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74 Cards in this Set

  • Front
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metabolic bone disease
- aka
- caused by

Nutritional or hormonal imbalances
Metabolic bone disease

4 main types
Osteoporosis (osteopenia)

Fibrous osteodystrophy


Hormones affecting bone growth
Thryoid hormone
Sex steroids
Increased corticosteroids
- affect on bone
Osteoporosis dt decr rate of bone formation
Decreased GH & IGF-I
- affect on bone
Proportional dwarfism
- progenitor cell differentiation
- chondrocyte proliferation
- affect on bone
Neonatal mortality

Postnatal exposure: retarded growth
- affect on bone
Osteoporosis prob dt negative metabolic balance
Sex steroids
- affect on bone
Osteoblasts have both estrogen & progesterone receptors

Hypoestrogenism > osteoporosis (menopause)
Define osteoporosis & osteopenia
Osteopenia: reduced mass of normal quality bone tissue (can be clinically silent)

Osteoporosis: reduced mass of normal bone quality OF CLINICAL SEVERITY
5 general causes of osteoporosis
1. Starvation - protein/calorie malnutrition
2. Gastrointestinal parasitism
3. Specific deficiency
4. Disuse atrophy
5. Endocrine associated osteoporosis
4 specific deficiencies that can lead to osteoporosis
- calcium
- phosphorus
- copper
- vitamin C
Osteoporosis from most causes is due to impaired deposition of bone
- except for which two causes?
Disuse atrophy and calcium deficiency lead to ACCELERATED RESORPTION of bone and thus osteoporosis
Histology of osteoporotic bone
- what feature indicates whether dt increased resorption or decreased production of bone?
Less trabeculae if increased resorption

Normal no. of thin trabeculae if decreased production
2 main consequences of osteoporosis
Pathological fractures & epiphyseal separation

Hypocalcaemic crises
- weaned lambs
- lactating ewes
What are you seeing
Osteoporotic bone with thinned and porous cortices
What might you see in an osteopenic bone during starvation or specific mineral deficiencies?
Serous atrophy of marrow
Metaphyseal growth arrest lines
Widely spaced trabeculae
Why, in some circumstances, doesn't osteoporotic bone return to normal when nutrients balance resumes?
Trabeculae surfaces are required for the formation of new bone by apposition
What are common sites of epiphyseal separation (4)
Femoral head
Humeral head
Ischial tuberosity
How does copper deficiency lead to osteoporosis?
Copper is required for adequate production of matrix collagen
What causes fibrous osteodystrophy
Prolonged and excessive exposure to PTH
What is the aetiology of fibrous osteodystrophy
Prolonged & excessive PTH ->

Increased osteoclastic resorption (>porosity), AND

Proliferation of osteoprogenitor cells to produce excess fibrous and fibro-osseus tissue
List the 4 sources of increased PTH secretion
Tumours of the PTH gland (rare)

Paraneoplastic secretion of PTH-like hormone by malignancies (lymphoma, anal gland tumour)

Secondary nutritional hyperparathyroidism

Secondary renal hyperparathyroidism
How can secondary nutritional hyperparathyroidism occur?
Occurs in response to relative Ca deficiencies (ratio Ca:P = 1:1)
- diet low in Ca, high in P (ratio imbalance)
- bran is high in P (horses)
- carnivores on offal (high P)
How does secondary renal hyperparathyroidism occur?
Renal failure leads to

- failure to excrete P (thus depression of Ca)

- reduced synthesis of active VitD
This horse was fed a diet in bran. What is this disease and cause?
Nutritional fibrous osteodystrophy ("Bighead" or "bran disease")
Bran high in P, Ca:P imbalance, PTH oversecretion, increased deposition of fibrous material in bone
Some tropical grasses can lead to fibrous osteodystrophy. How?
High in oxalates which band Ca++ in the gut and prevent absorption leading to hyperparathyroidism
Softening of bone (can be cut with a knife) dt deficiency of phosphrous or of vitamin D -> failure of bone matrix to mineralise
Deficiency of phosphrous or of vitamin D -> failure of cartilage AND bone matrix to mineralise
How are osteomalacia and rickets similar and different
Both are dt vit D or P deficiency
- Osteomalacia: bone affected
- Rickets: cartilage AND bone fail to mineralise

Osteomalacia is aka adult rickets
What are the two main causes of osteomalacia in cattle & sheep?
VitD deficiency in pastured animals where winter sun is low on the horizon (sheep more susceptible)

Phosphorous deficiency dt grazing deficient pastures (uncommon: cattle more susceptible)
List 4 sequential changes in rickets
1. Failure of mineralisation & vascular invasion of the hypertropic zone

2. Failure of replacement of the growing cartilage with woven bone

3. Formation of osteoid (not bone) on persistent cartilage with irregular osteochondral junctions

4. Metaphyseal compression fractures with fibrosis & deformities of the shape & structure of bone
What is the simplest and earliest anatomic manifestation of rickets
Widening of the physis
What condition is this most likely to be? What processes can be seen?
What's this? Why?
Rachitic rosary

Enlarged joints at the costo-chondral junctions.
What are the causes of rickets in calves, sheep, pigs, puppies & kittens and Alpaca crias?
Calves: P-deficient pastures, sunlight deficiency

Young sheep: sunlight deficiency, green feed low in VitD

Pigs: sunlight deficiency, VitD deficiency (feed errors), insufficient activation of VitD in kidney

Puppies & kittens: same as pigs

Crias: common bouts of severe GI disease -> electrolyte loss (Ca & P)
What is florid rickets?

What is it commonly seen in pigs?
"Florid" = quick, flamboyant

Occurs in pigs as they are frequently weaned early and the grow rapidly
What animal species is mostly affected by osteomalacia?
What is scurvy?
Vitamin C deficiency in animals requiring an exogenous source (guinea pigs, primates)
What is the aetiology of scurvy?
Vit C required for collagen formation

Thus failure of osteoid formation

Cartilage calcification is unaffected leading to a distinctive line of calcified cartilage spicules without newly formed osteoid "SCORBUTIC LATTICE"
Review physis biology
Causes of toxic osteodystrophies (3)

VitD toxicity

VitA toxicity
- how?
- who's affected?
- What's affected?
- CS?
Chronic exposure to excess fluoride leading to lack of mineralisation of teeth and bones


Teeth (toxic to odontoblasts) & bones (toxic to osteoblasts)

Teeth: mottling enamel, rapid wear, chipping
Bones: compensatory periosteal bone formation -> shifting lameness. Also spontaneous fractures
VitD toxicity
- 3 sources
- increased by?
Dietary supplementation

VitD toxicity increased with high dietary levels of calcium
VitD toxicity
- acute responses
Hypercalcaemia & hyperphosphatemia (dt incr osteoclast activity initially)

Metastatic mineralisation of soft tissue

Renal failure
VitD toxicity
- chronic responses
Early: incr. osteoclast activity -> removal of primary spongiosa

Then: incr. osteoblast activity and incr mineralisation -> osteosclerosis ("hardening")
- role in bone
Stimulate osteoclast activity
VitA deficiency
- causes in LA & SA
Cattle, pigs: unsupplemented rations or old hay

Carnivores: lean meat (no liver)
VitA deficiency
- main effects
Defective remodelling of membranous bone in skull & spine -> cerebellar herniation into foramen magnum

Also blindness, deafness, CNS signs
VitA toxicity
- how?
Esp cats fed almost exclusive diet of raw liver
VitA toxicity
- effect on growing animals & adults
Growing animals:
- degeneration & necrosis of chondrocytes & osteoblasts
- premature closure of growth plates, deformity, OSTEOPOROSIS

- paradoxical stimulation of osteoblasts
-> OSTEOSCLEROSIS, periosteal bone formation, exostoses, spondylosis
Fused cervical vertebrae, cat: Name and likely cause
Deforming cervical spondylosis: VitA toxicity
From here on, have given a definition of each term.
May expand later
- 6 causes
- 1 potential consequence of importance
1. Inflammatory diseases
2. Infiltration neoplasma
3. Peripheral vasoconstriction
4. Emboli (gas or fat)
5. Impaired lipid metabolism

Bone infarction can lead to OSTEOSARCOMA
Aseptic necrosis of bone
- aka ?
- bone death dt ischaemia (infarction)
Legg-Calve-Perthes disease
Which is the affected side?
Left (avascular)
Legg-Calve-Perthe disease
- what is it?
- who's most affected
Avascular necrosis of the femoral head

Poodles, Westies, Yorkies
Canine hypertrophic osteodystrophy (HOD)
- aka
- what is it?
- who's affected?
Metaphyseal Osteopathy
Initial lesion - neutrophilic osteomyelitis of metaphysis
Young, fast-growing large breeds
Most resolve spontaneously
Consequence of metaphyseal osteopathy?
Subphyseal infraction
Craniomandibular osteopathy
- aka
- who?
- what?
Lion jaw
- terriers (4-7mo)
- endosteal & periosteal proliferation of woven bone in mandible, occipital & temporal bones
Canine panosteitis
- who?
- what?
- effect?
Young, fast growing, large breed dogs (esp male GSD)
Inflammatory process, unknown cause
Waxes 7 wanes -> mild-severe lameness
Marie's disease
- aka
- commonly associated with?
- effects? why?
Hypertrophic osteopathy
Commonly assoc with a space occupying lesion of thorax (lung or chest wall) esp Spirocerca in dogs

Primarily a vascular disease leading to deposition of periosteal bone
Osteochondritis dissecans
- who?
- aetiology
Young, fast growing animals

Multifactorial (genetic, trauma, nutrition, excess dietary ca, cu def, hormones) but

Main histological features of osteochondrosis
Persistence of hypertrophic cartilage at physis
Name different types of bone tumours
Ossifying fibroma
Fibroblastic osteosarcoma
Giant cell osteosarcoma
Plasma cell myeloma
Enzootic bovine leukosis
What cells type can lead to primary neoplasms of bone
Myeloid cell lineages
Lymphoid cell lineages
Ossifying fibrtoma
- frequency?
- progression
Most common pirmary neoplasm of dogs & cats

Rapidly progressive - 14-22w survival
- classification
6 histological categories
- poorly differentiated (agressive)
- osteoblastic
- chondroblastic
- fibrobalstic (last aggressive)
- telangiectatic (most aggressive)
- giant cell
- common sites in dogs
Away from the elbow, towards the knee
Name 2 cartilage forming tumours

- what?
- where?
Benign tumour of cartilage
Mainly flat bones (scapula, ribs)
From articular cartilage?
- what?
- where?
Malignant tumour of cartilage
Arise from existing growth plate cartilage or metaplastic cartilage NOT articular cartilage
Some more to do briefly
Some more to do briefly