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Week 11- Musculoskeletal > Bone fracture healing > Flashcards

Bone fracture healing Flashcards

1
Q

What are the functions of bone?

A
  • mechanical: support, protection and movement
  • Mineral storage: calcium and phosphate
  • haematopoiesis in the marrow
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2
Q

Describe the structure of bone

A
  • Diaphysis is the shaft
  • Epiphysis are the ends
  • Metaphysic is the transitional flared area between the diaphysis and epiphysis
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3
Q

explain what cortical bone is

A
  • Compact or tubular bone
  • The diaphysis of long bone
  • Haversian systems/osteons
  • Slow turnover rate and metabolic activity
  • Stornger, greater resistance to torsion and bending than cancellous bone
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4
Q

Where are osteocytes located?

A

In the lacuna

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5
Q

What allows the communication of osteocytes

A

Canaliculi

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6
Q

Explain what cancellous bone is

A
  • Spongy/trabecular bone
  • metaphysic and epiphysis of long bones
  • Centrally in cuboid bones
  • 3 dimensional lattice structure
  • higher turnover rate and undergoes greater remodelling
  • less dense and less strong than cortical bone
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7
Q

What are the bone cells?

A
  • Osteoprogenitor (stem cell)
  • Osteocyte (maintains bone tissue)
  • Osteoblast (forms bone matrix)
  • Osteoclast (resorbs bone)
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8
Q

What makes up the matrix in bone?

A

•Organic - 40%

  • collagen
  • non-collagenous proteins
  • mucopolysaccharides

•Inorganic

  • calcium
  • phosphorus
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9
Q

What is the role of osteoblasts?

A

Produce osteoid

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10
Q

What are the potential fates of osteoblasts?

A
  • Osteocytes
  • Bone lining cell
  • Apoptosis
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11
Q

What type of cell is an osteoclast?

A

Large multinucleate cells

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12
Q

What is the role of the inorganic component of the bone matrix?

A
  • Responsible for compressive strength

* Reservoir for calcium, phosphorus and sodium and potassium

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13
Q

What is the role of the organic component of the bone matrix

A

Tensile strength of bone

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14
Q

What is a unique feature of children’s bone?

A

Physis - lies between the epiphysis and the metaphysic and is repsonsible for skeletal growth

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15
Q

What is the role of the physis?

A
  • responsible for skeletal growth
  • Allows remodelling of angular deformity after fracture
  • If physeal blood supply is damaged, will lead to growth arrest
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16
Q

What does fracture healing depend on?

A
  • Which bone is fractured
  • Mechanism of injury
  • closed or open fracture
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17
Q

What is indirect fracture healing?

A 
•Via callus formation 
•Formation of bone via a process of differential tissue formation until skeletal continuity is restored 
•Inflammation, repair and remodelling 
1. Fracture haematoma and inflammation 
2. fibrocartilage soft callus 
3. Bony hard callus 
4. bone remodelling
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18
Q

Describe fracture haematoma and inflammation

A
  • Blood from broken vessels forms a clot
  • 6-8 hours after the injury
  • Swelling and inflammation with removal of dead bone/tissue cells at fracture site
19
Q

Describe fibrocartilage callus

A
  • Lasts about 3 weeks
  • New capillaries organise fracture haematoma into granulation tissue (pro callus)
  • Fibroblast and osteogenic cells invade the pro callus
  • Collagen fibres are made with ends connected together
  • Chondrocytes begin to produce fibrocartilage
20
Q

Describe bony callus

A
  • After 3 weeks and lasts about 3-4 months

* osteoblasts make woven bone

21
Q

Bone remodelling in indirect fracture healing

A
  • Osteoclasts and osteoblasts remodel woven bone into compact bone and trabecular bone
  • Often will be no sign of fracture line on x-ray
22
Q

Explain the effect of movement on indirect fracture healing

A
  • A degree of movement is desirable to promote tissue differentiation
  • Excessive movement disrupts the healing tissue and affects cellular differentiation
23
Q

What is direct fracture healing?

A
  • Unique artificial surgical situation

* Direct formation of bone without the process of callus formation to restore skeletal continuity

24
Q

What does direct fracture healing rely upon?

A

Reduction and compression of the bone ends and for the fracture to be stable (no movement under physiological load)

25
Q

Explain the physiological process of direct bone healing

A
  • No callus
  • Cutting cone cross fracture site
  • Direct formation of bone via osteoclastic resorption and osteoblastic formation
26
Q

Explain blood supply of the bone

A
  • Endosteal: inner 2/3rds by nutrient artery, under high pressure
  • Periosteal: outer 1/3rd by capillaries from the muscle attachments, under low pressure
  • Metaphyseal-epiphyseal vessels supply ends
27
Q

What is the blood supply to the femoral neck?

A
  • Medial and lateral circumflex arteries
  • Extracapsular arterial ring at the base of femoral neck
  • Ascending cerbial vessels/reinacular vessels form a sub synovial ring
  • Epiphyseal branches supply the head
28
Q

Which fractures are more prone to have problems with union/avascualr necrosis?

A
  • Proximal pole of scaphoid fractures
  • Talar neck fractures
  • Intrascapular hip fractures
  • Surgical neck of humerus fracture
29
Q

What patient features lead to inhibition of fracture healing?

A
  • Increasing age
  • diabetes
  • Anaemia
  • malnutrition
  • Peripheral vascular disease
  • hypothyroidism
  • Smoking
  • Alcohol
30
Q

Which medications can inhibit bone healing

A
  • NSAIDs
  • Steroids (inhibit osteoblasts)
  • Bisphosphonates
31
Q

How do NSAIDs inhibit bone healing?

A
  • Reduce local vascularity at fracture site

* Additional reduction in healing effect independent of blood flow

32
Q

How do bisphosphonates inhibit bone healing?

A
  • Inhibits osteoclastic activity
  • There are also recognised bisphosphonate associated fractures
  • Delay fracture healing as a result
  • Long half life (takes several years to be rid from bone)
33
Q

What is avascular necrosis of bone?

A

Bone infarction (tissue death caused by an interruption of the blood supply) near a joint

34
Q

What can avascular necrosis cause?

A
  • Infarction of sub-chondral bone i.e. the bone right under the joint surface
  • collapse of the joint surface and end stage arthritis
35
Q

Where is AVN/osteonecrosis most common?

A

The hip

36
Q

What are the risk factors of avascular necrosis?

A
  • alcohol abuse
  • Steroid/sickle cell disease
  • Idiopathic
  • Trauma
  • Gout/Gaucher’s disease
  • Rheumatoid/radiation
  • Infection/inflammatory arthritis
  • Pancreatitis/pregnancy
  • SLE/smoking
  • Chronic renal failure/chemotherapy/caisson disease
  • Hyperlipidaemia
37
Q

What could cause an interruption to the blood supply of bone?

A
  • Extraosseous e.g. trauma
  • Intraosseous e.g. microcirculation from sickle cell
  • increased extravascular pressure e.g. steroid induced fat cell hypertrophy
38
Q

Describe the pathophysiology of AVN in the early stages

A
  • Necrosis always involves the medullary bone first
  • Cortex is spared due to the collateral supply
  • Articular cartilage is spared as it receives nutrition from the synovial fluid
39
Q

Describe the pathophysiology of AVN in the later stages

A
  • If bone doesn’t remodel, micro damage does not get repaired and the mechanical properties of the bone are impaired
  • Sub-chondral bone weakens and collapses
  • Joint surfaces become irregular and no longer smooth
  • Further damage to surrounding articular cartilage - arthrosis
40
Q

What is the clinical presentation of AVN of the femoral head?

A
  • Groin pain
  • Worsens with weight bearing and motion
  • Less commonly thigh and buttock pain
41
Q

What are the early X ray changes in AVN?

A
  • Mild density changes

* Followed by sclerosis and cystic areas

42
Q

What are the later x ray changes in AVN

A
  • Subchondral radiolucency ‘crescent sign’ precedes subchondral collapse
  • Loss of sphericity and collapse of the femoral head
  • Joint space narrowing and degenerative changes
43
Q

What are the treatment options of osteonecrosis?

A
  • Depends on the stage of the disease at presentation
  • Reduce the risk: minimise systemic corticosteroid to the minimum effective dose, modify risk factors
  • Education of patients at higher risk
  • Early symptom awareness: partial weight bearing, bisphosphonates
  • At early stages: Core decompression +/- bone graft, stem cell therapy, or vascularised bone graft
  • Later stages: total joint replacement

Week 11- Musculoskeletal (11 decks)

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