Figure 1.

Peripheral and central mechanisms of pain sensitization in inflammatory arthritis. Synovitis can induce the production of molecules responsible for both nociception and neuropathic pain (through the damage of the nerves and the recruitment of macrophages in the nerves themselves and in the dorsal root ganglion). Repeated nociceptive stimuli can modify the function of the diffuse noxious inhibitory control (DNIC), with augmented pain perception as a consequence. Inflammatory cells stimulate, at the level of the central nervous system, the glial cell proliferation. Glial cells in turn provoke neural alterations responsible, at least in part, for hyperalgesia and allodynia. Pain sensitization is also strongly influenced by the psychological baggage.