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4 tenets of bone healing

mechanics, scaffold, growth factors and cells


In a fracture gap model in which compression is applied after 4 weeks of healing describe the different forces felt by the cells of the callous in different locations of the callous and what effect that has on these cells

Cells in the middle of the callous feel the compression while cells on the periphery experience tension
Stemcells under tension tend toward osteoblastic lineage and bone is formed (think distraction osteogenesis)
Stemcells under compression tend toward chondroblastic lineage and cartilage is formed


Describe stress protection and how to avoid it

Inadequate amounts of stress is imparted to the fracture site so cell aren't stimulated to propagate and differentiate (healing is retarded)
Avoid limiting strain to less than 1-2%
Rule of thumb - simple fracture with a few to several millimeters of gap or comminution can tolerate 5-10% strain


Using axial strain as an example define strain

Strain is a measure of the amount of motion relative to the span over which the motion occurs.
Axial strain is the degree of compression across a gap
The decrease in the width of the gap divided by the total width of the gap


Describe the ideal relationship of stiffness to load ( aka activity level)

At low load (activity) levels stiffness should also be low (i.e. some movement at fracture site)
As load level increases stiffness should increase


According to Tobias the two predominant forces of the skeleton

Compressive and tensile (bending is a combo of both - compression on the concave aspect and tensile on the convex aspect)


Which force acting on a fracture is least tolerated
How is this force generated with oblique vs transverse fractures?

Oblique in axial load
Transverse in rotation load


What is the clinical enigma of the term delayed union

It assumes eventual healing - which can't be guaranteed until it has or has not healed


Negative intrinsic factors associated with bone healing

Diaphyseal cortical bone, decreased/compromised vascularity of the periosteum, sparse soft tissue attachments, aged and or ill patient


Negative extrinsic factors associated with bone healing

ORIF (approach, lavage, removal of hematoma etc.. all clear out the cellular and humoral components of early healing)
Armament - some less biologic than others (plate luting for e.g.)


What is the principle cell type of early bone healing and what is an important source of this cell type

Mesenchymal stem cell and the cambium layer of the periosteum is an important source. They are richest in areas of thick and vascular periosteum


What is a delayed union?

A prolongation in time for fracture healing. This time will vary depending on intrinsic and extrinsic factors.


Whats the most common cause of delayed union

Intrinsic factors of the patient and or fracture. Regardless of root cause results in inadequate cellular activity


Two broad categories of Non-unions and broad characteristics of each

Viable - biologic environment is adequate (which may or may not be noted via evidence of healing on x-rays) so healing can occur with improved fixation
Non-viable - Biologically inactive so that osteosynthesis cannot occur even with adequate fixation.


Types of viable non-unions

Hypertrophic (elephants foot/horses foot) and Oligotrophic


Hypertrophic non-union - appearance, most likely cause and treatments

Considerable callous on either side of the fracture line.
Typically due to excessive motion at fracture site
Debride fibrous tissues at fracture site, re-establish communication with medullary canal of bones.
Consider bone graft
Rigid fixation with dynamic compression is recommended to ensure an axial load is preferred (not shear)


Oligotrophic non-union

Hard to diff from non-viable on rads because its defined as viable non-union without radiographic evidence of biologic activity.
Problem here is both instability and disrupted cellular activity. Loose cerclage is common culprit
Gotta improve stability, remove loose shit and give cellular activity a boost - graft


Types of non-viable non-unions

dystrophic, necrotic, defect, atrophic


Dystrophic non-union

Non-viable bone on one or both sides of fracture. Compromise to the blood supply has occurred so there is no living bone tissue on the ends.


Necrotic non-viable non-union

Implies a sequestrum


Defect non-viable non-union

Gap too big. Gets filled with with tissue other than living bone. Typically fibrous tissue or muscle


Atrophic non-viable non-union

Usually a result of a defect non-viable non-union. Body resorbs dead bone without a healing or restorative process.


Components of a necrotic non-viable non-union

Sequestrum - the dead non-viable piece of bone inhibiting complete healing
Involucrum - the new bone grown surrounding the sequestrum


Treatment recommendations for Atrophic non-viable non-union

Remove all non-viable bone and regenerate new bone -
Rigid fixation and stimulation of regeneration via autologous cancellous graft, commercially available growth factors (rhBMP-2 or -7) with suitable matrix material, or distraction osteogenesis.
Challenging, guarded prognosis and relatively higher complication rate so amputation often chose


Additional ways to stimulate bone regeneration/growth

Extracorporeal shock wave, pulsed magnetic field, low-intensity ultrasonongraphy


Tissues within a callous from most to least tolerant to strain

fibrous tissue, cartilage and lastly bone


T or F
Small strains encourage healing in small fracture gaps?

30% strain was better than 7% for 1mm gap