Abstract
Fluor osteopathy, as the authors suppose, is a morphologic repetition of phylogenesis early stages in osteogenesis. Thus, osteosclerosis and osteoporosis demonstrated by X-ray should be considered as manifestation of bone fluorosis. Fluor-induced changes of bone tissue could not be adequately termed as “osteoporosis” and “osteosclerosis”, so is defined as “fluor osteopathy”.
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Effect of fluoride on osteoclast formation at various levels of receptor activator of nuclear factor Kappa-B ligand (RANKL).
Receptor activator of nuclear factor kappa-B ligand (RANKL) acting on osteoblasts is an essential cytokine for osteoclast formation. Recent studies have shown that fluoride (F) can stimulate RANKL expression of osteoblasts. However, the effect of F under various levels of RANKL on osteoclast formation is not clear. In this study,
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Long-term exposure to the fluoride blocks the development of chondrocytes in the ducks: The molecular mechanism of fluoride regulating autophagy and apoptosis.
Highlights Long-term fluoride exposure blocks the development of chondrocytes. Excessive fluoride could induce chondrocytes apoptosis. Long-term excessive fluoride triggered autophagy. Fluoride-induced chondrocytes apoptosis is associated with CytC/Bcl-2/P53 pathways. Long-term exposure to excessive fluoride causes chronic damage in the body tissues and could lead to skeletal and dental fluorosis. Cartilage damage
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Skeletal fluorosis causing high cervical myelopathy
Skeletal fluorosis is endemic in some parts of the world and is the result of life-long ingestion of high amounts of fluoride in drinking water. Its clinical presentation is characterized mostly by bone and dental changes with later ossification of many ligaments and interosseous membranes. We present a rare case of high cervical myelopathy
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Expression of core-binding factor a1 and osteocalcin in fluoride-treated fibroblasts and osteoblasts
To study the effects and importance of fluoride on FBs in the development of extraperiosteal calcification and the ossification of skeletal fluorosis, the presence of the osteogenic phenotype, which is indicated by the expression of core-binding factor a1 (Cbfa1) and osteocalcin (OCN), in an FB cell line (L929) and in
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Recovery from skeletal fluorosis
Kurland et al.(1) reported a fascinating case of skeletal fluorosis in a man who probably ingested significant quantities of fluoride from toothpaste. They report that after withdrawal of fluoride, there was a short initial period of rapid bone loss, followed by a prolonged period of slow BMD loss from the
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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.
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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.
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Variability in Radiographic Appearance of Skeletal Fluorosis
Osteosclerosis (dense bone) is the bone change typically associated with skeletal fluorosis, particularly in the axial skeleton (spine, pelvis, and ribs). Research shows, however, that skeletal fluorosis produces a spectrum of bone changes, including osteomalacia, osteoporosis, exostoses, changes resulting from secondary hyperparathyroidism, and combinations thereof. Although the reason for this radiographic variability is not yet fully understood, it is believed to relate to the dose of fluoride consumed, the individual's nutritional status, exposure to aluminum, genetic susceptibility, presence of kidney disease, and area of the skeleton examined.
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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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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.
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