How Aging Affects the Structure of Our Skin
by Diana L. Howard Ph.D.
Vice President Technical Development
The International Dermal Institute
Published in Dermascope July 2003

As the global population reaches middle age and beyond, there has been a marked interest in research into age related changes that affect our skin. Ultimately, the goal is to understand how aging affects our skin’s structure, so that we may utilize new technology to treat the manifestations of aging skin more effectively.

Age related skin changes are the result of both intrinsic factors, or genetically programmed changes, and extrinsic influence which includes the environmental wear and tear on the skin. Both factors result in changes to the skin structure and function with extrinsic factors causing the more pronounced changes. Some estimates state that from 80-99% of what we see on our skin as adults is the result of these environmental influences, in particular exposure to the sun.

Intrinsically aged skin is smooth and generally unblemished. There are exaggerated expression lines on the skin but by and large, the skin is well preserved. Under the microscope we will see some signs of epidermal degeneration, flattening of the epidermal rete ridges (the finger-like protrusions of epidermis that extend into the glove-like extensions of the dermis) as well as, a breakdown of the dermal tissue. Collagen fibrils are still prevalent but not noticeably thickened or cross-linked.

In direct contrast, extrinsically aged skin such as that found on our face, hands and chest, shows signs of premature aging as a result of environmental influences. The main antagonist in prematurely aging skin is exposure to the sun’s ultraviolet radiation, which results in a condition known as photo damaged skin. The consequences of chronic sun exposure are readily apparent when one compares the exposed skin of the face, hands or neck to unexposed skin of the buttocks or inner thigh. While the sun is not the sole source of skin aging it is a major contributor to photoaging.

Extrinsically aged skin shows characteristic traits that include wrinkles, a sallow skin color, pigmented lesions such as freckles and lentigines, areas of hyper- and hypopigmentation. This is often accompanied by a loss of tone and elasticity, increased fragility, areas of purpura caused by blood vessel weakness and benign lesions such as keratoses, telangiectasias and skin tags. Under the microscope discreet changes are evident in the collagen and elastin structure and organization. Collagen becomes more fragmented and with thicker fibers while elastin fibers fragment and show signs of cross-linking and calcification.

From a clinical perspective we see wrinkles, which are depressions in the skin’s surface that may be classified as either coarse or fine, depending on their depth. Although the exact mechanism of wrinkle formation is not known, we do know that it is accompanied by several structural changes in the skin. Wrinkles occur as a result of a reduction in muscle mass and skin thickness. This is accompanied by a loss of elasticity and a restructuring of the dermal collagen and elastin along with dehydration of the stratum corneum. The latter may be associated with the decline in hyaluronic acid in the dermis as we age. These changes not only result in visible wrinkles on the surface of the skin, but in a loss of hydration, mechanical strength and elasticity as well.

Aside from wrinkles, the other obvious attribute of aging skin is discoloration. Often we see in aged skin an increase in yellow coloration which is the result of a decrease in brown melanin pigment and red & blue colored capillaries. Studies have also shown this yellow color to be attributed to a breakdown product of elastin protein. This yellow-colored breakdown product of elastin is especially prevalent in cigarette smoker’s skin. This overall skin discoloration is often accompanied by an increase in broken veins, especially on the face and legs, which is a result of dilated blood vessels which become more apparent as skin thins. The latter condition is often referred to as telangiectasis.

As skin ages there is also an increase in solar lentigos. As the name suggests, these are the result of sun exposure and often occur after the age of fifty, hence they are also referred to as senile lentigos . They are characterized by an increased number of melanocytes with increased melanin pigmentation, as well as, clubbed or elongated rete ridges that are infiltrated with an excess of melanin at the epidermal-dermal junction. Interestingly, they do not occur on sun protected areas of the skin. While it is difficult to distinguish solar lentigos from freckles or ephelides with the naked eye, under the microscope one can distinguish freckles by their lack of elongated rete ridges and the usual complement of melanocytes.

Age related changes to the Dermis
Studies of aged skin tissue indicate the majority of age-dependent changes take place in the dermis. These changes include a loss of the vascular system accompanied by a loss of cell structure and form. The dermis as a whole can lose from 20-80% of its thickness while aging. Fibroblasts, the cells responsible for collagen, elastin and glycosaminoglycans (ie hyaluronic acid) biosynthesis, degenerate slowing down production of new protein and GAGs which may account for the overall dermal atrophy in aged skin and its inability to repair itself as quickly.

Just below the epidermis a new band of tissue, referred to as the Grenz Zone, appears in aging skin; it contains densely packed collagen fibrils that are organized in rope-like bundles which are in disarray when compared to the organized pattern that is seen in younger skin. The overall collagen content per unit area of skin surface decreases approximately 1% per year after we reach 30 years. Despite the loss of collagen as we age, the network appears more dense due its haphazard organization.

In the past decade, studies have demonstrated that UV radiation activates collagen degrading enzymes (ie collagenase) within hours of UVB exposure. Long term elevation of this enzyme, which is typically found in people with prolonged exposure to sunlight, results in disorganized and clumped collagen that is characteristic of photodamaged skin. Additional damage occurs as a result of UVA rays that penetrate deep into the dermis inducing free radicals that contribute to the cross-linking of collagen, and inactivation of enzymes which impairs fibroblasts, keratinocytes, Langerhans cells and melanocytes.

Like collagen, elastin also shows changes in aging skin. Changes in our elastic fibers are so characteristic in photoaged skin that the condition known as elastosis is considered a hallmark of photoaged skin. This is characterized by an accumulation of amorphous elastin protein and a breakdown in the typical structural layout that is evident in younger skin. While elastin production slows, there is a progressive cross-linking, calcification and deposition of lipids that occurs with age. Although reduced in number, the elastin fibers expand and increase in size, ultimately forming a broad sheet rather than a distinct cylindrical fiber. This change in structure results in a decrease in skin elasticity, extensibility and tensile strength. This phenomenon accounts for why mature skin takes longer to assume its original position when extended or compressed.

Like the collagen and elastin protein of the dermis, the ground substance also undergoes age related changes. Not only is there less ground substance as we age, but the distribution changes as well. Studies have shown that the amount of hyaluronic acid found in the dermis starts to diminish as early as our forties. This most likely accounts for the dehydrated state that skin assumes as we age. In young skin, hyaluronic acid is found at the periphery of collagen and elastin fibers and at the interface of these fibers. In aged skin, the hyaluronic acid connection is lost. Decreases in the amount of hyaluronic acid, leading to its lack of association with collagen and elastin and decreased water binding , may in fact account for the changes associated with aging skin, in particular, loss of turgidity, wrinkling and altered elasticity.

Age related Epidermal Changes
Less affected by aging than the dermis, the epidermis does display some age related characteristics. The most obvious structural change is the flattening of the rete ridges, the finger-like protrusions that interface at the epidermal-dermal junction. This is accompanied by a decrease in dermal-epidermal cohesion which results in an easier separation of the two layers in aging skin as well as, a decrease in the connecting surface area. This loss of surface area may lead to increased fragility of the skin and less nutrient transfer between dermis and epidermis. It has been suggested that the flattening out of the rete pegs may account for why the epidermis is said to “thin” with age. In fact, while the layers of epidermis remain constant, the retraction of rete pegs may be responsible for the decrease in epidermal proliferation associated with aging. It is believed that the epidermal stem cells responsible for proliferation are located at the tips of the rete.

Other changes include a reduction in the number of melanocytes; there is a decline of 6-8% per decade after age 30, which accounts for the lighter skin color with aging and a diminished protective capacity against UV exposure. This decline in the number of melanocytes is similar for both sun protected and exposed tissue. The reduction in melanin along with impaired melanosome transfer into keratinocytes, accounts for the mottled pigmentation so characteristic of photoaged skin.

Along with a decline in melanocytes there is a decline in the other dendritic cell of the epidermis, the Langerhans cells, which results in a diminished immune response for the skin. Not only is there a decline in the number, but functionality diminishes as well. This results in decrease immune surveillance which may account for the increased incidence of premalignant and malignant lesions in maturing skin.

The other significant change in the structure of the epidermis concerns the stratum corneum (SC). Studies have indicated a reduction in moisture content of the SC as skin ages. This is most likely due to a reduction in the stratum corneum lipids which results in an inefficient ability to bind and retain water; the result is the appearance of fine lines and scales which are really aggregates of stratum corneum cells. Fortunately, application of moisturizers can alleviate this problem to a certain extent. It should be noted that there are strong disagreements with regards to the water content and thickness of the epidermis as a function of age. Some studies indicate the epidermis thins with age but other studies do not concur. Most are in agreement however, that the pH of the skin does increase from pH 4.5 to 5.0. In addition, the surface of the stratum corneum becomes more irregular and smoothness and luster is reduced with age.

A discussion of the effects of aging on the epidermis would not be complete without including the effects of aging on cell turnover rates. Studies indicate that the epidermal turnover rate slows from 30 to 50% between our thirties and eighties. Studies demonstrated that in young adults the stratum corneum transit time was as quick as 15-20 days, whereas, in older adults it stretched to 30 days or more. This prolonged stratum corneum replacement rate also coincides with a subsequent slowing of the wound healing process that is typical in older people. In fact doctors report that older patients take twice as long to reepithelialize after dermabrasion resurfacing procedures when compared to younger patients. The slow down in the cell cycle is combined with a less than efficient desquamation process that typically occurs in older people and accounts for the characteristic dull, rough skin surface that is seen in maturing skin.

Ingredients to fight the signs of Aging
So now that we know what happens to our skin as we age what ingredients can we look for in skin care products to affect these changes? Since the introduction of AHAs in the early 90’s the use of certain ingredients and their impact on the skin has literally changed the face of the cosmetic industry.

A new generation of cosmeceutical skin care products containing ingredients that are specific for aging skin include retinoids (ie retinol or vitamn A; tretinoin), ascorbic acid (vitamin C), alpha hydroxy acids (ie lactic acid), glycosaminoglycans (ie. hyaluronic acid), antioxidants (ie green tea extract, tocopherol or vitamin E), bioflavonoids (ie green tea, gingko biloba and licorice extracts), pigment brightening botanicals (ie bearberry extract, rice extract etc.) and sunscreens. While this list is certainly not all inclusive it does represent some of the more readily available ingredients to look for in selecting skincare products.

Retinoids
Retinol or vitamin A and its derivatives (retinyl palmitate or retinyl acetate) have been most successful in addressing skin changes associated with aging. Retinoic acid is the only FDA approved drug for reversing aging effects on skin, including smoothing the skin, reducing wrinkles and treating uneven pigmentation; it also increases epidermal thickness and stimulates deposition of new collagen. Retinol, which is much weaker than retinoic acid, has been shown to convert to retinoic acid in the skin and is much less aggressive than retinoic acid. It is an important regulator of epidermal cell growth and can modulate collagen synthesis in the skin. Like retinoic acid, retinol helps normalize skin cells that are precancerous. Retinol improves skin’s water barrier properties and has been shown to reduce number and depth of wrinkles. Likewise, studies on retinyl palmitate have demonstrated a significant biological effect on the skin as well. Increases in skin elasticity, epidermal thickness and normalization of photodamaged skin have all been demonstrated with this retinoid derivative.

Ascorbic Acid and its derivatives
Studies have demonstrated that topically applied ascorbic acid can induce a three fold increase in collagen content while providing antioxidant protection to the skin. Its main protective role is to prevent lipid peroxidation induced by the formation of free radicals Vitamin C is also used in treating hyperpigmentation.

Tocopherol and its derivatives
In its free form, tocopherol provides antioxidant protection not only for the product but for the skin, protecting cell membrane lipids and DNA from free radicals. In addition to slowing down the aging process, it provides moisturization properties, protection against photosensitivity and photodamage, and smoothes the skin. Studies have also shown that tocopheryl acetate improves skin smoothness by 36% compared to the control product without any vitamin E present and it helps to enhance the performance of UVB sunscreens.

Antioxidants
Antioxidants are often used in a skin care formulation to not only protect the integrity of the formula but to protect the skin while scavenging free radicals. Skin is rich in lipids, proteins and DNA all of which are prone to free radical attack. While vitamins C and E have been used most frequently for this reason, recent studies have shown that many of the plant based extracts rich in bioflavonoids are actually more effective in scavenging free radicals.

Bioflavonoids
Often referred to as the vitamins of the dermis for their anti-aging affect , bioflavonoids consist of over 4,000 different molecules that display superior antioxidant properties, protecting collagen, elastin and GAGs of the dermis, while stimulating collagen biosynthesis. Studies have shown that aggressive AHA treatments, peels, and dermabrasion can cause capillaries to become fragile, cracked and weak. Topical application of bioflavonoids can prevent and reverse this. Bioflavomids are found in the following plant extracts: Camellia sinensis (Green Tea), Ginkgo biloba, and Grapeseed Extracts.

Hydroxy acids (AHAs and BHAs)
AHAs and BHAs not only stimulate cell renewal, smooth the skin, reduce wrinkles, repair sun damage and treat uneven skin pigmentation. Alpha hydroxy acids such as lactic acid affect intercellular bonds of the stratum corneum allowing for cells to slough off more readily. The result is a reduction in the outermost layer, bringing to the surface a smoother, softer skin. Unlike glycolic acid which only affects cell renewal, lactic acid has the added benefit of moisturizing the skin, enhancing barrier lipids of the epidermis and reducing hyperpigmentation spots. Beta hydroxy acids, such as salicyklic acid, are believed by many researchers to actually be more effective than AHAs in treating signs of skin aging.

Hyaluronic acid
Studies on Hyaluronic acid, one of the most abundant GAGs in the dermis, have shown a decline with aging. In young skin hyaluronic acid is plentiful allowing for mobility of cells by increasing water content and hence dermal fluidity; as the dermis matures, the levels decline. Because hyaluronic acid can bind up to 1000 times its own volume in water, it helps to regulate the water binding capabilities of the dermis.

Pigment Brighteners
To treat skin discoloration and hyperpigmentation in particular, look for safe, botanical alternatives to hydroquinone. These include: Bearberry, Licorice, Yeast, Rice extract, Paper Mulberry, Yellow Dock, Vitamin C and Lactic acid; the latter has been shown to lighten pigmentation when used in concentrations greater than 5%.

Sunscreens
For obvious reasons,there is no point in treating the signs of aging if we are remiss about preventing further photo damage to the skin. For this reason The International Dermal Institute always recommends the use of a sunscreen with minimum SPF 15 to protect the skin from further damage and insult.

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