Primary intention healing occurs when a wound is closed within hours of injury through surgical or mechanical approximation of wound edges. Delayed primary healing allows time for wound debridement before closure to prevent infection. Secondary intention healing involves closure of full thickness wounds through wound contraction and epithelialization without surgical closure. Wound healing progresses through inflammatory, proliferative, and remodeling phases regardless of closure method and can move between phases based on intrinsic and extrinsic patient factors.

2. Occurring when a wound is closed within a few
hours of its creation. Wound edges are surgically or mechanically
approximated, and collagen metabolism provides long-term strength.
Occurs when a poorly delineated wound
is left open to protect against wound infection. The open wound allows
for the natural host defense to debride the wound before closure.
Occurs when an open full thickness wound is
allowed to close by wound contraction and epithelialization.
Thickness Wounds – Occurs when a partial-
thickness wound is closed primarily by epithelialization. This wound
healing involves the superficial portion of the dermis. There is minimal
collagen deposition, and an absence of wound contraction.

4. Whether wounds are closed by primary intention, subject
to delayed primary closure or left to heal by secondary
intention1, the wound healing process is a dynamic one which
can be divided into three phases. It is critical to remember
that wound healing is not linear and often wounds can
progress both forwards and back through the phases
depending uponintrinsic and extrinsic forces at work within
the patient

8.  Two types of factor influence the wound healing :
A. Local feature :
1. infection.
2. Poor blood supply.
3. Movement.
4. Foreign body.
5. Exposure to ultraviolet ray.
6. Types , size and local of injury.

9.  Systemic feature:
 Age.
 Infection.
 Nutrition :arginine and vita A.
 Hypoxia.
 Anemia.
 Hypo perfusion.
 Metabolic disorder : D.M. And uremia .
 Steroid and radiation.

10.  Infection.
 Epidermal cyst formation.
 Pigmentation.
 Deficient scar formation.
 Incision hernia.
 Hypertrophied scars and keloid formation.
 Extensive contraction.
 Neoplasia.

14. Growth factor Abbreviation Main origin Effects
Epidermal growth factor EGF •Macrophages. Granulation
•Salivary gland. tissue formation.
•Keratinocytes.
Transforming growth TGF-α •Hepatocyte and
factor-α epithelial cell
proliferation.
•Activated
•Expression of
macrophages
antimicrobial
•T-lymphocytes
peptides.
•Keratinocytes
•Expression of
chemotactic
cytokines.
Hepatocyte growth factor HGF Mesenchymal Epithelial
cells and endothelial
cell proliferation
Hepatocyte
motility
Vascular endothelial growth VEGF Mesenchymal Vascular
factor cells permeability
Endothelial cell
proliferation

15. Platelet derived growth PDGF Granulocyte,
factor macrophage,
fibroblast and
smooth muscle
•Platelets cell chemotaxis
•Macrophages Granulocyte,
•Endothelial macrophage and
cells fibroblast
•Smooth muscle activation
cells Fibroblast,
•Keratinocytes endothelial cell
and smooth
muscle cell
Fibroblast growth factor 1 FGF-1, -2 Macrophages Fibroblast
and 2 Mast cells chemotaxis
T-lymphocytes Fibroblast and
Endothelial cells keratinocyte
Fibroblasts proliferation
Keratinocyte
migration
Angiogenesis