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Retrospective analysis identifies clinical features of cicatricial alopecia, highlighting its implications in hair loss populations.
tural skin changes may be present.Histologically, damaged HFs replaced with fibrous tissues are present (1).Cicatricial alopecias may be classified as primary, in which the HF itself is the direct target of inflammation, or secondary, occurring due to incidental follicular damage from unrelated inflammatory processes such as infections, sarcoidosis, burns, radiation, or malignancies (1, 2).Although irreversible destruction of the stem cells of epithelial HFs is thought to play a role in primary CA (PCA), its exact etiopathogenesis remains unknown (1).PCA iis further histologically classified according to the predominant inflammatory cell type into lymphocytic, neutrophilic, mixed, or nonspecific forms.Lymphocytic types include chronic cutaneous lupus erythematosus (CCLE), lichen planopilaris (LPP-C: classic type; FFA: frontal fibrosing alopecia; Graham-Little syndrome), pseudopelade of Brocq (PPB), central centrifugal cicatricial alopecia (CCCA), keratosis follicularis spinulosa decalvans (KFSD), and alopecia mucinosa.Neutrophilic types include folliculitis decalvans (FD) and dissecting cellulitis (DC), while mixed forms include acne keloidalis, acne necrotica, and erosive pustular dermatosis (Fig. 1) (3).Although the exact prevalence is unknown, the frequency of PCA among patients presenting with hair loss has been reported to range between 2.1% and 7.3% (4-6).zkesici Kurt et al. reported that PCA accounted for 6% of all hair diseases (7).Given the
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Zorlu et al. (2026) studied this question.
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