Musculoskeletal Growth, Injury & Repair Flashcards
Describe bone growth:
Blood vessels grow inside
Secondary ossification centres along longitudinal bone growth
At either end; spongy bone- absorbs shock load
Middle diaphyseal bone which is very resistant to bending
Describe a long bone’s anatomy (e.g. the femur):
Diaphysis (Shaft)
Metaphysis (Flare at the end of the shaft)
Epiphysis (On joint side of physis)
Physis Growth (Plate)
Medullary canal
(Long diaphysis with a big central canal in the middle with nutrient vessels; the reason it is hollow is to keep it lighter)
Name some characteristics of CORTICAL BONE which differenciates it from CANCELLOUS BONE:
Cortical:
DIAPHYSIS (the shaft of a long bone)
Resists bending and torsion
Laid down CIRCUMFERENTIALLY
LESS biologically active
Name some characteristics of CANACELLOUS BONE which differenciates it from CORTICAL BONE:
Metaphysis (narrow portion of a long bone containing the growth plate)
Resists/ absorbs compression
Site of LONGITUDINAL GROWTH (physis)
VERY BIOLOGICALLY ACTIVE
What is a fracture?
BREAK in the structural continuity of bone
May be a crack, break, split, crumpling, buckle
What is the shorthand sign for a fracture?
its the HASHTAG sign
Why do bones fail?
HIGH ENERGY TRANSFER in normal bones: TAKES A LOT FOR A BONE TO FAIL
Repetitive STRESS in normal bones: Stress fracture (e.g. road runners or footballers)
LOW ENERGY TRANSFER in abnormal bones: osteoporosis, osteomalacia, metastatic tumour, other bone disorders
(older; bone is thinner and weaker- therefore takes less energy to break your bone
Osteomalacia- abnormality of laying down bone due to vitamin d problems)
Describe FRACTURE BIOLOGY:
Mechanical and structural failure of bone
Disruption of blood supply
Regenerative process: NO SCAR, 4 STAGES
(you have to regrow a blood supply back to regrow the bone
Its the only structure in the human body to regrow without a scar)
What are the 4 stages of Fracture repair?
1) Inflammation
2) Soft callus
3) Hard callus
4) Bone remodeling
STAGE 1: INFLAMMATION; DESCRIBE;
If patients in pain: give NSAIDs
If these drugs work, they’ve reduced inflammation
NSAIDs reduce inflammation so may potentially affect healing
How might we affect: NSAID’s, loss haematoma: open fractures, surgery
Extensive tissue damage: poor blood supply
Describe platelet concentrates:
“Buffy coat”
Platelet-derived growth factor (PDGF)
Transforming growth factor-beta (TGF-B)
Insulin like growth factor (IGF)
Vascular endothelial growth factor (VEGF)
(Picture on the right : top is platelet rich plasma then below is buffy coat which contains PDGF and TGFB
They increase the blood supply, which increase inflammation which aids healing)
When does ‘STAGE 2 SOFT CALLUS’ begin?
begins when pain and swelling subside
when does ‘stage 2 soft callus’ last until?
lasts until bony fragments are united by carilage or fibrous tissue
describes what happens during stage 2- SC?
some stability of fracture
angulation can still occur
continued increase in vascularity
(stage 2- the inflamm starts to subside
the fibroblasts throw collagen out in a big lump around the fracture and provides stability- stops shortening of the fracture)
How might we affect stage 2 soft callus?
Replace cartilage: DMB (demineralised bone matrix)
Jump straight to bone: bone graft, bone substitutes
(DMB has proteins that stimulate bone growth
Bone graft- takes bits of bone out where patients don’‘t need them but put them where they do)
Whats the “GOLD STANDARD” type of bone graft?
AUTOGENOUS CANCELLOUS BONE GRAFT
Describe Autogenous Cancellous Bone graft:
gold standard
osteoconductive
osteoinductive
best chance for the majority of bone graft needs
(Its the gold standard if you are going to put bone in
Inductive; stimulates bone to form
conductive- bone can form along it)
Describe osteoconduction:
Conduction- put something in and the bone grows on either end
What is allograft bone?
(from a donor)
cortical
cancellous
fresh
prepared
structural
osteoconductive
NOT osteoinductive
creeping substitition (donor bone replaced with your own bone)
Risk of disease transmission
describe stage 3- hard callus:
conversion of cartilage to woven bone
(Woven bone is just thrown down- it points every direction- doesn’t have a fixed orientated structure- responds to force from any direction and thus a more useful structure)
stage 3: hard callus: describe the 2 types of bone formation that occurs in stage 3 in a typical long bone fracture
- endochondral bone formation
- membranous bone formation
describe the structural changes that occur in stage 3- hard callus
Increasing rigidity
- “secondary” bone healing
- obvious callus
(callus means the bone has healed but you will limp as the body tries to keep the forces going through the bone to a specific amount)
describe stage 4- bone remodeling:
- conversion of woven bone to lamellar bone
- medullary canal is reconstituted
- bone responds to loading characteristics Wolff’s Law
(body converts the extra bone back to lamellar bone
if you stimulate bone in a particular direction, it will orientate in that direction and create more bone)
describe fracture biology:
mechanical properties of tissue and their environment are critical for the progression of fracture healing
What is strain?
the degree of INSTABILITY is best expressed as magnitude of strain; % change of initial dimension
what happens if strain is too low?
If strain is too low mechanical induction of tissue differentiation fails
what happens if strain is too high?
too high and healing process does not progress to bone formation
(you never move from soft callous to hard callous because its moving too much)
what is delayed union?
failure to heal in expected time
bad fracture to start with (smoker ??)
Give some causes of DELAYED UNION (delayed healing):
high energy injury
distraction (increased osteogenic jumping!)
instability
infection
steroids
immune suppressants
smoking
warfarin
NSAID
ciprofloxacin
(if you are a smoker- you have a 50% extension on your time for union)
(stops or hasn’t healed- non-union; failure of calcification; instability)
what is NON UNION?
failure to heal
describe non union:
- failure calcification fibrocartilage
- instability ;excessive osteoclasis
- abundant callus formation
- pain + tenderness
- persistent fracture line
- sclerosis (excessive bone around the edges)
With delayed healing, what are some alternative managements you could do?
- different fixation
- dynamisation
- bone grafting
(predict the ones who will get delayed union and intervene)
