WOUND HEALING PROCESS

Sita Saraswat
 PENYEMBUHAN
(REGENERASI & REPAIR)

REGENERASI
• Penggantan sel rusak/mat akibat jejas dengan jenis
sel yang sama

REPAIR
• Penyembuhan dengan cara penggantan dengan
jaringan ikat

3
 WOUND HEALING PROCESS
Injury

Algogene.Fibrin Tissue damage & 20 - 30

menutup luka haemorrhage menit

Inflamasi primer.
Inflamasi neurogenik
24 - 36 jam
Gejala radang Inflamaton

Proliferasi Produksi
Remodeling
Cell pertahanan produksi collagen resorbsi collagen,
& fibroblast maksimal penyesuaian bentuk
semula
 Stage 1: Acute Inflammatory

 Increase blood flow to the area that brings

cells and chemicals to begin the healing
process.

Phagocytes- Eat up dead cells.

Leukocytes- Infecton fightng white blood cells.
Platelets-Carry blood clotting materials.
 Vascular changes
– Vasoconstriction – immediately; decreased blood
flow to area (approx. 5-10 mins.); platelet plug
formed; blood coagulation; produces local anemia

– Vasodilation – increased blood flow; increased

hydrostatic pressure in blood vessels ( capillary
permeability, plasma proteins leak out; proteins
attract H2O = edema)

THIS STAGE LASTS FOR ABOUT 2 DAYS

 HAEMODINAMIC CANGE
• PHASE I = vasoconstriction (momentary
constricton of small blood vessels in the
area).
 Vascular spasm begins very quickly (30 sec.)
after the injury at it last a few minutes.
 The mechanism of spasm is nervous –
through catecholamine liberated from
sympatric nerves endings.
• PHASE II = active vasodilation (through catabolism
products that act through receptors and directly
stmulates vascular dilaton – nervous mechanism).
– Dilaton of arterioles and capillaries (redness =
rubor);
– Blood flow increases and gives pulsate sensaton;
– Actve hyperemia in skin territory and increased
metabolism leads to higher local temperature
(heat = calor).
 HAEMODINAMIC CHANGE
• PHASE III = passive vasodilation
 Blood vessels in the affected area loose
their reactvity to nervous  passive
vasodilaton occurs.
 Progressively fluid move into the tssues
(increased vascular permeability and
structural alteraton of blood vessels) and
cause swelling (tumor), pain, and impaired
functon.
 HAEMODINAMIC CHANGE
 The exudaton or movement of the fluid
out of the capillaries and into the tssue
spaces dilutes the offending agent.
 As fluid moves out of the capillaries,
stagnaton of flow and clotting of blood in
the small capillaries occurs at the site of
injury.
 This aids in localizing the spread of
infectous microorganisms
 Phase I: Acute Inflammatory Phase

• Goal
– Protect,
– Localize,
– Decrease injurious agents,
– Prepare for healing and repair
 Cardinal Signs of Inflammation

Redness Heat Swelling Pain Loss of

Function
Caused by Increased Caused by Direct injury Increased
dilation of chemical accumulation of nerve pain/ swelling
arterioles/ activity & of blood & fibers,
increased increased damaged tissue pressure of
blood flow blood flow to cells hematoma on n.
skin surface endings
Chemical
irritants –
bradykinin,
histamine,
prostaglandin
 Chronic Inflammation
• Inflamasi akut yang tak tertangani dengan baik
akan berubah menjadi inflamasi kronis
• Sering kali di bedakan dari segi waktu :
– 1-36 jam → inflamasi akut
– 3-15 hari→ inflamasi sub akut
– 2-3 minggu → chronic inflamaton
• Khusus untuk penggunaaan Modalitas/
elektrofisika perhatkan sensitftasnya/aktualitas
 Phase 2: Proliferaton/Repair

• The injured area has been

filled with the blood,
cells, and chemicals
needed to rebuild the
injury
– Fibroblasts begin building
fibers across the injury and
form the scar.

THIS PROCESS LASTS FROM 6

WEEKS TO MONTHS.
 Phase II: Proliferation Phase
• Phase removes debris & temporary repair
– SCAR FORMATION (fibroplasia)

Dependent on levels of:

• Debris removal,
• Skin cell production,
• Production of fibroblasts
 Phase II: Proliferation Phase
• Repaired through 3 phases
– Resolution - dead cells & cellular debris are
removed (tissue left with original structure
& function in tact)
• fibroblast (tissue cells) formation
Phase II: Proliferation Phase
– Regeneration – damaged tissue is replaced
by cells of the same type (structure retains
some or all of its original structure &
function)
• synthesis of collagen (fencing)
– Repair – original tissue is replaced with scar
tissue (original structure & function is lost)
• tissue alignment
 Phase 3: Remodeling
• Goal
– Builds tssue strength in the repaired/replaced
tssue of the tendons, ligaments or muscles in
order to withstand stress applied to the body.

THIS STAGE TAKES UP TO A YEAR OR MORE.

 Phase III: Remodeling Phase

• Usually begins @ week 3

• Purpose is to increase strength of

repaired/replaced tissues
– First 3-6 weeks involves laying down of collagen
and strengthening of fibers
– 3 months to 2 years allowed for enhanced scar
tissue strength

• Balance must be maintained between

synthesis & lysis
– Build up (synthesis) and break down (lysis)
 Note!

• Varying issues exist for all soft tissues

relative to healing (cartilage, muscle,
nerves)
• Blood supply and nutrients is necessary for
all healing
• Healing in older athletes or those with poor
diets may take longer
• Certain organic disorders (blood
conditions) may slow or inhibit the healing
process
 Factors That Impede Healing

• Extent of • Atrophy
injury • Infection
• Edema
• Hemorrhage • Health, Age,
• Poor Vascular and Nutrition
Supply
• Muscle Spasm
 Types of Tissues and their Healing

Cartilage
• Limited capacity to heal
• Little or no direct blood supply
• Articular cartilage that fails to clot heals
very slowly
Ligaments/ Tendons

• Long full healing process (12 months)

• Decent blood supply
• Requires a lot of collagen being laid
down
• Bone
– Severity of injury
• Soft tissue damage
• Amount of necrotic tissue
• Disruption of blood supply
• Displacement of fragments
– Open fractures disrupts blood supply,
severe soft tissue damage
– Union v Displaced/malunion fractures
• Skeletal Muscle
– Initial bleeding followed by laying down a ground
substance
– Healing could last 6-8 weeks depending on muscle
injured
Guideline