Oral Microbiota Identifies Patients in Early Onset Rheumatoid Arthritis

Esberg, Anders; Johansson, Linda; Johansson, Ingegerd; Rantapää-Dahlqvist, Solbritt

doi:10.3390/microorganisms9081657

Cited by 32 publications

(40 citation statements)

References 57 publications

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“…Since genetic variations in TAS2R38 have functional consequences that, in addition to taste perception, may contribute to antimicrobial responses [18,20], we investigated the buccal microbiome in our RA and non-RA control subjects, many of whom were at risk for developing future RA, and compared the microbiome across TAS2R38 genotypes. Our findings are consistent with other reports finding the enrichment of periodontal pathogens in oral, pulmonary, and gastrointestinal microbiomes obtained from individuals at risk for RA [35][36][37][38][39][40]. Relative depletion of P. gingivalis has been reported in RA patients compared to anti-citrullinated protein autoantibody (ACPA)-positive individuals who are at risk for developing future RA [38].…”

Section: Discussionsupporting

confidence: 92%

Association of Bitter Taste Receptor T2R38 Polymorphisms, Oral Microbiota, and Rheumatoid Arthritis

Jesus

Singh

Schroth

et al. 2021

CIMB

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The association of taste genetics and the oral microbiome in autoimmune diseases such as rheumatoid arthritis (RA) has not been reported. We explored a novel oral mucosal innate immune pathway involving the bitter taste G protein-coupled receptor T2R38. This case–control study aimed to evaluate whether T2R38 polymorphisms associate with the buccal microbial composition in RA. Genomic DNA was obtained from buccal swabs of 35 RA patients and 64 non-RA controls. TAS2R38 genotypes were determined by Sanger sequencing. The buccal microbiome was assessed by Illumina MiSeq sequencing of the V4-16S rRNA gene. Bacterial community differences were analyzed with alpha and beta diversity measures. Linear discriminant analysis effect size identified taxa discriminating between RA versus non-RA and across TAS2R38 genotypes. TAS2R38 genotype frequency was similar between RA and non-RA controls (PAV/PAV; PAV/AVI; AVI/AVI: RA 42.9%; 45.7%; 11.4% versus controls 32.8%; 48.4%; 18.8%, chi-square (2, N = 99) = 2.1, p = 0.35). The relative abundance of Porphyromonas, among others, differed between RA and non-RA controls. The relative abundance of several bacterial species also differed across TAS2R38 genotypes. These findings suggest an association between T2R38 polymorphisms and RA buccal microbial composition. However, further research is needed to understand the impact of T2R38 in oral health and RA development.

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Section: Discussionsupporting

confidence: 92%

Association of Bitter Taste Receptor T2R38 Polymorphisms, Oral Microbiota, and Rheumatoid Arthritis

Jesus

Singh

Schroth

et al. 2021

CIMB

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“…This supports the hypothesis that the oral microbiome, and specifically Pg, may be important in the initiation of some cases of RA [84,85]. Notably, dysbiosis of the oral microbiome might contribute to RA independently of periodontal status, as concluded in another study, also showing that patients with early RA had enriched levels of Prevotella pleuritidis, Treponema denticola, Porphyromonas endodontalis, and Filifactor alocis and species in the Porphyromonas and Fusobacterium genera with functions linked to ornithine metabolism, glucosylceramidase, beta-lactamase resistance, biphenyl degradation, fatty acid metabolism, and 17-beta-estradiol-17-dehydrogenase metabolism [76].…”

Section: 1mentioning

confidence: 76%

“…Indeed, in conditions such as hypoxia, human enzymes may be much less effective than enzymes of anaerobic bacteria from microbiota are. Whether genes of metabolism contribute to shape the profile of microbiota DNA found in human synovium and cartilage is a question that makes sense, especially as RA is strongly associated with the metabolic profile of synovial fluid [48], and host metabolism strongly shapes the oral microbiota [76].…”

Section: Translocation Of Oral Bacteria In Blood Has Been Observed Including In Patients With Ramentioning

confidence: 99%

Another Look at the Contribution of Oral Microbiota to the Pathogenesis of Rheumatoid Arthritis: A Narrative Review

Berthelot¹,

Bandiaky

Goff³

et al. 2021

Microorganisms

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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.

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“…In contrast, in preterm birth, diabetes, Alzheimer's disease, atherosclerosis, and one of the autoimmune diseases, rheumatism, the involvement of gram-negative obligate anaerobic bacilli, such as P. gingivalis and Treponema denticola, which are classified as periodontal pathogens, is strongly suspected; however, it is rare that the causative organism is specifically detected in the lesion. Various studies have been undertaken into the pathogenic mechanism of these bacteria, but there are many unclear points (41)(42)(43).…”

Section: The Oral Biotamentioning

confidence: 99%

Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role of Porphyromonas gingivalis

et al. 2022

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Gut microbiota play many important roles, such as the regulation of immunity and barrier function in the intestine, and are crucial for maintaining homeostasis in living organisms. The disruption in microbiota is called dysbiosis, which has been associated with various chronic inflammatory conditions, food allergies, colorectal cancer, etc. The gut microbiota is also affected by several other factors such as diet, antibiotics and other medications, or bacterial and viral infections. Moreover, there are some reports on the oral-gut-liver axis indicating that the disruption of oral microbiota affects the intestinal biota. Non-alcoholic fatty liver disease (NAFLD) is one of the systemic diseases caused due to the dysregulation of the oral-gut-liver axis. NAFLD is the most common liver disease reported in the developed countries. It includes liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer. Recently, accumulating evidence supports an association between NAFLD and dysbiosis of oral and gut microbiota. Periodontopathic bacteria, especially Porphyromonas gingivalis, have been correlated with the pathogenesis and development of NAFLD based on the clinical and basic research, and immunology. P. gingivalis was detected in the liver, and lipopolysaccharide from this bacteria has been shown to be involved in the progression of NAFLD, thereby indicating a direct role of P. gingivalis in NAFLD. Moreover, P. gingivalis induces dysbiosis of gut microbiota, which promotes the progression of NAFLD, through disrupting both metabolic and immunologic pathways. Here, we review the roles of microbial dysbiosis in NAFLD. Focusing on P. gingivalis, we evaluate and summarize the most recent advances in our understanding of the relationship between oral-gut microbiome symbiosis and the pathogenesis and progression of non-alcoholic fatty liver disease, as well as discuss novel strategies targeting both P. gingivalis and microbial dysbiosis.

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Oral Microbiota Identifies Patients in Early Onset Rheumatoid Arthritis

Cited by 32 publications

References 57 publications

Association of Bitter Taste Receptor T2R38 Polymorphisms, Oral Microbiota, and Rheumatoid Arthritis

Association of Bitter Taste Receptor T2R38 Polymorphisms, Oral Microbiota, and Rheumatoid Arthritis

Another Look at the Contribution of Oral Microbiota to the Pathogenesis of Rheumatoid Arthritis: A Narrative Review

Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role of Porphyromonas gingivalis

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