## 4 Discussion  
In this study we analyzed the presence of implant failures, and in particular the number of implants lost due to peri-implantitis, in two different types of implant surfaces, Ti-Unite(tm) surface and Ossean(r). Both surfaces present a common characteristic that is roughness of its surface. A review by [PERSON] et al. (2018), analyzing a total of over 17,000 implants with at least 10 years of follow-up, showed a high survival rate of implants with Ti-Unite(tm) surfaces; in fact, this anodised surface showed the lowest probability of failure compared with other different surface modifications such as plasma-sprayed titanium [30]. A meta-analysis by [PERSON] and [PERSON] (2017), based on 106 publications, reported a 10-year survival rate of Ti-Unite implants of 95.14%. Of these studies, 18% (19 studies) investigated the prevalence of peri-implantitis in Ti-Unite(tm) surface: in a total of 1229 patients, 64 underwent peri-implantitis, with a prevalence of 5.2% and a mean follow-up of 47.89 months [31]. In contrast, [PERSON] et al., in 2017, reported a considerably higher percentage of peri-implantitis with anodized implant surface (28.3% of the implants evaluated) [29]; the same author, instead, reported a considerably lower percentage of peri-implantitis with machined implant surfaces (1.8% of all the implants examined) [32]. Our findings are in contrast with the results obtained by [PERSON] et al. regarding rough surfaces [33]; in fact, we observed 1.6% of peri-implantitis with Ti-Unite(tm) surface and 1.5% of peri-implantitis with Ossean(r) surface. This conflict could be explained by differences in classifications of peri-implantitis: only a few authors pay specific attention to the role of bacteria's role in peri-implantitis etiology; [PERSON] et al. suggested a classification including the research of specific bacteria such as _Porphyomonas gengivalis_, _Prevotella intermedia_, _Fusobacterium nucleatum_, _Tannerella forystthia_, _Aggregatibacter actinomycetemitans_, and _Treponema denticola_[34; 35; 36]. Moreover, [PERSON] et al. stated that there is no evidence of a major risk of peri-implantitis due to bacterial contamination related to rough surfaces, without differences in the prevalence of peri-implantitis in 5-year and 10-year follow-up data between smooth and rough surfaces [37; 38]. In the non-surgical therapy of periodontal diseases the persistence of specific sub-gingival species including _A. actinomycetemcomitans_, _P. gingivalis_, and _T. denticola_ (their ability to invade the subjacent periodontal tissues) has been associated with poor response to treatment by scaling and root planing [39]. Also peri-implantitis have been associated with specific microbiota that make it difficult to remove with non-surgical therapy alone [40]. [PERSON] et al. [15] in a recent meta-analysis evaluated 49 articles but only 7 met the strict inclusion criteria regarding quality assessment. The studies included those by [PERSON] et al. [41], [PERSON] et al. [16], [PERSON] et al. [42], [PERSON] et al. [43], [PERSON] et al. [44], [PERSON] et al. [45], and [PERSON] et al. [46] who concluded that \"a high-power diode laser may have some effect on peri-implant pathogens causing peri-implantitis, whereas Er:YAG laser application shows no significant effect on oral bacteria in the long term. aPDT (antimicrobial photodynamic [PERSON]) has the ability to reduce the total count of the different bacterial strains associated with peri-implantitis, e.g., _A. actinomycetemcomitans_, _P. gingivalis_, _P. intermedia_, _T. denticola_, _T. forystthia_, _F. nucleatum_, and _C. rectus_\". In addition, outcomes of surgical/regenerative treatment are strictly associated with the presence of high bacterial load and specific pathogen complexes in deep periodontal pockets (also associated with intra-bony defects) [47]. In peri-implantitis, instead, surgical therapies aim at improving implant surface cleanability and modifying bone and soft tissue morphology to reach a possibility of new osseointegration [40].