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Skin Pharmacol Physiol 2012;25:227–235
DOI: 10.1159/000338978
Received: July 18, 2011
Accepted after revision: April 20, 2012
Published online: June 20, 2012
Oily Skin: An Overview
Thais H. Sakuma Howard I. Maibach
University of California, San Francisco, Calif., USA
Oily skin (seborrhea) is a common cosmetic problem that occurs when oversized sebaceous glands produce excessive
amounts of sebum giving the appearance of shiny and
greasy skin. This paper overviews the main concepts of sebaceous gland anatomy and physiology, including the biosynthesis, storage and release of sebum, as well as its relationship to skin hydration and water barrier function. We
also address how skin oiliness may vary according to diet,
age, gender, ethnicity and hot humid climates. The deeper
understanding of this skin type provides the opportunity to
better guide patients regarding skin care and also assist in
the development of sebosuppressive agents.
Copyright © 2012 S. Karger AG, Basel
Oily skin (seborrhea) is common, affecting men as
well as women and typically starting just before puberty.
Oily skin looks shiny and greasy, and is frequently accompanied by large pores. It contributes to the development of acne and may be a cosmetic problem. It can
negatively affect the patients’ self-image and have detrimental psychosocial effects. Many individuals feel em© 2012 S. Karger AG, Basel
Fax +41 61 306 12 34
E-Mail [email protected]
Accessible online at:
barrassed and annoyed with the appearance of their oily
skin, and the unpleasant feeling of uncleanness is also a
source of complaint [1–3].
The relevance of a seemingly trivial matter becomes
evident when we realize its constant frequency in women’s magazines or beauty websites and, most impressively,
numerous products marketed by the cosmetics industry
intended for this skin type. However, together with its
popularity come speculation, controversy and myths. It
is common to read inaccurate information conveyed by
the media. In this manner, this overview attempts to fill
the information gap of this common cosmetic problem,
bridging scientific data to clinical practice.
Skin Surface Oil Source
The sebaceous gland, through its holocrine activity,
excretes a complex mixture of lipids called sebum onto
the skin surface. Other lipid sources are the epidermal
keratinocytes, which, during their final stages of differentiation, extrude lamellar granules into intercellular
spaces of the stratum corneum. They consist of lipid
packages that fill these intercellular spaces like mortar or
cement, ensuring the skin permeability barrier [4–6].
This paper is dedicated to the memory of Prof. Albert M. Kligman and
Prof. Walter B. Shelley.
Thais H. Sakuma
252 Swain Way
Palo Alto, CA 94304 (USA)
Tel. +1 650 919 4842
E-Mail thais.sakuma @
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Key Words
Oily skin ⴢ Sebum ⴢ Sebaceous gland ⴢ Skin care
Skin Surface Oil Composition
The average composition of human sebum in adults
consists of 57.5% triglycerides and their hydrolysis products, 26.0% wax esters, 12.0% squalene, 3.0% cholesterol
esters and 1.5% cholesterol [9]. Among these, squalene
and wax esters are unique to human sebum and not found
anywhere else in the body nor among the epidermal surface lipids [5, 12–15].
By comparison, the human epidermal (stratum corneum) lipid is comprised of 50% ceramides, 25% cholesterol, 15% of free fatty acids [16] as well as smaller amounts
of cholesterol esters and cholesterol sulfate [17]. In contrast to the free-flowing oils of the sebaceous gland, the
epidermal lipids are in a solid state at room temperature.
Sebaceous Gland Anatomy
The sebaceous gland is located in the reticular dermis,
where it is usually found in association with hair follicles,
forming the pilosebaceous unit [8, 14]. The lanugo pilosebaceous units of the face can be of two types: the most
common is superficial, tiny and its ostia and minute hairs
Skin Pharmacol Physiol 2012;25:227–235
are invisible to the naked eye. Its sebaceous glands are
disproportionately large, as are all lanugo follicles. The
less numerous type have multilobular sebaceous glands
of extravagant size and depth, greater in volume than the
much smaller glands of the superficial, tiny follicles. It
empties to the skin surface through a wide duct, which is
in fact the follicle, and is joined by a tiny hair of insignificant proportions. Their ostia are easily visible as the
pores of adult facial skin and the gaping orifices are highly prominent in many oily patients, especially on the
cheeks. This type of sebaceous follicles is practically limited to the face, scalp and upper trunk. The tiny superficial hair follicles outnumber these huger sebaceous follicles by a ratio of about 3:1, being evenly dispersed among
them. The hairs associated with the huge sebaceous follicles are larger than those of the superficial hair follicles
and are the ones generally seen with the naked eye [18].
This type of sebaceous follicles contributes by far to the
greatest quantity of facial sebum. The oily appearance
commonly found on the ‘T’ zone (forehead, nose and
chin) reflects the dominance of these sebaceous follicles.
Pagnoni et al. [19] found that sebum output and density
of follicles followed a centrolateral decreasing gradient,
and Lopez et al. [20] showed that such a ‘T’-like distribution could indeed be clearly observed even in the women
presenting the lowest mean value of sebum casual level1.
We conclude that all skins are of a ‘combination’ type,
with increased sebum values on the ‘T’ zone compared to
the rest of the face, regardless if the skin is oily or not.
Biosynthesis, Storage and Release of Human Sebum
The quantity of lipids delivered in a given time per unit
area is proportionate to the total glandular volume (size
and number of glands), a function of the total number
of sebaceous cells generated. Miescher and Schonberg
[22] performed planimetric measurements of glandular
size (actually surface area) in biopsy specimens and
showed that the ratio between lipid delivery and glandular size was constant; that is, the larger the glands, the
more sebum produced in a given time [18].
The fully developed adult sebaceous gland contains sebocytes at different stages of differentiation. Its peripheral
zone is composed of mitotically active sebocytes, which
differentiate towards the center of the gland. During this
The sebum casual level (CL) is defined as the amount of lipids present
at equilibrium when the skin surface remains untouched for several hours
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The relative contribution of lipid from each source depends upon the number of sebaceous glands present at the
site sampled [7, 8], with as many as 900 glands/cm2 on the
face to less than 50 on the forearm [7]. On sebaceous
gland-rich areas, such as the face, lipids produced by the
epidermal cells represent an insignificant fraction of the
total extractable surface lipid. In adults, the amount of
surface lipid on the forehead, for example, normally varies
between 150 and 300 ␮g of lipid/cm2, of which the epidermal contribution is only 5–10 ␮g or 3–6% [9, 10]. However, when sebaceous gland development is minimal, as in
the prepubertal child, or absent, as in the palms and soles,
epidermal lipids constitute the major surface lipid [5].
Sebum forms an amorphous sheet of variable thickness on the skin. It can be !0.5 ␮m or even negligible in
sebum-poor areas, or 1 4 ␮m in some areas of the sebumrich face [11].
With the knowledge that the face is rich in sebaceous
glands and that the epidermal lipids are probably delivered
to the surface at a constant rate as epidermal cells mature
[5], we conclude that a global overvolume of sebaceous
glands is the cause of oily skin. Areas commonly affected
include those that have a higher sebaceous gland density,
such as the face, ears, scalp and the upper trunk [8].
process, they lose their mitotic activity, increase their size
and accumulate lipid droplets. Then, the terminally differentiated sebocytes disintegrate and release their content
to the skin surface via holocrine secretion. This continuous differentiation activity is under the control of paracrine, endocrine and neural mediators acting on a wide
array of receptors expressed by sebocytes [12, 14].
Until 1947, researchers stated that the sebum accumulated on the skin surface was the chief force regulating the
gland’s excretory activity. Surface loss would accelerate
sebum production, and skin surface saturation would
lead the gland to shut down. However, Kligman and Shelley [18] performed experiments that dismissed this concept, termed by them as the ‘positive feedback theory’.
Instead, they proposed that the sebaceous gland functions continuously, without regard to what is on the surface [18]. They demonstrated that the remarkable ability
of sebum to spread over the skin surface could lead to the
false impression that the sebaceous glands were in ‘sleep
mode’. After preventing sebum from flowing away or being wiped off during the lipid’s collection, they obtained
an average of 3.13 mg of sebum per 10 cm 2 on the volunteer’s forehead, compared to the amount of 1.4 mg per 10
cm2 when such precaution was not taken. Hence, the reason why the values of sebum collected from the skin are
relatively constant is related to the fact that after a few
hours, the skin surface of the studied site (e.g. the forehead) becomes saturated, and the excess spreads over to
surrounding areas of the face.
The ‘positive feedback’ theory was questioned after
the explanation of a curious phenomenon that led many
workers to support it. Literature data demonstrate that
the more frequently sebum is collected from a given area,
the larger the sum that will be obtained in equivalent time
periods; for example, the sum of the quantities of lipids
collected at several short intervals greatly exceeds the
amount collected at a single removal at the end of the
same length of time.
Kligman and Shelley [18] ascribed this phenomenon
to the follicular reservoir (the duct which connects the
sebaceous gland located in the dermis to the skin surface), whose importance was later demonstrated by
Downing et al. [23]. They measured sebum secretion in
human skin over a period of 24 h and observed that it declines over a period of 12 h and then remains constant for
the remaining 12 h. It was inferred that the final, sustainable rate represents the true rate at which sebum is secreted by the sebaceous glands, and that the additional
sebum collected at earlier intervals was obtained from an
accumulation in the stratum corneum or in the follicular
canals. In this manner, Millns and Maibach [24] stated
that the sebum measured on the skin surface should be
seen as the end product of what they called a ‘multifunctional sebaceous apparatus’, which involves not only sebum production but also sebum storage (a volume function) and surface delivery (a rate function).
With this three-component model in mind, it is easier
to elucidate the ‘positive feedback’ misunderstanding.
The lipid which rapidly reappears on the skin surface
soon after defatting of a sebaceous-rich area, such as the
face, is actually derived from preformed sebum stored in
the follicular reservoir. This preformed sebum would
flow out of the follicular reservoir into the meshy spaces
of the stratum corneum, through a capillarity mechanism, refilling the space previously occupied by the removed sebum.
The rate of replenishment is proportional to the size,
number of glands and the amount of preformed sebum
that can be stored in the follicular reservoir. On the forehead, total replacement of the removed sebum is expected
after 3 h (if sebum run off is prevented), and sometimes
even after 2 h in oily skin volunteers [18]. After defatting
the skin by wiping the skin several times with an ethersoaked cloth, Butcher and Parnell [25] observed clear follicular droplets of sebum under the stereoscopic microscope (!12) within 15 min. These became visible to the
naked eye in 40 min, giving the skin a star-spangled appearance under bright light.
Kligman and Shelley [18] also demonstrated that it is
probably impossible to exhaust the forehead follicular
reservoirs completely. After applying absorbent cigarette
papers to the forehead of 2 volunteers every 10 min for
6 h, large oil globules could still be expressed by hemostat
compression. Also, neither ether nor absorptive papers
significantly removed oil from the follicular reservoir.
The authors stated that there is no physiological way to
empty it [18].
Based on these data and contrary to what many think,
overwashing the skin does not cause sebum overproduction, but just leads preformed sebum to flow up through
a capillarity mechanism.
Oily Skin
Skin Pharmacol Physiol 2012;25:227–235
Skin Oiliness Assessment
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Sebum present at the skin surface can be objectively
measured non-invasively using one of several methods
based on absorbent paper pads, photometric assessment
(e.g. Sebumeter쏐 SM810; CK electronic), bentonite clay
and lipid-sensitive tapes (e.g. Sebutape쏐; CuDerm Corp.).
Sebaceous Gland Function Regulation
The sebaceous gland is an androgen target organ,
stimulated to produce sebum at puberty and beyond by
androgens [27]. Akamatsu et al. [28] demonstrated that
Skin Pharmacol Physiol 2012;25:227–235
testosterone and 5-alpha-dihydrotestosterone (5␣-DHT)
stimulated the proliferation of facial cultured human sebocytes in a significant dose-dependent manner. Also,
according to their experiments, the effect of testosterone
and 5␣-DHT on the proliferation of cultured human sebocytes may depend on the localization of the sebaceous
glands at different skin regions. Androgens are more effective in increasing the proliferation of facial than nonfacial sebocytes [27, 28].
It has been proposed that, besides abnormal circulating androgen levels, sebum production can be increased
by overproduction of androgens in the pilosebaceous
units due to enhanced expression and activity of androgenic enzymes or/and by overexpression or hyperresponsiveness of androgen receptors [29].
Conversion of testosterone to 5␣-DHT (an intracellular metabolite of testosterone and the most active androgen in upregulating sebum production) is induced by the
enzyme 5␣-reductase. 5␣-reductase type 1 activity is significantly higher in sebaceous glands compared to other skin compartments. Furthermore, facial sebaceous
glands exhibit higher 5␣-reductase type 1 activity than
sebaceous glands from non-acne-prone areas.
Using the human sebocyte culture model, thyroidstimulating hormone, hydrocortisone and, especially, insulin significantly stimulated proliferation of human sebocytes maintained in a serum-free medium in a dosedependent manner. These results indicate that not only
androgens but also other hormones may modulate sebocyte activity, leading to a complex regulation of the sebaceous gland [27].
Sebum Secretion: Role of Diet
Diet may be an important source of substrate for sebum synthesis. It is synthesized de novo in the gland from
several sources (e.g. glucose, acetate and fatty acids); however, some dietary lipids (especially fatty acids) can also
pass unchanged from the circulation to the sebaceous
cells. It is presumed that undifferentiated cells of the sebaceous gland acquire the dietary lipids whilst in the basal layer exposed to the circulation [15].
Fulton et al. [30] measured the effect of excessive chocolate ingestion on 5 healthy adult male volunteers. All
volunteers ingested two chocolate bars daily for 1 month.
Although the authors concluded that chocolate and fat
did not alter sebum composition and output, at the end
of the study, an increase in collected sebum was observed
in 3 of the 5 volunteers [30]. Pochi et al. [31] investigated
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Since many environmental and biological factors influence the data, rigorous methodological designs are mandatory. The Sebumeter SM810 and Sebutape are widely
used. The Sebumeter affords direct photometric reading
of the lipid collected on a probe of opaque plastic strip
after a 30-second skin contact. Increases in transparency
are directly proportional to the sebum present. The digital read-out displayed as micrograms per square centimeter provides estimated total amount of lipids present on
the skin at one time point. The Sebutape is a white porous
tape that traps oil and becomes translucent. After removal from the skin, it is laced in a black background. A pattern of dots of variable sizes and density develops, proportional to the amount of sebum delivered. This pattern
is matched to a grading scale to generate a numerical report (details provided in [22, 26]).
Arbuckle and colleagues [1, 2] developed and validated
the content of two questionnaires focusing on the patients’ self-assessment of skin oiliness. The first one, the
‘Oily Skin Self-Assessment Scale’ (OSSAS), measures facial oily skin severity and consists of three questionnaires
that assess subjects’ oily facial skin through visual perception of oily skin, tactile perception of oily skin and
sensation of oily skin questions. The second one, the ‘Oily
Skin Impact Scale’ (OSIS), assesses the emotional impact
of oily skin using two questionnaires. One evaluates the
subjects’ annoyance and the other their self-image/selfconcept. OSSAS scales have low correlations with the Sebumeter data [2]. As the validity of the Sebumeter has not
been demonstrated, it is difficult to interpret this result.
Note that the reliability of self-assessment questionnaires
might be affected by numerous environmental (e.g. humidity, season of the year) and biological conditions (e.g.
hormonal fluctuations), and, most importantly, it depends on the individuals’ subjective perception of skin
oiliness. Self-perception of physical appearance may not
always correspond with the biophysical measurements.
Another validated questionnaire is the Oily Skin SelfImage Questionnaire (OSSIQ), developed with 18-item
questions to assess perception as well as behavioral and
emotional consequences associated with oily skin. In
contrast to previous studies, OSSIQ scores accorded with
objective sebum level measurements [3].
Oily Skin
Genetic Influence
A twin study investigating sebum secretion in 20 pairs
of adolescent acne twins found that, differently from dizygotic twins, the sebum secretion rate was homogeneous
between monozygotic twins [38]. Several genes regulate
sebaceous gland function. Overexpression of the ageingassociated gene Smad7 in adult transgenic mice has been
correlated with hyperplasia of the sebaceous gland, and
c-myc overexpression has been shown to be associated
with enhanced sebaceous lipid synthesis and to have a
drastic decrease with age. Parathyroid hormone-related
protein knock-out mice presented hypoplastic sebaceous
glands, whereas parathyroid hormone-related protein
overexpression led to sebaceous gland hyperplasia [39].
Age, Gender, Ethnic and Seasonal Variation
Differences in sebum secretion at various times of life
have been associated with concomitant changes in endogenous androgen production. Sebaceous glands are
well developed in neonates, but their size decreases dramatically a few weeks after birth, starts to rise again with
the adrenarche and reaches its maximum in young adults.
While the number of sebaceous glands remains the same
during life, sebum secretion rates are highest in the
15–35-year-olds and decline continuously throughout
the adult age range [40]. At any age range, the mean sebum values in men exceed those of women. Although
surface lipid levels fall with age, paradoxically, the sebaceous glands become larger, rather than smaller, as a result of decreased cellular turnover [5, 39, 41–43]. This
could explain the larger pores observed on the elderly
Black subjects have larger sebaceous glands which
contribute to the increased sebum secretion. Hillebrand
et al. [44] reported that African-Americans showed significantly more sebum excretion than East Asians. African-Americans also had a greater pore count fraction, but
the number of pores increased with age in all races [45].
Kligman and Shelley’s [18] comparative racial study also
confirmed these observations. Blacks presented higher
sebum casual levels compared to Whites [18]. However,
the results of Pochi and Strauss [46] and Grimes et al. [47]
showed no consistent difference in sebaceous gland activity between black and white skin.
Experiments of Cunliffe et al. [48] demonstrated that
the sebum excretion rate varies directly with temperature, so that an increase in temperature of 1 ° C produces
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the response of the sebaceous gland to total caloric deprivation in 18 obese patients undergoing fasts for periods
of 4–8 weeks. Sebum release reduced in an average of 40%
[31]. These data may indicate that the composition and
quantity of food could, when changed significantly, produce measurable variation in the sebaceous gland product [32].
Diets rich in carbohydrates with a high glycemic index
are associated with hyperglycemia, reactive hyperinsulinemia and increased formation of insulin-like growth
factor-1 (IGF-1). Except for cheese, milk and all dairy
products also have potent insulinotropic properties, far
exceeding those expected from their low glycemic indexes [33]. Insulin and IGF-1 levels also peak during late puberty and gradually decline until the third decade [34].
Insulin and IGF-1 stimulate sebaceous gland lipogenesis
in vitro by increasing the expression of a transcription
factor (SREBP-1) that regulates numerous genes involved
in lipid biosynthesis [35]. IGF-1 also mediates the induction of androgen production and stimulation of peripheral androgen metabolism. Its signaling alleviates androgen receptor repression by the repressive protein Foxo1,
resulting in androgen receptor gain-of-function. Thus,
IGF-1 has direct influence on the intracrine androgen
regulation of the skin and potentiates androgen signaling
by the induction of 5␣-reductase activity and activation
of the androgen receptor [34].
Vora et al. [36] compared facial sebum levels with serum IGF-1 levels in 16 patients (mean age 19.5 8 2 years)
with acne. They found a positive correlation between the
mean facial sebum excretion (␮g cm–2) and serum IGF-1
[36]. Smith et al. [34] compared the endocrine effects of
an experimental low glycemic-load diet with a conventional high glycemic-load diet on 43 patients with acne.
After 12 weeks, the low glycemic-load diet group showed
a significant improvement in insulin sensitivity and a reduction in testosterone bioavailability and DHEAS concentrations [34].
Smith et al. [15] found that volunteers on a low glycemic-load diet demonstrated an increase in the saturated
fatty acid/monounsaturated fatty acid ratio compared to
a decrease in the control group. However, they did not
detect an effect of the dietary intervention on sebum output [15]. Recent evidence suggests that only monounsaturated fatty acids induce hyperkeratinization and epidermal hyperplasia similar to that seen in comedo formation, whereas saturated fatty acids have little effect [37].
Further studies are required to better clarify the underlying role of diet in sebaceous gland physiology.
Table 1. Correlations between sebum secretion and diet, genetic influence, age, gender as well as ethnic and seasonal variation
Genetic influence
Age, gender, ethnic variation
Seasonal variation
– Composition and
quantity of food, when
changed significantly, may
produce variation in sebum
secretion [30, 31]
– Insulin and IGF-1
stimulate sebaceous gland
lipogenesis in vitro [35]
– Vora et al. [36] found a
positive correlation between
mean facial sebum excretion
and serum IGF-1
– Differently from dizygotic
twins, sebum secretion is
homogeneous between
monozygotic twins [38]
– Overexpression of the
ageing-associated gene Smad7
in adult transgenic mice has
been correlated with
hyperplasia of the sebaceous
gland [39]
– Secretion rates are highest in
15–35-year-olds and decline
continuously throughout the adult
age range [40]
– At any age, mean sebum values
in men exceed those found in
– Some studies demonstrate no
consistent difference in sebaceous
gland activity between black and
white skin, although others show
that Blacks present higher sebum
casual levels compared to whites
[5, 18, 39, 41–43, 45]
– An increase in temperature
of 1° C produces an increase in
the sebum excretion rate in
the order of 10% (due to
alterations in sebum viscosity,
not in sebum production) [48]
– Warming or cooling the skin
changes the flow to the surface
by making the preformed
sebum either more or less
viscous [49]
Skin Pharmacol Physiol 2012;25:227–235
sual levels. In general, the casual levels were not higher in
those whom they estimated to be greasier. In fact, the two
highest levels in the group were in subjects judged to be
non-greasy. They concluded that marked and persistent
greasiness truly reflects increased quantities of surface
lipids, but sudden or intermittent greasiness is more likely due to sweating. Warming or cooling the skin changes
the flow to the surface by making the preformed sebum
either more or less viscous. Therefore, after defatting the
skin, the flow to the surface can be expected to be strongly temperature dependent. Furthermore, the wicking
power of the emptied capillary reservoir will be greater
when the liquid is less viscous. The increased greasiness
of the face in the summer or in tropical climates may simply be an expression of increased eccrine sweating or a
decreased sebum viscosity [18]. Correlations between sebum secretion and diet, genetic influence, age, gender as
well as ethnic and seasonal variations are summarized in
table 1.
Sebum: Protective Effects
The functions attributed to sebum in humans include
the delivery of fat-soluble antioxidants to the skin surface
and antimicrobial activity [12]. Sebum mantles the epidermis, representing the ultimate barrier of the body
against exogenous oxidative insults. It is believed to deliver antioxidants to the surface in the form of vitamin E
(␣-tocopherol) and CoQ10 [52].
Squalene is the first human skin surface lipid targeted
by oxidative stresses such as sun light and, as a conseSakuma/Maibach
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an increase in the sebum excretion rate in the order of
10%. This result might reflect a change in the rate of delivery of sebum to the skin surface due to alterations in
sebum viscosity, or an increase in the rate of absorption
by the collecting papers. The possibility of sebum production increase was dismissed as the changes occurred
within 90 min and the sebaceous gland turnover rate approximates 7 days [48–50]. Youn et al. [51] measured facial sebum secretion seasonally for 1 year and found summer to be the highest sebum-secreting season.
Kligman and Shelley [18], while comparing lipoid deliveries in atropinized and non-atropinized sites of sweating subjects, made an observation of clinical significance.
Although visible oil droplets formed in the dry atropinized sites, the skin showed no evidence of being greasy or
oily. In the symmetrical sweating site, oiliness was prominent. According to them, the clinical impression of oiliness would not be a reliable index of surface lipids (this
could explain the differences observed between the Sebumeter measurements and the subjective questionnaire results obtained by Arbuckle et al. [1]). The presence of
sweat would impart the clinical appearance of oiliness.
According to the authors, how oily a subject will appear
at any one time will be influenced by the chance of his/
her having recently sweated or having been in an environment of high humidity. It is easy to understand why
oiliness is less prominent in winter and, conversely, so
marked in hot humid climates. Possibly, it is the emulsification of sweat with oil that is responsible for the oily
Kligman and Shelley [18] also graded 12 white males
in terms of clinical greasiness and determined their ca-
Sebum: Undesirable Effects
Besides surface oiliness, excess sebum blocks pores,
provides nourishment to bacteria that live upon the skin
(Propionibacterium acnes) and contributes to acne flareups. Along with increased sebum secretion rate, quantitative modifications of sebum are also likely to occur in
acne [12].
Sebum participates in the induction of comedo formation, which represents the retention of hyperproliferating
ductal corneocytes in the pilosebaceous duct [56]. Upon
oxidative challenge (e.g. UV radiation), squalene is readily oxidized to squalene peroxide, which is comedogenic.
Comedones have been triggered by exposing rabbit ears
to irradiated squalene. A positive correlation exists between the degree of squalene peroxidation and the size of
the comedones elicited. In addition, marked hyperplasia
and hyperkeratosis of the epithelium in the follicular infundibulum and marked proliferation of sebaceous
glands were observed.
In vitro data showed that squalene peroxide beyond
the induction of HaCaT keratinocytes proliferation led
Oily Skin
also to the upregulation and release of inflammatory mediators, which indicate a pro-inflammatory activity of
by-products of squalene oxidation. The strategy that skin
adopts to limit the potentially harmful effects of peroxidated squalene relies on the vitamin E supply to the skin
surface, mentioned previously [12].
Sebum and Water Barrier Function
The stratum corneum is an efficient biological barrier
membrane, protecting the underlying living tissue from
water loss, etc. Despite being on the skin surface, sebum
does not seem to influence this function. Fluhr et al. [57]
studied asebia J1 mice, which display profound sebaceous
gland hypoplasia, and found transepidermal water loss
levels comparable to those of control animals, and the
ability to acutely restore permeability barrier function to
normal after acute disruption was unchanged [58].
Sebum and Hydration
Note that skin oiliness is a property of the sebaceous
glands and that skin moisture is largely a property of the
stratum corneum. Low sebum secretion and high water
content are considered main features of fair skin. The latter is dependent upon the rates of water movement into
and out of this tissue (barrier function), as well as upon
the ability of the stratum corneum to retain water [59, 60].
Hydrated skin is soft and smooth, and reflects the optimum water content in the superficial stratum corneum.
It results from the complex and perfect interaction of water-holding substances, (i.e. amino acids produced by
proteolysis of filaggrin that occurs during their slow upward movement in the stratum corneum), lactate and potassium derived from sweat as well as intercellular lipids,
specially their major component ceramides that play a
crucial role in providing barrier function to the stratum
corneum [59]. In conjunction with cholesterol, free fatty
acids and cholesterol sulfate, they form arrays of hydrophobic chains, constructing lipid bilayers with closely
packed interiors which dramatically reduce their permeability to water and solutes. Commonly used tools to assess skin hydration are the Corneometer쏐 (CK electronic), the Skin Surface Hygrometer (Skicon-200) and the
DermaPhase meter (Nova DPM 9003), which measure
capacitance, conductance and impedance-based capacitance, respectively [61].
Skin Pharmacol Physiol 2012;25:227–235
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quence, is depleted where a toxic photo-oxidation product (squalene monohydroperoxide isomers) is produced
[53]. Passi et al. [54] demonstrated that exposure of sebum to UV irradiation (4 MED) depleted 84.2% of vitamin E, 70% of CoQ10 and only 13% of squalene, while
10-MED UV exposure produced a 26% loss of squalene.
The same UV dose when applied in the absence of vitamin E and CoQ10 produced a 90% decrease in squalene
[54]. This antioxidant function of sebum is important as
the buildup of reactive oxygen species on the skin surface
can cause a breakdown of the skin barrier and signs of
aging [8].
Sebocytes are part of the innate immune system. By
sonicating total sebum into bacterial culture medium,
Wille and Kydonieus [55] observed that the Gram-positive bacteria tested (Staphylococcus aureus, Streptococcus
salivarius) were exceedingly susceptible to sebum, with a
significant (1 4 orders of magnitude) decrease in the
number of viable cells. However, most Gram-negative
bacteria tested (Escherichia coli, Pseudomonas aeruginosa
and Echinococcus faecalis) were unaffected. Fractionation
of the human sebum lipids showed that the C16:1⌬6 isomer of palmitoleic acid (cPA) was the most active antibactericidal fatty acid component and the most active
fraction in blocking the adherence of a pathogenic strain
of Candida albicans to the porcine stratum corneum [55].
Harsh cleaners or overwashing the skin to remove excess sebum might remove these lipids from the stratum
corneum surface, resulting in excessive skin drying. Another essential factor to guarantee minimally permeable
water barrier is the physical state of the lipid chains in the
non-polar regions of the bilayers. Due to their high melting point, at physiological temperature they are mainly in
a solid crystalline or gel state, enabling low lateral diffusional properties. Contrary to the permeability barrier
results, Fluhr et al. [57] found that the water-holding capacity of the stratum corneum was reduced in asebia J1
mice. This appeared to be due to a decrease in glycerol, a
well-known humectant and a potential catabolic product
of sebaceous gland-derived triglycerides.
We conclude that the intuitive belief that a low sebum
secretion rate is the main cause of dry skin is not accurate,
although sebum seems to play a minor role in skin hydration. It is also inappropriate to use the term dry skin as
the opposite of oily skin. If dry skin represented the opposite of greasy skin, one should expect little sebum in
xerotic conditions. In many types of xerosis, however, sebum excretion remains in the physiological range [8]. The
skin should be better referred as oily or non-oily when
referring to the sebum content or, when regarding water
content, dry or non-dry.
Oily skin is a common cosmetic problem that occurs
when oversized sebaceous glands produce excessive
amounts of sebum, giving the appearance of shiny and
greasy skin. These glands are under androgen control of
and appear influenced by increased IGF-1 generation by
high glycemic-index diets. Age, gender, ethnicity and hot
humid climates may also play a role in skin oiliness variations. With this overview, we shed some scientific light
to some common daily questions and misconceptions,
such as why overwashing the skin does not cause sebum
overproduction but may cause dryness, why all skin are
of a ‘combination’ type and why dry skin is not the opposite of oily skin. The deeper understanding of this type
of skin provides the opportunity to better guide patients
regarding skin care and also assist in the development of
sebosuppressive agents.
Disclosure Statement
The authors have no conflicts to declare.
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