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
Gastroenterologyjournal_title
Gastroenterologyauthors
Lin CL,Moniz C,Chambers TJ,Chow JWdoi
10.1053/gast.1996.v111.pm8898640subject
Has Abstractpub_date
1996-11-01 00:00:00pages
1263-71issue
5eissn
0016-5085issn
1528-0012pii
S0016508596004817journal_volume
111pub_type
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