Rheumatology Advance Access originally published online on November 12, 2007
Rheumatology 2007 46(12):1749-1750; doi:10.1093/rheumatology/kem292
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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The Vitamin D Paradox
Musculoskeletal Research Group, School of Clinical Medical Sciences, University of Newcastle-upon-Tyne, UK.
Correspondence to: R. M. Francis, Bone clinic, Musculoskeletal Unit, Freeman Hospital, Newcastle-upon-Tyne, NE7 7DN, UK. E-mail: RMFrancis@compuserve.com
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Vitamin D is essential for musculoskeletal health, as it promotes calcium absorption from the bowel, mediates the mineralization of osteoid tissue within bones and plays an important role in bone turnover and muscle function [1, 2]. The most obvious consequence of vitamin D deficiency is the development of vitamin D deficiency osteomalacia, where a failure of mineralization leads to the accumulation of unmineralized osteoid within the skeleton. This is generally only seen when the serum 25-hydroxyvitamin D (25OHD) concentration falls below 20 nmol/l. It has become increasingly apparent that less severe vitamin D deficiency or insufficiency may lead to secondary hyperparathyroidism that contributes to parathyroid hormone (PTH)-induced bone loss, development of osteoporosis and an increased risk of low-trauma fractures [2–4].
There is no universal consensus on what constitutes vitamin D insufficiency [
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