Although RA has been extensively researched, its cause is still unclear. Studies
in families have shown that susceptibility to the disease is inherited. However, not every predisposed
individual actually develops RA. Researchers suspect that there are external triggering factors such
as bacteria or viruses which may cause onset
of RA.
In patients with RA, the
immune system mistakenly attacks its own joint cartilage. This raises a question like the chicken and
the egg, which came first? In RA, is the misdirected immune response the driving force for cartilage
destruction or merely a reaction to tissue that has already been destroyed (for other reasons)? It is
worth noting that inflammation originates in the synovium and then spreads to other regions of the joint. Successive waves of inflammation lead to the formation of an invasive and erosive (synovial) tissue called pannus. This contains proliferating and destructive inflammatory cells including macrophages which in turn produce
pro-inflammatory cytokines. Cytokines are molecules that act as messengers between immune cells to facilitate
processes such as differentiation, inflammatory mediator release, recruitment of more inflammatory cells
to the site and programmed cell death. Examples of cytokines involved in RA include tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) , interleukin 6 (IL-6) and interleukin 10 (IL-10).
