Scalp Rosacea: Current Evidence

Abstract

Scalp rosacea, also known as red scalp disease (RSD), is an inflammatory dermatosis that remains underrecognized and frequently misdiagnosed because of its clinical overlap with other inflammatory scalp disorders and the relative nonspecificity of its findings. It is characterized by diffuse scalp erythema, dry scaling, vascular alterations, and inflammatory papules or pustules, often accompanied by pruritus or burning sensations. Despite being described several decades ago, scalp rosacea has only recently gained attention, and no standardized diagnostic criteria or therapeutic guidelines have yet been established. The prevalence of scalp rosacea is unknown; however, it appears to predominantly affect middle-aged men and has been associated with androgenetic alopecia, suggesting a potential role for increased ultraviolet exposure. Current evidence supports a multifactorial pathogenesis involving genetic susceptibility, dysregulation of the innate immune response, neurovascular alterations, and environmental triggers. Keratinocyte activation by exogenous stimuli induces cathelicidin/LL-37-driven inflammation, promoting macrophage activation, vasodilation, and angiogenic signaling. In addition, Demodex folliculorum infestation may contribute to disease persistence, with the scalp acting as a potential reservoir. Clinically, scalp rosacea presents with diffuse erythema and scaling, with sparse, non-follicular papules or pustules surrounded by dilated capillaries. Trichoscopy has emerged as a valuable diagnostic tool, revealing characteristic vascular and perifollicular patterns that aid in distinguishing scalp rosacea from other inflammatory scalp conditions. Histopathology, when required, demonstrates vascular ectasia and perifollicular inflammation without follicular destruction, confirming its non-scarring nature. Management relies on topical and systemic therapies extrapolated from facial rosacea, with oral tetracyclines as first-line treatment. Overall, prognosis is favorable, as progression to cicatricial alopecia does not occur. The aim of this review is to synthesize current evidence on the pathogenesis, clinical presentation, trichoscopic and histopathologic features, differential diagnosis, and therapeutic approaches to scalp rosacea, in order to improve its recognition and clinical management.

Key Summary Points

Scalp rosacea is an underrecognized inflammatory dermatosis that often mimics other scalp conditions, with unclear prevalence and no established diagnostic or treatment consensus.

Increasing awareness is needed because of its frequent misdiagnosis, nonspecific trichoscopic features, and overlap with disorders such as psoriasis, seborrheic dermatitis, and cicatricial alopecias.

This review aimed to summarize current evidence on the epidemiology, pathogenesis, clinical, trichoscopic and histopathologic features, differential diagnosis, and management of scalp rosacea.

Available data indicate that scalp rosacea presents with characteristic vascular and perifollicular patterns on trichoscopy, is associated with immune dysregulation and Demodex proliferation, and responds to topical therapies and systemic agents, particularly oral tetracyclines.

Despite the lack of standardized guidelines, improved recognition and use of trichoscopy and histopathology can enhance diagnostic accuracy and management, with a generally favorable prognosis as the condition does not progress to scarring alopecia.

Introduction

Scalp rosacea, also known as red scalp disease (RSD), is an inflammatory dermatosis that is frequently underrecognized or misdiagnosed, primarily because its clinical features resemble those of other scalp conditions and its trichoscopic findings are often nonspecific [1, 2]. It is characterized by diffuse erythema, inflammatory papules and pustules, dry scaling, and vascular changes [3, 4]. Patients may seek consultation because of scalp pruritus or burning sensations [1, 4]. The term “extrafacial rosacea” was first introduced by Fountain and Sarkany in 1967 [5]; however it was not until 1975 that Gajewska [6] reported four patients with rosacea affecting both the face and the scalp, without areas of alopecia due to the scalp disease. More recently, additional clinical characteristics of this entity have been described. Nevertheless, to date, no consensus has been reached regarding its diagnostic criteria or therapeutic algorithms. This review aims to consolidate the currently available evidence on the pathogenesis, clinical presentation, trichoscopic and histopathologic features, differential diagnoses, and therapeutic approaches to scalp rosacea. This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors. Written informed consent was obtained from all patients for the publication of their clinical information and anonymized clinical photographs included in this manuscript.

Epidemiology

The exact prevalence of scalp rosacea remains unknown, as it is considered an underdiagnosed condition. It predominantly affects men aged 40 and 60 years, with a reported mean age of 47.95 years [2, 4]. Androgenic alopecia has been proposed as a potential predisposing factor, as the increased solar exposure of the affected scalp may enhance vulnerability and further support the pathogenic role of ultraviolet radiation [2, 4, 7]. Additional associations include genetic predisposition and aberrant immune responses against Demodex folliculorum and Helicobacter pylori, while environmental triggers are also believed to contribute to disease development [3, 7, 8]. While Dall’Oglio et al. [4] demonstrated that the condition is more frequent in men and fair phototypes, they did not find a clear association with androgenetic alopecia, ultraviolet exposure, or the frequency of facial flares.

Pathogenesis

The etiology and pathogenesis of RSD have not been fully elucidated. They are currently believed to be associated with genetic susceptibility, immune dysregulation, and neurovascular alterations [9, 10]. However, it is important to note that no studies have specifically investigated the pathogenic mechanisms underlying scalp rosacea. Consequently, current concepts regarding RSD pathogenesis are largely extrapolated from data obtained in facial rosacea. Future studies evaluating the scalp microenvironment, including local immune responses, neurovascular alterations, microbiome composition, and barrier function, are needed to clarify whether RSD represents a site-specific manifestation of rosacea or possesses distinct pathogenic features.

Among the proposed mechanisms, dysregulation of the innate immune response has emerged as a central feature in the pathogenesis of rosacea, including its scalp variant. Keratinocytes exposed to external stimuli—such as ultraviolet radiation, alcohol, microbial flora, and psychological stress—release cathelicidin (hCAP18), which is proteolytically processed into LL-37, thereby promoting macrophage activation and downstream inflammatory signaling [10]. Activated macrophages secrete pro-inflammatory cytokines and mediators—including interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNFα)—as well as chemokines such as CXCL8/IL-8, promoting leukocyte recruitment, inflammation, and reactive oxygen species (ROS)-mediated oxidative stress. These pathways contribute to persistent vasodilation, endothelial dysfunction, and vascular remodeling (including angiogenic signaling), ultimately leading to diffuse erythema and telangiectasia [10]. Furthermore, macrophages link innate and adaptive immunity through crosstalk with Th1/Th17 responses, amplifying inflammation [9, 11].

In addition, demodicosis can present either as a primary disease or as a complication of scalp rosacea. Forton and De Maertelaer [12], in a large cohort, reported that scalp involvement was frequent in both rosacea and demodicosis. Later, Trave et al. [7] investigated the presence of Demodex spp. on the face and scalp of patients with papulopustular rosacea and demonstrated a significantly higher frequency of Demodex-positive biopsies compared with controls, particularly on the scalp (35% vs. 0%, p = 0.033). Demodex folliculorum was the predominant species, identified in over 90% of positive samples. Interestingly, facial positivity frequently coincided with scalp involvement, suggesting that the scalp may act as a Demodex reservoir and contribute to recurrent disease [3, 7].

Finally, scalp rosacea has also been reported as an adverse event following photodynamic therapy for the treatment of multiple actinic keratoses and field cancerization [13].

Clinical Presentation

Recent studies have highlighted the distinctive clinical profile of scalp rosacea. Patients typically complain of hair loss associated with diffuse scalp erythema and dry scaling, frequently accompanied by pruritus or a burning sensation [1, 7, 12]. Interestingly, most patients do not exhibit the classic features of facial rosacea, aside from worsening of scalp symptoms following sun exposure, which is often identified only through direct questioning [1, 4].

On closer examination, a limited number of small papules and pustules may be observed (Fig. 1). These lesions are usually sparse, non-follicular, and surrounded by dilated capillaries that are easily appreciable with manual dermoscopy [4]. Such findings appear to be more common in patients with moderate disease severity and in those with Demodex positivity [7]. Follicular or peripilar scaling represents a frequent clinical and trichoscopic finding in scalp rosacea. These keratotic accumulations surrounding the follicular ostia may be observed throughout the disease course and tend to be more prevalent in patients with greater disease severity, ocular involvement, and higher Demodex densities. Notably, follicular scaling can also be detected in patients with minimal or even absent inflammatory lesions, supporting its role as an early and persistent marker of scalp rosacea [3, 12].

Fig. 1.

Clinical features of scalp rosacea. a Diffuse scalp erythema, with mild background inflammation. b Close-up view showing erythematous papules on an erythematous scalp, without follicular destruction or scarring

Trichoscopy

Trichoscopy is an easy and useful tool that supports the identification of characteristic patterns of scalp rosacea. In practice, findings can be organized into two main trichoscopic profiles: an interfollicular pattern, characterized by diffuse erythema, folliculocentric pustules, and prominent vascular abnormalities; and a follicular pattern, mainly represented by perifollicular changes such as peripilar scaling. Notably, the characteristic vascular pattern consists of a thicker linear vessel with multiple shorter, thinner ramifications along its length, and resembling caterpillar hair [2].

In a pilot study of 21 biopsy-confirmed cases, Lin et al. reported “caterpillar hair vessels” (86%), thin arborizing vessels (76%), rhomboid polygonal structures (71%), and thick arborizing vessels (67%) as the most frequent vascular findings, often occurring in combination (Fig. 2) [2]. Additional features included tubular scales (38%), Demodex tails (29%), and follicular keratotic plugs, which correlated with histological evidence of dilated and angulated capillaries [2].

Fig. 2.

Trichoscopic features of scalp rosacea. a Diffuse background erythema with signs of increased hair shedding (blue arrows) and prominent arborizing vessels (red circles). b Persistent erythema, arborizing vessels (red circle), and characteristic caterpillar hair vessels (white circle)

Similarly, Vázquez-Herrera et al. emphasized peripilar scaling as a consistent finding, frequently associated with arborizing vessels and increased hair shedding [5, 9]. Importantly, peripilar scaling in scalp rosacea lacks the concentric arrangement typically observed in lichen planopilaris. Overall, the trichoscopic vascular profile observed in scalp rosacea differs from those described in other inflammatory scalp disorders. Seborrheic dermatitis typically displays comma-shaped and atypical non-branching red vessels; psoriasis is characterized by red dots, globules, and glomerular vessels; while discoid lupus erythematosus and dermatomyositis more commonly show tortuous arborizing and serpentine vessels, together with red dots and red blood cell extravasation [2].

Histopathology

In cases where the clinical evaluation and trichoscopy are not sufficient to perform a correct diagnosis, histopathology can be diagnostic. Histopathological features of rosacea vary according to disease stage [5, 14]. Early lesions typically exhibit edema with vascular ectasia in the superficial and mid-dermis. As the disease advances, a perivascular and perifollicular lymphohistiocytic infiltrate becomes apparent, mainly around the follicular infundibulum and isthmus, frequently harboring multiple Demodex spp. mites within the infundibular lumen [9]. In granulomatous variants, non-caseating epithelioid granulomas surrounded by lymphocytes may be observed, occasionally with necrobiotic changes (Fig. 3). Late stages are characterized by sebaceous gland hyperplasia [5, 9]. Notably, the absence of epithelial destruction, sebaceous gland atrophy, and fibrosis underscores the non-scarring nature of the disease.

Fig. 3.

Histopathological features of scalp rosacea. Hematoxylin and eosin (H&E) staining showing nodular granulomatous dermatitis, consistent with scalp rosacea. Magnification × 10

Diagnosis

The diagnosis of scalp rosacea relies on the integration of clinical, trichoscopic, and histopathological findings, as previously outlined. A dermoscopy-guided biopsy is recommended in areas displaying follicles with peripilar scaling and dilated arborizing vessels. This approach is crucial for diagnostic accuracy, since chronic inflammation at the level of the follicular infundibulum and isthmus may induce papulopustular changes and peripilar scaling that closely resemble the features of folliculitis decalvans and lichen planopilaris [9, 10].

The classification of this condition within the rosacea spectrum is supported by the aforementioned findings together with its reported response to conventional rosacea therapies. Although scalp rosacea frequently occurs in association with facial disease, diagnosis should not be based solely on the presence of facial rosacea. Isolated scalp involvement has also been reported in the literature, indicating that facial rosacea is not a prerequisite for diagnosis.

The absence of validated diagnostic criteria highlights the need for further studies to better define this entity and distinguish it from other inflammatory scalp disorders.

Differential Diagnosis

Differential diagnosis of scalp rosacea is broad and includes causes of scalp erythema such as psoriasis, seborrheic dermatitis, contact dermatitis, lichen planopilaris, folliculitis decalvans, dermatomyositis, and discoid lupus erythematosus [1, 15]. All of these conditions may present with pruritus or a burning sensation in varying degrees. Frequently, discerning between scalp rosacea and these entities relies on the combination of clinical and trichoscopic findings. In some cases, a scalp biopsy may be required to confirm the diagnostic suspicion [15].

The main trichoscopic findings of the most relevant differential diagnoses of scalp rosacea are summarized below.

In psoriasis, characteristic trichoscopic features include diffuse silver-white scaling and perifollicular scaling, together with regularly distributed twisted red loops, dotted (glomerular) vessels, and punctate hemorrhages (hemorrhagic dots) [16, 17].

The main trichoscopic feature of seborrheic dermatitis is diffuse yellowish scaling. Thin, irregularly arranged arborizing and linear vessels, as well as red structureless areas, may also be observed [18].

In contact dermatitis, trichoscopy usually reveals diffuse white-yellowish scaling and yellow exudate, occasionally accompanied by perifollicular tubular scaling. The most common vascular patterns include dotted vessels, comma vessels, and single loops, frequently involving the hairline, retroauricular region, or neck [19, 20]. In this setting, a detailed history of recent scalp exposure to new products is essential for diagnosis.

Lichen planopilaris in diffuse pattern is characterized by perifollicular hyperkeratosis and hair casts, erythema, and white scarring patches with loss of follicular openings, findings not observed in scalp rosacea. Folliculitis decalvans may share some of these features; however, it more commonly presents with perifollicular pustules, yellowish crusts, and prominent tufted hairs [15, 20].

Among connective tissue diseases with scalp involvement, diffuse erythema represents the classical trichoscopic finding. Dermatomyositis shows prominent vascular alterations, particularly fine linear telangiectasias [21–24]. Peripilar casts and interfollicular scaling may also be present; however, follicular pustules are absent in contrast to scalp rosacea [12].

In discoid lupus erythematosus, trichoscopic features vary according to disease activity. Active lesions commonly exhibit red dots, blue-gray dots, and adherent scaling, whereas inactive/chronic disease more often shows structureless white areas with reduced follicular openings, exaggerated honeycomb pigmentation, and arborizing vessels. Follicular keratotic plugs and telangiectasia may be found in both stages with variable frequency [21].

In patients with systemic lupus erythematosus, trichoscopy most commonly reveals black dots, scattered brown pigmentation, a speckled blue-gray pattern, and prominent thick arborizing vessels [22, 23].

Acneiform eruptions of the scalp may also mimic scalp rosacea, particularly in patients with follicular papules or pustules on erythematous skin. Trichoscopy reveals central follicular pustules, yellow-brown crusts, and a lattice-like pattern of dilated vessels, often with perifollicular erythema and reactive scaling.

Unlike scalp rosacea, vascular changes are less uniform, and findings tend to reflect suppurative folliculitis, favoring an acneiform process when predominant [24].

Other differential considerations may include infectious processes—such as dermatophyte infections, Candida, Malassezia-associated dermatitis, or bacterial infestations—as well as non-infectious entities such as Ofuji syndrome and early-stage folliculitis decalvans, which may partially overlap in clinical or trichoscopic appearance [1, 15, 24].

To support diagnostic accuracy, Table 1 summarizes the clinical, trichoscopic, and histopathological features that differentiate scalp rosacea from other conditions that may present with scalp erythema.

Table 1.

Key clinical, trichoscopic, and histopathologic features of scalp rosacea and its main differential diagnoses

Condition	Clinical clues	Trichoscopic findings	Histopathology
Scalp rosacea	Persistent scalp erythema; telangiectatic background; follicular papules/pustules; burning/stinging; poor or absent response to corticosteroids; often mild/silent facial involvement	Arborizing/polygonal vessels; perifollicular white/yellow scaling; dilated follicular ostia; orange-yellow perifollicular areas; dilated vessels	Dilated venules; perifollicular lymphohistiocytic infiltrate at infundibulum/isthmus; neutrophils in pustules; Demodex frequently within follicular lumen
Psoriasis	Erythematous plaques with silvery-white scale; may cross hairline; plaques on elbows/knees/sacrum; non-cicatricial shedding	Glomerular/dotted vessels, twisted red loops; silver-white scaling; hemorrhagic dots	Parakeratosis with neutrophils; elongated rete ridges; Kogoj micropustules; dilated papillary dermal vasculature
Seborrheic dermatitis	Pruritus with yellow-greasy scale; winter flares; facial seborrheic areas involved	Thin arborizing vessels; yellow scaling; red structureless areas; vessel pattern non-uniform	Psoriasiform hyperplasia; spongiosis; shoulder parakeratosis along follicular openings
Contact dermatitis	Onset after new product/exposure; pruritus; extension to hairline/ears/neck	Yellow serous crust/exudate; dotted/comma/linear vessels; hemorrhagic dots	Spongiosis; vesiculation; perivascular lymphocytes/neutrophils; dilated capillaries
Diffuse lichen planopilaris	Diffuse erythema + thinning; trichodynia; mucosal/nail LP signs	Loss of follicular openings; perifollicular erythema/scale; white/sclerotic patches; tufting	Lichenoid interface dermatitis at isthmus/infundibulum; lamellar perifollicular fibrosis; follicular dropout
Dermatomyositis	Painful/itchy scalp; poikiloderma; hair fragility; heliotrope rash/Gottron; proximal weakness	Tortuous/arborizing vessels; perifollicular/interfollicular pigmentation; scaling	Epidermal atrophy; vacuolar interface change; dermal mucin; sparse perivascular lymphocytes
Discoid lupus	Scarring alopecia; dyspigmentation; follicular atrophy; photodistributed plaques; chronic course	Loss of follicular ostia; follicular keratotic plugs; telangiectasias; pigmentary changes	Interface dermatitis; follicular plugging; basement membrane thickening; mucin; perifollicular fibrosis; ↓ follicles/sebaceous glands
Acneiform eruption	Follicular papules/pustules or crusts; erythematous painful lesions; occasional bleeding or purulent exudate; may mimic infectious or inflammatory folliculitis	Central pustules on inflamed background; lattice-pattern dilated vessels; crusts ranging red → yellow–brown; perifollicular erythema	Suppurative folliculitis in superficial dermis; neutrophilic infiltrate; dilated sebaceous glands; intra-infundibular hyperkeratinization with lamellar retention plugs

Treatment and Prognosis

There are still no consensus or guidelines on scalp rosacea-specific treatments. Nonetheless, the available evidence suggests a favorable prognosis, as the condition does not progress to cicatricial alopecia. The therapeutic approach to scalp rosacea includes both topical and systemic options. Topical agents such as azelaic acid, metronidazole, and ivermectin have been reported to be beneficial, with solution-based formulations generally preferred because of the cosmetic limitations of creams and gels on the scalp [5, 9, 25]. In addition, oral tetracyclines remain a cornerstone of therapy, with regimens including lymecycline 150–300 mg/day, doxycycline 40–200 mg/day, or minocycline 100 mg/day for 4–8 weeks, followed by gradual tapering to the lowest effective dose [9, 26]. Oral ivermectin at a dose of 200 µg/kg administered as a single dose, which may be repeated after 7–14 days depending on the clinical response, has also been used effectively [5]. In severe or refractory cases, low-dose isotretinoin (0.1–0.2 mg/kg/day) may be considered [27]. Other systemic antibiotics, such as azithromycin or erythromycin, can serve as alternative therapeutic options when tetracyclines are contraindicated or not tolerated [25, 27]. Adjunctive probiotic therapy may also be considered; formulations containing Bifidobacterium breve BR03 and Lactobacillus salivarius LS01 (1 × 10⁹ CFU each, twice daily) have been reported to improve clinical response and support microbiome balance, particularly when used in combination with oral tetracyclines [26]. Furthermore, beyond pharmacologic therapy, patients should be advised to avoid exacerbating factors such as corticosteroids (topical or systemic), sun exposure, hot beverages, and potential contact irritants [5].

The prognosis of scalp rosacea is generally favorable, even in chronic or long-standing cases. Importantly, the condition does not progress to scarring alopecia, regardless of disease extent or duration, although transient hair shedding may occasionally occur [1, 9]. Oral tetracyclines remain the most consistently effective systemic therapy, with improvements reflected clinically by a reduction in scalp erythema and symptom burden, and trichoscopically by decreased peripilar scaling. Moreover, concomitant facial rosacea often shows parallel improvement, underscoring the systemic therapeutic benefits of this approach.

A practical therapeutic approach is summarized in Fig. 4, which outlines a stepwise treatment algorithm based on disease severity and response.

Fig. 4.

Diagnostic and treatment algorithm for scalp rosacea based on disease severity (LPP lichen planopilaris, FD decalvans folliculitis, CLD dissecting cellulitis)

Conclusions

Scalp rosacea represents an underrecognized variant of rosacea that poses significant diagnostic challenges due to its clinical overlap with other inflammatory scalp disorders. Scalp involvement is frequently underrecognized and often misinterpreted as other inflammatory conditions, underscoring the need for systematic scalp examination to avoid misdiagnosis. Advances in trichoscopy and histopathology have facilitated a better understanding of its distinctive vascular and perifollicular patterns, allowing early diagnosis. Although standardized therapeutic algorithms are lacking, both topical and systemic agents, particularly oral tetracyclines, have shown consistent efficacy, with prognosis generally favorable since progression to cicatricial alopecia does not occur. Continued awareness and further research are essential to refine diagnostic criteria and optimize management strategies for this overlooked condition.

Declarations

Conflict of Interest

Michela Valeria Rita Starace is an Editorial Board member of Dermatology and Therapy. Michela Valeria Rita Starace was not involved in the selection of peer reviewers for the manuscript nor any of the subsequent editorial decisions. Valeria Olvera Rodríguez has nothing to disclose. Francesca Pampaloni has nothing to disclose. Andrea Sechi has nothing to disclose.

Ethical Approval

This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors. Written informed consent was obtained from all patients for the publication of their clinical information and anonymized clinical photographs included in this manuscript.