Major step in Rheumatoid Arthritis?

Introduction
The etiology of rheumatoid arthritis (RA) is unknown,
but both environmental and genetic factors are likely to
play roles in its pathogenesis. Periodontal disease (PD),
an inflammatory disease of tooth-supporting structures,
may be an environmental trigger for RA. Compared
with healthy controls, PD is more frequent in RA
patients, both in those with new-onset and in those with
long-standing disease, even when potential confounding
factors such as smoking are taken into account [1-5].
Furthermore, there is increasing evidence of a role for
PD pathogens, particularly Porphyromonas gingivalis (Pg),
in RA pathogenesis. Pg is the only prokaryote known to
possess a peptidylarginine deiminase (PAD), an enzyme
that catalyzes the posttranslational modification of arginine residues to citrulline. Although citrullination may
occur more generally in sites of inflammation, antibodies
to citrullinated proteins (anti-cyclic citrullinated peptide
(anti-CCP) antibodies) are specific for RA and are now
valuable diagnostic markers for the disease [6]. CCP antibodies are associated with a more aggressive course [7]
and may be detected prior to the onset of clinical disease
[8], suggesting a role in RA pathogenesis. Pg, through its
PAD enzyme, may citrullinate host or bacterial proteins
[9], altering their antigenicity and triggering autoimmunity
and RA in predisposed individuals [9,10]. Further support
for this hypothesis comes from animal models. Pg enolase
has been found to cause arthritis in DR4-IE-transgenic
mice [11], and Pg infection has been shown to exacerbate
collagen antibody-induced arthritis [12].

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