Researchers including an Indian origin have discovered the first-ever mouse model of "diffuse idiopathic skeletal hyperostosis" or DISH - the second most common form of arthritis after osteoarthritis.
This breakthrough could lead to a better understanding of the disease that until now has eluded scientists.
DISH affects between six and 12 percent of North Americans, usually people older than 50. It is classified as a form of degenerative arthritis and is characterized by the formation of excessive mineral deposits along the sides of the vertebrae in the neck and back. Symptoms of DISH include spine pain and stiffness and in advanced cases, difficulty swallowing and damage to spinal nerves. The cause of DISH is unknown and there are no specific treatments.
The first-ever mouse model of this disease was identified by researchers at Western University's Bone and Joint Initiative, with collaborator Doo-Sup Choi at the Mayo Clinic in Rochester, Minnesota.
"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," said corresponding author Cheryle Seguin of the Skeletal Biology Laboratories and the Department of Physiology and Pharmacology at Western's Schulich School of Medicine and Dentistry.
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 (mineralization) of spinal structures.
Changes in the backbone of these mice were characterized by an interdisciplinary team which included: Sumeeta Warraich, Diana Quinonez, Hisataka Ii, Maria Drangova, David Holdsworth and Jeff Dixon.
Their findings established that spinal mineralization in these mice resembles DISH in humans and point to a role for adenosine in causing abnormal mineralization in DISH.'
Their work has been published online in the Journal of Bone and Mineral Research.(ANI)