Biomedical Engineering Reference
In-Depth Information
This fl uence will vary depending on the pulse width and
spot size.
In addition to improvement in erythema and fl attening of
scars, there is a clear reduction in itching and pain as well as
optimization of skin texture (31).
Not all reports have been as positive. Allison et al. (43) found
the PDL to be effective in alleviating the intense pruritus that
often occurs during the healing of a burn injury but did not reveal
signifi cant reduction in scar redness or improvement in height
and texture of the scars. In a similar manner, Chan et al. (44)
treated one-half of each of 27 hypertrophic scars using 585 nm,
5-mm spot, 7-8 J/cm 2, and 2.5-ms pulse with three to six treat-
ments. They found signifi cant improvement in pain and touch
sensitivity on the treated side, but no improvement in thickness
or elasticity of the treated side. Perhaps the small spot site and
relatively high fl uence had some negative effects on their out-
come. Karsai et al. (42) report that 5-10 PDL sessions lead to only
a moderate reduction in hypertrophy but a signifi cant decrease in
pain and irritation.
The mechanism of action of the PDL on scars is unclear.
The laser's specifi c targeting of vessels may damage the micro-
vasculature directly, leading to hypoxia and an increase in col-
lagen degradation. In addition, superheating of collagen fi bers
can result in the dissolution of disulfi de bonds (45) and subse-
quent collagen fi ber realignment with decreased fi broblast
proliferation as well as release of histamine (13). It is interest-
ing how similar this thesis is to the proposed mechanism of
action of the argon laser, another vascular-targeting laser.
These hypotheses are supported by work done by Reiken et al.
on hypertrophic scar implants in athymic mice (46). The degree
of inhibition of scar growth was found to be proportional to
PDL fl uence that was used, ranging from 6 to 10 J/cm 2 . They
also found maximum effect at the lowest wavelength tested
(585-600 nm). On histological examination, signifi cant vessel
wall necrosis was seen in the treated scars, confi rming that the
microvasculature is the primary target. A decrease in mast cells
was also seen after treatment and this is thought to alter fi bro-
blast proliferation and contribute to success as well (45).
Alster and Williams (34) reported that their biopsy studies
showed a proliferation of mast cells. These mast cells could indi-
rectly infl uence the proliferation of fi broblasts through the
release of histamine, which may contribute to keloid develop-
ment (47). Histamine would be released right after treatment
and prolonged mast cell activity has been associated with
increased scar “activity,” because histamine is capable of enhanc-
ing collagen synthesis (48).
Biochemical studies performed by Kuo et al. (49,50) have
shown a decrease in the induction of transforming growth
factor-beta1 (TGF-
CTGF will attenuate only pathologic scarring (55) and the
PDL role in this regard is likely to be one of its mechanisms of
action on keloids.
The optimum time for treatment has not been defi nitively
determined, but most clinicians agree that early treatment is
preferable. McCraw and colleagues (51) have promoted early
postoperative initiation of PDL treatment in order to prevent
excessive scar formation. They described scar prevention
effects by treating surgical wounds either 2 weeks after surgery
or 1-2 weeks after suture removal. Scar induration and redness
were diminished as was the incidence of hypertrophic scar-
ring. This concept is supported by Mancini et al. (5) who
showed that keloid fi broblasts do not deviate from their nor-
mal pattern for at least 3 weeks after surgery. Therefore, initiat-
ing treatment at 2-3 weeks after surgery may be preventative.
Nouri et al. (55) treated one-half of each surgical scar in
11 patients starting on the day of suture removal, twice more
at monthly intervals using the PDL. A defi nite improvement in
the treated half was seen using the Vancouver Scar Scale. They
also recommend using a larger spot size.
The most common adverse side effect of 585-nm PDL treat-
ment is purpura, which usually takes 7-10 days to resolve.
Hyperpigmentation has been reported to occur in 1-24% of
patients (56,57). Transient hypopigmentation and blistering
have also been reported (37,44).
nonablative fractional
resurfacing for scars
In 2004, Manstein and Anderson introduced a new concept of
skin treatment called fractional photothermolysis (FP) that
delivers an array of microscopic treatment zones (MTZs) of
thermal damage of controlled depth, width, and density to the
skin (58). These MTZs are surrounded by untreated areas of
viable epidermis and dermis that allow for rapid repair of
these small volumes of thermal heating and tissue damage.
Laubach and colleagues provided a detailed histologic study
on the biologic response to nonablative fractional resurfacing
(NAFR) using a prototype diode laser (59). Within 1 hour after
laser irradiation, well-defi ned columns of epidermal and der-
mal thermal damage are evident, but the overlying stratum
corneum remains intact. The importance of preserving the
stratum corneum is that it protects against possible bacterial
infection as it serves as a barrier function of the skin and also
enhances hydration of the underlying wound. Within 24 hours,
viable cells from the periphery of the MTZs migrate and prolif-
erate rapidly to replace the thermally damaged epidermis (60).
Exfoliation of coagulated tissue occurs from the formation of
microepidermal necrotic debris (MENDs). Studies have shown
that MENDs comprise thermally damaged epidermal and der-
mal cells along with melanin and elastin (61,62). MENDs
undergo transepidermal extrusion between 3 and 7 days, and
initiation of a biologic signaling cascade is seen by an increased
expression of cellular markers of dermal wound healing and
neocollagenesis such as heat shock protein 70, proliferating cell
nuclear antigen,
1) and upregulation of matrix metallopro-
teinase (MMP) expression in keloid tissue treated with a
585-nm PDL. This would favor collagen degradation and fi bro-
blast apoptosis. They reported 50% improvement in 26 of
30 patients with keloids after fi ve to six treatments using 585 nm,
0.45-ms pulse, 5-mm spot, and 10-18 J/cm 2 (51).
A study (52) has shown that PDL treatment of keloids
downregulates the expression of connective tissue growth fac-
tor (CTGF) in greater than 80% of patients studied. CTGF is
not found in normal skin but found only in pathological scar
tissue, specifi cally keloids (53). Blocking TGF-
β
α
-smooth muscle actin, collagen III, and
TGF-
(58,59).
Clinically, fractional resurfacing with nonablative micro-
scopic delivery of high energies to targeted depths in the der-
mis has allowed signifi cant clinical improvement, including
photodamage, scarring, and dyspigmentation. The fractional
β
will affect
both normal and pathologic scarring (54), whereas blocking
β
 
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