Difference between revisions of "Bones Metabolic - Pathology"

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#REDIRECT[[:Category:Bones - Metabolic Pathology]]
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{{review}}
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{{toplink
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|backcolour =CDE472
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|linkpage =Musculoskeletal System - Pathology
 +
|linktext =Musculoskeletal System
 +
|maplink = Musculoskeletal System (Content Map) - Pathology
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|pagetype =Pathology
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|sublink1=Bones Degenerative - Pathology
 +
|subtext1=BONES DEGENERATIVE
 +
}}
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<br>
 +
===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 Gland - Pathology#Pituitary Hyperfunction|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 [[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|osteoporosis]]
 +
 
 +
 
 +
===Gonads===
 +
 
 +
*Oestrogen and androgens
 +
**Affect growth of skeleton
 +
**Accelerate epiphyseal closure
 +
*Oestrogen
 +
**Stimulates [[Bones - normal#Normal structure|osteoblasts]] to produce matrix
 +
**Inhibits [[Bones - normal#Normal structure|osteoclasts]]
 +
*'''Hypogonadism''' in growing skeleton -> delayed epiphyseal closure and skeletal maturation
 +
 
 +
 
 +
===Adrenal glands===
 +
 
 +
*[[Adrenal Glands - Pathology#Adrenal Hyperfunction|Hyperadrenocorticism]]
 +
**Causes [[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|osteoporosis]]
 +
**Reported in dogs with Cushing's disease
 +
 
 +
 
 +
===[[Parathyroid Glands - Pathology#Hyperparathyroidism|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
 +
 
 +
=====<u>'''Primary hyperparathyroidism'''</u>=====
 +
 
 +
*This is increased production of PTH not related to calcium or phosphorus levels
 +
*Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
 +
*Rare
 +
 
 +
=====<u>'''Secondary hyperparathyroidism'''</u>=====
 +
 
 +
*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
 +
[[Image:Renal osteodystrophy.jpg|right|thumb|100px|<small><center>Renal osteodystrophy (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
*'''Renal hyperparathyroidism'''
 +
**Pathogenesis:
 +
***[[Kidney Renal Failure - Pathology#Chronic|Chronic renal failure]]
 +
****-> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
 +
*****-> [[Kidney Renal Failure - Pathology#Uraemia|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) +/- [[Bones Metabolic - Pathology#Osteomalacia|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===
 +
[[Image:Rickets in dog.jpg|right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
*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 systems|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 [[Bones - normal#Normal structure|osteoclastic remodelling]] resulting in bone overgrowth and nerve compression
 +
*Optic nerves particularly affected
 +
 
 +
 
 +
===Hypervitaminosis A===
 +
[[Image:Hypervitaminosis A.jpg|right|thumb|100px|<small><center>Hypervitaminosis A (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
*Main lesions:
 +
**Injury to growth cartilage -> [[Bones - normal#Physis (Growth plate)|premature closure of growth plate]]
 +
**[[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|Osteoporosis]]
 +
**'''Exostoses'''
 +
**[[Musculoskeletal Terminology - Pathology|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 Palate|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:
 +
***Gastrointestinal haemorrhage
 +
***Foci of [[Myocardial Mineralisation|myocardial discoloration]]
 +
**Microscopically:
 +
***Mucosal haemorrhage
 +
***Necrosis of crypts
 +
***Focal myocardial necrosis
 +
***Mineralisation of intestinal mucosa, [[Arterial Calcification#Medial calcification|blood vessel walls]], [[Lungs Degenerative - Pathology#Calcification|lungs]] and kidneys
 +
*'''Chronic poisoning'''
 +
**Grossly:
 +
***Intense [[Bones - normal#Normal structure|osteoclastic activity]] -> active resorption of bone, especially [[Bones - normal#Bone organisation|trabecular]]
 +
**Microscopically:
 +
***Excessive production of [[Bones - normal#Normal structure|osteoid]] - appears both eosinophilic and basophilic in different places
 +
***Marrow cavity may be obliterated
 +
***Mineralisation of soft tissues, especially [[Arterial Calcification|blood vessel walls]]
 +
**Due to inhibition of [[Bones - normal#Bone resorption|PTH]] and increase of [[Bones - normal#Bone resorption|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" = [[Bones Developmental - Pathology#Retention of elongated primary trabeculae|growth retardation lattice]]

Revision as of 13:46, 1 July 2010

 This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing.


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()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
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