Cause of alopecia
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causes of alopecia classification types
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Causes of Alopecia
Alopecia (hair loss) is broadly divided into two major categories: scarring (cicatricial) and non-scarring. This distinction is clinically and etiologically fundamental - scarring alopecia destroys the follicle permanently, while non-scarring alopecia preserves the follicle and is often reversible.
I. NON-SCARRING ALOPECIA
In non-scarring alopecia, hair shafts are absent or miniaturized but the hair follicles are preserved, which explains its reversible nature.
1. Androgenetic Alopecia (Pattern Baldness)
- The most common cause of hair loss in both men and women
- Caused by the effect of dihydrotestosterone (DHT) on genetically susceptible hair follicles
- The 5alpha-reduction of testosterone is increased in balding scalp, yielding excess DHT; androgen-inducible TGF-beta1 from dermal papilla cells mediates hair growth suppression
- In men: bitemporal recession + vertex thinning; in women: diffuse crown thinning with preserved frontal hairline
- Polygenic inheritance; androgen receptor gene implicated in early-onset disease (<30 years)
- In women, elevated androgens may signal ovarian/adrenal dysfunction or neoplasm; signs of virilization warrant investigation for tumor
- Mechanism: progressive shortening of the anagen phase, follicular miniaturization, terminal hairs replaced by vellus hairs
2. Telogen Effluvium
- Diffuse hair shedding caused by premature shift of many follicles from anagen (growth) to telogen (resting)
- Common triggers:
- Physical stress: major surgery, high fever, severe illness, postpartum (2-3 months after delivery)
- Psychological stress
- Nutritional deficiencies: iron, zinc, protein, biotin
- Rapid weight loss / crash dieting
- Thyroid disorders (hypothyroidism and hyperthyroidism both cause diffuse thinning)
- Hormonal changes: stopping oral contraceptives
3. Alopecia Areata
- Autoimmune origin - T-cell mediated attack on hair follicles
- Presents as well-circumscribed, oval/round patches of complete hair loss, often with "exclamation mark" hairs at the periphery
- Can progress to alopecia totalis (entire scalp) or alopecia universalis (entire body including eyebrows, eyelashes)
- Associated with other autoimmune diseases: thyroid disease, vitiligo, type 1 diabetes
4. Tinea Capitis
- Fungal infection of the scalp (most common dermatophytes: Trichophyton and Microsporum species)
- More common in children
- Features: scaly, pruritic patches; "black dot" pattern if hair shafts break at the scalp surface
- Can cause kerion (boggy inflammatory mass) - risk of scarring if untreated
5. Drug-Induced Alopecia
- Most drugs cause a telogen effluvium; chemotherapy agents cause anagen effluvium (hair loss within weeks of starting)
- Drugs implicated (from Harrison's 22E):
- Anticoagulants: warfarin, heparin
- Antithyroid: propylthiouracil, carbimazole
- Retinoids: isotretinoin, acitretin
- Mood/psychiatric: lithium, amphetamines, interferons
- Cardiovascular: beta-blockers
- Other: colchicine, chemotherapy agents (daunorubicin - anagen effluvium)
- Hair typically regrows after stopping the offending agent
6. Systemic Disease - Associated
- Lupus erythematosus (SLE): two forms - non-scarring alopecia coinciding with flares ("lupus hairs" - multiple short hairs at the frontal scalp); and scarring from discoid lesions
- Secondary syphilis: "moth-eaten" alopecia - scattered, poorly circumscribed patches
- Hypothyroidism / Hyperthyroidism: diffuse thinning
- Iron deficiency anemia
7. Traumatic Alopecia
- Traction alopecia: chronic tension from tight hairstyles (braids, cornrows, ponytails); repeated tension damages follicles
- Trichotillomania: compulsive hair-pulling; irregular patches with broken hairs of varying lengths (psychological/psychiatric cause)
II. SCARRING (CICATRICIAL) ALOPECIA
Characterized by fibrosis, inflammation, and permanent destruction of hair follicles. The scalp shows a smooth surface with decreased follicular openings.
Primary Cutaneous Disorders (most common causes)
| Condition | Key Features |
|---|---|
| Lichen planopilaris (LPP) | Perifollicular violet macules at periphery; associated with oral lichen planus |
| Discoid lupus erythematosus (DLE) | Erythematous scaly active border, hypopigmented center with rim of hyperpigmentation; may occur without systemic lupus |
| Central centrifugal cicatricial alopecia (CCCA) | Begins at crown, spreads outward; most common in women of African descent |
| Folliculitis decalvans | Follicular pustules at the active periphery; patients may develop reactive arthritis |
| Frontal fibrosing alopecia (FFA) | Frontotemporal hairline recession with loss of eyebrows; band-like scarring |
| Linear scleroderma (morphea) | Sclerotic plaques; "en coup de sabre" pattern on the frontoparietal scalp |
Systemic/Other Causes of Scarring Alopecia
- Sarcoidosis: multiple morphologies - plaques, macular lesions mimicking alopecia areata, diffuse alopecia; biopsy shows non-caseating dermal granulomas; virtually always seen in African/African American women
- Chemotherapeutic agents (rarely, permanent anagen effluvium)
- Cutaneous metastases
- Radiation therapy: permanent follicle destruction at high doses
Summary Table
| Category | Common Examples | Reversible? |
|---|---|---|
| Androgenetic | DHT-mediated, genetic | Partial (with treatment) |
| Telogen effluvium | Stress, nutritional, postpartum | Yes |
| Alopecia areata | Autoimmune | Often yes |
| Tinea capitis | Fungal infection | Yes (if treated early) |
| Drug-induced | Warfarin, lithium, beta-blockers, chemo | Usually yes |
| Systemic disease | SLE, syphilis, thyroid disorders | Variable |
| Traumatic | Traction, trichotillomania | Usually yes |
| Scarring (primary) | LPP, DLE, CCCA, FFA | No |
| Scarring (systemic) | Sarcoidosis, metastases | No |
Sources:
- Harrison's Principles of Internal Medicine 22E (2025), Chapter 61 - Table 61-4 & 61-5 on Alopecia
- Andrews' Diseases of the Skin - Clinical Dermatology, Chapter 33 on Pattern Alopecia
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