Difference between revisions of "Hyperparathyroidism"

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[[Image:parathyroidadeoma.jpg|thumb|right|100px|Parathyroid adenoma. Image courtesy of Biomed Archive.]]
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Also Known As: '''''HPT — Parathyroid Hyperplasia — Parathyroid Adenoma — Fibrous Osteodystrophy — Grain Overload — Bran Disease — Big Head Disease — Millers Disease — Rubber Jaw — [[Metabolic Bone Disease]]'''''
+
===Primary===
 +
* Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia. [[Image:parathyroidhyperplasia.jpg|thumb|right|100px|Parathyroid hyperplasia. Image courtesy of Biomed Archive.]]
 +
* Rare.
 +
===Secondary===
 +
* Secondary hyperparathyroidism causes [[Hyperparathyroidism|fibrous osteodystrophy or "rubber jaw"]].
 +
* In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect.
 +
* There are two common forms of secondary hyperparathyroisism:
 +
*# [[Hyperparathyroidism#Nutritional Hyperparathyroidism|'''Nutritional Hyperparathyroidism''']]
 +
*#* This includes [[Metabolic Bone Disease|Metabolic Bone Disease]].
 +
*# [[Hyperparathyroidism#Renal Hyperparathyroidism|'''Renal Hyperparathyroidism''']]
 +
* Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise. 
 +
** Flat bones of the skull swell.
 +
** Fibrous tissue is seen around the tooth roots.
 +
** Bone softens in adult animals.
 +
*** This is what gives rise to the term "rubber jaw".
 +
***  Long bones become soft with thin cortices.
 +
**** These fracture easily.
 +
====Nutritional Hyperparathyroidism====
 +
[[Image:secondaryhyperparathyroidism.jpg|thumb|right|100px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]]
 +
* Nutritional hyperparathyroidism is also known as nutritional osteodystrophy.
 +
* This occurs  most commonly in:
 +
** Young, fast-growing animals
 +
** Animals with a poor diet, for example:
 +
*** Swine fed unsupplemented cereal grain
 +
*** Dogs and cats fed all-meat diets
 +
*** Horses fed bran
 +
**** In this case, nutritional hyperparathyroidism is known as "bran disease".
 +
=====Pathogenesis=====
 +
* Pathogenesis follows low calcium/high phosphate diets.
 +
** These lead to decreased serum calcium levels, stimulating [[Calcium#Parathyroid Hormone (PTH)|PTH]] release.
 +
** The increase in PTH gives an increase in bone resorption, causing pathology.
  
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==Introduction==
+
=====Pathology=====
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[[Image:parathyroidadeoma.jpg|thumb|right|200px|Parathyroid adenoma. Image courtesy of Biomed Archive.]]
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* '''Gross'''
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[[Image:secondaryhyperparathyroidism.jpg|thumb|right|200px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]]
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** Severe cases may show:
−
[[Image:renalhyperparathyroidism.jpg|thumb|right|200px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]]
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*** Maxillary and mandibular swelling
−
[[Image:Renal_osteodystrophy.jpg|thumb|right|200px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]]
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*** [[:Category:Teeth - Anatomy & Physiology|Teeth]] lost or buried in soft tissue
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[[Image:parathyroidhyperplasia.jpg|thumb|right|200px|Parathyroid hyperplasia. Image courtesy of Biomed Archive.]]
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*** Nasal and frontal bone enlargement, leading to dyspnoea
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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)]]'''. This in turn results in chronic hypercalaemia. It occurs in many veterinary species and can be primary or secondary.
+
*** Long bone fracture
 +
*** Detatchment tendons and ligaments
 +
** Early or less severe cases are characterised by shifting lameness and ill thrift.
 +
* '''Histological'''
 +
** Osteoclastic resorption
 +
** Fibrous replacement
 +
=====Metabolic Bone Disease=====
 +
* Metabolic bone disease affects lizards in captivity, particularly young green iguanas
 +
* The condition is caused by:
 +
** Dietary deficiency of calcium and vitamin D
 +
*** For example, due to poor lighting (which diminishes viatmin D production).
 +
** Dietary excess of phosphorus
 +
** Certain toxicities
 +
** Diseases of the kidneys, [[Liver - Anatomy & Physiology|liver]] or parathyroid
 +
*** This aetiology is rare
 +
* Clinical signs include:
 +
** Lethargy
 +
** Inability to support weight
 +
** Rounded skull
 +
** Spontaneous fractures
 +
** Adult animals also show signs of [[Hypocalcaemia|hypocalcaemia]]
 +
* The skeleton shows reduced density on radiography.
 +
====Renal Hyperparathyroidism====
 +
* Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease.
 +
=====Pathogenesis=====
 +
[[Image:renalhyperparathyroidism.jpg|thumb|right|100px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]]
 +
# Chronic renal disease results in reduced glomerular filtration.
 +
# As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys.
 +
# Hyperphosphataemia develops due to phosphate retention.
 +
#* Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels.
 +
# PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects:
 +
#* Parathyroid hyperplasia
 +
#** I.e. '''renal secondary hyperparathyroidism'''.
 +
#* Soft tissue mineralisation
 +
#** Particularly seen in dogs
 +
#** Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces.
 +
#** Calcification also occurs in other sites, e.g. [[Monogastric Stomach - Anatomy & Physiology|stomach]] wall, lungs, kidneys.
 +
#* Increased bone resorption
 +
#** This causes fibrous osteodystrophy, or "rubber jaw".
 +
=====Pathology=====
 +
[[Image:Renal_osteodystrophy.jpg|thumb|right|100px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]]
 +
* Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism.
 +
* '''Gross'''
 +
** The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
 +
*** The maxillae and mandible appear swollen.
 +
*** Radiographically, bone shows reduced density, and [[:Category:Teeth - Anatomy & Physiology|teeth]] hence appear embedded in soft tissue.
 +
*** However, only a few cases of chronic renal disease show such severe bone lesions.
 +
** Other lesions may also be seen.
 +
*** Intercostal muscles may be calcified.
 +
*** Bone marrow lesions may cause anaemia.
 +
*** The lung may show oedema, and have calcified alveolar walls.
 +
* '''Histological'''
 +
** Osteoclastic resorption
 +
** Fibrous replacement
  
  
−
<big>'''Primary hyperparathyroidism'''</big> originates within the parathyroid gland itself and can be due to '''glandular hyperplasia or [[Neoplasia - Pathology|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>Merck Veterinary Manual, '''Primary Hyperparathyroidism''', accessed online 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/40407.htm</ref>
 
  
 +
==From musculoskeletal==
  
−
<big>'''Secondary hyperparathyroidism'''</big> is usually diffuse hyperplasia of the parathyroid glands due to relative hypocalcaemia and can be either renal or nutritional in origin:
+
*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
  
−
Secondary '''renal hyperparathyroidism''' is a complication of '''chronic renal failure'''. This is due to relative '''hyperphosphataemia developing as a result of impaired glomerular filtration rate'''. '''Reduced vitamin D''' synthesis or absorbtion is also thought to contribute to low serum calcium levels and subsequent stimulation of the parathyroid gland. Renal production of [[Calcium#Calcitriol|calcitriol]] (active Vitamin D3) is also reduced, exacerbating the resulting [[hypercalcaemia]].
+
=====<u>'''Primary hyperparathyroidism'''</u>=====
  
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Secondary '''nutritional''' hyperparathyroidism is caused by excessive '''phosphorus intake''' causing a total or relative calcium deficiency by '''binding calcium in the gut and decreasing its absorption'''.  This category encompasses '''bran disease in horses and also [[Metabolic Bone Disease|metabolic bone disease]] in reptiles'''.
+
*This is increased production of PTH not related to calcium or phosphorus levels
 +
*Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
 +
*Rare
  
−
==Signalment==
+
=====<u>'''Secondary hyperparathyroidism'''</u>=====
−
'''Primary''' hyperparathyroidism is seen '''infrequently in dogs and cats''', but is documented in German Shepherd Dogs.
 
  
−
'''Secondary renal''' hyperparathyroidism is seen '''frequently in dogs and occasionally in cats.'''
+
*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:
 +
***[[Chronic Renal Failure|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|osteomalacia]]
  
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'''Nutritional''' secondary HPT can affect '''horses of all breeds and ages''' that are either supplemented with large amounts of grain based concentrates or bran, or those that escape and break into a grain store or similar. It is also seen '''occasionally in dogs and cats fed all meat diets and pigs fed unsupplemented cereal''' feed. It is most commonly seen in '''young growing animals.'''
 
  
−
'''[[Metabolic Bone Disease]] occurs in a wide range of captive reptiles, particularly young green iguanas'''. It is also seen in some small mammals, e.g. chinchillas and degus.
 
  
−
Any disease in ruminants is very rare and usually mild.
+
*'''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'''''
  
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==Clinical Signs==
 
−
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.
 
  
−
Sequelae of hyperparathyroidism include '''fibrous osteodystrophy and organ failure due to metastatic calcification.'''
+
[[Category:Bones - Metabolic Pathology]]
  
−
'''Osteodystrophy is the [[Bones - Anatomy & Physiology#Cells|osteoclastic resorption]] of bone and replacement by weaker fibrous tissue'''. When this occurs in the '''long bones it causes shifting lameness''' and weakened bones that are '''prone to [[Fractures|fracture]]'''. Compression fractures may also occur spontaneously and if this occurs in the vertebrae, nerve dysfunction results.<ref>Merck Veterinary Manual, '''Metabolic Osteodystrophies: Fibrous Osteodystrophy: Primary Hyperparathyroidism''', accessed online 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/90313.htm</ref> Weakened bones may also cause '''tendon and ligament avulsions.'''
+
[[Category:Parathyroid Glands - Pathology]]
  
−
Fibrous osteodystrophy in the '''flat bones of the skull and face causes facial hyperostosis'''. This is seen in Bran disease or grain overload in horses and also in dogs with primary hyperparathyroidism. The face and head become '''grossly disfigured''' by excessive amounts of fibrous tissue laid down in an attempt to consolidate the weakened lamellar bone. In advanced cases, the '''mandible may become pliant''' and '''[[Teeth - Anatomy & Physiology|teeth]] may loosen''', hence the colloquial name, “rubber jaw”. This may interfere with mastication and cause '''pain, dysphagia and consequent weight loss.'''
+
[[Category:To Do - Clinical]]
  
−
'''Grain overload''' is also an important cause of '''severe [[Colic in Horses|colic in horses]]'''. The sudden '''increase in fermentation results in enodtoxaemia and acidosis which can be fatal.'''
+
[[Category:To Do - Steph]]
−
 
 
−
Animals affected by secondary renal HPT may exhibit '''classical signs of renal insufficiency such as polydipsia, polyuria, weight loss, vomiting and dehydration'''.
 
−
 
 
−
'''[[Metabolic Bone Disease]] in reptiles is caused by inadequate UVB light''' which diminishes '''Vitamin D production''' in the skin. In small mammals it is usually a straightforward dietary deficiency. Affected animals often have '''limb deformities, pathological fractures, are lethargic, very weak and inappetant and may also show signs of concurrent [[Hypocalcaemia|hypocalcaemia]]'''. They may also exhibit '''[[Dysecdysis|dysecdysis]].''' Rodents may have loose or deformed teeth and faces.
 
−
 
 
−
==Diagnosis==
 
−
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.
 
−
 
 
−
'''Urinary excretion of phosphorus''' and sometimes also calcium is increased. This can result in urolithiasis in some cases.
 
−
 
 
−
'''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. A '''high PTH assay along with high creatinine and blood urea nitrogen is indicative of possible renal secondary HPT'''.
 
−
 
 
−
'''Exploratory surgery''' of the cervical region may identify enlarged parathyroid glands if no other test is available or to confirm the diagnosis.
 
−
 
 
−
Animals with '''secondary renal hyperparathyroidism''' may demonstrate signs of bone loss radiographically. The bones of the '''jaw''' are affected first - with loss of the '''lamina dura, interdental and interradicular regions'''. Eventually bone loss generalises and widespread radiographic signs can be seen.
 
−
 
 
−
In cases of '''nutritional hyperparathyroidism, serum calcium is normal or low''' compared to high in other pathogeneses. '''Urinary excretion of phosphorus is markedly increased''' and serum PTH high. Radiographs will identify bony resorption and pathological fractures with fibrous tissue calluses.
 
−
 
−
'''[[Metabolic Bone Disease|MBD]]''' is usually identified by '''clinical signs and radiographic evidence''' of a poorly mineralised skeleton.
 
−
 
 
−
==Treatment==
 
−
Treatment for '''primary hyperparathyroidism''' usually requires '''surgical excision'''. [[Hypocalcaemia]] is a known post-operative complication and supplementation may be required in the short or long term management. If the hypercalcaemia persists, metastatic disease should be suspected and investigated.
 
−
 
 
−
Renal secondary HPT therapy is directed at '''control of the renal disease by way of specialised diet and rehydration along with supplementation of calcitriol and phosphorus binders'''.
 
−
 
 
−
'''Horses with bran disease should be confined until radiographs show normal bone density'''. Diet should be rectified if inadequate, and '''calcium: phosphorus ratio maintained at 1:1-3:1 for the first 2-3 months''' followed by a normal ration. If horses have also been feeding on plants high in oxalates (which can also bind calcium in the intestine) then these should be removed from the diet and limestone can be added to the diet to prevent or treat any associating signs.
 
−
 
 
−
Horses with colic as a result of '''grain engorgement''' require '''aggressive [[:Category:Fluid Therapy|fluid therapy]] and analgesia, and a nasogastric tube''' should be passed to alleviate any reflux. Measures should also be taken to try and prevent [[Laminitis - Horse|laninitis]] such as specialised shoes.
 
−
 
 
−
{{Learning
 
−
|flashcards = [[Hyperparathyroidism Flashcards]]<br>[[Small Mammals Q&A 19]]<br>[[Veterinary Dentistry Q&A 12]]
 
−
}}
 
−
 
 
−
==References==
 
−
<references/>
 
−
Lavoie, J-P., Hinchcliff, K. W (2008) '''Blackwell’s Five-Minute Veterinary Consult: Equine 2nd ed'''. ''Wiley-Blackwell, Oxford'', pp524-525.
 
−
 
 
−
Merck Vet Manual, '''Renal Secondary Hyperparathyroidism''', accessed 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/90314.htm
 
−
 
 
−
Merck Vet Manual, '''Nutritional Diseases''', accessed 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/182606.htm&word=nutritional%2csecondary
 
−
 
 
−
Verstraete, F. J. M. (1998) '''Self-Assessment Colour Review - Veterinary Dentistry''' ''Manson''
 
−
 
 
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{{review}}
 
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−
{{OpenPages}}
 
−
 
 
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[[Category:Endocrine Diseases - Dog]] [[Category: Endocrine Diseases - Cat]] [[Category:Bones - Metabolic Pathology]] [[Category:Parathyroid Glands - Pathology]] [[Category:Colic in Horses]][[Category:Endocrine Diseases - Horse]]
 
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[[Category:Expert Review]]
 

Revision as of 14:11, 26 July 2011

Parathyroid adenoma. Image courtesy of Biomed Archive.

Primary

  • Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia.
    Parathyroid hyperplasia. Image courtesy of Biomed Archive.
  • Rare.

Secondary

  • Secondary hyperparathyroidism causes fibrous osteodystrophy or "rubber jaw".
  • In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect.
  • There are two common forms of secondary hyperparathyroisism:
    1. Nutritional Hyperparathyroidism
    2. Renal Hyperparathyroidism
  • Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise.
    • Flat bones of the skull swell.
    • Fibrous tissue is seen around the tooth roots.
    • Bone softens in adult animals.
      • This is what gives rise to the term "rubber jaw".
      • Long bones become soft with thin cortices.
        • These fracture easily.

Nutritional Hyperparathyroidism

Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.
  • Nutritional hyperparathyroidism is also known as nutritional osteodystrophy.
  • This occurs most commonly in:
    • Young, fast-growing animals
    • Animals with a poor diet, for example:
      • Swine fed unsupplemented cereal grain
      • Dogs and cats fed all-meat diets
      • Horses fed bran
        • In this case, nutritional hyperparathyroidism is known as "bran disease".
Pathogenesis
  • Pathogenesis follows low calcium/high phosphate diets.
    • These lead to decreased serum calcium levels, stimulating PTH release.
    • The increase in PTH gives an increase in bone resorption, causing pathology.
Pathology
  • Gross
    • Severe cases may show:
      • Maxillary and mandibular swelling
      • Teeth lost or buried in soft tissue
      • Nasal and frontal bone enlargement, leading to dyspnoea
      • Long bone fracture
      • Detatchment tendons and ligaments
    • Early or less severe cases are characterised by shifting lameness and ill thrift.
  • Histological
    • Osteoclastic resorption
    • Fibrous replacement
Metabolic Bone Disease
  • Metabolic bone disease affects lizards in captivity, particularly young green iguanas
  • The condition is caused by:
    • Dietary deficiency of calcium and vitamin D
      • For example, due to poor lighting (which diminishes viatmin D production).
    • Dietary excess of phosphorus
    • Certain toxicities
    • Diseases of the kidneys, liver or parathyroid
      • This aetiology is rare
  • Clinical signs include:
    • Lethargy
    • Inability to support weight
    • Rounded skull
    • Spontaneous fractures
    • Adult animals also show signs of hypocalcaemia
  • The skeleton shows reduced density on radiography.

Renal Hyperparathyroidism

  • Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease.
Pathogenesis
Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.
  1. Chronic renal disease results in reduced glomerular filtration.
  2. As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys.
  3. Hyperphosphataemia develops due to phosphate retention.
    • Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels.
  4. PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects:
    • Parathyroid hyperplasia
      • I.e. renal secondary hyperparathyroidism.
    • Soft tissue mineralisation
      • Particularly seen in dogs
      • Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces.
      • Calcification also occurs in other sites, e.g. stomach wall, lungs, kidneys.
    • Increased bone resorption
      • This causes fibrous osteodystrophy, or "rubber jaw".
Pathology
"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.
  • Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism.
  • Gross
    • The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
      • The maxillae and mandible appear swollen.
      • Radiographically, bone shows reduced density, and teeth hence appear embedded in soft tissue.
      • However, only a few cases of chronic renal disease show such severe bone lesions.
    • Other lesions may also be seen.
      • Intercostal muscles may be calcified.
      • Bone marrow lesions may cause anaemia.
      • The lung may show oedema, and have calcified alveolar walls.
  • Histological
    • Osteoclastic resorption
    • Fibrous replacement


From musculoskeletal

  • 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
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