Therapy of osteoporosis with fluoride

Controversy continues whether as to and under which conditions fluoride-induced bone is sufficiently stable. The unique selectivity of fluoride ions to induce osteoblast proliferation and matrix synthesis is unquestioned; however, fluoride is accumulated in the newly formed bone in depending on the concentration and, when exceeding a toxic level, deteriorates the mechanical strength by changing the bone crystal structure. In addition, fluorides delay the mineralisation time and, if used above the toxic threshold, induce osteomalacia-like changes which are even worse when calcium deficiency develops. The favourable osteoblast-stimulating effect can be expected in a narrow therapeutic window between 5 and 10 mu mol fluoride while the toxic accumulation in bone increases in linear proposition with the fluoride serum concentration. Hence, sustained-release or retarded sodium fluoride preparations are now preferred which are mainly absorbed in the small bowel and produce fewer gastrointestinal side effects. Another experimental treatment approach used recently is the intermittent application of fluoride. Controlled clinical studies during the last ten years show inconsistent results. Although bone density increased substantially, some controlled studies could not detect a significant effect on the spinal fracture rate. Other studies, however, using low-dose and slow-release preparations or in connection with intermittent, cyclical application with sufficient additional calcium, demonstrated an impressive decrease of the spinal fracture rate in postmenopausal women. In conclusion, several important details of fluoride therapy are still unclear and no standardised therapeutic scheme has been developed so far. Therefore, fluoride does not meet the criteria of evidence-based medicine and continues to be an experimental drug which cannot be recommended for general practice.