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| − | ===Pituitary===
| + | #REDIRECT[[:Category:Bones - Metabolic Pathology]] |
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| − | *Growth hormone
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| − | **Secreted by the anterior pituitary
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| − | **Influences the size of the skeleton and soft tissue
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| − | ====Pituitary dwarfism====
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| − | *Rare in animals, reported in German Shepherd Dogs
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| − | *Deficiency of growth hormone
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| − | *Proportionate dwarfism
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| − | *Growth plates remain open for up to 4 years
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| − | *Disorganised proliferating chondrocytes
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| − | ====Pituitary gigantism (Acromegaly)====
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| − | *Occurs in humans with pituitary adenoma
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| − | *Due to [[Acromegaly|pituitary hyperfunction]]
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| − | *Overgrowth of cranial bones, chin, hands and feet
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| − | *Reported in dogs '''?(and cats)?'''
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| − | ===Thyroid===
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| − | *Thyroid hormones affect maturation of growth of cartilage
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| − | ====Hypothyroidism====
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| − | *In young animals
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| − | *Retardation of growth and development of endochondral bone
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| − | *Stunted growth
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| − | *Skeletal abnormalities
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| − | *In neonatal foals, Giant Schnauzers and Scottish Deerhounds
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| − | ====Hyperthyroidism====
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| − | *In young animals causes accelerated maturation of growth plate
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| − | *In adults causes [[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|osteoporosis]]
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| − | ===Gonads===
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| − | *Oestrogen and androgens
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| − | **Affect growth of skeleton
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| − | **Accelerate epiphyseal closure
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| − | *Oestrogen
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| − | **Stimulates [[Bones - Anatomy & Physiology|osteoblasts]] to produce matrix
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| − | **Inhibits [[Bones - Anatomy & Physiology|osteoclasts]]
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| − | *'''Hypogonadism''' in growing skeleton -> delayed epiphyseal closure and skeletal maturation
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| − | ===Adrenal glands===
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| − | *[[Hyperadrenocorticism]]
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| − | **Causes [[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|osteoporosis]]
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| − | **Reported in dogs with Cushing's disease
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| − | ===[[Hyperparathyroidism|Hyperparathyroidism]]===
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| − | *Can arise in a number of ways but single common factor is elevated PTH
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| − | *Results in increased resorption of bone and replacement by fibrous connective tissue
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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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| − | *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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| − | *Regardless of pathogenesis, the result is:
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| − | **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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| − | ***[[Kidney Renal Failure - Pathology#Chronic|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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| − | *****-> [[Kidney Renal Failure - Pathology#Uraemia|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) +/- [[Bones Metabolic - Pathology#Osteomalacia|osteomalacia]]
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| − | *'''Nutritional hyperparathyroidism''' (nutritional osteodystrophy)
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| − | **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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| − | ===Rickets===
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| − | [[Image:Rickets in dog.jpg|right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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| − | *Essentially the same disease as osteomalacia
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| − | *Caused by Vitamin D and phosphorus deficiency
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| − | *In young animals
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| − | *Failure of:
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| − | **Mineralisation of osteoid at sites of membranous growth
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| − | **Cartilage vascularisation and mineralisation at sites of endochondral ossification
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| − | *Osteoid and catilage build up at those sites
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| − | *Histologically:
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| − | **Lines of hypertrophic cartilage cells are lenghtened and disorganised
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| − | **Ossification at metaphysis is poor
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| − | **Persisting osteoid and cartilage -> shaft modelling failure
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| − | **Thuckened physes due to normal chondrocyte proliferation but defective removal
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| − | *Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis
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| − | **Most affected:
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| − | ***Proximal humerus
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| − | ***Distal radius
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| − | ***Ulna
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| − | ***Ribs
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| − | ****Enlargement of costochondral junction - called 'rachitic rosary'
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| − | *Weight bearing leads to:
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| − | **Thickening of the physis and
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| − | **Flaring of the excess matrix at the metaphysis
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| − | *Histological lesions heal whn diet corected
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| − | *Minor deformities correct but major deformities remain
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| − | *Occurs after weaning because:
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| − | **''In utero'' and in milk - adeqaute nutrients obtained at expense of dam
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| − | *In Foals
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| − | **Rare - long nursing period and relatively slow rate of growth
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| − | *In Calves and lambs
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| − | **When diet deficeint of phosphorus and poor exposure to sunlight
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| − | *In Puppies, Kittens and Piglets
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| − | **Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet
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| − | ===Osteomalacia===
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| − | *Failure of mineralisation of osteoid / softening of the bones
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| − | *Active resorption of bone replaced by excess osteoid on trabeculae, endosteum of cortices and [[Bones - Anatomy & Physiology#Bone Remodeling|Haversian canals]]
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| − | *Decreased resistance to tension -> osteoid build-up at tendon insertions
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| − | *In advanced disease
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| − | **Bones break easily and become deformed
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| − | **Tendons may separate from bones
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| − | *Caused by prolonged phosphorus and Vitamin D deficiency
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| − | **Vitamin D maintains normal plasma levels of calcium and phosphorus through acting on the intestines, bones and kidneys
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| − | *In mature animals
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| − | *Mainly grazing ruminants following gestation and lactation
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| − | **Sunlight is important for production of vitamin D in the skin of ruminants
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| − | **Vitamin d is also present in sun-dried hay
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| − | **Mostly seen where there is long grass growing season with poor sunlight
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| − | ===Hypovitaminosis A===
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| − | *Vitamin A is essential for normal bone growth in foetus and neonates
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| − | *Hypovitaminosis from dietary deficiency of dam -> teratogenic in pigs and large cats
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| − | *More commonly, deficiency in neonates (puppies, kittens, calves, piglets) on vitamin-deficient diets
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| − | *Dietary deficiency -> failure of [[Bones - Anatomy & Physiology|osteoclastic remodelling]] resulting in bone overgrowth and nerve compression
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| − | *Optic nerves particularly affected
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| − | ===Hypervitaminosis A===
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| − | [[Image:Hypervitaminosis A.jpg|right|thumb|100px|<small><center>Hypervitaminosis A (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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| − | *Main lesions:
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| − | **Injury to growth cartilage -> [[Bones - Anatomy & Physiology|premature closure of growth plate]]
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| − | **[[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|Osteoporosis]]
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| − | **'''Exostoses'''
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| − | **[[Musculoskeletal Terminology - Pathology|Osteophyte]] formation in prolonged exposure
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| − | *In cats fed bovine liver for prolonged periods
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| − | **Rich in vitamin A in grazing animals
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| − | **Vertebrae fuse with each other due to bone proliferation - '''cervical spondylosis''' ('''ankylosing exostosis''' of the vertebral column), especially in the neck
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| − | *Can also be teratogenic, especially in pigs ([[Cleft Palate|cleft plate]] and abortions)
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| − | ===Hypervitaminosis D===
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| − | *May be of dietary or iatrogenic origin (has narrow safety margin)
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| − | *Key features are hypercalcaemia with metastatic calcification of soft tissues
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| − | *'''Acute poisoning'''
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| − | **In dogs and cats often from rodenticides containing cholecalciferol
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| − | **Grossly:
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| − | ***Gastrointestinal haemorrhage
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| − | ***Foci of [[Myocardial Mineralisation|myocardial discoloration]]
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| − | **Microscopically:
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| − | ***Mucosal haemorrhage
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| − | ***Necrosis of crypts
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| − | ***Focal myocardial necrosis
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| − | ***Mineralisation of intestinal mucosa, [[Arterial Calcification#Medial calcification|blood vessel walls]], [[Pulmonary Calcification|lungs]] and kidneys
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| − | *'''Chronic poisoning'''
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| − | **Grossly:
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| − | ***Intense [[Bones - Anatomy & Physiology|osteoclastic activity]] -> active resorption of bone, especially [[Bones - Anatomy & Physiology|trabecular]]
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| − | **Microscopically:
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| − | ***Excessive production of [[Bones - Anatomy & Physiology|osteoid]] - appears both eosinophilic and basophilic in different places
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| − | ***Marrow cavity may be obliterated
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| − | ***Mineralisation of soft tissues, especially [[Arterial Calcification|blood vessel walls]]
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| − | **Due to inhibition of [[Calcium|Parathyroid Hormone (PTH)|PTH]] and increase of [[Calcium#Calcitonin|calcitonin]]
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| − | ===Fluorine poisoning===
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| − | *F is widespread in nature
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| − | *Pastures may be contaminated by industrial processes (e.g. brick manufacture)
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| − | *'''Acute poisoning''':
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| − | **Gastroenteritis
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| − | **Nephrosis
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| − | *'''Chronic poisoning''':
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| − | **''Dental abnormalities''
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| − | ***Intoxication during teeth development
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| − | ***Foci of poor enamel formation - yellow, dark brown/black, chalky
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| − | ***Irregular wear of teeth, chip easily
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| − | **''Osteodystrophy = Fluorosis''
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| − | ***Generalised skeletal disturbance
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| − | ***Most affected are metatarsals and mandibles
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| − | ***Periosteal hyperostosis + endosteal bone resorption -> thickened bones with enlarged marrow cavities
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| − | ===Lead poisoning===
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| − | *Lead can bind to mineral portion of bone and cartilage
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| − | *In young animals ingesting large dose at once
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| − | ** -> Lead induced malfunction of osteoclasts
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| − | ** -> Transverse band of increased density on radiographs of metaphysis = "lead line" = [[Bones Developmental - Pathology#Retention of elongated primary trabeculae|growth retardation lattice]]
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| − | [[Category:Musculoskeletal System - Pathology]]
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