2. • Wound is a break in the integrity of skin or
tissues; associated with disruption and
function.
3. • Injury to tissue may result in cell death &
destruction
• The inflammatory response to microbes and
injured tissues not only serves to eliminate
these dangers, but also sets into motion the
process of repair.
• Healing is an attempt to restore the normal
structure and function
4. What is Repair????
• Repair or healing refers to the restoration of
tissue architecture and function after an
injury.
5. • Repair of damaged tissues occurs by two types
of reactions:
1. Regeneration by proliferation of residual
(uninjured) cells and maturation of tissue
stem cells
2. Deposition of connective tissue to form a scar
6. REGENERATION
• Some tissues are able to replace the damaged
components and essentially return to a
normal state
• Occurs by proliferation of cells that survive the
injury and retain the capacity to proliferate
7. Connective tissue deposition (scar
formation)
• If the injured tissues are incapable of
complete restitution, or if the supporting
structures of the tissue are severely damaged,
repair occurs by the laying down of connective
(fibrous) tissue SCAR
8. • Types of cells on the basis of regeneration
capacity—
1. Labile cells(continuous proliferation
throughout life) Bone marrow cells, cells
lining skin, GIT, transitional cell of bladder
2. Stable cell(undergo replication only when
stimulated) Liver, renal tubules,
chondroblasts, osteoblasts
3. Permanent cells( do not replicate after
birth) Neurons, skeletal muscle, cardiac
muscle cells
9. STEPS IN SCAR FORMATION
• Angiogenesis/Neovascularisation.
• Formation of granulation tissue.
• Remodelling of connective tissue
10. ANGIOGENESIS(NEOVASCULARISATION)
• Formation of new blood vessels, which supply
nutrients and oxygen needed to support the
repair process.
• New vessels sprout from the parent vessels
and migrates towards the area of damage.
11. STEPS IN ANGIOGENESIS
• Vasodilation and increased permeability
• Separation of pericytes from the abluminal
surface and breakdown of the basement
membrane to allow formation of a vessel
sprout
• Migration of endothelial cells toward the area
of tissue injury
12. • Proliferation of endothelial cells just behind
the leading front of migrating cells
• Recruitment of periendothelial cells (pericytes
for small capillaries and smooth muscle cells
for larger vessels) to form the mature vessel
• Suppression of endothelial proliferation and
migration and deposition of the basement
membrane.
14. GRANULATION TISSUE FORMATION
• Migration and proliferation of fibroblasts and
deposition of loose connective tissue,
together with the vessels and interspersed
leukocytes granulation tissue
16. DEPOSITION OF CONNECTIVE TISSUE
• The laying down of connective tissue occurs in
two steps:
1. Migration and proliferation of fibroblasts
into the site of injury.
2. Deposition of ECM proteins produced by
these cells
17. FACTORS INFLEUNCING TISSUE REPAIR
• Infection
• Diabetes
• Nutritional status
• Foreign bodies
• Mechanical factors
• Type and extent of tissue injury
• Location of injury
19. HEALING BY FIRST INTENTION
• Injury involving only the epithelial layer.
• The incision causes only focal disruption of
epithelial basement membrane continuity and
death of relatively few epithelial and
connective tissue cells
20. • Wounding causes the rapid activation of
coagulation pathwaysblood clot on the
wound surface .
• The clot serves to stop bleeding .
• As dehydration occurs at the external surface
of the clot, a scab covering the wound is
formed.
21. FIRST 24 HOURS
• Neutrophils are seen at the incision margin,
migrating toward the fibrin clot.
• They release proteolytic enzymes that begin
to clear the debris.
• Basal cells at the cut edge of the epidermis
begin to show increased mitotic activity.
22. 24 to 48 HOURS
• Epithelial cells from both edges have begun to
migrate and proliferate along the dermis,
depositing basement membrane components
as they progress.
• The cells meet in the midline beneath the
surface scab, yielding a thin but continuous
epithelial layer that closes the wound.
23. BY DAY 3
• Neutrophils have been largely replaced by
macrophages, and granulation tissue
progressively invades the incision space.
• Collagen fibers are now evident at the incision
margins.
• Epithelial cell proliferation continues, forming
a covering approaching the normal thickness
of the epidermis
24. DAY 5
• Neovascularization reaches its peak as
granulation tissue fills the incisional space.
• The fibroblasts produce ECM proteins and
collagen fibrils become more abundant and
begin to bridge the incision.
• The epidermis recovers its normal thickness as
differentiation of surface cells yields a mature
epidermal architecture with surface
keratinization.
26. END OF FIRST MONTH
• Scar comprises a cellular connective tissue
largely devoid of inflammatory cells and
covered by an essentially normal epidermis.
• However, the dermal appendages destroyed in
the line of the incision are permanently lost.
• The tensile strength of the wound increases
with time.
27. HEALING BY SECOND INTENTION
(SECONDARY UNION)
• When cell or tissue loss is more extensive,
such as in large wounds, abscesses, ulceration,
and ischemic necrosis in parenchymal organs,
the repair process involves a combination of
regeneration and scarring.
28. • Inflammatory reaction is more intense, there
is development of abundant granulation
tissue, accumulation of ECM and formation of
a large scar and wound contraction by the
action of myofibroblasts.