A reduced bone mineral density has been reported in inflammatory bowel disease (IBD). To assess the mechanisms of bone disease in IBD. We studied in 90 patients (61 with Crohn's disease, 22 with ulcerative colitis, 7 with indeterminate colitis) biochemical markers of bone metabolism in serum and bone mineral density by peripheral quantitative computed tomography at the forearm. Forty-five percent of the patients had a reduced bone density (Z score <-1). Serum calcium was normal in most patients, vitamin D deficiency was documented in 17%. Osteocalcin, a serum marker of bone formation, was decreased in 26%(1.2±0.1 ng/ml). whereas the carboxyterminal cross-linked telopeptide of type 1 collagen (ICTP), a recently described serum parameter of bone breakdown, was stimulated in 38%(10.4±2.3 µg/L). Of 33 patients with increased ICTP levels, 19 showed a decreased bone density (Z score <-1), and 2 of them never received steroids. An active status of the underlying disease in most patients with increased ICTP levels suggests a direct effect of the underlying IBD. In the whole series of patients with a history of active disease (n= 34), 47% had signs of an increased hone degradation (ICTP > 5 µg/L; mean, 12.9±4.7 µg/L). Data derived from a retrospective survey of 245 patients with IBD suggest that the prevalence of bone fractures in IBD is unexpectedly high, particularly in patients with a long duration of disease, frequent active phases, and high cumulative doses of corticosteroid intake. Several mechanisms may be involved in IBD-associated bone disease:(1) a high inflammatory activity directly induces hone degradation via yet unknown pathways,(2) treatment with corticosteroids may exert catabolic effects on tbe bone, or (3) malabsorption and vitamin D deficiency may activate bone turnover.