It is quite possible, and indeed likely, that current fluoride exposures contribute to and worsen the bone disease (renal osteodystrophy) that many people with advanced kidney disease suffer. This possibility is supported by the fact that patients with advanced kidney disease accumulate a large quantity of fluoride in their bone, and the spectrum of bone changes found in renal osteodystrophy closely resemble the spectrum of bone changes found among individuals with skeletal fluorosis. It is also supported by recent evidence showing that the levels of fluoride in the bones of dialysis patients are significantly associated with osteomalacic changes. (Ng 2004). Osteomalacia, a bone-softening disease which makes bone more subject to fracture, is a well-established effect from excessive fluoride exposure and is often found in people with skeletal fluorosis.
Even when fluoride is causing or exacerbating a patient’s renal osteodystrophy, fluoride’s role is likely to go undetected. As noted by Dr. Helmut Schiffl:
“The National Kidney Foundation in its ‘Position Paper on Fluoride—1980’ as well as the Kidney Health Australia express concern about fluoride retention in kidney patients. They caution physicians to monitor the fluoride intake of patients with advanced stages of kidney diseases. However, a number of reasons will account for the failure to monitor fluoride intake in patients with stages 4 and 5 of chronic kidney diseases and to detect early effects of fluoride retention on kidneys and bone. The safety margin for exposure to fluoride by renal patients is unknown, measurements of fluoride levels are not routine, the onset of skeletal fluorosis is slow and insidious, clinical symptoms of this skeletal disorder are vague, progression of renal functional decline is multifactorial and physicians are unaware of side effects of fluoride on kidneys or bone.”
Similarities between Skeletal Fluorosis and Renal Osteodystrophy
“Renal osteodystrophy may be difficult to distinguish from skeletal fluorosis on imaging studies.”
SOURCE: National Kidney Foundation. Fluoride Intake in Chronic Kidney Disease. April 15, 2008. [See full statement]
“As other causes of osteosclerosis, osteopenia, and calcification of ligaments and tendons are common in end-stage kidney disease, fluorosis may be overlooked until it reaches a late stage.”
SOURCE: Applbaum YK. (2010). Imaging of the skeleton and the joints in CKD. p. 208. In: The Spectrum of Mineral and Bone Disorders in Chronic Kidney Disease. (Olgaard K, Salusky IB, Silver J, eds.) Oxford University Press.
“The differential diagnoses included osteopetrosis, Paget disease, hyperparathyroidism, renal osteodystrophy, osteomalacia, and skeletal fluorosis. Given the patient’s history of well-water and instant-tea consumption, radiographic findings, and increased plasma fluoride [7 umol/L], the diagnosis of skeletal fluorosis was given.”
SOURCE: Isbel TS, Villareal-Armamento R. (2010). What Is Your Guess? A Case of Thick but Brittle Bones and Instant Tea. Clinical Chemistry 56(6):1041-42.
“Fluoride is bone-seeking due to its high affinity for calcium phosphate and therefore accumulates in bone. Radiological changes can be quite similar to changes of renal osteodystrophy, and therefore the diagnosis may be missed unless specifically investigated.”
SOURCE: Bansal R, Tiwari SC. (2006). Back pain in chronic renal failure. Nephrology Dialysis Transplantation 21:2331-2332.
“[E]levated bone fluoride content is frequently found in patients with uremia. Increased bone radiodensity, thus, appears to be related to the positive effects of parathyroid hormone on new bone formation in some patients with renal failure, and to fluoride accumulation in others.”
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38:833-35.
“[R]enal disease and fluoride cause similar changes. This overlap makes it very difficult to assess the effect of fluoride per se in these patients.”
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.
“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.”
SOURCE: Posen GA, et al. (1971). Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water. Fluoride 4: 114-128.
“The findings of osteosclerosis, osteomalacia and increased bone resorption have been confirmed in experimental fluorosis in animals. It can be seen, therefore, that fluoride bone disease could mimic renal osteodystrophy.”
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.
“[T]he 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.”
SOURCE: Posen GA, et al. (1971). Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water. Fluoride 4: 114- 128.
“Osteosclerosis from chronic renal disease associated with secondary hyperparathyroidism may produce similar changes (as fluorosis), and indeed may have intensified the findings (of fluorosis) in one of our patients.”
SOURCE: Morris JW. (1965). Skeletal fluorosis among indians of the American Southwest. American Journal of Roentgenology, Radium Therapy & Nuclear Medicine 94: 608-615.
In the fluoride-treated patients, “we observed osteoclasts resorbing bone beneath osteoid seams, and fragments of osteoid isolated in the bone marrow. This type of resorption beneath unmineralized bone matrix is often observed in osteomalacia, particularly that caused by renal abnormalities and associated secondary hyperparathyroidism.”
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.
“During our field studies our attention was drawn to the high incidence of bone disease and bony leg deformities with clinical invalidism in children exposed to high intake of endemic fluoride in drinking water. Due to variable and unusual clinical features, these children (with fluorosis) had often been mistaken for rickets, renal osteodystrophy, osteosclerosis and hereditary osteopathies etc.”
SOURCE: Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian Journal of Pediatrics 65:371-81.
“A 40-year-old American Indian woman with chronic pyelonephritis and renal failure complained of progressive muscular weakness, fatigue, and increasingly severe pain in her ribs, low back, and left hip. X-ray study of these areas showed evidence of osteosclerosis, compatible with either renal osteodystrophy or skeletal fluorosis… No other pathologic changes were apparent in the bones or ligaments…”
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.
Print 
PDF