Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
42 Cards in this Set
- Front
- Back
Indirect bone healing
|
healing by intermediate callus formation:
inflammation repair remodeling |
|
Direct Bone healing:
|
primary osteonal reconstruction
contact healing gap healing |
|
When does indirect bone healing occur?
|
with unstable mechanical environment and motion between fracture fragments
when gap between fracture fragments in >1 mm- impaired blood supply or impaired revascularization transient extraosseous blood supply develops |
|
Describe the inflammatory stage of indirect bone healing
|
begins immediately after fracture and lasts 3-4 days, development of clot at fracture site causes release of osteoinductive growth factors which stimulate angiogenesis and bone formation. Abundant mast cells are also present- vasoactive substances-new vessel formation
Extraosseous blood supply within hours. |
|
Describe the repair stage of indirect bone healing
|
clot changes into granulation tissue (mononuclear cell and fibroblasts) and there is a slight gain in mechanical strength with formation of a soft callus
Mesenchymal cells become osteoblasts which form a medullary and external callus (fibrocartilage). Resorption and mineralization of fibrocartilage forming a hard callus. Bony union is achieved. |
|
In what phase of indirect bone healing is bony union achieved?
|
Repair
|
|
How long does the repair stage of indirect bone healing last?
|
approx. 2 months
|
|
How long does the inflammatory stage of indirect bone healing last?
|
3-4 days
|
|
What happens during the inflammatory stage of indirect bone healing?
|
clot develops-> lots of mast cells --> new vessel formation--> Extraosseous blood supply (hours)
|
|
What happens during the repair stage of indirect bone healing?
|
clot--> granulation tissue--> soft callus --> osteoblasts form external callus (fibrocartilage)--> mineralization--> hard callus--> bony union
|
|
Describe the remodeling stage of indirect bone healing
|
May last 6-9 years in humans.
Accounts for 70% of total healing time Acts to provide optimal function and strength balance of osteoclast resorption and osteoblast depostion Governed by Wolfe's Law |
|
How long does the remodeling stage of indirect bone healing last?
|
6-9 years, makes up 70% of total healing time
|
|
What is the purpose of the remodeling stage of indirect bone healing?
|
provie optimal function and strength to repaired bone
|
|
What governs remodeling stage of indirect bone healing?
|
Wolfe's Law
compression- osteoblasts tension- osteoclasts Balance of osteoclast resorption and osteoblast deposition |
|
Describe direct bone healing
|
direct filling of fracture site with bone without callus formation. occurs by direct osteonal proliferation and requires precise reduction and rigid fixation that minimizes osteoprogenitor cells. Can take 6-12 months for appropriate mechanical strength
|
|
How long does it take to reach mechanical strength in direct bone healing?
|
6-12 months
|
|
How can we initiate direct Contact bone healing?
|
Contact healing, defect between fracture site must be < 0.01 mm
with an interfragmentary straing <2% |
|
How does bony union differ between indirect and direct contact bone healing vs. gap healing?
|
when bones heal by indirect healing bony union occurs during the repair phase BEFORE remodeling. In direct bone healing bony union is concurrent with remodeling. In gap healing bony union and remodeling are separate steps
|
|
Describe gap healing
|
Direct bone healing with a fracture gap of <1mm. Osteoblasts deposit laminar bone in fracture gap perpendicular to long axis. Mechanically weak at fracture ends.
|
|
How does cancellous bone heal?
|
metaphyseal fractures invovlving trabecular or cancellous bone are more stable than cortical bone fractures and do not heal by callus formation. Woven bone is deposited on trabeculae bridging of fracture site occurs before union of cortical shell
|
|
How do physeal fractures healed/
|
Fracture zone of hypertrophy will heal by continued growth of physeal cartilage.
Fracture of zone of proliferation will heal by endochondrial ossification prevent normal physeal function premature physeal closure |
|
How does stability of fracture influence the type of bone healing?
|
absolutely stable fracture will induce direct bone healing while unstable fracture will induce indirect bone healing
|
|
What factors affect fracture healing?
|
location of fracture, stability, method of fixation, biological environment, blood supply, biomechanical vs. biological osteosynthesis
|
|
Explain the biomechanical approach to fracture healing?
|
anatomical reduction, rigid fixation, will compromise soft tissue to achieve
|
|
Explain fracture healing by biological osteosynthesis.
|
emphasizes the role of soft tissue integrity, restores overall length, restores overall alignment, limit surgical approach, limit soft tissue disruption, look but do not touch, emphasizes use of bone grafts
|
|
What are some types of bone implants and how do they affect type of bone healing
|
plates and ESF- direct (contact or gap)
pins with wires/ESF/interlocking nails- direct and/or indirect casts and splints- indirect healing no fixation- indirect healing |
|
How do implants effect blood supply to bone?
|
may disrupt endosteal blood supply and block medullary flow when in contact with endosteal surface. Bone plates impair blood supply to outer layer of cortical bone.
|
|
Which types of implants do not impair vascularity?
|
cerclage wires and external fixator pins
If loose may significantly damage blood supply (cerclage wires) |
|
What is the advatange of using bone grafts
|
bone grafts enchance healing but will not compensate for unstable mechanical environments
|
|
What are some indications for bone grafts?
|
at initial fracture repair: comminuted fractures, fractures with bone loss, delayed or nonunion fractures, arthrodeses.
|
|
What are some functions of bone grafts?
|
osteogenesis-laying down new bone by osteoblasts
osteoinduction: recruitment of host mesenchymal cells to form new bone or osteogenesis Osteoconduction- providing a scaffold for the growth of new bone. |
|
Advantages for autogenous cancellous bone grafts
|
gold standard of bone graphs, promotes osteogenesis (provides cells directly, osteoinduction, osteoconduction), readily available and avoides immune reactions
|
|
Disadvantages for autogenous cancellous bone grafts
|
mechanically weak, increased surgical time, limited storage time, pain at donor site, intrapoerative blood loss.
|
|
Advantages of cancellous bone allograph
|
available as frozen chips or powder
decreased surgical time readily available no donor site problems |
|
Disadvantages for cancellous bone allograph
|
expensive
lack osteogenic properites can mix with autograft to increase volume |
|
Describe the phases of cancellous bone graft effect
|
phase 1- inflammation (w/in hrs)
phase 2- revacularization and osteoinduction (2 weeks) phase 3 - osteoconduction (3-4 wks) phase 4 - mechanical support (up to 12wks) |
|
What is the purpose of cortical bone grafts
|
provide structural support, osteoconductive properties, highly comminuated fractures/ bone tumors
|
|
Whare cortical autographs harvested?
|
ribs, ulna, fibula, ilial wing
|
|
What are the phases of cortical bone graft effect?
|
Osteoclasts move into graft and resorb bone. Osteoblasts follow and lay down new bone. Mechanical strength of graft maintained. Termed "creeping substitution"
|
|
Describe cortical-cancellous bone grafts.
|
Graft containing both cortical and cancellous bone. Provides immediate mechanical support, promotes osteogenesis, osteoinductive, osteoconductive, autogenous graft obtained directly from patient.
|
|
Which type of graft is considered a "gold standard" and why?
|
Cancellous autographs are most common. They are readily available, highly cellular, but mechanically weak. They have superior osteogenic and osteoinductive properties but lack osteoconductiveness
|
|
What is the deal with cortical bone grafts?
|
excellent mechanical support, osteoconductive, acellular with no osteogenic properties.
|