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Avci et al. Page 4 environmental influences are responsible for the aging process of skin; however photodamage seems to be one of the most important causes of these changes. Several modalities have been developed in order to reverse the dermal and epidermal signs of photo- and chronological aging. The main concept of most of these modalities is removing the epidermis and inducing a controlled form of skin wounding in order to promote collagen biosynthesis and dermal matrix remodeling. The most commonly used interventions as of today are retinoic acid (a vitamin A derivative), dermabrasion, chemical peels, and ablative laser resurfacing with carbon dioxide (CO2) or erbium: yttrium- aluminum-garnet (Er:YAG) lasers or a combination of these wavelengths.25–27 However, these procedures require intensive post-treatment care, prolonged downtime and may lead to complications such as long-lasting erythema, pain, infection, bleedings, oozing, burns, hyper- or hypopigmentation and scarring.28,29 These limitations created a need for the development of alternative rejuvenation procedures that were safer, more effective, had fewer side effects and minimum postoperative care and downtime, which in turn led to the emergence of non-ablative rejuvenation technologies.30–32 Non-ablative skin rejuvenation aims to improve photoaged and aging skin without destroying the epidermis.31,32 Irregular pigmentation and telangiectasia can be treated with intense pulsed light sources (IPL), 532 nm potassium-titanyl-phosphate lasers (KTP), and high-dose 585/595 nm pulsed dye lasers (PDL)33. Wrinkle reduction and skin tightening through thermal injury to the dermis (photothermolysis) can be achieved by other IPL sources (ie, low-dose 589/595 nm PDLs, 1064 & 1320 nm neodymium:yttrium-aluminum-garnet lasers, (Nd:YAG) 1450 nm diode lasers, and 1540 nm erbium fiber lasers).33 LED which is a novel light source for non-thermal, non-ablative skin rejuvenation has been shown to be effective for improving wrinkles and skin laxity (Figure 3).34–40 It is not a new phenomenon since the first reports of LLLT effects on increased collagen go back to 1987. Studies by Abergel et al. and Yu et al. reported an increase in production of pro-collagen, collagen, basic fibroblast growth factors (bFGF) and proliferation of fibroblasts after exposure to low-energy laser irradiation in vitro and in vivo animal models (Figure 4).41,42 Furthermore, LLLT was already known to increase microcirculation, vascular perfusion in the skin, alter platelet-derived growth factor (PDGF), transforming growth factor (TGF-β1) and inhibit apoptosis (Figure 4).1,43,44 Lee et al. investigated the histologic and ultrastructural changes following a combination of 830 nm, 55 mW/cm2, 66 J/cm2 and 633 nm, 105 mW/cm2, 126 J/cm2 LED phototherapy and observed alteration in the status of MMPs and their tissue inhibitors (TIMPs).33 Furthermore, mRNA levels of IL-1β, TNF-α, ICAM-1, and connexin 43 (Cx43) were increased following LED phototherapy whereas IL-6 levels were decreased (Figure 4) 33. Finally, an increase in the amount of collagen was demonstrated in the post-treatment specimens 33. Pro-inflammatory cytokines IL-1β and TNF-α are thought to be recruited to heal the intentionally formed photothermally-mediated wounds associated with laser treatments, and this cascade of wound healing consequently contributes to new collagen synthesis.33 LED therapy may induce this wound healing process through non-thermal and atraumatic induction of a subclinical ‘quasi-wound’, even without any actual thermal damage which could cause complications as in some other laser treatments.33 TIMPs inhibit MMP activities, so another possible mechanism for the Semin Cutan Med Surg. Author manuscript; available in PMC 2014 August 08. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPDF Image | Low-level laser (light) therapy (LLLT) in skin: stimulating, healing, restoring
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