biologic process of wound repair1
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8/11/2019 Biologic Process of Wound Repair1
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Oedijani SantosoBagian/SMF Gigi dan Mulut
FK Undip/RSUP dr Kariadi
Semarang
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Factors Which Impede Healing
(Systemic)
- Age
- Mal-nourishment
- Corticosteroids/NSAIDs
- Diabetes- Anti-coagulants
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Factors Which Maximize Healing(Systemic)
- Adequate nutrition
- Calcitonin
- Vitamin A
- Glucosamine- Anabolic Steroids
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Factors Which Impede Healing(Local)
- Prolonged immobilization
- Rigid fixation
- Excessive soft tissue gap
- Excessive motion or stress/repeatinjury
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Factors Which Maximize Healing
(Local)
- Electrical stimulation- Injectable growth factors
- Surgical gap closure/surgical
- Controlled motion
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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
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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
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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
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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
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Cells Involved in Wound Repair
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3. Chemotactic Mediators
= subtances that promote migration of
cells
= can be through several mechanismand pathway :
* complement system
* immune system
* phagocytotic system
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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
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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
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Movement during inflammatoryphase:
Improves blood flow
Decreases swelling
Relieves pain
Increases phagocytosisPrevents joint stiffness and muscle
weakness in related areas
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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
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NORMAL REPAIR
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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
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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
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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
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Movement during proliferation
phase:Increases tensile strength
Increases tissue metabolismPromotes extensibility of scar tissue
Maintains and improves joint range
of movement & muscle strength
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= 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↓
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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
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Prevent unwanted adhesions
[abnormal deposits of collagen that
disrupt gliding between adjacentstructures]
Restore functional activity
Address intrinsic and extrinsic causes
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Movement during remodellingphase:
Restores full range of movement and
muscle strength
Counteracts scar contraction
Restores functionRestores confidence
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= 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
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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
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Systemic= Malnutrition
= Smoking ↓ osteoblast
nicotine vaso constr
blood flow in fracture site ↓
= DM collagen defect
= aging compromise in vascularity,
osteoporosis
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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
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= 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
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1. Initial stage :
Hematoma formation concurrent with
inflammatory response cellularproliferation (8-12 hours) fibroblast
collagen + capillary network
granulation tissue oxygen tension& pH ↓ cartilage
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Secondary Bone Repair
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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
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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
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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
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Secondary Bone Repair
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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
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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
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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
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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
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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
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Wound Healing
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