Author Affiliations: Department of Dermatology and Cutaneous Surgery, University of Miami, Miller School of Medicine, Miami, Florida.
Background Alopecia areata is a common cause of hair loss seen in 3.8% of patients in dermatology clinics and in 0.2% to 2.0% of the general US population. The pathology of the disease remains poorly understood. Hair loss in alopecia areata can range from a single patch to 100% loss of body hair. When hair regrowth occurs in alopecia areata, the new hair may demonstrate pigment alterations, but a change in hair texture (ie, curly or straight) has rarely been reported as a consequence of alopecia areata.
Observations We report a case of a 13-year-old African American boy who experienced an alteration of hair shape following regrowth after alopecia areata. The new hair recapitulated his hair shape from early childhood.
Conclusions The precipitating factor for a change in hair texture in alopecia areata may be a result of treatment, pathophysiologic changes, or a combination of both. Whether the change is triggered at the level of stem cell differentiation, by cytokine or hormonal influences, gene expression during hair follicle development, a combination of all of these, or an unknown cause is a question that remains to be answered.
Alopecia areata (AA) is a common cause of hair loss seen in 3.8% of patients in dermatology clinics1,2 and 0.2% to 2.0% of the general US population.3,4 Usually up to 50% of patients recover within 1 year of treatment, but spontaneous remissions5 and frequent relapses have been reported in up to 90% of cases.6 Initially during regrowth, the new hair may have a smaller shaft size and may show pigment alterations ranging from total achromia to mild hypopigmentation, with a tendency toward total repigmentation over time.7 A review of the literature has shown that the shape (ie, curly or straight) of the new hair after regrowth is usually similar to the shape of the hair prior to the AA episode, although rare reports of hair shape changes have been documented.8 Herein, we report a case of an alteration in hair shape following regrowth in a male adolescent patient with AA, where the regrowth resembles the patient's hair shape from early childhood.
A 13-year-old African American boy presented with “a few months of hair loss. ” His medical history included seborrheic dermatitis limited to the scalp, self-treated with an over-the-counter medicated shampoo; and seasonal allergic rhinitis and hypersensitivity to cat allergens, both treated with a mometasone furoate monohydrate nasal spray as needed. His family history was significant for hypothyroidism diagnosed in his mother and maternal grandmother, and negative for AA.
Physical examination revealed a 5 × 3-cm patch of hair loss on the right supratemporal hairline and a 3.5 × 2.0-cm patch of hair loss on the vertex of the scalp, with evidence of partial regrowth. There was no evidence of cicatricial alopecia or skin lesions suggestive of discoid lupus erythematosus. In addition, nail pitting was not seen. Relevant laboratory findings included mild elevation in the serum level of free thyroxine.
After the clinical diagnosis of AA was made, the patient was treated with clobetasol propionate foam, 0.05%, once daily; triamcinolone acetonide cream, 0.1%, twice daily Monday through Friday; and clobetasol propionate cream, 0.05%, twice daily Saturday through Sunday.
After 3 months, the patient returned for a follow-up visit and showed evidence of substantial hair regrowth in both areas of prior alopecia. In addition, the newly growing hair in the 2 areas of prior alopecia displayed a different shape (ie, straight), in contrast to the curly shape seen on the rest of the patient's scalp (Figure). The patient's mother confirmed that the hair shape displayed in those specific areas of prior AA was similar to the hair shape seen in the patient during childhood. At a 1-year follow-up visit, the patient had not developed any new alopecic patches, and the hair growing in the areas of prior AA continued to display a straight shape, in contrast to the rest of the hair on his scalp.
Figure. The areas of prior alopecia displayed a different shape (ie, straight) in contrast to the curly shape seen on the rest of the patient's scalp.
Hair shape, or curliness, is a spectrum ranging from straight hair to tightly curled (frizzy) hair.9 Prior classifications of hair shape included 3 categories based on ethnicity: African, Asian, and European. Recently, several morphologic parameters have been used to broaden the hair shape classification to 8 types, independent of ethnicity. These parameters include the curve diameter, the curl index (which measures the ratio of the stretched length of the hair related to its length at rest), the highest number of waves in the hair when it is pulled to four-fifths of its length, and the number of twists detected along the fiber.9,10
There are several theories as to what generates the degree of hair curvature. In mouse models, mutations in transforming growth factor α (TGF- α), TGF- α receptor, and ETS2 (transcription factor receptor) cause mice to develop wavy hair and a change in follicular structure.11 Another theory suggests that morphologic parameters of the hair shaft, such as the diameter and geometric contour, determine hair shape and are frequently related to ethnicity. Examination of hair shafts in cross-section reveals that thicker, curly hair, such as that of some African Americans, is ellipsoid, whereas the hair of European Americans is thin, with a spheroid appearance (this correlates with a straight hair phenotype). Immunohistochemical and in vitro studies performed by Thibaut et al12 suggest that hair shape is more of a dynamic process, affected by the expression of certain proteins regulated by the hair bulb as well as by mechanical stress induced by myofibroblasts. Proliferative markers, specifically Ki-67, show increased expression in an asymmetrical manner on the convex side of curly hairs within the matrical cells, which may contribute to curving.12,13 Similarly, α –smooth muscle actin expression, a marker for myofibroblasts, is increased on the concave surface creating a mechanical imbalance, which may contribute to kinking.14 Interestingly, when the proximal portion of curly hair is cultured in vitro, it maintains its shape; this suggests that at the very least, hair shape can be maintained by the follicle with no input from other adnexal structures.12
Acquired straightening of the hair has been described patients with human immunodeficiency virus as well as in patients with chronic malnutrition15,16 and has been ascribed to mineral deficiencies and hormonal dysfunction. Kinking of the hair (in addition to pigmentation changes) has also been reported with the use of acitretin and etretinate, which are thought to be associated with a change in keratinization patterns within the inner root sheath.17,18
To our knowledge, this is the first report of a patient with AA who experienced a change in hair structure that recapitulated the patient's hair texture as a child. The precipitating factor for this change may have been a result of treatment of AA, pathophysiologic changes associated with the AA, or a combination of both.
The pathogenesis underlying AA is yet to be fully understood. It is clear that immune dysregulation consisting of cytokines, hormones, and T cells cause the hair cycle to become dysfunctional and come to a halt.19 When the hair follicle reenters anagen, the same signaling molecules active during morphogenesis (ie, WNT and SHH) trigger hair growth.11,20 In their work on hair follicle development, Legu é et al21 suggest that each hair cycle is a distinct morphogenetic event during which hair stem cells, under the influence of growth factors and cytokines, migrate from the bulge to promote new follicle growth, mostly maintaining their omnipotent properties.
In our patient, hair regrowth was achieved, but the pathologic changes induced by inflammation and/or treatment caused an alteration of hair texture. Whether the change was triggered at the level of stem cell differentiation, by cytokine or hormonal influences, by gene expression during hair follicle development, a combination of these, or an unknown cause is a question that remains to be answered. Elucidating triggers in hair texture change could help us further understand AA. Furthermore, it could have a major impact on the world of hair grooming, where countless hours are spent by people attempting to change their hair texture.
Correspondence: Lawrence Schachner, MD, Department of Dermatology and Cutaneous Surgery, University of Miami, Miller School of Medicine, 1600 NW 10th Ave, RMSB, Room 2023A (R250), Miami, FL 33136 (email@example.com).
Accepted for Publication: March 24, 2011.
Published Online: July 18, 2011. doi:10.1001/archdermatol.2011.192
Author Contributions: All authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Valins, Vega, Amini, and Schachner. Acquisition of data: Vega and Woolery-Lloyd. Analysis and interpretation of data: Amini and Woolery-Lloyd. Drafting of the manuscript: Valins, Vega, and Amini. Critical revision of the manuscript for important intellectual content: Valins, Amini, Woolery-Lloyd, and Schachner. Administrative, technical, and material support: Valins, Vega, and Amini. Study supervision: Woolery-Lloyd and Schachner.
Financial Disclosure: Dr Schachner has received grants from Stiefel, Astellas, Novartis, and Organogenesis.
Thank you for submitting a comment on this article. It will be reviewed by JAMA Dermatology editors. You will be notified when your comment has been published. Comments should not exceed 500 words of text and 10 references.
Do not submit personal medical questions or information that could identify a specific patient, questions about a particular case, or general inquiries to an author. Only content that has not been published, posted, or submitted elsewhere should be submitted. By submitting this Comment, you and any coauthors transfer copyright to the journal if your Comment is posted.
* = Required Field
Disclosure of Any Conflicts of Interest*
Indicate all relevant conflicts of interest of each author below, including all relevant financial interests, activities, and relationships within the past 3 years including, but not limited to, employment, affiliation, grants or funding, consultancies, honoraria or payment, speakers’ bureaus, stock ownership or options, expert testimony, royalties, donation of medical equipment, or patents planned, pending, or issued. If all authors have none, check "No potential conflicts or relevant financial interests" in the box below. Please also indicate any funding received in support of this work. The information will be posted with your response.
Some tools below are only available to our subscribers or users with an online account.
Download citation file:
Web of Science® Times Cited: 1
Customize your page view by dragging & repositioning the boxes below.
Enter your username and email address. We'll send you a link to reset your password.
Enter your username and email address. We'll send instructions on how to reset your password to the email address we have on record.
Athens and Shibboleth are access management services that provide single sign-on to protected resources. They replace the multiple user names and passwords necessary to access subscription-based content with a single user name and password that can be entered once per session. It operates independently of a user's location or IP address. If your institution uses Athens or Shibboleth authentication, please contact your site administrator to receive your user name and password.