Arch Dermatol Res (2012) 304:683687
DOI 10.1007/s00403-012-1254-0
ORIGINAL PAPER
The association of oxidative stress and disease activity
in seborrheic dermatitis
Selma Emre Ahmet Metin Duriye Deniz Demirseren
Gulsen Akoglu Aynure Oztekin Salim Neselioglu
Ozcan Erel
Received: 3 April 2012 / Revised: 29 May 2012 / Accepted: 1 June 2012 / Published online: 15 June 2012
Springer-Verlag 2012
Abstract The pathogenesis of seborrheic dermatitis (SD)
has not been clearly identified, and many factors are
thought to play a role in its development. Recently, new
studies have focused on increased oxidative stress (OS) in
T cell-mediated skin diseases like psoriasis, contact der-
matitis, and atopic dermatitis. However, there is no study
investigating the status of OS in SD. In this study, we
aimed to determine the status of OS in SD and the corre-
lation of disease severity with OS. Fifty-four patients who
were clinically and/or histopathologically diagnosed with
SD were included in the study. Fifty-four healthy volun-
teers constituted the control group. Disease severity in
patients with SD was scored according to the Seborrheic
Dermatitis Area and Severity Index (SDASI). Serum total
antioxidant status (TAS) and total oxidative status (TOS)
were measured, and the oxidative stress index (OSI) was
calculated in all patients and control subjects. The mean
TAS values were significantly lower in the patient group
than in the control group (p = 0.024). However, patients
had significantly higher TOS and OSI values than the
controls (p \ 0.05). There was no correlation between
SDASI and TAS, TOS, and OSI values. In this study, the
association of oxidative stress and disease activity has first
investigated in seborrheic dermatitis. It was found that OS
S. Emre (&)  A. Metin  D. D. Demirseren  G. Akoglu 
A. Oztekin
Clinic of Dermatology, Ataturk Training and Research Hospital,
Bilkent, Ankara, Turkey
e-mail: dr_semre@yahoo.com
S. Neselioglu  O. Erel
Clinic of Biochemistry, Ataturk Training and Research Hospital,
Ankara, Turkey
was significantly higher in SD patients than in healthy
subjects. In conclusion, our findings point to the possible
role of the OS for the etiopathogenesis of SD.
Keywords Seborrheic dermatitis  Oxidative stress 
Oxidant status  Antioxidant status
Introduction
Seborrheic dermatitis (SD) is an inflammatory skin disor-
der characterized by greasy scaling with an erythematous
background on the sebum-rich areas of the skin. Scalp,
eyebrows, ears, nasolabial folds, presternal and interscap-
ular regions, axillae, and inguinal folds are the most
affected sites of the body. Seborrheic dermatitis affects
210 % of healthy adults and it is more common in males,
young adults, and adolescents [37].
The pathogenesis of SD has not been clearly identified.
Many factors are suggested to play a role in the develop-
ment of SD lesions. Although SD is mainly observed on
sebum-rich areas, it is not defined as a sebaceous gland
disease. The high frequency of the disease in adolescents
and young adults, whose sebum production is maximum,
and the localisation of the lesions on the skin abundant with
sebaceous glands are the clues that SD is related to sebum
[16]. However, sebum levels are not higher in patients with
SD than normal population [17]. The higher frequency in
males and the onset of symptoms during puberty point that
androgens may involve in the pathogenesis of SD [16].
Psychological stress, depression, neurological diseases, and
dry and polluted air have negative effects on SD [17, 28].
Although no evidence has been provided, it has been pro-
posed that the inflammatory response is triggered by toxic
metabolites of Malassezia species (Malassezia spp.), non-
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immunogenic irritations, and reactive oxygen species
(ROS) [14, 26, 28].
Malassezia spp. which are accepted to be members of
the normal flora of the skin in 7598 % of healthy indi-
viduals have been demonstrated to have a main role in the
pathogenesis of SD [1]. In recent studies, the most common
detected types were M. globosa, M. furfur, M. restrica, and
M. sympodialis in the lesions of SD. Malassezia spp. were
suggested to induce or aggravate the disease in patients
who are susceptible to SD [15, 35]. Regression of SD
lesions observed using antifungal therapies that are effec-
tive against Malassezia spp. also supports the role of these
microorganisms in SD [8, 35]. However, the current
knowledge is not sufficient to explain the exact role of
Malassesia in SD pathogenesis [15].
Recently, new studies have focused on the increased
oxidative stress (OS) in T cell-mediated skin diseases like
psoriasis, contact dermatitis, and atopic dermatitis [2, 33].
However, there is no study investigating the status of OS in
SD. In this study, we aimed to determine the status of OS in
SD and the correlation of disease severity with OS.
Materials and methods
This study was performed in accordance with the guide-
lines of good clinical practice and the Helsinki declaration
between July 2009 and July 2010. Clinical Research Ethics
Committee of the hospital approved the study. Fifty-four
patients who were clinically and/or histopathologically
diagnosed with SD and 54 healthy controls were included
in the study. Neither patients nor control subjects were on
any local and/or systemic treatments with anti-inflamma-
tory and/or anti-mycotic drugs at participation. Pregnant or
nursing women, patients who had cardiac, renal or hepatic
disease, diabetes mellitus, a positive HIV test, allergies, or
active infection were excluded from the study. Disease
severity in patients with SD was scored according to the
Seborrheic Dermatitis Area and Severity Index (SDASI)
(range of scores 012.6) modified by Comert et al. [8]. All
participants were informed about the study and signed
informed consents were obtained.
Measurement of serum total oxidant status (TOS)
The total oxidant status (TOS) of the serum was studied at
658 nm using the fully-automated colorimetric method
with an autoanalyzer (Advia 2400 Clinical Chemistry
System, Siemens Healthcare Diagnostics, Tarrytown, New
York, USA). Assay Diagnostics (Turkey) kits developed
by Erel [12] were used to study TOS. The oxidants present
in the sample oxidize the ferrous ion-o-dianisidine complex
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Arch Dermatol Res (2012) 304:683687
to ferric ion in this method. The oxidation reaction was
enhanced by glycerol molecules, which are abundantly
present in the reaction medium. The ferric ion produced a
coloured complex with xylenol orange in an acidic med-
ium. The colour intensity, which could be measured
spectrophotometrically, was related to the total amount of
oxidant molecules present in the sample. The assay was
calibrated with hydrogen peroxide (calibrator concentra-
tion 10 lM, analytical range 0300 lM) and the results are
expressed in terms of micromolar hydrogen peroxide
equivalent per litre (lmol H2O2 Eq/L).
Measurement of serum total antioxidant status (TAS)
The total antioxidant levels (TAS) of the serum was mea-
sured using an automated colorimetric measurement
method for TAS [11]. This method is based on the
bleaching of characteristic colour of a more stable ABTS
(2,20 -azino-bis[3-ethylbenzothiazoline-6-sulphonic acid])
radical cation by antioxidants. The results were expressed
as mmol Trolox (Rel Assay) equivalent/L.
Determination of oxidative stress index (OSI)
The ratio of TOS to TAS was accepted as oxidative stress
index (OSI). The OSI value is calculated according to
below formula [23] in which TAS values were converted to
lmol/L: OSI (arbitrary unit) = [TOS (lmol H2O2 Eq/L)/
TAS (lmol Trolox Eq/L)] 9 100.
Statistical analysis
KolmogorovSmirnov test was used for the comparisons to
determine the distribution of all variable groups. Non-
parametric variables were compared using MannWhitney
U test. Cross tabulation statistics were used for the com-
parison of categoric variables. The association between the
variables (for symmetrically distributed data) was deter-
mined by the Pearson correlation test. The statistical
analyses of the determined data were performed by SPSS
16.0 software. Statistical significance was accepted as
p \ 0.05.
Results
The study included 33 females (61.1 %) and 21 males
(38.9 %) in the patient group and 37 females (68.5 %) and
17 males (31.5 %) as controls. There was no statistically
significant difference between the two groups in regard to
age and gender (p = 0.283 and p = 0.420, respectively)
(Table 1). Fifty-one (94.4 %) patients had scalp lesions, 13
(24.7 %) had nasolabial sulcus involvement, 7 had
Arch Dermatol Res (2012) 304:683687 685

Table 1 Baseline characteristic of patients and controls status is firstly investigated in SD, which is a chronic
Patients (n = 54) Controls (n = 54) p
inflammatory skin disease.
Reactive oxygen species are the most important com-
Age (years) ponents of the oxidative system [4, 31]. Exposure of
Median (range) 25 (1854) 25 (1854) 0.283 keratinocytes to chemical irritants, allergens, or inflam-
Gender matory agents such as UVA and UVB radiation causes
Male (n/%) 21/38.9 17/31.5 0.420 ROS activation. The ROS may act as a second messenger
Female (n/%) 33/61.1 37/68.5 in biological processes and play a triggering role in the
pathogenesis of allergic reactions and inflammation in the
skin [6, 13]. They cause lipid peroxidation in the cell
Table 2 Oxidative stress parameters of patients and controls
membrane, DNA damage, and the secretion of inflamma-
Patients Controls p tory cytokines, eliciting an immune and inflammatory
response [4, 33].
TAS (lmol Trolox Eq/L) 3.33 0.45 3.52 0.43 0.024
(mean SD) Immunohistochemical studies in SD patients have
TOS (lmol H2O2 Eq/L) 12.20 9.85 0.007 shown increased production of cytokines such as IL-1a, IL-
(median, range) (6.5146.35) (1.0541.57) 1b, TNF a, IFNc, IL-12, and IL-4 in the lesional skin
OSI (arbitrary unit) 0.38 0.30 0.001 compared with nonlesional skin [13]. A significant increase
(median, range) (0.221.09) (0.030.99) in the ratio of IL-1RA: IL-1a and IL-8 and overproduction
TAS total antioxidant status, TOS total oxidative status, OSI oxidative of histamine have been detected in the scalp skin of
stress index patients with dandruff and SD when compared to healthy
individuals [1, 22]. Oxidative stress is thought to produce
Table 3 Correlation between disease severity (SDASI) and oxida- this inflammatory response observed in SD [14].
tive stress parameters including total antioxidant status (TAS), total The TOS indicates the total oxidative products in the
oxidant status (TOS), and oxidative stress index (OSI)
body. Serum levels of oxidative products such as ROS,
TAS TOS OSI reactive nitrogen species, hydrochloric acid, malonyldial-
dehyde, and lipid peroxides constitute TOS [12, 33]. In this
SDASI
study, the measurements of TOS levels were significantly
r -0.082 0.065 0.114
higher in the patients with SD than the healthy controls.
p 0.556 0.638 0.414
However, there was no correlation between TOS and dis-
SDASI Seborrheic Dermatitis Area and Severity Index ease severity.
There are antioxidant defence systems that eliminate the
(12.9 %) eyebrow, 4 (7.4 %) had postauricular, 3 (5.5 %) harmful effects of ROS in the body [16, 20]. The plasma
had inguinal, and 3 (5.55) had sternal lesions of SD. The concentrations of antioxidant molecules can be measured
mean SDASI of the patients was 2.25 0.99 with a score separately; however, this method is very difficult and time-
range of 0.55.1. Complete blood count and biochemistry consuming. The fully-automated method which provides
results were within normal limits and similar in both the ability to measure the total serum concentrations of
patients and controls. Mean TAS values were significantly antioxidant molecules was used in the present study [11].
lower in the patient group than the control group The mean TAS value was significantly lower in the patient
(p = 0.024). However, TOS and OSI values of the patients group than in the control group. There was no correlation
were significantly higher than controls (p \ 0.01) between TAS levels and disease severity of SD.
(Table 2). There was no correlation between disease In cases of extremely elevated levels of ROS, the pro-
severity and TAS, TOS, and OSI values (Table 3). duction of antioxidant enzymes also increases in order to
protect the structural and functional integrity of the organ-
ism [33]. Therefore, measurement of isolated TAS or TOS
Discussion levels may be inadequate to show the exact OS status in the
organism. The OSI is obtained by the ratio of TAS/TOS,
Oxidative stress emerges as a result of overproduction of which is the most crucial factor in determining OS [2]. In this
oxygen radicals or inadequate antioxidant defence mech- study, the values of OSI were significantly higher in the
anisms. To date, it has been shown that OS plays a role in patients than controls, indicating the presence of higher OS
the pathogenesis of more than 100 disorders, including in SD. On the other hand, no significant correlation was
allergic diseases, inflammatory skin diseases, vitiligo, observed between disease severity and OSI.
psoriasis, acne vulgaris, atopic dermatitis, Behcets dis- The role of OS in inflammatory skin diseases including
ease, and skin cancers [2, 19, 20, 24]. In this study, OS psoriasis, atopic dermatitis, and allergic contact dermatitis

123
686
has been investigated widely in dermatology [6]. Although
the pathogenesis of SD is not clearly established, SD has
similar clinicopathological properties with psoriasis and
atopic dermatitis [21, 22]. The scalp and facial lesions of
SD may not be sometimes distinguishable from psoriasis
[15]. Despite spongiosis in the histopathological examin-
ations supports SD rather than psoriasis, the late lesions of
SD may have psoriasiform features with less or absence of
spongiosis [35]. Involvement of T cells and increase in
counts of NK T cells and CD16? cells were demonstrated
in the inflammation of SD, which was similar in the cel-
lular alterations observed in psoriasis [3, 13]. The infantile
form of SD may closely resemble atopic dermatitis and SD
was suggested to be a variant of atopic dermatitis [34].
Unclarified complex mechanisms including cutaneous
microflora, cutaneous immunity, genetics, and environ-
mental factors, which involve in atopic dermatitis and
psoriasis, were also suggested to have important effects in
the pathogenesis of SD [15, 21, 22, 33]. However, there is
no study investigating the status of OS in SD to explain
whether OS may involve in the pathogenesis of the disor-
der. The present study is the first one that investigated the
association of OS and disease activity in SD. The main
finding of our study was that a higher level of systemic OS
was present in SD patients than in healthy individuals. An
increase in oxidative products together with inadequate
amounts of antioxidants in the whole organism might
contribute to a systemic OS in SD.
It is known that SD is more common in patients with
Parkinsons disease (PD) [16], HIV/AIDS [29], various
cancers [7], and Downs syndrome [10] than in the normal
population. However, the reason of association of SD with
these disorders has not been clearly understood [16].
Mitochondrial functional impairment causing increased
lipid peroxidation and OS in PD, and increased OS were
considered to have a role in the onset and progression of
the symptoms of this disease [5, 9, 30, 38, 39]. Interest-
ingly, OS was determined to be significantly increased in
patients with HIV/AIDS [36, 37] and a chronic OS was
shown in Downs syndrome [18, 27] and cancer [25, 39]. It
is likely that diseases in which SD is frequently observed
may have an increased systemic OS in common.
Polyunsaturated fatty acids (PUFA) which exist in the
composition of membrane phospholipids have a critical
role for the maintenance of normal structures and functions
of epidermal cells. Previous studies have shown that
abnormalities in essential fatty acid metabolism may play a
role in atopic eczema, acne, and psoriasis [32, 40]. Plasma
deficiency of PUFA in animals induces manifestations on
the skin characterized by scaly dermatosis, hyperprolifer-
ation of epidermis, hyperkeratosis, hypergranulosis,
achanthosis, and erythema. In an another study, levels of
serum vitamin E, PUFA of phospholipids, and erythrocyte
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Arch Dermatol Res (2012) 304:683687
glutathione peroxidase have been detected to be lower both
in HIV-positive and HIV-negative patients with SD than
healthy individuals without SD. The authors suggested that
these findings involve in the pathogenesis of SD [32]. Our
results also point the lower levels of antioxidants in SD in
parallel to their conclusion. In our study, although a higher
OS was detected in patients with SD, none of them had SD
induced by comorbidities such as PD, AIDS, Downs
syndrome, or malignancy. Therefore, the findings of
increased OS may only be related to the presence of SD in
the patients.
The present study has introduced a systemic OS in
patients with SD. Since total serum oxidants and antioxi-
dants were measured at the same point in time, we cannot
conclude an exact cause and effect relationship according
to the cross-sectional design of the study. However, this
study may give important suggestions about the patho-
genesis of SD. The patients who are susceptible to develop
SD because of genetical, immunological, or environmental
factors may have a chronic permanent systemic OS. When
exposed to triggering factors of SD, the lesions of SD may
easily develop in these patients. One of the remarkable
results of this study is the lack of correlation between
disease severity and OS. This finding may suggest that OS
may be a main preparative or triggering factor leading the
onset of SD that does not directly affect the severity of the
disease. On the other hand, OS may be a chronic condition
that provides the persistence of the disease. To clarify this
suggestion in detail, some further studies are needed. The
local measurement of OS in the lesions of SD and com-
parison of the local OS parameters with circulating ones in
the whole organism may be helpful. Besides, to demon-
strate a relationship between OS markers and disease
severity, a longitudinal assessment of OS status before and
after SD therapies with or without oral antioxidant sup-
plementation may be considered. Since our study is the first
one that highlights a systemic OS is present in patients with
OS, we think that the results of our study will give rise to
further studies about OS in SD to explain the pathogenesis
of this disorder. Although the presence of a systemic OS is
detected in SD, we cannot point the origin of the OS and
cannot establish the systemic changes related to OS in
patients with SD in the scope of our study. These are also
the other important issues to be investigated in future
studies.
In conclusion, our findings point to the possible role of
the OS for the etiopathogenesis of SD. We think that this
study has important results since it is the first one that
demonstrates the role of OS in SD. The higher levels of OS
in SD also suggest that new treatment alternatives targeting
OS may be effective in SD. Further studies are needed
to support our findings and identify the pathogenetic
mechanisms.
Arch Dermatol Res (2012) 304:683687
Conflict of interest None.
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