CAUSES OF FACIAL AGING

Cutaneous aging is a complex biological process that involves many cellular components of the skin. The aging process is inevitable, but there are substantial differences in the way people age depending on genetics and lifestyle. Two biologically distinct processes affect skin aging. Natural, or intrinsic, aging represents internal and chronologic changes; and environmental, or extrinsic, aging represents the external influences and lifestyle choices that both compound and exaggerate the natural intrinsic aging process.

Both intrinsic and extrinsic aging lead to a progressive degradation of physiological functioning and structural support, but histologically, they are very different. Intrinsic skin aging is characterized by the slow and inalterable internal process of cellular aging influenced by genetics. These changes are insidious, and fine lines or wrinkles, laxity, lack of luster, and drier skin are the obvious visual effects. Seborrheic keratoses, benign epithelial neoplasms appearing as early as the third decade, are good markers of intrinsic aging.

The natural decline of hormones and dermal and epidermal growth factors also play a role in chronological skin aging. A decrease in estrogen causes thinning and drying of the dermis, and supplementation has been shown to improve and reverse aging changes of the skin.

The end product of these processes is the deterioration of collagen, elastin, and the extracellular matrix of the dermis. Histologically, although few changes in the epidermis occur, the dermal-epidermal junction shows flattening of the epidermal ridges, which decreases the area of surface contact, leading to diminished nutrition of the epidermis and a slowing of epidermal cell turnover. In the dermis, there is a generalized decrease in cells.

Environmental or extrinsic aging results from preventable external influences that include exposure to the sun, pollution, tobacco smoking, diet, alcohol intake, and other lifestyle choices. The most common contributor to extrinsic aging is sun exposure; therefore extrinsic aging is commonly referred to as photoaging. In contrast to intrinsically aged skin, the clinical hallmarks of photoaging are the appearance of leathery or inelastic skin, sallow coloring (yellow) with a loss of translucency (the pink, radiant glow indicative of young, healthy skin), coarse texture (deep wrinkles), blotchy irregular pigmentation (dark spots or lentigines), and telangiectasias (superficial vasculature of 1 mm or less).

Photoaging not only compounds the effects of innate intrinsic aging but is also distinguished by unique cellular changes. The histologic hallmark of photoaging is solar elastosis, characterized by a massive deposition of abnormally structured elastin fibers that are thickened, tangled, and clumped in the superficial dermis. This abnormal elastoic material eventually replaces collagen fibers in the dermal matrix. Solar elastosis is responsible for the “leathery” look and feel of sun-damaged skin.

Free radical activity, exacerbated by extrinsic influences, causes considerable damage to cell membranes and increases matrix metalloproteinases (MMPs). MMPs are enzymes that increase collagenase (catabolic proteins that “eat up” and degrade collagen, “Pacman”-style) and create an environment of chronic oxidative stress resulting in inflammation and shortening of telomeres. Shorter telomeres interfere with DNA replication, leading to an irreversible and planned arrest of cell function followed by cell death (apoptosis).

The abnormalities in the structural protein of the extracellular matrix are responsible for a dry appearance and wrinkling. This is a complex situation because sun-damaged skin has a paradoxical increase in water content. In undamaged skin, water binds with proteins (collagen and elastin) and mainly with glycosaminoglycans (GAGs) in the dermis, responsible for hydration of the skin. In photoaged skin, the GAGs are abnormally attached to the aberrant proteins and unavailable to bind with water. The unbound water binds to itself in a tetrahedral form, resulting in a loss of turgor or buoyancy and clinically “drier” skin.

Cumulative ultraviolet radiation from the sun further damages skin by causing DNA mutations that interfere with the normal immune mechanisms that police carcinogenic cells. Increased skin cancer rates have been seen in “baby boomers,” a generation that has lived the longest with the most exposure to outdoor recreational activities and long-term sun exposure.

The important clinical implication is that a vast population of patients, from young to old, are seeking to improve the early signs of aging skin, to minimize established wrinkles, and to improve the appearance of sun damage.

Croton oil peeling now offers a single modality, one powerful tool that can not only improve the early signs of aging, wrinkles, and sun damage, but can reverse extensive skin damage and deep wrinkling and perhaps even prevent skin cancer.

PROCESS OF FACIAL AGING

The process of facial aging, although complex, can be subdivided into three main categories: (1) structural or gravitational changes, (2) correction of volume depletion or facial deflation, and (3) treatment of rhytids, creases, and texture.

Structural or gravitational changes are the most obvious and familiar changes to surgeons and lay individuals, who may notice them when they pull the skin back while looking in a mirror. A multitude of surgical procedures address these structural changes, and most aesthetic surgeons are well within their comfort zone in performing them. These operations understandably dominate meetings and publications, because surgeons are familiar with them and are able to read or hear about a new technique and successfully perform it.

In recent years, an important factor that has received increased attention is the correction of volume depletion or even facial deflation. Historically, alloplastic implants have played an important role in specific areas, and taking a cue from other specialties, injectable dermal fillers are commonplace in modern plastic surgical practices. In the last decade, the enormous value of autologous fat transfers has become recognized not only for generalized volume replacement but for the action of stem cells and growth factors. The qualitative improvement to be gained by harnessing the intangible power of these techniques is an exciting new frontier discussed elsewhere in this book.

The treatment of well-established rhytids, creases, and textural changes is perhaps the most difficult, and certainly the least talked about, category among aging-related changes. Surgeons are intimidated by this aspect of the specialty and tend to surrender their patients to aestheticians or use nonablative superficial techniques that, as well as being minimally invasive, are minimally effective.

The most common tactic is to simply ignore the issue. Regrettably, in doing so, surgeons are missing the opportunity to deliver a more complete rejuvenation and improve such a fundamental aspect of aging. Surgeons tend to concentrate on the things they can fix and lose sight of the fact that perioral rhytids can be more notable to a patient than jowls or loose skin. If textural changes are unaccounted for, the very best facelift, although a technical success, can paradoxically accentuate deep creases around the mouth or forehead and result in an aesthetic failure.

Why this aversion to resurfacing? Admittedly, the techniques traditionally available seem difficult and fraught with problems. Moreover, although surgeons are quite willing to cut and sew skin, they seem ill-equipped to treat the skin itself, whether because this seems to lie more in the realm of aestheticians or dermatologists or simply because plastic surgeons have not had the training or exposure.

The main purpose of this chapter is to demystify and systematize the process of modern chemical peeling so that practitioners may be motivated to try them and offer significant improvement to their patients.