A Systematic Approach to Hair Loss and Scalp Dermatoses

At the Rapids 2026 conference in Fort Lauderdale, Eileen Cheever sat down with Dr. Asempa to discuss practical, systematic frameworks for diagnosing and managing hair loss. From the nuances of trichoscopy to the pathophysiology of scarring versus non-scarring alopecia, Dr. Asempa shared essential clinical pearls for dermatology practitioners.

1. The Systematic Framework for Hair Loss Evaluation

To ensure diagnostic accuracy and prevent cognitive bias, Dr. Asempa emphasizes a standardized evaluation protocol for every patient presenting with hair loss:

1. Detailed Clinical History: Documenting precise onset, progression, and exacerbating factors.
2. Global Examination: Evaluating the scalp from a distance and manually parting the hair to assess distribution. Physical palpation and direct scalp visualization are mandatory.
3. Trichoscopy: Utilizing dermoscopy to provide a microscopic view of the epidermis and follicular units.
4. Histopathology: Utilizing a scalp biopsy when trichoscopic features are insufficient for a definitive diagnosis.
5. Laboratory Evaluation: Reviewing previous labs and ordering targeted serology (e.g., iron panels, thyroid function, hormonal metrics).
6. Therapeutic Response Review: Re-evaluating the initial diagnosis if a patient fails to respond to standard therapy, rather than assuming treatment failure alone.

2. Master Class in Trichoscopy: The 5 Key Features

Trichoscopy bridges the gap between clinical examination and histopathology. Dr. Asempa trains residents to systematically evaluate five distinct features during every dermoscopic exam:

• Hair Shaft Morphology: Assess fiber caliber, variability, and the number of shafts emerging from each follicular orifice (terminal vs. vellus-like hairs).
• Pigmentation Patterns: Look for interfollicular hyperpigmentation, hypopigmentation, or specific structures like the perifollicular "dirty dots" or "honeycomb" patterns.
• Vascular Architecture: Identify erythema, pinpoint vessels, or dilated, twisted loops that signal active inflammation.
• Interfollicular Space: Evaluate the distance between follicular units to assess true density and identify areas where follicles have been entirely replaced by fibrous tissue.
• Scale Characteristics: Document the presence, quality, and location of desquamation. Is it diffuse (interfollicular) or localized around the hair base (perifollicular)?

3. Differentiating LPP from CCCA

Distinguishing between Lichen Planopilaris (LPP) and Central Centrifugal Cicatricial Alopecia (CCCA) can be challenging because both present as scarring alopecias. However, key clinical and trichoscopic differences guide the differential diagnosis:

Clinical and Trichoscopic Comparison

4. Pathophysiology: Loss of Immune Privilege

Understanding why certain alopecias cause permanent scarring while others do not comes down to follicular anatomy and immune privilege.

Alopecia Areata (Non-Scarring)

The hair bulb normally maintains an immune-privileged site, shielded from systemic immune surveillance. In alopecia areata, this immune privilege collapses, causing $T\text{ lymphocytes}$ to target the bulbar area (resembling a "swarm of bees"). Crucially, this intense inflammation spares the follicular bulge, where epithelial stem cells reside. Because the stem cells are preserved, the potential for hair regrowth remains intact.

Lichen Planopilaris (Scarring)

In contrast, conditions like LPP present with lichenoid inflammation that specifically targets the isthmus region and the follicular bulge. By directly destroying the stem cell niche, the follicle loses its capacity to regenerate, leading to permanent fibrotic replacement (scarring).

5. Managing Acne Keloidalis Nuchae (AKN)

Dr. Asempa notes that Acne Keloidalis Nuchae (AKN) is a misnomer: it is not a true form of acne, does not form true keloids, and can extend far beyond the nuchal region up into the vertex or crown of the scalp.

Pathogenesis

AKN is multifactorial, driven by:

• Androgenic influences (highly prevalent in male patients).
• Mechanical friction (hats, helmets, collars).
• An aberrant immune response to commensal skin flora, including Staphylococcus aureus and Demodex mites.

Treatment Protocol

Management requires a stepped therapeutic strategy tailored to the severity of the disease:

• First-Line (Mild/Early): Topical antibiotics combined with topical anti-inflammatories to reduce bacterial load and initial erythema.
• Second-Line (Moderate): Intralesional corticosteroid injections directly into papules and early plaques to arrest localized inflammation and flatten lesions.
• Third-Line (Severe/Acute Flare): Systemic retinoids or extended courses of systemic antibiotics to manage widespread or deeply infiltrative disease.
• Refractory Cases: Wide surgical excision of the fibrotic plaque, often down to the fascial plane, followed by healing by second intention or grafting.

Patient Counseling & Compliance

Counseling must be approached with cultural competence, as hair-styling practices are deeply personal and tied to identity. Rather than issuing absolute prohibitions, clinicians should focus on risk mitigation:

• Avoid Close Shaving: Advise against clean-shave razor passes directly on the skin, as this can induce inflammatory foreign-body reactions when curved hairs re-enter the dermis.
• Reduce Mechanical Friction: Minimize constant rubbing from tight headwear. Dr. Asempa uses a standardized, letter-graded "Hairstyle Guide" (A to F) to objectively assess how a patient's preferred hairstyle affects scalp health, enabling a collaborative approach to treatment compliance.

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