INTRODUCTION
Aging alters the structure and function of all organs of the body, including the skin. The skin protects the body from harmful external stimuli (e.g., microorganisms, trauma, radiation) and has defense mechanisms, including immunologic and wound healing responses, to repair compromised tissue. The skin also contributes to one’s external appearance, making skin health an important component of facial aesthetics. The cutaneous manifestations of aging include atrophy, pigmentation, decreased ability for wound healing, and rhytides.1 Under the cumulative influence of gravity, thinning dermis, and degradation of collagen fibers, the structure of the face changes.2 The desire to preserve youth is prevalent in modern society, as a youthful appearance is associated with perceived well-being and physical attractiveness.3,4,5 Understanding the biology of cutaneous aging is important as life expectancies have increased and individuals may seek to preserve cutaneous function and structure.
Intrinsic aging of the skin occurs as a result of DNA damage accumulated through cell division, leading to altered production of biomolecules and functional decline of normal cellular processes.6 Genes relating to basic biologic processes such as protein metabolism, cell division, DNA repair, and oxidative stress response, have been demonstrated to be expressed at higher levels in younger patients compared to older patients.7 The slow decline in function of the epidermis is due to reactive oxygen species (ROS) damage to telomeres and other cellular components.8 Extrinsic aging of the skin is caused by modifiable factors such as ultraviolet (UV) radiation exposure and smoking, which generate ROS that indirectly damage DNA.8 Sun damage causes fragmentation of type I collagen, the most abundant collagen in the body, and decreased tension on fibroblasts.6,9 Fibroblasts respond by producing less collagen and more matrix metalloproteinases (MMPs), creating a vicious cycle that manifests clinically as thinning skin.6,9
The interactions between light and the skin are complex and are not fully understood. UV light has various biologic effects on the skin that may cause disease or provide therapeutic benefits. While unprotected exposure to both UVA (320 – 400 nm) and UVB (280 – 320 nm) radiation causes skin damage, UVA contributes to over 80% of premature aging of the facial skin.10,11 UVB phototherapy is widely used in dermatology for the treatment of skin disorders such as psoriasis; however, there are short-term and long-term deleterious side effects associated with UVB irradiation including the increased risk of skin cancer.12 In recent years, different forms of visible light (400–700 nm) have been studied as a treatment modality to manage age-related skin changes. Phototherapy using visible light, such as light emitting diodes (LEDs), is currently being used for a wide spectrum of medical and aesthetic dermatologic conditions.13
LEDs produce non-coherent light in the near-infrared, visible, and UV ranges using high-efficiency semiconductors.14 LEDs are utilized as part of low level light therapy (LLLT) and photodynamic therapy (PDT) for various medical conditions. Other
Intrinsic aging of the skin occurs as a result of DNA damage accumulated through cell division, leading to altered production of biomolecules and functional decline of normal cellular processes.6 Genes relating to basic biologic processes such as protein metabolism, cell division, DNA repair, and oxidative stress response, have been demonstrated to be expressed at higher levels in younger patients compared to older patients.7 The slow decline in function of the epidermis is due to reactive oxygen species (ROS) damage to telomeres and other cellular components.8 Extrinsic aging of the skin is caused by modifiable factors such as ultraviolet (UV) radiation exposure and smoking, which generate ROS that indirectly damage DNA.8 Sun damage causes fragmentation of type I collagen, the most abundant collagen in the body, and decreased tension on fibroblasts.6,9 Fibroblasts respond by producing less collagen and more matrix metalloproteinases (MMPs), creating a vicious cycle that manifests clinically as thinning skin.6,9
The interactions between light and the skin are complex and are not fully understood. UV light has various biologic effects on the skin that may cause disease or provide therapeutic benefits. While unprotected exposure to both UVA (320 – 400 nm) and UVB (280 – 320 nm) radiation causes skin damage, UVA contributes to over 80% of premature aging of the facial skin.10,11 UVB phototherapy is widely used in dermatology for the treatment of skin disorders such as psoriasis; however, there are short-term and long-term deleterious side effects associated with UVB irradiation including the increased risk of skin cancer.12 In recent years, different forms of visible light (400–700 nm) have been studied as a treatment modality to manage age-related skin changes. Phototherapy using visible light, such as light emitting diodes (LEDs), is currently being used for a wide spectrum of medical and aesthetic dermatologic conditions.13
LEDs produce non-coherent light in the near-infrared, visible, and UV ranges using high-efficiency semiconductors.14 LEDs are utilized as part of low level light therapy (LLLT) and photodynamic therapy (PDT) for various medical conditions. Other