Beyond inflammation – exploring chronic pain mechanisms in rheumatoid arthritis
In Europe 1 in 5 adults suffer from chronic pain, which is associated with dramatically reduced quality of life for the individual and significant costs for society. Rheumatoid arthritis (RA) is a chronic autoimmune disease with joint pain as a major problem. Recent work has shown that joint pain and presence of autoantibodies may exist for many years before the patient develops the disease.
Antibodies mediates the inflammation that causes joint swelling and destruction of cartilage and bone in RA and the general consensus is that pain in RA is driven by factors produced during the inflammatory process. However, we propose that antibodies, when targeting specific structures such as cartilage, can directly activate pain fibers and thereby act as pain-inducing molecules, completely uncoupled from the inflammatory process. In addition, our pilot data have led us to the hypothesis that neurons express antibody receptors (Fc-gamma receptors) and that long-term activation of these have “nerve-damaging” effects, leading to spinal glial activation and an increased risk to develop a state that resembles neuropathic pain.
We trust our studies to be important as they have potential to:
i) explain the reason for joint pain in early RA
ii) point to mechanisms that drive persistent pain in RA patients that seemingly receive adequate disease control and
iii) provide important clues to pain pathology and reveal novel targets for analgesia, not only in RA, but also other autoimmune diseases.