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Pembimbing
dr. Deddy Saputra, Sp. BP-RE
Chapter 6
Wound Healing: Normal and Abnormal
Mechanisms and Closure Techniques
Phases Of Wound Healing
Cytokines/Chemokines and Growth Factor
Disturbances Of Wound Healing
Chronic Wounds and Abnormal Scar
Formation
Wound Closure
Early Phases
Intermediate Phases
Late Phases
Terminal phases
In first 24 hours after injury, thickening of the basal cell layer begins.
Marginal basal cells elongate, detach from the underlying basement
membrane, and migrate into the wound as a monolayer across the
denuded area. Migrating orient themselves along collagen fibers
and exhibit what is called contact guidance.
Basal cells at the edge of the denuded area begin to divide 48 to72
hours after injury. Epithelial cell proliferation contributes new cells to
the advancing epithelial monolayer. Cells migrate until they reach
cells migrating from a different direction( contact inhibition)
differentiate into more basal-like cells with hemidesmosomes.
Cellular proliferation continues in the new basal cells as a
multilayered epidermis is reestablished. Subsequently, new surface
cells begin to keratinize.
Local Factor
Infection
Hypoxia and Smoking
Delivery of oxygen to healing tissues is critical for
prompt wound repair. Oxygen is necessary for
cellular respiration and for hydroxylation of proline
and lysine residues.
Smoking can impair tissue oxygenation as it
acutelystimulates vasoconstriction
Radiation
Fibroblasts that migrate into irradiated tissue
are often abnormal, Collagen is sinthesized
to an abnormal degree in irradiated tissue,
causing a characteristic fibrosis.
The decreased vascularity and increased
fibrosis limits the ability of platelets and
inflammatory cells to gain access to
wounds in the area. The quantity of
cytokines released is therefore limited.
Systemic Factors
Malnutrition
Collagen synthesis essentially stops in the absence of protein
intake resulting in impaired healing
Wound healing slows when carbohydrate or fat stores are
limited.
Vitamin C is a necessary cofactor for hydroxylation of
lysine and proline during collagen synthesis
Vitamin A is essential for normal epithelialization,
proteoglycan synthesis, and normal immune function
Vitamin D is required required for bone healing.
Exogenous vitamin E impairs wound healing in rats, most
likely by influencing theinflammatory response in a
corticosteroid-like manner
Zinc deficiency can therefore result in an inhibition of cellular
proliferation and deficient granulation tissue formation and
healing
Cancer
Cancer-induced cachexia, which manifests itself as weight
loss, anorexia, and asthenia, significantly limits healing.
glucose turnover may be increased,leading to glucose
intolerance, protein catabolism may be accelerated, unable to
alter their metabolism to conserve energy by relying on fat for
most of their energy needs. Vitamin C may be preferentially
taken up by some tumors
Macrophages do not migrate or function normally in cancer
patients. Inflammatory cell dysfunction may limit the
availability of cltokines required for healing and may also
predispose to
infection.
Advanced Age
The elderly have been shown to heal less
efflciently than younger individuals.
Diabetes
Diabetes is associated with impaired
neutrophil chemotaxis and phagocytic
function
Chemotherapeutic Agents
Chemotherapeutic agents impair healing
primarily through inhibitidn of cellular
proliferation
CHRONIC WOUNDS
Any wound that is affected by compromising
factors may become a chronic wound. Chronic
wounds do not respond to standard care and
remain substantially unhealed beyond the 6week period typically required for normal wound
healing. They are also characteized by slow
progression of either re-epithelialization or
contraction.