Structure and function of the

epidermal barrier
R. Randall Wickett, PhD,a and Marty O. Visscher, PhDb
Cincinnati, Ohio

The skin is divided into 2 main structural layers: the epidermis and the dermis. The epidermis is generally considered to be sub-
divided into 5 separate strata: basal, spinous, granular, lucid, and corneum. The vital barrier function of the skin resides primarily
in the top stratum of the epidermis, the stratum corneum (SC). The SC is the barrier to the passive diffusion of water out of the skin,
allowing us to live in air without suffering from dehydration, and is the barrier to other molecules including irritants into the skin.
The epidermis also has immunologic functions and provides some protection of the skin from ultraviolet light via the pigment
system. This paper will review the structure and function of the epidermal barrier and the response to environmental challenges
such as repeated handwashing. Emphasis will be placed on the SC, the front line of the skin’s defense against the insults of the
outside world. (Am J Infect Control 2006;34:S98-110.)

The skin is the largest organ of the human body,
accounting for approximately 16% of total body weight.
Its vital role is to prevent loss of water and other compo-
nents of the body to the environment and protect the
body from a variety of environmental insults. The skin
also has important immune and sensory functions,
helps to regulate body temperature, and synthesizes vi-
tamin D. For a review of the overall structure of the skin
including the dermis and skin appendages, see Odland.1
Any discussion of the structure of skin will necessar-
ily refer to layers. The various layers of the skin work in
concert to provide strength and flexibility and perform
the multiple functions of the skin. This review will
focus on the barrier function residing in the top layer
of the skin, the epidermis. The barrier function of the
skin has been called ‘‘la raison d’etre’’ of the epidermis.2
The epidermal barrier serves to limit passive water loss
from the body, reduce the absorption of chemicals
from the environment, and prevent microbial infec-
tion. These defensive functions reside primarily in
the top stratum of the epidermis, the stratum corneum
(SC), at which they are integrated with SC formation
and homeostasis.3,4 Thus, proper development and
maintenance of the SC are keys to its remarkable ability
to defend the body against both chemical and microbi-
ologic attack as well as dehydration.
From the College of Pharmacy,a University of Cincinnati; and Cincinnati
Children’s Hospital Medical Center, Cincinnati, OH.b
Correspondence should be addressed to R. Randall Wickett, PhD,
Professor of Pharmaceutics and Cosmetic Science, University of Cin-
cinnati, College of Pharmacy, 3223 Eden Ave, Cincinnati, OH 45267.
E-mail: randy.wickett@uc.edu.
0196-6553/$32.00
Copyright ª 2006 by the Association for Professionals in Infection
Control and Epidemiology, Inc.
doi:10.1016/j.ajic.2006.05.295
The epidermis is itself divided into several layers or
strata starting with the basal layer or stratum basale
just above the dermis proceeding upward through the
prickle and the granular layers to the top layer, the
SC. Figure 1 is a diagram representing the major strata
of the epidermis. English and Latin nomenclature of
the epidermal strata are given in Table 1.
The predominant cell type of the epidermis is the
keratinocyte. Keratinocytes exist from the basal layer
to the granular layer at which they transform into the
corneocytes of the SC. Keratinocytes make keratin
and many other proteins. Keratins are the major struc-
tural proteins of the SC.5 There are 2 other important
cell types in the epidermis: melanocytes and Langer-
hans cells. These 2 cells types are shown in the micro-
graph in Fig 2.
Melanocytes are the pigment-producing cells of the
skin and hair in all mammals. In the skin, they are
found at the basal layer of the epidermis at which
they make pigment granules called melanosomes con-
taining melanin. The melanosomes are transferred
from the melanocytes to the epidermal keratinocytes
at which they impart some protection to the cell nu-
cleus from ultraviolet (UV) light and give the skin its
color. The process of melanin synthesis and transfer
of melanosomes occurs continuously as the epidermis
renews but can be speeded up in response to UV expo-
sure to produce tanning.
Another epidermal cell shown in Fig 2 is the Langer-
hans cell. Langerhans cells are dendritic immune cells
that are the antigen-presenting cell of the skin.6-8 They
are important to the immune barrier of the epidermis
and also participate in contact allergy.
FORMATION OF THE SC BARRIER
The granular layer or stratum granulosum (SG) is
named for the granules that appear in the cells at this

S98
 Wickett and Visscher
Fig 1. Diagram of the epidermis showing the main
layers. The clear layer (not shown) is only found in
the very thick epidermis of the palms and soles.
point in the epidermis. Although it is only a few cells
thick, it is a vital component of the epidermis because it
is here that the key transformations that form the SC bar-
rier occur. Two types of granules are formed at the SG:
keratohyalin granules,1 which are full of protein, and
lamellar bodies,9,10 which contain lipids. In the SG, the
cells are transformed into the corneocytes or squames
that form the SC. The nucleus is digested, the cytoplasm
disappears, the lipids are released into the intercellular
space, the keratin intermediate filaments aggregate to
form microfibrils, and the cell membrane is replaced by
a cell envelope made of cross-linked protein with lipids
covalently attached to its surface. The corneocyte or
squame that results from this transformation is a flat
cell that tends to be in the shape of either a hexagon or
pentagon approximately 25 mm on a side with a surface
area of approximately 1000 mm2 and a thickness of
approximately 0.5 to 1.0 mm.11,12 On most body sites,
the SC is 12 to 16 cell layers thick, but it can vary from
as little as 9 cell layers of the forehead or eyelids to as
much as 25 on the dorsum of the hand and up to 50 or
more on the palms or the soles of the feet.13,14 To discuss
the structure and formation of the SC in more detail, we
will refer to a common conceptual model of the SC
barrier, the ‘‘bricks and mortar’’ model.15,16
THE BRICKS AND MORTAR MODEL
OF THE SC BARRIER
The SC is often modeled as a brick wall (Fig 3). The
SC corneocytes with their resistant cell envelopes and
December 2006 S99
Table 1. Nomenclature for epidermal strata
English Latin Alternative
Basal cell layer Stratum Basale S Germinativium,
Malpighian layer
Prickle layer S Spinosum Malpighian layer
Granular layer S Granulosum Malpighian layer
Clear layer S Lucidum
Horny layer S Corneum
keratin microfibrils are considered to be the bricks,
and the layers of lipids found between the cells are
considered to be the mortar.15 The lipid ‘‘mortar’’ is
the main barrier to water passing out through the
SC.17 The permeability of lipid soluble molecules is
modeled by considering them to wind their way around
the corneocyte bricks by diffusing through the lipid
mortar.18 Both the bricks and the mortar of the SC are
produced by keratinocytes at the SG at which keratino-
cytes release the lipids of the mortar into the space
between the cells as they are being transformed into
the corneocytes ‘‘bricks.’’ A major difference between
the current and the earliest versions of the model is
that we now know that the bricks are linked by deso-
mosomes as illustrated in Fig 3 and discussed below.
The bricks (corneocytes)
The SC is approximately 60% keratin by dry
weight.19 Keratins are members of a family of proteins
called intermediate filaments that form part of the cyto-
skeleton of nucleated cells5,20,21 and are major struc-
tural proteins of skin, hair, and nail. When keratins
are made by the cell, an acidic type I keratin is made
at the same time as a neutral to basic type II keratin.
Acidic proteins have more negatively charged amino
acid side chains (aspartic or glutamic acid), and basic
proteins have more positively charged side chains
(lysine, arginine, or histidine at low pH). This allows
the 2 a helical proteins to interact with each other, form-
ing a structure called the coiled-coil.5,21,22 Coiled-coils
are important to the structure of the keratinocyte
and help maintain its integrity. Improper assembly
of coiled-coils can lead to fragile keratinocytes, which
rupture easily causing blistering diseases.21,23-25 At
the SG as keratinocytes are transformed into the corne-
ocyte ‘‘bricks,’’ the coiled-coils aggregate to form struc-
tures called microfibrils, which are thought to lie
parallel to the surface of the skin serving to reinforce
the corneocytes and limit SC swelling in the plane of
the skin surface.26,27
Two proteins from the keratohyalin granules, filag-
grin and loricrin, play key roles in the formation of the
‘‘bricks.’’ Filaggrin is an acronym for filament-aggregating
S100 Vol. 34 No. 10 Supplement 2
Fig 2. Micrograph of the upper dermis and
epidermis showing the layers and major cell types.
(Figure courtesy of Steve B. Hoath, MD, used with
permission.)
protein.28-31 Filaggrin contains a high level of positively
charge amino acids and participates in the aggregation
of the keratin coiled-coils,32 which have an overall neg-
ative charge. After filaggrin performs this function, it is
modified to come off the keratin microfibrils and is
then digested by proteolytic enzymes to produce the
amino acid components of the natural moisturizing
factor (NMF) of the SC.33-35 NMF consists of lactate,
amino acids from filaggrin breakdown, and pyrollidone
carboxylic acid (PCA) formed from the amino acid glu-
tamine.36-38 These natural moisturizers are important
to maintain proper hydration of the SC, allowing it to
be flexible and to desquamate properly.39-43
In the lower layers of the epidermis, the keratinocyte
has a typical phospholipid bilayer cell membrane.
Phospholipid membranes are far too permeable to
water to survive exposure to air in a dry environment.
At the SG, the cell membrane of the keratinocyte is
transformed into the resistant cell envelope of the cor-
neocyte.44 The transformation is brought about by the
membrane-bound enzyme transglutaminase45 (T-gase).
T-gase cross-links 2 proteins together by connecting a
glutamine side chain of one to a lysine side chain on
the other, resulting in the formation of an isopeptide
bond as illustrated in Fig 4.
Several proteins participate in cross-linking reac-
tions. The most predominate is loricrin, a globular pro-
tein released from the keratohyalin granules that is rich
in hydrophobic amino acids and cysteine.46-48 The cy-
toplasm contains involucrin, a highly helical protein
that is also a major substrate for T-gase and an impor-
tant component of the cell envelope.49-51 An early
step in formation of the cell envelope is cross-linking
between involucrin and loricrin.50 Other proteins
Wickett and Visscher
Fig 3. A ‘‘Bricks and Mortar’’ model for human
stratum corneum illustrating the corneocyte
‘‘Bricks,’’ the Intercellular lipid ‘‘Mortar,’’ and the
desmosomes connecting the corneocytes.
participate in cross-link formation, especially some
small proteins rich in the amino acid proline, known
as SPRs.52-54 Eventually, the entire cell membrane is
replaced by cross-linked proteins.55 Keratin fibers are
also cross-linked to the envelope,56 and lipids (ceram-
ides) are covalently attached to involucrin on the outer
surface.57,58 These attached ceramides are important
to the barrier function of the SC.59 The new structure
is known as the resistant cell envelope. A schematic
of the SC cell envelope based on the work of Peter
Steinert is shown in Fig 5.
Recent studies indicate that the cell envelope is not
always completely formed in at the SG/SC interface and
that some incompletely formed envelopes may persist
into the SC.60 Harding et al61 have classified cell enve-
lopes into 2 types: completely formed robust cell enve-
lopes and incompletely formed fragile envelopes. The
ratio of fragile to robust envelopes was reported to
increase in dry and damaged skin.
SC desomosomes
Desomosomes are structures composed primarily
of glycoproteins, which join cells together. The deso-
mosomes joining corneocytes in the SC are modified
from those that join epidermal keratinocytes by the ad-
dition of a protein called corneodesmosine,62-65 and SC
desmosomes are sometimes referred to as corneodes-
mosomes. For proper desquamation of the SC to occur,
the desmosomes must be digested by proteolytic en-
zymes.62,65,66-70 At least some of the keratin fibers are
thought to connect to the desmosomes as illustrated
in Fig 4. Figure 5 shows electron micrographs of des-
mosomes in the SC.70 In the lower SC, desmosomes
 Wickett and Visscher
Fig 4. Formation of the isopeptide bond by
transglutaminase.
are intact, but they are gradually digested by the time
the skin surface is reached (Fig 6).
In SC that is desquamating at its normal rate, corne-
ocytes persist in the SC for approximately 2 weeks,
depending on body site, before being shed into the
environment.71-74 On average, about one layer of cor-
neocytes is shed each day from the surface and re-
placed by keratinocytes at the SG. The corneocytes
that are shed each day can have a significant bacterial
load and may be a source of contamination of the
environment.71,75-77
The mortar
The lamellar bodies that appear at the SG contain
lipids, which are released into the intercellular space as
the SC forms. These lipids are glucosyl ceramides, choles-
terol, cholesterol esters, and long-chain fatty acids. In the
intercellular space, the glucosyl cermides are converted
to ceramides.78,79 The lipids spontaneously organize
into multiple layers between the SC cells.80 These layers
are illustrated in Fig 7, which shows lipid layers in the
lower SC after the overlaying SC has been removed by
stripping with cellophane tape.70
This lipid ‘‘mortar’’ is critically important to the bar-
rier function of skin, and ceramides are vital to the or-
ganization and functioning of the barrier.81 Ceramides
are sphingolipids linked to long-chain fatty acids.
There are several ceramides found in the SC, including
ceramides 1 and 2 shown in Fig 8.
The SC contains no phospholipids. The phospho-
lipids from the keratinocytes of the viable layers are
broken down by phospholipases82-84 in the lower SC.
December 2006 S101
Fig 5. The corneocyte envelope as proposed by
Steinert.53-55
This produces fatty acids, which are necessary for the
development of a functional SC barrier and may play
a role in producing the acid pH of the SC.82 The SC
has a surface pH of approximately 4 to 5.5, and this
acidic pH, the so-called ‘‘acid mantle’’ of the skin,85-88
may play a role in protecting against colonization of
the skin surface by harmful bacteria.3,89,90
Elias et al91 and Schurer and Elias92 have proposed
that the lipids released from lamellar granules in the
SG are precursor or probarrier lipids that must be pro-
cessed in extracellular spaces.92 The necessity of this
extracellular lipid processing emphasizes the dynamic
nature of the SC. The SC can no longer be considered
as a Saran wrap (SC Johnson, Racine, WI)-like covering
of the skin. It is a dynamic tissue that is metabolically
active, even if it is not a living tissue in the classic sense.
For more details on the dynamic SC and the ‘‘updated’’
bricks and mortar model, see the excellent review by
Harding.93
The lamellar bodies of the SC release other impor-
tant molecules into the intercorneocyte spaces in
addition to the lipids that form the permeability barrier.
The proteolytic enzymes involved in desmosome hy-
drolysis94,95 as well as inhibitors of those enzyme to
control rates of desquamation96 are released by the
lamellar bodies, as are antimicrobial peptides called
defensins,97 which may play a role in protecting the
skin from infection.98 Production of these peptides is
increased in skin with psoriasis but not in skin with
atopic dermatitis (eczema).99,100 This may account for
the much higher susceptibility of eczema sufferers to
skin infection, and eczematous skin may be more
likely to spread nocosomial infections.101
S102 Vol. 34 No. 10 Supplement 2 Wickett and Visscher

Fig 6. Electron micrographs of tape strippings of normal skin. Degradation of desmosomes toward the surface of the
stratum corneum: (A) First strip; desmosome fully degraded. (B) Second strip; partially degraded and encapsulated by
lipid lamella. (C) Second strip; desmosome partially degraded. (D) Third strip; normal desmosome; lipid envelopes in
direct contact with desmosome. (magnification, 3200,000) Reprinted from Rawlings et al70 with permission of the
Society of Cosmetic Chemists.

The very specialized ‘‘bricks and mortar’’ of the SC
work together to produce a covering for the skin that
is both flexible and superbly protective.3,4 When the
SC is functioning properly, it defends us against dehy-
dration, external toxins, and bacterial assault as well
as protecting the more fragile keratinocytes below
from mechanical disruption.
HAND HYGIENE AND EPIDERMAL
BARRIER FUNCTION
Surfactants
Most handwash products rely on surfactants for
their cleansing action. Surfactants are surface-active
molecules. They have a hydrophobic portion referred
 Wickett and Visscher
Fig 7. Normal lipid lamella at the third tape strip.
(magnification, 3200,000) Reprinted from Rawlings
et al70 with permission of the Society of Cosmetic
Chemists.
to as the tail and a hydrophilic portion referred to as the
head group. A ball and stick representation of an ionic
surfactant is shown in Fig 9.
Surfactants are classified primarily by the character-
istics of the head groups. Natural soaps are the metal
salts of fatty acids, so the head group is a carboxylic
acid and the X is either sodium or potassium. The ma-
jor classifications of surfactants are anionic, cationic,
ampotheric, and nonionic, depending on whether the
head group has a negative (anionic) or positive charge
(cationic) or both (amphoteric) or is uncharged (non-
ionic).102 The hydrophobic tail can vary in length and
structure, but hydrocarbon chains of various lengths
are the most common. The structure of one of the
most frequently used anionic surfactants, sodium
lauryl sulfate (SLS), is shown below. Here, the hydro-
phobic tail is the 12 carbon hydrocarbon chain, and
the head group is the sulfate moiety.
CH3-CH2-CH2-CH2-CH2-CH2-CH2-CH2-CH2-CH2-CH2-
CH2-O-S-O32 NA1
Surfactants have a wide variety of applications and
are especially useful for cleansing. They can form asso-
ciation structures such as micelles, which can dissolve
oils directly. The hydrophobic tail can associate with
oils on a surface causing it to lift up from the surface,
and they can help to break up other types of soil.
Nearly all products for cleansing skin or hair contain
surfactants.
Surfactants effects on the bricks and mortar
Unfortunately, the very characteristics of surfactants
that make them so useful for cleaning allow them to
damage both the bricks and mortar of protective bar-
rier of the SC. Repeated washing of the skin with soaps
and surfactants can negatively impact the multiple
functions of the epidermal barrier. The skin problems
that can be engendered by the necessity of repeated ex-
posures in a health care environment are multiple. Skin
damage from surfactants can be further exacerbated
by occlusion from wearing gloves and the mechanical
December 2006 S103
Fig 8. Ceramides 1 and 2.
Fig 9. Ball and stick representation of a surfactant
molecule.
action of scrubbing the hands. The negative effects
that soaps and surfactants can have on the epidermal
barrier are illustrated in Fig 10.
Surfactant molecules are well-known to bind to pro-
teins,103-106 causing changes in their structure, and
have been shown to bind to the SC.107 Surfactants
known to be aggressive to the skin such as SLS bind
more strongly than milder surfactants such as isethio-
nates. Surfactants cause swelling of the SC in vitro, pre-
sumably by interaction with SC proteins,27,103,108,109
and the degree of swelling is well correlated with the
harshness of either individual or mixtures of surfactant
mixtures.109,110
The lipid mortar is the major barrier to permeability
of the SC, and surfactants are well-known to increase
the ability of exogenous compounds to penetrate the
skin111,112 and to increase the rate of water loss through
the skin,113-123 presumably because of their effects on
the lipid barrier SC.2,112,124,125 An obvious mechanism
for the decrease in barrier function after surfactant treat-
ment could be direct removal of SC lipids and removal of
SC lipids by surfactant treatment, an effect that has been
reported in some studies.126,127 Other studies on surfac-
tant-induced irritation indicate that, rather than greatly
reducing the total lipid content, the main effects are to al-
ter lipid composition70,128 and disorder the lamellar
structure of SC lipids.70,129-133 Figure 11 illustrates the
extreme disordering of the SC lamellar lipid structure
for soap-induced, winter-dry skin.70
Surfactant effects on the acid mantle
As discussed above, the SC has a surface pH of
approximately 4 to 5.5, and this acidic pH, the so-called
S104 Vol. 34 No. 10 Supplement 2 Wickett and Visscher

Fig 10. Schematic of surfactant interactions with the epidermis. (A) Surfactant molecules enter the SC, binding to
proteins and disrupting lipid structures, and eventually reach the viable epidermis. (B) Water depletes NMF after lipid
disruption and corneocytes swelling. (C) The formation of the SC is up-regulated by inflammatory factors leading to
improper barrier function. (D) Incomplete hydrolysis of desmosomes leads to scale formation.

‘‘acid mantle’’ of the SC,85,87,88,134 may play a role in
protecting against colonization of the skin surface by
harmful bacterial.3,4,90 Bar soaps made from natural
soap are alkaline by their very nature and can raise
the pH of the skin during washing.88,90,135 Trobaugh
and Wickett135 reported that a single washing with typ-
ical bars soaps raised the pH from the normal range of
5.0 to 5.5 to approximately 7.5. Washing with a bar
soap based on the synthetic detergent sodium cocoyl
isethionate did not have this effect. The pH of soap-
washed skin gradually declined toward normal over
the next several hours because SC has components
(fatty acids) that naturally provide buffering
capacity.136,137 Trobaugh and Wickett135 further re-
ported that washing 10 times per day with soap over-
came the skin’s natural buffering capacity to some
extent, and, within 3 days, the skin surface pH was con-
sistently above 6.0, suggesting that the mechanism for
maintaining the acid mantle was disrupted. In addition,
cracking (fissuring) grades increased (worsened) from
1.5 to 3.0 on a 5.0-point scale. The authors interpreted
the cracking as due to the harsh nature of natural soap
bars and not simply to the high pH of the soap bars.
Newman and Seitz138 found similar increases in skin
surface pH on repeated soap washing paralleled by
similar increases in cracking grade. Korting et al90
 Wickett and Visscher
also reported increases in skin pH following the use of
natural soaps and a concomitant increase in skin colo-
nization by coagulase-negative staphylococci.
Surfactant effects on SC hydration
and flexibility
Since the pioneering work of Blank,139,140 we have
known that water is a key factor for maintaining the
pliability of the SC. Studies with isolated SC have found
that well-hydrated SC is very flexible and dry SC is very
stiff and brittle.139,141,142 Many in vivo studies have
also found hydration to increase the elasticity of the
skin.143-149 Loss of elasticity in surfactant-damaged
dry skin can lead to cracking of the skin, especially
around the knuckles at which stretching and flexing
of the skin is required for movement.
Effects on SC metabolism and desquamation
In addition to the requirement of water for SC flexibil-
ity, we now understand that adequate hydration of the
SC is required for the important metabolic processes
occurring in the SC, such as conversion of probarrier
lipids to barrier lipids82,91,150-152 to maintain barrier
function and the hydrolysis of desmosomes67-70,153,154
necessary for normal desquamation. Skin in good
condition maintains SC water content at approximately
30% by weight (except at the very surface), whereas
very dry skin can be as low as 10% to 15% water
throughout most of the SC down to nearly the level of
the SG.155 The natural moisturizing factors of the SC
are very important to maintaining SC hydration.156-160
NMF is easily lost from the skin, especially after the
barrier is perturbed,157,161,162 and it is likely that NMF
removal is a major factor in the development of dry
skin following repeated hygiene procedures.
The desmosomes connecting SC cells (Fig 6) are
gradually digested by a cascade of proteolytic en-
zymes.67,163 In dry and in dry, damaged skin, these en-
zymes are not able to perform their function properly,
thereby causing intact desmosomes to persist into the
upper SC.69,70 This results in shedding of large scales
or flakes rather than individual cells. It also increases
the surface area of the SC available for bacterial adhe-
sion and may be a factor in the increased presence
of colonizing bacteria on damaged hands.90,164
Surfactant effects on cytokines-
hyperproliferation
Surfactants can induce the release of inflammatory
cytokines (cell-signaling molecules). Interleukins, par-
ticularly interleukin-1a, are released upon surfactant
exposure.165-167 There are 2 mechanisms that can
contribute to this effect. Surfactants are clearly able
to penetrate the SC and encounter keratinocytes in the
December 2006 S105
Fig 11. Disordering of lipids in the outer SC in
soap induced winter dry skin. Reprinted from
Rawlings et al70 with permission of the Society of
Cosmetic Chemists.
viable layers of the epidermis. The interaction of sur-
factants with keratinocytes is known to induce cyto-
kine release.166,168
Interleukin-1a is also released as a natural response
of the epidermal barrier to disruption169 as part of the
protective process intended to stimulate repair of the
barrier. In surfactant-irritated skin, these effects may
combine to produce overstimulation, causing the skin
to hyperproliferate.170 The overstimulated skin has an
increased rate of cornification that does not permit suf-
ficient time for the complex events that must occur in
the SG to form a fully functional SC. A normal SC lipid
profile will not be produced,70,171 and SC cell envelopes
that incompletely formed and are thus ‘‘fragile’’ will
form in higher than normal proportion.61 Cells with
fragile envelopes will lose their NMF easily and not
have good barrier properties. These effects will combine
to lead to SC with impaired barrier function. This result-
ing barrier will have weaknesses in both the bricks and
the mortar. Consequently, it will be increasingly suscep-
tible to further surfactant damage and less able to hold
water to allow SC enzymes to function. The result will
be a vicious cycle of skin damage.161
Breaking the dry skin cycle
The challenge in the health care environment is
to somehow break this dry skin cycle while meeting
hygiene guidelines that require frequent cleansing
of the hands. Multiple approaches are required. The
first step is to use cleansers formulated with mild
S106 Vol. 34 No. 10 Supplement 2
surfactants such as isethionates,172 amphodiacetates,
and sulfosuccinates. Blending surfactants together in
appropriate ratios can also significantly improve their
mildness.110 The use of alcohol-based hand sanitizers
that contain appropriately formulated emollients may
also help to improve hand condition.173-175
Although improving the surfactant cleansing system
will help reduce skin problems, it is likely to be neces-
sary to use well-formulated therapeutic lotions to help
break the cycle and reestablish the formation of nor-
mal SC. Glycerin has been shown to be an effective
skin-conditioning agent when incorporated into a
lotion at 5% or higher.176,177 It has several positive
effects on the physical properties of the SC, including
increasing hydration178-180 and improving elastic-
ity.146,147,178 Glycerin has been reported to normalize
the rate of desmosome hydrolysis in dry skin,181 and
glycerin has been shown to accelerate the repair of
the SC barrier after damage by SLS.182
Petrolatum is an effective treatment for dry skin183
both as a single ingredient and as a component of creams
and lotions. Petrolatum is an occlusive agent that reduces
the rate of water loss through skin, increasing hydration
by causing buildup of water in the upper SC. Petrolatum
has been shown to penetrate deeply into damaged skin
and enhance recovery of SC barrier function.184 Use of
lotions and creams outside of work may have significant
benefits for health care workers and should be stressed as
part of the routine hand hygiene practices. Two factors
must be considered while using lotions in the health
care environment. One is the possibility that oils such
as mineral oil and petrolatum in the lotion may com-
promise the integrity of latex gloves.185 The other is that
lotions formulated with anionic emulsifiers may inacti-
vate the residual activity of chlorhexidine gluconate on
the skin.186,187 These issues can be addressed by pro-
viding lotions that contain lower levels of oils such as
petrolatum and mineral oil and that use either nonionic
or cationic emulsifers while using latex gloves and
chlorhexidine gluconate-containing cleansers.188 The
consistent use of mild cleansers, alcohol rubs with
emollients, and effective skin lotion both during and
outside of work should go far to help maintain the pro-
tective function of the SC, keeping both the ‘‘bricks’’ and
the ‘‘mortar’’ intact while meeting the hand hygiene
requirements of the health care worker.
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2. Madison KC. Barrier function of the skin: ‘‘la raison d’etre’’ of the
epidermis. J Invest Dermatol 2003;121:231-41.
3. Elias PM, Choi EH. Interactions among stratum corneum defensive
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4. Elias PM. Stratum corneum defensive functions: an integrated view.
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5. Steinert PM. Structure, function and dynamics of keratin intermedi-
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