FLUOR IN THE TREATMENT OF OSTEOPOROSIS - AN OVERVIEW OF 30 YEARS CLINICAL RESEARCH

It has long been known that fluoride ''hardens'' mineralized tissues. Fluoride ingestion through drinking water in areas naturally rich in fluoride leads to osteosclerosis, known as endemic fluorosis. The first suggestion that fluoride be used in the treatment of osteoporosis was made in 1964. However, despite 30 years of research, the treatment remains controversial. Fluoride has a dual effect on osteoblasts. On the one hand, it increases the birthrate of osteoblasts at tissue level by a mitogenic effect on precursors of osteoblasts, while on the other hand it has a toxic effect on the individual cell with mineralization impairment and reduced apposition rate resembling osteomalacia. Fluoride has a positive effect on axial bone density, but the axial bone gain is not matched by similar changes in cortical bone. Furthermore, approximately one third of patients are non-responders. The effect of the addition of fluoride to the drinking water on fracture rate is not clear. It probably only has a small relative impact on total hip fracture rates. In two controlled fluoride therapy studies the incidence of vertebral fractures decreased, while in two other studies it increased. Experience teaches that denser bones are not necessarily better bones. The major side effects of fluor therapy are skeletal fluorosis, gastrointestinal intolerance, and painful lower extremity syndrome. Fluoride is the single most effective agent for increasing axial bone volume in the osteoporotic skeleton; however, its therapeutic window is narrow. The best candidates for fluoride therapy are patients with axial osteoporosis but with good peripheral bone density. They should have a good renal function and vitamin D status. Favourable candidates are also patients with corticosteroid induced osteoporosis in middle age.