Abstract
Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six others developed the disease within a year of fluoridated dialysis. However, in all patients, the disease progressed despite recommended therapy (including high doses of vitamin D). The mean pre-dialysis serum fluoride level was 16 + 4 uM which rose to 28 + 3 post-dialysis. The bone fluoride content ranged from 800 to 22,500 ppm on a dry fat-free basis. Toxic effects have been reported at these levels and could complicate underlying renal osteodystrophy. Further studies are required to delineate the role of fluoride in this condition.
In our hemodialysis center, opened in April 1964, fluoridated dialysis began with the fluoridation of the city water supply in November 1965. Our subsequent therapeutic failure was completely unexpected and a possible explanation was suggested by the observation of Taves et al. that the serum fluoride levels in patients chronically hemodialyzed with fluoridated water are comparable to those that cause fluorotic bone disease. Thus, the study of fluoride levels in our patients became of particular interest because several of them had been on fluoridated dialysate for much longer periods than those patients reported by Taves et al… Clinically, radiologically, and histologically, the disease seen in these patients was indistinguishable from uremic osteodystrophy, although the manifestations of bone disease tended to appear sooner and in more severe form in our patients maintained on fluoridated dialysate. . . .
Histologically and radiographically, these patients showed features of uremic osteodystrophy instead of the fluorosis characterized by exostoses and osteosclerosis. Nervertheless, the observed changes (osteomalacia, osteitis fibrosa and osteoporosis) were similar to those induced by high doses of fluoride in humans and experimental animals, in which widened osteoid seams have been observed, and where increased areas of resorption due to secondary hyperparathyroidism may be seen. Therefore, it seems likely that fluoride was aggravating the underlying renal osteodystrophy in our patients, and that this effect was enhanced by concomitant administration of high doses of vitamin D.
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