Difference between revisions of "Bones Metabolic - Pathology"
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− | # | + | {{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 - Pathology#Osteomalacia|osteomalacia]] | ||
+ | |||
+ | |||
+ | |||
+ | *'''Nutritional hyperparathyroidism''' (nutritional osteodystrophy) | ||
+ | **Also called '''fibrous osteodystrophy, “rubber jaw”''' or '''“bran disease”''' | ||
+ | **More common in young, fast-growing animals | ||
+ | **Pathogenesis: | ||
+ | ***Low calcium / high phosphate diets | ||
+ | ****-> Decreased calcium levels in serum | ||
+ | *****-> Parathyroid gland stimulated (may become enlarged) | ||
+ | ******-> Increased PTH | ||
+ | *******-> Increased bone resorption | ||
+ | **Caused by poor diet | ||
+ | ***Cattle and sheep - usually mild disease | ||
+ | ***'''Swine''' fed un-supplemented cereal grain, usually mild disease | ||
+ | ***'''Dogs/cats''' fed all-meat or offal diets (Ca:P often as high as 1:20) | ||
+ | ****Few weeks after weaning | ||
+ | ****Provision of calcium alone correct the problem | ||
+ | ****Very brittle bones -> sponataneous fractures | ||
+ | ****Extreme porosity of the whole skeleton on radioghraphs | ||
+ | ***'''Horses''' fed bran | ||
+ | ****Very susceptible to high phosphorus diet | ||
+ | ****Any time after weaning, susceptibility declines after seventh year | ||
+ | ****Early signs: | ||
+ | *****Mild changes of gait | ||
+ | *****Stiffness | ||
+ | *****Transient shifting lameness | ||
+ | ****Advanced signs: | ||
+ | *****Swelling of mandible and maxilla - 'Big head' | ||
+ | *****Dyspnoea caused by swelling of nasal and frontal bones | ||
+ | *****Teeth lost or buried in softened jaw | ||
+ | *****Fractures from mild trauma | ||
+ | *****Detached tendons and ligaments | ||
+ | *****Histologically: | ||
+ | ******Marked loss of bone | ||
+ | ******Replacement by proliferative tissue | ||
+ | ****Often called '''''Osteodystrophia fibrosa''''' | ||
+ | |||
+ | ===Rickets=== | ||
+ | [[Image:Rickets in dog.jpg|right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Essentially the same disease as osteomalacia | ||
+ | *Caused by Vitamin D and phosphorus deficiency | ||
+ | *In young animals | ||
+ | *Failure of: | ||
+ | **Mineralisation of osteoid at sites of membranous growth | ||
+ | **Cartilage vascularisation and mineralisation at sites of endochondral ossification | ||
+ | *Osteoid and catilage build up at those sites | ||
+ | |||
+ | *Histologically: | ||
+ | **Lines of hypertrophic cartilage cells are lenghtened and disorganised | ||
+ | **Ossification at metaphysis is poor | ||
+ | **Persisting osteoid and cartilage -> shaft modelling failure | ||
+ | **Thuckened physes due to normal chondrocyte proliferation but defective removal | ||
+ | *Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis | ||
+ | **Most affected: | ||
+ | ***Proximal humerus | ||
+ | ***Distal radius | ||
+ | ***Ulna | ||
+ | ***Ribs | ||
+ | ****Enlargement of costochondral junction - called 'rachitic rosary' | ||
+ | |||
+ | *Weight bearing leads to: | ||
+ | **Thickening of the physis and | ||
+ | **Flaring of the excess matrix at the metaphysis | ||
+ | *Histological lesions heal whn diet corected | ||
+ | *Minor deformities correct but major deformities remain | ||
+ | *Occurs after weaning because: | ||
+ | **''In utero'' and in milk - adeqaute nutrients obtained at expense of dam | ||
+ | *In Foals | ||
+ | **Rare - long nursing period and relatively slow rate of growth | ||
+ | *In Calves and lambs | ||
+ | **When diet deficeint of phosphorus and poor exposure to sunlight | ||
+ | *In Puppies, Kittens and Piglets | ||
+ | **Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet | ||
+ | |||
+ | |||
+ | ===Osteomalacia=== | ||
+ | |||
+ | *Failure of mineralisation of osteoid / softening of the bones | ||
+ | *Active resorption of bone replaced by excess osteoid on trabeculae, endosteum of cortices and [[Haversian systems|Haversian canals]] | ||
+ | *Decreased resistance to tension -> osteoid build-up at tendon insertions | ||
+ | *In advanced disease | ||
+ | **Bones break easily and become deformed | ||
+ | **Tendons may separate from bones | ||
+ | *Caused by prolonged phosphorus and Vitamin D deficiency | ||
+ | **Vitamin D maintains normal plasma levels of calcium and phosphorus through acting on the intestines, bones and kidneys | ||
+ | *In mature animals | ||
+ | *Mainly grazing ruminants following gestation and lactation | ||
+ | **Sunlight is important for production of vitamin D in the skin of ruminants | ||
+ | **Vitamin d is also present in sun-dried hay | ||
+ | **Mostly seen where there is long grass growing season with poor sunlight | ||
+ | |||
+ | |||
+ | ===Hypovitaminosis A=== | ||
+ | |||
+ | *Vitamin A is essential for normal bone growth in foetus and neonates | ||
+ | *Hypovitaminosis from dietary deficiency of dam -> teratogenic in pigs and large cats | ||
+ | *More commonly, deficiency in neonates (puppies, kittens, calves, piglets) on vitamin-deficient diets | ||
+ | *Dietary deficiency -> failure of [[Bones - normal#Normal structure|osteoclastic remodelling]] resulting in bone overgrowth and nerve compression | ||
+ | *Optic nerves particularly affected | ||
+ | |||
+ | |||
+ | ===Hypervitaminosis A=== | ||
+ | [[Image:Hypervitaminosis A.jpg|right|thumb|100px|<small><center>Hypervitaminosis A (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Main lesions: | ||
+ | **Injury to growth cartilage -> [[Bones - normal#Physis (Growth plate)|premature closure of growth plate]] | ||
+ | **[[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|Osteoporosis]] | ||
+ | **'''Exostoses''' | ||
+ | **[[Musculoskeletal terminology|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]] |
Revision as of 19:18, 18 August 2008
|
Pituitary
- Growth hormone
- Secreted by the anterior pituitary
- Influences the size of the skeleton and soft tissue
Pituitary dwarfism
- Rare in animals, reported in German Shepherd Dogs
- Deficiency of growth hormone
- Proportionate dwarfism
- Growth plates remain open for up to 4 years
- Disorganised proliferating chondrocytes
Pituitary gigantism (Acromegaly)
- Occurs in humans with pituitary adenoma
- Due to pituitary hyperfunction
- Overgrowth of cranial bones, chin, hands and feet
- Reported in dogs ?(and cats)?
Thyroid
- Thyroid hormones affect maturation of growth of cartilage
Hypothyroidism
- In young animals
- Retardation of growth and development of endochondral bone
- Stunted growth
- Skeletal abnormalities
- In neonatal foals, Giant Schnauzers and Scottish Deerhounds
Hyperthyroidism
- In young animals causes accelerated maturation of growth plate
- In adults causes osteoporosis
Gonads
- Oestrogen and androgens
- Affect growth of skeleton
- Accelerate epiphyseal closure
- Oestrogen
- Stimulates osteoblasts to produce matrix
- Inhibits osteoclasts
- Hypogonadism in growing skeleton -> delayed epiphyseal closure and skeletal maturation
Adrenal glands
- Hyperadrenocorticism
- Causes osteoporosis
- Reported in dogs with Cushing's disease
Hyperparathyroidism
- Can arise in a number of ways but single common factor is elevated PTH
- Results in increased resorption of bone and replacement by fibrous connective tissue
Primary hyperparathyroidism
- This is increased production of PTH not related to calcium or phosphorus levels
- Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
- Rare
Secondary hyperparathyroidism
- Regardless of pathogenesis, the result is:
- Increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise
- Flat bones of the skull swell, including maxillary and nasal bones
- Long bones become soft with thin cortices which fracture easily
- Renal 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
- -> Increased bone resorption
- -> Increased PTH output
- -> Hyperphosphataemia and hypocalcaemia (high P depresses Ca)
- -> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
- Chronic renal failure
- 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
- Pathogenesis:
- 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
- -> Increased PTH
- -> Parathyroid gland stimulated (may become enlarged)
- -> Decreased calcium levels in serum
- Low calcium / high phosphate diets
- 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
- 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'
- Most affected:
- Weight bearing leads to:
- Thickening of the physis and
- Flaring of the excess matrix at the metaphysis
- Histological lesions heal whn diet corected
- Minor deformities correct but major deformities remain
- Occurs after weaning because:
- In utero and in milk - adeqaute nutrients obtained at expense of dam
- In Foals
- Rare - long nursing period and relatively slow rate of growth
- In Calves and lambs
- When diet deficeint of phosphorus and poor exposure to sunlight
- In Puppies, Kittens and Piglets
- Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet
Osteomalacia
- Failure of mineralisation of osteoid / softening of the bones
- Active resorption of bone replaced by excess osteoid on trabeculae, endosteum of cortices and Haversian canals
- Decreased resistance to tension -> osteoid build-up at tendon insertions
- In advanced disease
- Bones break easily and become deformed
- Tendons may separate from bones
- Caused by prolonged phosphorus and Vitamin D deficiency
- Vitamin D maintains normal plasma levels of calcium and phosphorus through acting on the intestines, bones and kidneys
- In mature animals
- Mainly grazing ruminants following gestation and lactation
- Sunlight is important for production of vitamin D in the skin of ruminants
- Vitamin d is also present in sun-dried hay
- Mostly seen where there is long grass growing season with poor sunlight
Hypovitaminosis A
- Vitamin A is essential for normal bone growth in foetus and neonates
- Hypovitaminosis from dietary deficiency of dam -> teratogenic in pigs and large cats
- More commonly, deficiency in neonates (puppies, kittens, calves, piglets) on vitamin-deficient diets
- Dietary deficiency -> failure of osteoclastic remodelling resulting in bone overgrowth and nerve compression
- Optic nerves particularly affected
Hypervitaminosis A
- Main lesions:
- Injury to growth cartilage -> premature closure of growth plate
- Osteoporosis
- Exostoses
- Osteophyte formation in prolonged exposure
- In cats fed bovine liver for prolonged periods
- Rich in vitamin A in grazing animals
- Vertebrae fuse with each other due to bone proliferation - cervical spondylosis (ankylosing exostosis of the vertebral column), especially in the neck
- Can also be teratogenic, especially in pigs (cleft 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 discoloration
- Microscopically:
- Mucosal haemorrhage
- Necrosis of crypts
- Focal myocardial necrosis
- Mineralisation of intestinal mucosa, blood vessel walls, lungs and kidneys
- Chronic poisoning
- Grossly:
- Intense osteoclastic activity -> active resorption of bone, especially trabecular
- Microscopically:
- Excessive production of osteoid - appears both eosinophilic and basophilic in different places
- Marrow cavity may be obliterated
- Mineralisation of soft tissues, especially blood vessel walls
- Due to inhibition of PTH and increase of calcitonin
- Grossly:
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
- Dental abnormalities
Lead poisoning
- Lead can bind to mineral portion of bone and cartilage
- In young animals ingesting large dose at once
- -> Lead induced malfunction of osteoclasts
- -> Transverse band of increased density on radiographs of metaphysis = "lead line" = growth retardation lattice