Treatment for Scarring Alopecia
The primary goal in scarring alopecia is disease stabilization with corticosteroids and immunosuppressive agents, as hair follicles are permanently destroyed and cannot regenerate; newer biologics targeting TNF-α, IL-17, and JAK inhibitors show the most promise for halting progression when conventional therapy fails. 1
Understanding Scarring vs. Non-Scarring Alopecia
Scarring (cicatricial) alopecia fundamentally differs from conditions like alopecia areata because the hair follicles are permanently destroyed and replaced by scar tissue—making hair regrowth impossible. 2 The treatment approach must therefore focus entirely on stopping disease progression rather than stimulating regrowth. 1
Key Pathophysiologic Distinction
- Primary scarring alopecias directly target and destroy hair follicles through inflammatory processes, with lymphocytic types (discoid lupus erythematosus, lichen planopilaris, frontal fibrosing alopecia, central centrifugal alopecia) being most common, followed by neutrophilic types (folliculitis decalvans, dissecting cellulitis). 2, 3
- Recent gene expression studies reveal that lichen planopilaris, frontal fibrosing alopecia, and central centrifugal alopecia share common dysregulated pathways—particularly mast cell infiltration, downregulation of cholesterogenic pathways, and upregulation of fibrosis genes—suggesting similar treatment approaches may be effective across these subtypes. 4
Diagnostic Confirmation Before Treatment
Histopathological confirmation via scalp biopsy is essential before initiating therapy, as clinical diagnosis alone is unreliable and treatment differs fundamentally from non-scarring alopecias. 3
- Biopsy allows classification into lymphocytic vs. neutrophilic subtypes, which guides therapeutic selection. 3
- Reflectance confocal microscopy (RCM) can identify epidermal disarray, interface dermatitis, peri- and intra-adnexal inflammatory cell infiltration, and dermal sclerosis—features that correlate with histopathology and can monitor treatment response non-invasively. 5
First-Line Treatment Algorithm
For Lymphocytic Scarring Alopecias (LPP, FFA, DLE, CCCA)
Start with intralesional or systemic corticosteroids combined with hydroxychloroquine for discoid lupus variants, or with topical/oral immunosuppressants for lichen planopilaris variants. 1, 2
- Corticosteroids remain the cornerstone but offer inconsistent disease improvement, particularly in advanced stages. 1
- Immunosuppressive agents (methotrexate, mycophenolate mofetil, cyclosporine) are added when corticosteroids alone fail to halt progression. 1
For Neutrophilic Scarring Alopecias (Folliculitis Decalvans, Dissecting Cellulitis)
Initiate long-term oral antibiotics (doxycycline, rifampin combinations) targeting bacterial colonization and inflammation. 2
- These conditions often involve Staphylococcus aureus colonization requiring prolonged antimicrobial therapy. 2
Second-Line and Emerging Therapies
When conventional therapy fails to stabilize disease after 3-6 months, consider:
Biologics with Strongest Evidence
- TNF-α inhibitors (adalimumab, infliximab) demonstrate the most consistent benefit for refractory cases. 1
- IL-17 inhibitors (secukinumab, ixekizumab) show promise, particularly given the inflammatory pathways involved. 1
- JAK inhibitors (tofacitinib, baricitinib, ruxolitinib) offer potential through modulation of immune-mediated pathways, with emerging evidence supporting their use. 1
Biologics with Moderate Evidence
- IL-23 inhibitors (guselkumab, risankizumab) show some benefit in case reports. 1
- Interferon Alpha Receptor 1 inhibitors demonstrate limited but positive results. 1
Treatment Monitoring Strategy
Use reflectance confocal microscopy or serial dermoscopy to monitor inflammatory activity non-invasively, as clinical examination alone may miss subclinical progression. 5
- RCM can detect reduction in epidermal, junctional, and dermal inflammation during treatment, providing objective evidence of therapeutic response. 5
- Continued inflammation on RCM despite clinical stability warrants treatment escalation. 5
Critical Treatment Principles
What Does NOT Work
The treatments effective for alopecia areata (intralesional corticosteroids for regrowth, contact immunotherapy, minoxidil) are irrelevant for scarring alopecia because destroyed follicles cannot regenerate. 6, 1
Treatment Goals Are Different
- Primary goal: Halt disease progression and prevent further follicular destruction. 1
- Secondary goal: Manage symptoms (pruritus, pain, burning). 1
- Unrealistic goal: Hair regrowth in scarred areas (impossible once follicles are destroyed). 2
Common Pitfalls
- Delaying biopsy and treating empirically as alopecia areata—this wastes time while irreversible scarring progresses. 3
- Stopping treatment once inflammation appears controlled clinically—subclinical inflammation may persist and require ongoing suppression. 5
- Expecting hair regrowth in areas of established scarring—counsel patients that treatment preserves remaining hair but cannot restore lost follicles. 2
- Failing to recognize that patient satisfaction with conventional therapy is often poor, particularly in severe disease, warranting earlier consideration of biologics or JAK inhibitors. 1
Practical Treatment Timeline
- Months 0-3: Initiate first-line corticosteroids ± immunosuppressants; perform baseline RCM or dermoscopy. 1, 5
- Month 3: Reassess with clinical examination and RCM—if inflammation persists or progresses, escalate to biologics/JAK inhibitors. 1, 5
- Month 6+: Continue maintenance therapy indefinitely if disease is stabilized; any treatment cessation risks reactivation and further scarring. 1