C h a p t e r 4
Cell Proliferation and Tissue Regeneration and Repair
83
Blood vessel
Fibrous scar
Wound
contraction
Wound Contraction and
Remodeling Phase.
This phase
begins approximately 3 weeks after
injury with the development of the
fibrous scar, and can continue for 6
months or longer, depending on the
extent of the wound. During this
phase, there is a decrease in vascu-
larity and continued remodeling of
scar tissue by simultaneous synthesis
of collagen by fibroblasts and lysis
by collagenase enzymes. As a result
of these two processes, the architec-
ture of the scar becomes reoriented
to increase its tensile strength, and
the scar shrinks so it is less visible.
3
The role of minerals in wound healing is less clearly
defined. The major minerals, including sodium, potas-
sium, calcium, and phosphorus, as well as trace min-
erals such as copper and zinc, must be present for
normal cell function. Zinc is a cofactor in a variety
of enzyme systems responsible for cell prolifera-
tion. In animal studies, zinc has been found to aid in
reepithelialization.
Blood Flow and Oxygen Delivery
Impaired healing due to poor blood flow and hypoxia
may occur as a result of wound conditions (e.g., swell-
ing) or preexisting health problems.
24,25
Arterial disease
and venous pathology are well-documented causes
of impaired wound healing. In situations of trauma,
a decrease in blood volume may cause a reduction in
blood flow to injured tissues.
For healing to occur, wounds must have adequate
blood flow to supply the necessary nutrients and to
remove the resulting waste, local toxins, bacteria,
and other debris. Molecular oxygen is required for
collagen synthesis and killing of bacteria by phago-
cytic white blood cells. It has been shown that even
a temporary lack of oxygen can result in the forma-
tion of less-stable collagen.
24
Wounds in ischemic tis-
sue become infected more frequently than wounds
in well-vascularized tissue. Neutrophils and macro-
phages require oxygen for destruction of microorgan-
isms that have invaded the area. Although these cells
can accomplish phagocytosis in a relatively anoxic
environment, they cannot digest bacteria. Oxygen also
contributes to signaling systems that support wound
healing. Recent research suggests that almost all cells
in the wound environment are fitted with specialized
enzymes to convert oxygen to reactive oxygen species
(ROS).
24
These ROS function as cellular messengers
that support wound healing, stimulating cytokine
action, angiogenesis, cell motility, and extracellular
matrix formation.
The availability of respired oxygen to wound tis-
sues depends on vascular supply, vasomotor tone, the
partial pressure of oxygen (PO
2
) in arterial blood, and
the diffusion distance for oxygen (see Chapter 21). The
central area of a wound has the lower oxygen level,
with dermal wounds ranging from a PO
2
of 0 to 10 mm
Hg centrally to 60 mm Hg in the periphery, while the
PO
2
of arterial blood is approximately 100 mm Hg.
24
Transcutaneous oxygen sensors are available for use
in measuring wound oxygenation. From a therapeu-
tic standpoint oxygen can be given systemically or
administered locally using a topical device. Although
topical oxygen therapy is not likely to diffuse into the
deeper tissues, it does have the advantage of oxygen-
ating superficial areas of the wound not supported by
intact vasculature. Hyperbaric oxygen therapy delivers
100% oxygen at two to three times the normal atmo-
spheric pressure at sea level.
26
The goal of hyperbaric
oxygen therapy is to increase oxygen delivery to tissues
by increasing the partial pressure of oxygen dissolved in
(
text continued from page 81
)
