Abstract
Bone fragility during fluoride therapy for osteoporosis was observed in 24 (37.5%) of 64 patients treated with sodium fluoride, calcium, and vitamin D for 2.5 years who developed episodes of lower-limb pain during treatment. Eighteen (28%) of these patients had clinical and roentgenographic features of 41 stress fractures and 12 new spinal fractures. There were 26 periarticular, six femoral neck, three pubic rami, three tibia and fibula, one greater trochanter, and two subtrochanteric fractures. Vertebral fractures appeared first, then periarticular, then femoral neck, and lastly long-bone shaft fractures. All fractures were spontaneous in onset. The peripheral fracture rate during treatment was three times that in untreated osteoporosis. Roentgenograms must be repeated at intervals of three to four weeks before the pathognomonic callus becomes visible, and the diagnosis can be made. Trabecular stress fractures tend to occur in the first 18 months of treatment, and cortical stress fractures occur after 30 months of therapy.
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Patterns of fracture among the United States elderly: geographic and fluoride effects
The purpose of this study was to examine whether geographic area or water fluoride were related to the occurrence of fractures among the elderly in the United States. We used a 5% sample of the white U.S. Medicare population, aged 65 to 89 years during the period 1986-1990, to identify
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Marked decrease in trabecular bone quality after five years of sodium fluoride therapy--assessed by biomechanical testing of iliac crest bone biopsies in osteoporotic patients
Sodium fluoride has for more than 2 decades been a commonly used therapeutic agent for established osteoporosis because of a repeatedly documented anabolic effect on trabecular bone mass. Recently, however, three controlled trials have failed to demonstrate any therapeutic advantage of NaF over placebo with respect to vertebral fracture rate.
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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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Abnormal bone mineralization after fluoride treatment in osteoporosis: a small-angle x-ray-scattering study
Sodium fluoride treatment of osteoporosis is known to stimulate bone formation and to increase bone mass, but recent clinical trials failed to prove its antifracture effectiveness. The formation of bone with abnormal structure and, therefore, increased fragility is discussed as a possible explanation. Until now, however, exact information on the
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Fluorosis as a probable factor in metabolic bone disease in captive New Zealand native frogs (Leiopelma species)
This report describes the investigations into the cause and treatment of metabolic bone disease (MBD) in captive native New Zealand frogs (Leiopelma spp.) and the role of fluoride in the disease. MBD was diagnosed in Leiopelma archeyi and Leiopelma hochstetteri in 2008 at three institutions: Auckland Zoo, Hamilton Zoo, and
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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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"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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Clinical Trials: Fluoride Treatment & Bone Fracture in Osteoporosis Patients
Due to its ability to increase bone mass, fluoride has been used as an experimental treatment for osteoporosis. The results, however, have generally been disastrous. Rather than prevent bone fractures in osteoporosis patients, fluoride therapy (at doses of 20-34 mg/day) was repeatedly found to increase fracture rates. One of the most
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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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In Vitro Studies on Fluoride & Bone Strength
The "in vitro" research on fluoride and bone strength confirms what has repeatedly been found in animal and human studies: the more fluoride a bone has, the weaker the bone becomes. In an in vitro bone study, the researcher directly exposes a human or animal bone to a fluoride solution
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