Abstract

Rabbits of similar age and body weight received sodium fluoride (NaF) (50 mg/kg body weight/day) intragastrically for up to 136 days. The acid-soluble collagen of bone, tendon, trachea and skin was extracted and purified. Aldehyde associated with the collagen was determined spectrophotometrically. Bone collagen, which had maximum aldehyde content in normal conditions, showed maximum reduction after sodium fluoride ingestion, as compared to other tissues. The mode of action of fluoride appears variable from tissue to tissue. The collagen fibres produced during fluoride toxicity would be defective due to inadequate cross-links. Thus sodium fluoride interferes with the maturation and normal metabolism of tissue collagen.

Excerpt:

NaF [sodium fluoride] produces abnormal collagen fibres which provide an abnormal environment for calcification. The formation of defective collagen fibres during fluoride poisoning may explain the development of neobone in fluorosis. NaF is suggested to interfere with maturation of collegen fibres by exerting an adverse effect on cross-link precursors.

Print PDF

• Related Studies :

  • Effect of slow-release sodium fluoride on cancellous bone histology and connectivity in osteoporosis

    We have previously demonstrated that a treatment regimen of slow-release sodium fluoride (SRNaF) and continuous calcium citrate increases lumbar bone mass, improves cancellous bone material quality, and significantly reduces vertebral fracture rate in osteoporotic patients. In order to assess whether such treatment also improves trabecular structure, we quantitated cancellous bone

  • Fluoride-induced changes in 60 retired aluminum workers

    Orthopedic, radiological and analytical examinations were performed in a group of 60 retired disabled workers of an aluminum factory. Occupational disease had previously been recognized in this group because of disturbances in the respiratory and circulatory systems. The age of those examined averaged 49.6 years; the duration of exposure averaged

  • Addition of monofluorophosphate to estrogen therapy in postmenopausal osteoporosis: a randomized controlled trial

    INTRODUCTION: Treatment of osteoporosis with high-dose fluoride alone does not reduce fracture risk. We hypothesized that the antifracture efficacy of fluoride could be optimized by its use in low doses combined with an antiresorptive agent. EXPERIMENTAL SUBJECTS: Subjects included 80 women with postmenopausal osteoporosis who had been taking estrogen for at least 1

  • [Dermatoglyphic indices in assessing the predisposition to occupational fluorosis].

    Dermatoglyphic investigations which prove the existence of genetic predisposition to occupational fluorosis in workers of aluminum and criolite plants were carried out. Mathematical methods of pattern recognition were used for the multifactorial analysis. It was found that the complex analysis of ten the most informative dermatoglyphic parameters permits to prognosticate

  • Endemic fluorosis: a study of the factors involved in the production of mottled enamel in children and severe bone manifestations in adults

    Summary and Conclusions A detailed study of the factors involved in the production of "mottled enamel" in children and severe bone manifestations in adults; as a result of the ingestion of fluorides in drinking water, has been made during the last three years. This study revealed: 1. "Mottled enamel" in children was

• Related FAN Content :

  • "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.

  • 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.