New research indicates that pain is not a symptom of arthritis; rather it is a cause of the condition.
The study led by University of Rochester Medical Centre suggests that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis.
Moreover, the nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, 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, D.D.S., Ph.D., associate professor of Dentistry at the University of Rochester Medical Centre.
"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.
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In the study conducted using genetically engineered mice, the research team assessed the levels of a pro-inflammatory signalling chemical called interleukin 1-beta (IL-1ß).
The experiments showed that higher levels of the chemical in a peripheral joint caused higher levels IL-1ß 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.
"Our study results confirm that joints can export inflammation in the form of higher IL-1ß along sensory nerve pathways to the spinal cord, and that higher IL-1ß inflammation in the spinal cord is sufficient in itself to create osteoarthritis in peripheral joints," Kyrkanides said.
"We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor," he added.
The study is published in journal Arthritis and Rheumatism.