It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride’s bone effects. As discussed in the following studies, fluoride increases the skeleton’s need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and vitamin D is available to mineralize the osteoid, the bone develops mineralization defects that can both weaken the bone and lead to clinical osteomalacia. As summarized by the National Research Council of Canada:
“There is . . . definite evidence that fluoride supplementation creates a greater metabolic requirement for calcium in humans. Much of this evidence has accrued from attempts to treat human osteoporosis by means of high doses of fluoride… If the calcium insufficiency is not corrected, fluoride supplementation can induce osteomalacia… Kyle et al. (1975) commented that “in the absence of additional calcium, the bone is incompletely mineralized. If fluoride administration continues…the net result will be osteomalacia and increased bone resorption.” To prevent osteomalacia, the calcium supplement must be “administered concurrently” with fluoride (Riggs and Jowsey 1972). Jowsey et al. (1972b) and Kyle et al. (1975) recommend that, in high-fluoride therapy, the calcium supplements, given concomitantly, should be 35 to 40 times the fluoride supplement, by weight… If this same fluoride-to-calcium proportionality applies to chronic daily intake of fluoride, then the ingestion of 5 mg of fluoride per day would require a supplemental intake of 200 mg calcium per day. This extrapolation may not be justified, but it serves to emphasize the need for an adequate intake of dietary calcium during long-term exposure to fluoride.””
SOURCE: Marier J, Rose D. 1977. Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.
Fluoride Increases Metabolic Requirement for Calcium & Vitamin D:
“Osteomalacia may be observed in fluorotic individuals with a reduced or suboptimal intake of calcium.”
SOURCE: World Health Organization. (2002). FLUORIDES. Environmental Health Criteria 227. World Health Organization, Geneva
“Recent evidence suggests that fluoride may cause osteomalacia by stimulating bone formation to the extent that there is inadequate calcium absorption to support the demand for increased mineral deposition. Fluoride could cause a calcium deficiency osteomalacia.”
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.
“When calcium intake is inadequate, the administration of fluoride also results in an impairment of mineralization.”
SOURCE: Lindsay R. (1990). Fluoride and bone: quantity versus quality (editorial). New England Journal of Medicine 322: 845-846.
“The prevalence of osteomalacia was much higher with high-dose NaF (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; although the numbers were too small for this difference to be significant, the increase was substantially greater in the absence of vitamin D. All patients on high-dose NaF had a dietary calcium intake of at least 1.5 g daily, but they might have benefited from a higher dose.”
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.
“When osteomalacia was observed in initial trials with fluoride, the mineralization defect was prevented by supplementation with calcium and vitamin D. An increasing number of studies have, however, found indications that mineralization defects may develop in spite of supplementation.”
SOURCE: Kragstrup J, et al. (1989). Effects of sodium fluoride, vitamin D, and calcium on cortical bone remodeling in osteoporotic patients. Calcified Tissue International 45(6):337-41.
“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… When fluoride is given with an adequate calcium intake, the newly formed matrix may become adequately mineralized.”
SOURCE: Pak CY. (1989). Fluoride and osteoporosis. Proceedings of the Society for Experimental Biology and Medicine 191: 278-86.
“Fluoride does, however, produce a high-turnover state in bone, and requirements for vitamin D and calcium may therefore be increased.”
SOURCE: Kragstrup J, et al. (1984). Experimental osteo-fluorosis in the domestic pig: a histomorphometric study of vertebral trabecular bone. Journal of Dental Research 63: 885-889.
“supplementary calcium improves therapeutic efficiency in two ways. It decreases the formation of excessive unmineralized osteoid by a mechanism that is not as yet understood. In addition, it prevents the increase in bone resorption which occurs when sodium fluoride is given alone.”
SOURCE: Riggs BL. (1983). Treatment of osteoporosis with sodium fluoride: An appraisal. Bone and Mineral Research 2: 366-393.
“Impaired bone mineralization producing thick osteoid seams has been a consistent histomorphometric finding in patients treated with sodium fluoride alone… The mineralization defect is less marked, and indeed, is sometimes absent when calcium supplements, with or without vitamin D, are given to patients treated with moderate doses.”
SOURCE: Riggs BL. (1983). Treatment of osteoporosis with sodium fluoride: An appraisal. Bone and Mineral Research 2: 366-393.
“The effect of fluoride on bone is dependent on the duration and degree of dosage and the concomitant use of such other agents as calcium, vitamin D, and estrogen.”
SOURCE: Vigorita VJ, Suda MK. (1983). The microscopic morphology of fluoride-induced bone. Clinical Orthopaedics and Related Research 177:274-282.
“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.
“Concurrent administration of supplementary calcium with or without vitamin D, however, is required to prevent or minimize defective bone mineralization that may occur when fluoride is given alone.”
SOURCE: Riggs BL, et al. (1980). Treatment of primary osteoporosis with fluoride and calcium: Clinical tolerance and fracture occurrence. Journal of the American Medical Association 243(5): 446-449.
“Morphologic studies of bone biopsy samples have shown that the predominant effect of fluoride therapy on the skeleton is osteoblastic stimulation. The newly formed osteoid tissue is poorly mineralized, resulting in the histologic picture of osteomalacia… We have shown that, when combined with vitamin D and calcium supplements, a dose of fluoride can be given which produces an increase in the formation of morphologically normal bone with a decrease in bone resorption.”
SOURCE: Jowsey J, et al. (1972). Effect of combined therapy with sodium fluoride, vitamin D and calcium in osteoporosis. American Journal of Medicine 53: 43-49.
“The microradiographic examination suggests that the tissue present within the NaF induced areas of new bone formation is atypical. Further experimentation is required to determine whether it is possible to eliminate this pathological mineralization of the matrix by combining NaF therapy with vitamin D, and, if necessary, calcium.”
SOURCE: Kuhlencordt F, et al. (1970). The histological evaluation of bone in fluoride treated osteoorosis. In: TL Vischer, ed. (1970). Fluoride in Medicine. Hans Huber, Bern. pp.169-174.
“a retardation of osteoid mineralization became obvious, showing its maximum after 40 weeks of treatment. In later periods of treatment, an apparent recovery from the mineralization delay was noted which might be partly due to reduction of the daily intake of sodium fluoride, and/or additional application of vitamin D. However, vitamin D, when administered together with F from the beginning, could not prevent a temporary surface osteomalacia.”
SOURCE: Reutter FW, et al. (1970). Fluoride in osteoporosis: clinical and quantitative histological studies on bone structure and bone remodelling. Fluoride 3: 209.
“If calcium and vitamin D are not administered wtih the fluoride, the new bone is largely uncalcified; however, if an increase in calcium absorption is produced, then the new bone tissue appears relatively normal.”
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.
“The study shows that elevated levels of calcium in the diet are capable of preventing the osteomalacic effects of high levels of fluoride.”
SOURCE: Burkhart JM, Jowsey J. (1968). Effect of variations in calcium intake on the skeleton of fluoride-fed kittens. Journal of Laboratory and Clinical Medicine 72: 943-50.
“The failure of mineralization of new tissue coincided with low calcium or phosphate levels in the serum.”
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.
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