- 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.
Diagnosis of endemic skeletal fluorois: clinical examination vs. X-rays.
Objective: To compare the diagnosis of endemic skeletal fluorosis by means of clinical examination to diagnosis by x-ray, in order to provide a foundation for revising standards of clinical diagnosis for endemic osteofluorosis. Method: The study was carried out using existing data. The fluoride levels of 15 villages in the Qianan
Prevention of bony fluorosis in aluminum smelter workers. A 15-year retrospective study of fluoride excretion and bony radiopacity among aluminum smelter workers -- Pt. 4
1. Fifty six aluminum smelter workers with 10 to 43 years' occupational exposure, and who had been previously studied medically, were re-x-rayed. Average urinary fluoride concentrations since 1960 were estimated to range from 2.78 mg/liter preshift and 7.71 mg/liter postshift. 2. Roentgenographic studies in 1960-66 and 1974 failed to reveal
Effects of fluoride on the ultrastructure and expression of Type I collagen in rat hard tissue
Long-term excessive fluoride (F) intake disrupts the balance of bone deposition and remodeling activities and is linked to skeletal fluorosis. Type I collagen, which is responsible for bone stability and cell biological functions, can be damaged by excessive F ingestion. In this study, Sodium fluoride (NaF) was orally administrated to
Fluoride osteosclerosis simulating carcinoma of the prostate with widespread bony metastasis: a case report
A case of extensive fluoride osteosclerosis is presented because of its roentgenographic similarity to carcinoma of the prostate with widespread bony metastasis. Roentgenographic manifestation of the effects of fluoride in human bones occurs only rarely and is infrequently recognized. Although no treatment is indicated in this condition, it should be
Dental and early-stage skeletal fluorosis in children induced by fluoride in brick-tea
Fluorosis from brick-tea was discovered during the last decade in western and northern parts of China. Dental fluorosis has a high prevalence among children in these brick-tea endemic areas, but skeletal fluorosis does not normally become apparent until adulthood. In July 2002 we examined 132 primary school children, age 8
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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.
X-Ray Diagnosis of Skeletal Fluorosis
In 1937, Kaj Roholm published his seminal study Fluorine Intoxication in which he described three phases of bone changes that occur in skeletal fluorosis. (See below). These three phases, which are detectable by x-ray, have been widely used as a diagnostic guide for detecting the disease. They describe an osteosclerotic bone disease that develops first in the axial skeleton (the spine, pelvis, and ribs), and ultimately results in extensive calcification of ligaments and cartilage, as well as bony outgrowths such as osteophytes and exostoses. Subsequent research has found, however, that x-rays provide a very crude measure for diagnosing fluorosis since the disease can cause symptoms and effects (e.g., osteoarthritis) before, and in the absence of, radiologicaly detectable osteosclerosis in the spine.
Fluoride & Spondylosis; Spondylitis
Among individuals with skeletal fluorosis, the fluoride-induced changes to the spine, and the accompanying symptoms, can bear a close resemblance to spondylosis and spondylitis (as well as DISH). Spondylosis is a (non-inflammatory) degenerative disease of the spine marked by bony outgrowths (spurs) which can produce nerve cord compression. Spondylitis, by contrast, is an inflammatory form of arthritis that causes inflammation in the joints between the vertebrae. Whereas spondylosis is generally asymptomatic, spondylitis generally causes significant pain and stiffness in the spine.
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