Photodermatology, An Issue of Dermatologic Clinics
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2 - Photodermatology [Seite 2]
3 - copyright [Seite copyright]
- 3 [Seite 3]
4 - Contributors [Seite 4]
5 - Contents [Seite 8]
6 - Dermatologic Clinics [Seite Dermatologic Clinics]
- 12 [Seite 12]
7 - Preface [Seite Preface]
- 14 [Seite 14]
8 - Introduction to Photobiology [Seite 16]
8.1 - Key points [Seite 16]
8.2 - Introduction [Seite 16]
8.3 - UVR [Seite 16]
8.3.1 - Solar Radiation [Seite 16]
8.3.2 - UVR [Seite 17]
8.3.3 - Light-Skin Interactions [Seite 17]
8.3.3.1 - Reflection, scattering, and absorption [Seite 17]
8.3.3.2 - Photochemical reactions [Seite 18]
8.4 - Basic principles of phototherapy [Seite 18]
8.4.1 - MED [Seite 19]
8.4.2 - Acute and Chronic Effects of UVR [Seite 20]
8.4.3 - UV Damage on a Molecular Level [Seite 20]
8.4.3.1 - DNA damage and repair [Seite 20]
8.4.3.2 - UVR-induced apoptosis [Seite 21]
8.4.3.3 - Role of lipids [Seite 21]
8.4.3.4 - Role of proteins [Seite 21]
8.4.4 - UV Damage on a Clinical Level [Seite 21]
8.4.4.1 - Sun exposure: acute and chronic effects [Seite 21]
8.4.4.1.1 - Sunburn and tanning [Seite 21]
8.4.4.1.2 - Vitamin D production [Seite 22]
8.4.4.1.3 - Photoaging [Seite 22]
8.4.4.1.4 - Carcinogenesis [Seite 24]
8.4.4.2 - Phototherapy [Seite 24]
8.4.5 - Phototesting with Artificial Light Sources [Seite 24]
8.4.5.1 - Arc lamps [Seite 25]
8.4.5.2 - Excimer [Seite 25]
8.4.5.3 - Fluorescent lamps [Seite 25]
8.4.5.4 - Light-emitting diodes [Seite 25]
8.4.5.5 - Lasers [Seite 25]
8.5 - Summary [Seite 26]
8.6 - References [Seite 26]
9 - Evaluation of Patients with Photodermatoses [Seite 28]
9.1 - Key points [Seite 28]
9.2 - Overview [Seite 28]
9.3 - History [Seite 29]
9.3.1 - Age of Onset [Seite 29]
9.3.2 - Seasonal Variation, Interval Before Onset, Duration of the Eruption [Seite 30]
9.3.3 - Family History [Seite 30]
9.3.4 - Systemic Abnormalities [Seite 30]
9.3.5 - Window Glass [Seite 30]
9.3.6 - Exposure to Photosensitizers [Seite 31]
9.4 - Epidemiology and prevalence [Seite 31]
9.5 - Pathophysiology [Seite 32]
9.6 - Clinical findings [Seite 32]
9.6.1 - Histology [Seite 33]
9.6.2 - Laboratory and Photobiology Tests [Seite 33]
9.6.2.1 - Blood tests [Seite 33]
9.6.2.2 - Phototesting [Seite 34]
9.6.2.3 - Photopatch testing [Seite 34]
9.7 - Treatment [Seite 35]
9.8 - Summary [Seite 35]
9.9 - References [Seite 35]
10 - Photoimmunology [Seite 38]
10.1 - Key points [Seite 38]
10.2 - Evidence of photoimmunologic effects of UV radiation in humans [Seite 38]
10.3 - Experimental evidence for the photoimmunologic effects of UV radiation [Seite 39]
10.4 - Mechanisms of UV-induced immune suppression [Seite 39]
10.4.1 - Regulatory T Cells [Seite 39]
10.4.2 - APCs [Seite 40]
10.4.3 - Initial Molecular Events [Seite 41]
10.4.4 - Cytokines and Other Soluble Mediators [Seite 42]
10.4.5 - TLRs and Innate Immunity [Seite 43]
10.5 - Photoimmunologic diseases [Seite 44]
10.5.1 - PMLE [Seite 44]
10.5.2 - Chronic Actinic Dermatitis [Seite 44]
10.5.3 - Cutaneous Lupus Erythematosus [Seite 44]
10.6 - Photoimmunologic effects of phototherapy [Seite 46]
10.7 - Summary [Seite 47]
10.8 - References [Seite 47]
11 - Photoaging [Seite 52]
11.1 - Key points [Seite 52]
11.2 - Introduction [Seite 52]
11.3 - History [Seite 52]
11.4 - Epidemiology [Seite 52]
11.5 - Pathogenesis [Seite 53]
11.6 - Clinical manifestations [Seite 54]
11.7 - Histology [Seite 54]
11.8 - Photobiologic evaluation [Seite 54]
11.9 - Treatment [Seite 55]
11.9.1 - Topical Retinoids [Seite 56]
11.9.2 - Cosmeceuticals [Seite 56]
11.9.3 - Chemical Peels [Seite 57]
11.9.4 - Neuromodulators [Seite 57]
11.9.5 - Soft Tissue Fillers [Seite 58]
11.9.6 - Light Sources [Seite 58]
11.10 - Summary [Seite 59]
11.11 - References [Seite 59]
12 - Photocarcinogenesis [Seite 62]
12.1 - Key points [Seite 62]
12.2 - Introduction [Seite 62]
12.3 - Biologic effects of UV [Seite 62]
12.3.1 - DNA Damage [Seite 63]
12.3.2 - Cell-Cycle Arrest [Seite 63]
12.3.3 - DNA Repair [Seite 64]
12.3.4 - Apoptosis [Seite 64]
12.3.5 - UV Effects on the Immune System [Seite 64]
12.4 - Nonmelanoma skin cancer [Seite 65]
12.4.1 - Epidemiology [Seite 65]
12.4.2 - Genetic Predisposition for NMSC [Seite 65]
12.4.3 - Sporadic Formation of NMSC [Seite 65]
12.4.4 - Occupational Exposure and NMSC [Seite 66]
12.4.5 - Indoor Tanning and NMSC [Seite 67]
12.5 - Melanoma [Seite 67]
12.5.1 - Genetic Predisposition to Melanoma [Seite 68]
12.5.2 - Sporadic Melanoma [Seite 69]
12.5.3 - Occupational Exposure and Melanoma [Seite 69]
12.5.4 - Indoor Tanning and Melanoma [Seite 69]
12.6 - UVR, vitamin D, and skin cancer [Seite 70]
12.7 - Summary [Seite 71]
12.8 - References [Seite 71]
13 - Polymorphous Light Eruption [Seite 76]
13.1 - Key points [Seite 76]
13.2 - Introduction [Seite 76]
13.3 - History [Seite 77]
13.4 - Epidemiology [Seite 77]
13.4.1 - General Epidemiology [Seite 77]
13.5 - Clinical manifestations [Seite 77]
13.5.1 - Quality of Life [Seite 78]
13.5.2 - Relation to Lupus Erythematosus [Seite 78]
13.6 - Histology and immunohistochemistry [Seite 79]
13.7 - Photobiologic evaluation [Seite 79]
13.7.1 - Waveband Aspects [Seite 79]
13.8 - Pathogenesis [Seite 80]
13.8.1 - Genetics [Seite 80]
13.8.2 - Potential Antigens in PMLE [Seite 80]
13.8.3 - General Immunologic Aspects [Seite 81]
13.8.4 - Cell Migration Patterns and Cytokines [Seite 82]
13.8.5 - Antimicrobial Peptides [Seite 84]
13.8.6 - Hormonal Factors [Seite 84]
13.8.7 - Vitamin D [Seite 85]
13.8.8 - Relation to Skin Carcinogenesis [Seite 85]
13.9 - Management [Seite 86]
13.9.1 - Prevention [Seite 86]
13.9.2 - Photohardening [Seite 86]
13.9.3 - Established Treatments [Seite 87]
13.9.4 - Experimental Approaches [Seite 87]
13.10 - Summary and perspectives [Seite 88]
13.11 - Acknowledgments [Seite 88]
13.12 - References [Seite 88]
14 - Actinic Prurigo [Seite 96]
14.1 - Key points [Seite 96]
14.2 - Introduction [Seite 96]
14.3 - History [Seite 96]
14.4 - Epidemiology [Seite 97]
14.5 - Pathogenesis [Seite 97]
14.6 - Association with HLA [Seite 98]
14.7 - Clinical manifestations [Seite 98]
14.8 - Histology [Seite 99]
14.9 - Laboratory findings [Seite 99]
14.10 - Photobiological evaluation [Seite 100]
14.11 - Treatment [Seite 100]
14.12 - Summary [Seite 102]
14.13 - References [Seite 102]
15 - Hydroa Vacciniforme and Solar Urticaria [Seite 106]
15.1 - Key points [Seite 106]
15.2 - Hydroa vacciniforme [Seite 106]
15.2.1 - History [Seite 106]
15.2.2 - Epidemiology [Seite 106]
15.2.3 - Pathogenesis [Seite 107]
15.2.4 - Clinical Manifestations [Seite 107]
15.2.4.1 - Mucocutaneous manifestations [Seite 107]
15.2.4.2 - Systemic manifestations [Seite 107]
15.2.5 - Histology [Seite 108]
15.2.6 - Differential Diagnosis [Seite 108]
15.2.7 - Laboratory Findings [Seite 108]
15.2.8 - Photobiological Evaluation [Seite 108]
15.2.9 - Management [Seite 108]
15.3 - Solar urticaria [Seite 108]
15.3.1 - History [Seite 108]
15.3.2 - Epidemiology [Seite 109]
15.3.3 - Clinical Manifestations [Seite 109]
15.3.4 - Associated Conditions [Seite 109]
15.3.5 - Differential Diagnosis [Seite 109]
15.3.6 - Pathogenesis and Classification [Seite 109]
15.3.7 - Action Spectrum [Seite 109]
15.3.8 - Inhibition Spectrum [Seite 110]
15.3.9 - Augmentation Spectrum [Seite 110]
15.3.10 - Photobiological Evaluation [Seite 110]
15.3.11 - Management [Seite 110]
15.3.11.1 - Medical therapy [Seite 110]
15.3.11.1.1 - Antihistamines [Seite 110]
15.3.11.1.2 - Cyclosporine [Seite 111]
15.3.11.1.3 - Methotrexate [Seite 111]
15.3.11.1.4 - Intravenous immunoglobulin [Seite 111]
15.3.11.1.5 - Omalizumab [Seite 111]
15.3.11.1.6 - a-Melanocyte stimulating hormone analogue [Seite 111]
15.3.11.2 - Procedural therapy [Seite 111]
15.3.11.2.1 - Phototherapy and photochemotherapy [Seite 111]
15.3.11.2.2 - Plasmapheresis [Seite 112]
15.3.12 - Prognosis [Seite 112]
15.4 - References [Seite 112]
16 - Chronic Actinic Dermatitis [Seite 116]
16.1 - Key points [Seite 116]
16.2 - History [Seite 116]
16.3 - Epidemiology [Seite 116]
16.4 - Pathogenesis [Seite 117]
16.5 - Diagnosis [Seite 117]
16.5.1 - Clinical Manifestations [Seite 117]
16.5.2 - Differential Diagnoses [Seite 117]
16.5.3 - Histology [Seite 117]
16.5.4 - Photobiological Evaluation [Seite 117]
16.5.5 - Laboratory Evaluation [Seite 118]
16.6 - Management [Seite 118]
16.7 - Prognosis [Seite 119]
16.8 - Summary [Seite 119]
16.9 - References [Seite 120]
17 - Drug-Induced Photosensitivity [Seite 124]
17.1 - Key points [Seite 124]
17.2 - Introduction [Seite 124]
17.3 - Epidemiology [Seite 125]
17.4 - Pathogenesis [Seite 125]
17.5 - Clinical manifestations [Seite 126]
17.6 - Laboratory findings [Seite 126]
17.7 - Photobiological evaluation [Seite 126]
17.8 - Management [Seite 127]
17.9 - References [Seite 128]
18 - The Cutaneous Porphyrias [Seite 130]
18.1 - Key points [Seite 130]
18.2 - Introduction [Seite 130]
18.3 - History [Seite 130]
18.4 - Pathogenesis of skin lesions [Seite 131]
18.5 - Diagnostic approach in cutaneous porphyria [Seite 132]
18.6 - General photoprotection [Seite 133]
18.7 - Porphyrias presenting with acute photosensitivity [Seite 133]
18.7.1 - Erythropoietic and X-Linked Dominant Protoporphyria [Seite 133]
18.7.1.1 - Epidemiology [Seite 133]
18.7.1.2 - Clinical features [Seite 134]
18.7.1.3 - Differential diagnosis [Seite 134]
18.7.1.4 - Laboratory findings [Seite 135]
18.7.1.5 - Management [Seite 135]
18.8 - Porphyrias presenting with fragile skin [Seite 135]
18.8.1 - Porphyria Cutanea Tarda [Seite 135]
18.8.1.1 - Epidemiology and pathogenesis [Seite 135]
18.8.1.2 - Clinical features [Seite 136]
18.8.1.3 - Differential diagnosis [Seite 136]
18.8.1.4 - Laboratory findings [Seite 136]
18.8.1.5 - Management [Seite 137]
18.8.1.6 - Complications [Seite 137]
18.8.2 - The Autosomal Dominant Acute Porphyrias [Seite 137]
18.8.2.1 - Epidemiology [Seite 137]
18.8.2.2 - Pathogenesis of acute attacks [Seite 137]
18.8.2.3 - Clinical manifestations [Seite 138]
18.8.2.4 - Laboratory findings [Seite 138]
18.8.2.5 - Management [Seite 138]
18.8.3 - Congenital Erythropoietic Porphyria [Seite 139]
18.8.3.1 - Epidemiology [Seite 139]
18.8.3.2 - Clinical manifestations [Seite 139]
18.8.3.3 - Laboratory findings [Seite 140]
18.8.3.4 - Differential diagnosis [Seite 140]
18.8.3.5 - Management [Seite 140]
18.8.3.6 - Complications [Seite 141]
18.9 - Rare porphyria variants [Seite 141]
18.10 - References [Seite 141]
19 - Photoaggravated Disorders [Seite 146]
19.1 - Key points [Seite 146]
19.2 - Introduction [Seite 146]
19.3 - Diseases usually exacerbated by UVR [Seite 147]
19.3.1 - Cutaneous Lupus Erythematosus [Seite 147]
19.3.1.1 - Introduction [Seite 147]
19.3.1.2 - History [Seite 147]
19.3.1.3 - Epidemiology [Seite 147]
19.3.1.4 - Pathogenesis [Seite 148]
19.3.1.5 - Clinical manifestations [Seite 148]
19.3.1.6 - Histology [Seite 149]
19.3.1.7 - Laboratory findings [Seite 149]
19.3.1.8 - Management [Seite 149]
19.3.2 - Darier Disease [Seite 150]
19.3.2.1 - Introduction [Seite 150]
19.3.2.2 - History [Seite 150]
19.3.2.3 - Epidemiology [Seite 150]
19.3.2.4 - Pathogenesis [Seite 150]
19.3.2.5 - Clinical manifestations [Seite 150]
19.3.2.6 - Histology [Seite 150]
19.3.2.7 - Management [Seite 150]
19.3.3 - Dermatomyositis [Seite 151]
19.3.3.1 - Introduction [Seite 151]
19.3.3.2 - History [Seite 151]
19.3.3.3 - Epidemiology [Seite 151]
19.3.3.4 - Pathogenesis [Seite 151]
19.3.3.5 - Clinical manifestations [Seite 151]
19.3.3.6 - Histology [Seite 151]
19.3.3.7 - Laboratory findings [Seite 152]
19.3.3.8 - Photobiologic evaluation [Seite 152]
19.3.3.9 - Management [Seite 152]
19.3.4 - Lichen Planus Actinicus [Seite 152]
19.3.4.1 - Introduction [Seite 152]
19.3.4.2 - Epidemiology [Seite 152]
19.3.4.3 - Pathogenesis [Seite 152]
19.3.4.4 - Clinical manifestations [Seite 152]
19.3.4.5 - Histology [Seite 152]
19.3.4.6 - Management [Seite 152]
19.3.5 - Pellagra [Seite 152]
19.3.5.1 - Introduction [Seite 152]
19.3.5.2 - Epidemiology [Seite 152]
19.3.5.3 - Pathogenesis [Seite 152]
19.3.5.4 - Clinical manifestations [Seite 153]
19.3.5.5 - Laboratory findings [Seite 153]
19.3.5.6 - Management [Seite 153]
19.3.6 - Rosacea [Seite 153]
19.3.6.1 - Introduction [Seite 153]
19.3.6.2 - History [Seite 153]
19.3.6.3 - Epidemiology [Seite 153]
19.3.6.4 - Pathogenesis [Seite 153]
19.3.6.5 - Clinical manifestations [Seite 153]
19.3.6.6 - Histology [Seite 153]
19.3.6.7 - Management [Seite 153]
19.3.7 - Smith-Lemli-Opitz Syndrome [Seite 154]
19.4 - Diseases sometimes exacerbated by UVR [Seite 154]
19.4.1 - Atopic Dermatitis [Seite 154]
19.4.2 - Pemphigus [Seite 154]
19.4.3 - Psoriasis [Seite 154]
19.5 - References [Seite 155]
20 - UV-Based Therapy [Seite 160]
20.1 - Key points [Seite 160]
20.2 - Introduction [Seite 160]
20.3 - History [Seite 160]
20.4 - UV-B [Seite 161]
20.4.1 - Mechanism of Action [Seite 161]
20.4.2 - Modes of Delivery [Seite 161]
20.4.2.1 - BB-UV-B phototherapy [Seite 161]
20.4.2.2 - NB-UV-B phototherapy [Seite 161]
20.4.3 - Targeted Phototherapy: Excimer Lasers and Lamps [Seite 162]
20.4.4 - Indications [Seite 162]
20.4.5 - Contraindications [Seite 162]
20.4.6 - Treatment Protocol [Seite 163]
20.4.7 - Expected Outcome [Seite 165]
20.4.8 - Side Effects [Seite 165]
20.5 - PUVA and UV-A1 [Seite 165]
20.5.1 - Mechanism of Action [Seite 165]
20.5.2 - Modes of Delivery [Seite 166]
20.5.2.1 - PUVA [Seite 166]
20.5.2.2 - UV-A1 [Seite 166]
20.5.3 - Indications [Seite 166]
20.5.4 - Contraindications [Seite 166]
20.5.5 - Expected Outcome [Seite 166]
20.5.6 - Treatment Protocol [Seite 167]
20.5.7 - Side Effects [Seite 167]
20.6 - Summary [Seite 169]
20.7 - References [Seite 169]
21 - Photodynamic Therapy [Seite 176]
21.1 - Key points [Seite 176]
21.2 - Introduction [Seite 176]
21.3 - Historical perspective [Seite 176]
21.4 - Mechanism of action [Seite 177]
21.5 - Sensitizer [Seite 177]
21.6 - Light source [Seite 177]
21.7 - Therapeutic applications and expected outcomes [Seite 178]
21.7.1 - Photorejuvenation [Seite 178]
21.7.2 - Acne Vulgaris [Seite 179]
21.7.3 - Verrucae [Seite 180]
21.7.4 - Actinic Keratosis [Seite 180]
21.8 - NMSC [Seite 181]
21.8.1 - Bowen Disease [Seite 181]
21.9 - BCC [Seite 182]
21.10 - Management of adverse events [Seite 182]
21.10.1 - Pain [Seite 182]
21.10.1.1 - Cold air [Seite 183]
21.10.1.2 - Injectable anesthetics [Seite 183]
21.10.1.3 - Interruption of treatment [Seite 183]
21.10.1.4 - Topical anesthetics [Seite 184]
21.10.2 - Phototoxicity [Seite 184]
21.10.3 - Infection [Seite 184]
21.10.4 - Immunosuppression [Seite 184]
21.10.5 - Scarring [Seite 184]
21.10.6 - Pigmentation [Seite 184]
21.10.7 - Risk of Carcinogenesis [Seite 185]
21.11 - Summary [Seite 185]
21.12 - References [Seite 185]
22 - Sunscreens [Seite 188]
22.1 - Key points [Seite 188]
22.2 - Introduction [Seite 188]
22.3 - Mechanism of action [Seite 189]
22.4 - Health benefits of using sunscreen [Seite 189]
22.4.1 - Prevention of AK and SCC [Seite 190]
22.4.2 - Reduction of Basal Cell Carcinoma [Seite 191]
22.4.3 - Prevention of Melanoma [Seite 192]
22.4.4 - Prevention of Skin Aging [Seite 192]
22.4.5 - Management of Photodermatoses [Seite 192]
22.5 - FDA regulation on sunscreen labeling and effectiveness testing [Seite 192]
22.6 - Controversies associated with sunscreens [Seite 195]
22.6.1 - Safety of Oxybenzone [Seite 195]
22.6.2 - Safety of Nanoparticles [Seite 195]
22.6.3 - Sunscreen-Induced Vitamin D Deficiency [Seite 196]
22.7 - Limitations of sunscreen use [Seite 196]
22.8 - Summary [Seite 196]
22.9 - References [Seite 196]
23 - Photoprotection [Seite 200]
23.1 - Key points [Seite 200]
23.2 - Introduction [Seite 200]
23.3 - Photoprotection by glass [Seite 200]
23.3.1 - Main Types of Glass [Seite 200]
23.3.2 - UV Transmission Through Residential Glass [Seite 201]
23.3.3 - UV Exposure in Automobiles [Seite 201]
23.3.4 - Automobile Glass [Seite 201]
23.3.4.1 - UV transmission through automobile glass [Seite 202]
23.3.4.2 - Window films [Seite 202]
23.4 - Photoprotection with sunglasses [Seite 203]
23.4.1 - UV Exposure and the Eye [Seite 203]
23.4.2 - Sunglasses Guidelines [Seite 203]
23.5 - Photoprotection by clothing [Seite 204]
23.5.1 - Methods for Assessing the UPF of Textiles [Seite 204]
23.5.1.1 - In vitro method [Seite 204]
23.5.1.2 - In vivo method [Seite 205]
23.5.2 - Influence of Fabric Parameters on UPF [Seite 206]
23.5.3 - Porosity, Weight, and Thickness [Seite 206]
23.5.4 - Type of Fabric [Seite 206]
23.5.5 - Color of Fabrics [Seite 206]
23.5.6 - Laundry [Seite 206]
23.5.7 - Moisture Content [Seite 206]
23.5.8 - Stretch [Seite 207]
23.5.9 - Fabric to Skin Distance [Seite 207]
23.5.10 - Fabric Processing [Seite 207]
23.5.11 - UV Absorbers [Seite 207]
23.6 - Summary [Seite 207]
23.7 - References [Seite 208]
24 - Index [Seite 210]
Introduction to Photobiology
Elma D. Baron, MDa∗elma.baron@uhhospitals.org and Amanda K. Suggs, MDb, aDepartment of Dermatology, University Hospitals Case Medical Center, Louis Stokes Cleveland Veterans Affairs Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Lakeside 3500, Mailstop 5028, Cleveland, OH 44106-5028, USA; bDepartment of Dermatology, University Hospitals Case Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA
∗Corresponding author.
Photobiology is the study of the local and systemic effects of incident radiation on living organisms. Solar radiation is made up of ultraviolet, visible and infrared radiation. Ultraviolet radiation is made up of UV-C, UV-B, and UV-A. Sun exposure can lead to sunburn, tanning, vitamin D production, photoaging, and carcinogenesis. Phototherapy is the use of nonionizing radiation to treat cutaneous disease. Various types of artificial light sources are used for photo testing and phototherapy.
Keywords
Ultraviolet radiation
Ultraviolet light
Phototherapy
Photobiology
Sunburn
Melanogenesis
Vitamin D production
Photoaging
Key points
• Solar radiation is made up of ultraviolet, visible, and infrared radiation.
• Ultraviolet radiation is made up of UV-C, UV-B, and UV-A.
• Most ultraviolet radiation that reaches the earth is UV-A.
• Sun exposure has a wide range of biological effects, including sunburn, tanning, vitamin D production, photoaging, and carcinogenesis.
• Phototherapy uses properties of ultraviolet light that are useful in the treatment of certain dermatologic conditions.
Introduction
Photobiology deals with the local and systemic effects of incident radiation on living organisms. This introductory article on cutaneous photobiology focuses on the effects of ultraviolet (UV) radiation (UVR), both from its natural source (ie, the sun) and artificial sources (ie, those used in phototherapy), on skin function and diseases. Although visible light and infrared radiation also have effects on skin cells, there is more information on UVR.
Phototherapy is the use of nonionizing radiation to treat cutaneous disease. For more than a century, phototherapy has played a pivotal role in the treatment of dermatologic diseases. In 1903, Niels Finsen received the Nobel Prize in Medicine for using light to treat a cutaneous mycobacterial disease. In the middle of the 20th century, advancements in UV-B light therapy expanded treatment options for patients with psoriasis. In the 1970s, photochemotherapy (ie, using psoralen as a photosensitizer in combination with UV-A radiation [PUVA]) made its debut. PUVA became an established player in the treatment of skin diseases in the last quarter of the 20th century. More recent advances in the last few decades (ie, narrowband UV-B therapy, laser therapy, targeted phototherapy, photodynamic therapy [PDT], UV-A1) have also revolutionized photodermatology.1,2
UVR
Solar Radiation
The rays of the sun hit the earth in the form of UVR, visible, and infrared radiation. These 3 entities are components of the electromagnetic spectrum, which also includes radiowaves, microwaves, radiographs, and γ radiation (Fig. 1). Solar radiation is made up of approximately 50% visible light, 40% infrared, and 9% UVR.3 Visible radiation is that which is perceived by the human eye.4 Each color of visible light represents a different wavelength range (see Fig. 1). UVR is the area of the electromagnetic spectrum that is considered most biologically active and therefore of greatest impact on health and disease.
Fig. 1 Electromagnetic spectrum.
UVR
UVR spans the wavelengths 100 to 400 nm and is subdivided into UV-C, UV-B, and UV-A. There are subtle differences in the subdivisions described in the literature. In this article, the subdivision most commonly chosen in photobiology is used (ie, UV-C, 200–290 nm; UV-B, 290–320 nm; and UV-A, 320–400 nm).4 Other ranges referenced in the literature include: UV-C at 200 to 280 nm, UV-B at 280 to 320 nm, UV-A at 320 to 400 nm, UV-C at 200 to 280 nm, UV-B at 280 to 315 nm, and UV-A at 315 to 400 nm.5 The stratospheric ozone prevents wavelengths shorter than approximately 290 nm from hitting the earth. Most UV radiation that reaches the earth is UV-A. Only a small percentage (approximately 5%) of UV-B is present in terrestrial sunlight. UV-C is typically filtered by the ozone layer.6 The amount of solar energy at a specific wavelength that can affect the earth varies with season, region, altitude, pollution, and the path that the solar radiation traverses through the ozone.7 The amount of UV in sunlight also varies throughout the day. Being of a longer wavelength, UV-A is present consistently from sunrise to sunset, whereas UV-B peaks around noon. Approximately 50% of UV-A exposure occurs in the shade as a result of surface reflection and its penetration to cloud cover. Windows and automotive glass do not shield against UV-A but do shield against UV-B.8
For the purposes of phototherapy, UV-B has been further subdivided into broadband UV-B (290–320 nm) and narrrowband UV-B (311 nm–313 nm). UV-A radiation has been subdivided into UV-A1 (340–400 nm) and UV-A2 (320–340 nm), primarily because the biological effect of UV-A2 is closer to that of UV-B. The specific applications of these modalities are discussed in more detail in the article by Rkein and Ozog elsewhere in this issue.
Light-Skin Interactions
Light has both the properties of waves and particles known as photons. In cutaneous photobiology, it is important to understand what happens to photons when they encounter the skin surface. They can undergo reflection, scattering, or absorption. According to the Grothus-Draper law, light can have a biological effect only if it is absorbed. Once radiation is absorbed by molecules in the skin (termed chromophores), energy is transferred to produce heat or drive photochemical reactions. This process results in detectable responses at the cellular and molecular levels that could lead to a clinical outcome (Fig. 2).9,10
Fig. 2 Light-skin interaction pathway.
Reflection, scattering, and absorption
Reflection happens at the skin surface. Light reflected from the skin can be used for diagnostic purposes but does not have much of a therapeutic role. Scattering alters the direction of the light transmission through the skin. How deep a photon can go is influenced by how much it is scattered by structures in the skin. Most scattering takes place in the dermis as a result of the presence of collagen. Scattering of radiation is also wavelength dependent; shorter wavelengths scatter more, whereas longer wavelengths penetrate deeper.9,10
The depth of light penetration is critical for phototherapy. UV-B is generally absorbed in the epidermis and upper dermis, whereas UV-A (because of its longer wavelengths) penetrates well into the dermis (Fig. 3). Shorter wavelength visible light such as blue light can be used in PDT for epidermal growths (such as actinic keratoses). Red light, which is of a longer visible wavelength, can target deeper structures such as sebaceous glands and thicker lesions.11 Nonetheless, penetration depth is only 1 part of the equation. The light must also be of the appropriate wavelength to be absorbed by the target molecule or chromophore. Only on absorption can a photon exert a clinical effect.
Fig. 3 UV wavelength and depth of skin penetration.
Different wavelength(s) target different chromophores, which results in a variety of cutaneous effects.11 Chromophores can be cellular/molecular components, such as amino acids, nucleotides, lipids, and 7-dehydrocholesterol (a vitamin D precursor). They can also be porphyrins (exogenous or endogenous), tattoo pigments, or photosensitizing drugs (eg, psoralens).10 DNA directly absorbs UV-B and is therefore a chromophore targeted by UV-B phototherapy. In cosmetic laser treatments, endogenous chromophores targeted are mainly hemoglobin, melanin, and water.12 Exogenous substances (ie, aminolevulinic acid solution, which converts to protoporphyrin IX) may also be used to act as chromophores, depending on the phototherapeutic modality.
Absorption is wavelength dependent and is influenced by the physicochemical structure of the chromophore.4,10 Each chromophore has an absorption spectrum, which is the range of wavelengths that are absorbed by that molecule. For example, the absorption spectrum for melanin is 250 to 1200 nm.13 The...
