Bones Metabolic - Pathology

Hypervitaminosis D

• May be of dietary or iatrogenic origin (has narrow safety margin)
• Key features are hypercalcaemia with metastatic calcification of soft tissues
• Acute poisoning
  • In dogs and cats often from rodenticides containing cholecalciferol
  • Grossly:
    • Gastrointestinal haemorrhage
    • Foci of myocardial discoloration
  • Microscopically:
    • Mucosal haemorrhage
    • Necrosis of crypts
    • Focal myocardial necrosis
    • Mineralisation of intestinal mucosa, blood vessel walls, lungs and kidneys
• Chronic poisoning
  • Grossly:
    • Intense osteoclastic activity -> active resorption of bone, especially trabecular
  • Microscopically:
    • Excessive production of osteoid - appears both eosinophilic and basophilic in different places
    • Marrow cavity may be obliterated
    • Mineralisation of soft tissues, especially blood vessel walls
  • Due to inhibition of Parathyroid Hormone (PTH)|PTH and increase of calcitonin

Fluorine poisoning

• F is widespread in nature
• Pastures may be contaminated by industrial processes (e.g. brick manufacture)
• Acute poisoning:
  • Gastroenteritis
  • Nephrosis
• Chronic poisoning:
  • Dental abnormalities
    • Intoxication during teeth development
    • Foci of poor enamel formation - yellow, dark brown/black, chalky
    • Irregular wear of teeth, chip easily
  • Osteodystrophy = Fluorosis
    • Generalised skeletal disturbance
    • Most affected are metatarsals and mandibles
    • Periosteal hyperostosis + endosteal bone resorption -> thickened bones with enlarged marrow cavities

Lead poisoning

• Lead can bind to mineral portion of bone and cartilage
• In young animals ingesting large dose at once
  • -> Lead induced malfunction of osteoclasts
  • -> Transverse band of increased density on radiographs of metaphysis = "lead line" = growth retardation lattice