Abstract

We grouped mice [strains: C57BL/6J (n=32) and C3H/HeJ (n=32)] to address the influence of bone density on fluoride‘s (F’s) biological effects. These animals received low-fluoride food and water containing 0 (control group) or 50ppm of F for up to 28days. The upper left central incisor was extracted, and the left maxilla was collected at 7, 14, 21, and 28days for histological and histomorphometric analysis to estimate bone neoformation. Our results showed bone neoformation in all of the evaluated groups, with the presence of bone islets invading the center of the alveoli when replacing the existing connective tissue. Curiously, this biological phenomenon was more evident in the C57BL/6J strain. The histomorphometric analysis confirmed the histological findings in relation to the amount of new bone tissue and showed a decrease in C3H/HeJ mice (control group). Altogether, our results showed differential effects of fluoride bone metabolism, confirming a genetic component in susceptibility to the effects of fluoride.

• Related Studies :

  • Bone response to fluoride exposure is influenced by genetics

    Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined. A label-free proteomics approach was employed to identify and evaluate changes in bone protein expression in two mouse strains having different susceptibilities to develop dental fluorosis and to alter bone

  • The genetic influence on bone susceptibility to fluoride

    INTRODUCTION:  The influence of genetic background on bone architecture and mechanical properties is well established. Nevertheless, to date, only few animal studies explore an underlying genetic basis for extrinsic factors effect such as fluoride effect on bone metabolism. MATERIALS AND METHODS:  This study assessed the effect of increasing fluoride doses (0

  • [Qualitative and quantitative variation of serum proteins in fluorosis patients].

    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

  • Fluoride reduces bone strength in older rats

    In response to recent concerns about the effect of water fluoridation on hip fracture rates, we studied the influence of fluoride intake on bone strength. Four groups of rats were fed a low-fluoride diet ad libitum and received 0, 5, 15, or 50 ppm of fluoride in their drinking water.

  • Aberrant DNA methylation of Cyclind-CDK4-p21 is associated with chronic fluoride poisoning.

    Endemic fluorosis is a serious problem in public health, affecting thousands of people. Abnormal proliferation and activation of osteoblasts in skeletal fluorosis lesions play a leading role and osteoblast proliferation is finely regulated by the cell cycle. There are a few reports on fluoride-induced DNA methylation. However, the role of

• 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.

  • 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

  • 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.

  • 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

  • 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.