Hair stimulation following laser and intense pulsed light photo-epilation: Review of 543 cases and ways to manage it

Abstract

BACKGROUND Stimulation of terminal hair growth following photo- epilation is a poorly understood problem with significant clinical relevance. We have observed this problem in a number of patients in our dermatologic laser practice in Basque Country Spain. To better evaluate the incidence and character of this phenomenon a retrospective chart review was performed on all patients who received laser and intense pulsed light (IPL) photo-epilation at this single center within the 5-year period from December 1998 to December 2003. Patient images before and after treat- ments were compared (digital images after 1999 and non- digital images before year 1999) and the medical history reviewed. METHODS Five hundred forty-three patients with Fitzpatrick skin types II, III, and IV (13%, 68%, and 19%, respectively) ranging in age from 16 to 52 years received laser and/or IPL hair photo-epilation of the beard, neck and chin areas, excluding the upper lip. The number of treatments received by each patient ranged from 3 to 23. Hair epilation treatments were performed using a long pulsed 755 nm alexandrite laser (Gentlelase, Candela, Wayland, MA) and IPL source (Epilight, Lumenis, Santa Clara, CA) and a 1,064 nm Nd:YAG (Lyra, Laserscope, San Jose, CA). Only 10% of the treatments were performed with the 1,064 nm Nd:YAG laser. Treatments were usually performed every 2-3 months. The alexandrite laser was used in 85% of the treatments, IPL in 10% and Nd:YAG in 5%. The parameters used are listed in Table 1. RESULTS Of the 543 patients who received laser/IPL hair photo- epilation, 57 (10.49%) demonstrated an increase in hair growth compared to baseline. The increased hair growth occurred within the area that was treated and also in the areas bordering the treated area, and appeared thicker and darker than the hairs initially treated (Figs. 1 and 2). An additional 44 (8.10%) patients demonstrated no apparent reduction in hair growth following treatment. Four hundred twenty-four patients (78.08%) demonstrated a decrease in hair growth with ongoing treatments. Only 14 patients (2.5%) were discharged from the clinic due to near complete hair reduction. These results are summarized in Table 2. The increased terminal hair growth occurred mostly in areas in which fine hair or both fine and coarse hair was present prior to initiation of treatment. Hair growth occurred with greater frequency in patients treated with the Alexandrite and IPL devices compared those treated with the Nd:YAG, however, the later device was used less frequently. Patients that developed terminal hair growth were in the following age groups: 19-31 years, 44 patients; 30-40 years, 8 patients; greater than 40 years, 5 patients. The onset of increased terminal hair growth was noted between the third and tenth treatment in 39 (72.2%) of 57 patients, and 11 (19%) of 57 between the third and fourth treatment. Most patients had a normal hormonal history. Sixteen patients had irregular menses or documented ovarian cysts. Because the terminal hair growth occurred both within the treated areas and also at the periphery of treated areas it was thought that sub-therapeutic thermal energy delivered to nearby follicles induced terminal hair growth. Subsequent application of cold packs surrounding the treatment area during treatments and treating all patients with two passes has minimized the incidence of terminal hair growth (Fig. 3). Since we have instituted this method in our clinic 2 years ago, we have treated over 200 patients and have not had any patients with hair growth stimulation. DISCUSSION

Full text

Lasers in Surgery and Medicine 39:297–301 (2007)
Hair Stimulation Following Laser and Intense Pulsed Light
Photo-Epilation: Review of 543 Cases and Ways to Manage It
Andrea Willey, MD,
1
* Jaioae Torrontegui, RN,
2
Jose Azpiazu, MD,
2
and Nerea Landa, MD
2
1
Oregon Health & Science University, Portland, Oregon 97239
2
Dermitek Clinic, Bilbao, Basque Country, Spain
BACKGROUND
Stimulation of terminal hair growth following photo-
epilation is a poorly understood problem with significant
clinical relevance. We have observed this problem in a
number of patients in our dermatologic laser practice in
Basque Country Spain. To better evaluate the incidence
and character of this phenomenon a retrospective chart
review was performed on all patients who received laser
and intense pulsed light (IPL) photo-epilation at this single
center within the 5-year period from December 1998 to
December 2003. Patient images before and after treat-
ments were compared (digital images after 1999 and non-
digital images before year 1999) and the medical history
reviewed.
METHODS
Five hundred forty-three patients with Fitzpatrick skin
types II, III, and IV (13%, 68%, and 19%, respectively)
ranging in age from 16 to 52 years received laser and/or IPL
hair photo-epilation of the beard, neck and chin areas,
excluding the upper lip. The number of treatments received
by each patient ranged from 3 to 23. Hair epilation
treatments were performed using a long pulsed 755 nm
alexandrite laser (Gentlelase, Candela, Wayland, MA) and
IPL source (Epilight, Lumenis, Santa Clara, CA) and a
1,064 nm Nd:YAG (Lyra, Laserscope, San Jose, CA). Only
10% of the treatments were performed with the 1,064 nm
Nd:YAG laser. Treatments were usually performed every
2– 3 months. The alexandrite laser was used in 85% of the
treatments, IPL in 10% and Nd:YAG in 5%. The parameters
used are listed in Table 1.
RESULTS
Of the 543 patients who received laser/IPL hair photo-
epilation, 57 (10.49%) demonstrated an increase in hair
growth compared to baseline. The increased hair growth
occurred within the area that was treated and also in
the areas bordering the treated area, and appeared thicker
and darker than the hairs initially treated (Figs. 1 and 2).
An additional 44 (8.10%) patients demonstrated no
apparent reduction in hair growth following treatment.
Four hundred twenty-four patients (78.08%) demonstrated
a decrease in hair growth with ongoing treatments.
Only 14 patients (2.5%) were discharged from the clinic
due to near complete hair reduction. These results are
summarized in Table 2.
The increased terminal hair growth occurred mostly in
areas in which fine hair or both fine and coarse hair was
present prior to initiation of treatment. Hair growth
occurred with greater frequency in patients treated with
the Alexandrite and IPL devices compared those treated
with the Nd:YAG, however, the later device was used less
frequently. Patients that developed terminal hair growth
were in the following age groups: 19–31 years, 44 patients;
30–40 years, 8 patients; greater than 40 years, 5 patients.
The onset of increased terminal hair growth was noted
between the third and tenth treatment in 39 (72.2%) of 57
patients, and 11 (19%) of 57 between the third and fourth
treatment. Most patients had a normal hormonal history.
Sixteen patients had irregular menses or documented
ovarian cysts.
Because the terminal hair growth occurred both within
the treated areas and also at the periphery of treated areas
it was thought that sub-therapeutic thermal energy
delivered to nearby follicles induced terminal hair growth.
Subsequent application of cold packs surrounding the
treatment area during treatments and treating all
patients with two passes has minimized the incidence of
terminal hair growth (Fig. 3). Since we have instituted this
method in our clinic 2 years ago, we have treated over 200
patients and have not had any patients with hair growth
stimulation.
DISCUSSION
Despite the widespread use of lasers and IPL for hair
reduction, the biologic mechanism of photo-epilation is
largely unknown. Upon treatment with a laser or IPL
device, light is absorbed over millisecond pulse durations by
melanin contained within melanosomes in the hair matrix
and within keratinocytes in the hair shaft [1,2]. Heat
energy is transferred from the follicular matrix to the
surrounding non-pigmented follicular epithelium and
perifollicular dermis [1–4]. Sufficient thermal injury to
the follicle and its surrounding tissue results in miniatur-
ization of follicles such that they become clinically unap-
parent for a variable duration of time [2]. The precise target
of thermal injury from adjacent melanosomes or the
*Correspondence to: Andrea Willey, MD, Oregon Health &
Science University, Portland, OR. E-mail: willeya@ohsu.ed
Accepted 27 December 2006
Published online 25 April 2007 in Wiley InterScience
(www.interscience.wiley.com).
DOI 10.1002/lsm.20485
ß2007 Wiley-Liss, Inc.

subsequent biologic events that lead to clinical hair
reduction is not understood. Potential targets include cells
critical for follicular cycling, including the follicular stem
cells located within the bulge area of the outer root sheath
and cells of the follicular papilla [5]. This may include cell
populations necessary for communication during follicular
cycling as well as cell populations essential for follicular
morphogenesis itself.
Histological studies have shown that within a photo-
epilated area not all of the follicles are thermally injured
TABLE 1. Laser Hair Epilation Devices and Parameters
Device
Wavelength
(nm)
Fluence
(J) Spot size
Pulse duration
(milliseconds) Cooling
Alexandrite gentle plus
(Candela
TM
)
755 12– 18 12 and 18 mm 3 Cryogen spray
40 milliseconds/
30 milliseconds
IPL (Epilight
TM
) 645, 690, and 735 35– 38 4.5 cm 0.5 cm 3– 20 Cold gel
Long pulsed Nd:YAG (Lyra
TM
) 1,064 24– 30 10 mm 35– 50 Cold gel
Fig. 1. A: Before photo-epilation. B: Terminal hair growth
stimulation within and around the photo-epilated area after
12 sessions. [Figure can be viewed in color online via
www.interscience.wiley.com.]
Fig. 2. A: Before photo-epilation. B: Terminal hair growth
stimulation within and around photo-epilated area after five
sessions. [Figure can be viewed in color online via www.
interscience.wiley.com.]
298 WILLEY ET AL.

[1,6], which suggests that some follicles are more suscep-
tible to photo-thermal injury than others. Differences in the
content of melanin associated with differing stages in the
hair cycle may account for this, since melanogenesis ceases
during catagen and telogen, commencing again during
anagen. Follicles in early anagen have been thought to be
most susceptible to photo-epilation since they contain
melanin which is located high in the dermis relative to late
anagen follicles residing deep in the subcutaneous tissue
beyond the optical penetration of red and near infrared
wavelengths [1,6]. Although the degree of melanin within
growing hairs is associated with efficacy of treatment [1,2],
the degree to which melanin in the shaft versus the matrix
plays a role in affecting efficacy depends upon whether the
target of thermal injury is primarily in the follicular stem
cells located in the bulge or the follicular papilla; heat
transferred from the shaft may heat primarily the follicular
infundibulum, whereas heat transferred from the matrix
may affect primarily the lower segment of the follicle.
Clearly, the efficacy of laser hair epilation is fluence
dependent, with the greatest amount of hair loss occurring
with higher fluences [1,2]. Our observations that stimula-
tion of hair growth occurred at the periphery of treated
areas and that such hair growth could be minimized in the
same patients by applying cold packs to the surrounding
area and by using double passes with each treatment
suggests that sub-therapeutic fluences at the periphery of
treated areas induce terminal differentiation of hair
growth rather than miniaturization. In other words,
instead of inducing miniaturization with a subsequent
prolonged telogen phase, follicles are instead shifted
towards terminal anagen hair growth.
Acquired localized hypertrichosis has been described in
various other settings of dermal injury, including terminal
hair growth at the periphery of a burn [7], transient limb
hypertrichosis associated with casting [8,9] peri-incisional
hypertrichosis following knee surgery or fracture sites
[10,11], distal hair growth following lymphadenectomy
[12], terminal hair growth at the site of bug bites [13]
and verruca vulgaris [14], local reactions to measles
[15], smallpox [16] and other vaccines [17], and chronic
rubbing, scratching, and biting associated with various
clinical situations [18,19]. Common to these widely varied
clinical presentations is the hypothesis that local hyper-
emia or inflammation may lead to localized terminal hair
growth.
Consonant with this idea, in addition to the complex
orchestrated events of follicular cycling that lead to
transformation of the follicle proper, the surrounding
follicular epithelium, associated dermal components, and
follicular vasculature undergo spectacular morphogenesis
with each growth cycle [5]. A pronounced increase in
follicular vascularization occurs during anagen that is
accompanied by the upregulation of vascular endothelial
growth factor (VEGF) in outer root sheath keratinocytes
[20]. This is followed by a rapid regression in perifollicular
vessels during catagen. Indeed growing follicles have much
higher perfusion requirements than resting follicles. These
accounts taken together with our observations raise the
compelling possibility that sub-therapeutic thermal injury
to the follicular vasculature may affect follicular cycling in
such a way to induce terminal hair growth rather than
miniaturization. Alternate hypotheses include the possibi-
lity that sub-therapeutic injury to the follicle may result in
the release of factors that alter follicular angiogenesis and
influence hair cycling. Additionally, both ultrastructural
and light microscopic studies have demonstrated the
uniform induction of perifollicular inflammation associated
with photo-epilation that persists for up to 2 weeks. Thus, it
follows that this local inflammatory response may also
affect follicular cycling in such a way to induce terminal
hair growth. While feasible, this idea does not explain why
some follicles react in this way and others do not, since
inflammation is not selective and thus not limited to less
thermally injured areas.
In our experience, there are five key factors associated
with failure to epilate and risk of hair stimulation:
(1) The thickness of treated hair: thicker hair is easier
to heat because the follicle reaches a high enough
temperature to destroy the cells critical for follicular
cycling; thinner hairs derived from follicles with less
chromophore absorb light energy less efficiently.
This explains the failure to epilate fine hair that
occurred on areas on the face with fine hair growth
Fig. 3. The use of cold packs to prevent peripheral stimulation
of hair growth. [Figure can be viewed in color online via
www.interscience.wiley.com.]
TABLE 2. Results
Subjects (%) Response
57 (10.49) Increased terminal hair growth
(equally distributed in all skin types)
44 (8.10) No change in hair growth
424 (70.08) Reduced hair growth (continued
treatment)
14 (2.5) Persisting reduction in hair growth
(discharged from clinic)
LASER– INTENSE PULSED LIGHT PHOTO-EPILATION 299

and at other sites such as the abdomen, linea alba,
and back and shoulders in men.
(2) The color of treated hair: melanin within melano-
cytes of the follicular matrix and shaft is the
chromophore absorbed during photo-epilation, thus
darker hair is more efficiently heated.
(3) The depth of treated hair: optical penetration of
light may not be deep enough to adequately
thermally injure deeply growing anagen hairs in
some areas. This is only a hypothesis, however, since
we do not have in vivo real time sequences of lasers
reaching the target cells. It is possible that telogen
or late anagen follicles that are located in the dermis
may be more susceptible to hair growth stimulation.
Based on these observations, our current photo-epilation
protocol includes the use of ice packs for all patients with
fine hair growth on facial or body areas. In addition, we
have observed in side to side studies that two passes with a
long pulsed 755 nm Alexandrite laser using an 18 mm spot
size is more effective than a single pass (unpublished work
by N.L.). Our current technique is to use 12–14 J/cm
2
followed 1 minute later by a second pass using 8 –10 J/cm
2
.
Therefore, the amount of energy delivered is important in
definitive destruction of the key cells responsible of normal
follicular cycling. Sub-optimal energies seem to stimulate
these cells and induce longer thicker hairs as a consequence
of accelerating the transition from vellus to terminal
follicles. This phenomenon by which heat induces hair
growth has been previously observed [9,10].
In our cases, the presence of fine hair prior to treatment
appeared to be the most important factor for increased risk
of paradoxical terminal hair growth. In addition, some
areas appeared to be at higher risk: terminal hair growth
occurred most often in the low maxillary or ‘‘beard’’ area,
neck, lateral cheeks and chin areas in young women with
either skin types II, III, or IV. Patients with hair
stimulation were found in all skin types. Differences in
skin type likely matters only in that lower energies may be
used in patients with darker skin types, and thus it was
probably easier to deliver sub-optimal energies. In these
darker skinned patients, the use of double passes at lower
energies should be attempted. Alternatively, a single
treatment using one pass followed by a second single pass
treatment 1 week later may also be tried. Terminal hair
growth was mostly noted between third and fourth
treatment, but also occurred as late as after the tenth
treatment. The application of cold packs surrounding the
treatment area during treatments and use of double pass
technique appears to minimize the incidence of terminal
hair growth within and around photo-epilated areas.
Referral to an electrologist may be considered for patients
who are at high risk.
Previous descriptions of hair stimulation have occurred
with the use of various devices, including 694 nm Ruby,
755 nm Alexandrite, and 810 nm Diode lasers in addition to
IPL sources [21–26]. It is unclear if hair removal with the
1,064 nm Nd:YAG laser is less inclined to cause hair
stimulation or if it is simply used less often as is the case
in our practice. The more common occurrence of hair
stimulation on the lower face in females observed in this
study is also consistent with other reports, however reports
on the back of men have also been described. Females with
vellus hair on facial ‘‘beard area’’ should be anticipated a
chronic treatment with on multiple going sessions for
years.
Although the majority of women in this study had no
history of hormonal abnormalities, the true hormonal
status cannot be certain from historical data. Thus,
hormonal abnormalities may or may not be directly
involved hair growth stimulation. Nevertheless, hirsute
individuals may be at an increased risk regardless of
hormonal status. It is our observation that the amount of
vellus facial hair may change with different hormonal
cycles or may be induced by laser epilation during different
treatment sessions. In our experience photo-epilation
should be performed more frequently and with higher
energies to optimize efficacy in these patients.
Previous reports of paradoxical hair growth associated
with laser-IPL photoepilation suggest the incidence is
uncommon [21–26]. In addition, because the majority of
the reported cases occurred in individuals of Fitzpatrick
skin types III–V it has been felt that these patients are at
greatest risk. Our observations suggest that hair growth
stimulation following laser/IPL photo-epilation may be
more common than previously recognized and that indivi-
duals of Fitzpatrick skin type II are also susceptible.
REFERENCES
1. Grossman M, Diericks CC, Farinelli WA, Flotte T, Anderson
RR. Damage to hair follicles by normal mode ruby laser
pulses. J Am Acad Dermatol 1996;35:889– 894.
2. Diericks CC, Grossman M, Farinelli WA, Anderson RR.
Permanent hair removal by normal mode ruby laser. Arch
Dermatol 1998;134:837– 842.
3. Svaasand LO, Nelson SJ. On the physics of laser induced
selective photothermolysis of hair follicles: Influence of
wavelength, pulse duration, and epidermal cooling. J Biomed
Optic 2004;9:353– 361.
4. Altshuler GB, Anderson RR, Manstein D, Zenzie HH,
Smirnov MZ. Extended theory of selective photothermolysis.
Laser Surg Med 2001;29:416– 432.
5. Stenn KS, Paus R. Controls of hair follicle cycling. Physiol
Rev 2001;81:449– 494.
6. Liew SH, Cerio R, Sarathchandra P, Grobbelaar AO, Gault
DT, Sanders R, Green C, Linge C. Ruby assisted hair
removal: An ultrastructural evaluation of cutaneous damage.
B J Plast Surg 1999;52:636– 643.
7. Shafir R, Tsur H. Local hirsutism at the periphery of burned
skin. B J Plast Surg 1979;32:93.
8. Leung A, Kiefer GN. Localized acquired hypertrichosis
associated with fracture and cast application. J Nat Med
Assoc 1989;81:65– 67.
9. Bergen D. Localized hirsutism following Colles’ fracture. Can
Med Assoc 1983;128:368.
10. Ravin N. New hair growth over fracture sites. New Engl J
Med 1990;323:350.
11. Gupta S, Gupta S, Kanwar AJ, Kumar B. Hypertrichosis
surrounding scar of knee replacement surgery. J Am Acad
Dermatol 2003;50:802– 803.
12. Finck SJ, Cochran AJ, Vitek CR, Morton DL. Local hirsutism
after radical inguinal lymphadenectomy. New Engl J Med
1981;305:958.
13. Tisocco LA, Del Campo DV, Bennin B, Barsky S. Acquired
localized hypertrichosis. Arch Dermatol 1981;117:127– 128.
300 WILLEY ET AL.

14. Egawa K, Honda Y, Miyawaki Y. Local hypertrichosis
associated with a human papillomavirus type 1-induced
wart. B J Dermatol 2005;153:1229– 1247.
15. Ozkan H, Dundar NO, Ozkan S, Kumral A, Duman N,
Gulcan H. Hypertrichosis following measles immunization.
Pediatr Dermatol 2001;18:458– 459.
16. Kumar LR, Goyal BG. Pigmented hairy scar follow-
ing smallpox vaccination. Indian J Pediatr 1968;35:283–
284.
17. Pembroke AC, Marten RH. Unusual cutaneous reactions
following diphtheria and tetanus immunization. Clin Exp
Dermatol 1979;4:345– 348.
18. Wendelin DS, Pope DN, Mallory SB. Hypertrichosis. J Am
Acad Dermatol 2003;48:161– 179.
19. Olsen EA. Hypertrichosis. In: Disorders of hair growth, 2nd
ed. New York, NY: McGraw Hill; 2003;401–430.
20. Yano K, Brown LF, Detmar M. Control of hair growth and
follicle size by VEGF-mediated angiogenesis. J Clin Invest
2001;107:409– 417.
21. Hirsch RJ, Farnelli WA, Laughlin SA, Campos V, Dover
JS, et al. Hair growth induced by laser hair removal. Lasers
Surg Med 2003;32:63 (abstract).
22. Bernstein E. Hair growth induced by diode laser treatment.
Dermatol Surg 2005;31:584– 586.
23. Alaijilan A, Shapiro J, Rivers JK, MacDonald N, Wiggin
J, Lui H. Paradoxical hypertrichosis after laser epilation. J
Am Acad Dermatol 2005;53:85– 88.
24. Vlachos AP, Kontoes PP. Development of terminal hair
following skin lesin treatments with an intense pulsed light
source. Aesthetic Plast Surg 2002;26:303– 307.
25. Moreno-Arias GA, Vlachos SP, Savva MP, Kontoes PP.
Efficacy of long and short pulse alexandrite lasers compared
with an intense pulsed light source for epilation: A study on
532 sites in 389 patients. J Cosmet Laser Ther 2003;5:140–
145.
26. Kontoes P, Vlachos S, Konstanttinos M, Anastasia L, Myrto
S. Hair induction after laser-assisted hair removal and its
treatment. J Am Acad Dermatol 2006;54:64–67.
LASER– INTENSE PULSED LIGHT PHOTO-EPILATION 301