Background: The pathogenesis of CN is still unknown. An increase of the bone blood supply seems to be one of the mechanisms involved. A feature of CN is a bone reabsorption. IGF-1 can influence the bone tissue by various mechanisms but its vasodilatory effects in others tissues are well-known. Alendronate have an inhibitory effect on bone reabsorption. Aim of this study is to evaluate the effect of alendronate on foot bone density in CN and above all if this effect can be mediated by a modification in IGF-1 levels.

Methods: Twenty patients with a diagnosis of acute CN of the foot were enrolled. According to the randomization, 11 patients were treated with 70 mg of alendronate per os once a week (TG) and 9 patients were followed as control group (CG). Markers of bone turnover [urinary hydroxyprolin, serum collagen carboxyl-terminal telopeptide of type 1 collagen (ICTP), serum bone alkaline phosphatase (B-ALP)], IGF-1 and BMD by dual energy X-ray absorptiometry (DEXA).

Results: ICTP didn’t show significant difference between the two groups (0,54±0,05 ng/ml vs 0,56±0,06 ng/ml p< 0,6) at the outset, after six months the treated group had a significant decrease of this parameter (0,54±0,05 ng/ml vs 0,30±0,03 ng/ml p< 0,05).

In TG hydroxyprolin followed the same trend showing a significant decrease after the six month treatment (18±3,2 mg/l vs 13±3,6 mg/l p< 0,05).

At the same time B-ALP reduction was almost significant (36±4,8% vs 23±3,9% p=0,06)

DEXA demonstrated an improvement in total foot mineralization in the TG(0,18±0,06 g/cm2 vs 0,24±0,08 g/cm2 p< 0,05) and in the distal phalanxes (0,194 g/cm2 vs 0,242 g/cm2 p< 0,01) (fig. 3). Only the TG showed a significant decrease of IGF-1 throughout the trial (142,8±24 vs 123,5±41 ng/ml p< 0,05).

Conclusions: The increase in bone blood flow could be linked to the vascular effects of IGF-1. Alendronate in acute phase helps to stop bone reabsorption and this effect could be mediated by the decrease of IGF-1 levels.