Bovis ISSN 2398-2993

Fluorosis

Synonym(s): Dental fluorosis, Osteofluorosis

Contributor(s): Ben Dustan , Alexander Corbishley

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Introduction

  • Cause: exposure and ingestion of excessive fluorides (eg sodium fluoride, sodium fluorosilicate).
  • Signs: see below.
  • Diagnosis: see below.
  • Treatment: no specific antidote.
  • Prognosis: moderate to poor. See below.

Pathogenesis

Etiology

  • Chronic ingestion of >1-2mg/kg bodyweight/day, or >12 - 27 ppm of the diet in cattle will result in lesions.
    • Suttie et al 1957 reported fluorosis in dairy cows after 3-5 years at 50 mg F /kg DM when ingested as NaF.
    • Shupe et al 1963 reported lower tolerances in calves of 30 mg F/kg DM when ingested as NaF.
    • Higher tolerances are reported to the fluoride in rock phosphate, CaF2 and defluorinated feed phosphate.
  • Rapid ingestion of any amount significantly above levels stated above will result in acute toxicosis signs. The greater the toxic load the more severe the clinical presentation.
  • The most common sources of excess dietary fluorides are:
    • Water with naturally high fluoride content (eg geothermal springs).
    • Forages contaminated with fluorides, from irrigation with water high in fluorides or from nearby industrial plants (eg phosphate-processing plants, aluminum plants, smelters).
    • Mineral (nondefluorinated rock phosphorus) and feed supplements.
    • Volcanic activity depositing high fluoride containing ash over soil, plants water.

Pathophysiology

  • Pathognomonic lesions of chronic fluorosis involve teeth and bones:
    • Dental fluorosis:
      • Chalky/mottled teeth and excessive attrition are the result of hypoplastic pitting of the enamel.
      • Affected teeth become shortened, down to gum level in severe cases, because of the rapid wear.
      • Dental lesions only develop when fluorosis is present/active when the tooth is being formed.  Once fully formed the tooth is unaffected, hence why deciduous teeth are rarely affected.
      • Partial placental barrier reduces fluoride accumulation within the fetus.
    • Osteoflurosis:
      • Most pronounced in metacarpals, metatarsals and mandible.
      • Bone becomes thicker, heavier (hyperosteosis) and the marrow cavity decreases.
      • Periosteal proliferation is often accompanied by formation of exostoses (<0.5cm length) leading to clinical manifest stiffness/lameness.
      • Articular surfaces are not involved - a useful diagnostic discriminatory factor.

Timecourse

  • Acute fluorosis: hours - days after severe toxic ingestion event.
  • Chronic fluorosis: years for dental and osteofluorosis to develop and clinical manifest, depending upon ingested volume.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Schultheiss W A & Godley G A (1995) Chronic fluorosis in cattle due to the ingestion of a commercial lick. J S Afr Vet Assoc 66 (2), 83-4 PubMed.
  • Jubb T F, Annand T E, Main D C & Murphy G M (1993) Phosphorus supplements & fluorosis in cattle - a northern Australian experience. Australian Veterinary Journal 70 (10), 379-83 PubMed.
  • Shupe J L, Bruner R H, Seymour J L & Alden C H (1992) The pathology of chronic bovine fluorosis: A Review. 20 (2), 274-85 PubMed.
  • Krook L, Maylin G A, Lillie J H & Wallace R S (1983) Dental fluorosis in cattle. Cornell Veterinarian 73 (4), 340-62 PubMed.

Other sources of information

  • Andrews A H, Blowey R W, Boyd H & Eddy R G (2008) Bovine Medicine. 2nd edn.
  • Smith B P (2002) Large Animal Internal Medicine. In: Diseases of the bones, joints and connective tissue. 3rd edn.
  • Jones T C, Hunt R D & King N W (1997) Veterinary Pathology. In: Diseases due to extraneous poisons. 6th edn.


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