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Rheumatology Advance Access originally published online on May 3, 2005
Rheumatology 2005 44(8):1067-1068; doi:10.1093/rheumatology/keh675
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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@oupjournals.org

LETTER TO THE EDITOR

Association of apolipoprotein E polymorphism with bone mineral density in postmenopausal women with rheumatoid arthritis

S. I. Lee, S. Y. Lee1 and W. H. Yoo

Department of Internal Medicine and 1 Diagnostic Radiology, Chonbuk National University Medical School and Research Institute of Clinical Medicine, Republic of Korea.

Correspondence to: W. H. Yoo, Division of Rheumatology, Department of Internal Medicine, Chonbuk National University Medical School and Research Institute of Clinical Medicine, #634-18, Keumamdong, Dukjingu, Jeonju, Jeonbuk, 561–712, Korea. E-mail: ywhim@moak.chonbuk.ac.kr

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SIR, Pathological bone loss can occur by marginal erosions, juxta-articular osteoporosis and generalized osteoporosis in rheumatoid arthritis (RA) [1]. Several studies demonstrated that these different types of bone involvement are similarly mediated by receptor activator of nuclear factor {kappa}B ligand (RANKL), a factor stimulating osteoclast differentiation [2, 3]. Therefore, generalized osteoporosis has been suggested as a risk factor for severe joint destruction in RA. In fact, joint erosions related to generalized osteoporosis and high Larsen scores associated strongly with bone mineral density (BMD) reduction have been found in patients with . . . [Full Text of this Article]


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