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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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 quality in fluoride-exposed populations: A novel application of the ultrasonic method.
Highlights A novel ultrasonic bone quality biomarker was tested in a population with low to high exposure to F.- Negative associations were found between F- exposure and bone quality Decreased bone quality reflects net bone loss, abnormal mineralization and altered collagen. The finding highlights that F- exposure has complex
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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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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: 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 Reduces Bone Strength Prior to Onset of Skeletal Fluorosis
The majority of animal studies investigating fluoride's impact on bone strength have found that fluoride has either no effect, or a detrimental effect, on bone strength. Importantly, several of the animal studies that have found fluoride reductes bone strength have reported that this reduction in strength occurs before signs of skeletal fluorosis
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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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