Abstract
The purpose of this review is to summarise contemporary knowledge of sinonasal tissue remodelling during chronic rhinosinusitis (CRS), a chronic disease involving long-term inflammation of the paranasal sinuses and nasal passage. The concept of tissue remodelling has significant clinical relevance because of its potential to cause irreversibility in chronic airway tissues. Recent studies have indicated that early surgical treatment of CRS may improve clinical outcome. Tissue remodelling has been described in the literature extensively with no consensus on how remodelling is defined. This review describes various factors implicated in establishing remodelling in sinonasal tissues with a special mention of asthma as a comorbid condition. Some of the main histological features of remodelling include basement membrane thickening and collagen modulation. This may be an avenue of research with regard to targeted therapy against remodelling in CRS.
Highlights
Epidemiological data suggest chronic rhinosinusitis (CRS) affects at least 5% of the general population [1]
We summarise the current knowledge of remodelling in idiopathic CRS. e association of extracellular matrix (ECM), stromal cells, cytokines, the influence of thrombin, sinonasal inflammation, and the sinus microbiome on tissue remodelling are discussed
A reduction in the expression of POSTN was observed following successful functional endoscopic sinus surgery (FESS), suggesting POSTN is a possible CRS biomarker that correlates with postoperative disease resolution [30]
Summary
Epidemiological data suggest chronic rhinosinusitis (CRS) affects at least 5% of the general population [1]. Ese observations suggest remodelling may occur early in the disease process in CRS. E association of ECM, stromal cells, cytokines, the influence of thrombin, sinonasal inflammation, and the sinus microbiome on tissue remodelling are discussed. Eosinophils and collagens I, III, and V deposition in the ECM and TGFβ-1 can be detected in the mucosa of CRS tissues. E basement membrane (BM) thickening in CRS by secretion of TGF-β by eosinophils results in activation of fibroblasts and increased production of ECM proteins [27]. A reduction in the expression of POSTN was observed following successful functional endoscopic sinus surgery (FESS), suggesting POSTN is a possible CRS biomarker that correlates with postoperative disease resolution [30]. OPN expression is markedly upregulated in CRSsNP and CRSwNP tissues compared to inferior turbinate tissues from patients without CRS disease. What remains unclear is how early, in CRS pathogenesis, POSTN and OPN overexpression occurs and how these influence subsequent tissue remodelling in late-stage CRS
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