Risedronate is a pyridinyl bisphosphonate that can be administered ora
lly in lower dosages than other antiresorptive bisphosphonates. Like o
thers of its class risedronate inhibits osteoclast-mediated bone resor
ption. In experimental models of osteoporosis, risedronate inhibited b
one loss and improved trabecular architecture. In patients with Pager'
s disease, pain diminished or disappeared and serum alkaline phosphata
se levels decreased after treatment with oral risedronate 30 mg/day fo
r less than or equal to 3 months. Risedronate 30 mg/day orally for 2 m
onths significantly reduced pain, whereas etidronate 400 mg/day orally
for 6 months tended to reduce pain, in a randomised double-blind tria
l of patients with Paget's disease. Oral risedronate 5 mg/day for less
than or equal to 2 years increased bone mass in postmenopausal women
with low or normal bone mass. Risedronate 2.5 mg/day prevented bone lo
ss in postmenopausal women treated with glucocorticoids for rheumatoid
arthritis. The incidence of gastrointestinal or other adverse events
was similar in patients treated with risedronate or placebo in clinica
l trials.