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A 32-year-old man presents with hair loss along with chronic pustular eruptions of his scalp. Previous biopsy has shown folliculitis decalvans. He has had many courses of antibiotics, but the hair loss continues to progress. The active pustular lesions are cultured and grow out methicillin-resistant Staphylococcus aureus. The patient is treated with trimethoprim-sulfamethoxazole twice daily and mupirocin to the nasal mucosa, twice daily for 5 days. Two weeks later, the pustular lesions are less prominent although the alopecia is permanent (Figures 189-1 and 189-2).
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Scarring alopecia is a group of inflammatory disorders in which there is permanent destruction of the pilosebaceous unit. Although it is mostly seen on the scalp, it can involve other areas, such as the eyebrows.
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In primary cicatricial alopecia, the hair follicle is the primary target of destruction by inflammation. In secondary cicatricial alopecia, the follicular destruction is incidental to a nonfollicular process such as infection, tumor, burn, radiation, or traction.
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Primary cicatricial alopecias are rare.
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The annual incidence rate of lichen planopilaris (LPP) in 4 hair loss centers in the United States varied from 1.15% to 7.59% as defined by new biopsy-proven LPP—all new patients with hair loss seen over a 1-year period.1
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Scarring alopecia occurs when there is inflammation and destruction of the hair follicles leading to fibrous tissue formation.2
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Hair loss in scarring alopecia is irreversible because the inflammatory infiltrate results in destruction of the hair follicle stem cells and the sebaceous glands.3
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The inflammatory infiltrates are either predominantly lymphocytic, neutrophilic, or mixed. These differences are used to classify the scarring alopecias. See Table 189-1.
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Scarring alopecias can vary by distribution and appearance. Most patients will need a biopsy to confirm the clinical impression and determine the specific type of alopecia.
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Clinical Presentation
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