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Evaluation and diagnosis of hair loss

Evaluation and diagnosis of hair loss
Literature review current through: Jan 2024.
This topic last updated: Oct 04, 2023.

INTRODUCTION — "Hair loss" is a common clinical complaint that is a manifestation of a wide variety of disorders. Although the cause of hair loss is easily diagnosed in some cases, such as in patients who present with classic male pattern hair loss or patchy hair loss due to alopecia areata, the diagnosis of hair loss also can be challenging.

An overview of the basic principles of hair biology, potential causes of hair loss, and the assessment of patients who present with a complaint of hair loss is provided here. Specific types of hair disorders are reviewed in greater detail separately.

(See "Acne keloidalis nuchae: Pathogenesis, clinical manifestations, and diagnosis".)

(See "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis".)

(See "Central centrifugal cicatricial alopecia".)

(See "Alopecia related to systemic cancer therapy".)

(See "Alopecia areata: Clinical manifestations and diagnosis".)

(See "Dissecting cellulitis of the scalp".)

(See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis".)

(See "Folliculitis decalvans".)

(See "Lichen planopilaris".)

(See "Telogen effluvium".)

(See "Tinea capitis".)

(See "Traction alopecia".)

(See "Hair shaft disorders".)

HAIR BIOLOGY

Anatomy — The human scalp contains approximately 100,000 to 150,000 hair follicles [1]. Each hair follicle sits above a dermal papilla, a collection of mesenchymal tissue with inductive properties (figure 1). The dermal papilla induces the development of hair follicles in the fetus and appears to play an important role in follicular cycling and hair growth [2]. (See 'Hair cycle' below.)

Hair follicles consist of four segments: the bulb, suprabulbar region, isthmus, and infundibulum (figure 1) [3]. The bulb, the lowest portion of the hair follicle, is the site of the hair matrix, a group of rapidly proliferating keratinocytes responsible for the production of hair [2]. The suprabulbar region of the follicle extends from the bulb to the isthmus, which is the portion of the follicle between the insertion of the arrector pili muscle and the insertion of the sebaceous gland. The uppermost portion of the follicle, the infundibulum, extends from the insertion of the sebaceous gland to the interfollicular epithelium.

The hair shaft is a layered structure that consists of three major components. The medulla, the innermost layer, is surrounded by the cortex and cuticle. Between the hair bulb and the isthmus, the hair shaft is surrounded by the inner root sheath, a structure that is composed of the cuticle of the inner root sheath, Huxley layer, Henle layer, and companion layer. The inner root sheath plays an important role in the shaping of the hair shaft [2]. The outer root sheath surrounds both the inner root sheath and the hair shaft and extends from the hair bulb to the epidermis. The outer root sheath and each of the components of the hair shaft and inner root sheath have distinct keratin profiles [4].

A region near the insertion of the arrector pili muscle, referred to as the bulge region of the hair follicle, has been identified as a site that harbors hair follicle stem cells that are essential for follicular cycling and hair growth [5]. The loss of the hair follicle stem cells in the bulge is postulated to contribute to permanent loss of hair in cicatricial alopecias (see 'Cicatricial alopecia' below) [5,6]. Mouse studies have demonstrated that hair follicle stem cells may also support wound healing by contributing to repopulation of interfollicular epithelial cells [7].

Hair types — The two major types of hair follicles on the human body are terminal hair follicles and vellus hair follicles. Terminal hair follicles are larger than vellus hair follicles and extend into the subcutaneous fat (2 to 5 mm from the skin surface) during hair growth. In contrast, the lowest portions of vellus hair follicles generally extend only into the reticular dermis. Hairs produced by terminal hair follicles are usually at least 0.06 mm in diameter while vellus hairs are short, fine, and usually less than 0.03 mm in diameter [8]. The term "intermediate hairs" has been used to describe hairs with characteristics that are between vellus and terminal hairs (0.03 to 0.06 mm) [9,10].

At birth, terminal hairs are found on the scalp, eyebrows, and eyelashes, and vellus hairs populate the remaining hair-bearing areas. During puberty, vellus hairs in certain areas, such as the genital area and axilla, are stimulated to become terminal hairs. Transitioning between terminal and vellus hair follicles may also occur in pathologic states. Abnormal transitioning of vellus hairs to terminal hairs occurs in hirsutism in women, and transitioning of terminal hairs to vellus hairs (follicular miniaturization) is a classic feature of androgenetic alopecia. (See "Pathophysiology and causes of hirsutism" and "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis" and "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis".)

Hair cycle — Once formed, hair follicles undergo lifelong cycling characterized by periods of growth (anagen), transformation (catagen), and rest (telogen). In humans, hair cycling is not synchronous, meaning that individual follicles cycle independently, preventing en mass shedding of hair. Although the lower portion of the hair follicle undergoes growth and regression during cycling, the isthmus and infundibulum remain stable:

Anagen – At any given time, approximately 90 percent of scalp hair follicles are in the anagen phase [11]. The rate of hair growth and the duration of anagen vary with the type of hair and location. On the scalp, the growth rate of terminal hair is approximately 0.3 mm per day and the duration of anagen ranges from two to six years [9,11]. In contrast, eyebrow hair grows only at a rate of 0.1 mm per day and has an anagen phase of two to three months [2,9]. The abbreviated anagen phase accounts for the relatively short maximum length of eyebrow hair. Similarly, a short anagen phase is responsible for the short maximum length of vellus hairs (typically less than 20 mm) [8].

Catagen During catagen, the lower portion of the hair follicle regresses and hair production ceases. The deepest part of the hair follicle tracts upward toward the isthmus, and the dermal papilla migrates from within the subcutaneous fat into the reticular dermis. The duration of catagen on the scalp is usually around three weeks [9]. Less than 1 percent of follicles on the scalp are in catagen [11].

Telogen – The telogen phase, also known as the resting phase, follows catagen and lasts for two to three months on the scalp [11]. Normally, up to 10 percent of scalp follicles are in telogen [11]. Telogen is characterized by the presence of a club hair (a fully keratinized hair with a club-shaped proximal end) that is ready for shedding from the hair follicle (picture 1) [2]. The term "exogen" has been used to describe the exact time point at which the hair is shed. Normally, between 50 and 150 telogen hairs are shed per day [2].

Anagen follows the telogen phase, resulting in the production of a new hair. Prolongation of the telogen phase, as may occur in telogen effluvium, can result in a reduction in hair density due to a failure of follicles to reenter anagen following shedding. The term "kenogen" has been used to describe a delay in the entry into anagen following shedding of a telogen hair [12].

CLASSIFICATION — Hair loss disorders are a large, heterogenous group of conditions that have various clinical features, pathologic findings, and etiologies. Hair loss may occur due to disorders of hair cycling, inflammatory conditions that damage hair follicles, or inherited or acquired abnormalities in hair shafts.

The major dividing lines for the various forms of hair loss are the distinction between cicatricial (scarring) alopecia, nonscarring alopecia, and structural hair disorders. Cicatricial alopecias are conditions that lead to the irreversible cessation of hair cycling and permanent hair loss. As noted above, the loss of hair follicle stem cells in the bulge region of the hair follicle is thought to contribute to the development of cicatricial alopecia (see 'Anatomy' above). In nonscarring alopecias, the hair follicle is not permanently damaged, making spontaneous or treatment-induced regrowth a possibility. Structural hair disorders that lead to hair loss demonstrate abnormalities within the hair shafts that result in hair fragility. (See 'Scalp and hair examination' below.)

Cicatricial alopecia — Primary cicatricial alopecias are inflammatory disorders of the scalp that lead to permanent hair loss. The primary cicatricial alopecias are subdivided by the type of inflammation detected on histologic examination. The three major classes are lymphocytic primary cicatricial alopecias, neutrophilic primary cicatricial alopecias, and mixed primary cicatricial alopecias [13].

Examples of the primary cicatricial alopecias are provided below. A summary of the clinical and histologic features of the cicatricial alopecias is provided in a table (table 1A):

Lymphocytic primary cicatricial alopecia:

Alopecia mucinosa Alopecia mucinosa (also known as follicular mucinosis) may result in scarring or nonscarring alopecia. Permanent hair loss results from the replacement of hair follicles by mucin, rather than from fibrosis. Patients usually present with erythematous or skin-colored indurated plaques of alopecia on the face or scalp (picture 2). Follicular papules may also be present.

Two types of alopecia mucinosa have been described, idiopathic alopecia mucinosa and alopecia mucinosa that occurs as a manifestation of mycosis fungoides or cutaneous T cell lymphoma. However, some authors believe that these disorders may represent aspects of a single disease spectrum [14]. Whether all cases designated as idiopathic alopecia mucinosa are actually indolent forms of mycosis fungoides remains uncertain [15]. (See "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides".)

Central centrifugal cicatricial alopecia – Central centrifugal cicatricial alopecia is a form of cicatricial alopecia that primarily affects women of African descent. Alopecia occurs on the crown of the scalp and gradually progresses in a centrifugal manner to the parietal areas (picture 3). Perifollicular hyperpigmentation and the emergence of multiple hairs from a single follicle may be present. Symptoms may include itching, tenderness, or prickling sensations [14]. (See "Central centrifugal cicatricial alopecia".)

Discoid lupus erythematosus – Discoid lupus erythematosus (also known as a form of chronic cutaneous lupus erythematosus) may occur in the absence of systemic disease but may also occur in the setting of systemic lupus erythematosus. Patients typically present with well-demarcated inflammatory plaques that develop into atrophic scars (picture 4A-B). Follicular hyperkeratosis (follicular plugging, aka patulous follicles), telangiectasias, hypopigmentation, and hyperpigmentation are common clinical features [16]. When the scalp seems to be the primary site of involvement, examination of the conchal bowls for patulous follicles can aid in differentiating discoid lupus erythematosus from other forms of scarring alopecia. (See "Overview of cutaneous lupus erythematosus", section on 'Discoid lupus erythematosus'.)

Keratosis follicularis spinulosa decalvans (KFSD) Keratosis follicularis spinulosa decalvans is a rare genetic disorder that commonly is associated with a mutation in the membrane-bound transcription factor protease site 2 (MBTPS2) gene on the X-chromosome (MIM #308800) [17]. Familial cases of KFSD that demonstrate an autosomal dominant inheritance pattern have also been reported (MIM #612843) [18,19]. Patients first present in infancy with follicular papules with keratotic spines on the scalp. Eyebrow, eyelash, and other involvement of hair-bearing skin may develop (picture 5A-B). Photophobia is common [18]. Progression of the disease improves during puberty, leaving atrophic scars. (See "Keratosis pilaris atrophicans", section on 'Keratosis follicularis spinulosa decalvans'.)

Lichen planopilaris – Lichen planopilaris is a follicular variant of lichen planus that typically manifests with perifollicular erythema and follicular hyperkeratosis (picture 6A-B) [20]. The areas of alopecia may be discrete or confluent, especially on the crown. Itching, burning, pain, or skin sensitivity are often present. (See "Lichen planopilaris".)

Frontal fibrosing alopecia – In this disorder, patients present with band-like alopecia affecting the frontal scalp. Follicular hyperkeratosis and perifollicular erythema may be seen. Concomitant eyebrow involvement is common and may precede the hair loss [21]. Facial involvement may manifest as small rough follicular papules that have a predilection for the temporal area [22]. (See "Lichen planopilaris", section on 'Frontal fibrosing alopecia'.)

Pseudopelade of Brocq Pseudopelade of Brocq is an idiopathic cicatricial alopecia that presents with small, skin-colored patches of alopecia on the scalp [16]. The pattern of the disorder has been described as "footprints in the snow" [23]. Follicular hyperkeratosis and erythema are minimal or absent. Some clinicians believe pseudopelade of Brocq is a late stage of lichen planopilaris.

Neutrophilic primary cicatricial alopecia:

Dissecting cellulitis of the scalp – Dissecting cellulitis of the scalp (also known as perifolliculitis capitis abscedens et suffodiens of Hoffman or dissecting folliculitis) is a form of cicatricial alopecia that may occur independently or in association with acne conglobata and hidradenitis suppurativa as part of the "follicular occlusion triad." The condition most commonly occurs in young Black men [24]. Patients develop follicular papules, pustules, fluctuant nodules, and abscesses on the scalp (picture 7A-B). Purulent drainage is common. Over time, hypertrophic or keloidal scars may develop.

Folliculitis decalvans – Folliculitis decalvans often begins on the vertex of the scalp. Patches of alopecia, inflamed papules, pustules, and follicular hyperkeratosis are common features (picture 8A-B) [25]. Tufted folliculitis (multiple hairs emerging from a single inflamed follicle) is a characteristic feature, but is not exclusive to this disorder. Pain, itching, and burning are common. Staphylococcus aureus colonization and a defect in host cell-mediated immunity may be contributing factors [25]. (See "Folliculitis decalvans".)

Mixed:

Acne keloidalis nuchae – Acne keloidalis nuchae primarily occurs in young Black men [26]. Affected patients present with dome-shaped follicular papules, pustules, and plaques on the occipital scalp (picture 9). Keloid-like plaques also may develop. (See "Acne keloidalis nuchae: Pathogenesis, clinical manifestations, and diagnosis".)

Acne necrotica Acne necrotica is a rare form of cicatricial alopecia that is characterized by the development of umbilicated papules on the scalp that undergo central necrosis. Patients usually experience pruritus or pain. Individual lesions resolve with small varioliform or pox-like scars [27,28].

Erosive pustular dermatosis of the scalp Erosive pustular dermatosis of the scalp is a rare disorder that primarily occurs in older adults. The condition often develops after trauma or surgery on the scalp [29,30]. It may also develop after treatment of actinic keratoses with topical agents or photodynamic therapy [31]. Patients develop sterile pustules, erosions, and crusted plaques on the scalp that lead to scarring (picture 10) [29,30].

A wide variety of conditions or events may cause secondary cicatricial alopecia. Inflammation from a condition that is not a primary scalp disease and physical trauma are potential causes. Examples include tinea capitis, neoplasms, radiation therapy, and surgical scars. (See "Tinea capitis".)

Nonscarring alopecia — In nonscarring alopecias, clinical signs of inflammation are usually mild or absent and destruction of the hair follicle does not occur. Recognition of the distribution of nonscarring alopecia is useful for narrowing the differential diagnosis (table 1B):

Focal hair loss:

Alopecia areata – Alopecia areata is a relatively common form of nonscarring alopecia in which an autoimmune process contributes to the loss of hair on the scalp or other areas. Most frequently, hair loss occurs in patches (picture 11A-B). Another common pattern is loss at the occipital scalp margin, called ophiasis. Occasionally, alopecia areata progresses to loss of all scalp or body hair. A diffuse variant of alopecia areata that manifests with diffuse hair thinning also occurs. (See "Alopecia areata: Clinical manifestations and diagnosis".)

Alopecia syphilitica – Secondary syphilis can present with patchy hair loss on the scalp, which has been described as "moth-eaten" alopecia (picture 12). Hair loss may also occur in other sites. (See "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV", section on 'Clinical manifestations'.)

Pressure-induced (postoperative) alopecia Pressure-induced alopecia describes transient hair loss that occurs in areas of prolonged pressure on the scalp, as may occur during general anesthesia for long operative procedures [32,33]. Hair loss usually develops a few weeks after the event. Regrowth occurs in most patients.

Temporal triangular alopecia Temporal triangular alopecia (also known as congenital triangular alopecia) is a lifelong condition that is usually first noted in infancy or childhood as a triangular or oval patch of alopecia in the temporal area (picture 13) [34,35]. The area of involvement is usually only a few centimeters in diameter. Most cases are unilateral, though bilateral involvement may also occur. Fine vellus hairs are visible in the affected area with close inspection. Hair transplantation is an effective treatment [36,37].

Traction alopecia – Traction alopecia results from prolonged pull or tension on the hair follicle, usually due to hairstyles such as tight ponytails or braids. Traction alopecia from braids or hair weaves is most commonly detected along the frontal and temporal hair lines (picture 14). Longstanding traction can result in a transition to cicatricial alopecia with permanent hair loss. (See "Traction alopecia".)

Patterned:

Androgenetic alopecia in men (male pattern hair loss) – Androgenetic alopecia in men is characterized by the slow, progressive loss of hair in a characteristic distribution (picture 15A-C). The condition is mediated by the action of androgens on androgen-sensitive hair follicles in genetically susceptible males. (See "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis".)

Female pattern hair loss – Female pattern hair loss most frequently presents as hair thinning on the frontal and crown areas of the scalp with relative sparing of the occipital scalp (picture 16A-B). The frequency of this condition increases with age. (See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis".)

Trichotillomania Trichotillomania is a disorder in which individuals repeatedly pluck hairs from the scalp or other hair-bearing areas (picture 17A-C) [38]. The areas of alopecia may have irregular, bizarre shapes.

Diffuse:

Anagen effluvium Anagen effluvium occurs as a result of an acute interruption of the anagen phase and leads to extensive hair loss without transition of follicles into the catagen or telogen phase. Hair loss typically occurs within two weeks of an inciting event. Chemotherapeutic agents are a major cause of anagen effluvium. (See "Alopecia related to systemic cancer therapy".)

Loose anagen syndrome Loose anagen syndrome usually presents in young children (ages two to five years) as slowly growing hair that can easily be pulled out without pain [39]. The hair density may appear normal or reduced (picture 18). Affected children are often females with blond hair. Loose anagen syndrome is characterized by the light microscopic finding of anagen hairs with a ruffled cuticle and an absent inner root sheath (picture 19). The condition often improves with age and may be sporadic or familial.

Telogen effluvium Telogen effluvium is a common cause of diffuse hair loss that usually presents with acute or chronic loss of hair due to an abrupt shift of numerous hair follicles in anagen to the telogen phase (picture 20A-B). Chronic telogen effluvium may also occur. Examples of factors that may stimulate acute telogen effluvium include major physical or psychologic stressors, childbirth, dietary restriction, and medications. Hair loss usually occurs two to three months after the inciting event. Arsenic, thallium, or mercury poisoning can also result in telogen effluvium [40]. (See 'Medical and family history' below.)

Other Alopecia areata and female pattern hair loss may present with diffuse hair thinning. Additional rare causes of diffuse nonscarring hair loss include atrichia with papular lesions (MIM #209500), a condition caused by a mutation in the hairless gene that results in hair loss within the first year of life (picture 21) [41], and hypotrichosis simplex. Hypotrichosis simplex consists of a group of hereditary alopecias in which diffuse hair loss usually begins in early childhood and progresses until adulthood [42]. Multiple gene mutations have been linked to this condition [42].

Nonscarring alopecia may also occur as a direct consequence of scalp involvement with acute or chronic inflammatory skin diseases. As examples, psoriasis, atopic dermatitis, seborrheic dermatitis, and contact dermatitis may result in focal or diffuse hair loss. In addition, patients with systemic lupus erythematosus may develop "lupus hair," which is described by dry, coarse hair along the frontal hair line that usually occurs in association with disease flares [43]. Patients with systemic lupus erythematosus may also develop telogen effluvium as a consequence of disease exacerbations or medical treatments [43].

Inherited and acquired structural hair disorders — Structural hair abnormalities that result in brittle or fragile hair can lead to hair breakage or the appearance of a failure of hair to grow. The hair fragility may result from abnormal hair formation or external insults that damage the hair shaft. The most common structural hair abnormalities are acquired trichorrhexis nodosa and trichoptilosis, both of which may occur as a result of harmful hair care practices, such as chemical processing, excessive brushing or teasing of hair, or the application of excessive heat. Trichorrhexis nodosa is characterized by disruption of the protective cuticle and fraying of the hair shaft (picture 22A). Trichoptilosis is a term that describes splitting and fraying of the distal end of the hair shaft, which is commonly referred to as "split ends." Bubble hair (bubble-like structures within the hair shaft) is another microscopic finding that may be seen in heat-damaged hair. (See "Hair shaft disorders".)

Examples of genetic conditions that cause hair fragility and excessive hair breakage include:

Menkes disease Patients with Menkes disease (MIM #309400), an X-linked disorder associated with a defect in copper transport, develop hair fragility that is most prominent during childhood. The mutation is in the gene encoding a copper transporting ATPase (ATP7A) [44]. Sparse, short, and brittle hair with a kinky or steel wool-like quality is present (picture 23). Microscopic examination of the hair shaft reveals pili torti (flattened, twisted hair) (picture 22C). Pili torti may also be seen as an isolated congenital disorder or a manifestation of other genetic conditions. (See "Overview of dietary trace elements", section on 'Menkes disease'.)

Monilethrix Monilethrix (MIM #158000) is a genetic condition that is usually associated with an autosomal dominant pattern of inheritance. Most cases occur due to mutations in the hair cortex keratin genes, KRT81, KRT83, or KRT86 [45]. Patients present with short, brittle hair (picture 24). Microscopic examination of the hair shaft reveals elliptical nodes, resulting in a beaded appearance (picture 22D). Examples of other potential findings in monilethrix include brittle nails, keratosis pilaris, cataracts, and tooth abnormalities.

Trichothiodystrophy Trichothiodystrophy (MIM #601675) is an autosomal recessive disorder that manifests with sulfur-deficient, short, brittle hair (picture 25). Microscopic examination of the hair reveals trichoschisis (transverse fractures of hair) (picture 22B). Examination of the hair shaft under polarized light demonstrates alternating light and dark bands that resemble a "tiger tail" pattern. Patients may have accompanying features such as photosensitivity, ichthyosis, intellectual impairment, decreased fertility, and short stature. Mutations in the XPD, XPB, and p8/TTDA subunits of the transcription/repair factor TFIIH have been linked to trichothiodystrophy with photosensitivity [46].

Trichorrhexis invaginata Trichorrhexis invaginata (also known as "bamboo hair" or "ball and socket" deformity) is a hair shaft disorder that results from intussusception within the hair shaft (picture 22E). Trichorrhexis invaginata is a pathognomonic finding of Netherton syndrome (OMIM #256500), but may also occur as a sporadic disorder or in combination with other hair shaft disorders. (See "Netherton syndrome".)

Individuals with Netherton syndrome (OMIM #256500), an autosomal recessive disorder, develop atopy, ichthyosis (ichthyosis linearis circumflexa), and short, sparse hair (picture 26A-B). Mutations in the SPINK5 gene encoding the serine protease inhibitor lymphoepithelial Kazal-type related inhibitor (LEKTI) lead to this disorder [47]. Clinicians should be aware that trichorrhexis invaginata is not evident in every hair. Multiple hairs may need to be examined before trichorrhexis invaginata is detected.

Examples of other rare inherited conditions that may result in hair fragility include inherited trichorrhexis nodosa, Björnstad syndrome, ectodermal dysplasias, and argininosuccinic aciduria.

Structural hair disorders may also occur without associated hair fragility. Examples include pili annulati, uncombable hair syndrome (picture 27), and woolly hair.

PATIENT INTERVIEW — The patient interview, if performed carefully, can provide valuable clues for diagnosis. In general, the interview should include an assessment of the nature of hair loss, the patient's medical history (including medication and supplement use), the patient's hair care practices, and the patient's family history as it relates to hair loss and potential causes of hair loss.

Description of hair loss — Questioning about the nature of hair loss consists of an assessment of the course and pattern of hair loss, as well as associated symptoms. This can be particularly helpful for narrowing the differential diagnosis in patients with physical findings that suggest nonscarring alopecia:

Duration and rate of progression of hair loss – Knowledge of the duration and progression of hair loss is useful for differentiating between congenital and acquired disorders, and between acute, chronic, or transient conditions.

Location and pattern of hair loss In conjunction with the physical examination, the patient's description of the distribution of hair loss may help to distinguish focal, patterned, and diffuse hair loss (see 'Nonscarring alopecia' above). Since some disorders characterized by scalp hair loss may involve other hair-bearing areas, patients should also be asked about the presence of additional sites of hair loss.

Extent of hair loss When evaluating patients with a complaint of diffuse hair loss, the knowledge that normal hair loss ranges from 50 to 150 hairs per day is useful for comprehending the magnitude of the patient's complaint [2]. Of note, for patients who shampoo hair infrequently, marked increases in hair loss may be noted on shampoo days due to the manual dislodging of telogen hairs that would have been progressively shed with more frequent manipulation of the hair.

Patient descriptions of physical changes noted (eg, a thinning ponytail or increased visibility of the scalp through hair) and review of prior photographs also may be useful for assessing the degree of hair loss. On average, a 30 percent decrease in hair density occurs before hair loss is easily appreciated by individuals other than the affected patients [43]. In particular, patients with thick, coarse hair at baseline may not appear to have clinically concerning hair loss until a major reduction in hair density has occurred.

Associated symptoms Although symptoms such as pain, tenderness, pruritus, or burning sensations are not always consistently detected in specific types of hair loss, the recognition of associated symptoms can be useful for supporting a diagnosis. In addition, in patients who appear to have a form of hair loss that is typically asymptomatic, the presence of symptoms may indicate the presence of an additional disorder (eg, pruritus from seborrheic dermatitis in a patient with androgenetic alopecia).

Differentiation of hair shedding from hair breakage Patients who are focused on their hair loss may be able to communicate information that helps to distinguish hair shed from the follicle from hair breakage. Patients with disorders associated with shedding of telogen hairs from follicles may describe the hair loss as occurring from "the roots," meaning that they have noticed a small white bulb at the proximal end of lost hairs (picture 1). In contrast, the follicular portion of the hair shaft is absent in broken hairs.

Hair care practices – Questions about hair care practices are particularly relevant in patients with features suggestive of hair breakage or traction alopecia. Hair care practices that damage the hair shaft are a common cause of hair breakage and prolonged traction of hair by tight braids, ponytails, or other means can lead to traction alopecia.

Medical and family history — Questions about the patient's medical and family history may be useful for diagnosis. As an example, for women with clinical features suggestive of patterned hair loss, questions about irregular menses, hirsutism, infertility, and signs of virilization may provide clues about an underlying hormonal disorder as a contributor to the condition. (See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis", section on 'Diagnosis' and "Evaluation of premenopausal women with hirsutism" and "Diagnosis of polycystic ovary syndrome in adults".)

In addition, telogen effluvium, one of the most common causes of nonscarring hair loss, may be induced by factors that can be detected via a medical history (see "Telogen effluvium"). Potential contributing factors include [40]:

Drugs (table 2)

Poor diet (caloric or protein restriction)

Medical disorders and medical events:

Major illness or surgeries

Major psychologic stress

Significant weight loss

Chronic iron deficiency

Thyroid disorders

Childbirth

Poisoning from arsenic, mercury, or thallium

The clinical history may also be useful when a diagnosis that may present with associated clinical findings is being considered. Examples of questions that may be useful include inquiries about a history of lichen planus in a patient with lichen planopilaris and questions about a history of hidradenitis suppurativa or severe acne in a patient with dissecting cellulitis of the scalp. (See "Lichen planus", section on 'Clinical features' and "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)

Obtaining a family history of similar hair loss can be useful because genetics play a role in susceptibility to multiple hair diseases. Sometimes patients will deny a family history of hair loss because their parents were not fully bald. Asking about both hair thinning and balding is helpful for identifying a family history of alopecia.

PHYSICAL EXAMINATION — The physical examination of the patient with a complaint of scalp hair loss involves the examination of the scalp, hair, and other body sites.

Scalp and hair examination — Ideally, the scalp and hair examination should be performed with the patient in a position that allows the clinician to examine the scalp from above comfortably, such as the clinician in a standing position and the patient seated in a chair. Good lighting is essential. Examination techniques such as trichoscopy and the hair pull test may be helpful.

Visual inspection — The first step of the physical examination consists of inspection of the entire scalp for physical clues that may aid with diagnosis, such as erythema, scales, papules, pustules, erosions, or excoriations. The presence or absence of follicular ostia (the pinpoint openings from which hair emerges from the scalp) within affected areas also should be noted; a lack of follicular ostia suggests a scarring alopecia. Among the primary cicatricial alopecias, pustules are most likely to be seen in neutrophilic or mixed cicatricial alopecias.

The examination of the hair should include an assessment of the distribution and density of hair on the scalp to identify the pattern and degree of hair loss. Hair density is best assessed by parting the hair and noting the amount of space between the parts [48]. Comparing the frontal hair density to the occipital hair density is particularly useful for female pattern hair loss. In female pattern hair loss, hair density on the frontal and vertex scalp is reduced, while hair on the occipital scalp is relatively spared. A Christmas-tree-like pattern of hair loss (with a wider part at the frontal hairline) is often evident in the involved area (picture 16A-B). (See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis", section on 'Physical examination'.)

The hair shafts are then evaluated for caliber, length, shape, fragility, and texture. Distinguishing between terminal and vellus hairs is particularly helpful for the diagnosis of male and female pattern hair loss, disorders in which terminal hairs transition to vellus hairs. Broken hairs, which suggest a structural hair disorder, may also be noted during this step. Hair fragility can be further assessed by grasping a cluster of hair fibers in two places and tugging in opposite directions [48].

Features associated with certain forms of hair loss may also be detected during examination of the hair and may aid in diagnosis. Examples include exclamation point hairs in alopecia areata (picture 28), tufted folliculitis in folliculitis decalvans and other cicatricial alopecias (picture 8B), follicular plugging in discoid lupus erythematosus (picture 4A), and keratotic follicular papules in lichen planopilaris (picture 6B).

A tool that can be helpful during the hair examination is a small piece of white or black paper. The color should contrast with the color of the patient's hair (eg, white paper for a patient with dark hair). Placing the paper behind the hairs being examined facilitates visualization of the hairs [48]. This procedure also is helpful for differentiating the tapered tips of regrowing hairs from the blunt tips of broken or cut hairs.

Trichoscopy — Dermoscopy, a technique in which a handheld magnifier is used to visualize skin structures, can aid in the examination of patients with hair loss. Some devices are equipped for photography. (See "Overview of dermoscopy".)

Dermoscopy of the hair and scalp (trichoscopy) facilitates the examination of the epidermis, follicular ostia, hair shafts, perifollicular scale and erythema, and blood vessels [49]. Certain dermoscopic findings have been linked to particular forms of hair loss [49-54]. (See "Overview of dermoscopy of the hair and scalp".)

Examples of trichoscopic features of follicular ostia that may aid in diagnosis include [49]:

Absence of follicular ostia (suggests cicatricial alopecia)

Black dots (indicates hairs broken or destroyed at the level of the scalp as may occur in alopecia areata, dissecting cellulitis, tinea capitis, and some other disorders)

Yellow dots (indicates accumulation of keratotic material or sebum, as may occur in alopecia areata, discoid lupus erythematosus, male or female pattern hair loss, and some other disorders)

Fibrotic white dots (indicates fibrosis as may occur in primary cicatricial alopecias)

Examples of hair shaft abnormalities that may be detected with trichoscopy include [49]:

Exclamation point hairs (as may occur in alopecia areata, trichotillomania, or chemotherapy-induced alopecia) (picture 28)

Comma or corkscrew hairs (as may occur in tinea capitis) (picture 29)

Pohl-Pinkus constrictions (thinning of the hair shaft), as may occur in alopecia areata; chemotherapy-induced alopecia; blood loss; malnutrition; or chronic intoxication

Increased proportion of vellus hairs (as may occur in male or female pattern hair loss or alopecia areata)

Hair shaft changes correlating with genetic hair shaft disorders

Hair pull test — A hair pull test identifies active hair loss and should be performed on every patient who presents with a complaint of hair loss. It is important to consider that patients with hair loss may have concerns about pulling out additional hair; therefore, good communication is essential.

To perform the test, 50 to 60 hair fibers are grasped close to the skin surface and tugged from the proximal to the distal end. The easy extraction of more than six hair fibers suggests the presence of active hair loss. The proximal ends of hairs obtained by the hair pull test can be microscopically examined to determine the type of hairs removed (eg, telogen, anagen, dystrophic, or broken hairs) (picture 1).

Examination of other sites — Some hair loss disorders are associated with abnormalities in areas other than the scalp. Depending on the disorder, additional hair, nail, skin, tooth, or other abnormalities may be seen. Examining the entire skin surface, nails, and teeth at the time of the initial evaluation is useful for identifying additional sites of involvement and associated features.

DIAGNOSTIC TECHNIQUES — If the cause of hair loss remains uncertain following the patient history and physical examination, additional tests may assist with diagnosis. Microscopic examination of hair shafts and scalp biopsies are commonly performed in clinical practice.

Microscopic examination — When patients present with diffuse hair shedding, microscopic evaluation of the proximal ends of shed hairs is useful for determining the type of hairs that are being shed (eg, telogen, anagen, or dystrophic anagen hairs). For patients with hair breakage, microscopic examination of the hair shaft may identify structural abnormalities that contribute to hair fragility (picture 22A-E); this is done by cutting hairs close to the scalp surface.

The use of 1 to 2 drops of a mounting medium (eg, Permount) when placing the hair shafts between a glass slide and a coverslip optimizes the examination [48]. Examinations for pili torti are an exception; the shadows and twists of pili torti are best visualized when the hair is examined dry, without a mounting medium [48].

Of note, microscopic examination under polarized light is necessary for visualization of the "tiger-tail" pattern seen in patients with trichothiodystrophy. (See 'Inherited and acquired structural hair disorders' above.)

Scalp biopsies — Scalp biopsies can be a useful tool for the evaluation of hair loss when the diagnosis is uncertain. Scalp biopsies can distinguish scarring from nonscarring alopecia, and can provide information that further narrows the differential diagnosis. We perform scalp biopsies to confirm the diagnosis in all patients with cicatricial alopecia. Scalp biopsies are not usually performed for the diagnosis of hair shaft disorders due to the ability to diagnose these disorders with light microscopic examination of the hair shaft. However, in genetic structural hair disorders, abnormalities also may be evident when the intrafollicular portion of the hair shaft is seen on histologic examination.

Cicatricial alopecia — In patients with suspected cicatricial alopecia, scalp biopsies for diagnosis should be performed in sites of active disease. Features that suggest sites of active disease include the presence of primary lesions, symptoms, or a positive pull test [14]. The peripheral margin of an area of alopecia usually is the preferred site for a biopsy. Some hair should remain in the biopsy site; areas of end-stage, complete balding should be avoided.

Many dermatopathologists prefer to receive two punch biopsy specimens, since this allows for evaluation of the tissue in both vertical and transverse sections [14]. We usually perform two 4 mm punch biopsies. If only one biopsy can be performed, transverse sections are preferred [13,14]. The punch biopsies should be performed at an angle that mimics the direction of hair growth. (See "Skin biopsy techniques", section on 'Punch biopsy'.)

The vascular nature of the scalp can lead to significant bleeding during surgical procedures. To decrease bleeding, we inject 1% lidocaine with epinephrine for anesthesia and wait up to 10 minutes prior to performing the biopsy.

Nonscarring alopecia — Scalp biopsies are less frequently performed in patients with nonscarring alopecias, since the clinical picture and patient history often provide the diagnosis. However, when the diagnosis remains uncertain, scalp biopsies can be useful for ruling in or ruling out certain diagnoses (table 1A-B). Pathologic assessment of the proportion of anagen, catagen, and telogen follicles; the proportion of terminal and vellus hairs; the follicular structure; and the degree of inflammation can aid in distinguishing among the different types of nonscarring alopecia and can provide important information for treatment selection and setting patient expectations. Scalp biopsies are particularly useful for distinguishing among the diffuse presentations of alopecia areata, telogen effluvium, and female pattern hair loss.

A single scalp biopsy processed with transverse sections usually is sufficient for the evaluation of patients with clinical features suggestive of nonscarring alopecia [40].

Trichograms and phototrichograms — Trichograms and phototrichograms are techniques for the evaluation of nonscarring hair loss that are primarily used in research studies and specialized hair centers. Trichograms and phototrichograms can be used to assist with diagnosis and following the response to treatment.

To perform a trichogram, approximately 25 to 50 hairs are grasped close to the scalp with a needle holder. The hairs are then sharply plucked from the scalp. Following this, the proximal ends of the hairs are microscopically examined to evaluate the proportion of hairs in each stage of the hair cycle and to determine whether dystrophic hairs are present.

A phototrichogram is a less traumatic procedure in which hairs in a defined area are clipped to a length of approximately 1 mm and photographed. This baseline photograph can be used to assess hair density and the proportion of vellus, intermediate, and terminal hairs [55]. The same site is photographed two to three days after the initial photograph to assess hair growth. Since only anagen hairs grow substantially, catagen hairs elongate only slightly, and telogen hairs remain stable, the proportion of anagen, catagen, and telogen (resting) hairs can be estimated by comparing the two photographs [56].

Phototrichogram technology has evolved to include contrast-enhanced phototrichograms. Contrast-enhanced phototrichograms involve the use of high-resolution photography and hair dye that augments the contrast between hair color and skin color [56]. In addition, a software-based system for performing phototrichograms (TrichoScan) has been developed [57].

Laboratory studies — Depending on the type of hair loss suspected, serologic and microbiologic studies may also be useful for obtaining information to support the diagnosis and to detect associated disorders. For patients with new-onset diffuse, nonscarring hair loss without a clear cause, an initial laboratory evaluation focused on identifying potential causes can be performed. Suggested initial laboratory tests for the primary care setting include thyroid stimulating hormone to assess for thyroid disease as well as serum iron and ferritin to assess for iron deficiency. In addition, a rapid plasma reagin test to rule out syphilitic alopecia is appropriate for patients with patchy hair loss without visible inflammation or scarring.

Laboratory evaluation for hyperandrogenism can be beneficial for women presenting with both pattern hair loss and other signs of hyperandrogenism, and testing for thyroid stimulating hormone is typically performed for patients with alopecia areata, based upon an association of alopecia areata with thyroid disease. The suggested laboratory work up for specific forms of alopecia is discussed in detail in dedicated topic reviews in UpToDate. (See "Telogen effluvium", section on 'Evaluation for cause' and "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis", section on 'Laboratory tests' and "Alopecia areata: Clinical manifestations and diagnosis", section on 'Additional evaluation'.)

INDICATIONS FOR REFERRAL — Patients with signs of cicatricial alopecia (eg, hair loss with absent follicular ostia) should be referred to a dermatologist for evaluation and management. Referral to a dermatologist is also indicated if the cause of hair loss is unclear. Patients with extensive alopecia areata or chronic telogen effluvium may also benefit from referral.

PATIENT SUPPORT — Due to the cosmetic value placed upon hair in many societies, hair loss can be a highly distressing condition. In addition to diagnosis and treatment of the hair loss disorder, the clinician must also address the emotional and psychologic well-being of the patient. Organizations such as the National Alopecia Areata Foundation and the Scarring Alopecia Foundation can provide information and support for patients with hair loss. The American Hair Research Society is an additional source for information.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Alopecia".)

SUMMARY AND RECOMMENDATIONS

Hair cycle Throughout life, hair follicles undergo cycling characterized by periods of growth (anagen), involution (catagen), and rest (telogen). At any given time, 90 percent of hair follicles on the scalp are in anagen. The duration of the anagen phase determines maximum length of hair growth. (See 'Hair cycle' above.)

Classification Hair loss disorders can be divided into cicatricial (scarring) alopecias, nonscarring alopecias, and structural hair disorders:

Cicatricial alopecias When not treated early, cicatricial alopecias are characterized by irreversible damage to the hair follicle that results in permanent hair loss. The primary cicatricial alopecias are subdivided into lymphocytic, neutrophilic, and mixed inflammatory disorders (table 1A). (See 'Classification' above and 'Cicatricial alopecia' above.)

Nonscarring alopecias Nonscarring alopecias are conditions in which the hair follicle is not destroyed; in many cases of alopecia areata or telogen effluvium hair loss, spontaneous or treatment-induced hair regrowth can occur. Recognition of the distribution of hair loss is useful for the diagnosis of nonscarring alopecias (table 1B). (See 'Nonscarring alopecia' above.)

Structural hair disorders Structural hair disorders result in fragile hair and may be inherited or acquired. Damaging hair care techniques are a common cause of hair fragility. (See 'Inherited and acquired structural hair disorders' above and "Hair shaft disorders".)

Diagnosis:

History and physical examination Assessment of the patient with hair loss begins with obtaining a description of hair loss from the patient as well a medical history and family history. The physical examination incorporates inspection of the scalp, hair, and other body sites. (See 'Patient interview' above and 'Physical examination' above.)

Additional techniques When the diagnosis remains uncertain after the patient history and clinical examination have been performed, diagnostic techniques such as microscopic examination of cut or plucked hair fibers and scalp biopsies may provide additional information that is helpful for diagnosis. Depending on the differential diagnosis, additional laboratory studies may be performed. (See 'Diagnostic techniques' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Nina Otberg, MD, who contributed to an earlier version of this topic review.

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References

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