Psoriatic Alopecia: Clinical Features, Pathogenesis, and Emerging Treatment Strategies

Abstract

Background

Psoriatic alopecia is a distinct but underrecognized manifestation of psoriasis, leading to both non-scarring and scarring hair loss. While scalp involvement is common in psoriasis, the mechanisms underlying follicular damage and hair loss remain poorly understood. Diagnosis is challenging due to clinical and histopathological overlap with other alopecias, and treatment responses are often variable.

Summary

This review examines the clinical presentation, pathogenesis, and management of psoriatic alopecia. The inflammatory process, primarily driven by the Th17/IL-23 axis, contributes to hair follicle disruption, sebaceous gland atrophy, and in severe cases, permanent alopecia. Trichoscopy and histopathology aid in diagnosis, but standardized criteria are lacking. Treatment strategies include topical corticosteroids, vitamin D analogs, and systemic biologics, but some patients remain refractory to conventional therapies. Paradoxical psoriatic alopecia induced by TNF inhibitors further complicates management, necessitating individualized treatment approaches.

Key Messages

Psoriatic alopecia requires greater clinical recognition and research to improve diagnosis and treatment. A deeper understanding of its pathogenesis, particularly immune-mediated follicular damage, could lead to more effective therapies. Personalized treatment approaches, including novel biologics, hold promise for improving patient outcomes, but further studies are needed to optimize long-term management strategies.

Introduction

Psoriasis is a chronic, immune-mediated inflammatory disease that affects the skin and other organs, with an estimated global prevalence ranging from 0.51% to 11.43% in the adult population [1]. Scalp involvement occurs in 45–56% of individuals with psoriasis and is often one of the first areas affected. However, despite its high prevalence, psoriatic alopecia remains a much less common manifestation [2]. While the cutaneous manifestations of psoriasis are well documented, its effects on hair and hair growth, referred to as psoriatic alopecia, remain relatively underexplored. This specific complication was first described by Shuster in 1972 [3] and is characterized by hair loss or abnormalities in hair growth occurring in individuals with psoriasis [4, 5].

Although the scalp is one of the most commonly affected sites in psoriasis, the mechanisms and clinical features of psoriatic alopecia are not fully understood. Psoriatic alopecia can be considered a specific, less frequent, but clinically distinct manifestation within the spectrum of scalp psoriasis, with follicular inflammation and damage potentially leading to non-scarring or scarring hair loss. Understanding this continuum is crucial for accurate diagnosis and tailored therapeutic strategies. It remains unclear whether hair loss is a direct consequence of the inflammatory processes underlying psoriasis, a secondary effect of physical trauma, or related to other local factors such as changes in the scalp microenvironment. Moreover, the limited number of studies addressing psoriatic alopecia has resulted in a lack of consensus on its pathogenesis, classification, and optimal management strategies.

The aim of this review was to bridge these gaps by providing a comprehensive analysis of the clinical manifestations, underlying pathophysiology, and treatment options for psoriatic alopecia. By synthesizing existing knowledge and highlighting emerging evidence, this article seeks to enhance the understanding of this condition and its implications for patient care.

Methods

This review follows a scoping review methodology. We systematically searched PubMed database using keywords including “psoriatic alopecia,” “scalp psoriasis,” “TNF inhibitors,” “biologics,” and “trichoscopy” from inception to date, critically selecting relevant papers to comprehensively review the clinical features, diagnosis, pathogenesis, and treatment strategies.

Pathophysiology

Role of the Th17/IL-23 Axis

The inflammatory process in psoriatic alopecia involves the Th17/IL-23 axis, similar to plaque psoriasis. IL-23 activates Th17 cells, leading to secretion of IL-17, IL-22, and other inflammatory mediators, contributing to hair follicle disruption. Although the general mechanisms overlap with psoriasis, localized follicular inflammation and associated sebaceous gland dysfunction specifically contribute to hair loss in affected areas [6].

Impact of Inflammation on Hair Follicles

Psoriatic lesions are rich in cytokines such as TNF-α, IL-1β, and IFN-γ, which disrupt the anagen phase of the hair cycle, inhibiting hair follicle activity [7, 8]. However, overt hair loss in scalp psoriasis is uncommon due to the protective role of growth-promoting factors like IGF-1, VEGF, and Wnt signaling, which are upregulated in psoriatic skin. These factors help maintain the hair follicle and sustain the hair growth cycle despite the inflammatory environment [7, 9, 10].

Mechanisms of Psoriatic Alopecia

In psoriatic alopecia, the balance between inflammation and growth promotion tips in favor of pro-inflammatory cytokines. Chronic inflammation prematurely shifts anagen follicles into the telogen phase, leading to a significant increase in telogen hairs, with rates reported as high as 86% in active cases. Additionally, hyperkeratotic plaques on the scalp can adhere to hair shafts, causing mechanical trauma during plaque removal or treatment. This often results in synchronized shedding of telogen hairs in clumps (tufts), exacerbating the visual impact of hair loss [4].

Sebaceous Gland Atrophy

Sebaceous gland atrophy has been observed in psoriatic lesional skin, with an inverse correlation to the thickness of the psoriatic epidermis. This atrophy alters the scalp’s microenvironment, potentially weakening hair shafts and contributing to hair loss in affected areas. These changes underscore the importance of sebaceous gland health in maintaining hair follicle integrity [11–13].

The Köbner Phenomenon and Wound-Healing Pathways

The Köbner phenomenon, a hallmark of psoriasis, describes the appearance of new psoriatic lesions on previously unaffected skin following trauma [14]. A similar mechanism occurs in hair follicles, where trauma such as hair shaft depilation triggers telogen follicles to reenter the anagen phase. However, pro-inflammatory cytokines released during this process, including TNF-α, IL-1β, and IL-6, can inhibit hair growth [7, 15].

Interestingly, Wnt signaling plays a dual role in this context. While it drives hyperproliferation in psoriatic epidermis, it also activates stem cells in hair follicles, inducing anagen initiation. Trauma-induced Wnt activity, facilitated by the reduction of inhibitors and macrophage-released signals, highlights the complex interplay between psoriasis-related hyperproliferation and hair follicle dynamics [7, 15].

Itch in Psoriatic Alopecia

Pruritus is a significant but often underrecognized issue in scalp psoriasis, contributing to scratching and further mechanical trauma, potentially exacerbating hair loss. Addressing itch therapeutically may thus improve patient quality of life and potentially ameliorate hair shedding [16].

Clinical Features and Diagnosis

Psoriatic alopecia presents with diverse clinical manifestations, first categorized by Shuster [3, 17] into three distinct types.

• 1.Hair loss confined to psoriatic lesions: This is the most common presentation, characterized by hair loss localized within psoriatic plaques on the scalp. Shuster [3, 17] noted an excessive number of dystrophic hair bulbs in plucked hairs from the affected areas, reflecting follicular involvement in the disease process [18].
• 2.Acute telogen effluvium: This form of hair loss extends beyond psoriatic lesions and is typically observed in cases of severe psoriasis. It manifests as a diffuse shedding of hair in response to the systemic inflammatory state, with hair follicles prematurely entering the telogen phase [3, 17].
• 3.Scarring alopecia: The least common and most severe type, scarring alopecia involves follicular destruction and perifollicular inflammation, as confirmed by histopathological examination. Initially described as permanent by Shuster [3, 17], subsequent reports, including a case of hair regrowth after 10 years, suggest that this form of alopecia may not always be irreversible. Several other cases have also documented regrowth, emphasizing the potential for recovery under certain conditions [4, 19–21]. It is characterized by cicatricial patches of hair loss accompanied by atrophic skin and surrounded by adherent scales with positive pull test [4, 22].

Patterns of Hair Loss

Runne and Kroneisen-Wiersma [4] further expanded on these presentations by analyzing 47 patients with psoriatic alopecia. The study described hair loss occurring in tufts due to the mechanical attachment of hair shafts to hyperkeratotic plaques. This adherence caused clustering of telogen hairs into conglomerates, with significant hair loss observed during plaque removal, whether by therapeutic intervention or mechanical force. The alopecia was classified into two patterns.

• Circumscribed alopecia: localized patches of hair loss.

• Diffuse alopecia: more widespread thinning of the hair.

Most patients experienced hair loss within the first 3 months of plaque onset [4].

Scalp Psoriasis

Scalp psoriasis is characterized by thickened, well-demarcated, scaly, erythematous plaques, often accompanied by pruritus. Lesions commonly appear in the retroauricular and cervical regions, though they may involve any part of the scalp. The severity of the disease varies, ranging from mild fine scaling to extensive thick, erythematous, crusted plaques affecting the entire scalp. These plaques frequently extend beyond the hairline, involving adjacent facial skin. In severe cases, psoriatic plaques can lead to alopecia [2].

Trichoscopy

Trichoscopic findings in scalp psoriasis and psoriatic alopecia are largely similar, with both conditions demonstrating diffuse white scaling and multiple clusters of dotted vessels across the scalp. However, psoriatic alopecia is distinguished by reduced hair density and an increased proportion of vellus hairs, which are not characteristic features of non-alopecic scalp psoriasis [23]. In cases of psoriatic scarring alopecia, distinctive trichoscopic features include interfollicular twisted red loop characteristic of scalp psoriasis, loss of follicular openings, and yellowish and silvery scales [22]. Accurate identification of interfollicular twisted red loops typically requires higher magnification (at least ×20, optimally ×50), beyond the standard ×10 dermatoscopes.

Trichogram

A trichogram analysis conducted on 29 patients revealed a pathologically elevated telogen rate in 13 cases. Notably, patients experiencing acute hair loss exhibited telogen rates as high as 63%, whereas those with chronic hair loss showed rates reaching up to 36% [4].

Histopathological Findings

Skin Histopathology

The key histopathological features of psoriatic alopecia, including psoriatic scarring alopecia, are summarized in Table 1. Most patients displayed typical psoriatic alterations along with a reduced number of hair follicles [4, 18, 24]. In some cases, psoriatic changes were absent, but an increased number of telogen hairs were observed. Additional findings included follicular abnormalities such as thinning or dilatation of the follicular infundibulum, perifollicular lymphocytic inflammation, and perifollicular fibrosis [4]. In cases of psoriatic scarring alopecia, chronic inflammatory infiltrates surrounding blood vessels and eccrine glands were noted, as well as fibrous tracts replacing follicular units [3, 23, 25].

Table 1.

Histopathological findings of psoriatic alopecia

Study	Year	Patients, n	Key findings
Non-scarring psoriatic alopecia
Iamsumang et al. [18]	2017	1	Psoriatic changes, decreased terminal hairs, sebaceous gland atrophy
Runne and Kroneisen-Wiersma [4]	1992	33	Follicular hyperkeratosis, increased telogen hairs, lymphohistiocytic infiltrates, spongiotic changes, epithelial thinning, granulomatous infiltrates, fibrosis, and digitate papillomas (1 case)
Silva et al. [24]	2012	31	Psoriatic changes, infundibular dilatation (87%), follicular thinning (55%), perifollicular inflammation (68%), fibrosis (77%), fibrous tracts (28%), sebaceous gland absence (60%), atrophy (25%), or normal (15%)
Scarring psoriatic alopecia
Almeida et al. [23]	2013	1	Psoriatic changes, moderate chronic inflammation around vessels/eccrine glands, and fibrous tracts
Bardazzi et al. [25]	1999	4	Psoriatic changes, reduced follicular units replaced by fibrotic tracts, abnormal remaining follicles
Shuster [3]	1972	Unknown	Follicular paucity, perifollicular inflammation, destructional folliculitis, fibrous tissue

Sebaceous Gland Pathology

Psoriatic alopecia is frequently associated with a decreased number, absence, or atrophy of sebaceous glands, as reported in numerous studies [4, 18, 23–25]. Rittié et al. [13] attributed this phenomenon to inflammation and cytokine activity, particularly IL-17, which inhibits lipid biosynthesis critical for sebaceous gland function. This results in significant downregulation of lipid-related genes, reduced sebum production, and a striking 91% decrease in sebaceous gland volume in psoriatic lesional skin. Dysfunction of the pilosebaceous unit disrupts the detachment of the inner root sheath from the hair shaft, leading to follicular elongation and visible hair loss [13].

A recent cross-sectional study further confirmed that sebaceous gland atrophy is a defining feature of psoriatic alopecia. It demonstrated that sebaceous glands in psoriatic alopecia are significantly smaller, with a mean surface area reduced by 50%, and are predominantly composed of immature sebocytes (70%) compared to those in alopecia areata (AA) [26].

Differential Diagnosis

Psoriatic alopecia shares overlapping clinical, dermoscopic, and histopathological features with other hair disorders, making accurate diagnosis challenging. Table 2 provides a detailed comparison of key distinctions between psoriatic alopecia and conditions such as telogen effluvium, AA, and seborrheic dermatitis.

Table 2.

Key clinical, dermoscopic, and histopathological differences between psoriatic alopecia and common differential diagnoses

Differential diagnosis	Clinical features	Dermoscopic findings	Histopathological features
Psoriatic alopecia	Red, scaly plaques; localized or diffuse hair loss [27]	Reduced hair density, vellus hairs, and diffuse white scaling [23]	Psoriatic changes, sebaceous gland atrophy, and reduced hair follicles [4, 18, 24]
Telogen effluvium	Diffuse hair shedding; no inflammation or visible scalp pathology [28–31]	Numerous short, regrowing hairs with uniform density [28, 31]	Increased telogen hairs; no inflammation or structural abnormalities [28–30]
AA	Patchy or total hair loss; immune-mediated [32]	Yellow dots, black dots, broken hairs, and exclamation-mark hairs [32, 33]	Peribulbar lymphocytic infiltrates (acute), follicular miniaturization (chronic); larger sebaceous glands compared to psoriatic alopecia [26, 34]
Seborrheic dermatitis	Erythematous lesions with greasy, yellowish scales [35, 36]	Diffuse yellowish/white scales on erythematous background; arborizing vessels [35, 37]	Spongiosis, parakeratosis, and mixed inflammation; overlaps with sebaceous atrophy [12, 35, 36, 38]

Telogen effluvium lacks inflammation and scalp pathology, with uniform regrowing hairs on trichoscopy, whereas psoriatic alopecia shows red, scaly plaques, vellus hairs, and white scaling. Histologically, telogen effluvium exhibits increased telogen hairs without structural changes, unlike psoriatic alopecia, which shows psoriatic alterations and sebaceous gland atrophy.

AA presents as patchy hair loss with yellow dots and broken hairs on trichoscopy, differing from the diffuse scaling and smaller sebaceous glands seen in psoriatic alopecia. Seborrheic dermatitis is histologically distinct from psoriatic alopecia, showing spongiosis and mixed inflammation. Accurate diagnosis requires integrating clinical, dermoscopic, and histological findings. Seborrheic dermatitis typically is present with arborizing vessels dermoscopically, distinguishing it clearly from the dotted vessel characteristic of psoriatic alopecia.

Drug-Induced Psoriatic Alopecia

Psoriatic alopecia can be induced or exacerbated by tumor necrosis factor-alpha inhibitors (TNFi), a phenomenon first reported by Papadavid et al. in 2007 [39]. Since then, more than 30 cases have been documented, with infliximab and adalimumab being the most frequently implicated agents [39–52]. This manifestation, termed TNF-α inhibitor-associated psoriatic alopecia (TiAPA), typically is present months to years after initiating TNFi therapy and predominantly affects patients treated for systemic conditions such as Crohn’s disease, rheumatoid arthritis, psoriasis, or psoriatic arthritis. Interestingly, many patients developing TiAPA lack a personal or family history of psoriasis, though cases in patients with preexisting psoriasis are increasingly recognized, indicating a broader spectrum of presentation [39–52].

Clinically, TiAPA is present as erythematous, scaly alopecic lesions on the scalp, often accompanied by psoriasiform plaques on other body areas. Some patients may develop severe forms, including pustular or palmoplantar psoriasis [39, 40, 42]. Histopathological findings include psoriasiform epidermal hyperplasia, parakeratosis, intracorneal neutrophils, and an increased proportion of catagen/telogen follicles with follicular miniaturization [39–45, 48–53]. Notably, sebaceous gland atrophy or absence, a hallmark of psoriatic alopecia, has been observed in some cases [42, 44, 45, 48]. A distinguishing feature of TiAPA is the presence of peribulbar inflammatory infiltrates composed of lymphocytes, eosinophils, and plasma cells, as outlined in the diagnostic criteria established by Doyle et al. [40].

The underlying mechanism of TiAPA involves dysregulation of cytokine networks, notably through TNFi-induced elevation of interferon-alpha (IFN-α). Normally, TNF-α inhibits plasmacytoid dendritic cell maturation, suppressing IFN-α production. However, TNFi therapy disrupts this regulatory mechanism, leading to enhanced IFN-α production, recruitment of inflammatory cells, and subsequent development of psoriatic lesions [41, 42].

Diagnostic criteria proposed by Doyle et al. [40], later modified by Melé-Ninot et al. [54], emphasize the temporal relationship with TNFi initiation and clinical presentation of alopecic patches with psoriasiform features. Notably, the absence of a prior psoriasis history is no longer mandatory, recognizing the occurrence of TiAPA even in patients with preexisting psoriasis [5, 45, 54–56].

Management includes either discontinuation of TNFi therapy or transitioning to other biologics, especially IL-23 inhibitors or ustekinumab. Concurrent topical or systemic corticosteroids may also aid in managing inflammation [39–46, 48–53]. Given the overlapping clinical and histological features between idiopathic psoriatic alopecia and TNFi-induced cases, recognition of this phenomenon is crucial for appropriate patient management, emphasizing the importance of individualized treatment strategies.

Treatment of Psoriatic Alopecia

Management of psoriatic alopecia, including both idiopathic and TiAPA, generally mirrors treatment strategies for scalp psoriasis. However, certain considerations specific to hair loss should guide therapeutic decisions [4, 18, 22, 40, 43, 45].

Topical Treatments

Topical corticosteroids remain the first-line treatment, with high-potency formulations often required to penetrate the scalp [57]. Foam, gel, solution, and spray vehicles enhance adherence and cosmetic acceptability [58]. Occlusion may further improve efficacy but should be used with caution. Vitamin D analogs, while effective for maintenance, show only modest benefit when used as monotherapy. Combination with corticosteroids may reduce adverse effects and improve tolerability [59].

Nonsteroidal topicals are emerging as promising adjuncts. Topical calcineurin inhibitors, such as tacrolimus and pimecrolimus, have shown benefit in sensitive areas like the face and intertriginous zones and may offer value in mild or steroid-intolerant cases, though data for alopecia are limited [60, 61]. Roflumilast, a topical PDE4 inhibitor, has shown efficacy in scalp psoriasis, with favorable tolerability, but its role in psoriatic alopecia is yet to be defined [62]. A detailed comparison between topical treatments is presented in Table 3.

Table 3.

Efficacy of topical therapies in scalp psoriasis and considerations for psoriatic alopecia

Treatment	Efficacy in scalp psoriasis	Considerations for psoriatic alopecia
Topical corticosteroids	Superior efficacy compared to vitamin D analog monotherapy [57]. Betamethasone valerate foam improves scalp psoriasis more than corticosteroid lotions [59]	Foam, gel, solution, shampoo, and spray formulations enhance adherence and cosmetic appeal [58]
		Common side effects: burning and itching [59]
Vitamin D analog	Used in combination with corticosteroids for maintenance therapy and long-term control. Has been associated with fewer treatment withdrawals due to side effects [57, 60]	May help reduce hyperkeratosis and inflammation in psoriatic alopecia, though evidence is limited. Combination with corticosteroids is preferred for synergistic effect. Not known to promote hair regrowth directly, but may aid in scalp normalization to support hair recovery
Coal tar	Limited evidence for scalp psoriasis, with concerns about staining affecting adherence [60–62]	Rarely used in psoriatic alopecia due to lack of robust data and potential for local irritation. Its anti-inflammatory and antiproliferative properties might theoretically benefit scalp lesions, but the risk of staining and unpleasant odor often limit long-term adherence
Calcineurin inhibitors	Tacrolimus: 28.6% of individuals achieved S-IGA 0/1 within 8 weeks [63]	Mainly used in mild-moderate cases [63]. No available data regarding the efficacy in psoriatic alopecia
	Pimecrolimus: 65.5% of facial psoriasis patients showed IGA improvement within 8 weeks [64]
Roflumilast	59.1% achieved S-IGA 0/1 compared to 11.4% in the placebo group [62]	Main reported side effects were diarrhea and hypotension; both were very rare [62]

S-IGA, Scalp Investigator Global Assessment.

Phototherapy

There are no specific data for psoriatic alopecia, but ultraviolet B comb therapy has shown benefits in scalp psoriasis, reducing relapse rates compared to topical corticosteroids [65–67].

Systemic Treatments

Systemic treatments are reserved for moderate-to-severe cases or those unresponsive to topical therapy. TNF inhibitors, while effective for scalp psoriasis, may paradoxically induce alopecia (TiAPA) in up to 5% of cases [68–72]. Discontinuation often leads to resolution, and switching to ustekinumab or IL-23 inhibitors may be beneficial [41, 45, 53, 56].

IL-17 and IL-23 inhibitors have demonstrated high efficacy in scalp psoriasis. IL-17 inhibitors (e.g., ixekizumab, brodalumab) offer rapid response [73–75], while IL-23 inhibitors (e.g., guselkumab, risankizumab) provide durable outcomes and may be preferable in TiAPA settings [64, 76, 77]. There is no direct evidence comparing their efficacy in psoriatic alopecia, but theoretical advantages exist: IL-17 inhibition may better target follicular inflammation, whereas IL-23 blockade may offer a more favorable safety profile and scalp tolerability.

PDE4 inhibitors such as apremilast have shown moderate efficacy in scalp psoriasis, with the advantage of oral administration and a favorable safety profile, although their role in alopecia remains to be elucidated [78–82]. JAK inhibitors, while not yet studied specifically in psoriatic alopecia, may be relevant in future given their success in other hair disorders. A detailed comparison between the systemic drugs is presented in Table 4.

Table 4.

Efficacy of systemic therapies in scalp psoriasis and considerations for psoriatic alopecia

Treatment	Efficacy in scalp psoriasis	Considerations for psoriatic alopecia
TNFi	Adalimumab, infliximab: ∼92% PSSI75 at 48 weeks [68, 69]	May induce alopecia (TiAPA), occurring in ∼5% of TNFi users [72]. Discontinuation often leads to improvement [41, 45, 53, 56]
IL-17 inhibitors (brodalumab, secukinumab, ixekizumab)	Brodalumab: 89% PSSI75, 63.4% PSSI100 at 12 weeks [75]. Ixekizumab: 74.6% PSSI100 [76]	Effective for scalp psoriasis, but role in TiAPA is unclear. Common side effects: nasopharyngitis, folliculitis [64, 75, 76]
IL-23 inhibitors (guselkumab, risankizumab, mirikizumab)	Guselkumab: 85% achieving ss-IGA 0/1, outperforming adalimumab [64]. Risankizumab: 97.6% achieving sc-PGA 0/1 at 52 weeks [78]	Potential alternative for TiAPA. Some patients transitioning from TNFi to IL-23 inhibitors show favorable responses [41, 45, 53, 56]
IL-12/23 inhibitor (ustekinumab)	97.5% achieved PSSI75 in 48 weeks [68]	Patients switching from TNFi to ustekinumab for TiAPA showed improvement, but it is unclear if this was due to TNFi discontinuation or ustekinumab efficacy [41, 45, 53, 56]
PDE-4 inhibitors (apremilast)	38.4%–46.5% achieved scPGA 0/1 within 16 weeks [80–83]	Effective for scalp psoriasis, but the role in scalp psoriasis is unclear

TNFi, tumor necrosis factor inhibitors; TiAPA, TNF-α inhibitor-associated psoriatic alopecia; PSSI, psoriasis scalp severity index; PGA, physician’s global assessment.

Management Considerations

• Mild cases: High-potency topical steroids with or without vitamin D analogs are usually sufficient (online suppl. Fig. 1; for all online suppl. material, see https://doi.org/10.1159/000545835).

• Refractory or extensive disease: Systemic biologics, particularly IL-17 or IL-23 inhibitors, are preferred.

• TiAPA: Withdrawal of TNFi and transition to alternative biologics is often effective.

• Scalp-specific considerations: Choose treatments with cosmetically acceptable formulations to maximize adherence. The scalp’s high follicular density may favor therapies that penetrate deeply or modulate perifollicular inflammation.

Current Challenges in Treatment and Diagnosis

Diagnosing psoriatic alopecia is challenging due to its overlap with other inflammatory and scarring alopecias, requiring trichoscopy and often histopathology for confirmation. Treatment is equally complex, particularly for patients unresponsive to conventional therapies, as the efficacy of IL-17 and IL-23 inhibitors in promoting hair regrowth remains uncertain. Additionally, TiAPA complicates therapeutic choices. Environmental factors such as smoking, obesity, and stress, along with mechanical trauma and sebaceous gland atrophy, may influence disease progression and treatment response. A personalized, multidisciplinary approach is essential for optimizing outcomes.

Future Research and Knowledge Gaps

Despite growing recognition of psoriatic alopecia, many aspects of the condition remain unexplored, including its exact pathogenesis, the role of sebaceous gland atrophy, and its distinction from other scarring and non-scarring alopecias. A deeper understanding of the inflammatory and immune mechanisms driving hair follicle involvement in psoriasis is needed to identify novel therapeutic targets. Additionally, research should focus on biomarkers that predict disease progression and treatment response, paving the way for personalized treatment strategies. Future studies should also evaluate the long-term efficacy of biologics and emerging therapies in restoring hair growth, ensuring more tailored and effective management approaches.

Summary and Conclusions

Psoriatic alopecia is a distinct yet often overlooked manifestation of psoriasis, presenting with a spectrum of non-scarring and scarring hair loss. Its diagnosis remains challenging due to overlapping clinical, trichoscopic, and histopathological features with other inflammatory alopecias. Understanding the underlying disease mechanisms, including chronic inflammation, sebaceous gland dysfunction, and the impact of mechanical trauma, is essential for refining diagnostic criteria and improving patient management. The limited response to conventional psoriasis treatments in some cases further underscores the need for targeted therapeutic approaches.

Recognizing psoriatic alopecia as a separate clinical entity is crucial for advancing research and optimizing treatment strategies. The development of personalized therapies, particularly within the expanding landscape of biologics and novel immunomodulators, has the potential to improve both hair regrowth and overall disease control. By bridging existing knowledge gaps and refining treatment protocols, clinicians can offer patients a more effective and tailored approach, ultimately enhancing their quality of life.

Conflict of Interest Statement

Y. Ramot received speaker honoraria, consultancy fees, or travel support from Pfizer, AbbVie, Novartis, Janssen, Sanofi, BI, Neopharm, Dexcel Pharma, Taro, BMS, and Lilly. E. Pirov has no conflicts of interest to declare.

Funding Sources

The authors have no funding to declare.

Author Contributions

Conceptualization, writing – review and editing, and supervision: Y.R.; data curation and writing – original draft preparation: E.P. and Y.R.

Funding Statement

The authors have no funding to declare.