Peripheral and Central Mechanisms in Chronic Joint Pain

In the individual patient with osteoarthritis (OA) little association is found between joint damage and pain as peripheral/central sensitisation amplify the nociceptive drive. The degree of centralised sensitisation (spreading extra-segmental sensitisation), descending pain control, and central temporal/spatial integration are some of the individual factors explaining the disconnect between joint damage and the pain intensity perceived. Although the peripheral sources of pain in OA are not well understood we know that continuous nociceptive barrage from joint and extraarticular nociceptors will provoke centralised sensitisation. It has consistently been shown that pain intensity, pain durations, and number of OA locations are important drivers for such central sensitisation in OA. Various animal models of OA have been established investigate the consequences of experimental OA on central nociceptive processing but many of those studies do not translate very well into humans. Better understanding of the individual fundamental pain mechanisms may improve patient profiling, help individualising management, suggest new treatment options and thereby advance development of new therapies.

Techniques for assessing sensitisation in OA have been developed and provide opportunities to quantify pain mechanisms and hence phenotype OA patients. Such biomarkers have recently also been used to predict pain outcomes after e.g. total knee replacement surgery.