Alopecia: A review of laser and light therapies
Published Web Locationhttps://doi.org/10.5070/D31jt041t2
Alopecia: A review of laser and light therapiesDepartment of Dermatology, MD Anderson Cancer Center, University of Texas, Houston, Houston, Texas
Sophia Rangwala AB, Rashid M Rashid MD PhD
Dermatology Online Journal 18 (2): 3
Since the 1980s, laser technology has become increasingly popular to treat a variety of cutaneous conditions. Its successful use as an epilator comes with the rare but interesting side effect of paradoxical hypertrichosis. In this review, we summarize cases describing hair growth after photoepilation, as well as studies testing laser and light sources as treatment for alopecia, particularly androgenetic alopecia and alopecia areata. We also discuss the possible biologic mechanisms by which phototherapy induces hair regeneration.
Initially used to treat benign vascular tumors, laser therapy is now considered first-line for removal of pigmented lesions, tattoos, scars, wrinkles, and unwanted hair. The ability of lasers to induce hair growth was incidentally noted in 1967 when Mester and colleagues used low-level laser therapy (LLLT) to treat cancer in mice with shaved backs . Since then, a number of studies have suggested the use of lasers as an effective way to treat alopecia, particularly androgenetic alopecia and alopecia areata, but there is still a paucity of independent, peer-reviewed blinded clinical trials. In this review, we discuss reports of paradoxical hair growth after laser treatment, studies that utilize lasers to treat different types of alopecia, and finally, mechanisms of photo-biomodulation that may explain these clinical findings.
2. Paradoxical hair growth after laser therapy
Since approval by the Food and Drug Administration (FDA) in 1996, lasers and intense pulsed light (IPL) sources have become a popular way to terminate growth of unwanted hair because of the relative safety and efficacy of these treatments . Photoepilation uses wavelengths in the red and infrared range (600-1100 nm) and is believed to work by delivering pulsed light energy to melanin in hair shafts. After absorption, the light converts to thermal energy, destroying the progenitor cells of the hair follicle while sparing surrounding tissue . The biologic mechanism, however, is likely more complex than just selective photothermolysis.
Hypertrichosis is a rare but significant side effect that usually occurs after several months within and/or proximal to areas treated with laser devices  (Table 1). First described in 2002 with IPL therapy , this phenomenon has now been widely acknowledged and also referred to as paradoxical hypertrichosis, terminalization, induction, or terminal hair growth  The incidence rate ranges from 0.6 percent to 10 percent and appears to occur with low fluences and all laser types , such as diode lasers [6, 7], neodymium:yttrium-aluminum-garnet (YAG) lasers [6, 8], IPL [8, 9, 10], and alexandrite lasers [6, 8, 9, 11]. This side effect most often occurs on the face and neck, and in patients with darker skin types (III-IV), dark coarse hair, and/or co-existing hormonal imbalances [4, 8]. Interestingly, pili bigeminy has been reported in 4 cases following alexandrite or ruby laser treatment for hair removal [12, 13] and is thought to be the result of suboptimal fluences that are too low to induce thermolysis, but high enough to stimulate follicular growth . Although the face and neck area appear to be most susceptible to hair induction effects, the relative sensitivity of the scalp to these effects is not known because patients do not usually seek laser hair removal for this area.
3. Androgenetic alopecia
Androgenetic alopecia, also known as male or female pattern hair loss, is a hereditary condition in which disruption of proper androgen signaling results in decreased proliferation of follicle epithelia and progressive miniaturization of terminal hairs on the scalp . A recent study found that in these patients, follicular stem cell populations were preserved but downstream progenitor cell populations were significantly reduced, thus suggesting a defect in conversion from a stem cell to progenitor cell phenotype . Currently, the only FDA-approved medications are finasteride and minoxidil. Because androgenetic alopecia is so common, many treatment modalities are marketed, such as topical products, supplements, and hair transplantation, but few have led to satisfactory results.
LLLT has recently increased in popularity as a stand-alone or adjunctive treatment, and is available in a home, salon, or clinical setting. The cost of available devices ranges from hundreds to thousands of dollars and the recommended course of treatment is 6 to 12 months . Companies marketing these products advertise them as both thickening and inducing growth of existing follicles. In 2007, the HairMax Laser Comb® received 510(k) clearance from the FDA for the treatment of androgenetic alopecia in men . This clearance means that the HairMax Laser Comb is considered a moderate-risk medical device by the FDA and is thereby solely screened for safety, not efficacy. The FDA approves a device for both safety and efficacy when it is regarded as high-risk. The HairMax Laser Comb has only been tested once in a company-sponsored study of 110 male patients, which claimed a significant increase in mean terminal hair density when compared to a sham device .
A consensus written by hair loss experts states that based on anecdotal experience, LLLT, particularly 650 to 900 nm wavelengths at 5 mW, may be an effective treatment option for patients. This group also found that even if no regrowth was appreciated, patients noted improvement in the texture and quality of hair . Avram and Rogers conducted the first independent blinded study of LLLT and hair growth. The study had 7 patients and found that on average, there was a decrease in the number of vellus hairs, an increase in the number of terminal hairs, and an increase in shaft diameter. However, this data was found not to be statistically significant. Of note, this study used a laser “hood” and the authors acknowledge that there may have been insufficient light delivery to the scalp using this system .
4. Alopecia areata
Alopecia areata is the most common cause of hair loss after androgenetic alopecia. This form of hair loss usually presents as round non-scarring patches, but may have a more diffuse or complete distribution. The pathophysiology of this autoimmune disease is unknown, but recent evidence suggests it involves both innate and adaptive immune components that may be triggered by an upregulation of ULBP ligands, which in turn activate NKG2D receptors on natural killer cells . Hair regrowth recurs once the inflammatory response is suppressed and the undamaged stem cells are able to regenerate the hair follicle . Intralesional corticosteroids are the first-line treatment for adults and have been used for about 50 years. Despite the emergence of other topical and systemic immunomodulatory therapies in the past decade, little progress has been made for refractory cases. These treatments can also have significant side effects and a high rate of relapse . Oral and topical psoralen plus UVA (PUVA) radiation has been considered in the past and although response rates have ranged from 15 percent to 70 percent in uncontrolled settings, there was no improvement over the spontaneous remission rate in large retrospective studies. In addition, high relapse rates and an increased risk of non-melanoma skin cancer have made it an unattractive option [23, 24, 25]. Photodynamic therapy has also been found to be ineffective [26, 27].
Recent case reports and clinical trials have demonstrated the 308 nm excimer laser as an effective and safe alternative for patients resistant to conventional therapies (Table 2). This laser system delivers high doses of long-wave monochromatic UVB radiation. A left-right controlled pilot study first explored the possibility of using narrowband UVB therapy via a non-laser source, but the data was not statistically conclusive because of a small sample size . The first report employing a laser was in 2004 . It described two patients with alopecia areata of the scalp who experienced thick and homogenous regrowth after a 9- to 11-week period of approximately weekly xenon chloride excimer laser therapy. Since this case series, only 4 additional small studies of adults and children have been published. In these reports, the excimer laser appears to produce better results for alopecia areata partialis of the scalp, as compared to alopecia areata partialis of the beard and extremities, alopecia totalis, and alopecia universalis [30, 31, 32]. With this laser, 60 percent to 77 percent of refractory patients had a complete response. Most studies compared the experimented area with a control area, with the control showing no appreciable hair growth in any study [30, 31, 32, 33]. All the published studies also indicate good tolerability by the patient, with the most common side effects being mild to moderate erythema or hyperpigmentation of the treated area. Atopic diathesis, generally a poor prognostic indicator for alopecia areata patients, was also negatively correlated with the efficacy of the excimer laser. A 308 nm excimer non-laser device showed promising results in one study, with 4 out of 8 patients demonstrating complete hair growth after a mean of 3 weekly treatments .
Other laser and light techniques have been effective against recalcitrant alopecia areata patches (Table 1), but need confirmation by additional studies. The Super Lizer, a Japanese linear polarized infrared light system traditionally used to treat arthralgias and neuralgias, was shown to expedite hair growth by 1.6 months for about 50 percent of patients with mild disease . Another group found that a pulsed 604 nm infrared diode laser was able to induce hair growth in 94 percent of patches otherwise resistant to conventional treatments, whereas control patches remained unchanged . Ninety percent of the responsive patches demonstrated terminal hair growth, whereas the remaining 10 percent had vellus hair growth.
Ho Yoo and colleagues found that weekly treatment with fractional photothermolysis induced complete hair growth after 6 months in a patient with patchy alopecia of the scalp . No relapse was appreciated during the 6-month follow-up period. Fractional laser therapy is a recently introduced laser system that produces columns of “microthermal treatment zones” that extend down to the reticular dermis . Because the emitted energy is absorbed mostly by water, the stratum corneum is not thermally damaged and thereby has a better side effect profile relative to other lasers.
Whereas the results mentioned above are encouraging, randomized controlled trials are needed to assess and compare these laser devices and to establish optimal therapeutic parameters. Also, combination therapies with the various other treatment modalities for alopecia areata should be tested.
5. Biologic mechanisms
The biologic events by which laser and light sources produce hair growth is unclear, but several theories have been proposed.
Hypertrichosis is the result of follicles converting from telogen (the resting phase) to anagen (the active phase), or vellus follicles transforming into terminal follicles. Sunlight has been recognized as a promoter of hypertrichosis. Although the pathogenesis is unknown, evidence shows UV radiation may upregulate production of prostaglandin E2 [39, 40], an inflammatory mediator that is known to induce reversible eyelid hypertrichosis  and to stimulate hair growth when applied topically on animal models .
When performing photoepilation, thermal energy at low fluences may not be sufficient to epilate the hair, but can still cause a perifollicular inflammatory response that persists for up to 2 weeks [4, 7]. The role of inflammation in hair induction is supported by the finding that using a cold pack after laser hair removal procedures markedly reduces the rate of hypertrichosis . Local hypertrichosis has also been appreciated with other stimuli that induce local inflammation , such as heavy friction [44, 45, 46], burns , surgical incision [48, 49], and vaccinations [50, 51, 52], as well as underlying fractures [53-58], thrombophlebitis, and chronic osteomyelitis . There have also been two cases in which hair induction occurred in a port wine stain and a tattoo treated with an IPL source .
On a cellular level, inflammation may result in increased local blood flow and release of inflammatory factors that promote follicular vascularization . In normal skin tissue, the anagen phase is accompanied by follicular angiogenesis and upregulation of vascular endothelial growth factor (VEGF) in outer root sheath keratinocytes. This vasculature rapidly regresses during catagen phase. Thus, enhanced vasculature induced by inflammation may promote the development of healthy follicles. Additionally, the heat shock associated with low levels of thermal energy may upregulate heat shock proteins such as HSP-27, which have a role in follicular stem cell growth and differentiation .
The wound healing associated with thermal injury may also contribute to hair growth. Ito and colleagues showed that in wounds of genetically normal adult mice, de novo hair follicles form from epidermal stem cells outside the follicle . Other mediators of wound healing linked to hair growth include polypeptide thymosin beta-4  and cyclopentyladenosine . The ability of laser treatment to induce regenerative healing has been seen in skin and many other tissues [64, 65].
In the case of alopecia areata, laser radiation may work by decreasing inflammation.
Although this is not a traditional idea, similar hypotheses exist for medicines otherwise not considered as immune modulators, particularly statins . Light energy may promote T-cell apoptosis as well as induce perifollicular lymphocytes to “scatter” [29, 37]. In fact, UV-mediated immunosuppression has been well studied , with several studies demonstrating that exposure can inhibit contact hypersensitivity reactions [68, 69, 70] and delayed-type hypersensitivity [71, 72, 73]. Cis-urocanic acid, a chromophore and a mediator of UV-induced immune suppression, is maximally produced when skin is exposed to 280-310 nm UVB light . Moreover, an immunosuppressive action spectrum for UV light, which measured suppression of nickel contact dermatitis in sensitive individuals, peaked at 300 nm . These peaks correlate with the operative wavelength of the 308 nm excimer laser and thus may provide a mechanistic rationale for this laser in alopecia areata patients.
Apart from immunomodulation, direct light stimulation may activate dormant follicles, or synchronize follicles into anagen phase so that the hair density appears to be thicker . Finally, follicle regeneration may be induced from a dispersal or suppression of inhibitory cells that prevent progression of follicle stem cells to progenitor cells in a manner analogous to the “scattering” of T cells in alopecia areata .
6. Laser hair transplantation
Lasers have also been suggested as auxiliary devices for patients undergoing autologous hair transplantation, a common surgical option for patients with extensive hair loss. Starting in 1995, carbon dioxide laser tissue ablation was proposed as an effective way to generate implantation holes and slits because of its efficiency and ability to significantly decrease damage to surrounding tissue and recovery time [76, 77]. However, the carbon dioxide laser wavelength of 10,600 nm is in the far-infrared spectral region and can result in minor thermal damage to the scalp .
Patients with scarring or cicatricial alopecia, a diverse group of rare inflammatory disorders that ultimately result in permanent follicular damage and irreversible hair loss, often seek hair transplantation. Yet, because of low perfusion of the scarred recipient tissue in these patients, it is imperative that minimal trauma be done when creating implantation holes and slits . The Erbium:YAG laser, with an infrared emission of 2940 nm, permits “cold” ablation with greater absorption and less thermal damage than the carbon dioxide laser system. One study found that using a fluence of 80-120 J/cm² and 8-12 pulses was particularly effective and resulted in a 95 percent mini- and micrograft survival rate .
Even though laser treatments for alopecia are currently available in a non-clinic setting, none are FDA-approved. Notably, no laser studies are currently available for telogen effluvium, but a group of hair loss experts believe that if laser devices are used in the pre- and post-surgical periods, the risk of post-surgical telogen effluvium may be minimized and an earlier regrowth of transplanted hair may be promoted . A better understanding of paradoxical hypertrichosis after photoepilation can help design more effective lasers and target more appropriate populations with alopecia. For instance, the patient groups most susceptible to hypertrichosis with laser epilation, namely those with dark skin and/or darker, coarser hair, may be more likely to benefit from laser treatment. Additional mechanistic studies and large-scale randomized trials will help elucidate whether laser therapy can increase hair growth and/or prevent further hair loss for those living with alopecia.
ACKNOWLEDGEMENT: Sophia Rangwala gratefully acknowledges support from the North American Hair Research Society.
References1. Mester E, Szende B, Gartner P. The effect of laser beams on the growth of hair in mice. Radiobiol Radiother. 1968;9(5):621-6. [PubMed]
2. Tanzi EL, Lupton JR, Alster TS. Lasers in dermatology: four decades of progress. J Am Acad Dermatol. 2003 Jul;49(1):1-31; quiz 31-4. [PubMed]
3. Wanner M. Laser hair removal. Dermatol Ther. 2005 May-Jun;18(3):209-16. [PubMed]
4. Desai S, Mahmoud BH, Bhatia AC, Hamzavi IH. Paradoxical hypertrichosis after laser therapy: a review. Dermatol Surg. 2010 Mar;36(3):291-8. [PubMed]
5. Moreno-Arias G, Castelo-Branco C, Ferrando J. Paradoxical effect after IPL photoepilation. Dermatol Surg. 2002 Nov;28(11):1013-6. [PubMed]
6. Bouzari N, Tabatabai H, Abbasi Z, Firooz A, Dowlati Y. Laser hair removal: comparison of long-pulsed Nd:YAG, long-pulsed alexandrite, and long-pulsed diode lasers. Dermatol Surg. 2004 Apr;30(4 Pt 1):498-502. [PubMed]
7. Bernstein EF. Hair growth induced by diode laser treatment. Dermatol Surg. 2005 May;31(5):584-6. [PubMed]
8. Willey A, Torrontegui J, Azpiazu J, Landa N. Hair stimulation following laser and intense pulsed light photo-epilation: review of 543 cases and ways to manage it. Lasers Surg Med. 2007 Apr;39(4):297-301. [PubMed]
9. Kontoes P, Vlachos S, Konstantinos M, Anastasia L, Myrto S. Hair induction after laser-assisted hair removal and its treatment. J Am Acad Dermatol. 2006 Jan;54(1):64-7. [PubMed]
10. Radmanesh M. Paradoxical hypertrichosis and terminal hair change after intense pulsed light hair removal therapy. J Dermatolog Treat. 2009;20(1):52-4. [PubMed]
11. Alajlan A, Shapiro J, Rivers JK, MacDonald N, Wiggin J, Lui H. Paradoxical hypertrichosis after laser epilation. J Am Acad Dermatol. 2005 Jul;53(1):85-8. [PubMed]
12. Ye JN, Prasad A, Trivedi P, Knapp DP, Chu P, Edelstein LM. Pili bigeminy induced by low fluence therapy with hair removal alexandrite and ruby lasers. Dermatol Surg. 1999 Dec;25(12):969. [PubMed]
13. Bukhari IA. Pili bigemini and terminal hair growth induced by low-fluence alexandrite laser hair removal. J Cutan Med Surg. 2006 Mar-Apr;10(2):96-8. [PubMed]
14. Olsen EA, Messenger AG, Shapiro J, Bergfeld WF, Hordinsky MK, Roberts JL, Stough D, Washenik K, Whiting DA. Evaluation and treatment of male and female pattern hair loss. J Am Acad Dermatol. 2005 Feb;52(2):301-11. [PubMed]
15. Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, Stanton DC, Carrasco L, Spiegel JH, Tobias JW, Cotsarelis G. Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells. J Clin Invest. 2011 Feb 1;121(2):613-22. [PubMed]
16. Avram MR, Leonard RT, Jr., Epstein ES, Williams JL, Bauman AJ. The current role of laser/light sources in the treatment of male and female pattern hair loss. J Cosmet Laser Ther. 2007 Mar;9(1):27-8. [PubMed]
17. Finlay CA, Hinds PW, Levine AJ. The p53 proto-oncogene can act as a suppressor of transformation. Cell. 1989 Jun 30;57(7):1083-93. [PubMed]
18. Leavitt M, Charles G, Heyman E, Michaels D. HairMax LaserComb laser phototherapy device in the treatment of male androgenetic alopecia: A randomized, double-blind, sham device-controlled, multicentre trial. Clin Drug Investig. 2009;29(5):283-92. [PubMed]
19. Avram MR, Rogers NE. The use of low-level light for hair growth: part I. J Cosmet Laser Ther. 2010 Apr;12(2):116. [PubMed]
20. Petukhova L, Duvic M, Hordinsky M, Norris D, Price V, Shimomura Y, Kim H, Singh P, Lee A, Chen WV, Meyer KC, Paus R, Jahoda CA, Amos CI, Gregersen PK, Christiano AM. Genome-wide association study in alopecia areata implicates both innate and adaptive immunity. Nature. 2010 Jul 1;466(7302):113-7. [PubMed]
21. Paus R, Cotsarelis G. The biology of hair follicles. N Engl J Med. 1999 Aug 12;341(7):491-7. [PubMed]
22. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part II. Treatment. J Am Acad Dermatol. 2010 Feb;62(2):191-202, quiz 203-4. [PubMed]
23. Taylor CR, Hawk JLM. PUVA treatment of alopecia areata partialis, totalis and universalis: audit of 10 years' experience at St John's Institute of Dermatology. Br J Dermatol. 1995 Dec;133(6):914-8. [PubMed]
24. Mohamed Z, Bhouri A, Jallouli A, Fazaa B, Kamoun MR, Mokhtar I. Alopecia areata treatment with a phototoxic dose of UVA and topical 8-methoxypsoralen. J Eur Acad Dermatol Venereol. 2005 Sep;19(5):552-5. [PubMed]
25. Healy E, Rogers S. PUVA treatment for alopecia areata—does it work? A retrospective review of 102 cases. Br J Dermatol. 1993 Jul;129(1):42-4. [PubMed]
26. Bissonnette R, Shapiro J, Zeng H, McLean DI, Lui H. Topical photodynamic therapy with 5-aminolaevulinic acid does not induce hair regrowth in patients with extensive alopecia areata. Br J Dermatol. 2000 Nov;143(5):1032-5. [PubMed]
27. Fernández-Guarino M, Harto A, García-Morales I, Pérez-García B, Arrazola JM, Jaén P. Failure to treat alopecia areata with photodynamic therapy. Clin Exp Dermatol. 2008 Aug;33(5):585-7. [PubMed]
28. Bolduc C, Hobbs L, Shapiro J, McLean D, Lui H. Efficacy of narrow-UVB in the treatment of alopecia areata. Tokyo: Poster Presented at Third Intercontinental Meeting of Hair Research Societies
29. Gundogan C, Greve B, Raulin C. Treatment of alopecia areata with the 308-nm xenon chloride excimer laser: case report of two successful treatments with the excimer laser. Lasers Surg Med. 2004;34(2):86-90. [PubMed]
30. Zakaria W, Passeron T, Ostovari N, Lacour JP, Ortonne JP. 308-nm excimer laser therapy in alopecia areata. J Am Acad Dermatol. 2004 Nov;51(5):837-8. [PubMed]
31. Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata. Dermatol Surg. 2007 Dec;33(12):1483-7. [PubMed]
32. Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata in children. Pediatr Dermatol. 2009 Sep-Oct;26(5):547-50. [PubMed]
33. Raulin C, Gundogan C, Greve B, Gebert S. Excimer laser therapy of alopecia areata--side-by-side evaluation of a representative area. J Dtsch Dermatol Ges. 2005 Jul;3(7):524-6. [PubMed]
34. Aubin F, Vigan M, Puzenat E, Blanc D, Drobacheff C, Deprez P, Humbert P, Laurent R. Evaluation of a novel 308-nm monochromatic excimer light delivery system in dermatology: a pilot study in different chronic localized dermatoses. Br J Dermatol. 2005 Jan;152(1):99-103. [PubMed]
35. Yamazaki M, Miura Y, Tsuboi R, Ogawa H. Linear polarized infrared irradiation using Super Lizer is an effective treatment for multiple-type alopecia areata. Int J Dermatol. 2003 Sep;42(9):738-40. [PubMed]
36. Waiz M, Saleh AZ, Hayani R, Jubory SO. Use of the pulsed infrared diode laser (904 nm) in the treatment of alopecia areata. J Cosmet Laser Ther. 2006 Apr;8(1):27-30. [PubMed]
37. Yoo KH, Kim MN, Kim BJ, Kim CW. Treatment of alopecia areata with fractional photothermolysis laser. Int J Dermatol. 2010 Jul;49(7):845-7. [PubMed]
38. Tierney EP, Kouba DJ, Hanke CW. Review of fractional photothermolysis: treatment indications and efficacy. Dermatol Surg. 2009 Oct;35(10):1445-61. [PubMed]
39. Orengo IF, Gerguis J, Phillips R, Guevara A, Lewis AT, Black HS. Celecoxib, a cyclooxygenase 2 inhibitor as a potential chemopreventive to UV-induced skin cancer: a study in the hairless mouse model. Arch Dermatol. 2002 Jun;138(6):751-5. [PubMed]
40. Gresham A, Masferrer J, Chen X, Leal-Khouri S, Pentland AP. Increased synthesis of high-molecular-weight cPLA2 mediates early UV-induced PGE2 in human skin. Am J Physiol. 1996 Apr;270(4 Pt 1):C1037-50. [PubMed]
41. Cohen JL. From serendipity to pilot study and then pivotal trial: bimatoprost topical for eyelash growth. Dermatol Surg. 2010 May;36(5):650-1. [PubMed]
42. Uno H, Zimbric ML, Albert DM, Stjernschantz J. Effect of latanoprost on hair growth in the bald scalp of the stump-tailed macacque: a pilot study. Acta Derm Venereol. 2002;82(1):7-12. [PubMed]
43. Wendelin DS, Pope DN, Mallory SB. Hypertrichosis. J Am Acad Dermatol. 2003 Feb;48(2):161-79. [PubMed]
44. Camacho F. Acquired circumscribed hypertrichosis in the 'costaleros' who bear the 'pasos' during Holy Week in Seville, Spain. Arch Dermatol. 1995 Mar;131(3):361-3. [PubMed]
45. Ressmann AC, Butterworth T. Localized acquired hypertrichosis. AMA Arch Derm Syphilol. 1952 Apr;65(4):458-63. [PubMed]
46. Tisocco LA, Del Campo DV, Bennin B, Barsky S. Acquired localized hypertrichosis. Arch Dermatol. 1981 Mar;117(3):127. [PubMed]
47. Shafir R, Tsur H. Local hirsutism at the periphery of burned skin. Br J Plast Surg. 1979 Apr;32(2):93. [PubMed]
48. Gupta S, Kanwar AJ, Kumar B. Hypertrichosis surrounding scar of knee replacement surgery. J Am Acad Dermatol. 2004 May;50(5):802-3. [PubMed]
49. Finck SJ, Cochran AJ, Vitek CR, Morton DL. Localized hirsutism after radical inguinal lymphadenectomy. N Engl J Med. 1981 Oct 15;305(16):958. [PubMed]
50. Kumar LR, Goyal BG. Pigmented hairy scar following smallpox vaccination. Indian J Pediatr. 1968 Jun;35(245):283-4. [PubMed]
51. Pembroke AC, Marten RH. Unusual cutaneous reactions following diphtheria and tetanus immunization. Clin Exp Dermatol. 1979 Sep;4(3):345-8. [PubMed]
52. Ozkan H, Dundar NO, Ozkan S, Kumral A, Duman N, Gulcan H. Hypertrichosis following measles immunization. Pediatr Dermatol. 2001 Sep-Oct;18(5):457-8. [PubMed]
53. Nielsen JS. Localized hirsutism following Colles' fractures. Can Med Assoc J. 1983 Aug 1;129(3):229. [PubMed]
54. Harper MC. Localized acquired hypertrichosis associated with fractures of the arm in young females. A report of two cases. Orthopedics. 1986 Jan;9(1):73-4. [PubMed]
55. Chang CH, Cohen PR. Ipsilateral post-cast hypertrichosis and dyshidrotic dermatitis. Arch Phys Med Rehabil. 1995 Jan;76(1):97-100. [PubMed]
56. Leung AK, Kiefer GN. Localized acquired hypertrichosis associated with fracture and cast application. J Natl Med Assoc. 1989 Jan;81(1):65-7. [PubMed]
57. Kara A, Kanra G, Alanay Y. Localized acquired hypertrichosis following cast application. Pediatr Dermatol. 2001 Jan-Feb;18(1):57-9. [PubMed]
58. Ravin N. New hair growth over fracture sites. N Engl J Med. 1990 Aug 2;323(5):350. [PubMed]
59. Schraibman IG. Localized hirsuties. Postgrad Med J. 1967 Aug;43(502):545-7. [PubMed]
60. Vlachos SP, Kontoes PP. Development of terminal hair following skin lesion treatments with an intense pulsed light source. Aesthetic Plast Surg. 2002 Jul-Aug;26(4):303-7. [PubMed]
61. Ito M, Yang Z, Andl T, Cui C, Kim N, Millar SE, Cotsarelis G. Wnt-dependent de novo hair follicle regeneration in adult mouse skin after wounding. Nature. 2007 May 17;447(7142):316-20. [PubMed]
62. Philp D, St-Surin S, Cha HJ, Moon HS, Kleinman HK, Elkin M. Thymosin beta 4 induces hair growth via stem cell migration and differentiation. Ann N Y Acad Sci. 2007 Sep;1112:95-103. [PubMed]
63. Sun LL, Xu LL, Nielsen TB, Rhee P, Burris D. Cyclopentyladenosine improves cell proliferation, wound healing, and hair growth. J Surg Res. 1999 Nov;87(1):14-24. [PubMed]
64. da Silva JP, da Silva MA, Almeida AP, Lombardi Junior I, Matos AP. Laser therapy in the tissue repair process: a literature review. Photomed Laser Surg. 2010 Feb;28(1):17-21. [PubMed]
65. Posten W, Wrone DA, Dover JS, Arndt KA, Silapunt S, Alam M. 2005. Low-level laser therapy for wound healing: mechanism and efficacy. Dermatol Surg. 2005 Mar;31(3):334-40. [PubMed]
66. Egesi A, Sun G, Khachemoune A, Rashid RM. Statins in skin: research and rediscovery, from psoriasis to sclerosis. J Drugs Dermatol. 2010 Aug;9(8):921-7. [PubMed]
67. Ullrich SE. 2005. Mechanisms underlying UV-induced immune suppression. Mutat Res. 2005 Apr 1;571(1-2):185-205. [PubMed]
68. Cooper KD, Oberhelman L, Hamilton TA, Baadsgaard O, Terhune M, LeVee G, Anderson T, Koren H. UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose, CD1a-DR+ epidermal macrophage induction, and Langerhans cell depletion. Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8497-501. [PubMed]
69. Damian DL, Halliday GM, Barnetson RS. Broad-spectrum sunscreens provide greater protection against ultraviolet-radiation-induced suppression of contact hypersensitivity to a recall antigen in humans. J Invest Dermatol. 1997 Aug;109(2):146-51. [PubMed]
70. Kelly DA, Seed PT, Young AR, Walker SL. A commercial sunscreen's protection against ultraviolet radiation-induced immunosuppression is more than 50% lower than protection against sunburn in humans. J Invest Dermatol. 2003 Jan;120(1):65-71. [PubMed]
71. Cestari TF, Kripke ML, Baptista PL, Bakos L, Bucana CD. Ultraviolet radiation decreases the granulomatous response to lepromin in humans. J Invest Dermatol. 1995 Jul;105(1):8-13. [PubMed]
72. Damian DL, Halliday GM, Taylor CA, Barnetson RS. Ultraviolet radiation induced suppression of Mantoux reactions in humans. J Invest Dermatol. 1998 May;110(5):824-7. [PubMed]
73. Moyal D. Immunosuppression induced by chronic ultraviolet irradiation in humans and its prevention by sunscreens. Eur J Dermatol. 1998 Apr-May;8(3):209-11. [PubMed]
74. McLoone P, Simics E, Barton A, Norval M, Gibbs NK. An action spectrum for the production of cis-urocanic acid in human skin in vivo. J Invest Dermatol. 2005 May;124(5):1071-4. [PubMed]
75. Matthews YJ, Halliday GM, Phan TA, Damian DL. A UVB wavelength dependency for local suppression of recall immunity in humans demonstrates a peak at 300 nm. J Invest Dermatol. 2010 Jun;130(6):1680-4. [PubMed]
76. Ho C, Nguyen Q, Lask G, Lowe N. Mini-slit graft hair transplantation using the Ultrapulse carbon dioxide laser handpiece. Dermatol Surg. 1995 Dec;21(12):1056-9. [PubMed]
77. Grevelink JM. Laser hair transplantation. Dermatol Clin. 1997 Jul;15(3):479-86. [PubMed]
78. Smithdeal CD. Carbon dioxide laser-assisted hair transplantation. The effect of laser parameters on scalp tissue--a histologic study. Dermatol Surg. 1997 Sep;23(9):835-40. [PubMed]
79. Otberg N, Wu WY, McElwee KJ, Shapiro J. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008 Jan-Feb;7(1):19-26. [PubMed]
80. Podda M, Spieth K, Kaufmann R. Er:YAG laser-assisted hair transplantation in cicatricial alopecia. Dermatol Surg. 2000 Nov;26(11):1010-4. [PubMed]
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