Lichen planopilaris: A clinicopathologic study

Frontal fibrosing alopecia presenting with components of Piccardi-Lassueur-Graham-Little syndrome

“…1,10 Furthermore, both conditions affect mostly postmenauposal women. [11][12][13] However, the hypothesis of FFA being a variant of LPP can be challenged by two facts. First, the presence of eyebrow thinning in 50% to 81% 1,8 of FFA cases cannot be accounted for by cutaneous or follicular LP.…”

Update on primary cicatricial alopecias

“…A tumid, plaque form of LP with prominent follicular involvement often affecting the retroauricular portion of the scalp has been described but does not cause cicatricial alopecia. 102,103 The pathogenesis of lichen planopilaris appears to resemble that of classic LP on the basis of shared histopathology and immunohistochemical staining patterns. 104 An antigenic trigger has been postulated to initiate disease, given the observation of increased numbers of Langerhans cells in affected epithelium early in disease 104,105 and the occurrence of scalp lichen planopilaris or LP after ingestion of gold, 106 atabrine, 107 or quinacrine, 108 hepatitis B vaccination, 109 hepatitis C infection, 110 arguably, and in association with microbial overgrowth in an epidermal nevus.…”

“…In a case of concomitant alopecia areata and lichen planopilaris affecting the scalp, disease involvement with lichen planopilaris stopped abruptly at the border between the two conditions. 10 Terminal hairs can be affected exclusively, 101 in combination with vellus hairs, 103 or limitedly, as occurs in a condition called ''fibrosing alopecia in a pattern distribution,'' which has histopathologic features of lichen planopilaris and preferentially affects the miniaturized secondary vellus hairs in those with androgenetic alopecia (AGA). 111 Ultimately, these disparate etiologic stimuli are postulated to elicit lesional expression of common keratinocyte autoantigens 104 and an ensuant Tcellemediated lichenoid response with destruction of follicular basilar epithelium by CD8 1 activated T cells.…”

Primary cicatricial alopecias: clinicopathology of 112 cases

“…[8][9][10][11][12][13] On the scalp, the classic clinical features include the presence of follicular hyperkeratotic papules, perifollicular erythema, and scaling at the periphery of the cicatricial process. Onychodystrophy was recorded in 40% of LPP and we thought that associated nail changes might not be that uncommon in LPP.…”