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Soft Tissue Healing

Online Course: Injury and Heal…

Introduction

After
an
injury,
soft
tissue
structu
res in
the
body
underg
oa
natural
healing
process
throug
h
specific phases of healing.

The timeline for healing depends on: the

individual; the extent of the injury; age;
overall health status.
Physiotherapy helps facilitate healthier
healing - resulting in a smaller risk of re-
injury, chronic pain and dysfunction.
One of the main risks of future injury is how
the soft tissue was rehabilitated or recovered,
from previous injury/ surgery.
Soft tissue healing is defined as the replacement
of destroyed tissue by living tissue in the body.[1]
This process consists of two parts - regeneration
and repair.[2] Note - There are no defined
boundaries between stages as the wound healing
response “transitions” into the next stage of
healing[3].

During the regeneration component,

specialized tissue is replaced by the
proliferation of surrounding undamaged
specialized cells.
In the repair component, lost tissue is
replaced by granulation tissue which matures
into scar tissue.[2]
The cellular reaction after injury depends on the
tissue type as well as the extent of the wound.

In injury to CNS tissue that damages neurons

and the supporting glial cells, the body’s
response is unforgiving, as regeneration of
lost neurons is not possible. Activated
astrocytes wall off the lesion, creating a glial
scar.
In contrast, in non-CNS tissue, a single tissue
type can have multiple responses depending
on the magnitude of injury.[3]

Phases of Healing

The different healing phases are not mutually

exclusive and tend to overlap quite a lot.[2]

Bleeding Phase

Short
phase
immedi
ately
after
injury -
lasting
about
6-8
hours,
up to
24
hours
after a
crush
injury.

Time of the bleeding will depend on the

extent of the soft tissue injury and the
management thereof.
The more vascular the injured structures, the
more bleeding will occur.[2]

Inflammation Phase

The goal of the inflammation phase is to stop the

bleeding phase.

This phase starts rapidly within a 6-8 hours

after the soft tissue injury, reaches the
maximal reaction between 1-3 days and
gradually resolves in a few weeks.[2]
Achieved by vasoconstriction, retraction of
injured blood vessels, fibrin deposition and
clotting.
The blood supply to the area increases in this
time, causing oedema and redness.
Phagocytosis ("the engulfing and usually the
destruction of particulate matter by
phagocytes that serves as an important
bodily defence mechanism against infection
by microorganisms and against occlusion of
mucous surfaces or tissues by foreign
particles and tissue debris[4]") happens
during this phase.[2]

1. The acute inflammatory response involves

activities that generate exudates - plasma-
like fluid that exudes out of tissue or its
capillaries and is composed of protein and
granular leukocytes (white blood cells).[5]
2. The chronic inflammatory response is of
prolonged duration and involves the
presence of nongranular leukocytes and
the production of scar tissue.
The acute phase involves three mechanisms that
act to stop blood loss from the wound:[5]

1. Local vasoconstriction occurs, lasting a

few seconds to as long as 10 minutes.
Larger vessels constrict due to
neurotransmitters and capillaries and
smaller arterioles and venules constrict
due to the influence of serotonin and
catecholamines released from platelets.
The resulting reduction in the volume of
blood flow in the region promotes
increased blood viscosity or resistance to
the flow, which further reduces blood loss
at the injury site.
2. The platelet reaction provokes clotting as
individual cells irreversibly combine with
each other and with fibrin to form a
mechanical plug that occludes the end of a
ruptured blood vessel. The platelets also
produce an array of chemical mediators in
the inflammatory phase: serotonin,
adrenaline, noradrenaline, and histamine.
Also, ATP is used for energy in the healing
process.
3. Fibrinogen molecules are converted into
fibrin for clot formation.
Approximately 1-hour post-injury, swelling or
oedema, occurs as the vascular walls become
more permeable and increased pressure within
the vessels forces a plasma exudate out into the
interstitial tissues. This happens in:

Mild trauma - for a few minutes with a return

to normal permeability in 20-30 minutes.[5]
More severe traumas - can result in a
prolonged state of increased permeability,
and sometimes result in delayed onset of
increased permeability, with swelling not
apparent until some time has elapsed since
the original injury.
Bradykinin, a major plasma protease present
during inflammation, increases vessel
permeability and stimulates nerve endings to
cause pain[5].

Proliferation Phase

This phase starts between 24-48 hours after

injury, lasts up to 2-3 weeks when the bulk of the
scar tissue is formed.[2]

Fibroplasia and Granulation Tissue

Formation

The central event during the proliferative

phase.
Occurs 3-5 days following an injury and
overlaps with the preceding inflammatory
phase.
Granulation tissue includes inflammatory
cells, fibroblasts, and neovasculature in a
matrix of fibronectin, collagen,
glycosaminoglycans, and proteoglycans.[6]

Epithelialization

Formation of epithelium over a denuded surface.

The process begins within hours of tissue injury.

Involves the migration of cells at the wound

edges over a distance of less than 1 mm, from
one side of the incision to the other. Incisional
wounds are epithelialized within 24-48 hours
after injury. This epithelial layer provides a
seal between the underlying wound and the
environment.[6]
Epidermal cells at the wound edges undergo
structural changes, allowing them to detach
from their connections to other epidermal
cells and to their basement membrane.
Intracellular actin microfilaments are
formed, allowing the epidermal cells to creep
across the wound surface.
Occlusive and semiocclusive dressings
applied in the first 48 hours after injury may
maintain tissue humidity and optimize
epithelialization.[6]
When epithelialization is complete, the
epidermal cell assumes its original form,[6]

Fibroplasia

Fibroplasia begins 3-5 days after injury and may

last as long as 14 days.

Skin fibroblasts and mesenchymal cells

differentiate to perform migratory and
contractile capabilities.
Fibroblasts are responsible for the production
of collagen, elastin, fibronectin,
glycosaminoglycans, and proteases.
Fibroblasts fill the defect left by an open
wound as the number of inflammation cells
decrease.[6]
As granulation tissue matures, the fibroblasts
produce less type III collagen and become
more spindly in appearance. They begin to
produce the much stronger type I collagen

Angiogenesis

Angiogenesis results in greater blood flow to the

wound and, consequently, increased perfusion of
healing factors. Angiogenesis ceases as the
demand for new blood vessels ceases. New blood
vessels that become unnecessary disappear by
apoptosis.[6]

A rich blood supply is vital to sustaining

newly formed tissue (as is appreciated in the
erythema of a newly formed scar).
The macrophage is essential to the
stimulation of angiogenesis and produces
macrophage-derived angiogenic factor in
response to low tissue oxygenation.[6]

Contr
actio
n

Con
trac
tion
resu
lts
in a
decr
ease
in wound size eg a 2-cm incision may
measure 1.8cm after contraction.
Loose tissues contract more than tissues with
poor laxity, and square wounds tend to
contract more than circular wounds.
Wound contraction depends on the
myofibroblast located at the periphery of the
wound, its connection to components of the
extracellular matrix, and myofibroblast
proliferation.[6]
Radiation and drugs, which inhibit cell
division, have been noted to delay wound
contraction.

Remodelling Phase

This phase starts around the peak of the

proliferation phase. The result of this phase is an
organised, quality and functional scar similar to
the tissue it is busy repairing.[2]

The ultimate endpoint following remodelling

depends on the tissue type.

Non-central nervous system (CNS) tissue that

undergoes primary healing, very little
remodelling occurs because of the lack of
extracellular matrix produced during the
repair. Secondary healing, in contrast,
involves fibre alignment and contraction to
reduce the wound size and to reestablish
tissue strength. Complete recovery of original
tissue strength is rarely obtained in
secondary healing because repaired tissue
remains less organized than non-injured
tissue, which results in scar formation.[6]
Collagen-rich scars are characterized
morphologically by a lack of specific
organization of cellular and matrix elements
that comprise the surrounding uninjured
tissue.
CNS tissue - there is no repair or regeneration
of injured neurons, relatively little
reestablishment of structural integrity in the
region. During CNS remodelling, activated
astrocytes wall off the lesion, creating a glial
scar. These activated astrocytes may prevent
further tissue damage, although neuron
axonal regrowth is inhibited.[3][6]

Types

Primary
Intention

Restoration of
continuity occurs
directly by fibrous adhesion, without the
formation of granulation tissue; it results in a
thin scar.[7]

Secondary Intention

Wound healing occurs by union by adhesion of

granulating surfaces when the edges of the
wound are far apart and cannot be brought
together. Granulations form from the base and
sides of the wound toward the surface.[7]

Tertiary
Intention

Wound healing occurs by the gradual filling of a

wound cavity by granulations and a cicatrix.[7]

Physiotherapy Management

This classification is based on a treatment

protocol of Clanton et al.[8], but it is similar to
other classifications. It is possible that some
phases overlap, dependable on the individual
response to healing and the type of injury. Not
every patient undergoes all phases to achieve full
rehabilitation.

Phase 1: Acute Phase (1 - 7 Days)

Goal: Minimize inflammation and pain.

Treatment:

RICE-method: Rest, ice, compression and

elevation
Pain-free range of motion with
cryotherapy

Phase 2: Subacute Phase (Day 3 - <

3 Weeks)

This phase starts when signs of inflammation

begin to reduce. Inflammation signs are heat,
swelling, redness and pain.

Goal: Prevent muscle atrophy

Treatment:

Pain-free full range of motion: concentric

strengthening
If any pain present: decrease the intensity
of exercises

Phase 3: Remodelling Phase: ( 1 - 6

Weeks)

Stretching to avoid a decrease in flexibility

Eccentric strengthening
It is important to make sure that the muscle
is already regenerated, to prevent risk of re-
injury

Phase 4: Functional Phase: (2

Weeks - 6 Months)

Goal: Return to sport without re-injury.

Treatment:

Increase their strength, endurance, speed,

agility, flexibility and proprioception
Sport-specific activities

Phase 5: Return to Competition

Phase: (3 Weeks to 6 Months)

Goal: Avoid a re-injury

Criteria: Full range of motion, strength,
coordination and psychological readiness
Treatment:

Address deficits in criteria

Progressive agility and trunk
stabilization[9]

Soft tissue injury and the heali…

[10]

Clinical Bottom Line

Soft tissue healing is a natural process that

occurs in the body after an injury. This process
happens without the need for medication and
therapy, but this can play an important role in
cases where problems are identified in this
natural process, such as repeated trauma,
inhibited response or delayed reactions. The aim
would then be to facilitate and stimulate the soft
tissue healing process.[2] It is also important to
realise that inappropriate therapy will inhibit
these events. It is thus very important to be
selective of the most appropriate therapy at each
stage.

Practical
Assessment and
Treatment of
Cervicogenic
Headaches
An online course by Ari Kaplan

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