Fracture Healing Flashcards

1
Q

what does an osteoblast do?

A
  1. make bone matrix (aka osteoid)
  2. initiates mineralization of said matrix
  3. initiate resoprtion of this matrix via osteoclasts

bonus: help with calcium homeostasis and detection of use/damage to bone

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2
Q

what are osteocytes?

A

osteoblasts that have been surrounded by mineralized bone matrix

they sit in spaces called lacunae and extend long cytoplasm through canaliculi tunnels in bones to touch other osteocytes/blasts

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3
Q

what purpose do these canaliculi serve?

A
  • facilitate Ca++ shifting (w/o bone structure change)
  • detect changes in stress/strain/micro cracks in bone
  • signal to osteoblasts –> initiate bone formation or resorption
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4
Q

what are osteoclasts?

A

multinucleate cells that do the bone resorbing

need access to mineralized surface of bone to do their work (they can’t bind to unmineralized bone)

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5
Q

how to osteoclasts resorb bone?

A

cell brush border needs to contact with mineralized bone

brush border secretes H+ ions = dissolves mineral and proteinases that cleave collagen within the matrix

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6
Q

what protects the surface of the bone from osteoclasts?

A

surface has continuous layer of osteoblasts as well as a thin layer of unmineralized bone mineral matrix

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7
Q

what gives bone its strength and flexibility?

A
  • collagen content
  • lamellar arrangement
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8
Q

what are the two developmental bone formation pathways? what’s the main difference?

A

intramembranous ossification
endochondral ossification

intramembranous - bone tissue formed directly
endochondral - hyaline cartilage template first, then bone

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9
Q

what is bone modelling? what are the two types and what differences between these types?

A

bone modelling = process by which primary (new) bone is formed by osteoblasts or resorbed by osteoclasts on a given bone envelope

types:
1. formation modelling = done by osteoblasts (bone deposited where it wasn’t before); stimulated by increase in bone strain
2. resorptive modelling = done by osteoclasts (bone removed to alter shape of primary bone); stimulated by decrease in bone strain

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10
Q

define Wolff’s Law

A

a principle describing how bone remodels in response to its mechanical environment: “bone adapts to the load under which it is placed”

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11
Q

explain Wolff’s Law

A

If the stresses in a region of bone increase, osteogenesis is
stimulated and the bone becomes stiffer and stronger.

If the stresses in a region of bone decrease, osteoclasts are stimulated to make the bone less stiff and strong.

= biofeedback system
* energy expenditure maintaining the bone is balanced against the strength of the bone needed for load-bearing, which makes for optimal bone structure

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12
Q

strength vs stiffness of bones

A

strength = ultimate load a material can stand before catastrophic failure

stiffness = rate at which material deforms when load is applied

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13
Q

how do you interpret a load-displacement curve?

A

elastic modulus / stiffness= slope of ascending linear portion of curve
* steeper slope = stiffer material
* here, displacement is elastic because material can return to original state

yield point = load exceeds ability for material to recover = material is permanently deformed
* permanent deformation = plastic deformation

ultimate point of failure = where material can withstand no more load –> material fails

total area under curve = toughness
* total energy absorbed during loading process

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14
Q

what type of material is bone?

A

viscoelastic

ability of bone to handle particular load depends on rate that load is applied to it

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15
Q

how to describe the behaviour of bone as material?

A

anisotropic

mechanical behaviour of material varies depending on direction in which the force is applied

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16
Q

fracture patterns: tensile loading

A

application of uniaxial tensile load (stretching force) = bone pulled apart in transverse fracture

17
Q

fracture patterns: compressive loading

A

compressive stress in axial direction + tensile stress in circumferential direction = oblique fracture

18
Q

fracture patterns: torsional loading

A

normal tensile forces act in oblique direction + shear stresses acting in axial & transverse direction = spiral fracture

19
Q

fracture patterns: bending

A

usually initiated on tension side of bend then propagate to compression side = transverse fracture (some shearing forces can be strong enough to form short oblique fracture creating butterfly segment)

20
Q

fracture patterns: combined loads

A

compression induced bending (buckling) + torsion = communited fracture

21
Q

order these forces from when bone is strongest to weakest: shear, tension, compression

A

compression > shear > tension

22
Q

do smaller or larger gaps experience greater strain potential?

A

smaller gaps have greater interfragmentary strain

23
Q

what is primary bone healing?

how does the fracture heal here (ossification type)?

A

aka direct bone healing or primary osteonal reconstruction

occurs under conditions of:
1. absolute stability
2. strain at fracture site is less than 2% (via treatment with anatomic reconstruction, compressiong of fragments, rigid fixation of bone column)

here the fracture heals via intramembranous ossification where surviving osteoblasts/clasts deposite bone at the fracture site

24
Q

what is secondary bone healing?

A

= an organized healing process wherein fractures are not anatomically reconstructed and stabilized with rigid fixation

this healing is expected after external computation or semi-rigid internal fixation of fractures. Surgically stabilized comminuted fractures will heal this way.

25
Q

what is the basics of “biological osteosynthesis” healing?

A

this emphasizes the role of soft-tissue integrity in bone healing, with a “less-than-rigid” fixation of the fracture

26
Q

what is the “biomechanical” approach to fracture management?

A

aims for anatomic reduction and rigid fixation

27
Q

list the 7 stages of fracture healing (simplified!)

A
  1. hematoma
  2. granulation tissue
  3. connective tissue
  4. cartilage (cartilaginous callus)
  5. cartilage mineralization
  6. woven bone formation
  7. remodelling to lamellar bone
28
Q

what are malunions and why do they happen?

A

= bone heals but alignment and function of healed bone is inappropriate

happens due to failure of mechanical re-establishment of form and function of the fracture ex. healing without surgery, poor surgical reduction, failure of surgical fixation

29
Q

delayed union vs nonunion

A

delayed union - prolonged fracture healing time

nonunion - fracture does not heal

30
Q

what causes delayed union?

A

mechanical causes: excessive fracture gaps & motion at fracture site

biological causes: inadequate cellular actiity

31
Q

how can we pre-emptively treat a delayed union?

A

if we know there is minimal biologic activity or decreased callus formation – use bone morphogenic proteins, demineralized bone matrix or autogenous bone graft

32
Q

what causes nonunion?

A

failure of adequate mechanical environment, biological environment, or both

if bio environment of callus is OK and we get healing response, this is a viable nonunion

33
Q

what is hypertrophic nonunion? how to treat?

A
  • considerable callus is produced
  • elephant’s foot appearance on either side of fracture line (due to excessive movement that exceeds tissue strain tolerance = fibrous/cartilaginous tissues persist)

treatment? rigid fixation, dynamic compression

34
Q

what is oligotrophic nonunion? What is cause? Treatment?

A

viable nonunion without evidence of biologic activity and thus difficult to distinguish from a biologically inactive (non-viable) nonunion

cause: lack of cellular activity

treatment: remove loose implants, get rid of inter-fragmentary motion, re-install bioactive environment

35
Q

what is a nonviable nonunion?

A

biologically inactive so that osteosynthesis cannot occur even with adequate fixation

36
Q

briefly list and define four types of nonviable nonunions.

A
  1. dystrophic nonunion = bone vasculature compromised, nonviable bone on one/both sides of fracture
  2. necrotic nonunion = infected bone (sequestrum), bone is dead which prevents union
  3. defect nonunion = gap at site that is too large for normal process to occur, and is filled with tissue other than bone
  4. atrophic nonunion = result of defect nonunion, when dead bone of fracture is removed by host without healing or restoring