The second most common form of arthritis after osteoarthritis is 'diffuse idiopathic skeletal hyperostosis' or DISH.
Researchers at Western University and the Mayo Clinic in Rochester were studying mice that had been genetically modified to lack a specific membrane protein that transports adenosine and found that these mice developed abnormal calcification (mineralisation) of spinal structures.
Changes in the backbone of these mice were characterised by an interdisciplinary team, which included Indian-origin graduate student, Sumeeta Warraich, technician, Diana Quinonez, postdoctoral fellow, Hisataka Ii, imaging scientists Maria Drangova and David Holdsworth, and skeletal biologist, Jeff Dixon.
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.
DISH is classified as a form of degenerative arthritis and is characterised by the formation of excessive mineral deposits along the sides of the vertebrae in the neck and back.
The cause of DISH is unknown and there are no specific treatments.
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"This model will allow us for the first time to uncover the mechanisms underlying DISH and related disorders," said corresponding author Cheryle Seguin at Western's Schulich School of Medicine & Dentistry.
"Knowledge of these mechanisms will ultimately allow us to test novel pharmacological treatments to reverse or slow the development of DISH in humans," Seguin said in a statement.
The research was published in the Journal of Bone and Mineral Research.