Abstract
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 rat at 150mgL–1 for 60 and 120d. We examined the effects of excessive F ingestion on the ultrastructure and collagen morphology of bone in rats by using transmission electron microscopy (TEM). Furthermore, we investigated the effect of F consumption on the expression levels of COL1A1 and COL1A2 in the bone tissues of rats by using quantitative real time (qRT)-PCR, to elucidate the molecular mechanisms of F-induced collagen protein damage. Our results showed that F affected collagen I arrangement and produced ultrastructural changes in bone tissue. Meanwhile, the mRNA expression of COL1A1 and COL1A2 were reduced and the COL I protein levels decreased in the fluorosis group. We concluded that excessive F ingestion adversely affected collagen I arrangement and caused ultrastructural changes in bone tissue. Reduced COL1A1 mRNA expression and altered COL I protein levels may contribute to the skeletal damage resulting from F exposure.
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Circulating levels of sialic acid and glycosaminoglycans: a diagnostic test for ankylosing spondylitis
The circulating levels of sialic acid (N-acetylneuraminic acid) and glycosaminoglycans (GAGs) were measured in 69 patients with spinal disorders of orthopaedic interest (ankylosing spondylitis 17, osteofluorosis 6, idiopathic backache 10, osteoarthrosis 16, osteoporosis 20). The serum GAG levels showed no statistically significant change from control values in the five disorders
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Excessive ingestion of fluoride and the significance of sialic acid: glycosaminoglycans in the serum of rabbit and human subjects
The levels of sialic acid and glycosaminoglycans were explored in the sera of rabbit and human subjects who ingested fluoride and had clinical manifestation of fluorosis. Changes observed in the level of these chemical constituents in sera possibly reflect changes occurring in calcified and noncalcified tissues due to fluoride intoxication. The
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[Histomorphometric profile of bone fluorosis induced by prolonged ingestion of Vichy Saint-Yorre water. Comparison with bone fluorine levels].
Nine transiliac bone biopsies from 7 patients with skeletal fluorosis due to prolonged ingestion of often high quantities of Vichy Saint-Yorre water were analyzed. Four of these patients also suffered from a chronic renal failure. A histomorphometric study was possible in 8 out of the 9 biopsies. The measurement of bone fluoride
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Toxic effect of fluoride on biochemical parameters and collagen metabolism in osseous and non-osseous tissues of rats
The present study was carried out to assess the effects of fluoride exposure on collagen metabolism by evaluating the level of hydroxyproline in both osseous and non-osseous tissues along with serum biochemical parameters in rats. Eight week old female rats were divided into two equal groups of six rats each.
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Histopathological assessment of endemic skeletal fluorosis
Nine patients with skeletal fluorosis were subjected to iliac crest biopsy because they presented with stiffness and bone pains. The histopathological findings are correlated with the clinical course, X-ray and laboratory data. All but one of the patients showed an increase in bone surfaces lined by osteoid and in these
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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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"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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Skeletal Fluorosis in the U.S.
Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.
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Fluoride & Arthritis
The doses that American adults now routinely ingest overlap the doses that may cause chronic joint pain.
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