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%); Tables 1 and 2 provide the complete results.

Fig. 1.

(A) Non alopecic patches in vertex area. (B) Perifollicular erythema and scaling and loss of follicular openings.

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.

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.