Dysbiotic relationship between arthritis and the oral‐gut microbiome. A critical review

Abstract

Arthritis and prosthetic joint infections (PJIs) overall are associated with reduced quality of life and limited work capacity. Multiple, overlapping factors contribute to these conditions. Some investigations have suggested a dysbiotic association between the oral‐gut microbiome and pathogenesis of arthritis and PJIs. A better understanding of the role of the oral‐gut microbiota in arthritis and PJI pathophysiology can shed light into how its disequilibrium can discharge a pro‐inflammatory response, and impact the health of patients susceptible to arthritis or with established joint disease. A review of published in vivo and clinical data suggested that alterations in oral and gut microbiota can lead to a disturbance of immunoregulatory properties, and may be associated with joint infections and arthritis. This review brings new insights into the current status of the evidence on the potential molecules and inflammatory biomarkers disrupted by an oral‐gut microbial dysbiosis. Normal commensals and pathogenic oral and gut microflora homeostasis are important not only to prevent infections per se but also its potential progression. Further experiments, especially controlled clinical trials, are needed to ascertain how microbiome manipulation and other microbiota‐directed approaches can help control inflammation and effectively prevent and treat arthritic diseases. Additionally, studies on the effects of the long‐term oral diseases, such as chronic periodontitis, on arthritis and PJIs need to be conducted.

Periodontal and microbiological data in patients with mucous membrane pemphigoid in a French population in 2021–2022: A pilot cross‐sectional study

“…Finally, the vascular diffusion of antigens, antibodies and immune complexes to the joints is thought to promote local activation of osteoclasts and low-noise inflammation. 62 Second, these metagenomic studies could eventually reveal a relationship between the oral and intestinal microbiota of gMMP patients, as observed by Imai et al ( 2021) 63 for Crohn's disease. The prospective, controlled study they conducted showed that patients had oral dysbiosis in addition to intestinal dysbiosis, with significant quantitative and qualitative differences in their microbiota compared with control subjects.…”

“…Research into the existence of a link between periodontitis and other autoimmune inflammatory diseases makes this approach relevant. For example, in rheumatoid arthritis, clinical studies have shown that the oral microbiota of patients, compared with controls, was enriched in periodontopathogenic pathogens, including Porphyromonas gingivalis 62 . This bacterium is thought to be able of inducing joint changes during the preclinical inflammatory phase via one of its virulence factors, peptidylarginine desiminase (PAD), which converts the arginine associated with a peptide into peptidylcitrulline.…”

“…The presentation of these citrullinated proteins to lymphocytes by antigen‐presenting cells then leads to the production of anti‐citrullinated peptide antibodies. Finally, the vascular diffusion of antigens, antibodies and immune complexes to the joints is thought to promote local activation of osteoclasts and low‐noise inflammation 62 …”

“…For example, in rheumatoid arthritis, clinical studies have shown that the oral microbiota of patients, compared with controls, was enriched in periodontopathogenic pathogens, including Porphyromonas gingivalis. 62 This bacterium is thought to be able of inducing joint changes during the preclinical inflammatory phase via one of its virulence factors, peptidylarginine desiminase (PAD), which converts the arginine associated with a peptide into peptidylcitrulline. The pathological mechanism behind a breakdown in immune tolerance is thought to be based on the hypercitrullination of numerous bacterial and host proteins within periodontal pockets.…”

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“…For example, P. gingivalis and Fusobacterium nucleatum are the most well-known pathogens of periodontal disease that influence and disturb the structure of the intestinal microbiota community, actively participate in the destruction of the intestinal barrier by increasing the permeability of the intestinal mucus and implicitly in the systemic inflammatory response [29]. Recent studies have shown that dysbiosis in periodontal disease was directly correlated in the long term with RA and when RA was properly treated, oral microbiota dysbiosis was restored [30].…”