Pain from the arthritic joint

Abstract

Nociceptive input from the joint is processed in spinal cord neurons which are either only activated by mechanical stimulation of the joint and other deep tissue, e.g. adjacent muscles, or in neurons which receive convergent inputs from joint, muscles and skin. Neurons with joint input show pronounced hyperexcitability during development of joint inflammation (enhanced responses to mechanical stimulation of the inflamed joint as well as to healthy adjacent deep structures, reduction of mechanical threshold in high threshold neurons and expansion of the receptive field). This state of hyperexcitability is maintained during persistent inflammation. The neurons are under strong control of descending inhibition which increases at least during the acute phase of inflammation. Both the induction of inflammation-induced spinal hyperexcitability and its maintenance are dependent on glutamate, substance P, neurokinin A, and CGRP. Spinal prostaglandin E2 supports the induction of spinal hyperexcitability. By contrast, spinal prostaglandin D2 rather attenuates spinal hyperexcitability during established inflammation.