There are a number of changes, which occur within the skin and subcutaneous tissues with increasing age. The majority of these changes relate to atrophy or reduced numbers of cells resulting in a reduction in overall tissue depth. The ratio of collagen subtypes also changes with age. In the skin there is usually a far higher proportion of type I collagen to type III ratio (4:1) with aging; this ratio changes as proportionally more type III collagen is present. Other histologic changes in the skin include thinning of both the dermis and epidermis, with flattening of the dermal–epidermal junction. This results from cellular apoptosis and is affected by genetic predisposition. There is also a decrease in the number of Langerhans cells and melanocytes, blood vessels, fibroblasts, and mast cells. The stratum corneum becomes more disorganized, with collagen and elastin becoming less well ordered. Beneath the skin, there is atrophy of the subdermal fat. All of the above contribute to reducing the overall thickness and quality of the skin and subcutaneous tissues with advancing age. This has clinical relevance in many areas of plastic surgery, including approaches to facial rejuvenation.
Extrinsic aging results from skin exposure to a number of environmental factors including UV radiation, dehydration, inadequate nutrition, temperature extremes, physical damage, and traumatic injuries. In addition, smoking will have a profound effect on the extrinsic aging process of the skin. Of all of these factors, actinic damage from UVA radiation is the major cause of extrinsic aging. UVB radiation is primarily responsible for sunburns. UV radiation generally results in DNA damage within the nucleus and mitochondria. More specifically, UVA results in damage through the creation of free radicals in the form of reactive oxygen species.
The extrinsic aging process results in thickening of the stratum corneum, atrophy of the epidermis with cellular atypia, irregular dispersion of melanin, collagen fragmentation, and abnormal deposition of elastin. These changes can be observed clinically with the presence of keratosis, which are associated with actinic damage and development of nonmelanoma skin malignancies such as squamous cell carcinoma. Telangiectasia is a common finding in sun-damaged skin; however, it is not specifically associated with development of cutaneous malignancies. Instead, it is a feature of basal cell carcinomas and can be a distracting finding in such patients. Irregular pigmentation is observed in the aging skin with solar lentigines and freckle development. Almost all adult patients will have a combination of intrinsic and extrinsic aging that can be accelerated by environmental factors and genetic predisposition.1–3
The appearance of normal skin is poorly defined in classic dermatology and plastic surgery textbooks, but it is an infant’s skin qualities that really define and illustrate healthy skin. The skin of an infant and hence healthy skin will have a smooth surface, an even color/pigmentation, firmness and tightness, adequate hydration, and fullness in contour with an absence of static rhytids, scars, and pigmentary imperfections. Collectively, the constituents of the skin and subcutaneous tissues will each impact upon these features. However, glycosaminoglycan content of the tissues will have the most significant impact on skin hydration, as glycosaminoglycans carry a large volume of fluid. Their role as a cosmetic filler takes advantage of this feature such that when such fillers are injected into the tissues, they not only increase volume by their presence, but they also draw in fluid to the area and further plump up the skin and soft tissues. Skin smoothness reflects the surface of the skin and is affected mainly by the effects of exfoliation where soft keratin remains, and harder keratin is removed. Uniform color or pigmentation reflects normal melanocyte function. With aging or unhealthy skin, there is an increase in pigmentation abnormalities. Firmness and tightness of the skin represent healthy elastin and collagen levels and organization, respectively.1
The KMC is the amount of time for a new keratinocyte to ascend through the epidermis and exfoliate. It is typically 40 days, i.e., 6 weeks’ duration. This is an important concept for treating skin with topical agents and chemical peels as pretreatment and treatment durations are both prescribed in units of the KMC. A keratinocyte is formed from mitosis of the basal layer of the skin, and takes approximately 28 days to mature. The keratinocyte then undergoes denucleation to become a corneocyte in the stratum corneum and exfoliates in approximately 12 days. The normal KMC is therefore approximately 6 weeks because it includes both of these phases (28 + 12 days).
A skin cycle is defined as the KMC and lasts for 6 weeks. This comprises a 4-week (28-day) process for a keratinocyte to develop and mature, plus a further 12 days (approximately 2 weeks) for it to denucleate and exfoliate. Treatment duration is prescribed in terms of skin cycles. It is usual to pretreat skin with topical agents for at least one skin cycle before peeling or commencing a therapeutic treatment plan. A typical course of medical topicals (therapeutic skin care) without a peel is three skin cycles. Although this is the standard approach, other aspects of the patient’s health will need to be considered, as certain disease processes will accelerate or slow down the KMC. For example, KMC is accelerated in psoriasis, skin cancers, and verrucae. Conversely, it is prolonged in intrinsic aging, photoaging, and when using topical moisturizers and steroids. Skin complexion will also impact treatment cycles and patients with darker and complex skin types should be treated with topicals for more than one skin cycle before peeling.
Overuse of moisturizers can have a number of detrimental effects on skin including a reduction in barrier function and a contribution to development of sensitive skin. In addition, overuse of moisturizers can increase the skin cycle turnover time or KMC which has implications for selecting duration of pretreatment and treatment plans. It is important therefore to educate patients on appropriate use of moisturizers and ensure that overuse is not undertaken as the effectiveness of the topical treatment program may be reduced, prolong the KMC, reduce barrier function, and contribute to “sensitive” skin.
Medical skin care is the use of prescription-based topicals to induce clinically significant changes in the skin. Prescription-based topicals are primarily tretinoin and hydroquinone. These are used in combination with cleansers, toners, alpha hydroxy acids (AHAs), antioxidants, and sunscreens to form a customized regimen for the patient, rather than a “standard recipe.” Medical skin care should therefore be directed by a physician and not available over the counter. Although the majority of the program is delivered topically, oral prescriptions for skin diseases, e.g., isotretinoin or antibiotics for acne or rosacea, may also be added into the medical skin care regimen.
Sunscreens prevent photoaging by reducing UV light absorption through the skin. There are three types of UV light: A, B, and C. However, only UVA and UVB are clinically relevant as UVC does not penetrate the earth’s atmosphere. UVA is associated with skin aging leading to formation of rhytids, while UVB is associated with sunburn and skin cancer development. Some sunscreen’s active ingredients will affect UVA only, such as Avobenzone or Anthranilates, which are both chemical agents that have limited absorption spectrums (320–360 nm). Others affect UVB only such as Padimate A and Padimate O which are chemical agents based on p-aminobenzoic acid and its esters. These agents absorb the entire UVB spectrum (280–320 nm). Avobenzone is tolerated cosmetically but can produce allergic reactions. In contrast, physical sunblocks will reflect or scatter both UVA and UVB spectra. Titanium dioxide and micronized zinc oxide are the most common forms of physical sunblocks and are well tolerated by patients, as they do not produce contact sensitivity, phototoxicity, or photoallergy.
Sun protection factor (SPF) is the ratio of UV radiation dose that produces the first sign of erythema in sunscreen- protected skin to unprotected skin. As the SPF value increases, sunburn protection increases. So for example, SPF 30 blocks 96.7% of UV radiation (not 30 or 70%). If a person develops sunburn in 10 minutes on unprotected skin, then it will take 300 minutes to sunburn with SPF 30 sunscreen, i.e., 30 times longer. In contrast, an SPF 15 blocks 93.3% of UV radiation, and if a person develops sunburn in 10 minutes on unprotected skin, then it will take 150 minutes to sunburn with SPF 15 sunscreen. However, an SPF 30 sunscreen is not active or effective any longer than an SPF 15 sunscreen; therefore, both should be reapplied every 2 hours during direct sun exposure. SPF therefore is primarily showing the level of protection provided against UVB rather than UVA. In addition to the SPF rating, there is also a star rating used for sunscreens. This relates to the UVA protection. The stars range from 0 to 5 and indicate the percentage of UVA radiation absorbed by the sunscreen in comparison to UVB, i.e., the ratio between the level of protection by UVA and UVB. In general, therefore it is both advisable to have a high SPF and a high star rating combined in a single product ( http://www.bad.org.uk/skin-cancer/ sunscreen-fact-sheet).
Tretinoin is a derivative of vitamin A (not vitamin D) and represents the gold standard for the topical treatment of facial rhytids and photoaging. Unfortunately, while it is an effective medication, it can often cause skin irritation leading to redness, dryness, scaling, burning, and peeling, so patients must be advised of this prior to commencing treatment. Tretinoin induces epidermal hyperplasia and deposition of glycosaminoglycans. It also increases the thickness of the stratum corneum and reduces both keratinocyte and melanocyte atypia. Its use increases collagen types I and III in the papillary dermis through the inhibition of metalloproteinases. Changes within the epidermis are usually seen within 3 to 6 months (not a few days), while dermal changes are seen later at 9 or 12 months. The most common formulations for tretinoin are 0.025, 0.05, and 0.1% concentrations, not 5 or 10%.
Hydroquinone (HQ) is a melanin-modifying agent commonly used to treat skin hyperpigmentation such as melasma, solar lentigines, and postinflammatory hyperpigmentation due to injury, acne, dermatitis, lupus, or peels. The mechanism of action is to block conversion of dihydroxyphenylalanine (DOPA) to melanin by inhibition of tyrosine. HQ thereby inhibits melanocytes and prevents formation of melanosomes. It is used in concentrations of 2–4% and is frequently combined with other agents such as tretinoin, glycolic acids, and steroids to improve efficacy and decrease side effects. Side effects, although uncommon, may include redness, dryness, irritation, hypersensitivity, and allergic reactions. Prolonged topical HQ use can induce a condition called “exogenous ochronosis,” resulting in dark, blue-black, speckled pigmentation in treated areas. An interruption in HQ therapy is therefore recommended every 5 to 6 months for a minimum period of 3 months before reinitiating therapy.1 Kojic acid is another tyrosinase inhibitor with a similar but less effective action than HQ. It is derived from a Japanese mushroom, and side effects include contact dermatitis and hypersensitivity. Glycolic acid is an AHA used to treat acne, keratosis, warts, psoriasis, and photoaging. The mechanism of action is uncertain but may be related to the removal of calcium ions from the epidermal corneocytes producing exfoliation of the stratum corneum. Side effects include burning, pain, and erythema. Coenzyme Q10 (CoQ 10), usually available as alpha-lipoic acid, is a cellular antioxidant, which stabilizes free radicals. Clinically, CoQ 10 reduces UVB-induced erythema and improves photoaging. α-Tocopherol is a form of vitamin E and is used to protect cell membrane viability, which may reduce UV-induced erythema.
Hydroxy acids represent a group of compounds (AHAs, beta-hydroxy acids [BHAs], polyhydroxy acids [PHAs], and bionic acids) found in many cosmetic formulations used to treat acne, keratosis, warts, psoriasis, photoaging, and other disorders. They are used as chemical peel/exfoliating agents. BHAs have a hydroxy group in the beta-position and are hydrophobic. Salicylic acid is the most commonly used BHA. BHAs are lipophilic and indicated for use in oily areas of the face such as the chin, nose, and central forehead. The AHAs are the most commonly used hydroxy acids overall for skin treatment and include glycolic, lactic, mandelic, malic, and pyruvic acids. Of these, glycolic acid is the most frequently used. AHAs have a hydroxy group in the alpha-position and are water-soluble. The mechanism of action is thought to be related to the removal of calcium ions from the epidermal keratinocytes producing exfoliation of the stratum corneum. Daily application results in epidermal exfoliation, early thinning of the stratum corneum, and late thickening of the skin related to increased glycosaminoglycan and collagen deposition. PHAs have limited dermal penetration due to their larger molecular size compared to other AHAs and so are less commonly used; however, they do result in less burning and skin irritation. Common forms of PHAs are gluconolactone and lactobionic acid. They can have improved cell turnover and act as a humectant and antioxidant. Alpha-lipoic acid and L-ascorbic acid are both antioxidants used in topical treatment regimens, but neither are used as chemical peel or exfoliating agents. Alpha-lipoic acid is the most common form of coenzyme Q10 that is a cellular antioxidant, which stabilizes free radicals. Clinically, it reduces UV-induced erythema and improves photoaging. L-ascorbic acid is the active form of vitamin C, which acts as an antioxidant and as a promoter of collagen synthesis. It may be used to improve skin hydration and reduce fine rhytids by reducing inflammation and UV-induced immunosuppression.1,2
The Fitzpatrick skin classification is commonly used in dermatology and plastic surgery circles. It describes the skin color and response to sun exposure in terms of tanning. While it may be relevant in skin cancer patient management, its use in skin rejuvenation is limited because it fails to accurately predict a patient’s response to topical treatments and peels (Table 103.1).
Following pretreatment, patients will cycle between therapeutic and maintenance skin care and the mainstays of a therapeutic regimen are tretinoin, hydroquinone, and an AHA, such as glycolic acid. These topicals act synergistically to induce visible changes in the skin. Therapeutic skin care is usually a 5-month (not 3) regimen (i.e., three skin cycles) to treat a specific skin condition, e.g., hyperpigmentation, photoaging, acne, or rosacea. After the skin condition is treated, therapeutic skin care is stopped and maintenance skin care is initiated. If the skin condition recurs, then therapeutic skin care is initiated once again. The clinician should be able to provide both therapeutic and maintenance skin care guidance throughout the lifetime of the patient. Maintenance skin care usually involves weaning a patient from hydroquinone, changing from tretinoin to retinol (if there are patient tolerance issues), and maximizing antioxidant and sun protection use. Table 103.1 Fitzpatrick Skin Type Classification Skin Type Characteristics Sun Exposure History I Pale white, freckles, blue eyes, blond or red hair Always burns, never tans II Fair white, blue/green/hazel eyes, blond or red hair Usually burns, minimally tans III Cream white, any hair or eye color Sometimes burns, tans uniformly IV Moderate brown (Mediterranean) Rarely burns, always tans well V Dark brown (Middle Eastern) Rarely burns, tans easily VI Dark brown to black Never burns, tans easily (From Janis JE. Essentials of Aesthetic Surgery, Thieme, 2018.)