Skip Navigation



Rheumatology Advance Access published online on March 31, 2003
Rheumatology, doi:10.1093/rheumatology/keg220
Rheumatology © British Society for Rheumatology 2003; all rights reserved
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
42/6/784    most recent
keg220v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Hooiveld, M. J. J.
Right arrow Articles by Lafeber, F. P. J. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hooiveld, M. J. J.
Right arrow Articles by Lafeber, F. P. J. G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2003 British Society for Rheumatology 2003; all rights reserved

Original Papers

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

M. J. J. Hooiveld 1*, G. Roosendaal 2, H. M. van den Berg 2, J. W. J. Bijlsma 3, F. P. J. G. Lafeber 3*

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

* Corresponding author. E-mail: f.lafeber{at}azu.nl.

Received 3 September 2002 ; accepted 28 November 2002

Abstract

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 1{beta} (IL-1{beta}; 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-1{beta} 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-1{beta} 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-1{beta}, Hydroxyl radical formation, Joint damage, Cartilage damage, Red blood cells, Mononuclear cells.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.