HAIR AND SCALP CARE 75 A B 120 ns 110 ns 100 90 80 Control Si (eq 0.25%) C
140 130 120 110 100 90 80
Control +30% * +28% * AD (eq 0.25%) SiAd (0.25%) +13% *
D
ns
180 160 140 120 100 80 60
Si (eq 0.25%) AD (eq 0.25%) SiAd (0.25%) Control
+42% * +38% *
ns
Si (eq 0.25%)
AD (eq 0.25%)
SiAd (0.25%)
Figure 4: The SiAd complex stimulates HFDPC number and growth factor secretion. Schematic representation of the adenosine-dependent signaling pathway leading to the production of GF (adapted from Hyun 2021, Kim 2022, and Perez-Mora 2023) (A). HFDPC were treated with silicium (Si, eq. 0.25%), adenosine (Ad, eq. 0.25%), or the SiAd complex (0.25%) for 24 hours. Quantification of HFDPC number (B). Quantification of VEGF (C) and KGF (D) secreted using an ELISA assay. Mean ± SEM. *p-value<0.05, **p-value<0.01 versus control.
keratinocytes and melanocytes responsible for hair growth and colour respectively) together with the inner and outer root sheaths (responsible for the hair anchorage in both the dermis and the hypodermis of the scalp). Meanwhile, the dermal papilla will burrow
itself into the hypodermis for the whole hair growth period which can last for years. All along, HFDPC secrete growth factors (KGF and VEGF) responsible for stimulating the proliferation of hair matrix cells. The keratinocytes of the matrix will later accumulate keratin and will ultimately become the hair shaft. At the end of the growth phase, the hair
follicle enters into the catagen phase. During this regression phase, the bulb gets thinner (as the matrix cells undergo apoptosis), with lower melanin content and is separated from the papilla before migrating toward the border of the permanent zone. Meanwhile, the expression of anchoring proteins (such as β1-integrin) is decreased thus leading to a looser attachment of the hair to its sheath. The ‘old hair’ then enters the telogen phase
where it waits to be shed (exogen phase). The papilla in turn migrates back up close to the bulge, waiting for other stem cells in order to start a new cycle.
www.personalcaremagazine.com This cycle is sensitive to exposome, hormones
and ageing, often causing growth slow down or even hair loss. For example, especially in people affected with male (or female) hair loss pattern, testosterone and DHT may reduce the duration of the growth phase and precipitate the entry into catagen by prematurely inducing apoptosis of the hair matrix cells. By accelerating the cycles, more hair is falling at the same time which may cause alopecia. Furthermore, the number of cycles a hair can
undergo is limited (approximately 20 to 25) due to the fixed number of stem cells in the bulge. Once the stem cells pool is depleted, no new terminal hair may be produced and the newformed hair remains as a vellus, nearly invisible thus giving the impression of hairless skin (baldness). This process is known as ‘miniaturization’.13 Hair loss, or alopecia, is a multifactorial
condition affecting individuals of all ages and genders.14
Its causes range from genetic
predisposition and hormonal imbalance to stress and medication. There are several different types of alopecia:
■ Androgenic alopecia is the most common type as it affects 70-80% of men and 30-40% of women (often after menopause), ■ Alopecia areata is an autoimmune disorder
that causes patchy hair loss, ■ Telogen effluvium is a temporary hair shedding due to stress or illness, ■ Traction alopecia is caused by a physical pull of the hair (e.g. combing) Although pharmacological treatments such
as minoxidil and finasteride are widely used and their activity clinically proven, their application is often associated with side effects—including scalp irritation, hormonal disturbances, and poor patient compliance.11,15 Moreover, many compounds that promote
hair growth may be poorly tolerated by the scalp, especially during long-term treatments. This highlights the need for active ingredients that are both effective and well tolerated. Adenosine has been described to stimulate
hair growth by increasing growth factor secretion by HFDPC (Figure 4A).6
In order to assess the
ability of the SiAd complex to stimulate HFDPC proliferation while also increasing their secretion of both VEGF and KGF involved in angiogenesis and hair growth respectively, HFDPC were treated with SiAD (0.25%), or by an equivalent concentration of silicium or adenosine alone (Figure 4B,C,D). The SiAd complex stimulated HFDPC
proliferation by 13% while also increasing the September 2026 PERSONAL CARE MAGAZINE
VEGF secreted (% of control)
KGF secreted (% of control)
HFDPC number (% of control)
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