WikiPathWikiPath Banner.png
()Map MUSCULOSKELETAL SYSTEM (Map)
BONES DEGENERATIVE



Pituitary

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

Pituitary dwarfism

  • Rare in animals, reported in German Shepherd Dogs
  • Deficiency of growth hormone
  • Proportionate dwarfism
  • Growth plates remain open for up to 4 years
  • Disorganised proliferating chondrocytes

Pituitary gigantism (Acromegaly)

  • Occurs in humans with pituitary adenoma
  • Due to pituitary hyperfunction
  • Overgrowth of cranial bones, chin, hands and feet
  • Reported in dogs ?(and cats)?


Thyroid

  • Thyroid hormones affect maturation of growth of cartilage

Hypothyroidism

  • In young animals
  • Retardation of growth and development of endochondral bone
  • Stunted growth
  • Skeletal abnormalities
  • In neonatal foals, Giant Schnauzers and Scottish Deerhounds

Hyperthyroidism

  • In young animals causes accelerated maturation of growth plate
  • In adults causes osteoporosis


Gonads

  • Oestrogen and androgens
    • Affect growth of skeleton
    • Accelerate epiphyseal closure
  • Oestrogen
  • Hypogonadism in growing skeleton -> delayed epiphyseal closure and skeletal maturation


Adrenal glands


Hyperparathyroidism

  • Can arise in a number of ways but single common factor is elevated PTH
  • Results in increased resorption of bone and replacement by fibrous connective tissue
Primary hyperparathyroidism
  • This is increased production of PTH not related to calcium or phosphorus levels
  • Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
  • Rare
Secondary hyperparathyroidism
  • Regardless of pathogenesis, the result is:
    • Increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise
    • Flat bones of the skull swell, including maxillary and nasal bones
    • Long bones become soft with thin cortices which fracture easily
Renal osteodystrophy (Image sourced from Bristol Biomed Image Archive with permission)
  • Renal hyperparathyroidism
    • Pathogenesis:
      • Chronic renal failure
        • -> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
          • -> Hyperphosphataemia and hypocalcaemia (high P depresses Ca)
            • -> Increased PTH output
              • -> Increased bone resorption
                • -> Fibrous osteodystrophy - increased osteoclastic resorption of cancellous and cortical bone + proliferation of fibrous tissue
    • Mainly in dogs
    • Affects whole skeleton but mainly skull
    • Bones soft and pliable
    • Canine teeth easily removed - rubber jaw
    • Microscopically - Osteodystrophia fibrosa (above = fibrous osteodystrophy) +/- osteomalacia


  • Nutritional hyperparathyroidism (nutritional osteodystrophy)
    • Also called fibrous osteodystrophy, “rubber jaw” or “bran disease”
    • More common in young, fast-growing animals
    • Pathogenesis:
      • Low calcium / high phosphate diets
        • -> Decreased calcium levels in serum
          • -> Parathyroid gland stimulated (may become enlarged)
            • -> Increased PTH
              • -> Increased bone resorption
    • Caused by poor diet
      • Cattle and sheep - usually mild disease
      • Swine fed un-supplemented cereal grain, usually mild disease
      • Dogs/cats fed all-meat or offal diets (Ca:P often as high as 1:20)
        • Few weeks after weaning
        • Provision of calcium alone correct the problem
        • Very brittle bones -> sponataneous fractures
        • Extreme porosity of the whole skeleton on radioghraphs
      • Horses fed bran
        • Very susceptible to high phosphorus diet
        • Any time after weaning, susceptibility declines after seventh year
        • Early signs:
          • Mild changes of gait
          • Stiffness
          • Transient shifting lameness
        • Advanced signs:
          • Swelling of mandible and maxilla - 'Big head'
          • Dyspnoea caused by swelling of nasal and frontal bones
          • Teeth lost or buried in softened jaw
          • Fractures from mild trauma
          • Detached tendons and ligaments
          • Histologically:
            • Marked loss of bone
            • Replacement by proliferative tissue
        • Often called Osteodystrophia fibrosa

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
    • Grossly:
    • 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 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