Cicatricial Alopecia
Scarring hair loss (cicatricial alopecia or scarring alopecia) is a serious and complex group of scalp disorders in which hair follicles are permanently destroyed and replaced by fibrotic tissue. Unlike non-scarring forms (such as pattern hair loss or alopecia areata), scarring alopecia causes permanent, irreversible hair loss once the follicular stem cells have been destroyed.
At its core, scarring alopecia is driven by inflammation that targets the bulge region of the hair follicle, home to the follicular stem cells:
- Attack on stem cells in the follicular bulge: The bulge holds the stem cells that regenerate the hair at the start of each new anagen (growth) cycle. When autoimmune inflammation or infection destroys this area, the follicle loses all ability to recover.
- Loss of immune privilege and inflammatory response: Depending on the main type of inflammatory cell involved, primary scarring alopecias fall into these groups:
- Lymphocytic: Autoreactive T cells attack and destroy the follicle (as in lichen planopilaris, frontal fibrosing alopecia, or discoid lupus erythematosus).
- Neutrophilic: Intense acute inflammation and infection cause abscesses and tissue necrosis (as in folliculitis decalvans and dissecting cellulitis).
- Mixed: A combination of lymphocytes, neutrophils, and foreign-body giant cells (as in acne keloidalis nuchae).
- Fibrosis and loss of follicle openings: After the inflammatory phase, fibroblasts multiply rapidly and replace the follicle entirely with tough bands of collagen, sealing off and erasing the follicle openings on the scalp surface.
At Haute-Derma, we treat scarring hair loss as a medical emergency. The first goal is not to regrow hair in areas that have already scarred, but to shut down active inflammation right away and protect as many of the remaining follicles as possible.
Clinical Features and Differential Diagnosis
Examining a patient with scarring hair loss means looking for signs of active inflammation around the follicle openings, together with the characteristic loss of those openings:
- Complete loss of follicular ostia: The bald scalp is smooth, shiny, and flat, either thin and atrophic or firm and thickened, with no natural follicle openings left. This is the single most important clinical sign separating it from non-scarring hair loss.
- Signs of active inflammation at the edge:
- Scaling around the follicle openings (peripilar erythema and keratosis): Follicles at the edge of the patch are red, slightly swollen, and wrapped in tube-like collars of scale.
- Tufted hairs (polytrichia): Several hairs (3–10) bundled together and emerging from a single distorted follicle opening (typical of folliculitis decalvans).
- Pustules, draining tracts, and keloid-like scars: Deep pustules, firm keloid-like bands, or interconnected tracts that drain foul-smelling pus.
- Marked symptoms: Patients often live with burning, intense itching, stinging, or deep scalp tenderness, even to a light touch.
- Trichoscopy (scalp dermoscopy) and biopsy:
- Complete absence of follicular openings.
- Redness and thick scale around the follicle openings (peripilar casts).
- Scalp biopsy: The gold standard for diagnosis. A 4 mm punch biopsy is taken from the active edge of the bald patch so histopathology can identify the exact subtype (lymphocytic or neutrophilic).
How Haute-Derma Diagnoses and Treats the Condition
- Urgent diagnosis and biopsy to identify the subtype: The doctor uses trichoscopy to find the actively inflamed areas and arranges an early scalp biopsy to classify the inflammatory pattern (lymphocytic or neutrophilic). This lets us start targeted treatment before more follicles are lost.
- Controlling inflammation according to the cause:
- Lymphocytic types (LPP, FFA, DLE):
- Control inflammation with a super-potent topical corticosteroid (clobetasol) under occlusion or with intralesional injections (ILTAC).
- Add a systemic immunomodulator: hydroxychloroquine, doxycycline (anti-inflammatory dose), isotretinoin, or dapsone.
- Neutrophilic types (folliculitis decalvans, dissecting cellulitis):
- Long courses of high-dose combined oral antibiotics (rifampicin plus clindamycin) to eradicate bacteria (Staphylococcus aureus) and reduce inflammation.
- Topical antiseptic washes combined with oral isotretinoin to control the sebaceous glands.
- Lymphocytic types (LPP, FFA, DLE):
- Medical technology and newer targeted drugs:
- JAK inhibitors: Targeted drugs such as tofacitinib and baricitinib for treatment-resistant lichen planopilaris (LPP) or frontal fibrosing alopecia (FFA), to block the IFN-γ inflammatory signaling pathway.
- Anti-fibrotic PRP / PRF micro-injections: Once inflammation is under control, the patient's own growth factors are used to calm the dermis, reduce stiffness, and protect neighboring follicles.
- Long-term cosmetic restoration: For areas that have become completely smooth scar and where the disease has been stable (no signs of inflammation for at least 1–2 years), the doctor assesses whether hair transplantation into the scar is feasible, or recommends cosmetic alternatives such as scalp micropigmentation (SMP).
