Cradle cap
Cradle cap, also known as infantile seborrheic dermatitis, is a common, self-limiting skin condition characterized by scaly, greasy, yellowish patches on an infant's scalp, typically appearing between the third week and first few months of life and peaking around 3 months of age.[1] It affects approximately 10% of infants in the first three months, with prevalence reaching up to 70% at its peak, and shows no predilection for gender or race.[1]Introduction and epidemiology
Definition
Cradle cap, medically termed infantile seborrheic dermatitis, is a common, non-contagious non-inflammatory skin disorder that primarily affects the scalp of infants, presenting as scaly, greasy patches due to overproduction of sebum and involvement of skin flora.[1][2] It is considered a benign, self-limiting condition that typically resolves without scarring or long-term complications in most cases.[1][2] The condition usually emerges between 2 weeks and 6 months of age, with peak incidence around 3 months, coinciding with the maturation of the infant's sebaceous glands influenced by maternal hormones.[1][2] Unlike infectious dermatoses, cradle cap does not spread between individuals and is not associated with systemic illness.[1] Historically, the term "cradle cap" derives from its characteristic scaling on the infant scalp, resembling a cap, and distinguishes this pediatric manifestation from adult seborrheic dermatitis, though both share etiological links to Malassezia yeast and seborrhea; the infantile form is transient and hormonally driven, resolving spontaneously by 12 months without recurrence in early childhood.[1][2]Epidemiology
Cradle cap, or infantile seborrheic dermatitis, is a prevalent condition among infants, with estimates indicating it affects 10% to 70% during the first year of life.[3][1] Prevalence is approximately 10% in the initial three months, rising to a peak of about 70% around 3 months of age before declining to 7% in children aged 1 to 2 years.[3][1] Demographic patterns show a slight predominance in males, with rates of 10.4% reported in boys compared to 9.5% in girls during early infancy, though overall there is no strong gender predilection.[1] The condition exhibits no significant racial or geographic biases, occurring across diverse populations without notable variations in distribution.[1][4] Temporal trends reveal onset typically in the neonatal period, between the third week and the first few months of life, with peak incidence at 3 months.[1][4] The majority of cases resolve spontaneously by 12 months of age, and persistence into childhood is rare.[1][4]Clinical presentation
Signs and symptoms
Cradle cap, a form of infantile seborrheic dermatitis, primarily manifests on the scalp with greasy, yellowish-white scales or crusts that adhere firmly to the skin.[5][1] These scales often cover oily or dry skin and may appear in patchy areas, sometimes accompanied by mild erythema, or redness, underneath.[5][6] Temporary hair loss can occur in the affected regions due to the buildup of scales, though hair typically regrows once the condition resolves.[7] The condition usually starts in the first few months of life as fine, white flakes resembling dandruff, which can evolve into thicker, more adherent plaques over time.[6][5] In infants, cradle cap is rarely itchy or painful, distinguishing it from other scalp conditions.[6] Associated mild symptoms include dandruff-like flaking of the skin.[7][5]Warning signs
While cradle cap typically presents as benign, yellowish scales on an infant's scalp, certain developments may indicate secondary bacterial or fungal infection, necessitating prompt medical evaluation. These include the presence of pus-filled bumps, oozing fluid from the affected areas, increased redness or swelling around the scales, and accompanying fever, which can signal bacterial overgrowth such as from Staphylococcus or Streptococcus species.[8][9][10] Signs that the condition has extended beyond its usual localized form or has become more severe also warrant professional attention to rule out underlying issues or complications. A widespread rash extending to areas like the face, neck, ears, or diaper region, persistent scaling that does not resolve after 12 months of age, or a sudden worsening despite home care efforts may suggest atypical seborrheic dermatitis or alternative diagnoses.[11][5][8] In rare cases, more alarming features can emerge, highlighting the need for immediate intervention to prevent further distress or systemic involvement. Bleeding from manipulated scales, significant irritability or crying due to discomfort from the lesions, or associated systemic symptoms such as poor feeding and lethargy may indicate severe inflammation or secondary infection.[8][11][9]Causes and pathophysiology
Etiology
The etiology of cradle cap, also known as infantile seborrheic dermatitis, is multifactorial and not fully elucidated, involving interactions between hormonal, microbial, genetic, and immunological factors.[1] A primary contributing factor is the persistence of maternal hormones, such as androgens, that cross the placenta during late pregnancy and stimulate hyperactivity in the infant's sebaceous glands after birth. This leads to excessive sebum production on the scalp, creating an oily environment conducive to scale formation and adherence.[12][5] Overgrowth of Malassezia yeast species, particularly M. globosa and M. restricta, plays a central role by colonizing sebum-rich areas and metabolizing lipids into irritant-free fatty acids, which may exacerbate skin scaling. These yeasts are present in over 80% of cases across age groups, supporting their etiologic significance in the sebum-abundant scalp of infants.[13][14] Genetic influences, including a family history of atopic dermatitis, asthma, or seborrheic conditions, heighten susceptibility, suggesting heritable components in immune regulation and skin barrier function.[15][16] Environmental factors, such as exposure to household allergens, may interact with these genetic predispositions. The immature immune system of newborns, characterized by underdeveloped T-cell responses, likely contributes by mounting an inadequate or exaggerated reaction to Malassezia and sebum components.[17][18]Pathophysiology
Cradle cap, or infantile seborrheic dermatitis, arises from hyperactivity of the sebaceous glands in the scalp, driven by exposure to maternal androgens during the perinatal period. This hormonal influence stimulates excessive sebum production, resulting in a lipid-rich environment on the infant's skin that promotes the adhesion of desquamated corneocytes rather than their normal shedding.[1][19] The proliferation of Malassezia yeast species, such as M. globosa and M. restricta, within this seborrheic milieu contributes to scale formation. These yeasts metabolize sebum lipids into unsaturated fatty acids.[1] Concurrently, the immature skin barrier in infancy contributes to the condition's persistence through dysfunction characterized by reduced ceramide levels and altered lipid composition. This impairment increases transepidermal water loss, facilitates microbial penetration, and enhances irritation, thereby promoting the adherence of scales to the scalp surface.[19]Diagnosis and differential diagnosis
Clinical evaluation
The clinical evaluation of cradle cap begins with a detailed history taking from the caregiver to contextualize the presentation. Key elements include the age of onset, which typically occurs between the third week and the first few months of life, peaking around 3 months.[1] Inquiries also cover family history of skin conditions such as eczema or atopy, which may signal a predisposition to related dermatoses.[1] Additionally, recent use of scalp products, including shampoos or oils, and the frequency of hair washing are assessed to identify potential irritants or exacerbating factors.[20] Physical examination focuses on visual inspection of the scalp for characteristic greasy, yellowish, adherent scales, often on the vertex or forehead, which are typically non-inflammatory and asymptomatic.[1] Palpation gently assesses for tenderness, which is usually absent, confirming the lack of pain or pruritus.[1] The exam also evaluates for spread to adjacent areas like the face, ears, or skin folds, noting any erythematous plaques or extension beyond the scalp.[1] Non-invasive tools are rarely required, as diagnosis relies primarily on clinical appearance alone.[20] However, if a fungal infection such as tinea capitis is suspected in atypical cases, a Wood's lamp examination may be used to detect fluorescence indicative of dermatophytes, though this is not routine for typical cradle cap.[21]Differential diagnoses
Cradle cap, or infantile seborrheic dermatitis, can be mimicked by several other dermatological conditions in infants, necessitating careful clinical differentiation to ensure accurate diagnosis.[1] Common mimics include atopic dermatitis, which typically presents with more intense pruritus affecting the cheeks, extensor surfaces, and flexural areas, often leading to sleep or feeding disturbances due to scratching, unlike the generally asymptomatic scaling of cradle cap.[1][22] Psoriasis in infants may resemble cradle cap on the scalp but is distinguished by sharply demarcated, bright red plaques with silvery scales that can extend to the diaper area or involve nails, and it lacks the greasy yellow crusts characteristic of seborrheic dermatitis.[1][22] Tinea capitis, a fungal infection, often causes patchy scaling with hair breakage or "black dot" hairs and associated cervical lymphadenopathy, which are absent in cradle cap; diagnosis is confirmed by positive potassium hydroxide (KOH) preparation or fungal culture.[1][17] Rare differentials include Langerhans cell histiocytosis, which may present with scalp involvement but features purpuric or brownish-red nodules, ulcerations, and systemic symptoms such as organ involvement or failure to thrive, requiring biopsy for confirmation.[1][22] Allergic contact dermatitis is suggested by a history of exposure to irritants like soaps or fabrics, resulting in itchy, vesicular lesions often in intertriginous or eyelid areas, contrasting with the non-pruritic, seborrheic distribution of cradle cap.[22] Key distinguishing features of cradle cap include the absence of significant itching, alopecia, or inflammatory changes beyond mild erythema, with lesions confined to seborrheic areas like the scalp and face; biopsy is rarely needed unless atypical features such as pus or purpura suggest an alternative diagnosis like infection or histiocytosis.[1][17]| Condition | Key Distinguishing Features | Diagnostic Aids |
|---|---|---|
| Atopic Dermatitis | Pruritic, flexural/extensor involvement, scratching | Clinical observation |
| Psoriasis | Sharply demarcated plaques, silvery scales, nail changes | Clinical; biopsy if needed |
| Tinea Capitis | Hair breakage, lymphadenopathy, patchy scaling | KOH prep or fungal culture |
| Langerhans Cell Histiocytosis | Purpuric nodules, ulcerations, systemic symptoms | Biopsy |
| Allergic Contact Dermatitis | Vesicular, exposure history, intertriginous sites | History; patch testing if chronic |