Abstract
Young rats were maintained, over a 2-week period, on laboratory chow and distilled water or water supplemented with 200 ppm fluoride. Metaphyseal and diaphyseal bone of the femurs and tibias of control and treated rats were analyzed. After fluoride treatment there was a decrease of lipid and citrate content and a decreased glucose utilization and lactate formation. The decrease in lipid content in bone from fluoride-treated rats was not mediated through diminished food intake or diminished weight gain of the experimental animals. It was accompanied by a significant decrease in, and alteration of the pattern of, lipid formation from acetate-J4C and citrate-1% . The decrease in citrate content was due to neither a decreased formation from exogenous acetate nor to an increased utilization of citrate. In contrast to bone, there was no fluoride effect on the total lipid or citrate content of liver. Femurs of fluoride-treated rats exhibited a decrease in mechanical strength as manifested by a decrease in ultimate stress to breaking as well as decrease in limit and modulus of elasticity.
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Effect of sodium fluoride on bone biomechanical and histomorphometric parameters and on insulin signaling and insulin sensitivity in ovariectomized rats
Osteoporosis is a systemic disease characterized by bone degradation and decreased bone mass that promotes increased bone fragility and eventual fracture risk. Studies have investigated the use of sodium fluoride (NaF) for the treatment of osteoporosis. However, fluoride can alter glucose homeostasis. The aim of this study was to evaluate
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Anaesthesia and fluorosis.
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The genetic influence on bone susceptibility to fluoride
INTRODUCTION: The influence of genetic background on bone architecture and mechanical properties is well established. Nevertheless, to date, only few animal studies explore an underlying genetic basis for extrinsic factors effect such as fluoride effect on bone metabolism. MATERIALS AND METHODS: This study assessed the effect of increasing fluoride doses (0
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Changes in the concentration of fluoride in the serum and bones of female rats with streptozotocin induced diabetes.
The aim of this study was to determine if streptozotocin-induced diabetes in rats as a model for Type-1 human diabetes causes changes in the levels of fluoride (F) and biogenic elements in the bones and serum in the initial stage of the disease. Twenty-two female Wistar rats were given streptozotocin
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Changing the structurally effective mineral content of bone with in vitro fluoride treatment
Bovine femur cortical bone specimens were tested in tension after being treated in vitro for 3 days with sodium fluoride solutions of different molarity (0.145, 0.5, and 2.0M). The treatments alter the mechanical properties of the bone samples with different degrees as compared to control samples (untreated). The mechanical properties
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Fluoride & Insulin
Insulin is a hormone produced by the pancreas that is responsible for maintaining appropriate levels of glucose in the blood. Insulin allows the body’s cells to take up glucose from the blood, and either use it as an energy source or store it as glycogen. Blood glucose levels in diabetics
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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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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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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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