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Results for “FLUORIDE POISONING”

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At least 613 records · Page 34Linked to original sources
PubMed1977

An electron microprobe analysis of osteofluorosis in the rabbit.

Osteofluorosis was induced in rabbits by the ingestion of 500 ppm F in their drinking water over a period of 30 days. The tibiae from experimental and control animals were selected for macroscopic, microscopic and microradiographic observation. Transverse sections of 100 mum thickness were prepared for an electron-microprobe analysis to determine Ca, P and F concentrations and to display the topographical distribution of F as revealed by the X-ray image of its Kalpha1 radiation. Variation in amount of periosteal and endosteal deposition was observed along the length of the bone. Changes, including numerous mottled osteones, were seen in the compact zone of bone which had been formed prior to the start of the experiment. The Ca/P ratio appeared to show a variation related to the F concentration.

Animals↗
PubMed1996

Gastroduodenal manifestations in patients with skeletal fluorosis.

A prospective case-controlled study was performed to evaluate the gastrointestinal symptoms and mucosal abnormalities occurring in patients with osteofluorosis. Ten patients with documented osteofluorosis and ten age- and sex-matched healthy volunteers were included in the study. Clinical evaluation, real-time ultrasound, and upper gastrointestinal endoscopy and biopsy from the gastric antrum and duodenum were performed in all subjects. The biopsies were subjected to a rapid urease test and light and electron microscopic examinations. Ionic fluoride levels were estimated in the drinking water, serum, and urine using an ION 85 ion analyzer. All patients with osteofluorosis had gastrointestinal symptoms, the most common being abdominal pain. Endoscopic abnormalities were found in seven patients with osteofluorosis. In all 7 of these patients, chronic atrophic gastritis was seen on histology. Electron microscopic abnormalities were observed in all 10 patients with osteofluorosis. These included loss of microvilli, cracked-clay appearance, and the presence of surface abrasions on the mucosal cells. None of the control subjects had any clinical symptoms or mucosal abnormalities. It was concluded that gastrointestinal symptoms as well as mucosal abnormalities are common in patients with osteofluorosis.

Abdominal Pain↗
PubMed2000

Changed cellular membrane lipid composition and lipid peroxidation of kidney in rats with chronic fluorosis.

An animal model of chronic fluorosis was produced by subjecting Wistar rats to high doses of fluoride in drinking water for a prolonged period. Phospholipid and neutral lipid contents in rat kidney were then analyzed by high-performance liquid chromatography (HPLC), and fatty acid compositions from individual phospholipids were measured by gas chromatography. Lipid peroxidation was detected by the thiobarbituric-acid-reactive substance assay. Results showed that the total phospholipid content significantly decreased in the kidney of the rats treated with high doses of fluoride and the main species influenced were phosphatidylethanolamine (PE) and phosphatidylcholine (PC). Decreased proportions of polyunsaturated fatty acids were observed in PE and PC in kidney of fluoride-treated animals compared to controls. No changes could be detected in the amounts of cholesterol and dolichol in kidneys between the rats treated with fluoride and controls. A significant decrease of ubiquinone in rat kidney was observed in the groups treated with excessive fluoride. High levels of lipid peroxidation were detected in kidney of the rats with fluorosis. It is plausible that the specific modification of lipid composition results from lipid peroxidation. The oxidative stress and modification of cellular membrane lipids may be involved in the pathogenesis of chronic fluorosis and provide a possible explanation for the gross system damage observed in the body, especially in soft tissues and organs.

Animals↗
PubMed1998

[Cervical spondylolisthesis in skeletal fluorosis. A case report].

The authors report an uncommon complication in cervical skeletal fluorosis. It is a cervical spondylolisthesis at C5-C6 level complicated by a radiculomyelopathy described in a man living in an endemic area for fluorosis. After 3 years, a spontaneous stabilization of the cervical spine with a posterior calcification of the supraspinal and interspinal ligaments has caused an improvement of the neurological symptomatology.

Adult↗
PubMed1994

Serum haptoglobin and C-reactive protein in human skeletal fluorosis.

Circulating levels of haptoglobin and C-reactive protein were studied in patients of skeletal fluorosis and compared with two types of controls. The first type of control included normal healthy individuals consuming water containing permissible levels of fluoride (up to 1 mg/L). The second type of control included individuals consuming water contaminated with fluoride (1.2-14.5 mg/L) but not exhibiting clinical manifestations of skeletal fluorosis. A significant increase in the levels of haptoglobin (p < 0.01) and C-reactive protein (p < 0.01) as well as a raised erythrocyte sedimentation rate were seen in patients of skeletal fluorosis as compared to both types of controls. The present study suggests the possibility of a subclinical inflammatory reaction occurring in patients with skeletal fluorosis.

Blood Sedimentation↗
PubMed1981

Zinc Depletion following experimental fluorosis in mice.

The effect of fluoride administration on zinc levels in liver, kidney and bone, and on protein content (microgram/mg tissue wt) in liver and kidney was investigated by subjecting albino mice for 16 weeks to different concentrations of fluoride (0 ppm - control; 10 ppm - group I; 25 ppm - group II; 50 ppm - group III; 100 ppm - group IV; and 200 ppm- group V) in drinking water. Zinc levels decreased significantly in liver and bone of groups III, IV and V; the decrease being 17%, 25% and 44% (P less than 0.005) in the case of liver, and 14% (p less than 0.01), 24% (p less than 0.005), and 39% (p less than 0.005) in the case of bone in groups III, IV and V respectively. Zinc depletion in the kidney of the fluoridated animals was only statistically significant (p less than 0.005) in groups IV and V. Similarly the protein content also decreased in liver and kidney (in liver significant at p less than 0.005, p less than 0.01, and p less than 0.005; in kidney significant at p less than 0.005, p less than 0.05 and p less than 0.005 in groups III, IV and V respectively). The experimental animals, especially in groups IV (100 ppm F) and V (250 ppm F), also exhibited retardation in growth.

Animals↗
PubMed1989

Endemic skeletal fluorosis in children: hypocalcemia and the presence of renal resistance to parathyroid hormone.

Although endemic skeletal fluorosis has been reported in children, hypocalcemia has not been previously noted. In a prevalence study of 260 schoolchildren living in an endemic fluorosis area in South Africa (water fluoride content 8-12 ppm), hypocalcemia was documented in 23%. Furthermore in a separate study of nine children with skeletal symptoms due to endemic fluorosis, hypocalcemia was found in six. 1,25-Dihydroxyvitamin D levels were elevated in the seven children in whom it was measured. Parathyroid hormone (PTH) stimulation tests on admission revealed evidence of impaired phosphaturic responses, typical of acquired pseudohypoparathyroidism type II, and a direct correlation between serum calcium values and the degree of phosphaturia was noted. Repeat tests performed in two of the children after correction of the hypocalcemia by dietary means, revealed a return of normal renal responsiveness. Serum calcium values also correlated inversely with the degree of osteomalacia on iliac crest bone histomorphometry. It is suggested that low dietary calcium intakes might exacerbate the severity of the bone lesions in children living in areas of endemic fluorosis.

Adolescent↗
PubMed1995

[Spinal cord compression in bone fluorosis. Apropos of 4 cases].

The authors report four cases of spinal cord compression (three at cervical level and one at dorsal level) due to vertebral osteosclerosis secondary to chronic fluoride intoxication. Roentgenograms showed typical diffuse densification of vertebral bodies, calcifications of bony insertions of many ligaments, discs and interosseous membranes. Urinary fluoride was markedly increased in two cases. In the other two cases the bone biopsy was suggestive of skeletal fluorosis. Spinal computed tomography showed severe cord compression due to posterior osteophytes. Good improvement was observed after surgical decompression in one case. Fluorosis was described as a consequence of endemic exposure to high fluoride content in soil and natural ground water in North Africa. Fluorotic myelopathy was due to bone excrescences mainly affecting the spine.

Bone Diseases↗
PubMed1988

Intraosseous schwannoma of the cervical spine associated with skeletal fluorosis.

Intraosseous Schwannoma of the cervical spine is very rare. Its association with skeletal fluorosis is also extremely rare. A case of successfully treated intraosseous neurofibroma of the cervical spine associated with skeletal fluorosis causing tetraparesis is reported. The clinical features, diagnostic aspects and the management is described and the literature is reviewed.

Calcinosis↗