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Evidence for neurogenic inflammation in lichen planopilaris and frontal fibrosing alopecia pathogenic mechanism
Author(s) -
Doche Isabella,
Wilcox George L.,
Ericson Marna,
Valente Neusa S.,
Romiti Ricardo,
McAdams Brian. D.,
Hordinsky Maria K.
Publication year - 2020
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13835
Subject(s) - scalp , pathogenesis , medicine , scarring alopecia , calcitonin gene related peptide , pathology , inflammation , calcitonin , immunohistochemistry , dermatology , neuropeptide , immunology , receptor
Lichen planopilaris ( LPP ) and frontal fibrosing alopecia ( FFA ) are lymphocytic scarring alopecias affecting primarily the scalp. Although both diseases may share some clinical and histopathological features, in the last decade, FFA has become an “epidemic” particularly in Europe, North and South America with unique clinical manifestations compared to LPP , thus, raising the idea that this disease may have a different pathogenesis. Symptoms such as scalp burning, pruritus or pain are usually present in both diseases, suggesting a possible role for nerves and neuropeptides in the pathogenesis of both diseases. Based on some previous studies, neuropeptides, such as substance P ( SP ) and calcitonin gene‐related peptide ( CGRP ), have been associated with lipid metabolism and many chronic inflammatory disorders. In this study, we asked if these neuropeptides are associated with LPP and FFA scalp lesions. Alteration in the expression of SP and CGRP in affected and unaffected scalp skin from patients with both diseases was found with examination of sections using immunohistochemical techniques and confocal microscopy. We then quantitatively assessed and compared SP and CGRP expression from control, LPP and FFA scalp biopsies. Although LPP and FFA share similar histopathologic findings, opposite results were found in affected and unaffected scalp in the ELISA tests, suggesting that these diseases may have different pathogenic mechanisms. We also found presence of histopathological inflammation irrespective of evident clinical lesions, which raises the possibility that both diseases may be more generalized processes affecting the scalp.