TISSUE INJURY AND REPAIR
SKIN STRUCTURE
ANATOMY:
Epidermis:
stratified, keratinized
avascular
a. Stratum germinativum (basal layer)
- hemodesmosomes connect basal
cells to basement membrane
- melanocytes melanin –
keratinocytes
b. Stratum spinosum
- desmosimes connect cells spiny
appearance
c. Stratum granulosum
- cyltoplasm contains granules that
later contribute to keratin
d. Stratum lucidum
- layer of dead cells without nuclei
e. Stratum corneum
- nearly acellular layer of keratin
Dermis:
a. Papillary dermis
- superficial thin layer of loose
vascular tissue
b. Reticular dermis
- deeper layer of denser tissue, less
vascular
contains sweat glands, hair follicles,
sebaceous glands, nerve endings &
blood vessels
fibroblasts, adipocytes, macrophages,
collagen, & ground substance
ADNEXA:
hair follicle
eccrine sweat gland
apocrine sweat gland
COLLAGEN:
Type I: skin, tendon, mature scar
Type II: cartilage
Type III: blood vessel & immature scar
Type IV: basement membrane
Vitamin C (ascorbic acid) – coenzyme
involve in hydroxylation of praline & lysine
NORMAL WOUND HEALING:
WOUND CLOSURE:
a. Primary closure
b. Delayed primary closure
c. Secondary closure
PHASES OF WOUND HEALING:
1. INFLAMMATORY PHASE
- begins at time of injury; lasts 2-3
days
- vasoconstriction platelet plug
clotting cascade fibrin deposition
- platelet release PDGF and TGF-β
attracting inflammatory cells
(macrophages)
- vasodilatation
- neutrophils peak at 24 hours
- monocytes enter wound
macrophages
- lymphocytes arrived later
- macrophages produce PDGF & TGF-
β attracting fibroblasts & collagen
formation
2. PROLIFERATIVE PHASE
- day 3 to week 3
- collagen synthesis (Type III),
angiogenesis, epithelialization
- total collagen content increases for 3
weeks until collagen production =
collagen breakdown
3. REMODELLING PHASE
- 6 months to 1 year
- Type I collagen replaces Type III
- wound strength increases
- vascularity decreases
- wound contraction – fibroblasts &
myofibroblasts
FACTORS CONTRIBUTING TO IMPAIRED
WOUND HEALING:
1. Local Factors
a. arterial insufficiency
b. venous insufficiency
c. edema
d. infection
e. pressure
f. radiation
g. foreign material or necrotic tissue
2. Systemic Factors
a. diabetes mellitus
b. malnutrition
c. vitamin deficiency
d. chemotherapy
e. smoking
f. aging
g. glucocorticoids
CHRONIC WOUND:
wounds that do not heal in 3 months
Approach:
1. adequate debridement
2. treatment of infection
3. appropriate wound dressings
4. treatment of local & systemic factors
EXCESSIVE WOUND HEALING:
KELOIDS:
scar tissue that extends beyond the
boundaries of the incision or wound
etiology: not understood, growth factor
inherited autosomal dominant pattern
common in earlobes & areas of tension
Treatment:
- excision alone is rarely successful
- corticosteroid injection may cause
some reduction in keloid size
- excision followed by corticosteroid
injection locally is more successful
- excision should be followed by
radiation therapy for severe cases
- recurrence is common
HYPERTROPHIC SCARS:
scar tissue that does not extend beyond
the boundaries of the incision or wound
etiology: prolonged inflammatory phase
of healing, increased wound tension
less genetic component than keloids
tendency decreases with age
more common in areas of tension:
presternal area
Treatment:
- corticoid injection, silicone sheeting
and pressure
- surgical excision