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CH. Low-level light therapy for androgenetic alopecia: a 24-week, randomized, double-blind, sham
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The Evolution
ofPhotobiomodulation
fortheTreatment ofHair Loss
RobertHaber
5
Hair loss has been a persistent concern for humanity throughout history. From ancient remedies to
modern medical innovations, various approaches
have been explored to address this cosmetic issue.
One such innovative approach is light-based therapy, which involves the use of specic wavelengths
of light to stimulate hair follicles and promote hair
growth. Over the years, light-based therapy for hair
loss has undergone signicant evolution, merging
ancient wisdom with cutting-edge technology. This
chapter will explore the development of light-based
therapy for hair loss, from its early roots to its contemporary applications.
The use of light as a therapeutic agent traces
back to ancient civilizations. Historical records
indicate that ancient Egyptians and Greeks recognized the potential of sunlight in promoting
general health and treating various ailments,
including hair loss. The concept of heliotherapy,
or sun therapy, prevailed as a practice to enhance
well-being. Although these early civilizations
didn’t have a precise understanding of the underlying mechanisms, their observations laid the
groundwork for future developments.
In ancient India, Ayurvedic medicine emphasized the holistic approach to health and healing.
Ayurvedic texts mentioned techniques involving
massage, herbal remedies, and sun exposure to
R. Haber (*)
Clinical Professor of Dermatology, Case Western
Reserve University School of Medicine, Cleveland,
OH, USA
address hair loss. The holistic philosophy of
Ayurveda recognized the interconnectedness of
the body, mind, and spirit, which contributed to
the integration of light-based therapies in the
treatment of hair-related issues.
The scientic understanding of light and its
effects on biological systems progressed signicantly in the nineteenth and twentieth centuries.
Pioneers like Niels Finsen, a Danish physician,
won the Nobel Prize in Physiology or Medicine
in 1903 for his work on light therapy for diseases
like lupus vulgaris, a skin tuberculosis. Finsen’s
research laid the foundation for comprehending
the therapeutic potential of light in medical
applications.
In the mid-twentieth century, the concept of
low-level laser therapy (LLLT) began to emerge.
The Hungarian researcher Endre Mester conducted experiments on mice, demonstrating that
low-level laser irradiation could stimulate hair
growth and wound healing [1]. Mester’s ndings
sparked interest in exploring the potential of
lasers for hair loss treatment.
The late twentieth century witnessed signicant advancements in laser technology, enabling
the development of devices specically designed
for hair loss treatment. Laser hair combs and helmets became commercially available, offering
individuals a non-invasive approach to address
hair thinning and balding. These devices utilized
low-level lasers or light-emitting diodes (LEDs)
to deliver controlled light energy to the scalp.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
P. J. Panagotacos, H. Maibach (eds.), Hair Loss, Updates in Clinical Dermatology,
https://doi.org/10.1007/978-3-031-74314-6_5
65
66
R. Haber
Eventually, clinical studies sought to establish
the efcacy of light-based therapy for hair loss.
Rigorous research methodologies were employed
to evaluate the benets of these treatments.
Several studies demonstrated positive outcomes,
showing increased hair density and improved
hair growth in participants who underwent lightbased therapy.
The accumulating clinical evidence led to regulatory approvals from organizations such as the
U.S.Food and Drug Administration (FDA). Laser
devices for hair loss treatment gained recognition
as safe and effective options for individuals seeking non-pharmacological interventions. These
approvals provided a signicant boost to the
credibility and acceptance of light-based therapy
within the medical community.
During the formative years of this eld of
study, non-specic and inaccurate terminology
was introduced and entered mainstream use,
including low level laser therapy and low level
light therapy, among many others. A more scientically accurate terminology was needed,
and as early as 2003 Juanita Anders, PhD along
with her scientic team coined the more accurate term photobiomodulation. Unfortunately, it
was not until 2016 that photobiomodulation
therapy was added to the National Library of
Medicine’s MeSH database as a search term,
following an article published by Dr. Anders
etal. the prior year [2].
Photobiomodulation (PBM) is the mechanism
by which non-ionizing optical radiation in the
visible and near-infrared spectral range is
absorbed by endogenous chromophores to elicit
photo-physical and photo-chemical events at various biological scales.
Photobiomodulation therapy (PBMT) is a
photon therapy based on the principles of PBM.It
involves the use of non-ionizing forms of light
sources including lasers, LED’s, and broadband
light, in the visible and infrared spectrum to
cause physiological changes and therapeutic benets. The putative target for PBM is the mitochondria, the cellular engine critical for cell
health and survival. Any cell with mitochondrial
downregulation will not function properly, and
PBM, by targeting mitochondrial chromophores,
upregulates this structure resulting in improved
cellular function. Hair follicle cells, due to their
proximity to the skin surface, can be reached by
externally applied light sources, thus the role of
PBM in the treatment of hair loss.
While there is a wide assortment of therapeutic devices available for consumer use, there
remains a paucity of scientic data regarding the
ideal treatment wavelength, power output and
duration of therapy. As clinicians, we are asked
by our patients if PBM actually works, and if it
does, which devices and protocols are best. The
eld of hair loss treatment has also long been tarnished by unethical practitioners hawking ineffective remedies, so it is incumbent upon ethical
practitioners to be aware of the development of
treatment devices and justications for treatment
recommendations.
The goal of a clinician reading a chapter about
PBM is to glean information that can be applied
in the ofce setting. Clinicians are bombarded
with claims of superiority when it comes to light
based devices, whether it be wavelength, power,
comfort, efcacy or some combination, and our
patients expect us to distill these claims into a
specic recommendation.
Ideally, data would exist to scientically
specify the ideal wavelength, power and treatment time. Unfortunately, such data does not in
fact exist, in spite of the high level research that
has been performed by experts such as Mike
Hamblin and Juanita Anders among others, and
it’s possible that some questions will never be
answered. Therefore, to utilize PBM we must
instead rely on partial data and personal
experience.
All clinicians experienced with photobiomodulation have responders and non-responders, and
the proportion of each will color our enthusiasm
for this treatment modality. As with many treatments, patient selection is important, but just as
the ideal treatment parameters are unknown, so
are ideal patient characteristics unknown.
Hair loss specialists have a limited selection
of treatments to choose from, and thus PBM,
even with all of its unknowns, will be used since
it is well documented to provide benets to the
correct patient population. It’s also cost effec-
5 The Evolution ofPhotobiomodulation fortheTreatment ofHair Loss
67
tive, as it’s the only treatment that gets cheaper
the longer one uses it as there are no consumables associated with its use. PBM also has
good peer reviewed support in the literature. In
fact, there is more peer reviewed support for
photobiomodulation than for platelet rich
plasma (PRP) treatments, another popular hair
loss treatment [3–16].
Photobiomodulation rst became commercially available to clinicians in the 1990’s in the
form of large ofce-based devices from companies such as Sunetics (Sunetics International
Marketing Group LLC, Dallas, Texas) (Fig.5.1).
Patients were required to visit an ofce several
times each week to undergo treatments (Fig.5.2).
This was inconvenient, but at the time there was
no alternative.
In 2003, the rst helmet-based device appeared
on the market (iRestore Laser, Irvine, CA)
(Fig.5.3), but this was cumbersome and not discrete, and had limited consumer acceptance. The
Lasercomb was introduced in 2004 containing a
small linear array of laser diodes, and instructions directed the user to move the device on the
scalp every 4s for a 15min period (Fig.5.4). This
translates to 225 movements per treatment session, and while effective if performed properly,
long term compliance was very difcult to
achieve outside of a research environment. In
2008 the Theradome was introduced (Theradome,
Inc. Pleasanton, California) which functionally
and visually added little to the available devices
and was certainly not something a patient would
wear in public (Fig.5.5).
While all of these devices were functional,
each had features that negatively impacted compliance and patient acceptance. The eld needed
Fig. 5.1 Example of large, ofce based Sunetics PBM
device
Fig. 5.2 Ofce based devices require patients to visit the
ofce several times each week for treatments. Image courtesy of Dr. Robert Leonard
68
R. Haber
Fig. 5.3 The iRestore device has a hard shell resembling
a bicycle helmet
Fig. 5.4 The HairMax Lasercomb requires frequent hand
movements during each treatment session
something disruptive, and two important advancements happened in 2009. First, Leavitt, etal. published the rst peer reviewed report presenting a
PBM device granted 510(k) clearance by the FDA
Fig. 5.5 The Theradome is another hard shelled device
resembling a bicycle helmet
[3]. This groundbreaking study of the Lasercomb
(Lexington Intl., LLC, Boca Raton, Fl) set the
stage for all subsequent treatment devices. Second was the introduction of the LaserCap (Transdermal Cap, Inc., Highland Heights, Ohio) which
was the rst discrete, powerful wearable device to
deliver photobiomodulation therapy (Fig. 5.6).
The device could t inside any ballcap or other
hat, was powered by a belt mounted battery, and
thus could deliver high energy while the wearer
was performing other routine activities. The
LaserCap changed the entire industry, and its success spawned a series of imitators including
Capillus in 2013, followed by Kiierr, Bosley and
others over the next decade.
As mentioned previously, there is no proven
ideal treatment wavelength, power output or duration of therapy. However, sound scientic principles can be used to make treatment
recommendations. Importantly, the depth of penetration into the skin is determined purely by wavelength and is not affected by power or treatment
duration. And as the hair follicles are fairly
supercial, deeply penetrating wavelengths do not
offer therapeutic advantages. Red light lasers and
diodes emitting in the 650nm wavelength range
are readily available and penetrate to the hair follicle depth, and thus are the most commonly used
in consumer devices. Devices offering additional
wavelengths do so for marketing benet and generally without data to support those wavelengths.
5 The Evolution ofPhotobiomodulation fortheTreatment ofHair Loss
Fig. 5.6 The LaserCap
administers higher laser
power than other
devices, and is discrete
when worn
69
Power and duration are important, as the mitochondria need to receive sufcient energy to
undergo upregulation, even if the exact amount of
energy is not known. Most experts recommend
treatments of 30min duration every other day. It
is possible to expose the mitochondria to too
much energy and this will result in an inhibitory
effect. Therefore, patients should be discouraged
from utilizing these devices on a daily basis, or
for many hours at a time. Devices that recommend treatment durations of less than 10min are
most likely underdosing and often these devices
also provide lower power output.
As with all hair loss therapies, most patients
will benet from reduced shedding and subsequent stabilization of hair loss. A small percentage
will enjoy increased visible density. Subtle results
are all we can sometimes expect with photobiomodulation, generally seen as a reduction in part
width, a common clinical assessment of treatment
efcacy (Fig. 5.7a–c). Patients will often also
report subjective improvements in hair texture and
shine, and this along with the increased density
generally results in high patient satisfaction.
Research in this eld continues to expand,
investigating optimal wavelengths, energy doses,
and treatment protocols. In addition, further
understanding of the mechanism of action of
PBM may reveal effects on blood circulation and
nutrient delivery to the scalp, as well as promoting cell proliferation and reducing inammation.
Photobiomodulation may also play a role in
reducing inammation and accelerating hair
growth after hair restoration surgery.
The landscape of light-based therapy for hair
loss continues to evolve with advancements in
technology and scientic understanding. Today, a
wide array of devices, ranging from wearable
helmets to handheld combs, is available for consumers. These devices often combine different
wavelengths of light and innovative features to
enhance treatment outcomes.
Moreover, researchers are exploring the synergistic effects of light-based therapy with other
treatments, such as topical medications and
regenerative therapies. The combination of multiple modalities aims to maximize hair growth
potential and provide comprehensive solutions
for individuals experiencing hair loss.
The journey of light-based therapy for hair
loss encompasses a rich historical tapestry, from
ancient civilizations recognizing the healing
power of sunlight to modern-day clinical applications backed by scientic evidence. This innovative approach bridges tradition and technology,
offering individuals an alternative avenue for
managing hair loss. As technology continues to
advance and research deepens our understanding,
the future holds promise for further renement
and customization of light-based therapy, providing hope for those seeking effective solutions to
hair loss.
70
R. Haber
a
b
c
Fig. 5.7 (a–c) In each of the examples, a signicant
reduction in part width can be seen after therapy with the
LaserCap
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Alopecia Areata: JAK Inhibitors—PRP
andExosomes
DorisDay
6
Description
Alopecia Areata typically manifests as one or
several round or oval non-scarring patches of hair
loss. The skin appears normal, without signs of
inammation or scarring [1]. A tell-tale sign of
alopecia areata are “exclamation point hairs,
which are short, broken hairs that are narrower
near the scalp and wider at the broken or tapered
end, resembling an exclamation point” [2]. They
are often seen at the edges of the bald patches in
individuals with alopecia areata.
Exclamation point hairs are considered a clinical sign of active hair loss and are indicative of
the disease’s autoimmune nature. They result
from inammation and damage to the hair follicles in alopecia areata, causing the hair to become
weak and break off at the scalp [2].
Over time, multiple patches can occur, coalesce,
or expand, leading to more widespread hair loss.
Alopecia Totalis (AT). This form is characterized
by the complete loss of all hair on the scalp. It can
emerge as a progression from the patchy form, or
it can present as the initial manifestation. Alopecia
Universalis (AU) the most severe form, involves
hair loss across the entire body, including eyebrows, eyelashes, and even nasal and ear hair [3].
D. Day (*)
NYU Langone Health, New York, NY, USA
e-mail: drday@dorisdaymd.com
This condition often signies a broader and more
aggressive autoimmune response.
Diagnosis
The diagnosis for AA, AT, and AU primarily
remains clinical, but more extensive presentations might require more intensive investigations
to rule out associated autoimmune disorders or
underlying triggers and to ascertain if there are
concomitant autoimmune conditions.
Clinical Examination
Pull Test: Gentle traction is applied to affected
areas. Positive results indicate active disease.
Dermoscopy: This can reveal yellow dots
(dilated follicular orices lled with keratin), black
dots (broken hairs), and short vellus hairs [2, 4].
Biopsy andHistology
When clinical features are ambiguous, a 4-mm
punch biopsy is performed where the hair is
sparsest within the alopecic patch [5]. In AA,
early lesions show peribulbar lymphocytic
inammation (“swarm of bees”) around anagenphase hair follicles. Advanced lesions may
exhibit brosis [6].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
P. J. Panagotacos, H. Maibach (eds.), Hair Loss, Updates in Clinical Dermatology,
https://doi.org/10.1007/978-3-031-74314-6_6
71
72
D. Day
Pathophysiology
The onset and progression from AA to AT or AU
depend on a complex interplay of genetic factors,
immune dysregulation, and potentially environmental triggers. The hair follicles in the anagen
phase become the target of immune cells, with
the exact trigger remaining elusive.
Molecular Mechanisms
At the molecular level, AA is characterized by
the presence of autoreactive T cells which target
the hair follicles, primarily in their active growth
(anagen) phase. This immune-mediated attack
leads to the disruption of the hair growth cycle.
Immune Cell Inltration
Histological analysis of AA lesions commonly
reveals a peri-follicular lymphocytic inltrate.
CD8+ NKG2D+ effector T cells target the hair follicle, releasing pro-inammatory cytokines such
as IFN-γ and TNF-α, culminating in hair loss.
Cytokine Disruption
There’s an upregulation of the Th1 cytokines
(like IFN-γ) in the affected scalp areas. This cytokine milieu pushes hair follicles from the anagen
(growth) phase to the telogen (rest) phase, inhibiting hair growth.
The treatment goal for all forms of AA, including AT and AU, is to suppress the immune
response against the hair follicles and promote
hair regrowth [8]. The treatment goal for all
forms of AA, including AT and AU, is to suppress
the immune response against the hair follicles
and promote hair regrowth [9].
Topical Treatments
Topical corticosteroids: Corticosteroids: Act by
suppressing the local immune response.
Topical Steroids: Patient Selection: Ideal for
those with <25% scalp involvement.
Application: Potent corticosteroid cream/ointment is applied to bald patches once or twice daily.
Duration: Continued for a few weeks then
intermittently as needed, with regular follow up
to ensure no atrophy noted.
Localized treatments
Intralesional Corticosteroids: Patient Selection:
Those with limited patchy AA or patients in
which topical treatments are ineffective.
Drug Selection: Triamcinolone acetonide
0.1% (2–5mg/ml).
Administration: Injected into the mid-toupper dermal layer. Repeat treatments at 4–6week intervals as needed.
Systemic treatments
Genetic Predisposition
Genetic factors undeniably play a role.
Genome- wide association studies have identied several potential genes located on various
chromosomes that may heighten susceptibility
to hair loss [7].
Treatment Paradigms
Modern treatments encompass traditional methods and cutting-edge technologies and techniques.
Oral Corticosteroids and Immunosuppressants:
These suppress the overarching immune response,
sometimes offering relief in more extensive cases.
Broad-spectrum immunosuppressants:
Methotrexate, cyclosporine, or azathioprine can
be useful, especially in treatment-resistant cases.
Cutting-Edge Therapeutic Interventions
JAK Inhibitors: These represent the newest class
of FDA-approved drugs that interrupt the Janus
kinase-signal transducer and activator of tran-