Biomedical Engineering Reference
In-Depth Information
functions. It serves as an energy-absorbing pad that minimizes mechanical injury
to skin. It also serves as an energy reservoir (packaged in the form of lipids) which
can be easily accessed, and catabolized on demand.
4.3
Wound repair and scar formation
In normal skin, the dermis and epidermis exist in a steady-state equilibrium
(with many complex and interdependent components), forming a protective
barrier against the external environment. When the protective barrier is broken,
the structural
integrity is compromised, the underlying vasculature is disrupted
and the physiological process of wound healing is immediately set in motion.
The classic model of wound healing involves dividing the process into four
sequential phases: (1) hemostasis, (2) inflammatory, (3) proliferative and (4)
remodeling. Although each phase is distinct, there is considerable overlapping
between them.
In brief, upon injury to the skin, platelets aggregate at the injury site to
degranulate, thereby initiating the clotting cascade. Within minutes, a fibrin clot is
formed and hemostasis is achieved. Within 24 hours, neutrophils arrive at the
wound site, ushering in the inflammatory phase (which lasts 3-4 days.)
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Neutrophils
scavenge for foreign materials, bacteria and damaged tissue for phagocytosis.
Macrophages appear thereafter (in day 1-2) to continue the task of phagocytosis
and in addition, secrete cytokines. Once non-essential debris has been removed,
fibroblasts (either mature or perhaps a precursor form) and endothelial cells (or
progenitors) are recruited into the wound microenvironment, signaling the begin-
ning of the proliferative phase. During the proliferative phase (occurring from day
4 to day 14), fibroblasts propagate and proliferate, depositing new matrix materials
(mainly collagen.) Concurrently, vascular endothelial cells (or precursors) assem-
ble themselves to form microvascular structures. During the remodeling phase
(which begins after week 2, and lasts between weeks and months), excess matrix
materials are removed, collagen fibers are cross-linked (strengthening the matrix)
and contraction of the ECM (by myofibroblasts) occurs.
Alternatively, cutaneous wound healing may be described in terms of an 'early
phase' and a 'cellular phase'. This would render less overlapping of the many
elements involved. In the early phase, hemostasis is accomplished and cytokines
are released, initiating the inflammation process. In the cellular phase, an inflam-
matory response is mounted, the dermis is repopulated, wound coverage is
achieved (re-epithelialization) and a scar is formed.
4.3.1
Early phase
The early phase of wound healing begins immediately following injury. Damage
to dermal structures, especially blood microvessels, triggers a cascade of mole-
cular and cellular events, resulting in a hemostatic plug covering the wound site.
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