Joints are richly innervated with a range of sensory nerve fibres that convey information to the central nervous system about forces exerted on articular tissues by both low and high threshold mechanical stimuli. High threshold nociceptive afferents terminate primarily in the synovium and periosteum, and normally respond only to movement of the joint beyond the working limits. Following joint damage, two factors combine to alter the mechanical sensitivity of articular nociceptors. Firstly, physical changes (joint effusion and tissue oedema) alter the resting and movement-induced forces exerted on the joint tissues and secondly, inflammatory mediators released within the damaged tissue sensitize articular nociceptive afferents by binding to receptors on the nerve endings. These factors result in a reduction of the mechanical threshold for activation of articular nociceptors such that manipulation of the joint within the normal range is easily sufficient to activate them. Acute and chronic animal models of joint inflammation have been used to study the mechanisms of articular nociceptor sensitization and a number of inflammatory mediators and their receptors have been implicated. The focus of this paper will be to introduce some of the important issues involved in the sensitization of nociceptive articular afferents.