Abstract

The effect of drinking water fluoridation on the fluoride content of human bone, on cancellous bone strength and on the mineral density of bone was studied by analysing 158 autopsy samples of the anterior iliac crest from persons from two different areas. In the samples from the town of Kuopio, where drinking water has been fluoridated since 1959, the fluoride concentrations were considerably higher than in samples from the surrounding area where low-fluoride drinking water is used. The fluoride content of bones from Kuopio increased significantly with age, while considerably less change with age was found in samples from outside Kuopio. The highest fluoride content in bone ash was observed in women with severe osteoporosis. Cancellous bone strength measured by a strain transducer was statistically significantly higher in women with chronic immobilizing disease from Kuopio, compared with the corresponding group from outside Kuopio. No statistically significant differences in bone strength were found in men. There were no statistically significant differences in bone mineral density, as measured by gamma ray attenuation, between the samples from the fluoridated and non-fluoridated areas

• Related Studies :

  • The Effects of Calcium, Magnesium, Phosphorus, Fluoride, and Lead on Bone Tissue.

    Bones are metabolically active organs. Their reconstruction is crucial for the proper functioning of the skeletal system during bone growth and remodeling, fracture healing, and maintaining calcium-phosphorus homeostasis. The bone metabolism and tissue properties are influenced by trace elements that may act either indirectly through the regulation of macromineral metabolism,

  • Effects of fluoride on bone metabolism in patients with hemodialysis

    The maior pathway of fluoride elimination from the human body is the kidney. The discharge of fluoride into urine depends on the clearance of the kidney. Fluoride in serum of hemodialysis patients is higher than that of healthy subjects. Fluoride is not reduced sufficiently with hemodialysis. Those patients are in

  • Human vertebral bone: relation of strength, porosity, and mineralization to fluoride content

    Radiographically normal vertebral bone cylinders from 80 male subjects were tested mechanicallly by static compression and analyzed for porosity, fluoride and ash content. As a group, they had low fluoride content, suggesting little prior intake, consonent with this geographic area. Nevertheless, increasing levels of fluoride were associated with bulkier bone,

  • Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water

    Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six

  • Non-Endemic Skeletal Fluorosis: Causes And Associated Secondary Hyperparathyroidism (Case Report and Literature Review).

    Highlights Fluorocarbon “huffing” is an under-appreciated cause of skeletal fluorosis (SF) We present a SF case with hyperparathyroidism, osteosclerosis, and osteomalacia SF may go undetected due to variation in symptoms, radiology, and biochemistry Dietary calcium, prior bone health, and skeletal F exposure influence SF features SF is common in

• Related FAN Content :

  • "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.

  • 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.

  • 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.

  • Skeletal Fluorosis Causes Bones to be Brittle & Prone to Fracture

    It has been known since as the early as the 1930s that patients with skeletal fluorosis have bone that is more brittle and prone to fracture. More recently, however, researchers have found that fluoride can reduce bone strength before the onset of skeletal fluorosis. Included below are some of the

  • 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