Wounds

&
Wound Healing
Prepared by:
Dr. Sarmad M. Mohammad
1st year PG senior house officer
Oral & maxillofacial department
The skin

• Epidermis
▫ Keratin layer
• Dermis
▫ Support
▫ Nutrition
▫ Nerves

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What are Wounds?

• A defect or breach in the continuity of the skin.
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Aetiology of Wounds
•
• • Trauma
• • Infection
•
• Vascular
•
• • Thermal
• Chemical
• Radiation
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Wound Pathology
•
• Ischemia
•
• • Venous stasis
• • Oedema
• • Neuropathic
•
• Infection (systemic)
•
• Malignancy
•
• Connective tissue disorders
• Blood dyscrasias
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Physiology of wounds
• Traumatic
(Intentional)

• Ischemic
(pressure wounds)
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Classification of wounds
• Clean

• Contaminated

• Infectious
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Wound Types
•
• Puncture
•
• • Surgical
• • Laceration
• • Ulceration
•
• Burn
•
• Contusion (bruise)
•
• Avulsion
• Abrasion
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Lacerated Wound
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Abrasion Wound
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Burn Wound
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Ulceration wound
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Puncture Wound
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Surgical Wound
 Wound & WoundHealing
By Dr. Sarmad
M.Mohammad

Different Tissues have Different Capacities

to Heal
Regenerative capacity varies:
High capacity
▫ epithelial, lymphoid, hematopoietic, mesenchymal
tissues (cell types include fibroblasts, smooth
muscle cells, osteoblasts, chrondrocytes, and
endothelial cells)
▫ Highly vascularized
Low capacity
▫ Nerve, muscle (skeletal and cardiac), cartilage
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Wound Healing
is the effort of injured tissues to restore their normal
function and structural integrity after injury.
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Introduction

• Following injury, wounds progress through a series of stages.

Many of these stages may be occurring in different areas of the
wound at the same time.
• The stages are:
• • Vascular response (Haemostasis)
• Inflammation
• Proliferation
- Angiogenesis
- Granulation
• Contraction
• Epithelialisation
• Maturation
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Vascular Response

• Haemostasis is achieved by clotting at the wound surface.

• • Platelets contact molecules from damaged endothelium such as
collagen and fibronectin.
• The platelets stick to the endothelium and flatten out in matter of
seconds, increasing their surface area.
• The platelets release factors (ADP) to produce thrombin and cause
further platelet aggregation.
• The thrombin activates fibrinogen to fibrin and with tissue factors
from the clotting cascade create irreversible links between platelets.
• A platelet/fibrin plug is formed.
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Inflammatory Stage
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Inflammation

• Vasodilatation and increased vascular permeability is

initiated by factors and serum proteins from the
clotting and complement cascades.
• The platelets release growth factors and chemical
attractants into the wound site.
• This enables more cells to move through the
endothelium .
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Inflammation continued...

• Immune cells migrate into the wound through

the endothelium.
• Neutrophils (leukocytes) engulf bacteria through
phagocytosis and produce chemotactic molecules and growth
factors.
• Macrophages phagocytise bacteria and damaged tissue and
produce chemotactic molecules and growth factors.
• Lymphocytes produce antibodies (B cells) and mediate the
bodies response to viruses, fungus and foreign material (T cells).
• The growth factors (cytokines) cause inflammation –
redness, swelling, heat and pain.
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Proliferative Stage
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Proliferation M.Mohammad

- Angiogenesis and Granulation

• Fibroblasts migrate into the wound and divide in response to macrophage Platelet
Derived Growth Factor (PDGF).

• New extra cellular matrix (ECM) is formed by fibroblasts.

• ECM comprises collagen, elastin, glycoproteins, proteoglycans and

glygosaminoglycans

• Collagenase (a Matrix Metaloprotease) is produced by fibroblasts to remodel

ECM

• The new ECM forms a scaffold into which capillaries can grow. The new
capillary growth is stimulated by growth factors (19 known growth factors) from
macrophages, fibroblasts, neutrophils, mast cells, keratinocytes and platelets.
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Proliferation continued...
- Angiogenesis and Granulation

• Blood vessels may be new extensions to existing vessels.

• The capillaries form loops in the naïve tissue which have
a red/pink granular appearance – granulation tissue.
• The granulation tissue produces increased exudates from
the wound bed.
• The granulation tissue must form a flat bed and fill the
wound to enable epithelialisation.
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Contract Contraction
• .

• Specialised fibroblasts (myofibroblasts) draw the

edges of the wound
• together allowing wound
contraction.
• Contraction reduces the size of the wound reducing
the potential for infection and helping to bring
damaged tissue together
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Epithelialisation
Epithelialisation
•
• Epithelial cells (keratinocytes) migrate across the wound bed
•
from the wound edge.
•
• The peri-wound surface is extremely fragile.
•
• The keratinocytes divide and form layers or strata.
• Once the stratified layer is complete, the keratinocytes undergo
a morphological change
• to become the epidermis, the normal
barrier layer of the skin.
• The new tissue continues to be remodelled. Numbers of
fibroblasts fall and capillary bundles become organised.
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MaturationMaturation
•
• Remodelling of tissue continues for months or up to 2
•
years.
• Collagen fibres •are reorganised to increase tensile strength.
• The type of collagen
•
produce changes ( type III to type I).
• The scar initially has about 5% of the tissue’s pre-injury
strength. The scar may mature to 80% of its original
strength.
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Primary Intention
PrimaryHealing
Intention
Healing
• Wounds healing by primary intention have minimal loss
•
of tissue and apposing edges to the wound.
•
• These wounds occur following injury or an operation.
• Edges of the wound
• are brought together (approximation)
by suturing or application of adhesive strips.
•
• The wound surface normally forms initial closure within
24 to 48 hours. •
• Primary intention healing can lead to linear scarring.
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Secondary Secondary Intention

Intention Healing
Healing
• Wounds healing by secondary intention have some
loss of tissue at the wound
• site.
• These wounds occur following injury or an operation
•
where tissue is excised.
• The wound is left open
• to allow exudates to drain,
removing bacteria and proteases that slow wound healing.
•
• Necrotic tissue must be debrided.
•
• The wound base is treated to encourage granulation tissue to provide a base to
support re-growth of epithelium.
• Skin grafting may be •applicable when granulation
tissue has formed.
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TertiaryHealing
Tertiary Intention Intention
Healing
• Wounds healing by tertiary intention have gross loss of
•
tissue at the wound site.
•
• These wounds occur following injury or an operation where
tissue is excised and foreign material or infection is present.
•
• Necrotic tissue must be debrided. Often revision surgery to
remove dead tissue
• is necessary.
• The wound is kept open to allow exudates to drain,
preventing the spread of deep infection and aiding
granulation.
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TertiaryHealing
Tertiary Intention Intention continued...
Healing continued...
• The wound base is treated to encourage granulation
•
tissue growth.
•
• The edges of the wound will begin to contract aiding
•
closure.
• When foreign material has been removed, necrotic
tissue debrided and infection is no longer present, the
wound edges are brought together to achieve closure
(delayed primary closure).
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Wound Strength
Tensile strength of a wound is related to the deposition of
collagen in the short term and the remodeling of collagen
over an extended recovery period.
Remodeling(degradation & redeposition) results in
alignment of fibers along lines of tension and fiber cross
linking, tensile strength rarely (if ever) returns to pre-
injury levels.
1 week after a clean wound (when the stitches are
removed) wound strength is ~10% of uninjured tissue,
by 3 months deposition and remodeling result in ~70-
80% strength.
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Optimum Healing Environment

• Moist wound surface
• Oxygen & perfusion
• Wound interface temperature….37*C
• pH of wound interface…dressings which reduce
the pH may help to prevent infection &
positively affect healing
• Nutrition…glucose (post trauma), protein,
vitamins ACE &K, zinc, iron & copper.
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Factors affecting healing

M.Mohammad

Systemic Local
•      Age • Mechanical injury
•    Nutrition •    Infection
•    Trauma •    Edema
•    Metabolic diseases •    Ischemia/necrotic tissue
•    Immunosuppression •    Topical agents
•    Connective tissue disorders •    Ionizing radiation
•    Smoking •    Low oxygen tension
•    Foreign bodies
Complications of Cutaneous Wound Healing
There are 3 general
categories
1. Inadequate formation of
granulation tissue or
assembly of scar resulting
in:
▫ Wound dehiscence, most
common in wounds under
mechanical tension
▫ Ulceration, most often due
to inadequate
vascularization
(atherosclerotic peripheral
vascular disease, diabetes).

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 Complications of Cutaneous Wound Healing
2. Excessive formation of repair
components:
▫ Hypertrophic scar, the excess
accumulation of collagen, if this
accumulation extends beyond the
boundary of the original wound it
is a keloid.
▫ Exuberant granulation tissue
protrudes above the level of the
surrounding epithelium impairing
re-epithelialization.
▫ Desmoids (aggressive
fibromatosis) a proliferation of
fibroblast in incisional scars or
traumatic injuries that acquire
some neoplastic characteristics.

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Complications of Cutaneous Wound Healing
3. Formation of
contractures:
▫ An exaggeration of wound
contraction this results in
tissue deformities, they
are prone to formation on
the palms, soles and
anterior thorax. They are
commonly associated
with burns and can
severely compromise
joint ROM. The etiology
is related to impaired
collagen remodeling

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 Fibrosis
This process of excess connective
tissue (scar) formation is usually a
component of a process (hepatic
cirrhosis, inhalation
pneumoconiosis, chronic
pancreatitis, etc.). In contrast to
orderly wound healing where
deposition is self-limited,
persistence of the inflammatory
signal results in WBC interactions
that sustain the synthesis and
secretion of growth factors and
fibrogenic cytokines, proteolytic
enzymes and other biologically
active molecules. A common cause
of delayed fibrosis is ionizing
radiation in cancer treatment.
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Types of Dressing
M.Mohammad

• Absorbent Dressings
• Nonadherent Dressings
• Occlusive and Semiocclusive Dressings
• Hydrophilic and Hydrophobic Dressings
• Hydrocolloid and Hydrogel Dressings
• Alginates
• Absorbable Materials
• Medicated Dressings
• Mechanical Devices
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Negative Pressure–Assisted
Wound Closure
• The exact mechanism of the improvement in has yet to be
determined.
• Many authors initially believed that the is:
-Removal of wound exudates
-Keeping the wound moist.
-There is a fivefold increase in blood flow to cutaneous tissues.
-An increase in capillary caliber
-Stimulated endothelial proliferation and angiogenesis.
• Interestingly, increased bacterial loads result in slowed wound
healing; however, with negative-pressure therapy, has shown to
result in increased bacterial counts.
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Bone Healing
• Bone healing after a fracture has many features
similar to skin healing except that it also
involves calcification of the connective tissue
matrix.
• Bone heals by regeneration rather than repair.
• Fractured bone is capable of restoring itself
spontaneously through sequential tissue
formation and differentiation (indirect healing).
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Bone Healing continue……

• As in skin the interfragmentary thrombus that forms
shortly after injury staunches bleeding from ruptured
vessels in the haversian canals, marrow, and periosteum.
Necrotic material at the fracture site elicits an immediate
and intense acute inflammatory response which attracts the
polymorphonuclear leukocytes and subsequently
macrophages to the fracture site. The organizing hematoma
serves as a fibrin scaffold over which reparative cells can
migrate and perform their function. Invading inflammatory
cells and the succeeding pluripotential mesenchymal cells
begin to rapidly produce a soft fracture callus that fills up
interfragmentary gaps.
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Summary of Wound Healing

1. Initially there is a variable inflammatory response
2. This is followed by the formation of granulation tissue
3. Followed by tissue remodeling and scar formation
4. Differing mechanisms at different times triggers the
release of signals that modulate the migration,
proliferation and differentiation of cells and
remodeling of ECM contents.
5. These signals also set in motion the processes
involved in terminating the reparative process.
6. A number of systemic & local factors influence this
process.