Bone Fracture Healing and AVN Flashcards
What are the functions of bone?
- mechanical support
- protection
- movement
- mineral storage (calcium and phosphate)
- haematopoiesis
Describe the structure of cortical bone
- 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
Describe the structure of cancellous bone
- 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
What are the 3 fates of the osteoblast?
- osteocyte (inactive)
- bone lining cell
- apoptosis
What is the role of the osteoclast?
- bone resorption
- contains acid phosphatase in lysosomes
- forms a ruffled border when making contact with the bone surface to increase surface area
Describe the role and contents of the inorganic bone matrix
- responsible for compressive strength
- made up of calcium phosphate
- reservoir for: Ca, P, Na and K
Describe the role and contents of the organic bone matrix
- 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)
What is the physis?
- 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
What are the 3 phases of indirect fracture healing?
- inflammation (haematoma)
- repair (callus formation)
- remodelling (maturation)
Describe the events in the inflammation stage of indirect fracture healing
- 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
Describe the events in the repair stage of indirect fracture healing
- 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
Describe the events in the remodelling stage of indirect fracture healing
- osteoclasts and osteoblasts remodel woven bone into compact bone and trabecular bone
- leaves no trace of fracture line on x-ray
Is movement good for indirect healing of fractures?
- a degree of movement is good to promote tissue differentiation
- excessive movement disrupts the healing tissue and affects cellular differentiation
Describe direct fracture healing
- 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
Describe the blood supply of the long bone
- 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)
Describe the blood supply of the femoral neck
- 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
What fractures encounter problems in healing due to compromised blood supply?
- proximal pole of scaphoid
- talar neck
- intracapsular hip
- surgical neck of humerus
What patient factors can inhibit healing of fractures?
- increasing age
- diabetes
- anaemia
- malnutrition
- peripheral vascular disease
- hypothyroidism
- smoking
- alcohol
What medications can inhibit fracture healing and how?
- NSAIDs (inhibit vascularity at fracture site)
- steroids (inhibit osteoblasts)
- bisphosphonates (inhibit osteoclastic activity which inhibits remodelling) - particularly subtrochanteric femoral fractures
What is avascular necrosis and its consequences?
- 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
What are the risk factors for AVN?
- 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))
Describe the pathophysiology of AVN
Interruption to blood flow:
- can be interosseous (eg. microcirculatory problems)
- can be extraosseous (eg. trauma)
- can be due to extravascular pressure
- necrosis starting in medullary bone and spreading
- cortex forms collaterals to try compensate
- articular cartilage is spared due to receiving nutrients from the synovial fluid
Describe the clinical presentation of AVN
- asymptomatic (found incidentally on imaging)
- pain, limp, restricted motion
- eg. hip (AVN femoral head) causes groin pain worse when weight-bearing
What are the x-ray signs of AVN
- 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)
What are the treatment aims for AVN?
- 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
How would you treat early stage AVN?
- try to reperfuse and heal infarcted region
- core decompression and possible bone graft
- vascularised bone therapy
- stem cell therapy
How would you treat later stage AVN?
- total joint replacement
- reperfusion of infarcted area will not restore joint surface
