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BackgroundThere is increasing evidence that biofilms are critical to the pathophysiology of chronic infections including chronic rhinosinusitis (CRS). Until relatively recently, our understanding of biofilms was limited. Recent advances in methods for biofilm identification and molecular biology have offered new insights into the role of biofilms in CRS. With these insights, investigators have begun to investigate novel therapeutic strategies that may disrupt or eradicate biofilms in CRS.ObjectiveThis review seeks to explore the evidence implicating biofilms in CRS, discuss potential anti-biofilm therapeutic strategies, and suggest future directions for research.ResultsThe existing evidence strongly supports the role of biofilms in the pathogenesis of CRS. Several anti-biofilm therapies have been investigated for use in CRS and these are at variable stages of development. Generally, these strategies: 1) neutralize biofilm microbes; 2) disperse existing biofilms; or 3) disrupt quorum sensing. Several of the most promising anti-biofilm therapeutic strategies are reviewed.ConclusionsA better understanding of biofilm function and their contribution to the CRS disease process will be pivotal to the development of novel treatments that may augment and, potentially, redefine the CRS treatment paradigm. There is tremendous potential for future research.

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Background-Nasal polyps influence the burden of aspirin exacerbated respiratory disease (AERD) by contributing to eicosanoid production. AERD is diagnosed through graded aspirin challenges. It is not known how sinus surgery affects aspirin challenge outcomes.Objective-To investigate the effects of endoscopic sinus surgery (ESS) on aspirin-induced reaction severity and on the levels of eicosanoids associated with these reactions.Methods-Twenty-eight AERD patients were challenged with aspirin before and 3-4 weeks after ESS. Respiratory parameters and plasma and urine levels of eicosanoids were compared before and after challenges.Results-Before ESS, AERD diagnosis was confirmed in all study patients by aspirin challenges that resulted in hypersensitivity reactions. After ESS, reactions to aspirin were less severe in all patients and twelve out of twenty-eight patients (43%, p<0.001) had no detectable reaction. A lack of clinical reaction to aspirin was associated with lower peripheral blood eosinophilia [0.1 K/μL