitant asthma aims to optimize the classification of CRS and its staging modes and to develop novel therapies.

Remodeling and Repair in Rhinosinusitis

Electrical Impedance and Expression of Tight Junction Components of the Nasal Turbinate and Polyp.

Introduction: Nasal polyposis is a progressive inflammatory disease that reduces the quality of life. The role of apoptotic and autophagic pathways in nasal polyposis pathogenesis is not yet clearly known. Objective: In this study we aimed to investigate apoptotic (MAPK/JNK), anti-apoptotic (PI3K/mTOR) and autophagic (LC3) pathways which are related each other in the nasal polyposis tissues. Methods: Twenty patients with nasal polyps and fifteen patients going through an inferior turbinate reduction were included in this study. Patients with asthma, Samter triad and allergic fungal sinusitis were excluded from the study. The apoptotic and autophagic pathways were investigated in paraffin-embedded nasal tissue sections of 20 NP and 15 samples from inferior turbinate reduction by H&E and immunohistochemistry with h-score. TUNEL method with apoptotic index was used to demonstrate apoptotic cells. Results: Decreased immunoreactivity of P38 MAPK (p <0.005) and JNK (p <0.005) were observed in nasal polyposis compared to material from inferior turbinate reduction. This decrease may indicate a downregulation of apoptosis as demonstrated by decreased TUNEL staining in nasal polyposis (p <0.005). The PI3K (p <0.002) and mTOR (p <0.005) immunoreactivities were increased in nasal polyposis. This increase indicates a downregulation of autophagy as demonstrated by decreased LC3 staining in nasal polyposis (p <0.001). Conclusion: Deficient apoptosis and autophagy through MAPK/JNK and PI3K/mTOR pathways may have a role in the pathogenesis of nasal polyposis.

High PI3K/mTOR and low MAPK/JNK activity results in decreased apoptosis and autophagy in nasal polyposis

Purpose of reviewBasic science studies directed at understanding the inflammatory mechanisms in chronic rhinosinusitis (CRS) are increasing, yet their relevance to the underlying disease process is often conflicting and confounded by the enrollment of a heterogeneous CRS population. This review is a

Confounding factors in rhinological research.

The understanding of the inferior turbinate (IT) function, role in nasal obstruction, and its management for symptomatic relief has evolved. We aim to provide a comprehensive review of the anatomy, contribution to nasal function and response of the IT to sinonasal disease. Techniques to study the nasal physiology are expanding; these include the computational flow dynamics that has allowed a better understanding of the function and role of the inferior turbinate in normal respiration and airway obstruction. The IT function includes warming, moisturizing, and filtering the air prior to the entrance to the lower airways. More sophisticated techniques have been developed to study the nasal physiology, though not widely used in clinical practice.

The Inferior Turbinate: Role in Normal Respiration and Airway Obstruction

Both inferior turbinate hypertrophy and nasal polyp formation entail the enlargement of the nasal mucosa caused by rhinosinusitis, but their macro/microscopic and clinical findings differ markedly. This study aimed at investigating differences in the expressions of erbB1/2 and the tight junction proteins, claudin-1 and tricellulin, in the two tissues. Ten inferior turbinates and ten nasal polyps were collected. The expressions of erbB1/2, claudin-1, and tricellulin were examined by fluorescence immunohistochemistry and by quantitative real-time transcription-polymerase chain reaction (qRT-PCR). The eosinophil count and % of nasal gland area in the mucosa were also measured. The fluorescence intensities in the inferior turbinates were higher for erbB1/2 and lower for claudin-1 than those in the nasal polyps. The results of qRT-PCR were consistent with the immunohistochemical findings for erbB1/2. The quantity of tricellulin mRNA was significantly higher in the inferior turbinates than in the nasal polyps. The % of nasal gland area was significantly higher but the eosinophil count was significantly lower in the inferior turbinate than in the nasal polyp. These results suggest that the underlying pathogenesis of hypertrophic inferior turbinates and nasal polyps is likely to differ with respect to regeneration/proliferation and thus the remodeling process.

Khac-Hung Nguyen

Papers

Different expressions of erbB1/2 and tight junction proteins in hypertrophic inferior turbinates and nasal polyps.