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/ Health News / 2008 / September 2008 / September 30, 2008 Pain is more a cause of arthritis than a symptom |
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How cancer prevention drives aging
For the first time, researchers have found how cellular senescence, the well-known mechanism for preventing cancer, can trigger aging and age-related disease by changing the local tissue environment. ANI
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A new study has revealed that psychiatric disorders appear to be common among 18- to 24-year-olds, with overall rates similar among those attending or not attending college. ANI
Pain is not a symptom of arthritis, it is a cause of the condition, according to a new research.
Washington, Sept 30 : Pain is not a symptom of arthritis, it is a cause of the condition, according to a new research.
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.
The research team found that the two-way "crosstalk" might first enable joint arthritis to transmit inflammation into the spinal cord and brain, eventually leading to it spreading through the central nervous system.
"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.
The common ground between arthritis and dentistry: the jaw joint is a common site of arthritic pain.
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.
ANI
