Abstract

Comparison between patients with occupational fluorosis, a group of healthy workers, and a sample from the general population revealed differences in concentrations of some polymorphic serum proteins. These differences depended on phenotypes of patients. TF 1-2, PI 1-2, and HP 2-1 patients exhibited a decreased concentration of transferrin (TF), a decreased concentration of proteinase inhibitor (PI), and an increased concentration of haptoglobin (HP), respectively.

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  • [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

  • Prolactin rs1341239 T allele may have protective role against the brick tea type skeletal fluorosis

    OBJECTIVE: Prolactin (PRL) has been reported to be associated with increased bone turnover, and increased bone turnover is also a feature of skeletal fluorosis (SF). Autocrine/paracrine production of PRL is regulated by the extrapituitary promoter and a polymorphism in the extrapituitary PRL promoter at -1149 (rs1341239) is associated with disturbances

  • A case of bone fluorosis of undetermined origin

    After predominant theories on the causes of fluorosis are described and remarks made about the metabolism of fluoride, an observation of bone fluorosis in a 64-year-old patient is reported. Because, despite painstaking research, none of the known causes of bone fluorosis could be found in our patient, a new pathomechanism is being offered for discussion, i.e.,

  • Preliminary screening of fluorine-stained osteoblastic apoptosis-related microRNA.

    This article has been accepted for publication and undergone full peer review but has not been through the copy editing, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ar.24709. Endemic fluorosis is a chronic systemic

  • Modifying role of GSTP1 polymorphism on the association between tea fluoride exposure and the brick-tea type fluorosis

    BACKGROUND:  Brick tea type fluorosis is a public health concern in the north-west area of China. The association between SNPs of genes influencing bone mass and fluorosis has attracted attention, but the association of SNPs with the risk of brick-tea type of fluorosis has not been reported. OBJECTIVE:  To investigate the

• Related FAN Content :

  • Factors which increase the risk for skeletal fluorosis

    The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.

  • 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.

  • 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.

  • "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.

  • Kidney Patients Are at Increased Risk of Fluoride Poisoning

    It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients