Abstract
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 investigated in the present study. Although osteoporosis and osteoarthrosis showed a decrease in serum sialic acid (SA) levels, the mean ratio (SA/GAG) demonstrated no change from control values. Idiopathic backache showed no difference in any of the parameters studied when compared with control values. Ankylosing spondylitis and osteofluorosis had a remarkable similarity in their clinical and radiological features, but a divergent mean value of ratio was noted. The mean ratio of both the conditions also showed a statistically significant difference from the control value. This suggests that the SA/GAG ratio can be used as a diagnostic test in ankylosing spondylitis.
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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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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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Fluorosis-induced hyperparathyroidism mimicking a giant-cell tumour of the femur
We report the case of a young woman who, over a period of five years was diagnosed and treated for a giant-cell tumour of bone, osteomalacia and fluorosis. A review of the literature revealed a correlation between these three diagnoses, the primary pathology being fluorosis and the remaining symptoms being secondary manifestations. It
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Effect of ultrastructural changes on the toughness of bone.
The ultrastructure of bone can be considered as a conjunction between the biology and the biomechanics of the tissue. It is the result of cellular and molecular activities of bone formation, and its organization dominates the mechanical behavior of bone. Following this perspective, the objective of this review is to
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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 Causes Bones to be Brittle & Prone to Fracture
It has been known since as the early as the 1930s that patients with skeletal fluorosis have bone that is more brittle and prone to fracture. More recently, however, researchers have found that fluoride can reduce bone strength before the onset of skeletal fluorosis. Included below are some of the
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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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