Abstract
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 the same condition as being exposed to high level of fluoride for a long time.
In this study, serum fluoride and bone mineral density (BMD) were measured in 93 patients (45 males and 48 females, aged 29 – 86) to clarify effects of fluoride on the bone metabolism. BMD of the third lumbar spine and the distal 1/3 of the radius were measured by dual energy X-ray absorptiometry.
Both in male and female patients, serum fluoride and BMD of the lumbar spine increased and BMD of the radius decreased for a year. Relative changes of BMD of the lumbar spine had a high correlation with those of serum fluoride (male: r=0.81, p<0.05, female: r=0.74, p<0.01).
BMD of the lumbar spine was mainly influenced by fluoride in serum.
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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
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Fluoride and strontium accumulation in bone does not correlate with osteoid tissue in dialysis patients
BACKGROUND: Osteomalacia is now a rare disease in dialysis patients in developed countries since the withdrawal of aluminium overload. The involvement of fluoride and strontium in the pathogenesis of the disease has been suggested. The aim of this study was to investigate a possible association between osteomalacia in dialysis patients
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High fluoride concentrations in the serum and bone of patients with chronic renal failure
The aim was to study the effect of ingested fluoride in patients with chronic renal failure (CRF). Serum fluoride concentrations were measured in 104 subjects, who formed three groups: nondialyzed CRF, dialyzed CRF, and a control group. The iliac bone fluoride was measured in 20 subjects. Serum, urine and water
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Serum ionic fluoride levels in haemodialysis and continuous ambulatory peritoneal dialysis patients
High serum fluoride (F-) in patients with chronic renal failure (CRF) and end-stage renal disease (ESRD) is associated with risk of renal osteodystrophy and other bone changes. This study was done to determine F- in normal healthy controls and patients with ESRD on haemodialysis (HD) or peritoneal dialysis (PD). Seventeen
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Exposure to excessive fluoride during hemodialysis
Discussion These data indicate that a patient maintained by hemodialysis in a community using fluoridated water may be exposed to a fluoride concentration higher than that present in tap water if the deionizer is allowed to become exhausted while the patient is being dialyzed. The concentration reached 520 uM in the
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Fluoride & Osteomalacia
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid content of bone. Osteoid is unmineralized bone tissue. When bones have too much of it, they become soft and prone to fracture -- a condition known as osteomalacia. As shown below, fluoride has repeatedly been
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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 in the U.S.
Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.
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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
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