Repair

Department of pathology
healing Cutaneous wound

Divided into 3 phases

1. Inflammation (early & late)
2. Granulation tissue formation &
re – epithelialisation
3. Wound contraction
healing Cutaneous wound - types

Skin wounds heal in two ways depending on the nature of wound:

1. Healing by first intention (primary union) (wounds with opposed
edges or surgical wounds)
2. Healing by secondary intention (secondary union) (wounds with
separated edges)
healing First intention

• It is the healing of clean,

uninfected, surgical incision
• The wound edges are
approximated by sutures
• Limited epithelial & connective
tissue loss is seen;
• Basement membrane is
disrupted
healing First intention

Incisional space fills up with clotted

Blood;

Dehydration of the surface clot leads

to scab formation
Healing by First intention

Within 24 hours
• Neutrophils appear at the
margins of the incision &
migrate into fibrin clot
• Basal cells at edges increase
mitotic activity
24 – 48 hours
• Epithelial cells migrate and
proliferate
• Deposition of basement
membrane
Healing by First intention

3 – 7 days
• Macrophages replace
neutrophils
• Neovascularization
• Granulation tissue formation
• Deposition of collagen bundles
• Bridging of wound
• Epithelial cells continue to
proliferate
Healing by First intention

Week 2 ( day 14)

• Collagen accumulation
continues to increase
• Fibroblast proliferation
• WBC and edema decreases
• Vascular channels regress
• Blanching
4 weeks
• scar formed by fibroblasts and
collagen
• Few inflammatory cells
• Tensile strength increases
Healing by Second Intention

Injury is more extensive with excessive tissue

Loss
• More inflammation
• More fibrin
• More granulation tissue
• More complex repair process
• wound contracts – original wound is reduced
to 5 – 10% of its original size; it is due to
action of actin containing fibroblasts &
myofibroblasts.
• There is more substantial scar formation
Healing by Second Intention – wound strength

• At suture removal: 10% of the original tensile strength

• Rapid increase over next 4 weeks
• At third month: 70-80%
Factors which might impair wound Repair
Systemic Factors Local factors

1. Age – very young and old

2. Disorders of nutrition
3. Vitamin C deficiency (collagen)
4. Glucocorticoids
(immunosuppression, interfere
with formation of granulation
tissue and wound contraction)
5. Diabetes/ immunosuppression
(increase susceptibility to low
virulence organisms)
1. Infection
2. Poor blood supply
3. Foreign bodies
4. Type and volume of tissue
injured
5. Location of the injury
6. movement
Complications of wound healing
Wound dehiscence

1. Wound dehiscence
2. Implantation(epidermal inclusion ) cyst
3. Pigmentation
4. Weak scar
5. Incisional hernia
6. Keloid formation
7. Contractures
8. Adhesions
9. Exuberant granulation tissue (proud
flesh)

proud flesh
Complications of Scarring

1. Loss of function:
• Scar tissue lacks specialized structures; LOSS OF STRUCTURE =
LOSS OF FUNCTION!
2. Contractures and Obstructions: Scar tissue is not elastic and
shortens over time;
• Decreased movement;
• Results in fixation/deformity of joint (contracture)
• Shortening of scar tissue results in shortening or narrowing
(stenosis) esp. of tubes and ducts
3. Adhesions: Bands of scar tissue; Joins 2 surfaces that are normally
separate; Prevent normal movement and can cause distortion or
twisting
Complications of Scarring
1. Hypertrophic scar & keloid

contracture
Complications of Scarring - Keloid

1. Keloids are overgrowth of dense fibrous

tissue that usually develops after healing
of a skin injury. The tissue extends
beyond the borders of the original
wound, does not usually regress
spontaneously, and tends to recur after
excision.
2. As many as 16% of people in a random
sampling of black Africans reported
having keloids.
3. Associated with HLA-B14, HLA-B21, HLA-
Bw16, HLA-Bw35, HLA-DR5, HLA-DQw3,
and blood group A.
Complications of Scarring - hypertrophic scars

• hypertrophic scars are characterized by

erythematous, pruritic, raised fibrous lesions
that typically do not expand beyond the
boundaries of the initial injury and may
undergo partial spontaneous resolution.
Hypertrophic scars are common after
thermal injuries and other injuries that
involve the deep dermis.
Healing in liver
1. Hepatocytes have excellent
regenerative capacity
2. If Hepatic architecture is
excessively damaged, poor
reconstruction leading to
fibrosis, sometimes cirrhosis, a
combination of parenchymal
regeneration & Scar formation
Healing of Fracture
Phase I:
1. Bleeding & fracture hematoma
forms
2. Inflammation
3. Next 2-3 Days, granulation tissue
formation
4. Osteogenic Cells invade tissue
and lay down osteoid
Healing of Fracture

Phase II
1. At 3 weeks a soft callus forms consisting of
osteoid (woven bone) and cartilage
2. Hard tissue callus (woven bone is
converted to lamellar bone) forms in 6 -
12 weeks
3. Clinical union of bone ends occurs in 12 -
16 weeks
Phase III
8. Remodeling of united fracture
Healing of renal tissue

1. Epithelium regenerates: so
tubular damage can regenerate
2. Architecture loss is not
restored; so glomerular
damage is permanent & is
replaced by scar with loss of
filtration capacity
3. Interstitial damage leads to
fibrosis
Healing of muscle injury

1. Cardiac and smooth muscle – permanent population and are

replaced by scar tissue

2. Voluntary (skeletal) muscle – limited capacity for regeneration from

satellite cells; regeneration depends on intact muscle sheath
Neural tissue

1. Neurons are permanent cells; so central nervous system does not

repair effectively
2. Glial cells proliferate in response to injury to produce a glial scar or
gliosis.
3. Peripheral nerve damage shows wallerian degeneration distal to
trauma and recovery depends on alignment and continuity
Neural tissue

When nerve fibers are cut, the end of the fiber

farthest from the brain dies, while the sheath
stays intact, leaving empty tubes. The end that
is closest to the brain does not die, and after
some time may begin to re-grow. If the sheath
was not cut, the nerve fibers may grow down
the empty tubes until reaching a muscle or
sensory receptor. If both the nerve and sheath
have been cut and the cut ends are not
sutured/ realigned, the growing nerve fibers
may grow into a ball at the end of the cut,
forming a mass called a ‘neuroma’.