Psoriasis is characterized by an increase of epidermal proliferation. The consequence of psoriasis on hair growth is not well known. It was previously suggested that both psoriatic epidermal lesions and anagen hair growth shared the same “switch-on” mechanism based on the comparison of the Koebner phenomenon and wound-induced hair growth.1 We provide new data to support this hypothesis.
We studied 7 consecutive patients (including the patient in the index case) with sharply demarcated, chronic, untreated psoriatic plaques on their scalps (Table). The index case involved a 41-year-old man with androgenetic alopecia and a history of flares of cutaneous psoriasis who decided to shave his scalp completely. After shaving, he developed psoriatic plaques on his scalp, and when his hair started to grow back, he noticed that the hair appeared to be denser in the areas affected by the psoriatic plaques than in other areas of the scalp. He had 1 plaque in the occipital region (Figure 1) and 2 plaques in the vertex region (Figure 2).
Index case (case 1). Increased density of hair in psoriatic plaque.
The 6 cases other than the index case were studied with videomicroscopic analysis. The psoriatic areas of the scalp (Figure 3, A) were compared with adjacent nonaffected areas (Figure 3, B). Videomicroscopic analysis demonstrated that the denser appearance of the plaques was attributable to a higher hair count, not to the length of the hair, which was always the same in both the normal areas and the areas with the psoriatic plaques.
Videomicrosopic images showing psoriatic scalp areas (A) and adjacent normal areas (B) in cases 2 through 7.
We report an increased density of hair in psoriatic plaques. Psoriasis- and wound-induced hair growth may share the same switch-on mechanism. In 1956, Argyris2 reported that wounding of the skin induced hair growth. Recently, Osaka et al3 demonstrated the critical involvement of macrophages in wound-induced hair growth in a model of mice. Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase family that is required for the recruitment and activation of macrophages. Wound-induced hair regrowth is impaired in ASK1-deficient mice. It activates both c-Jun NH2-terminal kinase and p38 mitogen-activated protein kinase pathways in response to inflammatory cytokine and physical stress. Transplantation of cytokine-activated bone marrow–derived macrophages also strongly induces hair growth in both ASK1-deficient and wild-type mice. Interestingly, recent studies provide support for a major contribution of monocytes and macrophages in psoriasis initiation. Marble et al4 demonstrated an increase of macrophages and dermal dendritic cells in prepsoriatic skin.
The role of psoriasis in hair growth induction is further supported by the recent finding of an increased level of nuclear β-catenin in the suprabasal psoriatic epidermis compared with uninvolved or normal skin.5 β-Catenin is known to control the hair cycle, and its expression is correlated with the induction of the anagen phase and the differentiation of stem cells. The ability to induce growth of new hair follicles by transiently activating β-catenin signaling in adult mouse epidermis is additional corroborating evidence.6
In conclusion, we suggest that scalp psoriasis may be caused by an increase in the recruitment of stem cells, resulting in a switch-on entry in the anagen phase. As compared with wound-induced hair growth, monocytes and macrophages could have a key role in this cascade of events in psoriasis by upregulation of the Wnt/β-catenin pathway.
Correspondence: Dr Descamps, Department of Dermatology, Bichat-Claude Bernard Hospital, Paris 7 University, Assistance Publique des Hôpitaux de Paris, 46 rue Henri Huchard, 75018 Paris, France (email@example.com).
Author Contributions: Dr Descamps had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Descamps. Acquisition of data: Sawan and Descamps. Analysis and interpretation of data: Descamps. Drafting of the manuscript: Descamps. Critical revision of the manuscript for important content: Sawan and Descamps. Administrative, technical, or material support: Sawan and Descamps. Study supervision: Descamps.
Financial Disclosure: None reported.
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