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. 2021 Apr 26;7(5):382–386. doi: 10.1159/000514565

Scalp Rosacea: Rethinking Peripilar Scaling

Norma Elizabeth Vázquez-Herrera a,*, Diana Miroslava Zamora-Benze a, Juana Irma Garza-Chapa b, Angélica Beatriz Rodríguez-Baca a, Antonella Tosti c
PMCID: PMC8436626  PMID: 34604328

Abstract

Introduction

Scalp rosacea is scarcely reported in the literature, but it is probably not uncommon. Trichoscopic findings have not been specifically established for this entity.

Case Presentation

We report 4 cases of chronic scalp rosacea with trichoscopic evidence of peripilar scaling that resolved without scarring after treatment.

Discussion/Conclusion

Chronic and persistent inflammation around the isthmus produced in scalp rosacea may form peripilar scaling resembling that found in lichen planopilaris.

Keywords: Peripilar scaling, Scalp rosacea, Dermoscopy, Trichoscopy

Established Facts

  • Scalp rosacea is an uncommon diagnosis with only few cases reported in the literature.

  • Dermoscopic findings that have been associated with rosacea include vascular polygons, linear branching vessels, follicular plugs, dilated follicles, white scales, yellow scales, and orange-yellowish areas.

  • Peripilar scaling has previously been linked to scarring alopecia, predominantly lichen planopilaris and frontal fibrosing alopecia.

  • Scalp rosacea presents with an inflammatory infiltrate centered on the superficial vessels and/or pilosebaceous units.

Novel Insights

  • Peripilar scaling is found in patients with scalp rosacea.

Introduction

Extrafacial rosacea is generally found in sun-exposed skin including the scalp [1]. Scalp involvement is usually observed in the granulomatous variant of rosacea [2]. Scalp rosacea is an uncommon diagnosis with only few cases reported in the literature [3]. It primarily affects men, and because of its atypical pattern, it becomes a diagnostic challenge as in most cases it is associated with [4] only mild facial lesions [2].

Several factors have been implicated in the etiopathogenesis of extrafacial rosacea, such as vascular reactivity disorders, genetic factors, solar elastosis in chronically sun-exposed skin, and an immune response against Demodex folliculorum and Helicobacter pylori [2, 4].

Dermoscopy has a high diagnostic accuracy for distinguishing common inflammatory skin disorders. Dermoscopic findings that have been associated with rosacea include vascular polygons, linear branching vessels, follicular plugs, dilated follicles, white scales, yellow scales, and orange-yellowish areas [5]. Trichoscopic findings, however, have not been specifically established for scalp rosacea.

Peripilar scaling is defined as concentrically arranged scales encircling an emerging hair shaft [6]. This trichoscopic finding is typically seen in scarring alopecia, predominantly lichen planopilaris and frontal fibrosing alopecia [6]. The severity of peripilar scaling has shown positive correlation with the grade of perifollicular infiltrate in the histopathology of frontal fibrosing alopecia, thus becoming a marker of inflammation [7].

On histopathology, initial stages of rosacea present with edema and dilated vessels in the superficial and mid-dermis. In latter stages, a perivascular and perifollicular lymphocytic infiltrate with presence of Demodex mites in the follicular infundibulum can be observed. In its granulomatous form, noncaseating granulomas are observed [8, 9]. Chronic and persistent inflammation produced in scalp rosacea may form peripilar scaling resembling that found in lichen planopilaris. We report 4 cases of chronic scalp rosacea with peripilar scaling present on trichoscopy, which resolved without scarring after treatment (Fig. 1, 2, 3, 4, 5, 6, 7).

Fig. 1.

Fig. 1

Peripilar scaling in trichoscopy of a patient with scalp rosacea.

Fig. 2.

Fig. 2

Peripilar scaling and dilated arborizing vessels in trichoscopy of a patient with scalp rosacea.

Fig. 3.

Fig. 3

Perifollicular lymphocytic infiltrate around the isthmus and infundibulum in trichoscopy-guided biopsy of a follicle with peripilar scaling in a patient with scalp rosacea.

Fig. 4.

Fig. 4

Dilated arborizing vessels and peripilar scaling.

Fig. 5.

Fig. 5

Biopsies were guided by trichoscopy, focusing on follicles with peripilar scaling present.

Fig. 6.

Fig. 6

Multiple Demodex spp. mites in follicular canals.

Fig. 7.

Fig. 7

Multiple Demodex spp. mites in follicular canals.

Case Presentation

A detailed case presentation is provided in Table 1.

Table 1.

Case presentation

Case 1 Case 2 Case 3 Case 4
Patient 41-year-old Hispanic male patient presented with a chief complaint of hair loss 23-year-old Hispanic female with a past medical history of facial and chest rosacea presented with a 4-year history of hair loss and scalp pruritus 67-year-old Caucasian female with a medical history of papulopustular rosacea presented with scalp redness, itching, and patterned hair loss 34-year-old Hispanic male patient with hair loss and scalp pruritus

Clinical examination Patterned alopecia Scalp erythema Scalp erythema Scalp erythema

Trichoscopic findings Hair shaft variability, peripilar scaling (shown in Fig. 1), and dilated arborizing blood vessels (shown in Fig. 2) Dilated arborizing vessels and peripilar scaling (shown in Fig. 4, 5) Hair shaft variability, dilated arborizing vessels, and peripilar scaling Hair shaft variability, dilated arborizing vessels, and peripilar scaling

Biopsies Two dermoscopy-guided punch biopsies were taken from the scalp targeting follicles surrounded by peripilar scaling and arborizing vessels

Pathology results Nonscarring alopecia with increase in vellus hairs and perifollicular lymphocytic infiltrate around the isthmus and infundibulum (shown in Fig. 3) with the presence of Demodex spp. in the follicular infundibula Inflammatory nonscarring alopecia, with the presence of multiple Demodex spp. in the follicular infundibulum (shown in Fig. 6, 7) Inflammatory nonscarring alopecia with the presence of Demodex spp. in the follicular infundibula Multiple Demodex spp. in the follicular infundibulum and perifollicular lymphocytic infiltrate around the isthmus and infundibulum

Treatment 8 weeks of 150 mg of oral lymecycline QD with significant improvement of the hair shedding 12 weeks of 150 mg of oral lymecycline QD and 6 weeks of topical metronidazole on the scalp 12 weeks of oral doxycycline QD 12 weeks of 150 mg of oral lymecycline QD

Evolution Decrease in scalp erythema and reduction of peripilar scaling on trichoscopy Significant improvement of hair shedding. Complete clearance of facial rosacea and reduction of peripilar scaling severity on trichoscopy Decrease in scalp erythema and reduction of peripilar scaling on trichoscopy Decrease in scalp erythema and pruritus. Reduction of peripilar scaling on trichoscopy

Discussion/Conclusion

Scalp rosacea is rarely mentioned in the scientific literature. Because of the high prevalence of facial rosacea, it can be assumed that scalp rosacea is an underdiagnosed entity [3]. Clinically, scalp rosacea may present with erythema and sometimes with papules and pustules [4]. In one study, vascular polygons, hyperkeratosis, and plugging of follicular ostia were found on trichoscopy [4]. However, specific trichoscopic findings have not yet been established. Histopathologically, rosacea presents as a lymphocytic inflammatory infiltrate around superficial vessels and pilosebaceous units [8].

All of our patients presented with increased hair shedding, with a positive pull test for telogen hairs and erythema; 3 out of 4 of them presented with hair thinning and miniaturization in an androgenetic pattern. On trichoscopy, arborizing dilated blood vessels, hair shaft variability, and peripilar scaling were observed. Histopathology showed a perifollicular lymphocytic infiltrate located between the isthmus and infundibulum associated with the presence of multiple Demodex spp. inside follicular canals, as well as miniaturization of hair follicles. There was no interface damage to the hair epithelium, sebaceous glands were present with no signs of atrophy, and no evidence of scarring was noted in any of the biopsies. Patients reported significant improvement after treatment with oral tetracyclines and topical metronidazole, showing decreased erythema, reduced hair shedding, increased hair density, and decreased peripilar scaling severity on trichoscopy.

Our cases show that peripilar scaling is not always a sign of scarring alopecia. In scarring alopecia, peripilar scaling severity has been associated with the severity of the inflammatory lymphocytic infiltrate involving the isthmus and infundibulum, but not with the degree of scarring. In our patients with scalp rosacea, peripilar scaling was a sign of active inflammatory disease. There are no reported cases of scarring alopecia due to rosacea, and the presence of peripilar scaling is a consequence of the location of the inflammation in this disease. This is relevant since it is probably an unusual presentation of peri­pilar scaling in a nonscarring alopecia, but it raises the question of whether chronic scalp rosacea may cause scarring alopecia due to the inflammation surrounding the upper portion of the hair follicle.

Statement of Ethics

All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1964, as revised in 2013. All subjects have given their written informed consent to publish their case and images. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity.

Conflict of Interest Statement

Antonella Tosti served as a consultant or advisor for DS Laboratories, Monat Global, Almirall, Thirty Madison, Pfizer, and Leo Pharmaceuticals. All other authors have no conflicts of interest to disclose.

Funding Sources

The authors did not receive any funding.

Author Contributions

N.E.V.-H. conceived the presented idea and contributed to the design of the work and acquisition of data. D.M.Z.-B. was responsible for drafting the work. J.I.G.-C. and A.R.-B. collaborated with the interpretation of pathology. A.T. supervised the findings of this work and gave the final approval of the version to be published. All authors discussed the results and contributed to the final manuscript.

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