One of fluoride’s most well-defined effects on bone tissue is it’s ability to increase the osteoid content of bone. Osteoid is unmineralized bone tissue. When bones have too much of it, they become soft and prone to fracture — a condition known as osteomalacia. As shown below, fluoride has repeatedly been found to cause osteomalacia, in humans and animals alike. Fluoride’s ability to cause osteomalacia has been demonstrated in:

• dialysis patients receiving dialysis from systems that fail to filter out the fluoridated water (1 mg/l);
• osteoporotic patients receiving high-dose fluoride treatment to build bone mass (20+ mg/day),
• humans suffering from skeletal fluorosis, including children with fluoride-induced rickets; and
• animals suffering from skeletal fluorosis.

Fluoridated Water & Dialysis Patients

Fluoride’s ability to cause osteomalacia began to first receive attention in the late 1960s when it was found that kidney patients receiving dialysis from units that did not filter fluoridated water out of the dialysate were experiencing high rates of severe and painful osteomalacia. After several studies (see excerpts below) confirmed that fluoridated water was causing osteomalacia in these patients, dialysis centers began using systems that filtered out the fluoride from water.

While the decision to begin filtering fluoridated water out of dialysate helped reduce the risks that dialysis patients face, dialysis patients continue to remain at risk from daily fluoride exposures, including fluoridated drinking water and tea. In a recent study, for example, the fluoride content in the bones of dialysis patients in a major fluoridated urban area (Toronto, Canada), were found to be significantly correlated with the severity of osteomalacia. (Ng 2004).  These results were largely consistent with previous research from France which found that dialysis patients with osteomalacia had extremely high levels of fluoride (average = 5,700 ppm), far higher than healthy controls (average = 1,300 ppm). (Cohen-Solal 2002; 1996). As noted by the French authors:

“Bone fluoride levels were increased in osteomalacic patients (0.57 + 0.1%) compared with normal controls (0.13 + 0.01%, P 0.5%) in 7/11 patients. These data show that mineralisation defects observed in hemodialyzed patients are frequently associated with high bone fluoride content. Fluoride may be considered as a potential etiological factor of osteomalacic osteodystrophy.” (Colen-Solal 1996)

Bone Fluoride & Osteomalacia in the General Population

Consistent with the research on dialysis patients, studies of the general population in Finland and the United States have found significant correlations between the fluoride and osteoid content of bone (i.e., the more fluoride, the more osteoid). (Arnala 1985; Stein & Granik 1980). Human cadaver bones from a New Jersey hospital, for example, were found to have “[c]hanges associated with increasing fluoride [that] were similar to those of osteomalacia in direction albeit not in degree.” (Stein & Granik 1980).

Excerpts from the Scientific Literature

1) Dialysis Patients in 1970s (when dialysis units were not filtering fluoride out of water):

To learn more about the controversy surrounding the failure by medical centers in the 1960s and 1970s to filter fluoridated water out of dialysis units, click here

“Five of the six patients exposed to fluoridated dialysate for an average of 23 months suffered bone pain and fractures, and three of these patients had incapacitating symptoms. . . . Osteomalacia was significantly more severe in the fluoridated group.”
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

“The risk of severe osteomalacia is reduced with the use of fluoride-free dialysate.”
SOURCE: Lough J, et al. (1975). Effects of fluoride on bone in chronic renal failure. Archives of Pathology 99: 484-487.

“Because we had not seen such severe bone disease in a patient while on relatively high concentrations of dialysate calcium when fluoride-free water had been employed, we recommended in October, 1968, that a commercial mixed-bed deionizer be installed to remove the fluoride.. Bone resorption decreased and osteomalacia improved, coincident wtih the lowering of dialysate, serum and bone concentrations of fluoride… The excessive amounts of osteoid seen in the bone biopsy specimen and the decrease in osteomalacia subsequent to correcting the deionizer operation are consistent with a fluoride effect.”
SOURCE: Johnson WJ, Taves DR. (1974). Exposure to excessive fluoride during hemodialysis. Kidney International 5: 451-454.

“The markedly increased incidence of osteomalacia in the fluoridated group supports previous reports that fluoride is an important factor… Since our patients in the fluoridated group were living in widely separate areas with different water supplies it seems unlikely that there was another common factor other than fluoride responsible for the higher incidence of osteomalacia. It is possible that the presence of other substances in untreated water is necessary before the toxic effects of fluoride become manifest… Forty-one patients on our chronic hemodialysis program were assessed for the degree of progression of bone disease over a period of 46 months. Four of 7 patients using fluoridated water (in diaylsis) developed florid osteomalacia, as opposed to none of the 34 patients in the non-fluoridated group… We conclude that the presence of fluoride in the dialysate, perhaps in conjunction with other substances, is associated with an increased incidence of osteomalacia. It therefore seems prudent to use non-fluoridated water in long-term hemodialysis.”
SOURCE: Cordy PE, et al. (1974). Bone disease in hemodialysis patients with particular reference to the effect of fluoride. Transactions of the American Society of Artifical Internal Organs 20: 197-202.

“The use of fluoride-free dialysate decreases the risk of severe morphologic osteomalacia.”
SOURCE: Jowsey J, et al. (1972). Effects of dialysate calcium and fluoride on bone disease during regular hemodialysis. Journal of Laboratory and Clinical Medicine 79: 204-214.

“We conclude that the osteomalacia that occurs in dialysis patients is due to multiple factors that are removed by deionization. Fluoride may be one of the contributing factors.”
SOURCE: Posen GA, et al. (1972). Comparison of renal osteodystrophy in patients dialyzed with deionized and non-deionized water. Transactions of the American Society for Artificial Internal Organs 18: 405-411.

2) Fluoridation & Dialysis Patients (Present Day):

“Increase in bone fluoride was associated with increased osteoid parameters and decreased bone microhardness… Fluoride interfered with bone mineralization and increased osteoid content, which was most evident in osteomalacia and the mixed bone disorder. In addition, fluoride may interact with aluminum to worsen the osteomalacic lesion.”
SOURCE: Ng AHM, et al. (2004). Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy. Bone 34: 216-224.

“[B]one fluoride content was significantly higher in the entire dialysis population than in controls (0.33 + 0.04% vs 0.13 + 0.018%, P=0.04). Bone fluoride levels were increased in osteomalacic patients (0.57 + 0.1%) compared with normal controls (0.13 + 0.01%, P 0.5% in 7/11 patients. These data show that mineralisation defects observed in hemodialyzed patients are frequently associated with high bone fluoride content. Fluoride may be considered as a potential etiological factor of osteomalacic osteodystrophy.”
SOURCE: Cohen-Solal ME, et al. (1996). Osteomalacia is associated with high bone fluoride content in dialysis patients. Bone 19: 135S.

“In the current study, concentrations of fluoride in the serum of patients with hemodialysis, for both male and female patients, were remarkably higher than those in healthy subjects… From the results obtained, it is suggested that the characteristic change of BMD in patients with hemodialysis, such as increase in BMD of the lumbar spine in spite of the decrease in that of the radius may be contributed to continuance of high concentration of fluoride in the serum. To control serum fluoride at an adequate level constantly, intake of fluoride should be controlled and also fluoride level maintenance system of the hemodialysis is desirable. Furthermore, frequent and long term monitoring of serum fluoride and BMD with hemodialysis patients are highly necessary.”
SOURCE: Takahashi Y. (1995). Effects of fluoride on bone metabolism in patients with hemodialysis. Bulletin of the Osaka Medical College 41: 27-35.

“From these results, it was suggested that absorbed F strongly affected the metabolism of bone, especially cancellous bone in the patients with long-term hemodialysis.”
SOURCE: Tanimura Y. (1994). Studies on serum fluoride and bone metabolism in patients with long term hemodialysis. Bulletin of the Osaka Medical College 40: 65-72.

3) Human Non-Dialysis Populations Exposed to Low Levels of Fluoride in Water:

“The main histolological change induced by fluoride is the increase of osteoid volume… This increase in osteoid parameters was observed in our study already at fluoride concentrations above 1.5 ppm.”
SOURCE: Arnala I, et al. (1985). Effects of fluoride on bone in Finland. Histomorphometry of cadaver bone from low and high fluoride areas. Acta Orthopaedica Scandinavica 56(2):161-6.

“Changes associated with increasing ash fluoride were similar to those of osteomalacia in direction albeit not in degree. . . . Mineralization of this bone . . . was an inverse function of fluoride content, indicating either reduced mineral fixation per unit volume of bone during formation or later leaching of bone mineral. . . . The fact that our subjects were low in fluoride content further suggests that these effects have no threshold.”
SOURCE: Stein ID, Granik G. (1980). Human vertebral bone: Relation of strength, porosity, and mineralization to fluoride content. Calcified Tissue International 32: 189-194.

4) Human Clinical Trials Using High Doses of Fluoride (20 mg+/day):

“[F]luoride therapy is not considered to be a therapeutic agent for bone in part because of its side effects of high incorporation of fluoride ion in bone and the associated osteomalacia.”
SOURCE: Lau KH, et al. (2002). Bone cell mitogenic action of fluoroaluminate and aluminum fluoride but not that of sodium fluoride involves upregulation of the insulin-like growth factor system. Bone 30: 705–711

“The prevalence of osteomalacia was much higher with high-dose NaF (sodium fluoride group) (42.8% for generalized, 85.7% for any) than with low-dose NaF (3.8% for generalized, 7.7% for any). With low-dose NaF, osteomalacia only developed in patients who were not taking vitamin D at the time of the second biopsy…”
SOURCE: Balena R, et al. (1998). Effects of different regimens of sodium fluoride treatment for osteoporosis on the structure, remodeling and mineralization of bone. Osteoporosis International 8: 428-435.

“[T]his study clearly documents in a prospective manner that fluoride therapy results in osteomalacia… Definitive evidence for osteomalacia is a prolonged mineralization lag time, which following fluoride treatment was found to be increased 9-fold in the second biopsy and 4-fold in the third biopsy.”
SOURCE: Lundy MW, et al. (1995). Histomophometric analysis of iliac crest bone biopsies in placebo-treated versus fluoride-treated subjects. Osteoporosis International 5:115-129.

“True osteomalacia existed in… two patients with mild impairment of renal function. This points out the harmful effect of even mild renal failure in fluoride-treated patients.”
SOURCE: Orcel P, et al. (1990). Stress fractures of the lower limbs in osteoporotic patients treated with fluoride. Journal of Bone and Mineral Research 5(Suppl 1): S191-4.

“Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients… Eight (fluoride-treated) patients showed a true histological osteomalacia with both a significantly increased osteoid width and a significantly decreased mineral apposition rate.”
SOURCE: Boivin G, et al. (1989). Skeletal fluorosis: histomorphometric analysis of bone changes and bone fluoride content in 29 patients. Bone 10:89-99.

“When fluoride is given, especially at a high dosage without calcium, osteomalacia may develop. The newly formed matrix may be abnormal and may not undergo adequate mineralization. Thus, a typical histomorphometric picture is represented by a pronounced increase in osteoid (nonmineralized matrix) and reduced calcification front.”
SOURCE: Pak CY. (1989). Fluoride and osteoporosis. Proceedings of the Society for Experimental Biology and Medicine 191: 278-86.

“In our patient, fluoride therapy induced typical bone fluorosis: elevated bone fluoride level (5,100 ppm), abornmal bone pattern on microradiography and an osteomalacia-like picture on histological examination.”
SOURCE: Van Linthoudt, Ott H. (1987). Supraacetabular and femoral head stress fracture during fluoride treatment. Gerontology 33:302-306.

“True clinical osteomalacia can be induced by fluoride in the right circumstances, as a direct side effect of fluoride.”
SOURCE: Kleerekoper M. (1983). Surgeon General’s Ad Hoc Committee on ‘Non-Dental Health Effects of Fluoride.” Transcript of Proceedings, National Institutes of Health, Bethesda, Maryland, April 19.

“Combinations of osteomalacia, osteoporosis, and osteosclerosis (in fluorosis) result in a spectrum of bone changes from an early age.”
SOURCE: Christie DP. (1980). The spectrum of radiographic bone changes in children with fluorosis. Radiology 136:85-90.

“Fluoride alone leads to accumulation of unmineralised bone, producing the histological picture of osteomalacia. The addition of calcium or vitamin D, or both, is believed to prevent this complication. We report a case where osteomalacia developed during sodium fluroide treatment despite large doses of vitamin D…”
SOURCE: Compston JE, et al. (1980). Osteomalacia developing during treatment of osteoporosis with sodium fluoride and vitamin D. British Medical Journal 281: 910-1.

5) Humans with Skeletal Fluorosis:

The studies referenced here concern osteomalacia in adult skeletal fluorosis. To see the studies on osteomalacia (i.e., “rickets”) in childhood skeletal fluorosis (rickets”), click here.

“An iliac crest bone biopsy revealed an increased amount of thick unmineralized osteoid as well as a large number of osteoclasts and associated resorption cavities, consistent with osteomalacia.”
SOURCE: Hallanger Johnson JE, et al. (2007). Fluoride-related bone disease associated with habitual tea consumption. Mayo Clinic Proceedings 82(6):719-24.

“Heavy and prolonged consumption of tea may be capable of inducing fluoride-related osteomalacia manifesting as unexpected spontaneous bone fractures.”
SOURCE: Hayem G, Ballard M, Palazzo E, Somogyi N, Roux F, Meyer O. (2004). Insufficiency bone fractures due to fluorosis in heavy tea drinkers. Annals of the Rheumatic Diseases 63(Suppl 1): 488.

“Skeletal fluorosis caused by endemic fluorine poisoning was once thought to result merely in osteosclerosis, causing marblelike changes. Later, various radiologic features were found, including osteosclerosis, osteomalacia, and osteoporosis. Although this disorder has a wide variety of appearances, little attention has been given to the spectrum of radiologic appearances.”
SOURCE: Wang Y, et al. (1994). Endemic fluorosis of the skeleton: radiographic features in 127 patients. American Journal of Roentgenology 162:93-8.

“High F intakes have been associated wtih a wide spectrum of bone diseases including osteosclerosis, osteoporosis, osteomalacia and exostoses… The pathogenic mechanisms underlying fluorosis of the mineralizing tissues have been studied extensively, but are still a matter of controversy.”
SOURCE: Kragstrup J, et al. (1989). Effects of fluoride on cortical bone remodeling in the growing domestic pig. Bone 10:421-424.

“Osteomalacia and osteoporosis may occur in older persons who ingest excessive fluorides (over 10-25 mg/d for 10-20 years).”
SOURCE: Ellenhorn MJ, Barceloux DG. (1988). Medical Toxicology: Diagnosis and Treatment of Human Poisoning. Elsevier; New York. pp. 534.

“It is evident that osteomalacia is a feature of fluorosis, particularly in children and young males.”
SOURCE: Krishnamachari KA. (1986). Skeletal fluorosis in humans: a review of recent progress in the understanding of the disease. Progress in Food and Nutrition Sciences 10(3-4):279-314.

“Metabolic bone disease occurred more frequently in residents of endemic (fluorosis) areas than in residents of nonendemic areas whose nutritional status was comparable. Common metabolic bone disorders, associated with endemic skeletal fluorosis, were osoteoporosis (bone resorption), rickets, osteomalacia, and parathyroid bone disease.”
SOURCE: Teotia SPS, et al. (1984). Environmental fluoride and metabolic bone disease: an epidemiological study (fluoride and nutrient interactions). Fluoride 17: 14-2.

“Some cases showed axial osteosclerosis exclusively, others axial osteosclerosis in association with peripheral osteoporosis or osteomalacia.”
SOURCE: Daijei H. (1984). Further observations on radiological changes of endemic foodborne skeletal fluorosis. Fluoride 17: 9-14.

“The osseous changes in fluorosis have been described as osteosclerosis, exostosis, hyperostosis, osteoporosis, osteomalacia, and rickets. Many questions arise as to why sometimes one type of osteopathy is induced and another at other times.”
SOURCE: Krook L, Maylin GA. (1979). Industrial fluoride pollution. Chronic fluoride poisoning in Cornwall Island cattle. Cornell Veterinarian. 69(Suppl 8): 1-70.

5) Fluoride-Exposed Animals:

“Our study also demonstrated evidence of osteomalacia in rats receiving 15 ppm fluoride, or the equivalent of 3 ppm fluoridated water for humans.”
SOURCE: Turner CH, et al. (1996). High fluoride intakes cause osteomalacia and diminished bone strength in rats with renal deficiency. Bone 19:595-601.

“The effect of fluoride on bone appears to be one of increased turnover with matrix formation exceeding resorption. Mineralization of newly-formed matrix is imperfect and much of the bone appears as woven or immature bone with components of unmineralized matrix resembling osteomalacia.”
SOURCE: Riggins RS, et al. (1974). The effects of sodium fluoride on bone breaking strength. Calcified Tissue Research 14: 283-289.

“The osteofluorotic lesions may be porosis, sclerosis, hyperostosis, osteophytosis, and malacia, depending on the interacting factors influencing the degree of fluorosis.”
SOURCE: Shupe JL, Olson AE. (1971). Cinical aspects of fluorosis in horses. Journal of the American Veterinary Association 158: 167-174.

“The changes produced in experimental animals… have been described as resembling osteomalacia by Roholm (1937), osteoporosis by Kellner (1939) and osteomalacia and rickets by Bauer (1945).”
SOURCE: Faccini JM. (1969). Fluoride and bone. Calcified Tissue Research 3:1-16.

“a small number of studies in animals and in man have indicated that osteomalacia is the prevailing response to administration of fluoride.”
SOURCE: Jowsey J, et al. (1968). Some results of the effect of fluoride on bone tissue in osteoporosis. Journal of Clinical Endocrinology 28:869-874.

“Very high levels of fluoride resulted in severe osteomalacia.”
SOURCE: Johnson LC. (1965). Histogenesis and mechanisms in the development of osteofluorosis. In: H.C.Hodge and F.A.Smith, eds : Fluorine chemistry, Vol. 4. New York, N.Y., Academic press. 424-441.

“The effects of fluorine on the osseous system are complicated, which may explain some of the apparently contradictory experimental observations. Both diffuse sclerosing processes, and a generalized condition resembling osteomalacia are observed.”
SOURCE: Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the literature and some experimental investigations. London: H.K. Lewis Ltd.

“For practical reasons the bone affection resulting from the severe fluorine intoxication, accompanied by general symptoms, has been called osteomalacia… Common features are the reduced strength of the bones, the tendency to form exostoses, bone atrophy, and a deficient calcification.”
SOURCE: Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the literature and some experimental investigations. London: H.K. Lewis Ltd.