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Submitted on November 12, 2003
Accepted on January 8, 2004
Department of Pathology, Tokushima University School of Dentistry (T.Y., N.I., R.A., M.K., T.I., Y.H.), Tokushima 770-8504; Department of Orthodontics, Tokushima University School of Dentistry (T. Y., T.I., K.M.), Tokushima 770-8504
* To whom correspondence should be addressed. E-mail: hayashi{at}dent.tokushima-u.ac.jp.
The aim of this study was to evaluate the in vivo effects of estrogen-deficiency in MRL/lpr mice as a model for rheumatoid arthritis (RA), and to analyze the possible relationship between immune dysregulation and RANKL-mediated osteoclastogenesis. Experimental studies were performed in ovariectomized (Ovx)-MRL/lpr, Ovx-MRL-+/+, sham-MRL/lpr, and sham-MRL-+/+ mice. Severe autoimmune arthritis developed in younger Ovx-MRL/lpr mice until 24-week-old, while these lesions were entirely recovered by pharmacologic levels of estrogen administration. A significant elevation in serum RF, anti-ds-DNA, and anti-CII was found in Ovx-MRL/lpr mice, and recovered in mice underwent estrogen administration. A high proportion of CD4+ T cells bearing RANKL was found, and an enhanced expression of RANKL mRNA and an impaired osteoprotegerin (OPG) mRNA was detected in the synovium. An increase in both osteoclast formation and bone resorption pits was found. These results indicate that estrogen deficiency may play a crucial role on acceleration of autoimmune arthritis associated with RANKL-mediated osteoclastogenesis in a murine model for RA.
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