Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself

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Open AccessResearch Article
Allergy & Therapy
Eberting et al., J Allergy Ther 2014, 5:5
http:/t/dx.doi.org/10.4172/2155-6121.1000187
J Allergy Ther
ISSN:2155-6121 JAT an open access journal Volume 5 • Issue 5 • 1000187
Keywords: Skin barrier repair; Ceramide; Phytosphingosine;
Cholesterol ester; 18-β Glycyrrhetinic acid; Niacinamide; pH; Calcium
chelation; Silicone; Paran
Abbreviations: ACD: Allergic Contact Dermatitis; AD: Atopic
Dermatitis; AHAs: Alpha Hydroxy Acids; GLU: Gluconolactone; ICD:
Irritant Contact Dermatitis; PPAR: Peroxisome Proliferator Activated
Receptor; TEWL: Transepidermal Water Loss
Introduction
A compromised skin barrier plays a major role in many dermatoses
including irritant and allergic contact dermatitis, atopic dermatitis,
dry skin, aged skin, xerosis, rosacea, and acne [1–5]. Many of these
conditions share common defects in the skin barrier and an association
with inammation [4,6]. e knowledge we have regarding specic
lipid deciencies, pH aberration, inammation, irregular calcium
gradients, and susceptibility to contact sensitization can be leveraged to
address many aspects of the disrupted skin barrier. By addressing these
major points of vulnerability the skin’s inherent ability to heal itself can
be optimized for skin barrier repair.
Dermatitis is a term that includes irritant and allergic contact
dermatitis, atopic dermatitis and many other conditions that are
explained by skin barrier disruption and dysfunction. An association
with inammation and, in many cases, exacerbation from chemical
irritants and allergens is common (Figure 1). We will discuss the
commonalities of skin barrier compromise in dermatitis and other
forms of skin barrier disruption. We will discuss the role that skin
barrier dysfunction plays in these conditions, how to leverage the
strengths of the skin’s barrier repair pathways to stimulate skin barrier
repair, and the optimal features of skin barrier repair products.
ACD and ICD are associated with skin barrier defects that may be
a result of exogenous (the nature of an irritant or allergen, exposure
concentration, duration, chronicity, and other mechanical factors) and
endogenous factors [7]. In atopic dermatitis, there are several known
inherent skin barrier defects including specic lipid deciencies
and llagrin null mutations [8–10]. ough the specic etiology of
ACD, ICD and AD may be variable, all three conditions have similar
deciencies that drive the disease state. All three conditions are
initiated as a result of skin barrier defects that lead to the activation of
inammatory mediators such as IL-1 and TNFα [5,11,12]. ese pro-
inammatory mediators set into motion inammatory cascades in an
eort to induce reparative processes and restore skin barrier function
[13]. Unfortunately, the role of inammation may overshoot the skin
barrier repair mechanisms and result in dry, scaly, inamed, and
irritated skin.
For protection, the skin utilizes the following types of barriers:
physical, biochemical, redox, and immune [4]. e epidermis makes
up the physical barrier that is the rst line of defense, mostly attributed
to the protective eects of the stratum corneum which includes the
lipid bilayer, the acid mantle (one contributor to the acidic pH of the
epidermis), a calcium gradient which inuences desquamation and
cellular turnover and dierentiation of the epidermis, and the many
aspects of the cutaneous immune system [14]. e epidermis is able to
provide protection from solids, liquids, and gases in addition to warding
o attacks from viruses, bacteria, fungi, and other microbes [15].
Points of Vulnerability
A disrupted skin barrier has many points of vulnerability including
excessive water loss, slow/decient lipid production, an imbalance in
content and ratio of skin lipids, a dry skin barrier, an elevation of pH,
susceptibility to infection and inammation, and susceptibility to contact
sensitization [16–19]. ere have been many approaches to induce and
enhance skin barrier repair in chronic dermatitis. Some products have
focus on skin barrier protection or physiologic skin lipid replacement
or inammation. To eectively heal the skin barrier, trans-epidermal
water loss (TEWL) must be minimized and the skin must be protected
*Corresponding author: Cheryl Lee Eberting, 144 South Main St. Suite
300, Alpine, Utah 84004, USA Tel: 8017637107; Fax: 8017637607; E-mail:
CherylLee@CherylLeeMD.com
Received May 16, 2013; Accepted August 11, 2014; Published August 18, 2014
Citation: Eberting CL, Coman G, Blickenstaff N (2014) Repairing a Compromised
Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself. J Allergy Ther
5: 187. doi:10.4172/2155-6121.1000187
Copyright: © 2014 Eberting CL, et al. This is an open-access article distributed
under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Abstract
Skin barrier defects play a major role in many dermatoses including irritant and allergic contact dermatitis, atopic
dermatitis, dry skin, aged skin, xerosis, rosacea, acne and more. Skin barrier repair technology has heretofore
focused on physiologic skin lipid replacement and skin protection without addressing the myriad other areas of
compromise such as an elevated pH, balance of the microbiome, inammation, succeptibility to infection, aberrant
calcium gradients and the proclivity for contact sensitization. By changing the paradigm from physiologic skin lipid
supplementation to that of supplementing the epidermis with lipids that have recently been found to be particularly
decient from the disrupted skin barrier, and by simultaneously addressing the many facets of vulnerability, the skin
barrier can be effectively repaired. This model of advanced skin barrier repair wherein physiologic deciencies are
supplemented and/or augmented may be an effective method for restoring the ability of xerotic and dermatitic skin
to heal itself.
Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the
Skin’s Ability to Heal Itself
Cheryl Lee Eberting1*, Garrett Coman2 and Nicholas Blickenstaff2,3
1CherylLeeMD, Sensitive Skin Care, Alpine, Utah, USA
2,3University of Utah School of Medicine, Salt Lake City, Utah, USA

Citation: Eberting CL, Coman G, Blickenstaff N (2014) Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself.
J Allergy Ther 5: 187. doi:10.4172/2155-6121.1000187
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ISSN:2155-6121 JAT an open access journal Volume 5 • Issue 5 • 1000187
from further contact with irritants, allergens, and infectious organisms
[20]. Ideally, the skin pH would be optimized to encourage natural
ceramide production and to discourage the growth of pathogens while
encouraging the growth of a healthy microbiome [21,22]. Modulation
of the disrupted calcium gradient may restore appropriate levels of
desquamation [23]. Inammation must also be minimized while all
sensitizers, irritants and proinammatory mediators should be avoided
[24]. By addressing all of these points of vulnerability simultaneously,
the skin’s ability to itself may be optimized.
Skin Barrier Heal
Current medical and scientic literature provides insight to the
characteristics, features, and classes of ingredients able to address the
aforementioned vulnerabilities of the disrupted epidermis in chronic
dermatitis.
Lipid Replacement
Close examination has revealed that much of the barrier protection
from the epidermis comes from stratum corneum lipids. e lipids are
arranged in a highly organized structure with controlled ratios. When
these ratios or structure are interrupted or unbalanced, barrier function
is compromised which gives microbes and allergens unencumbered
entrance to the deeper layers of the skin where inammatory pathways
are triggered [15,25].
Current therapeutic options include products which address skin
barrier repair by supplementing the skin with lipids in physiologic
ratios, while other products have employed behentrimonium
methosulfate, a cationic surfactant quaternary ammonium salt, as
part of a dynamic lipid delivery system [20,26]. Several specic lipid
deciencies have been elucidated in many forms of chronic dermatitis.
Phytosphingosine-containing ceramides such as ceramide 3 [27–29],
and possibly phytosphingosine itself are decient in conditions such
as dry skin, aged skin, and in atopic skin. In fact, as dryness levels of
the skin increase, so does the degree of phytosphingosine-containing
ceramide deciency [27,30,31]. Marked deciency in ceramide 3
(N-Acyl phytosphingosine) has also been well-documented in atopic
skin and correlated to increased TEWL [32].
Cholesterol esters are decient relative to cholesterol in xerotic skin
[33] and in SDS-induced dry skin (Figure 2). e overall sterol content
is preserved, but the ratio of cholesterol to cholesterol esters is increased
with an excess relative concentration of cholesterol [27,33]. When
SDS-induced dry skin treated with 1% cholesterol base was compared
to 1% cholesterol ester base, the cholesterol ester treated skin showed
improved conductance values while the cholesterol-treated skin did
not [34]. Atopic skin has also been shown to have abnormally elevated
levels of cholesterol [32]. Cholesterol esters are esteried to short,
medium, long, and very long chain fatty acids. Based on these studies
of chronic dermatitis conditions where the cholesterol:cholesterol ester
ratio has been shown to be elevated as compared to normal skin, it may
be optimal to supplement the skin with cholesterol esters rather than
with cholesterol as has traditionally been done by many physiologic
skin lipid replacement products. Indeed, it may not be necessary
and may possibly be less ecacious, to supplement, xerotic, atopic,
and SDS-induced dry skin with unesteried cholesterol, because the
cholesterol:cholesterol ester ratios in these conditions have been shown
to be abnormally elevated. (Figures 2-5) Of note however, cholesterol
itself was shown to aid barrier recovery in a tape stripping model in
aged skin, but not in young skin [35]. e aged skin in this study was
not controlled for ingestion of cholesterol lowering medications. Of
note, a disease of unknown etiology in aged skin, Grover’s disease, is
Figure 1: The epidermal barrier plays an important role in many dermatoses. Copyright of Cheryl Lee Eberting, M.D.

Citation: Eberting CL, Coman G, Blickenstaff N (2014) Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself.
J Allergy Ther 5: 187. doi:10.4172/2155-6121.1000187
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ISSN:2155-6121 JAT an open access journal Volume 5 • Issue 5 • 1000187
frequently beneted from cholesterol ester-containing skin barrier
repair products. Author’s experience, CLE (Figure 6).
Fatty acid deciency also contributes to a disrupted skin barrier.
Long chain fatty acids like palmitic (C16) and stearic acids (C18) are
known to be decient in atopic skin [36], but more recent studies have
shown a particular deciency in the very long chain fatty acids cerotic
(C26) montanic, (C28), and melissic (C30) acids [37]. Very long chain
fatty acids are naturally occuring in candelilla wax. Candelilla wax
is accessible, aordable, and has only one reported case of contact
sensitization [38].
Inammation
e use of molecules with inherent anti-inammatory qualities has
been shown to be eective in many forms of skin barrier disruption
[39]. Glucocorticoids are most commonly prescribed for this purpose,
but non-glucocorticoid molecules also show anti-inammatory
qualities [40]. An over the counter petrolatum and lanolin-based
product that employs bisabolol as an anti-inammatory agent has
shown comparable ecacy to a prescription medical device cream [41].
Increasing numbers of contact sensitization to this product are being
reported in patients who are using it to treat dermatitis. ose who
are sensitized to bisabolol should be counseled to avoid any bisabolol-
containing products [42–44].
18β-Glycyrrhetinic acid exhibits corticosteroid-like anti-
inammatory, anti-allergic activity, and many other benets in
contact dermatitis. In vitro, glycyrrhetic acid is known to inhibit Δ4β-
reductase, an enzyme that competitively inactivates steroid hormones,
and 11β-hydroxysteroid dehydrogenase, an enzyme that deactivates
cortisol [45]. Inhibiting the metabolism of naturally occurring cortisol
enhances the body’s natural anti-inammatory capacity by potentiating
the activity of endogenous (and possibly even exogenously applied)
corticosteroids. When used in formulation by it or with a glucocorticoid,
glycyrrhetinic acid may augment and extend the eectiveness of
glucocorticoids, allowing the use of less-potent glucocorticoids and/or
a shorter course of treatment. is could limit overall glucocorticoid
exposure and associated side eects. When a metabolic precursor to
18β-glycyrrhetinic acid was given intraperitoneally, it suppressed
contact dermatitis in mice with higher ecacy than prednisolone.
When administered orally, it was ineective [46]; possibly highlighting
the necessity to deliver the active molecule directly to the area of
contact dermatitis. is same molecule is bactericidal to MRSA and has
anti-candidal eects [47,48], a benecial characteristic when treating
disrupted skin that particularly is susceptible to these organisms.
is molecule has skin brightening and lightening eects [49] and
thus may have additional benets for dermatitis associated with
Figure 2: Irritant “Lip-licker’s Dermatitis” Before and eight hours after
a single application of a preservative-free ointment that contains skin
barrier lipids, isostearyl isostearate, petrolatum, parafn wax and 18-β
glycyrrhetinic acid. Photos copyright of Cheryl Lee Eberting, M.D.
Figure 3: Atopic and allergic contact dermatitis due to lanolin. R. arm was
treated with 0.1% Triamcinolone ointment and L. arm was treated with
a preservative-free ointment that contains skin barrier lipids, isostearyl
isostearate, petrolatum, parafn wax and 18-β glycyrrhetinic acid. Photos
copyright of Cheryl Lee Eberting, M.D.
Figure 4: Severe Xerosis before and 30 seconds after application of a
preservative-free ointment that contains skin barrier lipids, isostearyl
isostearate, petrolatum, parafn wax 18-β glycyrrhetinic acid. Photos
copyright of Cheryl Lee Eberting, M.D.
Figure 5: Atopic Dermatitis before and after ten days twice daily application
of a hypoallergenic skin barrier repair cream that contains skin barrier
lipids, isostearyl isostearate, petrolatum, niacinamide, gluconolactone,
18-β glycyrrhetinic acid, gluconolactone and EDTA. Photos copyright of
Cheryl Lee Eberting, M.D.
Figure 6: Grover’s Disease before and after ten days of twice daily
application of a preservative-free ointment that contains skin barrier lipids,
isostearyl isostearate, petrolatum, parafn wax and 18-β glycyrrhetinic
acid. Photos copyright of Cheryl Lee Eberting, M.D.

Citation: Eberting CL, Coman G, Blickenstaff N (2014) Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself.
J Allergy Ther 5: 187. doi:10.4172/2155-6121.1000187
Page 4 of 8
J Allergy Ther
ISSN:2155-6121 JAT an open access journal Volume 5 • Issue 5 • 1000187
post-inammatory hyperpigmentation in light and darker-skinned
individuals [49]. is molecule also has photoprotective benets. Aer
UV exposure, it reduced ROS, NF-KB, cytochrome c, and caspase 3
levels and inhibited hyaluronidase, possibly by inhibition of MMP1
activation by modulating NF-KB signaling [50]. Feeding mice with this
molecule prior to UVB radiation caused delays in tumor appearance,
multiplicity, and size [51]. is molecule also oers protection from
UVB radiation damage in humans [52].
Niacinamide, a B vitamin and possible Peroxisome Proliferator-
Activated Receptor (PPAR) ligand, has been shown to up regulate
llagrin and involucrin synthesis [53]. It has been proven eective
in the treatment of many forms of a disrupted skin barrier [54-
56]. Niacinamide also suppresses antigen-induced lymphocytic
transformation, an added benet that may minimize rates of
contact sensitization. Niacinamide also inhibits 3'-5' cyclic AMP
phosphodiesterase, and blocks the inammatory actions of iodides
[57]. Niacinamide increases the thickness of the epidermis [58]
while inducing de novo ceramide production through up-regulated
expression of serine palmitoyltransferase, the rate-limiting enzyme in
sphingolipid synthesis [59]. Ceramides are eective in blocking the
reduction, and even stimulating the synthesis, of collagen aer UV
irradiation [60]. Niacinamide shows improved facial wrinkle appearance
and tolerability compared to tretinoin [61]. Additionally, a niacinamide-
containing moisturizer applied with tretinoin therapy enhanced the
response to tretinoin, improved the stratum corneum, and decreased
tretinoin-associated side-eects [62]. Niacinamide is well tolerated
by the skin and provided signicant improvements versus control in
ne lines/wrinkles, hyperpigmentation spots, texture, red blotchiness,
elasticity, and skin yellowing versus an oil in water moisturizer control
[63,64]. Both niacinamide and 18-β glycyrrhetinic acid are optimal
anti-inammatory molecules for optimizing repair of the compromised
skin barrier.
pH Modulation
e pH of the epidermis becomes abnormally elevated in the setting
of dermatitis, infection, or from contact with alkaline substances such
as soap, bleach, solvents and even tap water [65]. e optimal pH of
the skin is between 4.6 and 5.6 which is ideal for ceramide production.
e skin lipid-producing enzymes β-glucocerebrosidase and acid
sphingomyelinase both have optimal levels of activity within this pH
range [21,22]. When the skin is overly alkaline, both serine protease-
mediated inactivation and metabolism of the β-glucocerebrosidase
and acid sphingomyelinase enzymes take place. Ceramide and lipid
production slows or comes to a halt [66]. e disrupted and alkaline
skin barrier is unable to support a healthy microbiome. Staphylococcus
aureus, Candida, and Propionibacterium acnes all grow more
eectively in an alkaline environment. Natural skin ora also become
compromised at an elevated pH [67,68]. is shi in the microbiome
of the skin may lead to a cycle of increased alkalinity, infection, and
a disrupted epidermal barrier. Additionally, as the pH reaches and
exceeds 5.7, there is inhibition of lamellar body secretion and corneo-
desmosome-constituent proteins can be degraded [66].
Acidication and even hyper-acidication of the epidermis has
been shown to decrease TEWL [69]. In fact, a common technique for
acidifying topical skin care formulations is the addition of acidic salts,
such as citric or lactic acids. ese acids are uncommon sensitizers,
but are prone to crystallization, which can result in irritation of the
skin. Alpha Hydroxyacids (AHAs) are also used to modulate the
pH of the skin and to enhance stratum corneum desquamation and
improve skin appearance. Unfortunately, AHAs result in sunburn cell
formation and increase the risk of skin cancer. e FDA now requires
a sun-burn warning on products containing AHAs [70]. A natural
polyhydroxy acid, Gluconolactone (GLU) is a free radical scavenger
and is a superior TEWL inhibitor when compared to several other acids
[69,71]. Additionally, GLU is known to enhance stratum corneum
desquamation, improve skin appearance, prevent skin irritation, and
is protective against UV radiation-induced elastin promoter activation
[71]. GLU treatment does not result in a signicant increase in sunburn
cells. UV absorption of GLU is low, so the UV protective eect must be
due to other mechanisms, such as its ability to function as a chelating
agent and free radical scavenger [71]. Additionally, GLU does not
crystalize and become an irritant to the skin as easily as citric and
lactic acid, making it an optimal epidermal acidier (CLE, unpublished
author observation).
Skin Barrier Protection
Eective transepidermal water loss inhibition
TEWL measurements can be used as a marker for skin barrier
integrity. Improvements in TEWL have been tied to improvements
in SCORAD scores in atopic dermatitis and are considered a marker
for stratum corneum integrity and hydration [20]. In addition to the
TEWL lowering benets of sphingolipid and cholesterol ester fractions,
TEWL inhibitors like petrolatum, dimethicone and other lipid fractions
are commonly used as skin protectants. Petrolatum is considered to be
the gold standard TEWL inhibitor [72]. In an eort to explore possible
alternatives to petrolatum, the author subjectively tested countless
plant-based petrolatum substitutes and was unable to nd one that
matched the characteristics of petrolatum including: hypoallergenicity,
hydration, taste, viscosity, melting temperature, and non-desiccating
eects on palmar and lip skin (as these areas tend to become most-
easily irritated/tight when they are desiccated). Petrolatum is a complex
semi-solid combination of paran wax, microcrystalline wax and
white mineral oil. Paran wax is even more impermeable to water than
petrolatum and when combined with petrolatum, is also an extremely
ecient TEWL inhibitor.
Dimethicone, a man-made polymer of the naturally occurring
element silica or silicon, is a very common skin protectant. Silicon
is naturally present in very small amounts in the human body and
may be associated with bone health [73]. Silicone and dimethicone
are manufactured by polymerizing silicon with carbon, hydrogen
and oxygen. e human body does not have the ability to metabolize
these polymers and in fact, when human monocytes were incubated
on dimethicone, they secreted variable levels of IL-1 beta, IL-6 and
TNF-alpha [24]. Furthermore, dimethicone has the potential to cause
an inammatory reaction when implanted [74]. When ve dierent
silicone materials were tested for skin sensitization potential, the murine
local lymph node assay showed weak to moderate skin sensitization
potential for four of the ve materials. Sensitization via cutaneous
contact or via injection or implantation is increasingly reported in the
literature. Reactions include allergic contact dermatitis, granuloma
formation, systemic sclerosis, and a psoriasiform eruption, among
others [75-78]. Rates of sensitization to silicone and silicone polymers
are increasing in both topical and implanted exposures [79-81].
While it is technically dicult to objectively study a skin protectant’s
ability to prevent penetration of allergens, irritants, and microbes
into the skin, there are three objective measures that may be used to
determine a product's or ingredient’s eectiveness in these areas: 1)
if a product or molecule has superior hydrophobicity; 2) lower water
solubility; and 3) a higher melting point than another, it may be more

Citation: Eberting CL, Coman G, Blickenstaff N (2014) Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself.
J Allergy Ther 5: 187. doi:10.4172/2155-6121.1000187
Page 5 of 8
J Allergy Ther
ISSN:2155-6121 JAT an open access journal Volume 5 • Issue 5 • 1000187
dicult to wash o and therefore more ecient at preventing contact
with irritants, allergens and pathogens. Solvent permeability and
penetration characteristics are also to be considered.
Hydrophobicity
Hydrophobicity is the measure of a product or ingredient’s degree of
repellency from a mass of water. Hydrophobic molecules are non-polar
and prefer other neutral molecules. e hydrophobicity of a skin barrier
product or ingredient can be objectively measured by determining the
contact angle, or the angle measured through the liquid where a liquid/
vapor interface meets a solid surface, of a drop of water applied to the
product in question. e contact angle is also directly correlated with a
molecule’s ability to adhere to a surface. While there are many variables
that can alter the contact angle of a molecule, hydrophobicity can be
subjectively measured by observing how easily water will bead and
roll o of the skin. A product that is very hydrophobic will have a high
contact angle, causing water to bead more eciently [82]. e higher
the contact angle, the more hydrophobic and adherent to the skin the
molecule is. e largest contact angles measured between water and
a smooth surface are with paran. Paran is a mixture of saturated
aliphatic hydrocarbons and is considered to be the most hydrophobic
water-repelling agent [83]. By comparison, to reach this range of
hydrophobicity, dimethicone must be applied to a smooth surface such
as glass and then must be baked on [84]. e contact angle of paran
is between 106 and 112 degrees and is dependent on the texture of
the surface and the purity of the paran [83]. Paran is composed of
non-polar alkane chains that, like the methyl groups in silicone uid,
have hydrophobic properties. ey interact very weakly with water
molecules so water stays in a drop and does not wet the paran wax.
Melting point
e melting points of skin protectant molecules may be another
indicator of their persistence on the skin aer washing and eectiveness.
e melting point of paran wax ranges from 47°C up to 65°C
depending on which grade of wax is used [85]. e melting point of
dimethicone is generally below 50°C (depending on which polymer is
used) [86].
Water solubility
Water solubility is an objective variable that can be used to assess the
eectiveness of a skin protectant. e water solubility of an ingredient
is an important indicator of its ability to protect the skin from water,
allergens and irritants. e water solubility of dimethicone is 33-77 g/l,
while paran wax is insoluble in water [87].
In addition to petrolatum, paran wax, and dimethicone, many
lipid-based TEWL inhibitors have also been investigated. ese lipids
include glyceryl monoisostearate, isopropyl isostearate, isostearyl
isostearate, cetyl alcohol, potassium cetyl phosphate, cetyl behenate and
behenic acid [88,89]. Isostearyl Isostearate has been proven to be the
most eective lipid-based TEWL inhibitor in these studies [88].
Calcium chelation
Forslin et al. were able to use a scanning nuclear microprobe to map
calcium distribution in cross sections of normal, atopic, and psoriatic
skin. In normal skin, calcium localizes to the uppermost granular layer
of the epidermis as well as to the basal and spinous layers. Forslind et
al. found that psoriatic and dry atopic skin had an epidermal calcium
gradient higher than normal skin [90]. Calcium is a necessary part of
the apoptotic process, and increased intracellular calcium may induce
the activation of endonuclease, transglutaminase, and morphological
changes [90]. Lee et. al., showed that removal of extracellular calcium
stimulates both lamellar body secretion and lipid synthesis, while also
blunting those responses when extracellular calcium concentration
was raised for hairless mice [91]. Calcium also seems to impair
corneodesmin hydrolysis with incomplete desquamation at alkaline pH
and without the presence of EDTA [23]. e nal step appears to be
inhibited by calcium, resulting in incomplete desquamation and residual
intercorneocyte cohesion in cases of skin barrier disruption. e skin’s
naturally occurring chelating agent is unknown, but calcium chelation
in a lower pH environment and in the presence of EDTA allows this
step to proceed [92]. erefore, weak calcium chelation may benet
a disrupted skin barrier by improving desquamation. Gluconolactone
and EDTA are both mild chelating agents that can safely be used in skin
barrier repair formulations to help optimize desquamation.
Susceptibility to contact sensitization
ose with llagrin null mutations have been found to have
increased rates of ACD particularly to lanolin and p-tert-butylphenol-
formaldehyde resin [93]. Research regarding the relevance of ACD in
atopic dermatitis is emerging [17,94,95]. ose with atopic dermatitis are
more likely to develop contact sensitization to certain chemicals relative
to non-atopics. Formaldehyde-releasers [18], cocamidopropylbetaine
[96] nickel, cobalt, chromium [16], Kathon CG, fragrance, neomycin
[97], and propolis (from beeswax but found in cough syrup, pills,
cosmetics, and vitamins) are advisably avoided in atopic dermatitis in
the setting of contact dermatitis as atopics are possibly more likely to
develop contact dermatitis [96].
Discussion
Techniques that optimize skin barrier repair include skin
lipid replacement, pH modulation/optimization, the use of anti-
inammatory molecules, the use of mild calcium chelation, and the
overt avoidance of known skin irritants and allergens in formulation.
e eectiveness of a skin barrier repair and protectant product may
also be determined by its ability to adhere to the skin and its ability
to prevent the contact of water, irritants, allergens, and solvents from
coming in contact with the skin. ese qualities may be a function of a
product’s hydrophobicity, melting point, and water solubility.
Conclusion
A healthy skin barrier protects from pathogens, allergens, toxins,
and irritants. When the skin’s leading physical barrier, the stratum
corneum, is damaged as a result of disease or acute destruction, the
deeper layers of the epidermis and dermis are vulnerable to further
irritation and sensitization. Finding ways to protect the skin and repair
its natural barrier qualities is a major goal in reducing the incidence of
chronic dermatitis. Utilizing the large amount of existing and recent
data on dierent chemicals’ interaction with the stratum corneum
and the skin barrier to create novel products based on evidence-
based medicine is essential to improving treatment outcomes. Further
research and investigation into the skin’s barrier function and our
ability to enhance its protective qualities is paramount to the future
treatment of these patients.
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Citation: Eberting CL, Coman G, Blickenstaff N (2014) Repairing a Compromised Skin Barrier in Dermatitis: Leveraging the Skin’s Ability to Heal Itself.
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