Abstract
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 ratio of sialic acid content vs glycosaminoglycans revealed there was a 50% reduction in rabbit and human sera. The test is recommended for evaluating the prognosis of fluoride poisoning/fluorosis.
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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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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
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Bone mineral structure after six years fluoride treatment investigated by backscattered electron imaging (BSEI) and small angle x-ray scattering (SAXS): a case report
NaF, a bone formation stimulating agent, is used for the treatment of osteoporosis. Controversy exists concerning the quality of the newly formed bone and the antifracture effectiveness. We report about a 70 years old woman, who had received 50 mg NaF/d for about 6 years. Calcium or Vit D supplements
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Bone and joint pathology in fluoride-exposed workers
Clinical and radiological investigations were performed for 2,258 aluminum workers exposed to fluoride for an average of 17.6 yr (standard deviation = 7.6). Changes in bone and joints were presented in detail in three groups: (1) exposed up to 5 yr (135 cases), (2) exposed from 6-32 yr (1,463 cases),
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The relationship between water-borne fluoride, dental fluorosis and skeletal development in 11-15 year old Tanzanian girls
Dental fluorosis was evaluated by a classification system, previously shown to be sensitive, and skeletal changes evaluated by bone maturity and structure. Dental fluorosis was more severe in posterior than in anterior teeth in both jaws irrespective of fluoride concentration of the drinking water. There appeared to be no dependence between fluoride content
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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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"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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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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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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