Hyperparathyroidism

Parathyroid adenoma. Image courtesy of Biomed Archive.

Primary

• Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia.
  

  Parathyroid hyperplasia. Image courtesy of Biomed Archive.
• Rare.

Secondary

• Secondary hyperparathyroidism causes fibrous osteodystrophy or "rubber jaw".
• In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect.
• There are two common forms of secondary hyperparathyroisism:
  1. Nutritional Hyperparathyroidism
     • This includes Metabolic Bone Disease.
  2. Renal Hyperparathyroidism
• Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise.
  • Flat bones of the skull swell.
  • Fibrous tissue is seen around the tooth roots.
  • Bone softens in adult animals.
    • This is what gives rise to the term "rubber jaw".
    • Long bones become soft with thin cortices.
      • These fracture easily.

Nutritional Hyperparathyroidism

Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.

• Nutritional hyperparathyroidism is also known as nutritional osteodystrophy.
• This occurs most commonly in:
  • Young, fast-growing animals
  • Animals with a poor diet, for example:
    • Swine fed unsupplemented cereal grain
    • Dogs and cats fed all-meat diets
    • Horses fed bran
      • In this case, nutritional hyperparathyroidism is known as "bran disease".

Pathogenesis

• Pathogenesis follows low calcium/high phosphate diets.
  • These lead to decreased serum calcium levels, stimulating PTH release.
  • The increase in PTH gives an increase in bone resorption, causing pathology.

Pathology

• Gross
  • Severe cases may show:
    • Maxillary and mandibular swelling
    • Teeth lost or buried in soft tissue
    • Nasal and frontal bone enlargement, leading to dyspnoea
    • Long bone fracture
    • Detatchment tendons and ligaments
  • Early or less severe cases are characterised by shifting lameness and ill thrift.
• Histological
  • Osteoclastic resorption
  • Fibrous replacement

Renal Hyperparathyroidism

• Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease.

Pathogenesis

Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.

1. Chronic renal disease results in reduced glomerular filtration.
2. As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys.
3. Hyperphosphataemia develops due to phosphate retention.
   • Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels.
4. PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects:
   • Parathyroid hyperplasia
     • I.e. renal secondary hyperparathyroidism.
   • Soft tissue mineralisation
     • Particularly seen in dogs
     • Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces.
     • Calcification also occurs in other sites, e.g. stomach wall, lungs, kidneys.
   • Increased bone resorption
     • This causes fibrous osteodystrophy, or "rubber jaw".

Pathology

"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.

• Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism.
• Gross
  • The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
    • The maxillae and mandible appear swollen.
    • Radiographically, bone shows reduced density, and teeth hence appear embedded in soft tissue.
    • However, only a few cases of chronic renal disease show such severe bone lesions.
  • Other lesions may also be seen.
    • Intercostal muscles may be calcified.
    • Bone marrow lesions may cause anaemia.
    • The lung may show oedema, and have calcified alveolar walls.
• Histological
  • Osteoclastic resorption
  • Fibrous replacement