Rheumatoid arthritis (RA) is an inflammatory autoimmune disease that causes chronic erosive polyarthritis, and further evolves towards extra-articular complications and permanent disability. Whereas complex gene-environment interactions underpin the development of RA, its exact etiopathogenesis remains poorly understood. Typically, RA starts in genetically predisposed individuals with a long period of serologically detectable autoimmunity, described as the pre-clinical phase of the disease. Because this pre-clinical phase is devoid of signs of arthritis, it has been surmised that RA-related autoimmunity is triggered outside of the joints. Growing evidence points towards the involvement of incipient dysbiosis at mucosal surfaces, among which the oral periodontium, as one early trigger of the immune onset of RA. Gathering a better understanding of these mechanisms would be essential to elucidate the exact aetiology of the disease, would significantly improve the risk assessment in at-risk individuals, and would have direct applications for the design of prophylactic strategies.
Epidemiological associations between RA and periodontitis, i.e., the inflammation of the periodontium driven by microbial dysbiosis, have been long-established. However, the underlying cross-talk between the oral microbiota, mucosal and systemic immunity have just started to surface. Several lines of investigation suggest indeed a dysbiotic microbiota to cause the local production of citrullinated peptides and thereby to contribute to the immune onset of RA. Potential mechanisms involved include the loss of the mucosal barrier function, the induction of anticitrullinated peptides autoantibodies (ACPA) along with molecular mimicry and epitope spreading between microbial and host citrullinated epitopes. Whereas increasing evidence supports this so-called “mucosal origins hypothesis” of RA, it remains difficult to connect the dots between these findings and grasp a comprehensive understanding of the path to autoimmunity.
The goal of this Research Topic is to provide novel insights into potentially causal associations between oral microbial profiles and the development of RA. The Topic additionally aims to shed light upon the various processes through which a dysbiotic oral microbiota may contribute to the local initiation, and systemic spread, of the characteristic ACPA response observed in RA.
We welcome the submission of Original Research, Brief Research Reports (pre-clinical and clinical) as well as Systematic and Narrative Reviews, mini-Reviews or Opinion-type papers.
More specifically, themes may include but are not limited to:
• Associations between taxonomic oral microbial profiles and the development of RA.
• Relationships between functional oral microbial patterns, and/or microbial effectors, and RA-related autoimmunity.
• Insights into the potential cascade of events between the development of oral dysbiosis, periodontal inflammation and local ACPA production.
• Dynamics between the local production of citrullinated peptides, the local generation of ACPAs and the ensuing systemic ACPA response.
Rheumatoid arthritis (RA) is an inflammatory autoimmune disease that causes chronic erosive polyarthritis, and further evolves towards extra-articular complications and permanent disability. Whereas complex gene-environment interactions underpin the development of RA, its exact etiopathogenesis remains poorly understood. Typically, RA starts in genetically predisposed individuals with a long period of serologically detectable autoimmunity, described as the pre-clinical phase of the disease. Because this pre-clinical phase is devoid of signs of arthritis, it has been surmised that RA-related autoimmunity is triggered outside of the joints. Growing evidence points towards the involvement of incipient dysbiosis at mucosal surfaces, among which the oral periodontium, as one early trigger of the immune onset of RA. Gathering a better understanding of these mechanisms would be essential to elucidate the exact aetiology of the disease, would significantly improve the risk assessment in at-risk individuals, and would have direct applications for the design of prophylactic strategies.
Epidemiological associations between RA and periodontitis, i.e., the inflammation of the periodontium driven by microbial dysbiosis, have been long-established. However, the underlying cross-talk between the oral microbiota, mucosal and systemic immunity have just started to surface. Several lines of investigation suggest indeed a dysbiotic microbiota to cause the local production of citrullinated peptides and thereby to contribute to the immune onset of RA. Potential mechanisms involved include the loss of the mucosal barrier function, the induction of anticitrullinated peptides autoantibodies (ACPA) along with molecular mimicry and epitope spreading between microbial and host citrullinated epitopes. Whereas increasing evidence supports this so-called “mucosal origins hypothesis” of RA, it remains difficult to connect the dots between these findings and grasp a comprehensive understanding of the path to autoimmunity.
The goal of this Research Topic is to provide novel insights into potentially causal associations between oral microbial profiles and the development of RA. The Topic additionally aims to shed light upon the various processes through which a dysbiotic oral microbiota may contribute to the local initiation, and systemic spread, of the characteristic ACPA response observed in RA.
We welcome the submission of Original Research, Brief Research Reports (pre-clinical and clinical) as well as Systematic and Narrative Reviews, mini-Reviews or Opinion-type papers.
More specifically, themes may include but are not limited to:
• Associations between taxonomic oral microbial profiles and the development of RA.
• Relationships between functional oral microbial patterns, and/or microbial effectors, and RA-related autoimmunity.
• Insights into the potential cascade of events between the development of oral dysbiosis, periodontal inflammation and local ACPA production.
• Dynamics between the local production of citrullinated peptides, the local generation of ACPAs and the ensuing systemic ACPA response.