Abstract

This study examined the relationship between transient peak plasma fluoride levels (subcutaneous injections) as well as lower but relatively constant levels (subcutaneous constant infusion) and the occurrence of disturbances in the enamel mineralization of the rat incisor as determined microradiographically. The fluoride doses were administered for 1 week, and the animals were killed 2 weeks later. Once daily peak plasma fluoride levels of 10 µM were uniformly associated with disturbances in the mineralization of the enamel, but once daily peak levels of 5 µM were not. Neither were twice daily 5-µM peaks. Relatively constant plasma fluoride levels, which averaged 3.3 µM, were associated with an increased incidence of changes in enamel formation and levels of 4.7 µM consistently associated with disturbances in enamel mineralization. These findings suggest that (1) the rat is a better model for the study of human enamel fluorosis than previously believed, and (2) slightly elevated but relatively constant plasma fluoride levels are more likely to be associated with the occurrence of fluorotic disturbances in the mineralization of enamel than are the more rare high and transient peak levels.

• Related Studies :

  • Developmental and post-eruptive defects in molar enamel of free-ranging Eastern Grey kangaroos (Macropus giganteus) exposed to high environmental levels of fluoride

    Dental fluorosis has recently been diagnosed in wild marsupials inhabiting a high-fluoride area in Victoria, Australia. Information on the histopathology of fluorotic marsupial enamel has thus far not been available. This study analyzed the developmental and post-eruptive defects in fluorotic molar enamel of eastern grey kangaroos (Macropus giganteus) from the

  • Exposure to lead exacerbates dental fluorosis.

    AIM: Our aim was to test the hypothesis that co-exposure to lead and fluoride alter the severity of enamel fluorosis. MATERIALS AND METHODS: Wistar rats were allocated in four groups: control, and 3 groups that received water containing 100 ppm of fluoride (F), 30 ppm of lead (Pb), or 100 ppm of F

  • Short exposure to high levels of fluoride induces stage-dependent structural changes in ameloblasts and enamel mineralization.

    We tested the hypothesis that the sensitivity of forming dental enamel to fluoride (F-) is ameloblast developmental stage-dependent and that enamel mineralization disturbances at the surface of fluorotic enamel are caused by damage to late-secretory- and transitional-stage ameloblasts. Four-day-old hamsters received a single intraperitoneal dose of 2.5-20 mg NaF/kg body

  • Histone acetyltransferase promotes fluoride toxicity in LS8 cells.

    Highlights Fluoride activates histone acetyltransferase (HAT) in enamel organ-derived LS8 cells. HAT inhibitors suppressed fluoride-mediated acetylation of p53 and cell toxicity. Modulation of HAT activity may be a potential target to mitigate fluoride toxicity. Previously we demonstrated that fluoride increased acetylated-p53 (Ac-p53) in LS8 cells that are derived from mouse enamel

  • Fluoride affects enamel protein content via TGF-B1-mediated KLK4 inhibition

    Dental fluorosis is caused by chronic high-level fluoride (F-) exposure during enamel development, and fluorosed enamel has a higher than normal protein content. Matrix metalloproteinase 20 cleaves enamel matrix proteins during the secretory stage, and KLK4 further cleaves these proteins during the maturation stage so that the proteins can be

• Related FAN Content :

  • Mechanisms by Which Fluoride Causes Dental Fluorosis Remain Unknown

    When it comes to how fluoride impacts human health, no tissue in the body has been studied more than the teeth. Yet, despite over 50 years of research, the mechanism by which fluoride causes dental fluorosis (a hypo-mineralization of the enamel that results in significant staining of the teeth) is not

  • Dental Fluorosis Is a "Hypo-mineralization" of Enamel

    Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin

  • Diagnostic Criteria for Dental Fluorosis: The TSIF ("Total Surface Index of Fluorosis")

    The traditional criteria (the "Dean Index") for diagnosing dental fluorosis was developed in the first half of the 20th century by H. Trendley Dean. While the Dean Index is still widely used in surveys of fluorosis -- including the CDC's national surveys of fluorosis in the United States -- dental

  • Moderate/Severe Dental Fluorosis

    In its "moderate" and severe forms, fluoride causes a marked increase in the porosity of the enamel. After eruption into mouth, the porous enamel of moderate to severe fluorosis readily takes up stain, creating permanent brown and black discolorations of the teeth. In addition to extensive staining, teeth with moderate to severe fluorosis are more prone to attrition and wear - leading to pitting, chipping, and decay.

  • Dental Fluorosis in the U.S. 1950-2004

    Before the widespread use of fluoride in dentistry, dental fluorosis was rarely found in western countries. Today, with virtually every toothpaste now containing fluoride, and most U.S. water supplies containing fluoride chemicals, dental fluorosis rates have reached unprecedented levels. In the 1950s, it was estimated that only 10% of children in