Fluoride's Effect on Bone and Related Factors

by T.C. Schmidt

Introduction

Bone tissue has long been recognized as a key accumulation site for some toxic substances. This is significant because fluoride actually accumulates in skeletal tissue, concentrating in the surface layers. Bone samples from cadavers show that fluoride content of the bone tissue can be correlated with that of the drinking water -- with certain bone changes becoming markedly increased when water fluoride contentexceeds 1.5 ppm (parts per million).

Thus, daily intake of fluoride that is supposed to be beneficial for developing teeth, may lead to skeletal fluorosis of varying degrees, plus certain disorders that are now becoming common in both the middle-aged and elderly if ingested throughout adult life. This was recently substantiated in a review showing that osteoporosis in the long bones may provide the earliest indicators of fluorosis, including calcification and/or ossification of the attachments of the soft-tissue structures to bone. Elevated parathyroid hormone is not uncommon in fluorosis and can play a major role in nervous system dysfunction and development of hypertension .

Lessons Learned from Treatment

Water fluoridation proponents like to tout that fluoride is used as a "treatment" for osteoporosis. Despite more than several decades of research controversy remains and it has not been approved by FDA. Even adherents now recommend that clinical trials include certain restrictions and very close monitoring for side effects that include gastro-intestinal problems. Clearly, bones that have more density are not necessarily more desirable.

While increased bulk may offset the reduced strength of vertebral bone, which is an indication of the fluoride content, it may also become more brittle and more likely to fracture on impact. Other studies regarding changes in mineral/collagen composite helped to explain the reduction in bio-mechanical properties due to fluoride treatment that were found in earlier research. These studies concluded that "the increase in bone mass during fluoride treatment does not translate into an improved bone strength -- rather, bone quality declines".

Additionally, this density is "achieved at the expense of bone-mineral in the peripheral cortical skeleton" (the hard shell encasing the bone). In further prospective clinical trials comparing fluoride treatment vs. a placebo, not only was there was no decrease in vertebral fracture rate, but there was an increase in non-vertebral (hip) fractures although that study included the use of calcium. The result was a 35% increase in bone mass but "the new bone was weak and structurally abnormal". Indeed, the difference in rate of hip fractures for fluoride treated patients vs. non-treated is ten-times higher than would normally be expected.

Likewise, fluoride treatment was found to result in a nine-fold increase in definitive osteomalacia, a condition which includes muscle weakness and bone loss.This was attributed to a prolonged mineralization lag time, as well as a resultant relative calcium deficiency. Although the deficiency might be expected to improve by incorporating calcium supplements, such a double blind clinical trial showed this to be no more effective than placebo in retarding the progression of spinal osteoporosis.

Similarly, fluoride with both calcium and vitamin D, is no more effective than calcium and vitamin D alone. That fluoride cannot be recommended to prevent fractures, the primary adverse health outcome of osteoporosis, is supported by studies using patient bone biopsies. These studies showed a significantincrease in bone fluoride level after one year and five years, however, after five years of "treatment," decreases in long bone strength and quality were 45% and 58%, respectively.

While the increased fragility and "abnormal texture" of bone tissue caused by fluoride treatment has been attributed to both hypo and hypermineralization, the net result is "identical to that of heavy fluorosis". This is characterized by the presence of additional large crystals, located outside the collagen fibrils. These calcium-fluoride crystals, which are not present before the fluoride treatment, contribute to increased mineral density with no improvement in mechanical properties.U.S. randomized double blind study shows no beneficial effect.Therefore, subsequent FDA Guidelines for Pre-clinical and Clinical Evaluation of Agents Used in the Prevention of Treatment of Postmenopausal Osteoporosis states "the relation between increased bone mass density and reduced fracture risk has been validated for patients receiving estrogens, but not fluoride".

Related Considerations

Fluoride is a cumulative toxin, adversely affecting the homeostasis of bone mineral metabolism. Total ingested fluoride is the most important factor determining the clinical course of osteo-fluorosis, which is on the increase world-wide. ;Research has shown that levels of 4-10 ppm in drinking water causes progressive ankylosis, or loss of cartilage, in various joints as well as crippling deformities regardless of other variables. Animal studies showed fluoridated water equivalent to only 3 ppm in humans results in reduced bone strength after six monthswhen accompanied by renal deficiency.

During treatment with fluoride for spinal osteoporosis, some patients suffered spontaneous bilateral hip fractures. Examination revealing severe osteo-fluorosis -- attributed to excessive retention of fluoride due to renal insufficiency. Fluoride can cause lesions in the kidney tubule. Acute renal failure results from accidental industrial exposure to fluoride, with the toxic effects on the kidneys related to serum fluoride level. Because fluoride is eliminated through the kidney, this results in aluminum deposition into bone. Decreased kidney function results in increasing serum fluoride thus initiating a vicious cycle. There is ample evidence of the toxic renal and other effects caused by a bottled mineral water at 8.5 ppm yet the Center for Disease Control calls for a normal control range for school fluoridation systems of up to 6.5-ppm

Some studies indicate that men may have an even greater susceptibility to the detrimental effects of fluoride on bone strength. A comparison of fluoridated and non-fluoridated areas revealed a significant increase in bone cancer among males under 30-years of age the animal model also produces bone cancers. For this reason a gender-specific physiologically based model has been developed to describe the absorption, distribution and elimination of fluoride. Testosterone deficiency is a major risk factor for male osteoporosis and fluoride use correlates with decreased testosterone levels as well as reduced sperm count and motility. It could be argued that this is the causative factor for reduced fertility rate in areas of the U.S. having fluoride levels of at least 3-ppm. That is, based on the deleterious testicular effects in three different animal modelsthis decrease in the total fertility rate due to ingested fluoride is paternal in nature.

Just as ingested fluoride has a deleterious effect on bone, the same is true for developing teeth. Dental fluorosis or mottling of the teeth is now having an incidence of 35-60% in fluoridated areas of North America. Most studies show no statistically significant decrease in the incidence of dental cavities from ingested fluoride. Cavities in permanent teeth increase with increasing dental fluorosis. The odds ratio for developing dental fluorosis increases with decreasing age of exposure, so children are at the greatest risk for this condition. There is also a correlation between fluoridation and elevated blood lead levels, with the heavily fluoridated North Eastern U.S. having a greater incidence than the less fluoridated Western portions.

A separate study found that increased brain lead concentrations was the cause of a significantly higher level of learning disabilities in the children of a community in the North East. The cause of the higher lead concentrations was the fluoride in the water supply. Just as fluoride is used by industry to etch metal, it also leaches lead from the solder joints of metal piping popular in the North East.

There is some consensus that any decrease in cavities over the past fifty years is not due to water fluoridation but to fluoridated dentifrice. The extent of that is now being questioned, with speculation as to the actual cause including changes in oral microbial flora. At the same time there is also evidence that detrimental effects on kidney function may occur at fluoride levels associated with the "misuse" of fluoridated dentifrice by children.

As CDC now "celebrates" the fifty-years of water fluoridation as being one of the greatest public health advances of the century, there has been documentation of a very significant (approximately 50%) decrease in human semen quality (both seminal volume and mean sperm density) coinciding with a very significant (300-400%) increase in testicular cancer over the past fifty-years While those references assert that this must be due to some (albeit undetermined) environmental pollutant, research shows decreased total fertility rate in the areas of the U.S. with water fluoride levels of at least 3-ppm.

In addition to being a "reproductive effector"(due to both paternal and maternal effects) the compound descriptors for sodium-fluoride in the NIOSH Registry of Toxic Effects of Chemical Substances (RTECS) also include "tumorigen" and "mutagen". The latter is based on more than 40 positive results including the following -- unscheduled DNA synthesis and DNA inhibition of human fibroblast, mutation in human lymphocyte and DNA inhibition in the human lung. Similarly, another review of genetic toxicity states that gene mutations in human cells were produced in the majority of cases, and "the weight of the evidence leads to the conclusion that fluoride does result in increased chromosome aberrations".

The "painful lower extremity syndrome" from fluoride treatment attributed to stress fractures may also have a connection with fibromyalgia, which is associated with chronic fatigue syndrome. There is a relationship between chronic fatigue and pineal gland calcification, with the latter consisting of crystals similar in size and structure to dentin and bone. Thus, fluoride’s potential to exacerbate certain tissue pathologies in general, deserves further consideration.

Similarly, the cognitive difficulties that result from exposure to fluoride are accompanied by general malaise and fatigue. Intolerance to low levels of environmental chemicals is an indication of chronic fatigue, fibromyalgia, etc. resulting from an immunological and/or a neurogenic triggering of somatic symptoms and inflammation. The earliest subjective symptoms of osteo-fluorosis are arthritic in nature.

Side-effects of fluoride treatment also include gastro-intestinal problems simply referred to as -- "symptoms" "intolerance" and "complaints". In two separate studies, the comparative results between patients receiving fluoride treatment for 3-12 months et al. and those having documented osteo-fluorosis were identical: 70% intestinal abnormalities and cellular inflammation, 70-90% chronic gastritis and 100% cellular abnormalities such as loss of intestinal microvilli. Moreover, these affects were also qualitatively similar to a study that correlated dyspepsia, a chronic intestinal condition, with ingested fluoride level.

As with osteoporosis, fluoride has been proposed as a preventive measure against Alzheimer’s Disease (AD) based on the presumption that by direct competition in the gut, fluoride would decrease aluminum uptake. Rather, such antagonism is due to the formation of aluminum-fluoride complex. Ithas been substantiated that fluoride can set of the potential for aluminum to be toxic for the brain. Also, fluoride decreases protein content of brain tissue with 7-months of exposure to 30 ppm fluoride resulting in a 10% decrease in total brain phospholipid content – as well as changes in brain levels of coenzyme-Q. Osteo-fluorosis is endemic in certain regions of China with detrimental effects of fluoride on the IQ of children now being documented.

Except for the introductory sentence (from a textbook); one CDC document; one study; two FDA documents; and the NIOSH RTECS the technical basis for this review has been LIMITED on purpose ONLY to those citations which are retrievable on-line from the National Library of Medicine (PubMed MEDLINE and/or Internet Grateful Med TOXLINE.