美絲 Sunetic 激光活髮

本中心特從美國訂購了一部,與 Dr Friedman 生髮研究中心相同型號的激光罩 Sunetic LaserHood ,用於強化毛囊。Sunetic 已通過 美國食品和藥物安全局 的 510(k) 驗証,能有效改善成年男性和女性的遺傳性脫髮 (Androgenetic Alopecia),促進毛囊再生,可用於改善:

•   男士脫髮 - 促進頭髮生長以改善 (雄性禿第二至五期)
•   女士脫髮 - (Ludwig Savin 第一、二期; Fitzpatrick 第一至五期)


也被稱為低能量激光療法、光療、冷激光治療,光生物調整,生物刺激及光線療法,這些療法已在餘千的出版刊物、廣泛流傳、證明了光療能有效地維持毛囊細胞的正常生長和功能,可用於改善雄性禿及其他類型的脫髮問題。已有餘千的出版刊物,報導激光或低能量激光能有效地增加細胞的存活,增殖和功能。激光的光波被細胞的線粒體 mitochondria 吸收後,會增加細胞呼吸,並通過活性氧的誘導,激活細胞核的轉錄因子的。臨床對照試驗顯示,激光能夠刺激和保存受雄激素性脫髮及其他脫髮症影响毛囊。

在 2009 年美國藥物管理局 FDA 經業界評議研究,決定批准激光合法成為激發頭髮重新生長的產品。壞死或嚴重萎縮的毛囊,雖然不能死裡跑生,但若在脫髮初期便進行光療,相信能顯著改善頭髮的密度和質量。 已有臨床研究報導激光能刺激體外培養的人類毛囊中,並加速小鼠毛髮的再生長。一般男士或女士脫髮均可適用。更可用與植髮藥物治療一并使用,得到更顯著的改善。其功效包括:

•   增加細胞代謝,速進毛囊的血液循環
•   刺激皮脂腺讓頭髮更亮麗
•   增加毛囊的黑色素分泌讓頭髮更烏黑


激光生髮療法, 也被稱為低能量激光療法、光療、冷激光治療,光生物調整,生物刺激及光線療法,這些療法已在餘千的出版刊物、廣泛流傳、證明了紅激光或低能量激光能有效地增加細胞的存活,增殖和功能。紅激光的光波被細胞的線粒體 mitochondria 吸收後,會增加細胞呼吸,並通過活性氧的誘導,激活細胞核的轉錄因子。以下收錄光學專家 Dr Hamblin 的一篇著作。

Scientific Study - Low Level Laser Therapy for Hair Growth 2009

Since the first pioneering publication of Mester [1] reported stimulation of hair growth in mice, there have been virtually no follow-up studies on LLLT stimulation for hair growth in animal models. Mester’s study involved delivering 1 J of pulsed light (1 millisecond pulse duration) into a 1 cm2 spot from a ruby laser at 694-nm to the depilated abdominal area of black C57 and white Balb/c mice every week for up to 11 weeks. Before each successive treatment the skin was again depilated. Increased hair growth in the irradiated spot growth was observed in all black animals between the 5th and 7th treatment. This reaction continued to the 9th treatment and it was characteristic of the hair growth intensity that in places that were completely bare at the time of the respective irradiation, hair growth as dense as on other body parts was observed only 4 – 6 days after the irradiation. On the other hand, it was found after the 9th irradiation that hair growth stopped in the irradiated locations only. Instead, a peripheral, ringshaped hair growth was observed around the irradiated area. This ring-shaped hair growth first appeared in the animal on which the central growth stimulation was first observed. The peripheral growth appeared in all treated black mice between the 7th and 9th irradiation with the intensity varying from mouse to mouse. In white mice no effect on hair growth was detected up to the 8th irradiation. The central growth described for black mice only began to form after the 8th irradiation. Further irradiation caused the hair growth just described in some of the mice, but the peripheral hair growth characteristic of the 2nd phase was already appearing in some as well. The hair growth of the control animals developed as follows: The depilated skin grew hair slowly and diffusely. However, on half of the control animals (both among black and white mice), no further hair growth whatsoever was observed. At the same time, a diffuse hair growth appeared on some animals, but in other animals an uncharacteristic, sometimes diagonal strip appeared.

Despite the fact that LLLT devices are widely marketed and used for hair regrowth, there have been only a few literature reports containing some observations of LLLT-induced hair growth in patients, and amelioration or treatment of any type of alopecia. A Japanese group reported [49] on the use of Super Lizer (a linear polarized light source providing 1.8W of 600 – 1600-nm light) to treat alopecia areata. Three minute sessions every one or two weeks produced significant hair growth compared to non-treated lesions in 47% of patients. A Spanish group has reported [50, 51] on the use of HeNe laser for both alopecia androgenic and areata. A report from Finland [52] compared three different light sources used for male-pattern baldness (HeNe laser, InGaAl diode laser at 670-nm and non-coherent 635-nm LED and measured blood flow in the scalp.

Recent work has uncovered some biological mechanisms involved in the regulation of hair growth that could be good candidates to explain the stimulating effects of LLLT. Peters et al [53] found that nerve growth factor (NGF) promotes proliferation via its high affinity receptor (TrkA). and identified NGF and p75 as important hair growth terminators. By rtPCR we found, that NGF/proNGF mRNA levels peak during early anagen in murine back skin while NGF/proNGF protein levels peak during catagen, indicating high turnover in early anagen and protein accumulation in catagen. By immunohistochemistry, NGF and TrkA were found in the proliferating compartments of the epidermis and hair follicle throughout the cycle. Commercial 7S NGF, which contains both NGF and proNGF, promotes anagen development in organ-cultured early anagen mouse skin, while it promotes catagen development in late anagen skin. Therefore the data suggest an anagen-promoting/-supporting role for NGF/TrkA.

Another report from this group [54] studied the expression and function of p75 neurotrophin receptor (p75NTR), which is implicated in apoptosis control in spontaneous catagen development in murine skin. They found that p75NTR alone was strongly expressed in TUNEL+/Bcl2- keratinocytes of the regressing outer root sheath, but both p75NTR and TrkB and/or TrkC were expressed by the nonregressing TUNEL- /Bcl2+ secondary hair germ keratinocytes. There was significant catagen retardation in p75NTR knockout mice as compared to wild-type controls. Instead, transgenic mice over expressing NGF (promoter: K14) showed substantial acceleration of catagen.Schwartz et al [55] reported in 2002 that helium/neon laser irradiation (3J/cm2) augmented the level of NGF mRNA fivefold and increased NGF release to the medium of myotubes cultured in vitro. This correlated with a transient elevation of intracellular calcium in the myotubes. Yu and coworkers found a significant increase in nerve growth factor release from cultured human keratinocytes. [27]. Therefore it is postulated that LLLT may influence hair regrowth via the NGF/ p75NTR signaling system.

Zcharia and colleagues [56] identified the endoglycosidase, heparanase, as an Important regulator of murine hair growth. Degradation of the extracellular matrix barrier formed by heparan sulfate by heparanase enables cell movement through extracellular barriers and releases growth factors from extracellular matrix depots, making them bioavailable. This allows follicular stem cell progeny migration and reconstitution of the lower part of the follicle, which is a prerequisite for hair shaft formation. Heparanase contributed to the ability of the bulge-derived keratinocytes to migrate through the extracellular matrix barrier in vitro. In heparanase-overexpressing transgenic mice, increased levels of heparanase enhanced active hair growth and enabled faster hair recovery after chemotherapy-induced alopecia. Thymosin beta4 (TB4) is a 43-amino acid polypeptide that is an important mediator of cell migration and differentiation, also promotes angiogenesis and wound healing [57]. Philp et al [58] reported that TB4 stimulated hair growth in normal rats and mice. A specific subset of hair follicular keratinocytes in mouse skin expressed TB4 in a highly coordinated manner during the hair growth cycle. These keratinocytes originated in the hair follicle bulge region, a niche for skin stem cells. Rat vibrissa follicle clonogenic keratinocytes, closely related, if not identical, to the bulge-residing stem cells, were isolated and their migration and differentiation increased in the presence of nanomolar concentrations of TB4. Expression and secretion of the extracellular matrix degrading enzyme matrix metalloproteinase-2 were increased by TB4. Thus, TB4 accelerated hair growth, in part, due to its effect on critical events in the active phase of the hair follicle cycle, including promoting the migration of stem cells and their immediate progeny to the base of the follicle, differentiation, and extracellular matrix remodeling.

A recent report [59] identified the transforming growth factor-beta family member activin is a potent regulator of skin morphogenesis, repair and hair growth. Mice overexpressing the secreted activin antagonist follistatin, however, have the reduced hair growth. Mice expressing a dominant-negative activin receptor IB mutant (dnActRIB) in keratinocytes had unaltered architecture of adult skin, but delays were observed in postnatal pelage hair follicle morphogenesis and in the first catagen-telogen transformation of hair follicles.As yet there are no reports of LLLT affecting heparanase, TB4, or activin expression levels in tissue culture or in mouse skin, but these molecules are good candidates for further study to explain the hair growth-induction by LLLT.