Author(s) : Rodney D Sinclair, James R Schwartz, Heather L Rocchetta, Thomas L Dawson Jr, Brian K Fisher, Knut Meinert, Elizabeth A Wilder , Department of Dermatology, St. Vincent’s Hospital Melbourne, University of Melbourne, P.O. Box 2900 Fitzroy Victoria Australia 3065, Sharon Woods Innovation Center, The Procter & Gamble Company, Cincinnati, Ohio, USA, Miami Valley Innovation Center, The Procter & Gamble Company, Ross, Ohio, USA, Darmstadt Technical Center, The Procter & Gamble Company, Darmstadt, Germany. |
ARTICLE
Auteur(s) : Rodney D Sinclair1, James R Schwartz2,
Heather L Rocchetta2, Thomas L Dawson Jr3,
Brian K Fisher3, Knut Meinert4, Elizabeth A
Wilder3
1Department of Dermatology, St. Vincent’s
Hospital Melbourne, University of Melbourne, P.O. Box 2900
Fitzroy Victoria Australia 3065
2Sharon Woods Innovation Center, The Procter &
Gamble Company, Cincinnati, Ohio, USA
3Miami Valley Innovation Center, The Procter &
Gamble Company, Ross, Ohio, USA
4Darmstadt Technical Center, The Procter & Gamble
Company, Darmstadt, Germany
Dandruff/seborrheic dermatitis (D/SD) is a common chronic
inflammatory condition. Inflammation, possibly initiated by
microflora such as Malassezia sp., results in flakes, erythema and
itch. The impact of D/SD on associated hair has not been studied
previously; we report the results of evaluations of hair from a
D/SD population in comparison to a control group.
Female volunteers providing informed consent from the Xi’an
region of China with a hair length of at least 12 cm and who
had refrained from use of an antidandruff shampoo, hair colorant
and permanent treatment for at least one year were considered for
inclusion. Based on expert dermatologist grading of D/SD severity
(adherent scalp flaking score, ASFS [1]), women were classified as
affected (ASFS ≥ 27) or controls (ASFS ≤ 15). Hair was cut from a
2.5 cm2 area (for the D/SD group it was from the
highest flaking area). This area was then clipped to about
1 mm hair length prior to imaging using a Hi-Scope system.
Objective image capture and analysis methodology [2] provided hair
diameter as well as growth rate via image acquisition, initially
and 24 hours post hair-clipping. Isolated hair was gently but
thoroughly washed prior to subsequent blinded assessments. Surface
hardness was assessed by a slight modification of a
nano-indentation technique [3]. Shine was assessed [4] by
evaluation of the height and full width at half maximum (FWHM) of
the shine band; the more narrow the band, the more intense the
shine.
Population parameters and experimental data are summarized in
table 1. The D/SD group exhibited a
reduced hair diameter compared to that of the normal subjects
(p-value 0.068). The hair derived from D/SD scalp was significantly
(p: 0.027) less shiny than hair from normal scalp. Finally, using
the nano-indentation technique, the surface hardness of hair was
found to be harder (p: 0.08) for D/SD hair than normal hair.
These observations indicate for the first time that D/SD
symptoms extend to hair quality as assessed by objectively-measured
shine and supported by directional changes in diameter and surface
hardness. The higher surface hardness may encourage superficial
damage that results in reduced shine. While this study was limited
to one gender and ethnic group, we feel these results are generally
relevant based on analogous observations in psoriasis and lead to a
broader and more complete description of D/SD symptoms.
Psoriasis is also a chronic inflammatory condition with similar
cutaneous symptoms to D/SD; negative effects on associated hair
have been described. Hair from psoriatic scalp areas tends to be
abnormally narrow and has surface irregularities such as micropits
and abraded cuticle surfaces ([5] and references therein). These
independent observations in D/SD and psoriatic conditions suggest
that, in general, chronic inflammatory scalp conditions affect the
associated hair as well as the skin.
While there is no specific data available determining the impact
of scalp atopic dermatitis (AD) to hair, it is possible, based on
the role of nonspecific immunity to Malassezia in this condition
[6], that scalp AD also causes negative hair manifestations.
We hypothesize that the similarities between the skin and hair
symptoms of psoriasis and D/SD are due to common pathogenic
pathways involving chronic inflammation. Psoriasis is thought to
result from an exaggerated immune response to an unknown skin
autoallergen and D/SD an immunological response to increased skin
colonization by Malassezia sp. On histology, both conditions
display chronic dermal inflammation, irregular psoriasiform
acanthosis, hypogranulosis, and parakeratosis, resulting in many
similarities. We have demonstrated in this work that the hair
quality effects of both conditions are qualitatively similar. This
is represented schematically in figure 1. While hair loss
may occur in association with scalp psoriasis [5, 7] further
research is needed to ascertain whether the common pathogenic
pathway with D/SD leads to enhanced hair loss rates for D/SD
sufferers as well.
Acknowledgements
This work was funded by the Procter & Gamble Company. We thank
Maaike Bose and Dr. Xuemin Wang for study execution and Megan Copas
for statistical analysis. Dr. Carl Schmidt, Dr. Gregory Tormos and
Mr. Brandon Dunphy are acknowledged for hair technical evaluations.
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