The influence of experimental colitis, induced by trinitrobenzenesulphonic acid with ethanol, on bone mineralisation and mineral metabolism was investigated in male rats. Three days after colitis induction, there was a significant rise (p < 0.01) in urinary calcium excretion, which was still present 20 days later (p < 0.05). Three weeks after colitis induction, urinary hydroxyproline excretion was significantly increased (p < 0.01), while urinary cyclic AMP and phosphorus decreased. Colitis was associated with reduced bone density (p < 0.025), ash weight (p < 0.05) and calcium/volume ratio (p < 0.05), whereas no change was found for bone volume and the phosphorus/volume and magnesium/volume ratios. Serum minerals remained unchanged. We conclude that chronic experimental colitis in the rat leads to resorptive hypercalciuria, increased urinary hydroxyproline and osteopenia. Considering site of inflammation, diet, sex, and absence of therapy, inflammatory mediators, e.g. cytokines, with known catabolic effects on bone, might be involved in the pathogenesis of osteopenia.
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