THE EFFECT OF ETIDRONATE ON TRABECULAR BONE REMODELING IN POSTMENOPAUSAL SPINAL OSTEOPOROSIS - A RANDOMIZED STUDY COMPARING INTERMITTENT TREATMENT AND AN ADFR REGIME

Thirty-seven patients were randomized to receive intermittent cyclic etidronate (400 mg/day oral for 2 weeks, followed by 13 weeks off treatment) or an ADFR treatment (100-mu-g/day oral triiodothyronine for 7 days, followed by 400 mg/day etidronate for 2 weeks and 12 weeks off treatment). Supplemental calcium (120 mg/day) and vitamin D3 (400 IU/day) were given throughout the study period to all patients. Biochemical analyses, iliac-crest bone biopsies, and lumbar bone mineral content (BMC) measurements were performed before and during 60 weeks of treatment. Sixteen patients in the intermittent cyclic etidronate group and 15 in the ADFR group completed 60 weeks of treatment. Serum alkaline phosphatase decreased from 185 (43) (mean, (SD)) to 144 (35) (p < 0.001) and from 221 (69) to 156 (43) (p < 0.002) during intermittent cyclic etidronate treatment and ADFR treatment, respectively, without any significant changes in renal hydroxyproline excretion. Final resorption depth, trabecular bone activation frequency, and bone formation rate decreased significantly from 51.5 (48.4/60.0) mu-m (median (25%/75% quartiles)) to 44.0 (39.6/46.2) mu-m (p < 0.04), from 0.30 (0.17/0.62) year-1 to 0.10 (0.02/0.19) year-1 (p < 0.03) and from 0.035 (0.020/0.081) mu-m3/mu-m2/day to 0.015 (0.002/0.025) mu-m3/mu-m2/day, p < 0.03 respectively, during intermittent cyclic etidronate treatment, but were unchanged during ADFR treatment. No significant changes in trabecular bone volume, bone balance per remodeling cycle, or BMC were noted in either treatment group; no evidence of osteomalacia was found. Intermittent cyclic etidronate treatment may be effective in preventing bone loss and in decreasing the risk of trabecular plate perforation, and thereby maintaining the integrity of bone architecture, in postmenopausal osteoporosis. The absence of positive results after 60 weeks of ADFR treatment with triiodothyronine and etidronate suggest that a change in the choice of activator and/or depressor is necessary.