Fluorosis

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.