Alopecia

Descriptive text is not available for this image BASICS

Absence of hair from areas where it normally grows

DESCRIPTION

  • Phases of the hair follicle cycle
    • Anagen phase (growth phase): 90% scalp hair follicles, lasts 2 to 6 years
    • Catagen phase (transition phase): regression of follicle, <1% follicles, lasts 3 weeks
    • Telogen phase (resting phase): club hair ready for shedding, lasts 2 to 3 months
  • Scarring (cicatricial) alopecia
    • Inflammatory disorders leading to permanent follicle destruction and hair loss
    • Includes lymphocytic, neutrophilic, and mixed cicatricial alopecia
  • Nonscarring (noncicatricial) alopecia
    • Mild or no inflammation, no destruction of follicle
    • Includes focal (alopecia areata [AA], traction alopecia), patterned (androgenic alopecia, female pattern hair loss), or diffuse hair loss (telogen effluvium, anagen effluvium)
  • Structural hair disorders: Brittle hair from abnormal hair formation/external insult

EPIDEMIOLOGY

Prevalence

  • Androgenic alopecia:
    • In males, 30% Caucasian by 30 years of age, 50% by 50 years of age, and 80% by 70 years of age
    • In females, 70% of women >65 years of age
  • AA: 1/1,000 with lifetime risk 1–2%; men and women are affected equally.
  • Scarring alopecia: rare, 3–7% of all hair disorder patients

ETIOLOGY AND PATHOPHYSIOLOGY

  • Scarring (cicatricial) alopecia
    • Inflammatory disorders leading to permanent destruction of the follicle
    • Slick smooth scalp without follicles evident
    • Three subtypes based on inflammation: lymphocytic, neutrophilic, and mixed
    • Primary scarring includes discoid lupus, lichen planopilaris, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, acne keloidalis nuchae, folliculitis decalvans, dissecting cellulitis of scalp, primary fibrosing, among others
    • Secondary scarring from infection, neoplasm, radiation, surgery, and other physical trauma, including tinea capitis
    • Central centrifugal cicatricial alopecia is the most common form of scarring hair loss in African American women; etiology unknown but possibly from hair care practices
  • Nonscarring (noncicatricial) alopecia
    • Focal hair loss
      • AA: patchy hair loss, usually autoimmune, T cell–mediated inflammation resulting in premature transition to catagen and then telogen phases
        • May progress to alopecia totalis (entire scalp) or alopecia universalis (loss of all hair)
        • Nail disease frequently seen (10–20% of patients with AA)
        • High psychiatric comorbidity
      • Alopecia syphilitica: “moth-eaten” appearance, secondary syphilis
      • Pressure-induced alopecia: hair loss from long periods of pressure on one area of scalp
      • Temporal triangular alopecia: congenital patch of hair loss in temporal area
      • Traction alopecia: due to physical stressor of tight braids, ponytails, hair weaves
    • Patterned hair loss
      • Androgenic alopecia: hair transitions from terminal to vellus hairs
      • Male pattern hair loss: thinning in bitemporal or vertex areas (Hamilton-Norwood Scale, stages I to VII); results from increased androgen receptors, and increased 5-α reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT); this leads to decreased follicle size and vellus hair
      • Female pattern hair loss: thinning on frontal and vertex areas; unclear etiology, possible association with polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia
    • Trichotillomania: intentional pulling of hair from scalp; presents various patterns
  • Diffuse
    • Telogen effluvium: sudden shift of many follicles from anagen to telogen phase, resulting in decreased hair density but not bald areas
      • May follow major stressors, including childbirth, injury, illness; occurs 2 to 3 months after event
      • Can be chronic with ongoing illness (SLE, renal failure, IBS, HIV, thyroid/pituitary dysfunction)
      • Adding or changing medications (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, β-blockers, ACE inhibitors, colchicine, cholesterol-lowering medications, etc.)
      • Malnutrition from malabsorption, eating disorders; poor diet can contribute.
    • Anagen effluvium
      • Interruption of the anagen phase without transition to telogen phase; days to weeks after inciting event
      • Chemotherapy is the most common trigger. Radiation, anticancer drugs, and severe protein-calorie malnutrition can also trigger.
  • Inherited and acquired structural hair disorders
    • Multiple inherited hair disorders including Menkes disease, monilethrix, and so forth; these result in the formation of abnormal hairs that are weakened.
    • May also result from chemical or heat damaging from hair processing treatments

Genetics

Family history of early patterned hair loss is common in androgenic alopecia, also in AA.

RISK FACTORS

  • Genetic predisposition
  • Chronic illness including autoimmune disease, infections, cancer
  • Physiologic stress including pregnancy and childbirth
  • Poor nutrition
  • Medication, chemotherapy, radiation
  • Hair chemical treatments, braids, weaves/extensions

GENERAL PREVENTION

Minimize risk factors if possible.

COMMONLY ASSOCIATED CONDITIONS

  • See “Etiology and Pathophysiology.”
  • Vitiligo—4.1% patients with AA, may be the result of similar autoimmune pathways

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