Fracture healing and wound healing

Fracture healing and wound
healing
Dr shermil sayd
KMCT dental college

Types of Bone
• Lamellar Bone
• Woven Bone or immature bone (non-lamellar)

Fracture
• Fracture is defined as a break in the continuity of
bone
• Fracture results in loss of its mechanical stability
and also partial destruction of blood supply
• Healing means to make whole or sound again, to
cure, leaving a scar behind. But following fracture
a scar is not formed, instead a bone has formed a
new at the original fracture site. So rather than
bone healing the appropriate nomenclature
would be BONE REGENERATION

TYPES OF FRACTURES(7,8,9)
• ON BASIS OF ETIOLOGY
- Traumatic fracture
- pathologic fractures due to some
diseases
- stress fracture
• ON BASIS OF DISPLACEMenT
- undisplaced
- displaced
translation ( shift )
angulation ( tilt )
rotation ( twist )

• ON BASIS OF RELATIONSHIP WITH EXTERNAL
ENVIRONMENT
- simple / closed fracture
- open fracture
• ON BASIS OF PATTERN
- transverse
- oblique
- spiral
- comminuted
- segmental

HEALING AFTER FRACTURE FIXATION
• DIRECT/PRIMARY:

• Mechanism of bone healing seen when there is no
motion at the fracture site (i.e. rigid internal fixation).
• Does not involve formation of fracture callus.
• Osteoblasts originate from endothelial and perivascular
cells.

• INDIRECT/SECONDARY:

• Mechanism for healing in fractures that are not rigidly
fixed.
• Bridging periosteal (soft) callus and medullary (hard)
callus re-establish structural continuity.
• Callus subsequently undergoes endochondral

ossification.

TYPES OF BONE HEALING
• PRIMARY
1. CONTACT HEALING: When there is direct contact between the
cortical bone ends, lamellar bone forms directly across the fracture
line , parallel to long axis of the bone, by direct extension of
osteons.
2. GAP HEALING: Osteoblasts differentiate and start depositing
osteoids on the exposed surfaces of fragment ends, mostly
without a preceding osteoclastic resorption which is later

converted into the lamellar bone

• SECONDARY:
It is usual type consisting of formation of callus
either of cartilaginous or fibrous. This callus is

later replaced by lamellar bone. It is comparable
to healing of soft tissue by filling of gaps with

vascular granulation tissue

MECHANISM OF BONE FORMATION
1. Cutting Cones
2. Intramembranous Bone Formation
3. Endochondral Bone Formation

CUTTING CONES
• Primarily a mechanism

to remodel bone.
• Osteoclasts at the front
of the cutting cone
remove bone.
• Trailing osteoblasts lay
down new bone

INTRAMEMBRANOUS BONE
FORMATION(PERIOSTEAL)
• Mechanism by which a long bone grows in
width.
• Osteoblasts differentiate directly from pre
osteoblasts and lay down seams of osteoid.
• Does NOT involve cartilage

ENDOCHONDRAL BONE FORMATION
• Mechanism by which a long bone grows in
length.
• Osteoblasts line a cartilage precursor.

• The chondrocytes hypertrophy, degenerate and
calcify (area of low oxygen tension).
• Vascular invasion of the cartilage occurs followed
by ossification (increasing oxygen tension).

STAGES OF FRACTURE HEALING
• There are 3 major phases with sub divisions:

• A. Reactive Phase:
– i. Fracture and inflammatory phase.
– ii. Stage of hematoma formation.
– iii. Granulation tissue formation.

• B. Reparative Phase:
– iv. Cartilage Callus formation.
– v. Lamellar bone deposition.

• C. Remodeling Phase:
– vi. Remodeling to original bone contour.

Components of Bone Formation
• Cortex

• Periosteum
• Bone marrow

• Soft tissue

A.REACTIVE PHASE
• I .Fracture & inflammatory

phase :
After fracture the first change
seen by light and electron
microscopy is the presence of
blood cells within the tissues
which are adjacent to the
injury site. Soon after
fracture, the blood vessels
constrict, stopping any further
bleeding

• ii. Stage of Hematoma
formation:
Within a few hours after
fracture, the extravascular blood
cells form a blood clot, known as
a hematoma. All of the cells within
the blood clot degenerate and die.
The fracture hematoma
immobilizes & splints the fracture.
The fracture haematoma provides
a fibrin scaffold that facilitates
migration of repair cells.

iii. Granulation Tissue Formation:

Within this same
area, the fibroblasts survive and
replicate. They form a loose
aggregate of cells, interspersed with
small blood vessels, known
as granulation tissue which grows
forward, outside and inside the bone
to bridge the fracture.
They are stimulated by vasoactive
mediators like serotonin and
histamine

B. REPARATIVE PHASE
•

iv. Cartilage Callus formation :

Days after the # the periosteal cells
proximal to the fracture gap and
fibroblasts develop
into chondroblasts which
form hyaline cartilage.
The periosteal cells distal to the
fracture gap develop
into osteoblasts which form woven
bone. These 2 tissues unite with
their counterparts and culminate
into new mass of heterogenous
tissue called Fracture Callus
restoring some of its original
strength.

• v. Lamellar bone deposition:
Or consolidation ..where hyaline
cartilage and woven bone is replaced
by lamellar bone. This process is
called Endochondral ossification.
At this point, the mineralized matrix
is penetrated by channels, each
containing a microvessel and
numerous osteoblasts.
This new lamellar bone is in the
form of trabecular bone which
restores bone’s original strength

C. REMODELLING PHASE
• vi. Remodelling to original bone
contour:
The remodeling process substitutes
the trabecular bone with compact
bone. The trabecular bone is first
resorbed by osteoclasts, creating a
shallow resorption pit known as a
"Howship's lacuna".
Then osteoblasts deposit compact
bone within the resorption pit.
Eventually, the fracture callus is
remodelled

STAGES BASED ON REACTION TO
TORSIONAL TESTING
• STAGE 1- A healing bone subjected to torsion fails
through original # site with a low stiffness pattern.
• STAGE 2- The bone still fails through the # site , but the
characteristic indicate high stiffness pattern(hard
tissue pattern)
• STAGE 3 – The bone fails partly through the original #
site and partly through the previously intact bone with
a high stiffness pattern .
• STAGE 4 –Failure does not occur through the # site
duplicates the mechanical properties of uninjured
tissue

# HEALING IN CANCELLOUS BONE
1.Cancellous bone heals by “CREEPING SUBSTITUTION” New blood vessels
can invade the trabeculae of cancellous bone
and bone opposition may take place directly on
to the surface of trabeculum.

2.Heals at the point of direct contact:
•

Cancellous bone certainly can unite very rapidly, but it
unites rapidly only at the points of direct contact.

3.No bridging callus :
Cancellous bone unites only by contact, not by throwing out
callus even when it is cut of due to dense attachment of the

periosteum.

4.No death of osteocytes:
Takes place in the cut edges of divided trabeculae in
cancellous bone. This must be because of the blood
supply is good and large surface area of the trabecular
spaces combined with relatively thin trabeculae, keep
the osteocytes nourished.
5.Has tendency for late collapse :
This lack of callus production by cancellous bone explains
the tendency to late collapse which have been
distracted. Eg: after reduction of colle’s fracture a
hallow cavity is left in the cancellous end of the radius

FRACTURE HEALING IN CHILDREN
• Compared with the relatively static mature bone
of adult, the changing structure and
function, both physiological and
biomechanical, of immature bones make them
susceptible to different patterns of fracture.
• Fracture in children are more common and are
more likely to occur after seemingly insignificant
trauma. Damage involving specific growth regions
such as the physis or epiphyseal ossification
center may lead to acute and chronic growth
disturbances.

FRACTURE REPAIR IN CHILDREN
Fracture healing in children follow same pattern of adults
but with some peculiarities :
PERIOSTEUM:
• In the contrast to adults, the periosteum strips away
easily from the underlying bone in children. Allowing
fracture haematoma to dissect along the diaphysis and
metaphysis and this is evident in the subsequent
amount of new bone formation along the shaft.
• Dense attachment of the periosteum into the zone of
ranvier limit subperiosteal hematoma formation to the
metaphysic and diaphysis

REMODELLING IN CHILDREN
• The remodelling phase is the longest phase
and in children may continue until skeletal
maturation. Remodelling is better in children
compared to adult, This is in response to
constantly changing stress patterns in children
during skeletal growth and development

FACTORS INFLUENCING BONE
HEALING
1.
2.
3.
4.
5.
6.

LOCAL FACTORS
CHEMICAL FACTORS.
VASCULAR FACTORS.
SYSTEMIC FACTORS
ELECTROMAGNETIC FACTORS
TREATMENT FACTORS

1.LOCAL FACTORS
A. Type of bone:
Cancellous (spongy) bone or cortical bone.
B. Degree of Trauma:
Extensive soft tissue injury and comminuted
#‘s V/s Mild contusions
C. Vascular Injury:
Inadequate blood supply impairs healing. Especially
vulnerable areas are the femoral head, talus, and
scaphoid bones.

D. Degree of Immobilization:
Immobilized for vascular ingrowth and bone healing to occur.
Repeated disruptions of repair tissue, especially to areas with
marginal blood supply or heavy soft tissue damage, will impair
healing.
E. Type of Fractures:
Intraarticular fractures communicate with synovial fluid, which
contains collagenases that retard bone healing
Open fractures result in infections
Segmental fractures have disrupted blood supply.
F.Soft Tissue Interposition:
G.others: Bone death caused by radiation, thermal or chemical
burns or infection.

2.CHEMICAL FACTORS

1.MESSENGER
SUBSTANCES
-Serotonin
-Prostaglandins
Polypeptides
-Histamines
-Thromboxane

2.GROWTH 3.PERMEABILITY
FACTORS
FACTORS
-Transforming GF
-Proteases
-Fibroblast GF
- Amines
- Platelet derived GF
-BMP
-Insulin like GF

34

• 1.MESSENGER SUBSTANCE:
A.CYTOKINES-IL-1,4,6,11, macrophage and granulocyte/macrophage (GM) (CSFs) & (TNF)
stimulate bone resorption.
-IL-1 ,6 synthesis is decreased by estrogen

B. PROSTAGLANDINS of the E series-Stimulate osteoblastic bone formation and inhibit activity of isolated
osteoclasts.

C.LEUKOTRINESStimulate osteoblastic bone formation and enhance the capacity of isolated
osteoclasts to form resorption pits

2.GROWTH FACTORS:
A. Transforming growth factor(TGF):
Superfamily of growth factors (~34 members)
Act on serine/threonine kinase cell wall receptors
Promotes proliferation and differentiation of
osteoblasts, osteoclasts and chondrocytes
Stimulates both endochondral and intramembranous
bone formation and collagen type 2 synthesis.
B.Fibroblast growth factors(FGF):
Both acidic (FGF-1) and basic (FGF-2) forms
Increase proliferation of chondrocytes and osteoblasts
Enhance callus formation & stimulates angiogenesis.

C.Platelet derived growth factor(PDGF):

A dimer, genes PDGF-A and PDGF-B
Stimulates bone cell growth
Increases type I collagen synthesis by increasing the number
of osteoblasts.
PDGF-B stimulates bone resorption.
D.Insulin like growth factor(ILGF):
Two types, IGF1 &IGF2, out of which IGF1 is produced in liver
and stimulated by growth hormone.
Stimulates bone collagen & matrix synthesis and replicates
osteoblasts . It also inhibits collagen degradation.

• E.Bone Morphogenic Proteins (BMP):
BMP was discovered by Marshall Urist in 1965. They are
Osteoinductive proteins initially isolated from
demineralized bone matrix
FUNCTIONS: 1. Induce cell differentiation : BMP
3(osteogenin).
2. Promote endochondral ossification: BMP 2 & 7.
3. Regulate extracellular matrix production :BMP1.
4.Increase fusion rates in Spinal fusions): BMP 2
5.Non unions: BMP 7 as good as bone grafting
These are included in the TGF-β family except BMP 1. Must be
applied locally because of rapid systemic clearance .

3.PERMEABILITY FACTORS:
-Protease – Plasmin , Kalikrein, Globulin permeability
factor.
-Polypeptides –leucotaxime, Bradykinin, Kallidin
-Amines – Adrenalin, nor-adrenalin, Histamine
These factors work in ways that :
–
–
–
–
–
–
–

Increase capillary permeability
Alteration in diffusion mechanism in intracellular matrix
Cellular migration
Proliferation & differentiation
New blood vessel formation
Matrix synthesis
Growth & development

3.VASCULAR FACTORS
A. Metalloproteinases
Degrade cartilage and bones to allow invasion of vessels

B. Angiogenic factors:
Vascular-endothelial growth factors mediate neoangiogenesis & endothelial-cell specific mitogens
C. Angiopoietin (І & ІІ)
Regulate formation of larger vessels and branches.

4.SYSTEMIC FACTORS
A.Age:
Young patients heal rapidly and have a remarkable ability
to remodel V/S old .

B.Nutrition:
An adequate metabolic stage with sufficient
carbohydrates and protein is necessary.
C.Systemic Diseases:
And those causing an immunocompromised state will
likely delay healing. Illnesses like Marfan’s syndrome and
Ehlers-Danlos syndrome cause abnormal musculoskeletal
healing

D.HORMONES:
• Estrogen
Stimulates fracture healing through receptor mediated mechanism.

• Thyroid hormones
Thyroxine and triiodothyronine stimulate osteoclastic bone resorption.

• Glucocorticoids
Inhibit calcium absorption from the gut causing increased PTH and
therefore increased osteoclastic bone resorption.

• Parathyroid Hormone
• Growth Hormone: Mediated through IGF-1 (Somatomedin-C)
Increases callus formation and fracture strength

5.ELECTROMAGNETIC FACTORS
In vitro bone deformation produces
piezoelectric currents and streaming potentials.
Electromagnetic (EM) devices are based on
Wolff’s Law that bone responds to mechanical
stress: Exogenous EM fields may simulate
mechanical loading and stimulate bone growth
and repair

6.TREATMENT FACTORS
 APPOSITION OF FRACTURE FRAGMENTS.


LOADING AND MICROMOTION .



FRACTURE STABILIZATION.



RIGID FIXATION.



BONE GRAFTING.

RECENT ADVANCES
• GROWTH FACTOR THERAPY(3)
Due to their ability to stimulate proliferation and
differentiation of mesenchymal and osteoprogenitor cells they have
shown great promise for their ability to promote fracture repair .
•

APPLICATION OF PLATELET RICH PLASMA(4)
Injecting platelet rich plasma at fracture site helps in fracture
healing .

•

TISSUE ENGINEERING, STEM CELLS AND GENE THERAPIES(5)
In past decade tissue culture and stem cells have been
implicated in enhancing fracture healing and articular cartilage
regeneration.

• Nanotechnology(1)
based on understanding cell-implant interactions. Cells
do not interact directly with an implant but instead
interact through a layer of proteins that absorb almost
instantaneously to the implant after insertion.
Scientists have improved numerous implant
materials, including titanium and titanium
alloys, porous polymers, bone cements and
hydroxyapatite, by placing nanoscale features on their
surfaces. The bulk materials' properties remain
unchanged, maintaining their desirable mechanical
properties, but the surface changes enhance the
interactions with proteins. This causes bone-forming
cells to adhere to the implant and activates them to
grow more bone.

COMPLICATIONS OF
FRACTURE HEALING
• MALUNION
• DELAYED UNION
• NONUNION

MAL UNION
• A MALUNITED Fracture is one that has healed
with the fragments in a non anatomical
position
• CAUSES
1 INACCURATE REDUCTION
2 INEFFECTIVE IMMOBILIZATION

MALUNION can IMPAIR FUCNTION by
ABNORMAL JOINT SURFACE
ROTATION or ANGULATION
OVERRIDING
MOVEMENT OF NEIGHBOURING JOINT MAY
BE BLOCKED

CHARACTERISTICS FOR ACCEPTABILITY
OF FRACTURE REDUCTION
ALIGNMENT (MOST IMPORTANT)
 ROTATION
 RESTORATION OF NORMAL LENGTH
ACTUAL POSITION OF FRAGMENTS
(LEAST IMPORTANT)

Correction
• Operative treatment for most malunited
fracture should not be considered until 6 to 12
months but in INTRA ARTICULAR fracture early
operative treatment is needed.
• Surgeon should look for before surgery- OSTEOPOROSIS
 SOFT TISSUE
 HOW MUCH FUNCTION CAN BE GAINED

ILIZAROV TECHNIQUE is BEST
Simultaneous restoration of
ALIGNMENT
 ROTATION

LENGTH

Delayed Union
• The exact time when a given fracture should
be united cannot be defined
• Union is delayed when healing has not
advanced at the average rate for the location
and type of fracture (Btn 3-6 mths)
• Treatment usually is by an efficient cast that
allows as much function as possible can be
continued for 4 to 12 additional weeks

• If still nonunited a decision should be made to
treat the fracture as nonunion
• External ultrasound or electrical stimulation
may be considered
• Surgical treatment should be carried out to
remove interposed soft tissues and to oppose
widely separated fragments
• Iliac grafts should be used if plates and screws
are placed but grafts are not usually needed
when using intramedullary nailing, unless
reduction is done open

Nonunion
• FDA defined nonunion as “established when a
minimum of 9 months has elapsed since
fracture with no visible progressive signs of
healing for 3 months”
• Every fracture has its own timetable (ie long
bone shaft fracture 6 months, femoral neck
fracture 3 months)

Delayed/Nonunion
Factors contributing to development:
• Systemic
• Local

Systemic factors:
• Metabolic
• Nutritional status
• General health
• Activity level
• Tobacco and alcohol use

Local factors
• Open
• Infected
• Segmental (impaired blood supply)
• Comminuted
• Insecurely fixed
• Immobilized for an insufficient time
• Treated by ill-advised open reduction
• Distracted by (traction/plate and screws)
• Irradiated bone
• Delayed weight-bearing > 6 weeks
• Soft tissue injury > method of initial treatment

Nonunited fractures form two types of
pseudoarthrosis:
• Hypervascular or hypertrophic
• Avascular or atrophic

Hypervascular or
Hypertrophic:
1. Elephant foot
(hypertophic, rich in
callus)
2. Horse foot (mildly
hypertophic, poor in
callus)
3. Oligotrophic (not
hypertrophic, no callus)

Hypervascular nonunions. A, "Elephant foot"
nonunion. B, "Horse hoof" nonunion.
C, Oligotrophic nonunion (see text). (Redrawn
from Weber BG, Cech O, eds:
Pseudarthrosis, Bern, Switzerland, 1976, Hans
Huber.)

Vascular or Atrophic
• Torsion wedge
(intermediate fragment)
• Comminuted (necrotic
intermediate fragment)
• Defect (loss of fragment
of the diathesis)
• Atrophic (scar tissue with
no estrogenic potential is Avascular nonunions. A, Torsion wedge
nonunion. B, Comminuted nonunion. C, Defect
replacing the missing
nonunion. D, Atrophic nonunion (see text).
fragment)
(Redrawn from Weber BG, Cech O, eds:
Pseudarthrosis, Bern, Switzerland, 1976, Hans
Huber.)

Classification (Paley et al)
•
Type A<2cm of bone loss
A1 (Mobile deformity)
A2 (fixed deformity)
A2-1 stiff w/o
deformity
A2-2 stiff w/ fixed
deformity
•
Type B>2cm of bone loss
B1 with bony defect
B2 loss of bone length
B3 both

A, Type A nonunions (less than 1 cm of bone loss):
A1, lax (mobile); A2, stiff (nonmobile) (not shown);
A2-1, no deformity; A2-2, fixed deformity. B, Type B
nonunions (more than 1 cm of bone loss): B1, bony
defect, no shortening; B2, shortening, no bony
defect; B3, bony defect and shortening.

Treatment:
1. Electrical
2. Electromagnetic
3. Ultrasound
4. External fixation (ie deformity, infection, bone loss)
5. Surgical
•
•
•

Hypertrophic: stable fixation of fragments
Atrophic: decortications and bone grafting
According to classification:
type A : restoration of alignment, compression
type B : cortical osteotomy, bone transport or
lengthening

Surgical guidelines:
• Good reduction
• Bone grafting
• Firm stabilization

Reduction of the fragments:
• Extensive dissection is undesirable, leaving
periosteum, callus, and fibrous tissue, to
preserve vascularity and stability, resecting
only the scar tissue and the rounded ends of
the bones
• External fixator, Intramedullary nailing, Ilizarov
frame

Bone Grafting origins:
• Autogenous “the golden standard”
• Allograft
• Synthetic substitute

Bone grafting techniques:
• Onlay
• Dual onlay
• Cancellous insert
• Massive sliding graft
• Whole fibular transplant
• Vascularized free fibular graft
• Intramedullary fibular graft

CRITERTIA FOR SUCCESSFUL BONE
GRAFT
• OSTEOCONDUCTION
• OSTEOGENICITY
• OSTEOINDUCTION

Stabilization of bone fragments:
• Internal fixation (hypertrophic #):
intramedullary, or plates and screws
• External fixation(defects associated#):
ie Ilizarov

Factors complicating nonunion
• Infection
• Poor tissue quality
• Short periarticular fragments
• Significant deformity

Healing
Primary Healing
• In rigid fixation techniques
• Lag screws, compression plates, Recon
plate, external fixation, Wire
fixation, Miniplate fixation
• No callus formation
• Question of bone resorption

Secondary bone healing
• Callus formation
• Remodeling and strengthening
• MMF, Wire fixation, Miniplate fixation

Closed Reduction
• Favorable, non-displaced fractures
• Grossly comminuted fractures when
adequate stabilization unlikely
• Severely atrophic edentulous mandible
• Children with developing dentition

• Length of MMF
– De Amaratuga – 75% of children under 15
healed by 2 weeks, 75% young adults 4 wks
– Juniper and Awty – 82% had healed at 4 wks
– Longer period for edentulous fractures 610wks

Open Reduction
• Displaced unfavorable fractures
• Mandible fractures with associated midface
fractures
• When MMF contraindicated or not possible
• Patient comfort
• Facilitate return to work

Intraosseous wiring
• Semirigid fixation
• Cheap
• Technically difficult
• Primary and Secondary bone healing

Lag Screws
• Rigid fixation (Compression)
• Good for anterior mandible fractures, Oblique
body fractures, mandible angle fractures
• Cheap
• Technically difficult
• Injury to inferior alveolar neurovascular
bundle

Compression plates
• Rigid fixation
• Allow primary bone healing
• Difficult to bend
• Operator dependent
• No need for MMF

• Miniplates
– Semi Semi-rigid fixation
– Allows primary and secondary bone healing
– Easily bendable
– More forgiving
– Short period MMF Recommended

Reconstruction Plates
• Good for comminuted fractures
• Bulky, palpable
• Difficult to bend

External Fixation
• Alternative form of rigid
fixation
• Grossly comminuted
fractures,
contaminated
fractures, non-union
• Often used when all
else fails

MAXILLARY FRACTURES
• Fractures of the maxilla occur less frequently
than those of the mandible or nose due to the
strong structural support of this bone
• Reestablishing continuity of these buttresses
is the foundation on which maxillary fracture
treatment is based.

LeFort classification of midfacial
fractures.

• The Lefort I fracture, or transverse
fracture,extends through the base of the
maxillary sinuses above the teeth apices
essentially separating the alveolar
processes, palate, and pterygoid processes from
the facial structures above. This transverse
fracture across the entire lower maxilla separates
the alveolus as a mobile unit from the rest of the
midface. Fracture dislocations of segments of the
alveolus may be associated with this fracture.

• A pyramidal fracture of the maxilla is synonymous
with a LeFort II fracture. This fracture pattern
begins laterally, similar to a LeFort I, but medially
diverges in a superior direction to include part of
the medial orbit as well as the nose.
• The fracture extends diagonally from the
pterygoid plates through the maxilla to the
inferior orbital rim and up the medial wall of the
orbit to the nose. This separates the maxillary
alveolus, medial wall of the orbit and nose as a
separate piece

• A LeFort III fracture or craniofacial dysjunction
denotes a complete separation of the midface
or facial bones from the cranium. This fracture
transverses the zygomaticofrontal
suture, continues through the floor of the
orbit, and finally through the nasofrontal
suture. The bones of the orbit are separated
through the lateral wall, floor, and medial wall.

Treatment
• by reduction and immobilization
• Establishment of preinjury occlusion and midface
buttress alignment
• reestablish normal height and projection of the face
• To accomplish this, the structural buttress of the
maxilla must be aligned and stabilized to provide the
necessary support and contour to the midface.
• The proper occlusal relationship between the dental
arches is established with intermaxillary fixation
(IMF), or more appropriately termed
maxillomandibular fixation

Wound Healing
• Wound- Discontinuity of the
skin, mucous membrane or tissue
caused by physical, chemical or
biological insult
• Wound healing is a complex and dynamic process
of restoring cellular structures and tissue layers
• There are 3 distinct phases
• There are various categories of wound healing
 the ultimate outcome of any healing process is
repair of a tissue defect

• The types of wound healing:
o 1° healing
o Delayed 1° healing
o 2° healing
o (Epithelialisation)
Even though different categories exist, the
interactions of cellular and extracellular
constituents are similar.

Primary wound healing
• Also known as “healing by primary intention”
• Think of a typical surgical wound: the wound
edges are approximated
• Minimal number of cellular constituents die
• Results in a small line of scar tissue
• Minimizes the need for granulation tissue so
scarring is minimized

The importance factors for good
wound healing
•
•
•
•
•
•
•

Technique
Choice of suture
Choice of needle
Training
Instruments
Antibiotics
Aftercare

Delayed Primary healing
• Occurs if wound egdes are not approximated
immediately
• May be desired in contaminated wounds
• By day 4: phagocytosis of contaminated
tissues has occurred
Usually wound is closed surgically at this stage
If contamination is present still : chronic
inflammation ensues leading to prominent
scar eventually

Secondary Healing
• Also called healing by secondary intention
• A full thickness wound is allowed to heal by
itself: there is no approximation of wound
edges
• Large amounts of granulation tissue formed
• Wound eventually very contracted
• Takes much longer to heal

2 weeks post op – healing by 2
intention

Epithelialization
• Epithelization is the process by which
epithelial cells migrate and replicate via
mitosis and traverse the wound
• Common in the healing of ulcers and erosions
• Occurs by one of 2 mechanisms

Epithelialization: Mechanisms
• Mechanism 1
If basement membrane is intact ie some
dermis or dermal appendages remain
Epithelialization occurs by epithelial cells
migrating upwards

• Mechanism 2
Occurs in a deeper wound
A single layer of epithelial cells advance from
the wound edges to cover the wound
They then stratify so wound cover is complete

Normal Wound Healing
•
I.
II.
III.

There are 3 phases
Inflammatory phase: Days 0-4
Proliferative phase : Days 5-21
Remodelling phase: Days 22-60

•
I.
II.
III.
IV.

It can also be classified in 4 stages:
Haemostasis
Inflammation
Granulation
Remodelling

Haemostasis
•
•
o
o
o

Injury causes local bleeding
Vasoconstriction is mediated by :
Adrenaline
Thrombaxane A2
Prostaglandin 2α

• Platelets then adhere to damaged
endothelium and discharge ADP
o Which promotes thrombocyte clumping and
“dams” the wound
• Inflammation is initiated by cytokine release
from platelets

• α-granules from platelets release:
Platelet Derived Growth Factor (PDGF)
Platelet factor IV
Transforming Growth Factor β
• Thrombocyte dense bodies release:
Histamine
Serotonin

• PDGF attracts fibroblasts chemotactically
Leading to collagen deposition in later stages
of wound healing

• Fibrinogen → Fibrin
Thus providing the structural support for the
cellular components of inflammation

Inflammatory Phase
• Capillary dilatation occurs due to:
Histamine
Bradykinin
Prostaglandins
• This dilatation allows inflammatory cells to
reach the wound site

• These PMNs or leukocytes have several
functions:
• Scavenge for debris
• Debride the wound
• Help to kill bacteria by:
-oxidative burst mechanisms
-opsonisation

• Opsonin
“factor which enhances the efficiency of
phagocytosis because it is recognized by
receptors on leucocytes
2 major opsonins are:
fragment of IgG
A product of complement, C3b

• Monocytes now enter the wound and become
macrophages
• They have numerous functions
-Secretion of numerous enzymes and cytokines
 Collagenases and elastases
-To break down injured tissues
 PDGF, TGFβ, IL, TNF
-To stimulate proliferation of
fibroblasts, endothelial and smooth muscle cells

• Angiogenesis
The formation of new blood vessels
Formed by endothelial cells becoming new
capillaries within the wound bed
Angiogenesis stimulated by TNFα

Proliferative Phase
• Collagen deposition
Type III collagen is laid down by fibroblasts
Fibroblasts are attracted by TGFβ and PDGF
Total collagen content increases until day 21
• Granulation Tissue
Is the combination of collagen deposition and
angiogenesis

Granulation Tissue
• Definition:
Newly formed connective tissue, often found
at the edge or base of ulcers and wounds
made up of :
capillaries, fibroblasts, myofibroblasts, and
inflammatory cells embedded in a mucin rich
ground substance during healing

Occasionally overgranulation can occur (as above following a
flexor tendon repair)
Treatment is steroid topical cream (1% hydrocortisone cream)

• Re-epithelialization occurs next:
By upward migration of epithelial cells if BM is
intact
Or from wound edges

Remodelling Phase
• Fibroblasts become myofibroblasts
And wound begins to contract
Can contract 0.75mm per day
Can over contract however
Contraction allows wound to become smaller
A large wound can contract by up to 40-80%

• Type III collagen is degraded
 And replaced with Type I
• Water is removed from the scar, allowing collagen
to cross-link
• Wound vascularity decreases
• Collagen cross linkage allows:
 Increased scar strength
 Scar contracture
 Decreased scar thickness

Wound Strength
• During phase 1 and 2 (inflammatory and
proliferative phases)
Wounds have very little strength
• During remodelling:
Wounds rapidly gain strength
o @ 6 weeks: wound is 50% of final strength
o @12 months: wound is maximal strength: but
this is only 75% of pre-injury tissue strength

Abnormal Scars
• Hypertrophic Scars
• Keloid Scars

Hypertrophic Scars
•
•
•
•
•
•

Raised, red and thickened
Limited to boundaries of scar
Occurs shortly after injury
Common on anterior chest and deltoids
Regresses over time
Related to wound tension and prolonged
inflammatory phase of healing

• Treatment:
Surgical excision
Intralesional Triamcenelone acetate injection

Keloid Scars
•
•
•
•
•
•
•
•
•

Raised, red and thickened scar
Extends beyond original scar boundary
Occurs months after injury
Does not regress
Commoner in darker skinned people
Familial tendency
Autoimmune phenomenon
Worsened by surgery and in pregnancy
Regresses post menopause

• Treatment:
Surgical excision : caveat- recurrence = 65%
Compression treatment
CO2 lasers
Cryotherapy

Factors influencing scarring
• These can be broken down into:
i. Patient factors
ii. Surgical factors

Patient Factors
• Age
Elderly scar well
• Skin type
Celtics : hypertrophic scar tendency
Dark skinned: keloid scars

• Anatomic region
Midline
Deltoid region
Sternotomy
• Patient morbidity
Nutritional state
Diabetes
Wound infections

• Local tissue
Oedema
Previous radiotherapy
Vascular insufficiency

Surgical factors
• Atraumatic skin handling
• Eversion of wound edges
Inversion places keratinised epidermis
between the healing surfaces = delayed
healing
• Tension free closure
• Clean and healthy wound edges

• Scar orientation
Parallel to lines of relaxed skin tension
Langers lines
• Suture tension
Over-tight: pressure necrosis
Under-tight: wound gaping and widened scar

Acute Inflammation
•
o
o
o

Definition
The cellular and vascular response to injury
Short in duration
Has cellular and chemical components

Acute Inflammation: Causes
• Injury by:
o Pathogens
 Bacteria, viruses, parasites
o Chemical agents
 Acids, alkalis
o Physical agents
 Heat, trauma (surgery), radiation
o Tissue death
 Infarction

Stages of Acute Inflammation
• Dilatation of local capillaries
• ⁭ endothelial permeability
• Leakage of protein-rich fluid into interstitial
space – including fibrinogen
• Fibrinogen → fibrin
• Margination of leukocytes to peripheries of
capillaries
Mostly neutrophils

Stages of Acute Inflammation
• Acute Inflammation is mediated by:
Chemicals: interleukins and histamine
Proteins: complement cascade

Complement Cascade
•
•


I.
II.


Component of innate immune system
Cascade of proteins
Resulting in formation of MembraneAttack-Complex (MAC) which can
Destroy invading bacteria
Recruit other cells ie neutrophils
Can also act as opsonins: enhancing
phagocytosis

Complement Cascade
•
I.
II.

2 main activating arms of CC:
Classic pathway: consists of antigenantibody complexes
Alternative pathway: activated directly by
contact with micro-organisms

Chronic Inflammation
•
o
o
o

Definition
Tissue response to persistent injury
Long in duration
Cellular components differ from acute
inflammation

• Causes
Foreign bodies: ie sutures
Bacteria: ie TB
Chronic abscess: ie osteomyelitis
Transplant: ie chronic rejection
IBD
Progression from AI

• Key points
Histological pattern not as predictable as
acute inflammation
There may be areas of acute inflammation
occurring simultaneously
Granulation tissue and fibrosis may both be
present: indicating the tissues attempts at
repair

Lymphocytes predominate
Macrophages present too
• In granulomatous inflammation they fuse
forming multinucleate Langhans giant cells
Plasma cells are also present

• Macrophages
Derived from monocytes
Phagocytosis and killing of pathogens by
lysosomes
Langhans giant cell formation

Chronic Inflammation: Effects
•
•
•
•

Secondary infection ie chronic epithelial injury
Scarring
Resolution: restoration of normality
Local lymphadenopathy

The Surgical Wound
• It is often said that it is “controlled trauma”
Carried out in a sterile environment
Under aseptic conditions

• Many protocols are put in place to prevent
infections in surgical wounds
o Hand washing
o Gowns and gloves
o Painting and draping
o Drains
o Antibiotics
o Laminar flow theatres
o Sterile instruments
o Sterile dressings

Surgery
• But wound infections can occur despite these
measures causing:
• Death
• Morbidity
• Longer hospital stays
• Cosmetically displeasing wounds

Operation Types
• The risk of a wound infection depends on the
operation
• For that reason, operations are classified into
distinct types
o Clean
o Clean-Contaminated
o Contaminated
o Dirty

Class I :Clean wounds
•
•
•
•

Elective operations (non emergency)
Non traumatic injury
Good surgical technique
Respiratory, gastrointestinal, biliary and
genitourinary tracts not breached
• Risk of infection < 2%
• Eg: mastectomy, hernia repair

Class II: Clean - Contaminated
• Urgent or emergency case that is otherwise
clean
• GI, GU or respiratory tracts entered
electively, no spillage or unusual
contamination
• Minor break in sterile technique occurred
• Endogenous flora involved
• Risk of infection: <10 %
• Eg: appendicectomy, bowel resection

Class III: Contaminated
• Non-purulent inflammation
• Gross spillage from GIT, entry into GU or biliary
tract in the presence of infected bile/urine.
• Major break in technique
• Penetrating trauma < 4hrs old
• Chronic open wounds
• Risk of infection: 20%
• Eg: GSW, rectal surgery

Class IV : Dirty
• Purulent inflammation (abscess)
• Pre-operative perforation of GI, GU, biliary or
respiratory tract
• Penetrating trauma > 4 hrs
• Existing acute bacterial infection or a
perforated viscera is encountered (clean tissue
is transected to gain access to pus).
• Risk of infection: 40%

Signs of Infection
• The cardinal points of acute inflammation
I. Calor
II. Rubor
III. Dolor
IV. Tumour
V. Functio Laesa

Signs of Infection
• Patient may be systemically unwell
↑ Temp
Tachycardic
Hypotension
Wound breakdown
Wound discharge
Warm peripheries
Septic shock

Prevention
•
•
•
•
•
•
•

Aseptic technique
Good technique
Prophylactic antibiotics where appropriate
Microbiology input
Clean operating theatre
Elective surgery
Good post op care

Conclusion
• Fracture and wound healing is influenced by
many variables including mechanical
stability, electrical environment, biochemical
factors and blood flow etc…
• Our ability to enhance fracture and wound
healing will increase as we better understand
the interaction between these variables.

References
1.

Opportunities for nanotechnology-enabled bioactive bone implants
Phong A. Tran, Love Sarin, Robert H. Hurt and Thomas J. Webster, J. Mater.
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9.Müller ME, Nazarian S, Koch P, et al (1990) The Comprehensive Classification of
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11. FUNDAMENTAL OF PEDIATRIC ORTHOPAEDICS By Lynn T. Stahel
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15. Treatment of Mandible Fractures using Bioabsorbable plates”, Plastic and
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16. Ellis, E. “Treatment Methods for Fractures of the Mandibular Angle." Journal of
CraniomaxillofacialTrauma, vol. 28. 1999: 243-252
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20. Oral and maxillofacial surgery, daniel m
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