Dear Editor,
Lichen planopilaris (LPP) is a primary lymphocytic cicatricial alopecia characterized by inflammation targeting the follicular infundibulum and isthmus, in which CD8+ T-cells attack autoantigens located in the follicular promontory, leading to irreversible follicular destruction.1, 2 Traditionally, it presents as well-defined alopecic patches with perifollicular erythema and scaling.3, 4 However, recent evidence has broadened the clinical spectrum of LPP, including diffuse non-patch variants that even mimic non-scarring alopecias.5 This article aims to describe epidemiological, clinical, trichoscopic, and histopathologic features of a localized non-patch form of LPP confined to specific scalp regions.
We performed a multicenter retrospective study involving 74 patients from 20 trichology referral centers. All cases were confirmed by trichoscopy and histopathology. Patients were excluded if they had androgenetic alopecia, frontal fibrosing alopecia, Fibrosing Alopecia in a Pattern Distribution (FAPD), or diffuse LPP. We compared our findings with the largest case series of diffuse variants of scalp LPP to date.5
Patients were mostly female (82.4%), with a mean age at onset of 41-years and a mean disease duration before diagnosis of 3.72-years. The vertex was most affected (82.4%). Scalp erythema was observed in 75.6% of cases. The predominant subjective symptom was mild to moderate pruritus (71.6%). The main trichoscopic features were perifollicular scaling (95.9%), perifollicular erythema (93.2%), and loss of follicular openings (73%). (Fig. 1A‒B). Histopathological examination revealed follicular dropout (100%), perifollicular concentric lamellar fibrosis (86.5%), reduction in the number of follicles (60.6%), and loss or reduction of sebaceous glands in 52.7% of patients. The most prescribed treatment was topical corticosteroids (98.6%), followed by topical tacrolimus (65.8%) and oral minoxidil (64.9%); Table 1, Table 2 provide the complete results.
Fig. 1.
(A) Non alopecic patches in vertex area. (B) Perifollicular erythema and scaling and loss of follicular openings.
Table 1.
Demographic and clinical characteristics of patients with lichen planopilaris.
| Variables | Categories | Statistics | |
|---|---|---|---|
| Demographic Characteristics and Individual History | |||
| - Female Gender: n (%) (n = 74) | |||
| - Phototype: n (%) (n = 74) | II | 16 | (21.6) |
| III | 41 | (55.4) | |
| IV | 12 | (16.2) | |
| V | 5 | (6.8) | |
| - Body Mass Index: n (%) (n = 74) | Normal | 67 | (90.5) |
| Overweight | 7 | (9.5) | |
| - Family history of LPP: n (%) (n = 74) | 7 | (9.5) | |
| - Menopause (n = 61): n (%) (n = 74) | 26 | (42.6) | |
| - Age: mean (SD) // median // min; max (n = 74) | 44.9 (13.8) // 44 // 14;74 | ||
| - Age at onset: mean (SD) // median // min; max (n = 71) | 41.3 (13.8) // 42 // 13;71 | ||
| - Disease duration (years): mean (SD) // median // min; max (n = 71) | 3.7 (3.9) // 3 // 0; 20 | ||
| Exposures and Habits | |||
| - Sun exposure: n (%) (n = 74) | 42 | (56.8) | |
| - Sun exposure minutes/day: mean (SD) // median // min; max (n = 29) | 53.6(49.0) //30 // 15;240 | ||
| - Sunscreen use on scalp: n (%) (n = 74) | 3 | (4.1) | |
| - Other photoprotection: n (%) (n = 74) | 16 | (21.6) | |
| - Hair dye use: n (%) (n = 74) | 37 | (50.0) | |
| - Chemical damage/discoloration: n (%) (n = 74) | 12 | (16.2) | |
| - Smoking: n (%) (n = 74) | 15 | (20.3) | |
| - Chemical hair straightening: n (%) (n = 74) | 9 | (12.2) | |
| - Alcohol use: n (%) (n = 74) | 7 | (9.5) | |
| - Hormone use: n (%) (n = 74) | 7 | (9.5) | |
| Medical History and Comorbidities: n (%) (n = 74) | |||
| - Autoimmune diseases | 5 | (6.8) | |
| - Hashimoto's thyroiditis | 3 | (4.1) | |
| - High blood pressure | 3 | (4.1) | |
| - Hypercholesterolemia | 2 | (2.7) | |
| - Other | 15 | (20.3) | |
| Localization: n (%) (n = 74) | |||
| - Vertex | 36 | (48.6) | |
| - Vertex + mid scalp | 25 | (33.8) | |
| - Other combinations | 13 | (17.6) | |
| Clinical Symptoms and Signs: n (%) | |||
| - Pruritus (n = 74) | 53 | (71.6) | |
| - Pruritus intensity (n = 53) | Mild | 29 | (54.7) |
| Moderate | 20 | (37.7) | |
| Severe | 4 | (7.5) | |
| - Pain (n = 74) | 28 | (37.8) | |
| -- Pain intensity (n = 27) | Mild | 20 | (74.1) |
| Moderate | 7 | (25.9) | |
| - Burning | 23 | (31.1) | |
| -- Burning intensity (n = 27) | Mild | 13 | (61.9) |
| Moderate | 7 | (33.3) | |
| Severe | 1 | (4.8) | |
| - Positive pull test (n = 74) | 12 | (16.2) | |
| - Disease spreading (n = 74) | No | 52 | (70.3) |
| Indeterminate | 10 | (13.5) | |
| Yes | 12 | (16.2) | |
| Disease activity score: mean (SD) // median// min; max (n = 71) | 2.9 (1.8) // 2.6 // 0.3; 9.0 | ||
Table 2.
Trichoscopic, histopathological and treatment characteristics of patients with lichen planopilaris.
| Variables | Statistics | ||
|---|---|---|---|
| Trichoscopic Findings (n = 74) | n | (%) | |
| Inflamatory Signs | |||
| -- Scalp erythema | Absent | 14 | (18.9) |
| Mild | 36 | (48.6) | |
| Moderate | 20 | (27.0) | |
| Severe | 4 | (5.4) | |
| -- Perifollicular erythema | Absent | 5 | (6.8) |
| Mild | 32 | (43.8) | |
| Moderate | 36 | (49.3) | |
| Severe | 1 | (1.4) | |
| -- Perifollicular scaling | Absent | 3 | (1.4) |
| Mild | 32 | (43.2) | |
| Moderate | 30 | (40.5) | |
| Severe | 9 | (12.2) | |
| -- Absent follicular openings | 54 | (73.0) | |
| -- Perifollicular tubular casts | 42 | (56.8) | |
| -- White structureless areas | 36 | (48.6) | |
| -- Milky red areas | 32 | (43.2) | |
| -- Fibrotic white dots | 31 | (41.9) | |
| -- Arborizing vessels | 25 | (33.8) | |
| -- Small tufts | 15 | (20.3) | |
| -- Pili torti | 14 | (18.9) | |
| -- Broken hairs | 13 | (17.6) | |
| -- Scattered pigmentation | 13 | (17.6) | |
| -- Loss of honeycomb pattern | 11 | (14.9) | |
| -- Perifollicular gray to blue-gray structures | 10 | (13.5) | |
| -- Hairpin vessels | 9 | (12.2) | |
| -- Black dots | 8 | (10.8) | |
| -- Red globules | 7 | (9.5) | |
| -- Dotted vessels | 6 | (8.1) | |
| -- Linear vessels | 5 | (6.8) | |
| -- Perifollicular blue-gray dots | 3 | (1.4) | |
| -- Target sign | 3 | (1.4) | |
| -- Circular hairs | 3 | (1.4) | |
| -- Interfollicular brown globules | 3 | (1.4) | |
| Histopathological Findings (n = 74): n (%) | |||
| -- Perifollicular lamellar fibrosis | 64 | (86.5) | |
| -- Reduction in number of individual follicles | 43 | (58.1) | |
| -- Loss/reduction of sebaceous glands | 39 | (52.7) | |
| -- Basal layer vacuolar degeneration | 30 | (40.5) | |
| -- Outer root sheath thining | 24 | (32.4) | |
| -- Perifollicular mucin | 8 | (10.8) | |
| -- Colloid bodies | 7 | (9.5) | |
| Treatments (n = 74): n (%) | |||
| -- Topical corticosteroids | 73 | (98.7) | |
| -- Topical tacrolimus | 48 | (64.9) | |
| -- Oral minoxidil | 48 | (64.9) | |
| -- Tetracyclines | 25 | (33.8) | |
| -- Hydroxychloroquine | 20 | (27.0) | |
| -- Systemic steroids | 15 | (20.3) | |
| -- Dutasteride | 9 | (12.2) | |
| -- Methotrexate | 3 | (1.4) | |
| -- Other (Pioglitazone/JAK inhibitors) | 1 | (1.4) | |
Starace et al. analyzed 40 patients with diffuse variants of scalp LPP.5 Our group was notably younger and predominantly premenopausal compared with both Lichen Planopilaris Diffuse Pattern (LPPDP) and Cicatricial Pattern Hair Loss (CPHL) – which might not represent a distinct disease entity but a post-inflammatory or residual form of cicatricial alopecia (Table 3). Our cohort showed milder symptoms (less pain/pruritus) and preserved sebaceous glands in 47.3% vs. 0% in both comparator groups, with moderate to severe hair loss (Table 3). Although the mean disease duration of 3.7-years supports an early or mild form in most patients, the presence of longer disease duration in isolated cases suggests that this localized, non-patch presentation may represent a stable, indolent phenotype within the LPP spectrum rather than a purely initial phase. These findings indicate less severe/chronic follicular injury. Unlike diffuse LPP, inflammation was localized ‒ predominantly at the vertex ‒ with lower activity (mean LPPAI 2.9), aligned with Miteva,6 who performed trichoscopy-guided biopsies in 43 patients presenting with scalp pruritus or sensitivity, but without obvious patches and presumed to have subtle or early-stage LPP. Notably, 70% showed no spread beyond the initial focus, and trichoscopy revealed early inflammatory signs before overt alopecia, consistent with a mild, early disease stage and supporting frequent use of topical-only therapy.
Table 3.
Comparison of study findings (n = 74) with Starace et al. (2020) (n = 40) findings.
| Variables | Present study finding | Comparison to Other Groups: Starace et al. (2020) | p-values for differences among groups |
|---|---|---|---|
| Demographic characteristics | |||
| Age (Mean) | Youngest mean age (44.9 yrs) | Significantly younger than CPHL (56.9 yrs) and LPPDP (53.0 yrs) | <0.001 |
| Menopause | Lowest rate of menopausal women (42.6%) | Significantly lower than CPHL (92.9%) and LPPDP (63.6%) | 0.001 |
| Gender (Female %) | Highest percentage of females (82.4%) | Higher than CPHL (70.0%) and LPPDP (55.0%) | 0.034 |
| Clinical symptoms/Histopathology | |||
| Pain | Lowest prevalence (37.8%) | Significantly lower than LPPDP (100.0%) and CPHL (80.0%) | 0.001 |
| Pruritus (Itching) | Lowest prevalence (71.6%) | Significantly lower than LPPDP (100.0%) and CPHL (90.0%) | 0.004 |
| Loss/Reduction of Sebaceous Glands | Nearly half showed preservation (47.3%) | Both CPHL and LPPDP reported 0.0% preservation, with high rates of moderate/severe loss | 0.001 |
| Trichoscopic findings | |||
| Perifollicular Erythema | Varied degree, with a high rate of moderate/severe (50.7%) | LPPDP was 100.0% mild (level 1); CPHL not reported | 0.001 |
| Small Tufts | Presence (20.3%) | Higher than CPHL (0.0%) but lower than LPPDP (45.0%) | 0.001 |
| Broken Hairs | Presence (17.6%) | Higher than CPHL (0.0%) but lower than LPPDP (45.0%) | 0.001 |
Notes: CPHL, Cicatricial Pattern Hair Loss; LPPDP, Lichen Planopilaris Diffuse Pattern.
Sun exposure was frequent (56.8%) with a mean duration of 53.6 minutes per day. However, scalp photoprotection was minimal (4.1%), and only 21.6% reported any form of physical protection. The vertex, a chronically sun-exposed area, could be predisposed to UV-induced disruption of follicular immune privilege, promoting localized autoimmune inflammation in susceptible individuals.7, 8 The use of hair dye and chemical hair straightening reinforces the hypothesis that chronic chemical and photo-oxidative stress may act as triggering factors.9, 10
FAPD is an important differential diagnosis, though non-patch LPP does not present miniaturized hair. Other inflammatory scalp conditions should also be ruled out as they depict different erythema and scaling patterns.
To our knowledge, this is the first case series focused exclusively on the localized non-patch form of LPP. Moreover, our study pointed out that this condition may represent an early stage of classic or diffuse LPP. Finally, recognizing this presentation is crucial, as timely anti-inflammatory treatment may halt disease progression and scarring. Trichoscopy-guided biopsy of symptomatic yet non-alopecic areas can confirm diagnosis and guide intervention. Further studies are warranted to determine whether this form remains localized or progresses to classic patchy or diffuse non-patch LPP, and to clarify the roles of UV exposure and cosmetic habits in disease onset.
ORCID ID
Maria Andrea Ocampo: 0000-0002-8857-6180
Rita Fernanda Cortez de Almeida: 0000-0001-7904-998X
Michela Starace: 0000-0002-3981-1527
Bianca Maria Piraccini: 0000-0001-6537-9689
Gener Alejandro Mancilla: 0000-0002-3333-503X
Lidia Rudnicka: 0000-0002-8308-1023
Adriana Rakowska: 0000-0001-6117-3704
Anna Waskiel-Burnat: 0000-0003-4984-3589
Asmahane Souissi: 0000-0002-0058-0645
Awatef Kelati: 0000-0003-2570-4584
Kuzma Khobzei: 0009-0002-2879-9240
Tatiana Siliuk: 0000-0001-9118-2396
Andrei Doroshkevich: 0009-0009-8093-7269
Renan Minotto: 0000-0002-1451-0461
Cecilia Navarro Tuculet: 0000-0003-0613-9962
Maria Eugenia Cappetta: 0009-0006-8798-789X
Luis Enrique Sánchez-Dueñas: 0000-0002-2136-1230
Maria Julia Mojardin-Lopez: 0009-0004-4252-7537
Mariana Lavia: 0009-0008-8134-6113
Boris Sanchez: 0000-0002-6096-136X
Daniela Lynett: 0000-0003-1338-4384
Sebastian Augusto Mercau: 0009-0001-2384-5159
Aldo Gálvez-Canseco: 0000-0002-8644-634X
David Saceda-Corralo: 0000-0001-6315-5462
Carla Jorge Machado: 0000-0002-6871-0709
Daniel Fernandes Melo: 0000-0002-8807-2556
Financial support
None declared.
Authors’ contributions
Claudia Montoya, Maria Andrea Ocampo, Rita Fernanda Cortez de Almeida, André Luiz Vairo Donda: Data collection, analysis and interpretation of data; writing of the manuscript and critical review of important intellectual content; data collection, analysis and interpretation, critical review of the literature; final approval of the final version of the manuscript.
Michela Starace, Bianca Maria Piraccini, Gener Alejandro Mancilla, Lidia Rudnicka, Adriana Rakowska, Anna Waskiel-Burnat, Asmahane Souissi, Awatef Kelati, Kuzma Khobzei, Tatiana Siliuk, Andrei Doroshkevich, Renan Minotto, Cecilia Navarro Tuculet, Maria Eugenia Cappetta, Luis Enrique Sánchez-Dueñas, Maria Julia Mojardin-Lopez, Mariana Lavia, Boris Sanchez, Daniela Lynett, Sebastian Augusto Mercau, Aldo Gálvez-Canseco, David Saceda-Corralo: Data collection; intellectual participation in the propaedeutic and therapeutic conduct of the studied cases; final approval of the final version of the manuscript.
Carla Jorge Machado: Statistical analysis; critical review of important intellectual content; final approval of the final version of the manuscript.
Daniel Fernandes Melo: The study concept and design; data collection, analysis and interpretation of data; critical review of important intellectual content; intellectual participation in the propaedeutic and therapeutic conduct of the studied cases; critical review of the literature; final approval of the final version of the manuscript.
Research data availability
The entire dataset supporting the results of this study was published in this article.
Conflicts of interest
None declared.
Editor Neusa Yuriko Sakai Valente.
Footnotes
Study conducted at the Clinical appointments and documentation were carried out at the authors’ respective affiliation.
References
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