biologic process of wound repair1

8/11/2019 Biologic Process of Wound Repair1

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Oedijani SantosoBagian/SMF Gigi dan Mulut

FK Undip/RSUP dr Kariadi

Semarang

Factors Which Impede Healing

(Systemic)

- Mal-nourishment

- Corticosteroids/NSAIDs

- Diabetes- Anti-coagulants

Factors Which Maximize Healing(Systemic)

- Adequate nutrition

- Calcitonin

- Vitamin A

- Glucosamine- Anabolic Steroids

Factors Which Impede Healing(Local)

- Prolonged immobilization

- Rigid fixation

- Excessive soft tissue gap

- Excessive motion or stress/repeatinjury

Factors Which Maximize Healing

(Local)

- Electrical stimulation- Injectable growth factors

- Surgical gap closure/surgical

- Controlled motion

1. Primary Intention epithelization 24 hoursseals the wound from bacterial

2. Delayed Primary Closure contaminated

wounds host inflammatory and immuneresponses

3. Secondary Intention natural biologic healing

processes without surgical interventionepithelization & collagen deposition in the

spontaneous closure of large open wounds

I. Inflammation : - vascular response - cellular infiltrate

- neovascularization - synth granulation

tissue

II. Proliferation : - cell proliferation - collagen synthesis- endothelial cell proliferation

- mature formation of granulation tissue

- increase in mechanical strength

III. Maturation : - collagen remodeling- increase in wound strength

- decrease in vascularity

- formation of scar tissue

1. Vascular Reaction

= Hemostasis deposition fibrin blood clot

= Transient constriction local vessels 5-10mtleuko, erythro, platelet adherent to endothelium

= vasoconstriction followed by active vasodilatation

vasopermeability mediators ↑ : histamine,

prostaglandin, norepinephrine permeability ↑

endothelial cells swell separation between

themselves

2. Cellular Movement= PMN leukocytes , macrophage

penetrated the vessel wall

phagocytosis function 1-2 days

= fibroblast and capillaries

(neovascularization) appear 1-10 days

= fibroblast glycosaminoglycans

collagen

Cells Involved in Wound Repair

3. Chemotactic Mediators

= subtances that promote migration of

= can be through several mechanismand pathway :

* complement system

* immune system

* phagocytotic system

Inflammation is an essential part of

healing, but as an "all or nothing"

response can be harmful.

Excessive or prolonged inflammationexcessive scar formation

•pain

•oedema•secondary tissue ischaemia

•loss of movement and weakness

Physiotherapy aims to

control inflammation:

•prevent disruption of new blood vessels

and collagen fibrils

•minimise bleeding•promote collagen and ground substance

synthesis

•reduce oedema ; protect healing tissue

•provide pain relief

Movement during inflammatoryphase:

Improves blood flow

Decreases swelling

Relieves pain

Increases phagocytosisPrevents joint stiffness and muscle

weakness in related areas

1. Epithelization

= 3 separate but overlapping phases of

epithelial activity :

* migration

* proliferation

* differentiation

= migration and proliferation of epithelial

cells 24-48 hours after injury at the

wound margin

NORMAL REPAIR

2. Fibroblast

= migrate along strands of fibrin deposited in blood clotproliferation glycosaminoglycans collagen

3. Collagen

Type I Fibroblast Bone,tendon,skin,dentin(90%) ligament, arteries, uterus

Type II Chondrocyte Hyaline cartilage

Type III Fibroblast arteries, spleen, intestine

Smooth muscle

Type IV Epithel Basement membrane

4. Tensile Strength= collagen deposition tensile strength↑

= is defined as the load per cross-sectional

area that can be supported by the wound

= a sufficient quantity of collagen

fibroblast in the wound diminishes

disappearance of fibroblasts marks the end

of phase II

Use therapeutic techniques to help

control pain and swelling; reduce relianceon support and strapping; progress activity

levels. Applying tension through exercise

or manual therapy

•increase collagen synthesis,

•promote better collagen alignment •increase tensile strength

Movement during proliferation

phase:Increases tensile strength

Increases tissue metabolismPromotes extensibility of scar tissue

Maintains and improves joint range

of movement & muscle strength

= Microscopically : a random collagen fibers

organized pattern

= Loss of the size of collagenous mass depend on :

physical factors (tension, pressure), oxygen supply,patient’s age

= Interplay between collagen deposition and

degradation : breakdown > production scar softer;

Production > breakdown hypertrophy scar/keloid

= after scar matured scar density ↑ fluid and

volume↓

Physiotherapy aims to help the tissuesregain as near normal structure and

function as possible and control tissue

overload by modifying intrinsic andextrinsic factors

Achieve and maintain flexibility of

healing tissues

Prevent unwanted adhesions

[abnormal deposits of collagen that

disrupt gliding between adjacentstructures]

Restore functional activity

Address intrinsic and extrinsic causes

Movement during remodellingphase:

Restores full range of movement and

muscle strength

Counteracts scar contraction

Restores functionRestores confidence

= unique structure with several specific function

= major reservoir of calcium

= insertion of musc & protect vital soft tissue str= body support and strength, 1/10 body weight

= extremely strong, has a flexible and elastic str

= undergoing spontaneous regeneration= injured bony str regain preinjury strength &

function

Local:

= Soft tissue injury

= Interruption of local blood supply

= Interposition of soft tissue at fracture

site= Bone death cause by radiation,

thermal, chemical burn or infection

Systemic= Malnutrition

= Smoking ↓ osteoblast

nicotine vaso constr

blood flow in fracture site ↓

= DM collagen defect

= aging compromise in vascularity,

osteoporosis

1. Primary intention occurs when:

excellent anatomic reduction, minimal /

no mobility, good vascular supply at the

fracture site

2. Secondary intention intermediate

fibrous tissue is formed within thefracture gap through adaptation &

remodelling form and function similar

preinjury bone

= occurs when enough rigidity

= osteogenic cells and capillary

proliferation in medullary bone on bothsides of the fracture forming new bone

= without intermediate cartilaginous callus

formation

= 2 way : gap healing and contact healing

1. Initial stage :

Hematoma formation concurrent with

inflammatory response cellularproliferation (8-12 hours) fibroblast

collagen + capillary network

granulation tissue oxygen tension& pH ↓ cartilage

Secondary Bone Repair

2. Cartilaginous callus (Soft callus)

= while external callus is forming

internal callus between the bone ends

also form

= this area better blood supply, less

necrosis osteoblast form an internal

bony callus= callus strength & stiffness of bone ↑

especially resistance against bending &

torsion, during the healing period

3. Bony callus (Hard callus )= cartilaginous callus undergoes

calcification

= osteoblast deposit osteoid on calcifiedcartilage calcification

process forming bone

= initially, woven bone lamellar bone

during final stage

4. Remodeling= familiar pattern of lamelar bone

= osteoclast (resorption of bone) +

remodeling factors (bone

morphogenetic protein = BMP) as a

mitogenic and transforming growth

factor induce differentiation of

mesenchymal cells bone formation

Secondary Bone Repair

1. Inflammatory reaction – Hematoma

stage (0-5 days after fracture)

= inflammatory reaction involves PMNleukocytes, lymphocytes, macrophages,

monocytes

= hematoma also contains platelets

produce PDGF mitogenic for

fibroblasts

2. Callus formation stage (4 – 40days after fracture)

= periosteal & endosteal mesenchymal

cells fibrocartilaginuos callus

= chondroblast produce cartilage

growth factor cartilage-sp type2

collagen & hyaluronic acid cell

proliferation

1. Growth factors:

-TGF = transforming growth factor

- BMP = bone morphogenetic protein

- FGF = fibroblast growth factor

- PDGF = platelet-derived growth factor

- IGF = insulin-like growth factor

2. Cytokine

Spesific factors stimulation of osteoblast & osteoclastCytokine Bone formation Bone resorption

IL-1 + +++

TNFα + +++TNFβ + +++

TGFα - - +++

TGFβ ++ ++PDGF ++ ++

IGF-1; IGF-2 +++ 0

FGF +++ 0

3. Prostaglandine/leukotrient :

stimulate osteoblastic bone formation

4. Hormone:

- Estrogen : stimulate fracture healing- Glucocorticoid : stimulate osteoclastic

bone resorption

- Parathyroid GH: ↑ bone formation

↑ callus formation

5. Growth factor antagonist

Wound Healing

biologic process of wound repair1

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