Pain Isnt Just a Symptom of Arthritis
Reported October 01, 2008
(Ivanhoe Newswire) — Pain is often thought to be a debilitating symptom of osteoarthritis. But new research suggests pain is more than a symptom, its a damaging part of the disease itself.
According to a new study, pain signals originate in arthritic joints and the biochemical processing of those signals as they reach the spinal cord actually worsen and expand arthritis. Furthermore, researchers found that nerve pathways that carry pain signals transfer inflammation from arthritic joints to the spine and back again to the joint — causing disease at both ends.
The process of pain signals being transmitted from the sight of origin to the processing centers in the spinal cord and back is called nociception — a type of crosstalk within the body. According to the study, its this crosstalk that enables joint arthritis and inflammation to be transmitted to the spinal cord and brain and consequently spread throughout the central nervous system.
Researchers have identified likely drugs that can interfere with the crosstalk of arthritis pain through inflammatory receptors on sensory nerve cells. This could be an effective new approach to treating osteoarthritis — a condition that affects 21 million Americans.
Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging, Stephanos Kyrkanides, D.D.S., Ph.D., associate professor of Dentistry at the University of Rochester Medical Center, was quoted as saying. 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.
Researchers also believe that if joint arthritis can have an effect on neuro-inflamation, it could have a role in conditions like Alzheimers disease, dementia and multiple sclerosis.
SOURCE: Arthritis and Rheumatism, 2008;58:3100-3109