## 1 Introduction  
Dental Implantology is, nowadays, a technique with highly predictable results and, for this reason, represents a preponderant part of the range of therapeutic alternatives in the treatment of partially and totally edentulous patients [1]. The application of implant-supported prosthetics in dentistry began towards the end of the 1980s, even if their technical development occurred at the beginning of 1960, when [PERSON]'s group introduced new and revolutionary concepts deriving from the knowledge of the biological phenomena that occurred in the interface between bone and implant. The term of osseointegration was introduced to define the formation of strict and functional link between bone and implant fixture, subjected to prosthetic loading, without connective tissue interposition [2]. However, dental implants over time can present pathological changes in the surrounding tissues, which can cause osseointegration defects. These pathological conditions, indicated by the term \"mucositis\" and \"peri-implantitis\" (PI) (respectively, if the inflammatory processes affect only the marginal gingiva or the deep peri-implant tissues), have increased in recent years, in proportion to the grater insertion of the dental implant. Peri-implantitis (PI) concerns complex phlogistic phenomena that occur in the tissues surrounding a functionally active implant. A bad balance between pathogenic bacterial load and host response could trigger an inflammatory cascade that would first affect the superficial peri-implant soft tissues (mucositis) and then progress into the deep layers, with a loss of implant support bone which can be clinically and radiologically highlighted (peri-implantitis) [3]. PI is therefore an infectious disease in which the bacteria colonizing the dental implant's surface and participating in the development of the biofilm are responsible for the genesis of an inflammatory response and inhibiting the integration of bone cells to the surface of the implant [4; 5]. Clinical diagnosis of PI is based on the following findings: bleeding on light peri-implant probing, an increase in probing depth, and marginal bone loss (however, subsequent to the physiological remodeling that is observed following the placement and the loading of the dental implants) [6]. Based on a review article published by [PERSON] and his co-worker, the prevalence of PI was rated in the order of 10% of implants and 20% of patients 5-10 years after implant loading [7; 8]. However, the authors also acknowledge that this statement derives from the analysis of clinical studies reporting rather variable and difficult-to-compare data, and for this reason, it is not definitively representative of the diffusion of PI among patients. Peri-implant treatment is still challenging; although several treatments have been proposed, no consensus on which is the most predictable, reproducible and effective procedure has been reported in the literature. In the treatment of PI, it is mandatory not only to remove all the inflammatory soft tissue around the peri-implant pocket and eventually apply bone augmentation techniques, but also to decontaminate the infected fixtures parts. Several approaches for implant decontamination aimed to eliminate bacterial biofilm are noted: mechanical and pharmacological decontamination, implantoplasty and laser irradiation. However, none of the curative protocols reported in the literature has proven to be effective in the treatment of PI [9]. Therapeutic performances of mechanical or chemical modalities seem to be limited due to resistant bacterial strains, limited access to inflamed area and pharmacologic limitations such as in-site drug dosage or insufficient antibacterial effect. Moreover, mechanical strategies such as metallic curettes, ultrasonic metal tip scalers and air powder abrasion may develop a roughened implant surface, which itself increases bacterial colonization and biofilm formation [10].