Nagaia Ciacci

Titanium shows optimal biocompatibility properties; however, its gray color may be a limit for aesthetic results of dental rehabilitations. Some surface treatments that change the color of the material have been proposed. The aim of this study is to, in vitro, investigate the biocompatibility of the surfaces subjected to titanium nitride (NiT) coating and anodic-oxidized (AO) treatment and their propensity to impair bacterial proliferation. The viability of primary human gingival fibroblasts (HGFs) has been evaluated through a methyl thiazolyl tetrazolium (MTT) assay in three experimental groups: uncoated titanium (UNCOATED), titanium nitride (NiT)-coated surface, and anodic-oxidized (AO) titanium. Bacterial proliferation experiments were performed using a Streptococcus gordonii clinical isolate in contact with the three different above-mentioned materials. The treated surfaces (NiT and AO) showed a significantly higher fibroblast proliferation than the uncoated titanium alloy (p < 0.05). In contrast, Streptococcus gordonii growth was significantly higher on the untreated titanium (p < 0.05).

Stenotrophomonas maltophilia is an emerging global opportunistic pathogen, responsible for a wide range of human infections, including respiratory tract infections. Intrinsic multidrug resistance and propensity to form biofilms make S. maltophilia infections recalcitrant to treatment. Colistin is among the second-line options in case of difficult-to-treat S. maltophilia infections, with the advantage of being also administrable by nebulization. We investigated the potential synergism of colistin in combination with N-acetylcysteine (NAC) (a mucolytic agent with antioxidant and anti-inflammatory properties) against S. maltophilia grown in planktonic phase and biofilm. Eighteen S. maltophilia clinical isolates (comprising three isolates from cystic fibrosis (CF) and two trimethoprim-sulfamethoxazole (SXT)-resistant strains) were included. Checkerboard assays showed a synergism of colistin/NAC combinations against the strains with colistin Minimum Inhibitory Concentration (MIC) >2 µg/mL (n = 13), suggesting that NAC could antagonize the mechanisms involved in colistin resistance. Nonetheless, time–kill assays revealed that NAC might potentiate colistin activity also in case of lower colistin MICs. A dose-dependent potentiation of colistin activity by NAC was also clearly observed against S. maltophilia biofilms, also at sub-MIC concentrations. Colistin/NAC combinations, at concentrations likely achievable by topical administration, might represent a valid option for the treatment of S. maltophilia respiratory infections and should be examined further.