Fluoride Action Network


At two x ray examinations in 1957 and 1967, 17 cases of skeletal fluorosis were identified among long term cryolite workers in Copenhagen. In 1982 four of these patients were alive, eight to 15 years after exposure had ended. Radiographs were obtained, and the urinary fluoride excretion was measured. A similar picture emerged in all four cases: extensive fading of the sclerosis of trabecular bone in ribs, vertebral bodies, and pelvis, whereas cortical bone thickening and calcification of muscle insertions and ligaments remained virtually unchanged. The fluoride excretion was increased in three cases (with the shortest exposure free period). These findings indicate that with continuous remodelling of bone tissue trabecular sclerosis is slowly reversible and the excess fluoride is excreted in the urine.



The reversibility of skeletal fluorosis suggested by Roholm2 has been studied in more detail by Fritz.7 Seven of 42 German patients with skeletal fluorosis showed a decreased degree of osteosclerosis 13-19 years after exposure ceased. Three cases were described in detail, but little information was given on other cases of fluorosis known to Fritz. Thus the evidence presented suggests that reversibility of osteosclerosis occurred in at least seven cases. Schlegel mentioned five patients who, two to three years after retirement, experienced both a decrease in fluoride content of bone tissue and a decreased bone density on the radiographs.8 Franke et al noted that in two patients osteosclerosis faded within two to five years, though in nine other patients, no appreciable improvement could be seen after five years without occupational exposure to fluoride.4 These studies support the notion that reversibility of osteosclerosis is possible. In patients with slight degrees of skeletal fluorosis any improvement of the condition after a few years of retirement may be difficult to recognise. Thus over longer periods considerable improvement would be more likely. The present study indicates that reversibility may be a normal course of trabecular osteosclerosis after exposure has ended. Thus all patients who were alive 15 years after their last examination showed a remarkable decrease in osteosclerosis, although the resulting diffuse, blurred trabeculation was not normal.

The earlier studies referred to above suggest a characteristic pattern: decrease of trabecular bone density but unchanged cortical sclerosis, subperiosteal growths, and calcification of ligaments. These observations are entirely in agreement with the present study. One particular form of possible fluorosis followed a different pattern, however. In the 1950s several patients in Spain suffered a “periostitis deformans,” apparently related to adulteration of wine with large amounts of fluoride.9 The patients initially developed some osteosclerosis that later reverted into a definite osteoporosis. Further, the subperiosteal nodules tended to disappear spontaneously.9 Thus the wine related bone disease seems to differ from occupational fluorosis.

The reversibility of the osteosclerosis may be related to the continued excretion of fluoride accumulated in the body. Brun et al found increased fluoride concentrations in the urine of cryolite workers several years after retirement.5  After defluoridation of the drinking water in a Texas community, local residents continued to excrete
excess fluoride in the urine for at least 113 weeks.10 These observations are in agreement with the present study. More than 99% of the body burden of fluoride is retained in the calcified tissues, and the continued excretion must be related to a slow release from the bones. After a period of high fluoride exposure, experimental subjects excrete fluoride in amounts that decrease exponentially with time. “I Calculations based on these data suggest that half of the fluoride accumulated in the body would be excreted in about eight years.’2 Other data indicate that the annual turnover, or remodelling, rate of bone tissue is 2*5% and 10% for cortical and trabecular bone, respectively.13 Spine and pelvis appear to have average turnover rates of 7-8%,13 which would correspond to a half life of about nine years. The information available indicates that fluoride, after incorporation into skeletal tissues, is later released in relation to the normal remodelling of the bones. If high fluoride exposures are no longer present normal bone tissue is then formed.

Other “bone seekers,” such as lead, may be released slowly from the skeletal stores and may then prevent blood concentrations frovreturning to normal even several years after exposure has ended.’4 Similarly, continued release of accumulated fluoride could prevent blood fluoride concentrations from returning to normal and could cause a continued exposure of other body tissues to fluoride. The reversibility of skeletal fluorosis and skeletal storage of fluoride could then, theoretically, lead to chronic effects. A mortality study of cryolite workers is in progress and may offer a possible answer to this question in the near future.

Patients records from past examinations were kindly made available by Dr F Gyntelberg, department of
occupational medicine, Rigshospitalet. Fluoride and creatinine determinations were performed by Jytte Molin Christensen of the Danish National Institute of Occupational Health.


1. Moiler PF, Gudjonsson SV. Massive fluorosis of bones and ligaments. Acta Radiol 1932;13:269-94.

2. Roholm K. Fluorine intoxication. London: Lewis, 1937.

3. Hodge HC, Smith FA. Occupational fluoride exposure. JOM 1977;19:12-39.

4. Franke J, Runge H, Fengler F. Endemic and industrial fluorosis. In: Courvoisier B, Donath A, Baud A, eds. Fluoride and bone. Bern: Hans Huber, 1978:129-43.

5. Brun GC, Buchwald H, Roholm K. Die Fluroausscheidung im Harn bei chronischer Fluorvergiftung von Kryolitharbeitern. Acta Med Scand 1941;106:261-73.

6. Neefus JD, Cholak J, Saltzman BE. The determination of fluoride in urine using a fluoride-specific ion electrode. Am Ind Hyg Assoc J 1970;31:96-9.

7. Fritz H. Besonderheiten des Verlaufs der Knochenfluorose. Radiol Diagn 1964;5:393-403.

8. Schlegel HH. Industrielle Skelettfluorose. Vorliaufiger Bericht iiber 61 Falle aus Aluminiumhultten. Sozial Pravendvmed 1974;19:269-74.

9. Soriano M. Periostitis deformans. Rev Clin Espanola 1965;97:375-88.

10. Likins RC, McClure FJ, Steere AC. Urinary excretion of fluoride following defluoridation of a water supply. In: McClure FJ, ed. Fluoride drinking waters. US Public Health Service Publ. No 825, 1962;421-3.

11. Largent EJ. Fluorosis. The health aspects of fluorine compounds. Columbus: Ohio State University Press, 1961.

12. World Health Organisation. Fluorides -and human health. Geneva: WHO 1970.

13.  International Commission on Radiological Protection. Report of the task group on reference man. Oxford: Pergamon Press, 1975.

14. Grandjean P, Kon SH. Lead exposure of welders and bystanders in a ship repair yard. Am J Ind Med 1981;2:65-70.