Rheumatoid Arthritis Clinical Trial
Official title:
Study of the Articular Microbiota in Rheumatoid Arthritis.
The cause of rheumatoid arthritis (RA) remains unknown, although major advances have been
done these last ten years in the comprehension of its pathophysiology.
The aim of this study is to described a synovial microbiota specific for rheumatoid
arthritis.
The cause of rheumatoid arthritis (RA) remains unknown, although major advances have been
done these last ten years in the comprehension of its pathophysiology. One of the most
significant discoveries was the post-translational modification of various self-proteins
resulting in the replacement of arginine residues by citrulline. This conversion results in
modifications of the basic charge of the peptides, of its primary and secondary structure,
and the transformed peptides can then bound to some HLA-DR molecules (HLA-DR4, HLA-DR1), that
are the best well known genetic factors of rheumatoid arthritis (RA). This leads to
immunization to citrullinated peptides in genetically predisposed patients, which is now
identified as the most characteristic auto-immun phenomenon of RA. Anti-citrullinated peptide
antibodies (ACPA) have become the most relevant biologic test for the diagnosis of RA.
The conversion to citrulline is due to the action of an enzyme, the peptidyl arginine
deiminase (PAD). Endogenous PADs have been identified in humans, but their activation needs
high concentrations of calcium in the cells that are not physiological. Thus, the activation
of self-PADs occurs only in extreme conditions, such as apoptosis, or major stresses
resulting from toxic or infectious process. But some bacteria also contain PADs that are
involved in their energetic metabolism. Two main factors have yet been identified to lead to
citrullination of self-peptides and are now recognized as important environment risk factors
for RA: smoking and periodontitis. Periodontitis is the consequence of an infection that is
mainly due to Porphyromonas gingivalis, one of the bacteria processing a PAD. These facts
reinforce the old hypothesis of an infectious origin of RA.
However, all RA patients are neither smoker nor affected by periodontitis, and many other
bacteria have PADs and may be involved in the pathophysiology of RA. Moreover, it has been
demonstrated that citrullination process and ACPA production can precede RA for years, while
the citrullination and ACPA production are located to a mucous membrane (oral, pulmonary…).
How these processes reach the joint remains a mystery.
The hypothesis is that the involved bacteria translocate to the joint, inducing local
citrullination of synovial peptides, inflammation and production of ACPA within the joint,
and resulting in arthritis.
The aim of this study is to demonstrate this translocation of bacteria in the synovium, and
to described a synovial microbiota specific for rheumatoid arthritis .
Pilot study, including only few patients, just to demonstrate the validity of the
translocation concept and the performance of the procedures.
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