Biomechanics
Team Member：Chin Lin Wang
Chung Chun Lin
Ken Chung Chen
2010/12/30
Basic Orthopaedic Biomechanics and Mechano-Biology, 3rd Edition
Editors: Mow, Van C.;
Huiskes, Rik
Copyright ©2005
Lippincott Williams &
Wilkins
 Biomechanics of Fracture
Fixation and Fracture Healing
Contents
1
Mechanical Principles of Fracture Fixation
2
Biomechanics of Fracture Healing
3
Biomechanical Monitoring of Fracture Healing
Introduction
Up to the nineteenth century, fracture treatment
was performed by external splinting




Alignment
Stabilize
External loading and muscle activity
Tissue strain and the cellular reaction
As a consequence, the operative treatment of
fractures, which involved new fixation systems
and implants, was developed in the twentieth
century
Mechanical Principles of Fracture Fixation
Splinting
 Plaster Cast and Brace
External Fixation
Internal Fixation




Intramedullary Nail
Compression Plate
Lag Screws
Tension band systems
Plaster Cast and Brace
The classical way to stabilize a
fracture is plaster cast fixation.
Instability due to bending movements
and torque must be limited by a good
fit between the plaster cast and the
outer shape of the extremity.
External Fixator
When a fracture is accompanied
by an open soft-tissue wound, a
plaster cast or brace is often not
possible.
In such cases, an external
stabilization of the fracture can be
performed by using an external
fixator.
The distance between two connecting bars (L3)
and the distance between two screws in one fragment (LS).
The greater the distance, the higher the stability.
Bilateral open tibia fractures stabilized by two
external fixators. Left leg: monolateral double
tube fixator; right leg: biplanar external fixator.
There are limitations. From a
biological point of view, it
cannot be proposed to
increase the number or the
diameter of the screws as
much as possible to achieve
maximal stability.
External fixator with four 5mm screws showed
interfragmentary movements
of 1 to 3 mm under partial
axial loading (300 N).
Intramedullary Nail
Intramedullary nailing is a generally accepted
internal splinting technique. The conventional
Küntscher nail is a longitudinally slotted tube that
is inserted into a long bone under prestress.
The reaming of the bone
can cause a considerable
rise in intramedullary
pressure and temporary
damage to the bone's
blood supply .
Interfragmentary Compression
Interfragmentary compression (N) created by a
lag screw, for example, has to neutralize external
forces and moments to achieve stability of the
fracture.
Lag Screws
Interfragmentary compression created by two
spongy bone lag screws in the epiphyseal fracture
of the distal femur.
Therefore, an internal fixation of a fracture with
lag screws alone is rarely stable enough to allow
load bearing of the operated extremity. In most
cases, a lag screw is used in combination with a
plate.
Compression Plate
Application of interfragmentary compression by a
tension device pulling on the plate.
Compression hole principle
Compression hole principle. When the screw is
inserted into the bone, the screw head moves
toward the bone, sliding on the slope and pushing
the plate in horizontal direction (Δ axial).
Compression holes can be used to close fracture
gaps and create interfragmentary compression.
Interfragmentary Compression by Tension Band Principle
The application of the tension band principle by a
plate fixed on the tensile force site of a fractured
bone.
Tension band systems
Tension band principle applied for the cerclage
fixation of a patella fracture.
Key Point
The fracture type
The fracture position
The loading direction
Wolf’s law
Biomechanics of Fracture Healing
Bone Healing under Interfragmentary Movement
Fracture Healing under Interfragmentary
Compression
Delayed Healing and Nonhealing under Unstable
Fixation
Bone Healing under Interfragmentary Movement
Fracture healing under interfragmentary
movement occurs by callus formation that
mechanically unites the bony fragments.
After trauma and fracture, a hematoma occurs
that undergoes tissue differentiation.
The sequence of fracture healing




Inflammation
Soft callus
Hard callus
Remodeling
Stages in the Healing of a Bone Fracture
Hematoma
formation
 Torn blood vessels
hemorrhage
 A mass of clotted
blood (hematoma)
forms at the
fracture site
 Site becomes swollen,
painful, and inflamed
Stages
in
the
Healing
of
a
Bone
Fracture
Fibrocartilaginous
callus forms
Granulation tissue (soft
callus) forms a few
days after the fracture
Capillaries grow into
the tissue and
phagocytic cells begin
cleaning debris
Stages
in the
Healing of a Bone Fracture
Bony
callus
formation
 New bone trabeculae appear
in the fibrocartilaginous
callus
 Fibrocartilaginous callus
converts into a bony (hard)
callus
 Bone callus begins 3-4
weeks after injury, and
continues until firm union is
formed 2-3 months later
Stages in the Healing of a Bone Fracture
Bone remodeling
 Excess material on
the bone shaft
exterior and in the
medullary canal is
removed
 Compact bone is
laid down to
reconstruct shaft
walls
Schematic drawing of the callus healing process. Early
intramembranous bone formation (a), growing callus
volume and diameter mainly by enchondral ossification
(b), and bridging of the fragments (c).
Figure from Brighton, et al, JBJS-A, 1991.
A: Roentgenogram of a callus healing in a sheep tibia with
the osteotomy line still visible (6 weeks p.o.).
B: Histological picture of a sheep tibia osteotomy (fracture
model) after bone bridging by external and intramedullary
callus formation. A few areas of fibrocartilage remain at the
level of the former fracture line (dark areas).
Bone Healing under Interfragmentary Movement(cont.)
The flexural and torsional rigidity of a fracture
depends on the material properties and the second
moment of inertia (rigidity = EI) of the callus.
 Particularly the increase in callus diameter has a
significant effect on the stabilization of the
fracture.
 Linear relation to the mechanical quality of the
callus tissue (E),
The rigidity is proportional to the fourth power of
the diameter (IBending = πd4/64, ITorsion = π d4/32)
Bone Healing under Interfragmentary Movement(cont.)
The interfragmentary movement under external
loading decreases with healing time in relation to
the rigidity of the callus.
 Finally, the hard callus bridges the bony
fragments and reduces the interfragmentary
movement to such a low level that a healing of the
fracture in the cortex can take place (Fig).
When this has happened, the callus tissue is no
longer required and is resorbed by osteoclasts.
 Finally, after a remodeling process, the shape and
strength of the normal bone are reconstituted.
Healed osteotomy of a sheep metatarsal with bony bridging of
the cortical osteotomy gap and only small remaining callus volume.
Fracture Healing under Interfragmentary Compression
 implants and external loads  Compression forces
compression and close contact ( the external traction forces
=> the internal compression preload )
 compression preload +friction between the
fragmentsrelative movement between the fragments is
avoided.
 Under this absolutely stable fixation, bone healing can
occur by direct osteonal bridging of the fracture line with
minimally or no callus formation .
 In areas with direct contact, remodeling starts a few weeks
after fracture fixation, which leads to bridging of the
fragments by newly formed osteons .
Fracture Healing under Interfragmentary Compression(cont.)
Haversian osteons with osteoclasts in their cutter
heads resorb bone, create a tunnel that crosses the
fracture line, and fill the tunnel with new bone in a
process of osteoblastic activity.
In areas with a gap between the fragments, a
filling of the gap by woven bone occurs as a first
step before the Haversian osteons can cross the
fracture area .
In reality a mixture of contact and gap healing will
occur.
Osteon with bone-resorbing osteoclasts (left) that drill a
tunnel into the bone and osteoblasts that lay down new bone
(osteoid) and fill the tunnel with a new bone layer (original
magnification 100×)
Osteoclas
t
Osteoblast
New
bone
Contact healing with osteons crossing the fracture line (left).
Healing of a fracture gap (right). Woven bone fills the gap
before the osteons can bridge the fracture area.
Fracture Healing under Interfragmentary Compression(cont.)
An advantage of absolute stability is that the blood
vessels may cross the fracture site more easily and
lead to faster revascularization .
 In contrast to callus healing, there is no increased
bone diameter under direct osteonal healing.
This limits the load-bearing capacity of the healing
bone, which consequently requires a longer period
of protection by the implant.
Delayed Healing and Nonhealing under Unstable Fixation
 When the interfragmentary movement is too large, the
bony bridging of the fragments is delayed or even
prevented.
 Large interfragmentary movements cause large tissue
strains and hydrostatic pressures in the fracture that
prevent the vascularization of the fracture zone.
 Without this vascularization bone cells cannot survive,
bone cannot be built, and only fibrocartilage can be
formed .
 Because the resisting fibrocartilage layer in between the
two bony fragments looks like the image of a joint, the
nonunion is also called pseudarthrosis (false joint).
MAIN FACTORS INFLUENCING
THE BIOMECHANICS OF
FRACTURE HEALING
Inter Fragmentary Movement-Axial Movement
Small interfragmentary(IFM) movements
stimulate callus formation
Small fracture gaps
 Cyclic axial movement 
stimulated callus volume
Large fracture gaps
 Callus formation seems to be
limited and bridging of the fracture gap is delayed
 A more stable fixation with smaller interfragmentary
movements seems to be advantageous
Axial Movement
Very stiff fixation of a fracture can suppress the
callus formation and delay healing. In such cases,
an externally applied interfragmentary movement
can be used to stimulate callus healing.
-- Kenwright J, Goodship AE. Controlled mechanical stimulation in the treatment of tibial fractures. Clin
Orthop 1989:36-47.
However, when the fracture fixation itself allows
axial movements to a sufficient extent to stimulate
callus formation, an additional external
application of interfragmentary movements does
not lead to further improvement of the healing
process.
--Augat P, Merk J, Wolf S, et al. Mechanical stimulation by external application of cyclic tensile
strains does not effectively enhance bone healing. J Orthop Trauma 2001;15:54-60.
Shear Movement
Shear movement delays the fracture healing ?
 Impede vascularization and promote fibrous tissue
differentiation
 Oblique tibial fracture (shear movements : 4 mm)
-- treated with functional bracing show rapid natural healing
Shear movement to induce delayed unions and
nonunions ?
 Control
• Shear movement
• Osteotomies of oblique or transverse type
Comparison
Timing, magnitude, and/or gap size
Tibial osteotomy in sheep
 3-mm osteotomy gap
 Give axial or plane shear movement
of 1.5 mm
(Augat et al., 2003)
 Loading of the tibia during gait
Tibial osteotomy




2.4-mm osteotomy gap
25% axial compression (0.6 mm)
Torsional shear (7.2°)
A displacement-controlled hydraulic actuator
(Bishop et al., 2003)
Blood Supply
Sufficient blood supply
 Nutrition of the healing zone
 A delayed union or even an atrophic nonunion
 Trauma or smoking
Under unstable fixation
 Capillaries required for osseous repair are constantly
ruptured
fibrocartilaginous tissue
 Large interfragmentary movement
• Non-ossified callus tissue
• Tissue strains
prevent revascularization
• Hydrostatic pressure
a collapse of the blood vessels
Biomechanical Monitoring of Fracture Healing
The interfragmentary movement can be used for
the monitoring of the bone healing process for
patients with fracture treatment by external
fixation
As the healing process progresses, the callus
increases in size and rigidity and shares more and
more of the external load
The load at the external fixator decreases, which
leads to decreasing deformation of the fixation
frame
Therefore, the measurement of fixator
deformation allows an indirect determination of
the interfragmentary movement and stiffness of
the callus
Mechanobiology of Fracture Healing
Mechanical Stimulation of Fracture Callus Cells
 Mechanoregulation of Fracture Healing
Mechanoregulation of Tissue Differentiation
Mechanoregulation Models of Fracture Healing
Mechanical Stimulation of Fracture Callus Cells
Fracture healing
Early phase of fibroplastic stage
 The progenitor cells are believed to arise from the
periosteum, endosteum, marrow, and surrounding
extracortical soft tissue
 Multipotential progenitor cells begin to invade the
granulation tissue callus
 Differentiate into various cell phenotypes and proliferate
within the callus
Fracture healing
Early phase of fibroplastic stage
 away from the fracture gap and along the periosteum and
endosteum, the cells differentiate into osteoblasts and
begin to directly produce bone
 within the callus and the gap, the progenitor cells
differentiate into fibroblasts or chondrocytes, proliferate,
and begin to produce a fibrous connective tissue or
cartilage matrix, respectively
 this soft tissue bridges the fragment ends and stabilizes the
fracture to some degree
Contemporary oral and
maxillofacial surgery 5e
Fracture healing
Late phase of fibroplastic stage
 chondrocytes at the hard and soft tissue interface proliferate,
hypertrophy, and calcify, forming bone
 fibroblasts and connective tissue are slowly replaced by
chondrocytes and cartilage
 creeping substitution of bone from the distal ends of the
callus until an initial osseous bridge of the fracture gap
 When the gap is filled with woven bone, the fracture is
considered healed
Contemporary oral and
maxillofacial surgery 5e
Final remodeling stage
 osteoclasts begin to resorb the woven bone in the
extraperiosteal callus as osteonal remodeling occurs across
the gap
Contemporary oral and
maxillofacial surgery 5e
Mechanical Stimulation of Fracture Callus Cells
Various cells found in the callus are modulated by
the local mechanical environment
Cyclic hydrostatic pressure applied to in vitro cell
cultures of bone marrow-derived mesenchymal stem
cells were found to enhance differentiation into
chondrocytes and stimulated cartilaginous matrix
Angele P, Yoo JU, Smith C, et al
production
Mechanical compression was also found to regulate
synthesis of distinct proteoglycan types by fibroblasts
in tendon explants
Koob TJ, Clark PE, Hernandez DJ, et al.
Mechanical Stimulation of Fracture Callus Cells
 When intermittent hydrostatic pressure was applied
to embryonic bone organ cultures, hypertrophy of
chondrocytes and mineralization were accelerated
van't Veen SJ, Hagen JW, van Ginkel FC, et al.
Osteoblasts have also been demonstrated to be
sensitive to mechanical stimuli. Cyclic tensile strain
has been found to increase their proliferation and
osteoid production
Kaspar D, Seidl W, Neidlinger-Wilke C, et al.
In contrast, biaxial stretch was found to regulate
apoptosis and proliferation of osteoblasts in a
differential fashion dependent on their state of
differentiation
Weyts FA, Bosmans B, Niesing R, et al.
Mechanical Stimulation of Fracture Callus Cells
Mechanical loading applied to the callus tissue
produces local biophysical stimuli sensed by the
cells
 regulate cell phenotype, proliferation/apoptosis, and
anabolic and catabolic synthesis activities
 with alteration of the extracellular matrix and the associated
changes in material properties of the tissue
Mechanical Stimulation of Fracture Callus Cells
In normal fracture healing
 this feedback process reaches steady state when the callus
has ossified and the original cortex has regenerated
However, this feedback process may also explain
some complications of fracture healing such as
delayed or nonunions where the tissue properties
combined with loading may promote the
persistence of soft tissues
Thus, the mechanobiology of callus cells is integral
to understanding the biomechanics of fracture
healing.
Mechanoregulation of Fracture Healing
Mechanoregulation of Tissue Differentiation
Mechanoregulation Models of Fracture Healing
Mechanoregulation of Tissue Differentiation
Late 1800s ,Roux introduced his theory of
functional adaptation
He proposed that the mechanical environment or
“irritations” actually stimulated the formation of
particular types of connective tissue
Compression stimulated the formation of bone
Tension for connective tissue
In combination with compression or tension for
cartilage
Mechanoregulation of Tissue Differentiation
Almost a century later, Pauwels proposed a more
rigorous mechanoregulation theory based on
continuum mechanics
 He analyzed the mechanical environment with a
healing fracture callus and hypothesized that the
invariants of the strain and stress tensors guided
the differentiation pathway
Mechanoregulation of Tissue Differentiation
 Perren and Cordey
 believed that tissue differentiation was a result of tissue
disruption
 if stresses exceeded the tissue strength or tissue elongation
resulted in rupturing, the tissue would change its phenotype
such that tissue failure would not occur
 using finite-element analysis (FEA) to calculate the
complex tissue strain in the callus at the beginning of
healing
Mechanoregulation of Tissue Differentiation
 Cheal et al.
 compared histology of the fracture callus with magnitudes
of strain
Although they did not demonstrate tissue damage,
they found an association of
 high strain levels with soft tissues and bone resorption
 low strain levels with bone formation
Mechanoregulation of Tissue Differentiation
Carter et al.
 proposed local stress or strain history as a method to allow
a range of cyclically applied loads to influence tissue
differentiation over time
Mechanoregulation of Tissue Differentiation
Claes and Heigele was initially presented in
quantitative terms
Mechanoregulation of Tissue Differentiation
Finally, Prendergast, Huiskes, and colleagues have
developed a different mechanoregulation concept
taking into consideration that connective tissues are
poroelastic and comprise both fluid and solid
Mechanoregulation of Tissue Differentiation
They all propose that
 higher magnitudes of tissue deformation result in the
stimulation of softer fibrous connective tissue
 cartilage and bone are formed in the presence of lower
strains
Mechanoregulation Models of Fracture Healing
The models are generally divided into two parts
 In one part, the tissue deformations and stresses
are calculated using FEM of the healing fracture
with tissue morphology, material properties, and
loading conditions as the input
Mechanoregulation Models of Fracture Healing
In the other part, the mechanoregulation
algorithm is described by a set of mathematical or
logical rules and used to predict changes in tissue
material properties
Mechanoregulation Models of Fracture Healing
 Now that these complex models have been developed
 The next challenge will be to compare them with known in
vivo results demonstrating the mechanosensitivity of tissue
differentiation during fracture healing
 With such comparisons, the most significant
mechanobiological interaction can be resolved and
mechanically guided tissue transformation functions
defined
 These could then be combined with dramatically
improving computer and imaging technology (computed
tomography, nuclear magnetic resonance) and
musculoskeletal loading simulations to develop fracture
healing models that would enable us to optimize fracture
treatment for individual patients from a biomechanical
point of view
Thanks for your attention!