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[[Image:parathyroidadeoma.jpg|thumb|right|100px|Parathyroid adenoma. Image courtesy of Biomed Archive.]]
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Also Known As – '''''Parathyroid hyperplasia – Parahyroid adenoma - Fibrous Osteodystrophy – Grain Overload – Bran Disease – Bran-head Disease '''''
===Primary===
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* Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia. [[Image:parathyroidhyperplasia.jpg|thumb|right|100px|Parathyroid hyperplasia. Image courtesy of Biomed Archive.]]
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* Rare.
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===Secondary===
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* Secondary hyperparathyroidism causes [[Hyperparathyroidism|fibrous osteodystrophy or "rubber jaw"]].
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* In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect.
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* There are two common forms of secondary hyperparathyroisism:
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*# [[Hyperparathyroidism#Nutritional Hyperparathyroidism|'''Nutritional Hyperparathyroidism''']]
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*#* This includes [[Metabolic Bone Disease|Metabolic Bone Disease]].
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*# [[Hyperparathyroidism#Renal Hyperparathyroidism|'''Renal Hyperparathyroidism''']]
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* Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise. 
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** Flat bones of the skull swell.
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** Fibrous tissue is seen around the tooth roots.
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** Bone softens in adult animals.
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*** This is what gives rise to the term "rubber jaw".
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***  Long bones become soft with thin cortices.
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**** These fracture easily.
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====Nutritional Hyperparathyroidism====
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[[Image:secondaryhyperparathyroidism.jpg|thumb|right|100px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]]
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* Nutritional hyperparathyroidism is also known as nutritional osteodystrophy.
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* This occurs  most commonly in:
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** Young, fast-growing animals
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** Animals with a poor diet, for example:
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*** Swine fed unsupplemented cereal grain
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*** Dogs and cats fed all-meat diets
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*** Horses fed bran
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**** In this case, nutritional hyperparathyroidism is known as "bran disease".
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=====Pathogenesis=====
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* Pathogenesis follows low calcium/high phosphate diets.
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** These lead to decreased serum calcium levels, stimulating [[Calcium#Parathyroid Hormone (PTH)|PTH]] release.
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** The increase in PTH gives an increase in bone resorption, causing pathology.
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=====Pathology=====
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==Introduction==
* '''Gross'''
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Hyperparathyroidism is an [[Endocrine System – Anatomy & Physiology|endocrine]] disease caused by overactivity of the [[Parathyroid Glands – Anatomy & Physiology|parathyroid gland]] and consequent raised body levels of [[Calcium#Parathyroid Hormone|parathyroid hormone (PTH)]]. It occurs in many veterinary species and can be primary or secondary.  
** Severe cases may show:
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*** Maxillary and mandibular swelling
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*** [[:Category:Teeth - Anatomy & Physiology|Teeth]] lost or buried in soft tissue
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*** Nasal and frontal bone enlargement, leading to dyspnoea
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*** Long bone fracture
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*** Detatchment tendons and ligaments
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** Early or less severe cases are characterised by shifting lameness and ill thrift.
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* '''Histological'''
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** Osteoclastic resorption
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** Fibrous replacement
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=====Metabolic Bone Disease=====
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* Metabolic bone disease affects lizards in captivity, particularly young green iguanas
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* The condition is caused by:
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** Dietary deficiency of calcium and vitamin D
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*** For example, due to poor lighting (which diminishes viatmin D production).
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** Dietary excess of phosphorus
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** Certain toxicities
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** Diseases of the kidneys, [[Liver - Anatomy & Physiology|liver]] or parathyroid
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*** This aetiology is rare
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* Clinical signs include:
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** Lethargy
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** Inability to support weight
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** Rounded skull
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** Spontaneous fractures
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** Adult animals also show signs of [[Hypocalcaemia|hypocalcaemia]]
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* The skeleton shows reduced density on radiography.
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====Renal Hyperparathyroidism====
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* Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease.
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=====Pathogenesis=====
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[[Image:renalhyperparathyroidism.jpg|thumb|right|100px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]]
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# Chronic renal disease results in reduced glomerular filtration.
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# As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys.
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# Hyperphosphataemia develops due to phosphate retention.
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#* Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels.
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# PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects:
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#* Parathyroid hyperplasia
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#** I.e. '''renal secondary hyperparathyroidism'''.
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#* Soft tissue mineralisation
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#** Particularly seen in dogs
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#** Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces.
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#** Calcification also occurs in other sites, e.g. [[Monogastric Stomach - Anatomy & Physiology|stomach]] wall, lungs, kidneys.  
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#* Increased bone resorption
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#** This causes fibrous osteodystrophy, or "rubber jaw".
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=====Pathology=====
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[[Image:Renal_osteodystrophy.jpg|thumb|right|100px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]]
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* Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism.
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* '''Gross'''
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** The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
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*** The maxillae and mandible appear swollen.
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*** Radiographically, bone shows reduced density, and [[:Category:Teeth - Anatomy & Physiology|teeth]] hence appear embedded in soft tissue.
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*** However, only a few cases of chronic renal disease show such severe bone lesions.
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** Other lesions may also be seen.
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*** Intercostal muscles may be calcified.
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*** Bone marrow lesions may cause anaemia.
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*** The lung may show oedema, and have calcified alveolar walls.
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* '''Histological'''
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** Osteoclastic resorption
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** Fibrous replacement
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Primary hyperparathyroidism originates within the parathyroid gland itself and can be due to glandular hyperplasia or [[Neoplasia – Pathlology|neoplasia]]. It is most commonly due to a solitary benign [[Adenoma|adenoma]] of either the [[Parathyroid Glands – Anatomy & Physiology|internal or external parathyroid gland]].<ref name=Merck1>Merck Veterinary Manual, '''Primary Hyperparathyroidism''', accessed online 24/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/40407.htm</ref>
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==From musculoskeletal==
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==Signalment==
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*Can arise in a number of ways but single common factor is elevated PTH
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==Clinical Signs==
*Results in increased resorption of bone and replacement by fibrous connective tissue
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The main effect of hyperparathyroidism is [[Hypercalcaemia|hypercalcaemia]] which causes a range of clinical signs. Polydipsia, polyuria, anorexia, lethargy and depression are the most common signs but animals may also be constipated, weak, stiff-gaited, shivering and vomiting. Mild hypercalcaemia may not generate any overt clinical signs.
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=====<u>'''Primary hyperparathyroidism'''</u>=====
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*This is increased production of PTH not related to calcium or phosphorus levels
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==Diagnosis==
*Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
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*Rare
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=====<u>'''Secondary hyperparathyroidism'''</u>=====
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Electrolyte imbalances on blood biochemistry profiles are highly suggestive. Hypercalcaemia with a normal to low serum phosphorus and a low urine specific gravity are fairly consistent findings.
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*Regardless of pathogenesis, the result is:
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Serum PTH levels may be useful in diagnosing primary hyperparathyroidism, but only in animals with normal renal function, i,e, those with normal creatinine and blood urea nitrogen.  
**Increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise
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**Flat bones of the skull swell, including maxillary and nasal bones
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**Long bones become soft with thin cortices which fracture easily
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[[Image:Renal osteodystrophy.jpg|right|thumb|100px|<small><center>Renal osteodystrophy (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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*'''Renal hyperparathyroidism'''
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**Pathogenesis:
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***[[Chronic Renal Failure|Chronic renal failure]]
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****-> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
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*****-> Hyperphosphataemia and hypocalcaemia (high P depresses Ca)
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******-> Increased PTH output
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*******-> Increased bone resorption
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********-> '''Fibrous osteodystrophy''' - increased osteoclastic resorption of cancellous and cortical bone + proliferation of fibrous tissue
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**Mainly in dogs
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**Affects whole skeleton but mainly skull
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**Bones soft and pliable
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**Canine teeth easily removed - rubber jaw
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**Microscopically - ''Osteodystrophia fibrosa'' (above  = fibrous osteodystrophy) +/- [[Osteomalacia|osteomalacia]]
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Exploratory surgery of the cervical region may identify enlarged parathyroid glands if no other test is available or confirmatory.
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==Treatment==
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Treatment for primary hyperaparathyroidism usually required surgical excision.
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*'''Nutritional hyperparathyroidism''' (nutritional osteodystrophy)
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==Control==
**Also called '''fibrous osteodystrophy, “rubber jaw”''' or '''“bran disease”'''
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**More common in young, fast-growing animals
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**Pathogenesis:
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***Low calcium / high phosphate diets
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****-> Decreased calcium levels in serum
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*****-> Parathyroid gland stimulated (may become enlarged)
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******-> Increased PTH
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*******-> Increased bone resorption
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**Caused by poor diet
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***Cattle and sheep - usually mild disease
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***'''Swine''' fed un-supplemented cereal grain, usually mild disease
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***'''Dogs/cats''' fed all-meat or offal diets (Ca:P often as high as 1:20)
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****Few weeks after weaning
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****Provision of calcium alone correct the problem
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****Very brittle bones -> sponataneous fractures
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****Extreme porosity of the whole skeleton on radioghraphs
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***'''Horses''' fed bran
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****Very susceptible to high phosphorus diet
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****Any time after weaning, susceptibility declines after seventh year
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****Early signs:
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*****Mild changes of gait
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*****Stiffness
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*****Transient shifting lameness
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****Advanced signs:
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*****Swelling of mandible and maxilla - 'Big head'
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*****Dyspnoea caused by swelling of nasal and frontal bones
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*****Teeth lost or buried in softened jaw
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*****Fractures from mild trauma
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*****Detached tendons and ligaments
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*****Histologically:
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******Marked loss of bone
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******Replacement by proliferative tissue
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****Often called '''''Osteodystrophia fibrosa'''''
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{{Learning
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|flashcards = [[Hyperparathyroidism Flashcards]]
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}}
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[[Category:Bones - Metabolic Pathology]]
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==References==
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<references/>
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Lavoie, J-P., Hinchcliff, K. W (2008) '''Blackwell’s Five-Minute Veterinary Consult: Equine 2nd ed'''. ''Wiley-Blackwell, Oxford'', pp.
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[[Category:Parathyroid Glands - Pathology]]
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Haskell, S (2008) '''Blackwell’s Five-Minute Veterinary Consult:Ruminant'''. ''Wiley-Blackwell, Oxford'', pp.
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[[Category:To Do - Clinical]]
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[[Category:To Do - Manson review]] [[Category: Diseases - Horse]] [[Category:]]
 
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[[Category:To Do - Steph]]
 
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