Is Animal Ketoconazole The Same For People?
J Clin Investig Dermatol. Writer manuscript; available in PMC 2016 May ii.
Published in final edited form as:
J Clin Investig Dermatol. 2015 December; 3(two): 10.13188/2373-1044.1000019.
Published online 2015 Dec 15. doi:10.13188/2373-1044.1000019
PMCID: PMC4852869
NIHMSID: NIHMS754376
Seborrheic Dermatitis and Dandruff: A Comprehensive Review
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 peel without visible inflammation. SD tin affect the scalp as well as other seborrheic areas, and involves itchy and flaking or scaling skin, inflammation and pruritus. Various intrinsic and ecology 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, nosotros 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 farther insight on the pathophysiology and strategies for better treatment.
Keywords: Seborrheic dermatitis, Dandruff, Sebaceous gland, Malassezia, Epidermal barrier
Introduction
Seborrheic Dermatitis (SD) and dandruff are common dermatological issues that bear upon the seborrheic areas of the body. They are considered the same basic condition sharing many features and responding to similar treatments, differing simply in locality and severity. Dandruff is restricted to the scalp, and involves itchy, flaking pare without visible inflammation. SD affects the scalp besides as face, retro-auricular area, and the upper breast, causing flaking, scaling, inflammation and pruritus, and tin can have marked erythema. Flaking in SD and dandruff is usually white-to-yellowish, and may exist oily or dry.
It is estimated that SD and dandruff combined touch on half of the developed population. Despite such high prevalence, their etiology is non well understood. Various intrinsic and environmental factors, such equally sebaceous secretions, peel surface fungal colonization, individual susceptibility, and interactions between these factors, all contribute to the pathogenesis. Genetic, biochemical studies and investigations in animate being models farther provided insight on the pathophysiology and strategies for better treatment. In this comprehensive review, we summarize the electric current cognition on SD and dandruff, and endeavour to provide directions for future investigations and treatments.
Epidemiology
SD is a common dermatological disorder in the U.s.a. and worldwide [1]. Its incidence peaks during three age periods - in the first three months of life, during puberty, and in machismo with an apex at xl to sixty years of historic period [ane–iv]. In infants up to three months of age, SD involves the scalp (termed "cradle cap"), the face, and diaper area. Incidence can exist up to 42% [4–6]. In adolescents and adults, SD affects the scalp and other seborrheic areas on the confront, upper-chest, axillae, and inguinal folds [4,7,8]. Incidence is ane–iii% of the full general adult population [3,9]. Men are affected more frequently than women (iii.0% vs. 2.six%) in all age groups, suggesting that SD may be associated with sexual activity hormones such as androgens [i,3,8]. No apparent differences were observed in SD incidence between ethnic groups [3].
SD is more than prevalent in immune-compromised patients such equally 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,x]. Most cases of SD in HIV patients are diagnosed with CD4+ T lymphocyte counts between 200 and 500/mm3 [3,fourteen,xv], and decreased CD4+ counts are ofttimes associated with worse SD. Fewer cases of SD were reported when CD4+ T cells were more than 500/mm3 [xiv]. These observations suggest that immunological defects may play a role in SD.
SD is also associated with neurological disorders and psychiatric diseases, including Parkinson's disease, neuroleptic induced parkinsonism, tardive dyskinesia, traumatic brain injury, epilepsy, facial nervus palsy, spinal cord injury and mood depression [4,five,16,17], chronic alcoholic pancreatitis, hepatitis C virus [18,19], and in patients with built disorders such every bit Down syndrome [xx]. Furthermore, seborrhea-like dermatitis of the face up may also develop in patients treated for psoriasis with psoralen and ultraviolet A (PUVA) therapy [21].
Comparison with SD, dandruff is much more common, and affects approximately 50% of the general developed population worldwide. It is also more than prevalent in males than females [22,23]. Dandruff starts at puberty, reaches tiptop incidence and severity at the age of almost 20 years, and becomes less prevalent amid people over l [23]. Incidence varies between unlike ethnic groups: in a study in the U.South. and China, dandruff prevalence was 81–95% in African Americans, 66–82% in Caucasians, and 30–42% in Chinese [23].
Brunt of Disease
It is estimated that at least 50 meg Americans suffer from dandruff, who spend $300 1000000 annually on over-the-counter products to treat scalp itching and flaking [22]. Also physical discomfort such every bit itching, dandruff is socially embarrassing and negatively impacts patients' self-esteem [22].
While SD is much less prevalent, outpatient office visits alone toll $58 million in the United states in 2004, and $109 million were spent on prescription drugs [24]. Together with over-the-counter products and infirmary services, the total direct costs of SD were estimated to exist $179 meg, plus another $51 one thousand thousand indirect costs in the form of lost work days [24]. In addition, because SD frequently occurs on the face up and other visible areas, it has pregnant negative effects on patients' quality of life (QOL) in the grade of psychological distress or depression self esteem; the willingness to pay for relief of the symptoms was $one.2 billion [24]. Furthermore, although the QOL impact in SD patients ranked lower than in patients with atopic or contact dermatitis, it was constitute to be higher than skin ulcers and solar radiation impairment, and women, younger patients, and subjects with higher educational level were more afflicted [24].
Clinical Presentation and Diagnosis
Clinical presentations
The clinical presentations of SD and dandruff in children and adults are summarized in Table 1. SD oft presents as well-delimited erythematous plaques with greasy-looking, xanthous 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 breast. Distribution of the lesions is by and large symmetrical, and SD is neither contagious nor fatal. SD has a seasonal design, presenting more than frequently during winter, and improving usually during summer [v,25,26]. Additionally, aggravation of SD has been associated with sleep deprivation and stress [7,27,28].
Tabular array 1
Clinical presentations of seborrheic dermatitis (SD) and dandruff.
| Features | ||
|---|---|---|
| Dandruff | Calorie-free, white to yellow and dispersed flaking on the scalp and pilus without erythema. Absent to mild pruritus. Can spread to hairline, retro-auricular area and eyebrows. | |
| SD in Infants | Scalp | Cradle Cap: Most Common. Red-yellow plaques coated past thick, greasy scales on vertex, appearing within iii months of age. |
| Face up/Retro-auricular area | Erythematous, flaky, salmon-colored plaques on forehead, eyebrows, eyelids, nasolabial folds, or retro-auricular areas. | |
| Torso folds | Lesions have moist, shiny, not-scaly aspects that tend to coalesce on neck, axillae or inguinal area. | |
| Torso | More extensive form: Sharply limited plaques of erythema and scaling that cover lower abdomen. | |
| Generalized | Leiner'southward Illness: Unusual, associated with immunodeficiency. Absent to mild pruritus. Concurrent diarrhea and failure to thrive. Spontaneous clearing inside weeks to few months. | |
| SD in Adults | Scalp | From mild desquamation to honey-colored crusts fastened to scalp and hair leading to alopecia. May reach into forehead as scaly erythematous border known as "corona seborrheica". |
| Face/Retro-auricular area | Forehead, eyebrows, glabella or nasolabial folds. May spread to malar regions and cheeks in butterfly distribution. | |
| Eyelids: Yellowish scaling between eye lashes. Tin can pb to blepharitis with honey-colored crusts on free margin. | ||
| Retro-auricular area: Crusting, oozing and fissures. May expand to external canal, with marked itching on occasionally secondary infection (otitis externa). | ||
| Upper Breast | Petaloid type (mutual): small, reddish follicular and peri-follicular papules with oily scales at onset that get patches resembling a medallion (flower petals). | |
| Pityriasiform type: Widespread 5–fifteen mm oval-shaped, scaly macules and patches. Distributed forth the skin tension lines (similar to extensive pityriasis rosea). New eruptions can continue for >3 months. Commonly on face and intertriginous areas. | ||
| Torso Folds | Moist, diminished appearance with erythema at the base and periphery on axillae, umbilicus, breast fold, genital or inguinal surface area. May progress to fissures and secondary infection. | |
| SD with allowed-suppression * | Extensive, astringent and refractory to treatment. In both children and adults with AIDS†. Unusual sites involved such as extremities. More widespread with CD4 counts <200 cells/mm3. Associated with rosacea, psoriasis and acne. | |
In infants, SD may present on the scalp, face, retro-auricular area, body folds, and body; rarely information technology may be generalized. Cradle cap is the most common clinical manifestation. SD in children is usually self-limited [3,15]. On the other hand, in adults, SD is a chronic or relapsing status, featured past erythematous patches, with flaky, large, oily or dry out scales in sebum-rich areas such every bit face (87.seven%), scalp (lxx.three%), upper trunk (26.8%), lower extremities (two.3%), and upper extremities (1.3%) [5,7,29]. Pruritus is non an obligatory feature, just it is often present, mainly in scalp involvement [2]. The principal complexity is secondary bacterial infection, which increases the redness and exudate and local irritation [iii,15].
In allowed-suppressed patients, SD is oftentimes more extensive, intense, and refractory to treatment [3,26,30]. It is considered an early skin presentation of AIDS in both children and adults [14]. SD may also exist a cutaneous sign of the immune reconstitution inflammatory syndrome in patients with highly active antiretroviral therapy (HAART) [31]. Withal, there accept also been reports of SD regression with HAART [10].
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 bear on similar locations as SD, typical lesions in psoriasis are thicker and present as plaques sharply limited with silver white scales [8,32]. Lesions in atopic dermatitis usually do not announced until later on 3 months of age, while lesions in SD usually appear before and rarely affect extensor areas. Tinea capitis, a highly contagious affliction, typically shows scaly patches of scalp pilus loss associated with "black dots", which represent distal ends of broken hairs [33]. Conversely, SD is not associated with pilus loss. Rosacea usually targets the malar areas on the face, sparing the nasolabial folds, and practise not have scales; on the other paw, facial SD lesions are usually scaly, and touch on the nasolabial folds, eyelids, and eyebrows, without associated flushing or telangiectasias [7,8,34]. Finally, peel lesions in SLE ofttimes follow a clear photo distribution, such equally astute flares of bilateral malar rash, and may be associated with extra-cutaneous abnormalities such equally arthritis, oral cavity ulcers, glomerulonephritis or cardiomyopathy [viii,35]; SD does not have a photo distribution blueprint, and does not affect organ systems other than the pare.
Table 2
Differential diagnosis of seborrheic dermatitis and dandruff.
| Diagnosis | Diagnostic Clues | |
|---|---|---|
| Psoriasis | Normally involves extensor, palmar, plantar, nails and extensor areas. Thick plaques sharply limited with silvery white scales. Positive family history. Arthritis present in 10% of patients. Uncommon in children. | |
| Atopic Dermatitis | Offset advent subsequently 3 months of historic period, pruritus and restlessness are mutual. Frequently involves scalp, cheeks and extensor areas. Flexures involvement is more frequent in older ages. Family history of atopy such equally eczema, allergic rhinitis and asthma. Self resolved by age 12. | |
| Tinea Capitis | Commonly seen in children, frequently accompanied by hair loss patches with "blackness dots" (broken hair). Highly contagious. KOH examination of the hair shaft and fungal culture ostend the diagnosis. Household members of patient should be examined. | |
| Rosacea | Normally targets the face up. Papulopustules and telangiectasias on the malar, olfactory organ and perioral regions with slight desquamation. Recurrent edema and flushing. | |
| Systemic Lupus Erythematous (SLE) | In astute stage, butterfly rash on face that spares the olfactory organ bridge or nasolabial folds. Photosensitivity is common. Skin lesions are more often than not associated with other clinical signs of SLE. Histology and serologic tests such every bit antinuclear autoantibodies ostend the diagnosis. | |
| Others | Pemphigus Foliaceous | Erythema, scaling and crusting that beginning present on the scalp and face tin expand to chest and back. Histology, direct immunofluorescence with anti-desmoglein antibodies confirm diagnosis. |
| Pityriasis Rosea | Abrupt onset, appearance of herald patch and resolution inside weeks. | |
| Secondary syphilis | Peripheral lymph-adenopathy, mucosal lesions and palmoplantar macula-papules. Serology tests such equally VDRL/ RPR, FTA-ABS* ostend diagnosis. | |
| Diaper Dermatitis | Occurs on convex pare surfaces in contact with diaper, such as lower abdomen, genitalia, buttocks and upper thighs. Spares skin folds. Pustules are common. | |
| Langerhans cell histiocytosis | Multisystem disease. Brown to purplish papules prone to coalesce on the scalp, retro-auricular areas, axillae and inguinal folds. Possible lytic os lesions, liver, spleen and lung involvement. Histology confirms diagnosis. | |
Other less mutual atmospheric condition that may resemble SD are pemphigus foliaceous, pityriasis rosea, secondary syphilis, diaper dermatitis and cutaneous Langerhans cell histiocytosis [three,4,vii,thirty], which are summarized in Table 2. The bulk of these conditions can be differentiated by clinical presentation and history; although syphilis, pemphigus foliaceous and SLE may require laboratory confirmation.
Additionally, some drugs (griseofulvin, ethionamide, buspirone, haloperidol, chlorpromazine, IL-2, interferon-α, methyldopa, psoralens) and nutritional deficiencies (pyridoxine, zinc, niacin and riboflavin) may induce an SD-like dermatitis, although the mechanism remains unknown [36,37]. These weather condition can coexist with SD as well, making the diagnosis more challenging.
Pathology
Diagnosis of SD is typically fabricated past history and physical exam. In rare cases, a skin biopsy is needed for differential diagnosis. Histologically, the development of SD can exist divided into two stages. In the astute and sub-acute stages, SD shows superficial perivascular and perifollicular inflammatory infiltrates, equanimous mainly of lymphocytes and histiocytes in clan with spongiosis and psoriasiform hyperplasia, and tin can exist coupled with parakeratosis effectually follicular opening ("shoulder parakeratosis"). Neutrophils can besides exist found in the scale chaff at the margins of follicular ostia. On the other mitt, in chronic lesions, marked psoriasiform hyperplasia and parakeratosis can be present with dilation of the venules of surface plexus which resembles psoriasis [iii,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 equally SD in histology, such equally epidermal hyperplasia, parakeratosis, and Malassezia yeasts surrounding the parakeratotic cells [23]. Whereas inflammatory cells such as lymphocytes and NK cells may be nowadays in slap-up 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].
Handling
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 about mutual treatment is topical antifungal and anti-inflammatory agents (Tabular array three). Other widely used therapies are coal tar, lithium gluconate/ succinate and phototherapy (Table 3). New therapies have besides emerged including allowed modulators such as topical calcineurin inhibitors, and metronidazole, but their efficacy remains controversial [5]. Culling therapies have been reported too, such every bit tea tree oil [40,41]. Some factors to be considered before selecting a treatment include efficacy, side effects, ease of utilize/compliance, and age of the patient [v]. Systemic therapy is needed but in widespread lesions and in cases that do non respond to topical handling [3,26].
Table iii
Treatment of seborrheic dermatitis and dandruff.
| Medication | Dose/ Formulation | Regimen | Mechanisms | Side Furnishings | References | ||
|---|---|---|---|---|---|---|---|
| TOPICAL | Antifungals | Ketoconazole | ii% Shampoo, foam, gel or foam | Scalp or skin: Twice/week × four weeks, so once/week for maintenance. | Inhibition of fungal prison cell wall synthesis. | ICD† in <1% of patients. Itching, burning sensation and dryness in 3% of patients. | [2,8,26,97–101] |
| Bifonazole | 1% shampoo, cream or ointment | Scalp: every other day or once daily. Skin: once daily. | ICD in 10% of patients. | [8,26,99,102] | |||
| Miconazole | Foam | Pare: 1–2 times daily. | ICD, itching, burning sensation. | [47,97,103] | |||
| Ciclopirox Olamine | 1.5% shampoo, foam, gel or lotion | Scalp: 2–3 times/week × 4 weeks, then in one case/week for maintenance. Skin: twice daily. | Inhibition of metal-dependent enzymes. | ICD in <1% of patients. Itching, called-for sensation in 2% of patients. | [8,47,97,99,104,105] | ||
| Selenium sulfide | 2.5% shampoo | Scalp: Twice/week × ii weeks, and so once/week × 2 weeks. Echo afterwards 4–6 weeks. | Cytostatic and keratolytic. | ICD in ~iii% of patients. Orange-chocolate-brown scalp discoloration. | [8,97,106,107] | ||
| Zinc Pyrithione | i% shampoo | Scalp: two–3 times/calendar week. | Increased cellular copper interferes with iron-sulfur proteins. | ICD in ~iii% of patients. | [eight,97,99,101,108,109] | ||
| Cortico-steroids | Hydrocortisone | 1% cream | Skin: 1–ii times daily. | Anti-inflammatory, anti-irritant. | Take a chance of skin atrophy, telangiectasias, folliculitis, hypertrichosis, and hypopigmentation with prolonged apply. | [8,9,97,99,103,108] | |
| Betamethasone dipropionate | 0.05% balm | Scalp and skin: i–ii times daily. | [8,47,110] | ||||
| Desonide | 0.05% balm, gel | Scalp and pare: 2 times daily. | [8,111–113] | ||||
| Fluocinolone | 0.01% shampoo, balm or cream | Scalp or pare: Once or twice daily. | [seven,114] | ||||
| Immuno-modulators | Pimecrolimus | 1% cream | Skin: one–2 times daily. | Inhibition of cytokine production by T-lymphocyte. | Adventure of skin malignancy and lymphoma with prolonged apply. | [47,98,115–118] | |
| Tacrolimus | 0.one% ointment | Skin: 1–2 times daily × 4 weeks, then twice/week for maintenance. | [26,97,109,118–120] | ||||
| Miscellaneous | Coal tar | 4% shampoo | Scalp: one–2 times/calendar week. | Antifungal, anti-inflammatory, keratolytic, reduces sebum production. | Local folliculitis, ICD on fingers, psoriasis bedevilment, skin atrophy, telangiectasias, hyper-pigmentation. Take chances of squamous prison cell carcinoma with prolonged use. | [4,8,47,117,121] | |
| Lithium gluconate/succinate | 8% ointment or gel | Pare: twice daily × viii weeks. | Anti-inflammatory via increased IL-10 and decreased TLR2 and TLR4 in keratinocytes. | ICD in <x% of patients. | [viii,122–124] | ||
| Metronidazole | 0.75% gel | Pare: twice daily × four weeks. | Anti-inflammatory via inhibition of free radical species. | Rare contact sensitization with prolonged use. | [5,47,125,126] | ||
| Phototherapy | UVB: Cumulative dose of ix.eight J/cm2 | 3 fourth dimension/week × 8 weeks or until immigration. | Immuno-modulation and inhibition of jail cell proliferation. | Burning, itching awareness during/later therapy. Risk of genital tumor with prolonged use. | [26,127–129] | ||
| SYSTEMIC | Itraconazole | Oral: 200 mg | Once daily × 7 days, then once daily × ii days/month for maintenance. | Inhibition of fungal cell wall synthesis. Anti-inflammatory via inhibition of 5-lipoxygenase metabolites. | Rare liver toxicity. | [97,130,131] | |
| Terbinafine | Oral: 250 mg | One time daily × 4–6 weeks or 12 days monthly × 3 months. | Inhibition of cell membrane and cell wall synthesis. | Rare tachycardia and indisposition. | [132–134] | ||
Pathophysiology
Despite the high prevalence, the pathogenesis of SD and dandruff is non well understood. However, studies have identified several predisposing factors, including fungal colonization, sebaceous gland activeness, as well equally several factors that confer individual susceptibility [2].
Fungal colonization
Several lines of show 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,vii,47]. Studies take detected Malassezia on the scalp of dandruff patients [45,48], and higher numbers of Malassezia (1000. globosa and 1000. restricta) correlate with SD appearance/severity [iv,49,fifty]. Additionally, among the multiple chemical entities that are effective in treating SD and dandruff, such as azoles, hydroxypyridones, allylamines, selenium and zinc, the sole mutual mechanism of action is antifungal activity [47–49]. Furthermore, Malassezia was shown to have lipase activity, which hydrolyzes human being sebum triglycerides and releases unsaturated fatty acids such every bit oleic and arachidonic acid [51,52]. These metabolites cause aberrant keratinocytes differentiation, resulting in stratum corneum abnormalities such equally 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-1α, IL-6, IL-8 and TNF-α, thus prolonging the inflammatory response [39,54]. Furthermore, arachidonic acrid tin can be a source of prostaglandins, which are pro-inflammatory mediators that tin crusade inflammation via neutrophil recruitment and vasodilation [38]. Interestingly, Malassezia infection has likewise been reported in goats, dogs and monkeys with seborrhea (dry or greasy) and dermatitis [55– 59].
While these observations support a pathogenic function for Malassezia in SD and dandruff, there is also stiff evidence suggesting that private predispositions and host interactions with Malassezia, rather than the mere presence of Malassezia, contribute to SD and dandruff pathogenesis. For instance, Malassezia was detected on normal peel 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 not-dandruff subjects, it acquired 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].
Sebaceous gland activity
Sebaceous glands (SGs) are distributed over the entire skin surface in humans, except on the palms and soles. Secretion of sebum is highest on the scalp, face and chest [44]. Sebum product is under hormonal control, and SGs are activated at nativity under the influence of maternal androgens via androgen receptors in sebocytes [sixty]. SGs are activated over again at puberty nether the control of circulating androgens [38,61], resulting in increased sebum secretion during adolescence, which is kept stable between 20 and thirty years of historic period and is then reduced [62]. During the menstruation of active sebum secretion, the secretion charge per unit is higher in males and stays high longer, betwixt xxx and 60 years of age; in females, the rate drops fast later on menopause [44]. Thus, SD and dandruff have a potent time correlation with SG activity, with cradle cap after birth, increased incidence throughout the teens, between tertiary and sixth decades and then decreasing [3,four,9]. Yet, SD patients may have normal sebum production, and individuals with excessive sebum production sometimes don't develop SD [38,63]. These findings suggest that while SG activity strongly correlates with SD and dandruff, sebum production by itself is not a decisive cause.
In addition to the level of sebum product, abnormalities of lipid composition may too play a role in SD development, likely through a favorable milieu for Malassezia growth [64]. In patients with SD, triglycerides and squalene were reduced, but free fatty acids and cholesterol were considerably elevated [38,44]. The elevated levels of costless fat acids and cholesterol may be the event of triglyceride degradation by Malassezia's lipase, and these metabolites promote Malassezia growth and lead to recruitment of inflammatory infiltrates in the pare [64].
Individual susceptibility
As well 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 function 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 past specialized intercellular cell adhesion structures called corneodesmosomes [66]. Whatsoever 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) office [66].
Normally, sebum may influence intercellular lipid organization to aid desquamation [66,67]. In SD and dandruff, still, 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,seventy]. These observations betoken that disrupted EPB function tin contribute to the aggravation of dandruff. Recent genetic studies in humans and animals suggest that disrupted barrier function may fifty-fifty directly crusade SD-like conditions [71]. Biochemical analysis farther demonstrated that dandruff pare displayed altered poly peptide profiles besides 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 direction 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 institute in Malassezia levels betwixt individuals with and without SD in this population, it is probable that an immune or inflammatory reaction could be the predisposition [5,9]. Indeed, one report found elevated levels of human leukocyte antigens HLA-AW30, HLA-AW31, HLA-A32, HLA-B12 and HLA-B18 in SD [three,73,74]. Additionally, increased levels of total serum IgA and IgG antibodies have been detected in SD patients [75]. However, no increment in the titers of antibodies against Malassezia was detected, suggesting that the elevated immunoglobulin production occurs rather as a response to yeast metabolites [26,75,76]. The strong inflammatory reaction provoked by these metabolites includes infiltration of Natural Killer (NK) cells and macrophages, with concurrent local activation of complement and an increased local production of inflammatory cytokines, such as IL-1α, IL-1β, IL-6 and TNF-α in affected skin areas [54]. The lack of increase in anti-Malassezia antibodies also indicates a change in cellular immune response instead of humoral response [76,77]. The specific function of lymphocyte activity remains controversial [76–79].
Genetic factors
The genetic components of SD and dandruff had been nether-appreciated until recently, when studies in animate being models and humans identified inherited dominant and recessive forms of SD and dandruff. In the autosomal recessive "inherited seborrheic dermatitis" (seb) mice, a spontaneous mutation in the outbred Him:OF1 mice acquired seborrhea, rough coat, alopecia, growth retardation, and sometimes abnormal pigmentation in homozygous mutants [fourscore]. Histological exam revealed enlarged sebaceous glands, hyperkeratosis, parakeratosis, acanthosis and inflammatory infiltrates in the epidermis and dermis. Neither yeasts nor dermatophytes were detected. These mice were the first animal model of SD to evidence a articulate mode of inheritance, though the underlying mutation remains unidentified [eighty,81].
Consistent with a part for altered amnesty in the pathogenesis of SD, transgenic mice carrying the 2C T cell receptor (TCR) transgene in the DBA/2 background developed extremely inflammatory phenotype in seborrheic areas, such every bit the ears, around the eyes, and muzzle area [82]. Additionally, positive fungal staining by PAS was consistently detected in lesional pare but not readily apparent in non-lesional skin from diseased mice or from DBA/2 control mice. Furthermore, antifungal treatment reversed clinical and pathology presentations, and reduced PAS staining [82]. These observations support the notion that immune compromise and fungal infection play active roles in SD.
Another spontaneous mutant mouse strain that shows SD-like phenotype is the crude coat (rc) mice, which showed sebaceous hypertrophy and greasy hair coat, baldness, and growth retardation [83]. The rc is transmitted in an autosomal recessive mode. Nosotros have since identified the cause of the rc phenotype to be a missense mutation in the Mpzl3 gene, which is expressed in the superficial layers of the epidermis [84,85]. Our Mpzl3 knockout mice recapitulated the rc phenotype, and mice with white hair coat developed more than severe and persistent inflammatory skin phenotype and dandruff in the seborrheic areas [85]. We have shown that the early on-onset inflammatory skin phenotype was not caused by immune defects [85]. However, skin abnormalities in Mpzl3 knockout mice and perturbed epidermal differentiation in organotypic human pare models with MPZL3 knockdown indicate that MPZL3 is a key regulator of epidermal differentiation [85,86]. Interestingly, a frame-shift mutation in ZNF750, a transcription cistron controlling epidermal differentiation and an upstream regulator of MPZL3, caused autosomal dominant seborrhea-like dermatitis in patients [71,86]. These studies in humans and animal models underscore the consequence of abnormal epidermal differentiation in the pathogenesis of SD and dandruff, and accept provided the genetic footing for some of the predisposing factors discussed in a higher place. These animal models will exist important tools to dissect the underlying pathways that will identify novel targets for better treatment of these disorders.
Neurogenic factors and emotional stress
The loftier incidence of SD in patients with Parkinson's illness [17,87,88] and neuroleptic-induced Parkinsonism [89,ninety] has long been observed, peculiarly in those with severe seborrhea, which provides favorable atmospheric condition for Malassezia proliferation. Bilateral seborrhea has been observed in patients with unilateral Parkinsonism, suggesting that these sebum changes were probable regulated neuro-endocrinologically rather than purely neurologically [5,26,91]. Consequent with this notion, α-melanocyte stimulating hormone (α-MSH) levels were elevated in Parkinson patients, maybe due to inadequate dopaminergic input. Moreover, treatment with L-dopa reduced α-MSH, and re-established the synthesis of MSH-inhibiting factor, reducing sebum secretion [26,92].
Additionally, there is testify for a link between neurological damage (e.one thousand. traumatic brain, spinal cord injury) and SD [93]. Facial immobility of Parkinsonian patients (mask-like face) and immobility due to facial paralysis tin induce elevated sebum aggregating and lead to SD, but only on the afflicted side [26,43,94]. Considering poor hygiene has been implicated in SD, these observations advise that sustained reservoirs of rest sebum associated with immobility may influence the manifestation of the disease [3,22,26,88]. SD is besides more than usually seen in depressive disorders and emotional stress [5,xvi].
Other factors
In the past, nutrition has been studied as a possible contributing factor for SD. Zinc deficiency in patients with acrodermatitis enteropatica, riboflavin, pyridoxine and niacin deficiency can manifest seborrheicdermatitis-like rash [26,36]. Other medical conditions, such every bit familial amyloidotic polyneuropathy and Down syndrome, have also been associated with SD [95,96].
In summary, multiple predisposing factors have been identified in the pathogenesis of SD and dandruff (Figure 1). The presence and abundance of Malassezia yeast, host epidermal conditions and sebaceous secretion, combined with various other factors, and interactions between these factors, determine an individual'south susceptibility to SD and dandruff. In a likely scenario, there may be aberrant epidermal bulwark function due to genetic predisposition, and excessive or altered sebum composition would exacerbate EPB disruption and provides a favorable milieu for Malassezia colonization. Disrupted EPB function facilitates entry of Malassezia and its metabolites, and irritates the epidermis and elicits host's immune response. The host inflammatory response further disturbs epidermal differentiation and bulwark germination, and pruritus and subsequent scratching would impairment the bulwark even farther, leading to cycles of immune stimulation, aberrant epidermal differentiation, and barrier disruption.
Predisposing factors and their interactions in the pathogenesis of seborrheic dermatitis and dandruff.
Conclusions
SD and dandruff are of a continuous spectrum of the aforementioned disease that affects the seborrheic areas of the body (Table 4). They share many common features and reply to similar treatments. Various intrinsic and ecology factors, such every bit Malassezia yeast, host epidermal atmospheric condition, 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 every bit pruritus, and general scalp and skin wellness to help maintain remission. Studies in humans and animal models to investigate the genetic and biochemical pathways will aid identify new targets for the development of more efficacious treatment with less side furnishings, and meliorate management of these conditions.
Table 4
Comparing of seborrheic dermatitis and dandruff.
| Seborrheic Dermatitis | Dandruff | References | |
|---|---|---|---|
| Epidemiology | Up to 40% of infants within iii months of age, 1–3% of the general adult population. | fifty% of developed population. | [1–three,22,23] |
| Location | Scalp, retro-auricular area, face (nasolabial folds, upper lip, eyelids, eyebrows), upper chest. | Scalp. | [ii,seven,15] |
| Presentation | Erythematous patches, with big, oily or dry scales. | White to yellow flakes dispersed on the scalp and hair; without erythema. | [ii,3,26] |
| Histology | Acanthosis, hyperkeratosis, spongiosis, parakeratosis, Malassezia yeasts. | [3,23,38] | |
| Vasodilation and perivascular and perifollicular inflammatory infiltration; "shoulder parakeratosis". | Subtle neutrophil infiltration or no inflammatory infiltration. | ||
| Treatment | Antifungal shampoos and topical. | [2,8,26,47,97] | |
| Topical corticosteroids, allowed modulators, phototherapy, systemic treatment. | |||
| Predisposing Factors and causes | Sebaceous gland activity, fungal colonization, and private susceptibility (epidermal barrier integrity, host allowed response, genetic factors, neurogenic factors and stress, diet, etc.). | [2,3,9,15,26,44,66] | |
Acknowledgments
This work was supported past AR059907 from NIH/NIAMS, (T.C.Due west.), the Brian 5. Jegasothy M.D. Basic Scientific discipline Enquiry Award (T.C.W.) and a Dermatology Souvenir Fund from the Department of Dermatology and Cutaneous Surgery, Academy of Miami Miller School of Medicine (T.C.W.).
Abbreviations
| AIDS | Acquired Allowed-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 Enquiry Laboratory |
Footnotes
Reviewed & Approved by: Dr. Craig Yard Burkhart, Clinical Professor, Section of Medicine, Ohio University, USA
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869/
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