What’s new in hair — April 2016 | Dr. Claire A. Higgins

All hairstyles are not created equal: What the dermatologist needs to know about black hairstyling practices and the risk of traction alopecia (TA).

J Am Acad Dermatol. 2016 Apr 21. pii: S0190-9622(16)01398-0.
doi: 10.1016/j.jaad.2016.02.1162

Traction alopecia is caused by prolonged tension on the hair root, and is frequently seen as a result of black hairstyling techniques.  It is difficult for physicians to recommend management plans other than “avoid tight hairstyles”.  In this review, Haskin and Aguh describe different black styling techniques, categorising them by risk of causing traction alopecia.  Practices such as chemical straightening, braids and dreadlocks are seen as high risk hair styles.  Comparatively, thermal straightening or permanent waving represent moderate risk hair styling techniques.  The authors recommend a way to manage traction alopecia is to suggest patients move towards a safer hairstyling practice.

 

Treatment of an alopecia areata patient with tofacitinib results in regrowth of hair and changes in serum and skin biomarkers.

Exp Dermatol. 2016 Apr 27. doi: 10.1111/exd.13060.

In the past couple of years we have seen a number of research group’s trialling Jak inhibitors for treatment of alopecia areata.  One of these studies is being spearheaded by Columbia University, and there currently is an open-label pilot trial ongoing to assess the efficacy of oral tofacitinib.  In this paper, Jabbari et al detail the specifics of one of the patients enrolled.  The patient, who had alopecia for 5 years prior to enrolment initially responded very well to a 5mg dose of tofacitinib twice daily.  After three months, scalp hair regrowth was at 94%.  However, upon cessation of treatment near-complete hair loss resumed.  When the authors assessed the patients ALADIN score, which is used as a biometric marker of disease state, it seemed that their signature had altered from the baseline signature, but was not restored to the same level as unaffected controls.  Perhaps the timeframe for treatment should be guided by this biomarker assessment, as it will likely vary from patient to patient.

 

Low-level laser therapy as a treatment for androgenetic alopecia.

Lasers Surg Med. 2016 Apr 25. doi: 10.1002/lsm.22512.

Androgenetic alopecia affects 50% of men aged 50, and increases in prevalence with age.  Low level laser therapy (LLLT) has been proposed as a safe treatment, however most of the studies to assess efficacy are small and it is difficult to interpret the results.  In this paper, Afifi et al review 11 studies comprising 444 men and 236 women, which tested LLLT for androgenetic alopecia.  The duration of treatment, the wavelength or power of LLLT used varied between studies assessed, which may confound results.  However, in reviewing the literature the authors found that 9 or the 11 studies reported positive results after LLLT.  This included an increased hair count after treatment, indicating that LLLT may activate kenogen follicles to re-enter anagen.  Larger and more thorough studies, without variation in test parameters, are required to evaluate the efficacy of LLLT in the future.

 

Signaling Networks among Stem Cell Precursors, Transit-Amplifying Progenitors, and their Niche in Developing Hair Follicles.

Cell Rep. 2016 Mar 29;14(12):3001-18. doi: 10.1016/j.celrep.2016.02.078.

Building on their recent characterisation of skin during development, the Rendl group has now characterised transcriptome signatures of 14 cell populations in adult skin.  In this paper, Rezza et al used elegant transgenic mouse models to isolate 14 distinct cell populations from 5 day old mouse skin/hair follicles.  Using RNA-Seq to characterise each cell population, they were able to detect differences between hair follicle stem cells, outer root sheath cells, transit amplifying precursors and matrix cells.  In addition, in mouse back skin there are 4 follicle subtypes; guard, awl, auchene and zigzag hairs.  Guard hairs develop first, and are largest, but only cover 1% of the coat.  Zigzag hairs form last, making up 80% of the coat.  Rezza et al found that dermal papilla from each hair type were relatively similar, and only expressed a few signature genes.  For example, Gpx3 was highest in awl and auchene papilla, compared to zigzag or guard hairs.  It would be interesting to know if human follicles on different body sites, such as the eyebrow or arm, could be categorised into distinct subtypes based on their papillae signature.

 

Development and Characterization of a 3D Printed, Keratin-Based Hydrogel.

Ann Biomed Eng. 2016 Apr 29. doi: 10.1007/s10439-016-1621-7

Natural biomaterials need to be biodegradable, and support cell attachment, growth and migration.  The most common natural biomaterial is collagen, however, in this paper Placone et al use human hair to make keratin hydrogels.  Hair keratin has specific cell binding motifs, LDV and RGD, which support cell attachment.  To extract keratin, human hair was oxidised, then purified with filtration and dialysis.  Resultant keratin was printed with a 3D printer, resulting in honeycombed scaffolds with pores sizes between 10-30μm.  Cells grown within the hydrogels had normal levels of metabolic activity and were viable, indicating that keratin from human hair is indeed a good natural biomaterial.  Given the large amount of human hair discarded every day at hair salons, hair as a source of keratin for scaffolds makes economic sense.

 

STAT5 activation in the dermal papilla is important for hair follicle growth phase induction.

J Invest Dermatol. 2016 Apr 27. pii: S0022-202X(16)31064-8. doi: 10.1016/j.jid.2016.04.014.

The dermal papilla is a mesenchymal compartment located at the base of the hair follicle, which has roles controlling growth and cycling of the follicle.  In this paper Legrand et al evaluate the expression of inactive and phosphorylated forms of STAT5 throughout the hair cycle.  They find expression localised to the dermal papilla of murine hair follciles, with the highest amounts expressed during competent telogen and anagen.  To determine the role of STAT5 within the dermal papilla, the authors generate a mouse where STAT5 is conditionally knocked out in the dermal papilla at birth. They find that knocking out STAT5 resulted in a delayed anagen entry during the second hair cycle, suggesting a role for JAK-STAT signalling in anagen entry.

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