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Background:

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.

Aim:

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

Methods:

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).

Results:

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.

Conclusions:

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.