Jurnal Dermatitis Seboroik
Jurnal Dermatitis Seboroik
Jurnal Dermatitis Seboroik
Abstract
Seborrheic Dermatitis (SD) and dandruff are of a continuous
spectrum of the same disease that affects the seborrheic areas of
the body. Dandruff is restricted to the scalp, and involves itchy, flaking
skin without visible inflammation. SD can affect the scalp as well as
other seborrheic areas, and involves itchy and flaking or scaling skin,
inflammation and pruritus. Various intrinsic and environmental factors,
such as sebaceous secretions, skin surface fungal colonization,
individual susceptibility, and interactions between these factors,
all contribute to the pathogenesis of SD and dandruff. In this
review, we summarize the current knowledge on SD and dandruff,
including epidemiology, burden of disease, clinical presentations
and diagnosis, treatment, genetic studies in humans and animal
models, and predisposing factors. Genetic and biochemical studies
and investigations in animal models provide further insight on the
pathophysiology and strategies for better treatment.
Abbreviations
AIDS: Acquired Immune-Deficiency Syndrome; FTA-ABS:
Fluorescent Treponemal Antibody-Absorption; HAART: Highly
Active Antiretroviral Therapy; HIV: Human Immune-Deficiency
Virus; ICD: Irritant Contact Dermatitis; QOL: Quality of Life;
RPR: Rapid Plasma Regain; SC: Stratum Corneum; SD: Seborrheic
Dermatitis; VDRL: Venereal Disease Research Laboratory
Introduction
Seborrheic Dermatitis (SD) and dandruff are common
dermatological problems that affect the seborrheic areas of the body.
They are considered the same basic condition sharing many features
and responding to similar treatments, differing only in locality
and severity. Dandruff is restricted to the scalp, and involves itchy,
flaking skin without visible inflammation. SD affects the scalp as well
as face, retro-auricular area, and the upper chest, causing flaking,
scaling, inflammation and pruritus, and can have marked erythema.
Flaking in SD and dandruff is usually white-to-yellowish, and may
be oily or dry.
It is estimated that SD and dandruff combined affect half of the
adult population. Despite such high prevalence, their etiology is not
well understood. Various intrinsic and environmental factors, such
as sebaceous secretions, skin surface fungal colonization, individual
susceptibility, and interactions between these factors, all contribute
to the pathogenesis. Genetic, biochemical studies and investigations
in animal models further provided insight on the pathophysiology
and strategies for better treatment. In this comprehensive review, we
summarize the current knowledge on SD and dandruff, and attempt
to provide directions for future investigations and treatments.
Open Access
Review Article
Journal of
Epidemiology
SD is a common dermatological disorder in the United States and
worldwide [1]. Its incidence peaks during three age periods - in the
first three months of life, during puberty, and in adulthood with an
apex at 40 to 60 years of age [1-4]. In infants up to three months of
age, SD involves the scalp (termed cradle cap), the face, and diaper
area. Incidence can be up to 42% [4-6]. In adolescents and adults,
SD affects the scalp and other seborrheic areas on the face, upperchest, axillae, and inguinal folds [4,7,8]. Incidence is 1-3% of the
general adult population [3,9]. Men are affected more frequently than
women (3.0% vs. 2.6%) in all age groups, suggesting that SD may be
associated with sex hormones such as androgens [1,3,8]. No apparent
differences were observed in SD incidence between ethnic groups [3].
SD is more prevalent in immune-compromised patients such as
HIV/AIDS patients [7,10], organ transplant recipients [11,12], and
patients with lymphoma [13]. The incidence among HIV patients
ranges from 30% to 83% [9,10]. Most cases of SD in HIV patients
are diagnosed with CD4+ T lymphocyte counts between 200 and
500/mm3 [3,14,15], and decreased CD4+ counts are often associated
with worse SD. Fewer cases of SD were reported when CD4+ T
cells were more than 500/mm3 [14]. These observations suggest that
immunological defects may play a role in SD.
SD is also associated with neurological disorders and
psychiatric diseases, including Parkinsons disease, neuroleptic
induced parkinsonism, tardive dyskinesia, traumatic brain injury,
epilepsy, facial nerve palsy, spinal cord injury and mood depression
[4,5,16,17], chronic alcoholic pancreatitis, hepatitis C virus [18,19],
and in patients with congenital disorders such as Down syndrome
[20]. Furthermore, seborrhea-like dermatitis of the face may also
develop in patients treated for psoriasis with psoralen and ultraviolet
A (PUVA) therapy [21].
Comparing with SD, dandruff is much more common, and affects
Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
ISSN: 2373-1044
Features
Dandruff
Scalp
SD in Infants
Burden of Disease
Trunk
Generalized
Scalp
Clinical presentations
The clinical presentations of SD and dandruff in children and
adults are summarized in Table 1. SD often presents as well-delimited
erythematous plaques with greasy-looking, yellowish scales of
varying extents in regions rich in sebaceous glands, such as the scalp,
the retro-auricular area, face (nasolabial folds, upper lip, eyelids and
eyebrows), and the upper chest. Distribution of the lesions is generally
symmetrical, and SD is neither contagious nor fatal. SD has a seasonal
pattern, presenting more frequently during winter, and improving
usually during summer [5,25,26]. Additionally, aggravation of SD has
been associated with sleep deprivation and stress [7,27,28].
SD in Adults
Body Folds
SD with
immunesuppression*
Differential diagnosis
The main differential diagnosis of SD and dandruff includes
psoriasis, atopic dermatitis (mainly in the pediatric form of SD),
tinea capitis, rosacea, and systemic lupus erythematous (SLE) [3,7,8]
(Table 2). While psoriasis can affect similar locations as SD, typical
lesions in psoriasis are thicker and present as plaques sharply limited
with silvery white scales [8,32]. Lesions in atopic dermatitis usually
do not appear until after 3 months of age, while lesions in SD usually
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Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
ISSN: 2373-1044
Table 2: Differential diagnosis of seborrheic dermatitis and dandruff.
Diagnosis
Diagnostic Clues
Psoriasis
Atopic
Dermatitis
Tinea Capitis
Rosacea
Systemic
Lupus
Erythematous
(SLE)
Others
Secondary
syphilis
Diaper
Dermatitis
appear earlier and rarely affect extensor areas. Tinea capitis, a highly
contagious disease, typically shows scaly patches of scalp hair loss
associated with black dots, which represent distal ends of broken
hairs [33]. Conversely, SD is not associated with hair loss. Rosacea
usually targets the malar areas on the face, sparing the nasolabial folds,
and do not have scales; on the other hand, facial SD lesions are usually
scaly, and affect the nasolabial folds, eyelids, and eyebrows, without
associated flushing or telangiectasias [7,8,34]. Finally, skin lesions
in SLE often follow a clear photo distribution, such as acute flares
of bilateral malar rash, and may be associated with extra-cutaneous
abnormalities such as arthritis, mouth ulcers, glomerulonephritis
or cardiomyopathy [8,35]; SD does not have a photo distribution
pattern, and does not affect organ systems other than the skin.
Other less common conditions that may resemble SD are
pemphigus foliaceous, pityriasis rosea, secondary syphilis, diaper
dermatitis and cutaneous Langerhans cell histiocytosis [3,4,7,30],
which are summarized in Table 2. The majority of these conditions
can be differentiated by clinical presentation and history; although
syphilis, pemphigus foliaceous and SLE may require laboratory
confirmation.
Pathology
Diagnosis of SD is typically made by history and physical
examination. In rare cases, a skin biopsy is needed for differential
diagnosis. Histologically, the development of SD can be divided into
two stages. In the acute and sub-acute stages, SD shows superficial
perivascular and perifollicular inflammatory infiltrates, composed
mainly of lymphocytes and histiocytes in association with spongiosis
and psoriasiform hyperplasia, and can be coupled with parakeratosis
around follicular opening (shoulder parakeratosis). Neutrophils can
also be found in the scale crust at the margins of follicular ostia. On the
other hand, in chronic lesions, marked psoriasiform hyperplasia and
parakeratosis can be present with dilation of the venules of surface
plexus which resembles psoriasis [3,4,38]. However, in psoriasis
parakeratosis is often associated with thinning or loss of the granular
layer due to accelerated keratinocyte differentiation.
Dandruff shows many common features as SD in histology,
such as epidermal hyperplasia, parakeratosis, and Malassezia yeasts
surrounding the parakeratotic cells [23]. Whereas inflammatory cells
such as lymphocytes and NK cells may be present in great numbers
in SD, dandruff shows subtle neutrophil infiltration or no infiltration.
These findings support the notion that dandruff and SD are of a
continuous spectrum of the same disease entity with different severity
and location [39].
Treatment
Treatment of SD and dandruff focuses on clearing signs of the
disease; ameliorating associated symptoms, especially pruritus; and
maintaining remission with long-term therapy. Because the main
underlying pathogenic mechanisms involve Malassezia proliferation
and local skin irritation and inflammation, the most common
treatment is topical antifungal and anti-inflammatory agents (Table
3). Other widely used therapies are coal tar, lithium gluconate/
succinate and phototherapy (Table 3). New therapies have also
emerged including immune modulators such as topical calcineurin
inhibitors, and metronidazole, but their efficacy remains controversial
[5]. Alternative therapies have been reported as well, such as tea tree
oil [40,41]. Some factors to be considered before selecting a treatment
include efficacy, side effects, ease of use/compliance, and age of the
patient [5]. Systemic therapy is needed only in widespread lesions and
in cases that do not respond to topical treatment [3,26].
Pathophysiology
Despite the high prevalence, the pathogenesis of SD and dandruff
is not well understood. However, studies have identified several
predisposing factors, including fungal colonization, sebaceous gland
activity, as well as several factors that confer individual susceptibility
[2].
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Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
ISSN: 2373-1044
Table 3: Treatment of seborrheic dermatitis and dandruff.
Cortico-steroids
Immunomodulators
TOPICAL
Antifungals
Medication
Miscellaneous
Regimen
Mechanisms
Side Effects
References
Ketoconazole
2% Shampoo, cream,
gel or foam
Bifonazole
1% shampoo, cream
or ointment
Miconazole
Cream
Ciclopirox Olamine
1.5% shampoo,
cream, gel or lotion
Selenium sulfide
2.5% shampoo
Scalp: Twice/week x 2
weeks, then once/week x
2 weeks. Repeat after 4-6
weeks.
Zinc Pyrithione
1% shampoo
Hydrocortisone
1% cream
Betamethasone
dipropionate
0.05% lotion
Desonide
Fluocinolone
Pimecrolimus
1% cream
0.1% ointment
Tacrolimus
Inhibition of cytokine
production by
T-lymphocyte.
[8,26,99,102]
[47,97,103]
[8,9,97,99,103,108]
[8,47,110]
[8,111-113]
[7,114]
[47,98,115-118]
Risk of skin malignancy
and lymphoma with
[26,97,109,118-120]
prolonged use.
Lithium gluconate/
8% ointment or gel
succinate
Anti-inflammatory via
increased IL-10 and
decreased TLR2 and
TLR4 in keratinocytes.
Metronidazole
0.75% gel
Anti-inflammatory via
inhibition of free radical
species.
Rare contact
sensitization with
prolonged use.
[5,47,125,126]
Phototherapy
Immuno-modulation
and inhibition of cell
proliferation.
Burning, itching
sensation during/after
therapy. Risk of genital
tumor with prolonged
use.
[26,127-129]
[97,130,131]
[132-134]
Coal tar
SYSTEMIC
Dose/
Formulation
4% shampoo
Itraconazole
Oral: 200 mg
Inhibition of fungal
cell wall synthesis.
Once daily x 7 days, then
Anti-inflammatory
once daily x 2 days/month for
via inhibition of
maintenance.
5-lipoxygenase
metabolites.
Terbinafine
Oral: 250 mg
Inhibition of cell
Once daily x 4-6 weeks or 12
membrane and cell wall
days monthly x 3 months.
synthesis.
[8,122-124]
Note: Shampoos, foams and lotions are better suited for treating seborrheic dermatitis and dandruff on the scalp; gels, creams and ointments are used to treat
seborrheic dermatitis on body locations other than the scalp.
ICD: Irritant Contact Dermatitis.
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Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
ISSN: 2373-1044
Fungal colonization
Several lines of evidence suggest a pathogenic role for yeasts of
the genus Malassezia in SD and dandruff [42-46]. Malassezia are
lipophilic yeasts that are found mainly on seborrheic regions of
the body [5,7,47]. Studies have detected Malassezia on the scalp of
dandruff patients [45,48], and higher numbers of Malassezia (M.
globosa and M. restricta) correlate with SD appearance/severity
[4,49,50]. Additionally, among the multiple chemical entities
that are effective in treating SD and dandruff, such as azoles,
hydroxypyridones, allylamines, selenium and zinc, the sole common
mechanism of action is antifungal activity [47-49]. Furthermore,
Malassezia was shown to have lipase activity, which hydrolyzes
human sebum triglycerides and releases unsaturated fatty acids
such as oleic and arachidonic acid [51,52]. These metabolites cause
aberrant keratinocytes differentiation, resulting in stratum corneum
abnormalities such as parakeratosis, intracellular lipid droplets, and
irregular corneocyte envelope [53]. Such changes lead to disrupted
epidermal barrier function and trigger inflammatory response, with
or without visible local inflammation. In addition, these metabolites
induce keratinocytes to produce pro-inflammatory cytokines such
as IL-1, IL-6, IL-8 and TNF-, thus prolonging the inflammatory
response [39,54]. Furthermore, arachidonic acid can be a source of
prostaglandins, which are pro-inflammatory mediators that can
cause inflammation via neutrophil recruitment and vasodilation [38].
Interestingly, Malassezia infection has also been reported in goats,
dogs and monkeys with seborrhea (dry or greasy) and dermatitis [5559].
While these observations support a pathogenic role for Malassezia
in SD and dandruff, there is also strong evidence suggesting that
individual predispositions and host interactions with Malassezia,
rather than the mere presence of Malassezia, contribute to SD and
dandruff pathogenesis. For example, Malassezia was detected on
normal skin of majority of healthy adults, making it a commensal
organism [2,5,26]. Moreover, while topical application of oleic acid
did not induce visible changes in non-dandruff subjects, it caused
skin flaking on the non-lesional scalp of dandruff patients [48]. These
observations are suggestive of intrinsic epidermal barrier defects in
the pathogenesis of SD and dandruff [48].
Individual susceptibility
Besides sebaceous activity and Malassezia colonization, other
factors also contribute to the pathogenesis of SD. Epidermal barrier
integrity, host immune response, neurogenic factors and emotional
stress, and nutritional factors have all been shown to play a role in
individual susceptibility.
Epidermal barrier integrity: The stratum corneum (SC), the
anucleated outer layers of the epidermis, functions as a barrier
against water loss and entry of microorganisms and harmful agents
from the environment [65]. The SC consists of several layers of
terminally differentiated keratinocytes, the corneocytes, encased in
lipid lamellae, held together by specialized intercellular cell adhesion
structures called corneodesmosomes [66]. Any changes in the lamellar
lipid composition, corneocyte size or shape, corneodesmosome
number and SC thickness, could lead to alterations in the epidermal
permeability barrier (EPB) function [66].
Normally, sebum may influence intercellular lipid organization
to aid desquamation [66,67]. In SD and dandruff, however, altered
corneodesmosomal hydrolysis may disrupt lipid organization and
disturb the desquamation process, leading to aberrant barrier function
[53,68]. In support of this notion, barrier structural abnormalities have
been detected in dandruff scalp by electron microscopy that included
intercellular Malassezia yeasts, changes in corneocyte shape and
corneodesmosomes, and disrupted lipid lamellar structure [23,53,66].
Consistent with the structural findings, dandruff patients have been
found to be more reactive (higher itch perception or flaking) than
controls to topical applications of histamine or oleic acid to the scalp
[48,69,70]. These observations indicate that disrupted EPB function
can contribute to the aggravation of dandruff. Recent genetic studies
in humans and animals suggest that disrupted barrier function may
even directly cause SD-like conditions [71]. Biochemical analysis
further demonstrated that dandruff skin displayed altered protein
profiles as well as those of SC ceramides and free fatty acids, in the
absence of apparent inflammation [72]. These studies underscore
the importance of barrier restoration and maintenance in the
management of SD and dandruff.
Immune response: Both the incidence and severity of SD are
associated with immune-suppression, particularly in HIV/AIDS
patients. Because no clear differences were found in Malassezia
levels between individuals with and without SD in this population,
it is likely that an immune or inflammatory reaction could be the
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Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
ISSN: 2373-1044
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Citation: Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investigat Dermatol. 2015;3(2): 10.
ISSN: 2373-1044
Table 4: Comparison of seborrheic dermatitis and dandruff.
Seborrheic Dermatitis
Dandruff
Up to 40% of infants
within 3 months of age, 50% of adult
1-3% of the general adult population.
population.
Epidemiology
Location
Presentation
Scalp, retro-auricular
area, face (nasolabial
folds, upper lip, eyelids,
eyebrows), upper chest.
Scalp.
Erythematous patches,
with large, oily or dry
scales.
White to
yellow flakes
dispersed on
the scalp and
hair; without
erythema.
References
References
[1-3,22,23]
[2,7,15]
Histology
[2,3,26]
Topical corticosteroids,
immune modulators,
phototherapy, systemic
treatment.
Predisposing
Factors and
causes
[3,23,38]
[2,8,26,47,97]
Conclusions
SD and dandruff are of a continuous spectrum of the same disease
that affects the seborrheic areas of the body (Table 4). They share
many common features and respond to similar treatments. Various
intrinsic and environmental factors, such as Malassezia yeast, host
epidermal conditions, sebaceous secretion, immune response, and
the interactions between these factors, may all contribute to the
pathogenesis. Effective management of SD and dandruff requires
clearing of symptoms with antifungal and anti-inflammatory
treatment, ameliorating associated symptoms such as pruritus, and
general scalp and skin health to help maintain remission. Studies in
humans and animal models to investigate the genetic and biochemical
pathways will help identify new targets for the development of more
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ISSN: 2373-1044
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Acknowledgements
This work was supported by AR059907 from NIH/NIAMS, (T.C.W.),
the Brian V. Jegasothy M.D. Basic Science Research Award
(T.C.W.) and a Dermatology Gift Fund from the Department of
Dermatology and Cutaneous Surgery, University of Miami Miller
School of Medicine (T.C.W.).
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