||This article may require cleanup to meet Wikipedia's quality standards. (June 2011)|
Photoaging or photoageing (also known as "Dermatoheliosis") is a term used for the characteristic changes induced by chronic UVA and UVB exposure.:29 Tretinoin is the best studied retinoid in the treatment of photoaging
The deterioration of biological functions and ability to manage metabolic stress is one of the major consequences of the aging process. Aging is a complex, progressive process which also leads to functional and esthetic changes in the skin. This process could result from both intrinsic, such that it is genetically determined, as well as extrinsic processes which include environmental factors.
Photoaging is a process of aging of the skin attributed to continuous, long-term exposure to ultraviolet (UV) radiation of approximately 300–400 nm, natural or synthetic, on an intrinsically aged skin. Photoaging is thus also known as aging of the skin of the face, ears, neck and hands, caused by UVA and UVB rays.
Effects of UV light 
UV and molecular and genetic changes
UVB ray is considered as a primary mutagen that can only penetrate through the epidermal or outermost layer of the skin, resulting in DNA mutations. These DNA mutations arise due to chemical changes, the formation of cyclobutane pyrimidine dimers and photoproducts formed between adjacent pyrimidine bases. These mutations may be clinically related to specific signs of photoaging such as wrinkling, increasing in elastin and collagen damage.
The epidermal layer does not contain any blood vessels or nerve endings but melanocytes and basal cells are embedded in this layer. Upon exposure to UVB rays, melanocytes will produce melanin, a pigment that gives the skin its color tone. However, UVB will cause the formation of freckles and dark spots, both of which are symptoms of photoaging. With constant exposure to UVB rays, signs of photoaging might appear and precancerous lesions or skin cancer may develop.
UVA rays are able to penetrate deeper into the skin as compared to UVB rays. Hence, in addition to the epidermal layer, the dermal layer will also be damaged. The dermis is the second major layer of the skin and it comprises collagen, elastin, and extrafibrillar matrix which provides structural support to the skin. However, with constant UVA exposure, the size of the dermis layer will be reduced, thereby causing the epidermis to start drooping off the body. Due to the presence of blood vessels in the dermis, UVA rays could lead to dilated or broken blood vessels most commonly visible on the nose and cheeks. UVA can also damage DNA indirectly through the generation of reactive oxygen species (ROS) which includes superoxide anion, peroxide and singlet oxygen. These ROS damage cellular DNA as well as lipids and proteins.
UV and pigmentation
UV exposure could also lead to inflammation and vasodilation which is clinically manifested as sunburn. UV radiation activates the transcription factor, NF-κB, which is the first step in inflammation. NF-κB activation will result in the increase of proinflammatory cytokines e.g. interleukin 1 (IL-1), IL-6 vascular endothelial growth factor and tumor necrosis factor, TNF-α. This would then attract neutrophils which lead to an increase in oxidative damage through the generation of free radicals.
Additionally, UV radiation would cause the down-regulation of an angiogenesis inhibitor, thrombospondin-1, and the up-regulation of an angiogenesis activator which is platelet-derived endothelial cell growth factor, in keratinocytes. These enhance angiogenesis and aid in the growth of UV-induced neoplasms.
UV and immunosuppression
It has also been reported that UV radiation would lead to local and systemic immunosuppression, due to DNA damage and altered cytokine expression. This has implications in cutaneous tumor surveillance. The langerhan cells would undergo changes in terms of quantity, morphology and functions due to UV exposure and eventually becomes depleted. One of the reasons suggested to account for the presence of immunosuppression mediated by the body is due to the need to suppress or prevent an autoimmune response to inflammatory products resulting from UV-mediated damage.
UV and degradation of collagen
UV exposure would also lead to the activation of receptors for epidermal growth factor, IL-1 and TNF-α in keratinocytes and fibroblasts, which then activates signalling kinases throughout the skin via an unknown mechanism. The nuclear transcription factor activator protein, AP-1, which controls the transcription of matrix metalloproteinases (MMP), is expressed and activated. MMP-1 is a major metalloproteinases for collagen degradation. This entire process is aided by the presence of reactive oxygen species (ROS) that inhibits protein-tyrosine phosphatases via oxidation, thereby resulting in the up-regulation of the above mentioned receptors. Another transcription factor NF-κB, which is also activated by UV light, also increases the expression of MMP-9.
The up-regulation of MMP can occur even after minimal exposure to UV, hence, exposure to UV radiation which is inadequate to cause sunburn can thus facilitate the degradation of skin collagen and lead to presumably, eventual photoaging. Thus, collagen production is reduced in photoaged skin due to the process of constant degradation of collagen mediated by MMPs.
In addition, the presence of damaged collagen would also down-regulate the synthesis of new collagen. The impaired spreading and attachment of fibroblasts onto degraded collagen could be one of the contributing factors to the inhibition of collagen synthesis.
UV and retinoic acids and photodamage
Retinoic acid (RA) is essential for normal epithelial growth and differentiation as well as for maintenance of normal skin homeostasis. UV radiation decreases the expression of both retinoic acid receptors (RARs) and retinoid X receptors (RXRs) in human skin, thereby resulting in a complete loss of the induction of RA-responsive genes. It also would lead to an increase in activity of AP-1 pathway, increasing MMP activity and thus also resulting in a functional deficiency of vitamin A in the skin.
Signs, symptoms and histopathology 
The early symptoms of photoaging includes the following:
- Dyspigmentation and the formation of wrinkles around regions of skin commonly exposed to sun, namely the eyes, mouth and forehead.
- Spider veins on face and neck
- Loss of color and fullness in lips
Symptoms of photoaging attributed to prolonged exposure to UV
- Wrinkles deepen and forehead frown lines can be seen even when not frowning.
- Telangiectasias most commonly seen around the nose, cheeks and chin.
- Skin becomes leathery and laxity occurs.
- Solar Lentigines (age spots) appears on the face and hands.
- Possibly pre-cancerous red and scaly spots (actinic keratoses) appear.
- Cutaneous malignancies
In addition to the above symptoms, photoaging could also result in an orderly maturation of keratinocytes and an increased in the cell population of the dermis where abundant; hyperplastic, elongated and collapsed fibroblasts and inflammatory infiltrates are found.
Photodamage could also be characterized as the disorganization of collagen fibrils which constitute most of the connective tissue and the accumulation of abnormal, amorphous, elastin-containing material.
Endogenous defense mechanism against UV radiation 
The endogenous defense mechanisms provide protection of the skin from damages induced by UV.
UV exposure which would lead to an increase in epidermal thickness could help protect from further UV damage.
It has been reported in many cases that fairer individuals who have lesser melanin pigment show more dermal DNA photodamage, infiltrating neutrophils, keratinocyte activation, IL-10 expression and increased MMPs after UV exposure. Therefore, the distribution of melanin provides protection from sunburn, photoaging, and carcinogenesis by absorbing and scattering UV rays.
Repair of DNA mutation and apoptosis
The damage of DNA due to exposure of UV rays will lead to expression of p53, thereby leading to eventual arrest of the cell cycle. This allows DNA repair mediated by endogenous mechanisms like the nucleotide excision repair system. In addition, apoptosis occurs if the damage is too severe. However, the apoptotic mechanisms decline with age and if neither DNA repair mechanism nor apoptosis occurs, cutaneous tumorigenesis may result.
Tissue inhibitors of MMPs (TIMPs)
TIMPs regulate the activity of MMP. UV rays have been shown in many studies that it would induce TIMP-1.
The skin consists of several antioxidants which include vitamin E, coenzyme Q10, ascorbate, carotenoids, superoxide dismutase, catalase and glutathione peroxidase. These antioxidants provide protection from ROS produced during normal cellular metabolism. However, too much exposure to UV rays could lead to a significant reduction in the antioxidant supply, leading to oxidative stress. Hence, these antioxidants are essential in the skin's defense mechanism against UV radiation and photocarcinogenesis.
Treatment of photoaging 
Treatment and intervention for photoaging can be classified into a unique paradigm based on disease prevention.
Primary prevention aims to reduce the risk factors before a disease or condition occurs. Primary prevention method involves mainly sun protection that comes in many forms like sun avoidance, protective clothing, and sunscreens.
The UV exposure would be the strongest between 10am and 4pm and sun avoidance between this period of time is highly encouraged. If one cannot avoid exposure to the sun, clothing, hats and sunglasses that protects one from sun exposure should be fully utilized. Wide spectrum sun screens that have a sun protection factor (SPF) of at least 30 should be used when one gets frequent sun exposure.
Secondary protection refers to early detection of disease, potentially while still asymptomatic, to allow positive interference to prevent, delay or attenuate the symptomatic clinical condition. This includes the following:
- Retinoids e.g. Tretinoin
- Antioxidants e.g. topical vitamin C, oral supplements, CoQ10, Lipoic acid
- Growth factors and cytokines.
Lastly, tertiary prevention is the treatment of an existing symptomatic disease process to ameliorate its effects or delay its progress. Such tertiary prevention includes the use of chemical peels, resurfacing techniques like micro-dermabrasion, the use of ablative and non-ablative laser systems, radiofrequency technology, the use of exotoxin Botulinum toxins and soft tissue augmentation, also known as fillers.
See also 
- Helfrich, Y. S. (Jun 2008). "Overview of skin aging and photoaging" (PDF). Dermatology nursing / Dermatology Nurses' Association 20 (3): 177–183; quiz 183. ISSN 1060-3441. PMID 18649702.
- Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0.
- James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.
- Stefanaki, C.; Stratigos, A.; Katsambas, A. (2005). "Topical retinoids in the treatment of photoaging". Journal of Cosmetic Dermatology 4 (2): 130–134. doi:10.1111/j.1473-2165.2005.40215.x. PMID 17166212.