(1)
Department of Dermatology, University of Pennsylvania, Penn Presbyterian Medical Center Medical Arts Building, Philadelphia, PA, USA
Abstract
This section focuses on diseases that cause hair loss or hair abnormalities. Clinically, scarring alopecia is suggested by loss of hair follicle ostia and smooth, shiny patches of skin between tufts of hair (like doll’s hairs). Non-scarring alopecias typically retain hair follicles despite loss of hair. With time, however, even non-scarring alopecias may show loss of follicular ostia. On pathology, scarring alopecias may show changes from minimal inflammation to perifollicular fibrosis and ultimately true follicular scars.
The hair cycle consists of: anagen/growth phase (~2–6 years), catagen/transition phase (~3 weeks), telogen/release phase (~3 months); mnemonic: rule of 3s, 3 years (anagen), 3 weeks (catagen), 3 months (telogen)
Keywords
AlopeciaScarring alopeciaNon-scarring alopecia9.1 Scarring Alopecia
9.1.1 Inflammatory Scarring Alopecia
(a)
Lymphoid scarring alopecia
I.
Discoid lupus (DLE)
Classically hyperkeratotic plaques with follicular plugging and scarring alopecia; typically on face, scalp, conchal bowls of ears
“Carpet tack sign” = horny plugs on undersurface when scale removed (non-specific)
“Lupus hairs” = short, fragile frontal hairs
See also Connective Tissue Diseases:Lupus
II.
Lichen planopilaris (LPP)
Classically scarring alopecia with perifollicular scaling
Frontal fibrosing alopecia = appears to be a pattern of LPP, mostly in postmenopausal women
Graham-Little-Piccardi-Lasseur Syndrome = LPP, KP, axillary/genital non-scarring alopecia
Recent interest in treating LPP with pioglitazone (a TZD medication) that is a PPAR-γ agonist. PPAR- γ’s activation may help prevent scarring alopecia
See also Papulosquamous:Lichenoid:Lichen Planus
III.
Central centrifugal cicatricial alopecia (CCCA)
Aka follicular degeneration syndrome
Aka “Hot comb” alopecia
Classically associated with history of chemical treatments, relaxing, perms, hot combs, although no strong evidence to support these associations
(b)
Neutrophilic scarring alopecia
I.
Folliculitis decalvans
Flat and boggy plaques of alopecia, can become pseudopelade
Usually treat with antibiotics, steroids
Some may use term almost interchangeably with dissecting cellulitis
II.
Dissecting cellulitis
Aka perifolliculitis capitis abscedens et suffodiens
Terrible name: not dissecting, not a cellulitis
Part of the follicular occlusion tetrad, see also Acneiform Diseases
Clinically more separate nodules/cysts in scalp with associated alopecia, can become pseudopelade
Some may use term almost interchangeably with folliculitis decalvans
May treat with tetracyclines, isotretinoin
(c)
Mixed infiltrate scarring alopecia
I.
Acne keloidalis nuchae
Exact etiology unclear, but may represent a scarring reaction to ingrown hairs (pseudofolliculitis), see also Acneiform Diseases
Name is at least partially a misnomer – it is not caused by acne and lesions are not keloidal (on pathology), though it does classically appear on the posterior neck
Commonly seen in African-American patients with short curly hairs and short haircuts (which all predisposes to pseudofolliculitis)
(d)
Pseudopelade of BrocqEnd stage of scarring alopecia, tufted doll’s hairs, “footprints in the snow”
9.1.2 Non-Inflammatory Scarring Alopecia
(a)
Trauma
(b)
Traction alopecia
Sometimes non-inflammatory, sometimes inflammatory
Typically non-scarring initially, but may become scarring
(c)
Aplasia cutis congenita (ACC)
A focal congenital loss of skin/hair in newborns, may evaluate with imaging/MRI (do not want to risk biopsy)
“Hair collar sign” = a collar of hair seen around the skin defect
Ddx nevus sebaceus
I.
Adams-Oliver syndrome = ACC with cutis marmorata telangiectatica congenita
II.
Bart’s syndrome = ACC with epidermolysis bullosa
9.2 Non-Scarring Alopecia
9.2.1 Non-Inflammatory Non-Scarring Alopecia
(a)
Androgenic/androgenetic alopecia
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Norwood classification describes the stages of male pattern hair loss
Path: small/miniaturized superficial hair follicles (normally deep in fat)
I.
Male pattern – vertex and bitemporal/frontal scalp
II.
Female pattern – central thinning on crown; usually not frontal (which is more likely from traction)Stay updated, free articles. Join our Telegram channel
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