Lifetime Skincare

Most cosmetic surgeons and patients would agree that the majority of cosmetic procedures are performed to repair the signs of extrinsic aging more so than intrinsic aging changes. While many patients turn to surgery, lasers, and other in-office treatments, there is merit to the idea that a good skincare regimen, in the right patient, can yield results that parallel those attained by more invasive procedures. This chapter details such skincare regimens and shows photographic documentation of the benefits of a well-designed daily skincare regimen.

The number of new skincare products on the market continues to grow strong, even in the face of the growth in the device industry. Patients have a desire to look their best while living longer, healthier lives. This means that many will try one product after another in search of better looking skin. Therefore, it is imperative that we address their concerns in both a clinically effective and cost-effective manner. Furthermore, we must help them decipher the Internet and magazine hype that follows the launching of a new product or device. Every cosmetic surgeon should be able to formulate a skincare regimen, individualized for each patient, which will help patients enhance the results of in-office treatments and surgery.

The author’s approach to skincare comes from 15 years’ experience treating patients of all skin types and with many skin concerns. The best way to cultivate a growing population of cosmetic patients is by building trust and confidence. Patients need to know that when they come to your office, they are going to receive a “medical” approach to their care that they cannot get from the multitude of aesthetic centers around town. It is not unusual to see patients who have spent a small fortune at other centers only to present with persistent acne, melasma, and photodamage.

Additional benefits of starting an effective skincare regimen for patients is that results can be seen within weeks, thus encouraging patients to continue with your advice and plan ( Fig. 12.1 ).

Fig. 12.1

(A) This patient has significant post-inflammatory hyperpigmentation due to acne. (B) The patient 6 weeks after starting a topical skincare regimen geared towards addressing acne and pigmentation utilizing retinoic acid, hydroquinone, and a mineral-based sunblock.

When selected properly, a topical regimen can often achieve results that are at least equal to, if not better than, current non-invasive lasers and microdermabrasion machines ( Fig. 12.2 ). A topical skincare regimen can also be used to prolong the results of in-office procedures.

Fig. 12.2

(A) This patient shows significant sun damage and requested a laser procedure for the brown spots. (B) The patient 3 weeks after starting a topical skincare regimen geared towards addressing sun damage, brown spots, and wrinkles utilizing retinoic acid, hydroquinone, an alpha-hydroxy lotion, and a mineral-based sunblock. (C) The redness and flaking of a retinoic acid dermatitis (not an allergic reaction) at 6 weeks of topical agents. She has a dramatic evening of her skin tone and discoloration. Fine lines are diminished. No lasers were used.

This chapter presents the author’s formalized approach to skin rejuvenation, including the understanding of skin biology and aging, as well as patient evaluation. A clear understanding of these topics will facilitate matching correct therapies and procedures to patients.

Skin Anatomy

Knowledge of skin anatomy and the function of the main cells that comprise the skin are critical to planning a skin rejuvenation regimen. The skin is divided into three layers that are in constant interaction: the epidermis, the dermis, and the subcutaneous fat ( Fig. 12.3 ). While there are many cells that play a role in skin function, this chapter focuses on the three cells most responsible for cosmetic improvement in skin texture and appearance: the keratinocyte, the fibroblast, and the melanocyte.

Fig. 12.3

The skin showing the epidermis, dermis, subcutaneous fat, and the adnexal structures within the skin.


The epidermis is the most superficial layer of the skin and consists of terminally differentiated stratified squamous epithelium (keratinocytes 80–90% of cells), melanocytes, Langerhans cells, and Merkel cells. It is the body’s first-line of defense, acting as both a mechanical and an antimicrobial barrier. Homeostasis is maintained with the skin protecting against water loss.

The epidermis is divided into four layers, each with characteristic cell shapes and intracellular proteins (top to bottom: stratum corneum, stratum granulosum, stratum spinosum, and stratum basale). The stratum corneum consists of anucleate cells containing fibrils of keratin that are cross-linked to form the cornified envelope. The cornified envelope contains a durable protein/lipid polymer containing ceramides that supply a barrier to water loss and mechanical protection. The natural moisturization factor (NMF) consists of filaggrin degradation products that allow the stratum corneum to remain hydrated even in drying conditions. Epidermal melanocytes are dendritic cells that produce melanin-containing packets (melanosomes) and distribute these melanosomes to the keratinocytes, thus giving skin its color.

A key concept in skin rejuvenation is that of the “skin turnover cycle” or the approximate epidermal turnover time. This is the time it takes a cell to mature from the basal layer to the stratum corneum and then to be exfoliated. The range is 52–75 days depending on anatomic location, with cells on the face turning over at a faster rate than cells on the feet, for example. The skin cycle is a useful measure to help patients understand how long it takes to see results from products and procedures. Normally, patients are instructed that to really begin to see change in their skin from topical agents, they usually need to wait 6 weeks, or one skin cycle. Results continue and can peak at 3–4 skin cycles.


The dermis is located between the epidermis and subcutaneous fat. Since the epidermis lacks a vascular supply, it derives its supply of nutrients from the dermis. Similarly to anatomic differences in epidermal thickness, there are anatomic differences in dermal thickness with the thinnest, <0.5 mm on the eyelids, and the thickest, >4 mm on the back. Fibroblasts in the dermis produce the components of the connective tissue matrix: collagen (mainly type I), elastin, proteoglycans (PGs), glycosaminoglycans (GAGs), and glycoproteins. Collagen gives the dermis tensile strength, while elastin helps return stretched or deformed skin back to its normal shape. PGs and GAGs are important in dermal hydration by binding up to 1000 times their volume in water.

Adnexal structures such as hair follicles, sebaceous glands, apocrine glands, and eccrine glands, arise embryologically from the epidermis and grow downward into the dermis. The presence or density of these structures varies with anatomic location with the face having more adnexal structure than the neck or chest. This must be taken into consideration when resurfacing the skin, since the wound reepithelializes from these adnexal structures. The dermal–epidermal junction (DEJ) supports the epidermis, allows for cell signaling, and protects against external shearing forces by creating an interface between the epidermis and dermis.

Subcutaneous Fat

The subcutaneous fat serves as the “cushion” of the skin and sits between the dermis and the muscular layer. Fat lobules are separated by connective tissue through which blood vessels pass. Furthermore, fat serves an essential role as an energy reserve and a cosmetic role through which it creates the molding of skin over the contours of the body.

Skin Aging

It is important to understand that there is an intrinsic and an extrinsic component to aging. Intrinsic aging is an inevitable and chronologic process that results from the biologic action of cellular senescence. Furthermore, it is now understood that in addition to cutaneous changes, there is progressive atrophy in bone, muscle, and fat, resulting in a complex ongoing alteration of facial proportions. These changes include alteration in facial shape, forehead height, eyebrow shape, eye size, inter-eye distance, nasal shape, lip volume, skin texture/clarity, and pigmentation ( Fig. 12.4 ).

Fig. 12.4

(A,C) Patient in her early 70s with extensive intrinsic and extrinsic aging resulting in wrinkles, precancerous lesions, and volume depletion. (B,D) Patient is shown 3 months after full face fractionated CO 2 laser resurfacing and autologous fat augmentation.

Intrinsic Aging

At the cellular level, there appears to be an age-related impairment in signal transduction, and a decrease in cell doubling (cell turnover) exhibited by melanocytes, fibroblasts, and keratinocytes. Within the dermis, there is an upregulation of cytokines and enzymes such as elastase, collagenase, stromelysin, and interleukin-1. These enzymes disrupt normal tissue integrity resulting in the clinical stigmata of aging skin: wrinkling, dermal fragility, and dermal thinning. Histologically, these changes can be seen as flattening of the epidermis at the DEJ and effacement of the dermal papillae and epidermal rete pegs, thus impairing nutrient transfer and making the skin more susceptible to trauma from shearing forces. Telomere shortening further complicates the aging process. Telomeres are tandem repeats of a short sequence TTAGGG that cap the terminal portion of chromosomes, preventing their fusion. With each cell division, the final 100–200 bases of the telomeres are lost. After a certain number of cell divisions, telomeres reach a critically short length, at which point the cell stops dividing and enters a state of replicative senescence.

After the age of 18 years, dermal collagen and elastin production declines by about 1% per year. Decades of such a decline in production result in thinning of dermal thickness, skin fragility, and delayed wound healing. While there is no histologic correlate for superficial or fine wrinkles, broadening and shortening of subcutaneous fat connective tissue septae may contribute to deep furrows. Over time, the decrease in lipid synthesis in the stratum corneum results in an impaired skin barrier function. This leads to patients developing “sensitive skin” and is further exacerbated in patients taking lipid-lowering medications.

Extrinsic Aging

In the most simplistic terms, extrinsic aging can be conceptualized as accelerated and exaggerated intrinsic aging. Extrinsic aging occurs insidiously through years and decades of exposure of the skin to environmental insults such as pollution, ultraviolet (UV) radiation, and chemicals. While tobacco use and sun exposure each accelerates the aging process, the combination of the two accelerates aging in a multiplicative manner.

The mechanisms by which photoaging occurs is: (1) impaired membrane/nuclear signaling; (2) mitochondrial damage; (3) protein oxidation; and (4) shortening of telomeres and reduced DNA repair capacity. UV radiation produces reactive oxygen species (ROS), which activate nuclear factor kappa beta (NF-κB) transcription and leads to increased expression of proinflammatory cytokines. These in turn stimulate the production of matrix metalloproteinases (MMPs), which then degrade collagen and elastin in the dermis.

In dermal fibroblasts, UV irradiation induces mtDNA “common deletion” leading to compromised synthesis of mitochondrial proteins, which further increases ROS and decreases the ability of the cell to generate energy. In vitro studies suggest that ultraviolet A (UVA) is a major contributor to protein oxidation in the skin. With reduced DNA repair capacity, sun damaged skin has a greater propensity than non-sun damaged skin to develop cutaneous malignancies.

Extrinsically aged or photodamaged skin has specific histologic findings distinct from intrinsically aged skin ( Fig. 12.5 ). The epidermis may be atrophied (late stage) or thickened with atypical keratinocytes. The most significant findings are seen in the dermis with significant collagen and elastin degeneration. Cumulatively, these changes can manifest clinically as wrinkles, solar elastosis, dyschromias, actinic keratosis, enlarged pores, and telangiectasias ( Fig. 12.6 ).

Fig. 12.5

(A) Hematoxylin and eosin stained specimen (H&E) of healthy skin showing normal stratum corneum, normal epidermal thickness, no atypical epidermal cells, normal rete ridges, and healthy collagen bundles. (B) H&E of photodamaged skin showing thinning of the epidermis, flattening of the rete ridges, and solar elastosis in the dermis.

Fig. 12.6

This patient has sun damaged skin showing dyschromia, wrinkles, actinic keratosis on the (A) face and (B) chest. There are also depigmented scars at previous biopsy sites.

Initial Consultation Goals

The goals of the topical regimen are to reverse actinic damage, slow the aging process by increasing collagen, elastin, and glycosaminoglycans (GAGs), minimize subsequent oxidative damage, and to address any active disease states (acne, rosacea, melasma). Returning the skin to a healthy state requires identification of the pathologic process, recognizing the level of the pathology, and choosing the correct skincare products to reach this goal.

Initial consultations are carried out in a well-lit room and patients are asked to remove all makeup. Patients are assessed with regards to their cosmetic concerns and any additional flaws are identified. Patients are given a handheld mirror so that they can follow along with their evaluation. Patients are then shown before and after photographs of other patients treated for similar conditions. These can simply be before and after using skincare regimens or can be of patients that have undergone extensive procedures to repair their skin (laser resurfacing, medium-depth peels, pigmentation lasers, vascular lasers, fat grafting). All patients receive written instructions on how to use the products and what reactions to expect while they start their new regimen. It is vital to educate the patient on correct product application and how to handle anticipated side-effects, so as to improve patient compliance. Patients are told that the goal of treatment is to return the skin back to its normal, healthy state.

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Sep 8, 2018 | Posted by in Aesthetic plastic surgery | Comments Off on Lifetime Skincare
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