Risedronate is a heterocyclic orally active aminobisphosphonate and it belongs to the
bisphosphonate category: these drugs are powerful
bone resorption inhibitors, thanks to their affinity for
hydroxyapatite crystals at bone
mineral matrix level and to their inhibiting effects on osteoclast activity, using the ability of inhibiting
enzyme FPPS. Recent observations have reported that
risedronate can decrease resorption entity, not only of the trabecular bone, but also of the cortical bone, modifying therefore the (bone compact) thickness and the cortical porosity entity, which is largely responsible of
femoral fracture especially among elderly patients. Various controlled studies have proved the efficacy of
risedronate in reducing fragility fracture risk significantly. In particular, it is able to lower in a very significant way the incidence of vertebral, non-vertebral and
femoral fractures, with precocity of effects after only six months of
therapy. The extension of protocols, moreover, has marked its efficacy even after seven years of treatment. Under the metabolic profile, these studies have also shown that
risedronate activity can reduce
bone resorption markers and increase bone density values at lumbar and femoral level. Results emerged from a group of women aged over 80 are relevant:
risedronate has proved capable of decreasing
femoral fracture risk. Also in male and steroidal
osteoporosis, clinical controlled studies have shown that
risedronate is effective in decreasing vertebral fracture incidence. Lastly, tolerability: the main side effects concern the gastrointestinal tract and they are usually rare, of minor entity and can be solved by sospending the treatment.
Acute phase reaction is rare, due to
risedronate oral administration; it is also valid for
osteonecrosis of the jaw and atypical fractures.