Literature DB >> 20854819

Histomorphometric analysis reveals reduced bone mass and bone formation in patients with quiescent Crohn's disease.

Angela E Oostlander1, Nathalie Bravenboer, Evelien Sohl, Paulien J Holzmann, Christien J van der Woude, Gerard Dijkstra, Pieter C F Stokkers, Bas Oldenburg, J Coen Netelenbos, Daniel W Hommes, Ad A van Bodegraven, Paul Lips.   

Abstract

BACKGROUND & AIMS: Crohn's disease (CD) is associated with an increased prevalence of osteoporosis, but the pathogenesis of this bone loss is only partly understood. We assessed bone structure and remodeling at the tissue level in patients with quiescent CD. We also investigated the roles of osteocyte density and apoptosis in CD-associated bone loss.
METHODS: The study included 23 patients with quiescent CD; this was a subgroup of patients from a large randomized, double-blind, placebo-controlled, multicenter trial. We obtained transiliac bone biopsy samples and performed histomorphometric analysis. Results were compared with data from age- and sex-matched healthy individuals (controls).
RESULTS: Trabecular bone volume was decreased among patients with CD compared with controls (18.90% vs 25.49%; P < .001). The low bone volume was characterized by decreased trabecular thickness (120.61 vs 151.42 μm; P < .01). Bone formation and resorption were reduced, as indicated by a decreased mineral apposition rate (0.671 vs 0.746 μm/day; P < .01) and a low osteoclast number and surface area compared with controls and published values, respectively. In trabecular bone of patients with CD, osteocyte density and apoptosis were normal. The percentage of empty lacunae among patients was higher than that of published values in controls.
CONCLUSIONS: In adult patients with quiescent CD, bone histomorphometric analysis revealed a reduction in bone mass that was characterized by trabecular thinning. The CD-associated bone loss was caused by reduced bone formation, possibly as a consequence of decreased osteocyte viability in the patients' past.
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Year:  2010        PMID: 20854819     DOI: 10.1053/j.gastro.2010.09.007

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


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