One of fluoride’s most well-defined effects on bone tissue is it’s ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture — a condition known as osteomalacia. When osteomalacia develops during childhood, it is called “rickets.” The potential for fluoride to cause rickets was first identified in the 1930s by a doctor in Texas. The doctor observed that, in one of Texas’s high-fluoride areas:

“Some of these babies have more tendency to bowing of the legs, even in the face of constant antirachitic therapy, thus suggesting the theory that the toxic fluorides interfere with the bone and dental metabolism.”
SOURCE: Lemmon JR. (1934). Mottled enamel in children: a resume with consideration of clinical and etiological factors. Texas State Journal of Medicine 30: 332-336.

In the wake of this study, the Director of Public Health for Oklahoma’s Panhandle District conducted physical examinations of children with dental fluorosis. Based on these examinations, the health officer stated:

“it would seem reasonable to think or assume and I think can safely be stated here that chronic fluorosis has a definite relation to child development and thus a predisposition to rickets, poor posture and under weight and possibly a predisposition to fractures.”
SOURCE: Blue JA. (1938). Mottled enamel in Oklahoma Panhandle, and its possible relations to child development. Journal of the Oklahoma State Medical Association 31:295-301.

Based on these findings and prior evidence suggesting that “a low calcium intake hastens the onset and development of this chronic fluorine poisoning,” the Oklahoma health officer recommended that children living in areas with elevated fluoride levels in the water receive extra calcium supplementation.

While little American research has since been done to understand the fluoride/rickets relationship, researchers in Africa, India, and China have repeatedly confirmed that fluoride can cause rickets, particularly in children with suboptimal calcium intake.

Research on Fluoride & Rickets

“Fluoride levels in drinking water sources were measured and the prevalence of DF [dental fluorosis] and deformities due to SF [skeletal fluorosis] were assessed in children attending school in the two villages. The assessment also recorded the source of drinking water as well as children’s height, weight and 3-day food diaries. Over one-quarter of the children in both villages had skeletal deformities [knock-knee, bowed legs, sabre tibia], despite one village having much higher levels of fluoride in its drinking water sources. More than 90% of children in both villages had DF. SF and DF are major problems in this area. Deformities relating to SF are common, but the reasons for individual susceptibility remain unclear and may include a low calcium diet, ingestion of magadi (local salt) with high fluoride, or genetic factors… Unlike DF, bone deformities caused by a high intake of fluoride do not necessarily occur during the first 2 years of life; rather, it is expected that these will appear during the first weight-bearing stages as the bones are still developing and will affect the major weight-bearing bones, i.e. the legs. Thus, if a population of all ages began drinking water high in fluoride at the same time, we would expect to see the most obvious deformities in younger children and to a lesser extent teenagers.”
SOURCE: Shorter JP, et al. (2010). Comparison of two village primary schools in northern Tanzania affected by fluorosis. International Health 2:269-74.

“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 had often been mistaken for rickets, renal osteodystrophy, osteosclerosis and hereditary osteopathies etc… The findings strongly suggest that children with calcium deficiency rickets reported in the literature should be re-investigated for possible fluoride interactions… This aspect has not been analysed in any of the reports published on calcium deficiency rickets. A greater index of clinical acumen is, therefore, necessary to differentiate calcium disorders in childhood from fluoride and calcium interaction syndromes of bone disease and deformities…”
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.

“Three children demonstrated some features resembling rickets in the form of fraying of metaphyses and apparent widening of the epiphyseal cartilage. These patients also had subperiosteal resorption of phalanges…A rickets-like picture may be a manifestation of the mineralization defects induced by fluoride toxicity…”
SOURCE: Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis: relationship with calcium intake. Skeletal Radiology 22: 257-61.

“In skeletal fluorosis mineralization defects in mineralized bone are common but are not specific of this pathology since (similar defects) have been reported in renal osteodystrophy, vitamin D-treated osteomalacia, vitamin D-resistant rickets…”
SOURCE: Boivin G, et al. (1989). Skeletal fluorosis: histomorphometric analysis of bone changes and bone fluoride content in 29 patients. Bone 10:89-99.

“Osteomalacia has been found in osteoporotic patients treated with sodium fluoride alone, and increased prevalence of rickets has been reported for children from a high fluoride area.”
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.

“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

“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. The pathogenesis of the osseous changes in fluorosis has not been uncovered. Hodge and Smith (1965) commented on the cellular mechanisms whereby the bone lesions are induced in fluorosis: ‘Questions are many, and answers are few, indeed, practically non-existent.'”
SOURCE: Krook L, Maylin GA. (1979). Industrial fluoride pollution. Chronic fluoride poisoning in Cornwall Island cattle. Cornell Veterinarian 69(Suppl 8): 1-70.

“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.

“the new tissue (formed under fluoride therapy) had the characteristic appearance of bone from patients with rickets.”
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.

“Fluoride has been reported to result in sclerosis of the skeleton; on the other hand, recent studies have shown that fluoride may also produce rickets in young animals and osteoid tissue in adult animals and in human beings.”
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.

“An abnormal number of haversian canals are filled with calcified connective tissue. There are osteocytes with adjacent low mineral-density tissue and wide osteoid borders, features characteristic of rickets.”
SOURCE: Adams PH, Jowsey J. (1965). Sodium fluoride in the treatment of osteoporosis and other bone diseases. Annals of Internal Medicine 63: 1151-1155.

“Some of the manifestations of fluoride feeding reported here and in previous work recall the classical rachitic syndrome: decreased growth, decreased and imperfect mineralization, hypertrophy of the costochondral junction, and overproduction of osteoid.”
SOURCE: Belanger LF, et al. (1958). Rachitomimetic effects of fluoride feeding on the skeletal tissues of growing pigs. American Journal of Pathology 34: 25-36.

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