Telogen effluvium is a common non-scarring hair cycle disorder in which an abnormal amount of hairs transitions from anagen phase to telogen phase, resulting in increased diffuse shedding of hair (19, 31). This growth cycle perturbation is usually due to medications, illness, surgery, metabolic disturbances, nutritional deficiencies, trauma, immunizations, and the postpartum state. However, no trigger is identified in one-third of cases (19, 31–34). Moreover, it is not uncommon for telogen effluvium to be superimposed on other forms of alopecia if patients experience an inciting event. Important differential diagnoses to consider include androgenetic alopecia (AGA), female pattern hair loss (FPHL), and diffuse AA (35, 36). Acute telogen effluvium occurs 3–4 months after an inciting event, lasts approximately 3 months, and spontaneously resolves, while chronic telogen effluvium usually lasts longer than 6 months. The hair pull test roughly estimates the percentage of telogen hairs. A positive hair pull test, particularly at the vertex and the scalp margins, is highly suggestive of telogen effluvium (19, 31, 33).

Patients can present after the phase of acute shedding has subsided. In these cases, patients report a period of increased shedding, while on exam, clinicians observe evidence of short hairs regrowing along the temporal and frontal hairline. A complete blood count and metabolic panel, with additional tests for metal poisoning and nutrition deficiencies, can help identify causes of telogen effluvium (19, 37). Acute telogen effluvium is completely reversible with removal of stressors and treatment of underlying disorders, if present. Prognosis is generally good with most patients regrowing hair within the year, though at a slow rate of approximately 1 cm/month (19). Treatment is not necessary except in cases of chronic telogen effluvium, but unfortunately, options are limited (38, 39). While topical minoxidil has mixed results in treating telogen effluvium in adults, its efficacy in children remains unknown (39).

Anagen effluvium is rapid hair loss that is rarely seen in the healthy pediatric population. It usually occurs within days or weeks after an inciting event resulting in profound alopecia affecting 90% of the scalp, corresponding to the number of hairs typically in the anagen phase (31, 40). Anagen effluvium should be suspected in a patient with a history of radiotherapy; antineoplastic agents (doxorubicin or vincristine) and other medications, including colchicine; toxic chemical exposure (mercury, boron, and thallium); and severe malnutrition (31, 40, 41). These insults acutely disrupt mitotic activity, thus the proliferating cells of the hair bulbs are preferentially targeted, while quiescent stem cells within the follicle remain unaffected (41). Thus, breakages occur at the fragile proximal hair shaft. Dystrophic anagen hairs will often have tapered fractures of hair shafts (31, 41). Once the insult is removed, most patients experience normal hair regrowth with a delay of 1–3 months; however, permanent alopecia may occur depending on the underlying cause (41). It is important to note that pediatric patients treated with myeloablative conditioning with busulfan have been reported to have permanent diffuse alopecia as a potential side effect. In one multicenter study of 240 childhood leukemia patients, 66 received busulfan and 174 received total body irradiation (TBI) as conditioning. In the busulfan group, 25.8% reported alopecia as a long-term side effect of treatment >10 years out from their stem cell transplant, whereas only 2.9% reported this in the TBI-treated group (42). Use of scalp hypothermia (scalp temperature <24°C), scalp compression, and topical minoxidil can reduce hair loss in some adult patients undergoing chemotherapy, but the techniques differed widely in these studies, and the benefit in children remains unclear (41, 43, 44).

Loose anagen syndrome is a relatively infrequent cause of hair loss, characterized by poor anchoring of anagen hairs to the follicle, resulting in frequent painless hair loss with gentle pulling (31, 45). Patients are born with sparse but normal hair, and generally present between 2 and 7 years of age with unruly hair that is slow growing. Light microscopy and trichogram reveal predominantly loose anagen hairs (>50%), misshapen anagen roots with absent external root sheaths, and ruffled cuticles (46). Trichoscopy findings include rectangular black granular structures, solitary yellow dots, and >90% of follicular units with single hairs (47). LAS is considered autosomal dominant with incomplete penetrance, and a keratin mutation is responsible for several familial cases (46, 48, 49). LAS may also be associated with heritable developmental conditions, such as Noonan syndrome (50, 51). Due to abnormal premature keratinization in the inner root sheath, hair and the inner root sheath are poorly adherent in LAS. Most cases require no treatment as hair spontaneously returns to normal within a few years, but avoiding hair products and styling, and gentle handling may prevent further hair loss (31, 48, 51). Topical minoxidil may benefit LAS patients, particularly those with severe symptoms (46, 49).

Short anagen syndrome is a rare cause of perceived hair loss in children, due to a shortened growth phase of the hair cycle. This is typically a sporadic congenital condition that can be inherited in an autosomal dominant fashion in some cases. Patients present with normal hair density but with very short hairs that never need to be cut, similar to LAS. However, a gentle hair pull in patients with SAS will reveal that the short hairs are shed in the telogen phase in contrast to being shed in the anagen phase in LAS. This condition is benign, and the majority of patients will improve by puberty (52, 53).

Trichotillomania is a not infrequently seen impulse control disorder characterized by repetitive, compulsive, and self-induced hair pulling from the scalp, eyebrows, and/or other parts of the body (19, 31). Although trichotillomania can occur in children under 6 years old, peak incidence is age 9–13 years with a strong female predominance (54, 55). Clinical presentation includes multiple non-scarring and focal patches of hair loss with irregular borders (Figure 5), little to no scale or excoriation, and presence of broken hairs of different lengths, often contralateral to the side of the body with the dominant hand (19, 56). Hair loss in trichotillomania frequently spares the occiput, as these hairs are more painful to pull out. Trichobezoars can be identified in patients who eat their pulled hairs, leading to gastrointestinal symptoms, including nausea and vomiting, abdominal pain, and bowel perforation (57). In trichotillomania, hair density is normal with a negative pull test; however, presence of flame hairs (proximal hair residue that remains after pulling anagen hairs), the “v-sign” (two hairs rising from the same follicular opening and broken at same level), and tulip hairs (short hairs with darker tulip-shaped ends) on trichoscopy are highly characteristic (58, 59). The main differential diagnosis of trichotillomania is AA. Distinguishing features that are more suggestive of trichotillomania include sparing of the lower occiput scalp, no discrete patches of complete hair loss, a geometric-shaped patch with hairs of all different lengths sometimes with associated evidence of scalp trauma (small pinpoint hemorrhagic spots on scalp). This is in contrast to a patch of hair loss that spontaneously regrows in patients with AA where the hairs typically are all the same length.

Trichotillomania is classified under obsessive–compulsive and related disorders in DSM-V. While its causes are unknown, higher rates of obsessive–compulsive disorder and psychiatric conditions are found in first-degree relatives (56, 60, 61). Management varies across age of presentation. Trichotillomania in preschool-aged children is considered a habit disorder similar to thumb sucking and has a benign course generally disappearing by school age. This can be managed conservatively with gentle reminders. In preadolescents and teenagers, trichotillomania often presents with other psychiatric comorbidities, and patients may benefit from a psychiatric evaluation if willing (19, 55, 56). In children and adolescents, behavioral therapy—positive reinforcement, habit reversal training, and self-monitoring—are effective when working with a skilled therapist (62, 63). Pharmacological interventions are limited. Studies showed mixed results for selective serotonin reuptake inhibitors and tricyclic antidepressants in adults, and data regarding their efficacy in children are lacking (55). While N-acetylcysteine is a promising agent that reduces symptoms in adults, no benefit was seen in children (64, 65).

Traction alopecia is a common pattern of traumatic hair loss caused by constant tensile forces exerted on scalp hair. Clinical presentation follows a predictable natural history, with early development of perifollicular erythema, pustules, scaling, and broken hairs and late sequelae of follicular scarring and permanent alopecia. In children, marginal hair loss along the temporal hairline is commonly observed, although non-marginal occipital and frontomarginal patterns can also occur depending on hairstyle (66). Fringe sign is the retention of hairs along the frontal or temporal rim (Figure 6A). Highly suggestive of excessive tension, tenting of hair follicles refers to the raising of skin on the scalp when hair is pulled extremely tightly (Figure 6B). Both are important exam findings for diagnosing traction alopecia (67, 68). The applied trauma is unintentional and often secondary to cultural and social practices given known associations with grooming accessories and particular hairstyles (68, 69). High-risk hairstyling practices include tights buns, ponytails, braids, cornrows, or dreadlocks; application of weaves, braids, or hair extensions to relaxed hair; and any hairstyles that cause pain, crusting, tenting, or pimples (68). Treatment involves adopting grooming practices that minimize traction, and antibiotics to address folliculitis if present (31). With early diagnosis and treatment, regrowth can occur within months; however, chronic traction alopecia may be irreversible despite discontinuation of traction.

Central centrifugal cicatricial alopecia is a form of scarring alopecia that starts with patchy hair loss at the vertex and gradually spreads centrifugally. Patients may complain of tender or pruritic bumps in this location of the scalp. Long thought to be secondary to damage from chemical relaxers and hair dyes, CCCA disproportionately affects middle-aged women of African descent and was previously rarely reported in children (70, 71). However, a recent pediatric case series suggests a familial mode of inheritance with earlier disease onset and greater penetrance in individuals of successive generations. A case series of six children with CCCA reported that the majority (83%) were of African descent, had no history of chemical treatment of hair, and had a positive family history of CCCA (72, 73). Although still a rare cause of hair loss in children, a low threshold of suspicion should be maintained for young African American patients presenting with vertex hair loss and symptoms. To the best of our knowledge, CCCA has not been reported in children of non-African descent. Early treatment with topical or intralesional steroids can decrease inflammation to slow or halt disease progression. This highlights the importance of recognizing CCCA in children with a positive family history to control progressive scarring alopecia.

Discoid lupus erythematosus is very rare in children. It is an inflammatory autoimmune disease that most commonly leads to erythematous, scaly patches on the head and neck that can spread to involve other areas of skin in some cases. The inflammation can lead to atrophy and scarring of the skin and permanent hair loss. Lesions may initially mimic tinea capitis or bacterial infections given the confluent erythema, but laboratory investigations will be negative and there will be a lack of response to anti-infectious agents. The diagnosis is typically made by scalp biopsy revealing basal vacuolization, increased dermal mucin, and a dermal, perivascular, and periadnexal lymphocytic infiltrate. Although there is a female predominance in adult DLE, there is no sex predilection in children. Antinuclear antibodies are uncommon in children (26%), as opposed to 43% positivity in adults; however, progression to systemic lupus erythematosus (SLE) is more common in children with 26% over a 3-year period developing SLE in contrast to only 5% of adults (74). One retrospective study of 40 children with DLE reported the greatest risk of progression to SLE was in the first year after DLE diagnosis. The majority of patients met SLE diagnostic criteria with mucocutaneous disease, cytopenia, and positive antibodies (75). Therefore, children with DLE should be very closely monitored for SLE development. Other goals of management involve controlling activity of disease to prevent further scarring and dyspigmentation. Treatments include potent topical steroids, hydroxychloroquine (4–6 mg/kg/day), and intralesional or systemic corticosteroids. There appears to be some genetic predilection, with DLE patients often reporting a family history of rheumatologic conditions.

Lichen planopilaris is an exceedingly rare cause of scarring alopecia in the pediatric population. The cause of LPP is unknown and seems to be sporadic. LPP in adults typically occurs in Caucasian, postmenopausal females. In contrast, LPP in children has no sex predilection and has been reported to occur more frequently in patients of East Indian and African descent. Patients present with scarring alopecia with perifollicular erythema and scales on exam, in contrast to the more confluent erythema and scaling seen in DLE. About half of LPP cases are asymptomatic and could be confused with the more common AA as a result. The clinical features of atrophy and perifollicular scale and erythema are strongly suggestive of LPP (76).

Transient neonatal hair loss encompasses the very common phenomenon of neonatal occipital alopecia and development of bald patches in other locations. Healthy babies have been observed to develop alopecic oval patches, most notably in the occiput, during the first 2 months of life. Friction was the presumed cause of TNHL, with the occiput particularly affected due to supine sleeping positions. However, recent retrospective studies found no association between TNHL and sleeping positions. TNHL has a benign course with no accompanying symptoms, and the hair spontaneously regrows (82, 83).

Congenital triangular alopecia, also known as temporal triangular alopecia or Brauer nevus, is a non-progressive, non-scarring infrequent cause of alopecia that primarily affects frontotemporal regions. Lesions are triangular or lancet shaped, with complete hair loss of the affected patch except a few vellus hairs. Most lesions are unilateral, predominantly left-sided, but can be bilateral in approximately 7.5–20% of cases (84, 85). A small subset of CTA is associated with known syndromes, including Down syndrome and phakomatosis pigmentovascularis. Although CTA can manifest at birth, most cases are reported after age 2 when the affected patch becomes more noticeable as children undergo vellus to terminal hair transition. Vellus hairs are a highly sensitive but not specific marker for CTA (86). Trichoscopy can demonstrate other features such as miniaturized terminal hair follicles, hair length diversity, and the absence of features characteristic for other types of alopecia, notably AA (85). CTA remains unchanged throughout adult life. Surgical intervention can produce satisfactory cosmetic results, and efficacy of topical minoxidil has been described in a 1-year-old patient (87–90).

Congenital atrichia and hypotrichosis comprise a group of rare congenital disorders that present with hair loss or reduction in hair volume (31). Caused by autosomal recessive mutations in the human hairless gene, atrichia congenita presents with either complete hair loss shortly after birth or permanent absence of scalp hair due to follicular agenesis or programmed follicular destruction and papular lesions on the face, scalp, and extremities (31, 91–93). Vitamin-D-dependent rickets is an important differential diagnosis to exclude (93, 94). Atrichia congenita is often mistaken for AU until patients fail to respond to steroid therapy (95). Congenital hypotrichosis is less severe than atrichia congenita with patients presenting after 2 years with diffusely thin hair and variation in quality and quantity of hair (31). Congenital hypotrichosis may be associated with other features, including epilepsy, chromosomal abnormalities, inborn errors of metabolism, and ocular, ectodermal, or skeletal abnormalities. If any associations are identified, workup for a syndromic cause should be performed and genetic counseling may be appropriate depending on the diagnosis (96). For many of these conditions, there is currently no effective treatment.

Androgenetic Alopecia (AGA) is characterized by relatively common non-scarring hair loss in androgen-dependent regions of the scalp, particularly the vertex and temporoparietal areas, with distinct and well-described male patterns (31, 97, 98). The most frequent cause of alopecia in adolescents, AGA presents gradually after puberty when enough testosterone is converted into dihydrotestosterone and is not generally observed in prepubertal patients without abnormal androgen levels (31, 99, 100). Trichoscopy reveals increased number of thin and vellus hairs, hair shaft thickness diversity, perifollicular pigmentation, and variable number of yellow dots. Biopsy commonly demonstrates perifollicular inflammation (100, 101). A strong genetic predisposition is observed, but no causative gene has been identified, although the androgen receptor gene has been posited (102, 103). Topical minoxidil can prevent progression of AGA in adolescents (99, 100). Finasteride with or without minoxidil is equally well-tolerated and increased hair density in a small cohort of adolescent boys (100). Recent studies have also demonstrated efficacy of low-level laser therapy for adult patients of both genders with AGA (104–106).

Female Pattern Hair Loss (FPHL) is a commonly seen non-scarring alopecia distinct from male AGA, presenting with diffuse central thinning beginning anytime after menarche or adrenarche (100, 107). Frontotemporal recession or vertex loss, a more “male pattern” baldness, is less common (107). Trichoscopy shows increased yellow dots, pilosebaceous units with only one hair, and perifollicular hyperpigmentation (108). Family histories for FPHL are often not straightforward, and androgens may not explain all cases of FPHL as many female patients demonstrate little to no biochemical or clinical evidence of increased androgens (107, 109). Signs of hyperandrogenism such as hirsutism and menstrual disturbances should prompt evaluation for polycystic ovarian syndrome, congenital adrenal hyperplasia, and other androgen-producing conditions (110, 111). Topical minoxidil is similarly well tolerated in adolescent girls and prevents progression of FPHL (100). In cases of hyperandrogenism, antiandrogen or 5-alpha reductase inhibitors, such as spironolactone, finasteride, and cyproterone acetate, can be used, though the efficacy of these treatments in children remains unclear (107, 112).