- Chronic excess dietary fluoride intake contributes to degenerative joint disease.
- Species differences in lesion location largely explained by biomechanics of gait.
- Irrespective of bone fluoride, koalas show higher baseline prevalence of DJD.
- Increasing bone fluoride associated with prevalence of moderate and severe lesions.
- Inconsistencies in relationship explained by the effect of selective survival bias.
One of the manifestations of chronic fluoride toxicosis in mammals is skeletal fluorosis, which can include lesions of degenerative joint disease (DJD). Although DJD lesions have been less commonly studied than bone or dental lesions in relation to the pathology and epidemiology of fluoride toxicosis, there have been multiple independent studies in various species that have concluded that there appears to be an effect. The mechanisms by which fluoride affects the joints are not clear, but our data provide evidence that chronic excess dietary fluoride intake contributes to DJD. Our study is the first to specifically address the association between fluoride exposure and DJD in multiple species of free-ranging mammals. We describe levels of DJD in six marsupial species (Macropus giganteus, Notamacropus rufogriseus, Wallabia bicolor, Phascolarctos cinereus, Trichosurus vulpecula and Pseudocheirus peregrinus) inhabiting high and low fluoride environments. Lesions occurred to varying extents in all species, and lesion distribution varied with biomechanical differences in gait. In addition, we show an association (independent of age) between increasing bone fluoride concentration (as a measure of fluoride exposure) and increasing prevalence of moderate and severe DJD in five species of marsupial, which we propose does not persist at the highest levels of fluoride exposure due to selective survival bias.
[Spinal cord compression in bone fluorosis. Apropos of 4 cases].
The authors report four cases of spinal cord compression (three at cervical level and one at dorsal level) due to vertebral osteosclerosis secondary to chronic fluoride intoxication. Roentgenograms showed typical diffuse densification of vertebral bodies, calcifications of bony insertions of many ligaments, discs and interosseous membranes. Urinary fluoride was markedly
Lipid peroxidation and antioxidant enzyme status of adult males with skeletal fluorosis in Andhra Pradesh, India.
Blood samples from 24 adult males, age 25 to 40, with endemic skeletal fluorosis, living in the Vaillapally village of the Nalgonda district, Andhra Pradesh, India, were examined and compared with samples from 15 matched controls for their antioxidant enzyme activity and lipid peroxidation. Elevated malondialdehyde (MDA) levels indicated an
[Bone fluorosis without occupational exposure in chronic renal insufficiency].
Report on a 70-year-old male with bone fluorosis which was ascertained radiologically, by section and fluor analysis in the bone ash. With empty professional anamnesis as cause was found the presence of a chronic renal insufficiency with simultaneously increased fluor content of drinking water. The decreased renal excretion of fluoride
Sketetal changes in endemic fluorosis
Summary 1. The skeletal changes in endemic fluorosis are described from an area of the Punjab where the fluorine content of water and soil is very high. 2. A detailed description of a fluorotic skeleton is given, with its various anthropometric measurements. 3. The vertebral changes demonstrated the pathogenesis of the neurological complications
Aberrant methylation-induced dysfunction of p16 is associated with osteoblast activation caused by fluoride.
Chronic exposure to fluoride continues to be a public health problem worldwide, affecting thousands of people. Fluoride can cause abnormal proliferation and activation of osteoblast and osteoclast, leading to skeletal fluorosis that can cause pain and harm to joints and bones and even lead to permanent disability. Nevertheless, there is
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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.
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.
Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
Tea Intake Is a Risk Factor for Skeletal Fluorosis
A number of recent studies have found that heavy tea drinkers can develop skeletal fluorosis - a bone disease caused by excessive intake of fluoride.
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