Title: High-intensity flashlamp photoepilation: a clinical, histological, and mechanistic study in human skin.
Authors: Sadick NS, Shea CR, Burchette JL Jr, Prieto VG
Journal: Arch Dermatol 1999 Jun;135(6):668-76
PMID: 10376694, UI: 99303187
Affiliated institution: Department of Dermatology, New York Hospital-Cornell Medical Center, New York, USA.
Cited in :
OBJECTIVE: To examine the clinical, histological, and immunohistological effects of flashlamp photoepilation.
DESIGN: Nonrandomized control trial with blinded histological study and follow-up of 1 to 20 months. SETTING: Private academic practice. SUBJECTS: Sixty-seven subjects (10 males and 57 females) with areas of excess body hair. INTERVENTIONS: Single (9 subjects) or multiple (58 subjects) treatments (noncoherent, 590-1200 nm, 2.9-3.0 milliseconds, 40-42 J/cm2) to hairy skin. From subjects given a single treatment, biopsy samples were taken immediately after treatment and at different intervals for up to 20 months.
MEAN OUTCOME MEASURES: Clinical measures include hair counts and morphologic features before and after treatment. Histological measures include terminal-vellus and anagen-other ratios, hair shaft diameter, and morphologic features (routine and immunohistochemical detection of bcl-2, bax, p53, Ki67, cyclin D1, and hsp70) before and after treatment.
RESULTS: Mean hair loss after photoepilation was 49%, 57%, and 54% for a single treatment and 47%, 56%, and 64% for multiple treatments at follow-up of less than 3 months, 3 to less than 6 months, and 6 months or longer, respectively (P<.05 for all comparisons). Transient erythema was seen in all subjects; no scarring occurred. Histologically, treatment caused morphologic damage confined to hair follicles and shafts. Terminal-vellus and anagen-telogen ratios, mean hair shaft diameter, and immunohistochemical profiles were not significantly modified by treatment. Treatment did not alter other skin adnexa, epidermis, or vessels.
CONCLUSIONS: Flashlamp treatment leads to significant, longlasting epilation. The predominant mechanism seems to be via selective photothermal damage to large, pigmented hair follicles rather than induction of a programmed state of follicular cycle arrest or follicular miniaturization.