Fracture Healing Flashcards
what does an osteoblast do?
- make bone matrix (aka osteoid)
- initiates mineralization of said matrix
- initiate resoprtion of this matrix via osteoclasts
bonus: help with calcium homeostasis and detection of use/damage to bone
what are osteocytes?
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
what purpose do these canaliculi serve?
- 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
what are osteoclasts?
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)
how to osteoclasts resorb bone?
cell brush border needs to contact with mineralized bone
brush border secretes H+ ions = dissolves mineral and proteinases that cleave collagen within the matrix
what protects the surface of the bone from osteoclasts?
surface has continuous layer of osteoblasts as well as a thin layer of unmineralized bone mineral matrix
what gives bone its strength and flexibility?
- collagen content
- lamellar arrangement
what are the two developmental bone formation pathways? what’s the main difference?
intramembranous ossification
endochondral ossification
intramembranous - bone tissue formed directly
endochondral - hyaline cartilage template first, then bone
what is bone modelling? what are the two types and what differences between these types?
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
define Wolff’s Law
a principle describing how bone remodels in response to its mechanical environment: “bone adapts to the load under which it is placed”
explain Wolff’s Law
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
strength vs stiffness of bones
strength = ultimate load a material can stand before catastrophic failure
stiffness = rate at which material deforms when load is applied
how do you interpret a load-displacement curve?
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
what type of material is bone?
viscoelastic
ability of bone to handle particular load depends on rate that load is applied to it
how to describe the behaviour of bone as material?
anisotropic
mechanical behaviour of material varies depending on direction in which the force is applied
fracture patterns: tensile loading
application of uniaxial tensile load (stretching force) = bone pulled apart in transverse fracture
fracture patterns: compressive loading
compressive stress in axial direction + tensile stress in circumferential direction = oblique fracture
fracture patterns: torsional loading
normal tensile forces act in oblique direction + shear stresses acting in axial & transverse direction = spiral fracture
fracture patterns: bending
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)
fracture patterns: combined loads
compression induced bending (buckling) + torsion = communited fracture
order these forces from when bone is strongest to weakest: shear, tension, compression
compression > shear > tension
do smaller or larger gaps experience greater strain potential?
smaller gaps have greater interfragmentary strain
what is primary bone healing?
how does the fracture heal here (ossification type)?
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
what is secondary bone healing?
= 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.
what is the basics of “biological osteosynthesis” healing?
this emphasizes the role of soft-tissue integrity in bone healing, with a “less-than-rigid” fixation of the fracture
what is the “biomechanical” approach to fracture management?
aims for anatomic reduction and rigid fixation
list the 7 stages of fracture healing (simplified!)
- hematoma
- granulation tissue
- connective tissue
- cartilage (cartilaginous callus)
- cartilage mineralization
- woven bone formation
- remodelling to lamellar bone
what are malunions and why do they happen?
= 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
delayed union vs nonunion
delayed union - prolonged fracture healing time
nonunion - fracture does not heal
what causes delayed union?
mechanical causes: excessive fracture gaps & motion at fracture site
biological causes: inadequate cellular actiity
how can we pre-emptively treat a delayed union?
if we know there is minimal biologic activity or decreased callus formation – use bone morphogenic proteins, demineralized bone matrix or autogenous bone graft
what causes nonunion?
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
what is hypertrophic nonunion? how to treat?
- 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
what is oligotrophic nonunion? What is cause? Treatment?
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
what is a nonviable nonunion?
biologically inactive so that osteosynthesis cannot occur even with adequate fixation
briefly list and define four types of nonviable nonunions.
- dystrophic nonunion = bone vasculature compromised, nonviable bone on one/both sides of fracture
- necrotic nonunion = infected bone (sequestrum), bone is dead which prevents union
- defect nonunion = gap at site that is too large for normal process to occur, and is filled with tissue other than bone
- atrophic nonunion = result of defect nonunion, when dead bone of fracture is removed by host without healing or restoring
