Which part of long bones are made from cortical bone and cancellou bone?
Cortical bone is found in the diaphysis (shaft)
Cancellous bone is found in the metaphysis (flare at the end of the shaft)
What does cortical bone resist?
It resists bending and torsion
What does cancelous bone resist?
Resists / absorbs compression
How is cortical bone laid down?
What type of bone is the site of longitudinal growth?
Which type of bone is more biologically active?
Cancellous bone - very biologically active
Cortical bone is less biologically active
What is a fracture?
Break in structural continuity of bone
May be a crack, break, split, crumpling, buckle
Why do bones fail?
High energy transfer in normal bones
- Takes a lot
Repetitive stress in normal bones
- Stress fracture
Low energy transfer in abnormal bones
- Osteomalacia, metastatic tumour
- Other bone disorders
What are the four stages of fracture repair?
Soft cell callus
Summary of fracture repair
The bone matrix is destroyed and the bone cells adjoining the fracture die.
The damaged blood vessels form a blood clot.
The blood clot, damaged bone matrix, and dead cells are removed by macrophages.
Granulation tissue forms in the site of the blood clot and condenses into connective tissue and later into a fibrocartilagenous callus.
At the same time, osteoprogenitor cells of the periosteum are activated and become osteoblasts that begin to deposit new bone. The new bone, which is a meshwork of trabeculae of primary bone, forms a bone callus around the fracture site.
A similar activation of cells of the endosteum results in deposition of bone around the fibrocartilagenous callus that is slowly eroded away and replaced by bone (endochondral ossification).
The spongy bone uniting the bones is transformed into compact bone by osteoblastic deposition of bone matrix, which gradually obliterates the spaces among the trabeculae.
Resorption of excess bone by osteoclasts reestablishes the marrow cavity and the normal surface contours of the bone.
What s involved in stage 1 inflammation?
Hematoma and fibrin clot
Platelets, PMN’s, Neutrophils, Monocytes, Macrophages
By products of cell death – lysosomal enzymes
Mesenchymal & Osteoprogenitor cells (osteoprogenitor cells are capable of producing osteoblasts and osteoclasts, Osteoprogenitor cells are located in the inner cellular layer of the periosteum, the endosteum and lining osteonic canals)
Transformed endothelial cells from medullary canal and/or periosteum
Osteogenic induction of cells from muscle and soft tissues
Oxygen gradient required (low)
Macrophages – produce angiogenic factors under hypoxic conditions
How might doctors affect infalammation of the fracture?
How might we affect ?
NSAID’s - releive pain and reduce inflammation. Evidence suggests that NSAIDs slow down the healing process of fractures.
- Open fractures
Extensive tissue damage
- Poor blood supply
( so if there is less blood supply - NSAIDs or extensive tissue damage, or there is loss of tha haematoma, possible by either open fractures of surgery)
What are platelet concentrates?
Platelet concentrates activate the bodies repair process and are used to boost the bodies supply of bioactive factors. Platelet activation is the first response to injury and is the first step in the repair process. Bioactvie factors are involved in processes such as angiogenesis and the recruitment of healing cells to the injury sites.
Platelet cocnentrates are used in a wide spectrum of musculoskeletal disorders or injuries, including osteoarthritis (OA), tendinopathies, rotator cuff tears, anterior cruciate ligament (ACL) injuries, and bone fractures.
What is meant by buffy coat?
The buffy coat is the fraction of an anticoagulated blood sample that contains most of the white blood cells and platelets following density gradient centrifugation of the blood.
What is contained within platelet concnetrates? (i.e what are the bioactive factors as mentioned previously)
Platelet-derived growth factor (PDGF)
Transforming growth factor-beta (TGF-B)
Insulin like growth factor (IGF)
vascular endothelial growth factor (VEGF)
When does soft callus formation begin and end?
Begins when pain and swelling subside
Lasts until bony fragments are united by cartilage or fibrous tissue
Angulation can still occur (the soft callus is still flexible)
Continued increase in vascularity
How can we affect the soft callus stage of repair?
- DMB (demineralised bone matrix)
- Autogenous cancellous bnoe graft (osteoconductive and osteoinductive)
Jump straight to bone
- Bone graft
- Bone substitutes
Osteoinduction is the when osteogenesis is induced. Immature cells are recruited and these are stimulated to mature into pre-osteoblasts.
Osteoconduction - allows bone growth on its surface.
What is allograft bone?
Allograft bone is a bone transplant usually from a cadaveric specimen from a bone bank. Bone transplant is sometimes needed. A bone has the ability to regenerate completely however it needs a small fracture space or a bone scaffold to do so. Most bone grafts are expected to be reabsorbed and replaced as the natural bone heals over a few months’ time.
What are the types of allograft bone?
What are the features of allograft bone?
Risk of Disease transmission
What happens durign stage 3?
Conversion of cartilage to woven bone
Typical long bone fracture
- Endochondral bone formation
- Membranous bone formation
There is increasing rigidity and is described as secondary bone healing - ther is an obvious callus on X-ray
What is stage 4?
Woven bone is converted to lamellar bone
Medullary canal is reconstituted
Bone reponds to loading characteristics (Wolff’s law)
Wolff’s law states that a bone adapts to the loads under which it is placed
What is the effect of strain on tissue healing?
If strain is too low then mechanical induction of tissue differentiation fails
If strain is too high then healing process does not progress to bone formation
Degree of instability is best expressed as magnitude of strain (% change of initital dimension)
What is meant by delayed union?
Failure to heal in expected time
What are some of the causes of delayed union?
•high energy injury
(increased osteogenic jumping!)
- immune suppressants
•failure calcification fibrocartilage
-excessive osteoclasis (surgical destruction of bone)
- abundant callus formation
- pain + tenderness
- persistent fracture line
- sclerosis (abnormal hardening of body tissue)
What are the alternative managements to delayed bone healing?
dynamisation - dynamization. a strategy for promoting bone healing in fractures by allowing some movement or compressive loading.