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Bones Metabolic - Pathology (view source)
Revision as of 19:15, 18 August 2008
, 19:15, 18 August 2008New page: {{toplink |backcolour =CDE472 |linkpage =Musculoskeletal System - Pathology |linktext =Musculoskeletal System |maplink = Musculoskeletal System (Content Map) - Pathology |pagetype =Patholo...
{{toplink
|backcolour =CDE472
|linkpage =Musculoskeletal System - Pathology
|linktext =Musculoskeletal System
|maplink = Musculoskeletal System (Content Map) - Pathology
|pagetype =Pathology
|sublink1=Bones Degenerative - Pathology
|subtext1=BONES DEGENERATIVE
}}
<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#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|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 ([[Oral Cavity - Cavity & Gingiva#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 - Pathology#Mineralisation|myocardial discoloration]]
**Microscopically:
***Mucosal haemorrhage
***Necrosis of crypts
***Focal myocardial necrosis
***Mineralisation of intestinal mucosa, [[Arterial Disease - Pathology#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 Disease - Pathology#Medial 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]]
|backcolour =CDE472
|linkpage =Musculoskeletal System - Pathology
|linktext =Musculoskeletal System
|maplink = Musculoskeletal System (Content Map) - Pathology
|pagetype =Pathology
|sublink1=Bones Degenerative - Pathology
|subtext1=BONES DEGENERATIVE
}}
<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#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|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 ([[Oral Cavity - Cavity & Gingiva#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 - Pathology#Mineralisation|myocardial discoloration]]
**Microscopically:
***Mucosal haemorrhage
***Necrosis of crypts
***Focal myocardial necrosis
***Mineralisation of intestinal mucosa, [[Arterial Disease - Pathology#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 Disease - Pathology#Medial 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]]