Bone fracture healing Flashcards
What are the functions of bone?
- mechanical: support, protection and movement
- Mineral storage: calcium and phosphate
- haematopoiesis in the marrow
Describe the structure of bone
- Diaphysis is the shaft
- Epiphysis are the ends
- Metaphysic is the transitional flared area between the diaphysis and epiphysis
explain what cortical bone is
- 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
Where are osteocytes located?
In the lacuna
What allows the communication of osteocytes
Canaliculi
Explain what cancellous bone is
- 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
What are the bone cells?
- Osteoprogenitor (stem cell)
- Osteocyte (maintains bone tissue)
- Osteoblast (forms bone matrix)
- Osteoclast (resorbs bone)
What makes up the matrix in bone?
•Organic - 40%
- collagen
- non-collagenous proteins
- mucopolysaccharides
•Inorganic
- calcium
- phosphorus
What is the role of osteoblasts?
Produce osteoid
What are the potential fates of osteoblasts?
- Osteocytes
- Bone lining cell
- Apoptosis
What type of cell is an osteoclast?
Large multinucleate cells
What is the role of the inorganic component of the bone matrix?
- Responsible for compressive strength
* Reservoir for calcium, phosphorus and sodium and potassium
What is the role of the organic component of the bone matrix
Tensile strength of bone
What is a unique feature of children’s bone?
Physis - lies between the epiphysis and the metaphysic and is repsonsible for skeletal growth
What is the role of the physis?
- responsible for skeletal growth
- Allows remodelling of angular deformity after fracture
- If physeal blood supply is damaged, will lead to growth arrest
What does fracture healing depend on?
- Which bone is fractured
- Mechanism of injury
- closed or open fracture
What is indirect fracture healing?
•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
Describe fracture haematoma and inflammation
- 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
Describe fibrocartilage callus
- 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
Describe bony callus
- After 3 weeks and lasts about 3-4 months
* osteoblasts make woven bone
Bone remodelling in indirect fracture healing
- Osteoclasts and osteoblasts remodel woven bone into compact bone and trabecular bone
- Often will be no sign of fracture line on x-ray
Explain the effect of movement on indirect fracture healing
- A degree of movement is desirable to promote tissue differentiation
- Excessive movement disrupts the healing tissue and affects cellular differentiation
What is direct fracture healing?
- Unique artificial surgical situation
* Direct formation of bone without the process of callus formation to restore skeletal continuity
What does direct fracture healing rely upon?
Reduction and compression of the bone ends and for the fracture to be stable (no movement under physiological load)
Explain the physiological process of direct bone healing
- No callus
- Cutting cone cross fracture site
- Direct formation of bone via osteoclastic resorption and osteoblastic formation
Explain blood supply of the bone
- 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
What is the blood supply to the femoral neck?
- 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
Which fractures are more prone to have problems with union/avascualr necrosis?
- Proximal pole of scaphoid fractures
- Talar neck fractures
- Intrascapular hip fractures
- Surgical neck of humerus fracture
What patient features lead to inhibition of fracture healing?
- Increasing age
- diabetes
- Anaemia
- malnutrition
- Peripheral vascular disease
- hypothyroidism
- Smoking
- Alcohol
Which medications can inhibit bone healing
- NSAIDs
- Steroids (inhibit osteoblasts)
- Bisphosphonates
How do NSAIDs inhibit bone healing?
- Reduce local vascularity at fracture site
* Additional reduction in healing effect independent of blood flow
How do bisphosphonates inhibit bone healing?
- 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)
What is avascular necrosis of bone?
Bone infarction (tissue death caused by an interruption of the blood supply) near a joint
What can avascular necrosis cause?
- Infarction of sub-chondral bone i.e. the bone right under the joint surface
- collapse of the joint surface and end stage arthritis
Where is AVN/osteonecrosis most common?
The hip
What are the risk factors of avascular necrosis?
- 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
What could cause an interruption to the blood supply of bone?
- Extraosseous e.g. trauma
- Intraosseous e.g. microcirculation from sickle cell
- increased extravascular pressure e.g. steroid induced fat cell hypertrophy
Describe the pathophysiology of AVN in the early stages
- 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
Describe the pathophysiology of AVN in the later stages
- 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
What is the clinical presentation of AVN of the femoral head?
- Groin pain
- Worsens with weight bearing and motion
- Less commonly thigh and buttock pain
What are the early X ray changes in AVN?
- Mild density changes
* Followed by sclerosis and cystic areas
What are the later x ray changes in AVN
- Subchondral radiolucency ‘crescent sign’ precedes subchondral collapse
- Loss of sphericity and collapse of the femoral head
- Joint space narrowing and degenerative changes
What are the treatment options of osteonecrosis?
- 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
