Researchers have found the molecular mechanism associated with development of osteoarthritis pain. The discovery may lead to better understanding and hopefully newer treatments for the painful condition.

Osteoarthritis is the most common form of arthritis. The condition causes pain and swelling in the joints, usually hands, knees, hips or spine. Osteoarthritis breaks down cartilage-the slippery tissue that covers the ends of bones in a joint. Loss of cartilage leads to rubbing of the bones in the joint that can cause bone deformity.

"Clinically, scientists have focused on trying to understand how cartilage and joints degenerate in osteoarthritis. But no one knows why it hurts," said Dr. Anne-Marie Malfait, associate professor of biochemistry and of internal medicine at Rush, who led the study, in a news release.

Researchers from Rush University Medical Center along with researchers at Northwestern University studied the progression of osteoarthritis in surgical mouse models. The team was able to monitor both pain behaviors and molecular mechanisms in neurons of the knee.

Researchers examined the development of pain that occurred with changes in dorsal root ganglia (DRG) - nerves that carry information from sensory organs to the brain. Study analysis found that chemokine called monocyte chemoattractant protein (MCP)-1 (CCL2) and its receptor, chemokine receptor 2 (CCR2), were associated with pain in the development of osteoarthritis. Previous research found that MCP-1/CCR2 is associated with pain that occurs after a nerve injury. MCP-1 is associated with regulation of migration and infiltration of monocytes into tissues where they restore macrophages that fight an infection.

The study mice had a temporary increase in levels of MCP-1, CCR2 mRNA and protein, and neuronal signaling activity was also elevated in the DRG at eight weeks after surgery. These mice also tended to avoid behaviors like walking or climbing.

Mice that lacked CCR2, too had osteoarthritis. However, these mice did not have behavioral changes that were seen in the mice that had CCR2.

Surprisingly, levels of MCP-1 and CCR2 reduced to normal levels by 16 weeks. Researchers believe that MCP-1 and CCR2 only initiates the changes in DRG.

The study is published in the journal Proceedings of the National Academy of Sciences.

According to Centers for Disease Control and prevention, arthritis causes disability in 21 million people in the U.S. There is no cure for the disease.