Abstract

Despite having an exceptionally high fluorine (F) concentration in their bones (up to 9000 µg/g in the present study), radiographs of mature Ade?lie penguins (Pygoscelis adeliae) do not show any symptoms of skeletal fluorosis. In this research, a series of chemical fractionation and speciation analyses for F gave a tentative explanation for this seemingly abnormal fact. The results showed that the inorganic fraction of F in penguin bones represented only about one-third of the total F with the rest bound organically, mostly in the form of fluorinated chitin or its derivatives. A laboratory experiment with rats on a high F intake indicated that chitin might prevent skeletal fluorosis by effectively combining with F and inhibiting abnormal mineralization, thereby decreasing the expected increase in bone mineral density.

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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.

  • 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: 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.

  • Factors which increase the risk for skeletal fluorosis

    The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.