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Highly Accessed Review

Arthritis and pain. Future targets to control osteoarthritis pain

Andy Dray1* and Simon J Read2

Author affiliations

1 AstraZeneca R&D Montreal, Frederick Banting St, Montreal H4S 1Z9, Canada

2 AstraZeneca R&D, Mereside, Alderley Park, Macclesfield, Cheshire SK10 4TG, UK

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Citation and License

Arthritis Research & Therapy 2007, 9:212  doi:10.1186/ar2178

Published: 30 May 2007

Abstract

Clinical presentation of osteoarthritis (OA) is dominated by pain during joint use and at rest. OA pain is caused by aberrant functioning of a pathologically altered nervous system with key mechanistic drivers from peripheral nerves and central pain pathways. This review focuses on symptomatic pain therapy exemplified by molecular targets that alter sensitization and hyperexcitability of the nervous system, for example, opioids and cannabinoids. We highlight opportunities for targeting inflammatory mediators and their key receptors (for example, prostanoids, kinins, cytokines and chemokines), ion channels (for example, NaV1.8, NaV1.7 and CaV2.2) and neurotrophins (for example, nerve growth factor), noting evidence that relates to their participation in OA etiology and treatment. Future neurological treatments of pain appear optimistic but will require the systematic evaluation of emerging opportunities.