Patients with Crohn’s disease are at risk of osteoporosis and premature fracture. However, the pathophysiology underlying bone loss remains poorly understood and the optimum treatment has not been established.


To investigate mechanisms of bone loss in Crohn’s disease using biochemical markers of bone turnover.


Bone mineral density was measured at the hip and spine using dual-energy X-ray absorptiometry in 117 patients (48 male) with Crohn’s disease. Bone turnover was assessed by measuring serum osteocalcin (BGP), pro-collagen carboxy-terminal propeptide (PICP), bone specific alkaline phosphatase (BALP) and urinary deoxypyridinoline (DPD); and compared to age-matched healthy controls (n = 28).


Bone mineral density was reduced (z-score < −1) in 48 (41%) patients with Crohn’s disease. Mean values for bone formation markers in patients with Crohn’s disease were all within the normal reference range (BGP 8.92 (± 3.23) ng/mL (normal range 3.4–10.0), BALP 17.6 (± 12.6) U/L (normal range 11.6–43.3), PICP 95.1 (± 46.5) ng/mL (normal range 69–163)) and were not significantly different to the control population. However, mean urinary DPD was significantly higher in patients with Crohn’s disease compared to healthy controls (10.97 (± 9.22) n M DPD/m creatinine vs. 5.02 (± 1.03) n M DPD/m creatinine, difference in means = 5.95, 95% CI: −9.6 to −2.3, = 0.00001) and compared to the UK reference range DPD levels were increased in 74 (63%) patients.


Bone resorption as evidenced by urinary DPD was frequently increased in patients with Crohn’s disease and was significantly higher than in an age-matched control population. The high levels of urinary DPD suggest increased bone collagen degradation may contribute to osteoporosis in patients with Crohn’s disease. These results suggest anti-resorptive agents such as the bisphosphonates may be effective treatment for osteoporosis in Crohn’s disease.