Perifollicular fibrosis and inflammation in androgenetic alopecia and seborrheic dermatitis: diagnostic challenges in differentiation from fibrosing alopecia in a pattern distribution<sup/>

Souza, Tatiane Elen de; Böer-Auer, Almut; Werner, Betina

doi:10.1016/j.abd.2026.501408

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ORIGINAL ARTICLE • An. Bras. Dermatol. 101 (4) • 2026 • https://doi.org/10.1016/j.abd.2026.501408 linkcopy

Perifollicular fibrosis and inflammation in androgenetic alopecia and seborrheic dermatitis: diagnostic challenges in differentiation from fibrosing alopecia in a pattern distribution^☆

Authorship SCIMAGO INSTITUTIONS RANKINGS

Background: Androgenetic Alopecia (AGA) and Seborrheic Dermatitis (SD) are scalp conditions that may show histopathological features overlapping with Fibrosing Alopecia in a Pattern Dis-tribution (FAPD), potentially leading to diagnostic confusion between non-scarring and scarring alopecias.

Objective: To identify histopathological features that distinguish AGA from SD and to evalu-ate findings overlapping with those described in FAPD, focusing on perifollicular fibrosis and inflammation.

Methods: Transverse scalp biopsy sections from 56 Caucasian male patients (21 AGA, 35 SD) were blindly evaluated. Quantitative follicular parameters and qualitative epidermal, follicular, inflammatory, and adnexal features were assessed and statistically compared.

Results: AGA showed higher vellus follicle counts (p = 0.029) and lower terminal follicle and anagen hair counts (p = 0.002; p = 0.045), confirming follicular miniaturization. Perifollicular fibrosis (infundibular and/or isthmic) was frequent in both conditions, limiting its specificity for scarring alopecias. Mild basal vacuolization (14.3%; p = 0.048) and eccrine duct dilatation (23.8%; p = 0.006) occurred exclusively in AGA, whereas polytrichia was observed only in SD (17.1%; p = 0.050). Perifollicular inflammation was common and non-specific in both groups, occasionally mimicking lichenoid patterns. Demodex spp. was more prevalent in AGA (p = 0.007). Necrotic keratinocytes were rare, with no significant differences. Study limitations: The study included only male patients and had a limited sample size, a cross-sectional design, and no FAPD comparison. Nonetheless, substantial histopathological overlap exists between AGA, SD, and features attributed to FAPD, particularly perifollicular fibrosis and inflammation. Careful clinicopathological correlation is essential to avoid misclassification, with prognostic and therapeutic implications.

KEYWORDS
Androgenetic alopecia; Dermatitis; seborrheic; Fibrosis; Inflammation; Cicatricial alopecia

Histopathologic Parameters	AGA (n = 21)	SD (n = 35)	p-value
Quantitative parameters
Total follicular units	14.24 (3.64)	13.82 (4.53)	0.72
Total hair follicles	35.30 (11.38)	42.12 (14.27)	*0.047*
Terminal follicles	24.35 (11.98)	34.29 (12.41)	*0.002*
Vellus follicles	10.95 (6.06)	7.79 (4.97)	*0.029*
Anagen hairs	33.45 (11.68)	40.53 (14.27)	*0.045*
Telogen hairs	1.75 (2.07)	1.29 (2.15)	0.49
Sebaceous gland size (mm)	0.53 (0.07)	0.51 (0.15)	0.27
Qualitative parameters
Epidermal spongiosis	4 (19.0%)	12 (34.3%)	0.22
Follicular spongiosis	16 (76.19%)	24 (68.57%)	0.54
Intrafollicular parakeratosis	12 (57.1%)	23 (65.7%)	0.52
Basal layer vacuolization	3 (14.3%)	0 (0.0%)	*0.048*
Necrotic keratinocytes - infundibulum	1 (4.8%)	1 (2.9%)	0.61
Necrotic keratinocytes - isthmus	3 (14.3%)	2 (5.7%)	0.27
Yeasts	0 (0.0%)	1 (2.9%)	0.43
Demodex - follicular canal	9 (42.9%)	4 (11.4%)	*0.007*
Demodex - sebaceous duct	8 (38.1%)	3 (8.6%)	*0.007*
Bacterial colonies	15 (71.4%)	21 (60.0%)	0.39
Perifollicular inflammation - infundibulum	16 (76.2%)	22 (62.9%)	0.30
Perifollicular inflammation - isthmus	15 (71.4%)	21 (60.0%)	0.39
Inflammation in terminal hair	17 (81.0%)	24 (68.6%)	0.31
Inflammation in vellus hair	8 (38.1%)	7 (20.0%)	0.14
Lichenoid-type inflammation	0 (0.00%)	0 (0.00%)	0.00
Eosinophils	0 (0.00%)	0 (0.00%)	0.00
Plasma cells	0 (0.00%)	0 (0.00%)	0.00
Acute neutrophilic folliculitis	0 (0.00%)	0 (0.00%)	0.00
Foreign body-type granulomatous reaction	0 (0.00%)	0 (0.00%)	0.00
Infundibular dilatation	6 (28.6%)	15 (42.9%)	0.28
Cicatricial fibrous tracts	1 (4.8%)	0 (0.0%)	0.38
Perifollicular fibrosis - infundibulum	9 (42.9%)	7 (20.0%)	0.067
Perifollicular fibrosis - isthmus	8 (38.1%)	5 (14.3%)	*0.044*
Fibrosis around terminal follicles	9 (42.9%)	7 (20.0%)	0.067
Fibrosis around vellus follicles	2 (9.5%)	0 (0.0%)	0.14
Sebaceous gland atrophy	0 (0.0%)	0 (0.0%)	0.00
Polytrichia	0 (0.0%)	6 (17.1%)	*0.050*
Eccrine duct dilatation	5 (23.8%)	0 (0.0%)	*0.006*

Histopathological Parameter	AGA (n = 21)	SD (n = 35)	FAPD
Follicular Miniaturization	+++ (p = 0.029,	- (0%)	++ (∼70%)
	significantly higher
	vellus follicles)
Perifollicular Fibrosis	+ (∼40% overall;	+/- (∼17%; 14.3%	+++ (79-93% of cases)
	38.1% isthmic, 42.9%	isthmic, 20.0%
	infundibular)	infundibular)
Perifollicular Inflammation	++ (> 70%)	++ (> 60%)	+++ (55-100%, often lichenoid)
Basal Layer Vacuolization	+/- (14.3%)	- (0%)	++ (∼57%, associated with interface
			changes)
Necrotic Keratinocytes	+/- (Uncommon,	+/- (Uncommon,	+ (29%)
	∼10%)	∼10%)
Polytrichia	- (0%)	+/- (17.1%)	+ (Exact frequency varies; reported
			in LPP variants)
Eccrine Duct Dilatation	+/- (23.8%)	- (0%)	+ (Exact frequency varies; reported
			in LPP variants)
Demodex Presence	+ (∼40%)	+/- (∼10%)	(Not reported in LPP/FAPD literature)
Yeasts of Malassezia	- (0%)	+/- (∼2.8%)	+/- (∼1.5%)

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Perifollicular fibrosis and inflammation in androgenetic alopecia and seborrheic dermatitis: diagnostic challenges in differentiation from fibrosing alopecia in a pattern distribution☆

Perifollicular fibrosis and inflammation in androgenetic alopecia and seborrheic dermatitis: diagnostic challenges in differentiation from fibrosing alopecia in a pattern distribution^☆