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Rheumatology Advance Access originally published online on June 14, 2005
Rheumatology 2005 44(9):1090-1096; doi:10.1093/rheumatology/keh640
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

REVIEW

Mechanisms of inflammation in gout

N. Dalbeth and D. O. Haskard

Eric Bywaters Centre, Faculty of Medicine, Imperial College London, Hammersmith Campus, Du Cane Rd, London W12 0NN, UK.

Correspondence to: D. Haskard. E-mail: d.haskard@imperial.ac.uk

The first 150 words of the full text of this article appear below.


   Introduction
 
The clinical manifestations of gout are due to interactions between monosodium urate (MSU) crystals and local tissues. This review article outlines recent advances in the understanding of the mechanisms of inflammation in gout. We focus on the cellular response to MSU crystals during acute arthritis, termination of the acute attack and maintenance of asymptomatic hyperuricaemia, and chronic tophaceous disease. We then propose a unifying model of gout involving the differential role of mononuclear phagocytes in the regulation of the inflammatory response to MSU crystals.


   The acute gout attack
 
Initiation of the acute gout attack
The acute attack of gout has all the hallmarks of an acute inflammatory response. Histological examination of the synovium in acute gout shows lining layer hyperplasia and intense infiltration of the membrane by neutrophils, mononuclear phagocytes and lymphocytes [1, 2]. Acute attacks of gout are often triggered by specific events, such as trauma, surgery, intercurrent illness, excess alcohol intake or drugs that alter . . . [Full Text of this Article]

Leucocyte recruitment
Amplification
Complement
Kininogen
Cellular amplification
Pain in the acute gout attack

   Termination of the acute attack and maintenance of asymptomatic hyperuricaemia
 
Stages of the inflammatory response in skin
Mediators of the resolution phase in acute gout
Changes in proteins that coat MSU crystals
Melanocortins
Peroxisome proliferator-activated receptor {gamma}
The role of monocyte-macrophage differentiation

   Tophaceous gout
 

   Conclusion
 

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