Soft tissue Wound healing

CONTENTS
Introduction
Wound
Classification of soft tissue wounds
Healing

Regeneration

Repair
Healing by first intention
Healing by second intention
Factors influencing wound healing
Complications of wound healing
Conclusion

INTORDUCTION
Medicine arouse out of the primary sympathy of Man
with Man, out of his desire to help those in sorrow,
disease and suffering.
Wound, a breach in the surface of the body, can be
caused by accident, assault, warfare & surgical
operations. The healing of such wounds has
always been central consideration in surgical
practice.

So, understanding of the various mechanism of

healing and factors affecting it is of Prime
importance for successful practice.

IF EVERY CELL REGENERATES

NO DEATH
LOST CELLS NOT REPLACED
NO LIFE
ALL ORGANISMS LIFE LIES
BETWEEN THESE TWO EXTREMITIES

INVERTIBRATES AND AMPHIBIANS

LOBSTERS REGROWS LOST
CLAWS
SALAMANDERS DEVELOPS NEW
LENS
NEWTS REPLACE LOST
EXTREMETIES
IN MAMMALS, GRANULATION
TISSUE
REPLACES LOST TISSUE

Tissue Destruction

Cell Death

Disruption of the normal

continuity of structures

A) Based on Tissue integrity

Open

Wound involving a break in skin Trauma by sharp object or blow

(surgical
incision,
gunshot
or mucous membranes
wound)
Part of body being struck by
Closed
Wound involving no break in blunt object (bone fracture,
tear of visceral organ)
skin

B) Causes of injury
Intentional:
Wound resulting from
therapy

Surgical incision

Unintentional:
Wound that occurs
unexpectedly

Traumatic
accident,

injury,

C) Severity of injury
Superficial:
Wound
that
involves
epidermal layer of skin

only

Penetrating

Wound involving break in epidermal

skin layer, as well as dermis and
deeper tissues or organs

Perforating

Penetrating wound in which

foreign object enters and exits
an internal

abrasion, first-degree burn,

shearing
Foreign object or instrument
entering deep into body tissues
(gunshot wound, stab wound)
(same as above entry)

D) Duration
Acute:
Short duration

Chronic:
Long duration

Trauma from a sharp object

Ulcers exposed to friction,

shear, moisture, pressure

E) Descriptive qualities:
Laceration:
Tearing of tissues with irregular
wound edges

Abrasion

Severe traumatic injury (knife

wound,
industrial
accident
involving machinery, tissues cut
by broken glass)

Wound often resulting from fall;

Superficial wound involving scraping or
wound
also
resulting
from
rubbing of skins surface
dermatological
procedure
for
removing scar tissue

Contusion

Bleeding in underlying tissues

Closed wound caused by a blow to
caused by blunt force against
body by blunt object; contusion or
body part
bruise characterized by swelling,
discoloration, and pain

F) Cleanliness
Clean:(<5%

infected)

Wound containing no pathogenic organisms

Clean-contaminated

Closed surgical wound

(2-10%

infected):
Wound made under aseptic conditions, but
Surgical wound
normally harbors microorganisms is likely
Contaminated (15-20% infected) Open, traumatic, accidental wounds;
surgical wound in which break in
Wound existing under conditions in which \
asepsis occurred
presence of microorganisms is likely
Any wound that does not properly heal
Infected (>30% infected)
and grows organisms, old traumatic
Bacterial organisms present in wound site,
wound, surgical incision into area
usually above 105 organisms per gram of
infected.
tissue
Chronic wound (vascular stasis ulcer,
Colonized
pressure ulcer)
Wound containing multiple microorganisms
(usually)

 Is the process in which body responds

to injury and attempts to restore
normal structure and function

Wound healing is a symphony of

biological process .

Healing involves two

process
Regeneration
Repair

REGENERATION
Definition : means proliferation of the
parenchymal cells resulting in
complete restoration of the original
tissues
It requires cell proliferation which is
largely regulated by micro
environment that can either
stimulate or inhibit cell growth

cell proliferation depends on the cell growth cycle

Which consists of
4 unequal phases.
1. G1 (pre synthetic) phase
2. S (DNA synthesis) phase +
3. G2 (pre mitotic) phase
4. M (mitotic) phase
quiescent or resting cells will be in a physiologic
state called G0.

Cells are usually classified into

three groups depending on
their capacity for regeneration.

Labile cells
Stable cells
Permanent cells

LABILE CELLS
- Also called continuously dividing cells
- Follow the cell cycle from one mitosis to
other
- Continue to proliferate throughout life,
replacing tissues that are continuously
destroyed
- E.g.

Stable cells
Also called
quiescent cells
However these cells
can undergo rapid
division in response
to a variety of
stimuli and capable
of reconstituting
the tissue of origin
E.g.

Permanent cells
- Also called non
dividing cells
- Have left the cell
cycle and cannot
undergo mitotic
division in post
natal life
- E.g.

Control of cell growth

cell growth is controlled largely by chemical
factors in the environment which either
stimulate or inhibits cell proliferation.
Although many chemical substances can
affect cell growth the most important are
polypeptide growth factors present in the
serum or produced by the cells.

Growth Factors involved

in Wound Healing
Molecule

Source

Action

Basic Fibroblast
Growth factor
(FGF)

Keratinocytes,
Macrophages

Stimulates
angiogenesis

Salivary gland

Stimulates
epidermal cell
proliferation

Platelets,
Endothelium

Stimulates
epidermal
hyperplasia in
combination with
EGF

Epidermal
Growth Factor
(EGF)
Platelet-Derived
Growth Factor
(PDGF)

Molecular events in cell

growth
Polypeptide growth factors bind to their
receptors and activates them
This activation posphorylates several
substrates that are involved in the
generation of second messengers
These intern transmit the signal to the
nucleus where activation of the
transcription factors leads to the
initiation of DNA synthesis and
ultimately cell division

In general
Regeneration of parenchymal cells
INVOLVES ..
1)Proliferation of original cells from the
margin of injury so as to cover the gap.
2)Proliferation of migrated cells with
subsequent differentiation and
maturation so as to reconstitute the
original tissue.

REPAIR
IS THE REPLACEMENT OF INJURED
TISSUE BY FIBROUS TISSUE.
PROCESSES INVOLVED INREPAIR:
1.GRANULATION TISSUE FORMATION
2. CONTRACTION OF WOUNDS

Granulation tissue formation

The term derives its name from slightly granular
and pink appearance of the tissue. Each granule
corresponds histologically to proliferation of new
small blood vessels which are slightly lifted on
the surface by thin covering of fibroblasts and
young collagen.
3 phases are observed in the formation of
granulation tissue
1. PHASE OF INFLAMMATION.
2. PHASE OF CLEARENCE
3. PHASE OF INGROWTH OF GRANULATIN TISSUE.

1.PHASE OF INFLAMMATION
After trauma blood clot occurs at the site
of injury. There is acute inflammatory
response with exudation of neutrophils
plasma cells and some monocytes within
24 hours.

2.PHASE OF CLEARANCE
Combination of the proteolytic
enzymes liberated from neutrophils,
autolytic enzymes from dead tissue
cells and phagocytic activity of
macrophages clear off the necrotic
tissue debris and red blood cells.

PHASE OF INGROWTH OF
GRANULATIN TISSUE
This phase consists of two main
processes :
1. Angiogenesis or neovascularization
2. Formation of fibrous tissue.

Angiogenesis or
neovascularization
- Formation of new blood vessel at the site of
injury.
- Takes place by proliferation of endothelial cells
from the margin of the severed blood vessel.
- Newly formed blood vessels are leaky,
accounting for the edematous appearance of
new granulation tissue.
- Soon, these blood vessels differentiate in to
muscular arterioles, thin walled venules and
true capillaries.

1) Pre-existing vessel

2) Mobilization of EPCs from

bone marrow

FACTORS INFLUENCING

FIBROUS TISSUE
FORMATION
Newly formed blood vessels are in amorphous
ground substance or matrix
The new fibroblasts originate from fibrocytes as
well as by mitotic division of fibroblasts
Some of the fibroblasts have morphogenic and
functional characteristic of smooth muscle cells
Collagen fibrils begin to appear about 6th day as
maturation proceeds more and more collagen is
formed while the number of active fibroblasts
and new blood vessel decreases
This results in formation of inactive looking scar
known as cicatrisation

CONTRACTION OF WOUNDS
Wound starts contracting after 2-3 days
of collagen formation, and the process
is completed largely by 14th day.
During this period wound is reduced by
approximately 70-80% of its original
size.
Contracted wound results in rapid
healing.

MECHANISM OF WOUND
CONTRACTION
1. Dehydration :as a result of removal
of fluid
2. Contraction of collagen
3. Discovery of myofibroblasts

Wound healing

Skin

Primary
intention

Oral soft tissue wounds

Secondary
intention

Healing by first intention

This is defined as healing of a wound which
has the
following characteristics:
- clean and uninfected
- surgically incised
- without much loss of cells and tissue
- edges of wound are approximated by
surgical sutures.

Initial hemorrhage
Acute inflammatory response
Epithelial changes
Organization
Suture tracks
A suture wound, thus, takes a little
longer to heal but the scar formed is neat
due to close apposition of the margins of
wound. The use of adhesive tapes at the
incised margins avoids this complication.

Secondary Intention
[ Secondary union ]
This is defined as healing of a wound
having the following characteristics:
Open with a large tissue defect, at times
infected
Having extensive loss of cells and tissues
The wound is not approximated by
sutures but is left open.

Initial hemorrhage
Inflammatory phase
Epithelial changes
Granulation tissue
Wound contraction

Complications of wound
healing
Deficient scar formation

Dehiscence

Ulceration
Excessive scar formation

Keliods

excess of fibrous tissue or Proud flesh

Excessive contraction
Contracture

Miscellaneous
Painful scars
Pigmentary
changes
Implantation

Factors that influence

wound healing
Local Factors
Infection single most important reason
for delayed wound healing

Foreign bodies
suture material, bone and wood splinters
.

Mechanical factors
Early movement
Pressure

 Ionising radiation : delays

granulation tissue formation
Ultra violate light : facilitates
healing
Type size and location

Systemic factors
Malnutrition
Protein deficiency delays wound healing
Vitamin C deficiency (inhibition of collagen
synthesis)
Metabolic status
e.g. Diabetes mellitus
Cortisone treatment
inhibits inflammation and collagen synthesis
Circulatory status
Inadequate blood supply due to arteriosclerosis
Varicose veins

 Age : Older patient at higher risk of

poor wound healing
Medication : Anti-inflammatory
(aspirin), cytotoxic,
immunosuppressive and
anticoagulant drugs all reduce
healing rates by interrupting cell
division or the clotting process.
Iron, required to transport oxygen.

 Minerals, zinc, copper, are important for enzyme

systems and immune systems. Zinc deficiency
contributes to disruption in granulation tissue
formation.
Vitamins A, B complex and C, are responsible for
supporting epithelialisation and collagen
formation. It is also important for the inflammatory
phase of wound healing.
Carbohydrates and fats. These provide the
energy required for cell function. When the patient
does not have enough, the body breaks down
protein to meet the energy needs. Fatty acids and
essential for wound healing.

Conclusion
For most people, wound healing is a natural,
uneventful process. For some individuals,
however, it becomes a complex medical
problem requiring specialized treatment
and care.
Since problem of wounds are often
associated with underlying medical
conditions, so it is the physicians duty to
understand the necessary of care level and
educating people to overcome the problems

References:
Robbins Pathologic Basis of Disease; 7th Ed
Vinay Kumar, Abbas, Fausto
Text book of Pathology;
Emanuel Rubin & John C Farbar
Short Practice of Surgery; 22nd Edition:
Bailey & Love.
Andersons Pathology; 10th Edition:
James Linder
Boyds text book of Pathology; 3rd Edition:
Ritchie.
Essentials of Pathology for Dental students;
9th Ed
Harsh Mohan
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