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Inflammatory pain forms part of nociception, the system of detecting harmful stimuli by the nervous system, which alerts the body to potential harm.
Inflammatory pain – an overview
Nociceptors are excitatory neurons with free nerve endings that branch out from the axon and innervate parts of the dermis and epidermis. They are responsible for "translating" noxious signals into action potentials.
Some of the hallmarks of inflammatory pain are the decrease in the threshold to nociceptor activation and the hypersensitization of the surrounding area even beyond the immediate site of inflammation (flare) to even innocuous stimuli (eg, sensitivity to touch).
At the cellular level, substance P and other neuropeptides released at the site of injury stimulate cytokines' secretion by resident immune cells (eg, Langerhans and mast cells). These, in turn, cause vasodilation (reddening) and plasma extravasation (swelling). Many secreted molecules also act directly or indirectly on nociceptor ion channels and receptors, resulting in hypersensitization.
What to expect
This pathway poster presents an overview of the cellular events at the injury site and the mechanisms of inflammatory nociceptor hypersensitization.