Clinical pain severity and experimental pain sensitivity in osteoarthritis

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Pain is the most common presenting symptom of osteoarthritis and an important outcome in most osteoarthritis intervention trials. However, the causes of pain among osteoarthritis patients are not well-understood, and studies of pain mechanisms have been limited. To date, most studies have relied on visual analog scales of overall pain or patient-reported pain at joint sites, but these measurements are subjective and prone to bias. Although osteoarthritis is often defined structurally by cartilage loss and joint space narrowing, population-based studies have indicated that the association between joint space narrowing and patient-reported pain is weak. Recent studies, however, suggest that correlations between structural changes and pain may be masked by other factors, such as central pain processing mechanisms, which differ between patients. To examine pain mechanisms, some studies have utilized quantitative sensory testing techniques, which rely on the application of defined, noxious, experimental stimuli to determine pain threshold and tolerance levels. These studies suggest that, compared to pain-free controls, osteoarthritis patients are more sensitive to experimental noxious stimuli at both joint and non-joint sites, indicating diffuse hyperalgesia, characteristic of central pain syndromes. Studies using quantitative sensory testing methods and functional neuroimaging have also indicated that osteoarthritis patients have impairments in conditioned pain modulation, also known as descending analgesia or diffuse noxious inhibitory controls. This talk will give an overview of the study of pain mechanisms in osteoarthritis, focusing on studies of experimental pain sensitivity in osteoarthritis patients, and the implications of these studies for future research and for the development of pain management strategies in osteoarthritis.