Chronic pain threshold in rheumatoid arthritis may be raised by altering brain chemistry. Pain is a common complaint in rheumatoid arthritis patients but little is known about the mechanisms which contribute to this pain.
In the U.S. alone the cost of treating rheumatoid arthritis is estimated at $128 billion and the condition affects nearly one percent of the population. Treating rheumatoid arthritis (RA) early on can help alleviate the pain felt by patients in the long run.
There is currently no cure for rheumatoid arthritis and so symptom management is the course of treatment which patients undergo. Not only does managing symptoms help alleviate pain but it can also help improve quality of life as well.
In rheumatoid arthritis joint inflammation is a key marker as the cause for pain and yet it has been well observed that pain exists in RA patients even without inflammation being present. Recent research aimed to explain this phenomenon as to why RA patients experience pain without inflammation.
The researchers found that injecting anti-citrullinated protein antibodies (ACPAs) into RA nice patients produces pain behaviors even without the presence of inflammation. ACPAs stimulated release of the chemokine C-X-C motif ligand 1 (CXCL1) from osteoclasts, the cells that resorb bone, while blocking the CXCL1 receptor, CXCR1/2, dampened pain sensitivity.
Marzia Malcangio from King’s College London wrote, “As autoantibodies are present in serum of RA patients even when joint inflammation is controlled, it is conceivable that they maintain pain in RA patients. This study suggests that CXCR1/2 antagonists may exert beneficial effects in the treatment of RA pain.”
Lead researcher, Camilla Svensson, wrote, “Knowing that joint pain is one of the very first signs of RA and that ACPAs also frequently occur in the preclinical phase of the disease made us ask if ACPAs (and other antibodies) can drive pain signaling via mechanisms that are uncoupled from the inflammatory process.”
A recent study found that arthritis patients can raise their pain threshold by altering brain chemistry. The findings come for the University of Manchester where they outlines that pain lasting for six months affects nearly 46 percent of the U.K. population and yet some people cope better with pain than others.
It is well known that the brain has receptors for pain which respond to natural painkilling opiates like endorphins but it is unknown how the receptors help increase pain threshold over the long-term. The researchers found that more opiate receptors in the brain increase pain threshold.
Dr. Christopher Brown said, “As far as we are aware, this is the first time that these changes have been associated with increased resilience to pain and shown to be adaptive. Although the mechanisms of these adaptive changes are unknown, if we can understand how we can enhance them, we may find ways of naturally increasing resilience to pain without the side effects associated with many pain killing drugs.”
Professor Anthony Jones is the director of the Manchester Pain Consortium added, “This is very exciting because it changes the way we think about chronic pain. There is generally a rather negative and fatalistic view of chronic pain. This study shows that although the group as a whole are more physiologically vulnerable, the whole pain system is very flexible and that individuals can adaptively upregulate their resilience to pain.”
“It may be that some simple interventions can further enhance this natural process, and designing smart molecules or simple non-drug interventions to do a similar thing is potentially attractive,” He added.
Professor of Cognitive Neuroscience at the University, Wael El-Deredy concluded, “Receptor imaging is challenging and requires the co-ordination of a large team to collect and analyse the images. We are very lucky to have this technique in Manchester. There are very few places in the world where this study could have been done.”
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