Bacteria adhering to implanted medical devices can cause invasive microbial infections, of e.g. skin, lung or blood. In dentistry, Streptococcus gordonii is an early oral colonizer initiating dental biofilm formation and also being involved in life-threatening infective endocarditis. To treat oral biofilms, antibacterial mouth rinses are commonly used. Such initial biomaterial-bacteria interactions and the influence of antibacterial treatments are poorly understood and investigated here in situ by quartz crystal microbalance with dissipation monitoring (QCM-D). A saliva-coated titanium (Ti) biosensor is applied to analyze possible specific signal patterns indicating microbial binding mechanisms and bactericide-caused changes in bacterial film rigidity or cell leakage caused by a clinically relevant antibacterial agent (ABA), i.e., a mouth rinse comprising chlorhexidine (CHX) and cetylpyridinium chloride (CPC). Apparent missing mass effects during the formation of microscopically proven dense and vital bacterial films indicate punctual, specific binding of S. gordonii to the saliva-coated biosensor, compared to unspecific adhesion to pure Ti. Coincidentally to ABA-induced killing of surface-adhered bacteria, an increase of adsorbed dissipative mass can be sensed, contrary to the prior mass-loss. This suggests the acoustic sensing of the leakage of cellular content caused by bacterial cell wall rupturing and membrane damage upon the bactericidal attack. The results have significant implications for testing bacterial adhesion mechanisms and cellular integrity during interaction with antibacterial agents.
Keywords: Antibacterial; Cellular leakage; Cetylpyridinium chloride; Chlorhexidine; QCM-D; Saliva-coated biosensor.
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