Open AccessPeriodontal pathogens alter the synovial proteome. Periodontal pathogens do not exacerbate macroscopic arthritis but alter the synovial proteome in mice
Author(s) -
Anna-Lena Buschhart,
Lennart Bolten,
Johann Volzke,
Katharina Ekat,
Susanne Kneitz,
Stefan Mikkat,
Bernd Kreikemeyer,
Brigitte MüllerHilke
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0242868
Subject(s) - porphyromonas gingivalis , aggregatibacter actinomycetemcomitans , arthritis , periodontitis , rheumatoid arthritis , immunology , medicine , proteome , dental alveolus , inflammatory arthritis , inflammation , synovial fluid , immune system , pathology , biology , bioinformatics , osteoarthritis , dentistry , alternative medicine
Rheumatoid arthritis (RA) and periodontitis (PD) are chronic inflammatory diseases that appear to occur in tandem. However, the mutual impact PD exerts on RA and vice versa has not yet been defined. To address this issue, we set up an animal model and analyzed how two prime inducers of periodontitis— Porphyromonas gingivalis (Pg) and Aggregatibacter actinomycetemcomitans (Aa)– differ in their pathogenic potential. Our experimental setup included collagen induced arthritis (CIA) in the mouse, oral inoculation with Pg or Aa to induce alveolar bone loss and the combination of both diseases in inverted orders of events. Neither pathobiont impacted on macroscopic arthritis and arthritis did not exacerbate alveolar bone loss. However, there were subtle differences between Pg and Aa with the former inducing more alveolar bone loss if PD was induced before CIA. On a molecular level, Pg and Aa led to differential expression patterns in the synovial membranes that were reminiscent of cellular and humoral immune responses, respectively. The Pg and Aa specific signatures in the synovial proteomes suggest a role for oral pathogens in shaping disease subtypes and setting the stage for subsequent therapy response.