Orthopaedics I: general principles

Principles of fracture healing

and disorders of bone union

energy the bone can absorb. With higher loading speeds, as in a

road traffic accident, more energy is absorbed, resulting in greater
damage to the bone and surrounding soft tissues (Figure 1).
Healing of a fracture depends on the blood supply to the bone,
the amount of force producing the fracture and the condition of
the soft tissues.

Rajeev Jahagirdar
Brigitte E Scammell

Fracture classification
Fractures can be classified based on:
cause (traumatic, stress, pathological)
fracture pattern (transverse, spiral, compression, oblique)

Abstract
This article describes the mechanisms of fracture healing (direct and
indirect), general fracture management, the influence of the surgeon
on the biology and biomechanical environment of bone healing, and
disorders of bone union.

Keywords delayed union; fracture callus; fracture healing; non-union

A fracture is defined as the structural failure of bone. Several factors, such as the load, rate of loading, direction of load and bone
properties, affect how a bone fractures.
Extrinsic factors: bone fails under applied compression, tension, rotation, shear or a combination of these forces. Depending
on the mechanical characteristics of the bone, loads applied in
a specific direction and rate will produce predictable patterns of
failure. For example, a bone that fractures as it is pulled apart in
tension will have a transverse fracture pattern, whereas one subjected to a twisting force will result in a spiral fracture pattern.
Intrinsic factors: these are factors related to the biomechanical characteristics and shape of the bone. Bone is a composite
tissue made up of inorganic mineral and cells surrounded by a
large volume of extracellular matrix, which is mainly type I collagen. Bones consist of an outer cortical layer, where the osteons
are organized into compact Haversian systems and the bone is
strong but brittle, and inner cancellous bone, where the Haversian systems are much less compact and are separated by large
areas of marrow or fat. The relative amounts of cortical and cancellous bone can determine how bones fracture; for example the
calcaneum, which is mainly cancellous bone with very little cortex, often sustains a crush or compression fracture.
Bone is anisotropic, which means that it has different mechanical properties when loaded in different axes. Bone absorbs more
energy before failure if a compressive load is applied along its
longitudinal axis compared to the same load applied in the transverse axis. Bone is also viscoelastic, which is a time-dependent
property and means that the rate of loading affects the amount of

Rajeev Jahagirdar MBBS MRCS is a Registrar in Orthopaedics at New

Cross Hospital, Wolverhampton, UK. Conflicts of interest: none
declared.
Figure 1 a At a low rate of loading, little energy is dissipated to the
surrounding soft tissues. b At a high loading rate much surrounding
soft tissue damage occurs.

Brigitte E Scammell DM FRCS(Orth) is a Reader and Honorary Orthopaedic

Consultant at Nottingham University Hospitals, Nottingham, UK.
Conflicts of interest: none declared.

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Orthopaedics I: general principles

and this is directly influenced by what method of fixation the

surgeon chooses.
Direct bony union or primary fracture healing occurs when
there is absolute stability (no motion between fracture surfaces
under functional load), as found with anatomical reduction and
rigid internal fixation.
If left alone, a broken bone will heal by callus formation. Callus
is natures response of living bone to interfragmentary movement
where there is relative stability (some controlled motion between
the fracture fragments under functional load). When a bone is
shown to have healed by visible callus formation on radiography,
it is said to have united by secondary or indirect bone healing.

displacement (displaced or undisplaced)

which section of the bone is fractured (intra-articular, metaphysis, diaphysis)
whether the skin is intact (closed fracture) or damaged (open
fracture).
Open vs closed
A closed fracture is one where the overlying skin is intact. An
open fracture is one in which a break in the skin and underlying
soft tissues leads directly to, or communicates with, the fracture
and its haematoma.
A fracture with a skin wound in the same limb segment must
be considered to be open until proven otherwise. Special challenges faced in open fractures result from:
bacterial contamination
crushing/stripping and devascularization of surrounding soft
tissues leading to increased susceptibility to infection
difficulty with immobilization
loss of function due to damage to muscles, tendons, nerves
and vessels.

Secondary or indirect bone healing

Fracture healing may be considered as a series of phases that
overlap and occur sequentially (Figure 2).
Initial haematoma: bone has an excellent blood supply. The
medullary cavity and inner two-thirds of the cortex are supplied
centrifugally by nutrient arteries within the bone, whereas the
outer third of the cortex is supplied by the periosteal arteries.
Bleeding from the bone and surrounding soft tissues results in a
fracture haematoma.
There is disruption of the Haversian systems and necrosis of
osteocytes at the fracture surfaces. The extent of bone cell death
depends on:

Fracture healing
Bone differs from other tissues owing to its remarkable ability
to repair itself and heal without leaving a scar. The processes
involved depend on the biomechanical stability of the fracture

Secondary fracture healing: bridging of a fracture by external callus

Fracture site
Periosteum
a Haematoma

Haematoma forms at the fracture site and the

periosteum is torn. The bone ends die and are
resorbed by osteoclasts

Cortex

Medullary canal

Haematoma
Dead bone at
fracture site

b Inflammation

Granulation tissue replaces the haematoma and

woven bone or hard callus starts to form the
abutments of the bridge from the cambium layer
of the periosteum by intramembranous
ossification
Granulation tissue
New woven bone/
external hard callus

c Repair
The fracture gap is bridged by soft callus or
cartilage. This is replaced with bone by the
process of endochondral ossification. The gap is
also bridged by hard external callus arching over
the soft cartilaginous callus as shown in the
lower half of the diagram. Internal or medullary
callus forms more slowly and finally cortical
continuity is restored
Cartilage/soft callus

Figure 2

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osteogenesis. Bone union by callus formation is the predominant

form of healing when simple fractures are treated by traction, sling
or plaster-cast immobilization, or external fixation or intramedullary nailing. The stage of repair lasts several weeks (Figure 3).

the degree of fracture comminution and displacement, and

thus disruption of the local blood supply
the amount of periosteal stripping, which affects the cortical
blood supply and removes the cambial layer of periosteal stem
cells from the surface of the bone.
In general, the greater the bone and surrounding soft tissue
damage, the slower the bone is to heal.
Within the haematoma, histamine is released from mast cells,
and platelets and other blood cells release cytokines. These result
in increased capillary permeability, chemotaxis and small vessel
dilatation. Along with these changes a clot of insoluble fibrin is
formed at the fracture site.

Stage of remodelling: once the fracture has been satisfactorily

bridged by callus the newly formed bone is remodelled. Any excess
callus is removed and the woven osteoid bone is remodelled into
lamellar bone. The medullary canal and bone shape are restored.
Bone is laid down in areas of excess stress and removed from
areas where there is too little (Wolffs law). Remodelling, which
is really just an extension of normal bone turnover, can continue
long after the fracture has healed clinically (up to 7 years).
In children remodelling is usually very effective at restoring shape; even completely displaced fractures may heal and
remodel without trace. The younger the child, the greater is the
propensity for remodelling, and the physis of a bent bone grows
eccentrically to help restore alignment and growth in bone length
and width to conceal deformity. There is some ability to correct
angulation but this decreases in adolescents, and axial malrotation must never be accepted as it will not remodel.
In adults there is very little correction of angulation or axial
rotation so both must be corrected before the bone unites, or
malunion will occur.

Stage of inflammation: the clot provides a framework of fibrin

fibres for the influx of various migrating cells (e.g. neutrophils, lymphocytes, monocytes, macrophages, mast cells, platelets). These
release various cytokines, including transforming growth factor-,
platelet-derived growth factor, fibroblast growth factor, and interleukin-1 and -6. Endothelial cells undergo mitosis to form capillaries and, together with fibroblasts, granulation tissue is formed.
Granulation tissue is able to form under conditions of high
strain, such as are found initially when the fracture surfaces are
very mobile. (Strain is the change in length of a given material
when a given force is applied.) Osteoblasts are able to tolerate
only very low strain (<1%), whereas immediately after a fracture the area between the bone fragments has a strain of more
than 100%, so bone cannot form. Initial healing is thus via granulation tissue, which tolerates very high strains.
Osteoclasts start to resorb the dead bone ends and phagocytes
remove other necrotic tissue. This phase lasts about a week.

Primary or direct bone healing

Primary bone repair or direct healing is the term given to fracture
repair when the fracture ends have been rigidly immobilized and
there is absolute stability under functional load. Healing of the
fracture occurs without radiographic evidence of callus. Under
these conditions strain is very low and bone can form directly.
With a fracture gap between the bone ends of less than 200 m
and absolute stability, osteoclasts can tunnel across the fracture
line, and establish a cutting cone across the fracture (Figure 4).
Osteoblasts follow, and lay down bone matrix and re-establish
continuity between the Haversian systems. Vessel ingrowth is
absent and the bone filling the interfragmentary gap appears without the intermediate formation of cartilage or connective tissue.

Stage of repair: as the granulation tissue matures, it reduces strain

at the fracture site as it forms in between the bone ends. Cartilage
forms when the strain is below 10% and then bone formation
eventually replaces the cartilaginous phase when the strain is less
than 1%. Callus formation requires angiogenesis and an intact
periosteum. The term hard callus refers to new woven bone that
is mineralized and therefore visible on radiographs. Soft callus
refers to the cartilaginous phase that occurs at the fracture gap
which then differentiates into hard callus. The process whereby
soft callus is replaced by hard callus is called endochondral ossification. The chondrocytes become hypertrophic, calcify and die,
allowing angiogenesis to occur, and osteoblasts lay down woven
bone on the collagen framework left by the chondrocytes.
External callus forms on the outside of the fractured bone to
bridge the gap. Internal callus forms more slowly from the medullary canal and, finally, cortical continuity is restored. External callus initially forms by intramedullary ossification from the
periosteum. If the periosteum is intact, a bridge of callus readily
forms from the cambium (inner) layer, arching over the dead
bone. If, however, the periosteum is ruptured, cuffs of callus
grow outwards from the living bone, eventually joining together
like the abutments to a bridge. Between the abutments of hard
callus, soft callus forms, which is seen as a gap on radiographs
and only becomes visible when it is replaced by endochondral
ossification into mineralized woven bone.
Cyclical micro-movements stimulate the growth of cartilage and
then bone. The optimal size of these movements is about 1mm.
As the callus grows in size, it becomes stiffer, thus facilitating

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Figure 3 Radiographs of a mid-shaft femoral fracture treated with a

locked intramedullary nail, showing union progressing by indirect
healing with external callus (from left to right). The third image shows
both hard external callus which is mineralized and therefore easily
visible, with central soft callus that is cartilaginous.

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Orthopaedics I: general principles

Primary bone healing

Fracture line

Cutting cone
with osteoclasts
resorbing bone

Closing cone
with osteoblasts
laying down
new bone
This schematic diagram shows a cutting cone tunnelling the bone from
left to right. The cutter head is at the right with multinucleated osteoclasts
to resorb the dead bone. The tail, with its conical surface, is lined with
osteoblasts (as seen on the left) laying down new bone. This is a slow
process which is also seen in normal turnover of bone. Direct bone
healing occurs without an intermediary cartilaginous phase

Figure 4

Fracture healing with the formation of new cortical bone

between the bone ends occurs slowly, and is essentially the same
biological process as occurs in normal bone turnover and late
remodelling.

Healing with different methods of stabilization

The pattern of bone healing can be modified by the mechanical
environment of the fracture and this can in turn be manipulated
by surgical intervention. The purpose of fracture stabilization is
to maximize the biology of fracture healing to aid early union
and restore function while minimizing complications. Generally,
the amount of callous formed is inversely proportional to the stability of the fracture. Extremely unstable fractures will, however,
not unite as the strain remains high, ossification fails and only
fibrous union occurs.
Relative stability techniques
Examples of relative stability techniques are shown in Figures 3
and 5.

Radiographs of fixation techniques with relative stability.

aComminuted intra-articular fracture of the distal radius with an
associated fracture of the ulna styloid stabilized by external fixation.
b Fracture of the distal third of the shaft of the femur stabilized
with a bridging plate. Both of these techniques will result in indirect
healing of the fracture with external callus formation.

Plaster casts prevent angulation and malrotation but provide

only relative stability. Secondary fracture healing takes place
with callus visible on radiographs. However, only transverse
fractures have axial stability in a cast, and oblique fractures may
displace and shorten.

Figure 5

Traction is considered old-fashioned, but is an effective and safe

way of maintaining reduction in some clinical situations. Here
again healing is by abundant callus formation.

used. There is always some movement at the fracture site so

external bridging callus is seen on the radiograph.
Unilateral external fixation is particularly useful if there is an
overlying soft tissue injury. All external fixators allow movement
at the fracture site, so promote healing with callus formation.

Intramedullary nails prevent angulation and provide axial stability. They also provide rotational stability if locking screws are

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Circular frames provide stability in three planes and allow axial

micro-movement to encourage callus formation. They are useful
if the fracture is very close to a joint and associated soft tissue
injuries preclude safe internal fixation.

There are different fixation methods for treating the same fracture, but an understanding of the type of healing one wishes
to achieve avoids adverse outcomes. An example of poor treatment is rigid internal fixation of a diaphyseal fracture with damage to surrounding soft tissues, and periosteal stripping without
achieving compression and leaving fracture ends separated. This
prevents primary bone healing because of a gap at the fracture
site and inhibits external bridging callus because of the absolute
stability, resulting in non-union and possible implant failure.

Internal fixation with relative stability permits some controlled

movement at the fracture site and encourages callus formation.
Examples are:
a buttress plate resists axial load by applying a force at 90 to
the potential deformity
a plate on the tensile surface of the bone resists tensile force
and dynamically compresses the far cortex
a bridging plate secures the two main fragments, leaving the
fracture zone undisturbed (so called biological plating).

Management
This includes initial assessment of the patient, then the injured
limb, followed by definitive fracture treatment.
Initial assessment and management
The Advanced Trauma Life Support protocol of airway, breathing and circulation must be applied to all patients. The history
should determine the situation, direction and magnitude of the
force. Antibiotics must be given as soon as an open fracture is
suspected, and the wound covered with a sterile dressing until formal exploration and debridement can take place in the operating
theatre. Antibiotics must cover Gram-positive and Gram-negative
organisms and anaerobes, depending on the local hospital protocol. Examples include intravenous cephalosporin or flucloxacillin,
plus an aminoglycoside. High-dose penicillin is added where clostridial infection (e.g. farmyard injuries) is a possibility. The status
of tetanus vaccination must be considered for open fractures.
Clinical examination must include assessment of the distal
neurovascular status of the limb. Radiological assessment should
include the whole of the fractured bone and the joint above and
below the fracture.
The principles of debridement include wound extension to
determine the extent of the injury, removal of all devitalized
tissues including bone, followed by irrigation of the wound with
at least 6 litres of warmed Hartmanns solution to reduce the

Absolute stability
Internal fixation with absolute stability: an anatomical reduction allows maximal friction at the fracture site. If this is combined with interfragmentary compression to prevent motion,
absolute stability is achieved. Absolute stability is when there
is no motion between the fracture surfaces under functional
load; there is very low strain across the fracture and primary
bone healing occurs without formation of external callus. This
is a slow process that relies on internal remodelling of the bone.
Interfragmentary compression can be achieved with a lag screw
across the fracture or a dynamic compression plate that causes
compression as the screws are tightened (Figure 6). Simple fractures, osteotomies and non-unions are best treated using a technique of absolute stability.
Anatomical reduction is required in two special situations:
the forearm: when the radius and ulna are fractured and displaced pronation and supination will be reduced unless anatomical reduction is achieved; the bones are held reduced
with a lag screw and plate
displaced intra-articular fractures to reconstruct the joint
surface.

Figure 6 Radiographs of a Galeazzi fracture.

Absolute stability is provided by the lag screw
across the fracture protected by a plate. The
fracture united without external callus.

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anagement and the biology of the compromised fracture site

m
must be respected when considering surgical intervention.

bacterial load. Patients with highly contaminated wounds and

severely damaged soft tissues should return to theatre every
48hours until the wound is clean and only healthy tissues
remain. If possible, a plastic surgeon should be present at the
initial debridement as exposed bone must be covered as soon as
possible (usually within 5 days).
The state of the soft tissue surrounding the fracture dictates
management, even in closed fractures. One must not operate
through bruised and highly swollen tissues where the wound
may be impossible to close or break down later.

Property of bone involved: there is a variation in the speed at

which bones heal in the same individual. Fractures of the upper
limb generally heal more quickly than fractures in the lower
limb. Clavicle fractures heal remarkably well; on the other hand,
tibial shaft fractures heal slowly.
Type of fracture: displaced and comminuted fractures frequently
result in delayed healing. The avascular fragments of splintered
bone require resorption, a more extensive inflammatory and callus phase, and more time to remodel. Transverse fractures take
longer to heal than spiral fractures because they usually have
more displacement of the periosteum and a smaller surface area
of contact.

Definitive fracture treatment

This involves reduction, stabilization and rehabilitation. Reduction can be achieved by closed methods (traction and manipulation) or open reduction (surgical). Stabilization can be achieved
by conservative techniques (plaster cast) in stable fractures, and
by surgery using either internal or external fixation in unstable or
potentially unstable fractures.

Infection in a fracture will delay or prevent healing. This is a

common cause of delayed or non-union. There is a prolonged
inflammatory phase and cellular activity is directed towards
fighting the infection rather than bone healing. A further problem is, in the presence of metalwork, that bacteria readily produce biofilms which render normal antibiotic dosage regimens
useless, as toxic concentrations of antimicrobials are required to
inhibit bacterial growth.

Factors affecting fracture healing

General
Age: childrens bones unite more rapidly; the speed decreases as
skeletal maturity approaches. Childrens bones also have great
capacity for remodelling (except for axial rotation).
Nutrition and drug therapy: poor nutrition and general health
reduce rates of healing. Smoking, and use of corticosteroids and
non-steroidal anti-inflammatory drugs impair the inflammatory
response and delay bone healing.

Biomechanical environment: there is an optimal balance

between stability and micro-motion to encourage callus formation. Small, cyclical movement of about 1 mm increase the rate
of healing by 25% and are a feature of many external fixation
devices.

Bone pathology: pre-existing bone disease such as malignancy

inhibits bone healing and screws in osteoporotic bone often fail.

Electromagnetic environment: direct current helps stimulate an

inflammatory-type response and pulsed electromagnetic fields
initiate calcification of fibrocartilage. Their therapeutic use is
controversial.

Type of bone: cancellous bone tends to heal faster than cortical bone. This is due to a large area of bony contact (e.g. in
the metaphysis) and the greater number of active bone cells
present.

Ultrasound: low-intensity pulsed ultrasound accelerates fracture

healing, and improves mechanical strength by increasing the
stiffness and torque of fracture callus. Its use is controversial.

Local
Mobility at fracture site: excess mobility at the fracture site will
interfere with vascularization of the fracture haematoma, cause
high strain and disrupt the bridging callus, thus interfering with
union.

High-dose irradiation is associated with a decrease in cellularity,

long-term changes within the Haversian system and an increased
risk of non-union.

Separation of the bone ends: bony union may be delayed or prevented if the bone ends are separated by interposed soft tissue, or
held apart with the fixation device or traction.

Disorders of bone union

Some fractures are slow to unite despite optimal treatment.

Disturbance of blood supply: a fundamental factor affecting

healing is the blood flow to the bone. Fractures compromising
blood flow to the fracture site or one of the fragments at the
fracture are slow to unite if they unite at all. Examples include
intracapsular fractures of the neck of femur and scaphoid
fractures where the blood supply to the bone is via an end
artery.
High-energy injuries resulting in comminution, loss of
soft tissue attachments and periosteal stripping heal slowly.
In these injuries the soft tissues dictate the definitive fracture

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Delayed union
Healing fails to occur within the expected time for the fracture. The
fracture proceeds through the normal stages of healing clinically
and radiologically but at a slower rate. This can be due to intrinsic factors (tibial diaphyseal fractures are often slow to unite), a
reduced blood supply or infection at the fracture site. Choosing a
technique of absolute stability and leaving a fracture gap of more
than 1 mm will also delay union as the rigid fixation will inhibit
healing by callus formation and the gap will delay or even inhibit
direct bone healing.
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appear sclerotic and flared owing to excess callus formation;

this gives a typical appearance on radiographs of an elephants
foot. Here the biomechanical environment is faulty, and the
gap between bone ends is filled by cartilage and fibrous tissue.
The blood supply at the bone ends is good and immobilizing
the fracture (e.g. with an intramedullary nail) usually results
in union.
Atrophic: in atrophic non-union, there is no attempt at healing,
the bone ends are resorbed and rounded; the bone biology is
faulty. The gap between the bone ends is filled by fibrous tissue (Figure 7). Rigid fixation with interfragmentary compression
and elimination of the fracture gap is required, and supplementary bone grafting may be required. Recombinant human bone
morphogenetic proteins are now commercially available and are
licensed for use in difficult non-union surgery.

Further reading
McRae R, Esser M, eds. Practical fracture management, 4th edn.
Edinburgh: Churchill Livingstone, 2002.
Redi TP, Buckley RE, Moran CG, eds. Practical fracture management,
2nd edn. New York: Thieme, 2007.
Standing S, ed. Grays anatomy, the anatomical basis of clinical
practice, 40th edn. Edinburgh: Churchill Livingstone, 2008.
Wraighte PJ, Scammell BE. Principles of fracture healing. The
Foundation Years 2007; 3(6): 24351.

Figure 7 Established atrophic non-union at 8 months after

intramedullary nailing. Treated with a lag screw across the fracture
gap and blade plate fixation. The fracture united with minimal callus
4months later.

Non-union
The healing process ceases to be active and this is usually thought
to be the case if by 6 months there is no progression to union.
Non-union occurs if there is wide separation of the bone ends,
soft tissue interposition, and lack of blood supply, infection or
an adverse biomechanical environment. There are two types of
non-union.

Acknowledgements
Thanks to Professor Christopher Moran and Mr Nitin Badhe for
their assistance with the images used in this article.

Hypertrophic: inadequate stability of the fracture leads to

hypertrophic non-union, with normally viable bone ends that

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