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MBChB3 > Bone Fracture Healing and AVN > Flashcards

Bone Fracture Healing and AVN Flashcards

1
Q

What are the functions of bone?

A
  • mechanical support
  • protection
  • movement
  • mineral storage (calcium and phosphate)
  • haematopoiesis
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2
Q

Describe the structure of cortical bone

A
  • forms the diaphysis of long bones
  • arranged in Haversian systems/osteons (concentric lamellae around vascular structures)
  • slow turnover rate and metabolic activity
  • stronger, greater resistance to torsion and bending than cancellous bone
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3
Q

Describe the structure of cancellous bone

A
  • spongy or trabecular bone (honeycomb lattice structure)
  • metaphysis and epiphysis of long bones
  • high turnover rate and greater remodelling
  • less dense and strong as cortical bone
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4
Q

What are the 3 fates of the osteoblast?

A
  • osteocyte (inactive)
  • bone lining cell
  • apoptosis
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5
Q

What is the role of the osteoclast?

A
  • bone resorption
  • contains acid phosphatase in lysosomes
  • forms a ruffled border when making contact with the bone surface to increase surface area
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6
Q

Describe the role and contents of the inorganic bone matrix

A
  • responsible for compressive strength
  • made up of calcium phosphate
  • reservoir for: Ca, P, Na and K
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7
Q

Describe the role and contents of the organic bone matrix

A
  • responsible for tensile strength of the bone
  • made up of type I collagen
  • contains: type V, XI collagen, bone specific proteoglycans and mucopolysaccharides, and non-collagenous matrix proteins (eg. osteonectin, osteopontin etc)
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8
Q

What is the physis?

A
  • the growth plate, between the epiphysis and metaphysis
  • responsible for skeletal growth in children
  • allows remodelling of angular deformity after fracture
  • if any damage to blood supply, growth will halt
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9
Q

What are the 3 phases of indirect fracture healing?

A
  • inflammation (haematoma)
  • repair (callus formation)
  • remodelling (maturation)
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10
Q

Describe the events in the inflammation stage of indirect fracture healing

A
  • blood from broken vessels form a clot (haematoma) 6-8hrs after injury
  • swelling and inflammation occur with the removal of dead bone and tissue cells (by osteoclasts and macrophages) at the fracture site
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11
Q

Describe the events in the repair stage of indirect fracture healing

A
  • new capillaries organise fracture haematomy into granulation tissue
  • fibroblasts and osteogenic cells invade procallus to connect collagen fibre ends
  • chondrocytes begin to produce fibrocartilage
  • lasts 3 weeks
  • osteoblasts then make woven bone (hard callus)
  • lasts 3-4 months
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12
Q

Describe the events in the remodelling stage of indirect fracture healing

A
  • osteoclasts and osteoblasts remodel woven bone into compact bone and trabecular bone
  • leaves no trace of fracture line on x-ray
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13
Q

Is movement good for indirect healing of fractures?

A
  • a degree of movement is good to promote tissue differentiation
  • excessive movement disrupts the healing tissue and affects cellular differentiation
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14
Q

Describe direct fracture healing

A
  • unique artificial surgical situation
  • direct formation of bone without process of callus formation to restore skeletal continuity (cutting cones across the fracture site - osteoclastic resorption and osteoblastic formation)
  • relies upon reduction and compression of the bone ends
  • fracture stable
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15
Q

Describe the blood supply of the long bone

A
  • endosteal supply (inner 2/3rds by nutrient artery at high pressure)
  • perisoteal supply (outer 1/3rd from capillaries from muscle attachments at low pressure)
  • metaphyseal-epiphyseal vessels (supply ends of long bones)
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16
Q

Describe the blood supply of the femoral neck

A
  • medial and lateral circumflex arteries (from the profunda femoris artery) form the extra-capsular ring at the base of the neck
  • ascending cervical vessels/retinacular vessels form the synovial ring (at risk of damage in a fracture!!)
  • the epiphyseal branches of this supply the head of the femur
17
Q

What fractures encounter problems in healing due to compromised blood supply?

A
  • proximal pole of scaphoid
  • talar neck
  • intracapsular hip
  • surgical neck of humerus
18
Q

What patient factors can inhibit healing of fractures?

A
  • increasing age
  • diabetes
  • anaemia
  • malnutrition
  • peripheral vascular disease
  • hypothyroidism
  • smoking
  • alcohol
19
Q

What medications can inhibit fracture healing and how?

A
  • NSAIDs (inhibit vascularity at fracture site)
  • steroids (inhibit osteoblasts)
  • bisphosphonates (inhibit osteoclastic activity which inhibits remodelling) - particularly subtrochanteric femoral fractures
20
Q

What is avascular necrosis and its consequences?

A
  • bone infarction (tissue death caused by an interruption of the blood supply) near a joint
  • can result in infarction of subchondral bone and collapse of joint surface and end-stage arthritis with the joint surface becoming irregular
21
Q

What are the risk factors for AVN?

A
  • alcohol
  • steroids/sickle cell (haemoglobinopathy)
  • idiopathic
  • trauma
  • Gaucher’s disease/gout
  • RA/radiation
  • infection/inflammatory arthritis
  • pancreatitis/pregnancy
  • SLE/smoking
  • chronic renal failure/chemo/caisson disease
  • hyperlipidaemia
    (AS IT GRIPS, C (ollapse) H(appens))
22
Q

Describe the pathophysiology of AVN

A

Interruption to blood flow:
- can be interosseous (eg. microcirculatory problems)
- can be extraosseous (eg. trauma)
- can be due to extravascular pressure

  1. necrosis starting in medullary bone and spreading
  2. cortex forms collaterals to try compensate
    - articular cartilage is spared due to receiving nutrients from the synovial fluid
23
Q

Describe the clinical presentation of AVN

A
  • asymptomatic (found incidentally on imaging)
  • pain, limp, restricted motion
  • eg. hip (AVN femoral head) causes groin pain worse when weight-bearing
24
Q

What are the x-ray signs of AVN

A
  • early: mild density changes followed by sclerosis/cystic areas
  • later: subchondral radiolucency ‘crescent sign’ preceding subchondral collapse
  • late stages: loss of sphericity and collapse of femoral head, joint-space narrowing and degenerative changes (end-stage arthritis)
25
Q

What are the treatment aims for AVN?

A
  • reduce risk by minimum effective dose of systemic corticosteroids and modify risk factors
  • increase awareness by advising at risk patients to report any alarming symptoms
26
Q

How would you treat early stage AVN?

A
  • try to reperfuse and heal infarcted region
  • core decompression and possible bone graft
  • vascularised bone therapy
  • stem cell therapy
27
Q

How would you treat later stage AVN?

A
  • total joint replacement
  • reperfusion of infarcted area will not restore joint surface

MBChB3 (100 decks)

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