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7 September 2026

Localised Alopecia Associated with Hairstyling Accessories: A Multicentre Case Series with Clinical, Trichoscopic, and Histopathological Evidence of Mixed Mechanical Injury

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1
Dermatology Department, Hospital Universitario de Toledo, 45007 Toledo, Spain
2
Trichology Unit, Instituto Médico Ricart, 28046 Madrid, Spain
3
Hair Disorders Unit, Grupo Pedro Jaén, 28002 Madrid, Spain
4
Department of Dermatology, Hospital Universitario La Paz, 28046 Madrid, Spain
Cosmetics2026, 13(5), 229;https://doi.org/10.3390/cosmetics13050229
This article belongs to the Special Issue Feature Papers in Cosmetics in 2026
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Abstract

Mechanical forces generated by hairstyling practices are recognised causes of hair and scalp disorders, particularly traction alopecia, but the effects of prolonged, localised exposure to hairstyling accessories remain poorly characterised. We conducted a multicentre retrospective study of 10 women evaluated at five centres with chronic localised alopecia anatomically corresponding to the site of repeated accessory contact, analysing clinical, trichoscopic, histopathological and outcome data. Mean age was 51.3 years and mean disease duration 5.8 years; nine patients had vertex involvement, and one had an interparietal patch. Trichoscopy showed vellus hairs, with variable broken hairs, black and yellow dots, dystrophic, bent and coiled hairs, perifollicular casts and loss of follicular openings. Histopathology, available in seven patients, showed scarring alopecia in four and non-scarring alopecia in three. Implicated exposures included hairpins, clips, buns, rollers and a hair prosthesis. After accessory removal and variable treatment, four patients showed partial regrowth, four remained stable, one worsened, and follow-up was unavailable for one. The anatomical correspondence between alopecic patches and accessory exposure, with overlapping pressure, traction and friction-related features, is consistent with a proposed mixed mechanical injury from chronic low-intensity stress. Recognising hairstyling accessories as a potential cause of localised alopecia may facilitate diagnosis and prevent progression to irreversible damage.

1. Introduction

Hairstyling practices are an integral part of cosmetic hair care and may involve repeated physical manipulation of the hair shaft and scalp. Although generally considered harmless, prolonged or excessive mechanical forces generated by certain hairstyles, hair extensions, head coverings and external devices can lead to hair shaft damage and follicular injury, with clinical manifestations ranging from reversible hair loss to permanent scarring alopecia [1]. The development and severity of mechanically induced hair loss appear to depend on the characteristics of the mechanical exposure, including the magnitude, duration and repetition of the applied force, as well as on individual susceptibility factors [1,2].
Among mechanically induced alopecias, traction alopecia is the best characterised and has been extensively associated with hairstyles that exert sustained or repetitive tension on the hair follicles. Pressure and friction, by contrast, have received comparatively little attention, despite contributing to hair loss through mechanisms that are distinct in principle but often overlap with traction in practice [3,4]. Hairstyling accessories such as hair clips, pins, elastics, rollers and hair systems are widely used across different age groups, often daily and for prolonged periods. These accessories are generally regarded as harmless cosmetic tools, and chronic localised alopecia related to their use is seldom considered in routine clinical practice. Consequently, patients may undergo extensive investigations or receive alternative diagnoses before the mechanical origin of the alopecia is recognised.
Pressure alopecia is an uncommon form of hair loss caused by local tissue ischaemia resulting from sustained or repetitive pressure on the scalp. It has traditionally been described after prolonged immobilisation during surgery or intensive care admission, particularly over pressure-bearing areas of the scalp [5]. However, pressure alopecia has also been reported in association with external devices, including orthodontic headgear, cervical collars, electroencephalographic monitoring equipment and hair systems, indicating that prolonged continuous immobilisation is not required for mechanically induced ischaemic follicular injury [6,7,8,9]. Depending on the severity and duration of the insult, pressure alopecia may be reversible or progress to follicular destruction, fibrosis and permanent scarring alopecia [10].
Traction alopecia results from sustained or repeated tension transmitted to the hair shaft and follicle and may similarly evolve from reversible follicular dysfunction to permanent follicular loss when the mechanical exposure persists [1]. Epidemiological and clinical studies suggest that the risk and severity of traction alopecia are influenced by the characteristics and duration of the mechanical exposure, associated hair-care practices and individual susceptibility [2,11,12]. A useful illustration of how far hairstyling practice itself can modulate this risk comes from the dermatological literature on Black hairstyling, in which hairstyles have been explicitly stratified into high-, moderate- and low-risk categories according to the tension, weight and duration of the styling technique involved [13]. To our knowledge, a comparable risk stratification has not yet been attempted for the broader range of everyday hairstyling accessories used across other patient populations.
Friction-related alopecia is less well characterised and is attributed to repetitive rubbing or contact, leading predominantly to hair shaft breakage and structural shaft damage [4]. Repetitive self-induced rubbing of the scalp, termed trichoteiromania, represents a related form of mechanical hair damage, and the largest series published to date underscores how substantial hair shaft damage from friction alone can be, even in the absence of any external device [14].
Although pressure, traction and friction alopecia have generally been described as distinct entities according to their predominant pathogenic mechanisms, mechanical forces encountered in everyday hairstyling practices may not necessarily act in isolation. External devices and hairstyling practices may simultaneously generate pressure, traction and friction, and the relative contribution of each force may vary according to the characteristics of the accessory or hairstyle, its anatomical position, fixation and duration of use.
Published reports describing accessory or device-related alopecia have mainly focused on individual accessories or specific external devices, including orthodontic headgear, electroencephalographic electrodes, cervical collars, headbands, hair prostheses and individual hairstyling practices [6,7,15,16]. Consequently, it remains unclear whether these apparently diverse presentations represent distinct clinicopathological entities or different manifestations of a common pattern of chronic mechanical follicular injury, which may not be adequately captured by the current classification of mechanical alopecias.
Despite the widespread use of hairstyling accessories, chronic localised alopecia developing at sites of repeated accessory contact has not been systematically characterised, and its relationship with established forms of mechanical alopecia remains poorly understood. Recognition of this presentation is clinically important because the causative exposure is potentially reversible, whereas delayed diagnosis may allow progression to scarring alopecia.
In this multicentre study, we describe a series of patients presenting with chronic localised alopecia of the vertex or interparietal scalp anatomically corresponding to sites of prolonged exposure to hairstyling accessories. The aim of this study was to characterise the clinical, trichoscopic and histopathological features of this presentation and to explore its potential underlying mechanical mechanisms. Our findings suggest that chronic exposure to hairstyling accessories may give rise to a mixed-pattern mechanical alopecia resulting from varying contributions of pressure, traction and friction, which may progress to scarring alopecia in some patients.

2. Materials and Methods

2.1. Study Design and Patient Selection

This multicentre retrospective case series included 10 patients evaluated at five centres in Spain between 2020 and 2025. Cases with a similar clinical presentation were identified by the participating dermatologists from their clinical practice, and clinical data were retrospectively collected from the corresponding medical records.
The study was conducted in accordance with the principles of the Declaration of Helsinki. All participants provided written informed consent for the use and publication of their de-identified clinical data and images.
Eligibility criteria were the presence of a chronic localised alopecic patch, available clinical and trichoscopic documentation, repeated use of a hairstyling accessory over the affected area, and anatomical correspondence between the site of accessory exposure and the alopecic patch. Cases in which an alternative diagnosis was considered more likely on the basis of the available clinical, trichoscopic and, when available, histopathological findings were excluded; concomitant hair disorders were not considered exclusion criteria when a history of repeated mechanical exposure and anatomical correspondence between the site of exposure and the alopecic patch were present. Histopathological examination was not required for inclusion.

2.2. Data Collection and Clinical, Trichoscopic and Histopathological Assessment

Demographic and clinical data were retrospectively collected from the medical records, including age, sex, location and duration of alopecia, associated symptoms, hairstyling practices and accessories used over the affected area, previous diagnoses and treatments, management after identification of the suspected mechanical trigger, and available follow-up information.
Clinical and trichoscopic findings were retrospectively collected from medical records and available clinical and trichoscopic images. Because of the retrospective multicentre design, trichoscopic examination and image acquisition were not performed according to a standardised protocol across participating centres. Trichoscopic findings were initially assessed by the treating dermatologist at each centre and subsequently reviewed centrally by one of the authors across all cases, in order to homogenise the recording of findings and reduce interobserver variability.
Scalp biopsy was performed according to clinical judgement and was not required for study inclusion. Histopathological findings were retrospectively collected from the original pathology reports, with histopathological images used as supplementary documentation when accessible. Histopathological assessment was not standardised across participating centres.
Removal or modification of the implicated hairstyling accessory was recommended in all patients. Additional treatment was prescribed according to clinical judgement. Clinical outcomes were retrospectively classified, according to the available follow-up records, as partial regrowth, stable disease or worsening; outcome could not be determined in one patient for whom follow-up data were unavailable.

2.3. Statistical Analysis

Descriptive statistics were used to summarise demographic, clinical, trichoscopic and histopathological findings. Continuous variables were expressed as mean and range, and categorical variables as absolute frequencies and percentages. No inferential statistical analyses were performed because of the descriptive nature of the study and the small sample size.

3. Results

3.1. Patient Characteristics, Clinical Presentation and Mechanical Exposure

The study included 10 women with a mean age of 51.3 years (range, 36–65 years). All patients were Caucasian, with Fitzpatrick skin phototypes II–III. The mean duration of alopecia at the time of evaluation was 5.8 years (range, 1–20 years). Nine patients presented with a localised alopecic patch involving the vertex, whereas one patient had an interparietal alopecic patch. One patient presented with two adjacent patches measuring 2 and 3 cm; in the remaining patients, the mean largest diameter of the alopecic area was 5.5 cm (range, 3.5–7 cm). The alopecic patches were asymptomatic in all patients, except for patient 6, who reported occasional pruritus attributed to concomitant seborrhoeic dermatitis. Two patients had a concomitant hair disorder, androgenetic alopecia and fibrosing alopecia in pattern distribution, respectively, affecting the scalp according to the pattern typical of each condition, independently of the alopecic patch described here. Clinical and demographic patient characteristics are summarised in Table 1, and representative clinical presentations are shown in Figure 1.
Table 1. Clinical, trichoscopic, histopathological and treatment characteristics of the patients.
Figure 1. Clinical presentation of the ten patients ((A–J), corresponding to Patients 1–10 in Table 1, respectively). The alopecic patch was located on the vertex in nine patients (A–E,G–J) and on the posterior interparietal scalp in one patient (F).
In all patients, the alopecic area anatomically corresponded to the site of repeated exposure to a hairstyling accessory or practice. Four patients reported the use of hairpins, two used a hair clip positioned over the vertex, one wore a bun or ponytail resting on the interparietal scalp, one routinely used a hair roller that remained in place overnight, one wore a hair prosthesis secured with hairpins, and one reported the use of either a hair clip or a bun over the affected area. Figure 2 shows representative examples of the hairstyling accessories implicated in this series.
Figure 2. Representative examples of the hairstyling accessories implicated in this series: (A) hairpins; (B–D) hair clips: barrette clip (B), snap clip (C) and claw clip (D); (E) hair roller.
Before recognition of the association with hairstyling practices, the recorded diagnoses included alopecia areata, pressure alopecia, lichen planopilaris, female androgenetic alopecia and fibrosing alopecia in pattern distribution (Table 1).

3.2. Trichoscopic Findings

Vellus hairs were observed in all patients (10/10, 100%) and represented the only finding consistently present throughout the series. Short regrowing hairs, broken hairs and dystrophic (pili torti-type) hairs were observed in five patients (50%), black dots, coiled hairs and loss of follicular ostia in four (40%), bent hairs and yellow dots in three (30%), white structureless areas in two (20%), and perifollicular casts in one patient (10%). Haemorrhages were documented in one patient (10%), who had concomitant seborrhoeic dermatitis with scaling; scratching related to this associated condition could not be excluded as a contributing factor. Trichoscopic findings are summarised in Table 1, and representative images are shown in Figure 3.
Figure 3. Trichoscopic findings (A–F). (A) Vellus hairs (light blue asterisks), black dots (green arrows), broken hairs (purple arrows) and bent hairs (yellow arrows). (B) Coiled hairs (red asterisks), loss of follicular ostia (orange arrows) and broken hairs (purple arrows). (C) Dystrophic hairs/pili torti (pink asterisk), short regrowing hairs (dark blue arrows) and black dots (green arrows). (D) White structureless areas (white circles) and yellow dots (black arrows). (E) Dystrophic hairs/pili torti (pink asterisk). (F) Perifollicular casts (red circles).

3.3. Histopathological Findings

Scalp biopsy was performed in seven patients. Histopathological examination showed scarring alopecia in four patients (57.1% of biopsied patients) and non-scarring alopecia in three (42.9%). One patient with scarring alopecia had concomitant fibrosing alopecia in pattern distribution, and the histopathological findings could not be attributed exclusively to mechanical injury.
Among the findings documented in the available histopathological data, reduction or loss of terminal follicles with relative preservation or increase in vellus follicles was described in five patients. Mild perifollicular lymphocytic inflammation was reported in two patients. Reduced follicular density and follicular streamers were also described in one patient. The histopathological findings of individual patients are detailed in Table 1, and representative histopathological images are shown in Figure 4.
Figure 4. Histopathological findings (A–C). Longitudinal (A) and transverse (B) sections showing non-scarring alopecia, with loss of terminal follicles, relative increase in vellus follicles and mild perifollicular lymphocytic inflammation (haematoxylin-eosin [H&E]; ×20 [A], ×10 [B]). (C) Longitudinal section showing scarring alopecia, with loss of terminal follicles and preservation of vellus follicles (H&E; ×20).

3.4. Management and Clinical Outcomes

Removal or modification of the implicated hairstyling accessory or practice was recommended in all patients. Nine patients received topical or oral minoxidil, either alone or in combination with other treatments according to associated hair disorders and clinical judgement.
Partial hair regrowth was documented in four patients (40%), and four patients (40%) remained clinically stable. One patient (10%) experienced worsening of the alopecia while continuing to use a hair prosthesis secured with hairpins. Follow-up data were not available for one patient (10%), who had been using an overnight hair roller. One patient who remained clinically stable under oral minoxidil subsequently underwent hair transplantation, achieving satisfactory hair regrowth (Table 1).

4. Discussion

In this multicentre retrospective case series, we describe 10 patients with chronic localised alopecia anatomically corresponding to sites of repeated exposure to hairstyling accessories. The main findings were the consistent presence of vellus hairs, a heterogeneous trichoscopic pattern including signs of hair shaft damage and follicular involvement, and histopathological findings ranging from non-scarring to scarring alopecia. Taken together, these observations suggest that chronic exposure to hairstyling accessories may produce a heterogeneous pattern of mechanical follicular injury, potentially involving the combined effects of different mechanical forces. Previous reports have proposed overlapping mechanisms of pressure and traction in alopecia associated with partial hair systems, providing a clinical precedent for the coexistence of different mechanical mechanisms in the same patient [15]. Our findings extend this concept to a broader range of everyday hairstyling accessories and suggest that the resulting presentations may not consistently fit within the classical categories of pressure, traction or friction alopecia.
Pressure alopecia has traditionally been described after prolonged immobilisation during surgery or intensive care admission, where sustained pressure on the scalp may lead to local tissue ischaemia and subsequent follicular injury [5,10]. Notably, the vertex, together with the occiput, is among the most frequently reported sites of classical pressure alopecia [5,8,17], indicating that this mechanism does not require a poorly vascularised area but rather localised, sustained compression of the microvasculature at the point of contact. Depending on the intensity and duration of the mechanical insult, hair loss may be reversible or progress to permanent scarring alopecia [8]. However, subsequent reports have expanded this classical clinical setting by describing localised alopecia associated with external devices including orthodontic headgear, cervical collars and electroencephalographic monitoring equipment [6,9,18,19,20,21]. A recent review classified this externally applied form as type 1 pressure alopecia, distinguishing it from a second, less familiar pattern (type 2 pressure alopecia) associated with cosmetic injectables such as hyaluronic acid, calcium hydroxyapatite, autologous fat grafting or mesotherapy, in which pressure from the injected volume is thought to compress local vasculature without direct intravascular occlusion, rather than from an external device, underlining that the pressure mechanism itself is broader than the postoperative model usually taught [8]. These observations indicate that pressure-related follicular injury from external pressure is not restricted to prolonged immobilisation and may also occur in response to repeated or localised mechanical exposure. The cases in our series further extend this spectrum to hairstyling accessories used in everyday life: none of the patients had a history of prolonged immobilisation, whereas all presented with chronic localised alopecia anatomically corresponding to the site of repeated accessory exposure. Unlike the acute or subacute onset typically reported in postoperative pressure alopecia, where hair loss usually becomes apparent within a few days to four weeks of the precipitating exposure [8], the prolonged duration of alopecia in our patients suggests that chronic, lower-intensity mechanical exposure may produce a distinct clinical presentation that can remain unrecognised for years.
The mechanical forces generated by hairstyling accessories are unlikely to act in isolation and may vary according to the type of accessory, its position and fixation, and the duration and repetition of exposure. A hairpin or clip positioned against the scalp may exert local pressure while simultaneously transmitting traction to the attached hairs, with repeated contact between the accessory and the scalp also generating friction. This interpretation is supported by the anatomical distribution observed in our series, in which the alopecic patch consistently corresponded to the precise site of accessory contact rather than to the wider area from which traction-bearing hairs originated, a pattern more consistent with a substantial contribution of localised pressure and friction than with traction acting alone. Similarly, other hairstyling accessories and hairstyles, such as rollers, buns and hair systems, may generate different combinations of pressure, tension and friction. Notably, the accessories implicated in our series are in widespread use across different populations and are not among the high-risk hairstyling practices already identified in the literature [13], suggesting that chronic low-intensity mechanical exposure, rather than an inherently aggressive styling technique, may be sufficient to produce this pattern of injury. Previous reports have already questioned the strict separation between mechanical alopecias. Gil-Redondo et al. described a series of six patients with hair system-induced alopecia in whom distinguishing between traction and pressure as the predominant mechanism was difficult, proposing instead a combined mechanism of action [15], while other reports have proposed combined traction and pressure-induced ischaemia in patients developing scalp ulceration and alopecia after prolonged mechanical exposure [7]. A similar overlap between friction and pressure has been described outside the context of hairstyling, in breakdancers who perform headspins, where repeated friction between the scalp and the floor combines with sustained pressure from the weight-bearing nature of the movement [22,23]. Our findings further support this concept and suggest that, in some patients, mechanically induced alopecia may be better understood according to the combination and cumulative effects of the physical forces acting on the scalp rather than as strictly separate forms of pressure, traction or friction alopecia.
The trichoscopic findings observed in our series largely overlap with those previously described in different forms of mechanical alopecia (Table 2). Broken hairs, black dots, yellow dots, vellus hairs and short regrowing hairs have been reported in both pressure and traction alopecia, whereas hair casts are considered a characteristic feature of traction alopecia [3,17,24,25,26,27,28,29]. In a series of 25 patients with turban-related traction alopecia, yellow dots and broken hairs were each present in 68% of cases and hair casts in 28%, with hair casts becoming markedly less frequent as traction duration increased, a pattern the authors attributed to progressive replacement of ongoing follicular traction by established follicular dropout [25]. Likewise, friction-induced hair disorders are characterised by hair shaft damage, including trichorrhexis nodosa and broom hairs, together with broken hairs and scaling [14,30,31]. Dystrophic hairs have similarly been reported as a non-specific finding in both pressure and traction alopecia, generally without further morphological characterisation [17,26]. In our series, hairs classified under this category consistently showed axial shaft rotation compatible with pili torti; acquired pili torti has previously been attributed, among other causes, to repetitive mechanical trauma, providing a plausible mechanistic link to the repeated accessory contact described in our patients [24]. Collectively, these findings support the concept that the trichoscopic phenotype associated with hairstyling accessories cannot be attributed to a single mechanical mechanism, but rather reflects varying contributions of pressure, traction and friction, depending on the type of accessory, its position, fixation and chronicity of use.
Table 2. Overlap of trichoscopic features reported in pressure, traction and friction alopecia with those observed in hairstyling accessory-associated alopecia.
Interestingly, several patients also exhibited hairs showing a single abrupt angulation of the shaft without complete shaft fracture (descriptively referred to here as bent hairs), which we distinguished from the pili torti-type hairs described above. Angulation or bending of the shaft has previously been described in other hair shaft disorders, such as the irregular torsional twisting of pili torti, the regularly spaced nodosities of monilethrix, and the multiple sharp-angled bends of zigzag hairs, the last of which have been reported as a rare finding in tinea capitis, alopecia areata and other conditions causing focal weakening of the hair shaft [32]. The bent hairs identified in most of our patients showed a single, isolated abrupt angulation of the shaft; in one patient, however, several such angulations were observed along the same hair shaft, more closely resembling a zigzag pattern. We are not aware of the single-angulation morphology having been specifically described in the context of pressure, traction or friction alopecia. Repeated multidirectional mechanical stress exerted by hairstyling accessories may plausibly deform the hair shaft at a single point, giving rise to this appearance. Further studies are warranted to determine whether this represents a distinct, under-recognised trichoscopic feature of chronic mechanical alopecia.
Histopathological findings also support the concept of a mixed-pattern mechanical alopecia. Previous studies have shown considerable overlap between pressure and traction alopecias, particularly in the early stages, where increased catagen/telogen follicles, pigment casts, and trichomalacia are common findings resulting from mechanical injury to anagen follicles [1,7,33]. In pressure alopecia specifically, additional features described include necrosis of hair bulb cells and vascular congestion, together with a shift of 70–90% of follicles out of anagen into catagen or telogen without a reduction in total follicle number; in end-stage scarring lesions, absence of the follicular epithelium and sebaceous glands is expected [8,34]. A chronic inflammatory infiltrate, at times with a foreign body granulomatous component, has also been reported in this context [7,8,27,34].
Friction has been less specifically characterised histologically than pressure or traction injury. In the largest reported series of trichoteiromania, in which repeated rubbing of the scalp is the underlying mechanism, an inflammatory infiltrate and epidermal hyperplasia were the most common biopsy findings, present in over 85% of cases [14]. Trichoteiromania, however, results from active, self-inflicted rubbing rather than the passive, repetitive friction generated by a hairstyling accessory, and whether comparable epidermal changes occur in the latter context remains uncertain [14]. Trichomalacia, pigment incontinence and intrafollicular or perifollicular haemorrhage have similarly been described as shared histopathological features of hair shaft damage in traction alopecia and trichotillomania, although trichomalacia is not invariably present and, unlike trichotillomania, an inflammatory infiltrate is not observed at any stage of traction alopecia [35]. Chronic lesions may additionally show perifollicular fibrosis, reduced terminal follicle density and preservation of vellus follicles, with variable degrees of permanent follicular loss depending on the severity and duration of mechanical damage [1,26,27,36].
Our histopathological findings are consistent with this concept. Biopsies demonstrated reduced or absent terminal follicles with relative preservation or increase in vellus follicles in several patients, together with mild perifollicular lymphocytic inflammation and reduced follicular density with follicular streamers in isolated cases, while four patients had already developed unequivocal scarring alopecia. The coexistence of features suggestive of ongoing follicular injury with more chronic architectural changes, such as terminal follicle loss, supports the hypothesis that repeated exposure to hairstyling accessories may induce a progressive spectrum of follicular damage rather than a single histopathological pattern. Sano et al. proposed that headband-induced alopecia may result from the combined effects of pressure, traction and friction. Although their observations were limited to a single type of accessory, our findings extend this concept to a broader range of hairstyling accessories, suggesting that different accessories may produce a common mixed-pattern mechanical alopecia through varying combinations of these mechanical forces [7].
The pathogenesis of this entity is likely multifactorial and cannot be fully explained by a single mechanical insult. Rather than acting independently, pressure, traction and friction probably contribute simultaneously to follicular injury, with the relative contribution of each mechanism varying according to the type of accessory, its position on the scalp, the degree of fixation and the duration and repetition of exposure. Chronic pressure may impair local microcirculation and promote ischaemic injury to the hair bulb, a mechanism well established in postoperative and device-related pressure alopecia [5,10], while sustained traction generates repeated tensile stress on the follicular unit, leading to catagen/telogen shift and, if persistent, follicular dropout [1,26]. Friction, in turn, is thought to contribute a more cumulative form of hair shaft damage through repetitive surface contact rather than through a distinct follicular injury pathway of its own [4]. In our series, this combination is illustrated by the diversity of accessories implicated: a hairpin or clip pressed against the scalp, a bun or ponytail resting on the vertex, and an overnight roller (Figure 2) each plausibly generate a different balance of these three forces, which may account for the heterogeneity of the trichoscopic and histopathological findings observed across patients. Together, these mechanisms may ultimately converge towards a common clinicopathological phenotype of chronic mechanical alopecia. It should be emphasised, however, that trichoscopic and histopathological markers specific and exclusive to each individual mechanism are not well established, which precludes any reliable quantification of their relative contribution in individual patients. The mixed-pattern model proposed here should therefore be regarded as a clinicopathological framework requiring further validation, rather than as an established disease entity.
An additional observation supporting this hypothesis is the apparent variability in individual susceptibility. Although the use of hairstyling accessories is extremely common, only a small proportion of individuals appear to develop clinically significant alopecia. This is consistent with observations in classical pressure alopecia, where only 7–14% of patients undergoing surgery of comparable duration developed the condition despite an identical mechanical trigger [5], indicating that individual susceptibility can be a major determinant of clinical expression even under well-defined, high-intensity exposure. This suggests that accessory-related mechanical stress alone is unlikely to be sufficient and that individual factors, including scalp anatomy, hair characteristics, tissue resilience or local vascular susceptibility, may influence the threshold for irreversible follicular damage. Similar concepts have previously been proposed in traction alopecia, where anatomical features of the hair shaft and follicle, as well as a family history of male pattern baldness, have each been proposed as markers of individual predisposition to mechanical hair loss [1,28,37].
Recognising this presentation also requires distinguishing it from other causes of localised alopecia that can mimic its clinical appearance. In our series, patients had previously been diagnosed with alopecia areata, pressure alopecia, lichen planopilaris, female androgenetic alopecia and fibrosing alopecia in pattern distribution before the association with a hairstyling accessory was identified. Alopecia areata typically shows exclamation mark hairs and a positive pull test, features not present in our patients. Lichen planopilaris can occasionally present as a single vertex plaque, closely resembling the presentation described here; in such cases, perifollicular erythema and scaling are the most useful distinguishing trichoscopic features, and were not prominent findings in our series. Central centrifugal cicatricial alopecia, which occurs almost exclusively in women of African descent and follows a centrifugal pattern of scarring, is not consistent with the Caucasian ethnicity of our patients. Pseudopelade of Brocq is a diagnosis of exclusion with generally non-specific trichoscopic features and a clinical course that is independent of external triggers; unlike its expected natural history, most of our patients showed stabilisation or partial regrowth following removal of the implicated accessory, an outcome not anticipated if the accessory had played no causal role. Androgenetic alopecia, in turn, follows a diffuse pattern of distribution rather than a discrete, localised patch. Trichotillomania should also be considered in the differential diagnosis of localised alopecia, particularly given the overlap of some trichoscopic features such as broken hairs of variable morphology, black dots and coiled hairs. However, trichotillomania typically presents with an irregular, geometric patch border and hairs of markedly variable length reflecting repeated episodes of pulling. Furthermore, the consistent anatomical correspondence between the alopecic patch and the site of accessory contact in all patients, rather than a distribution determined by manual accessibility, argues against a primary self-inflicted mechanism.
A concomitant hair disorder was identified in only two of ten patients, with androgenetic and fibrosing alopecia in pattern distribution, respectively; no other alopecic disorder was documented in the remaining eight. In these two patients, we cannot fully exclude that the underlying condition contributed to, or lowered the threshold for, follicular injury, with the accessory acting as an additional, localised insult rather than the sole cause. A more localised patch that does not conform to the trichoscopic and distribution pattern of the underlying disorder should raise suspicion and prompt active questioning about hairstyling accessories.
A targeted history about habitual hairstyling accessories and hairstyles should form part of the assessment of any unexplained localised alopecia before biopsy is considered. Early recognition and avoidance of the causative accessory may prevent progression to irreversible scarring alopecia. In patients with persistent alopecia despite removal of the causative accessory and appropriate medical management, hair transplantation may be considered once the alopecia has stabilised.
This study has several limitations, including its retrospective design, limited sample size, and the lack of a standardised trichoscopic and histopathological protocol across centres, which may have led to under-recognition of some findings and limits comparison of their frequencies. Histopathological evaluation was not available in all patients, and the heterogeneity of the hairstyling accessories precluded comparison between individual accessory types. Data on systemic comorbidities, smoking or alcohol use, psychiatric history and family history of traction alopecia were not systematically collected; no significant comorbidities were documented in the available records, although this does not exclude undocumented conditions. As an observational study, a causal relationship between individual accessories and alopecia cannot be definitively established. Additionally, follow-up outcome data could not be retrieved for one patient. Nevertheless, the consistent anatomical correlation between the habitual site of accessory use and the alopecic area, together with the reproducibility of the clinical, trichoscopic and histopathological findings across five centres, supports a causal association. Further studies with prospective, standardised data collection are warranted to validate the proposed pathophysiological model and better define predisposing factors and optimal management strategies.

5. Conclusions

In conclusion, we describe a distinctive pattern of localised alopecia arising from the chronic use of hairstyling accessories. The concordance of clinical, trichoscopic and histopathological findings is consistent with a proposed mixed-pattern mechanical injury involving varying combinations of pressure, traction and friction, rather than a single classical mechanism. This trigger is common and easily overlooked, but avoidable once suspected; a specific history of habitual hairstyling practices should therefore be part of the assessment of localised alopecia. Further studies in larger series, with standardised clinical, trichoscopic and histopathological protocols, are needed to confirm this pattern, clarify the factors underlying individual susceptibility, and define optimal management once the diagnosis is made.

Author Contributions

Conceptualization, C.R.-d.B. and A.G.-Z.; methodology, C.R.-d.B.; formal analysis, C.R.-d.B.; investigation, C.R.-d.B.; writing—original draft preparation, C.R.-d.B.; writing—review and editing, C.R.-d.B., A.G.-Z., R.G.-R., J.F.M.-B., N.A.-S., D.V.-D. and J.M.R.-V. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki. Ethical review and approval were waived for this study due to its retrospective, observational design, which involved the analysis of de-identified clinical data and images collected during routine clinical practice, with no additional intervention or risk to the patients.

Data Availability Statement

The original, unedited images supporting the findings of this study are available from the corresponding author upon reasonable request, due to privacy and ethical restrictions related to identifiable clinical images and patient information.

Conflicts of Interest

Rocío Gil-Redondo the author is the employee of Grupo Pedro Jaén. Juan Francisco Mir-Bonafé the author is the employee of TricologiaMir. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Grupo Pedro Jaén and TricologiaMir had no role in the design of the study; in the collection, analyses or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Abbreviations

The following abbreviations are used in this manuscript:
AAAlopecia areata
LPPLichen planopilaris
FAGAFemale androgenetic alopecia
FAPDFibrosing alopecia in pattern distribution
NRNot reported/not systematically assessed
yYears
H&EHaematoxylin-eosin

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