1 Facial Aging, Cosmetic Concerns, and Facial Cosmetic Procedures
Key Concepts
Facial aging results from both intrinsic and extrinsic factors.
Sunlight is the most significant external influence for aging of the skin.
Volume loss occurs at both the skeletal and soft tissue levels of the face.
Reversal of many of the signs of facial aging can be accomplished with the selection of appropriate techniques and technologies.
Introduction
This book presents and graphically illustrates frequently used surgical and minimally invasive techniques to correct many common facial cosmetic concerns. Cosmetic problems arise from aging, trauma, hereditary conditions, and exposure to powerful extrinsic factors, such as cigarette smoking and ultraviolet radiation. Changes occur superficially in both the epidermal and dermal skin components, as well as in the deeper aspects of the facial anatomy. Numerous methods and technologies are available to treat facial cosmetic problems. These “tools” can be categorized in many ways; however, most fall within the bounds of surgical procedures, light and laser technologies, chemical peels, and the use of injectable implants and fillers. A description of the aging process will help set the stage for discussion of the various technologies.
Facial Aging-Related Problems
Facial aging can result from a variety of causes. Some factors are intrinsic and uncontrollable; others are extrinsic and controllable to a certain degree. All human beings appear to age along a common progression; however, differences related to lifestyle, gender, and ethnicity can be seen. For example, it is noted that the Asian face ages with certain characteristics that are different from the Caucasian face.1 Similar comparisons can be noted among other ethnic groups. Furthermore, different ethnic groups may express cultural differences in their goals for aesthetic facial surgery, and these should be considered when planning procedures.
The apparent rate of biological aging varies among individuals. Intrinsic aspects of aging appear to be highly controlled by heredity and are not largely influenced by the individual. In contrast, extrinsic factors are heavily determined by a person′s habits, nutrition, and exposure to deleterious factors, such as ultraviolet light and cigarette smoking. Facial aging, for the individual, occurs with various accelerations and decelerations and does not appear to proceed at an even rate. What is apparent, however, is the commonality of progression across various ethnicities that enables certain generalities to be observed ( Fig. 1.1 ).
People either consciously or unconsciously assign an apparent age to themselves and others based on facial appearance. A person′s facial appearance is the visible declaration of the biological changes in the individual′s basic facial structures. Aging leads to sagging, alterations in texture, and changes in facial volume and the underlying skeleton, which affect the perception of age. Once these age-related changes have occurred, very few are reversible. However, they can be improved through makeup, cosmetic skin care, and cosmetic rejuvenative surgical and minimally invasive techniques.2
Changes in the Skin
The facial skin is continually exposed to a variety of external conditions, such as wind, cold, heat, and ultraviolet radiation. The last factor is the principal agent causing extrinsic aging of the skin, with effects that are significant enough to warrant the term “photoaging.” This exposure extends throughout an individual′s life, although it is postulated that the ultraviolet exposure occurring early in one′s life is responsible for most of the changes in the skin decades later. Some authors have speculated that ~50 to 75% of a person′s total lifetime ultraviolet radiation exposure occurs before 20 years of age.3 People with fairer complexions are most susceptible to the harmful effects of ultraviolet radiation.
Sun-damaged epidermis is histologically disorganized and thickened compared with nonexposed skin. Keratinocytes lose their distinctive alignment, and a progressive flattening of the cellular architecture occurs. Dyskaryotic changes are seen in the superficial layers of the epidermis. In response to long-term exposure to sunlight, epidermal melanocytes enlarge, proliferate, and migrate to higher levels of the epidermis. This chronic stimulation of melanocytes leads to dyschromias, spotty hyperpigmentation, and the proliferation of pigmented keratoses. These changes are reflected in the dull uneven texture and pigmentation of adult sun-exposed skin.
In the deeper layers of the skin, ultraviolet radiation causes different long-term changes in addition to those seen in the epidermis. In sun-damaged skin, the region immediately beneath the epidermis develops a band of densely packed collagen with little or no elastic content.3 Beneath this region is a broad zone of electron-dense, elastotic material. Here, curled entangled masses of the elastin-staining material are found among degenerated collagen fibrils. Elastotic degeneration of dermal architecture is a consistent histologic feature of cutaneous photo-damage. These occurrences are responsible for many of the changes seen as wrinkling.4
Part of the aging of the skin is an inevitable degenerative process with changes that are superimposed on the external aging factors in each individual, thus producing the endless variety of problems that present. As part of the intrinsic skin-aging process, the skin varies in thickness. Skin thickness in women reaches a maximum at ~ 35 years of age and decreases gradually thereafter. In men, the curve is different, with the peak thickness occurring at 45 years of age.5 There is a diversity of cell size and shape. The dermatoepithelial abutment is flattened with the loss of rete ridges, rendering skin fragile and susceptible to injury from shearing forces. The dermis of senescent skin is characterized by marked cellular atrophy and a corresponding reduction in metabolic activity. The percentage of newly synthesized collagen in the dermis decreases.6 As a result, the skin is less distensible, poorly resilient, and prone to fine wrinkling.7 As the dermis thins, there is a decrease in collagen content, degeneration of elastic fibrils, decreased water content, and the gradual addition of stable cross-links between collagen fibrils.8
Changes in Fat and Volume
Changes in the deeper soft tissue structures of the face complete the picture of the aging face. The face loses volume through several mechanisms. There appears to be actual fat atrophy, as well as a redistribution of fat. These alterations in the fat distribution are secondary to changes in the suspensory apparatus of the facial tissue. Principal among these suspensory mechanisms are the facial ligaments ( Fig. 1.2 ): (1) zygomatic ligament, (2) mandibular ligament, (3) masseteric-cutaneous ligament, and (4) platysmaauricular ligament.9
In addition to the exaggeration of age-related changes from subcutaneous fat atrophy, further malposition of fibrofatty tissues and muscles and atrophy of the facial skeleton create a relative excess of skin. Absorption of the skull and facial bones occurs with advancing age. This is most prominent in the areas of the maxilla, the mandible, and the anterior nasal spine, for example, in the widening of the width of the orbital aperture.
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