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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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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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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Fluoride and Biological Calcification I: Effect of Fluoride on Collagen-Induced In Vitro Mineralization and Demineralization Reactions.
An in vitro system employing collagen isolated from the sheep tendons to induce mineralization and demineralization reactions was used not only to study the effect of various concentrations of fluoride on the collagen-induced mineralization and demineralization reactions but also to compare their action with the inhibitors of mineralization and/or demineralization.
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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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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 Changes in Industrial and Endemic Fluorosis
Fluorotic changes in bones and joints were evaluated in 105 aluminum workers and 20 residents of an endemic fluorosis region in India.
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Fluoride & Spondylosis; Spondylitis
Among individuals with skeletal fluorosis, the fluoride-induced changes to the spine, and the accompanying symptoms, can bear a close resemblance to spondylosis and spondylitis (as well as DISH). Spondylosis is a (non-inflammatory) degenerative disease of the spine marked by bony outgrowths (spurs) which can produce nerve cord compression. Spondylitis, by contrast, is an inflammatory form of arthritis that causes inflammation in the joints between the vertebrae. Whereas spondylosis is generally asymptomatic, spondylitis generally causes significant pain and stiffness in the spine.
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