scholarly journals Host–microbiota interactions in rheumatoid arthritis

2019 ◽  
Vol 51 (12) ◽  
pp. 1-6 ◽  
Author(s):  
Yuichi Maeda ◽  
Kiyoshi Takeda
Keyword(s):  
Rheumatoid Arthritis ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Th17 Cell ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Oral Bacteria ◽  
Oral Microbiota ◽  
Periodontal Bacteria ◽  
Growing Body

AbstractThe gut microbiota has been proposed to be an important environmental factor in the development of rheumatoid arthritis (RA). Here, we review a growing body of evidence from human and animal studies that supports the hypothesis that intestinal microbiota play a role in RA. Previous studies from we and others showed an altered composition of the microbiota in early RA patients. A recent study demonstrated that Prevotella species are dominant in the intestine of patients in the preclinical stages of RA. In addition, Prevotella-dominated microbiota isolated from RA patients contributes to the development of Th17 cell-dependent arthritis in SKG mice. Moreover, it was reported that periodontal bacteria correlates with the pathogenesis of RA. In this review, we discuss the link between oral bacteria and the development of arthritis. However, many questions remain to be elucidated in terms of molecular mechanisms for the involvement of intestinal and oral microbiota in RA pathogenesis.

scholarly journals Oral Microbiota Identifies Patients in Early Onset Rheumatoid Arthritis

2021 ◽  
Vol 9 (8) ◽  
pp. 1657
Author(s):  
Anders Esberg ◽  
Linda Johansson ◽  
Ingegerd Johansson ◽  
Solbritt Rantapää Dahlqvist
Keyword(s):  
Rheumatoid Arthritis ◽  
Early Onset ◽  
Amplicon Sequencing ◽  
Oral Bacteria ◽  
Oral Microbiome ◽  
Rrna Gene ◽  
Oral Microbiota ◽  
Disease Manifestation ◽  
Periodontal Status ◽  
Quality Register

Rheumatoid arthritis (RA) is the most common autoimmune inflammatory disease, and single periodontitis-associated bacteria have been suggested in disease manifestation. Here, the oral microbiota was characterized in relation to the early onset of RA (eRA) taking periodontal status into consideration. 16S rRNA gene amplicon sequencing of saliva bacterial DNA from 61 eRA patients without disease-modifying anti-rheumatic drugs and 59 matched controls was performed. Taxonomic classification at 98.5% was conducted against the Human Oral Microbiome Database, microbiota functions were predicted using PICRUSt, and periodontal status linked from the Swedish quality register for clinically assessed caries and periodontitis. The participants were classified into three distinct microbiota-based cluster groups with cluster allocation differences by eRA status. Independently of periodontal status, eRA patients had enriched levels of Prevotella pleuritidis, Treponema denticola, Porphyromonas endodontalis and Filifactor alocis species and in the Porphyromonas and Fusobacterium genera and functions linked to ornithine metabolism, glucosylceramidase, beta-lactamase resistance, biphenyl degradation, fatty acid metabolism and 17-beta-estradiol-17-dehydrogenase metabolism. The results support a deviating oral microbiota composition already in eRA patients compared with healthy controls and highlight a panel of oral bacteria that may be useful in eRA risk assessment in both periodontally healthy and diseased persons.

scholarly journals Intestinal Dysbiosis and Rheumatoid Arthritis: A Link between Gut Microbiota and the Pathogenesis of Rheumatoid Arthritis

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Gabriel Horta-Baas ◽  
María del Socorro Romero-Figueroa ◽  
Alvaro José Montiel-Jarquín ◽  
María Luisa Pizano-Zárate ◽  
Jaime García-Mena ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Research Field ◽  
Autoimmune Process ◽  
Present Evidence ◽  
Intestinal Dysbiosis ◽  
Process Studies ◽  
Bacterial Groups ◽  
Pathogenic Effects

Characterization and understanding of gut microbiota has recently increased representing a wide research field, especially in autoimmune diseases. Gut microbiota is the major source of microbes which might exert beneficial as well as pathogenic effects on human health. Intestinal microbiome’s role as mediator of inflammation has only recently emerged. Microbiota has been observed to differ in subjects with early rheumatoid arthritis compared to controls, and this finding has commanded this study as a possible autoimmune process. Studies with intestinal microbiota have shown that rheumatoid arthritis is characterized by an expansion and/or decrease of bacterial groups as compared to controls. In this review, we present evidence linking intestinal dysbiosis with the autoimmune mechanisms involved in the development of rheumatoid arthritis.

scholarly journals The Gut Barrier, Intestinal Microbiota, and Liver Disease: Molecular Mechanisms and Strategies to Manage

2020 ◽  
Vol 21 (21) ◽  
pp. 8351
Author(s):  
Julio Plaza-Díaz ◽  
Patricio Solís-Urra ◽  
Fernando Rodríguez-Rodríguez ◽  
Jorge Olivares-Arancibia ◽  
Miguel Navarro-Oliveros ◽  
...  
Keyword(s):  
Liver Disease ◽  
Intestinal Microbiota ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Bacterial Species ◽  
Intestinal Barrier ◽  
Lifestyle Changes ◽  
Alcoholic Fatty Liver ◽  
Underlying Mechanisms

Liver disease encompasses pathologies as non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, alcohol liver disease, hepatocellular carcinoma, viral hepatitis, and autoimmune hepatitis. Nowadays, underlying mechanisms associating gut permeability and liver disease development are not well understood, although evidence points to the involvement of intestinal microbiota and their metabolites. Animal studies have shown alterations in Toll-like receptor signaling related to the leaky gut syndrome by the action of bacterial lipopolysaccharide. In humans, modifications of the intestinal microbiota in intestinal permeability have also been related to liver disease. Some of these changes were observed in bacterial species belonging Roseburia, Streptococcus, and Rothia. Currently, numerous strategies to treat liver disease are being assessed. This review summarizes and discusses studies addressed to determine mechanisms associated with the microbiota able to alter the intestinal barrier complementing the progress and advancement of liver disease, as well as the main strategies under development to manage these pathologies. We highlight those approaches that have shown improvement in intestinal microbiota and barrier function, namely lifestyle changes (diet and physical activity) and probiotics intervention. Nevertheless, knowledge about how such modifications are beneficial is still limited and specific mechanisms involved are not clear. Thus, further in-vitro, animal, and human studies are needed.

scholarly journals Direct impact of commonly used dietary emulsifiers on human gut microbiota

Microbiome ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Sabrine Naimi ◽  
Emilie Viennois ◽  
Andrew T. Gewirtz ◽  
Benoit Chassaing
Keyword(s):  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Animal Studies ◽  
Intestinal Inflammation ◽  
Ex Vivo ◽  
Food Additives ◽  
Polysorbate 80 ◽  
Microbiota Composition ◽  
Epidemiologic Evidence ◽  
And Function

Abstract Background Epidemiologic evidence and animal studies implicate dietary emulsifiers in contributing to the increased prevalence of diseases associated with intestinal inflammation, including inflammatory bowel diseases and metabolic syndrome. Two synthetic emulsifiers in particular, carboxymethylcellulose and polysorbate 80, profoundly impact intestinal microbiota in a manner that promotes gut inflammation and associated disease states. In contrast, the extent to which other food additives with emulsifying properties might impact intestinal microbiota composition and function is not yet known. Methods To help fill this knowledge gap, we examined here the extent to which a human microbiota, maintained ex vivo in the MiniBioReactor Array model, was impacted by 20 different commonly used dietary emulsifiers. Microbiota density, composition, gene expression, and pro-inflammatory potential (bioactive lipopolysaccharide and flagellin) were measured daily. Results In accordance with previous studies, both carboxymethylcellulose and polysorbate 80 induced a lasting seemingly detrimental impact on microbiota composition and function. While many of the other 18 additives tested had impacts of similar extent, some, such as lecithin, did not significantly impact microbiota in this model. Particularly stark detrimental impacts were observed in response to various carrageenans and gums, which altered microbiota density, composition, and expression of pro-inflammatory molecules. Conclusions These results indicate that numerous, but not all, commonly used emulsifiers can directly alter gut microbiota in a manner expected to promote intestinal inflammation. Moreover, these data suggest that clinical trials are needed to reduce the usage of the most detrimental compounds in favor of the use of emulsifying agents with no or low impact on the microbiota.

scholarly journals SAT0590 ORAL MICROBIOTA IDENTIFIES PATIENTS WITH EARLY RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1254.2-1254
Author(s):  
A. Esberg ◽  
L. Johansson ◽  
I. Johansson ◽  
S. Rantapää Dahlqvist
Keyword(s):  
Rheumatoid Arthritis ◽  
Porphyromonas Gingivalis ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Oral Bacteria ◽  
Diagnostic Tools ◽  
Oral Microbiota ◽  
Healthy Controls ◽  
Periodontal Pathogens ◽  
Specificity And Sensitivity ◽  
Periodontal Infection

Background:Several studies have suggested a link between the two chronic inflammatory diseases, rheumatoid arthritis (RA) and periodontitis (PD) [1]. The diseases share similar environmental and genetic risks factors,e.g.,smoking [2] and the HLA-DRB1 alleles [3]. Several serum markers used in the diagnosis of RA have also been found to be elevated in PD,e.g.,anti-citrullinated proteins antibodies (ACPA) and rheumatoid factor (RF) [4]. The connection between PD and RA has been suggested to be explained by several periodontal pathogens,e.g., Aggregatibacter actinomycetemcomitansandPorphyromonas gingivalis, which have been suggested to induce the production of autoantibodies [5, 6].Objectives:To investigate the composition of the concerted saliva microbiota and its role in the development of RA, with the aim of improving the diagnostic tools.Methods:16S ribosomal RNA gene sequencing of saliva bacterial DNA isolated from a total of 61 early RA (eRA) patients and 59 healthy controls was made. The eRA (symptoms ≤ 12 months) was diagnosed at an Early Arthritis Clinic (fulfilling the 1987 ARA criteria) and matched with the controls for sex and age, except for two of the elderly cases. None of the individuals included in the study had taken antibiotics during the preceding 3 months. No one of the cases were treated with anti-rheumatic drugs except for corticosteroids in 16 cases the latest month.Results:All participants were classified into three hierarchical cluster groups based on their saliva microbiota and the distribution of eRA cases versus controls differed distinctly between the cluster groups. The microbiota from the eRA had higher species richness, differed in beta-diversity, and was enriched for species in the Fusobacterium and Porphyromonas genera, and for the Alloprevotella tannerae, Campylobacter gracilis, Capnocytophaga leadbetteri, Filifactor alocis, Fusobacterium nucleatum subsp. polymorphum, Neisseria elongate, Porphyromionas endodontalis and Prevotella pleuritidis species compared to controls. Combining two topped ranked species,A. tanneraeandCatonella morbisignificantly predicted eRA with an AUC score of 0.86 and a specificity and sensitivity of 0.80 and 0.85, respectively.The predicted functions of the microbiota in eRA patients were dominated by fatty acid metabolism, ornithine metabolism, glucosylceramidase, sphingolipids, beta-lactamase resistance, biphenyl degradation and 17-beta-estradiol 17-dehydrogenase metabolism.Conclusion:In this study a difference in oral microbiota diversity between eRA patients and healthy controls could be shown. Some of the eRA-associated oral bacteria have previously been suggested to play an aetiological role in the development of RA, but others have not been recognized earlier, such as A. tannerae, F. alocis, F. nucleatum subsp. polymorphum, and P. endodontalis, and may therefore be useful in RA risk assessment.References:[1]Fuggle, N.R., et al.,Hand to Mouth: A Systematic Review and Meta-Analysis of the Association between Rheumatoid Arthritis and Periodontitis.Front Immunol, 2016. 7: p. 80.[2]Heliovaara, M., et al.,Smoking and risk of rheumatoid arthritis.J Rheumatol, 1993. 20(11): p. 1830-5.[3]Katz, J., et al.,Human leukocyte antigen (HLA) DR4. Positive association with rapidly progressing periodontitis.J Periodontol, 1987. 58(9): p. 607-10.[4]Mikuls, T.R., et al.,Periodontitis and Porphyromonas gingivalis in patients with rheumatoid arthritis.Arthritis Rheumatol, 2014. 66(5): p. 1090-100.[5]Konig, M.F., et al.,Aggregatibacter actinomycetemcomitans-induced hypercitrullination links periodontal infection to autoimmunity in rheumatoid arthritis.Sci Transl Med, 2016. 8(369): p. 369ra176.[6]Rosenstein, E.D., et al.,Hypothesis: the humoral immune response to oral bacteria provides a stimulus for the development of rheumatoid arthritis.Inflammation, 2004. 28(6): p. 311-8.Disclosure of Interests:None declared

scholarly journals The oral and gut microbiota: beyond a short communication

2021 ◽  
pp. 405-411
Author(s):  
Sabino CECI ◽  
Pula BERATE ◽  
Sebastian CANDREA ◽  
Anida-Maria BABTAN ◽  
Daniela AZZOLLINI ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Oral Bacteria ◽  
The Body ◽  
Cochrane Library ◽  
Oral Microbiota ◽  
Oral Diseases ◽  
Philosophical Approach ◽  
Gut Dysbiosis ◽  
Inflammatory Bowel

Introduction. The current treatment and prevention of oral disorders, dental caries, periodontal and gum diseases, follow a very non-specific control of plaque as the main causative factor. The main therapeutically approach is carried out on the sole perspective to keep the levels of oral bacteria in an acceptable range compatible with one-way vision of oral-mouth health, as something completely separated from a systemic microbial homeostasis (dysbiosis) concomitant present in the gut. A sealed compartmental view which sees separate and incommunicable responses to a specific condition without considering the presence of interacting confounding factors can negatively influence the diagnosis a diseases and of course its progression. A general non-specific antimicrobial with more general antiplaque therapy based mainly on oral care products together with surgery interventions represent at the moment the only mechanical responses in treating oral diseases. Material and method. The present paper is a narrative review concening interractions between oral and gut microbiota, with a focus on the interdisciplinary approach in antimicrobial treatment. Pubmed, Cochrane Library database were used for searching engines. Key words used were as follows: “inflammatory bowel syndrome (IBS)”, “ulcerative colitis”, “oral dysbiosis”, “gut dysbiosis”, “probiotics”, “periodontitis”. Results and discussions. Literature research showed that there are few issues to be discussed the ever increasing resistance to antibiotics, the high consumption of industrial food and sugars and their negatively effect on gut and oral microbiota. There is a need to highlight and develop a novel philosophical approach in the treatments for oral diseases that will necessarily involve non-conventional antimicrobial solutions. Such approaches should preferably reduce the consumption of both intestinal and oral microbiota, that are intimately connected and host approximately well over 1000 different species of bacteria at 108–109 bacteria per mL of mucous and saliva. Preventive approaches based upon the restoration of the microbial ecological balance, rather than elimination of the disease associated species, have been proposed. Conclusions. Having both oral-gut microbiota screened is an essential moment that influence the healthy immune modulatory and regenerative capacity of the body and, the new proposed formula integrates a wider screen on the patients where oral condition is strictly evaluated together with gut screen; therefore any proposed treatment will be inevitably sustained by the use of prebiotics and probiotics to promote health-associated bacterial growth. Keywords: inflammatory bowel syndrome (IBS), ulcerative colitis, oral dysbiosis, gut dysbiosis, probiotics, periodontitis,

scholarly journals Oral microbial dysbiosis linked to worsened periodontal condition in rheumatoid arthritis patients

2018 ◽  
Author(s):  
Jôice Dias Corrêa ◽  
Gabriel R. Fernandes ◽  
Débora Cerqueira Calderaro ◽  
Santuza Maria Souza Mendonça ◽  
Janine Mayra Silva ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Periodontal Disease ◽  
Bacterial Load ◽  
Oral Bacteria ◽  
The Body ◽  
Rrna Gene ◽  
Oral Microbiota ◽  
Periodontal Inflammation ◽  
The Impact ◽  
Subgingival Microbiota

AbstractRheumatoid arthritis (RA) is an autoimmune disorder associated with increased periodontal destruction. It is thought that RA increases the risk of periodontal disease; it is not known how it influences the oral microbiota. Our aim was to analyze the impact of RA on subgingival microbiota and its association with periodontal inflammation and RA activity. Forty-two patients with RA were compared to 47 control subjects without RA. Patients were screened for probing depth, clinical attachment level, bleeding on probing and classified as with or without periodontitis. Subgingival plaque was examined by Illumina MiSeq Sequencing of 16S rRNA gene V4 region and inflammatory cytokines were measured in saliva. RA was associated to severe periodontal disease. In addition, the severity of RA, reflected by the number of tender and swollen joints, was significantly correlated with the presence of pathogenic oral bacteria (i.e. Fusobacterium nucleatum and Treponema socransky). Non-periodontitis RA patients compared to healthy controls had increased microbial diversity and bacterial load, higher levels of pathogenic species (Prevotella, Selenomonas, Anaeroglobus geminatus, Parvimonas micra, Aggregatibacter actinomycetemcomitans) and reduction of health-related species (Streptococcus, Rothia aeria, Kingela oralis). Genes involved with bacterial virulence (i.e. lipopolysaccharide biosynthesis, peptidases) were more prevalent in the subgingival metagenome of subjects with RA. In addition, the degree of oral inflammation reflected by IL-2, IL-6, TNF-α, IFN-γ salivary levels was increased in non-periodontitis RA patients in comparison with controls. Our findings support the hypothesis that RA triggers dysbiosis of subgingival microbiota, which may contribute to worsening periodontal status.Author SummaryRheumatoid arthritis (RA) is an autoimmune disease characterized by joints inflammation, swelling, pain and stiffness. Exactly what starts this disease is still unclear. Some recent studies have suggested mucosal surfaces in the body, like those in the gums, could affect the disease process. It has been observed that people with RA have higher risk of periodontitis (a bacterial inflammatory disease of the gums), compared with the general population, and this may be the start of the autoimmune process. Also, periodontitis increases the severity of RA while interventions by treating periodontitis can improve the symptoms of RA. One of the possible mechanisms that link the higher prevalence of periodontitis in RA patients is the dysbiosis of the oral microbiota triggered by the chronic inflammation in RA. Increased levels of molecules of inflammation may affect the oral environment and change the type of bacteria that live there. Here, we examined RA patients and healthy subjects, screening their oral health and inflammatory markers. We collected their saliva and the dental plaque from the space between the teeth and the gum. We found that RA patients exhibited severe periodontitis, increased levels of inflammatory mediators on their saliva and distinct bacterial communities, with higher proportions of bacteria species linked to periodontal disease, even in patients without periodontitis. We also found that the presence of these bacteria species was linked to worse RA conditions. Our study provides new insights to understand the bi-directional mechanisms linking periodontal disease to the development of RA, showing that we need to pay attention to the oral cavity in patients with RA and refer people for dental evaluation. This practice might have a positive impact in the course of RA.

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

2021 ◽  
Vol 10 (1) ◽  
pp. 59
Author(s):  
Jean-Marie Berthelot ◽  
Octave Nadile Bandiaky ◽  
Benoit Le Goff ◽  
Gilles Amador ◽  
Anne-Gaelle Chaux ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Pathogenic Bacteria ◽  
Human Leukocyte ◽  
Autoimmune Disorder ◽  
Oral Bacteria ◽  
Narrative Review ◽  
Oral Microbiota ◽  
Cross Sectional ◽  
Leukocyte Antigens ◽  
Patients At Risk

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.

scholarly journals Role of Intestinal Microbiota on Gut Homeostasis and Rheumatoid Arthritis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Mingxin Li ◽  
Fang Wang
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Chronic Inflammatory Disease ◽  
Host Immune System ◽  
Healthy Controls ◽  
Gastrointestinal Microbiota ◽  
Intestinal Dysbiosis ◽  
Immune Mediated

Rheumatoid arthritis (RA) is a chronic inflammatory disease that is immune mediated. Patients typically present with synovial inflammation, which gradually deteriorates to investigate severe cartilage and bone damage, affecting an individual’s ability to perform basic tasks and impairing the quality of life. When evaluated against healthy controls, patients with RA have notable variations within the constituents of the gut microbiota. The human gastrointestinal tract mucosa is colonized by trillions of commensal microbacteria, which are key actors in the initiation, upkeep, and operation of the host immune system. Gut microbiota dysbiosis can adversely influence the immune system both locally and throughout the host, thus predisposing the host to a number of pathologies, including RA. Proximal intestinal immunomodulatory cells, situated in specific locales within the intestine, are a promising intermediary through which the gastrointestinal microbiota can influence the pathogenesis and progression of RA. In the early stages of the disease, the microbiota appear to differ from those present in healthy controls. This difference may reflect potential autoimmune mechanisms. Research studies evaluating intestinal microbiota have demonstrated that RA is associated with a bacterial population growth or with a decline when judged against control groups. The aim of this review is to examine the studies that connect intestinal dysbiosis with the autoimmune pathways implicated in the pathogenesis of RA.

scholarly journals Oral-Gut-Brain Axis in Experimental Models of Periodontitis: Associating Gut Dysbiosis With Neurodegenerative Diseases

2021 ◽  
Vol 2 ◽  
Author(s):  
Luis Daniel Sansores-España ◽  
Samanta Melgar-Rodríguez ◽  
Katherine Olivares-Sagredo ◽  
Emilio A. Cafferata ◽  
Víctor Manuel Martínez-Aguilar ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Neurodegenerative Diseases ◽  
Systemic Inflammation ◽  
Experimental Models ◽  
Oral Bacteria ◽  
Oral Microbiota ◽  
Low Grade ◽  
Vagus Nerves ◽  
Intestinal Dysbiosis ◽  
The Brain

Periodontitis is considered a non-communicable chronic disease caused by a dysbiotic microbiota, which generates a low-grade systemic inflammation that chronically damages the organism. Several studies have associated periodontitis with other chronic non-communicable diseases, such as cardiovascular or neurodegenerative diseases. Besides, the oral bacteria considered a keystone pathogen, Porphyromonas gingivalis, has been detected in the hippocampus and brain cortex. Likewise, gut microbiota dysbiosis triggers a low-grade systemic inflammation, which also favors the risk for both cardiovascular and neurodegenerative diseases. Recently, the existence of an axis of Oral-Gut communication has been proposed, whose possible involvement in the development of neurodegenerative diseases has not been uncovered yet. The present review aims to compile evidence that the dysbiosis of the oral microbiota triggers changes in the gut microbiota, which creates a higher predisposition for the development of neuroinflammatory or neurodegenerative diseases.The Oral-Gut-Brain axis could be defined based on anatomical communications, where the mouth and the intestine are in constant communication. The oral-brain axis is mainly established from the trigeminal nerve and the gut-brain axis from the vagus nerve. The oral-gut communication is defined from an anatomical relation and the constant swallowing of oral bacteria. The gut-brain communication is more complex and due to bacteria-cells, immune and nervous system interactions. Thus, the gut-brain and oral-brain axis are in a bi-directional relationship. Through the qualitative analysis of the selected papers, we conclude that experimental periodontitis could produce both neurodegenerative pathologies and intestinal dysbiosis, and that periodontitis is likely to induce both conditions simultaneously. The severity of the neurodegenerative disease could depend, at least in part, on the effects of periodontitis in the gut microbiota, which could strengthen the immune response and create an injurious inflammatory and dysbiotic cycle. Thus, dementias would have their onset in dysbiotic phenomena that affect the oral cavity or the intestine. The selected studies allow us to speculate that oral-gut-brain communication exists, and bacteria probably get to the brain via trigeminal and vagus nerves.

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