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Review
. 2021 Sep 16:2021:7428955.
doi: 10.1155/2021/7428955. eCollection 2021.

Sinonasal Tissue Remodelling during Chronic Rhinosinusitis

Satya Amirapu  1 , Kristi Biswas  1 , Fiona J Radcliff  2 , Brett Wagner Mackenzie  1 , Stephen Ball  1 , Richard G Douglas  1
Affiliations
Review

Sinonasal Tissue Remodelling during Chronic Rhinosinusitis

Satya Amirapu et al. Int J Otolaryngol. .

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.

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Conflict of interest statement

The authors declare that there are no conflicts of interest regarding the publication of this study.

Figures

Figure 1
Figure 1
Progression of disease in chronic rhinosinusitis. Inflammation observed in acute rhinosinusitis caused by viruses, bacteria, and fungi can resolve to a healthy state or can proceed to CRS if the inflammation persists longer than 12 weeks. The chronic nature of disease induces widespread tissue remodelling of the paranasal sinuses and nasal passage. Unresolved CRS often requires surgical intervention to remove purulent, stagnant mucous, and inflamed tissue.
Figure 2
Figure 2
Key histological features of sinonasal mucosa remodelling during chronic rhinosinusitis (CRS). The haematoxylin and eosin-stained sections display tissue remodelling in sinonasal tissues from patients with CRS. (a) Normal mucosa, (b) epithelial denudation, (c) basement membrane thickening, (d) oedema, (e) epithelial hyperplasia, (f) glandular hyperplasia, (g) goblet cell hyperplasia, and (h) fibrosis. All images are captured at 20.05 x magnification. Black arrows indicate the different regions of interest.
Figure 3
Figure 3
Cytokine expression in the pathogenesis of remodelling in chronic rhinosinusitis. Epithelial barrier disruption induces inflammation, initiating adaptive and innate immune response which creates a cascade of cytokines. This leads to fibrin deposition through coagulation factors like thrombin and Factor XIIIA, oedema through VEGF, and extracellular matrix deposition through TGF-β1. VEGF = vascular endothelial growth factor, TGF-β1 = transforming growth factor-β1, IL-1β = interleukin-1β, IL-8 = interleukin-8, TNF-a = tumor necrosis factor-a, IFN-γ = interferon gamma, TIMP-1 = tissue inhibitor of metalloproteinase-1, MMP = metalloproteinases, and tPA = plasminogen activator.
Figure 4
Figure 4
Staphylococcus aureus influences tissue remodelling in patients with chronic rhinosinusitis and nasal polyps. S. aureus drives inflammation via the production of endotoxins that act as superantigens to generate a T- and B-cell-mediated cascade. Moreover, through TGF-β and MMP-9 and MMP-2, the extracellular matrix may be laid down inducing remodelling. TGF-β1 = transforming growth factor-β1 and MMP 2,9 = metalloproteinases 2,9.
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