The local peri‐implant pH changes caused by sterile inflammation and bacterial and fungal infections are studied herein. Then, a sensing electrode based on polyaniline and poly(2‐methyl‐2‐oxazoline) on a titanium alloy support is developed for potentiometric detection of peri‐implant pH changes to enable early detection of the aforementioned pathologies. The infected endoprosthesis area is shown to have an average pH of 0.79 units lower than the aseptic sample. The pH measurements of the individual pathogenic bacteria or pathogenic yeast reveal that Escherichia coli decreased the pH by 1.24 units, Staphylococcus aureus decreased the pH by 1.33 units and the methicillin‐resistant Staphylococcus aureus bacteria decreased the pH from 7.2 to 5.6 during 10 h, followed by a subsequent increase to 6.4. The results are statistically significant (α = 0.01). Pseudomonas aeruginosa is not shown to change pH levels. On the other hand, the pathogenic yeast has the lowest recorded pH, which decreases from 5.8 to 4.8. This difference in pH can be used to identify the nature of the infection. The developed electrodes have a pH response between pH 5 and 8, with a Nernstian slope of −59.6/pH. The developed electrode can contribute to the next generation of biosensors.

Microbial resistance is one of the main problems of modern medicine. Recently, antimicrobial peptides have been recognized as a novel approach to overcome the microbial resistance issue, nevertheless, their low stability, toxicity, and potential immunogenic response in biological systems have limited their clinical application. Herein, we present the design, synthesis, and preliminary biological evaluation of polymer-antibacterial peptide constructs. The antimicrobial GKWMKLLKKILK-NH₂ oligopeptide (PEP) derived from halictine, honey bee venom, was bound to a polymer carrier via various biodegradable spacers employing the pH-sensitive or enzymatically-driven release and reactivation of the PEP’s antimicrobial activity. The antibacterial properties of the polymer-PEP constructs were assessed by a determination of the minimum inhibitory concentrations, followed by fluorescence and transmission electron microscopy. The PEP exerted antibacterial activity against both, gram-positive and negative bacteria, via disruption of the bacterial cell wall mechanism. Importantly, PEP partly retained its antibacterial efficacy against Staphylococcus epidermidis, Escherichia coli, and Acinetobacter baumanii even though it was bound to the polymer carrier. Indeed, to observe antibacterial activity similar to the free PEP, the peptide has to be released from the polymer carrier in response to a pH decrease. Enzymatically-driven release and reactivation of the PEP antimicrobial activity were recognized as less effective when compared to the pH-sensitive release of PEP.