Efficacy of Removal of Residual Dental Cement by Laser, Ultrasonic Scalers, and Titanium Curette: An In Vitro Study.

The purpose of this study was to conduct an in vitro evaluation of the efficacy of six dental lasers, two ultrasonic scalers, and a titanium curette in the removal of dental cement from the surface of an implant. The study used a total of 39 dental implants, representing three different surface textures. The implants were divided into 13 groups with one of each of the three surface textures in a group. A standardized amount of modified resin dental cement was applied to the implant surface. Each test instrument was used as a monotherapy. Additionally, three of the lasers were used as part of a dual therapy in conjunction with the piezo ultrasonic scaler. Laser irradiation was limited to 2 minutes. Following treatment, implants were graded visually and by scanning electron microscopy (SEM) for the presence of unremoved cement and concomitant damage, if any, to the implant surface. The results showed that no treatment removed all residual cement from any of the three implant surfaces, although specific protocols appeared more effective than others. Implant surface damage was frequently observed, both visually and by SEM, and appeared to result from laser irradiation and the use of ultrasonic scaling instruments.

The fatty acid signaling molecule cis-2-decenoic acid increases metabolic activity and reverts persister cells to an antimicrobial-susceptible state.

Persister cells, which are tolerant to antimicrobials, contribute to biofilm recalcitrance to therapeutic agents. In turn, the ability to kill persister cells is believed to significantly improve efforts in eradicating biofilm-related, chronic infections. While much research has focused on elucidating the mechanism(s) by which persister cells form, little is known about the mechanism or factors that enable persister cells to revert to an active and susceptible state. Here, we demonstrate that cis-2-decenoic acid (cis-DA), a fatty acid signaling molecule, is able to change the status of Pseudomonas aeruginosa and Escherichia coli persister cells from a dormant to a metabolically active state without an increase in cell number. This cell awakening is supported by an increase of the persister cells' respiratory activity together with changes in protein abundance and increases of the transcript expression levels of several metabolic markers, including acpP, 16S rRNA, atpH, and ppx. Given that most antimicrobials target actively growing cells, we also explored the effect of cis-DA on enhancing antibiotic efficacy in killing persister cells due to their inability to keep a persister cell state. Compared to antimicrobial treatment alone, combinational treatments of persister cell subpopulations with antimicrobials and cis-DA resulted in a significantly greater decrease in cell viability. In addition, the presence of cis-DA led to a decrease in the number of persister cells isolated. We thus demonstrate the ability of a fatty acid signaling molecule to revert bacterial cells from a tolerant phenotype to a metabolically active, antimicrobial-sensitive state.