Alopecia: Types and Patterns

PRIMARY CLASSIFICATION: Scarring vs. Non-Scarring

I. NON-SCARRING ALOPECIAS

1. Androgenetic Alopecia (AGA) - Pattern Alopecia

Male-Pattern (Hamilton-Norwood Classification)

• Begins in teens/twenties with recession at frontotemporal regions ("Geheimratswinkeln" / professor angles)
• Progresses to vertex thinning, then confluence over the crown
• Grades I-VII, with vertex-predominant and frontoparietal variants
• Follicles produce progressively finer, lighter hairs with each cycle

Female-Pattern (Ludwig / Sinclair Classification)

• Ludwig pattern (most common): diffuse centroparietal thinning with preservation of the frontal hairline. Graded I-III (Ludwig) or I-V (Sinclair scale).
• Christmas-tree pattern (Olsen): hair part widens anteriorly, creating a triangular zone of thinning pointing toward the frontal hairline.
• A small subset shows a male-type temporal recession pattern.
• Most women have normal menses and fertility; if hirsutism, menstrual irregularities, or acne are present, evaluate for hyperandrogenism (PCOS, adrenal/ovarian tumor).

2. Telogen Effluvium

• Surgery, high fever, severe illness
• Parturition (postpartum hair loss) - hair shed 3-5 months after delivery
• Crash dieting / protein deficiency
• Drugs: warfarin, heparin, beta-blockers, lithium, retinoids, propylthiouracil, interferons, colchicine
• Thyroid disease (hypothyroidism and hyperthyroidism)
• Iron deficiency

• Acute telogen effluvium: typically resolves within 6 months
• Chronic telogen effluvium: shortened anagen phase persists (>6 months); associated with pattern alopecia
• Diffuse hair thinning without a specific distribution

3. Alopecia Areata (AA)

• Exclamation mark hairs (tapered/broken at the scalp end) at the patch margins
• Nail pitting in ~20% of cases
• Associated with thyroiditis, vitiligo, and other autoimmune diseases
• Positive family history in ~25% of cases

4. Anagen Effluvium

• Chemotherapy (daunorubicin, taxanes, anthracyclines) - most common cause; hair loss within 1-2 months of high-dose therapy
• Radiation to the scalp
• Severe protein malnutrition, arsenic/thallium poisoning

5. Tinea Capitis

6. Traction Alopecia

7. Trichotillomania (Hair-Pulling Disorder)

8. Pressure Alopecia

II. SCARRING (CICATRICIAL) ALOPECIAS

A. LYMPHOCYTIC PRIMARY CICATRICIAL ALOPECIAS

1. Lichen Planopilaris (LPP)

• Predominant in White women, age 40-60
• Perifollicular scaling, erythema, burning/itching
• Targets the isthmus-bulge region (lymphocytic infiltrate)
• Trichoscopy: perifollicular scale, absent follicular openings
• Spectrum includes:
  • Classic LPP: patchy occipital/vertex involvement
  • Frontal Fibrosing Alopecia (FFA): progressive recession of the frontal and temporal hairline; loss of eyebrows/eyelashes; also affects Asian and African-heritage women
  • Graham Little-Piccardi-Lasseur Syndrome: triad of scalp cicatricial alopecia + non-scarring axillary/pubic alopecia + follicular keratosis of the trunk/limbs

2. Central Centrifugal Cicatricial Alopecia (CCCA)

• Most common scarring alopecia in Black women
• Begins at the crown/vertex, expands centrifugally
• Associated with hot combs, chemical relaxers, and certain hair care practices (though causation is debated)
• Histology: premature desquamation of the inner root sheath

3. Discoid Lupus Erythematosus (DLE)

• Erythematous plaques with adherent scale; central atrophy and hypopigmentation with a rim of hyperpigmentation
• Active inflammation at periphery, scarring at center
• Can occur isolated to skin or with systemic lupus (minority)

4. Alopecia Mucinosa (Follicular Mucinosis)

• Well-demarcated erythematous/skin-colored patches; follicular papules; mucin deposition in outer root sheath
• Not a true primary cicatricial alopecia (no fibrotic scar)
• Must rule out underlying cutaneous T-cell lymphoma / mycosis fungoides

B. NEUTROPHILIC PRIMARY CICATRICIAL ALOPECIAS

1. Folliculitis Decalvans (FD)

• ~11% of primary cicatricial alopecias; young-middle aged adults, slight male predominance
• Starts at vertex: erythematous patches + follicular pustules (Staphylococcus aureus)
• Tufted folliculitis: 5-15 hairs emerging from a single dilated orifice - pathognomonic
• Treatment: prolonged antibiotics (rifampicin + clindamycin combination), topical antiseptics

2. Dissecting Cellulitis of the Scalp

• Deep, fluctuant nodules/abscesses on the vertex/occipital scalp
• Part of the follicular occlusion tetrad (with acne conglobata, hidradenitis suppurativa, pilonidal sinus)

C. MIXED CICATRICIAL ALOPECIAS

D. SECONDARY CICATRICIAL ALOPECIAS

• Deep burns
• Radiation dermatitis
• Cutaneous malignancies / metastases
• Sarcoidosis
• Morphea (linear scleroderma)
• Necrobiosis lipoidica
• Cutaneous tuberculosis
• Chronic pressure/ischemia

QUICK REFERENCE SUMMARY

Hypopigmentation Patches - Causes and Classification

MASTER CLASSIFICATION (Harrison's 22E, Table 61-9)

I. Primary Cutaneous Disorders

A. Diffuse

• Generalized vitiligo

B. Localized / Patchy

1. Postinflammatory hypopigmentation
2. Idiopathic guttate hypomelanosis
3. Pityriasis (tinea) versicolor
4. Vitiligo
5. Chemical- or drug-induced leukoderma (e.g., topical imiquimod, oral imatinib)
6. Nevus depigmentosus / Blaschko-linear hypopigmentation (pigmentary mosaicism)
7. Progressive macular hypomelanosis
8. Piebaldism

II. Systemic Diseases

A. Diffuse

1. Oculocutaneous albinism (OCA types I-VII)
2. Hermansky-Pudlak syndrome (+ platelet storage defect, lung disease)
3. Chédiak-Higashi syndrome (+ giant lysosomal granules, recurrent infections)
4. Phenylketonuria (tyrosine deficiency reduces melanin synthesis)

B. Localized / Patchy

1. Systemic sclerosis (scleroderma) - perifollicular pigment retained
2. Melanoma-associated vitiligo-like leukoderma
3. Sarcoidosis (overlying cutaneous lesions)
4. Cutaneous T-cell lymphoma / Mycosis fungoides (hypopigmented MF variant)
5. Tuberculoid and indeterminate leprosy
6. Onchocerciasis ("leopard skin")
7. Blaschko-linear hypopigmentation (pigmentary mosaicism)
8. Incontinentia pigmenti (Stage IV)
9. Tuberous sclerosis (ash-leaf spots)
10. Waardenburg syndrome / Shah-Waardenburg syndrome
11. Vogt-Koyanagi-Harada (VKH) syndrome

KEY CONDITIONS IN DETAIL

1. Vitiligo

• Loss of melanocytes (autoimmune T-cell mediated destruction)
• Well-demarcated, chalk-white (truly depigmented) patches
• Distribution: periorificial (mouth, eyes, nose), hands, feet, flexor wrists, ankles, elbows, knees, body folds
• Associated: Hashimoto's thyroiditis (most common - up to 30%), Graves' disease, Addison's disease, pernicious anemia, alopecia areata, uveitis
• Wood's lamp: bright white fluorescence (accentuates depigmentation)
• Treatment: topical ruxolitinib (JAK inhibitor), tacrolimus, corticosteroids, phototherapy (NB-UVB)

2. Pityriasis (Tinea) Versicolor

• Malassezia furfur (yeast) infection - produces azelaic acid which inhibits melanin synthesis
• Fine, scaly, hypopigmented (or hyperpigmented) macules/patches on the trunk, upper arms, neck
• Wood's lamp: yellow-green fluorescence
• KOH: "spaghetti and meatballs" (hyphae + spores)
• Treatment: topical/oral azoles, selenium sulfide

3. Pityriasis Alba

• Common in children/adolescents; associated with atopic dermatitis
• Ill-defined, slightly scaly, hypopigmented patches on the face (cheeks), upper arms
• Post-inflammatory; improves with emollients and low-potency topical steroids

4. Leprosy (Hansen's Disease) - Tuberculoid / Indeterminate Type

• Few asymmetric hypopigmented patches with well-defined or ill-defined edges
• Key distinguishing feature: associated anesthesia, anhidrosis, and alopecia within the patch
• Palpable thickened peripheral nerves at borders
• Biopsy: dermal granulomas with very few/no bacilli (tuberculoid); sparse lymphocytic infiltrate (indeterminate)
• Must be differentiated from: pityriasis alba, vitiligo, progressive macular hypomelanosis, tinea versicolor, pityriasis rosea, sarcoidosis

5. Tuberous Sclerosis - Ash-Leaf Spots

• Earliest cutaneous sign of tuberous sclerosis (often present at birth)
• Lance-ovate (ash-leaf) or polygonal hypopigmented macules, 1-3 cm
• Pigment reduced (not absent); may need Wood's lamp examination in fair-skinned patients
• ≥3 hypopigmented macules ≥5 mm = major diagnostic criterion
• Associated: angiofibromas ("adenoma sebaceum"), shagreen patches, ungual fibromas, seizures, intellectual disability, CNS hamartomas, renal angiomyolipomas

6. Postinflammatory Hypopigmentation

• Follows any inflammatory skin disease: eczema, psoriasis, lichen planus, discoid lupus, impetigo, pityriasis rosea, chemical burns, laser therapy
• Distribution follows that of the primary disease
• Usually temporary and reversible

7. Idiopathic Guttate Hypomelanosis

• Most common cause of guttate (drop-like) hypopigmentation
• Well-demarcated white macules, 2-4 mm on sun-exposed skin (shins, forearms)
• Seen in adults >40 years, increases with age and UV exposure
• Benign, no treatment usually required

8. Progressive Macular Hypomelanosis

• Young adults, especially darker skin tones
• Non-scaly, ill-defined coalescing hypopigmented macules on trunk (centrifugally spreading)
• Associated with Cutibacterium acnes follicular colonization
• Wood's lamp: follicular red fluorescence

9. Nevus Depigmentosus

• Stable, congenital, well-circumscribed hypomelanotic patch (usually single)
• Present at birth; does NOT enlarge proportionally with age
• Normal melanocyte number, but abnormal melanosomes/transfer
• Multiple lesions → rule out tuberous sclerosis

10. Piebaldism

• Autosomal dominant; c-KIT mutation → defective melanoblast migration
• Congenital, stable white patches + white forelock (poliosis)
• Characteristic distribution: anterior scalp/forehead, mid-trunk, mid-limbs
• Associated with Waardenburg syndrome (+ sensorineural deafness, dystopia canthorum)

11. Oculocutaneous Albinism (OCA)

• Autosomal recessive; mutations in tyrosinase (Type I) or OCA2/P protein (Type II)
• Generalized diffuse hypopigmentation of skin, hair, and eyes
• Complications: ↓ visual acuity, nystagmus, photophobia, ↑ risk of squamous cell carcinoma

12. Systemic Sclerosis (Scleroderma)

• "Salt-and-pepper" pattern - hypopigmentation with retention of perifollicular pigment
• Distinguishes it from vitiligo

13. Hypopigmented Mycosis Fungoides (CTCL)

• Variant of cutaneous T-cell lymphoma - more common in darker-skinned individuals
• Hypopigmented, slightly atrophic patches; can mimic pityriasis versicolor or vitiligo
• Biopsy with epidermotropic atypical T-cell infiltrate confirms diagnosis

14. Vogt-Koyanagi-Harada (VKH) Syndrome

• Granulomatous uveitis + cutaneous/hair depigmentation (vitiligo-like) + neurological and auditory features
• Poliosis (white patches of hair), perilimbal vitiligo (Sugiura sign)

QUICK DIFFERENTIATOR TABLE