Mw. Pysklywec et al., ZOLEDRONATE (CGP-42446), A BISPHOSPHONATE, PROTECTS AGAINST METAPHYSEAL INTRACORTICAL DEFECTS IN EXPERIMENTAL INFLAMMATORY ARTHRITIS, Journal of orthopaedic research, 15(6), 1997, pp. 858-861
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.