30 and 31 It was demonstrated that even after tooth loss, key periodontal pathogens remain colonizing oral cavity20 and 16 and that periodontitis history was positively correlated to peri-implantitis and peri-implant bone loss.7, 8 and 28 Therefore, one plausible explanation for the relationship between periodontal and peri-implant diseases is associated

with the microbial component.24 In fact, clinically, similar microenvironments including sulcus/pockets are presented around dental implants and teeth, which could favour similar bacteria colonization. Although studies have shown that the subgingival microbiota associated with health and disease is similar around implants and teeth,32 the occurrences of key periodontal species according to different peri-implant and periodontal clinical conditions and their direct comparisons still need further evaluation. Therefore, the present study firstly aimed to verify if the frequencies of target periodontal Linsitinib order species would increase progressively throughout health, reversible (mucositis and gingivitis) and irreversible (periodontitis and peri-implantitis) established peri-implant and periodontal diseases. For peri-implant sites, overall, the results showed that the majority of the bacterial frequencies were higher Autophagy activator in peri-implantitis than in healthy implants, as demonstrated by previous studies.21 and 22

However, the results of the present study did not show clear differences between peri-implantitis and mucositis and, the hypothesis that the bacterial frequencies would increase gradually from healthy to mucositis and peri-implantitis was rejected. Maybe, the overlapping profile of microbial frequency between mucositis and peri-implantitis indicates that, similarly to what happens in gingivitis,33 mucositis, as an intermediate reversible stage, could progress to peri-implantitis in susceptible subjects or even be a self-limiting Amrubicin disease in resistant subjects. Renvert et al.34 did not observed marked differences in the proportions of 40 bacteria species and total bacterial load in relation to different peri-implant status. Maximo et al.,23 using chequerboard

hybridization technique, showed that T. forsythia counts were higher in peri-implantitis than peri-implant health and mucositis. In addition, although not statistically significant, P. gingivalis was the species found at the highest levels in the peri-implantitis when compared to the other clinical conditions. In support of our results, the authors found higher proportion of red complex species in the submucosal area around peri-implantitis, followed by mucositis and by the healthy implants. In the present study, as previously shown, 19 and 13 microbial differences among healthy and diseased periodontal clinical statuses were evident. Although the expected pattern of progressive increased frequency of detection from health to periodontitis was observed for T.