PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “FLUORIDE POISONING”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed2004

Ossification of the transverse atlantal ligament associated with fluorosis: a report of two cases and review of the literature.

STUDY DESIGN: Two cases of ossification of the transverse atlantal ligament (OTAL) are reported, and the literature is reviewed. OBJECTIVE: To report two cases of OTAL, which share fluorosis as a possible etiologic link. SUMMARY OF BACKGROUND DATA: OTAL, a rare phenomenon, may cause upper cervical canal stenosis and spastic quadriparesis. However, the incidence, etiology, and the best therapeutic options are currently unclear. METHODS: Two cases are reported. Included are pertinent history, physical examination, radiographic evaluation, nonsurgical interventions, and outcomes. The available literature is also reviewed. RESULTS: On systemic examination, these two cases were found to have ossification of many ligaments and interosseous membranes, i.e., the atlantal transverse ligament, posterior longitudinal ligament, and interosseous membranes of ribs, forearm, and leg. These findings were coupled with a history of high fluoride intake and dental fluorosis; the diagnosis of fluorosis was made. After 2 weeks of treatment with halo ring traction, and protection and stabilization with a hard cervical collar, the clinical symptoms significantly improved. CONCLUSION: The incidence of OTAL may be not as rare as has been thought. Although the complete etiology of OTAL is not known, fluorosis may be one of the etiologic factors related to OTAL, as well as the ossification of other ligaments and interosseous membranes. Nonsurgical treatment may be safe and effective.

Aged↗
PubMed1986

Immunoglobulin G in cystic lesions of rat enamel organ following fluoride intoxication.

Fluoride given as a high single dose to young rats with developing molars has earlier been shown to cause subameloblastic cysts with disorganized ameloblasts in the cystic wall and an irregular mineralization pattern of the underlying enamel. In the present study immunohistochemistry has been employed to determine if an increased permeability of the enamel organ occurred at the areas of cell disturbances. For this purpose 5-day-old rats were injected with 60 mg sodium fluoride per kg body weight. They were decapitated after 24 h, the maxilla prepared histologically and paraffin sections incubated for the demonstration of IgG according to the avidin-biotin-peroxidase complex method. Staining for IgG was present in the cystic lumina and in areas of disorganized ameloblasts. No reaction was observed in areas of unaffected ameloblasts. It was suggested that the fluoride-induced cell injury increased the permeability of the ameloblastic cell layer. Diffusion of IgG and most likely other substances as well, through the ameloblastic layer may have contributed to cyst formation and to the irregular mineral deposits that have been found in the ameloblastic layer and at the enamel surface.

Ameloblasts↗
PubMed1975

Skeletal fluorosis in immobilized extremities.

The effect of immobilization on skeletal fluorosis was studied in growing rabbits. One hind leg was immobilized by an external fixation device extending below the wrist joint and above the knee joint, the extremity being in a straight position after severance of the sciatic nerve. The animals, aged 7 weeks at the beginning of the experiment, were given 10 mg of fluoride per kg body weight and day during 12 weeks. In the tibiae, development of the skeletal fluorosis was more irregular than that observed in previous studies of normally active animals, being most excessive in the mobile bone. The immobilization effect was most profound in the femora as the cortical thickness and the femur score were significantly higher than those in the mobile femora. It was suggested that an altered muscular activity was the reason for the observed changes.

Animals↗
PubMed1993

Phosphorus supplements and fluorosis in cattle--a northern Australian experience.

Chronic fluoride toxicosis caused lameness, dental lesions and illthrift in an extensive beef cattle herd in northern Australia. Up to 15% of the herd was lame and the disease forced the culling of large numbers of cows. The source of fluoride was fertiliser-grade monoammonium and diammonium phosphate fed as part of a mineral supplement. Large quantities of mineral supplement were provided to the cattle because lameness was attributed to phosphorus deficiency, which is endemic in the area. Most lameness developed in the late dry season in the post-lactation phase. Severe lameness was caused by fractured pedal bones.

Animals↗
PubMed1998

Chronic gypsum fertiliser ingestion as a significant contributor to a multifactorial cattle mortality.

OBJECTIVE: To assess the validity of claims that heavy metal contamination from an open-cut mine caused the death of 226 cattle on a nearby farm over a period of 18 months, and to investigate other possible contributing factors. PROCEDURE: A retrospective assessment of previous investigations combined with additional chemical analyses. RESULTS: Extensive chemical analyses produced no evidence of heavy metal contamination associated with the mine. Analysis of bones indicated exposure to fluoride in greater than normal amounts. The main source of fluoride seems to have been gypsum that was included in a feed supplement and also ingested from fertiliser dumps on paddocks. The gypsum itself may have contributed significantly to the ill health. Other factors probably affected some classes of animals, notably the young calves. CONCLUSIONS: What originally seemed to be a disease problem of single aetiology probably was an expression of interacting multifactorial causes. This investigation has highlighted the potential toxicity of gypsum to livestock and the need for further studies to establish its basis.

Animal Feed↗
PubMed1968

Epidemiological, clinical, and biochemical study of endemic dental and skeletal fluorosis in punjab.

The incidence of dental fluorosis in 46,000 children in the Punjab was assessed and compared with the fluoride content of their water supplies. Ten villages were selected for more detailed studies of skeletal as well as dental fluorosis.Factors other than the fluoride contect of the drinking water which were found to influence the incidence and the severity of fluorosis were the chemical composition of the water and in particular its calcium content; the duration of exposure; sex and occupation; nutritional status; and climatic and geological variations. The role of fluoride-containing foodstuffs has yet to be assessed.

Adolescent↗
PubMed1983

Reversibility of skeletal fluorosis.

At two x ray examinations in 1957 and 1967, 17 cases of skeletal fluorosis were identified among long term cryolite workers in Copenhagen. In 1982 four of these patients were alive, eight to 15 years after exposure had ended. Radiographs were obtained, and the urinary fluoride excretion was measured. A similar picture emerged in all four cases: extensive fading of the sclerosis of trabecular bone in ribs, vertebral bodies, and pelvis, whereas cortical bone thickening and calcification of muscle insertions and ligaments remained virtually unchanged. The fluoride excretion was increased in three cases (with the shortest exposure free period). These findings indicate that with continuous remodelling of bone tissue trabecular sclerosis is slowly reversible and the excess fluoride is excreted in the urine.

Aged↗
PubMed1977

Fluorosis in dairy cattle.

The investigation of a high incidence of arthritis in 21 dairy herds disclosed elevated fluorine levels in bone samples. In every herd except one, where herbage and water was contaminated by industrial fall-out, the main source of the fluorine was from mineral supplements; In a few herds, purchased cake or grain balancers contributed to the abnormal levels. Over 100 cows with arthritis had fluroine levels in the bone of between 2000 and 8000 ppm, or were in herds whose diet contained excess fluorine. Characteristic tooth lesions often confirmed the link between arthritis and fluorosis. Sixteen out of 31 samples of mineral supplement contained dangerous levels of fluorine (3000 to 13000 ppm). Grain balancers contained up to 400 ppm F, and dairy cake had levels as high as 140 ppm F. There was a statistical correlation between a high incidence of damage to peri-articular structures, resulting in debility and loss of production, and elevated bone fluorine.

Acetabulum↗
PubMed1984

Experimental osteo-fluorosis in the domestic pig: a histomorphometric study of vertebral trabecular bone.

The experiment aimed at describing effects of fluoride on structure and remodeling of vertebral trabecular bone in pigs. Eight animals receiving a supplement of 2 mg F-/kg b.w. per day from age eight to 14 mo were compared with eight controls. Plasma fluoride increased from 0.7 +/- 0.1 microM/1 to 12.7 +/- 2.0 microM/1 in pigs receiving fluoride. At slaughter, the concentration of fluoride in dry fat-free bone was 149.3 +/- 10.5 mM/kg for fluorotic animals and 9.5 +/- 0.9 mM/kg for controls. Morphologic changes were assessed in un-decalcified specimens of the fourth lumbar vertebra by quantitative histology using fluorochromes as intra-vital tissue time markers. The volume of trabecular bone tissue (bone + marrow) was unchanged in fluorotic animals, but the volume density of bone was increased by 17%. Surface densities of cancellous bone were almost unchanged, whereas the thickness of trabeculae increased in fluorosis. Fluoride enhanced remodeling of trabecular surfaces: The fraction of surface occupied by resorption lacunae increased 40%, and the formative surface approximately 30%. No changes were demonstrated at surface points undergoing formation: Osteoid thickness, calcification rate, lamellar thickness, and completed wall thickness were normal. It is concluded that the observed findings cannot be explained by fluoride-induced changes in a single cell. Fluoride appears to affect all cells involved in remodeling by direct or indirect mechanisms.

Animals↗
PubMed1987

Fluoride in dental products: safety considerations.

This review summarizes the nature of acute fluoride toxicity, its time-course, and the fluoride doses that are involved. The generally accepted "certainly lethal dose" range for 70 kg adults, i.e., from 5 to 10 g of sodium fluoride or from 32 to 64 mg fluoride/kg, is discussed. Based on recent case reports of fluoride-induced fatalities, it is concluded that this dose range has little utility in cases involving young children. The concept of a "probably toxic dose" (PTD) is advanced. The PTD, 5.0 mg F/kg, is defined as the dose of ingested fluoride that should trigger immediate therapeutic intervention and hospitalization because of the likelihood of serious toxic consequences. The concentrations and quantities of fluoride in selected dental products are discussed in relation to the PTD. It is concluded that, as these products are currently packaged, most of them contain quantities of fluoride sufficient to exceed the PTD for young children. Recommendations are made to reduce the risk of toxicity associated with their use.

Animals↗