In an experimental study conducted in arthritic rats, the researchers at McGill university, Canada have found that the nervous system and nerve-growth factor (NGF) play a major role in arthritis.
The study by Longo and colleaguse has been published by Journal of Neuroscience. online on June 12,2013.
Adequate treatments for arthritis are yet to come and existing therapies are not without serious side effect. An effective treatment can be developed only when the process of arthritis is well understood.
Present study determined the importance of nervous system and nerve-growth factor in pain behavior of arthritis.
The findings also support the idea that reducing elevated levels of NGF – a protein that promotes the growth and survival of nerves, but also causes pain may be an important strategy for developing treatment of arthritis pain.
The researchers examined inflammatory arthritis in the ankle joint of rats to look for changes in the nerves and tissues around the arthritic joint.
They did this by using specific markers to label the different types of nerve fibres and allow them to be visualized with a fluorescence microscope.
Normally, sympathetic nerve fibers regulate blood flow in blood vessels. Following the onset of arthritis in the rats, however, these fibers began to sprout into the inflamed skin over the joint and wrap around the pain-sensing nerve fibers instead. More sympathetic fibers were detected in the arthritic joint tissues, as well.
The results also showed a higher level in the inflamed skin of nerve growth factor
The researchers also found that on blocking fibers’ function, a reduction in pain was noticed.
Drugs that aim at preventing the production of elevated levels of NGF in arthritic rats may help in treatment of the condition.
- Study points to role of nervous system in arthritis, McGill Press Newsroom.
- G. Longo, M. Osikowicz, A. Ribeiro-da-Silva. Sympathetic Fiber Sprouting in Inflamed Joints and Adjacent Skin Contributes to Pain-Related Behavior in Arthritis. Journal of Neuroscience, 2013; 33 (24): 10066