Pharmacological strategies for targeting biofilms in otorhinolaryngologic infections and overcoming antimicrobial resistance (Review)

Abstract

Biofilm formation is a key factor in the persistence and recurrence of otorhinolaryngology (ORL) infections, driving antimicrobial resistance and treatment failure. Chronic conditions, such as rhinosinusitis, otitis media and tonsillitis, are linked to biofilm-producing pathogens, forming protective extracellular matrices that shield bacteria from immune defenses and antibiotics. The present review explores emerging pharmacological strategies to disrupt biofilm integrity and improve treatment outcomes. Strategies such as quorum sensing inhibitors, antibiofilm peptides, enzymatic dispersal agents, and drug repurposing can potentially disrupt biofilms and counter-resistance mechanisms. Furthermore, novel therapies (including nanotechnology-based drug delivery systems, phage therapy and immunomodulation) offer innovative alternatives for managing biofilm-associated infections. However, clinical implementation remains challenging. Future research should prioritize optimizing drug formulations, refining delivery techniques, and exploring synergistic combinations to enhance biofilm eradication. Implementing these innovative strategies can improve the management of chronic ORL infections, reducing recurrence rates and enhancing patient outcomes.

Keywords: antimicrobial resistance; biofilm-associated infections; infectious diseases; otorhinolaryngology.

Figure 1

Biofilm formation, resistance mechanisms and therapeutic strategies in ORL infections. There are three key phases of biofilm development in otorhinolaryngologic infections: Attachment, growth and disaggregation. During the growth phase, bacteria produce extracellular polymeric substances, enabling resistance through quorum sensing, efflux pumps, altered metabolism, horizontal gene transfer and immune evasion. Various antibiofilm strategies have been shown, targeting different stages, including quorum sensing inhibitors, nanoparticle-based antibiotics, phage therapy, and enzymatic dispersal agents. This schematic highlights the persistence of biofilm infections and the need for targeted therapies.