Professional Documents
Culture Documents
WOUND HEALING
Preseptor:
dr. Deddy Saputra, Sp. BP-RE (K)
Disrupts
WOUNDING Tissue
Integrity direct
exposure of
extracellular
matrix to
platelets
Hemostasis
SUBENDOTHELIAL COLLAGEN vs PLATELET
• Platelet aggregation
• Degranulation
• Activation of coagulation cascade
FIBRIN CLOT
Inflammation
Fibrin clot Migration of inflammatory cells to wound
- Polymorphonuclear leukocytes (PMN, Neutrophil)
- Monocytes
1st PMN enter wound site (24-48hr)
- Increased vascular permeability
- Local prostaglandin release
Stimulate neutrophil migration
- Presence of chemotactic substances
- Bacterial products
neutrophils Phagocytosis of bacteria
Phagocytosis tissue debris
TNF-α angiogenesis
collagen synthesis
Inflammation
• 2nd Macrophages (48 to 96 hours post injury and remain present
until wound healing is complete)
• Derived from circulating monocytes
T-lymphocyte numbers peak at about 1 week post injury and truly bridge the
transition from the inflammatory to the proliferative phase of healing
Proliferation
• The proliferative phase is the second phase of wound healing and
roughly spans days 4 through 12.
• phase that tissue continuity is reestablished
• Fibroblasts and endothelial cells infiltrate the healing wound
• The strongest chemotactic factor for fibroblasts is PDGF (platelet-
derived growth Factor)
• Cytokines
Wound fibroblasts proliferate activated
Macrophages
• Growth factors
Proliferation
• The proliferative phase is the second phase of wound healing and
roughly spans days 4 through 12.
• phase that tissue continuity is reestablished
• Fibroblasts and endothelial cells infiltrate the healing wound
• The strongest chemotactic factor for fibroblasts is PDGF (platelet-
derived growth Factor)
• Fibroblasts synthesize collagen
• Additionally, lactate
adenosine diphosphate
(ADP)-ribosylation
Regulate collagen synthesis
Proliferation
- CYTOKINES
- GROWTH FACTORS Endothelial cells migrate
from intact venules to the wound
ANGIOGENESI
S
Matrix Synthesis
Biochemistry of Collagen
• Deposition
Functional integrity WOUND
COLLAGE • Maturation of the wound HEALING
N
• Remodeling
PROCOLLAGEN
FIBROBLAST 3 weeks
Major glycosaminoglycans in wounds = Dermatan sulfate
= Chondroitin sulfate
Proteoglycan Synthesis
• As scar collagen is deposited, the proteoglycans are incorporated into
the collagen scaffolding
Scar remodeling continues for many (6 to 12) months post injury, gradually resulting in a
mature, avascular, and acellular scar.
The mechanical strength of the scar never achieves that of the uninjured tissue.
Epithelialization
• Epithelialization is the final step in establishing tissue
integrity
• Characterized primarily by proliferation and migration of
epithelial cells adjacent to the wound
• Begins within 1 day of injury
• Seen as thickening of the epidermis at the wound edge
Layering of the epithelium is reestablished, and the
surface layer eventually keratinizes
Once the defect is bridged, the migrating epithelial cells lose
their flattened appearance, become more columnar in shape, and
increase their mitotic activity
Fixed basal cells in a zone near the cut edge undergo a series of rapid
mitotic divisions, and these cells appear to migrate by moving over
one another in a leapfrog fashion until the defect is covered
Marginal basal cells at the edge of the wound lose their firm
attachment to the underlying dermis, enlarge, and begin to migrate
across the surface of the provisional matrix
• Reepithelialization is complete in less than 48
hours in the case of approximated incised
wounds but may take substantially longer in
the case of larger wounds
?
FIBROBLAST
responsible for contraction, and it
differs from the normal fibroblast
in that it possesses a cytoskeletal
structure
HEALING IN SPECIFIC TISSUES
Gastrointestinal Tract
Repair and healing of the gastrointestinal tract is essential
NEURAPRAXIA
Focal demyelination Survival of axonal cell bodies
1.0-1.4: Normal
Chronic Wounds-Venous Stasis Ulcers
Theory:
Distention of the dermal capillaries with leakage of fibrinogen into the
tissues
Neutrophils adhere to the capillary endothelium and cause plugging
with diminished dermal blood flow
Venous hypertension and capillary damage lead to extravasation of
hemoglobin
Lipodermatosclerosis
1.0-1.4: Normal
Chronic Wounds-Diabetic Wounds
The major contributors to the formation of diabetic ulcers include
neuropathy, foot deformity, and ischemia
1.0-1.4: Normal
EXCESS HEALING
DRESSING
• ABSORBENT
• NONADHERENT
• OCCLUSIVE & SEMIOCCLUSIE
TYPES • HYDROPHILIC & HYDROPHOBIC
• HYDROCOLLOID & HYDROGEL
• ALGINATES
• etc
SKIN REPLACEMENTS
The use of skin grafts or bioengineered skin substitutes
and other innovative treatments (e.g., topically applied
growth factors, systemic agents, and gene therapy)
cannot be effective unless the wound bed is adequately
prepared.
1. Dermoinducive
• help provide cells and factors
that will activate healing
within the wound by inducing
tissue growth or inducing
granulation within the wound.
2. Democonductive
• provide scaffolding to a
wound ending in a neodermis
by allowing migration of
surrounding tissues across the
wound, and this helps healing.
Growth
factor
therapy
Oxygen
therapy
Biofilm and
Gene or cell chronic
therapy wound
healing
HERITABLE DISEASES OF CONNECTIVE TISSUE