Inflammatory pain pathway

Inflammatory pain forms part of nociception, the system of detecting harmful stimuli by the nervous system, which alerts the body to potential harm. 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.

The hallmarks of inflammatory pain include the decrease in the threshold to nociceptor activation and the hypersensitization of the surrounding area beyond the immediate site of inflammation (flare) to 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.