## 1 Introduction  
To achieve a successful oral rehabilitation, aimed at substituting one or more missing teeth via dental implants, such as titanium (Ti) element or titanium alloys [1], it is important not only to obtain implant osseointegration but also to limit, as much as possible, the risk of peri-implant disease [2]. As recently underlined [3], much has to be done in such topic. Peri-implantitis is a chronic, irreversible, multifactorial condition, triggered by microbial biofilm formation, and persistent inflammation around dental implants [3; 4; 5], especially in patients with insufficiently poor oral hygiene, smoking, diabetes, history of periodontitis, trauma, or fracture due to uncontrolled implant-overload [6; 7]. Massive and long-lasting inflammation of the surrounding area will bring to local tissue de-structuration, bone-degradation and eventually loss of the involved implant(s) [8]. It has also been hypothesized that some subjects are genetically predisposed to the onset and progression of peri-implantitis. This would be due to an incorrect modulation of the RANK/RANKL systems, regulators of immune responses, and bone physiology [9; 10; 11; 12; 13]. In particular, three molecules, the receptor activator of NF-kappa B (RANK), its ligand RANKL, and the decoy receptor of RANKL, osteopororegin (OPG), attracted the attention of scientists and pharmaceutical companies alike. Genetic experiments evolving around these molecules established their pivotal role as central regulators of osteoclast function [14]. Notoriously, microbial contamination and biofilm formation may take place onto biotic and abiotic surfaces, including dental implants. Once established as a sessile structure, microbial community acquires enhanced resistance to cleansing techniques, antimicrobial drugs, and host immune defenses with respect to their planktonic counterpart [15; 16]. Several studies [17; 18] focused on implant and abutment colonization, stating that the characteristics of their surface(s) significantly influence clinical outcome, affecting microbial localization on the device(s) and around the peri-implant area. Moreover, by an experimental study in dogs, [PERSON] et al. [19] demonstrated that peri-implantis progression is more rapid when using rough surface implants rather than machined ones. Over the years, different methods, such as mechanical and chemical systems or antimicrobial solutions, have been used for implant decontamination, thus achieving good results [20; 21]. Nevertheless, undesired alteration(s) of implant surfaces can happen to a different extent [22]. Current efforts are aimed to implement microbial biofilm removal, minimizing changes/damages on implant surface-structure(s) and, at meantime, maintaining the implant biologically adequate and favorable for adhesion and persistence of reparative host cells [23; 24]. Among several decontamination systems, Nickel Titanium brushes (Brush) and Air Polishing system with 40 \(\upmu\)m bicarbonate powder (BIC-40) are receiving interesting attention. The former is known to be resistant and high flexible material when undergoing heating/cooling variations [25]. The latter, employing bicarbonate powder, is often used by clinicians for its efficacy in mechanical removal of biofilm, providing satisfactory clinical outcomes [26]. The set-up of new experimental models, such as the recently described use of an engineered laboratory strain of _Pseudomonas aeruginosa_ (_P. aeruginosa_) to assess, in real time, biofilm formation onto medical devices [27], opens new pathways for a better comprehension of the events involved in microbial biofilm formation onto abiotic surfaces and its abatement by chemical and/or mechanical procedures. The aim of the present study was to compare two decontamination systems, Brush and BIC-40, in their ability to impair _P. aeruginosa_ contamination onto titanium disks by a bioluminescence-based assay.