Sách Giáo Khoa Về Lột Da Hóa Học (Chemical Peels – Ấn Bản 2)

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Textbook of Chemical Peels

Series in Cosmetic and Laser Therapy
Series Editors
Nicholas J. Gary P. Lask, and David J. Goldberg
Philippe Deprez, Textbook of Chemical Peels, Second Edition: Superficial,
Medium, and Deep Peels in Cosmetic Practice, ISBN 9781482223934
Jenny Kim, Gary Lask, and Andrew Nelson, Comprehensive Aesthetic
Rejuvenation: A Regional Approach, ISBN 9780415458948
David J. Goldberg and Alexander L. Berlin, Disorders of Fat and Cellulite:
Advances in Diagnosis and Treatment, ISBN 9780415477000
Neil S. Sadick, Paul J. Carniol, Deborshi Roy, and Luitgard Wiest, Illustrated
Manual of Injectable Fillers: A Technical Guide to the Volumetric Approach to
Whole Body Rejuvenation, ISBN 9780415476447
Kenneth Beer, Mary P. Lupo, and Vic A. Narurkar, Cosmetic Bootcamp
Primer: Comprehensive Aesthetic Management, ISBN 9781841846989
Anthony Benedetto, Botulinum Toxins in Clinical Aesthetic Practice, Second
Edition, ISBN 9780415476362
Robert Baran and Howard I. Maibach, Textbook of Cosmetic Dermatology,
Fourth Edition, ISBN 9781841847009
Neil Sadick, Diane Berson, Mary P. Lupo, and Zoe Diana Draelos,
Cosmeceutical Science in Clinical Practice, ISBN 9780415471145
Paul Carniol and Gary Monheit, Aesthetic Rejuvenation Challenges and
Solutions: A Global Perspective, ISBN 9780415475600
Avi Shai, Robert Baran, Howard I. Maibach, Handbook of Cosmetic Skin
Care, Second Edition, ISBN 9780415467186
Benjamin Ascher, Marina Landau, and Bernard Rossi, Injection Treatments in
Cosmetic Surgery, ISBN 9780415386517
David J. Goldberg, Laser Hair Removal, Second Edition, ISBN
9780415414128
Paul J. Carniol and Neil S. Sadick, Clinical Procedures in Laser Skin
Rejuvenation, ISBN 9780415414135
C. William Hanke, Gerhard Sattler, and Boris Sommer, Textbook of
Liposuction, ISBN 9781841845326
David J. Goldberg, Fillers in Cosmetic Dermatology, ISBN 9781841845098

Philippe Deprez, M.D.
Medical Director
Policlinica Estetica & Anti-Aging
Empuriabrava, Spain
Textbook of Chemical Peels
SECOND EDITION
Superficial, Medium, and Deep Peels
in Cosmetic Practice

CRC Press
Taylor & Francis Group
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Boca Raton, FL 33487-2742
© 2017 by Taylor & Francis Group, LLC
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Contents
Acknowledgment......vii
1. Definition and classification of chemical peels....................................................... 1
2. Prepeel care..................................................................................................................... 7
3. Postpeel care..................................................................................................................13
4. Factors influencing the skin’s reactions to chemical peels..................................29
5. Selection of the right peel.......................................................................................... 32
6. Alpha hydroxy acids: Chemistry, pH and pKa, and mechanism of action.......45
7. Alpha hydroxy acids: Histology and factors influencing penetration..............50
8. Alpha hydroxy acids: Indications and results........................................................52
9. Alpha hydroxy acids: Application as cosmetics and as peels.............................55
10. Alpha hydroxy acids: Side effects of AHAs...........................................................63
11. Alpha hydroxy acids: A new slow-release AHA complex with no
neutralization required...............................................................................................65
12. Trichloroacetic acid: General information, toxicity, formulations, and
histology......................................................................................................................... 74
13. Trichloroacetic acid: Indications and contraindications......................................89
14. Trichloroacetic acid: Classic semiology...................................................................98
15. Easy TCA and Easy TCA Pain Control: Description and basic protocols......102
16. Treating melasma, chloasma, and postinflammatory hyperpigmentation........ 116
17. Treating acne...............................................................................................................126
18. Treating multiple keratoses on the scalp...............................................................132
19. Treating aging skin of the hands and forearms..................................................136
20. Treating the neck and décolletage..........................................................................144
21. Stretch marks, scars, and pilar keratosis: Anterior chemabrasion..................152
22. Face and hands: Actinic keratoses and lentigines...............................................183
23. Trichloroacetic acid to the papillary dermis: Unideep.......................................198
24. Resorcinol: Unna’s paste/Jessner’s solution..........................................................206
25. Phenol: Chemistry, formulations, and adjuvants................................................213
26. Phenol: Properties and histology............................................................................221
27. Phenol: Skin penetration and detoxification........................................................226

vi      Contents
28. Phenol toxicity: Causes, prevention, and treatment...........................................230
29. Phenol: Choice of peel and combination treatments..........................................239
30. Phenol: Indications....................................................................................................250
31. Phenol: Contraindications, precautions, and safety...........................................264
32. Phenol: Prepeel preparation.....................................................................................269
33. Full-face phenol: Nerve block anesthesia and/or sedation................................275
34. Full-face phenol: Application..................................................................................285
35. Full-face phenol: Postpeel care................................................................................295
36. Phenol: Chemical blepharoplasty and cheiloplasty............................................307
37. Complications of chemical peels............................................................................325
38. Combination peels..................................................................................................... 374
Index................... 387

Acknowledgment
The publication of this work has been assisted by an educational grant from Skin Tech pharma
group ( and ).
It should be noted that this textbook is comprehensive about all available peel products
but that there are many ancillary products (such as sunscreens) manufactured in comparable
formulations about which it cannot be expected to be comprehensive; the author is most famil-
iar with and recommends those from Skin Tech but does not imply by this that other products
may not be comparable.

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1
Definition and classification of chemical peels
DEFINITION OF A CHEMICAL PEEL
A chemical peel is a skin treatment intended to visibly improve
the structure of treated tissue by the external application of a
caustic solution. It can simply accelerate the natural processes
of exfoliation, but can also completely destroy the epidermis
and a more or less large proportion of the dermis, essentially
by protein coagulation or lysis. The effect of any peel reaches
the dermis, directly or indirectly and to varying depths, where
the processes of regeneration are induced to a greater or lesser
degree, depending on the molecule or molecules used and the
application procedure.
Chemical peels are among the oldest forms of skin reju-
venation and form a group of treatments in their own right.
They are both flexible and effective, with a histological, chemi-
cal, toxicological, and clinical basis. They have an ancient his-
tory, have evolved rapidly, and can be adapted to almost any
circumstances within the limits of their indications.
Most peels, to varying degrees, cause the same types of
histological changes, whose clinical results lead to a more or
less rejuvenating effect on all or part of the skin.
Classification is always restrictive, as it forces highly
variable events into a rigid framework. So many different fac-
tors come into play that it becomes difficult to fit all chemical
peels into a simplified and rigid classification of “superficial,”
“medium,” and “deep.”
Let us take the well-known glycolic acid peel as an exam-
ple: its depth of action depends on the patient’s skin type; the
presence of associated disorders (e.g., seborrheic dermatitis);
skin preparation in the long, medium, and short term; the type
of presentation (gel, liquid, mask, or self-neutralizing pseudo-
gel); the concentration of the product; the m/m (or w/w), m/v
(or w/v), or m+v (or w+v) calculation, whether or not it is com-
bined with other acid molecules (e.g., lactic or kojic); the pH of
the solution (e.g., 0.5 or 3.5) and therefore the fraction of free
glycolic acid; what it is applied with (brush, cotton pad, etc.);
the number of coats; how forcefully it is applied; whether it is
applied on the face or body; the exact location on the face (e.g.,
nostrils or eyelids1); the contact time; how or whether it is neu-
tralized or diluted at the end of the peel; the immediate post-
peel care; the quality of care between peels; the number and
frequency of repeat sessions; and the list goes on.
It is clear that it does not take much to turn a very light
glycolic acid peel into a medium-depth peel that can even reach
the deeper layers of the dermis and risk discoloration or even
scarring. All it takes is for the peel not to be neutralized prop-
erly. The same is true for all of these caustic molecules, which is
why a thorough knowledge of chemical peels and skin anatomy
is necessary before undertaking this kind of treatment. Every
practitioner, through personal experience and practice, should
aim to standardize his or her treatments to eliminate the maxi-
mum number of variables. Fortunately, new chemical peel
formulas are easier, safer, and quicker to use, allowing young
physicians to get on with the job of peeling without losing sleep
or having postpeel nightmares. Sound knowledge and experi-
ence are still essential for peels to the papillary dermis.
CRITERIA FOR CLASSIFICATION
Molecular Dependence
It is very simple to understand that phenol is more aggressive
than lactic acid but less simple to understand that a light tri-
chloroacetic acid (TCA) peeling can give deeper results com-
pared to deep phenol peel, when it is applied after a physical
abrasion (see Combined peelings). Note that phenol peel should
not be applied after abrasion for toxicological reasons.
Doctor Dependence
Classification may be personal; it may be related to the practice
of one particular doctor who has standardized his methods of
treatment with a view to limiting uncontrollable variables. But
such a classification would not allow for any scientific exchange.
What would produce a superficial peel with one practitio-
ner could in fact result in a medium peel with another who uses
the same product with a different application technique. This is
why peels are often considered to be doctor-​dependent.
How can we give a valid classification for a treatment
that is doctor-dependent? We should also compare products of
the same type only, and yet the quality of the preparations and
excipients is highly variable and impossible to control.
Chemical Dependence
TCA crystals, for example, are very hydrophilic, which means
that they must be kept in perfect conditions so that the phar-
macist can prepare the solutions we prescribe properly. How
can we know how long the pharmacist’s bottle of TCA crystals
has been open? If the crystals have not been hydrated inadver-
tently (if the pharmacist closes the bottle immediately after tak-
ing out the required amount), the final concentration will be
correct. If, on the other hand, the crystals are mostly hydrated
(if the pharmacist leaves the bottle of TCA open while serving
another customer), the concentration of the solution provided
by the pharmacy will be abnormally low and not very effective.
Peels therefore are also considered to be chemical-dependent.
Patient Dependence
Each patient has a skin type that is genotypically and pheno-
typically unique. The doctor must know each patient’s skin
history. Stable products that are properly prepared and applied
with precise methodology, in the same way, by the same doc-
tor, on the same day, can produce different results on differ-
ent patients. Every morning, or maybe several times a day,
patients go through their own particular skincare routine that
the doctor doing the peel does not necessarily know about. For
example, some teenagers secretly apply large quantities of topi-
cal benzoyl peroxide for acne. It reduces the thickness of the
stratum corneum and makes the skin more permeable. This of

2        Textbook of Chemical Peels
course makes it easier for the acids used for skin peeling to pen-
etrate the skin and can, in some cases, cause unexpected burns.
A similar situation arises with patients who want to present
their doctors with perfectly clean skin and use abrasive creams.
Their intention is noble, but the consequences are sometimes
unpleasant. Therefore, a peel is also patient-dependent.
If we leave aside these variables, we can fit the different
types of peels into their appropriate slots. This is just for the
beauty of the exercise, however, as the variables still need to be
taken into account. It is clearly possible to perform a superficial
or medium peel using phenol. But, given the inherent toxicity of
phenol, what would be the point? What is more, 70% unbuffered
glycolic acid that is left for 10–15 minutes on a thin, sensitive
skin that has been prepared with retinoic acid can result in a
cosmetic disaster. It is possible to conduct good-quality, deep
peels with TCA, but the risks can be greater than if phenol is
used correctly.
PEELING CLASSIFICATION
Peelings are traditionally classified as superficial, medium,
and deep peels. While these classifications seem simple and
understandable, the literature gives us little comprehensive
data about the different depths. What some authors consider as
superficial is considered as medium by others, and what some
consider medium others may consider as deep. A link with the
concentration that is used is especially pointless, because, as
described in Chapter 12, many details about the usable acid
concentration interfere. The depth reached by a 25% TCA is dif-
ferent if the concentration is calculated in weight/weight (w/w),
weight/volume (w/v), weight plus volume (w+v), or by dilution
of a more concentrated solution prepared using one of these
methods. Dramatic differences appear, generating side effects.
Usually, acid concentrations are simply quoted in percentage,
without specifying %w/w or w/v for example. In addition, the
depth of action of an acid solution of x% will be different if one
coat or several coats are applied, if the skin is thick or thin, if the
skin is dry or oily, if the applicator is a brush or a gauze, if the
pressure is soft or strong on the skin, and so forth.
The usual classification as superficial, medium, or deep
is therefore obsolete.
In reality, it is better to determine the depth of a peel by
clinically observing what is happening to the skin during the
course of the treatment than by blindly applying preset recipes.
When we say, for example, that the result of a glycolic acid
peel is time-dependent, this does not mean having to watch the
clock but rather continuously analyzing how the skin is react-
ing to determine the best moment to start neutralization.
One basic principle must be respected: a peel should not
be unnecessarily deep or unnecessarily superficial. There is
no point in completely destroying the papillary dermis when
treating a purely epidermal problem, and it is both pointless
and ineffective to use an intraepidermal peel, even repeatedly,
to treat a dermal problem.
Depths of Peelings
I usually consider seven depths of peelings (Figure 1.1).
Depth 1: Exfoliation (Very High Security)
The most superficial peel consists of a simple exfoliation of
stratum corneum dead cells; it gives a good skin cleansing and
a touch of better hydration. This “hydration touch” in reality
results in skin damage: the peel removed the protective stratum
corneum layer and the fingers are now directly in contact with
superficial keratinocytes. Keratinocytes are living cells (only
the most superficial layers are near to death) containing more
water than stratum corneum cells.
Depth 2: Intraepidermal Peel (Very High Security)
The peel solution penetrates deeply into the epidermis, remov-
ing more cells; nevertheless, it does not touch any part of the
Stratum disjunctum
Basal layer peel
Grenz zone peel
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
GZ
Exfoliation
Very High Security
Intraepidermal peel
High Security
Papillary dermis peel
Still secure zone
Superficial reticular
dermis peel
Quite secure zone
Deep reticular dermis peel
Difficult, dangerous
Over peel
Unsecure
Hypodermis
Stratum compactum
Kertinocytes K
Basal layer
Lower limit of
papillary dermis
K
Figure 1.1  The seven possible depths of peel.

Definition and classification of chemical peels      3
dermis or even the basal layer. The final touch of the skin is still
more hydrated than in the case of a simple exfoliation, depth
1. After the peel, living keratinocytes are suddenly directly
exposed to air, sun, pollution, and dryness. They react, syn-
thesizing more tumor necrosis factor alpha (TNFa) (inducing
a faster transformation of keratinocytes into corneocytes) and
sending a message to the basal layer to stimulate the basal layer
turnover and substitute the removed cells with new ones. At
the same time another message reaches the fibroblasts, which
respond with a stronger synthesis of the entire dermal intercel-
lular matrix.
Intraepidermic peels (depth 2) give better results than
depth 1 peels and can be used for treating superficial epidermal
melasma and many keratinization problems.
Table 1.1  Exfoliation Level
Main types
Alpha hydroxy acid (AHA) peels are primarily used for exfoliation.
Action mode
The activity of AHA on the corneocytes seems to be secondary to an action on ionic charges, to the inhibition of
enzymes involved in the formation of ionic links. For example, AHAs could compete with sulfates and phosphates at
the level of sulfotransferases, phosphotransferases, or kinases, involved in the formation of sulfated or phosphorylated
mucopolysaccharides, glycoproteins, sterols, and lipids. This could produce a lower quantity of electrically negative
groups on the surface of keratinocytes and corneocytes and lower the adhesion forces with amines or basic aminated
acids (electrically positive).
AHAs penetrate between cells, unsticking the proteins responsible for corneo-desmosomes adhesivity (the adhesion is a
noncovalent, electric link) and allowing the cells to separate from each other, inducing a desquamation. Because there
is no strict chemical reaction during this process, AHAs are not consumed much and have to be neutralized. Rinsing
with a basic solution stops their action.
Clinical signs
Irritative erythema is usually the only visible sign.
Desquamation
Typically, no desquamation is seen.
Risks and
problems
In general, this is not a risky depth. The main risks are a higher sensitivity to the sun and a greater risk of skin infections.
Neutralization is the main problem: if too early, it gives no result; if too late, it could induce more side effects. We will
see later that this problem can be avoided by using specific slow-release and self-neutralizing AHA mixtures.
Table 1.2  Intraepidermic Peels
Main types
Alpha hydroxy acid (AHA), alpha-ketoacids, trichloracetic acid (TCA), resorcine, and salicylic acid peels can be used.
Action mode
TCA is a proteocoagulant chemical. When in contact with proteins, it coagulates them, modifying their tridimensional
structures in a way that does not allow their normal function. All membrane proteins are therefore damaged, making
the keratinocytes unable to survive. At the same time, intercellular proteins are also coagulated.
Clinical signs
Visible erythema can be seen, but no white pinpoints appear yet.
Desquamation
It can look like very thin dandruff.
Risks and
problems
Intraepidermic peels are usually not dangerous. Nevertheless, cases of postinflammatory hyperpigmentations (PIH) have
been seen, making the prevention of this side effect necessary when the skin is known to be sensitive. Neutralization
of AHAs remains the main problem because it must be done following difficult rules. Neutralization has to be done
when an erythema (always irregular erythema) appears and before any sign of protein coagulation that would appear
as skin frosting points. It is difficult to foresee the right moment for an ideal neutralization.
Regarding TCA, no neutralization can reverse the proteinic coagulation; therefore the total amount of TCA that is applied
on the skin has to be perfectly calculated in relation to skin permeability. The TCA application technique has to be
perfect for an even penetration. Resorcine and salicylic acid are phenol derivatives that are not widely used outside of
the United States; large surfaces treatments using phenol derivatives are suspected to potentially induce toxic
reactions. TCA and AHAs, on the other hand, are not toxic products.
Table 1.3  Basal Layer Peels
Main types
AHAs should not be used at this depth because side effects are likely here, are difficult to treat, and affect the
patient’s social life. TCA is the best choice for this depth if the right concentration, formula, and postpeel care are
selected.
Action mode
Keratinocyte destruction induces a basal layer strong reaction, dramatically stimulating the turnover of basal cells.
Clinical signs
TCA coagulates proteins, and its entry through the domes of papillae induces a specific proteinic coagulation; dermal
protein coagulation points occur, clinically appearing as little white marks (white pinpoints) called “frosting points.”
Desquamation
It looks like a sunburn desquamation and does not affect the patient’s social life in the majority of the cases.
Risks and
problems
Basal layer peels are usually not dangerous peels. The application technique is important because a perfect protocol
is very secure. If the peeling application is a bit too strong, basal layer peeling can nevertheless result in a vicious
cycle of inflammation based on free radical liberation that induces cell damage and other problems. If we allow a
self-stimulation of this inflammatory vicious cycle, melanocytes could react and cause postinflammatory
hyperpigmentations (PIH). Cases of PIH have been seen, making the control of this postpeel inflammatory vicious
cycle necessary. No herpes prevention is necessary. Problems primarily are linked to a melanocytary stimulation
that is too strong without adequate treatment, to an irregular application, to an application that is too deep, or to
infectious rebounds in case of acne. Prepeel skin conditioning can be used at this point if the peeling used does
not penetrate evenly or does not control the postpeel inflammatory reaction. Using the Easy TCA® peel or Easy
TCA® Pain Control, which is a stronger yet less painful form of Easy TCA®, no prepeel conditioning is necessary.
Except in cases of deep scratching and/or strong local infection, no scar is expected from this peel depth.

4        Textbook of Chemical Peels
Depth 3: Basal Layer Peel (High Security)
This is a very interesting peeling level because it is easily
reached and gives good results. Stratum corneum cells are
completely removed; keratinocytes are largely damaged up to
the level of basal layer keratinocytes.
Nevertheless, the epidermis is not completely destroyed.
Because many keratinocytes—less prone to damage by ultra-
violet (UV) light—live in deep epidermal papillae, skin regen-
eration is fast and easy.
Basal layer peels can be used, as serial peelings, to treat
aging skin (Glogau I–II), fine lines, epidermal melasma, kera-
toses, and acne (from black dots up to papule-pustule acne).
Together with a good control of melanin synthesis (Blending
Bleaching Cream), a TCA basal layer peel can treat many cases of
melasma. If the patient’s skin is adequately cleaned (black dots
removed, microcysts opened, etc.) and if the patient applies dis-
infecting creams and creams limiting sebum production, then
practitioners can treat active acne, usually without antibiotics.
Table 1.4  Grenz Zone Peels
Main types
TCA is a must for these depths. AHAs are not used because of their irregular penetration. It is difficult to use resorcine
and salicylic acids to reach the Grenz zone. Phenol should be reserved for other indications.
Action mode
TCA coagulates keratinocyte proteins and dermal proteins, inducing a wider skin “frosting.”
Clinical signs
No more pinpoints of frosting occur, but “frosting clouds” are seen, together with a diffuse erythema. Easy TCA® Pain Control
reaches the frosting clouds more quickly than the classic Easy TCA® because it contains minute amounts of phenol.
Desquamation
Desquamation looks like a strong sunburn, which is easy for fair-skinned patients to live with. Dead skin becomes dark
brown on darker phototypes.
Risks and
problems
For dark phototype patients, social life can be difficult for a few days. At the same time, the risk of PIH becomes higher,
making a “pigment synthesis sedation” quite interesting before and after this peel depth. PIH prevention is mandatory
if the patient is phototype Fitzpatrick 4 or more or works outside in a sunny environment. Infections are uncommon at
this depth because the immune system is still working. Herpes prevention is not required except in special cases of
frequent recurrent herpes attacks. Other problems are the same as for basal layer peels.
Table 1.5  Papillary Dermis Peels
Main types
AHAs, salicylic acid, alpha-ketoacid, and resorcine are not good choices. Phenol has been used to perform depth 5
peels, but the related toxicity (cardiac, renal, hepatic) contradicts its use at this depth. A TCA peel, correctly applied, is
the best choice for a safe and efficient papillary dermis peel.
Action mode
Same as the TCA action mode.
Clinical signs
After application, frosting clouds progressively or rapidly become pink-white uniform frosting that can progressively or
rapidly turn into a pure white frosting.
Why does this happen progressively or rapidly? Passing from clouds to even frosting is progressive when we use
relatively low concentrations, as with Unideep (23% w/w) or Easy TCA® Pain Control. This concentration allows the
practitioner to stop the application as soon as he or she sees the desired frosting begin to appear. An even, pure white
frosting rapidly appears when using higher TCA concentrations, such as 35% or 40% (w/w). In this case, it is not
possible to stop the TCA action. It can be compared to lighting the fuse of a firecracker; once lit, it is impossible to stop
it or to modify the course of future events. Similarly, it is impossible to undo TCA by using neutralization. Frosting
appears as pink-white, as long as the acids did not coagulate the blood vessel proteins. When acids have been strong
enough for coagulating the well-defended perivascular area, blood cannot pass until the top of the dermal papillae,
close to epidermis basal layer, and frosting tonality passes from pink-white to pure white.
At the same time the acids penetrate the dermis, they coagulate proteins, sticking epidermis to dermis, and “epidermal
sliding” appears. This sign will last for a while and disappear when dermal edema is strong enough for tensing the
epidermis over it.
Desquamation
It looks like a snake changing its skin and lasts from 6 days (Unideep Peel, Skin Tech) to 8–12 days (usual TCA in water
solution, pharmacy made). The patient usually can resume a normal social life the evening after the treatment but not
the next morning. Days 2 to 6 are days of reclusion during which the skin will peel in more or less dark plaques, in
relation to the patient’s phototype.
Risks and
problems
The most immediate risk is infection: viruses, bacteria, and mycoses find the skin totally open and without defenses. It is
easy for them to penetrate and locally proliferate. It is therefore mandatory to prevent viral infections using herpes
prevention (i.e., valacyclovir 3–4 days before and 4–5 days after the peel). Bacterial and mycotic infections can be
avoided by proper hand and material cleaning and by avoiding any other source of iatrogenic infections. The patient
must wash his hands before any contact with his skin (such as scratching), avoid direct contact with pets, and call the
doctor immediately with question or concerns. Scratching the skin after a papillary dermis peel usually induces
infection. Nontreated or poorly treated infections could induce PIH, depigmentation, or scarring.
Another risk results from the fact that some peeling solutions do not evenly penetrate the skin. Simple TCA-in-water
solutions irregularly penetrate the tissues and can give uneven results: some areas are too deeply treated (causing
local erythema, pigmentations, depigmentations, infections, scarring, etc.).
Because the real action of TCA is largely hidden during the application, damage can occur that the practitioner cannot
see immediately and cannot correct. Therefore, the concentration of the peeling solution and, more important, the total
amount of TCA applied to the skin must be strictly calculated before application. No neutralization of TCA is possible.
When using a simple TCA-in-water solution, skin conditioning is mandatory for four main reasons: to allow a more even
penetration, to allow a deeper penetration and hence a better result, to keep melanocytes in rest and limit the
occurrence of PIH, and to stimulate the basal layer turnover and facilitate postpeel skin regeneration. Mixtures of
AHAs, tretinoin, and hydroquinone are often used for this purpose.

Definition and classification of chemical peels      5
Depth 4: Grenz Zone Peel (High Security)
This is a very interesting peel level. These peels are easy to per-
form, are not very painful for the patient, present a low level of
risk, and offer good results. Stratum corneum and a large portion
of keratinocytes are destroyed. Acids penetrate slightly into the
more superficial layers of the papillary dermis, eliminating abnor-
mal cells from the epidermis (treatment of lentigines, keratoses),
and eliminating many keratinocytes excessively charged in mela-
nin and melanocytes producing the melanine (melasma). A Grenz
(German for “border area”) zone peel also directly stimulates the
superficial coats of the papillary dermis, allowing a strong colla-
gen and elastin deposit into the Grenz zone. Grenz zone peels and
basal layer peels are the types of peels I use most frequently.
Depth 5: Papillary Dermis Peeling (Secure)
A depth 5 peel is at the border between secure and insecure
depths. This type of peel reaches some limits. It reaches positive
limits in the sense that a depth 5 peel is able to treat many skin
defects such as lentigines, solar keratoses, melasma, freckles, and
fine lines. It reaches negative limits because a papillary dermis
peel is not able to treat real wrinkles or skin sagging.
When strictly respected, this depth is safe from scarring;
scars should never appear when a peel is strictly limited at the
level of the papillary dermis.
Depths 6 and 7: Reticular Dermis Peeling (from
“Quite Secure” to “Difficult/Dangerous”)
A reticular dermis peel can be considered the Holy Grail of
peeling: this depth of peel treats nearly all pigment problems,
tenses the skin, and removes wrinkles. However, patients with
thick and oily skin are not the best candidates for a reticular
dermis peel because these skin types resist the action of the
acids. Unfortunately, folds usually resist the action of deep
peelings. Often, practitioners have to present patients with two
therapeutic options: surgical lifting or deep peeling. At Hera
Clinic in Empuriabrava, Spain, our first guide is a simple list of
options (Table 1.6). Naturally, this list must be adapted to each
Table 1.6  Reticular Dermis Peels
Main types
Two main molecules are used for reaching this depth: TCA and phenol. I use concentrated TCA for focal deep peels and for
deeply treating lentigines and keratoses with diameters less than 1 cm (Only Touch, for example, is a 45% w/w TCA), but I
would not be keen to use it for large areas, such as a full-face peeling. In this case, phenol seems to be a better choice; its
activity depth can be more easily kept under control and the results of phenol are definitively better, even at a similar depth
as TCA. It seems that phenol has a stronger “rebuilding effect” on the skin than TCA. My favorite phenol peel is Lip & Eyelid
Formula by Skin Tech. It is an oil of phenol that penetrates the skin slowly, which limits its general toxicity (giving the liver, the
lungs, and the kidneys more time to detoxify it) and allows a longer contact time between phenol and skin proteins, inducing
potentially more protein coagulation and hence a better result. A lighter form of the Lip & Eyelid Formula, a hybrid peeling
between a TCA and a phenol peel, is the Easy Phen Light from Skin Tech. Both products are CE Class II certified.
Action mode
Phenol is proteolytic or proteocoagulant, depending on the concentration. Higher concentrations are proteocoagulant and
lower concentrations are proteolytic. For peeling purposes, the best concentration range is between 40 and 60% (w/w).
Nevertheless, many substances can interfere with its action and speed up or slow down its penetration. These
substances are described in Chapters 25–36.
Clinical signs
Acids reach the reticular dermis after having largely coagulated the papillary dermis, showing a pink- or pure-white frosting.
(Depending on the concentration, an aggressive peel will result in an immediate pure-white frosting, without first
resulting in a pink-white one.) Quite quickly after the typical papillary dermis frosting, the tonality will shift to a gray-white
or to a gray frosting.
It is possible to reach this depth by applying various acid concentrations. However, I always feel more secure using less
concentrated products and applying more coats. When we use proteocoagulant products, the final result depends on the
total amount of active acid molecules that have been able to interact with the skin proteins. A very strong and aggressive
peeling solution could induce a superficial thick coagulation, allowing the acids to pass only at the level of higher skin
permeability, which could induce irregular results and local overpeelings. When using a progressive application technique,
we can always decide to apply no more acid to the higher permeability areas and to keep applying acid to the areas
where the desired frosting did not appear. Using this method, I have performed no overpeels during the last 30 years.
Desquamation
Desquamation is a major issue that can force a patient into social retirement for 7–8 days. Dead skin layers should be kept
as natural protection and extracted only at around day 6 or 7, if this extraction is easy and atraumatic. A phenol peel can
be used under a complete 24-hour occlusion, inducing a maceration of the upper coats of the skin. During occlusion,
skin melts (in open techniques, skin usually dries) and has to be protected by using bismuth subgallate powder. On day
5 or 6, sterile petroleum jelly can be applied to the dead skin to help the desquamation. Occlusion makes the phenol
peel deeper and more efficient. TCA occlusion does not have the same result.
Risks and
problems
Histologically, there is only one reticular dermis, situated between the papillary dermis and subcutaneous tissues.
However, with regard to peelings, we face two different depths.
In the more superficial reticular dermis, overall at the face level, we still can find keratinocytes (mainly at the level of hair
roots and sebaceous glands; sebocytes are phenotypically differentiated keratinocytes, able to undifferentiate into normal
keratinocyctes when necessary to repair the skin). The superficial reticular dermis still has material to rebuild the skin. The
deep reticular dermis is devoid of this reservoir but contains large fibroblasts, also differentiated to be able to synthesize a
thick bundle of collagen that will stick to the neighboring fibroblast. The fibroblasts are considered contractile nonmuscular
cells, able to contract when necessary. They are one of the main groups of cells responsible for the scarring process:
when these cells are strongly stimulated during a self-maintained inflammatory vicious circle, scarring can appear.
All possible side effects can appear when using deep peelings. Pigment problems are common because deep TCA kills
melanocytes and phenol can make them impotent, which makes them unable to synthesize melanin. As a result, many cases
of unaesthetic depigmentation were seen in the past. A new formulation (Lip & Eyelid Formula from Skin Tech) seems to be
much safer in this regard because it primarily induces postinflammatory hyperpigmentations (PIHs) that are easy to treat
rather than “porcelain skin” that cannot be treated. Chapters 25–36 give details of many of the possible side effects.

6        Textbook of Chemical Peels
type of skin and situation. Typically, we will not recommend
a phenol peel to patients with thick, sagging skin and no sun
aging problems. On the other hand, we will not recommend
surgery to patients who have thin skin without sagging but
with important pigment or sun aging problems.
The quest for the Holy Grail is risky, as is deep reticular
peeling. Not only does the selected peeling solution have to be
perfectly adapted to the doctor’s and the patient’s aims, but the
application technique and postpeel care also have to be profes-
sionally done. Full-face reticular peeling is a very aggressive
treatment that does not allow rough improvisation. Any mistake
can result in scarring, and pigmentary problems are common.
Nevertheless, reticular peels are valuable treatments in
the good hands and minds of able practitioners. Because there
are no specific diplomas or certifications for these types of
peels, experience and knowledge are crucial.
Table 1.7  Summary of Skin Problems and Preferred Treatments
Problem
Preferred treatment
Pigmentary problems
Peelings
Wrinkles
Peelings
Photo aging
Peelings
Acne
Peelings
Acne scars
Anterior chemoabrasion
Sagging skin
Surgery
Pigmentation and
sagging
Surgery, followed by phenol peel in
6 months
Thick skin
Surgery or pixel peel
Thin skin
Peeling
Stretch marks
Anterior chemoabrasion
Deprez P. Chemical Peelings. In: Baran R, Maibach H, eds. Textbook of
Cosmetic Dermatology. 4th ed. London: Informa, 2010: 482–93.

2
Prepeel care
IS IT NECESSARY TO PREPARE THE SKIN?
Depending on the type of peel, preparing the skin can be essen-
tial, pointless, or even dangerous. The chapters devoted to the
different types of peels give details of the preparation recom-
mended in each particular case. This chapter deals with the
generalities of prepeel care.
Medium- and Long-Term Preparation
Alpha hydroxy acid (AHA) peels produce the best results if they
are preceded by careful preparation and followed by long-term
daily cosmetic care. Easy Phytic® solution, on the other hand,
does not allow any prepeel preparation that is likely to acceler-
ate penetration of the acids, as the stratum corneum must be
intact for the peel to be safe. In this specific case, prepeel condi-
tioning is to be avoided.
Classic trichloroacetic acid (TCA) peels, in a simple aque-
ous solution in gel or mask form (TCA–SAS = trichloroacetic
acid in simple aqueous solution) always require approximately
1 month of intensive prepeel preparation. This preparation
stimulates keratinocyte regeneration and reduces the risk of
postinflammatory pigmentary changes and scarring. It blocks
the first stages of the biochemical conversion of tyrosine into
indole groups and melanin, and limits the reaction of mela-
nocytes to ultraviolet light. Easy TCA® and Easy TCA® Pain
Control require no preparation under their basic protocol (until
scattered pinpoint or cloudy white frosting appears). The prep-
aration required for their special deep-peel protocol or when
combined with abrasion is discussed later in this book.
Resorcinol produces far better results and fewer compli-
cations if the skin is well prepared. Phenol usually does not
require any specific preparation but needs careful postpeel
care.
As a general rule, it is worthwhile to prepare the skin care-
fully with tyrosinase inhibitors (such as Blending Bleaching®
cream from Skin Tech) if there is any risk of postpeel pigmen-
tary changes or to optimize results when treating melasma.
Retinoic acid and sometimes glycolic acid are used to make
transepidermal penetration more even or to deepen the action
of the acid solution.
Immediate Prepeel Preparation
Generally, patients must wash their skin with soap and water
before going to the appointment. The doctor will disinfect the
skin with alcohol and degrease it with acetone or ether. These
degreasing products allow the peel solutions, which are usu-
ally hydrophilic and have difficulty penetrating the skin’s pro-
tective oils, to penetrate more deeply and evenly. The products
break down some of the proteins and phospholipids in the cell
membranes, which enhances the action of the acids applied
afterward.
AHA peels require very careful preparation before being
applied. The skin should be cleaned with soapy water, rinsed
thoroughly, degreased with acetone, and disinfected with alco-
hol. Unlike the classic AHA peels, with Easy Phytic®, the skin
must be cleaned with a gentle, non-aggressive cleansing foam
that contains only surfactants, so that the acids do not penetrate
the skin too quickly and saturate its natural buffer capacity,
making it impossible for it to neutralize the sudden inflow of
acids in time. Thorough cleansing and degreasing of the skin
before Easy Phytic® would oblige the doctor to neutralize it in
the classic manner; when there is no prior preparation, there is
no need to neutralize it.
For TCA–SAS, resorcinol, salicylic acid, azelaic acid,
or phenol peels, the skin needs to be thoroughly cleansed of
makeup, degreased, and disinfected. Easy TCA® solution, on
the other hand, contains saponins that make prepeel makeup
removal and degreasing unnecessary; the skin’s natural
defenses are only very slightly diminished by this peel, and
therefore there is no need for any particular prepeel prepara-
tion against infections.
PRODUCTS USED TO PREPARE THE SKIN
The products usually used to prepare the skin are sunscreens,
tretinoin, AHAs, and tyrosinase inhibitors. Jessner’s solution is
sometimes used as a prepeel preparation. It is often necessary
to take measures to prevent infection, especially herpes.
Prevention of Infection
Prevention of the herpes simplex virus is essential for patients
who have a history of the infection (a single incidence of her-
pes is enough). Herpes prevention is necessary with a peel to
the papillary dermis. It is also worthwhile when a more super-
ficial peel is usually accompanied by a severe inflammatory
reaction, as is the case with resorcinol, “classic” AHAs, and
TCA–SAS. It is not necessary when using Easy TCA® under
its basic protocol or Easy Phytic®. General infection preven-
tion measures should be taken, depending on the depth of the
peel. For more information, see the discussion of infections in
Chapter 37.
Prepeel Sun Protection
It can be beneficial to protect the skin against the sun before cer-
tain peels. Effective sun protection should start 2 weeks before
a medium or deep peel and even before a series of superficial
peels to inhibit melanocyte activity and avoid excessive stimu-
lation of melanin production before the peel.
Prevention of Pigmentary Changes
Before any “classic” peel, steps must be taken to limit the risk of
pigmentary changes. Preparing the skin with tyrosinase inhib-
itors (hydroquinone, kojic acid, azelaic acid, arbutin, Morus
Alba, licorice extracts, etc.) is especially recommended to curb
the enthusiasm that certain melanocytes have for converting

8      Textbook of Chemical Peels
tyrosine into melanin. Preventive measures should begin 3–4
weeks before a medium or deep peel.
Combinations of hydroquinone (2%–4%) plus kojic acid
(2%–3%) or hydroquinone (2%–4%) plus glycolic acid (8%–
10%) are effective, as are certain formulas containing several
tyrosinase inhibitors, antioxidants, and concentrated reti-
nol (Blending Bleaching® cream). Some patients may develop
hyperpigmentation, or even ochronosis, when treated with
hydroquinone. Patients with dark skin types are most at risk.
Long-term use of high-concentration hydroquinone can also
cause confetti-like depigmentation (Figure 2.1).
Hydroquinone is prohibited from sale as an ingredi-
ent in cosmetic or cosmeceutical products in many countries
(although it is available by medical prescription) and has been
successfully replaced by new formulas combining other tyrosi-
nase inhibitors. Creams containing azelaic acid (usually at a
concentration of 20%) are considered slightly bleaching when
used for at least 4–6 months. Azelaic acid is an irritant and is
used mainly when other formulations cannot be used. For oily
or thick skins, tyrosinase inhibitors can be prescribed in a gel
form that penetrates the skin more easily and allows instant
and easy application of makeup. For more information, see the
discussion of pigmentary changes in Chapter 37.
Even Penetration of Acids and
Stimulation of Skin Regeneration
To perform a medium or deep TCA–SAS peel, the active mol-
ecule in the peel solution has to penetrate more deeply and the
skin must regenerate more quickly. Two large groups of mol-
ecules are at the practitioner’s disposal: AHAs and retinoids.
AHAs (e.g., 10%–15% glycolic acid) break down corneodes-
mosomes that maintain intercorneocyte cohesion; they make
it easier to shed this layer of dead cells (which are, however,
essential to the skin’s defenses, as they are largely responsible
for maintaining the permeability barrier function in the skin as
a whole). The epidermis is thinned by the AHAs, making the
stratum corneum more permeable, and the acids can penetrate
more deeply and evenly. The risk with this preparation is that
the epidermis may become too permeable and the effect of the
peel can go too deep. A peel that is meant to reach the papillary
dermis could penetrate as far as the reticular dermis as a result
of too “strong” a preparation of AHAs. A peel that is meant
to remain intraepidermal could become intradermal and result
in postpeel complications and more downtime: an intraepider-
mal peel removes several layers of “skin-color” keratinocytes
in light flakes for around 3 days, whereas an intradermal peel
removes the entire epidermis in the form of strips of brownish
skin. The darker the skin type, the more visible the flaking.
Retinoids form a growing range of products with ever-
widening indications. The retinoid most used in prepeel
preparation is tretinoin. Among other things, it stimulates
keratinocyte growth in the basal layer and causes an overall
thickening of the epidermis but also a relative thinning of the
stratum corneum. The prepeel use of tretinoin enhances pen-
etration of the acids while stimulating the regeneration pro-
cesses in the keratinocytes of the basal layer.
Determining which of these molecules to use depends
on the condition of the patient’s skin. Tretinoin is not used if
the patient has many telangiectasias; AHAs are avoided if the
skin is very thin. Conversely, the two products can be mixed
in the same prescription, in variable concentrations, depending
on the patient’s skin type and the desired effect. The concentra-
tion of tretinoin would be increased to stimulate reepithelial-
ization; the concentration of glycolic acid would be increased to
improve and even out transcorneal penetration.
Tretinoin
Tretinoin (all-trans-retinoic acid, ATRA) is the carboxylic acid
form of vitamin A (retinol). It is one of the first-generation reti-
noids and has been used since the 1970s to treat acne complaints
and dyskeratosis. It is important to have full knowledge about
this molecule to obtain benefit from its actions.
Histological Changes
During long-term treatment with tretinoin, the results can
first be seen through a microscope, long before they are clini-
cally visible. These histological changes explain the indisput-
able clinical efficacy of continuous treatment. The epidermis
increases in thickness by 10%–40%, with a thickening of the
stratum granulosum to the detriment of the superficial stratum
corneum (which decreases by about 25%); the overall water con-
tent of the epidermis is thus increased and the skin appears
more hydrated. This epidermal hyperplasia is observed both on
the face and on the rest of the body, especially on the arms or
forearms. Unfortunately, it is not certain whether the improve-
ment is permanent, as some studies show a reversibility of the
action of tretinoin (a habituation phenomenon?) after 6 months’
treatment on the forearms and the disappearance of histological
improvement altogether 1 year after the start of the treatment,
whereas clinically the improvement persists. Normal epidermal
differentiation is restored and keratinocyte abnormalities grad-
ually decrease. The atypical keratinocytes are eliminated, and
the tretinoin prevents or delays keratoses from reappearing.
The melanocyte clusters in the basal layer gradually disperse
as a result of the increased cell turnover. The marks on the skin
thus tend to be more diffuse, or even to disappear. The overall
pigmentation in the epidermis decreases in patients with black
skin (32%1 and 23%2) and in patients with yellow skin (41%3).
One year after the start of treatment, the melanin content of the
epidermis continues to decrease and causes the skin to lighten
in the long term. As with chemical peels, a newly formed col-
lagen layer appears, in horizontal bands, just beneath the basal
membrane, in the Grenz zone. New active fibroblasts appear
in the dermis, and new elastic and collagen fibers are secreted.
Figure 2.1  Confetti-like depigmentation.

Prepeel care      9
An increase in glycosaminoglycans thickens the dermis, and
elastotic tissue is pushed deeper down.
After 26 months of daily treatment with 0.05% tretinoin,
the events described above are extensive enough to push the
elastotic tissue deep down and hide it under the new vascu-
lar, elastic, collagen, and epidermal growth. It must be noted,
however, that not all authors accept the existence of these histo-
logical changes in the dermis in the long term. In particular, a
study by Gilchrest4 on 500 biopsies carried out during a 5-year
observation of daily topical tretinoin treatments (in concentra-
tions between 0.001% and 0.1%) could not find any evidence of
histological changes in the dermal parameters. This is surpris-
ing and contradicts the established fact that clinically visible
angiogenesis exists.
Mechanism of Action
Tretinoin is a synthetic (all trans) retinoic acid. Retinol and
retinaldehyde are also converted into retinoic acid in the tar-
get cell where it participates in metabolic activity. The retinoic
acid penetrates the cell’s nucleus, where it binds with a retinoic
acid receptor (RAR). The complex formed by the retinoic acid
and the RAR (RA–RAR) interferes with certain areas of DNA
by modulating the expression of some genes. It appears that
retinoic acid alters the regulation of the cell cycle.4
For many years, tretinoin was considered capable of
reducing sebum production in the sebaceous glands, but seri-
ous doubt has been cast on this theory. It is generally thought
that the mode of action of tretinoin is essentially linked to the
increase in epidermal turnover and enhanced exfoliation of the
stratum corneum, which makes it easier for the pilosebaceous
units to drain. A reduction in melanin production has also been
observed. Used specifically as a prepeel preparation, tretinoin
evens out the thickness of the stratum corneum and reduces
overall skin thickness. In these conditions, skin permeability
increases significantly. Tretinoin also stimulates keratinocyte
division and thus facilitates the regeneration phase, which can
sometimes be too slow with certain peels. Topical tretinoin stim-
ulates fibroblast production of collagen as well as other compo-
nents of the dermal extracellular matrix, and sometimes creates
a new layer of “repair” collagen that is laid on top of the photo-
damaged collagen.
Indications
Clinical results appear slowly and gradually, after histological
improvement. The skin soon appears to be intensely hydrated,
once the erythema has disappeared or subsided. Clinically, it
takes a year for the rejuvenating action of tretinoin to show.
Patients who hope to see rapid improvement typically are not
pleased with these slow clinical results on aging skin. Progress
can sometimes be seen more quickly when treating dyschro-
mia: some results may be seen after 1 month of daily applica-
tion of 0.1% tretinoin cream.
Comedonal acne and acne rosacea respond well to treti-
noin. In fact, the anti-aging effect of tretinoin was first observed
in patients being treated with tretinoin for comedonal acne:
their skin texture and skin tone were gradually seen to improve.
Oral isotretinoin (9-cis-retinoic acid) is often used in
treating severe or stubborn acne rosacea. A 1994 study5 com-
pared the treatment of rosacea with 10 mg/day low-dose oral
isotretinoin, 0.025% low-dose topical tretinoin, and a combina-
tion of the two. The results showed that before the 16th week of
treatment, isotretinoin was more effective, but that afterward
there was no difference between tretinoin and isotretinoin. The
combination of systemic and topical treatment does not give
any further improvement in low doses.
It is generally accepted that tretinoin with a concentra-
tion of 0.05% is as active as 5% benzoyl peroxide. Topical treti-
noin makes the skin smoother: the same patients who benefited
from the visible rejuvenating effect of tretinoin when being
treated for acne noticed, among other things, that their skin had
become smoother and softer after treatment. The improvement
brought about by this topical treatment is therefore visual as
well as tactile.
The application of topical tretinoin improves senile atro-
phy of the skin. A decrease in cell abnormalities and dysplasias
can be seen, as well as an antitumor effect that persists after the
end of treatment if it has been administered correctly and for a
sufficiently long period.6
Topical tretinoin reduces the size and number of lentigi-
nes and other age-related discolorations. In some cases, how-
ever, because of its photosensitizing potential, tretinoin can
aggravate certain types of dyschromia. This can be problem-
atic for Asian patients, for whom hyperpigmentation is more
of a problem than wrinkles as they age. The study by Griffiths
and colleagues3 proved (clinically, histologically, and by colo-
rimetry) that 0.1% tretinoin significantly improved hyperpig-
mentation in these patients. There was a 41% improvement with
tretinoin, compared with a 37% aggravation in patients receiv-
ing the vehicle alone.
Postinflammatory hyperpigmentation is also improved
by tretinoin, as proved clinically, histologically, and by colo-
rimetry, in a study by Bulengo-Ransby and colleagues2 on
subjects with black skin. A 40% improvement can be expected
after 40 weeks of treatment with 0.1% tretinoin. In the treatment
of melasma, topical 0.1% tretinoin was studied in comparison
with the vehicle alone in black patients.1 A 10-month treatment
lightened the melasma by 32% (an improvement factor estab-
lished both clinically and by colorimetry).
Histological studies have shown a significant decrease in
epidermal pigmentation in patients treated with tretinoin com-
pared with placebo. Of the patients treated with tretinoin, 67%
developed only one side effect, a mild “retinoid dermatitis”
(which is to be expected when using a concentration of 0.1%).
This study also showed that the finest wrinkles disappeared
and other wrinkles improved. Overall, skin tone improves
because of the combination of histological events in the dermis
and epidermis described above. The skin takes on a rosier com-
plexion as a result of angiogenesis occurring deep down.
How to Prescribe Tretinoin
One study7 showed that a tretinoin concentration of 0.01% is
effective for the face, hands, and forearms, whereas another8
showed that there is no difference between placebo, 0.01% treti-
noin, and 0.001% tretinoin. A concentration between 0.05% and
0.1% is, on the other hand, always considered active. The average
concentration used is 0.05%, but different skin types or sensitivi-
ties may require different concentrations, and it is recommended
to start any treatment with a trial dose of 0.02% or 0.03%.
The following is one frequently used formulation
(0.025%):
Tretinoin 15 mg
Urea (carbamide) 6 g
Water 4 g
Neribase® cream ad 60 g, or
Eucerin® O/W ad 60 g

10      Textbook of Chemical Peels
If this dose is well tolerated, it is possible to go immedi-
ately or gradually to a concentration of 0.05%. This concentra-
tion is common in proprietary medicines, but if prescription
medicines are preferred, it is possible to prescribe 0.05% treti-
noin in the following formulation:
Tretinoin, 30 mg
Urea (carbamide), 6 g
Water, 4 g
Neribase® cream, ad 60 g, or
Eucerin® O/W, ad 60 g
Formulations in alcohol gels dry out the skin, increase
the penetration of the tretinoin, and make the treatment more
uncomfortable. Gels should only be used on thick and oily skin.
When the patient can tolerate a concentration of 0.05%
without any notable side effects, the concentration can gradually
be increased to 0.07%, 0.09%, and 0.1%. Concentrations higher
than this are rarely used. If, on the other hand, the skin is very
sensitive and becomes irritated in spite of a low concentration
of 0.025%, the concentration must be decreased to 0.0125%9 or
the patient should be asked to do one of the following. The skin
can be sprayed with warm water immediately before applying
a small quantity of cream. The cream will spread more easily,
and less of the active ingredient will be applied on the skin.
Alternatively, the tretinoin cream can be mixed in the palm of
the hand with an equal quantity of hydrating vitamin E cream10
to halve the final concentration.
If the skin is still sensitive to the treatment, as a last resort
the treatment can be applied every other day or once every 3
days for the first month. Experience shows that daily applica-
tion of low concentrations is a better way to prepare the skin for
higher doses than applying higher concentrations two or three
times a week. The “normal” concentration for daily application
(0.05%) is reached gradually over 2–3 months.
It makes little sense to combine tretinoin with a topical
corticosteroid to limit the inflammatory reaction. It may well
be that this combination is supposed to stop inflammation, but
inflammation is beneficial in that it stimulates the process of
skin repair. Furthermore, the combined effect of corticosteroid
and tretinoin could potentially cause telangiectasia. The treti-
noin would stop skin atrophy as a result of the application of
topical corticosteroid, whereas it should increase the thickness
of the epidermis overall. A large part of the effect would there-
fore be lost. Finally, corticosteroids should not be applied to the
skin for a prolonged period, whereas long-term application of
tretinoin is necessary.
If the skin is resistant from the start and does not respond
at all to the above formulation at 0.05%, a concentration of 0.1%
can be used. This high concentration has been shown to pro-
duce results rapidly but can often have serious side effects.
Therefore, before such a sudden increase in concentration, a
few “therapeutic tricks” can be tried: When the skin appears
not to respond to a single daily application of 0.05%, a 0.05%
cream can be applied twice a day—once in the morning fol-
lowed by a sunscreen and again in the evening. To increase the
effect, it is possible to prescribe an alcohol gel, starting with a
concentration of 0.05% and increasing to 0.1% if the patient can
tolerate this. To increase the potency of the tretinoin, the imper-
meability of the skin barrier can be decreased, either by apply-
ing a 10% glycolic acid cream 20 minutes before applying the
tretinoin or by using a mildly abrasive sponge (Buf-Puf®) on the
skin before using the tretinoin. In some extreme cases, a light
facial or body scrub twice a week increases skin permeability
and makes it easier for the tretinoin to penetrate. Very superfi-
cial microdermabrasion with corundum crystals or sandpaper
can also make the skin more permeable.
Age for Starting Treatment
The lighter the patient’s phototype, the better it is to start treat-
ment at a young age. For example, individuals with skin pho-
totype II can start treatment in their 20s, whereas individuals
with skin phototype IV should only start in their 30s.
Various Recommendations
Tretinoin cream should be kept out of direct sunlight and away
from heat sources, to which it is sensitive. In spite of these pre-
cautions, it gradually loses its efficacy and it is recommended
that the prescription be renewed every 3 months. Tretinoin is
sensitive to oxidation, heat, and ultraviolet light; the refrigera-
tor (4°C) seems to be the best place to store this cream. The by-
products of degradation turn the cream a yellowish color, in
which case it should no longer be used.
Tretinoin is photosensitizing, and it is therefore prefer-
able to apply the cream in the evening and to use a hydrating
antioxidant or a cream such as Blending Bleaching® combined
with a sunscreen (UVB + UVA + HSP [heat shock protein])
of factor 20 or above in the morning. The tretinoin cream is
applied after washing the skin with a mild soap (Avène® or
Skin Tech’s Pre-Peel Cleanser® pH5), and is rubbed gently onto
the face and neck (very gently on the neck where the skin is
more sensitive). It is striking to note that the earlobe is often
missed in skin rejuvenation or tretinoin cream treatments and
can be a telltale sign of a person’s real age.
When tretinoin is applied to skin with seborrheic der-
matitis (even when this is subclinical), it is common for ery-
thema to develop, often in the middle of the face. One week’s
preventive treatment with topical nystatin can often prevent
erythema, and considerably improves treatment compli-
ance. Men whose skin tends to become irritated or infected
after shaving can use Dermasebex® foam as a shaving foam
or the lotion as a chronic maintenance treatment for avoid-
ing seborrheic dermatitis flares. Shaving soon becomes more
comfortable: within 48 hours, the irritation or potential acne-
form dermatitis has subsided or disappeared altogether. A
tretinoin cream could be applied every day for at least 12–18
months and two or three times a week thereafter to maintain
the results. When the treatment ends, the effect does not last
indefinitely, and the skin slowly returns to a state close to its
original condition. However, if the treatment is followed with
one to three applications a week afterward, the positive effects
remain visible.11 When the treatment lasts 5–6 years, the elas-
totic material in the dermis is gradually replaced by new col-
lagen and elastic structures.12 The results should last a long
time if the skin is protected from factors that accelerate the
aging process.
Combining tretinoin and benzoyl peroxide could inacti-
vate the tretinoin. If absolutely necessary, benzoyl peroxide can
be applied in the morning and tretinoin in the evening.
Side Effects
Patients should be warned of the high probability of adverse
effects, which fortunately are only temporary. Tretinoin is more
irritant than glycolic acid. The irritation is usually mild but can
take the form of “retinoid dermatitis” if high concentrations are
used or if the skin is delicate.

Prepeel care      11
This dermatitis is in fact a positive side effect when treti-
noin is used to prepare for a TCA–SAS peel, at least to the level
of the papillary dermis, as it helps the TCA penetrate more
deeply and evenly. A concentration of 0.05% tretinoin should
be used once or twice a day (depending on the thickness and
sensitivity of the skin) for 1 week; the following week, the con-
centration is increased to 0.07% and the third week to 0.1%.
This relatively aggressive preparation improves the penetra-
tion, evenness, and reepithelialization of the TCA–SAS peel,
but will not improve the cosmetic results (or will do so only
very slightly).
If the skin is not properly hydrated during treatment with
tretinoin, it will usually flake visibly and fairly rapidly after a
few days of treatment.
Erythema is to be expected with effective tretinoin treat-
ment. This is not an adverse effect but rather is collateral and
natural. The skin of a patient properly treated with tretinoin
is pinker than normal, and this provides the doctor with an
essential means of observation. A patient showing no erythema
is undertreated or incorrectly treated.
Erythema that appears very rapidly, 2–3 days after treat-
ment begins, and that is localized in patches may be seborrheic
dermatitis; it soon clears up with nystatin cream. Erythema
that appears in the medium or long term, 1 or more weeks later,
can spread over the whole face and sometimes to the neck in
patients with very sensitive skin. If this should happen, treat-
ment should be stopped for 1–2 weeks and started again at a
lower dose, as explained above, to avoid excessive neoangio-
genesis. More often than not, retinoid erythema does not last
long in patients with a dark skin phototype, whereas patients
with a lighter phototype can suffer from persistent, if not per-
manent, retinoid erythema. Sometimes, the redness is more of
a passing flush than fully established erythema.
The skin becomes more sensitive to the sun, perfumes,
and detergents. In fact, from the start of treatment, the skin
becomes more sensitive to any irritant. Patients should beware
of chemical hair removal products, waxes, dyes, and similar
products.
People who use tretinoin often report that their skin is
more sensitive to the sun and burns more easily. This photo-
sensitization is better explained by the thinning of the stratum
corneum rather than by a photochemical reaction between the
tretinoin and the sun’s rays. It is therefore essential to recom-
mend the use of a sunscreen (SPF 25–50 UVA + UVB + HSP
induction) to patients being treated with tretinoin. It should
also be borne in mind that there is a potential risk of skin can-
cers developing as a result of the stratum corneum thinning
and the enhanced penetration of the sun’s rays. Nevertheless,
it appears that patients on long-term tretinoin treatment do
not have a higher incidence of skin cancers. Tretinoin has in
fact proved to be effective in the treatment of photoaging and
actinic keratoses.
Teratogenicity of Tretinoin
To date, and in spite of the fact that no teratogenicity has been
officially attributed to tretinoin,13 we do not have all the nec-
essary facts at our disposal to allow its unreserved use dur-
ing pregnancy or in women who wish to become pregnant.
Despite the fact that application of tretinoin under occlusion
on more than 30% of the body has not been found to lead to
any abnormal increase in plasma levels, and despite there being
no higher incidence of fetal deformities among the children of
women who have used tretinoin during the first months of
pregnancy, it is nonetheless possible for retinoic acid to pen-
etrate the cell nucleus and alter the expression of certain genes.4
Caution dictates that one should not go ahead with treatment
in a particular case until all the necessary facts are available
to allow a risk-free choice to be made. Hypervitaminosis A is
theoretically possible and could be insidious and chronic.14
Practitioners should remain on their guard and make sure that
patients are not taking extra vitamin A supplements.
BENEFITS OF SKIN PREPARATION
Major Benefits
Avoiding Various Side Effects
Preparing the skin before a TCA–SAS peel helps prevent her-
pes and bacterial and mycotic infections. It also helps reduce
the risk of inadequate results (thanks to combination with other
treatments).
Improved Penetration of the Active Product
Preparation with AHAs or tretinoin reduces the thickness of
the stratum corneum, the skin’s natural barrier. As the barrier
is not as thick, it is easier for the products applied to the skin to
penetrate to the basal layer of the epidermis and more deeply
into the dermis. It should be noted that not all peels require this
kind of preparation.15
Even Penetration of the Peel
The skin does not have the same thickness all over, and this can
produce differences in the level of penetration. Correct prepa-
ration with AHAs and/or tretinoin tends to even out the thick-
ness of the skin and allow the active products of the peel to
penetrate evenly.
Areas of hyperkeratosis (senile keratoses, and flat and
seborrheic warts) are a perfect example of this difference in the
level of penetration. Keratoses, which are characterized by a
localized thickening of the stratum corneum, are less perme-
able to the acids. Prepeel preparation with tretinoin evens out
the thickness of the stratum corneum and hence the overall
permeability of the epidermis.
Reduced Risk of Pigmentary Change
Patients with olive and dark skin, or of Hispanic or Asian
origin, are more prone to pigmentary changes than patients
of Caucasian origin. It should be remembered that genotype
does not always correspond to phenotype and that there
are light skins that react in the same way as dark skins.16
Tretinoin, even more than AHAs, disperses melanin granules
and reduces the overall quantity of melanin in the epidermis.
This reduces the risk of postinflammatory or postpeel pig-
mentary changes.
Tyrosinase inhibitors should be used in postpeel treat-
ment as well as in prepeel preparation (1 month before the peel
when there is a risk of pigmentary change, i.e., when TCA–SAS
or AHA peels are used).
Some commercial creams have interesting formulations
with AHAs (to enhance penetration of the other active prod-
ucts), tretinoin precursors, lactic acid, extracts of Morus Alba,
and kojic acid, combined with Transcutol®, an adjuvant that
concentrates the active products near the basal layer and the
melanocytes.
Accelerated Healing of the Skin
After a peel, the skin needs to heal as quickly as possible to
maintain homeostasis of the whole organism. Tretinoin

12      Textbook of Chemical Peels
accelerates reepithelialization if used before the peeling. For
this it must be used at a dose of 0.05%–0.1%, sometimes to the
point of irritative dermatitis. Ideally, the treatment should start
3–4 weeks before a TCA–SAS peel. It is accepted scientifically
that the preventive application of tretinoin promotes postpeel
healing of the skin. In contrast, applying tretinoin during the
postpeel period appears to slow down skin regeneration. Not
all peels require this help with re-epitheliazation.
Minor Benefits
Testing Patient Compliance
A patient who refuses to comply with instructions for pre-
paring the skin before a peel will not be naturally inclined to
heed advice for care during or after the peel sessions either. It
is always preferable not to “peel” a patient who is incapable of
understanding or accepting these instructions. Testing patient
compliance is all the more important because preparing the
skin and keeping up cosmetic care afterward affect the quality
of the results.
Getting an Idea of Follow-Up Care
For patients who accept it, preparation gives them a taste of
between- and postpeel care.
Monitoring Skin Preparation
Monitoring the preparation process can give the practitio-
ner an idea of how reactive and sensitive the skin is. Thus,
a patient who cannot tolerate hydroquinone during prepeel
preparation will tolerate it even less in the days following
the treatment as the skin becomes more sensitive to any irri-
tant. Similarly, if the patient develops an allergy to one of
the products used in the preparation, it can be isolated and
avoided after the peel.
Combination Treatments
Other treatments can be combined with the prepeel prepara-
tion: shave excision, electrocoagulation, ablations, botulinum
toxin, dermal filling, mesotherapy, and so forth. Some peels can
be used simultaneously with these techniques. For example, a
phenol peel can be immediately preceded by shave excision of
raised benign lesions. Easy TCA® can be immediately preceded
by botulinum toxin, dermal filling, electrocoagulation of tel-
angiectasias (Figure  2.2), mesolift, intense pulsed light (IPL),
depilation, and other treatments.
For more information about combination treatments,
please refer to Chapter 38.
NOTES

1. Kimbrough-Green CK, Griffiths CE, Finkel LJ, et al. Topical reti-
noic acid (tretinoin) for melasma in black patients. A vehicle-
controlled clinical trial. Archives of Dermatology. 1994; 130: 727–33.

2. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al.
Retinoic acid treatment for hyperpigmented lesions caused by
inflammation of the skin in black patients. New England Journal of
Medicine. 1993; 328: 1486–7.

3. Griffiths CE, Goldfarb MT, Finkel LJ, et al. Retinoic acid treat-
ment of hyperpigmented lesions associated with photoaging in
Chinese and Japanese persons. Journal of the American Academy of
Dermatology. 1994; 30: 76–84.

4. Gilchrest BA. Retinoids and photodamage. British Journal of
Dermatology. 1992; 127(Suppl 41): 14–20.

5. Ertl GA, Levine N, Kligman AM. A comparison of the efficacy
of topical tretinoin and low-dose oral isotretinoin in rosacea.
Archives of Dermatology. 1994; 130: 319–24.

6. Published studies disagree on the efficacy of tretinoin.

7. Andreano JM, Bergfeld WF, Medandorp SV. Tretinoin emollient
cream 0.01% for the treatment of photoaged skin. Cleveland Clinic
Journal of Medicine. 1993; 60: 49–55.

8. Olsen EA, Katz HI, Levine N, et al. Tretinoin emollient cream:
A new therapy for photodamaged skin. Journal of the American
Academy of Dermatology. 1992; 26: 215–29.

9. By altering the formulations given above: 7.5 mg tretinoin in 60 g
of cream.
10. Vit. E Anti-oxydant® (Skin Tech) or a similar cream.
11. Thorne EG. Long-term clinical experience with a topical reti-
noid. British Journal of Dermatology. 1992; 127 (Suppl 41): 31–6.
12. Not all studies endorse this long-term treatment.
13. Guzzo CA, Lazarus GS, Werth VP. Dermatological Pharmacology.
In: Hardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman
AG, eds. Goodman & Gilman’s The Pharmacological Basis of
Therapeutics. 9th ed. New York: McGraw-Hill, 1996: 1600.
14. Farnes SW, Setness PA. Retinoid therapy for aging skin and acne.
Postgraduate Medical Journal. 1992; 92: 191–6, 199–200.
15. For example, Easy TCA® and Easy Phytic® need no prepeel
preparation.
16. This is why it is important to question the patient.
Figure 2.2  Treatment of telangiectasias by (Ellman®) radiofre-
quency immediately before the application of Easy TCA®. Scattered
pinpoint frosting signals the penetration of the acid at each point
treated by radiofrequency. This combination significantly reduces
scabbing and includes a “pixillized” deeper peeling.

3
Postpeel care
IMMEDIATE POSTPEEL CARE
Immediate postpeel care is described in detail in the chapters
dealing with each type of peel. As a general rule, tretinoin and
creams with an alpha hydroxy acid (AHA) concentration of
more than 10% should be avoided before the exfoliation phase
is completely finished.
ABOUT ACIDS NEUTRALIZATION
Acids neutralization is a recurrent problem. Questions often
arise as to what should be neutralized and why, when neutral-
ization should be done, and how it should be performed.
The concept of neutralization emerged with the der-
matological use of AHAs. Preexisting peelings, such as with
phenol derivatives and trichloroacetic acid (TCA), had not and
could not be neutralized, because proteocoagulant molecules
definitively interact with the skin’s proteins, combining with
them and forming a conglomerate that cannot be separated. As
a result of this interaction, non-AHAs are largely and automati-
cally neutralized and trapped into destroyed proteins whose
tridimensional structure has changed, inducing the well-
known sign of “frosting.” Neutralization of proteocoagulant
acids is therefore impossible after their action has begun. At a
maximum we could neutralize an eventual floating excess over
the skin, before this excess could penetrate the skin.
However, is this even possible? Neutralizing proteoco-
agulant acids (such as TCA) is very challenging because we
have to consider timing: Frosting is a signature of past events.
The frosting that we see does not represent what is happening
but rather what happened to the skin some time ago. Frosting
events have a kind of invisible inertia; they are not an immedi-
ately appearing phenomenon. Proteocoagulation will continue
during the neutralization process. It is therefore very risky to
apply too much of the (phenol derivative or TCA) acid on the
skin, thinking that it will be possible to neutralize it after a
frosting appears. Applying too much of the acid can result in
overpeeling. Trying to neutralize TCA after seeing frosting can
be compared to trying to stop an arrow just before it touches
the target. Moreover, neutralizing a proteocoagulant acid never
reverses the potential damage to cellular proteins or matrix
proteins. When an acid combines with amino acids to form a
protein, it is transformed into a salt that sticks to the amino
acids and modifies the volumetric, tridimensional, proteinic
appearance.
A safe procedure is to rub on the skin the right amount
of acids to get the desired frosting, without any neutralization.
Remember that proteocoagulant acids pass through the epider-
mis in only a few seconds. Therefore, phenol induces skin anes-
thesia only 12 seconds after its application.
AHAs have a very low proteocoagulant power; they do
not easily combine with proteins. Their natural neutralization
by the skin occurs using the skin buffer potential, which is slow
acting. Without neutralization, pure, nonpartially neutralized
AHAs would eventually burn the skin.
We cannot neutralize an acid by adding water to it. When
we pour water into an acid solution, we just dilute the acid; a
huge dilution is necessary to lower the resulting pH. Pouring
water on the face after a peel therefore cannot be considered
neutralization. Pouring a basic solution in a recipient contain-
ing acid will induce chemical acid–base reactions; the acid will
become a salt that has no more protons to liberate in solution
and therefore is no longer an acid. Neutralization changes the
chemical structure of acids. Simple sodium bicarbonate in a
saturated solution can be used to neutralize AHAs.
The answer to the question of what should be neutral-
ized is simple: We neutralize AHAs, but we cannot neutralize
proteocoagulant molecules. A slightly basic solution, in good
volume, will be poured on the skin until the chemical reactions
(usually seen as little bubbles) cease. Neutralization of AHAs
should begin as soon as an erythema can be seen and before
any frosting appears.
The next question is: When should we neutralize AHAs?
A too early neutralization does not give the acids enough time
to interact with the skin, and the result will be very poor. A too
late neutralization allows the acids to burn the skin and induces
many side effects. For these reasons, the industry proposes par-
tially neutralized AHAs (pH 2.5, 3, 3.5), which are less danger-
ous. They can be washed with simple water because they are
between 10 and 1,000 times less aggressive (efficient) than pure
AHA solutions, without partial preneutralization.
One exception to this rule is Easy Phytic Solution® (EPS).
Despite the solution’s very acid pH (0.5–1) and an average total
acids concentration of 60%, this AHA solution does not need to
be neutralized. Its time-controlled technology permits a slow
release, a complete progressive penetration, and a full action
of all acids. Because neutralization is not necessary, this solu-
tion offers greater efficacy. The best indications for EPS are
acne treatment, and photoaging prevention and treatment. EPS
comprises three AHAs: glycolic acid, lactic acid, and mandelic
acid. AHA is adsorbed on the polar groups of keratin chains
and inhibits the reactions between these groups. This improves
the elasticity of the skin and AHAs are better for that than
beta hydroxy acids (BHAs) because the alpha position of the
hydroxyl group allows a better penetration between keratin
chains than the beta position.
The three AHAs show different velocities of penetra-
tion through the skin. Glycolic acid penetrates first, followed
by lactic acid and then mandelic acid. These acids begin their
action at the level of the upper layers of the epidermis. Because
there is no neutralization, they continue their action, slowly
moving down to the epidermis and reaching the dermis, with-
out interfering with the skin’s capacity to naturally neutral-
ize itself. The EPS acids progressively become less aggressive,
producing their full effect. Phytic acid is not an AHA but is a
large molecule of inositol hexaphosphoric acid that is consid-
ered an excellent antioxidant and an antityrosinase. It binds
out iron. Phytic acid cannot produce a peeling effect. So why is

14      Textbook of chemical peels
phytic acid in this peeling formula? Every peeling produces an
inflammation; this inflammation produces free radicals (FRs)
and vasodilatation. Vasodilatation brings more oxygen in situ,
allowing the formation of more FRs. FRs bind immediately
with the closest structure, damaging it. Therefore, a peeling
always promotes skin regeneration but induces many FRs that
can damage the structures that are supposed to regenerate the
skin during the postpeel period. Science generally identifies
FRs as among the major causes of cell degeneration in the aging
process. It is important to fight these FRs during the postpeel
period. Phytic acid slowly penetrates the skin, after the other
acids: It is present in the skin when FRs are produced, when
inflammation develops. Scavenging FRs stop the vicious cycle
of inflammation–vasodilatation–FR.
It is known that AHAs make a thicker epidermis, pro-
duce more polymuccosaccharides in the dermis, and make a
better quality elastin. The density of papillary dermis collagen
is better after application of the solution, and patients treated
with EPS describe a tightening sensation after peeling and a
visible difference in the skin.
To use EPS, first cleanse the skin twice with Skin Tech
Cleanser, rinse, and dry. Apply a maximum total volume of 2.5
cc of EPS on the face, using a small cotton ball that has been
dipped only once in the peeling solution. Apply EPS in succes-
sive coats, checking the face between every coat for uniform
application. Two or three coats are usually sufficient.
When the patient indicates that he or she feels a tingling
sensation, apply the last coat, using the same cotton ball. No
frosting should occur. DO NOT NEUTRALIZE. One excep-
tion: In the event of accidental frosting, neutralize immediately
(using a sodium bicarbonate solution). For more information
about the details of the application technique, please refer to
the directions provided with the solution or visit
tech.info.
Another neutralization system from Skin Tech is the
Easy Droxy Complex Peel & Versicolor Neutralizer. The peel is
a mixture of AHA, BHA, carboxylic acids, and kojic acid, in a
thick liquid crystal gel that is neutralized by the application of
a neutralizing cream that changes color when the skin is totally
neutralized. The cream is naturally blue; it turns yellow when
the skin is acid and green when the skin is at pH 7. This patented
system allows perfect control and uniform neutralization.
SUN PROTECTION
Every peel, even a very superficial one, reduces the thickness of
the stratum corneum that protects the skin against the effects
of radiation. The diffractive and reflective protection usually
afforded in these outermost layers is no longer available, and
the overall quantity of rays that penetrate the skin increases.
This extra radiation can cause actinic damage in cells that
are usually physically protected by the thickness of the skin.
Melanocytes are more strongly stimulated, and there is an
increased likelihood of pigmentary change. All peels thus allow
the sun’s rays to penetrate more easily to at least the basal layer
of the epidermis, where keratinocytes ensure reepitheliali­
zation and melanocytes can induce hyperpigmentations.
Greater irradiation increases the risk of these cells being
genetically modified. All peels put the skin at risk of light
stress, which makes the use of sun protection creams essential.
A powerful, broad-spectrum sunscreen provides greater pro-
tection. The deeper the peel, the more important it is to use sun
protection. After any medium or deep peel, the patient must
use an effective sunscreen of sun protection factor (SPF) 30 or
50+ (ultraviolet A [UVA] + ultraviolet B [UVB] + heat-shock pro-
tein [HSP] inducers) for 6–12 weeks (depending on the depth of
the peel) (Figure 3.1). The sunscreen should be applied imme-
diately after washing in the morning, preferably with a cleans-
ing lotion. Postpeel sun protection should be reapplied every 3
hours on average under any makeup, even if the makeup itself
is considered to be photoprotective. After a peel, sun protec-
tion is necessary even if the patient does not go outside and
even in foggy or cloudy weather: windows block out most UVB
but not UVA, and not all clouds filter UV. Halogen lamps and
spotlights and cathode-ray screens also appear to produce a
sufficient quantity of radiation to induce postinflammatory
hyperpigmentation (PIH) in sensitive individuals.
Effective Sun Protection Factor
The SPF should be even more “aggressive” when treating postin-
flammatory hyperpigmentation, and should protect against UVA
as well as UVB. Protection from the sun means not only avoiding
lying on the beach but also avoiding daylight. The skin is sub-
jected to many light shocks; it is constantly under attack from
the sun and daylight. One pitfall to be avoided is applying sun-
screens that contain tanning accelerators that could have a harm-
ful effect.1 Between peels and during the first few weeks after a
peel, a generous amount of Melablock HSP® 50+ sun cream, for
example, should be applied every 3 hours.2 Thereafter, daily sun
protection can be lighter: for example, Melablock HSP® 30 applied
at 9:00 a.m., 12:00 p.m., and 3:00 p.m. (Figure 3.1a). Patients should
be advised to keep their backs to the sun and to wear light protec-
tive clothing (Figure 3.1b). UV is not the only cause of hyperpig-
mentary reactions; infrared rays can also cause them.
Heat-Shock Proteins
The process of wound healing after thermal injury (e.g., from
laser treatment) involves reepithelialization that starts within
the first few hours after injury and continues throughout the
different proliferative phases of skin repair. Viable keratino-
cytes (Figure 3.2) that are at the edge of the wound and have not
suffered lethal or sublethal heat shock migrate horizontally and
centripetally to form an initial single cell layer of keratinocytes,
the “new basal layer,” before starting vertical growth that will
regenerate a normal epidermal structure.
Reepithelialization uses up a lot of proteins, both during
the synthesis of the temporary matrix that acts as a protein high-
way for the new keratinocytes and during the intense mitotic
activity that creates new skin cells. Proteins are absolutely
essential to cell life; each enzyme in the body is a protein whose
98
96
90
50
0
SPF0
SPF2
SPF10
SPF25
SPF50
110
100
90
80
70
60
50
40
30
20
10
0
% UVB blocked
Figure 3.1  An SPF of 50 protects the skin against 98% of UV. A
higher protection factor is not necessary.

Postpeel care      15
unique three-dimensional structure is responsible for its highly
specific action. Proteins have vital functions that are specific and
strictly linked to their three-dimensional structure. The spatial
structure of proteins is altered by even the slightest increase in
temperature;3 any thermal stress can “unfold” the cell proteins,
making them ineffective and leading to apoptosis (programmed
cell death). In laser or flashlamp treatments, the temperature of
the target must be raised in order to destroy it, but the normal
cells around the target also undergo sufficient heat stress to
induce apoptosis or severely disrupt cell function. The rise in
temperature thus creates a central zone of lesions that are lethal
to cells, surrounded by a peripheral zone of sublethal damage
in which the heat-damaged cells must be repaired or replaced.
As a result, skin regeneration may be slower than it should be
as the cells on the edge of the treated area grow and migrate.
Preventive protection of the proteins in the cells surrounding
the target, increasing their resistance to heat, can help enhance
the skin healing process and reduce the incidence of complica-
tions associated with slow reepithelialization.
Where there is sublethal damage, or very light damage, the
cells must eliminate or repair the damaged and ineffective pro-
teins, increase protection of the proteins that did resist the heat,
and synthesize new replacement proteins. This is where HSPs or
stress proteins are necessary. HSPs were discovered in the early
1960s in the fruit fly in response to an increase in cell temperature
of just a few degrees. These proteins were subsequently found in
all types of living cells; they are secreted in response to any kind
of stress, not only in response to increased temperatures. HSP70
and other similar stress proteins appear rapidly in the cytoplasm
and mitochondrial matrix of cells that are subjected to stress.
Essentially, their role is to ensure protein viability. HSP70 binds
to polypeptide chains as soon as the latter have been synthesized
in ribosomes (which translate RNA information into the amino
acid sequence of the polypeptide) and facilitate the folding of
these chains into the three-dimensional structure essential for
protein activity. HSP70 then separates from the folded protein.
HSP70 is a member of a group of diverse proteins (also including
HSP60 and the chaperonins) that play an essential role in creat-
ing the appropriate three-dimensional structures of other pro-
teins but do not themselves form part of that final structure. This
group of proteins are also known as molecular chaperones and
have a fourfold role: in addition to providing the correct spatial
structure for a new protein coming out of the ribosome, they also
protect the structure of existing proteins, repair damaged pro-
teins by refolding them correctly, and act as protein transporters,
carrying proteins from one place to another within the cell and
Figure 3.1a  Under Wood lamp: Melablock HSP 50+ has been
applied on the right half of the face of this patient. This shows that
there is no latency in the sun protective effect.
Peripheral damage
Laser
target
Figure 3.2  Diagram of the peripheral thermal damage after abla-
tive laser treatment. The number of lethal lesions is proportional to
the degree of shading. The skin is repaired from peripheral kerati-
nocytes: some have suffered sublethal damage. Heat-shock protein
(HSP) inducers help improve keratinocyte resistance to heat shock.
Figure 3.1b  Sun exposure of 2 hours, during summer: The back
was protected by white clothing and shows no erythema. The
shoulder was protected by one coat of Melablock HSP 50+, but the
patient could not correctly apply the sun protection cream on the
back side of the arm (triceps area). The protected area shows the
same absence of sun damage as the covered area. In the center,
there is a surface that was sun exposed without any protection:
dark erythema, edema, and blisters appeared.

16      Textbook of chemical peels
eliminating proteins that are irreparable. Some HSPs are con-
stitutional and others are inducible. The latter are synthesized
in greater numbers after stress and give the cell increased resis-
tance to future stress, thus allowing the cell more time to repair
itself without having to resort immediately to apoptosis.
With age, HSP function deteriorates in human skin, and
aging cells are increasingly more prone to protein destruction.
Sun Protection and HSPs
It is beneficial to boost the synthesis of HSPs in the cytoplasm and
mitochondrial matrix of cells subjected to heat and light stress,
thus improving not only their resistance but also their defenses
and better equipping them to repair proteins in case of stress.
An interesting disaccharide, trehalose (Figure 3.3), was isolated
from cells of organisms that can survive in extreme conditions
such as dehydration; having this disaccharide in sufficient con-
centrations allows these organisms to increase their resistance to
the lack of water. It has been shown4 that trehalose can stimulate
HSP70 production. An interesting experiment showed that this
disaccharide increases cell viability after exposure to UVB. The
study involved subjecting a culture of keratinocytes to a slight
increase in temperature of 3°C for 1 hour in order to induce
slight heat stress. The keratinocytes were then cultured for 6
hours either in a medium containing trehalose or in a medium
without the disaccharide. After 6 hours, the culture medium was
replaced by a physiological saline solution and the keratinocytes
were exposed to UVB radiation. Cell viability was studied after
48 hours. There was a huge difference in keratinocyte survival in
the cells from the different culture media: only around 4% of via-
ble keratinocytes remain when cultured without trehalose ester,
whereas the survival rate was nearer to 40% in the group of kera-
tinocytes cultured in the medium rich in trehalose (Figure 3.4).
SPECIFIC CARE FOR DIFFERENT PEELS
AHAs
If an AHA peel is done correctly, no particular medical care is
necessary, no matter what concentration or pH is used. In gen-
eral, after an AHA peel, all that is necessary is good hydration
and effective sun protection for 2 weeks. AHA peels weaken the
barrier function of the stratum corneum and thus increase its
permeability; they make it easier for the active molecules to pen-
etrate the epidermis when creams are applied both immediately
after and between peeling sessions. The type of cream depends
on the problem being treated. The results for acne treatment can,
for example, be improved by applying a layer of anti-acne cream
immediately after a “classic” AHA peel has been neutralized and
leaving it to act under an occlusive dressing5 for around 30 min-
utes. The patient can apply the same cream twice daily thereafter.
The same applies for melasma and aging or sagging skin.6 After
an AHA peel, the patient’s daily care routine plays an essential
role in determining the quality of the results. Mesotherapy can be
combined with AHA peels in a number of ways: the “mesolift”
mixture7 can be injected before the peel or immediately after the
peel has been neutralized and before creams are applied under
occlusion. There is no danger of the glycolic acid penetrating
beneath the skin through the perforations made by the mesother-
apy needle. Most often, however, the treatments are alternated
every other week: in the first week, the peel and the cream under
occlusion are applied, and in the following week, the mesolift is
injected, followed by the cream under occlusion. If an AHA peel
is done correctly, there is usually no downtime. Nevertheless,
there can be complications, which are described in Chapter 10.
Resorcinol
Resorcinol in paste form9 is used in a very specific manner:
the paste is usually applied three times, once a day for 3 days
in a row. Postpeel care is very important during the following
week: the skin should not be hydrated at all, as it has to dry out
completely for the peel to be effective and, above all, the patient
must not pull off or pick at the flaking skin. Only the doctor
can safely cut off any strips of flaking skin with sterile scissors.
Cosmeceutical creams for age spots, acne, aging or sagging skin,
and other conditions should only be applied after the skin has
flaked. Effective sun protection (UVA + UVB + HSP inducers)
is absolutely essential for approximately 6 weeks after the peel.
Downtime may be around 4–5 days. After the first appli-
cation of the paste, the patient can usually have a normal social
life, but subsequent applications dry out the skin and leave it
looking papery.
TCA–SAS
TCA in simple aqueous solution (TCA–SAS) involves pre-
peel preparation, application of the TCA–SAS solution to the
required depth (usually the papillary dermis), flaking, natural
skin regeneration, and postpeel care.
The postpeel period for TCA–SAS requires special atten-
tion and, even if the peel is applied correctly, pigmentary changes
are the most common and benign complication. It is clear from
the many illustrations in books on TCA–SAS peels that there is
HO
H
OH
HO
H
H
H
O
H
O
OH
H
HO
H
O
H
H
HO
OH
OH
H
Figure 3.3  Chemical structure of trehalose.
0%
0.5%
1%
Trehalose ester concentration
40
35
30
25
20
15
10
5
0
Keratinocytes
percentage survival
Figure 3.4  The viability of keratinocytes exposed to UV after a
3ºC increase in temperature is very low, only a few percent. When
cultivated in an environment rich in trehalose ester, the viability is
close to 40% under the same conditions.

Postpeel care      17
an astonishing variety of post-TCA pigmentary changes, with
varying degrees of severity. If prepeel prevention does not prove
effective, or in cases of localized overpeeling, postinflamma-
tory hyperpigmentation (PIH) usually appears within a week
after the peel in the form of dark patches or persistent erythema
that will become pigmented under the effect of the sun’s rays.
For more information, see the section on hyperpigmentation in
Chapter 37. These genuine pigmentary changes should not be
confused with the darkening of epidermal melasma appearing
the next day after the peeling, and caused by dehydration of the
hydrophilic spaces between melanosomes, which makes the
skin seem to have a greater concentration of melanin and hence
appear darker. This darkening, which is temporary, is a positive
sign and will fade at the end of the first week.
Flaking should not be helped along under any circum-
stances. Peeling off any bits of skin can result in uneven skin
tone, infection, hyperpigmentation, scars, or localized achro-
mia. It is also essential to take preventive measures against
infection after a papillary TCA–SAS peel, as the latter destroys
most of the skin’s defenses. An antibiotic cream is applied dur-
ing the first week after the peel. The skin should be cleaned
before each application of cream, and any occurrence of contact
allergies, which can sometimes be confused with secondary
infections, should be monitored.
The results of a TCA–SAS peel also depend on the qual-
ity and consistent use of cosmeceuticals after the peel. It is clear
that a melasma treatment will produce better results if the
TCA–SAS peel is followed by the application of a retinol–anti-
tyrosinase–antioxidant cream or a hydroquinone-based prepa-
ration. For acne or aging or sagging skin, the same comments
apply as for AHAs above. These creams can be applied as soon
as flaking is finished, usually on the seventh day.
Effective sun protection is essential and should be used
in the first few days after the peel, before the skin has stopped
flaking. Even a total sunblock is not enough to avoid pigmentary
changes altogether, and the patient should be told to completely
avoid exposure to the sun. Sun creams containing tanning accel-
erators should, of course, not be used after the peel.9 Chemical
tanning with sprays containing dihydroxyacetone should also
be avoided, as these products, which are nontoxic when picked
up by the corneocytes and eliminated within 1 week, are not
intended for keratinocytes, which are the cells exposed to the
external environment during the first days after a peel.
Downtime is around 1 week following a TCA–SAS peel,
after which makeup can be used from the eighth day to cover
up any persistent erythema.
Easy TCA®
Easy TCA is an exception among TCA peels, as is Easy TCA
Pain Control, and should be distinguished from TCA–SAS as
it does not require prepeel care in the medium term nor any
immediate prepeel preparation, and pigmentary changes are
very rare if the “basic protocol” is followed.10 Some brown dis-
coloration is possible after the first or second application, but
this should fade after the following peel. Flaking skin can be
peeled off or a light cosmetic scrub can be used. With deeper
protocols, which are not usually necessary with this peel, there
is a greater likelihood of complications.
Combining Easy TCA with appropriate postpeel cos-
meceuticals helps improve and maintain results. The cos-
meceuticals should be applied the day after the first peel and
continued between sessions and for at least 6 weeks after the
last application. As with any peel, effective sun protection is
necessary to make up for the temporary loss of the stratum
corneum. Easy TCA causes the skin to flake, but not so much
as to disrupt the patient’s social life, although certain activities
may be compromised: television presenting, customer contact
in the food industry, and so forth. Easy Phytic is recommended
in these cases as there is almost no visible flaking of the skin (see
Chapter 11).
Phenol
Phenol entails the most complex postpeel care: occlusive masks,
healing masks, and cosmetic care during the months follow-
ing the peel. Chapters 25–36 are devoted to this technique. The
expected downtime is between 7 and 15 days, depending on the
formula used. The patient will have to wear camouflage makeup
to hide any redness, which can last for several weeks or months.
POSTPEEL COSMETICS
Chemical peels do not always treat the underlying cause of a
skin problem. For example, there can be many causes of acne,
and chemical peels do not alter the synthesis of testosterone or
the potency of the 5-alpha reductase that converts testosterone
into its active derivative, dihydrotestosterone. Acne may also be
partly due to excessive cell cohesion that blocks the sebaceous
glands or to an immunodeficiency of genetic origin. Chemical
peels do not alter an individual’s genetic makeup. Follow-up
care should come after the peel, which is only the first phase of
the treatment. Topical anti-acne treatments or cosmetics should
be used between and after the peels to improve and prolong
results. The same goes for blemishes, melasma, and aging.
Peels can provide quick cosmetic results, but it is the care
between and afterward that improves and maintains them.
This is why the same peel may be indicated for the treatment
of acne, which typically affects young patients, as for aging,
which affects older patients. In short, we can say that chemical
peels regenerate, restructure, and stimulate the skin, and that
care between and after peels widens their indications to prob-
lems such as acne, dyschromia, and aging.11
Cosmetic products have been specially created for appli-
cation very soon after a peel. For example, products such as
Easy Phytic or Easy TCA can be used the morning after the
first AHA peel. With TCA–SAS, Only Touch®, or phenol peels,
cosmetics usually are not applied until the eighth day after
the peel. With Unideep®, an antioxidant cream (Nutritive ACE
Lipoic Complex®) can be applied two days after the peel. IPLase
Mask (Skin Tech) has a strong anti-erythema and anti-inflam-
matory efficiency, allowing its use after deep procedures gener-
ating pain, erythema, or swelling. It has been used with success
after papillary dermis peel, reticulary dermis peel, laser and
intense pulsed light (IPL) treatment, and even against radioder-
mitis, a side effect of anticancer radiotherapy treatments.
Treatment for Acne
Tretinoin should be avoided between and after sequential peels,
as it can irritate the skin and increase penetration of the acids dur-
ing the next peel. Other topical products can be used. Glycolic
acid can be applied in low concentrations (8%); it makes the skin
softer to the touch. Like retinol, it prevents pores from clogging,
helps the pilosebaceous units to drain, and stimulates skin turn-
over. Tocopheryl acetate can be used as an antioxidant to com-
bat the FRs generated by inflammation. Triclosan12 is antiseptic,
anti-inflammatory, and antimycotic. Glycyrrhetinic acid is used

18      Textbook of chemical peels
for its hydrating, antipruritic, and anti-allergic properties. It stops
patients scratching. Tea tree oil (Melaleuca alternifomlia) is extracted
from an Australian shrub and has a similar action to benzoyl
peroxide but without its peroxidative effects. It is antiseptic (anti-
bacterial: anti-gram-positive and -negative), anti-­inflammatory
(it can suppress the production of pro-inflammatory media-
tors), antimycotic (anticandida and antidermatophyte), and even
antiviral, acting before and after viral adsorption. Other topical
treatments can also be applied: azelaic acid, antibiotic creams,
disinfectants, and others. For more details, please see Table 17.2.
Treatment for Hyperpigmentation
Chemical peels are one of the preferred indications for hyperpig-
mentation. A number of cosmetics can be used between and after
peels. Hydroquinone has been used for a long time and still is
used in many countries. Its cosmetic use, however, is forbidden in
Europe. Many depigmenting derivatives can be used in its place.
Kojic acid can be used pure or as an extract of Aspergillus and
has an antityrosinase and antioxidant action. It even potential-
izes leukocyte phagocytosis. Glabridin (a licorice extract) inhibits
the pigmentation and erythema caused by UV; it is antityrosi-
nase and anti-inflammatory. Liquiritin contains glycyrrhizin and
glycyrrhetinic acid (which are anti-inflammatory as they inhibit
the degradation of endogenous cortisol) and antioxidant flavo-
noids. Extracts of Morus alba contain arbutin and mulberroside
F, which are both tyrosinase inhibitors. Mulberroside F is also an
antioxidant. Transcutol® helps build up a reserve of active prod-
ucts near the dermoepidermal junction and improves the action
of tyrosinase inhibitors. AHAs can be used to enhance penetra-
tion of active products through the skin. Lactic acid has also
been described as having a tyrosinase-inhibiting action. Finally,
vitamins (A, C, and E) can be used in the treatment of hyperpig-
mentation: they are antioxidant and anti-inflammatory, protect
against UV damage, and stimulate epidermal turnover.
The well-known Kligman’s formulas combine the action
of tretinoin, a corticosteroid, and hydroquinone but are more
irritating than medical cosmetics. The cosmetics used for
hyperpigmentation should be applied very soon after the peels
(if possible, the next day). If possible, they should be applied
two or three times a day, before effective sun protection. For
more information on topical depigmenting agents, see the sec-
tion on hyperpigmentation in Chapter 37.
Treatment for Aging
The author’s cosmetic postpeel treatment for aging skin is
described in the following paragraphs.
Patients under 40–45 Years Old
The main thrust of the treatment is daily oxidation. In the morn-
ing, an antioxidant cream with vitamin E should be applied,
and in the evening another antioxidant cream: Nutritive ACE
Lipoic Complex.
Vit. E Anti-oxydant® is a cream with a relatively complex
but complete formulation. It does not contain AHAs, so it can
be applied daily without the risk of interference with the pro-
tective function of the corneocytes. It has been specially for-
mulated for use very soon after a chemical peel. Its qualitative
formulation is listed in Table 3.1.
Nutritive ACE Lipoic Complex is ideal for dry skin and
can also be applied in the morning. With normal or oily skin, it
is better applied in the evening. It does not contain any AHAs,
for the reasons outlined earlier. Its qualitative formulation
includes the ingredients listed in Table 3.2.
Patients over 40–45 Years Old
The fight against aging should take into account not only the
damage caused by the various sources of cell oxidation but
also the drop in hormone levels. For menopausal or postmeno-
pausal women, a standard formula is testosterone propionate
100 mg, estrone 5 mg, estradiol benzoate 5 mg, and water in oil
excipient ad 100 g.
Extracts of Mexican wild yam (Dioscorea) can also be
used, or other estrogen precursors or dehydroepiandrosterone
Table 3.1  Vit. E Anti-oxydant®
Urea and glycerol
Moisturizers
Enoxolone
Anti-inflammatory
Enoxolone is a natural inflammatory whose structure, similar to cortisol, provides the
anti-inflammatory properties, without suffering the antimetabolic properties of cortisol.
It has a modulatory effect on neural signaling through gap junction channels.
For more information, see Chapter 15.
Ceramides
Natural components of
the epidermis. One
of the major natural
skin defenses.
Antiaging, hydrating, and protecting actions.
Encourage skin repair after different types of injury.
Reinforce the natural lipid barrier of dry and aging skin.
Improve long-term moisturizing and protect the skin from external influences.
Vitamin E
Alpha tocopherol
acetate
Protects against anti-free-radicals. The tocopheryl acetate used in this cream is one of
the most stable derivatives of vitamin E and forms a reservoir in the skin after
penetration.
Biosaccharides
Polymers of fucose
Filmogenic properties that induce immediate hydration.
Slowly metabolized on the surface of the skin, giving a long-term hydrating effect.
Anti-inflammatory effect.
Natural moisturizing
factor
Natural-like mixture of
hexoses and amino
acids
One of the major natural skin defenses and hydration systems: it increases the epidermal
water content. Physiological moisturizer adapts to the water-binding capacity of human
skin.
Sun protection
(UV-A)
Avobenzone
The original global gold standard for UV-A protection: absorbs the full spectrum of UV-A
rays. Its ability to absorb ultraviolet light over a wider range of wavelengths than many
other sunscreen agents has led to its use as a “broad spectrum” sunscreen.
Avobenzone has an absorption maximum of 357 nm.
Sun protection
(UV-B)
Ethylhexyl
methoxycinnamate
Considered by health agencies as giving a good protection against UV-B and a very low
toxicity.

Postpeel care      19
(DHEA). DHEA Phyto® cream contains Dioscorea extracts in a
moisturizing cream base that is similar to Vit. E Anti-oxydant
cream.
Tetra Antiaging System
Some newer cosmetics contain peptides. One of them is espe-
cially interesting because it allows adipocytes to accumulate
more fat. This subcutaneous local fat accumulation acts as a
deep filler for the skin. Atrofillin® has multiple actions as out-
lined in Table 3.3.
Table 3.2  Nutritive ACE Lipoic Complex®
Thioctic acid =
lipoic acid
Antioxidant, chelator, protective
Lipoic acid protects the natural enzymatic antioxidant defenses and exists in different racemic forms. Only the R form
is active (Figure 3.5). Lipoic acid is absorbed rapidly both orally and topically. Enzymes in cell cytoplasm convert it
into dihydrolipoate (DHLA). DHLA penetrates the cell and mitochondrial membranes easily. It is a mitochondrial
cofactor that boosts mitochondrial activity while protecting against excess production of free radicals. Lipoic acid has
the major advantage of being both fat-soluble and water-soluble, which means that it is active at all levels in the cell.
It recycles vitamin C, when it is converted into the ascorbyl radical after acquiring a free electron, thus restoring its
antioxidant activity. It also recycles vitamin E indirectly. Lipoic acid protects the natural enzymatic antioxidant
defenses, such as catalase, coenzyme Q-10, glutathione, and cysteine. It is an iron, copper, mercury, and aluminum
chelator (Figure 3.6). It combats excessive secondary cell apoptosis resulting from various stresses.
Ascorbic acid
Pure vitamin C, protected in cyclodextrins. Vitamin C deficiency is linked with a reduced immunity response, an
increased risk of infection, reduced collagen synthesis, poor angiogenesis, and higher capillary fragility.
Vitamin C is a powerful antioxidant, effective in aqueous solutions, that scavenges free radicals and prevents the
breakdown of protein chains. It protects other antioxidants, which is an advantage in situations involving oxidative
stress, such as infected or uninfected wounds and in the postpeel healing period. Vitamin C has many roles in
wound healing, and vitamin C deficiencies result in impaired healing.
Retinol
Pure vitamin A, protected in cyclodextrins. Retinol induces the expression of retinoic acid-binding protein (RABP) and
regulates cell migration in the skin epithelium, which is vital for skin regeneration after a peel. Retinol exerts a strong
antioxidant activity. Encapsulating retinol provides better bioavailability of the vitamin and protects the skin against
oxidation. Keratinocytes have the enzyme tools required to convert retinol into retinoic acid (the corresponding
carboxylic acid), which is the molecule ultimately responsible for the effect of vitamin A.
Retinol can be considered as a tretinoin precursor, because when encapsulated in cyclodextrins it enters easily into
the skin, and when liberated from the cyclodextrin it is transformed by epidermal enzymes into retynaldehyde and
finally retinoic acid.
Alpha tocopherol
acetate
Stable ester of vitamin E. The advantage of the acetate form is that it forms a reservoir that gradually releases the
vitamin E inside the skin. Vitamin E scavenges free radicals that could damage neighboring tissue. It blocks
oxidative chain reactions by inhibiting the formation of lipoperoxides inside the cell, and in this way protects the
nucleic acids and proteins. Vitamin E is an antioxidant, and its lipophilic properties allow it to stabilize cellular
membrane integrity. Vitamin E also shows anti-inflammatory properties and decreases the risk of scar formation.
Urea and glycerol
Moisturizers
Enoxolone
Anti-inflammatory
Enoxolone is a natural inflammatory whose structure, similar to cortisol,
provides anti-inflammatory properties without suffering the
antimetabolic properties of cortisol. It has a modulatory effect on neural
signaling through gap junction channels.
Ceramides
Natural components of the epidermis.
One of the major natural skin defenses.
Anti-aging, hydrating, and protecting actions.
Phytic acid
Antioxidant
Phytic acid is well known for its anti-tyrosinase and antioxidant action. It
is also an iron chelator. This molecule is therefore a good indication for
skin-lightening and antiaging treatments. Phytic acid scavenges the
free radicals produced by the inflammation that follow any peel and
breaks the usual vicious cycle of postpeel inflammation.
Sun protection
HO
O
S
S
H
Figure 3.5  Chemical structure of (R)-lipoic acid.
SH
S
O
O
O
S
S
Fe2+
O–
Fe2+
Figure 3.6  Iron chelation by lipoic acid.

20      Textbook of chemical peels
Table 3.3  Atrofillin®
Acetyl
hexapeptide 38
What it makes
Local increase in fat tissue volume, face, or body: fat droplets increase 32.4% in 10 days
Local increase of jaw fat: 12% in 14 days
Note: No fat, no action (“empty hands” or “empty temporal area” are not good indications)
How it works
61% more expression of PGC-1α (coactivator that interacts with PPARy—receptor of peroxysomes proliferation) and
modulates adipogenesis.
PGC-1α regulates mitochondrial activity.
Aging is associated with a lower renewal and activity of mitochondria.
“PGC-1α is a master regulator of energy metabolism and mitochondrial biogenesis”1
Maintenance of mitochondrial function is beneficial in the prevention or delay of age-associated diseases. A central
molecule seems to be the peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), which is the key
regulator of mitochondrial biogenesis.
Besides regulating mitochondrial function, PGC-1α targets several other cellular processes and thereby influences
cell fate on multiple levels”2
PGC-1α stimulates mitochondrial biogenesis and promotes the remodeling of muscle tissue.3
PGC-1α was investigated as a candidate gene for growth and fatness traits in chickens because of its prominent
role in muscle fiber specialization and adipogenesis.4
DMAE
Progressive effect:
• Decreases lipofuscine (lentigos)
• Increases collagen fiber thickness and dermal thickness
Immediate effect:
• Increases skin firmness: Increases myofibroblasts tension → better skin tension
• Anti-inflammatory
• Antioxidant (hydroxyl, ascorbyle, lipids radicals)
Kojic dipalmitate
Kojic acid (KA) is a hydroquinone derivative with antityrosinase action.
Known melanogenic inhibitor
Ester form more active and less irritant
KA esters have lower cytotoxic effect than kojic acid.
It works at least as good as hydroquinone.
Although hydroquinone is effective and has been available for years, kojic acid has the advantage of being
pharmaceutically more stable and, also, a tyrosinase inhibitor.
Fifty-one percent of patients responded equally to hydroquinone and kojic acid.1
Twenty-eight percent had a more dramatic reduction in pigment on the kojic acid side; 21% had a more dramatic
improvement with the hydroquinone formulation.
These results were not statistically different.5–7
How it works
Tyrosinase is known as a copper-containing enzyme, thus the capability of KA and KA esters to chelate metal ions
may chelate cooper in tyrosinase, changing its three-dimensional conformation to inhibit its enzymatic activity.
Efficacy study: KA versus esters (palmitate) of KA
Data obtained from control skin, ultraviolet (UV)-stimulated tissue and KA-treated UV-irradiated explants are
compared. Moreover, statistical analysis concerning keratinocytes discloses a significant decrease in the mean
pigmentation index when explants exposed to UV light were treated with KA.
KA monopalmitate gave slightly higher inhibition to melanin formation compared to other inhibitors at doses ranging
from 15.63 to 62.5μg/mL.
KA and KA esters also show antioxidant activity that will enhance the depigmenting effect. The potency of KA esters
to stabilize free radicals and chelate metal ions may help to reduce melanogenesis process and downregulate
hyperpigmentation.
Safety
KA esters derived in this study have very low cytotoxicity, even at very high doses (up to 500 μg/L).
KA esters derived from esterification of KA and palm-oil-based fatty acid have been demonstrated as safe and
nontoxic depigmenting agents with a satisfactory inhibitory effect on melanin formation and tyrosinase activity as
determined on α-MSH induced B16F1 melanoma cells. Thus, it can be suggested that these depigmenting
compounds have potential to be used in cosmetic formulations and to treat hyperpigmentation.5–7
Alanine-phosphinic
acid
Alanine-phosphinic acid is a non-cytotoxic anti-dopachrome tautomerase by inhibition of its spontaneous (oxydative)
polymerization or by inhibition of DCT.
Stabilizing dopachrome, it is a melanogenesis inhibitor (evidenced on mouse melanocyte and reconstituted human
pigmented skin). It is not an antityrosinase.
Mulberroside,
resveratrol
Competitive inhibition and tyrosinase enzyme expression suppression: oxyresveratrol and moracenin D have been
extracted and exhibit stronger tyrosinase inhibitory activities than that of kojic acid. These results suggest the
Morus root extract as a good source of natural tyrosinase inhibitors with a great potential to be used as a skin-
whitening agent.8

Postpeel care      21
Sagging Skin: DMAE
One of the common signs of aging is loss of skin elasticity.
The skin appears devitalized and slack. One substance that
is of special interest in the treatment of sagging skin is N,N-
dimethylaminoethanol (DMAE) (Figure 3.7).
DMAE has been used for several years as a topical appli-
cation to produce a “face-lift” effect. While there is no doubt
that it produces a tightening effect on the face, there is no
definitive evidence regarding its mode of action. The following
paragraphs describe what type of skin structures respond to
DMAE and why it would be difficult to explain this action by
an improvement in tension of the striated muscle mass of the
face. Actilift® cream contains pure DMAE and helps induce a
nice skin tension.
Chemistry of DMAE
DMAE (also called deanol, dimethylethanolamine, and nor-
choline) is a small hydrophilic molecule. Its low molecular
Table 3.3 (Continued)  Atrofillin®
Twelve compounds with tyrosinase binding activity were found in mulberry leaf extracts. The identities of these compounds
were characterized by HPLC-DAD-MS(n). Two compounds, quercetin-3-O-(6-O-malonyl)-β-D-glucopyranoside and
kaempferol-3-O-(6-O-malonyl)-β-D-glucopyranoside, were identified as new tyrosinase inhibitors.9
Mulberroside A was isolated from the ethanol extract of Morus alba roots. The enzymatic hydrolysis of mulberroside
A with Pectinex produced oxyresveratrol and oxyresveratrol-3-O-glucoside. Histological analysis with Fontana-
Masson staining confirmed that these compounds significantly reduced the melanin content in the epidermis of
UVB-irradiated guinea pig skin compared to the vehicle control. Thus, these compounds effectively reduced
pigmentation and may be suitable cosmetic agents for skin whitening.10
How it works
Mulberroside and resveratrol (from mulberry extracts) suppressed the expression of melanogenic enzymes
tyrosinase, tyrosinase-related protein-1. Mulberroside A is a glycosylated stilbene of oxyresveratrol; thus, the
deglycosylation of mulberroside A resulted in enhanced inhibition of melanogenesis.10
In mulberry extracts, the resveratrol is the most efficient part.
Mulberroside A and oxyresveratrol showed inhibitory activity against mushroom tyrosinase with an IC(50) of 53.6 and
0.49 micro M, respectively.
Inhibition kinetics showed mulberroside A to be a competitive inhibitor of mushroom tyrosinase with L-tyrosine and
L-DOPA as substrate. Oxyresveratrol showed mixed inhibition and noncompetitive inhibition against L-tyrosine and
L-DOPA, respectively, as substrates. The results indicate that the tyrosinase inhibitory activity of mulberroside A
was greatly enhanced by the bioconversion process.11
Mulberry extract acts as an antityrosinase and an antioxidant.
Resveratrol: Acts as antioxidant (limits auto-polymerization of dopachrome)
Mulberroside F: Acts as antityrosinase.
An investigation of the in vitro effects of an 85% methanol extract of dried Morus alba leaves on melanin biosynthesis
found that these extracts inhibited the tyrosinase activity that converts dopa to dopachrome in the biosynthetic
process of melanin.
Mulberroside F showed inhibitory effects on tyrosinase activity and on the melanin formation of melan-a cells.
This compound also exhibited superoxide scavenging activity that is involved in the protection against auto-oxidation,
but its activity was low and was weaker than of kojic acid.
Mulberroside F isolated from mulberry leaves might be used as a skin whitening agent.12–13
Notes:
  1. Gomez-Cabrera MC, Sanchis-Gomar F. Mitochondria as sources and targets of damage in cellular aging. Clinical Chemistry and
Laboratory Medicine. 2012 Feb 1; 50(8):1287–95.
  2. Wenz T. Mitochondria and PGC-1α in aging and age-associated diseases. Journal of Aging Research. 2011; 810619.
  3. Ward WF. American Journal of Clinical Nutrition. 2011 April; 93(4):
  4. Wu GQ, Deng XM, Li JY, Li N, Yang N. A potential molecular marker for selection against abdominal fatness in chickens. Poultry Science.
2006 Nov; 85(11): 1896–9.
  5. Garcia A, Fulton JE Jr. The combination of glycolic acid and hydroquinone or kojic acid for the treatment of melasma and related condi-
tions. Dermatologic Surgery. 1996 May; 22(5): 443–7.
  6. Vie K, Fitoussi R, Mathieu E, Benetti LD, Gooris E, Hemmerlé J. Ultrastructural assessments of the melanosome distribution patterns and
pigmentation features in human epidermal cells after UV irradiation and kojic acid treatment. International Journal of Cosmetic Science.
2009 Dec; 31(6): 461–73.
  7. Lajis AF, Hamid M, Ariff AB. Depigmenting effect of kojic acid esters in hyperpigmented B16F1 melanoma cells. Journal of Biomedicine
and Biotechnology. 2012; 952452. Published online 2012 October 2. doi: 10.1155/2012/952452. PMCID: PMC3468271.
  8. Zheng ZP, Tan HY, Wang M. Tyrosinase inhibition constituents from the roots of Morus australis. Fitoterapia. 2012 Sep; 83(6): 1008–13.
  9. Yang Z, Zhang Y, Sun L, Wang Y, Gao X, Cheng Y. An ultrafiltration high-performance liquid chromatography coupled with diode array
detector and mass spectrometry approach for screening and characterising tyrosinase inhibitors from mulberry leaves. Analytica Chimica
Acta. 2012 Mar 16; 719: 87–95. doi: 10.1016/j.aca.2012.01.018. Epub 2012 Jan 18.
10. Park KT, Kim JK, Hwang D, Yoo Y, Lim YH. Inhibitory effect of mulberroside A and its derivatives on melanogenesis induced by ultraviolet
B irradiation. Food and Chemical Toxicology. 2011 Dec; 49(12): 3038–45. doi: 10.1016/j.fct.2011.09.008. Epub 2011 Sep 16.
11. Kim JK, Kim M, Cho SG, Kim MK, Kim SW, Lim YH. Biotransformation of mulberroside A from Morus alba results in enhancement of
tyrosinase inhibition. Journal of Industrial Microbiology and Biotechnology. 2010 Jun; 37(6):631–7.
12. Lee SH, Choi SY, Kim H, Hwang JS, Lee BG, Gao JJ, Kim SY. Mulberroside F isolated from the leaves of Morus alba inhibits melanin
biosynthesis. Biological and Pharmaceutical Bulletin. 2002 Aug; 25(8): 1045–8.
13. Department of Herbal Pharmacology, Graduate School of East-West Medical Science, Kyunghee University, Seoul, Korea.

22      Textbook of chemical peels
(a)
(b)
(c)
(d)
(e)
Figure 3.7  A tightening effect can be seen after the first application of N,N-dimethylaminoethanol (DMAE) in the form of Skin Tech’s
Actilift®: (a) before; (b) after (photo courtesy of John Jairo Hoyos, Colombia). (c) Before and (d) 30 minutes after application of a thick coat
of Actilift® around the eyes (photo courtesy of Evgeniya Ranneva, Spain). (e) Before (photo courtesy of Evgeniya Ranneva, Spain).

Postpeel care      23
weight (89.1) allows it to penetrate the skin easily. DMAE is
a precursor of acetylcholine (ACh), via choline (Figure 3.8). It
is a viscous liquid, as transparent as water, that is often said
to smell like ammonia but is in fact more reminiscent of fish
long past its sell-by date. Anchovies, sardines, and salmon are
important natural sources of DMAE. It is naturally present in
the body, and there are traces of it in the brain. DMAE is a
very basic molecule (pH 11) that cannot be used in its pure state
without the risk of causing chemical skin burns. It must be par-
tially neutralized for use at pH 7. Many derivatives have been
used in its place (e.g., DMAE bitartrate or acetamidobenzoate),
but these are more suitable for oral rather than topical use.
DMAE formulations tend to give only the total dosage of
the DMAE derivative used, of which pure DMAE is only part of
the weight. For example, 100 mg of DMAE cyclohexylcarboxyl-
ate contains only 33 mg of pure DMAE, while 350 mg of DMAE
bitartrate contains 130 mg of pure DMAE. The author prefers
to use a formulation with DMAE lactate (Skin Tech’s Actilift®)
in order to benefit from the properties of an AHA (lactic acid)
combined with the DMAE.
Side Effects and Precautions  The high pH of DMAE means that
the pure compound should not be brought into contact with
strong acids, mucous membranes, or the eyes. Pure DMAE is also
incompatible with copper and zinc. DMAE is volatile and should
be contained in sealed tubes rather than bottles, to prevent its
evaporation. Some cases of allergic dermatitis have been reported
after prolonged contact with very high concentrations of DMAE,
and it should be applied with extreme caution around the eyelids
of atopic subjects. DMAE is not considered to be carcinogenic,
cocarcinogenic, or immunosuppressive. Chronic exposure to
concentrated fumes of DMAE in the workplace can cause visual
problems.
Toxicity  DMAE has mostly been used orally. It is most
widely available in 100  mg tablets for the treatment of
cognitive disorders associated with senile dementia, at a
dose of 600 mg/day. The LD50 for oral administration in rats
is 2 g/kg. The LD50 in rabbits after application to the skin is
1.370 mg/kg. For subcutaneous injection in mice, the LD50 is
961 mg/kg. In a human clinical study,13 oral administration
of 1600  mg/day showed no side effects. The doses used in
topical applications are nowhere near the theoretical toxicity
limit. It takes a twice-daily application of around 30–50 mg
of DMAE on the skin to improve skin tension and achieve
the “lifting” effect. It is important to remember that a topical
application, even if it is very effective, cannot as yet compete
with a surgical procedure.
DMAE and N,N-dimethylisopropanolamine (DMIPA)
solutions are used in high concentrations (45%–50%) in indus-
try, especially in the printing industry. They are used in sprays,
and a study was conducted on their role in the appearance
of intermittent corneal opacity in workers in certain types of
printing works.14 The corneal opacities caused workers to have
blurry vision on their way home from work. These problems
were evident only from Mondays to Thursdays and never at the
end of the week. Eye tests revealed the appearance of intermit-
tent and reversible corneal opacity, limited to the part of the
(g)
(f)
Figure 3.7 (Continued)  A tightening effect can be seen after the first application of N,N-dimethylaminoethanol (DMAE) in the form of
Skin Tech’s Actilift®: (f) during, and (g) 30 minutes after application of a thick coat of Actilift® around the eyes. (Photographs courtesy of
Evgeniya Ranneva, Spain.)
(CH3)2NCH2CH2OH
DMAE
(CH3)3N+CH2CH2OH
Choline
O
(CH3)3N+CH2CH2OCCH3
Acetylcholine
Figure 3.8  Chemical structures of N,N-dimethylaminoethanol
(DMAE), choline, and acetylcholine.

24      Textbook of chemical peels
cornea in contact with the droplets of vaporized solution and
lasting just a few hours. A complete study was undertaken that
put the blame on DMIPA but cleared DMAE of involvement.
Lowering the concentrations of DMIPA without changing the
concentrations of DMAE solved the problem and produced no
visual sequelae.
DMAE has also been claimed to be teratogenic. Studies
on this subject remain controversial: some have shown that
DMAE can be teratogenic in mouse embryos at high doses;15,16
other studies have shown no evidence of toxicity in rodents.17
To the author’s knowledge nothing has been published on tera-
togenic effects in humans, and no research has shown terato-
genicity in humans, despite the wide use of DMAE in industry.
Historical and “Usual” Use of DMAE  Procaine, which is used
widely in mesotherapy, is one of the active principles of the well-
known (and at times much criticized) Gerovital H3 developed
by Dr. Ana Aslan of Romania. Procaine or 2-diethylaminoethyl
4-aminobenzoate hydrochloride (Figure  3.9) was synthesized
in 1905 by the German chemist Alfred Einhorn, who called it
novocaine (from the Latin novus = new, with the added suffix
of cocaine, a gold-standard product up until then). Another
German, Dr. Heinrich Braun, introduced the use of novocaine
in medicine.
In the body, the ester link of procaine is hydrolyzed, yield-
ing p-aminobenzoic acid (PABA) and N,N-diethyl-aminoethanol
(DEAE), an analog of DMAE. It is PABA (Figure 3.10) that is
responsible for the large majority of allergic reactions to “pro-
caine”; it is excreted rapidly by the kidneys. PABA is most often
used as a sunscreen but is sometimes called “vitamin B-x,”
although it is not essential for humans and the body cannot
synthesize folate from PABA. According to some authors, the
“Aslan” method relies solely on the combined action of PABA
and DEAE/DMAE. It is assumed that the action of PABA is due
to its anti-free-radical properties.
Another local anesthetic used in mesotherapy, lidocaine,
goes through a different metabolic pathway from procaine,
being converted into monoethylglycine, xylididide (MEGX),
and acetaldehyde. Its action in this context must therefore have
a different basis from that of procaine.
As well as having an antioxidant18 and anti-inflamma-
tory effect, DMAE taken orally has been claimed to have many
properties: an antiaging effect; improvement of memory and
intelligence; increased synthesis of acetylcholine; amelioration
of depressive states; improvement in motor coordination;
improvement in compulsive, impulsive, hyperactive, or antiso-
cial behavior; reduction of chronic fatigue and improvement in
the quality of sleep; aid in giving up alcohol and tobacco; reduc-
tion of headaches; improved ability to concentrate; improve-
ment in schizophrenia; improved muscle tone; and overall
higher energy levels.
DMAE can be incorporated into the membrane structure
of cells, where its antioxidant properties improve membrane
resistance to the oxidative stress resulting from the release of
free radicals from the phospholipid bilayer and the ­production
of eicosanoids associated with skin inflammation. The degra-
dation of cell membranes and subsequent inactivation of the
transmembrane proteins and receptors are considered to be the
main factors responsible for cell aging.
Carbachol
(Figure 
3.11)
and
the
closely
related
bethanechol are powerful cholinergic agents (used to induce
miosis). Carbachol’s structure is similar to that of choline and its
precursor, DMAE. Other muscarinic agents (e.g., pilocarpine)
have a completely different chemical structure from choline.
Topical Skin Application of DMAE  Topical application of DMAE
has a visible tightening, firming effect, often called the “lifting
effect.” This tightening effect can already be felt 20–30 minutes
after the product has been applied to the skin, and when only
one side of the face is treated with DMAE, the difference in
tension between the two sides is clear. Skin tension continues
to improve during the first 6 months of twice-daily application,
with individual variations, and remains stable for 4–8 weeks
after topical treatment is finished. This would seem to indicate
that the product accumulates in the skin and forms a reservoir.
Potential Mode(s) of Action of DMAE  DMAE is a precursor of
choline; it also inhibits the metabolism of choline in the tissues.
As there is more choline available, the biochemical reactions
may tip the balance toward an increase in ACh synthesis.
DMAE may stimulate macrophage activity and improve the
skin’s defenses. The mode of action of DMAE is not yet fully
understood, and its action as a local application even less so. We
must therefore put forward several hypotheses in an attempt to
understand this tightening effect.
Action on the Striated Facial Muscles  Botulinum toxin
(BTX), which is used to “smooth the skin,” like DMAE, acts on
ACh, although its action is the reverse of that of DMAE. BTX
relaxes the muscles, whereas DMAE increases muscle tone. Are
these two compounds therefore incompatible? It appears not, as
they have different targets, and the muscle cells that are deacti-
vated by BTX are not the same as those activated by DMAE. BTX
is a large molecule with a high molecular weight, which means
that it cannot pass through the skin when applied topically. To
achieve a cosmetic result, BTX must be injected directly into the
muscle to be paralyzed. BTX has no effect on the epidermis or
NH2
CO.CH2CH2N(C2H5)2
O
Figure 3.9  Chemical ­structure of procaine.
NH2
C
O
OH
Figure 3.10  Chemical structure of p-aminobenzoic acid (PABA).
(CH3)3N+CH2CH2CNH2
O
Figure 3.11  Chemical structure of carbachol. Note the similarity
between part of the molecule and DMAE and choline.

Postpeel care      25
dermis, as it blocks cholinergic transmission in the neuromus-
cular junction of the striated muscles and in this way limits the
facial expressions that cause expression lines.
BTX is picked up immediately, and there is no chance of
it diffusing up through the hypodermal fat layer. DMAE, on the
other hand, is a very small hydrophilic molecule with a molec-
ular weight of 89.1 that can easily penetrate the epidermis and
the dermis but cannot penetrate the hypodermal fatty layer.
DMAE cannot act on the striated muscle groups that produce
voluntary facial movements, and so cannot counter the effects
of BTX. This physiological hypothesis is confirmed clinically
when the two treatments are used together. The physicochemi-
cal properties of DMAE give this molecule a great affinity for
the dermis and epidermis. As the action kinetics of DMAE lead
to the hypothesis of a cutaneous “reservoir,” this could only
be located in the deep epidermal layers, as, if it was in the der-
mis, this small molecule would soon be eliminated by venous
or lymphatic resorption because of its concentration gradient.
The way in which they are administered, their targets,
their characteristics and their different modes of action do not
make BTX and DMAE incompatible: administering one will not
alter the effectiveness of the other. There is no established link
between age-related sagging skin and muscles and a deficiency
in ACh in the muscles. Any action of DMAE on striated facial
muscles is thus not only unlikely but also pointless. We must
therefore look for other more likely modes of action than muscle
stimulation, especially as there have been reports of improve-
ments in tone and younger-looking skin around the eyes and
lips after only a few days of treatment. Given that it is accepted
that paralysis (or hypotonia) of the muscles by BTX “smooths”
the skin, it would be illogical to claim that stimulating the same
muscle groups (with DMAE) can give similar results. We must
therefore look elsewhere: in the skin structures that have cho-
linergic receptors.
Epidermal Action  Human keratinocytes express cholin-
ergic receptors in the cells of the stratum basale, the stratum
spinosum, and the stratum granulosum. They use ACh, among
other things, to stick together. They also synthesize, store,
degrade, and release ACh.
ACh synthesis has been shown to occur in the perinuclear
regions of human keratinocytes due to the presence of a cho-
line acetyltransferase (this enzyme converts acetyl coenzyme
A into ACh). On the other side of the cell, inside or near the
cell membranes, an acetylcholinesterase has been identified.
This enzyme degrades ACh in order to prevent a toxic buildup.
Keratinocytes can move, which is essential during the second
phase of healing, thanks to cytoplasmic myosin and actin: the
actin moves in relation to the myosin when the two interact,19
in the same way that an oar stroke moves a kayak or an athlete
runs on a treadmill (the athlete representing the myosin and
the treadmill the actin). It has recently been shown, by immu-
nohistochemistry, that there are free nerve endings in all of
the layers of the epidermis, and it is now suspected that kera-
tinocytes have a neurotropic function. The ACh acts locally, in
the epidermis, like a hormone that can also be a “messenger”
stimulating the dermis. We can then suppose that an epidermal
reservoir of DMAE can interact with the dermis via ACh, of
which it is a precursor.
DMAE is also assumed to inhibit formation and enhance
elimination of lipofuchsin, a waste product of the aging cell
metabolism of fatty acids. Experiments have shown that lipo-
fuchsin is eliminated from the liver by DMAE. This buildup,
which occurs in all organs, has not been associated with any
disorder apart from lentigines. Some authors have reported a
gradual reduction in lentigines on the hands with oral DMAE
treatment. To date, there have been no studies published on the
topical use of DMAE in the treatment of lentigines.
Dermal Action  DMAE is used for its antioxidant proper-
ties, membrane stabilization, and inhibition or repair of protein
cross-links that clearly play a role in the aging process. It could
thus help maintain good-quality collagen and elastin and slow
down dermal aging.
Vasomotor Effect  The dermal blood vessels are inner-
vated by adrenergic fibers, which cause vasoconstriction, and
cholinergic fibers, which cause vasodilation. DMAE, as a pre-
cursor of ACh, could cause vasodilation that is clinically unde-
tectable but sufficient to produce temporary edema, a buildup
of water in the hydrophilic structures of the dermis, and, as
a result, a tightening of the skin. This hypothesis only partly
explains the particular kinetics of topical DMAE. The fact that
treating one side of the face shows improvement on one side
only suggests that the DMAE has a purely local action and is not
converted into ACh throughout the organism. Local blood flow,
which decreases with age, is vital for the nutrition and defense
of the dermis and epidermis. Constant slight vasodilation
would thus improve skin perfusion—especially in ­smokers—
and by diffusion would bring in more of the elements that con-
tribute to the overall rejuvenating effect observed when DMAE
is applied topically.
Effect
on
Myofilaments
and
Smooth
Muscle
Cells 
Myofilaments make up the endoskeleton of a cell (Figure
3.12). They can be found in the smooth muscle cells (SMCs) and
in the cytoplasm of “nonmuscle” cells, where they are capable
of moving and contracting. SMCs can regulate contraction far
more subtly than striated muscle cells. SMCs can shorten to
a greater extent than striated muscle cells. Shortening of stri-
ated muscle cells is limited to movement within the sarcomere,
whereas with SMCs, the myosin filaments can move over a far
greater distance, along the network of actin filaments in the
+
Nucleus
Direction of displacement
Microtubule
Dense bodies
Cellular
center
+
+
+
+
+
+
+
+
+
“Stress” contractile fibers
Network tightened with
actin microfibrils
Radial network with
actin microfibrils
Loose network with
actin microfibrils
in all cytosol
Figure 3.12  Different types of organization of actin microfibrils
(MF) and microtubules (MT) in a moving cell; organized polariza-
tion of the MF and the MT.

26      Textbook of chemical peels
cytosol. The force generated by SMCs is less than that generated
by striated muscle cells but can be sustained for much longer.
The arrector pili muscle is under adrenergic control and
does not respond to a local increase in ACh concentration. The
fibroblasts and myofibroblasts (MFBs) are very interesting cells
as far as the possibilities of the action of DMAE are concerned.
Fibroblasts have cytoplasmic myofilaments that help them
move in the dermis when necessary.20 There are different types
of fibroblast subpopulations. Some authors maintain that these
different subpopulations expand when they are needed through
different phenotype expressions, whereas others believe that
these subpopulations coexist permanently in the dermis. These
two hypotheses are not incompatible. MFBs are phenotypically
modified fibroblasts that have the secretory capacity of fibro-
blasts, which helps them synthesize strong fibronectin fibers.
They express the phenotypic characteristics of “nonmuscle”
cells, but with the contractile capacities (of SMCs) that make
them responsible for most of the phenomena of fibrotic contrac-
tion in the body. The fibronectin fibers synthesized by the MFBs
serve as a support for them to “pull” on during contraction,
which helps the wound to close by as much as 40%.
MFBs synthesize far more actin fibers than “standard”
fibroblasts and also have myosin fibers that, when interacting
with actin, constitute the contractile motor activity of MFBs.
MFBs are found in healing tissue, of which they form 40% of the
total number of fibroblasts present. A large number of MFBs are
also found in the periprosthetic capsule of encapsulated breast
implants, while there is no evidence of MFBs if no capsule has
formed around the prosthesis. In pathology, abnormal quanti-
ties of MFBs are found in diseases such as pulmonary fibrosis
and Crohn’s disease. Many SMCs respond to a kind of para-
crine stimulation, where the mediator is released into the envi-
ronment of the target cells and diffuses towards the cell, where
it interacts with a membrane receptor.
MFBs are not linked to any synapse, which would make
it impossible for them to move, but the exposure of MFBs to
certain mediators causes significant contraction, comparable to
that in SMCs. We can imagine the contractile potential of these
SMCs when we recall that the nipples, as well as the scrotum,
have many contractile cells of this type that are sensitive to dif-
ferent stimuli. The difference is that the contraction of MFBs
during wound healing is irreversible. Fibroblasts and MFBs, like
many SMCs, have numerous receptors on their surface for dif-
ferent mediators: ACh, adrenaline (epinephrine), noradrenaline
(norepinephrine), oxytocin, vasopressin, histamine, angioten-
sin II and prostaglandins. As ACh is a small water-soluble mol-
ecule, its membrane receptor can be a ligand-gated ion channel
receptor or can be coupled with the heterotrimeric G proteins
(RCPGs) that control the activity of a target protein, which can
be an enzyme or an ion channel. Opening and closing of the ion
channels causes polarization or depolarization of the myofila-
ments, and the SMCs (e.g., endothelial cells) contract or dilate.
The G protein acts as a transducer. As ACh is a small ligand,
the N-terminus of the G protein in the extracellular environ-
ment will be small. The presence of a larger quantity of ACh in
the pericellular environment of the MFBs could then stimulate
certain membrane receptors more strongly and increase their
contractile potential. DMAE, a precursor of ACh, might then
stimulate the contraction of MFBs. However, there must be a
reactivity threshold for MFBs to ACh, to guard against unnec-
essary contraction of these cells and the formation of pathologi-
cal fibroses. The hypothesis put forward here is that a slight
increase in the extracellular concentration of ACh (by conver-
sion from DMAE) could slightly stimulate the contraction of the
fibroblasts and do so reversibly, without fibrosis setting in as,
clinically, the effect of a topical application of DMAE is revers-
ible 4–8 weeks after treatment has stopped. This improved
tone, the reversible contraction of the fibroblasts, could explain
the clinical kinetics of DMAE in a topical application.
Exocrine Glands  The sweat glands have cholinergic
innervation.21 The eccrine sweat glands, which open directly
onto the skin, have denser autonomous innervation than the
apocrine sweat glands associated with pilosebaceous units.
ACh is the active neurotransmitter at this level, and the
response of the sweat gland will depend on the dose of ACh
that stimulates it. The myoepithelial cells contract in response
to the ACh. In strong doses,22 the muscarinic receptors are
stimulated and the gland reacts by producing large drops of
sweat. At lower concentrations,23 the nicotinic receptor is stim-
ulated and the gland will react by producing tiny droplets of
sweat. The possible increase in ACh caused by the application
of DMAE cannot, of course, stimulate the muscarinic receptors,
and no profuse sweating has been noted after application of
DMAE. On the other hand, a slight increase in the concentra-
tion of dermal ACh could stimulate the sweat glands’ nicotinic
receptors—in a paracrine manner—and increase hydration of
the stratum corneum, making the skin more “supple” and resis-
tant. The sweat glands themselves are controlled by circulating
hormones and are not under cholinergic control. DMAE will
not alter their function.
Conclusions  DMAE is a precursor of ACh, a neuromediator that
is important to the skin. Keratinocytes, as well as fibroblasts,
myofibroblasts, sweat glands, and endothelial cells, have
receptors that respond to ACh. They are not stimulated pre- or
postsynaptically but by paracrine diffusion, which can activate
specific membrane receptors. The hypothesis is that DMAE
in a topical application cannot stimulate the striated muscle
fibers, to which it has no access. Furthermore, muscle sagging
associated with aging is not caused by a deficiency in ACh.
The tightening effect of DMAE may result from cholinergic
stimulation of the membrane receptors of (myo)fibroblasts and
stimulate the gradual contraction of the myofilaments in their
cytosol. DMAE also has anti-free-radical and anti-lipofuchsin
activities and repairs protein (collagen and elastin) cross-
linking. The mode of action of topical DMAE could therefore
stem from a combination of effects working together at different
levels: tension of the “nonmuscle” dermal cells, keratinocyte
cohesion and movement, hydration and suppleness of the
stratum corneum, improved skin nourishment and defense,
antioxidant, and skin tone evener. As a result, it is very effective
at improving skin tone and firmness.
Summary of the Main Cosmeceuticals
Used Postpeel
See Table 3.4 for a list of postpeel cosmeceuticals according to
skin type, together with their times of application.
TROLAMINE
Trolamine (triethanolamine salicylate, TEAS) is a salicy-
late derivative, which is also known as “topical aspirin.” It
is an amino alcohol that is used for its topical analgesic and

Postpeel care      27
anti-inflammatory properties. Like the better-known salicylate
derivative, methyl salicylate—which has a rubefacient action
used to good effect in sports injuries and rheumatism—TEAS
is rapidly absorbed through normal skin after topical applica-
tion. It is used widely for treating sunburn.
Mode of Action and Absorption
Various studies show that salicylate derivatives act as much
through direct local diffusion as through absorption by the
dermal blood vessels and redistribution of salicylates in the
whole body. The blood level of salicylates increases in direct
proportion to the quantity applied, the resorption surface and
the number of topical applications. A large amount of salicy-
lates can be absorbed through the skin.
When TEAS is applied unilaterally on one limb, the con-
centration of salicylates has been found to be identical in the cor-
responding tissues of the contralateral limb. This supports the
theory of action by redistribution through the blood. The use
of radiolabeled TEAS also shows renal and fecal elimination.
Phonophoresis helps salicylates penetrate further into the skin.
How to Apply Trolamine
Salicylate derivatives, especially trolamine, are applied to first-
and second-degree burns. A first-degree burn consists of mild
erythema. A superficial second-degree burn consists of painful
blisters but does not reach the dermis. Medical advice is essen-
tial before applying the product to a second-degree burn.
Precautions
Trolamine must not be applied in cases of infection: salicylates
can accelerate the penetration of microbes into the skin and
aggravate any preexisting infection. It has been shown to cause
local skin irritation and scabs to form on the areas to which it
has been applied. Skin irritation increases the more it is applied.
In smaller quantities, repeated application only induces epider-
mal hyperplasia. Some authors consider TEAS to be a potential
cytotoxic agent. It is a potential skin irritant that makes the skin
sensitive and can cause contact allergies.
Trolamine is a salicylate derivative, and salicylic acid is a
keratolytic agent that dissolves the intercorneocyte amorphous
matrix and impairs the barrier function of the stratum corneum.
Symptoms of salicylism can appear with chemical peels
when large amounts of salicylate derivatives are applied on the
skin, on large surface areas or repeatedly, causing a high blood
level of salicylates. In cases of toxic levels of salicylate in the
blood, an increase in oxygen consumption causes hyperther-
mia by the uncoupling of oxidative phosphorylation.
Trolamine should therefore not be used during the imme-
diate postpeel period.
TIPS FOR THE CARE OF SENSITIVE SKIN
•
Prolonged use of creams containing more than 8%–10% of
AHAs can make some skins more sensitive by reducing
the thickness of the stratum corneum for long periods.
•
Use cleansing milks, lotions, or mineral water sprays to
wash.
•
Do not let water dry on the skin; when it evaporates, it soon
dries the skin out. Damp skin should be dried with a soft
cloth or paper tissues.
•
Avoid exfoliating scrubs, repeated micropeels, and creams
containing microcrystals on sensitive skins. Do not use
any masks that might dry out the skin.
•
Do not use aggressive soaps.
•
Tretinoin (vitamin A acid) makes the skin more sensitive.
One Easy TCA® peel per week for 4 weeks can restruc-
ture the skin and eliminate any abnormal sensitivity. In this
indication, the cosmeceuticals that can be combined with it are
restricted to Vit. E Anti-oxydant® cream in the morning and
the more nourishing Nutritive ACE Lipoic Complex® cream in
the evening.
CHARACTERISTICS OF “NORMAL SKIN”
Normal skin should be:
•
Firm: Contain a sufficient quantity of elastin and collagen
•
Soft: Compact stratum corneum protected by skin lipids
•
Hydrated and unwrinkled: Hydrated keratinocytes and
dermis
Table 3.4  Main Cosmeceuticals Used Postpeel
Skin type
Daily care product
When and how often to apply
Sagging skin
Dimethylaminoethanol (DMEA): Actilift face
Morning and evening
cream or Actilift body lotion
Atrofillin
Morning and evening
Patients under 40–45: skin aging
Vit. E Anti-oxydant
Morning
Atrofillin®
Morning and evening
Lentigines
Nutritive ACE Lipoic Complex
Evening
Blending Bleaching Cream
Morning (all over)
Patients over 40–45: skin aging
DHEA–PHYTO®
Morning
Nutritive ACE Lipoic Complex
Evening
Lentigines
Nutritive ACE Lipoic Complex
Evening
Acne
Purifying cream or gel
Morning (all over)
Purifying cream or gel
Evening (only on the lesions)
Hyperpigmentation (melasma–lentigines)
Blending Bleaching Cream
Morning (all over)
(Avoid exposure to sun: Melablock® HSP
Blending Bleaching Cream
Evening (only on the lesions)
50+ at 9 a.m., 11 a.m., 2 p.m.; serious cases:
3–4 times a day)
Dry skin
Vit. E Anti-oxydant
Morning, midday, evening
Thin skin
Atrofillin
Morning, midday, evening

28      Textbook of chemical peels
•
High in color: Active microcirculation; pink color visible
through the skin
•
Resistant to external aggression: Active protective function
•
Unscarred: No stellate or secondary scars
NOTES

1. Even though this type of sunscreen can protect the skin against
free radicals, some sunscreens could also cause postinflamma-
tory hyperpigmentation.

2. SPF 50+ protects the skin against 98% of UV, while SPF 25+ pro-
tects against about 96% of UV.

3. A typical example of this is seen when cooking an egg white as it
goes from transparent to white as a result of structural modifica-
tion of the proteins under the effect of heat.

4. By polymerase chain reaction (PCR).

5. Occlusion consists of applying an impermeable plastic film.

6. In the case of sagging skin, Actilift® face or body can be applied
as appropriate.

7. Example of mesolift mixture: 2.5 cm3 non-cross-linked 2% hyal-
uronic acid + 2.5 cm3 organic silicium + 2 cm3 vitamin C + 2 cc of
NA-nocleinate + 1 cm3 lidocaine.

8. Unna’s paste (see Chapter 24).

9. Molecules similar to tyrosine are used, for example, Tyrosilane C®.
10. Summary of Easy TCA “basic protocol”: no prepeel treatment,
application of the solution until scattered pinpoint or cloudy
white frosting appears, application of the postpeel cream (tyros-
inase inhibiting, antioxidant, stimulating). Repeat this process
four times at weekly intervals.
11. This paragraph particularly concerns superficial peels or peels
to the Grenz zone. Papillary dermal peels are not indicated in
cases of active acne.
12. Triclosan can be used as it is or encapsulated in cyclodextrins.
13. Casey DE, Denney D. Dimethylaminoethanol in tardive dyski-
nesia. New England Journal of Medicine. 1974; 291: 797.
14. NIOSH Publications Office. Health Hazard Evaluation Report
2002–03 79-2901 Superior Label Systems. Cincinnati, OH: May
2003.
15. Fisher MC, Zeisel SH, Mar MH, Sadler TW. Inhibitors of choline
uptake and metabolism cause developmental abnormalities in
neurulating mouse embryos. Teratology. 2001; 64: 114–24.
16. Fisher MC, Zeisel SH, Mar MH, Sadler TW. Perturbations in cho-
line metabolism cause neural tube defects in mouse embryos in
vitro. FASEB Journal. 2002; 12: 619–21.
17. Leung HW, Tyl RW, Ballantyne B, Klonne DR. Developmental
toxicity study in Fischer 344 rats by whole-body exposure to
N,N-dimethylethanolamine vapor. Journal of Applied Toxicology.
1996; 16: 533–8.
18. The antioxidant effect of DMAE has been shown by electron spin
resonance (ESR) for the hydroxyl radical. It does not seem to have
any antisuperoxide action.
19. There are different types of myosin for different types of move-
ment; cell movements (myosin II) are not facilitated by the same
myosin that permits endocytosis (myosin VI) or the movement of
vesicles between cells (Myosin V).
20. For example, movement along the fibrin/fibronectin fibers dur-
ing the healing process.
21. Catecholamines, vasoactive intestinal peptide and natriuretic
peptide have also been detected near the sweat glands.
22. Intradermal injection of 0.1 mg of ACh: postganglionic choliner-
gic stimulation (The Biology of the Skin: 58).
23. Hurley HJ. The Eccrine Sweat Glands: Structure and Function.
In: Freinkel RK, Woodley DT (Eds.). The Biology of the Skin.
Lancaster: Parthenon Publishing, 2001: 47–76.

4
Factors influencing the skin’s reactions to chemical peels
ALLERGIES
These are common when using antibiotic creams or oint-
ments in the postpeel period: between 5% and 10% of allergies
should be expected when using antibiotic creams containing
neomycin after a peel. The temporary thinning of the stratum
corneum allows products applied on the skin after peels to pen-
etrate more easily, which promotes the development of contact
allergies.
INFECTIONS
These are more common when patients have to undertake com-
plex postpeel care themselves. The basic principles of sterility
are not widely known by the public and require special train-
ing to be effective. The more patients have to take part in the
postpeel care, the higher the risk of infection. For example,
patients do not easily understand that it is mandatory to care-
fully remove leftover skin cream before applying a new layer.
They also do not know that touching with nondisinfected
hands is the best way to infect skin whose epidermal or stratum
corneum protection has been destroyed by the peeling.
SCABS
Pulling off scabs often leads to infection, prolonged erythema,
and even scarring. The less frequently patients touch their skin,
the better.
SUN EXPOSURE
It should be remembered that direct exposure to the sun for
10 minutes is enough to trigger pigmentary changes in sensi-
tive individuals during the postpeel period. See the section on
effective sun protection in Chapter 3.
DEHYDRATION OF THE SKIN
After a peel, drying and flaking skin causes an irresistible urge
to scratch and therefore a risk of complications (including sec-
ondary infections, inflammation, and scars). Applying white
Vaseline immediately improves the pruritus and the feeling of
tightness in the skin after a medium or deep peel. Sterile white
Vaseline is an excellent topical ointment that can be applied to
the treated areas in the first few days after a medium peel or
after removing the healing mask (after the eighth day) follow-
ing a phenol peel. Only a thin layer need be applied to avoid
itching caused by the drying out of surface keratinocytes that
have not yet differentiated into corneocytes. The Vaseline cre-
ates an impermeable layer on the surface of the skin and pre-
vents the water in the epidermis from evaporating. The water
accumulates under the layer of Vaseline and provides instant
natural hydration that soon relieves the itching caused by the
keratinocytes drying out.
INFLUENCE OF AGE
Older Patients
Intraepidermal and dermal peels are performed as usual even
on patients aged 80 or over (see Figure 29.1). With elderly people,
there seem to be fewer pigmentary changes, but the theoretical
risk of infection is higher. In theory, the weakened capacities of
the keratinocytes to regenerate, the presence of numerous cell
abnormalities, dormant fibroblasts, and underlying vascular
sclerosis should slow down healing after a peel in older people.
In practice, the only real problem is increased susceptibility to
infection resulting from a weakened immune system. A more
important factor seems to be the degree of skin photoaging
rather than age itself. Many phenol peels have been performed
on patients who are well into their 80s, without any particular
problems.
Young Patients
At the other end of the scale, what is the minimum age for hav-
ing a chemical peel? The answer is simple: in the majority of
cases, a peel is only necessary for young patients if they have
acne. Acne responds extremely well to intraepidermal peels or
peels to the basal layer of the epidermis. Deeper peels are not
recommended when the skin is infected. Very young patients
benefit from relatively superficial techniques with a high safety
level (Easy Phytic). The presence of acne means that the young
patient’s developing hormone system has created an adult
skin—thick and oily and resistant to acids.
USE OF CORTICOSTEROIDS
Topical Corticosteroids
These are only indicated in cases of serious edema or pruritus
during the first few days after an aggressive peel. It is always
best to start with a short-acting corticosteroid (hydrocortisone
or betamethasone). A cortisone-based cream can be used dur-
ing the first few days after a peel to reduce excessive edema or
pruritus. The deeper the peel, the greater the need for emol-
lients. Hydration after a peel is vital (except after a peel with
Unna’s paste); the hydrating cream should contain no alcohol or
perfumes. Corticosteroids may be used after peeling in the case
where a strong inflammation or a pigment rebound is feared.
Oral Corticosteroids
These are rarely indicated in combination with peels, and then
only for specific problems (see Chapter 37).
Intravenous Corticosteroids
These can be used before a deep peel to limit edema immedi-
ately after the peel and avoid any allergic or laryngeal reactions.1
They reduce postpeel inflammation, which is necessary to initi-
ate the skin repair processes. If the degree of inflammation is

30      Textbook of Chemical Peels
reduced, there is a risk of slowing down the first stages of skin
regeneration.
UNDERSTANDING THE HEALING PROCESS
Understanding the skin healing process after a peel allows
evaluation of the risks of scarring, infection, and dyschromia.
For more information on how the skin heals in relation to the
depth of the peel and on risk evaluation, see the section on scars
in Chapter 37.
Histologically, the skin healing process follows a precise
sequence of stages. The process starts almost immediately:
Neutrophils enter the treated area as soon as the peel has been
applied, and stay there for 3–5 days. Macrophages are present
from the 3rd to the 10th day and lymphocytes from the 6th or
7th day. Reepithelialization starts just 24 hours after the peel
and first manifests as a centripetal migration of keratinocytes,
followed by rapid cell proliferation. After the reepithelializa-
tion phase, dermal collagen is regenerated over a 2- to 3-month
period. Assessing the final results of a peel calls for patience.
How quickly the skin regenerates after a medium peel
depends on the concentration of pilosebaceous units (PSUs)
in the treated area: the face has many PSUs, and the nose and
forehead have more than the cheeks and temples. Statistically,
the cheeks and temples prove more sensitive to scarring. The
dermis of the eyelids is thinner but denser than the rest of the
face, and the dermoepidermal junction is flatter. The skin on
the back of the hand has few PSUs and little subcutaneous fat.
Atrophy develops there fairly rapidly. The skin on the back is
very thick, and its dermis is dense in collagen. Nevertheless, it
has fewer PSUs than the face, and the risk of developing post-
peel scars there is higher. The dermis of badly sun-damaged
skin has a depleted cell population, and is thin and slower at
detoxifying acids. The effect of the acids is therefore increased,
and peels on sun-aged skin are more dangerous than on young,
well-hydrated skin. Moreover, skin with actinic damage has
fewer appendages (PSUs) and tends to regenerate more slowly.
Healing is slower when a wound is left to heal in the open
air than when the wound is covered. This does not matter much
for intraepidermal peels but is more important when dealing
with medium or deep peels. One advantage that peels have over
laser treatments is that they leave a layer of dead, but protective,
skin in place, and this enhances reepithelialization. The strips
of skin that remain after a peel should be left alone, as they pro-
tect the regenerating skin. Lasers, on the other hand, gradually
vaporize the layers of skin to be removed, and the skin is left to
heal uncovered. The colloid dressings available on the market
(e.g., Convatec, Omniderm, Vigilon) allow better-quality heal-
ing, in a moist environment, after laser treatment. The prob-
lem with occlusive dressings is that there is an increased risk of
infection and they need to be monitored carefully, as bacteria
are known to proliferate much more quickly under an occlu-
sive dressing than in the open air. As bacterial proliferation
increases under occlusive dressings and as the skin’s immune
defenses are reduced after a deep peel, it is often preferable for
the skin to heal “under a scab.” To do this, a mask of bismuth
subgallate should be used (see Figure 4.1 and Chapter 35).
PREPARING THE SKIN
Preparation of this skin is worthwhile when the patient is
willing and when it is carried out under medical supervi-
sion. Unsupervised or secret use of aggressive products by the
patient can sometimes cause problems for the doctor who has
not been informed of the patient’s self-administered treatment.
The doctor should watch out for unacknowledged use of treti-
noin or other retinoids, concentrated glycolic acid, benzoyl per-
oxide, or any other product that increases penetration of the
acids, making them penetrate more quickly and deeply than
originally intended. Some patients come to their appointment
with their skin thoroughly scrubbed (with an abrasive sponge
or creams) to impress the doctor with skin that is clean, but
such skin is also hyperpermeable and dangerous.
SKIN COLOR
This must be taken into account when choosing a peel:
Fitzpatrick skin phototypes I–III can tolerate any kind of peel.
Patients of type IV with light-colored eyes have fewer problems
with dyschromia after a peel than dark-eyed patients of the
same type. Types V and VI patients are at most risk with peels,
and it is recommended not to go beyond the papillary dermis
with these patients to avoid hypochromia. Type V patients are
also quick to develop hyperpigmentation. Special care should
be taken with patients who have prolonged hyperpigmentation
with mosquito bites or small wounds.
Localized phenol peels should only be carried out on
patients with a skin phototype lower than IV, so that the area
treated with phenol is not left lighter than the surrounding
skin, even if it has been treated with a medium peel to even
out the color. The same applies to patients with many freckles,
which mostly disappear after a peel to the papillary dermis.
CHEMICAL PEELS FOR MEN
There is an increasing demand from men for basic treatments.
Their skin is thicker, and results are not as good as for women.
On the other hand, as men have more PSUs, they heal more
quickly and pose fewer risks of scarring. The fact that in most
cases they cannot use camouflage makeup makes it difficult to
perform a local or full phenol peel. Moreover, phenol peels pro-
duce less spectacular results on thick skins than on thin skins.
Shaving does not pose a problem, as a peel to the basal layer of
the epidermis does not rule out shaving, even with a blade. For
a peel to the papillary or reticular dermis, it is best not to shave
Figure 4.1  After a phenol peel, the crust of bismuth subgallate
appears dry but actually helps healing in a moist environment.

Factors influencing the skin’s reactions to chemical peels      31
while the skin is flaking. It is usually possible to shave after
the eighth day. Alcohol-based aftershaves should be avoided,
and a hydrating, antioxidant, or firming cream should be used
instead, followed by effective sun protection.
MAKEUP
Patients often ask about makeup. The general principle is that it
is possible to wear makeup, even when the skin is flaking, after
an epidermal peel or a peel to the basal layer, but it is unlikely
to look good. After a peel to the papillary or reticular dermis,
makeup is usually allowed, and even recommended, on the
eighth day. Patients who do not like wearing makeup should
be warned of the likelihood of postpeel erythema, depending
on the depth of the treatment. Some patients are thus ruled out,
as their professional lives do not allow any visible erythema or
they cannot stand the idea of wearing makeup. In these cases, it
is recommended to repeat an Easy TCA® peel four times rather
than use Unideep®.2
SMOKING AND PEELS
It is generally accepted that the free radicals produced each
time smoke is inhaled contribute to the overall aging of the
body and of the skin in particular. Publications that show the
difference in skin quality between two twins, one of whom is
a smoker and the other not, speak for themselves, so marked is
the deterioration of the smoker’s skin. Smoking causes repeated
vasoconstriction and chronic microvascular damage, which
contribute to the overall impoverishment and aging of the skin.
There are no major problems, however, with heavy smokers
who have peels to the papillary dermis. Full-face phenol peels
should be performed with caution because of the increased
risk of laryngeal edema. A localized phenol peel does not pose
this kind of problem, and phenol can, for example, be applied
around the edges of the mouth (which is usually very damaged
in smokers), while the rest of the face is treated with a trichloro-
acetic acid peel to the papillary dermis.
MENTAL RETARDATION AND PEELS
The more severe the patient’s retardation, the more superficial
the peel should be. The same applies to hypersensitive patients.
NUTRITION AND PEELS
The patient’s nutritional condition at the time of a peel is an
important factor in the treatment. For all the phases of heal-
ing to take place correctly, a perfect balance of nutrition and
micronutrition is necessary. It is clear that poor nutritional bal-
ance will have more impact on healing after a deep peel than
after a light peel, which is all the more important to note as
deep peels, rather than light peels, are usually intended for
older people. Many proteins are synthesized during healing
after an intraepidermal peel: many amino acids are needed to
form the provisional matrix as well as to synthesize new col-
lagen. Catabolic patients, or patients who have recently had
significant, involuntary weight loss, do not have sufficient pro-
tein reserves for the skin to regenerate properly. A dermal peel
also induces stress, which causes a hypercatabolic state that is
more or less acute depending on the depth of the peel. Patients
with insulin-dependent diabetes or patients who have recently
undergone significant trauma or surgery, who have liver or kid-
ney deficiencies, or who suffer from chronic inflammation are
not the best candidates for dermal peels, as the need for pro-
tein increases sharply. The average daily protein requirement
is 1.5 g/kg per day. The amino acids considered most essential
include arginine and glutamine. However, to date, it has not
been proved that supplements improve the quality of wound
healing. Arginine is a precursor of proline and collagen, and
the recommended dose is 15–25 g/day. It acts as a local stimu-
lant of lymphocytes and a general stimulant of human growth
hormone (HGH) and insulin-like growth factor I (IGF-I) pro-
duction. Glutamine also stimulates the production of HGH,
and is an antioxidant and an energy source for fibroblasts,
keratinocytes, lymphocytes, and macrophages. A daily intake
of 10–30 g/day is recommended.
Carbohydrates and fatty acids are also necessary for
rapid and good-quality skin regeneration. The extracellular
matrix is made up of glycosaminoglycans and proteoglycans,
which are polysaccharides linked to proteins. Omega-6 fatty
acids are essential for cell membrane formation. Supplements
of linoleic and linolenic acid can be recommended when the
patient’s blood is not properly balanced.3
Numerous trace elements are necessary for many
enzymes to function properly: copper is needed for the for-
mation of the collagen network and the antioxidant action of
superoxide dismutase; iron is needed for collagen synthesis;
zinc is a cofactor for DNA and RNA polymerases, plays a part
in protein synthesis, and stimulates cell division.
Vitamins also play a role in the healing process. Vitamin
A is involved in angiogenesis and keratinocyte differentiation,
stimulates collagen synthesis, and enhances intercellular adhe-
sion and skin immunity. Vitamin E can be used as a lipophilic
antioxidant. Vitamin C is necessary for collagen synthesis
and for stabilizing the collagen triple helix. Between 500 and
1000 mg/day can be given before and after an intradermal peel.
NOTES
1. Preventing laryngeal edema in smokers undergoing a phenol
peel.
2. Unideep (Skin Tech) TCA peel: to the papillary dermis, with a
qualitative formulation based on Easy TCA® but with a more
concentrated solution and postpeel cream.
3. The Roman Pais laboratory in Nivelles, Belgium, provides—
among other nutritional and micronutritional tests—a very pre-
cise and scientifically annotated blood count of circulating fatty
acids.

5
Selection of the right peel
The possibilities for treatment with chemical peels are many and
depend on the agent chosen as much as on the way in which it
is used. We can take a narrow view of peels as the destruction
of damaged tissue with acid.1 From this perspective, a result can
be achieved only by “destroying beneath the lesion.” This is,
of course, often the case, but we must not forget that chemi-
cal peels help to stimulate as much as destroy. Many of their
positive effects are largely due to this stimulation. Consider gly-
colic acid, for example, whose action is mainly intraepidermal2
but which is associated with activation of the papillary dermal
fibroblasts. The destructive effect, which removes the stratum
corneum and even part of the epidermis (depending on the
concentration used), improves the appearance of rough skin,
while the effects of remote stimulation improve the extracellular
matrix constituents secreted by the fibroblasts.
Choosing the right peel is often stressful for a doctor who
is starting his or her career in peeling: opting for a technique
that is too superficial will satisfy neither patient nor doctor,
while using a medium-strength product could cause unex-
pected side effects that can be hard to cope with, especially
if the results are mediocre. Deep peels have their own indica-
tions and risks. Sometimes, only a deep peel can solve a cos-
metic problem, but the level of complexity and danger of such
peels means that they are often rejected by beginners, who will
instead attempt to push the limits of a peel and do a medium
peel with an agent that is intended to be superficial. They will
often pay for the consequences in cash.
When choosing a peel, a simple equation should be
taken into account: the results expected from the peel must be
greater than the sum of the fear of the treatment’s complexity,
the risk of complications, and the downtime and financial cost
for the patient. The ratio [Results/(complexity + complications
+ downtime + cost)] must always be positive. During the pre-
liminary consultation, the doctor should first discuss down-
time and treatment cost with the patient, who always expects
breathtaking results. It is easier to deal with these two factors
first before embarking on the complexity of the technique and
the potential risks and complications. In this way, the treatment
can quickly be oriented to what the patient is prepared to go
through. If patients immediately say that they cannot accept
any downtime or have limited funds, it is pointless to waste
their time, which is as precious as yours, explaining unneces-
sary technical details about deep peels.
A few logical rules make it easier to choose the right peel
(see Table  5.1). Nothing speaks louder than pictures when it
comes to chemical peels. We will look at different clinical cases
to discuss the choice of an appropriate peel.
START OF PHOTOAGING
The patient shown in Figure 5.1, who is approaching 40, has
a few lentigines and a thick and oily skin with dilated pores.
There are no wrinkles but a slight sagging of the skin that is
only noticeable in a standing position.
A deep peel would not be the best way to treat this
patient, as the ratio of results to complexity + complications +
downtime + cost would not be favorable. The possibility of a
medium peel to the papillary dermis could be discussed, if the
patient wanted fairly quick results or if she did not have enough
time for a series of lighter peels. She could also be advised to
have a series of peels, either intraepidermal (to remove the epi-
dermis) or down to the basal layer, combined with appropriate
daily care.
Another possibility would be one alpha hydroxy acid
(AHA) peel per week for 6–10 weeks or one Easy TCA® (pin-
point frosting) per week for 4 weeks.3 The daily care routine
should include DMAE4 to firm the skin, tyrosinase inhibitors
and antioxidants to limit melanin production,5 and, of course,
effective sun protection. If the lentigines do not clear quickly,
they should be treated locally with a single careful application
of Only Touch®, immediately before the last of the four Easy
TCA peels.
UNDER-EYE BAGS
Many patients want to get rid of or improve under-eye bags
(Figure 5.2) that leave them looking permanently tired. This
is a purely surgical problem, although it has been suggested
that local injections of phosphatidycholine could dissolve the
fat, but this treatment can be very risky.6 Peels and cosmetic
products cannot improve them. In some circumstances, a
phenol peel can improve bluish circles under the eyes if it
succeeds in making the thin skin in this area thicker. The best
treatment is to remove the weak veins of the inner and outer
canthus with a Müller hook, followed by treatment with blue
laser light.7
SAGGING SKIN
Apart from an improvement in overall skin quality and tone,
the patient shown in Figure 5.3 will not benefit from any peel-
ing technique—either repeated superficial peels or a deep phe-
nol peel. Actinic damage is light and there are not many lines or
wrinkles. On the other hand, the folds of sagging skin are very
marked in this patient, who is a heavy smoker. Examination
and palpation show that the dermis has emptied of its ground
substance and atrophied. The daily care routine should com-
bine powerful antioxidants,8 DMAE, and possibly DHEA. This
patient refused to have any surgical treatment and was treated
with a phenol peel in an attempt to get the skin to retract.
Unfortunately, on a dermal base totally emptied of ground sub-
stance, this treatment resulted in an “accordion effect.”9 This
patient would only benefit cosmetically from a surgical face-
lift, possibly followed by peels to the Grenz zone to improve the
quality of the skin.

Selection of the right peel      33
The patient in Figure  5.4, on the other hand, received
much benefit from the stimulating and evening effect of Easy
Phytic on the epidermis and dermis.
The skin tension is better and the yellow discoloration
caused by actinic damage has been reduced. The daily care rou-
tine also consists of Actilift (DMAE cream) and DHEA-Phyto;
see Chapters 2 and 3 for more information on these two prod-
ucts. When retightening is indicated, Easy Phytic can be applied
in a single layer every morning for several days, depending on
how the skin reacts. The results are surprisingly quick, and the
skin soon tightens visibly (see Chapter 11).
Table 5.1  Choosing an Appropriate Peel
Sagging skin
Better treated by surgery. Deep phenol peels are the ones giving the best results in term of skin tension but only
if the skin is relatively thin. Peels are not indicated for sagging in thick skins, or for nasolabial folds or for the
neck. Chemical peels cannot compete with surgical face-lifts when it comes to sagging skin; they cannot
stretch the skin as well as the latter do. Results are often disappointing when we want to act on the oval
shape of the face by performing peelings.
Neck
Responds poorly to chemical peels. Results are positive when we want to act on photoaging signs.
Expression wrinkles
Benefit from treatment with botulinum toxin prior to any peel; it allows the skin to regenerate on a nonmoving base.
Photoaging and
free-radical aging from
smoking and pollution
Can be treated with a peel; the speed and quality of the results depend on the depth of the treatment.
Active acne
Should only be treated by a medium peel after it has been treated medically and the infection has cleared up;
it can, however, be treated by lighter peels during the active infectious phase. Easy TCA allows a treatment of
the active phase of acne, as well as AHA peels (see Chapter 17).
Facial acne scars
Difficult to treat, sometimes even with a deep phenol peel. Acne scars on the back, décolletage, or face can
fade or improve with a very deep combined technique of chemical peeling and dermabrasion (anterior
chemoabrasion). It is still difficult, however, to eliminate them completely.
Hyperpigmentation
disorders
Results depend entirely on the depth of the problem and the depth of the treatment. They are frequently treated
with peels that reach or go beyond the Grenz zone, in conjunction with appropriate daily care. The only way to
treat melasma permanently is by completely destroying the cells that produce melanin, by peeling “beneath
the lesion” with an agent that is toxic to melanocytes, which is a fairly aggressive treatment. Another option is
to treat the skin more superficially to reduce the risk of complications. Only a certain proportion of
melanocytes are destroyed to lighten the melasma at the same time as stimulating keratinocyte turnover. The
relative increase in the number of keratinocytes compared with the number of melanocytes dilutes the
melanin produced in the epidermal cells (the blending effect). Melanogenesis is reduced with tyrosinase
inhibitors and antioxidants, which are applied in the long term and combined with effective sun protection
(bleaching effect).
Solar or senile
lentigines
Respond partially to peels to the Grenz zone and the papillary dermis. They sometimes require a focal peel to
the reticular dermis to eliminate them completely. This deep peeling can be local (see Chapter 22).
Stretch marks
Can only be treated definitively by applying aggressive treatments that can improve the epidermal and dermal
atrophy that accompanies them.
Hypertrophic scars
Peels are not indicated; treatment using corticoids intralesional injections and permanent compression with a
silicone sheet give the best results. Some fine facial scars (from a face-lift, for example) improve vastly after
local application of some phenol peels; others are improved by a combination of abrasion and peeling.
Body peels
Produce fewer results and more problems than facial peels.
Peels on the backs of
the hands
Very easy and cause few complications, for example with trichloroacetic acid in the form of Easy TCA, following
a specific protocol (see Chapter 19).
Figure 5.1  Stimulating superficial peels and appropriate daily
care are indicated for this patient.
Figure 5.2  A peel is not an indication for under-eye bags.

34      Textbook of Chemical Peels
COMEDONAL ACNE
Comedonal acne (Figure 5.5) can be treated with an intraepi-
dermal peel or a peel to the basal layer. A trichloroacetic acid
(TCA) peel to the papillary or reticular dermis could be consid-
ered, but such a deep treatment would be pointless for this type
of disorder, which can be treated with a lighter peel and, in any
case, requires long-term maintenance treatment.
It is essential to “clean” the skin beforehand with a com-
edone extractor to limit damage to the skin; the skin should
be cleaned in this way a week before an alpha hydroxy acid
(AHA) peel10 or immediately before each of four Easy TCA
peels. Removing the comedones helps produce quicker results
and prevents postpeel infections.
Macrocomedones and Large
Comedones (1–2 mm in Diameter)
These can be treated locally with Only Touch, a solution with
a high concentration of saponified and stabilized TCA. Either
the applicator provided with the product or the point of a
30G1/2 needle should be used to limit the action precisely
to the head of the comedone. In 95% of cases, comedolysis is
achieved. Macrocomedones (>2 mm in diameter) can benefit
from careful infiltration of Easy TCA or Easy Phytic solution
into the center of the comedone. Postpeel care, which is very
important, consists of avoiding comedogenic cosmetics;
having the skin cleansed professionally once a month; and
applying an anti-acne cream containing AHAs, tretinoin or
precursors, disinfectants, anti-inflammatories, tea-tree oil,
and so forth11 once or twice a day. For details of this treatment,
see Chapter 15.
LENTIGINES, ACNE, AND DYSCHROMIA
The patient shown in Figure  5.6(a) has numerous treatments
to choose from. She does, however, have an important restric-
tion to take into account: downtime must be minimal and the
overall cost low. Resorcinol, TCA to the papillary dermis, and
phenol are all automatically ruled out. However, a relatively
strong acid is needed to treat the lentigines that can be seen
at the top of Figure 5.6(a). For this, Only Touch can be used,
applied locally and precisely on the lentigines, with Easy TCA
being applied on the rest of the face to treat the dyschromia,
superficial lentigines, photoaging, and acne and to even out
the result. See Chapter 15 for details on applying this product.
Daily postpeel care should consist of an anti-acne cream and a
blending and bleaching cream to even skin tone. Figure 5.6(b)
shows the lentigines clearing up, an improvement in the overall
appearance of the skin, and the dyschromia evening out. This
improvement can still be seen 1 year after treatment.
Nevertheless, focal application of a deep TCA peel
induces 2 weeks of crusting and could induce long-term red-
ness on the facial skin, with potential postinflammatory hyper-
pigmentation (PIH). Therefore, we actually prefer treating it
using a “mosaic” technique: Easy TCA is applied focally, until
inducing a focal white frosting. After that, Easy TCA is applied
on the full face to obtain a uniform result.
PHOTOAGING
The more severe the photoaging, the more important it is to
consider the depth of the peel. The patient shown in Figure 5.7
Figure 5.3  General sagging of the skin with little actinic damage;
this is not a good indication for a peel.
(a)
(b)
Figure 5.4  (a, b) A moderate improvement in sagging skin can
sometimes be achieved by applying superficial peels: here, after
three Easy Phytic peels.
Figure 5.5  Comedonal acne.

Selection of the right peel      35
has a light skin type that is sensitive to the sun’s rays. She
has developed a number of solar lentigines and fine wrinkles
caused by UV rays. The eyelids are very wrinkled and the naso-
labial folds and marionette lines are slack.
In the long term, this patient’s nasolabial folds and mar-
ionette lines will only improve slightly, even with a deep peel.
Other techniques12 should be used to treat them. There are
many peels to choose from. The wrinkles on the lower eyelids
can be softened with a TCA peel to the Grenz zone (Easy TCA)
or to the papillary dermis (Unideep), but only phenol can be
guaranteed to get rid of them. Many lentigines respond to a
TCA peel to the basal layer of the epidermis, the majority to
a TCA to the papillary dermis, while the deepest should be
treated to the reticular dermis. Fine wrinkles on the cheeks
can improve with TCA,13 but only phenol can really eliminate
them and tighten the skin. There are two choices of treatment
open to this patient. The first option would be an aggressive
treatment, to be done in a single session: a full-face phenol
peel that will treat all the symptoms of photoaging at once
and tighten the skin. If the patient opts for this treatment, she
must accept at least 8 days’ downtime and a high treatment
cost. The second option is a less aggressive, more gradual and
stimulating treatment that can be combined with a local phe-
nol peel on the lower eyelids. Only Touch is applied locally
on the deeper lentigines and Easy TCA on the rest of the face
to even out the result and improve the fine wrinkles. A local-
ized phenol peel on the lower eyelids14 is recommended if the
patient wants to get rid of her eyelid wrinkles. If this course
of action is chosen, the possibility of combining a localized
phenol peel with Unideep, a TCA peel to the papillary dermis,
should be discussed. With phenol, the downtime is 8 days and
it might be more appropriate to combine the local phenol peel
with a single session of Unideep® that has a downtime of 5–6
days, instead of having four weekly sessions of Easy TCA.
As the results are comparable,15 the decision is often based
on cost or the risk of complications, which is higher with a
dermal peel. Depending on requirements, daily postpeel care
should include a vitamin E antioxidant cream, a blending and
bleaching cream, and/or a DMAE cream.16 Some solar and
senile lentigines may only respond to peels to the reticular
dermis as, histologically, the lentigines may be characterized
by deep dermal papillae and elongated rete ridges with golf
club–shaped extensions.
POSTINFLAMMATORY
HYPERPIGMENTATION AND SCARRING
The patient shown in Figure 5.8(a) was in a serious road acci-
dent 6 years before the treatment. The surgeon did a perfect job
given that the patient’s face had been completely lacerated by the
car’s windshield. Severe post-traumatic inflammation quickly
turned into PIH that the patient hid for years under camou-
flage makeup. Given the extent of the problems to be treated, a
full-face phenol peel was initially suggested but was then ruled
out because of the high cost of the treatment. The glabellar scar
Figure 5.7  More severe photoaging.
(b)
(a)
Figure 5.6  Combination of lentigines, acne, and dyschromia. (b) Results 1 year after combining Easy TCA and Only Touch.

36      Textbook of Chemical Peels
could not be improved by anything but a phenol peel, which
was then applied locally, as can be seen in Figure 5.8(b): this
photograph shows the pure white frosting resulting from the
local application of phenol. The skin color was evened out by
applying four Easy TCA peels until a cloudy white frosting was
achieved, combined with Blending Bleaching Cream that was
applied twice a day from the day after the first peel and contin-
ued for at least 6 months (Figure 5.8c). An effective sunscreen
(see Chapters 3 and 35) must be applied every day between
the four weekly peels and until the end of the maintenance
treatment.
SEVERE AGING OF THE SKIN
The patient shown in Figure 5.9 has thin skin marked by expres-
sion wrinkles, sagging skin, and photoaging. Using a peel that
does not reach the dermis is always disappointing in cases like
this. Some light peels might tighten the skin temporarily as a
result of the edema that occurs afterward. It would be impos-
sible to attempt to correct all of these wrinkles, even by fre-
quent repetitions of an intraepidermal peel or even a peel to the
Grenz zone. A peel to the papillary dermis might improve the
finer wrinkles and the quality of the skin, but only a full-face
phenol peel could tighten the skin definitively through a “three-
dimensional facelift.”17 The expression wrinkles should be
treated first—1 week before the phenol—with botulinum toxin,
which will allow the skin to regenerate without the movements
that would soon reimprint the wrinkles on a healing dermis.
PERIORAL WRINKLES
Perioral wrinkles (around the upper lip and chin) only respond
to very deep peels (Figure  5.10). Many different agents have
been tried, such as pyruvic acid, which has a high potential for
scarring. This particular agent, which is difficult to control in
concentrated solutions, is rarely used.
Chemical cheiloplasty can only be considered under
three conditions:
The natural skin color allows treatment without the risk of pig-
mentary changes.
The skin around the area to be treated is in good enough condi-
tion that the demarcation line will not be too obvious.
Other treatments (i.e., hyaluronic acid, collagen, etc.) would
have no effect.
Patients with skin phototype above IV are therefore ruled
out from this treatment, as are patients with a light skin photo-
type but a lot of freckles18 and patients whose skin is severely
photoaged. Phototype IV patients should make a choice
between deep wrinkles and a possible depigmentation.
Lip & Eyelid Formula was originally developed to treat
only the lips and eyelids before its indications were extended
to the full face. It can be applied locally without nerve blocks or
any kind of anesthetic (see Chapter 36). A TCA Unideep peel (to
the papillary dermis) is applied to the rest of the face immedi-
ately after the phenol peel has been applied locally (Figure 5.11).
(c)
(b)
(a)
Figure 5.8  (a) Post-traumatic scars and hyperpigmentation. (b) Following treatment with a local phenol peel. (c) Four Easy TCA peels and
Blending Bleaching Cream were applied to even out the skin color.

Selection of the right peel      37
Figure 5.9  Result at 3 months average, after one Lip & Eyelid full face deep phenol peeling.
(a)
(b)
(c)
Figure 5.10  (a) Deep wrinkles on the upper lip and chin. (b) Bismuth subgallate powder mask during the first few days after a phenol peel.
(c) Results after treatment of these wrinkles with Lip & Eyelid Formula (phenol peel—chemical cheiloplasty).

38      Textbook of Chemical Peels
The Unideep must not come into contact with the skin that has
been treated with phenol.
Botulinum toxin often has to be used at the same time
as a deep peel on patients with thick skins to limit the contrac-
tions of the orbicular muscle of the lips and to improve/main-
tain results. The horizontal fold between the lower lip and the
prominence of the chin does not usually respond well to peels,
even deep ones. It can easily be filled in, however, together with
the nasolabial folds 1–2 months after the phenol peel.
DERMAL ATROPHY
The wrinkles on the cheeks of the patient shown in
Figure  5.12(a) have been caused by dermal and hypodermal
atrophy. Only a deep peel could improve the cosmetic appear-
ance of this patient. Dermal fillers are, however, another pos-
sibility for treatment. Figure  5.12(b) shows the rejuvenating
effect of injecting 2.5 cm3 of Bioalcamid®19 in each cheek. The
deep wrinkles have completely disappeared and the shape of
the face has been restored to look like it did in a photograph
of the patient when younger. Note the persistent bruising in
the injected areas. This bruising can largely be avoided by
using a trocar or blunt-tipped needle instead of a conventional
needle. This treatment can of course be combined with a peel:
Bioalcamid can be used perfectly safely with Easy TCA in the
same session. The peel is performed after the liquid implant
has been injected. A deeper peel, on the other hand, should
only be applied a few weeks after the filling to avoid interfer-
ence with the necessary process of encapsulation that fixes the
filler material in place.
DEEP WRINKLES
If the patients in Figures 5.13(a) and 5.14(a) want quick rejuve-
nation that will last around 15 years, a phenol peel is the only
indication (Figures 5.13b and 5.14b). The extent of the problems
(a)
(b)
Figure 5.11  (a, b) Wrinkles on the upper lip treated with a single application of Lip & Eyelid, with the rest of the face being treated with a
Unideep peel in the same session. Note the excellent results for facial skin tension with TCA.
(b)
(a)
Figure 5.12  (a) This patient’s wrinkles are caused by severe skin atrophy. A peel is not the best indication. (b) Results of treatment with
a dermal filler: 2.5 cm3 of Bioalcamid in each cheek.

Selection of the right peel      39
(a)
(b)
Figure 5.13  (a) Deep wrinkles. (b) Results after a session of full-face Exoderm®.
(b)
(a)
Figure 5.14  (a) Deep wrinkles. (b) Results after a full-face phenol peel; second treatment of the upper lip.

40      Textbook of Chemical Peels
would be beyond dermal fillers, and if these were used, the
results would be temporary. Botulinum toxin, used alone,
would only partially improve the areas around the eyes, lips,
and cheeks. A surgical facelift would tighten the neck and the
cheeks, but it would not treat the crow’s feet satisfactorily and
would have no effect at all on the wrinkles on the lips and the
overall skin quality. A light peel would only improve skin qual-
ity and even out skin tone, but would not get rid of the wrinkles.
A peel to the papillary dermis would have a similar and more
noticeable effect, but would not eliminate the deep and long-
standing wrinkles. An experienced doctor could use full-face
dermabrasion. Full-face carbon dioxide laser treatment used to
be very popular but is gradually being abandoned because of
the serious complications faced by both patients and doctors. A
phenol peel will treat the sun-damaged skin and tighten these
patients’ faces. An inexperienced doctor should not, of course,
use this type of peel. Treating the deep wrinkles on the upper
lip often calls for a combination of techniques: phenol plus
dermabrasion, phenol plus botulinum toxin, second phenol
treatment, and so on.
MELASMA
Many techniques are now available for treating melasma.
Some are more aggressive, some more effective, and others
more costly or complex. Only one technique can provide a
definitive and effective treatment in one single session: a
phenol peel. After a phenol peel, melanocytes can no longer
produce melanin. If we rule out this treatment, which would
be extreme for melasma alone, then the basic principle is rela-
tively clear, if not always 100% effective. The existing mela-
nin reserves must be eliminated by carrying out one or more
peels, and melanin must be prevented from building up again
by long-term topical postpeel treatment and effective sun pro-
tection. How quickly the melanin reserves can be eliminated
depends on the strength of the peel: an intraepidermal peel
will be extremely slow, a peel to the basal layer will be slow, a
peel to the Grenz zone will be quicker, and a peel that destroys
most of the papillary dermis will be quicker still. This progres-
sion raises the following problems: if the peel acts too slowly,
either the patient will tire of the treatment, or the skin, once
exposed to the sun’s rays, will resynthesize the melanin as it is
being eliminated; if the peel is deeper, to the papillary dermis,
and the inflammation is not controlled, the skin might react
and develop PIH.
In any event, success depends on sun protection/avoid-
ance and long-term topical treatment. Patients who refuse to go
through with postpeel care should not be accepted for melasma
treatment. The choice of treatment for the patient shown in
Figure  5.15(a) was four sessions of Easy TCA (Figure  5.15b).
The solution was first applied to the melasma spots until cloudy
white frosting appeared; it was then applied to the whole face
to even out skin tone.20 One session was done per week. Anti-
tyrosinase and antioxidant Blending Bleaching Cream was used
(b)
(a)
Figure 5.15  (a) Melasma before treatment. (b) After four Easy TCA peels and Blending Bleaching Cream.