Headway in understanding DISH arthritis
A long-awaited breakthrough in understanding a common form of arthritis will help pave the way to more effective treatment that has eluded scientists until now. The second-most common form of arthritis after osteoarthritis is "diffuse idiopathic skeletal hyperostosis" or DISH, a degenerative variant characterised by the formation of excessive mineral deposits along the sides of the vertebrae in the neck and back.
Symptoms include spine pain and stiffness and in advanced cases difficulty swallowing and damage to spinal nerves. The cause is unknown and there are no specific treatments. It affects between six and 12 percent of North Americans, usually people older than 50 years, according to the Arthritis Society, the Journal of Bone and Mineral Research reports.
Now researchers at Western University's Bone and Joint Initiative, with collaborator Doo-Sup Choi at the Mayo Clinic in Rochester, Minnesota, have discovered the first-ever mouse model of this disease, according to a Western statement.
"This model will allow us for the first time to uncover the mechanisms underlying DISH and related disorders. Knowledge of these mechanisms will ultimately allow us to test novel pharmacological treatments to reverse or slow the development of DISH in humans," says study co-author Cheryle Seguin of the department of physiology and pharmacology at Western.
Graduate student Derek Bone, working under the supervision of pharmacologist James Hammond, was studying mice that had been genetically modified to lack a specific membrane protein that transports adenosine when he noticed that these mice developed abnormal calcification (mineralisation) of spinal structures.
Their findings established that spinal mineralisation in these mice resembles DISH in humans and point to a role for adenosine in causing abnormal mineralisation in DISH.