Am J Clin Dermatol 2012; 13 (5): 331-340

REVIEW ARTICLE 1175-0561/12/0005-0331/$49.95/0

Adis ª 2012 Springer International Publishing AG. All rights reserved.

Management of Acne Scarring, Part II

A Comparative Review of Non-Laser-Based, Minimally Invasive Approaches
Lauren L. Levy and Joshua A. Zeichner
Mount Sinai Medical Center, New York, NY, USA

Contents

Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331
1. Scar Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
2. Scar Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
3. Treatment Options for Acne Scars . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333
3.1 Atrophic Acne Scars . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333
3.1.1 Pharmacologic Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333
3.1.2 Procedural Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333
3.2 Hypertrophic Acne Scars . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335
3.2.1 Pharmacologic Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335
3.2.2 Procedural Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 336
4. Treatment Options for Hyperpigmentation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337

Abstract Acne scarring is a commonly encountered yet extremely challenging problem to treat for the dermatol-
ogist. As acne scarring can lead to significant psychological distress and low self-esteem, it is of utmost
importance to have effective and satisfying treatments in the physician’s armamentarium. However, many
treatments are unsatisfying, leading to patient disappointment and frustration.
Although early treatment of acne lesions and inflammation with isotretinoin is beneficial in preventing
acne scarring, many patients still present with troubling noticeable scars. Despite the advances in phar-
macology and technology, scar treatment still remains suboptimal and is tainted with several adverse effects.
However, some treatments can provide benefits.
This review article exhaustively discusses and analyzes the various minimally invasive approaches to the
treatment of acne scarring with an emphasis on pharmacologic agents, such as isotretinoin for atrophic acne
scars and corticosteroids and chemotherapeutic drugs for hypertrophic scars. Intralesional injections of
corticosteroids are efficacious in reducing keloid scar formation in addition to preventing recurrence fol-
lowing surgical excision. In-office and minimally invasive procedural management, including chemical
peels, dermabrasion, tissue augmentation, and punch excision is also discussed. Superficial chemical peels
are efficacious in treating atrophic scars with relatively few adverse effects and complications. Although
dermabrasion is used less often with the advent of laser resurfacing, this technique remains as a viable option
for those with atrophic scars. Post-inflammatory hyperpigmentation can be managed successfully with
topical agents such as azelaic acid and hydroquinone. The efficacy of various treatment modalities is
highlighted with a focus on choosing the correct modalities for specific scar types.

Acne vulgaris affects approximately 90% of adolescents and develop significant scarring.[4] Early intervention is important
up to 5% of older adults.[1-3] The prevalence of acne scarring is to minimize the appearance of acne scarring, which may be dis-
estimated to occur in up to 95% of acne patients and 30% may figuring and associated with depressive symptoms, low self-esteem,
332
and suicidal tendencies.[5-7] Acne scarring is permanent; how-
ever, the appearance can be improved with various medical,
laser, and surgical approaches. In this article, we review mini-
mally invasive approaches that can improve and mitigate acne
scarring. Laser treatment for scarring is discussed in the
accompanying review by Sobanko and Alster on pages 319-330.
1. Scar Pathogenesis
Acne vulgaris results from a complex interaction of sebum
production, follicular hyperkeratinization, Propionibacterium
acnes proliferation, and inflammation.[8-11] Factors leading
to scarring are less clearly understood, although the body’s
inflammatory response to acne lesions plays a key role. In-
flammation of affected pilosebaceous units leads to disrup-
tion of the follicle with extravasation of the follicular material
into the dermis. This further propagates the inflammatory re-
sponse.[12,13] An altered wound healing response following in-
flammation leads to scar formation.
Not every patient with acne develops scars. There is little
clinical data, however, to predict which patients are prone to
scar. A study by Holland et al.[14] demonstrated that patients
with a propensity to scar had a greater non-specific inflamma-
tory response lasting for a longer duration when compared with
those patients who did not form scars. Additionally, findings
suggest that scars may result from an ineffective immune re-
Table I. Classification of acne scars with corresponding treatment
Scar classification Clinical features
Atrophic Loss of dermal collagen
Most common form of post-acne scarring
Ice-pick Deep and narrow pitting of the skin
Usually less than 2 mm wide
Extends into the dermis or subcutaneous tissue
Rolling Wide and shallow
Width approximately 4–5 mm
Superficial skin tethered to dermis or subcutaneous tissue
Boxcar Round or oval
Can be either deep (>0.5 mm) or shallow (<0.5 mm)
Vertical edges with a wide base
Hypertrophic Excess collagen deposition
Hypertrophic Pink, raised, firm papule
Confined to the area of previous damage
Keloidal Red to purple papules or nodules
Can extend beyond original wound borders
a Discussed in the accompanying review by Sobanko and Alster on pages 319-330.
b May require several treatment session and result in complete resolution.
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Levy & Zeichner
sponse to damaged tissue and abnormal wound healing. Severe
disease, such as nodulocystic acne, is most likely to result in
scarring, but even patients with mild acne can develop scars.
2. Scar Classification
Acne scars are classified according to whether there is a loss
or gain of collagen in the lesion. Atrophic scars have an overall
loss of collagen, and may be subcategorized as ice-pick, boxcar,
or rolling scars.[15] These scars are depressed in the skin. On the
other hand, hypertrophic scars are raised with excess collagen
deposition. The type of scars present will help direct treatment
(see table I).
Atrophic scars are the most commonly observed type of acne
scars. They result from inflammation in the deep dermis that
destroys dermal structures. Contraction ultimately leads to
indentation of the overlying skin.[16] Atrophic scars are further
classified based on width, depth, and architecture. Ice-pick
scars are narrow (less than 2 mm), deep, punctiform lesions with
epithelial tracts that extend vertically deep into the dermis.
Rolling scars are usually wider (4–5 mm) and occur when the
dermis is tethered to the subcutis resulting in an undulating
appearance. Boxcar scars are round or oval depressions with
sharply demarcated edges that can be either shallow or deep
and range in diameter from 1.5 to 4 mm. They are wider at the
surface than ice-pick scars.[16,17]
Treatment modalities
Dermal fillers
Laser resurfacinga
Punch excision
Chemical peelsb
Dermabrasion
Subcision
Chemical peel
Dermabrasion
Punch excision with punch elevation
Silicone gel sheeting
Intralesional corticosteroids
Cytotoxic agents: bleomycin, 5-fluorouracil
Cryosurgery
Radiotherapy
Pulsed dye lasera
Am J Clin Dermatol 2012; 13 (5)
Management of Acne Scarring, Part II
Hypertrophic scars are less common than atrophic scars and
are characterized by firm, raised lesions that do not exceed the
margin of the original wound.[18-20] Contrastingly, keloid scars
spread outside the margins of the original wound and evolve
over time.[21] Post-acne keloidal scars are more likely to form in
male patients and occur on the trunk as opposed to the face.[4]
3. Treatment Options for Acne Scars
The best treatment for acne scarring is prevention through
early treatment of active acne.[22] Once scars have developed,
treatment should be individualized to suit the needs of the pa-
tient. Regardless of the approach, patients must be counseled
on possible options and realistic expectations must be set. The
current nonsurgical, minimally invasive treatment modalities
for acne scars include systemic and topical pharmacologic
agents, as well as procedures such as injections, dermabrasion,
and chemical peels. Finally, in-office procedure options include
punch elevation, excision, and scar subcision.
3.1 Atrophic Acne Scars
3.1.1 Pharmacologic Management
Isotretinoin
Isotretinoin is a synthetic vitamin A derivative that has been
the standard of care for treating severe, recalcitrant, nod-
ulocystic acne since it was approved by the US FDA in 1982.[23]
It addresses all four of the pathogenic acne factors[24-29] and
provides long-term remission for most patients.[24,30-32]
Isotretinoin is prescribed to a cumulative target dose of
120–150 mg/kg, usually over a 6-month course. Patients are
typically started at a dose of 0.5 mg/kg and titrated up to
1 mg/kg for the duration of treatment. Lower treatment doses
have been associated with an increased rate of relapse.[33] There
may be an acute worsening of acne lesions following initial
treatment due to release of proinflammatory cytokines as acne
lesions are disrupted, so some patients with more severe acne
are concurrently put on oral prednisone to reduce this in-
flammation.[34] Common dose-related adverse effects include
cheilitis, dermatitis, and xerosis.[31,35] Isotretinoin has also been
associated with depression and suicidal ideation.[36,37] Addi-
tionally, there is a possible association between the drug and the
development of ulcerative colitis.[38,39] Isotretinoin is a potent
teratogen, with a birth defect rate of approximately 30%. Fe-
male patients of childbearing potential must use two forms of
birth control while on treatment. All patients are enrolled in the
iPLEDGE program, a government-enforced registry, in order
to receive the drug.[40,41]
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333
While isotretinoin carries significant risks, early use reduces the
likelihood of scarring in patients with severe acne. Layton et al.[42]
evaluated the effect of early treatment with the standard dose of
isotretinoin on acne scarring in 107 patients with facial acne.
Following treatment completion, acne scarring was evaluated and
correlated with demographic data. Patients who had acne for a
duration greater than 3 years prior to isotretinoin initiation had a
significantly greater degree of scarring compared with patients who
had acne for less than 3 years prior to treatment initiation. Thus,
acne patients should be prescribed isotretinoin early in the disease
process to aid in the prevention of scar formation.[43]
Topical Retinoids
Retinoids are vitamin A derivatives that treat acne vulgaris
by regulating follicular hyperkeratinization and reducing in-
flammation.[44-46] Topical retinoids are recommended as
monotherapy for comedonal acne and as part of combination
treatment for inflammatory disease. Topical retinoids stimulate
collagen formation, improve elastic fibers, and have been
shown to increase dermal collagen synthesis, explaining their
action in damaged skin seen in both photoaging and scars.[47,48]
Monotherapy with topical retinoic acid can improve acne
scarring. Application of 0.05% tretinoin for 4 months improved the
appearance of facial ice-pick acne scars.[49] Additionally, three
times-weekly iontophoresis with tretinoin 0.025% gel was effica-
cious in improving acne scarring in 93% of patients evaluated. Bi-
weekly treatments each lasting for 15 minutes over the course of
3 months gave clinical improvements sustained for up to 1 year.[50]
Iontophoresis provides increased tissue concentrations of tretinoin.
Complications included post-procedure erythema and xerosis.
Clinical improvement following iontophoresis in combination with
tretinoin 0.025% gel was associated with a decrease in scar depth in
94% of patients in a second follow-up study.[51]
3.1.2 Procedural Management
Dermabrasion
Since the early 1900s, dermabrasion has been employed to
physically remove the superficial skin layers, allowing healing to
occur with a more cosmetically acceptable result. This procedure
has largely fallen out of favor with the advent of resurfacing
lasers, which are beyond the scope of this article.[52,53] Various
dermabrasion devices exist. Through the use of either a rotating
motorized hand piece with a wire brush or a diamond-tipped
hand piece, the procedure removes the epidermis and part of the
dermis. Reepithelialization and repigmentation occur from cells
within adenexal structures. The procedure requires local and
sometimes general anesthesia because of significant pain.[54]
Dermabrasion is particularly successful in treating superficial
Am J Clin Dermatol 2012; 13 (5)
334
atrophic scars, such as rolling or boxcar scars. However, deeper,
ice-pick scars are too deep to be effectively treated by dermabra-
sion.[55,56] The wound healing process is accompanied by new col-
lagen formation and a smoothed appearance of the scarred skin.[52]
Dermabrasion has many potential complications, most of
which are often operator and technique dependent. Photo-
sensitivity occurs universally post-procedure, and patients must
use strict sun protection while the skin re-epithelializes. Addi-
tionally, erythema after dermabrasion can last several weeks to
months, and can be treated in part with topical corticosteroids.
Post-inflammatory pigmentation alterations, especially hypo-
pigmentation, are frequent complications that can be perma-
nent.[54,57] Post-procedural hypertrophic scarring is a potential
risk. This phenomenon was first reported in patients under-
going dermabrasion after receiving a recent course of iso-
tretinoin therapy. As a result, it is currently recommended that
patients wait at least 6 months after completion of isotretinoin
therapy before undergoing a dermabrasion procedure.[53,58]
Despite this recommendation, there are reports of patients
undergoing dermabrasion with concurrent isotretinoin ther-
apy, without hypertrophic scar formation.[59]
Chemical Peels
The first reported use of chemical products on the skin for
the treatment of acne scars dates back to phenol in the 1950s.[60]
Today, various chemicals are used to peel the skin and acne
scars. Chemical peels differ in their depth of penetration into
the skin. Peels are appealing to patients because they are rela-
tively non-invasive and can simultaneously improve skin pig-
mentation and tone as well as texture. Risks of chemical peels
include post-inflammatory pigmentation and scarring. These
risks are higher with stronger, deeper peels.[61] Chemical peels
should be used with caution in patients with skin of color
(Fitzpatrick skin types IV-VI), given the propensity to hyper-
pigment. It is recommended that superficial peeling agents be
used in these patients, such as glycolic acid or Jessner’s solution
(resorcinol, salicylic acid, and lactic acid).[62]
Light peels include glycolic, lactic, or salicylic acid. Addi-
tionally, Jessner’s solution and low-concentration (20%) tri-
chloroacetic acid are considered light peels. These chemicals
affect only the epidermis. They may be used to treat the most
superficial of acne scars and may be better suited for improving
post-inflammatory skin pigmentation. Higher concentrations
of trichloroacetic acid, such as 30–40%, give what are consid-
ered medium-depth peels, extending down to the papillary
dermis. Deep chemical peels, such as 50% or greater trichloro-
acetic acid and phenol-based peels can extend to the reticular
dermis.[63] Medium and deep peels are more effective for deep
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Levy & Zeichner
atrophic scars, but carry a higher risk of complications, such as
milia, post-procedure pigmentary changes, and secondary in-
fection.[64] Phenol peels are currently used infrequently because
they require cardiopulmonary monitoring and intravenous hy-
dration due to direct cardiotoxicity from the chemical.
Chemical peels create damage to the skin, and allow for a con-
trolled wound healing process to occur with subsequent improve-
ment in skin appearance. Application of trichloroacetic acid to
the skin, for example, causes coagulative necrosis of the epidermis
and the affected dermal collagen. The dead cells are sloughed and
the skin undergoes re-epithelialization.[61] During this process,
there is an increase in the production of collagen, elastin, and
glycosaminoglycans.[65]
While full face peels are commonly performed, reports of
spot treatment to atrophic scars with high-concentration tri-
chloroacetic acid (65% or 100%) has demonstrated success with
minimal adverse events, after multiple treatments.[66] Animal
models have shown histologic evidence of significant skin re-
juvenation with new collagen deposition using the spot treat-
ment with high-concentration trichloroacetic acid compared
with traditional trichloroacetic acid application techniques.[67]
There is also evidence of clinical and histologic improvement
with focally applied high-concentration trichloroacetic acid for
patients with ice-pick scars and with skin of color.[68,69]
Soft Tissue Augmentation
Soft tissue augmentation techniques are most effective in
treating patients with superficial atrophic scars, such as rolling
scars.[70-73] These products replace soft tissue volume lost in the
aging process. At the same time, they stimulate collagen pro-
duction, which can improve the texture of the skin itself. With
the development of non-collagen fillers, injectable collagens
have fallen out of favor and have been replaced with products
containing hyaluronic acid, calcium hydroxyapatite, and poly-
L-lactic acid. All of these products can help improve the ap-
pearance of the acne scars to some degree.
Hyaluronic acid is a hydrophilic, linear polysaccharide that
occurs naturally in the body’s connective tissue.[74] Since hyal-
uronic acid contains no protein material, it has low antigenic
properties and does not require skin testing prior to adminis-
tration. Commercially available products are cross-linked to
provide stability and are manufactured in various particle sizes.
Injection of cross-linked hyaluronic acid stimulates collagen
synthesis and partially restores dermal matrix components,
proposed to result from mechanical stretching of the dermis
that leads to activation of dermal fibroblasts.[75] Hyaluronic
acid fillers may improve the appearance of atrophic acne scars
alone or in combination with subcision, injecting the product
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Management of Acne Scarring, Part II
beneath the subcised skin to maintain optimized wound heal-
ing.[76] Long-term improvements can be seen after one to three
treatments; however, the correction is temporary.[77]
Calcium hydroxyapatite is a semi-permanent dermal filler
comprised of calcium hydroxyapatite microspheres in a
hydrogel vehicle. The hydrogel provides immediate volume
correction, but is degraded over time. The microspheres stim-
ulate fibroblast production of collagen, which grows over the
calcium hydroxyapatite scaffold. The gel has the unique ability
to be molded, which avoids contour irregularities.[78] Calcium
hydroxyapatite can improve the appearance of shallow, atro-
phic acne scars, but not deeper ice-pick scars.[79] Improvement
in appearance can occur after a single injection with results
maintained for 1 year; however, an additional filler can be
placed 1 month following initial treatment.
Poly-L-lactic acid is a synthetic, biodegradable, long-lasting,
dermal filler. Initially approved for the treatment of HIV lipo-
atrophy,[80,81] it received cosmetic approval from the FDA in
2009.[82] Similar to the mechanism of action of calcium hydroxy-
apatite, poly-L-lactic acid stimulates collagen formation, which
grows around the poly-L-lactic acid deposited in the skin. Patients
often require multiple treatments with poly-L-lactic acid for
maximum improvement and injections can occur at 1-month in-
tervals. Besides restoring facial volume, clinical trials and several
case reports have documented improvement in facial, atrophic
acne scars after several treatments with poly-L-lactic acid.[71,72,83]
Subcision
Subcision is a technique that is useful for the treatment of
superficial atrophic acne scars. A needle inserted percuta-
neously adjacent to the scar is passed into the dermis beneath
the scar. Through manipulation of the needle, fibrous tissue
that pulls the scar down giving the skin a depressed appearance
is released. In the subcision process, bleeding is necessary in
order for clot formation to occur in the created potential space.
The formed blood clot is necessary to occupy the area and keep
the skin elevated from the scar tissue below. New collagen can
then form without pulling the skin towards the dermis.[84]
Multiple treatments may be necessary, and this technique is not
appropriate for deep boxcar or ice-pick scars. Complications
include bruising, bleeding, infection, and the possibility of acne
exacerbation if acne sinus tracts are disrupted during the pro-
cedure. This later complication may require intralesional cor-
ticosteroid injections. Subcision may be used alone or in
combination with dermal fillers, which occupy the space rather
than relying solely on the created blood clot.[85-87] A recent
study reported success using a combination therapy of sub-
cision with a skin suctioning treatment.[88]
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335
Punch Excision
Punch excision with subsequent closure is an effective
method of removing deep pitted scars, such as the ice-pick or
the deep boxcar subtype. This method employs a punch biopsy
(size is dependent on scar diameter) to excise the scar tissue. The
open area is then sutured and allowed to heal. The new scar
created from this procedure may be less noticeable than the
prior deep atrophic acne scar.[89] This technique may be
combined with subsequent treatment with a resurfacing laser or
dermabrasion, 4–8 weeks post-excision.[90,91]
In some cases, following punch excision of a deep scar a
replacement graft can be inserted, often from posterior auric-
ular skin.[91-93] Success of this technique is strongly dependent
on the skill of the practitioner. Post-procedure, there is a risk of
graft failure as well as a noticeable unevenly matched appear-
ance. Punch grafting provides long-term correction and is an
appropriate treatment option for deep ice-pick scars.[15,53]
Punch elevation is a hybrid technique that combines ele-
ments of punch excision and grafting. In punch elevation, the
scar is punched, but rather than removed, the skin is elevated
and then fixed into place at a plane even to the surface of the
skin, using either sutures or steri-strips. This treatment is ap-
propriate for deep boxcar scars, with sharp borders and less
than 3 mm of depression.[15,94] Both punch excision followed by
grafting or elevation can benefit from post-procedure re-
surfacing laser procedures.
There are many options for treating atrophic scars and
various treatment modalities can be combined for a more effi-
cacious result. For example, laser resurfacing can follow a
chemical peel and subcision or can be combined with a tri-
chloroacetic acid peel followed by punch grafting and elevation
with subsequent dermabrasion to complete resurfacing.[94,95]
Laser treatment as a monotherapy for atrophic scarring, such
as the ablative carbon dioxide and erbium:yttrium-aluminum-
garnet systems, is effective for atrophic scars with reported
improvement ranging from 25% to 90%, but is not without
complications, expense, and time commitment.[96] Non-ablative,
fractionated lasers have fewer complications than ablative la-
sers, with significant improvement in atrophic scars.
3.2 Hypertrophic Acne Scars
3.2.1 Pharmacologic Management
Corticosteroids
Evidence-based recommendations name intralesional corti-
costeroid injections as first-line therapy for keloids and hy-
pertrophic scars.[97] The proposed mechanisms of action
Am J Clin Dermatol 2012; 13 (5)
336
include decreased fibroblast proliferation and collagen syn-
thesis along with a reduction in inflammatory mediators.[98]
Triamcinolone acetonide is commonly injected directly into
the scar to reduce the size and thickness. The treatment regimen
is tailored to the patient depending on the extent of scarring.
Injections are usually given every 4–6 weeks, with concen-
trations of 10–20 mg/mL, or even as high as 40 mg/mL for very
thick scars. Dose-dependent adverse effects include hypo-
pigmentation, dermal atrophy, and telangiectasias. Efficacy is
usually >50%, and recurrence rates range from 9% to 50%.[99,100]
In some cases, intralesional corticosteroids are even given post-
operatively as prophylaxis in predisposed patients.[101,102]
Intralesional injection of inflammatory acne lesions, such as
cysts, can help prevent subsequent scarring by reducing active
inflammation.[103] Care must be taken not to over treat, espe-
cially on the face, as skin atrophy is a common potential adverse
event. Interestingly, it has been shown that oral and topical
retinoids may ameliorate atrophy caused by intralesional cor-
ticosteroids.[77,104]
Silicone Gel Sheeting
The international advisory panel for hypertrophic and ke-
loid management recommend silicone gel sheeting as a rea-
sonable first-line treatment choice for hypertrophic scars and
keloids.[97] It has been suggested the therapeutic effect results
from a combination of pressure and hydration rather than
the silicone itself. Hydration inhibits fibroblast production
of collagen and prevents wound desiccation.[105] Other proposed
mechanisms include a reduction in collagen formation, pre-
vention of bacterial invasion into the scar, and modulation of
fibroblast growth factor-b and transforming growth factor-b,
molecules that stimulate collagen production from fibroblasts.[106]
Additionally, silicone gel sheeting may reduce pruritus, hyper-
pigmentation, and patient-reported discomfort.[107,108] Reported
adverse effects, although rare, include pruritus and skin macer-
ation. Silicone sheets are cut to the size of the scar and should be
worn for 12 hours per day for approximately 2 months. They may
be applied as soon as skin re-epithelialization occurs.
Cytotoxic Agents
Intralesional administration of fluorouracil (5-FU) and
bleomycin, cytotoxic agents, can treat hypertrophic scars and
keloids.[109-111] 5-FU inhibits rapidly proliferating fibroblasts
found in dermal wounds.[112] The therapy is efficacious for fa-
cial acne scars as monotherapy,[113,114] and in combination with
intralesional corticosteroids and a 585 nm pulsed dye laser.[100]
Studies with 5-FU use a concentration of 50 mg/mL with a total
dose per session ranging from 50 mg to 150 mg and can be given
multiple times a week to increase treatment efficacy.[110,114]
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Levy & Zeichner
Clinical response to intralesional corticosteroids alone or in
combination with 5-FU, and the 585 nm pulsed dye laser was
evaluated in a prospective, randomized controlled trial. All
treatment groups had significant improvement from baseline
without any significant differences between the groups. How-
ever, intralesional injections provided a faster improvement
than treatment with the pulsed dye laser.[100] Common adverse
effects associated with 5-FU include pain and purpura fol-
lowing injection, which can be ameliorated through combining
5-FU with either a corticosteroid or lidocaine.[114]
Bleomycin is another antineoplastic agent that inhibits col-
lagen synthesis through cytotoxic effects on rapidly dividing
fibroblasts.[115] Clinical studies have shown flattening of hy-
pertrophic scars in 44–50% of patients after treatment with
bleomycin along with marked improvement of pruritus in over
80% of patients.[116,117] In these studies, bleomycin (1.5 IU/mL)
was topically applied to the lesion followed by the creation of
small puncture wounds to the lesion resulting in penetration of
the drug. Treatment was administered at various time points,
ranging from 2 weeks to 4 months, depending on clinical re-
sponse. Complications from treatment include possible ulcer-
ation at the treatment site and hyperpigmentation. Notably, no
pulmonary or hepatic adverse events were reported. However,
randomized, placebo-controlled studies are lacking and are
necessary in order to understand both efficacy and safety, es-
pecially compared with intralesional corticosteroids.
3.2.2 Procedural Management
Cryotherapy
Cryotherapy utilizing liquid nitrogen is another option for
treating keloidal acne scars with a reduction in keloid volume
achieved in up to 80% of treated scars.[118,119] Several treatment
sessions are often required for significant improvement. The er-
ythema resulting from cryosurgery may take several weeks to heal
and there is a significant risk of permanent hypopigmentation,
thus lesions on the face may be difficult to treat.[120,121] The
combination of cryotherapy and intralesional corticosteroid in-
jections may be synergistic suggested by a greater clinical re-
sponse to a combination treatment regimen compared with the
individual treatment modalities.[122]
Radiotherapy
Through decreasing fibroblast activity and causing cellular
apoptosis, radiotherapy can serve as an adjunct to surgical
excision to prevent recurrence.[123] Recurrence following sur-
gical excision is a common complication with reported rates
ranging from 45% to 100%, while perioperative radiation can
reduce the recurrence rate to 10%.[97,124] Despite these benefits,
Am J Clin Dermatol 2012; 13 (5)
Management of Acne Scarring, Part II
the adverse effects of radiation must be considered prior to
initiation therapy for a benign disease.
4. Treatment Options for Hyperpigmentation
Post-inflammatory hyperpigmentation (PIH) can result
following active acne lesions, especially in darker skinned in-
dividuals and those living in areas of intense sun exposure.[125]
Pigmentation changes following active acne lesions are usually
transient; however, when permanent, are a great cosmetic
concern. Topical agents for treating hyperpigmentation include
retinoids, azelaic acid, and hydroquinone. Hydroquinone, a
topically applied bleaching agent, is often the first-line and gold
standard for the treatment of PIH in darker skinned in-
dividuals.[126] Hydroquinone is readily accessible, as lower
concentration formulations can be purchased over the counter
without a prescription. The treatment is efficacious and results
typically occur 8–12 weeks following treatment initiation. Po-
tential adverse effects include hypopigmentation of surround-
ing normal skin (the ‘halo effect’) and the development of
contact dermatitis. It is recommended that patients test hy-
droquinone on a small test area prior to application to gener-
alized pigmented lesions.[127,128]
Topical tretinoin can lighten and improve the appearance of
facial hyperpigmentation in darker skinned individuals, but
may also lighten normal skin.[129] Azelaic acid, which possesses
anti-tyrosinase activity, inhibits the synthesis of melanin in
addition to acting as an anti-inflammatory agent.[130,131]
Application of azelaic acid gel twice daily for 16 weeks sig-
nificantly improved PIH in patients with Fitzpatrick skin types
IV-VI with improvement noted as early as 4 weeks.[132]
Superficial chemical peels, such as glycolic acid and salicylic
acid, are efficacious in treating PIH in darker skinned patients
(Fitzpatrick skin types IV-VI).[133,134] Medium depth peels can
result in further hyperpigmentation in darker skinned patients,
so careful patient selection is critical.[68]
Laser treatments may be a further option, but caution
should be used in patients with skin of color to reduce potential
pigmentary adverse events.[135,136]
5. Conclusion
Acne scarring is a source of great stress and concern for
many and should not be dismissed by the clinician. While the
treatment armamentarium for acne is broad, a vast number of
patients still develop permanent scars. It is important to treat
not only patients’ active acne, but all the residual marks left
from the disease. There are many medical and minimally in-
Adis ª 2012 Springer International Publishing AG. All rights reserved.
337
vasive procedural treatments for acne scars, although no single
strategy has emerged as first line. The clinician must individu-
alize the treatment of acne scars according to the type of scars
present as well as the patients’ preferences. In addition, it is
important to manage patient expectations and set realistic
goals. These procedures, alone or in combination with laser
therapies, can significantly improve the appearance of acne
scars and the quality of life of patients affected by them.
Acknowledgments
No sources of funding were received to prepare this article. The authors have
no conflicts of interest that are directly relevant to the content of this article.
References
1. Stathakis V, Kilkenny M, Marks R. Descriptive epidemiology of acne vulgaris
in the community. Australas J Dermatol 1997 Aug; 38 (3): 115-23
2. Ghodsi SZ, Orawa H, Zouboulis CC. Prevalence, severity, and severity risk
factors of acne in high school pupils: a community-based study. J Invest
Dermatol 2009 Sep; 129 (9): 2136-41
3. Goulden V, Stables GI, Cunliffe WJ. Prevalence of facial acne in adults. J Am
Acad Dermatol 1999 Oct; 41 (4): 577-80
4. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne
scarring and its incidence. Clin Exp Dermatol 1994 Jul; 19 (4): 303-8
5. Dunn LK, O’Neill JL, Feldman SR. Acne in adolescents: quality of life, self-
esteem, mood, and psychological disorders. Dermatol Online J 2011 Jan 15;
17 (1): 1
6. Halvorsen JA, Stern RS, Dalgard F, et al. Suicidal ideation, mental health
problems, and social impairment are increased in adolescents with acne: a
population-based study. J Invest Dermatol 2011 Feb; 131 (2): 363-70
7. Uhlenhake E, Yentzer BA, Feldman SR. Acne vulgaris and depression: a
retrospective examination. J Cosmet Dermatol 2010 Mar; 9 (1): 59-63
8. Bellew S, Thiboutot D, Del Rosso JQ. Pathogenesis of acne vulgaris: what’s
new, what’s interesting and what may be clinically relevant. J Drugs Der-
matol 2011 Jun; 10 (6): 582-5
9. Dessinioti C, Katsambas AD. The role of Propionibacterium acnes in acne patho-
genesis: facts and controversies. Clin Dermatol 2010 Jan-Feb; 28 (1): 2-7
10. Makrantonaki E, Ganceviciene R, Zouboulis C. An update on the role of the
sebaceous gland in the pathogenesis of acne. Dermatoendocrinol 2011 Jan; 3
(1): 41-9
11. Arora MK, Yadav A, Saini V. Role of hormones in acne vulgaris. Clin Bio-
chem 2011 Sep; 44 (13): 1035-40
12. Holland DB, Jeremy AH. The role of inflammation in the pathogenesis of
acne and acne scarring. Semin Cutan Med Surg 2005 Jun; 24 (2): 79-83
13. Jeremy AH, Holland DB, Roberts SG, et al. Inflammatory events are involved
in acne lesion initiation. J Invest Dermatol 2003 Jul; 121 (1): 20-7
14. Holland DB, Jeremy AH, Roberts SG, et al. Inflammation in acne scarring: a
comparison of the responses in lesions from patients prone and not prone to
scar. Br J Dermatol 2004 Jan; 150 (1): 72-81
15. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification system and
review of treatment options. J Am Acad Dermatol 2001 Jul; 45 (1): 109-17
16. Knutson DD. Ultrastructural observations in acne vulgaris: the normal sebaceous
follicle and acne lesions. J Invest Dermatol 1974 Mar; 62 (3): 288-307
17. Fabbrocini G, Annunziata MC, D’Arco V, et al. Acne scars: pathogenesis,
classification and treatment. Dermatol Res Pract 2010; doi:10.1155/
2010/893080
Am J Clin Dermatol 2012; 13 (5)
338
18. Wolfram D, Tzankov A, Pulzl P, et al. Hypertrophic scars and keloids: a
review of their pathophysiology, risk factors, and therapeutic management.
Dermatol Surg 2009 Feb; 35 (2): 171-81
19. Brown JJ, Bayat A. Genetic susceptibility to raised dermal scarring. Br J
Dermatol 2009 Jul; 161 (1): 8-18
20. Bayat A, Bock O, Mrowietz U, et al. Genetic susceptibility to keloid disease
and hypertrophic scarring: transforming growth factor beta1 common
polymorphisms and plasma levels. Plast Reconstr Surg 2003 Feb; 111 (2):
535-43; discussion 544-6
21. English RS, Shenefelt PD. Keloids and hypertrophic scars. Dermatol Surg
1999 Aug; 25 (8): 631-8
22. Goodman GJ. Acne and acne scarring: why should we treat? Med J Aust 1999
Jul 19; 171 (2): 62-3
23. Merritt B, Burkhart CN, Morrell DS. Use of isotretinoin for acne vulgaris.
Pediatr Ann 2009 Jun; 38 (6): 311-20
24. Ward A, Brogden RN, Heel RC, et al. Isotretinoin: a review of its pharma-
cological properties and therapeutic efficacy in acne and other skin dis-
orders. Drugs 1984 Jul; 28 (1): 6-37
25. Dalziel K, Barton S, Marks R. The effects of isotretinoin on follicular and
sebaceous gland differentiation. Br J Dermatol 1987 Sep; 117 (3): 317-23
26. Leyden JJ, McGinley KJ. Effect of 13-cis-retinoic acid on sebum production
and Propionibacterium acnes in severe nodulocystic acne. Arch Dermatol
Res 1982; 272 (3-4): 331-7
27. King K, Jones DH, Daltrey DC, et al. A double-blind study of the effects of
13-cis-retinoic acid on acne, sebum excretion rate and microbial population.
Br J Dermatol 1982 Nov; 107 (5): 583-90
28. Zelickson AS, Strauss JS, Mottaz J. Ultrastructural changes in open come-
dones following treatment of cystic acne with isotretinoin. Am J Dermato-
pathol 1985 Jun; 7 (3): 241-4
29. Seguin-Devaux C, Hanriot D, Dailloux M, et al. Retinoic acid amplifies the
host immune response to LPS through increased T lymphocytes number and
LPS binding protein expression. Mol Cell Endocrinol 2005 Dec 21; 245 (1-2):
67-76
30. Layton AM, Knaggs H, Taylor J, et al. Isotretinoin for acne vulgaris: 10 years
later: a safe and successful treatment. Br J Dermatol 1993 Sep; 129 (3): 292-6
31. Layton A. The use of isotretinoin in acne. Dermatoendocrinol 2009 May; 1
(3): 162-9
32. Ben Omar N, Arias JM, Gonzalez-Munoz MT. Extracellular bacterial min-
eralization within the context of geomicrobiology. Microbiologia 1997 Jun;
13 (2): 161-72
33. Layton AM, Cunliffe WJ. Guidelines for optimal use of isotretinoin in acne.
J Am Acad Dermatol 1992 Dec; 27 (6 Pt 2): S2-7
34. Borghi A, Mantovani L, Minghetti S, et al. Acute acne flare following iso-
tretinoin administration: potential protective role of low starting dose.
Dermatology 2009; 218 (2): 178-80
35. Rademaker M. Adverse effects of isotretinoin: a retrospective review of
1743 patients started on isotretinoin. Australas J Dermatol 2010 Nov; 51 (4):
248-53
36. Thakrar BT, Robinson NJ. Isotretinoin and the risk of depression. J Clin
Psychiatry 2009 Oct; 70 (10): 1475; author reply 1475-6
37. Hull PR, D’Arcy C. Isotretinoin use and subsequent depression and suicide:
presenting the evidence. Am J Clin Dermatol 2003; 4 (7): 493-505
38. Popescu CM, Popescu R. Isotretinoin therapy and inflammatory bowel dis-
ease. Arch Dermatol 2011 Jun; 147 (6): 724-9
39. Reddy D, Siegel CA, Sands BE, et al. Possible association between iso-
tretinoin and inflammatory bowel disease. Am J Gastroenterol 2006 Jul; 101
(7): 1569-73
40. Malvasi A, Tinelli A, Buia A, et al. Possible long-term teratogenic effect of
isotretinoin in pregnancy. Eur Rev Med Pharmacol Sci 2009 Sep-Oct; 13 (5):
393-6
Adis ª 2012 Springer International Publishing AG. All rights reserved.
Levy & Zeichner
41. Maloney ME, Stone SP. Isotretinoin and iPledge: a view of results. J Am Acad
Dermatol 2011 Aug; 65 (2): 418-9
42. Layton AM, Seukeran D, Cunliffe WJ. Scarred for life? Dermatology 1997;
195 Suppl. 1: 15-21; discussion 38-40
43. Cunliffe WJ, van de Kerkhof PC, Caputo R, et al. Roaccutane treatment
guidelines: results of an international survey. Dermatology 1997; 194 (4):
351-7
44. Thielitz A, Gollnick H. Topical retinoids in acne vulgaris: update on efficacy
and safety. Am J Clin Dermatol 2008; 9 (6): 369-81
45. Thielitz A, Abdel-Naser MB, Fluhr JW, et al. Topical retinoids in acne: an
evidence-based overview. J Dtsch Dermatol Ges 2010 Mar; 8 Suppl. 1: S15-23
46. Jones DA. The potential immunomodulatory effects of topical retinoids.
Dermatol Online J 2005 Mar 1; 11 (1): 3
47. Schiltz JR, Lanigan J, Nabial W, et al. Retinoic acid induces cyclic changes in
epidermal thickness and dermal collagen and glycosaminoglycan biosyn-
thesis rates. J Invest Dermatol 1986 Nov; 87 (5): 663-7
48. Varani J, Perone P, Griffiths CE, et al. All-trans retinoic acid (RA) stimulates
events in organ-cultured human skin that underlie repair: adult skin from
sun-protected and sun-exposed sites responds in an identical manner to RA
while neonatal foreskin responds differently. J Clin Invest 1994 Nov; 94 (5):
1747-56
49. Harris DW, Buckley CC, Ostlere LS, et al. Topical retinoic acid in the
treatment of fine acne scarring. Br J Dermatol 1991 Jul; 125 (1): 81-2
50. Schmidt JB, Binder M, Macheiner W, et al. New treatment of atrophic acne
scars by iontophoresis with estriol and tretinoin. Int J Dermatol 1995 Jan; 34
(1): 53-7
51. Schmidt JB, Donath P, Hannes J, et al. Tretinoin-iontophoresis in atrophic
acne scars. Int J Dermatol 1999 Feb; 38 (2): 149-53
52. Frank W. Therapeutic dermabrasion: back to the future. Arch Dermatol 1994
Sep; 130 (9): 1187-9
53. Goodman G. Post acne scarring: a review. J Cosmet Laser Ther 2003 Jun; 5
(2): 77-95
54. Gold MH. Dermabrasion in dermatology. Am J Clin Dermatol 2003; 4 (7):
467-71
55. Aronsson A, Eriksson T, Jacobsson S, et al. Effects of dermabrasion on acne
scarring: a review and a study of 25 cases. Acta Derm Venereol 1997 Jan; 77
(1): 39-42
56. Shamban AT, Narurkar VA. Multimodal treatment of acne, acne scars and
pigmentation. Dermatol Clin 2009 Oct; 27 (4): 459-71, vi
57. Hirsch RJ, Lewis AB. Treatment of acne scarring. Semin Cutan Med Surg
2001 Sep; 20 (3): 190-8
58. Katz BE, MacFarlane DF. Atypical facial scarring after isotretinoin therapy
in a patient with previous dermabrasion. J Am Acad Dermatol 1994 May; 30
(5 Pt 2): 852-3
59. Bagatin E, dos Santos Guadanhim LR, Yarak S, et al. Dermabrasion for acne
scars during treatment with oral isotretinoin. Dermatol Surg 2010 Apr; 36
(4): 483-9
60. Mackee GM, Karp FL. The treatment of post-acne scars with phenol. Br J
Dermatol 1952 Dec; 64 (12): 456-9
61. Collins PS. Trichloroacetic acid peels revisited. J Dermatol Surg Oncol 1989
Sep; 15 (9): 933-40
62. Grimes PE. Management of hyperpigmentation in darker racial ethnic
groups. Semin Cutan Med Surg 2009 Jun; 28 (2): 77-85
63. Fischer TC, Perosino E, Poli F, et al. Chemical peels in aesthetic dermatology:
an update 2009. J Eur Acad Dermatol Venereol 2010 Mar; 24 (3): 281-92
64. Bradley DT, Park SS. Scar revision via resurfacing. Facial Plast Surg 2001
Nov; 17 (4): 253-62
65. Brody HJ. Variations and comparisons in medium-depth chemical peeling.
J Dermatol Surg Oncol 1989 Sep; 15 (9): 953-63
Am J Clin Dermatol 2012; 13 (5)
Management of Acne Scarring, Part II
66. Lee JB, Chung WG, Kwahck H, et al. Focal treatment of acne scars with
trichloroacetic acid: chemical reconstruction of skin scars method. Dermatol
Surg 2002 Nov; 28 (11): 1017-21; discussion 1021
67. Cho SB, Park CO, Chung WG, et al. Histometric and histochemical analysis
of the effect of trichloroacetic acid concentration in the chemical re-
construction of skin scars method. Dermatol Surg 2006 Oct; 32 (10): 1231-6;
discussion 1236
68. Al-Waiz MM, Al-Sharqi AI. Medium-depth chemical peels in the treatment
of acne scars in dark-skinned individuals. Dermatol Surg 2002 May; 28 (5):
383-7
69. Yug A, Lane JE, Howard MS, et al. Histologic study of depressed acne scars
treated with serial high-concentration (95%) trichloroacetic acid. Dermatol
Surg 2006 Aug; 32 (8): 985-90; discussion 990
70. Barnett JG, Barnett CR. Treatment of acne scars with liquid silicone in-
jections: 30-year perspective. Dermatol Surg 2005 Nov; 31 (11 Pt 2): 1542-9
71. Beer K. A single-center, open-label study on the use of injectable poly-L-lactic
acid for the treatment of moderate to severe scarring from acne or varicella.
Dermatol Surg 2007 Dec; 33 Suppl. 2: S159-67
72. Sadick NS, Palmisano L. Case study involving use of injectable poly-L-lactic
acid (PLLA) for acne scars. J Dermatolog Treat 2009; 20 (5): 302-7
73. Epstein RE, Spencer JM. Correction of atrophic scars with artefill: an open-
label pilot study. J Drugs Dermatol 2010 Sep; 9 (9): 1062-4
74. Laurent TC, Laurent UB, Fraser JR. The structure and function of hyalur-
onan: an overview. Immunol Cell Biol 1996 Apr; 74 (2): A1-7
75. Wang F, Garza LA, Kang S, et al. In vivo stimulation of de novo collagen
production caused by cross-linked hyaluronic acid dermal filler injections in
photodamaged human skin. Arch Dermatol 2007 Feb; 143 (2): 155-63
76. Lee JW, Kim BJ, Kim MN, et al. Treatment of acne scars using subdermal
minimal surgery technology. Dermatol Surg 2010 Aug; 36 (8): 1281-7
77. Goodman GJ. Management of post-acne scarring: what are the options for
treatment? Am J Clin Dermatol 2000 Jan-Feb; 1 (1): 3-17
78. Redbord KP, Busso M, Hanke CW. Soft-tissue augmentation with hyalur-
onic acid and calcium hydroxyl apatite fillers. Dermatol Ther 2011 Jan-Feb;
24 (1): 71-81
79. Goldberg DJ, Amin S, Hussain M. Acne scar correction using calcium hy-
droxylapatite in a carrier-based gel. J Cosmet Laser Ther 2006 Sep; 8 (3): 134-6
80. Perry CM. Poly-L-lactic acid. Am J Clin Dermatol 2004; 5 (5): 361-6; dis-
cussion 367-8
81. Valantin MA, Aubron-Olivier C, Ghosn J, et al. Polylactic acid implants
(New-Fill) to correct facial lipoatrophy in HIV-infected patients: results of
the open-label study VEGA. AIDS 2003 Nov 21; 17 (17): 2471-7
82. Sculptra Aesthetic (injectable poly-L-lactic acid) [package insert]. Bridge-
water (NJ): sanofi-aventis U.S. LLC, Dec 2009
83. Sadove R. Injectable poly-L: -lactic acid: a novel sculpting agent for the
treatment of dermal fat atrophy after severe acne. Aesthetic Plast Surg 2009
Jan; 33 (1): 113-6
84. Orentreich DS, Orentreich N. Subcutaneous incisionless (subcision) surgery
for the correction of depressed scars and wrinkles. Dermatol Surg 1995 Jun;
21 (6): 543-9
85. Alam M, Omura N, Kaminer MS. Subcision for acne scarring: technique and
outcomes in 40 patients. Dermatol Surg 2005 Mar; 31 (3): 310-7; discussion 317
86. Sasaki GH. Comparison of results of wire subcision performed alone, with
fills, and/or with adjacent surgical procedures. Aesthet Surg J 2008 Nov-Dec;
28 (6): 619-26
87. Balighi K, Robati RM, Moslehi H, et al. Subcision in acne scar with and
without subdermal implant: a clinical trial. J Eur Acad Dermatol Venereol
2008 Jun; 22 (6): 707-11
88. Aalami Harandi S, Balighi K, Lajevardi V, et al. Subcision-suction method: a
new successful combination therapy in treatment of atrophic acne scars and
other depressed scars. J Eur Acad Dermatol Venereol 2011 Jan; 25 (1): 92-9
Adis ª 2012 Springer International Publishing AG. All rights reserved.
339
89. AlGhamdi KM, AlEnazi MM. Versatile punch surgery. J Cutan Med Surg
2011 Mar-Apr; 15 (2): 87-96
90. Grevelink JM, White VR. Concurrent use of laser skin resurfacing and punch
excision in the treatment of facial acne scarring. Dermatol Surg 1998 May; 24
(5): 527-30
91. Solotoff SA. Treatment for pitted acne scarring: postauricular punch grafts
followed by dermabrasion. J Dermatol Surg Oncol 1986 Oct; 12 (10): 1079-84
92. Mancuso A, Farber GA. The abraded punch graft for pitted facial scars.
J Dermatol Surg Oncol 1991 Jan; 17 (1): 32-4
93. Dzubow LM. Scar revision by punch-graft transplants. J Dermatol Surg
Oncol 1985 Dec; 11 (12): 1200-2
94. Whang KK, Lee M. The principle of a three-staged operation in the surgery of
acne scars. J Am Acad Dermatol 1999 Jan; 40 (1): 95-7
95. Kang WH, Kim YJ, Pyo WS, et al. Atrophic acne scar treatment using triple
combination therapy: dot peeling, subcision and fractional laser. J Cosmet
Laser Ther 2009 Dec; 11 (4): 212-5
96. Jordan R, Cummins C, Burls A. Laser resurfacing of the skin for the improve-
ment of facial acne scarring: a systematic review of the evidence. Br J Der-
matol 2000 Mar; 142 (3): 413-23
97. Mustoe TA, Cooter RD, Gold MH, et al. International clinical recommend-
ations on scar management. Plast Reconstr Surg 2002 Aug; 110 (2): 560-71
98. Jalali M, Bayat A. Current use of steroids in management of abnormal raised
skin scars. Surgeon 2007 Jun; 5 (3): 175-80
99. Roques C, Teot L. The use of corticosteroids to treat keloids: a review. Int
J Low Extrem Wounds 2008 Sep; 7 (3): 137-45
100. Manuskiatti W, Fitzpatrick RE. Treatment response of keloidal and hyper-
trophic sternotomy scars: comparison among intralesional corticosteroid, 5-
fluorouracil, and 585-nm flashlamp-pumped pulsed-dye laser treatments.
Arch Dermatol 2002 Sep; 138 (9): 1149-55
101. Gupta S, Sharma VK. Standard guidelines of care: keloids and hypertrophic
scars. Indian J Dermatol Venereol Leprol 2011 Jan-Feb; 77 (1): 94-100
102. Chowdri NA, Masarat M, Mattoo A, et al. Keloids and hypertrophic scars:
results with intraoperative and serial postoperative corticosteroid injection
therapy. Aust N Z J Surg 1999 Sep; 69 (9): 655-9
103. Verbov J. The place of intralesional steroid therapy in dermatology. Br J
Dermatol 1976 Mar; 94 Suppl. 12: 51-8
104. McMichael AJ, Griffiths CE, Talwar HS, et al. Concurrent application of
tretinoin (retinoic acid) partially protects against corticosteroid-induced
epidermal atrophy. Br J Dermatol 1996 Jul; 135 (1): 60-4
105. Sawada Y, Sone K. Hydration and occlusion treatment for hypertrophic scars
and keloids. Br J Plast Surg 1992 Nov-Dec; 45 (8): 599-603
106. Puri N, Talwar A. The efficacy of silicone gel for the treatment of hyper-
trophic scars and keloids. J Cutan Aesthet Surg 2009 Jul; 2 (2): 104-6
107. Borgognoni L. Biological effects of silicone gel sheeting. Wound Repair
Regen 2002 Mar-Apr; 10 (2): 118-21
108. Phillips TJ, Gerstein AD, Lordan V. A randomized controlled trial of hy-
drocolloid dressing in the treatment of hypertrophic scars and keloids.
Dermatol Surg 1996 Sep; 22 (9): 775-8
109. Wang XQ, Liu YK, Qing C, et al. A review of the effectiveness of antimitotic
drug injections for hypertrophic scars and keloids. Ann Plast Surg 2009 Dec;
63 (6): 688-92
110. Gupta S, Kalra A. Efficacy and safety of intralesional 5-fluorouracil in the
treatment of keloids. Dermatology 2002; 204 (2): 130-2
111. Saray Y, Gulec AT. Treatment of keloids and hypertrophic scars with der-
mojet injections of bleomycin: a preliminary study. Int J Dermatol 2005 Sep;
44 (9): 777-84
112. Huang L, Wong YP, Cai YJ, et al. Low-dose 5-fluorouracil induces cell cycle
G2 arrest and apoptosis in keloid fibroblasts. Br J Dermatol 2010 Dec; 163
(6): 1181-5
Am J Clin Dermatol 2012; 13 (5)
340
113. Apikian M, Goodman G. Intralesional 5-fluorouracil in the treatment of
keloid scars. Australas J Dermatol 2004 May; 45 (2): 140-3
114. Fitzpatrick RE. Treatment of inflamed hypertrophic scars using intralesional
5-FU. Dermatol Surg 1999 Mar; 25 (3): 224-32
115. Hendricks T, Martens MF, Huyben CM, et al. Inhibition of basal and TGF
beta-induced fibroblast collagen synthesis by antineoplastic agents: im-
plications for wound healing. Br J Cancer 1993 Mar; 67 (3): 545-50
116. Espana A, Solano T, Quintanilla E. Bleomycin in the treatment of keloids and
hypertrophic scars by multiple needle punctures. Dermatol Surg 2001 Jan; 27
(1): 23-7
117. Aggarwal H, Saxena A, Lubana PS, et al. Treatment of keloids and hyper-
trophic scars using bleom. J Cosmet Dermatol 2008 Mar; 7 (1): 43-9
118. Rusciani L, Rossi G, Bono R. Use of cryotherapy in the treatment of keloids. J
Dermatol Surg Oncol 1993 Jun; 19 (6): 529-34
119. Rusciani L, Paradisi A, Alfano C, et al. Cryotherapy in the treatment of
keloids. J Drugs Dermatol 2006 Jul-Aug; 5 (7): 591-5
120. Burge SM, Bristol M, Millard PR, et al. Pigment changes in human skin after
cryotherapy. Cryobiology 1986 Oct; 23 (5): 422-32
121. Zouboulis CC, Blume U, Buttner P, et al. Outcomes of cryosurgery in keloids
and hypertrophic scars: a prospective consecutive trial of case series. Arch
Dermatol 1993 Sep; 129 (9): 1146-51
122. Yosipovitch G, Widijanti Sugeng M, Goon A, et al. A comparison of the
combined effect of cryotherapy and corticosteroid injections versus corti-
costeroids and cryotherapy alone on keloids: a controlled study. J Derma-
tolog Treat 2001 Jun; 12 (2): 87-90
123. Akita S, Akino K, Yakabe A, et al. Combined surgical excision and radiation
therapy for keloid treatment. J Craniofac Surg 2007 Sep; 18 (5): 1164-9
124. Berman B, Bieley HC. Adjunct therapies to surgical management of keloids.
Dermatol Surg 1996 Feb; 22 (2): 126-30
125. Quarles FN, Johnson BA, Badreshia S, et al. Acne vulgaris in richly pig-
mented patients. Dermatol Ther 2007 May-Jun; 20 (3): 122-7
126. Spann CT. Ten tips for treating acne vulgaris in Fitzpatrick skin types IV-VI. J
Drugs Dermatol 2011 Jun; 10 (6): 654-7
Adis ª 2012 Springer International Publishing AG. All rights reserved.
Levy & Zeichner
127. Callender VD. Acne in ethnic skin: special considerations for therapy. Der-
matol Ther 2004; 17 (2): 184-95
128. Barrientos N, Ortiz-Frutos J, Gomez E, et al. Allergic contact dermatitis from
a bleaching cream. Am J Contact Dermat 2001 Mar; 12 (1): 33-4
129. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Topical
tretinoin (retinoic acid) therapy for hyperpigmented lesions caused by in-
flammation of the skin in black patients. N Engl J Med 1993 May 20; 328
(20): 1438-43
130. Schallreuter KU, Wood JW. A possible mechanism of action for azelaic acid
in the human epidermis. Arch Dermatol Res 1990; 282 (3): 168-71
131. Thiboutot D. Versatility of azelaic acid 15% gel in treatment of inflammatory
acne vulgaris. J Drugs Dermatol 2008 Jan; 7 (1): 13-6
132. Kircik LH. Efficacy and safety of azelaic acid (AzA) gel 15% in the treatment
of post-inflammatory hyperpigmentation and acne: a 16-week, baseline-
controlled study. J Drugs Dermatol 2011 Jun; 10 (6): 586-90
133. Grimes PE. The safety and efficacy of salicylic acid chemical peels in darker
racial-ethnic groups. Dermatol Surg 1999 Jan; 25 (1): 18-22
134. Garg VK, Sinha S, Sarkar R. Glycolic acid peels versus salicylic-mandelic acid
peels in active acne vulgaris and post-acne scarring and hyperpigmentation:
a comparative study. Dermatol Surg 2009 Jan; 35 (1): 59-65
135. Ho SG, Yeung CK, Chan NP, et al. A retrospective analysis of the manage-
ment of acne post-inflammatory hyperpigmentation using topical treatment,
laser treatment, or combination topical and laser treatments in oriental
patients. Lasers Surg Med 2011 Jan; 43 (1): 1-7
136. Kim S, Cho KH. Treatment of facial postinflammatory hyperpigmentation
with facial acne in Asian patients using a Q-switched neodymium-doped
yttrium aluminum garnet laser. Dermatol Surg 2010 Sep; 36 (9): 1374-80
Correspondence: Dr Joshua Zeichner, MD, Director Cosmetic and Clinical
Research, Department of Dermatology, Mount Sinai Medical Center, 5 East
98th Street, 5th Floor, New York, NY 10029, USA.
E-mail: Joshua.Zeichner@mssm.edu
Am J Clin Dermatol 2012; 13 (5)