Bones Metabolic - Pathology

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Pituitary

  • Growth hormone
    • Secreted by the anterior pituitary
    • Influences the size of the skeleton and soft tissue

Pituitary dwarfism

Pituitary gigantism (Acromegaly)

Thyroid

  • Thyroid hormones affect maturation of growth of cartilage

Hypothyroidism

Hyperthyroidism

Gonadal Effect on Bones

Adrenal glands


Hyperparathyroidism

Rickets

Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)
  • Essentially the same disease as osteomalacia
  • Caused by Vitamin D and phosphorus deficiency
  • In young animals
  • Failure of:
    • Mineralisation of osteoid at sites of membranous growth
    • Cartilage vascularisation and mineralisation at sites of endochondral ossification
  • Osteoid and catilage build up at those sites
  • Histologically:
    • Lines of hypertrophic cartilage cells are lenghtened and disorganised
    • Ossification at metaphysis is poor
    • Persisting osteoid and cartilage -> shaft modelling failure
    • Thuckened physes due to normal chondrocyte proliferation but defective removal
  • Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis
    • Most affected:
      • Proximal humerus
      • Distal radius
      • Ulna
      • Ribs
        • Enlargement of costochondral junction - called 'rachitic rosary'
  • Weight bearing leads to:
    • Thickening of the physis and
    • Flaring of the excess matrix at the metaphysis
  • Histological lesions heal whn diet corected
  • Minor deformities correct but major deformities remain
  • Occurs after weaning because:
    • In utero and in milk - adeqaute nutrients obtained at expense of dam
  • In Foals
    • Rare - long nursing period and relatively slow rate of growth
  • In Calves and lambs
    • When diet deficeint of phosphorus and poor exposure to sunlight
  • In Puppies, Kittens and Piglets
    • Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet


Osteomalacia

  • Failure of mineralisation of osteoid / softening of the bones
  • Active resorption of bone replaced by excess osteoid on trabeculae, endosteum of cortices and Haversian canals
  • Decreased resistance to tension -> osteoid build-up at tendon insertions
  • In advanced disease
    • Bones break easily and become deformed
    • Tendons may separate from bones
  • Caused by prolonged phosphorus and Vitamin D deficiency
    • Vitamin D maintains normal plasma levels of calcium and phosphorus through acting on the intestines, bones and kidneys
  • In mature animals
  • Mainly grazing ruminants following gestation and lactation
    • Sunlight is important for production of vitamin D in the skin of ruminants
    • Vitamin d is also present in sun-dried hay
    • Mostly seen where there is long grass growing season with poor sunlight


Hypovitaminosis A

  • Vitamin A is essential for normal bone growth in foetus and neonates
  • Hypovitaminosis from dietary deficiency of dam -> teratogenic in pigs and large cats
  • More commonly, deficiency in neonates (puppies, kittens, calves, piglets) on vitamin-deficient diets
  • Dietary deficiency -> failure of osteoclastic remodelling resulting in bone overgrowth and nerve compression
  • Optic nerves particularly affected


Hypervitaminosis A

Hypervitaminosis A (Image sourced from Bristol Biomed Image Archive with permission)
  • Main lesions:
  • In cats fed bovine liver for prolonged periods
    • Rich in vitamin A in grazing animals
    • Vertebrae fuse with each other due to bone proliferation - cervical spondylosis (ankylosing exostosis of the vertebral column), especially in the neck
  • Can also be teratogenic, especially in pigs (cleft plate and abortions)


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:
    • Microscopically:
      • Mucosal haemorrhage
      • Necrosis of crypts
      • Focal myocardial necrosis
      • Mineralisation of intestinal mucosa, blood vessel walls, lungs and kidneys
  • Chronic poisoning


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