Research Profile - Why does arthritis hurt so much?
Dr. James Henry
A team of Canadian researchers is studying the genetic roots of osteoarthritis and the pain it causes.
Ask any arthritis sufferer what they find most difficult about their illness, and they'll tell you it's the constant physical pain. According to a National Population Health Survey, 80% of people with arthritis take some type of painkiller. And yet, there has been very little research examining why arthritis hurts so much.
Dr. Frank Beier
That's why the Canadian Institutes of Health Research (CIHR) and the Canadian Arthritis Network came together to fund a team of researchers who are studying how nerves behave in joints affected by osteoarthritis (OA).
According to Dr. James Henry, a neurophysiologist at McMaster University and one of the leading members of the research team, OA pain could be the result of nerve cells taking on new roles.
"Much of the pain that OA sufferers experience could be neuropathic pain, or pain that results from the activation of nerves that are not normally pain receptors," explains Dr. Henry. "This could explain why much OA pain is so poorly managed, because neuropathic pain responds poorly to normal pain treatments."
At a Glance
Who: Dr. James Henry at McMaster University and Drs. Frank Beier, Suzanne Bernier and David Holdsworth at the University of Western Ontario.
Issue: Chronic pain is a major problem for people with osteoarthritis, but researchers have much to learn about the source of this pain and how to treat it.
Solution: These CIHR-funded researchers developed a new animal model that is improving our understanding of how nerves behave in arthritic joints.
Impact: Their research could lead to improved pain treatments for people with osteoarthritis.
Dr. Henry's research suggests that unusual chemical conditions in the joint cause sensory neurons that do not normally detect pain to suddenly start sending pain signals to the spinal cord and brain.
"We're not sure yet what causes this change, but we suspect it has something to do with a change in which genes are being expressed in the nerve cells," says Dr. Henry. "We should know soon which genes are being affected."
To identify these genes, Dr. Henry and his team are using a special animal model, a rat that shows many of the same symptoms as a person with OA. This model was developed in Dr. Henry's research group and became the basis for a CIHR-funded, multidisciplinary team of researchers that originally included Dr. Henry, as well as Dr. Frank Beier, Dr. David Holdsworth and the late Dr. Suzanne Bernier at the University of Western Ontario. Together, they used the model to begin uncovering the causes of pain and fatigue in OA.
For example, Dr. Beier has been working with this animal model to identify genes involved in cartilage development and breakdown. He and his colleagues at the University of Western Ontario have been studying genetic material from the joints of these arthritic rats. Through this study, they hope to figure out which genes are active and which genes aren't, and compare this to gene activity in non-arthritic joints. The team faces a large task.
"We are looking at all of the approximately 20,000 genes in the rat," says Dr. Beier. Their research will provide a better genetic picture of why OA develops and causes pain. With the help of a CIHR Community Alliances for Health Research grant, Dr. Henry will translate these findings into better diagnostic tests and treatments for the disease.
"We've already identified genes that are promising targets for diagnosing and slowing the progression of OA," says Dr. Beier. "We are now validating these targets in mice and rats, and we hope to eventually study these genes in humans."