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Inflammatory pain and the joint

  • Chapter
Pain and Neurogenic Inflammation

Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

Most of us discover for ourselves that joints have a sensory innervation: twisting an ankle or knee is acutely painful and may lead to longer-lasting pain and inflammation which eventually disappears as the joint heals. We distinguish between sharp transient pain, which signals that damage or potential damage is occurring and initiates a protective reflex, and the less intense but persistent dull inflammatory pain that causes us to immobilise and guard the affected joint while it heals. We thus know from personal experience that different types of “normal” pain exist, and that inflammation is part of the normal healing process. But what provokes the chronic pain of inflammatory joint disorders such as rheumatoid arthritis (RA) where the alarm or protective aspect of pain becomes intolerable and damaging to the suffer-er?

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  1. Department of Neuroscience, University of Edinburgh Medical School, 1 George Square, EH8 9JZ, Edinburgh, Scotland, UK

    Daniel S. McQueen

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  1. Cardiovascular Research Centre, Division of Biomedical Sciences, King’s College London, Manresa Road, SW3 6LX, London, UK

    Susan D. Brain

  2. Messengers and Signalling Group, Division of Biomedical Sciences, King’s College London, Manresa Road, SW3 6LX, London, UK

    Philip K. Moore

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McQueen, D.S. (1999). Inflammatory pain and the joint. In: Brain, S.D., Moore, P.K. (eds) Pain and Neurogenic Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8753-3_8

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  • DOI: https://doi.org/10.1007/978-3-0348-8753-3_8

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