Abstract
Bone mass and architecture in appendicular and most axial sites is controlled primarily by the tissue-loading history. We introduce a conceptual framework for understanding how fluoride treatment alters this control and can cause systemic increases in bone mass. Due to possible adverse influences of fluoride on the mineralized tissue physical characteristics, however, the increase in bone mass does not necessarily result in an increase in bone strength. Using engineering analyses of bone trabeculae, we calculate the losses in trabecular strength which can be caused by the presence of hypomineralized or hypermineralized fluorotic tissue. Significant increases in bone volume fraction and bone mass may be required to overcome these strength deficits.
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Osteoporosis Treatments Affect Bone Matrix Maturation in a Rat Model of Induced Cortical Remodeling.
The example of sodium fluoride (NaF) clearly demonstrates an instance where increasing bone mass while altering maturation can negatively affect drug efficacy. NaF was a promising osteoporosis treatment because it increased BMD.5 However, it became evident that the treated patients were at increased risk of fracture,6, 7 which was later
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The effect of tamoxifen and fluoride on bone mineral density, biomechanical properties and blood lipids in ovariectomized rats
The most important aspect of therapy with fluoride and tamoxifen concerns its influence on bone tissue and lipid metabolism. The aim of the study was to evaluate the effect of tamoxifen and natrium fluoride (NaF) on bone metabolism, biochemical properties and blood lipids levels in ovariectomized rats. The study was
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Three-year effectiveness of intravenous pamidronate versus pamidronate plus slow-release sodium fluoride for postmenopausal osteoporosis
All currently available and approved therapies for osteoporosis inhibit bone resorption. But, despite their great value, antiresorptive agents are generally not associated with dramatic increases in bone mass. In light of these data, the aim of our prospective, placebo-controlled, randomized clinical trial, with a 3-year follow up, was to examine
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Effect of fluoride treatment on the fracture rate in postmenopausal women with osteoporosis
Although fluoride increases bone mass, the newly formed bone may have reduced strength. To assess the effect of fluoride treatment on the fracture rate in osteoporosis, we conducted a four-year prospective clinical trial in 202 postmenopausal women with osteoporosis and vertebral fractures who were randomly assigned to receive sodium fluoride
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Elevated serum fluoride concentrations in women are not related to fractures and bone mineral density.
Epidemiologic studies of the relations between drinking-water fluoride levels and bone mineral density (BMD) and fracture are characterized by disparate conclusions and an absence of information about individual circulating fluoride levels. This study relates serum fluoride concentrations, which reflect individual fluoride exposures, to BMD and bone fractures. Data are from
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Mechanisms by which fluoride may reduce bone strength
Based on a large body of animal and human research, it is now known that fluoride ingestion can reduce bone strength and increase the rate of fracture. There are several plausible mechanisms by which fluoride can reduce bone strength. As discussed below, these mechanisms include: Reduction in Cortical Bone Density De-bonding of
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Fluoride & Spontaneous Hip Fractures in Osteoporosis Patients
Due to its ability to increase vertebral bone mass, fluoride has been used as an experimental treatment for osteoporosis (doses > 20 mg/day). Fluoride treatment, however, proved far more harmful than beneficial. Not only was fluoride therapy shown to increase fracture rates among the treated patients, it was also found to
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The Relationship Between Fluoride, Bone Density, and Bone Strength
Although fluoride has generally been found to reduce the bone density of cortical bone, it is well documented that fluoride can increase the density of trabecular bone (aka cancellous bone). Trabecular bone is the primary bone of the spine, whereas cortical bone is the primary bone of the legs and arms. While increases in
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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