Abstract

Multi-year follow-up of 358 workers of aluminum pot rooms, including 165 individuals suffering from fluorosis, has shown significant changes in the clinical picture of the chronic occupational fluorine intoxication, developed under modern conditions of production, at lower concentrations of fluorine compounds in the air of working area. In this connection, the pathology of the musculoskeletal system plays the dominating role in this clinical picture and has the large variability of combinations of the individual sections destructions of the bone tissue. The main criterion to establish the phase of the disease is still the number and severity of the signs of this destruction. The visceral pathology in contemporary production circumstances is registered with less frequency and loses a number of the previously described clinical manifestations, however, is still of some importance to identify the early signs of the disease and to prevent the fluorosis on time.

• Related Studies :

  • Brick tea fluoride as a main source of adult fluorosis

    An epidemiological survey was conducted in Naqu County, Tibet in September 2001 to investigate the manifestations of fluorosis in adults caused by the habitual consumption of brick tea. Profiles were obtained for the total daily fluoride intake, environmental fluoride levels and average urinary fluoride concentration, and a physical examination and a

  • Radiological criteria of industrial fluorosis

    The bone radiographs of 43 potroom workers in an aluminium factory, on whom the diagnosis of industrial fluorosis had been confirmed by bone biopsy, are compared with radiographs from 18 control subjects. A higher frequency of ossification of ligament, tendon, and muscle attachments is observed among the fluoride exposed subjects.

  • Elevated fluoride levels and periostitis in pediatric hematopoietic stem cell transplant recipients receiving long-term voriconazole

    Azole therapy is widely utilized in hematopoietic stem cell transplant (HCT) recipients for the treatment of aspergillus. Complications of voriconazole treatment related to its elevated fluoride content have been described in adults, including reports of symptomatic skeletal fluorosis. We review fluoride levels, clinical, and laboratory data in five pediatric HCT recipients

  • Diagnosis and treatment of deforming osteoarthrosis in subjects in contact with fluoride compounds

    A comparative study is presented of 378 workers with osteoarthrosis deformans (OD) contacting with fluorine compounds and in 106 patients with primary OD. The diagnostic criteria in these two categories of patients coincided. But the pain syndrome in the joints in professional fluorosis (PF) was associated with ossalgias (85%), tenderness

  • [Skeletal fluorosis: a case report].

    The authors report a case of skeletal fluorosis described in a 60 years old man living in south-west Tunisian. The main clinical sign is a severe functional legs disability. Radiographic examination has shown a diffused osteocondensation, with cervical spine degenerative discopathy, a pelvis bilateral osteoarthritis and an interosseous membrane ossification

• Related FAN Content :

  • 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.

  • "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.

  • 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.

  • Skeletal Fluorosis in the U.S.

    Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.

  • Variability in Radiographic Appearance of Skeletal Fluorosis

    Osteosclerosis (dense bone) is the bone change typically associated with skeletal fluorosis, particularly in the axial skeleton (spine, pelvis, and ribs). Research shows, however, that skeletal fluorosis produces a spectrum of bone changes, including osteomalacia, osteoporosis, exostoses, changes resulting from secondary hyperparathyroidism, and combinations thereof. Although the reason for this radiographic variability is not yet fully understood, it is believed to relate to the dose of fluoride consumed, the individual's nutritional status, exposure to aluminum, genetic susceptibility, presence of kidney disease, and area of the skeleton examined.