Alopecia: An Overview

Alopecia is a medical term for hair loss that can occur on the scalp or other parts of the body. While occasional hair shedding is normal as part of the hair growth cycle, alopecia refers to excessive, pathological hair loss that may have cosmetic, psychological, and medical consequences. Hair loss can be temporary or permanent, localized or diffuse, and can arise from genetic, autoimmune, infectious, endocrine, nutritional, or pharmacologic causes.

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1. Hair Growth Cycle

Understanding the hair growth cycle is fundamental to understanding alopecia. Human hair undergoes three distinct phases:

1. Anagen (growth phase)

   • Lasts 2–7 years depending on body site.

   • Hair grows actively at ~1 cm per month.

   • Most scalp hairs (~85–90%) are in this phase at any time.

2. Catagen (regression phase)

   • Lasts 2–3 weeks.

   • Hair follicle involutes and stops growing.

3. Telogen (resting phase)

   • Lasts 2–4 months.

   • Hair is shed at the end of this phase.

   • Normally, 50–100 hairs are shed daily.

Disruption of the cycle, follicular inflammation, or follicle destruction can lead to alopecia.

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2. Classification of Alopecia

Alopecia can be broadly categorized into non-scarring (non-cicatricial) and scarring (cicatricial) alopecia.

A. Non-Scarring Alopecia

Hair follicles remain intact; regrowth is possible if the underlying cause is treated. Common types include:

1. Androgenetic Alopecia (AGA)

   • Also called male-pattern baldness or female-pattern hair loss.

   • Etiology: Genetic predisposition and androgen sensitivity, particularly to dihydrotestosterone (DHT).

   • Pattern:

     • Males: Receding hairline and vertex thinning.

     • Females: Diffuse thinning over the crown with preserved frontal hairline.

   • Pathophysiology: Shortening of anagen phase, miniaturization of follicles.

   • Treatment: Minoxidil (topical), finasteride (oral, in men), hair transplantation.

2. Alopecia Areata (AA)

   • Etiology: Autoimmune attack on hair follicles.

   • Presentation: Sudden, patchy hair loss, usually round or oval; may involve scalp, eyebrows, eyelashes, or beard.

   • Variants:

     • Alopecia totalis: Total scalp hair loss.

     • Alopecia universalis: Complete loss of body hair.

   • Histology: Peribulbar lymphocytic infiltrate (“swarm of bees”).

   • Prognosis: Often unpredictable; spontaneous regrowth possible.

   • Treatment: Corticosteroids (topical, intralesional, systemic), immunotherapy, JAK inhibitors.

3. Telogen Effluvium (TE)

   • Etiology: Premature transition of hairs from anagen to telogen phase due to stressors.

   • Triggers: Severe illness, surgery, childbirth, high fever, nutritional deficiencies, medications.

   • Presentation: Diffuse hair shedding, often noticed months after trigger.

   • Prognosis: Usually self-limited; hair regrowth occurs within 6–12 months.

4. Anagen Effluvium

   • Etiology: Rapid hair loss during anagen phase, usually due to cytotoxic drugs (chemotherapy) or toxins.

   • Presentation: Sudden, diffuse loss of scalp and body hair.

   • Treatment: Usually reversible after discontinuation of the causative agent; scalp cooling can reduce chemotherapy-induced hair loss.

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B. Scarring (Cicatricial) Alopecia

Hair follicles are permanently destroyed by inflammation or fibrosis. These are rarer and often progressive.

1. Primary Cicatricial Alopecia

   • Cause: Inflammatory conditions target hair follicles.

   • Examples:

     • Lichen planopilaris: Autoimmune interface dermatitis destroys follicles.

     • Discoid lupus erythematosus (DLE): Chronic cutaneous lupus leads to scarring.

     • Central centrifugal cicatricial alopecia (CCCA): Common in African-descendant women, often related to hair care practices.

2. Secondary Cicatricial Alopecia

   • Hair loss due to destruction of follicles by infections, burns, trauma, or tumors.

   • Example: Folliculitis decalvans, radiation-induced alopecia.

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3. Etiology and Risk Factors

1. Genetic: Family history of androgenetic alopecia.

2. Hormonal: Androgen excess (PCOS), menopause, thyroid disorders.

3. Autoimmune: Alopecia areata, lupus erythematosus, lichen planus.

4. Infectious: Tinea capitis (fungal), bacterial folliculitis.

5. Nutritional deficiencies: Iron, zinc, biotin, protein-calorie malnutrition.

6. Medications: Chemotherapy, retinoids, anticoagulants, antithyroid drugs.

7. Physical/psychological stress: Surgery, trauma, severe emotional stress.

8. Environmental: Hair care practices causing traction alopecia.

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4. Clinical Evaluation

Evaluation involves history, examination, and investigations:

1. History

   • Onset, duration, pattern of hair loss

   • Family history

   • Associated symptoms (itching, pain, scaling)

   • Triggers (stress, medications, illness)

2. Physical Examination

   • Distribution: Patchy vs. diffuse

   • Presence of scarring, erythema, scaling

   • Hair shaft abnormalities (broken hairs, exclamation mark hairs)

3. Investigations

   • Laboratory tests: CBC, ferritin, thyroid function, ANA if autoimmune suspected.

   • Scalp biopsy: Indicated in cicatricial alopecia or atypical cases; helps identify inflammatory infiltrates.

   • Trichoscopy: Dermoscopy to visualize follicular patterns and hair shaft changes.

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5. Pathophysiology of Common Types

• Androgenetic alopecia: DHT binds to androgen receptors in hair follicles → follicular miniaturization → shorter anagen phase.

• Alopecia areata: T cell-mediated autoimmune attack on hair follicle immune privilege.

• Telogen effluvium: Stressors cause >10% of hairs to prematurely enter telogen phase.

• Anagen effluvium: Direct toxic effect on rapidly dividing hair matrix cells.

• Cicatricial alopecia: Inflammatory destruction of follicular stem cells in the bulge region → irreversible hair loss.

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6. Treatment Approaches

A. Medical Therapy

1. Androgenetic Alopecia

   • Topical minoxidil: Vasodilator, prolongs anagen phase

   • Oral finasteride (men only): 5α-reductase inhibitor reducing DHT

   • Spironolactone (women): Anti-androgen effect

2. Alopecia Areata

   • Corticosteroids: Topical, intralesional, systemic

   • Topical immunotherapy: Diphenylcyclopropenone (DPCP)

   • JAK inhibitors: Emerging therapy (tofacitinib, ruxolitinib)

3. Telogen Effluvium

   • Treat underlying cause

   • Nutritional supplementation if deficient

4. Anagen Effluvium

   • Mainly preventive (scalp cooling)

   • Supportive care

5. Cicatricial Alopecia

   • Early anti-inflammatory treatment to halt progression

   • Agents: Hydroxychloroquine, corticosteroids, immunosuppressants

   • Hair transplantation only after disease stabilization

B. Surgical and Cosmetic Approaches

• Hair transplantation in stable cases

• Scalp micropigmentation

• Wigs and prostheses

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7. Psychological Impact

Alopecia can lead to significant psychological distress, including:

• Anxiety and depression

• Low self-esteem

• Social withdrawal

• Body image disturbances

Psychological support and counseling are important components of management.

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8. Prognosis

• Non-scarring alopecia: Often reversible if underlying cause addressed (telogen effluvium, anagen effluvium).

• Androgenetic alopecia: Progressive but manageable.

• Alopecia areata: Variable; spontaneous regrowth possible but unpredictable.

• Cicatricial alopecia: Permanent; early intervention improves outcomes.

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9. Summary

Alopecia represents a heterogeneous group of hair loss disorders with diverse etiologies. Key points include:

• Classification: Non-scarring vs. scarring alopecia

• Non-scarring forms: Androgenetic alopecia, alopecia areata, telogen effluvium, anagen effluvium

• Scarring forms: Primary (lichen planopilaris, discoid lupus), secondary (infections, burns)

• Pathophysiology: Follicular miniaturization, autoimmune attack, premature follicle cycling, or inflammatory destruction

• Diagnosis: History, examination, lab tests, biopsy, trichoscopy

• Management: Treat underlying cause, medical therapy, immunomodulation, surgical options, psychological support

A multidisciplinary approach, addressing medical, cosmetic, and psychosocial aspects, is essential for optimal patient care.