Not merely a symptom, pain may cause arthritis

Washington, September 30: Joint pain is widely known as one of the prime symptoms of arthritis. But a new study has revealed that pain is more than a symptom of osteoarthritis, saying that it is a cause of the condition.

The study led by University of Rochester Medical Centre suggests that pain itself may be what makes the disease worst. There is a burst of chemical signals in the spine when a pain signal from an arthritic joint reaches there, worsening and expanding arthritis, the study explains.

More specifically, the study revealed that the spine becomes inflamed in the area where the nerve from the joint attaches due to this burst of signals. The nerve pathways carrying pain signals between the arthritic joints and the spinal cord transfer inflammation to the spine and then travel backward from the spine to the joint, causing disease at both ends.

"Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging," said Stephanos Kyrkanides, DDS, PhD, associate professor of dentistry at the school's Medical Center, and lead author of the study.

"Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing and suggests the mechanisms behind the effect," said
Kyrkanides.

Kyrkanides and colleagues, who reported their findings on Monday in the journal Arthritis and Rheumatism, say their research provides strong evidence that two-way "crosstalk" may first enable joint arthritis to transmit inflammation into the spinal cord and brain, and then lead it to spread through the central nervous system (CNS) from one joint to another.

"This cross talk is oil to the fire of arthritis," said Kyrkanides. "Trying to stop joint inflammation with the traditional drugs we have is inadequate because it tries to address the joint but fails to address this newly discovered mechanism where pain is progressing along the nerve from the spine."

To reach their findings, Kyrkanides and colleagues used genetically engineered mice and studied levels of a pro-inflammatory signaling chemical called interleukin 1-beta (IL-1B). In lab trials, the researchers found that after treating the arthritic mice with a gene therapy to block the chemical messenger, IL-1B the mice stopped their pain behavior and got their joints better.

"It proves the processing of pain in the joint actually contributes to arthritis itself," Kyrkanides says. "We were very impressed to see we could control arthritis progression and allow for spontaneous healing if, by targeting IL-1B, we could control the pain at the spinal cord or along the sensory nerves."

After the successful mouse experiments, Kyrkanides and colleagues are working on a gene therapy that could be used in humans. However, some existing arthritis drugs, such as Kineret (anakinra), already target relevant chemical signals along the pain circuit.

About Arthritis
Arthritis is a term that covers a number of conditions characterized by inflammation of the joints, usually accompanied by pain, swelling, and stiffness, and resulting from infection, trauma, degenerative changes, metabolic disturbances, or other causes.

The most common form of arthritis is Osteoarthritis (OA), which results from degeneration and wearing away of articular cartilage, a part of the joint that cushions the ends of the bones and allows easy movement of joints.

Known as the “wear-and-tear” kind of arthritis, OA is a chronic condition characterized by the breakdown of the joint’s cartilage. The breakdown of cartilage causes the bones to rub against each other, causing stiffness, pain and loss of movement in the joint.