Background & Aims: Idiopathic inflammatory bowel disease (IBD) is asso
ciated with bone loss in more than 30% of cases. Nevertheless, the pat
hogenesis of the bone loss is uncertain, The aim of this study was to
investigate the bone loss and underlying mechanisms using an animal mo
del of IBD. Methods: Severe colitis was induced by intrarectal adminis
tration of a hapten, 2,4,6-trinitrobenzenesulfonic acid (TNBS), Severi
ty of IBD was graded macroscopically and histologically, Bone histomor
phometry was performed on cancellous bone of the tibiae, Results: A fl
orid transmural colitis was observed 3 weeks after administration of T
NBS, In these animals, there was considerable cancellous bone loss of
33% compared with age-matched, pair-fed control animals. This was asso
ciated with a marked suppression of the cancellous bone formation rate
to <30% of that in control animals. Thereafter, bone formation rate i
ncreased in parallel with healing of colitis, Twelve weeks after TNBS
administration, the persistent increase in bone formation rate was ass
ociated with return of bone volume to control levels. Conclusions: The
data suggest that bone loss can occur rapidly in colitis and is assoc
iated with suppression of bone formation. This study also shows that t
he bone loss that occurs during TNBS-induced colitis is reversible.