Inflammation and tissue damage in crystal deposition diseases.
OBJECTIVE
The crystal-induced arthropathies are characterized by self-limiting episodes of acute inflammation and chronic tissue damage. This review summarizes recent advances in the understanding of the cellular responses to monosodium urate, calcium pyrophosphate dihydrate and basic calcium phosphate crystals.


RESULTS
Factors such as the myeloid related proteins, endothelin-1 and the complement membrane attack complex have been recently identified as mediators of acute crystal-induced inflammation. In addition, signalling pathways involved in both acute inflammation and tissue damage in crystal arthropathies have been further clarified. The potential of macrophage-derived transforming growth factor beta1 to play a key role in the resolution phase of acute gout has also been demonstrated.


CONCLUSIONS
Recent work has provided new insights into the regulation of both acute and chronic articular responses to inflammatory microcrystals. Further analysis of these responses may identify potential therapeutic targets for management of the crystal-induced arthropathies.
Dalbeth
Nicola
N
Eric Bywaters Centre, Faculty of Medicine, Imperial College London, Hammersmith Campus, London, UK.
Haskard
Dorian O
DO
D002130:Calcium Phosphates / Q000378:metabolism; D002131:Calcium Pyrophosphate / Q000378:metabolism; D002805:Chondrocalcinosis / Q000378:metabolism / Q000473:pathology*; D018450:Disease Progression; D006073:Gout / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007596:Joints / Q000378:metabolism / Q000473:pathology*; D014527:Uric Acid / Q000378:metabolism
D002130:Calcium Phosphates; D014527:Uric Acid; C020243:calcium phosphate; D002131:Calcium Pyrophosphate