**2. Traction alopecia**

#### **2.1. Introduction**

Traction alopecia (TA) is defined as loss of hair caused by repetitive or continuous and prolonged tension applied to the hair [26–28]. It was first described using the terminology *alopecia groenlandica* to refer to the hair loss attributed to tight ponytails which girls and women wear in Greenland [29]. Although TA is more prevalent among females of African ancestry, it has been described in a wide range of populations, including nurses, ballerinas, Sikh boys and men, to name a few [30–34]. Research has convincingly demonstrated that certain habitual practices of hairstyling are implicated in the pathogenesis of TA [35–39].

#### **2.2. Epidemiology**

Most of the population‐based studies concerning the prevalence of TA originate from South Africa [35–37]. Overall, TA was found to be more common in females compared to males and in women compared to girls, presumably due to a longer history of hairdressing [37]. Impor‐ tantly, in a large cohort of African adults in Cape Town, almost one‐third of women had findings consistent with TA on scalp examination [35]. Of note, 17.1% of South African schoolgirls had TA, with increasing prevalence rates from the first year of school to the last year of high school [36]. A similar rate (18.4%) was observed in another study examining a population of 201 African American girls from the United States [38]. In males, TA seems to be considerably less prevalent, however, two notable exceptions are Sikh boys and men, who adhere to the religious practice of tightly knotting their scalp and/or beard hair and boys/men wearing dreadlocks or cornrows [32–35, 40].

#### **2.3. Pathogenesis**

rating of hair pulling. Clomipramine was found to be more effective than placebo, although 3 of 10 participants receiving clomipramine dropped out because of drug‐related adverse effects

At last, in a recent meta‐analysis of 11 randomized trials, the efficacy of behavioral therapy and SSRI for the treatment of trichotillomania; the outcome measure was the standardized mean difference of change in hair pulling [22]. This publication demonstrated a large effect for behavioral therapy and only a moderate effect for SSRI. A greater treatment effect was reported

The side effects and limited efficacy of pharmacological treatment, especially in pediatric population and difficulty in long‐term maintenance of behavioral therapies require alternative options of treatment. The glutamatergic system dysregulation is involved in obsessive‐ compulsive disorders etiology and it has been reported that N‐acetyl‐cysteine (NAC) might have a therapeutic effect on these entities by acting on the glutamatergic system and reducing oxidative stress [23]. It was reported as a safe and effective treatment option given 1200 mg/d per os. The efficacy of the glutamate modulator NAC was evaluated in a small randomized trial including 50 adults with trichotillomania [24]. N‐acetylcysteine was more effective than placebo in reducing hair‐pulling symptoms as measured by the Massachusetts General Hospital Hair Pulling Scale. A subsequent trial in children and adolescents did not find any

Traction alopecia (TA) is defined as loss of hair caused by repetitive or continuous and prolonged tension applied to the hair [26–28]. It was first described using the terminology *alopecia groenlandica* to refer to the hair loss attributed to tight ponytails which girls and women wear in Greenland [29]. Although TA is more prevalent among females of African ancestry, it has been described in a wide range of populations, including nurses, ballerinas, Sikh boys and men, to name a few [30–34]. Research has convincingly demonstrated that certain habitual

Most of the population‐based studies concerning the prevalence of TA originate from South Africa [35–37]. Overall, TA was found to be more common in females compared to males and in women compared to girls, presumably due to a longer history of hairdressing [37]. Impor‐ tantly, in a large cohort of African adults in Cape Town, almost one‐third of women had findings consistent with TA on scalp examination [35]. Of note, 17.1% of South African schoolgirls had TA, with increasing prevalence rates from the first year of school to the last year of high school [36]. A similar rate (18.4%) was observed in another study examining a population of 201 African American girls from the United States [38]. In males, TA seems to

practices of hairstyling are implicated in the pathogenesis of TA [35–39].

[21].

228 Hair and Scalp Disorders

for clomipramine in two included trials [22].

beneficial effect of NAC compared with placebo [24, 25].

**2. Traction alopecia**

**2.1. Introduction**

**2.2. Epidemiology**

Traction alopecia is typically noncicatricial and reversible in its early stages, whereas it may progressively result in permanent scarring in the long term [27, 28, 41]. It is well recognized that traction causes an inflammatory, sometimes subclinical, folliculitis. The exact pathome‐ chanism leading from follicular inflammation to follicle damage and hair loss remains to be elucidated; however, follicular miniaturization is considered to play a possible role [28, 42–44].

#### **2.4. Predisposing factors**

The factors predisposing to the development of TA fall into two major categories: (1) traumatic hairstyling practices and (2) application of chemicals and/or heat to the hair [27]. It has been shown that the combination of both factors greatly increases the risk of TA, cautioning against the application of traction on chemically relaxed hair [36–38]. Importantly, hairdressing practices causing symptoms such as stinging, pain, or crusting are associated with an increased risk of TA [37, 39]. "Tenting" of the hair follicle, which manifests as elevation of the scalp skin due to tight pulling, has been interpreted as a sign of excessive tension [27, 39, 43]. A more recent literature review classified hairstyles into low risk, moderate risk and high‐risk [39]. Accordingly, the excessive use of very tight buns or ponytails belongs to the category of high‐ risk hairstyles, as do dreadlocks, cornrows and braids [38, 39, 45]. Another well‐recognized factor associated with TA is the use of hair extensions, especially if applied to relaxed hair [39, 46]. According to the aforementioned review, other hairstyles such as braids and/or weaves are considered high‐risk if they are combined with chemical relaxation of the hair [39]. Moreover, hairpins used to fix the nurse's cap to the scalp may be related to hair loss [30]. Alopecia initially presenting with a traumatic ulcer was described in association with hairstyles requiring multiple hairpins [47].

#### **2.5. Diagnosis**

#### *2.5.1. Clinical findings*

Two main categories of TA have been recognized: marginal and nonmarginal [46]. The for‐ mer is more common and typically presents as bandlike loss of hair along the temporopar‐ ietal margin or frontal hairline (**Figure 1**) [48]. Marginal TA is usually attributable to traumatic hairstyles, whereas nonmarginal TA may be caused by hairpins or buns [40, 47, 49]. A peculiar form of TA, termed "horseshoe pattern" by the authors, was described as a result of weft hair extensions [46]. Hair loss in nonmarginal localizations may sometimes present a diagnostic challenge and require more detailed history taking and/or histopatho‐ logical examination [27, 48].

**Figure 1.** Marginal traction alopecia along the frontal hairline **(A)** and temporoparietal margin **(B)** in a woman who applied excessive traction to her hair.

The earliest clinical sign of TA is considered to be perifollicular erythema in the areas of the scalp exposed to maximum tension, which may progress to folliculocentric papules and pustules. However, these initial findings may be unrecognized by the patient and physician alike [22, 28, 31]. The presentation may be acute or more commonly, chronic and progressive. Patients may provide a history of symptoms such as stinging or tenderness during hairdressing practices [27]. As noted earlier, the alopecia is typically nonscarring in the early stages, but may become irreversible later during the disease course, following a "biphasic" course [27]. Correspondingly, follicular markings tend to be decreased in the late stages of TA [27, 31, 43]. An important clinical caveat in the diagnosis of TA is the "fringe sign," defined as the presence of retained hairs along the frontal and/or temporal margin. This useful finding was observed in early and late stages of TA alike (**Figure 2**) [43].

In general, TA is considered to have no systemic associations. Nonetheless, there is an anecdotal report of a 25‐year‐old woman with prolonged traction resulting in a combination of TA, cutis verticis gyrata and intractable headache. Her headache resolved as she was advised to change her habitual hairstyle, which also stopped further hair loss [50].

**Figure 2.** "Fringe sign" demonstrated in a woman with longstanding traction alopecia as a group of retained hairs along the temporoparietal hairlines and located in front of the alopecic patches bilaterally.

#### *2.5.2. Dermoscopy*

**Figure 1.** Marginal traction alopecia along the frontal hairline **(A)** and temporoparietal margin **(B)** in a woman who

The earliest clinical sign of TA is considered to be perifollicular erythema in the areas of the scalp exposed to maximum tension, which may progress to folliculocentric papules and pustules. However, these initial findings may be unrecognized by the patient and physician alike [22, 28, 31]. The presentation may be acute or more commonly, chronic and progressive. Patients may provide a history of symptoms such as stinging or tenderness during hairdressing practices [27]. As noted earlier, the alopecia is typically nonscarring in the early stages, but may become irreversible later during the disease course, following a "biphasic" course [27]. Correspondingly, follicular markings tend to be decreased in the late stages of TA [27, 31, 43]. An important clinical caveat in the diagnosis of TA is the "fringe sign," defined as the presence of retained hairs along the frontal and/or temporal margin. This useful finding was observed

In general, TA is considered to have no systemic associations. Nonetheless, there is an anecdotal report of a 25‐year‐old woman with prolonged traction resulting in a combination of TA, cutis verticis gyrata and intractable headache. Her headache resolved as she was advised

to change her habitual hairstyle, which also stopped further hair loss [50].

applied excessive traction to her hair.

230 Hair and Scalp Disorders

in early and late stages of TA alike (**Figure 2**) [43].

Dermoscopy may be utilized as a useful aid to confirm the clinical diagnosis of TA and/or differentiate it from other entities presenting with hair loss. In a cross‐sectional study from Korea, broken hairs and black dots were observed in 100 and 92% of patients with TA, respectively. Of these findings, broken hairs were noted in all patients with trichotillomania, as well (**Figure 3**). Other dermoscopic findings associated with TA in this study were clustered short vellus hairs, yellow dots and atypical red vessels, with decreasing frequency [51]. The presence of hair casts has been emphasized as an important dermoscopic sign of TA, described as cylindrical structures encircling the proximal hair shafts [52]. It has been demonstrated that observation of hair casts on dermoscopic examination is an indicator of ongoing traction [53] and should be interpreted as a warning sign that hairstyle changes should be implemented to halt the progression of alopecia [52]. More recently, the trichoscopic finding of "flame hairs"was reviewed in a population of patients with various hair disorders. Of note, flame hairs were noted in slightly more than one half of the patients with trichotillomania, whereas they were observed in less than 5% of patients with TA. This disparity was attributed by the authors to the extent of the acute mechanical damage to the hair follicle being more prominent in trichotillomania compared to that in TA [54].

**Figure 3.** Broken and irregular coiled hairs, decreased hair density in dermoscopic examination.

**Figure 4.** (A) Perifollicular fibrosis on superficial dermis and an anagen follicule with hair shaft avulsion ‐ H&Ex100, **(B)** catagen/telogen hair follicules‐ H&Ex40, **(C)** intrafollicular erythrocytes and perifollicular fibrosis H&Ex400 and **(D)** an empty follicule with hair shaft avulsion H&E ×200.

#### *2.5.3. Histopathology*

Histologic findings of TA parallel the biphasic course of the disease mentioned previously [27]. Early stages of TA are considered to resemble trichotillomania, whereas more advanced stages of TA are similar to "burned‐out" forms of cicatricial alopecia [55]. More specifically, early TA is characterized by increased numbers of telogen and catagen hairs and trichomalacia. In contrast to primary scarring alopecias, sebaceous glands are generally preserved in TA (**Figure 4**). With prolonged traction, terminal follicles tend to decrease in number and are progressively replaced by fibrous tracts [27, 28, 43]. Furthermore, vellus‐sized hairs may be observed on histology which are thought to correspond to the aforementioned "fringe sign" noted on physical examination [27]. Differentiation of late‐stage TA from primary scarring alopecias may be challenging and it has been demonstrated that transverse sections may be advantageous compared to vertical sections in differential diagnosis [56].

#### **2.6. Differential diagnosis**

**Figure 3.** Broken and irregular coiled hairs, decreased hair density in dermoscopic examination.

**Figure 4.** (A) Perifollicular fibrosis on superficial dermis and an anagen follicule with hair shaft avulsion ‐ H&Ex100, **(B)** catagen/telogen hair follicules‐ H&Ex40, **(C)** intrafollicular erythrocytes and perifollicular fibrosis

Histologic findings of TA parallel the biphasic course of the disease mentioned previously [27]. Early stages of TA are considered to resemble trichotillomania, whereas more advanced stages of TA are similar to "burned‐out" forms of cicatricial alopecia [55]. More specifically, early TA is characterized by increased numbers of telogen and catagen hairs and trichomalacia. In contrast to primary scarring alopecias, sebaceous glands are generally preserved in TA (**Figure 4**). With prolonged traction, terminal follicles tend to decrease in number and are progressively replaced by fibrous tracts [27, 28, 43]. Furthermore, vellus‐sized hairs may be

H&Ex400 and **(D)** an empty follicule with hair shaft avulsion H&E ×200.

*2.5.3. Histopathology*

232 Hair and Scalp Disorders

The clinical differential diagnosis of TA depends on the distribution pattern of hair loss. For marginal type TA, the most important entities to be considered in the differential diagnosis are alopecia areata with an ophiasis pattern and frontal fibrosing alopecia [27, 43]. A notewor‐ thy caveat is that TA only affects scalp hair exposed to traction, whereas body hair, eyebrows and/or nails may be involved in alopecia areata or frontal fibrosing alopecia [27]. Another important differential diagnosis is androgenetic alopecia. These two conditions may also coexist and in fact androgenetic alopecia is thought to predispose an individual to the development of TA due to the miniaturized hairs [30, 40, 43]. Nonmarginal TA, on the other hand, may be considered within the differential diagnosis of a broad range of conditions, including alopecia areata, trichotillomania, telogen effluvium and discoid lupus erythemato‐ sus [40, 48].

Central centrifugal cicatricial alopecia (CCCA) is another condition mainly seen in females of African descent [57]. The relationship between traction/TA and CCCA remains controversial [58]. Ackerman and coauthors categorized CCCA as a form of TA, [59] and a retrospective comparative study detected a strong association between CCCA and the use of tractional hairstyles with artificial hair extensions [60]. However, a more recent study failed to reveal an association between CCCA and tractional hairstyles. Interestingly, among more than 1000 female participants, not a single individual had a concomitant diagnosis of CCCA and TA in the same study, suggesting that CCCA and TA may not be closely related [58].

#### **2.7. Prevention and treatment**

Prevention is an integral part of management of TA, as appropriate measures to eliminate traction can stop hair loss before it becomes permanent [27, 28, 61]. It is important to recog‐ nize that TA most often originates during childhood and adolescence, suggesting that public education should primarily focus on these at‐risk populations [27, 43, 44]. Prevention strat‐ egies have been detailed elsewhere [39, 44]. Briefly, management should rely on two main principles: preferring loose hairstyles and avoiding heat and chemicals [27, 39]. Patients may be encouraged to switch from high‐risk hairstyles to low‐risk hairstyles, such as loose buns and ponytails [39]. An important message is that pain during hairstyling be interpret‐ ed as a sign that excessive tension has been applied and that particular hairstyle should bet‐ ter be avoided [39, 44].

Medical or surgical treatment should only be considered after traction has been minimized [39]. There is a paucity of evidence‐based literature data with regard to the medical treat‐ ment of TA. Topical or intralesional corticosteroids and topical or systemic antibiotics may be utilized to suppress the inflammation in the early stages of the disease [61].Topical min‐ oxidil was described as effective in an anecdotal report [42] and recommended by some au‐ thors [27, 43, 61], although controlled trials are lacking. An interesting study demonstrated the protective effect of piloerection induced by topical phenylephrine against the develop‐ ment of TA, suggesting a potential role of α1‐adrenergic receptor agonists in the treatment of TA [41]. For extensive TA, surgical treatment has been described [45, 62]. Of note, a scoring system was developed ("M‐TAS score") to evaluate the severity of marginal type TA and facilitate assessment of treatment effectiveness [63].
