Photoaging

Photoaging

As life expectancy has increased and baby boomers have begun to enter middle age, interest has increased in slowing the aging process. Implied in this escalating interest is the confidence that greater scientific knowledge and advancements in technology may enable us to control the physical manifestations of aging.

Although dermatologists have discussed since the end of the 19th century, the notion that sunlight contributes to premature aging.

Skin aging
There are two main processes of skin aging, intrinsic and extrinsic. Intrinsic aging reflects the genetic background of an individual and results from the passage of time. Extrinsic aging is caused by external factors, such as smoking, excessive use of alcohol, poor nutrition, and sun exposure. The intrinsic processes is inevitable, meanwhile the extrinsic processes is not inevitable. It has been said that 80% of facial aging is attributable to sun exposure.

Intrinsic vs Extrinsic aging
Intrinsically aged skin is smooth and unblemished, but preservation of the normal geometric patterns of the skin. Under the microscope, this skin demonstrates epidermal atrophy, flattening of the epidermal rete ridges, and dermal atrophy. Collagen fibrils are not thickened but are increased in number with an increase in the collagen III/collagen I ratio.
Extrinsically aged skin appears predominately in exposed areas such as the face, chest, and extensor surfaces of the arms. It is a result of the total effects of a life time exposure to ultraviolet radiation (UVR). Clinical findings of photoaged skin include wrinkles, pigmented lesions such as freckles, lentigenes, and patchy hyperpigmentation, and depigmented lesions such as guttate hypomelanosis. This sun damage can be highlighted by using a wood’s lamp or an ultraviolet camera system.
The importance of sun protection in the prevention of these pigmented lesions that not only make the skin appear older, but are known to be associated with an increased risk of melanoma.

Characteristics of Aged Skin
Epidermis
Aged epidermis exhibits a flattening of the dermal-epidermal junction (DEJ) with a correspondingly smaller connecting surface area. This lost of DEJ surface area may lead to the increased fragility of the skin and may also result in less nutrient transfer between the dermis and epidermis.
The importance is epidermal turnover rate slows from 30-50 percent between the third and eighth decades of life. Consequently, many cosmetic dermatologists employ products to “speed up” the cell cycle, in the belief that a faster turnover rate produces improvements in skin appearance and speeds wound healing after cosmetic procedures.

Dermis
The three components of the dermis that have received the most attention in antiaging research are collagen, elastin, and glycosaminoglycans.

Collagen
As the skin ages, the ratio of type III to type I collagen increases (meaning that there is less type I collagen with aging). This correlates with the extent of photodamage.
It is known that the overall collagen content per unit area of skin surface decrease approximately 1 percent per year.
Anchoring fibrils (made of collagen VII), are important because they attach the basement membrane zone to the underlying papillary dermis (attach the epidermis to the dermis). Patients with chronically sun-exposed skin have significantly lower number of anchoring fibrils. A weakened bond between epidermis and the dermis because of loss of the anchoring fibrils leads to wrinkle formation.
The etiology of how UVR induces collagen damage has known now. UVR exposure dramatically up-regulates the production of several types of collagen-degrading enzymes known as matrix metaloproteinases (MMP), such as collagenase, gelatinase, and stromelysin. MMPs in humans, specifically collagenase and gelatinase, are induced within hours of UVB (Ultraviolet B) exposures. Because collagenase degrades collagen, long term elevations in collagenase and other MMPs likely result in the disorganized and clumped collagen seen in photoaged skin.
Extensive marketing touting the importance of collagen in the aging process has lead to many collagen-containing topical products. Other components such as Vitamin C and glycolic acid owe some of their popularity to the claims that this agents can increase collagen synthesis. These products are usually labeled as “anti wrinkle creams”.

Elastin
In aged elastic fibers, is thickened and coiling, resulting in reduced elasticity and resiliency of the skin. This loss of elasticity may account for much of the sagging skin seen in elderly individuals.

Glycosaminoglycans
Glycosaminoglycans (GAGs) are important molecules because they can bind water up to 1000 times their volume. There are many members of the GAG family, including hyaluronic acid (HA), chondroitin sulfate, and dermatan sulfate. Numerous studies report that GAGs, especially HA, are decreased in amount in photoaged skin. Decreases in amount of HA, leading to its lack of association with collagen and elastin and decreased water binding.

Melanocytes
The number of melanocytes decreases from 8 to 20 percent per decade. Because melanin absorbs carcinogenic ultraviolet light, the skin of older patients is less able to protect itself from the sun and, consequently, is at greater risk for developing sun-induced cancers. It is for this reason that sun protection is important, even for patient who feel it is “too late” to begin adding a sunscreen to their skin care regimens.


Vasculature
Many studies show that aged skin is relatively avascular. Reduction of vascularity results in decreased blood flow, diminished nutrient exchange, impaired thermoregulation, lower skin surface temperature, and skin pallor.

Subcutaneous tissue
Elderly skin displays both a loss and a gain of subcutaneous tissue that is site-specific. Subcutaneous fat is decreased in the face, dorsal aspects of the hands, and the shins. Other areas, however, such as the waist in women and the abdomen in men, accumulate fat with aging.

The Role of Free Radicals in Photoaging
Free radicals, also known as reactive oxygen species (ROS), are suspected to be the cause of, or at least a major contributor to, the aging process. Free radicals are composed of oxygen with unpaired electron and are created by UV exposure, pollution, stress, smoking, and normal metabolic processes. There is evidence to suggest that free radicals induce changes in gene expression pathway that lead to the degradation of collagen an accumulation of elastin that is characteristic of photoaged skin.

Dry Skin
Aged skin demonstrates increased transepidermal water loss (TEWL) and the recovery of damaged barrier functionis slower. It’s therefore susceptible to becoming dry in low humidity environments. This is caused by a combination factors including decreased amounts of lipids in lamellar bodies and a reduction in epidermal filaggrin.

Treatment
Although there are many treatments available for aged skin, prevention is still paramount and should be emphasized to all patients.
The preventions is :
- Sun avoidance, particularly between 10am-4pm, and any exposure to tanning beds
- Sunscreen should be recommended, even when the patient remains indoors. Patient should be reminded that UVA (Ultraviolet A) rays are able to pass through the glass.
- UVA shields can be placed on windows
- Use sun protective clothing, such as a broad-brimmed hat, glasses, and SPF 45 clothing.

Many patient believe that their sun exposure is minimal and does not warrant daily use of sunscreen. Use of a woods light to demonstrate solar damage is helpful way to convince patients of the necessity of sun avoidance. Extensive or severe photodamage can also be a precursor to the skin cancer. So, you must protect yourself from the UVR !!!