Folliculitis Decalvans
Folliculitis decalvans (FD) is an uncommon condition in the group of neutrophilic primary cicatricial alopecias. It follows a chronic course marked by recurrent follicular inflammation, pustules and crusting, with gradual destruction of hair follicles that ends in permanent scarring hair loss.
FD arises from a complex interplay between Staphylococcus aureus and an abnormal immune response:
- The Role of Staphylococcus aureus and Biofilm: S. aureus can be cultured from most active pustules in FD. Rather than causing a simple infection, the bacteria release superantigens that switch on large numbers of T lymphocytes and set off a surge of pro-inflammatory cytokines (such as IL-1β, TNF-α and IL-8).
- Acute Neutrophil Infiltration and Follicle Damage: IL-8 draws large numbers of neutrophils into the infundibulum and neck of the follicle. The neutrophils release protein-digesting enzymes (proteases) and free oxygen radicals that rupture the follicle wall and spill hair components such as keratin into the surrounding dermis.
- Foreign-Body Reaction and Loss of Follicular Stem Cells: The immune system treats the escaped keratin as foreign material and mounts a foreign-body granulomatous reaction. This intense inflammation destroys the bulge region, home of the follicular stem cells, so the follicle can no longer regenerate and is replaced by scar tissue (fibrosis).
- How Tufted Hairs Form (Polytrichia): When inflammation and scarring affect the upper follicle, neighboring follicles are pulled together. Fibrosis fuses adjacent infundibula so that several hairs emerge through a single widened opening, creating the characteristic paintbrush or doll's hair appearance.
Clinical Features and Trichoscopy Findings
FD mostly affects adult men (male-to-female ratio about 3:1) and usually begins on the crown and the back of the scalp:
- Symptoms: Patients often describe persistent soreness, stinging, burning or marked itching in the affected area. Lesions tend to weep and bleed easily when combed or touched.
- Typical Lesions:
- Clusters of follicular pustules along the advancing edge of the bald patch.
- Thick yellowish, honey-colored crusts stuck firmly around the hair bases.
- Smooth, shiny, atrophic skin with no follicular openings at the center of the patch.
- Tufted Hairs (Polytrichia): Between 5 and 20 hairs emerge together from one fused follicular opening. This is the most important clinical clue to FD.
- Trichoscopy (Scalp Dermoscopy) Findings:
- Active border: Obvious hair tufts (polytrichia), deep perifollicular erythema, follicular tubular scales and follicular pustules.
- Inactive scarred center: Ivory-white or pale pink areas with no follicular openings, sometimes with starburst-like telangiectasia.
Diagnosis and Specialist Treatment at Haute-Derma
Because FD destroys follicles quickly, it needs early, active treatment to bring acute inflammation under control, eradicate S. aureus and stop scarring from spreading.
Diagnostic Workup
- Microbiology (Bacterial Culture and Sensitivity Testing): Pus from an intact pustule is cultured for Staphylococcus aureus and tested for antibiotic sensitivity, including screening for methicillin-resistant strains (MRSA).
- Scalp Biopsy (4 mm Punch): Taken from the active border, where pustules or hair tufts are present.
- Histopathology: Early lesions show a dense neutrophilic infiltrate around the follicular infundibulum; later, plasma cells, macrophages, foreign-body giant cells and bands of fibrosis replace the follicle.
Systemic and Topical Treatment
Treatment goals: Eradicate S. aureus, switch off neutrophil-driven inflammation and halt the spread of scarring.
- Standard Combination Antibiotic Regimen (Gold Standard):
- Rifampicin + clindamycin:
- Dose: Rifampicin 300 mg twice daily plus clindamycin 300 mg twice daily.
- Duration: A course of 8–12 weeks.
- How it works: Rifampicin penetrates scar tissue well and kills intracellular S. aureus; clindamycin blocks bacterial protein and toxin production and dampens inflammation. Using them together prevents staphylococci from rapidly becoming resistant to rifampicin.
- Rifampicin + clindamycin:
- Alternative Regimens (If First-Line Treatment Fails or Is Not Tolerated):
- Doxycycline / minocycline (100 mg twice daily): Makes use of the strong anti-inflammatory effect of the tetracyclines.
- Dapsone (50–100 mg/day): Inhibits neutrophil migration and activation (G6PD levels must be checked before starting).
- Oral isotretinoin (0.5–1.0 mg/kg/day): Used for treatment-resistant cases; it reduces sebum production, shrinks the follicular infundibulum and makes the environment less hospitable to bacteria.
- Supportive Topical Treatment:
- Intralesional triamcinolone acetonide: Injected at 5–10 mg/mL into the red, pustular active border to quickly relieve pain and calm acute inflammation.
- Antiseptic Washes and Shampoos: Chlorhexidine 4% solution, benzoyl peroxide, or shampoos containing ketoconazole 2% or ciclopirox olamine help reduce the bacterial load on the scalp.
Comparing the Neutrophilic Cicatricial Alopecias
| Folliculitis Decalvans (FD) | Dissecting Cellulitis of the Scalp (DCS) | Acne Keloidalis Nuchae (AKN) |
|---|---|---|
| Pustules, yellow crusts and scarring hair loss spreading from the crown or back of the scalp. | Deep abscesses and interconnected nodules forming draining sinus tracts; very painful. | Papules and pustules on the nape that progress to hypertrophic or keloidal scars. |
| Tufted hairs (5–20 per opening) and perifollicular scaling. | Loss of follicular openings, dome-shaped pus collections, bridging fibrous bands. | Firm keratotic papules around nape follicles, loss of follicles, thick scar tissue. |
| Heightened sensitivity to S. aureus and its superantigens. | Follicular occlusion; part of the follicular occlusion triad. | Most common in men with skin of color; triggered by close shaving at the nape. |
