wound-healing-reading-chapters

SRPS Volume 10, Number 7, Part 1
tion include pain, pruritus, hyperpigmentation, disfigurement,
and decreased self-esteem (especially
in teenagers). Persistent pruritus is associated with
keloid formation. 274 Areas of the head and neck
that are spared include the eyelids and the mucous
membranes. 274
Rudolph 275 described a third type of abnormal
scar, the widespread scar, which apparently results
not from excessive collagen deposition but rather
from a mishap occurring during the third phase of
healing as a consequence of continued tension and
mobility of the wound. The typical widespread
scar is flat, wide, and often depressed.
ETIOLOGY AND PATHOGENESIS
The underlying mechanism of abnormal scars is
an excessive accumulation of collagen from increased
collagen synthesis or decreased collagen degradation.
276,277 A number of genetic and environmental
factors have been implicated in the pathogenesis of
hypertrophic scars and keloids (Fig 9).
Fig 9. Factors implicated in the pathogenesis of hypertrophic
scarring. (Reprinted with permission from Thomas DW et al: The
pathogenesis of hypertrophic/keloid scarring. Int J Oral Maxillofac
Surg 23:232, 1994.)
The most common triggering mechanism for
keloid formation is earlobe piercing, although
localized skin trauma, vaccination, hormonal excess,
increased skin tension, genetic factors, and other
minor factors have also been implicated. 278 Virtually
all abnormal scars are associated with trauma,
including surgery, lacerations, tattoos, burns, injections,
bites, vaccinations, and occasionally blunt
impact. 271 Skin tension is frequently implicated,
especially in hypertrophic scar formation. Areas of
high skin tension, such as the anterior chest, shoulders,
and upper back are commonly involved. 279,280
Brody and colleagues 281 point out that hypertrophic
scars may result from compressive forces across the
scar rather than excessive tension, as hypertrophic
scar contractures occur only on the flexor surfaces
of joints. Other local etiologic factors include wound
infection or anoxia, prolonged inflammatory
response, and a wound orientation different from
the relaxed skin tension lines.
Tissue hypoxia has been implicated in keloidal
scar formation. 282 The mechanism by which
hypoxia may lead to keloidal scar formation is
unclear. Vascular endothelial growth factor (VEGF)
is released from fibroblasts in response to hypoxia.
Gira et al 283 found that VEGF production was
abundant in keloids and the source of the VEGF
was the overlying epidermis. In contrast,
Steinbrech et al 284 found no difference in levels
of VEGF between keloidal fibroblasts and normal
dermal fibroblasts.
There is a theory that keloidal scars are caused
by an immune reaction to sebum. 285 Proponents
suggest random damage to pilosebaceous structures
in the skin. 286 This theory is supported by the following
observations: keloids are more common in
adolescence; they rarely occur on the palms and
soles; spontaneous keloids occur in skin areas with
sebaceous activity; and one scar may be keloidal
whereas an adjacent scar may be normal.
Keloids can be considered a mesenchymal neoplasm.
Keloid fibroblast have been shown to contain
the oncogene gli-1 and express the protein
Gli-1, 287 and in this regard are similar to basal cell
carcinomas. This oncogene is not expressed in
fibroblasts from normal tissue and non-hypertrophic
scars (no reports in the literature whether it is
expressed in fibroblasts of hypertrophic scars).
A detailed review of keloids, their etiology, pathogenesis,
and treatment by Shaffer et al 288 is highly
recommended. A brief discussion of the differences
between keloids and hypertrophic scars is
presented.
EPIDEMIOLOGY
Keloids are far more common in blacks than in
other races, whereas other abnormal scars do not
exhibit an ethnic predilection. Even though they
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