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Bone Mineralization in Celiac Disease
Author(s) -
Tiziana Larussa,
Evelina Suraci,
Immacolata Nazionale,
Ludovico Abenavoli,
Maria Imeneo,
Francesco Luzza
Publication year - 2012
Publication title -
gastroenterology research and practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.622
H-Index - 45
eISSN - 1687-630X
pISSN - 1687-6121
DOI - 10.1155/2012/198025
Subject(s) - medicine , osteoprotegerin , malabsorption , bone mineral , bone remodeling , osteoporosis , proinflammatory cytokine , vitamin d and neurology , endocrinology , gastroenterology , activator (genetics) , receptor , inflammation
Evidence indicates a well-established relationship between low bone mineral density (BMD) and celiac disease (CD), but data on the pathogenesis of bone derangement in this setting are still inconclusive. In patients with symptomatic CD, low BMD appears to be directly related to the intestinal malabsorption. Adherence to a strict gluten-free diet (GFD) will reverse the histological changes in the intestine and also the biochemical evidence of calcium malabsorption, resulting in rapid increase of BMD. Nevertheless, GFD improves BMD but does not normalize it in all patients, even after the recovery of intestinal mucosa. Other mechanisms of bone injury than calcium and vitamin D malabsorption are thought to be involved, such as proinflammatory cytokines, parathyroid function abnormalities, and misbalanced bone remodeling factors, most of all represented by the receptor activator of nuclear factor B/receptor activator of nuclear factor B-ligand/osteoprotegerin system. By means of dual-energy X-ray absorptiometry (DXA), it is now rapid and easy to obtain semiquantitative values of BMD. However, the question is still open about who and when submit to DXA evaluation in CD, in order to estimate risk of fractures. Furthermore, additional information on the role of nutritional supplements and alternative therapies is needed.

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