ABSTRACT
Introduction
Chronic rhinosinusitis (CRS) is characterized by inflammation of the paranasal sinus mucosa persisting for more than 12 weeks. This condition is associated with reduced quality-of-life and causes a high direct and indirect economic burden. Several pathogenic factors have been attributed to CRS, including bacterial and fungal biofilms on the sinonasal mucosa. Biofilms are well-established contributors to recalcitrance to treatment in other chronic inflammatory mucosal conditions such as cystic fibrosis and otitis media.
Areas covered
This review will present an overview of the role of biofilms in CRS, including the evidence for biofilms being present on the sinonasal mucosa and their implications for disease severity. Furthermore, the interactions between biofilms and host-mediated immune factors are explored.
Expert opinion
The eradication of biofilms has been a focus of research shortly after their recognition as a cause of disease. The currently available methodologies for identifying biofilms on mucosal surfaces are not sufficiently well-developed to be used in a clinical setting. A more accurate, cheaper, faster approach for biofilm detection is necessary, and molecular techniques may provide the possibility for this.
Article highlights
CRS is a highly complex multifactorial disease, and biofilms have been implicated as a contributor to the pathogenesis of this condition.
Several techniques, such as scanning electron microscopy and confocal laser scanning microscopy, have been utilized to detect mucosal biofilms. Several studies have reported a higher biofilm prevalence in CRS patients than in healthy controls.
Biofilm-positive CRS patients tend to have worse postoperative outcomes than biofilm-negative CRS patients in terms of quality-of-life, radiological and mucosal severity, and requirement for follow-up visits.
The mucosal immunological response to biofilms is complex and requires further investigation.
Acknowledgments
For their contribution to figures provided in this review, a special thanks to Sharon Thurlow-Waldvogel () and Vivian Ward ().
Declaration of interest
K Biswas is supported by the Garnett Passe and Rodney Williams Memorial Foundation. B Mackenzie is supported by the Auckland Medical Research foundation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.