Bone Growth and Fracture Healing Flashcards
1
Q
Bone growth
A
- Start with long bone
- Primary ossification center forms which allows it to grow (during development, this occurs during weeks 8-12)
- Further secondary ossification centers at each end
- A medullary cavity is formed as the bone continues to grow
- Epiphyseal plate forms at the end of the long bones which allow it to grow over time until finally the Epiphyseal plate closes at the end of growth and skeletal maturity is reached
2
Q
True or false: On a growing long bone you can find multiple growth plates
A
True
3
Q
Cortical/compact bone
A
- Compact structure
- Multiple concentric lamellae which contain blood vessels in the centre
- It’s role is to resist bending and torsion
- It’s laid down circumferentially
- Less biologically active - slow growing
4
Q
Cancellous bone
A
- Spongy substance designed to take load
- It resists/absorbs compression and is much more flexible than compact bone
- It lies in the metaphysis and the epiphysis at the end of long bones
- And is usually sandwhiched between layers of cortical bone on the external surface of bones
- It undergoes microinjury all the time - very biologically active (repair)
5
Q
Why do bones fracture?
A
- High energy transfer/high velocity injury - enough to injure normal bones
- Repetitive stress in normal bones - stress fracture - everytime you load a bone (particularly at the ends) you get micro-injuries and the bone is constantly turning over to repair these. If the injury>repair, then over time the structure becomes weaker and then fails i.e army, runners
- Low energy transfer/ low velocity injury in abnormal bones i.e osteoporosis, osteomalacia, metastatic tumour etc - common in elderly
6
Q
Stage 1 of Fracture repair
A
Stage 1 - inflammation - creates perfect inflammatory process to bring in repair
- Begins immediately after the fracture and can last up to 2 weeks
- A haematoma (blood that leaks into the surrounding tissue) coagulates to form a fibrin clot. Platelets, neutrophils, monocytes, macrophages etc are released into the area
- Local areas of cell death release lysosomal enzymes which create a biological soup that is designed to bring in new cells to initiate repair i.e fibroblasts, mesenchymal + osteoprogenitor cells move in.
- Angiogenesis - blood supply is required for repair. Low level of O2 in the centre of the fracture which drives the angiogenesis to recover from this. Macrophages produce angiogenic factors under hypoxic conditions i.e VegF
7
Q
In what ways can doctors/injuries impair fracture healing? (3)
A
- NSAIDs use - they reduce the inflammation in stage one of fracture repair.
- Haematoma loss from open fractures or removal during surgery - if you lose the haematoma, you also lose the biological driver to bring in the repair cells
- Extensive tissue damage i.e from open fracture - limits the ability to restore angiogenesis. A bigger zone of injury.
8
Q
Use of platelet concentrates
A
- This is used in clinical practice to improve fracture healing in patients where the haematoma/fibrin clot has been lost.
- The solution of platelets releases growth factors such as platelet-derived growth factor, TGF-B, Insulin like growth factor, VEGF. These factors are important in bringing in cells and blood vessels.
- If we replace the clot that has been lost with these concentrates it can improve healing.
9
Q
Stage 2 fracture repair
A
Stage 2 - soft callus
- This begins when pain and swelling subsides.
- After the initial inflammatory phase (10-14 days) you have a maximal increase in blood flow and high cellular activity.
- The fibroblasts have helped to lay down a collagen matrix to try and provide some stability in the fracture.
- The callus holds the bone together, but isn’t strong enough for the body part to be used. Over the next few weeks, the soft callus becomes harder.
- There is continued increase in vascularity
- Soft callus limits the movement of the bone
10
Q
How can orthopaedic surgeons manipulate the soft callus?
A
- Replace cartilage - If the haematoma is lost earlier on then there may not be much soft callus - in this case it can be replaced
- Can jump straight to bone - give bone graft or substitute and place it in the gap between the fracture
11
Q
What is an autogenous cancellous bone graft?
A
The gold standard bone graft - uses the patient’s own bone
- It is osteoconductive - meaning it allows cells to grow through it to create bone.
- It is also osteoinductive - contains many factors used to stimulate bone formation + also has a high concentration of cells that will produce bone.
12
Q
Stage 3 of fracture repair
A
Stage 3 - Hard callus
Conversion of cartilage to woven bone (without any structure - seen in growing babies in the womb)
Increasing rigidity
13
Q
Allograft bone
A
A bone bank - take bone out of patients at the time of surgery (i.e hip replacement) or death.
The bone can be…
- Cortical
- Cancellous
- Fresh - frozen
- Prepared - irradiated or treated to prevent disease transmission
- Structural
How does it work? It is replaced gradually by new bone growing into it in the patient.
14
Q
Stage 4 fracture repair
A
Stage 4 - bone remodelling
Conversion of woven bone to lamellar bone
- Woven bone responds to load in any direction and it gradually becomes thicker in those directions that it is required as it remodels. In adults it won’t repair 100% in the bone but in children it will go back to normal.
- The medullary canal is reconstituted
- Bone responds to loading characteristics - defined by Wolff’s Law - meaning where it needs to be thickened it thickens and where it needs to be thinned it thins out
15
Q
What is meant by ‘delayed union’? and what causes it?
A
When a fracture fails to heal in expected time
Causes:
- High energy injury - a lot of damage to repair
- Distraction - when the fracture ends aren’t close together and it’s quite a long way for the bones to be able to heal
- Instability - too much movement of the fracture end
- Infection
- Steroids or Immune suppressants - suppresses bone formation
- Smoking - affects bone healing
- Warfarin, ciprofloxacin or NSAIDs
