Mechanisms of pain in RA

Primary articular nerves consist of unmyelinated (IV, C fibers 80%) and myelinated (III, AS and II A(, 20%) fibers. A( fibers end in corpuscles. AS and C fibers are free nerve endings; in the normal joint these are widely distributed throughout the synovium, capsule, ligaments and bone. The synovial membrane is not only richly innervated with C fibers but also with sympathetic nerves, whereas cartilage has no innervation at all. In RA there is a loss of C fibers from the synovium, possibly due to the rapid growth of

Figure 10.2 X-ray changes of RA.

synovial tissue outstripping the capacity of the nerve supply. This results in a drop-out in laminae I and II of the dorsal horn. A( (proprioceptive) fibers replace the pain fibers in these laminae so normal joint movement can be perceived as pain.

Inflammation, such as that seen in RA, has little effect on A( fibers but AS and C become sensitized with an increased response to movement or pressure. Previously "silent" fibers develop mechanically sensitive fields so that simply moving the joint results in stimulation of pain afferents. The mechanisms responsible for this sensitization are complex and involve many mediators such as bradykinin and prostaglandins; hence the effect is blocked by aspirin and other NSAIDs. Peripheral sen-sitization also results in spinal cord changes, leading to expanded receptive fields so that a spinal neurone responds to stimuli from a wider area. Opioid receptors are found in the synovium and their expression may be increased with inflammation of the joint.

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