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Skeletal Fluorosis

“Although skeletal fluorosis has been studied intensely in other countries for more than 40 years, virtually no research has been done in the U.S. to determine how many people are afflicted with the earlier stages of the disease, particularly the preclinical stages." - Chemical & Engineering News

Skeletal Fluorosis

Prolonged, excessive exposure to fluoride can cause a debilitating bone disease known as skeletal fluorosis. The disease develops insidiously and can be difficult to distinguish from a number of other bone and joint diseases. Research shows that individual susceptibility to fluorosis varies greatly across the population, both with respect to the doses and duration of exposure that can cause the disease, and the skeletal manifestations and symptoms that result. Although skeletal fluorosis used to be considered a non-issue in the United States and other western countries, recent research suggests that many people — particularly heavy tea drinkers and those with kidney impairment — may unknowingly be suffering from some form of the disease.

Skeletal Fluorosis: A “Diagnostic Riddle”

One of the reasons doctors fail to detect skeletal fluorosis is because — whether in its early or late stages — the symptoms and appearance of fluorosis can closely resemble other, more commonly known, bone and joint diseases.

In the initial stages of fluorosis, known as the ”pre-skeletal“ phase, a patient may suffer a variety of symptoms in the absence of any detectable bone changes, including joint pains, joint stiffness, and gastric distress. (Czerwinski 1988; Cook 1971). The absence of bone changes makes this pre-skeletal phase difficult to diagnose, because the symptoms are indistinguishable from common forms of arthritis, such as osteoarthritis and rheumatoid arthritis.

Even when bone changes do develop, correct diagnosis can remain elusive. This is because the bone changes in skeletal fluorosis mimic the bone changes in other diseases, including osteoarthritis, renal osteodystrophy, spondylosis, DISH, Paget’s Disease, and osteopetrosis. In 2011, for example, a team of U.S. scientists reported that a Georgia woman with crippling skeletal fluorosis, as evident by her severe hunchback (“kyphosis”), had to wait up to 18 years before doctors were able to diagnosis her condition as being caused by fluoride. (Whyte 2011). Other U.S. studies have reported similar results. (Sauerbrunn 1965). If a doctor cannot diagnose fluorosis when it reaches the crippling stage, it is doubtful that he or she will be able to detect the earlier, subtler forms of the disease.

Outdated science

For over 40 years, U.S. health authorities insisted that skeletal fluorosis can not develop unless a person ingests 20 milligrams of fluoride per day for over 10 years. U.S. health authorities now concede, however, that skeletal fluorosis can occur at doses as low as 10 mg/day. (NRC 1993; Whitford 1996; IOM 1997; ATSDR 2003). This revised estimate, however, is itself outdated. This is evident, for example, by the following data from a large-scale study in China which found that average doses of just 6.2 to 6.5 mg/day were sufficient to cause stage 1 skeletal fluorosis (a form of fluorosis in which bone changes are detectable on x-ray). Since arthritic symptoms can occur prior to the bone changes of stage 1 fluorosis, the doses that can cause arthritic symptoms would appear to be less than 6 mg/day.

Another error underlying U.S. safety standards is the notion that skeletal fluorosis does not occur at water fluoride levels below 8 ppm. (IOM 1997; EPA 1985).  Studies in India and China have repeatedly documented skeletal fluorosis at levels as low as 0.7 to 1.5 ppm fluoride. Even studies in the United States — despite being very small in scope — have reported advanced skeletal fluorosis in kidney patients at 1.7 ppm, (Johnson 1979) and crippling skeletal fluorosis at just 2.2 to 3.5 ppm. (Sauerbrunn 1965).

Individual susceptibility to fluorosis varies greatly across the population

The claim that skeletal fluorosis cannot occur if an individual consumes less than 10 mg/day of fluoride obscures the individual variability, and complexity, of fluorosis. As with any other toxic substance, individual susceptibility to fluoride varies considerably across the population. Research has documented, for example, that:

  • some individuals can develop skeletal fluorosis despite having “safe” levels of fluoride in their bones and without any known excessive exposure to fluoride; (Sandberg 1985)
  • individuals receiving the same dose of fluoride can exhibit dramatically different bone responses; (Chachra 2010)
  • individuals with pre-skeletal fluorosis can suffer excruciating pain, while individuals with advanced fluorosis can remain symptom-free; (Franke 1975)
  • although U.S. health authorities claim that fluorosis only develops after 10 or more years of exposure, children can develop the disease in as little as 6 months, (Teotia 1998), and some adults have developed it in as little as 2 to 7 years (Gerser 1983; Fratzl 1995; Felsenfeld 1991).

Skeletal fluorosis looks different in different individuals 

Skeletal fluorosis is a far more complex disease than is generally perceived. This fact is highlighted by the very different forms the disease can take based on an individual’s nutritional status, health status, age, genetics, and exposure to aluminum. Whereas the dominant feature of skeletal fluorosis is generally considered to be hyper-dense bone in the spine (axial osteosclerosis), research has documented that:

  • some fluorosis victims can suffer primarily from osteoarthritis without noticeable osteosclerosis in the spine,
  • other fluorosis victims can suffer primarily from osteomalacia, osteoporosis, and/or secondary hyperparathyroidism without prominent  osteosclerosis.

To the extent that doctors rely on osteosclerosis in the spine as the telltale marker of fluorosis, victims will continue to fall through the cracks.

Common Causes of Fluorosis

Excessive fluoride exposure from any source — and from all sources combined — can cause skeletal fluorosis. Certain exposure pathways, however, present a uniquely high risk. These pathways include:

  • Fluoridated Water for Kidney Patients
  • Excessive Tea Consumption
  • High-Fluoride Well Water (more likely to be a factor among deep wells)
  • Industrial Fluoride Exposure
  • Fluorinated Pharmaceuticals (Voriconazole & Niflumic Acid)
  • Indoor coal burning (a common practice in China).
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