Pain More a Cause of Arthritis Than a Symptom
Nerve cells may help spur inflammation, study shows
MONDAY, Sept. 29, 2008 (HealthDay News) -- The pain caused by osteoarthritis may be as damaging as the disease itself, according to a new study.
According to a University of Rochester study published Monday in the journal Arthritis & Rheumatism, the nerve pathways carrying pain signals between the arthritic joints and the spinal cord transfer inflammation to the spine and surrounding cells and back again.
"Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging," Stephanos Kyrkanides, associate professor of dentistry at the school's Medical Center, said in a university news release. "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."
The study gives strong evidence that this two-way "crosstalk" may first enable joint arthritis to transmit inflammation into the spinal cord and brain, eventually leading to it spreading through the central nervous system.
The researchers genetically engineered mice to study levels of a pro-inflammatory signaling chemical called interleukin 1-beta. Their experiments showed that higher levels of the chemical in a peripheral joint caused higher levels to be produced in the dorsal horns of the spinal cord and in spinal cord cells called astrocytes, which cause more osteoarthritic symptoms in joints.
In the mouse experiments, shutting down the signaling reversed the crosstalk effects. Some existing arthritis drugs, such as Kineret (anakinra), block the ability of interleukin 1-beta to send a pain signal through its specific nerve cell receptor, and Kyrkanides' group is experimenting with them as in osteoarthritis treatment.
The Arthritis Foundation has more about osteoarthritis.