PHYSIOLOGY OF HEALING

The healing process is divided into three broad stages which are
not mutually exclusive and overlap considerably.

1.Initial vascular reaction

2.Inflammatory response
3. Proliferative phase
4. Remodeling

Wound healing refers to the body’s replacement of destroyed

tissue by living tissue (Walter & Israel 1987).
It comprises of two essential components whose differentiation
is based on resultant tissue:
Regeneration specialised tissues replaced by proliferation of
-

surrounding undamaged specialised cells e.g lung,liver tissue

and meniscus (O’Brien 1990)
Repair Injured tissue replaced by granulation tissue which
-

matures to form scar tissue.

INJURY:
Tissue damage produces capillary bleeding inhibiting cell
metabolism resulting in cell death.
Dead cells contain Iysosomes which release digestive enzymes.
Within 10-15 mins the damaged soft tissues contain disrupted
extracellular tissues, dead and dying cells and extravastated
blood.

The extravasated blood contains platelets and plasma. The

platelets die due to lack of oxygen and release thrombin which
changes fibrinogen to fibrin. The fibrin deposits an irregular
network of fibers to form a clot.
 INFLAMMATION:
Inflammation is a normal and necessary pre- requisite to healing
(Hardy 1989).

It may be a non- immunological or immunological event, whether by injury

or virus.
Inflammation is a localised protective response to injury” Triple Response”.
There is disagreement as to specific duration of this phase but it is reported to
last between 3-5 days.

It is stimulated by “a cascade chemical effect’ and its extent is dependent

upon the area of damage and severity of injury. The cardinal signs of
inflammation are:

Calor
Rubor
Tumor
Dolor
Functiolasea

Calor /Rubor:

Initial V/C is followed by V/D.

Blood vessels: : Increase calibre ( histamine,bradykinin,
PGE)

- Increase permeability (serotonin, bradykinin,

histamine, leukotrines)

- Increase blood flow / decrease flow

- WBC + platelets marginate to walls endothelial cells

swell. (4hrs)
Tumor:

Swelling is due to inflammatory exudate as chemicals released increase

permeability of local capillaries.

Fluid exudate contains gammaglobulins and fibrinogen

(antibodies)
Gammaglobulins fight infection.
Fibrin is formed from fibrinogen to construct a fibrin lattice.
Platelets, mast cells and basophils are present in all tissue. Chemical
mediators modulate the action of the cells. Leucocytes ( neutrophils,
basophils, oesinophils) and macrophages enter area and act as debriders
(phagocytosis) Mast cells release hylauronic acid which draws water into the
site and creates a gel which limits local fluid flow, and further traps various
particles and debris (Hardy 1989)

Dolor:

Pain is caused by mechanical and chemical nociception Mechanical tissue

-

pressure.
Chemical increase sensitivity of nerve endings ( bradykinin, PGE and
-

histamine)

Functiolasea:

Loss of function is a result of:

Neurological reflex inhibiting movement due to pain
Oedema mechanically restricting movement
PROLIFERATIVE PHASE:

This develops from around the third day while inflammation is still
going on.
It consists of two fundamental processes
1. Fibroplasia
2. Angiogenesis (new cells).

Macrophages, fibroblasts and capillaries infiltrate the wound.

Fibroplasia involves activation of fibroblast proliferation. Fibroblasts

initially produce predominantly type 111 collagen fibres which will become
type I as the repair process matures ( 7-12 days)

Angiogenesis involves mitosis in the cells surrounding the

capillaries. Capillary buds sprout and communicate with
existing capillaries.

This new capillary system + fibroblasts = granulation tissue.

The tensile strength of the new tissue is at its lowest level at
this stage.

Myofibroblasts are derived from fibroblasts and are

responsible for wound contraction.

Some authors believe that this phase lasts approx 21 days

REMODELING PHASE:

This phase will have the longest duration extending a year or

more.
 Macrophages, fibroblasts, capillaries and water content all
decrease.
Sensitivity is reduced and collagen is primarily type I. Initial
deposition of collagen produces fibrils with random
orientation, which in time becomes more orientated in line
with local stresses.
Tensile strength correlates with maturity of collagen.
TENSILE STRENGTH
t
Restoration to near normal tensile strength (NNTS) varies
with different tissues.

Muscle may reach NNTS in 7 II days ((Garrett 1990).

-

The extent and duration of inflammation is reportedly longer

in
experimental contusion injuries compared with strains
(Stauber1990).

Ligaments & tendons may take 4 months for 85-95 % of

NNST or some say 40-50 weeks. There ~s yet no uniform
answer.

Ligaments may differ in their repair process. The ACL does not
heal well but the collaterals do.
The cell arrangement & blood supply differ between them. The
ACLs main nutrition is from synovium. Synovial fluid has been
shown to adversely affect ACL fibroblast proliferation.(Andrish
1979) Synovial fluid washes away the clot from the site of
injury This may deplete growth factors necessary for
stimulating the healing response.
 Tendon healing is very controversial but generally day 5 is
considered to be the weakest point for tendon tensile strength
(Gillman 1968)
Complete immobilization of a tendon results in reduction in
glycosaminoglycan content and in the strength of the tendon.
Too early mobilisation can result in rupture. Poor nutrition is
proposed to contribute to poor healing.

Articular cartilage: Avascular has limited powers of repair and

-

tends towards calcification following injury.

FACTORS THAT MAY RETARD HEALING:(Walter Israel

1978)

General causes:
-Old age
-Starvation
-lack of vit C (Scurvy)
-Steroids (inhibitory effect)
-temperature (lower rate when cooler)

Local causes:
-lschaemia
-irritation (infection or haematoma)
- drying of the wound
-excessive movement (restarts inflammation)
-adhesion to underlying bone or other tissues.

MODIFYING FACTORS:

NSAIDs will enhance the healing process.

However they act by inhibiting prostaglandin production (is
this a good thing?)
There is evidence that they may also increase collagen
strength. NSAID have side effects such as:
Gastrointestinal (upto 1-2% get ulcers) Skin eruptions.
Patients with asthma, nasal polyps and aspirin intolerance
should not be treated with these drugs.
Approximately 50% of patients who receive NSAID may
experience an adverse reaction.

NSAID’s use may be justified in a professional athelete as

opposed to a recreational athelete.
The most important time to use them is during the first stage
as Herring 1990 reported that extended dosages may actually
impair tissue repair.

REHABILITATION PROGRAMME

Avoid a cookbook approach.

Acute phase:
Ice, Compression, Elevation and gentle movement. Ultrasound
has been shown to have beneficial results in early stages of
healing (Dyson 1978). lt is believed to affect cell membrane
permeability.

Restoration phase:
Mobility
Flexibility
I
Strength/ Endurance
Balance & coordination
Confidence.

Evidence exists that stress on forming collagen encourages the

alignment of greater scar tissue strength than without
application of stress.
It is easier to mechanically affect young scars than it is to
change old scars

REFERENCES:

1.Evans P. (1980)

“The healing proces”

Physiotherapy 66: 8 256-259

2,Barlow Y. Willoughby J. (1992)

“Pathophysiology of soft tissue repair”

British Medical Bulletin 48: 3 698-711

3.Burroughs P, Dahners L (1990)

“The effect of enforced exercise on the healing ligament”

American Journal of Sports medicine 18: 4 376-378

4.Houglum PA (1992)

“Soft tissue healing and its impact on rehabilitation

Journal of Sport Rehabilitation 119-39

5. Watson T. (1996) “Wound healing” Lecture notes.