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Rheumatology Advance Access originally published online on November 22, 2005
Rheumatology 2006 45(3):287-290; doi:10.1093/rheumatology/kei149
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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@oxfordjournals.org

Oxidative stress by glutathione depletion induces osteonecrosis in rats

T. Ichiseki, Y. Ueda1, S. Katsuda1, K. Kitamura, A. Kaneuji and T. Matsumoto

Department of Orthopaedic Surgery and 1 Department of Pathophysiological and Experimental Pathology, Kanazawa Medical University, Ishikawa, Japan.

Correspondence to: T. Ichiseki, Department of Orthopaedic Surgery, Kanazawa Medical University, Daigaku 1-1, Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan. E-mail: tsy-ichi{at}kanazawa-med.ac.jp

Objective. We recently implicated in vivo oxidative stress in the development of osteonecrosis in a steroid-induced osteonecrosis model in the domestic rabbit. In the present experiment we devised a new non-traumatic model using the rat to investigate the relationship between oxidative stress and the development of osteonecrosis.

Methods. Seven 24-week-old male Wistar rats were subcutaneously injected with the pro-oxidant buthionine sulphoximine (BSO) 500 mg/kg for 14 consecutive days (group B) and eight rats received injections of vehicle (physiological saline; group N). The rats in both groups were killed after 14 days, and their bilateral femurs were examined histopathologically. Blood levels of reduced glutathione (GSH), total cholesterol (T-cho) and triglycerides (TG) were also determined.

Results. GSH was significantly decreased in group B compared with group N (P<0.01). No significant differences were found in T-cho or TG. Osteonecrosis was not detected in any animal in group N in contrast to five of seven animals in group B (P<0.05).

Conclusion. BSO is an inducer of oxidative stress, in particular interfering with the synthesis of GSH in vivo. In the present study, GSH levels were markedly reduced by BSO, whereas neither T-cho nor TG was significantly changed. The high rate of osteonecrosis noted in group B suggests that oxidative stress alone may be sufficient to promote the development of osteonecrosis at certain sites.

KEY WORDS: Osteonecrosis, Oxidative stress, Rat, Glutathione


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