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Reduced bone formation in patients with osteoporosis associated with inflammatory bowel disease

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Abstract

The pathophysiology of bone loss associated with inflammatory bowel disease has not been clearly defined. In this study we have performed a detailed histomorphometric analysis of iliac crest bone obtained from 19 patients with inflammatory bowel disease in whom a diagnosis of osteoporosis had been made. Eleven subjects were receiving prednisolone at the time of their biopsy. Comparison with control values demonstrated a highly significant reduction in trabecular bone area in the patient group (p<0.001). Wall width, adjusted appositional rate and bone formation rate were all significantly reduced in the patient group (p<0.001) and the formation period was significantly increased (p<0.001). Resorption cavities were slightly smaller in the patient group, differences in maximum cavity depth and cavity length achieving statistical significance (p<0.005 andp<0.05 respectively). The mineral appositional rate was significantly reduced in the patients with inflammatory bowel disease (p<0.001) and the mineralization lag time significantly increased (p<0.001); however, osteoid area, perimeter and seam width were not significantly different from controls. These results demonstrate that osteoporosis associated with inflammatory bowel disease is characterized by reduced bone formation at the cellular and tissue level; the proportionately greater change in wall width than in resorption cavity depth is consistent with a negative remodelling balance. Although none of the patients had osteomalacia as defined by the criteria of increased osteoid seam width and mineralization lag time, the higher mineralization lag time in the patient group indicates a mild mineralization defect.

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Croucher, P.I., Vedi, S., Motley, R.J. et al. Reduced bone formation in patients with osteoporosis associated with inflammatory bowel disease. Osteoporosis Int 3, 236–241 (1993). https://doi.org/10.1007/BF01623826

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  • DOI: https://doi.org/10.1007/BF01623826

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