WOUND HEALING

IKEM O.M.

OUTLINE
INTRODUCTION
CAUSES OF TISSUE DAMAGE
TYPES OF WOUNDS
STAGES OF WOUND HEALING
TYPES OF WOUND HEALING
SURGICAL SIGNIFICANCE OF WOUND HEALING
FACTORS AFFECTING WOUND HEALING
COMPLICATIONS OF WOUND HEALING
CONCLUSION
REFERENCES

INTRODUCTION
A wound is defined as a breakdown in the
protective function of the skin; the loss of
continuity of epithelium, with or without loss of
underlying connective tissue as a result of
trauma, infection or pathological process (Leaper
& Harding, 1998) ulcer
Wound healing is a complex sequence of
overlapping events which are often described
separately for ease of explanation but in reality
form a continuum often referred to as the healing
cascade (Diegelmann and Evans,2004).

CAUSES OF TISSUE DAMAGE

Mechanical Agents
Chemical Agents
Radiant Energy
Pathogenic Micro-Organisms

CLASSIFICATION OF TYPES OF
WOUND
Based on the duration
Based on breach of the epithelium
Based on hygiene

BASED ON DURATION
ACUTE

An acute wound is one

that proceeds through
an orderly and timely
reparative process to
establish sustained
anatomic and
functional integrity

A chronic wound is one

CHRONIC
that has failed to proceed
through an orderly and
timely reparative process
to produce anatomic and
functional integrity or has
proceeded through the
repair process without
establishing a sustained
anatomic and functional

BASED ON BREACH OF EPITHELIUM

CLOSED- Contusion/Bruise
OPEN- Abrasion
Incision
Laceration
Puncture/Penetrating/Peforating
Avulsion
Amputation

Illustration showing closed wounds

Illustration showing types of open wounds

STAGES OF WOUND HEALING

Consist of 3 highly integrated and overlapping
phases:
Inflammatory
Proliferative or Fibroblastic
Maturation or Remodelling
These phases and their physiological functions
must occur in the proper sequence, at a specific
time and duration at an optimal intensity

INFLAMMATORY PHASE
Characterized by haemostasis and inflammation.
Collagen exposed as a result of the wound
activates the clotting cascade, initiating the
inflammatory phase.
The exposed cell membranes release
thromboxane A2 & prostaglandin 2- which are
potent vasoconstrictors.
The clot that forms is made of collagen, platelets,
thrombin, and fibronectin, and these factors
release cytokines and growth factors that initiate
the inflammatory response.

INFLAMMATORY PHASE
Chemotaxis and Activation
Immediately after the clot is formed, a cellular
distress signal is sent out and neutrophils are the
first responders.
Inflammatory mediators and prostaglandins
cause vasodilation to allow invasion of
neutrophils (chemotaxis) by Interleukin (IL)-1,
Tumor Necrosis Factor (TNF-), Transforming
Growth Factor (TGF-), Platelet Factor-4 (PF4),
and bacterial products.
Monocytes in the nearby tissue and in the blood
will be attracted and transform into macrophages,

INFLAMMATORY PHASE
Neutrophils aid in clearing the wound of invading
bacteria and cellular debris by release of
proteolytic enzymes that will digest bacteria and
nonviable tissue.
Numerous enzymes and cytokines are secreted
by the macrophage, including collagenases,
which debride the wound; Interleukins and TNF, which stimulate fibroblasts and promote
angiogenesis; and TGF, which stimulates
keratinocytes

PROLIFERATIVE/FIBROBLASTIC PHASE
(4-14Days)

Epithelialization, angiogenesis, granulation tissue

formation, and collagen deposition are the
principal steps in this phase.
The stimulus for epithelial proliferation and
chemotaxis is epidermal growth factor (EGF) and
TGF- produced by activated platelets and
macrophages.
IL-1 and TNF- upregulate the expression of
keratinocyte growth factor (KGF) gene in
fibroblasts leading to synthesis and secretion of
KGF-1, KGF-2, and IL-6, which simulate
neighbouring keratinocytes to migrate in the

PROLIFERATIVE/FIBROBLASTIC PHASE
(4-14Days)
Angiogenesis, stimulated by TNF-, is marked by
endothelial cell migration and capillary
formation. The migration of capillaries into the
wound bed is critical for proper wound healing.
Fibroblasts migrate into the wound site from the
surrounding tissue, become activated, and begin
synthesizing collagen and proliferate.
Platelet-derived growth factor (PDGF) and EGF
are the main signals to fibroblasts and are
derived from platelets and macrophages.

PROLIFERATIVE/FIBROBLASTIC PHASE
(4-14Days)
Fibroblasts already located in the wound site will
begin synthesizing collagen and transform into
myofibroblasts for wound contraction (induced by
macrophage-secreted TGF-); they have less
proliferation compared with the fibroblasts coming
in from the wound periphery.
In response to PDGF, fibroblasts begin synthesizing
a provisional matrix composed of collagen type III,
glycosaminoglycans, and fibronectin.1

MATURATION/REMODELLING STAGE
(Day8-1Yr)
The main feature of this phase is the
deposition of collagen in an organized and
well-mannered network.
Collagen synthesis will continue for at least 4
to 5 weeks after wounding.
The collagen that is initially laid down is
thinner than collagen in uninjured skin and is
orientated parallel to the skin.
Over time, the initial collagen threads are
reabsorbed and deposited thicker and
organized along the stress lines.

MATURATION/REMODELLING STAGE
(Day8-1Yr)
The collagen found in granulation tissue is

biochemically different from collagen from

uninjured skin.
Granulation tissue collagen has a greater
hydroxylation and glycosylation of lysine
residues, and this increase of glycosylation
correlates with the thinner fibre size.
The collagen in the scar (even after a year of
maturing) will never become as organized the
collagen found in uninjured skin. Wound strength
also never returns to 100 percent. At 1 week, the
wound has only 3 percent of its final strength; at

SUMMARY OF WOUND HEALING

TYPES OF WOUND HEALING

HEALING BY PRIMARY INTENTION (PRIMARY
CLOSURE)
Describes the process of wound closure within hours of
injury and is possible where the wound edges remain in
proximity to each other and there is little or no tissue loss
or damage.
HEALING BY SECONDARY INTENTION (SECONDARY
CLOSURE)
A process were healing takes place by contraction and
reepithelialisation as a result of more extensive tissue loss

TYPES OF WOUND HEALING

DELAYED PRIMARY WOUND CLOSURE
(TERTIARY INTENTION)
Wound closure occurs when wound closure is
delayed for 36 days due to adverse local
conditions such as poor vascularity, uncontrolled
bleeding or risk of infection (Gottrup, 1999).
Once conditions improve, wounds are closed.
Delayed primary closure is therefore a
compromise between immediate primary closure
and allowing local wound conditions to improve

BONE HEALING
Osteoblasts and osteoclasts are involved in the
reconstitution and remodeling of bone
Osteoblasts are derived from periosteum,
endosteum and circulating pluripotent
mesenchymal cells
Osteoclasts are derived from monocytes.
In the repair of bone, the phenomena of
haematoma formation, absorption of debris and
structural tissue production proceed with the
modification that osteoblasts, take the place of
the fibroblasts and lay down matrix which calcify
.

SURGICAL SIGNIFICANCE OF
WOUND HEALING
The surgeon can create conditions that augment or
impede the natural wound healing process.
Adherence to surgical principles facilitate optimal
wound healing, with re establishment of tissue
continuity minimization of scar size and restoration of
function.
The surgeons goal with respect to scar formation is
not to prevent a scar, but to produce a scar that
minimizes any compromise of function and looks as
inconspicuous as possible

FACTORS AFFECTING WOUND

HEALING
LOCAL
Ischaemia
Infection
Foreign body
Surgical Technique
Immobilization and Trauma

FACTORS AFFECTING WOUND

HEALING
Severe Constitutional
SYSTEMIC
Diseases-Diabetes
Mellitus, Chronic
Nephritis , Congestive
Cardiac Failure ,
Chronic Liver Disease
and Syphilitic lesions,
Cancer
Hormones
Age

Nutritional FactorsVitamins A&C, Protein

Deficiency:(Arginine &
Glutamine), Trace Elements
Deficiencies: Zinc
deficiency
Cytotoxic agents

Smoking

COMPLICATIONS OF WOUND
HEALING
Infection
Keloid formation
Hyperpigmentation
Implantation cysts
Neoplasia
Weak scars
Cicatrization

CONCLUSION
Wound healing is a complex process performed by
cells that are programmed to achieve wound closure.
Although the process of wound healing appears to be
simple, advances in molecular science have provided
a greater understanding of the complex interactions
involved.
Understanding of these dynamic physiological
processes improves treatment outcome and better
patient care.

REFERENCES
Badoe et al, Principles and practice of surgery including
pathology in the tropics: wound and wound healing. Pages
57-66, 2009.
George Broughton II, Jeffrey E. Janis, Christopher E. Attinger.
Wound Healing: An Overview. (Plast. Reconstr. Surg. 117: 1eS, 2006.)
Leaper DJ and Harding KG. Wounds: Biology and
Management. Oxford University Press. 1998
Madeleine Flanagan, Wound Healing and Skin Integrity
principles and practices: physiology of wound healing. Pages
33-49, Wiley Blackwell 2009