Skin Care Department

“Skin Facts” to Optimize Aesthetic Outcomes Connie Brennan, RN, CPSN, CANS, CPC

Aesthetic providers need to be well versed in the anatomy and intricacies of the skin. This foundational skin knowledge is critical in assessing clients’ aged skin during the aesthetic consultation. A sound understanding of the skin is also a prerequisite to any facial rejuvenation procedure. This article provides the aesthetic provider with the basics of skin anatomy and how the skin changes over time.

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common denominator in all facial rejuvenation procedures is the skin: how it presents given the client’s age; how exposure to sun and the elements affect it; and how prior surgeries and aesthetic procedures impact the appearance and function of the skin. Knowing the intricacies of the skin and how it changes as a function of time is critical for success as an aesthetic provider. This article focuses on the anatomy of the skin, the depth and characteristics of various layers, and how to leverage these “skin facts” to optimize the delivery of superior aesthetic outcomes.

NORMAL SKIN: STRUCTURE AND CHARACTERISTICS The saying “beauty is only skin deep” has particular relevance as it relates to facial aging, and a good understanding of the composition of skin—the different layers and respective thicknesses—is a prerequisite to be mindful of before treating clients with nonsurgical aesthetic procedures. In normal skin, adipose tissue stores fat-soluble vitamins (e.g., vitamins A, D, E, and K) and retinoic acids,

Connie Brennan, RN, CPSN, CANS, CPC, is currently the Director of Medical Aesthetic Education at the Center for Advanced Aesthetics at Life Time Fitness and President/Founder of Aesthetic Enhancement Solutions, LLC. She is a licensed registered nurse in 10 states and has earned advanced certifications in aesthetic injectables, laser resurfacing, skin care, sclerotherapy, and perioperative nursing over the course of 26 years in aesthetic medicine. She has worked as an expert alongside the ASPSN task force in creating the first Certified Aesthetic Nurse Specialist examination. The author is a consultant to Allergan, Inc., and Galderma L.P., but has not received any funding to write or publish this article. The author reports no conflict of interest. Address correspondence to Connie Brennan, RN, CPSN, CANS, CPC, Aesthetic Enhancement Solutions, LLC, 5905 Troy Lane, N, Plymouth, MN 55446 (e-mail: [email protected]). DOI: 10.1097/PSN.0000000000000082

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and it provides protection against physical injury (e.g., heat, cold, and mechanical stress). Skin is the human body’s largest organ, comprising 17% of the body’s weight. The skin primarily acts as the barrier between the internal environment and the world outside, as a formidable immune defense barrier, and as a protector of vital body components. The surface pH of normal adult skin averages 5.5. This cutaneous acidity discourages bacterial colonization; it also contributes to the skin’s moisture barrier as amino acids, salts, and other substances in the acid mantle absorb water. The skin also helps create that “first impression” upon meeting someone. Although human skin is incredibly durable, like all other organ systems, it is affected by aging. A sophisticated and dynamic organ, skin performs numerous functions beyond simply acting as a barrier: homeostatic regulation; prevention of percutaneous loss of fluid, electrolytes, and proteins; temperature maintenance; sensory perception; and immune surveillance (Farage, Miller, & Maibach, 2010). Skin is composed of the following major layers (Figure 1): 1. Epidermis. The epidermis is 150–200 μm thick (Bariya, Mukesh, Mehta, & Sharma, 2012), and it contains the following layers: stratum corneum (outermost layer of dead cells whose purpose is to provide a protective barrier to the elements and extracellular organisms); stratum granulosum (or granular layer is a thin layer of cells where keratinocytes [structural] cells from the stratum spinosum become granular cells in this layer); stratum spinosum (or spinous layer/prickle cell layer—spiny “arms” that help the 5–10 layers of cells reach out and bind to each other); and stratum basale (basal cells are responsible for maintaining the epidermis by continually renewing the cell population by producing keratinocyte cells—considered the stem cells of the epidermis). In healthy skin, approximately one layer of corneocytes desquamates every day, so that the whole stratum corneum replaces itself about every 2 weeks (Tagami, 2008). 2. Dermis. The dermis is 1.5–3 mm thick (Bariya et al., 2012), and it contains the supporting layer that cushions the body and provides tensile strength and elasticity. It contains blood vessels, nerve endings, collagen, elastin, and hyaluronic acid (HA)—a naturally Volume 35 „ Number 1 „ January–March 2015

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Skin Care Department

FIGURE 2. Aged skin. FIGURE 1. Younger skin.

occurring polysaccharide that acts as a scaffold for collagen and elastin, and it maintains tissue hydration because of its hydrophilic (i.e., water loving) nature. The dermis is tightly connected to the epidermis through a basement membrane. 3. Subcutaneous tissue. The subcutaneous tissue (also known as the hypodermis) is 3–100 mm thick (Bariya et al., 2012), and it contains a fatty layer that provides cushioning, insulation, and an energy reserve. It supports blood vessels, nerves, deeper hair follicles, and sweat glands. There are three commonly used scales designed to classify various aspects of skin; they include the following: 1. Wrinkle Assessment Scale (Glogau, 1996)—classifies the extent of photoaging; 2. Baumann Skin Typing System (Baumann, 2006)— evaluates four basic skin parameters to predict a patient’s reactivity to treatment; and 3. Fitzpatrick Classification Scale (Fitzpatrick, 1975)— assesses a patient’s reaction to facial treatment based on tolerance to sunlight.

AGING SKIN: STRUCTURE AND CHARACTERISTICS Over time, the progressive cumulative effects of aging transform the once full, angular, youthful face into a rectangular (or pear-shaped) face, which appears longer in configuration, aged, and fatigued (Binder, 2010). There is a decrease in the rate of cell production/turnover. As human beings age, the skin has a tendency to become thinner, drier, more wrinkled, and unevenly pigmented. A loss of subcutaneous fat, as well as underlying bone and cartilage, manifests as sagging skin and fallen nasal tips. Aging of the skin can also produce significant morbidity. In fact, most people over 65 years have at least one skin disorder, and many have two or more (Farage et al., 2010). Plastic Surgical Nursing

Epidermis The aging epidermis is thinner relative to healthy normal skin, which makes it less efficient at protecting the body from external influences (Figure 2); key “aging epidermis facts” include the following: The epidermis decreases in thickness with age. The unexposed epidermis thins by up to 50% between the ages of 30-80, but changes in epidermal thickness are most pronounced in exposed areas, such as the face, neck, upper part of the chest and extensor surface of the hands and forearms. Overall, epidermal thickness decreases at about 6.4% per decade decreasing faster in women than in men (Farage et al., 2010 and references therein). The water content of aged skin, particularly in the stratum corneum, is lower than that of younger skin. The water content of the stratum corneum decreases progressively with age and eventually falls below the level necessary for effective desquamation; this causes corneocytes to pile up and adhere to the skin surface, which accounts for the roughness, and scaliness, flaking that accompanies xerosis in aged skin. The integrity of the stratum corneum barrier is dependent on an orderly arrangement of critical lipids. However, the total lipid content of the aged skin decreases by as much as 65% (Farage et al., 2010 and references therein). The most widely observed structural change in aged skin is a flattening of the dermal-epidermal junction, which occurs as a result of the decreasing numbers and size of the dermal papillae. The flattening of the dermal-epidermal junction, observed by about the sixth decade, creates a thinner epidermis primarily because of retraction of the rete pegs, decreasing the thickness of the dermal-epidermal junction by 35%. The flattening of the dermal-epidermal junction may also contribute to wrinkle formation by increasing the potential for dermal-epidermal separation (Farage et al., 2010 and references therein). 43

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Skin Care Department Injury repair diminishes with age. Wound-healing events begin later and proceed more slowly. The tensile strength of healing wounds decreased after the age of 70. Barrier function requires twice as long to restore in the aged as compared to younger controls; stratum corneum renewal times were much longer in the aged (about 30 days compared to 20 days in normal skin) (Farage et al., 2010 and references therein).

Changes in the epidermis include thinning to atrophy, hyperplasia of melanocytes, and disturbances in the texture of keratinocytes (Hulmbold, 2010). Enzymatically active melanocytes decrease at a rate of 8%–20% per decade, resulting in uneven pigmentation in elderly skin (Philips & Kanji, 1994).

Dermis Dermal thickness, vascularity, and cellularity also decrease with age (Friedman, 2005). The loss of dermal collagen and elastin makes up most of the reduction in total skin thickness in elderly adults; for example, in postmenopausal women, a decrease in skin thickness of 1.13% per year parallels a 2% decrease per year in collagen content (Brincat et al., 1987). Dermal thickness decreases at the same rate in both sexes (McCallion & Li Wan Po, 1993). Skin atrophy is marked only after the fifth decade of human life and shows a plethora of histomorphologic changes, including epidermal thinning, flattening of the dermal–epidermal junction, loss of melanocytes, and immunocompetent Langerhans cells. There are also dermal changes such as reduced fibroblast population and sebaceous glands (Bhattacharyya, 2010). Decreased production of HA leads to skin losing its ability to retain water. The sweat and oil gland activity decreases, leaving the skin dry and potentially itchy. Skin dryness accentuates rhytids. With aging, degeneration of collagen and elastin leads to the appearance of rhytids, creases, folds, and furrows. Collagen and elastin fibers lose their ability to recover; therefore, skin elasticity decreases during the aging process, leading to sagging under the effects of gravity and rhytids. Morphometric measurement of collagen fibers from stained human skin biopsies further showed that collagen fiber density started decreasing from around 30 to 40 years, with thinner and more spaced fibers (Farage, 2008). The loss of structural integrity of the dermis leads to increased rigidity, decreased torsion extensibility and diminished elasticity, these properties eroding faster in women than in men, with a concomitant increase in vulnerability to shear force injuries (Farage et al., 2010 and references therein).

The pH of the skin is relatively constant from childhood to approximately age 70 years, and then rises significantly. This rise is especially pronounced in lower limbs, possibly because of impaired circulation (Farage et al., 2010). 44

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In older skin, capillaries and small blood vessels regress and become more disorganized, blood vessel density diminishes, and a 30% reduction in the number of venular cross sections per unit area of the skin surface occurs in nonexposed areas of the skin. The maximum level of blood flow diminishes as functional capillary plexi are lost. Facial skin temperatures were lower in aged subjects, and older people exhibited a wider temperature difference between groin and toes (Farage et al., 2010). Cumulative sun exposure adds to the inevitable changes seen with aging; it is the single largest factor in our clinical perception of aging skin (Tan & Glogau, 2008). Chronic ultraviolet light exposure of skin leads to typical effects: changes in the collagen and elastic tissue matrix is considered the characteristic histological finding in aged skin, followed by visible wrinkling and pigmentary changes (Hulmbold, 2010).

Subcutaneous Tissue (Hypodermis) Subcutaneous tissue loses much of its fatty cushion with age. The density of fat in the subcutaneous layer decreases, and it has the tendency to be redistributed in stretched skin. This redistribution of fat accentuates rhytids. The basement membrane, a very small fraction of the total skin thickness, actually increases in thickness with age (Väzquez, Palacios, Alen´a, & Guerrero, 1996). Lastly, changes in the intrinsic muscles of facial expression are

TABLE 1 Changes in the Structure of Aged Skin Structure Epidermis

Observed Effect of Aging Dermal–epidermal junction flattens Number of enzymatically active melanocytes decreases by 8%–20% per decade Number of Langerhans cells decreases Capacity of reepithelialization decreases Number of pores increases

Dermis

Thickness reduced (atrophy) Vascularity and cellularity decrease Collagen synthesis decreases Pacinian and Meissner’s corpuscles degenerate Structure of sweat glands becomes distorted, number of functional sweat glands decreases Elastic fibers degrade Number of blood vessels decreases Number of nerve endings reduced

Subcutaneous Distribution of subcutaneous fat changes layer (hypodermis) Overall volume decreases Adapted from Farage et al. (2010) and references therein. Volume 35 „ Number 1 „ January–March 2015

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Skin Care Department TABLE 2. Changes in the Function of Aging Skin Function

Change

Barrier function

Renewal time for stratum corneum increased by 50% Baseline transepidural water loss lower in elderly skin

Sensory and pain sensation

Loss in sensitivity, especially after age 50 years Increased itching

Thermoregulation

Decreased sweat production

Response to injury

Lower inflammatory response (erythema and edema) Decreased wound healing Reduced re-epithelization Increased vulnerability to mechanical trauma

Permeability

Decreased percutaneous absorption Decreased sebum production Decreased vascularization Decreased chemical clearance

Immune function

Decreased number of thymus derived lymphocytes Decreased risk and intensity of delayed hypersensitivity reactions

Miscellaneous

Decreased vitamin D production Reduced elasticity

Adapted from Farage et al. (2010) and references therein.

unique in that they insert directly into the skin. Years of facial expressions result in progressive development of rhytids with facial movement. These rhytids are more prominent in areas where the underlying muscles and fascia have more direct attachments to the skin, such as in the frontal, glabellar, nasolabial, perioral, and periocular areas (Tan & Glogau, 2008). The overall volume of subcutaneous fat typically diminishes with age, although the overall proportion of subcutaneous fat throughout the body increases until approximately age 70 years. Fat distribution changes as well; that in the face, hands, and feet decreases whereas a relative increase is observed in the thighs, waist, and abdomen. The physiological significance may be to increase thermoregulatory function by further insulating internal organs (Farage et al., 2010 and references therein). Descending and thinning skin may make it easier to see these important structures (e.g., bone and vascular and venous vessels). Table 1 describes the skin changes that occur with age as a function of the three key layers of the skin. Table 2 captures the key skin functions and associated changes that occur with age.

CONCLUSION Human skin undergoes many changes over a lifetime, yet it remains one of the body’s best defenses against patho-

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gens and environmental insults. Although the relative durability of skin is certainly an evolutionary advantage, the skin of aging adults is compromised in many ways. Structural changes lead to undesirable rhytids, as well as a decreased elasticity and resilience. The reduction of the skin’s neurosensory capacity increases the risk of unrecognized injury with age. The intrinsic drying of the skin makes the skin itchy and increasingly uncomfortable. Reduction in the skin’s ability to repair itself slows wound healing and re-epithelization. Taking these “skin facts” into consideration during the aesthetic consultation (Brennan, 2012) and the injection process will ensure clients receive an optimal aesthetic outcome with each appointment.

REFERENCES

Bariya, S., Mukesh, G., Mehta, T., & Sharma, O. (2012). Microneedles: an emerging transdermal drug delivery system. Journal of Pharmacy and Pharmacology, 64, 11–29. Baumann, L. (2006). Oily, resistant, pigmented and tight: ORPT. In: The skin type solution (pp. 138–155). New York: Bantam. Bhattacharyya, T. (2010). Skin aging in animal models: Histological perspective. In M., Farage, K., Miller, & H., Maibach (Eds.), Textbook of aging skin (pp. 5–12). Berlin: Springer-Verlag. Binder, W. (2010). Facial rejuvenation and volumization using implants. Facial Plastic Surgery, 27, 86–97. Brennan, C. (2012). Art of the aesthetic consultation. Plastic Surgical Nursing, 32(1), 12–16; quiz 17–18. Brincat, M., Kabalan, S., Studd, J. W., Moniz, C. F., de Trafford, J., & Montgomery, J. (1987). A study of the decrease of skin collagen content, skin thickness, and bone mass in the post menopausal woman. Obstetrics and Gynecology, 70, 840–845. Farage, M. (2008). Intrinsic and extrinsic factors in skin aging: a review. International Journal of Cosmetic Science, 30, 87–95. Farage, M., Miller, K., & Maibach, H. (2010). Degenerative changes in the aging skin. In M., Farage, K., Miller, & H., Maibach (Eds.), Textbook of aging skin (pp. 5–12). Berlin: Springer-Verlag. Fitzpatrick, T. B. (1975). Soleil et peau. Journal de Médecine Esthétique, 2, 33–34. Friedman, O. (2005). Changes associated with the aging face. Facial Plastic Surgery of Clinical North America, 13, 371–380. Glogau, R. (1996). Aesthetic and anatomic analysis of the aging skin. Seminars in Cutaneous Medicine and Surgery, 15(3), 134–138. Hulmbold, P. (2010). Basophilic (actinic) degeneration of the dermis: an easy histological scoring approach in dermal photoaging. In M., Farage, K., Miller, & H., Maibach (Eds.), Textbook of aging skin (pp. 13–18). Berlin: Springer-Verlag. McCallion, R., & Li Wan Po, A. (1993). Dry and photo-aged skin: manifestations and management. Journal of Clinical Pharmacology and Therapeutics, 18, 15–32. Philips, T., & Kanji, L. (1994). Clinical manifestations of skin aging. In C. Squire, & H. W., Hill (Eds.), The effect of aging in oral mucosa and skin. Boca Raton: CRC Press. Tagami, H. (2008). Functional characteristics of the stratum corneum in photo-aged skin in comparison with those found in intrinsic aging. Archives of Dermatology Research, 300(1 Suppl), S1–S6. Tan, S., & Glogau, R., (2008). Fillers esthetics. In J. Carruthers, & A. Carruthers (Eds.), Soft tissue augmentation (2nd ed, pp. 11–18). Philadelphia: Saunders Elsevier. Väzquez, F., Palacios, S., Alen´a, N., & Guerrero, F. (1996). Changes of the basement membrane and type iv collagen in human skin during aging. Maturitas, 25, 209–215.

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"Skin facts" to optimize aesthetic outcomes.

Aesthetic providers need to be well versed in the anatomy and intricacies of the skin. This foundational skin knowledge is critical in assessing clien...
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