ABSTRACT S. aureus plays a central role in chronic rhinosinusitis (CRS), contributing to acute exacerbations and persistent infections through biofilm formation. With rising antibiotic resistance, bioactive glasses such as F18 and 45S5 have emerged as potential alternative antimicrobial agents. To evaluate the antimicrobial effects of F18 and 45S5 on S. aureus isolates from CRS patients, focusing on planktonic growth, biofilm formation, and mechanisms of action. Clinical S. aureus isolates were exposed to F18 and 45S5 (0–512 μg/mL) using a modified Calgary Biofilm Device. Biofilm biomass was quantified by crystal violet staining and spectrophotometry. A pH‐controlled assay was performed to determine whether alkalinization mediated antibiofilm effects. Inductively coupled plasma analysis characterized F18 ion‐release kinetics. Expression of biofilm‐related genes (icaA, icaB, icaD, agrA, agrC) was quantified, and biofilm morphology was examined by scanning electron microscopy. Both bioglasses inhibited biofilm formation at concentrations ≥ 128 μg/mL but did not eradicate mature biofilms. At 512 μg/mL, F18 and 45S5 reduced the biofilm optical density by 78% and 67%, respectively. Although pH elevation occurred, biofilm inhibition was independent of pH variation. F18 exposure downregulated ica operon genes but not agr genes. Ion analysis demonstrated concentration‐dependent release of Ca and Si, with no evidence of apatite formation. SEM showed reduced extracellular matrix and altered bacterial organization. F18 and 45S5 inhibit S. aureus biofilm formation through pH‐independent mechanisms associated with ion release and suppression of matrix‐related genes, supporting their potential as adjunctive strategies in CRS management.
Caetano et al. (Fri,) studied this question.