Androgenetic alopecia is associated with increased scalp hardness

Journal of the European Academy of Dermatology and Venereology
Androgenetic alopecia is associated with increased scalp hardness
Chen, K.‐Y., Lin, S.‐H., Cheng, S.‐Y., Lo, T.‐K., Huang, H.‐Y., Tang, M.‐J., Yang, C.‐C.

The physical properties of a tissue, including hardness, play an important role in development,
homeostasis and disease pathogenesis. For hair follicles, physical properties of the surrounding
tissue regulates hair morphogenesis and growth. However, little is known about the role of tissue
hardness in hair loss diseases. Androgenetic alopecia (AGA) is caused by androgen and
susceptible genetic background. The disease process of AGA is also modified by other factors.3, 4
We hypothesized that AGA was associated with scalp hardness and thus this study was conducted
to confirm the hypothesis.

Subjects with AGA and without other alopecia were enrolled from our Dermatology Clinic.
The control non-AGA subjects were healthy volunteers without any alopecia. The study protocol
was approved by the Institutional Review Board of National Cheng Kung University Hospital. The
scalp hardness was measured by Durometer (Model DD-4, Type OO, Rex), which quantified the
hardness as 0-100 and reflected the average hardness of the epidermis, dermis and upper subcutis.
The hardness of scalp was measured at 15 designated anatomical points (Fig. 1a-b) before any
treatment of alopecia was initiated. Student’s t-test, with Bonferroni correction when required, was
used for comparison between subgroups. Generalized estimating equation (GEE) model was
utilized to analyze the association between variables.

Eighty male subjects, including 57 male-pattern AGA and 23 non-AGA subjects, and 80 female
subjects, including 54 female-pattern AGA and 26 non-AGA, were enrolled. There was no
difference in the mean age and BMI between AGA and non-AGA subjects. In non-AGA subjects,
the scalp hardness was the highest at the frontal area and the lowest at the occipital area (Fig.
1c-d). The scalp hardness in male and female non-AGA subjects was comparable, except the
crown area where male subjects had higher hardness than female subjects. The GEE model
showed that sex, age and BMI was not associated with scalp hardness.
In male subjects, the hardness at the frontal and vertex scalp was significantly higher in
Accepted Article

AGA subjects (Fig. 1e), compared to non-AGA subjects. The scalp hardness at the frontal and
vertex scalp was also higher in subjects with higher AGA severity (Fig. 1f). GEE model showed
that increased scalp hardness was associated with higher risk and increased severity of AGA
(Table 1).

In female subjects, however, there was no significant difference in the scalp hardness
between female AGA and non-AGA subjects (Fig. 1g). The vertex scalp of subjects with grade 3
AGA had higher hardness than subjects without AGA (Fig. 1h). GEE model showed no
association between scalp hardness and AGA occurrence or severity (Table 1).

Our data showed that the AGA-prone scalp (frontal and vertex scalp) correlated with higher
hardness, while the AGA-resistant scalp (temporal and occipital scalp) correlated with lower
hardness. Male AGA subjects had higher hardness at the AGA-affected scalp than non-AGA
subjects. The above findings suggest an association between AGA and scalp hardness. The
interaction between the scalp hardness and hair follicles in AGA are complicated. Transforming
growth factor β1 (TGF-β1) is the key growth inhibitor of the hair epithelium in AGA.

On the other hand, TGF-β1 also induces tissue fibrosis and increased tissue hardness.
Perifollicular fibrosis had actually been identified in AGA.7, 8 Fibrosis of the tissue can in turn activate latent
TGF-β1, and further inhibits the hair epithelium growth. TGF-β1 also potentiated the sensitivity
of androgen receptor in the DP cells from the bald scalp.

In conclusion, there was a pattern distribution of scalp hardness. The occurrence of AGA
and AGA severity was positively correlate with scalp hardness in men. Further investigation is
required to identify the underlying mechanism and to look for a new therapeutic strategy.

I think this is the key. Talking to many women in the hair/scalp industry they will tell you the same they observe in the men with hair loss. There is a clear change in the fascia. I have been studying fascia non related to this for a while and I can tell you many fascial changes occur indirectly or via a chain reaction. The work of Guy Voyer has been great to remodel most of the fascia in the body. I havent come across a good map of the scalp fascia yet, I know Carla Stecco from Italy has some stuff about it but I havent figured it out yet. I assume it will involve some segments of the thoracic spine and cervical spine which can be manipulated by Soma therapy. But I believe the TMJ may be a key point of manipulation also to change the scalp fascial tension. This is likely why hair transplants fail because the scalp "terrain" just isnt good.

Figuring out a permanent cure to hair loss will probably have to deal with remodeling the scalp fascia.

Interesting. I did the scalp massage on and off for a while but I never committed to it or did it for long time. Might go back to it I guess.

Wouldn't this also reinforce the positive results of the botox scalp study for male pattern baldness?