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 f luoride 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 re mains controversial. Fluoride has a dual effect on osteoblasts. On the one hand, it increases the birthrate of osteoblasts at tissue level b y 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. Fluori de has a positive effect on axial bone density, but the axial bone gai n is not matched by similar changes in cortical bone. Furthermore, app roximately one third of patients are non-responders. The effect of the addition of fluoride to the drinking water on fracture rate is not cl ear. It probably only has a small relative impact on total hip fractur e rates. In two controlled fluoride therapy studies the incidence of v ertebral 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, gast rointestinal intolerance, and painful lower extremity syndrome. Fluori de is the single most effective agent for increasing axial bone volume in the osteoporotic skeleton; however, its therapeutic window is narr ow. The best candidates for fluoride therapy are patients with axial o steoporosis but with good peripheral bone density. They should have a good renal function and vitamin D status. Favourable candidates are al so patients with corticosteroid induced osteoporosis in middle age.