Mease PJ, Hanna S, Frakes EP, and Altman RD Pain mechanism in osteoarthritis: Understanding the role of central pain and current approaches to its treatment. J Rheumatol 2011;38:1546-1551
- There is often discordance between the degree of articular pathology and pain experienced by patients with OA, suggesting the presence of individual variability in the central processing of nociceptive stimuli.
- Activation of central nociceptive pathways without involving peripheral nociceptrors can also generate pain.
- Although a key pathologic hallmark of OA is abnormal articular cartilage, cartilage is avascular and hence aneural. Therefore, damaged articular cartilage is incapable of directly generating the pain of OA.
- Inflammation in the joint triggers a cascade of events, resulting in peripheral sensitization, increased sensitivity of nociceptive primary afferent neurons, and hyperexcitability of nociceptive neurons in the central nervous systems.
- While pain associated with OA has long been considered nociceptive pain coupled with local inflammatory mechanism, there is a growing hypothesis that neuropathic mechanisms may also be contributing to the pain experience in some patients with OA.
- Central sensitization is defined as a state in which neurons activated by nociceptive stimuli are sensitized by such stimuli and become hyperresponsive to subsequent stimuli to the neuron’s receptor fields. Peripheral sensitization is thought to play an important role in the development and maintenance of central sensitization.
- Central sensitization contributes ot the temporal, spatial and threshold changes and the generation of pain hypersensitivity experienced in acute and chronic pain settings.
- Persistent nociceptive input from an osteoarthritic joint is believed to result in central sensitization.
- These results are consistent with the hypothesis that central sensitization and perhaps spinal glial cell activation contribute to pain sensitivity and modulation in OA.
- Evidence suggests that genetic variations, such as low COMT enzyume activity, may increase sensitivity to pain.
- In 2 randomized, double-blind, placebo-controlled trials, patients with OA of the knee treated with an SNRI had a significantly greater reduction in pain compared with placebo, and also demonstrated improvement in function.
- OA is characterized by degenerative and inflammatory processes affecting joints and surrounding tissues, which are clinically manifested by pain and functional disability. Pain manifestations in OA are thought to be driven by joint pathophysiology and abnormal excitability in peripheral and central pain pathways.
