Abstract

Fluorotic lesions were studied in cows and calves on farms belonging to 2 agricultural companies. From company HP 3 calves, 4 heifers and 2 cows were examined and from the other (B), 12 bull-calves. The material consisted of a carcass from 1 dead calf and skull, metacarpus and kidneys from slaughtered animals. The F content of feed and water samples was determined. In HP material extensive enamel defects and strong wear were found in the deciduous incisors. Fluorotic lesions in calves were not described previously. One calf had osteoporosis. In the rest of the material osteosclerosis and subperiosteal bone apposition and tubular atrophy in the kidneys were seen. Kidney lesions were not observed previously in bovine fluorosis. Dark furrows and enamel defects appeared in the teeth of the heifers and the cows. In the skeleton osteosclerosis and subperiosteal bone apposition were found. Microscopically the skeleton showed signs of repair. The F content of the skeleton varied between 135 and 300 ppm in the ash. In water samples 1.5-4.0 ppm of F were found. The mineral supply used contained 300-500 ppm of F. The fluorosis in these animals was caused by a combination of the F of the water and the mineral supplement. Considering the microscopic picture and the low skeletal F level, the lesions in the bull-calves of company B were interpreted as fluorosis in a process of repair. The ingested fluorine in these animals was reduced during the fattening period.

• Related Studies :

  • [A study of the genetic basis of susceptibility to occupational fluorosis in aluminum industry workers of Siberia].

    The phenotype frequency distributions of several classical blood genetic markers and dermatoglyphic characters were analyzed in workers of Siberian aluminum plants who had occupational fluorosis. Comparison with healthy workers revealed significant differences in frequencies of several markers. Phenotypes B (AB0), D (Rh), MN (MN), P1 (P), Le a (Lewis), Gc

  • The spectrum of radiographic bone changes in children with fluorosis

    Painful, crippling deformities in Tanzanian children from an area of endemic fluorosis are reported. Excessive fluoride ingestion in pregnant women may possibly poison and alter enzyme and hormonal systems in the fetus causing disturbances to osteoid formation and mineralization. Knock-knees, bowlegs, and saber shins develop when walking begins. Combinations of osteomalacia, osteoporosis,

  • Fluoride-related bone disease associated with habitual tea consumption

    Acquired osteosclerosis is a rare disorder of bone formation but an important consideration in adults with sclerotic bones or elevated bone density results. In such patients, malignancy, hepatitis C, and fluorosis should all be considered when making a diagnosis. We describe 4 patients evaluated at our Metabolic Bone Disease Clinic

  • Fluoride Sources, Toxicity and Fluorosis Management Techniques - A Brief Review.

    Highlights Overexposure to fluoride via drinking water causes several health effects including fluorosis Endemic fluorosis is still persisted in several countries even with advancement in research Most of fluorosis management techniques suggested in the past have come with their own drawbacks Defluoridation techniques based on aluminium materials pose serious

  • Association of dental and skeletal fluorosis with calcium intake and vitamin D concentrations in adolescents from a region endemic for fluorosis

    Objective: Patan, is a semi urban area in Gujarat, India where fluorosis is endemic (Fluoride concentration in ground water 1.96–10.85 ppm, Patel et al., 2008). Exposure to fluoride is likely to be higher in lower socio-economic class (SEC) due to lack of access to bottled water. Calcium intake and vitamin

• Related FAN Content :

  • 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.

  • "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.

  • Fluoridation, Dialysis & Osteomalacia

    In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on

  • Mayo Clinic: Fluoridation & Bone Disease in Renal Patients

    The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.

  • 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.