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The 5- and 10-year implant success rates in dentistry are nearly 90%. Prevalence of peri-implant diseases is 10% for peri-implantitis and 50% for peri-implant mucositis. To better understand these inflammatory pathologies of infectious origin, it is important to know if the composition of the peri-implant microbiota is comparable with the periodontal microbiota in healthy and pathological conditions. New generation sequencing (NGS) is a recent metagenomic method that analyzes the overall microorganisms present in an ecological niche by exploiting their genome. These methods are of two types: 16S rRNA sequencing and the shotgun technique. For several years, they have been used to explore the oral, periodontal, and, more specifically, peri-implant microbiota. The aim of this systematic review is to analyze the recent results of these new explorations by comparing the periodontal and peri-implant microbiota in patients with healthy and diseased sites and to explore the microbiological characteristics of peri-implantitis. A better knowledge of the composition of the peri-implant microbiota would enable us to optimize our therapeutic strategies. An electronic systematic search was performed using the medical databases PubMed/Medline, Cochrane Library, and ScienceDirect, and Periodontology 2000. The selected articles were published between January 2015 and March 2021. Inclusion criteria included clinical studies comparing healthy and pathological periodontal and peri-implant microbiota exclusively using 16S rRNA sequencing or shotgun sequencing, with enrolled populations free of systemic pathology, and studies without substantial bias. Eight articles were selected and reviewed. All of them used 16S rRNA sequencing exclusively. The assessment of these articles demonstrates the specific character of the peri-implant microbiota in comparison with the periodontal microbiota in healthy and pathological conditions. Indeed, peri-implant diseases are defined by dysbiotic bacterial communities that vary from one individual to another, including known periodontopathogens such as Porphyromonas gingivalis (P.g.) and genera less mentioned in the periodontal disease pattern such as Filifactor alocis. Examination of peri-implant microbiota with 16S rRNA sequencing reveals differences between the periodontal and peri-implant microbiota under healthy and pathological conditions in terms of diversity and composition. The pattern of dysbiotic drift is preserved in periodontal and peri-implant diseases, but when comparing the different types of pathological sites, the peri-implant microbiota has a specificity in the presence of bacteria proper to peri-implantitis and different relative proportions of the microorganisms present.

Although autoimmunity contributes to rheumatoid arthritis (RA), several lines of evidence challenge the dogma that it is mainly an autoimmune disorder. As RA-associated human leukocyte antigens shape microbiomes and increase the risk of dysbiosis in mucosae, RA might rather be induced by epigenetic changes in long-lived synovial presenting cells, stressed by excessive translocations into joints of bacteria from the poorly cultivable gut, lung, or oral microbiota (in the same way as more pathogenic bacteria can lead to “reactive arthritis”). This narrative review (i) lists evidence supporting this scenario, including the identification of DNA from oral and gut microbiota in the RA synovium (but in also healthy synovia), and the possibility of translocation through blood, from mucosae to joints, of microbiota, either directly from the oral cavity or from the gut, following an increase of gut permeability worsened by migration within the gut of oral bacteria such as Porphyromonas gingivalis; (ii) suggests other methodologies for future works other than cross-sectional studies of periodontal microbiota in cohorts of patients with RA versus controls, namely, longitudinal studies of oral, gut, blood, and synovial microbiota combined with transcriptomic analyses of immune cells in individual patients at risk of RA, and in overt RA, before, during, and following flares of RA.

Periodontitis is a common condition characterized by an exacerbated pro-inflammatory response, which leads to tissue destruction and, ultimately, alveolar bone loss. In this pilot study, we assess the microbiota composition and cytokine profile changes in patients with stage III/IV, grade B/C periodontitis, specifically by comparing healthy and diseased sites in the same oral cavity. Overall, we found that microbiota architecture was significantly disrupted between diseased and healthy sites, and that the clustering was driven, in part, by the increased relative abundances of Synergistetes in diseased sites, as well as the increased abundances of Firmicutes in healthy sites. We also observed that diseased sites were enriched in Synergistetes, TM7, SR1, Spirochaetes, Bacteroidetes and Fusobacteria, and depleted in Firmicutes, Proteobacteria, Tenericutes and Actinobacteria compared to healthy sites. We found that Interleukin-1b, Interleukin-4, Interleukin-10, and Interleukin-17A were significantly overexpressed in diseased sites, whereas Interleukin-6 and TNF-alpha do not differ significantly between healthy and diseased sites. Here, we observed concomitant changes in the subgingival plaque microbiota and cytokines profile, suggesting that this combined alteration could contribute to the pathobiology of periodontitis.

Although autoimmunity contributes to rheumatoid arthritis (RA), several lines of evidence challenge the dogma that it is mainly an autoimmune disorder. As RA-associated human leukocyte antigens shape microbiomes and increase the risk of dysbiosis in mucosae, RA might rather be induced by epigenetic changes in long-lived synovial presenting cells, stressed by excessive translocations into joints of bacteria from the poorly cultivable gut, lung, or oral microbiota (in the same way as more pathogenic bacteria can lead to "reactive arthritis"). This narrative review (i) lists evidence supporting this scenario, including the identification of DNA from oral and gut microbiota in the RA synovium (but in also healthy synovia), and the possibility of translocation through blood, from mucosae to joints, of microbiota, either directly from the oral cavity or from the gut, following an increase of gut permeability worsened by migration within the gut of oral bacteria such as Porphyromonas gingivalis; (ii) suggests other methodologies for future works other than cross-sectional studies of periodontal microbiota in cohorts of patients with RA versus controls, namely, longitudinal studies of oral, gut, blood, and synovial microbiota combined with transcriptomic analyses of immune cells in individual patients at risk of RA, and in overt RA, before, during, and following flares of RA. [ABSTRACT FROM AUTHOR]