Joint pain is a common symptom in various forms of arthritis. Unfortunately, the mechanisms involved in the pathogenesis of joint pain are not well understood, but probably include peripheral and central neural mechanisms. The sympathetic system appears to interact with sensory afferents under pathological conditions, and this may be mediated directly via receptors on sensory neurons, or indirectly via inflammatory mediators. Classical inflammatory mediators such as serotonin and bradykinin appear to activate some nociceptive afferents and serotonin may sensitise these afferents to non-noxious stimuli in an inflamed joint. A purely sensory function has traditionally been ascribed to sensory afferents, but unmyelinated C fibres have in addition a neurosecretory role and release peptides such as substance P which may contribute to inflammation. Lastly, central sensitisation in the spinal cord may play an important role in the pathogenesis of joint pain. Activation of N-Methyl-D-Aspartate (NMDA) receptors and the wind-up phenomenon may be involved in central sensitisation.