Summarized by: Esema Idemudia | The Ohio State University College of Medicine and Stephanie Trovato, MD | Board-Certified Dermatologist | Cleveland Clinic
Lichen planopilaris, discoid lupus erythematosus, folliculitis decalvans, and erosive pustular dermatosis are forms of primary scarring alopecias that cause permanent hair loss through follicular destruction. These scalp disorders involve chronic inflammation, and treatments aim to reduce inflammation. Consequently, both persistent inflammation and immunosuppressive therapies may increase the risk of non-melanoma skin cancers, including squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), on the scalp. Lee et al. examined this complex relationship between primary scarring alopecias and scalp skin cancer.
Lichen planopilaris most commonly affects middle-aged women, presenting with burning sensations and perifollicular erythema. Beyond the scalp, lichen planopilaris has been associated with SCC of the oral cavity, esophagus and genitals. Retrospective analyses report scalp SCC and BCC rates of 1.7-1.8% and 4.5- 4.7%, respectively. While some cases appear coincidental, related to Fitzpatrick skin type, others point to underlying immunologic factors. For instance, one case attributed BCC development in a hair-covered area following triamcinolone therapy to a decreased local antitumor response. Another report, showed SCC arising after eighteen years in a hairless region of the scalp with minimal sun exposure and regular hat use, suggesting chronic inflammation as the driving mechanism.
The association between discoid lupus erythematosus (DLE) and SCC has been recognized since 1953, with cancer developing 6 to 30 years after initial diagnosis. Clinically, DLE presents with scaling erythematous or hypopigmented plaques on the head and neck, where hypopigmented areas are prone to actinic damage, transformation and progression to SCC. Approximately 50% of reported SCCs in DLE occurr on the lips, while 7.4% appear on the scalp. Risk factors such as chronic ultraviolet radiation UVR exposure, human papillomavirus (HPV) further compounds this risk, creating a conducive environment for malignant change in patients with DLE.
Folliculitis decalvans primarily affects the vertex and occipital scalp in middle-aged adults, presenting with follicular pustules, erythema and crust. Although rare, four cases of SCC arising from folliculitis decalvans have been reported, all in men in their forties and fifties with long-standing disease, highlighting the role of chronic inflammation in cancer development. While the exact mechanism remains unclear, repetitive follicular destruction without adequate immune response likely contributed to cancer development.
Erosive pustular dermatosis typically affects older individuals with sun-damaged skin, often mimicking actinic keratoses or bacterial infections. To date, three cases of SCC and three cases of BCC have been reported. The repeated cycles of injury and repair, combined with impaired barrier function in photodamaged skin, likely play a role. These observations reinforce the broader theme across primary scarring alopecias, persistent inflammation remains a crucial factor in malignant transformation.
Chronic inflammation is likely the main factor contributing to increased risk of scalp skin cancer in primary scarring alopecias. Case reports show that patients with primary scarring alopecias treated with intralesional or oral corticosteroids were not heavily immunosuppressed. In contrast, those with non-scarring alopecia areata, who also use similar therapies, do not exhibit an increased risk of skin cancer. This contrast supports chronic inflammation, rather than immunosuppression, as the key pathogenic factor. Therefore, regular skin cancer screenings, consistent use of broad-spectrum sunscreen, timely biopsy and excision of lesions are essential in managing patients with primary scarring alopecias.
Reference: Juwon Lee, Ludovica de Gregorio, Antonella Tosti; Scarring Alopecia and Risk of Skin Cancer: A Literature Review. Skin Appendage Disord 6 October 2025; 11 (5): 424–431. https://doi.org/10.1159/000545345