## 4 Discussion  
Implant health will be achieved if a symbiosis is established between the host and the peri-implant biofilm; however, in the presence of peri-implantitis risk factors, dysbiotic changes can occur to the microbiota constituting the peri-implant biofilm, setting off peri-implant soft tissue inflammatory processes, leading to peri-implant mucositis and peri-implantitis [23]. The implant material has gained interest in recent years because it may participate in peri-implant biofilm dysbiosis [42]. As a result of the process of corrosion and attrition of the implant, caused by both the exposure of titanium for long periods to oral environment and the frictional forces developing physiologically at the implant-abutment interface, ions and nano- or microparticles of this metal may be released at the peri-implant soft tissue level [43]. To date, it is unclear whether such release of metallic material can establish a tissue inflammatory response and, in association with the presence of the microbial component, play an important role in the progression of peri-implant disease [44]. Figure 1: Number of research papers published until 2021. Regarding the implant material, the addition of niobium and zirconium to the titanium implant alloy has been shown to have a similar bacterial adhesion pattern compared to implants composed of titanium and vanadium, with a slight increase in adhesion of _A. naeslundii_ and _S. sanguinis_[28]. In the presence of poor oral hygiene for a period longer than three weeks, it has been found that dysbiosis of the peri-implant biofilm occurs, with bacterial proliferation of _Tannerella forystthia_, _Prevotella intermedia_, _Freitbacterium Fastidiosum_ and _Treponema denticola_[29]. Few systematic reviews have shown that the peri-implant microbiota is similar to the periodontal microbiota in health or disease [30; 45]. However, with the use of more recent molecular techniques, capable of analyzing and detecting with more precision a considerably higher number of microorganisms, the first microbial differences between submucosal biofilms, in implants, and subgingival biofilms, in teeth, have been highlighted [31]. Although logic might suggest that implants and adjacent teeth have a similar microbiota because they share a similar ecological niche, i.e., the interdental space, more recent studies suggest the presence of important differences in diagnosis and therapy, probably due to different anatomy, histology, and peri-implant immunological characteristics [46]. The first studies aimed to identify bacteria around healthy implants and, in the presence of peri-implant pathologies, used anaerobic cultures and phase-contrast microscopy, detecting Gram-positive cocci and non-motile bacilli at the level of healthy implants; in the presence of peri-implant mucositis, a greater presence of cocci, motile bacilli and spiro-chetes was observed, while other Gram-negative, motile and anaerobic species emerged in peri-implantitis [17]. Subsequently, with the advent of newer techniques such as polymerase chain reaction (PCR), fluorescence in situ hybridization (FISH), or checkerboard DNA-DNA hybridization (CKB), a more precise inventory of micro-organisms involved in peri-implant infections has been provided, often assessing the presence of periodonotopathogenic bacteria: this includes members of the \"red complex\" bacterial cluster, including _Porphyromonas gigiwalls_, _Tannerella forystthia_, _Treponema denticola_, but also _Treponema I-III_ and _Synergistetes cluster A_[24]. From these early studies, the main differences in the peri-implant oral microbiota compared to the periodontal microbiota indicated the presence of pathogens such as _Peptostreprooccus_ spp. or _Staphylococcus epidermidis_ and _Staphylococcus aureus_[32].