DOI: 10.1111/jdv.

13579 JEADV

REVIEW ARTICLE

The role of topical dermocosmetics in acne vulgaris

no2
E. Araviiskaia,1,* B. Dre
1
First Pavlov State Medical University of St. Petersburg, St. Petersburg, Russia
2
Department of DermatoCancerology, Nantes University, Nantes, France
*Correspondence: E. Araviiskaia. E-mail: arelenar@mail.ru

Abstract
Acne is a common chronic inflammatory disease and treatment modalities based on acne severity are well established.
The role of dermocosmetics in dermatology, and in particular acne, is becoming more important as more research eluci-
dates the mechanisms of action of products in the pathogenesis of acne. Dermocosmetics have the potential to be used
as monotherapy or in combination with medical treatment. Therefore, it has become important for dermatologists to
understand dermocosmetics to effectively and appropriately advise patients on their use. The objective of this review
was to provide new insights into the role of traditional and novel ingredients in dermocosmetics for the treatment of
acne, based on the authors’ objective assessment of the published literature. The type of products discussed include:
those which have a sebostatic effect, such as topical antioxidants and niacinamide; agents targeting abnormal kera-
tinization, such as salicylic acid, lipo-hydroxy acid, alpha-hydroxy acids, retinol-based products and linoleic acid; agents
targeting Propionibacterium acnes, such as lauric acid; and anti-inflammatory agents such as nicotinamide, alpha-linole-
nic acid and zinc salts. Despite the scientific advances in understanding these cosmetic ingredients, there still remains a
lack of rigorous controlled studies in this area.
Received: 4 September 2015; Accepted: 27 November 2015

Conflicts of interest
E Araviiskaia has served as a speaker for L’Oreal, La Roche Posay, Vichy, Bioderma, Pierre Fabre, Uriage,
Galderma, Glenmark, Merck Sharp &Dohme, Bayer Health Care, Merz and Stiefel/Glaxo Smith Kline and as a
European Global Alliance Acne Treatment, Brimonidine International Global Advisory Board member for
Galderma. B Dre
no has received honorarium from the following companies: Pierre Fabre Dermo-Cosme
tique, La
Roche-Posay, Galderma SA and Meda AB.

Funding sources

tique, France.
This work was supported by an unrestricted grant from Pierre Fabre Dermo-Cosme

Introduction
Acne is typically considered an adolescent disorder but is
becoming more prevalent in adulthood.1 Even though treatment
modalities based on acne severity are well established,2,3 acne is
considered a chronic and relapsing inflammatory disease that
can vary in severity, and may require long-term management.1
Dermocosmetics have become increasingly important in der-
matology, and provide another management strategy for patients
with long-term disease and during periods of relapse.4 Over the
past couple of decades, there has been more scientific research
assessing the mechanism of action of potential cosmetic formu-
lations.3,5 Understanding the efficacy and potential side-effects
of the active ingredients in dermocosmetics will help dermatolo-
gists to recommend appropriate options to patients, as well as be
aware of those that should be discontinued in the event of skin
irritation or other adverse effects.6
There are four main pathogenic pathways that are recognized
in acne: excess sebum production, abnormal keratinization, bac-
terial colonization by Propionibacterium acnes and inflamma-
tion.7 Particular ingredients used in dermocosmetics are known
to target these different pathways, and as such can be used as a
maintenance treatment option, monotherapy, or in combination
with pharmacological treatment. As well as having symptomatic
effect, there is some early evidence that antiacne dermocosmetics
can also impact pathogenesis of the disease, as well as aid side-
effects of other antiacne medications.
Among the vast range of cosmetics available, there is an
expanding group of products that have undergone more rigor-
ous clinical testing than was previously required and have
demonstrated efficacy and safety when used to treat specific skin
problems. There is a lack of good studies to support some prod-
ucts, however, and well-designed, adequately powered, blinded,

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Dermocosmetics in acne vulgaris
randomized, clinical trials are needed to better establish their
efficacy and tolerability and so help dermatologists to make opti-
mal recommendations for patients.6 In addition to clinical trials,
research in this field utilizes a range of non-invasive methods
including modern surface tests (e.g. 3D image analysis or non-
invasive ultraviolet light), biometric tests assessing sebum levels
on the skin, in addition to traditional in vitro and in vivo tech-
niques and patient-reported questionnaires.8–13
With so many approaches and outcomes measures being
used to assess antiacne dermocosmetics it makes it difficult
to make direct comparisons between treatment options, and
in spite of the move towards randomized controlled trials
there remains a lack of evidence in this area.6 Throughout
this review we have included additional details on the studies
discussed in Table 1.
Literature search
To identify the studies included in this narrative review comput-
erized searches were undertaken in Pubmed and Medline using
the term acne vulgaris in combination with: dermocosmetics,
active cosmetics, sebostatics, keratinization, salicylic acid (SA),
niacinamide/nicotinamide, benzoyl peroxide (BPO), lipo-
hydroxy acid (LHA), alpha-hydroxy acids (AHAs), retinoid,
linoleic acid (LA), P. acnes and zinc salts. Search results were
reviewed and further hand-searching of reference lists was com-
pleted to identify any additional studies and this augmented by
expert opinion when literature was sparse. Following careful
review, only papers deemed directly relevant were included in
this review.
Dermocosmetics and pathogenesis of acne
Acne is a multifactorial disease originating in the pilosebaceous
unit and resulting in acne lesions. Four main pathways have
been identified in acne: inflammatory mediators are released
into the skin; changes of the keratinization process, leading to
comedones; increased and altered sebum production; and follic-
ular colonization by P. acnes.6 The active cosmetic ingredients
influencing these four pathogenic pathways are summarized here
and in Table 2. Details of all the studies mentioned can be found
in Table 1.
Targeting abnormal sebum production
Increased and altered sebum production is a key factor in acne
pathogenesis but very few topical products have been proven to
target abnormal sebum production.6 Currently, masks and day
creams that have an active effect on the skin’s surface are used.
These absorb skin-surface lipids and reduce the appearance of
oiliness.14
Several active ingredients in dermocosmetics have been shown
to provide a sebo-suppressive function. There has been a grow-
ing role of topical antioxidants, such as fullerene (a strong oxy-
gen radical sponge) and epigallocatechin-3-gallate (EGCG; a
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927
major polyphenol found in green tea).15,16 Recently a double-
blind controlled trial evaluated the efficacy and safety of topical
Sodium L-ascorbyl-2-phosphate, an antioxidant derived from
vitamin C thought to prevent oxidation of sebum, in 25 patients
with acne. Compared with the vehicle group (n = 25), there was
a significant improvement in symptoms with a similar tolerabil-
ity profile.17
Moreover, topical niacinamide (also known as nicotinamide)
increases desquamation, and may reduce sebum production. A
study by Biedermann et al.18 found a dose-dependent sebo-sup-
pressive effect of topical niacinamide incubated in a cell culture
of human sebocytes. Draelos et al. also reported that topical 2%
niacinamide was effective in reducing the rate of sebum excre-
tion in 50 Japanese individuals over a 4-week period, and
decreased casual sebum levels, but not sebum excretion rates, in
30 Caucasian individuals after 6 weeks in two double-blind, pla-
cebo-controlled studies.10 Nicotinamide is also known to target
inflammation, as discussed below.
Targeting abnormal keratinization
In individuals prone to acne, because of an excess of keratin,
dead skin cells in the hair follicle are not shed properly,
resulting in clogged pilosebaceous glands and microcomedo
formation. It is now thought that inflammation precedes
ductal hypercornification (i.e. hyperkeratinization) which itself
may be caused by an increased rate of keratinocyte prolifera-
tion as well as reduced separation of ductal corneocytes and
increased cohesion between keratinocytes.19 This theory is the
idea behind using acidic formulations, such as acid peels in
acne scar therapy.
Alpha-hydroxy acids
As well as thinning the stratum corneum, AHAs also increase
epidermal thickness, disperse basal layer melanin and increase
collagen synthesis within the dermis.20,21 Glycolic acid peels are
the most common AHA peel, which target corneosome’s by
reducing their cohesiveness, enhancing breakdown and causing
desquamation.22 Since low concentrations of AHA (5–10%) act
on the superficial layers of the skin – by augmenting the healing
response by subcorneal epidermolysis, opening comedones and
unroofing pustules – many dermatologists feel that products
containing AHAs should not be classified as cosmetics.23 How-
ever, several studies (including a large multicentre, double-blind,
randomized, vehicle-controlled trial) have demonstrated the
safety and efficacy of a preparation containing a combination of
the AHA glycolic acid and retinaldehyde (a form of vitamin A)
in treating acne and post-inflammatory hyperpigmentation asso-
ciated with acne.24–26 Furthermore, a recent single-centre, dou-
ble-blind, randomized, placebo-controlled trial on 10% glycolic
acid monotherapy for mild acne showed significant improve-
ment in acne compared with the placebo after 90 days of treat-
ment.27
© 2016 European Academy of Dermatology and Venereology
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Araviiskaia and Dre

Table 1 Summary of the active cosmetic ingredients influencing pathogenic pathways of acne.

Agents Study details References

Abnormal sebum production
Antioxidants 8-week, open trial on topical fullerene gel Inui et al.15
11 patients; twice-daily application; 1% LipoFullerene gel; assessment of number of inflammatory lesions and
pustules at 0, 4 and 8 weeks of treatment; in vitro assays on sebum production
8-week randomized, double-blind, split-face controlled trial on 1 or 5% epigallocatechin-3-gallate (EGCG) solution Yoon et al.16
35 patients; twice-daily application; 1 or 5% EGCG vs. vehicle control (3% ethanol); efficacy (physician
assessment of lesions) assessed after 0, 1, 2, 4 and 8 weeks of treatment; in vitro assessment of biochemical
and genetic effects
12-week randomized, double-blind controlled trial on sodium L-ascorbyl-2-phosphate (APS) 5% lotion monotherapy Woolery-
50 patients; APS 5% lotion vs. vehicle; efficacy and tolerability (adverse events) assessed by various scales Lloyd et al.17
Niacinamide 4-week, double-blind, controlled trial on 2% niacinamide Draelos
(nicotinamide) 100 Japanese patients; 2% niacinamide moisturizer vs. placebo moisturizer; sebum excretion rate (SER) et al.10
assessed at 0, 2 and 4 weeks of treatment
6-week, randomized split-face study on 2% niacinamide
30 Caucasian patients; 2% niacinamide moisturizer vs. placebo moisturizer; SER and casual sebum levels
(CSL) assessed at 0 and 6 weeks of treatment
Abnormal keratinization
Alpha-hydroxy 90-day, open, multicentre trial on 0.1% retinaldehyde (RAL) + glycolic acid (GA) cream
no et al.24
Dre
acids 397 female patients; once-daily application of RAL/GA cream (without stopping majority of other acne
treatments); tolerance (by 4-point scale) and efficacy (lesion counting) assessed after 0, 30 and 90 days of
treatment
90-day, open trial on 0.1% RAL + 6% GA cream
no et al.36
Dre
1,709 patients; once-daily application of RAL/GA cream (without stopping majority of other acne treatments);
tolerance and efficacy assessed after 0 and 90 days of treatment
3 month, double-blind, randomized, multicentre vehicle-controlled trial on 0.1% RAL + 6% GA cream Poli et al.25
87 patients; mild–moderate acne; once-daily application of RAL/GA cream or vehicle (without stopping
majority of other acne treatments); tolerance (side-effects) and efficacy (lesion counting and sebumetry)
assessed after 0, 30 and 90 days of treatment
90-day, mono-centre, randomized, double-blind placebo-controlled trial on 10% GA cream Abels et al.27
120 patients; mild acne; once-daily application of GA cream or placebo; tolerance (reported adverse events)
and efficacy (lesion counting and physician assessment) assessed after 0, 45 and 90 days of treatment
8-week, split-face study comparing a novel combination treatment (salicylic acid, capryloyl Baumann
salicylic acid, HEPES, glycolic acid, citric acid and dioic acid) with 1% clindamycin + 5% benzoyl peroxide gel: et al.33
28 patients; mild–moderate acne; split-face application of both treatments as well as full-face application
of cleanser, moisturizer and sunscreen; tolerance (by patient questionnaire) and efficacy (physician visual
assessment) were assessed after 0 and 8 weeks of treatment
Salicylic acid (SA) 4-week, crossover study to compare 2% salicylic acid cleanser with 10% benzoyl peroxide wash Shalita29
30 patients; efficacy (comedone number) assessed after 0, 2 and 4 weeks (sequential 2-week treatment)
12-week, split-face randomized study comparing LHA and SA peels Levesque
20 patients; six peels at 2-week intervals; comedonal acne; safety (adverse events and global tolerance) and et al.32
efficacy (lesion counting) were assessed after 0 and 98 days of treatment
16-week, randomized study comparing oral isotretinoin with or without 20% salicylic acid peel
60 patients; moderate–severe acne; once-daily 20 mg oral isotretinoin with or without a 20% salicylic acid peel
every 2 weeks; efficacy (lesion counting and physician assessments) was assessed every 2 weeks Kar et al.30
Lipo-hydroxy acid 2-week, comparative study of a lipohydroxyacid (LHA) formulation vs. no treatment Uhoda et al.9
(LHA) 28 female patients; ‘acne prone’ photosensitive skin; twice-daily application of LHA formulation vs. no
treatment; tolerance (by patient questionnaire) and comedolytic effect (density of the follicular keratotic plugs)
were assessed after 0 and 2 weeks of treatment
12-week, randomized study to compare a LHA formulation with 5% benzoyl peroxide Bissonnette
80 patients; mild–moderate acne; twice-daily application of LHA formulation vs. 5% benzoyl peroxide; et al.31
tolerance and efficacy (inflammatory lesion number) were assessed after 0, 28, 56 and 87 days of treatment
12-week, split-face randomized study comparing LHA and SA peels Levesque
20 patients; six peels at 2-week intervals; comedonal acne; safety (adverse events and global tolerance) and et al.32
efficacy (lesion counting) were assessed after 0 and 98 days of treatment

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Dermocosmetics in acne vulgaris 929

Table 1 (Continued)

Agents Study details References

Retinol-based 90-day, open, multicentre trial on 0.1% retinaldehyde (RAL) + glycolic acid (GA) cream
no et al.24
Dre
products 397 female patients; once-daily application of RAL/GA cream (without stopping majority of other acne
treatments); tolerance (by 4-point scale) and efficacy (lesion counting) assessed after 0, 30 and 90 days of
treatment
90-day, open trial on 0.1% RAL + 6% GA cream:
no et al.36
Dre
1709 patients; once-daily application of RAL/GA cream (without stopping majority of other acne treatments);
tolerance and efficacy assessed after 0 and 90 days of treatment
In vitro assessment of vitamin A (all-trans retinoic acid) and vitamin D (1,25-dihydroxyvitamin D3) on P. acnes- Agak et al.34
induced inflammation:
Assays on human peripheral blood mononuclear cells were used to assess the inflammatory response
induced by P. acnes and the effects of vitamin A and D
Linoleic acid 1-month, double-blind, placebo-controlled, randomized, crossover study on topical 2.5% linoleic acid gel formulation Letawe et al.12
vs. vehicle
20 patients; mild acne; topical application; twice-daily application of 2.5% linoleic acid gel or vehicle (1-month
wash-out period between treatments); comedolytic activity (size of follicular casts and microcomedones via
digital image analysis) was assessed after 0, 4, 8 and 12 weeks of treatment
P. acnes follicular colonization
Lauric acid In vitro and in vivo assessment of topical lauric acid on P. acnes colonies Nakatsuji
Assays on cultured human sebocytes and tests in a murine model were used to assess the tolerance and et al.41
effects of lauric acid on P. acnes colonies
In vitro assessment of lauric acid on P. acnes colonies Yang et al.40
Assays on P. acnes cultures were used to assess the effect of various concentrations and formatulation of
lauric acid on P. acnes
Retinaldehyde Single application, healthy volunteer trial on 0.05% retinaldehyde vs. vehicle Peche re
22 patients; single application of 0.05% retinaldehyde or vehicle on the forearm; efficacy (skin bacterial et al.42
densities) assessed after 0, 2 and 5 h of treatment
2-month, healthy volunteer trial on 0.05% retinaldehyde vs. vehicle
22 patients; once-daily application of 0.05% retinaldehyde or vehicle on the forehead; efficacy (skin bacterial
densities) assessed after 0 and 2 weeks of treatment
Zinc 2-month, open trial on 30 mg zinc gluconate
no et al.43
Dre
30 patients; inflammatory acne; once-daily dose of 30 mg zinc gluconate; efficacy (bacteriologic sampling and
lesion counting) assessed after 0, 30 and 60 days of treatment; in vitro assessment of zinc salts on erythromycin
resistance in P. acne
Inflammatory mediator release
Niacinamide 8-week, double-blind, randomized trial comparing topical 4% nicotinamide gel with 1% clindamycin gel Shalita et al.46
(nicotinamide) 76 patients; moderate inflammatory acne; twice-daily application of either 4% nicotinamide gel or 1%
clindamycin gel; efficacy (physician evaluations and lesion counts) was assessed after 0, 4 and 8 weeks of
treatment
45-day, open trial of topical formulation containing nicotinamide, retinol and 7-dehydrocholesterol Emanuele
16 patients; inflammatory acne; twice-daily application of formulation (4% nicotinamide, 1% retinol, 0.5% et al.49
7-dehydrocholesterol in a moisturizer base); gene expression of pro-inflammatory molecules, efficacy
(physician evaluation) and tolerance (patient evaluation) assessed after 0 and 45 days of treatment
8-week, double-blind, randomized trial comparing topical 5% nicotinamide gel with 2% clindamycin gel Shahmoradi
60 patients; mild–moderate acne; twice-daily application of either 5% nicotinamide gel or 2% clindamycin gel; et al.47
efficacy (physician evaluations and lesion counts) was assessed after 0, 2, 4, 6 and 8 weeks of treatment
8-week, double-blind, randomized trial comparing topical 4% nicotinamide gel with 1% clindamycin gel Khodaeiani
80 patients; moderate inflammatory acne; twice-daily application of either 4% nicotinamide gel or 1% et al.48
clindamycin gel; efficacy (physician evaluation) and tolerance were assessed after 0, 4 and 8 weeks of
treatment
Alpha-linolenic, 10-week, randomized, prospective, double-blind, controlled trial of dietary omega-3 fatty acid and c-linoleic acid Jung et al.51
eicosapentaenoic 45 patients; mild–moderate acne; twice-daily dose of 500 mg EPA + 500 mg DHA or 200 mg c-linoleic acid;
(EPA) and control group received no treatment; efficacy (lesion counts, self-evaluation), safety (patient evaluation) and
docosahexaenoic histological changes (biopsy) were assessed after 0 and 10 weeks of treatment
(DHA) acids

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Araviiskaia and Dre

Table 1 (Continued)

Agents Study details References

Zinc salts In vitro assessment of Zinc Gluconate on P. acnes-induced inflammation Jarrousse
Assays on the effect of P. acnes in human keratinocytes treated with Zinc Gluconate for 3 h. Inflammation et al.54
response was assessed at the cellular level
In vitro and in vivo assessment of Zinc Gluconate on inflammatory acne lesions Isard et al.55
In vivo assays on inflammatory marker expression in biopsies of acne lesions and healthy skin and in vitro
assay of the effect of P. acnes in human keratinocytes treated with Zinc Gluconate or vehicle
In vitro assessment of Zinc calx on P. acnes and P. acnes-induced inflammatory pathways Sandeep
Assays on the effect of Zinc calx on P. acnes growth in culture and on inflammatory marker production and gene Varma et al.44
expression (TNF-ɑ and IL-8) in P. acnes-stimulated human monocytic cell line
Other ingredients 3-month, single-blind, randomized clinical trial comparing 5% tea tree oil gel with 5% benzoyl peroxide lotion: Bassett
124 patients; mild–moderate acne; application of either 5% tea tree oil gel or 5% benzoyl peroxide lotion; et al.58
efficacy (lesion counts) and tolerance (patient evaluation) was assessed after 0, 1, 2 and 3 months of
treatment
In vitro assessment of undecyl-rhamnoside vs. Zinc Gluconate on P. acnes-induced inflammation: Isard et al.56
Assays on the effect of P. acnes in human keratinocytes pre-treated with undecyl-rhamnoside or Zinc
Gluconate for 24 h. Inflammation response was assessed at the cellular level
6-week, double-blind, controlled trial on 3% SIG1273 gel Fernande
z
30 patients; ‘acne-prone’ skin; application of either 3% SIG1273 gel or vehicle; efficacy (physician evaluations, et al.57
lesion counts and P. acnes assessment) was assessed after 0 and 6 weeks of treatment
In vitro assessment of oat plantlet extract on immune regulators Mandeau
Assays on the effect of oat plantlet extract (a range of concentrations) in human keratinocytes, activated T et al.59
lymphocytes and dendritic cells on a range of inflammatory mediators

Table 2 Summary of the known effects and roles of dermocosmetic ingredients in acne treatment regimens.

Pathogenic factor Role in treatment regimen

Abnormal Abnormal P. acnes Inflammation Maintenance/ Adjunctive Side-effect
sebum keratinization follicular monotherapy therapy management
production colonization
Antioxidants U U U
Niacinamide (nicotinamide) U U U U
Alpha-hydroxy acids U U U
Salicylic acid U U U U U
Lipo-hydroxy acid U U U
Glycolic acid U U U
Linoleic acid U U
Lauric acid U U
Retinaldehyde U U U U
Zinc salts U U U U U
Fatty acids U U U
Oat plantlet extract U U U U

Salicylic acid SA in combination with other treatments is also effective. In a

Salicylic acid, a lipid-soluble phytohormone with comedolytic
properties, is moderately effective in the treatment of acne,
although it is less potent than topical retinoids.28 In a cross-
over study comparing a SA cleanser and a BPO wash (a topi-
cal bactericidal agent commonly used as a first-line treatment)
in the treatment of acne vulgaris, 30 patients who were treated
with a 2% SA cleanser for 2 weeks showed a significant
improvement in their acne (as judged by a reduction in num-
ber of comedones), which then worsened during use of the
BPO wash.29
comparative study of oral isotretinoin versus oral isotretinoin
with a 20% SA peel in 60 patients with active acne, the combina-
tion treatment was more effective than isotretinoin alone (a
reduction of 93% in lesion number, compared with 73%).30
Lipo-hydroxy acid
Lipo-hydroxy acid, a derivative of SA, has been shown to be as
effective as BPO in reducing the number of lesions in a random-
ized study of 80 patients with acne. Fifty-nine patients com-
pleted the trial: 28 treated with LHA and 31 with BP.31 In a

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Dermocosmetics in acne vulgaris
small split-face randomized study on comedonal acne, LHA
peels were shown to be slightly superior to SA peels in reducing
numbers of non-inflammatory lesions.32
Several combinations of acids have been shown to be effective
and to have good tolerability. In a split-face study of 60 individ-
uals with mild to moderate acne, a product containing salicylic,
capryloyl salicylic, glycolic, citric and dioic acids was compared
with a gel containing clindamycin and BPO.33 The results
demonstrated similar tolerance and efficacy across both treat-
ments as judged by physician assessment and patient question-
naires.
Retinol-based products
Topical retinoids are the mainstay of acne therapy as they target
different pathogenic factors. The best recognized is their come-
dolytic action by increasing epithelial turnover. Given recent evi-
dence that showed P. acnes-induced inflammatory response in
patients with acne, which in turn was regulated by vitamin A
(retinol is a derivative of vitamin A) and vitamin D, retinoids
will continue to be important in acne management.34 Retinalde-
hyde, the direct precursor of retinoic acid, has been shown to be
efficacious and safe when combined with erythromycin,35 and it
has been shown to be effective and less irritating than other reti-
noids in a large study of more than 1000 patients.36
Linoleic acid
Linoleic acid deficiency is associated with disturbed keratiniza-
tion of the follicular infundibulum.37 In a double-blind, pla-
cebo-controlled, randomized crossover study, a topical 2.5% LA
gel had a dramatic effect on microcomedones.12 Digital image
analysis of cyanoacrylate follicular biopsies demonstrated a sig-
nificant effect of LA vs. placebo on the size of follicular casts and
microcomedones, as well as a 25% reduction in their overall fol-
licular cast size.
Targeting P. acnes
Antibacterial resistance in P. acnes has stimulated new approaches
in dermocosmetics that target these bacteria.38 The antimicrobial
activities of medium-chain fatty acids, such as lauric acid or glyc-
eryllaurate, against P. acnes has been demonstrated in vitro.39,40
Nakatsuji et al. found a significant reduction in the number of P.
acnes colonies at the epidermal surface, with non-toxicity to sebo-
cytes, together with strong bactericidal properties of lauric acid in
in vivo studies.41 Moreover, lauric acid exerted an inhibitory effect
on the growth of skin bacteria such as P. acnes, S. aureus and S.
epidermidis at a concentration 15 times lower than that of BPO.
Preliminary studies on retinaldehyde42 and zinc43,44 have also
shown antimicrobial activity against P. acnes.
Targeting inflammation
Over recent years it has become apparent inflammatory
responses are involved in the earliest stages of acne lesion devel-
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opment, highlighting the importance of anti-inflammatory
properties in dermocosmetics.45
Nicotinamide
Topical nicotinamide, in addition to its sebostatic effects, is also
an effective anti-inflammatory agent. Several double-blind stud-
ies have been conducted comparing the effect of nicotinamide
gel with clindamycin gel on patients with acne, and all have
demonstrated its anti-inflammatory effect, reducing the number
of inflammatory papules and acne lesions to a level comparable
with clindamycin gel.46–48
Nicotinamide may also be effective in reducing inflammation
in combination treatments. In a pilot study using skin biopsies
from 16 patients, combination treatment of nicotinamide, reti-
nol and 7-dehydrocholesterol had an anti-inflammatory effect,
resulting in reduced levels of pro-inflammatory molecules asso-
ciated with acne.49
Alpha-linolenic acid
There is evidence that derivatives of a-linolenic acid, eicos-
apentaenoic and docosahexaenoic acids (EPA and DHA) may
modulate the cascade of inflammatory reactions in acne by
modulation of toll-like receptors (TLR-2 and TLR-4).50 A
recent small observational uncontrolled trial assessing the
clinical efficacy of dietary omega-3 fatty acid (containing EPA
and DHA) in 45 patients with mild to moderate acne showed
a significant decrease in the number of inflammatory and
non-inflammatory acne leasions,51 justifying further investiga-
tions in this field.
Zinc salts
A small in vitro study assessed the mechanism of zinc on cuta-
neous inflammatory acne lesions and found that zinc had strong
anti-inflammatory properties through inhibition of leucocyte
chemotaxis.52 A recent in vitro study on zinc calx (a mineral
commonly used in traditional medicine) also showed an inhibi-
tory effect on both P. acnes growth and on P. acnes-induced IL-8
and TNFɑ signalling in a monocyte cell line44 and further
in vitro and in vivo studies have shown that zinc impacts a range
of pro-inflammatory signalling pathways known to be involved
in acne and comedo formation.53–55 Data from these prelimi-
nary studies may justify further research into the anti-inflamma-
tory effect of topical zinc.
Other products
Worldwide, there are several other products with ingredients for
which the mechanisms of action are not fully understood or
whose efficacy is not yet established.6 Early in vitro studies in
normal human keratinocytes have found that a rhamnoside deri-
vate (undecyl-rhamnoside) has anti-inflammatory properties,
modulating P. acnes-induced pro-inflammatory pathways in a
similar manner to zinc salts.56 Other in vitro studies have shown
© 2016 European Academy of Dermatology and Venereology
932
that a novel cosmetic functional ingredient, SIG1273, inhibits P.
acnes-induced IL-8 production and inhibits P. acnes growth,
improving inflammatory lesions, microcomedone counts and
Sebutape scores in cultured human keratinocytes.57
The efficacy of natural ingredients has also been assessed, for
example 5% tea tree oil was evaluated in 124 patients with acne
in a single-blind, randomized clinical trial. There was significant
reduction in both inflammatory and non-inflammatory acne
lesions and, although it had a slower onset of action when com-
pared with 5% BPO lotion, the tea tree oil caused fewer side-
effects.58 Another natural ingredient that has been researched for
its potential efficacy in acne treatment is oat preparations which
are well-known to sooth and restore fragile skin. An oat plantlet
extract has been shown to have a range of anti-inflammatory
immunomodulatory effects in keratinocytes in vitro and recently
it has been shown to inhibit bacterial adhesion.59 Several other
natural ingredients possess antioxidant, anti-inflammatory, and/
or moisturizing properties, which may be useful additions for
more effective acne therapies. These include feverfew, liquorice,
aloe vera, chamomile, curcumin, soy, coffeeberry, mushroom
extracts, green tea, pine bark extract, vitamin E, vitamin C and
niacinamide.60 However, before these novel products can be
reliably recommended for treatment, further clinical studies
must be conducted and their efficacy and safety reliably con-
firmed.6
Role of dermocosmetics in acne treatment
Maintenance therapy
Acne lesions can typically recur for years and the strategy for
treating these patients with sustained acne remission today
includes an induction phase followed by a maintenance phase.3
Adjunctive cosmetic treatments can be used to maintain the level
of improvement and prevent the appearance of new lesions in
addition to targeting specific aspects of acne pathogenesis, par-
ticularly where they target more than one contributing factor
(e.g. AHAs).14
Despite evidence of dermocosmetics’ role in the preventing
the recurrence of acne, however, further studies are needed to
demonstrate their efficacy in maintaining long-term remission
of acne.
Role of dermocosmetics
Prevention and maintenance: Synergistic effect:
prevent appearance of new lesions target another pathogenic factor
and/or improve the efficacy of
another treatment
Figure 1 The role of anti-acne dermocosmetics as adjunctive therapy.
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no
Araviiskaia and Dre
Synergistic effect
Combination treatment regimens for acne, directed at two or
more key pathogenic factors, are now the first-line therapeutic
option in most mild to moderately severe cases.3,6,60 Several cos-
metic products targeting additional pathogenic factors may be
used as an adjunctive to a pharmacological regimen, including
cleansing lotions, and day/night compositions containing agents
with mild comedolytic and anti-inflammatory effects.
For example glycolic acid aids comedone extrusion and has a
synergistic effect in the treatment of acne vulgaris when com-
bined with tretinoin, which prevents new microcomedone for-
mation.61 In a case series of approximately 500 patients, Elson
showed that the combination of tretinoin and glycolic acid was
more effective than either agent alone.62
A recent open multicentre study of 397 adult women with
acne emphasized the synergistic properties of retinaldehyde with
glycolic acid, which could be of interest for this patient popula-
tion to use in combination with their usual acne products
(except retinoids) due to the improved tolerance/efficacy ratio.24
Management of side-effects
The physician’s responsibility to patients goes beyond simply
prescribing acne medication. In clinical practice some topical
and systemic antiacne medications are known to induce skin
irritation and when this occurs the treatment regimen is dis-
rupted.14,63 However, there may be other options: in a prospec-
tive, open-label, non-randomized study patients with retinoid
dermatitis were either managed with a ethanolic myrtle extract
and vitamin gel (n = 116) or a simple emollient cream (n = 48)
and the combination gel substantially improved overall clinical
outcome.64 Furthermore, dermatologists are now able to refer to
lists of substances to avoid in patients with a susceptibility to
develop comedones.65
Cleansing and moisturizing
Aggressive cleansing has long been known to aggravate acne and
the importance of gentle cleansing is emphasized to patients.66,67
Avoiding irritation can partly be achieved by selecting cleansers
that contain synthetic detergents with a pH adjusted to between
5 and 7.3, which is closer to that of normal skin and is therefore
less irritating.
Management of side effects:
alleviate side effects of other
treatments and potential skin barrier
defects
© 2016 European Academy of Dermatology and Venereology
Dermocosmetics in acne vulgaris
Draelos reported that non-comedogenic, non-acnegenic
moisturizer selection is important to counteract the drying effect
of some acne medications.68 Topical emollient compounds can
be used to reduce skin irritation by enhancing the stratum cor-
neum barrier function. A simple emollient cream, which was
used as an adjunctive treatment in an open-label, randomized
study on 30 patients receiving either oral isotretinoin or topical
tretinoin, significantly improved skin dryness, roughness and
desquamation.69 A ‘combination skin care’ including an acidic
foaming facial skin cleanser, an aqueous lotion with eucalyptus
extract and a moisturizing gel containing pseudo-ceramide and
eucalyptus extract proved to be effective in 4-week non-com-
parative study among 29 postadolescent Japanese women with
mild acne associated with dry and sensitive skin. The significant
decrease in acne as well as improvement of dry skin was
achieved.70
Patient adherence
Patient adherence is closely associated with the role of cosmetics
to delay or prevent the side-effects of antiacne medications;
compliance is improved if the skin is not irritated.71 Dr
eno et al.
assessed the adherence to acne treatment and the use of cosmet-
ics, such as moisturizers and cleansers, using a simple, validated
questionnaire in a worldwide cohort of 3339 patients.72 The
results of this survey proved that dermocosmetics can increase
the patients’ adherence to treatment.
Future prospects and further research
With the widening role of cosmetics in dermatology, more
research is needed on the mechanism of action of these formula-
tions on acne. Innovative approaches are needed to better target
the follicular shaft and the sebaceous gland and cosmetics pro-
vide an avenue to facilitate follicular penetration of other topical
drugs.
With the increasing impact of antibacterial resistance, P. acnes
is an important target for novel treatments. The mechanism of
action of P. acnes in acne is still not clear and recent research has
shown that responses vary and biofilms are thought to play a
central role.73,74 The skin’s overall microbioma may also be a
future avenue for research; a preliminary study on topical appli-
cation of an extract from Lactobacillus plantarum (a probiotic
bacteria), which produces antimicrobial peptides, appeared to
effectively reduce lesion size in mild acne as well as reducing
acne-induced erythema and total microflora in a small number
of patients.75
The role of antiacne dermocosmetics among specific popula-
tions is increasing.5 There is the potential for dermocosmetics to
be particularly useful as a mild maintenance or treatment option
during pregnancy and lactation, and they may be viewed as safer
than prescription drugs in this group. Recent guidelines demon-
strate that accessory cosmetic measures may be useful during
pregnancy.76
JEADV 2016, 30, 926–935
933
Conclusions
The use of adjuvant skin care is now integral to the management
of acne and dermocosmetics are evolving into a real manage-
ment option for dermatologists. Recent advances in science and
technology have created a new era in their development and
there is a drive towards robust clinical trials evaluating cosmet-
ics, comparable to those used in the development and evaluation
of pharmaceutical products. Even though there is a favourable
risk–benefit ratio for the use of cosmetics in acne, the growing
market of dermocosmetics has further highlighted this require-
ment to facilitate effective clinical decision-making and reflect
its new role in the clinic.
This review adds new insights into the role of well-known
ingredients, as well as new ones based on objective methods of
assessment. In addition, we have provided an overview of the
synergistic role of dermocosmetics in the treatment of acne vul-
garis, the prevention of side-effects of antiacne drugs, and adher-
ence to treatment.
Acknowledgements
This article was presented in part at the 13th Entretiens d’Avene
meeting entitled The changing face of acne (6 June 2014, Tou-
louse, France). The authors thank MedSense Ltd, High
Wycombe, UK, for providing editorial assistance, which was
funded by Pierre Fabre Dermo-Cosm
etique, France.
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