Colitis causes bone loss in rats through suppression of bone formation.

Abstract:

BACKGROUND & AIMS:Idiopathic inflammatory bowel disease (IBD) is associated with bone loss in more than 30% of cases. Nevertheless, the pathogenesis of the bone loss is uncertain. The aim of this study was to investigate the bone loss and underlying mechanisms using an animal model of IBD. METHODS:Severe colitis was induced by intrarectal administration of a hapten, 2,4,6-trinitrobenzenesulfonic acid (TNBS). Severity of IBD was graded macroscopically and histologically. Bone histomorphometry was performed on cancellous bone of the tibiae. RESULTS:A florid transmural colitis was observed 3 weeks after administration of TNBS. In these animals, there was considerable cancellous bone loss of 33% compared with age-matched, pair-fed control animals. This was associated with a marked suppression of the cancellous bone formation rate to < 30% of that in control animals. Thereafter, bone formation rate increased in parallel with healing of colitis. Twelve weeks after TNBS administration, the persistent increase in bone formation rate was associated with return of bone volume to control levels. CONCLUSIONS:The data suggest that bone loss can occur rapidly in colitis and is associated with suppression of bone formation. This study also shows that the bone loss that occurs during TNBS-induced colitis is reversible.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Lin CL,Moniz C,Chambers TJ,Chow JW

doi

10.1053/gast.1996.v111.pm8898640

subject

Has Abstract

pub_date

1996-11-01 00:00:00

pages

1263-71

issue

5

eissn

0016-5085

issn

1528-0012

pii

S0016508596004817

journal_volume

111

pub_type

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