Fluoride Therapy for Vertébral Osteoporosis

Vertébral osteoporosis is characterized by a prédominant atrophy of spongy bone inducing non-traumatic vertébral fractures. Because a low bone mass is the major déterminant of fracture risk, the idéal therapy for established vertébral osteoporosis should increase trabecular bone mass substantially, thereby decreasing the risk of new crush fractures. This idéal treatment should also be capable of restoring the normal architecture of bone in order to maintain its mechanical properties. Treatments acting by decreasing bone résorption can maintain existing bone mass or protect spongy bone architecture, but cannot substantially increase bone mass in order to decrease the occurrence of new vertébral fractures. Of the antiresorptive drugs, calcitonin has never been shown capable of reducing vertébral fracture rate in established osteoporosis, and the promising results recently obtained with an intermittent cyclical treatment with etidronate given for 2 years in osteoporosis (1) hâve not been confïrmed by a follow-up of 346 patients during the third year of treatment with the drug. In contrast, regimens that stimulate bone formation hâve the potential of increasing bone mass, and fluoride is one of the most effective of thèse regimens because of its ability to increase the osteoblast cell population. Fluoride was proposed as a curative therapy for vertébral crush fracture syndrome 30 years ago, and this idea was suggested by the massive increase in trabecular bone density ofthe axial skeleton that characterizes skeletal fluorosis radiologically and the low prevalence of osteoporosis in areas with moderately high fluoride concentrations in drinking water. Since 1961, several prospective open studies hâve shown that fluoride salts (sodium fluoride or monofluorophosphate) are effective in increasing trabecular bone mass. This was shown first by radiological techniques, then by histomorphometric analysis of iliac bone biopsies, and by measurements of the minerai bone density of the axial skeleton using dual photon absorptiometry, quantitative computed tomography, or neutron activation analysis. The stimulating effect on bone formation was confïrmed by the increase in sérum osteocalcin levels. Thèse data led to a gênerai agreement that sodium fluoride, combined with adéquate calcium supplementation, has an anabolic effect on vertébral bone mass, and fluoride therapy has been approved for the treatment of established vertébral osteoporosis in nine European countries (Aus-