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Abstract
Photodynamic therapy (PDT) uses a photosensitizer, light energy, and molecular oxygen to cause cell damage. Cells exposed to the photosensitizer are susceptible to destruction upon light absorption because excitation of the photosensitizing agents leads to the production of reactive oxygen species and, subsequently, direct cytotoxicity. Using the intrinsic cellular heme biosynthetic pathway, topical PDT selectively targets abnormal cells, while preserving normal surrounding tissues. This selective cytotoxic effect is the basis for the use of PDT in antitumor treatment. Clinically, PDT is a widely used therapeutic regimen for oncologic skin conditions such as actinic keratosis, squamous cell carcinoma in situ, and basal cell carcinoma. PDT has been shown, under certain circumstances, to stimulate the immune system and produce antibacterial, and/or regenerative effects while protecting cell viability. Thus, it may be useful for treating benign skin conditions. An increasing number of studies support the idea that PDT may be effective for treating acne vulgaris and several other inflammatory/infective skin diseases, including psoriasis, rosacea, viral warts, and aging-related changes. This review provides an overview of the clinical investigations of PDT and discusses each of the essential aspects of the sequence: its mechanism of action, common photosensitizers, light sources, and clinical applications in dermatology. Of the numerous clinical trials of PDT in dermatology, this review focuses on those studies that have reported remarkable therapeutic benefits following topical PDT for benign skin conditions such as acne vulgaris, viral warts, and photorejuvenation without causing severe side effects.
Highlights
The principle of photodynamic action was first described by Oscar Raab in 1890 when he noted the toxic effects of acridine orange, which showed activity as a photosensitizer when combined with light and oxygen by destroying Paramecium caudatum cells without apparent damage to the protozoa when used alone [1]
The fact that aminolevulinic acid (ALA) is a water-soluble amino acid, has low lipid solubility, and is unable to penetrate through the stratum corneum restricts its clinical application in photodynamic therapy (PDT) to superficial skin diseases such as actinic keratosis, Bowen’s disease, and superficial basal cell carcinoma (BCC) [19,20]
There is growing evidence that topical PDT is effective in the treatment of various benign skin conditions including viral warts, photodamaged skin, and acne vulgaris, and especially in lesions that are inflamed or oily and unresponsive to conventional therapies
Summary
The principle of photodynamic action was first described by Oscar Raab in 1890 when he noted the toxic effects of acridine orange, which showed activity as a photosensitizer when combined with light and oxygen by destroying Paramecium caudatum cells without apparent damage to the protozoa when used alone [1]. It can react directly with a substrate, such as intracellular molecules or cell membrane components, to form radicals, which interact with oxygen to generate ROS (type I reaction); Second, the activated photosensitizer can transfer its energy directly to oxygen to form the ROS singlet oxygen (1O2), which further oxidizes various substrates (type II reaction). These species can oxidize various substrates and initiate cytotoxic effects by inducing necrosis and apoptosis. Following a low light dose, PDT with various photosensitizers has been shown to modify cytokine expression and induce immune-specific responses, resulting in immunomodulatory effects in inflammatory skin disorders
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