Bones Metabolic - Pathology

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

Hyperadrenocorticism
- Causes osteoporosis
- Reported in dogs with Cushing's disease

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

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

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 (Image sourced from Bristol Biomed Image Archive with permission)

Main lesions:
- Injury to growth cartilage -> premature closure of growth plate
- Osteoporosis
- Exostoses
- Osteophyte formation in prolonged exposure
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)

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