Bone path 1 Flashcards
What are the functions of bone?
- Rigidity
- protection
- haematopoiesis
- resovoir for minerals (calcium and phosphorus)
What are the cellular components of bone?
Make bone or cartilage
- osteoblasts -> osteocytes
- line bone trabeculae
- produce osteoid
- once they are mineralised bone matrix = osteocytes
Remove bone (remodelling)
- Osteoclasts - multinucleate phagocytic cells that sit in Howships lacunae and secrete acid and proteinase. Increase PTH -> increase in osteoclast numbers and activity . Osteoclasts have calcitonin receptors, calcitonin inhibits osteoclasts and causes them to detatch from bone surgaces
Bone marrow
- stromal cells
- adipocytes
- erythroid and myeloid precursors
What are the matrix components of bone?
Cone extracellular fluid (bone tissue fluid)
- Functional membrane (osteoblasts and osteocytes) separates bone ECF from general ECF
- Allows regulation of Ca2+ and PO4- ion flow into and out of bone ECF
Lining tissues
- Periosteum
- endosteum
Vascular supply
- Provides nutrients, growth factors/hormones, mineral ions
- Removes waste, mineral ions
Key components of calcium homeostasis
- ## tightly regulated - particularly extracellular calcium (kept in a very narrow range). This is critical to cell signalling
How is calcium regulated?
o Parathyroid hormone
Bone
* ↑Ca2+ transfer across cellular barrier
* ↑Ca2+ resorption
Kidney
* ↑Ca2+ absorption in DCT
* ↓ Pi absorption in PCT
* Activation of Vit D
o Calcitonin
↓ Bone resorption
↓Ca2+ transfer across cellular barrier
o 1,25(OH)2 Vitamin D
GIT: ↑Ca2+ absorption
Bone: ↑Ca2+ resorption
Kidney: Activation of Vitamin D
Skin: Formation of Vitamin D (UV dependent)
What are the causes of hyperparathyroidism?
- Reaction to persistently high serum PO4 (renal failure, vit D toxicity)
- Persistent secretion of PTH or related proteins (lymphoma, anal sac adenocarcinomas)
What could lead to pathological fractures?
Osteodystrophy - sacrifice of skeletal calcium
How does parathyroid hormone influence calcium homeostasis?
Parathyroid hormone
- BONE: ↑Ca2+ transfer across cellular barrier and ↑Ca2+ resorption
- KIDNEY: * ↑Ca2+ absorption in DCT, ↓ Pi absorption in PCT and activation of Vit D
Calcitonin: ↓ Bone resorption and ↓Ca2+ transfer across cellular barrier
1,25(OH)2 Vitamin D
- GIT: ↑Ca2+ absorption
- Bone: ↑Ca2+ resorption
- Kidney: Activation of Vitamin D
- Skin: Formation of Vitamin D (UV dependent)
How does calcium flow between bone and extracellular fluid TO ADD
What might happen if damage occurs to the growth plate?
- Stunted bone growth
- Malformation
- If you get damage to only one section of the growth plate, you might see malformations/deviations in the growth of the bone
What might happen if damage occurs to the growth plate?
- Stunted bone growth
- Malformation
- If you get damage to only one section of the growth plate, you might see malformations/deviations in the growth of the bone
What could lead to imparied osteoclastic activity?
Think viral or toxic causes
- Canine distemper virus
- Bovine viral diarrhoea
- Lead poisoning
Explain Wolffs law
- Bone is deposited at sites where its needed and reabsorbed where it isnt. The abnormal use of a bone can result in a change in shape. Removal of mechanical forces can cause localised osteopenia.
- Net bone formation at sites of compression, net bone resorption at sites of tension. Trabecular bon aligns along the lines of stress
What is osteochondrosis?
disorder resulting from abnormal growth, injury, or overuse of the developing growth plate and surrounding ossification centers
What is osteonecrosis?
The death of bone cells due to decreased blood flow. Generally as a reslt of trauma/fractures, pressure from tumours or inflammatory lesions or mechanical pressure, and lastly vasoconstriction from cold or ergotism.
What response do we see in periosteal injury?
Injured periosteum often forms bone. Usually see spicular bone that is orientated perpendicular to the log axis of the cortex (nodular lesions = osteophytes, osteophytes at insertions or tendons or ligaments are referred to as enthesiophytes). This spicular bone may be admixed with cartilage (esp. under low oxygen tension).
What is ectopic mineralisation/ossification?
Ectopic mineralisation: Mineralisation in areas of the body outside of the skeletal system
Ectopic ossification: Ectopic ossification is a biologic process in which new bone is formed in tissues which normally do not ossify.
What are the forms of ectopic mineralisation?
Metastatic and dystrophic
Give an examle of metastatic forms of ectopic mineralisation
- Hypercalcaemia or hyperphosphataemia
Give an examle of dystrophic forms of ectopic mineralisation
- Calcinosis cutis - Mineralisation of collagen fibres in the skin, strongly assoicated with cell injury
- Tumouralcalcinosis/calcinosis crcumscripta - often near joints, mass lesion due to depostiion of chalky accumulation of calcium salts
What can cause bone fractures?
Either
- Traumatic fractures - excessive force on NORMAL bone
- Pathological fractures - abnormal bone, minimal trauma as a result of neoplasia, inflammatory disease, osteodystrophies
What are the types of fractures?
- Transverse/oblique/spiral
- comminuted
- greenstick
- physeal (salter-harris I-V) - refer to image
Why is the distal ulnar physis easy to damage?
Because its conically shaped
What are the stages of healing following a fracture?
→ Haematoma
→ Local ischaemic necrosis of bone ends and local tissues
→ Acute inflammation, fibrinolysis, phagocytosis
→ Proliferation of mesenchymal cells (periosteal, endosteal) -> dominated by periosteal proliferation in the beginning stages
→ Loose connective tissue callus
→ Mesenchymal cells differentiate into chondroblasts
→ Cartilaginous callus, while osteoclasts remove dead bone
→ Osteoblasts proliferate and make woven bone
→ Bony callus (primary callus)
→ Modelling to mature lamellar bone (secondary callus)
→ remodolling continues for the remainder of the animals life
How would you promote high vascularity to promote bone formation?
- Minimise dead space
- Minimise dead tissue present
What are the aims of the treatment of fractures?
aimed at ensuring stability, maintaining blood supply, removing infectious agents and promoting normal function to optimise the healing process
In fracture repair, what does poor oxygen tension promote?
Poor oxygen tension promotes increased cartilage in the callus -> ont as strong as woven bone but will eventually form bone via endochondrial ossification
What would a lack of stabilisation mean in fracture repair?
↑ movement & tension, promoting development of mature fibrous tissue in the callus and may lead to non-union Infection
What diseases might impact fracture repair?
Neoplasia and or degenerative bone disease
List some adverse outcomes of fractures
o Delayed union
o Non-union
o Malunion
o Osteomyelitis
o Disuse atrophy of bone and musculature
o Physical disruption of surrounding tissue by the callus
o Angular limb deformity
How can inflammation induce a pathological fracture?
Exudate may accumulate in the medullary cavity
- Increased intramedullary pressure
- Compression of vessels
- Thrombosis and infarction
Stimulation of bone resorption
- Inflammatory mediators stimulate bone resorption by osteoclasts
- Enzymes from inflammatory cells and activation of matrix metalloproteinases promote matrix resorption
In a pathological fracture, what would cause a change to the matrix?
- Cellular infiltration from inflammation or neoplasia
- Change to the composition/amount of matrix as a result of osteodystrophies or congenital abnormalities of the bone or cartilage
Name some specific diseases that can result in a pathological fracture?
- Osteoporosis
- legg-calve-perthes disease in small dogs -> ishaemic necrosis of the femoral head
- Slipped capital physis in cats -> usually in overwight males, disorganised cartilage with delayed physeal closure
- Bucked shins -> dorsal cortex of MCIII in horses, repetative stress may cause periosteal damage, microfractures are in cortical bone
