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Last updated: Sun, Aug 4, 2024
Pain that originates in joints has many of the characteristics of other deep tissue pain. It is often dull and aching and poorly localized.
Pain from OA can have additional qualities, since OA eventually can lead to damage to bone and bone marrow. Although OA is considered to be a “non-inflammatory” form of arthritis, in fact the fluids in a joint damaged by OA are rich in inflammatory chemicals including cytokines, and various researchers have found such joints to contain inflammatory immune system cells.1 About one-third of C fiber mechanical sensors have a normal pressure threshold so high that they are called “silent nociceptors” or “mechanically-insensitive.” These fibers become active in an inflammatory environment, increasing pain. During inflammation, immune cells can invade the dorsal root ganglia, leading to generalized mechanical and thermal hyperalgesia in the tissues serviced by the affected spinal nerve.2
Although short-term pain causes spinal motor reflexes to be enhanced, long-term inflammation may cause them to be inhibited, possibly contributing to the muscle shrinkage and loss of strength that accompanies joint disease.3 Although short-tern inflammation causes an increase in descending inhibition of pain, in long-term inflammation descending inhibition becomes inadequate and descending excitation may instead expand the receptive field into healthy areas.4
Researchers have noticed marked differences in the processing of painful signals in the brains of experimental animals with diseased joints, but it is not known whether this is the result of neuroplastic changes in the brain, or simply a reflection of the changes in the spinal cord. Imaging studies of human OA patients show loss of gray matter in the thalamus and cortex. These losses can, however, be largely recovered if the arthritic joint is replaced.
The central nervous system can actually work to increase inflammation in joints. This phenomenon is called neurogenic (nerve-caused) inflammation. Sensory neurons release inflammatory neuropeptides into joint tissue when they are subjected to noxious stimulation, as is the case with cutaneous injury (see The Pain System in Acute Injury). These chemicals can increase the migration of inflammatory immune-system cells into the joint. Neurons of the sympathetic nervous system release epinephrine and norepinephrine directly into tissues, while sympathetic release of these same substances from the adrenal glands affects the entire body. During chronic inflammation the body releases less cortisol, less testosterone, and less androgen from the adrenal gland. Since these substances all help to suppress inflammation, this restriction of output may tend to prolong and worsen inflammation and the pain that accompanies it.