Pain sensitisation in osteoarthritis

Treating chronic musculoskeletal pain, and chronic joint pain (osteoarthritis (OA)) in particular, is challenging as the peripheral and central pain mechanisms are not fully discovered, and safe and as efficient analgesic drugs are not available. In general, the preclinical models of OA are limited to provide fundamental understanding of the pain mechanisms involved in patients with chronic joint pain (1). The pain associated with joint discomfort is highly variable, often underestimated by clinicians, and shows only modest association with crude radiological scorings. One reason for the disconnect between the extent of structural damage and pain is neuroplastic changes occurring in the peripheral and central nervous system resulting in pain sensitisation impacting the patient's experience of pain. In recent years, a variety of human quantitative and mechanistic pain assessment tools (Quantitative Sensory Testing, QST) have been developed, providing new opportunities for diagnostic phenotyping of OA patients and the associated degree of sensitisation. Mechanistic phenotyping has revealed specific subgroups of specifically sensitised OA patients, and been used as a predictive guideline to evaluate which patients are most likely to experience continued chronic pain after an otherwise technically successful knee replacement (chronic postoperative pain). Furthermore, such techniques may be used to profile new or existing drugs together with other e.g. cognitive or behavioural therapies with the potential to manage joint pain.