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Beach RA, Wilkinson KA, Gumedze F, Khumalo NP. Sebum Transforming Growth Factor β1 Induced by Hair Products. Arch Dermatol. 2012;148(6):764–766. doi:10.1001/archdermatol.2011.3533
Author Affiliations: Division of Dermatology, University of Ottawa, Ottawa, Ontario, Canada (Dr Beach); Institute of Infectious Disease and Molecular Medicine (Dr Wilkinson), Department of Statistical Sciences (Dr Gumedze), Division of Dermatology, Groote Schuur and Red Cross Children's Hospitals (Dr Khumalo), University of Cape Town, Cape Town, South Africa.
Chemical hair processing is used by more than 60% of women with Afro-textured hair and is a suspected contributor to scarring alopecia. We recently reported changes in 6 proinflammatory cytokines on scalp sebum of 36 women.1 Baseline scalp interleukin (IL)-1α in all participants including those with natural hair was higher than expected (ie, 18 times IL-1ra levels), which may suggest a predisposition to scalp inflammation. However, there was no difference in levels of IL-1α when sebum from shampooed natural hair was compared with that treated with ammonium thioglycolate (permanent wave), sodium hydroxide (“lye”) and guanidine hydroxide (“no-lye”) relaxers. Changes in IL-1ra were significant on the vertex but not on the crown, which may suggest site-specific scalp predisposition to inflammation.
In this study, samples from 36 participants (12 natural, 24 chemically treated) were tested for the presence of the profibrotic cytokine transforming growth factor (TGF) β1. The original study1 was conducted at Groote Schuur Hospital in 2010 and approved by the faculty ethics committee. Sebum was collected by applying Sebutape (CuDerm Corporation) to the scalp crown and vertex at visit 1 (before and after scalp shampoo), visit 2 (before and after chemical treatments), and on follow-up (visit 3). Details of chemical hair treatments and sample preparation for detection of cytokines have been described previously.1 Concentrations of TGF-β1 were determined using the Quantikine Human TGF-β1 Immunoassay (R&D Systems) according to the manufacturer's instructions.
Data analyses were performed using Stata software, version 12 (StataCorp LP).
Comparisons of interest were TGF-β1 levels with anatomic site after various chemical treatments and on follow-up. These comparisons were performed using Pearson χ2 and Fisher exact tests. Statistical significance was defined at the 5% alpha level (P = .05) for a 2-tailed hypothesis test.
There was a significant difference (P = .02) in the age of participants with a positive TGF-β1 finding (Table), all detected in samples taken after shampoo or chemical treatment. Only 1 sample from natural hair tested positive for TGF-β1; this was after shampoo treatment. All samples that tested positive at visit 3 (when no shampoo or chemical treatment occurred) were previously chemically treated. Two participants had positive TGF-β1 test results (the first tested positive at both scalp sites on visit 1; the second had higher TGF-β1 levels detected on natural hair at visit 1 than on follow-up after treatment with a lye relaxer); a third participant had 3 detectable TGF-β1 levels on 2 visits.
The number of participants with chemically treated hair was double that with natural hair. Overall, 16 samples (from 12 participants) yielded a positive TGF-β1 result; all except 1 of these were from chemically treated (94%) vs (6%) natural hair (Table). However, there was no statistically significant difference in detected TGF-β1 levels between samples from natural hair and chemical treatment groups (P = .23) nor within groups or scalp regions on different visits.
As a pleiotropic cytokine, TGF-β1 has roles in cell differentiation, proliferation, and inflammation. In scalps, TGF-β receptors have been reported to be strongly positive in proximal anagen hair follicles2; TGF-β1 is thought to induce regression of the hair follicle in catagen.2 Abundant levels of TGF-β1 have been found in the scalp dermis of patients with folliculitis decalvans and lichen planopilaris.3 These conditions are chronic and lead to scarring alopecia; TGF-β1 is postulated to mediate their fibrosis. Comparing data from biopsy specimens may not be appropriate because sebum was tested in this study, but changes in surface cytokines have been reported in scalp inflammation.4 Central centrifugal cicatricial alopecia (CCCA) predominantly affects women with Afro-textured hair. Although relaxer-induced acute CCCA-like scarring has been reported,5 the role of TGF-β1 is yet to be elucidated.
The detection of TGF-β1 after shampoo or chemical treatments in healthy subjects may suggest chemical interactions. The TGF-β isoforms are synthesized as latent precursors complexed with latent TGF-β binding protein (LTBP) or noncovalently bound to the latency-associated peptide (LAP). Extracellular dissociation from LTBP or LAP releases biologically active TGF-β. There are several conditions associated with this dissociation (activation), one of which is acidic pH.6 Most commercial shampoos are acidic (thought to induce less hair damage). However, TGF-β1 was not detected across all samples despite exposure of all to shampoo. Detectable levels of TGF-β1 at more than 1 visit may suggest a genetic predisposition and potential for scalp fibrosis, which may be influenced by hair grooming. Detection of TGF-β1 occurred predominantly in chemically altered hair but was inconsistent and lacked statistically significant difference in levels compared with findings in natural hair or between scalp sites. Large studies that correlate sebum cytokine levels and histologic characteristics may elucidate the association between hair chemical use and scarring alopecia.
Correspondence: Dr Khumalo, Division of Dermatology, Ward G23, New Groote Schuur Hospital, Observatory 7925, Cape Town, South Africa (email@example.com).
Accepted for Publication: December 6, 2011.
Author Contributions: Dr Khumalo had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Khumalo. Acquisition of data: Beach, Wilkinson, and Khumalo. Analysis and interpretation of data: Beach, Wilkinson, Gumedze, and Khumalo. Drafting of the manuscript: Beach and Khumalo. Critical revision of the manuscript for important intellectual content: Wilkinson, Gumedze, and Khumalo. Statistical analysis: Gumedze. Obtained funding: Khumalo. Administrative, technical, and material support: Beach and Wilkinson. Study supervision: Khumalo.
Financial Disclosure: None reported.
Funding/Support: The original study was supported in part by the North American Hair Research Society (Dr Beach) and the Women's Dermatologic Society (Dr Beach). Dr Wilkinson is supported by the Medical Research Council (United Kingdom) and performed the laboratory work in facilities partially funded by Wellcome Trust grant 084323 and the Division of Dermatology, University of Cape Town. The cytokines for the current study were funded by a Galderma (South Africa) award for published work 2010 (Dr Khumalo).
Role of the Sponsors: The sponsors had no role in the design and conduct of the study; in the collection, analysis, and interpretation of data; or in the preparation, review, or approval of the manuscript.
Additional Contributions: We are indebted to Gail Todd, FCDerm, PhD, for enabling participant recruitment and scalp treatments and to Steven Glassman, MD, who supervised the Ottawa Health Research Institute ethics submission.