Updated: Jan 27, 2009
In 1907, the first example of traction alopecia was reported in girls and women from Greenland who styled their hair in a ponytail. A similar pattern of hair loss was later noted in Japanese women who wear a traditional hairdo. In Sikhism, one of the religions practiced in India, men grow both scalp hair and beard hair. To keep their hair from falling in front of their face, it is tightly pulled into a bun. This practice has led to traction alopecia in Sikh men.[1,2 ]The tight rolling of beard hair into a pocket in the submandibular region also results in a similar phenomenon. The use of hair extensions, a common treatment for male or female pattern baldness, is also associated with a similar type of hair loss.[3 ]
Traction alopecia is a common cause of hair loss due to pulling forces exerted on the scalp hair. This excessive tension leads to breakage in the outermost hairs. This condition is seen in children and adults, but it most commonly affects African American women. The 2 types of traction alopecia are marginal and nonmarginal. Unlike trichotillomania, a psychiatric disorder of compulsive hair pulling that leads to patchy hair loss, traction alopecia is unintentionally induced by various hairstyling practices (eg, use of braids, hair rollers, weaves, twists, locks, or "cornrows"). In the initial stages, this hair loss is reversible. With prolonged traction, alopecia can be permanent. Physicians, especially dermatologists, must recognize this condition early to prevent irreversible hair loss.
Typically, traction alopecia is associated with sustained tension on the scalp hair. In theory, this phenomenon can also occur on areas of the face where hair is grown and styled. Traction causes hair to loosen from its follicular roots; however, hair loss also occurs secondary to follicular inflammation and atrophy. Hair loss is often symmetric and along the frontotemporal hairline; occipital scalp involvement is less common. Vellus hair is usually spared in the affected area.
Traction alopecia tends to follow a series of progressive events. Initially, pruritus and perifollicular erythema may be present. These may be accompanied by hyperkeratosis, creating a seborrheic picture. Pustules and scales may form. Eventually, an abundance of broken hairs can be detected. With persistent traction, the follicles atrophy and no longer produce the typical long and coarse hair. Instead, thinner, fine, short hair is generated.
When tensile forces are chronically present, an irritant type of folliculitis develops. Follicular scarring and permanent alopecia may result. In some cases, peripilar hair casts form. The casts are fine, yellowish white keratin cylinders smaller than 1 cm in diameter that ensheathe the hair follicle. Often, peripilar hair casts occur in isolation; however, they have also been known to occur in association with hyperkeratotic scalp disorders. The hair loss pattern entirely depends on the specific grooming pattern of each patient. Marginal and nonmarginal types may be seen.
Alopecia linearis frontalis, more commonly known as marginal alopecia, is a hair-loss pattern that usually results from the use of tight curlers, rollers, or straighteners during childhood. In this condition, the distribution of hair loss follows a characteristic pattern in the temporal scalp, starting in the periauricular area and extending forward in a triangular manner. The involved area is approximately 1-3 cm in width in most cases. For example, the constant contraction of the muscles used in facial expression, in addition to the tension caused by braiding, may partially account for why this pattern is often seen in the temporal region.
On the other hand, chignon alopecia is a type of nonmarginal alopecia that is characterized by hair loss in the occipital scalp region where the bun rests.[4 ]This condition is seen in patients with a long-standing history of pulling their hair into a bun. The typical patient is a 40-year-old woman who initially complains of itching and dandruff localized to the occipital area. Similar to marginal alopecia, perifollicular erythema with occasional peripilar hair casts can be seen.
The natural history of chignon alopecia mirrors that of marginal alopecia, with the eventual formation of pustules and the development of folliculitis. Permanent alopecia can also result if this condition remains undetected and the traction continues. Sometimes, the frontomarginal part of the scalp may also be involved because the longest hair roots originate in this region, and may be subjected to traction. When an examining physician notices both chignon alopecia and marginal alopecia, the index of suspicion should be high, and the diagnosis of chignon alopecia should be considered.
This condition is most commonly seen in African American population because of the practice of styling the hair in tight braids or the use of chemical hair straighteners. An estimated three fourths of African American females straighten their hair. More recently, female athletes who pull their hair tightly have been found to develop from this problem. Traction alopecia is also reported in nurses who secure their nurse's caps to their scalp with bobby pins.[5,6 ]The exact frequency of traction alopecia in the United States has yet to be documented.
Traction alopecia is seen worldwide. Its frequency usually depends on cultural customs. Japanese women who wear a traditional hairdo, Sikh men in India, and others who wear ponytails are examples of individuals who may be affected.
Population studies show a prevalence of 17.1% in African schoolgirls (6-21 y) and of 31.7% in women (18-86 y).[7 ]
Traction alopecia may lead to permanent hair loss if it is undetected for a protracted period. For females especially, this can lead to significant emotional trauma. Changes in self-perception, including lower self-esteem and social problems, are frequently reported by women who have traction alopecia.
This condition can be seen most commonly in African Americans, Japanese women, and Sikh men in India. See Frequency above.
Traction alopecia is more common in women than in men because women are more involved with hairstyling practices such as braiding or chemical hair straightening, and they are more likely to use tight curlers and nylon brushes and to wear chignons.
Traction alopecia is initially seen in children and young adults.
Three basic mechanisms of traction alopecia have been proposed: trichotillomania, telogen conversion, and overprocessing. In all cases, immediate cessation of the underlying cause can reverse the alopecia.
| Alopecia Areata | Telogen Effluvium |
| Alopecia Mucinosa | Tinea Capitis |
| Anagen Effluvium | Trichorrhexis Nodosa |
| Androgenetic Alopecia | Trichotillomania |
| Aplasia Cutis Congenita | |
| Sarcoidosis | |
| Syphilis |
Discoid lupus erythematosus
Senescent alopecia
Circumscribed scleroderma
Congenital vertical alopecia
Familial focal aplasia
Occipital pressure alopecia
Central centrifugal cicatricial alopecia[9 ]
Khumalo and colleagues developed a Marginal Traction Alopecia Severity scoring system to help guide behavioral modification decisions. The odds ratio was higher in adults than in children (<18 y) (1.87 [P <.001; 95% confidence interval, 1.28-2.72]) and was higher with braiding-related than chemical-related symptoms. The highest risk of traction alopecia, compared with natural hair, occurred when traction was added to relaxed hair (odds ratio 3.47 [P <.001; 95% confidence interval, 1.94-6.20]). Greater than 80% of patients with traction alopecia reported symptoms related to hairdressing. The authors concluded that traction alopecia severity was associated with age group, current hairstyle, and hairdressing symptoms, but larger studies are required to validate the use of the severity scoring system for marginal traction alopecia management.[7 ]
Early in the condition, lymphocytes surround a lichenoid perifolliculitis with infundibula.[11 ]Later, as the process evolves, a zone of fibroplasia separates this infiltrate.
Fully developed traction alopecia involves a mild lymphocytic perivascular infiltrate, a markedly thinned lower infundibulum, and an isthmus surrounded by a band of fibroplasia. Foreign body granuloma may be evident. The late process has a reduced number of hair follicles and thickened fibrous bands in much of the reticular dermis that extend into subcutaneous fat.
In early in traction alopecia, a subacute perifollicular inflammation is accompanied by mild-to-moderate hyperkeratosis. In cases of prolonged traction, decreased hair follicle and sebaceous gland density, perifollicular fibrosis, and vertical bands of follicular scarring are seen. However, blood vessels and eccrine sweat glands remain unaffected.
The physician must identify traction alopecia early. Failure to do so places the patient at risk for irreversible alopecia.
Despite the lack of medical options for the treatment of late-stage traction alopecia, achieving cosmetically acceptable correction of alopecia by means of surgical hair transplantation procedures (eg, punch grafting, flap rotation) is possible.[12 ]
Sufficient levels of iron and protein in the diet may help promote normal hair growth.
Medical therapy has no role in the treatment of traction alopecia.
Kanwar AJ, Kaur S, Basak P, Sharma R. Traction alopecia in Sikh males. Arch Dermatol. Nov 1989;125(11):1587. [Medline].
Singh G. Letter: Traction alopecia in Sikh boys. Br J Dermatol. Feb 1975;92(2):232-3. [Medline].
Harman RR. Traction alopecia due to "hair extension". Br J Dermatol. Jul 1972;87(1):79-80. [Medline].
Trueb RM. "Chignon alopecia": a distinctive type of nonmarginal traction alopecia. Cutis. Mar 1995;55(3):178-9. [Medline].
Hwang SM, Lee WS, Choi EH, Lee SH, Ahn SK. Nurse's cap alopecia. Int J Dermatol. Mar 1999;38(3):187-91. [Medline].
Renna FS, Freedberg IM. Traction alopecia in nurses. Arch Dermatol. Nov 1973;108(5):694-5. [Medline].
Khumalo NP, Jessop S, Gumedze F, Ehrlich R. Determinants of marginal traction alopecia in African girls and women. J Am Acad Dermatol. Sep 2008;59(3):432-8. [Medline].
Ozcelik D. Extensive traction alopecia attributable to ponytail hairstyle and its treatment with hair transplantation. Aesthetic Plast Surg. Jul-Aug 2005;29(4):325-7. [Medline].
Whiting DA, Olsen EA. Central centrifugal cicatricial alopecia. Dermatol Ther. Jul-Aug 2008;21(4):268-78. [Medline].
Steck WD. Telogen effluvium: a clinically useful concept, with traction alopecia as an example. Cutis. Apr 1978;21(4):543-8. [Medline].
Ackerman AB, Walton NW III, Jones RE, et al. Hot comb alopecia/follicular degeneration syndrome in African American women is traction alopecia. Dermatopathol Pract Concept. 2000;6:320-36.
Earles RM. Surgical correction of traumatic alopecia marginalis or traction alopecia in black women. J Dermatol Surg Oncol. Jan 1986;12(1):78-82. [Medline].
Aaronson CM. Etiologic factors in traction alopecia. South Med J. Feb 1969;62(2):185-6. [Medline].
Callender VD, McMichael AJ, Cohen GF. Medical and surgical therapies for alopecias in black women. Dermatol Ther. 2004;17(2):164-76. [Medline].
Clore ER, Corey A. Hair loss in children and adolescents. J Pediatr Health Care. Sep-Oct 1991;5(5):245-50. [Medline].
Halder RM. Hair and scalp disorders in blacks. Cutis. Oct 1983;32(4):378-80. [Medline].
Hantash BM, Schwartz RA. Traction alopecia in children. Cutis. Jan 2003;71(1):18-20. [Medline].
Ikeda T, Yamada M. [Factors in telogen affluvium and traction alopecia]. Acta Dermatol Kyoto Engl Ed. May 1967;62(2):109-13. [Medline].
Kanwar AJ, Ghosh S, Thami GP, Kaur S. Alopecia and cutis verticis gyrata due to traction presenting as headache. Int J Dermatol. Sep 1992;31(9):671-2. [Medline].
Laude TA. Approach to dermatologic disorders in black children. Semin Dermatol. Mar 1995;14(1):15-20. [Medline].
Monk BE, Neill SM, du Vivier A. Fashion causes traction alopecia. Practitioner. May 1986;230(1415):401-2. [Medline].
Phillips JH 3rd, Smith SL, Storer JS. Hair loss. Common congenital and acquired causes. Postgrad Med. Apr 1986;79(5):207-15. [Medline].
Scott DA. Disorders of the hair and scalp in blacks. Dermatol Clin. Jul 1988;6(3):387-95. [Medline].
Shapiro J, Wiseman M, Lui H. Practical management of hair loss. Can Fam Physician. Jul 2000;46:1469-77. [Medline].
Sperling LC, Mezebish DS. Hair diseases. Med Clin North Am. Sep 1998;82(5):1155-69. [Medline].
Springer K, Brown M, Stulberg DL. Common hair loss disorders. Am Fam Physician. Jul 1 2003;68(1):93-102. [Medline].
Stroud JD. Diagnosis and management of the hair loss patient. Cutis. Sep 1987;40(3):272-6. [Medline].
traction alopecia, traumatic alopecia marginalis, chignon alopecia, nurse's cap alopecia, nonmarginal traction alopecia, alopecia linearis frontalis, hot comb alopecia, follicular degeneration syndrome, hair loss, marginal alopecia, trichotillomania
Basil M Hantash, MD, PhD, Instructor of Dermatology and Plastic Surgery, Department of Dermatology, Division of Plastic Surgery, Stanford University School of Medicine
Basil M Hantash, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.
James W Patterson, MD, Director of Dermatopathology, Professor of Pathology and Dermatology, Departments of Pathology and Dermatology, University of Virginia Medical Center
James W Patterson, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association, American Society of Dermatopathology, Medical Society of Virginia, Royal Society of Medicine, Society for Investigative Dermatology, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other
Warren R Heymann, MD, Head, Division of Dermatology, Professor, Department of Internal Medicine, University of Medicine and Dentistry of New Jersey
Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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