Frontiers in Lichen Planopilaris and Frontal Fibrosing Alopecia Research: Pathobiology Progress and Translational Horizons

Senna, Maryanne M.; Peterson, Erik; Jozic, Ivan; Chéret, Jérémy; Paus, Ralf

doi:10.1016/j.xjidi.2022.100113

Cited by 20 publications

(17 citation statements)

References 155 publications

(249 reference statements)

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“…A genetic predisposition seems likely from analysis of familial relationships [19,20], a possibility supported by identification of several genomic loci, including an HLA allele, associated with it by genome wide studies [21]. Lichen planopilaris and FFA have been hypothesized to result from damage to hair follicle stem cells due to an autoimmune inflammatory response upon collapse of immune privilege [22,23]. This collapse may be triggered by a loss of normal interferon (IFN)-γ and peroxisome proliferator-activated receptor (PPAR)-γ-mediated signaling and homeostasis in the folliculosebaceous unit [24].…”

Section: Introductionmentioning

confidence: 99%

“…This collapse may be triggered by a loss of normal interferon (IFN)-γ and peroxisome proliferator-activated receptor (PPAR)-γ-mediated signaling and homeostasis in the folliculosebaceous unit [24]. Factors suggested to contribute to the occurrence of FFA include alterations in hormone levels or hair follicle microbiomes, defective mitochondrial lipid metabolism, neurogenic inflammation, perturbed levels of aryl hydrocarbon receptor pathway components and environmental factors such as cutaneous allergens and fragrances from personal care products [23,25].…”

Section: Introductionmentioning

confidence: 99%

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Protein profiling of forehead epidermal corneocytes distinguishes frontal fibrosing from androgenetic alopecia

et al. 2023

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Protein profiling offers an effective approach to characterizing how far epidermis departs from normal in disease states. The present pilot investigation tested the hypothesis that protein expression in epidermal corneocytes is perturbed in the forehead of subjects exhibiting frontal fibrosing alopecia. To this end, samples were collected by tape stripping from subjects diagnosed with this condition and compared to those from asymptomatic control subjects and from those exhibiting androgenetic alopecia. Unlike the latter, which exhibited only 3 proteins significantly different from controls in expression level, forehead samples from frontal fibrosing alopecia subjects displayed 72 proteins significantly different from controls, nearly two-thirds having lower expression. The results demonstrate frontal fibrosing alopecia exhibits altered corneocyte protein expression in epidermis beyond the scalp, indicative of a systemic condition. They also provide a basis for quantitative measures of departure from normal by assaying forehead epidermis, useful in monitoring response to treatment while avoiding invasive biopsy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protein profiling of forehead epidermal corneocytes distinguishes frontal fibrosing from androgenetic alopecia

et al. 2023

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“…Primary cicatricial alopecias are a group of relatively uncommon and difficult‐to‐treat dermatoses with predominant lymphocytic, neutrophilic, or mixed cellular infiltrate 1 . Lichen planopilaris (LPP) is one type of cicatricial alopecia characterized by lymphocytic infiltrates around the follicular antigens 2 . Clinically, the disease presents as single or multiple scarring alopecic patches, most commonly at the vertex and parietal scalp, with perifollicular scaling, erythema, and a positive hair pull test.…”

Section: Introductionmentioning

confidence: 99%

“…Of note, recent research has proposed a down‐regulated tissue expression of genes required for lipid metabolism and peroxisome biogenesis in LPP, one of which was the expression of peroxisome proliferator‐activated receptor γ (PPAR‐γ). Decreased PPAR‐γ expression is postulated to result in the accumulation of inflammatory lipids, local inflammation, and subsequent destruction of the pilosebaceous unit typical of LPP 2,12,13 …”

Section: Introductionmentioning

confidence: 99%

“…Decreased PPAR-γ expression is postulated to result in the accumulation of inflammatory lipids, local inflammation, and subsequent destruction of the pilosebaceous unit typical of LPP. 2,12,13 Pioglitazone is a PPAR-γ agonist, and based on the mentioned assumptions, it could account for a possible therapeutic option for LPP. In this regard, several case reports and case series have investigated the effect of this agent in controlling LPP and reported promising results.…”

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confidence: 99%

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Efficacy and safety of oral pioglitazone in the management of lichen planopilaris in comparison with clobetasol: A randomized clinical trial

Lajevardi

Ghiasi

Balighi

et al. 2022

Dermatologic Therapy

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Lichen planopilaris (LPP) is a scarring alopecia for which no treatment with remarkable effect has been identified. Pioglitazone has been reported as a possible therapeutic option. To compare the efficacy and safety of pioglitazone with clobetasol in LPP. This randomized, double-blind, parallel-group was conducted at Razi hospital.Patients were treated either with pioglitazone 15 mg/daily or clobetasol lotion 0.05% once at night for 6 months. Patients were visited every 2 months to assess the lichen planopilaris activity index (LPPAI) and record probable adverse events. Forty patients (mean age: 43.6 years; 62.5% female) were randomized 1:1. The mean of LPPAI at baseline and last session were 4.68 ± 1.97 and 2.59 ± 0.97 in the clobetasol group and 5.01 ± 1.71 and 3.04 ± 1.36 in the pioglitazone group, respectively. Both treatments significantly decreased the LPPAI over the two-month interval visits (p < 0.001). No significant difference in the LPPAI reduction was detected between groups. Regarding the safety profile, three clobetasol-treated patients developed folliculitis, and two in the pioglitazone group developed mild headaches. Pioglitazone effectively controlled the signs and symptoms of the LPP with no serious side effects.

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The spectrum of fibrosing alopecias

Orlando

Piraccini

Starace

2022

JEADV Clinical Practice

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Lichen planopilaris (LPP) is a primary lymphocytic cicatricial alopecia considered the most common cause of scarring hair loss in adults. It has been classified into three clinical variants: classical LPP, frontal fibrosing alopecia (FFA) and Graham Little-Piccardi-Lassueur syndrome. Classical LPP usually presents as a circumscribed cicatricial patch on the vertex and FFA as a band-like scarring alopecia of the frontotemporal hairline. Fibrosing alopecia in a pattern distribution (FAPD) and lichen planopilaris diffuse pattern (LPPDP) are two recently described subtypes of LPP that exhibit a diffuse involvement of the androgen-dependent region or the whole scalp, respectively. Classical LPP, FFA, FAPD and LPPDP share trichoscopic (cicatricial areas, absence of follicular openings, perifollicular erythema and hyperkeratosis) and histologic features (interface dermatitis involving follicular epithelium and concentric fibrosing around the isthmus and infundibulum).The remarkable clinical and histological overlap between these entities has led to the concept that these diseases exist along a spectrum. In the effort to identify classical LPP, FFA, FAPD and LPPDP with an umbrella term, we suggest to use 'lichenoid alopecias', as the distinguishing hallmark of these diseases is the lichenoid bandlike inflammatory infiltrate in the superficial dermis involving the infundibulum and isthmus of the hair follicle.

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Frontiers in Lichen Planopilaris and Frontal Fibrosing Alopecia Research: Pathobiology Progress and Translational Horizons

Cited by 20 publications

References 155 publications

Protein profiling of forehead epidermal corneocytes distinguishes frontal fibrosing from androgenetic alopecia

Protein profiling of forehead epidermal corneocytes distinguishes frontal fibrosing from androgenetic alopecia

Efficacy and safety of oral pioglitazone in the management of lichen planopilaris in comparison with clobetasol: A randomized clinical trial

The spectrum of fibrosing alopecias

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