bone injury, healing and grafting Flashcards
1
Q
When do stress fractures occur?
A
- Cyclical loading with forces below the ultimate strength of the bone
2
Q
Is cortical bone stiffer than cancellous?
A
- Yes
- Tolerates less strain before fracture 2% cf cancellous which is 75%
- Anisotrophic
- strong in compression
- weak in tension > shear ( worst)
3
Q
What determines the energy of the force transferred to the bone?
A
- E= 1/2 mv2
- m = mass
- v = velocity
- thus the energy imparted increases as the square of the velocity of the injury
- bone is viscoelastic - the biomechanical properties vary with the rate of application of the load
- bone is stiffer, stronger and more brittle when loads are applied at a higher rate
- with rapid loading bone absorbs more energy than when loaded more slowly and this energyis released as it fractures
- therefore as the energy increases the more comminuted the fx is likely to be
4
Q
What 5 key factors determine the type of fractures created?
A
- Load
- Rate
- Direction
- Bone properties- shape/anatomical area/quality of bone
- Soft tissue forces
5
Q
What do compressive forces do to bone?
A
- Lead to shear forces
- fx at 45o to compressive load
- -> oblique fractures
6
Q
What do tensile forces do to bone?
A
- Arise at soft- tissue insertions to cancellous bone
- -> transverse fx due to debonding of cement lines adn pulliing of osteons e.g patella/oelcranon
7
Q
What do pure bending forces do to bone?
A
- transverse fx from tension on the convexity and compression on concavity with the neutral axis moving towards the fx
- a bending wedge ( butterfly) fragment may occur compression ( concave ) side especially with high energy injuries
- with combined bending and compression= a transverse fx on tension and oblique fx on compression side
8
Q
What do torsional forces do to bone?
A
- Spiral fx
- if torsion and compression combined = spiral wedge fx
9
Q
What do 4 point bending forces do to bone?
A
- segmental fx
- like hitting a car bumper
10
Q
When does primary bone healing occur?
A
- Anatomical reduction and interfragmentary compression
- -> absolute stability ( no motion between fx surfaces under functional load)
- this process is very intolerant of strain ( movement ) at the fx site
11
Q
Describes what happens in primary bone healing?
A
- In first few days there is minimal activity in areas of direct contact ( contact healing)
- New blood vessels grow into any small gpas that exist ( gap healing) and mesechymal cells differentiate into osteoblasts
- these lay down new bone in small gaps and woven bone in larger gaps
- subsequently Osetoclasts form cutting cones that tunnel across the fx site whereveer there is contact between the bone ends or minute gap
- this leaves a path for blood vessels and osteoblasts to follow in their wake, laying down lamellar bone in the form of new osteons
- the formation of osteons bridging the gap may take months and may be difficult to see on xray
12
Q
When does secondary bone healing occur?
A
- In the presence of relative stability
- ( some movement at the fx site)
13
Q
What are the 2 methods of secondary bone healing?
A
- Periosteal bony callus = Intramembranous ossification
- Fibrocartilaginous bridging callus = endosteal ossification
14
Q
What is Periosteal bony callus Intramembranous ossification?
A
- Multipotent cells in the periosteum differentiate into osteoprognitor cells which produce bone directly without first forming cartilage
- This hard callus forms early on at the periphery of the fracture site providing there hasn’t been extensive periosteal stripping
15
Q
What is Fibrocartilaginous bridging callus, endosteal ossification?
A
- This process occurs stimultaneously between adjacent bone ends and involes the formation of fibrocartilage that become calcified adn is then replaced by osteoud or woven bone.
- This process occurs within the surrounding soft tissue
16
Q
What are the stages of callus formation of endoosteal ossificaiton?
A
-
Stage 1 -haematoma and inflammation
- up to a week
- **Stage 2- Soft callus **
- 1 week - 1 month
-
Stage 3- hard callus
- 1-4 months
-
Stage 4- remodelling
- up to several years
17
Q
What happens in the stage I of callus formation?
A
- Haematoma from ruptured blood vessels -> fibrin clot
- damaged tissue and degranulated platelets release signalling moecules and growth factors
- Migration of inflammatory cells PMNs. macrophages and fibroblasts into haematoma, responding to local growth factors and cytokines - IL1, IL6, TGF-Beta< BMPs, PDGF
- Proliferation , differentiation and matrix synthesis as the haematoma is replaced by granulation tissue.
- capillary ingrowth ( angiogenesis) and recruitment of fibroblasts, mesechymal adn osteoprognitor cells. periosteum plays important role
- all necrotic bone ends, bone resorptionis mediated by OC, and removal of tissue debris by macrophages
18
Q
What happens in the stage 2 of callus formation?
A
- Increased celluarity , with proliferation and differentiation and soft callus revascularisation
- callus is a combination of fibrous tissue, cartilage and woven bone
- Intramembranous callus- primary callus reponse- type 1 collagen laid down from periosteal OB in the Cambium layer of periosteal body callus or woven bone. hard callus but doesn’t bridge the fx
-
endochondral callus- bridging external callus- multipotent cells differentiate to -> chondroblasts and fibroblasts within the granulating callus=> type 2 cartilaginous and fibrous elements of matrix
- chondroblasts then calcify the chondroid matrix -> calcified fibrocartilage/ soft callus
19
Q
What happens in the stage 3 of callus formation?
A
- Calcified soft callus is resorbed by chondroclasts adn invaded by new blood vessels
- these bring with them OB precursors that produce type 1 collagen and then mineralise it to form woven bone
- Soft calcifed chondroid callus becomes hard mineralised osteoid callus
- Bony bridging continues peripherally as subperiosteal new bone formation At this point the fx is united, solid and pain free to movement
20
Q
What happens in the stage IV of callus formation?
A
- Once the fx has united the hard callus is remodelled from woven bone to hard , dense lamellar bone by a process of osteoclastic resorption followed by osteoblastic bone formation. the medullary canal reforms at the end of this process
- this is the same mechanism as for direct cortical , osteonal or primary bone healing
- bone assumes a configuration and shape based on stresses acting upon it - wolfe’s law
- OB activity > on electro+ve Tension side
- OC activity > on elctro-ve compression side
21
Q
What is Perren’s strain theory of fx healing?
A
- After a fx fixation or immobilisation the fx will undergo some degree of movement or strain
- Strain at the fx site is decreased with increased fx gap or greater surface area e.g. metaphsyeal fx and in multifragmented or segmental fx
- Fx callus becomes increasingly stiff with time from the gelatinous granultation tissue ti soft callus and then hard bony callus each of these tissues tolerates a diff amount of strain
- granulation tissue up to 100%
- Fibrous connective tissue 17%
- Fibrocartilage 2-10%
- lamellar bone 2%
- the degree of interfragmentary strain appears to govern the cellular response and therefore the type of tissue that forms between fx fragments
- in absolute stablity ( compression plating/rigid ext fixation) the fragments are inital contact, so strain low allow primary bone healing. If fixed rigid but gap present then cutting cones won’t bridge gap and lack of strain inhibit callus formation-> atrophic non union
- in relative stability ( splint, IM nail, bridge plating) the more strain tolerant cartilaginous callus is required to stiffen the fx site before hard woven bony callus forming and replacing it. a larger strain -> bigger callus
- in complete instablity callus is unable to form as strain is too much for it to tolerate. the more strain tolerant fibrous tissue forms-> hypertrophic non union
22
Q
What are the factors affecting bone healing ?
A
Local
- Degree of soft tissue trauma
- Assoc NV injury
- Degree of bone loss
- Degree of immobilisation
- Open fx or presence of infection
- local pathological lesion ( tumour)
- Type of fx ( tibia 3-4/12, MC 4-6/52)
- Site of fx ( metaphysis vs diaphysis)
- Interposition of soft tissue or inadequate reduction
Systemic
- Smoking ( affects OB fucntion)
- Diabetes mellitus
- Nutrition
- Age
- Drugs ( steriods/nsaids)
- Horomones
- Assoc head injury ( enhances fx healing)
