Dierickx, 1998  Title: Permanent hair removal by normal-mode
ruby laser.
Authors: Dierickx CC, Grossman MC, Farinelli
WA, Anderson RR
Journal: Arch Dermatol 1998 Jul;134(7):837-42
PMID: 9681347, UI: 98344672
Affiliated institution: Wellman Laboratories
of Photomedicine, Harvard Medical School, Boston, Mass 02114,
USA.
Cited in:
Williams overview
Lin
Full text is available at the Archives
of Dermatology website
Abstract
Objective: To assess the permanence of hair removal
by normal-mode ruby laser treatment.
Methods: Hair removal was measured for 2 years after
a single treatment with normal-mode ruby laser pulses (694 nm,
270 microseconds, 6-mm beam diameter).
Observations: Six test areas on the thighs or backs
of 13 volunteers were exposed to normal-mode ruby laser pulses
at fluences of 30 to 60 J/cm2 delivered to both shaved and wax-epilated
skin. In addition, there was a shaved and wax-epilated control
site. Terminal hairs were manually counted before and after laser
exposure. Transient alopecia occurred in all 13 participants after
laser exposure, consistent with induction of telogen. Two years
after laser exposure, 4 participants still had obvious, significant
hair loss at all laser-treated sites compared with the unexposed
shaved and wax-epilated control sites. In all 4 participants,
there was no significant change in hair counts 6 months, 1 year,
and 2 years after laser exposure. Laser-induced alopecia correlated
histologically with miniaturized, velluslike hair follicles. No
scarring and no permanent pigmentary changes were observed.
Conclusions: Permanent, nonscarring alopecia can
be induced by a single treatment with high-fluence ruby laser
pulses. Miniaturization of the terminal hair follicles seems to
account for this response.
Article
UNWANTED HAIR is a major cosmetic and surgical problem.
Many temporary hair removal methods exist, including shaving,
wax epilation, and use of chemical depilatories.[1,2] Electrolysis
is a well-established method for permanent destruction of terminal
hair follicles. However, the method is tedious, and efficacy has
been reported to range from 15% to 50% permanent hair loss.[3]
Scarring can occur after electrolysis, especially if inexpertly
performed.[4]
Damage to hair follicles based on the theory of
selective photothermolysis[5] has been reported recently.[6] Thirteen
volunteers with brown or black hair were exposed to normal-mode
ruby laser pulses (694 nm, 270 microseconds, 6-mm beam diameter)
at fluences of 30 to 60 J/cm2 delivered to both shaved and wax-epilated
skin sites on the thighs or back. In all 13 participants, laser
exposures produced a hair growth delay consistent with induction
of telogen. Ruby lasers have been commercialized for hair removal,
but the question remains whether permanent hair loss can be induced
by selective photothermolysis. Four study participants[6] had
clinically obvious hair loss at the final follow-up visit 6 months
after exposure, each of these with less than 50% regrowth of terminal
hairs. We decided to follow up the participants of this first
study at 1 and 2 years after laser exposure to evaluate the permanence
of hair removal.
PARTICIPANTS AND METHODS
Thirteen adult volunteers (12 men and 1 woman) consented
to participate, as previously described.[6] All had fair skin
(Fitzpatrick type I, II, or III) and brown or black hair. Test
sites were chosen on the back or posterior aspect of the thighs
based on uniformity and density of terminal hairs. Eight 3x2-cm
areas were mapped and photographed. Baseline hair counts were
obtained from each site by manually counting and marking terminal
hairs. Before laser exposure, half of the test sites were shaved
and half were epilated with cold wax (My-Epil, Laboratoire Suzy,
Montreuil, France). Sites were irradiated with a normal-mode ruby
laser, described below, at fluences of 0 (unexposed control),
30, 40, and 60 J/cm2. Laser pulses were given in a contiguous,
nominally nonoverlapping pattern that covered the entire test
site.
Clinical evaluation, terminal hair counts, and photographs
were obtained 1, 3, 6, 12, and 24 months after laser exposure.
One participant who had obvious alopecia in all laser exposure
sites at all of these follow-up visits consented to biopsy examination.
Three-millimeter punch biopsy samples were obtained before treatment
and at 1 year after laser exposure from a site with alopecia treated
at 60 J/cm2 after shaving. Tissue specimens were processed for
light microscopy of horizontal sections with a technique using
trisection or quadrisection that maintains all sections in the
same anatomic orientation (deep to superficial) on the microscope
slides.[7] All specimens were stained with hematoxylin-eosin for
light microscopy.
DATA ANALYSIS
Hair loss was defined as the percentage of terminal
hairs absent after treatment compared with the number before treatment.
For each site, at each follow-up visit, hair loss was calculated.
Results for each experimental condition were pooled for all participants.
The mean±SD for each condition was calculated. A paired t test
was used to determine significant differences (P<.05) between
posttreatment and pretreatment hair counts for each experimental
condition at the 6-, 12-, and 24-month observation times.
LASER AND DELIVERY APPARATUS
A normal-mode, flashlamp-pumped, 694-nm ruby laser
with a 270-microsecond pulse duration and a 6-mm spotsize was
used (model 936R4H-2, Lasermetrics, Winter Park, Fla). The beam
was steered via an articulated arm into an actively cooled "hand
piece" designed to maximize delivery of light into the reticular
dermis while minimizing epidermal injury. A planoconvex sapphire
lens (approximately 20-mm focal length) was used to provide a
convergent beam at the skin surface and to increase beam coupling
into the skin compared with air as an external medium. The sapphire
lens was cooled to 4…C to provide heat conduction from the epidermis
before, during, and after each laser pulse. The convex surface
of the cold sapphire lens was pressed firmly against the skin
before delivery of each laser pulse. Delivered pulse energy into
air was measured with a laser energy meter (model 351, Scientech,
Boulder, Colo).
RESULTS
HAIR LOSS
Results at 6 months' follow-up have been published
previously[6] but did not address the question of permanent hair
loss. Of the 13 participants, 7 were followed up for 2 years after
laser exposure. At 1 year and 2 years after laser treatment, 4
of these 7 participants still had obvious hair loss confined to
laser-treated sites and 3 had complete or nearly complete hair
regrowth. In all 7 participants, there was no significant change
in terminal hair counts 6 months, 1 year, and 2 years after laser
exposure.
Figure 1, left, illustrates hair loss on a participant's
back 1 year after laser exposure. The hair loss is fluence dependent,
with the greatest loss at the highest fluence (60 J/cm2). Figure
1, right, illustrates the same sites 2 years after treatment.
The same amount of hair loss is still present. Figure 2, top and
bottom, show the same site on an upper thigh treated with 60 J/cm2
at 3 months and 2 years, respectively. No substantial change in
the clinical appearance of the alopecia is seen. Neither pigment
changes nor scarring was seen in any participant at the 12- and
24-month follow-up visits.
Figure 1. Left, Test sites on the back 1 year
after ruby laser treatment. Site 1 was treated with 30 J/cm2,
site 2 was treated with 40 J/cm2, and site 3 was treated with
60 J/cm2. Site 4 was left untreated and served as a control. A
fluence-dependent regrowthis apparent. Right, Two years after
a single laser treatment, the same degree of hair loss is still
present. Figure 2. Hair loss in a test site on the thigh
treated with 60 J/cm2 3 months (top) and 2 years (bottom) after
treatment. Alopecia is still present at 2 years.
Hair loss at 6, 12, and 24 months after a single
laser exposure in the 4 participants showing permanent hair loss
are plotted vs fluence in Figure 3. Sites treated with 60 J/cm2
(highest fluence) after shaving had the greatest hair loss, 64.3%±1.1%.
Statistically significant hair loss was seen at 6 months for all
fluences at both shaved and epilated sites compared with the unexposed
shaved and epilated control sites. At 1 year and 2 years, there
was significantly less hair only in the shaved sites for all fluences
compared with the untreated control site.
HISTOLOGICAL FINDINGS
Terminal and velluslike (miniaturized) hairs were
identified on the transverse sections and counted by established
criteria.[8-10] Terminal-velluslike hair ratios were calculated
from the follicular counts, and fibrous tracts were recorded as
absent or present. Results are shown in the Table 1. The total
number of hairs was identical in the control and laser-treated
sites. However, in the laser-treated sites, there was a reduction
in large terminal hairs with a reciprocal increase in small velluslike
hairs. The average hair shaft diameter measured from the histological
sections also decreased after laser treatment (Figure 4). There
were no signs of fibrous tracts, and normal-appearing sebaceous
glands were still present around the miniaturized hair follicles.
Figure 4. Routine hematoxylin-eosin-stained
section (magnification x40) of untreated (top) and normal-mode
ruby laser-treated (bottom) areas. Miniaturized follicles were
present after laser treatment; the mean (±SD) diameter of the
hair shafts diminished from 68.7±44.2 to 22.5±12.2 µm.
COMMENT
The results of this study show that permanent loss
of terminal (coarse) hair can result from a single treatment with
high-fluence, normal-mode ruby laser pulses. The lack of change
in any participant's terminal hair counts beyond 6 months after
laser exposure suggests that 6 months' follow-up may be sufficient
to assess final outcome after treatment for hair removal.
The mechanisms by which high-fluence, normal-mode
ruby laser pulses induce selective damage to hair follicles[6]
are based on the principles of selective photothermolysis.[5]
At 694 nm, light penetrates well into and through the dermis,
and follicular melanin is by far the dominant chromophore in the
dermis.[11] Laser pulse width also seems to play an important
role, as suggested by the thermal transfer theory.[5] Thermal
conduction during the laser pulse heats a region around each microscopic
site of optical energy absorption. The spatial scale of thermal
confinement and resulting thermal or thermomechanical damage is
therefore strongly related to laser pulse width. Q-switched (nanosecond
domain) laser pulses effectively damage individual pigmented cells
within hair follicles by confinement of heat at the spatial level
of melanosomes,[12] leading in animals to leukotrichia but not
to hair loss after Q-switched ruby laser pulses.[13] Consistent
with this behavior, permanent hair loss has not been reported
in humans after Q-switched laser treatment despite a decade of
widely using Q-switched ruby and Nd:YAG lasers for tattoo removal.
The thermal relaxation time of whole hair follicles is between
1 and 100 milliseconds, depending on size. Thermal relaxation
of human terminal hair follicles has never been measured but is
estimated to be about 10 to 50 milliseconds.[6,14,15]
The 0.27-millisecond ruby laser pulses used in this
study were clearly long enough to cause thermal coagulation and
vaporization injury of hair follicles,[6] leading to a growth
delay[6] in all participants and permanent hair loss in some.
However, in theory, the longer-pulse (3-millisecond) ruby laser
now commercially available for hair removal may be more ideal
for several reasons. First, it is still unknown which "targets"
in hair follicles are responsible for permanent hair loss. A somewhat
longer pulse width should allow more thermal conduction and damage
to nonpigmented regions of the hair follicle but retain confinement
on the spatial scale of the follicle itself. Second, the efficiency
of extracting heat from the epidermis during each laser pulse
into cold sapphire in contact with the skin surface should be
improved with the longer laser pulse.
The biologic mechanisms by which ruby laser pulses
cause permanent loss of terminal hair remain unknown. However,
this study strongly suggests that miniaturization of coarse terminal
hair follicles to velluslike hair follicles is involved, producing
nonscarring alopecia. Only 1 participant with laser-induced alopecia
was examined histologically 1 year after laser exposure, and more
should be studied as the number of people with laser-induced alopecia
grows. In this participant, however, there was an absence of fibrosis
or any remnant of laser-damaged hair follicles, a decrease in
terminal hair follicles, and a reciprocal increase in miniature
hair follicles. These histological findings are also consistent
with clinical observations. A miniaturized terminal hair or secondary
vellus hair is arbitrarily defined as having a cross-sectional
hair shaft diameter of less than 30 mm.[9] Because the size of
a hair depends on the size of the papilla and the hair bulb,[16]
ruby laser pulses seem to miniaturize the papilla and the bulb
either by direct photothermal injury or by injury to other structures
of the follicle that control formation of the bulb with each anagen
cycle.
The histological picture of miniaturized follicles
after ruby laser pulses corresponds with the histological picture
of androgenetic alopecia.[8,9,17] Male baldness is characterized
by a proportional reduction in size of the papilla and the matrix.[16]
Therefore, the terminal follicles are gradually transformed to
velluslike follicles. "Loss" of hair in androgenetic
alopecia only relates to the loss of terminal hairs and is similar
to "loss" of hair after ruby laser treatment. The follicles
are not actually lost but produce hairs that are shorter, finer,
and less pigmented. These miniaturized follicles still have arrector
pili muscles.[8] Pluripotent stem cells of the bulge—a region
of follicular epithelium near the insertion of the arrector pili
muscles—regenerate epidermis during wound healing.[18,19]
To the extent that ruby laser-induced alopecia is like male pattern
alopecia, wound healing should not be largely affected after laser
hair removal.
We hypothesize and suggest that the 2 distinct responses—growth
delay and permanent hair loss—are caused by induction of
telogen and miniaturization of terminal hair follicles, respectively.
Numerous observations are explained by this hypothesis. In all
13 participants, whether they had measurable permanent hair loss
or not, there was a growth delay consistent in length with telogen.
Presence of the hair shaft during laser exposure was not essential
to induce growth delay, which occurred at all fluences in both
shaved and epilated sites in all participants.[6] Presumably,
there is enough ample melanin present because epilation typically
breaks the hair shaft above, in the upper third of, or at the
midlevel of the bulb.[20] In contrast, permanent hair loss after
a single laser exposure was significant only in sites that were
shaved (hair shaft present) rather than wax epilated and was fluence
dependent. Both responses are clinically significant and may be
separately desirable to different patients. Growth delay that
provides a few months of hairless skin is far more reliable and
requires lower fluences than permanent hair loss. Permanent hair
loss occurred in this study in only 4 of the 13 participants after
a single treatment.
Knowledge of the hair cycle and particularly of
the length of telogen is essential for interpretation of the results
of this study. At present, no consensus exists on a definition
for treatment-induced "permanent" hair loss despite
frequent use of the term to describe the effects of electrolysis.
We suggest, and hereby use, the following specific definition:
"permanent" hair loss is a significant reduction in
the number of terminal hairs after a given treatment that is stable
for a period longer than the complete growth cycle of hair follicles
at the given body site. Telogen may last for 3 to 7 months on
the thighs and chest,[21,22] after which the follicle will recycle
into anagen, which also lasts 3 to 7 months on the body. Our observation
period of 24 months after a single laser treatment therefore spans
2 to 4 complete growth cycles, depending on the length of the
telogen phase. The data show gradual reappearance of terminal
hair up to 6 months after laser exposure, which is consistent
with recovery of terminal hair follicles within 1 growth cycle.
Thereafter, the data show no significant difference in hair counts
6 months, 1 year, and 2 years later, which is consistent with
no further recovery of terminal hair follicles. This strongly
suggests that whatever terminal hair follicles were inactivated
at 6 months were also missing for at least 2 years, although we
did not map and track individual hair follicles in this study.
For studies of laser or other treatments intended to induce hair
loss, we suggest that measurements be carried out until a steady
state is achieved, which in this study seems to be between 6 months
and 1 year. A distinction also needs to be made between permanent
and complete hair loss. Complete hair loss refers to a lack of
regrowing hairs (ie, a significant reduction in the number of
regrowing hairs to zero). Complete hair loss may be either temporary
or permanent. Ruby laser treatment usually produces complete hair
loss for 1 to 3 months, followed by partial permanent hair loss.
Finally, it is likely, but as yet unproven, that
the sensitivity of human hair follicles to laser pulses varies
with the hair growth cycle. In this study of responses after a
single treatment, the hairs "resistant" to permanent
inactivation by laser treatment may have been mainly in the telogen
stage at the time of exposure. On the thighs, up to 72% of the
hairs are in telogen.[21] Selective photothermolysis requires
absorption of light, and the bulb of a telogen hair is unpigmented
because of cessation of melanogenesis during catagen.[23] On the
other hand, as anagen progresses, the bulb and papillae descend
deeply into the dermis and beyond such that late anagen hairs
may also be relatively resistant to laser pulse injury. By this
reasoning, follicles should be most easily inactivated by laser
pulses during early anagen. If so, the reliable induction of telogen
with a single laser treatment, as we suggest, has profound clinical
implications. As the "surviving" terminal follicles
transition into anagen, after growth delay, a second treatment
may be more effective than the first. On the contrary, a second
treatment given too early or too late may have little effect.
We are presently investigating these interesting questions.
From the Wellman Laboratories of Photomedicine,
Harvard Medical School, Boston, Mass (Drs Dierickx and Anderson
and Mr Farinelli), and the Laser and Skin Surgery Center of New
York City, New York, NY (Dr Grossman).
Accepted for publication December 8, 1997.
This study was supported by funds from the Wellman
Laboratory of Photomedicine, Harvard Medical School, Boston, Mass.
Presented in part at the 1997 American Society
for Laser Medicine and Surgery, Phoenix, Ariz, April 4, 1997.
We thank Thomas Flotte, MD, for his assistance
with the histology slides.
Reprints: R. Rox Anderson, MD, Wellman Laboratories
of Photomedicine, Bartlett Extension 6, 50 Blossom St, Boston,
MA 02114.
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