ZOLEDRONATE (CGP-42446), A BISPHOSPHONATE, PROTECTS AGAINST METAPHYSEAL INTRACORTICAL DEFECTS IN EXPERIMENTAL INFLAMMATORY ARTHRITIS

This study investigated zoledronate (CGP 42'446), a bisphosphonate, as a potential prophylactic and therapeutic agent against intracortical defects in metaphyseal bone in an experimental model of inflammatory a rthritis. Inflammatory arthritis was induced in the right tibiofemoral joint of rabbits by the repeated injection of carrageenan. Three grou ps of animals were treated with the bisphosphonate daily, beginning at different points after the induction of arthritis. Cross sections of the right distal femoral metaphysis were prepared, and intracortical d efects were examined by computerized image analysis. The percentage of total bone area with defects (the ratio of void area to total bone ar ea) was greatly increased in the arthritic group compared with that in the normal group (p < 0.001). In all groups treated with the bisphosp honate, there was a significantly lower percentage of total bone area with defects compared with that in the arthritic group (p < 0.001). Tr eatment was likewise effective in reducing the zonal (anterior and pos terior) predilection for the formation of defects observed in arthriti s. Although inflammatory arthritis has a substantial effect in produci ng intracortical defects in metaphyseal bone, a bisphosphonate, zoledr onate, was considerably effective in preventing these changes from occ urring.