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Rheumatology Advance Access originally published online on March 31, 2003
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Rheumatology 2003; 42: 784-790
© 2003 British Society for Rheumatology

Haemoglobin-derived iron-dependent hydroxyl radical formation in blood-induced joint damage: an in vitro study

M. J. J. Hooiveld1,2, G. Roosendaal2, H. M. van den Berg2, J. W. J. Bijlsma1 and F. P. J. G. Lafeber1,

1 Rheumatology and Clinical Immunology and
2 Van Creveldkliniek (National Hemophilia Center), University Medical Center Utrecht, Utrecht, The Netherlands

Objective. It has been reported that joint bleeds cause cartilage damage and that the combination of red blood cells (RBC) plus mononuclear cells (MNC) causes the adverse effects. The present study is to elucidate the mechanism by which blood, as present in whole blood, may cause this cartilage damage.

Methods. Human cartilage samples were cultured for 4 days in the presence of 50% whole blood, isolated MNC plus RBC, CD14+ cells (monocytes/macrophages) plus RBC, or lysed RBC with interleukin 1ß (IL-1ß; a major catabolic product of activated monocytes/macrophages). Antioxidants were used to investigate the involvement of oxidative stress. A subsequent 12-day culture period in the absence of additions is referred to as the recovery period. Changes in cartilage proteoglycan synthesis were determined at days 4 and 16.

Results. Cartilage cultured in the presence of whole blood, MNC plus RBC, or monocytes/macrophages plus RBC resulted in a prolonged inhibition of proteoglycan synthesis (>90% inhibition at day 16; all three P<0.05). Lysed RBC together with IL-1ß also induced prolonged inhibition of proteoglycan synthesis (>56% of controls, P<0.05). Dimethylsulphoxide (DMSO), scavenging hydroxyl radicals, could reverse the inhibition of cartilage proteoglycan synthesis.

Conclusions. Based on these results we hypothesize that IL-1ß produced by activated monocytes/macrophages increases the production of hydrogen peroxide by chondrocytes. This in combination with haemoglobin-derived iron from the RBC will result in the formation of hydroxyl radicals in the vicinity of chondrocytes. This mechanism may result in chondrocyte damage and as such be involved in blood-induced cartilage damage.

KEY WORDS: Interleukin-1ß, Hydroxyl radical formation, Joint damage, Cartilage damage, Red blood cells, Mononuclear cells.

Correspondence to: F. P. J. G. Lafeber, Rheumatology and Clinical Immunology, Room F02.127, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands. E-mail: f.lafeber{at}azu.nl


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