REVIEW ARTICLE

Advanced Treatment Modalities for Vitiligo

NISHIT S. PATEL, MD, KAPILA V. PAGHDAL, PHARMD, MD, AND GEORGE F. COHEN, MD*

BACKGROUND Vitiligo is an acquired multifocal and polygenic dyschromia that affects 1% to 3% of the
world and presents as multiple depigmented macules and patches. Traditionally, the treatment of vitiligo
has focused on pharmacologic interventions, but nearly half of all treated patients fail to respond success-
fully.
OBJECTIVE Several advanced techniques exist that can aid dermatologists in treating vitiligo in patients
who do not respond favorably to traditional pharmacologic treatments. These advanced interventions
include the use of the 308-nm excimer laser, total body depigmentation therapy with monobenzyl ether of
hydroquinone, microdermabrasion, micropigmentation, khellin-UVA therapy, and surgical management
using miniature punch grafting, suction blister grafting, and epidermal cultures.
MATERIALS AND METHODS This article reviews the current literature on these advanced treatment
modalities for vitiligo and provides a practical guide for application of these techniques.
RESULTS AND CONCLUSION Our ability to treat vitiligo may be imperfect, but through appropriate
patient selection and careful application of one or more of these advanced therapies, successful treatment
of vitiligo, even in patients refractory to treatment, can be achieved.
The authors have indicated no significant interest with commercial supporters.

V itiligo is an acquired multifocal and polygenic

dyschromia that manifests primarily as depig-
mented macules and patches on the skin.1,2 Vitiligo
affects all ages, races, and sexes equally but is most
clinically apparent in patients with darker skin.
The prevalence of vitiligo is estimated to be
between 1% and 3% globally, with an incidence
of 1% in the United States. Vitiligo can cause sig-
nificant psychosocial distress in patients, ultimately
affecting their self-esteem, their personal relation-
ships, and even their employment. In certain cul-
tures, it may cause the patient to be ostracized,
because it may easily be confused with an infec-
tious process, such as leprosy.
Many competing theories of the etiology of vitiligo
have been proposed, but no single unifying model
has been adopted. The most prominent theories
include autoimmune, oxidative stress, neural, and
viral theories.1 The autoimmune theory suggests
that the melanocytic destruction seen in vitiligo is
the result of an autoimmune phenomenon. The
presence of autoantibodies against melanocyte sur-
face antigens in patients with vitiligo, combined
with the discovery of a correlation between quan-
tity of autoantibodies and level of disease, provides
strong support for this model. The significant asso-
ciation between vitiligo and other autoimmune
phenomena, including alopecia areata, diabetes
mellitus, Addison’s disease, pernicious anemia,
Graves disease, Hashimoto’s thyroiditis, systemic
lupus erythematosus, rheumatoid arthritis, psoriasis
and inflammatory bowel disease provides addi-
tional support.1,2 The oxidative theory postulates
that the melanocytic destruction seen in vitiligo is
the result of toxicity from free radicals. Low levels
of erythrocyte glutathione (a limiter of free radi-
cals) and high serum nitric oxide levels in patients

*All of the authors were affiliated with the Department of Dermatology and Cutaneous Surgery, University of South
Florida, Tampa, Florida

© 2012 by the American Society for Dermatologic Surgery, Inc.  Published by Wiley Periodicals, Inc. 
ISSN: 1076-0512  Dermatol Surg 2012;38:381–391  DOI: 10.1111/j.1524-4725.2011.02234.x

381
 ADVANCED TREATMENT MODALITIES FOR VITILIGO
with vitiligo provides support for the oxidative
model. The neural theory suggests that vitiligo
results from release of mediators from nerves,
which results in a significant decrease in melanin
production. Cases of segmental vitiligo and biopsy
evidence of degenerative changes to axons, as well
as high neuropeptide-Y levels support this theory.
The viral theory proposes that vitiligo is the result
of direct damage to melanocytes by viruses, and
skin biopsies of vitiliginous areas that show the
presence of cytomegalovirus, hepatitis C, and
Ebstein-Barr virus support it. A convergence theory
has also been proposed that views vitiligo as a
syndrome that results from a convergence of all
proposed hypotheses.1
Successful treatment of vitiligo is often difficult,
and treatment modalities have traditionally cen-
tered on a combination of camouflage products,
topical corticosteroids, topical immunomodulators,
psoralen plus ultraviolet A light therapy (PUVA),
and ultraviolet B (UVB) light therapy.2 Successful
repigmentation occurs only for approximately half
of treated patients, leaving many patients without
a solution. This article explores several advanced
techniques available for the treatment of vitiligo,
including excimer laser, khellin ultraviolet-A light
therapy (KUVA), depigmentation therapy, micro-
pigmentation, autologous skin grafting (including
miniature punch grafting, suction blister grafting,
and epidermal cultures), and microdermabrasion.
We briefly review each of these techniques below,
in addition to the strengths and limitations of each
modality.
Excimer Laser
The 308-nm excimer laser, formally known as the
xenon chloride (XeCl) excimer (excited dimer)
laser, works by delivering a monochromatic and
coherent beam of narrow-band UVB (NbUVB)
photons at 308 nm in short pulses to vitiliginous
areas.3–5 It is postulated that this therapy works by
inducing migration of reservoir melanocytes from
the outer root sheath of hair follicles, resulting in
382 DERMATOLOGIC SURGERY
repigmentation of the vitiliginous area. Addition-
ally, the 308-nm wavelength is particularly effec-
tive at inducing apoptosis of T-lymphocytes,
requiring only 95 mJ/cm2, versus the 320 mJ/cm2
that traditional NbUVB therapy requires.
The excimer laser’s use of an articulated arm with
spot sizes ranging from 14 to 30 mm is especially
helpful because it allows for delivery of the therapy
only to the vitiliginous areas, even in difficult areas
such as skin folds.4,5 This level of control prevents
hyperpigmentation of adjacent healthy skin and
minimizes exposure of adjacent normal skin to
damaging UV radiation.
The excimer laser, even without the aid of any top-
ical medication, is highly effective at treating viti-
ligo, resulting in a repigmentation rate of greater
than 75% in 20% to 60% of patients depending
on dosage and location of treatment.3–6 Prelimin-
ary investigations into the efficacy of combination
treatment using the 308-nm excimer laser and topi-
cal medications, such as tacrolimus, have shown
promise for an even greater response rate.3,6–8
Treatment with the 308-nm excimer laser involves
application to clean, dry skin approximately one to
three times weekly on noncontiguous days for at
least 25 to 30 treatments.2,4 The more frequently
the patient is treated, the quicker the repigmenta-
tion is found to occur, with three times weekly
being the most effective, although the most impor-
tant predictor of response is the total number of
treatments, rather than the frequency of treat-
ments.4,9 The dose used should be based on each
patient’s minimal erythematous dose (MED),
which is the minimal dose sufficient to produce
mild erythema in the vitiliginous area for 24 hours
after application. Despite the lack of pigment in
the vitiliginous patches, the MED still tends to be
higher in people with Fitzpatrick skin types III to
VI than in those with types I and II.10 Initial
repigmentation generally occurs perifollicularly and
from the peripheral margins, with eventual coales-
cence and resolution of the vitiliginous patch. The

level of response varies greatly based on the loca-
tion of the skin, with UV-sensitive areas such as
the face, neck, trunk, and proximal extremities
responding best to therapy using the 308-nm exci-
mer laser.6,10,11 UV-resistant areas such as knees,
elbows, hands, and feet are much less responsive to
therapy (Figures 1 and 2).
Treatment is generally well tolerated, with only
minimal side effects reported, including mild to
moderate erythema, edema, burning, and sting-
ing.4,6 Rarely, more-severe effects, including severe
erythema or blister formation, may occur, requir-
ing a reduction of the UV dose.
A major limitation to widespread use of 308-nm
excimer laser therapy is the cost of treatments and
equipment maintenance, as well as the difficulty in
treating patients with large body surface area
involvement (>20%) because of the 30-mm maxi-
mum size of the laser focus.5 Additionally, many
insurance providers will not cover this therapy, so
appropriate discussion regarding the potential cost
to the patient before initiation of treatment is
essential.
Figure 1. Clinical photograph of a man with multiple, coa-
lescing depigmented patches involving the bilateral face
and chin. 57 Reprinted with permission from: Mouzakis
JA, Liu S, Cohen G. Rapid response of facial vitiligo to
308-nm excimer laser and topical calcipotriene. J Clin Aes-
thet Dermatol 2011;4:41–4. Copyright 2011 Matrix Medical
Communications. All rights reserved.
PATEL ET AL
Figure 2. Clinical photograph showing follicular repigmen-
tation of the patient from Figure 1 after undergoing 20
treatments with the 308-nm excimer laser. 57 Reprinted
with permission from: Mouzakis J, Liu S, Cohen G. Rapid
response of facial vitiligo to 308-nm excimer laser and top-
ical calcipotriene. 2011;4:41–4. Copyright 2011 Matrix Med-
ical Communications. All rights reserved.
Khellin Plus Ultraviolet A Light
PPUVA is a commonly used therapy for the treat-
ment of vitiligo. Although generally well tolerated,
PUVA therapy has been associated with phototox-
icity and can lead to risk of malignancy because of
psoralen’s ability to cause DNA mutations through
cross-link formation.12,13 An emerging alternative
to PUVA, KUVA, has recently been tested. Khellin
is a furochromone that is derived from the Ammi
visnaga plant seed, which functions similarly to
psoralen but has been found to form fewer cross-
links in DNA and is therefore less carcinogenic.13
The exact mechanism of action of KUVA is not
entirely understood but is believed to repigment vi-
tiliginous patches through stimulation of melano-
genesis and melanocyte proliferation.
Studies of systemic and topical KUVA have been
conducted, with systemic KUVA therapy found to
be as effective as PUVA.12,14,15 Systemic khellin is
generally well tolerated, with side effects of only
nausea and transaminitis being reported. Initial
investigations into topical KUVA demonstrated
38:3:MARCH 2012 383
 ADVANCED TREATMENT MODALITIES FOR VITILIGO
mixed results. In vitro studies with KUVA found a
narrow therapeutic window with an optimal dose
of 0.1 mmol/L and significant cytotoxicity to mela-
nocytes and fibroblasts when khellin concentrations
exceeded 0.5 mmol/L. The mixed results with topi-
cal KUVA may be because of the usage of an
inhibitory or cytotoxic concentration of khellin.
KUVA represents a promising alternative treatment
for patients with vitiligo that are planning to or
are currently undergoing PUVA. With KUVA,
patients can benefit from khellin’s less-mutagenic
and -carcinogenic properties (than of psoralen) and
avoid phototoxic skin erythema (as seen with
PUVA) while having a similar level of efficacy.13,14
Depigmentation Therapy
Depigmentation therapy consists of application of
monobenzyl ether of hydroquinone (MBEH) to
normally pigmented skin to induce destruction of
epidermal melanocytes, ultimately resulting in
more-uniform pigmentation.1 The exact mechanism
of MBEH remains unclear, but recent investiga-
tions have hypothesized that it works through
induction of necrotic changes in melanocyte plasma
and nuclear membranes.16 MBEH is the only Food
and Drug Administration (FDA)-approved drug for
depigmentation and is sold in the United States
and Europe as a 20% cream that can be concen-
trated or diluted as needed.1,16 Typically, applica-
tion of MBEH requires twice-daily application for
6 to 18 months, with special care taken to avoid
contact with other individuals for up to an hour
after application to avoid accidental depigmenta-
tion in other people.1,17 Occasional spontaneous
repigmentation in areas treated with MBEH has
been reported, but this remains uncommon.18
Appropriate patient selection is the most important
factor in deciding whether to use depigmentation
therapy. Therapy should be reserved for patients
with depigmentation involving a large portion of
the surface area of their skin (>50%), disfiguring
lesions, and nonresponsive lesions and for those
384 DERMATOLOGIC SURGERY
with significant impairment in their professional or
person lives.1,19 Although depigmentation is an
excellent therapeutic option for these select
patients, it carries with it significant psychosocial
consequences. Additionally, given the tumultuous
racial history of the United States and the contro-
versy surrounding the late Michael Jackson’s skin
transformation, there is the possibility of a negative
connation with the “bleaching” of skin of color.
The ideal patient should be capable of informed
consent because depigmentation is, at present, irre-
versible.19 Additionally, the patient must under-
stand that choosing to undergo depigmentation
therapy eliminates any possibility of repigmenta-
tion should further advances in vitiligo therapy be
discovered in the future. Patients must also be
aware that depigmentation therapy places them at
high risk for sunburns and that they will need life-
long sun protection and live with restrictions on
future sun exposure. Additionally, treated patients
will be at greater risk for cutaneous malignancies
and premature aging.
In our experience, depigmentation is best
approached in stages, with the most-visible areas,
such as the face and hands, depigmented first. This
approach evens the skin in publically viewable
areas in 3 to 12 months and gives the patient an
immediate benefit (Figures 3 and 4). Subsequently,
depending upon the patient’s desire and agreed-
upon goals for total body depigmentation, one can
proceed to other stages over time.
The most common side effect of MBEH is contact
dermatitis, which is usually irritant in nature.20,21
We have found that discontinuing the 20%
MBEH, followed by treatment with a mid- to
high-potency topical corticosteroid, and reinstitut-
ing the compound at 10% to 15% usually allows
the patient to continue the depigmentation process.
Other side effects of MBEH use include pruritus,
xerosis, and much less commonly, corneal pigment
deposition and conjunctival melanosis.17,22 There
have also been some concerns regarding MBEH’s

Figure 3. Clinical photograph of a man with significant de-
pigmented patches involving more than 50% of the head
and neck.
Figure 4. Clinical photograph of the patient from Figure 3
after successful depigmentation therapy with monobenzyl
ether of hydroquinone.
risks of systemic toxicity, but it has never been
seen in any patient in the author’s (GC) 30-year
experience.
PATEL ET AL
Micropigmentation
Micropigmentation, or tattooing as it is more com-
monly known, is a technique that involves the
injection of small inert pigmented granules,
approximately 6 lm in size, into the superficial
dermis.23 The granules are composed of inert, non-
toxic, insoluble chemicals that, once inserted into
the dermis, become relatively permanent by resid-
ing in mononuclear cells and collagen fibers. The
most common chemical composition of pigment
used for medical micropigmentation is iron oxide,
which produces a light to dark brown appearance
when injected.23,24 Delivery of the pigment into
the dermis is achieved through the use of electrical
tattooing machines that typically consists of an
array of several 25-G needles that penetrate
approximately 1 to 2 mm deep and can achieve up
to 9,500 strokes per minute.23 Before injection,
color matching is achieved by creating a paste or
colloidal suspension by mixing various dyes with
water, saline, or alcohol.
The cosmetic outcome of micropigmentation is lar-
gely dependent on operator skill, because the most
important factor for permanent uniform pigmenta-
tion is depth of the injection of the pigment gran-
ules.23,24 Ideally, all pigment should be inserted
approximately 1.5 mm deep, between the upper
and mid-papillary dermis. Granules that are
injected more superficially will be expelled shortly
after the procedure, and macrophages will remove
pigment that is injected too deep. Additional
factors that affect the cosmetic outcome include
thickness of the pigment paste, the number of nee-
dles in the tattooing machine, and the thickness
and elasticity of the recipient skin.
Micropigmentation is generally well tolerated with
minimal side effects, including localized infection,
edema, bleeding, and crusting in the first several
days after the procedure.23,25 Although rare, there
have been reports of granuloma formation, allergic
reaction, keloid formation, and reactivation of her-
pes simplex virus with micropigmentation.23,25 The
38:3:MARCH 2012 385
 ADVANCED TREATMENT MODALITIES FOR VITILIGO
provider’s ability to produce an exact color match
to nearby normally pigmented skin and the fanning
and fading of pigment over time limit the wide-
spread use of the procedure.24,25
With sufficient training, micropigmentation serves
as a useful tool in the treatment of stable vitiligo,
especially in darker-skinned individuals.26,27 It is
particularly useful in areas such as lips, skin folds,
nipples, and areolae, where other interventions are
often limited.23,24 Although mild fading of pigment
may occur over time, it can often be managed with
additional tattooing every 1.5 to 2 years.26 Over-
all, micropigmentation is a quick, simple, safe
intervention, producing a satisfactory long-term
cosmetic outcome for many patients.
Surgical Management
Autologous minigrafting is an important tool avail-
able in the treatment of stable vitiligo, which is
defined as stable-sized hypopigmented patches for
longer than 2 years.28 Surgical management
becomes especially important when it is apparent
that reservoir melanocytes have been depleted and
in traditionally recalcitrant areas: distal extremities
(hands, feet, fingers, toes, palms, soles), elbows,
knees, nipples, eyelids, and lips.29,30 Several
options are available for the surgical transplanta-
tion of melanocytes, including miniature punch
grafting, suction blister grafting, transfer of noncul-
tured epidermal suspension, and transfer of
cultured melanocytes.30
As is the case with many treatments for vitiligo,
appropriate patient selection is the key to ensuring
the best outcome. Before proceeding with surgical
management, it is recommended that a test mini-
graft be performed to ensure that the patient is
likely to respond to the treatment.28 Additionally,
by performing a test before treatment, there is an
opportunity to exclude patients who respond with
a Koebner phenomenon at the donor site, which
may be a sign of active vitiligo and may indicate
poor response to treatment.31 Response to surgical
386 DERMATOLOGIC SURGERY
management is greatest when treating stable dis-
ease or focal or segmental vitiligo and in younger
patients28,31 Of all patients with successful repig-
mentation, a significant portion maintained the
repigmentation for longer than 5 years after
treatment.31
Miniature Punch Grafting
Mini-punch grafting has been shown to be one of
the cheapest, fastest, and easiest approaches of all
surgical treatments available.29,31–34 With this tech-
nique, 2- to 4-mm punch grafts are taken from a
normally pigmented donor site of similar thickness
and adnexal makeup to the recipient vitiliginous
site and are stored on normal saline-impregnated
guaze.32,35 Next, the recipient site is prepared by
taking multiple punch biopsies that are the same
size or 0.25 to 0.5 mm smaller than those taken
from the donor site. Alternatively, a hand engine-
mounted punch device may be used. Often, the
recipient site may be pretreated with phototherapy,
dermabrasion, cryotherapy, or laser irradiation
before transplantation.35 The grafted tissue from
the donor site is then secured into the vitiliginous
areas. Grafts that are 2 mm or smaller do not
require suturing, but larger grafts can be easily
secured to recipient areas using a figure eight stitch
(Figure 5). Immobilization of the recipient site is
critical and can be ensured by application of a pet-
rolatum impregnated pressure bandage for approx-
imately 1 week.36 Once the graft site is well
healed, further treatment with PUVA, NbUVB
(1–2 times weekly for 10–20 weeks) or excimer
laser (2–3 times weekly) can be used to further
promote repigmentation.32,35,36 Successful response
to mini-punch grafting, defined as repigmentation
of greater than 65%, occurs in 62% to 74% of
patients.34 Long-term follow-up 5 years after treat-
ment found greater than 65% repigmentation in
50% of all patients with vitiligo and in 89% of
patients with segmental vitiligo.31
Complications of punch grafting include infection,
hyperpigmentation, imperfect color matching,
 PATEL ET AL

Figure 5. Clinical photograph showing minigrafts sutured Figure 6. Clinical photograph showing a negative pressure
in place with the figure eight stitch. apparatus (evacuated syringe) in place to induce bullae
formation.

koebnerization at the donor site, keloid formation,

and most importantly, scarring at the donor or
graft site.28,34 An important limitation of punch
grafting is the possibility of cobblestone repigmen-
tation, ultimately requiring the use of camouflage
products for ideal cosmesis.32,37 The size and depth
of the grafts and the site being treated all affect the
likelihood of cobblestoning.32,34 The risk of cob-
blestoning is highest with larger punch biopsy
grafts, which has led some to propose that 1.5 mm
should be the upper size limit for punch biopsy
grafts on the trunk or extremities and 1 mm on the
face.32,37 Additionally, cobblestoning can be mini-
mized by creating recipient sites that are 1 mm
deeper or 0.5 mm narrower than the donor Figure 7. Clinical photograph revealing the formation of
multiple bullae after removal of the negative pressure
grafts.36,37 Fortunately, the cobblestoned appear- apparatus seen in Figure 6.
ance will often improve over time without inter-
vention. For those with persistent cobblestoning,
electrofulguration has been shown to be particu- epidermal blisters.34,36 One of the simplest ways to
larly efficacious.37 produce blisters on the donor sites is by using the
evacuated barrel of a syringe, which can generate
the negative pressure needed to create blisters38
Suction Blister Grafting
(Figures 6 and 7). The authors recommend apply-
Another useful tool available in the surgical man- ing a 20-mL syringe with the barrel removed to the
agement of vitiligo is grafting using epidermal suc- skin with lubricant to create a seal. Next, connect
tion blister. In this technique, a negative pressure a 60-mL syringe to the 20-mL syringe using a stop-
apparatus producing 300 to 500 mmHg of cock. The 60-mL syringe creates a vacuum, and
pressure is applied to the normally pigmented the stopcock maintains the negative pressure.
donor site to promote the formation of multiple Other options include using an angiosterrometer, a

38:3:MARCH 2012 387

 ADVANCED TREATMENT MODALITIES FOR VITILIGO
modified gastric suction pump, or a double syringe
device.36,37,39 The donor site may also be pretreat-
ed with PUVA to increase the number of melano-
cytes available for transplantation.36
The recipient site is prepared by removing the epi-
dermis through induction of suction blisters, appli-
cation of liquid nitrogen, PUVA, carbon dioxide
laser, yttrium aluminum garnet laser, or dermabra-
sion34,38,40,41 (Figure 8). The roofs of the blisters
at the donor site are subsequently removed and
transferred to the newly prepared recipient site. A
pressure bandage should be applied to the recipient
site for 1 week, and judicious use of antibiotic
ointment at both sites is recommended. Postopera-
tive UV therapy with PUVA or NbUVB has been
shown to improve repigmentation as well and can
be initiated as soon as the site is reepithelialized.36
Figure 8. Clinical photograph of dermabraded site with a
suction blister graft in place.
388 DERMATOLOGIC SURGERY
Review of the literature reveals that several investi-
gations have been conducted comparing the various
techniques for preparing the vitiliginous recipient
area. Use of suction blistering at the recipient area
has been shown to be particularly effective in that it
tends to result in immediate adherence of grafted
tissue and has the fastest rate of repigmentation.42–
44
Additionally, there is some evidence to support
the use of systemic corticosteroids perioperatively to
improve repigmentation rates.45
Epidermal suction blistering is highly effective,
with a response rate of 83% to 90%, and has been
shown to have an excellent side-effect profile, with
mainly hyperpigmentation of the donor sites and
imperfect color matching being reported.34 In addi-
tion, this technique does not cause the scarring or
cobblestoning commonly seen with miniature
punch grafting and allows for coverage of larger
areas.
Epidermal Cultures
The use of cultured melanocytes originated
30 years ago with the application of cultured epi-
dermis in the treatment of people with burns. Lerner
and colleagues,15 who successfully achieved repig-
mentation by transplanting autologous cultured
melanocytes, subsequently adapted the technology
for the treatment of vitiligo in 1987. Since then,
myriad techniques have been developed to culture
and prepare autologous melanocytes for transplan-
tation. In general, all of these techniques begin
with obtaining a small sample of epidermis using
suction blisters, electric dermatome, or scalpel. The
sample is then introduced into a medium that
typically contains enzymes, such as trypsin and
ethylenediaminetetraacetic acid, that cause
separation of the epidermis into a cell suspension.
The cell suspension is then washed and placed
into culture media containing various antibiotics,
growth factors, and bovine serum with or
without the patient’s serum.46,47 The most
commonly used growth factors are
12-O-tetradecynol-phorbol-13-acetate and cholera

toxin (which promote melanocyte proliferation)
and geneticin (which eliminate keratinocytes and fi-
broblasts).14,46,47 After a sufficient amount of
melanocyte proliferation occurs, the suspension is
typically transferred onto hyaluronic acid ester
polymer sheets for several weeks. Finally, these
sheets are grafted onto recipient vitiliginous sites
prepared using methods similar to those for suction
blister grafting.
Overall, autologous melanocyte culture is an effec-
tive tool in the treatment of vitiligo. Excellent
repigmentation is achieved in 41% to 52% of
patients and a good response in 7% to 19%.48,49
Several factors have been found that increase the
likelihood of successful melanocyte culturing,
including donor site selection and temperature of
the donor tissue.50 One of the most effective donor
sites is the forearm, because it has been found to
produce melanocytes that proliferate fastest when
cultured. In addition, warming of the donor site
has been shown to expedite the formation of the
suction blisters that are critical to the creation of
autologous melanocyte cultures.
The major advantage of autologous melanocytes
culture is its ability to treat a large vitiliginous area
using tissue from only a small donor site.46 Many
other popular methods, such as suction blister
grafting, would require a significantly greater
amount of donor tissue to achieve the same effi-
cacy. Despite this strength, its tremendous labora-
tory requirements and associated costs severely
limit the widespread implementation of autologous
melanocyte cultures. In addition, the use of growth
factors and bovine serum has raised some concerns
about possible teratogenicity of the transplanted
tissue,51 although initial investigations refute this
claim.52
Dermabrasion
Microdermabrasion, first introduced to the United
States in 1994, involves the application of a contin-
uous flow of aluminum oxide microcrystals over
PATEL ET AL
the skin with simultaneous negative pressure to
remove the crystals and skin debris. Many varia-
tions of this technique have been developed since
its initial introduction, including the application of
sodium chloride crystals, magnesium oxide crystals,
sodium bicarbonate crystals, and even particle-free
units that use solutions with positive pressure.53 As
outlined above, dermabrasion is a useful tool in
the preparation of the recipient site for multiple
methods of melanocyte transfer. In addition to this
important role, dermabrasion has been shown to
be effective in treating stable vitiligo even when
used as a monotherapy.54,55 It is hypothesized that
microdermabrasion or curettage monotherapy
works by activating follicular melanocyte reser-
voirs, stimulating peripheral epidermal melano-
cytes, and possibly by activating metabolically
inactive melanocytes in vitiliginous patches.54,56 A
recent study by Quezada and colleagues54 com-
pared melanocyte and keratinocyte transfer using a
sandpaper method with simple dermabrasion and
found both to be equally effective in successfully
inducing repigmentation in vitiliginous patches.54
Another study by Sethi and colleagues56 showed a
success rate of 63% with dermabrasion monother-
apy at 6 months after treatment. An even higher
success rate was achieved if 5-fluorouracil was add
to the dermabraded sites, although the time to
reepithelization was longer.
Conclusion
Our ability to treat vitiligo is imperfect, and there is
no single modality that is effective in all situations.
Although the standard of care for vitiligo has his-
torically consisted of pharmacologic management,
recent advances have led to many new, exciting
treatment opportunities. The expansion of technol-
ogies such as the excimer laser, dermabrasion, and
micropigmentation provide new tools that synergize
with conventional treatments to improve outcomes.
In addition, for the right patient, total body depig-
mentation with MBEH may be an excellent treat-
ment option. Recent advances in the surgical
management of vitiligo in the form of miniature
38:3:MARCH 2012 389
 ADVANCED TREATMENT MODALITIES FOR VITILIGO
punch grafting, suction blister grafting, and epider-
mal cultures provide even more avenues by which
treatment-resistant patients may be able to success-
fully undergo repigmentation.
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2. Al-Otaibi SR, Zadeh VB, Al-Abdulrazzaq AH, Tarrab SM,
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Address correspondence and reprint requests to: Nishit
Patel, MD, 12901 Bruce B Downs Blvd, MDC 79,
Tampa, FL 33612, or e-mail: npatel85@gmail.com
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