In the past, pain mechanisms in osteoarthritis (OA) have received surprisingly little attention, although this is now changing. Attempts to discriminate between OA and other rheumatologic disorders, such as rheumatoid arthritis, through verbal descriptions of pain have generally proved unsuccessful as the patterns of pain often overlap. Use-related pain in OA is common but rest pain and night pain sometimes occur, and a variety of patterns of pain are described by different patients, varying from a dull ache to sharp, stabbing pains. It seems probable that a variety of different mechanisms contribute to symptoms in this disorder and that the relative importance varies among individuals.
The presence and severity of joint pain correlate poorly with structural evidence of joint damage. Current evidence suggests that OA joint damage predisposes to pain, but that little correlation between pain severity and the extent of joint damage exists. The probable explanation of these observations lies in that fact that pain perception arises in response to a complex series of underlying neurophysiologic events involving transduction of stimuli, transmission of encoded information, and subsequent modulation of this activity at both peripheral and more central levels. In all but acute situations, the relation between tissue injury and resultant symptoms becomes less well defined and more susceptible to extraneous influences originating both within and external to the individual.
Minor injuries or damage within the joint produce short lived excitation of specialized high threshold nociceptors with brief, spatially localized pain. More severe tissue damage associated with the release of inflammatory mediators produces not only direct nociceptor excitation, but also modified response properties to subsequent stimuli (peripheral sensitization). Under these circumstances, the response to a noxious stimulus becomes exaggerated. Alternatively, normally innocuous stimuli such as standing or walking may produce pain.
HSS Journal, an academic peer-reviewed journal published three times a year, February, July and October. The Journal accepts and publishes peer reviewed articles from around the world that contribute to the advancement of the knowledge of musculoskeletal diseases and disorders.