1 The Aging Face

Aging is a physiologic process of the body in response to the passage of time. Since the beginning of time, people have sought treatments to retard or reverse aging, with little avail. Aging can be accelerated by intrinsic and extrinsic factors. Aging cannot be stopped or reversed, but its effects can be mitigated. Trying to make a 60-year-old patient look 30 is unreasonable; a 60-year-old patient who wants to look as good as possible for 60 is very reasonable.

It is imperative that cosmetic surgeons fully understand the pathophysiology of aging, and educating patients on this process also helps them appreciate the basis for rejuvenation. Although we may feel we know much about aging, in reality we know little. Most textbook descriptions of facial aging are very mechanical and relate to loss of volume and support. Although this is certainly a factor and important to reversing the effects of aging through cosmetic surgery, there are many other intrinsic factors that make aging happen. Most cosmetic facial surgery patients are female, and the nuisances of metabolic aging influences are significant. Menopause produces decreased estrogen levels with elevated androgen levels, which contribute to epidermal and dermal changes. The decrease in basal metabolic rates (in men and women) facilitates weight gain and fat distribution in unwanted places such as thighs, abdomen, hips, buttocks, face, and neck. Add the ravages of childbearing to the skin and muscle, and it is easy to understand the aging process in females. Subcutaneous fat also decreases, which affects the support of the skin. The face and neck are rich in glandular structures that are less frequently discussed in volume loss but are probably moderate contributors. Finally, osteoporosis plays a key role in bone resorption; the majority of women in their fifth decade are osteoporotic. Osteoporotic changes also occur in males and in both sexes contribute to facial skeletal and dental resorption. As the facial skeleton shrinks, even more soft-tissue support is lost.

One unique factor to facial aging is that in most cultures, the face is exposed. Clothes can masquerade somatic aging, but the face and hands give it all away.

Like all other theories or processes, surgeons and anatomists argue about what exactly happens during aging. Although most surgeons agree that atrophy, ligamentous laxity, and ptosis are causative factors, others argue against this. What is universally agreed upon is that aging is a gradual process of structural weakening, and its effects begin in the third decade and progress throughout an individual’s lifetime. Aging is basically a process of deflation, similar to the transition from grape to raisin (Figure 1-1).

FIGURE 1-1 The analogy of a grape transforming into a raisin symbolizes the loss of volume in facial aging.

Babies and toddlers have full, rounded faces with full, convex contours. Adolescence includes rapid but disharmonious growth of bone, cartilage, muscle, and fat, which produces a sometimes awkward appearance in the preteen years. Through the teen years, puberty produces secondary sexual characteristics, including rapid growth phases that produce hereditary but predictable and distinguishable facial changes. Middle age brings the onset of aging changes that progress until death, as described later in this chapter.

The youthful face is tapered like an upside down egg, owing to the distinct volume and tight tissue retention (Figure 1-2, A). The aging face is more a reverse taper, similar to a right-side-up egg, due to the descent of volume and fat-compartment changes (Figure 1-2, B).

FIGURE 1-2 The youthful face is the shape of an upside-down egg; the volume is in the midface, with a tapering lower face (A). The aging face has volume loss, descent of tissues, and loss of the taper, giving it a right-side-up egg shape (B).

Aging changes are not only from volume loss and support changes but also intrinsic and extrinsic factors ¹^–³ (Box 1-1). It is interesting that biological aging can sometimes exceed chronologic aging, and we all know 45-year-olds who look 60 (or the inverse).

Box 1-1 Etiology of Aging

Intrinsic Aging	Extrinsic Aging
• Cellular senescence • Decreased proliferative capacity • Decrease in cellular DNA repair capacity and chromosomal abnormalities • Hormone reductions • Oxidative stress • Gene mutation • Fat and muscle changes • Bone and cartilage remodeling • Loss of dental structure

• Ultraviolet radiation

• Environmental factors

• Smoking

• Ethanol abuse

• Gravitational effects

• Elasticity changes

• Emotional stress

Lifestyle and heredity are significant contributors to the aging equation. Some aging factors are controllable whereas others are not. Studies of monozygotic twins have revealed that aging is affected greatly by environmental and lifestyle factors, as measured by physical appearance. The factors that exert the greatest influence seem to be substance or alcohol abuse, sun exposure, and emotional distress.⁴ These aging changes are shown with supporting images in the various procedure chapters.

In the first clinic I wrote, Dr. Tom Faerber contributed a chapter on facial aging. To compare aging changes, he performed an interesting study in which he obtained computed tomography (CT) scans on his 9-year-old daughter, 42-year-old wife, and 75-year-old mother-in-law. These women’s ages were separated by roughly 35 years.⁵ Of particular note is that the youthful face is convex, whereas the aging face is concave due to fat atrophy, muscle atrophy, and gravitational and ptotic changes (Figure 1-3). A pattern of muscle atrophy was demonstrated in the masseter and buccinator muscles in the oldest family member. The parotid gland maintained its volume, but the surrounding perimuscular and subcutaneous fat showed atrophy. Fat and muscle atrophy in the temporal, buccal, and malar regions were also seen and contributed to the concavities in those regions that develop with age, as evidenced in the progressive CT scans.

FIGURE 1-3 A, Computed tomography (CT) scan showing the facial anatomy of a 9-year-old female. B, CT scan showing the facial anatomy of a 42-year-old female.C, CT scan showing the facial anatomy of a 75-year-old female.

(From Faerber TH: Evaluation of the aging face. In Niamtu J (ed): Cosmetic facial surgery. Oral Maxillofac Surg Clin North Am, pp 523–530, 2000.)

Osseous volume-loss changes have also been implicated in midfacial aging.⁶^,⁷ Other studies show osseous volume increases in the lower face.⁸

Regional Facial Aging

The most logical means to address facial aging and rejuvenation is to start at the top and work downward. If the novice surgeon keeps this in mind, an orderly progression is always completed with consultation, diagnosis, and treatment.

Skin

The most plentiful facial tissue is skin. The facial integumentary, like the exposed hands, rarely gets a rest from the ravaging effects of the environment. Photodamage from sun exposure is especially harmful and coupled with extrinsic factors such smoking can accelerate the effects of aging.

Photodamage describes aging changes of the skin from chronic ultraviolet (UV) light exposure. Cumulative photodamage can be seen in almost every patient by comparing the sun-exposed and sun-protected areas of skin (Figure 1-4). The most obvious clinical cutaneous aging changes include markedly increased skin roughness, increased mottled hyperpigmentation, increased loss of elasticity, increased wrinkling, and sallowness.

FIGURE 1-4 Sun damage is evident on most individuals, and the difference between the sun-protected and sun-exposed skin is obvious.

Genetic contributions to skin aging result in numerous biochemical, histologic, and physiologic changes: a reduction of vascularity, increased dermal/epidermal thickness, collagen changes, proteoglycan and dermal cellularity, and loss of elastic fibers.⁹^–¹¹

Photoaging causes functional and anatomic modifications in the exposed regions. Ultraviolet B (UVB) radiation produces direct damage to the DNA of skin cells and also modulates the activity of cytokines and adhesion molecules.¹²^,¹³ Ultraviolet A (UVA) radiation initiates the formation of reactive oxygen species (ROS), which also damage nuclear and mitochondrial DNA and activate matrix metalloproteinases (MMPs).¹³

Histologically, the effects of skin photoaging include epidermal thickening, keratinocyte atypia, loss of polarity, and increased melanogenesis ¹⁴ (Box 1-2). A fragmented and disorganized dermal fibrillar network is present and forms amorphous groups.¹⁵ Collagenous changes occur in the appearance of fragmented collagen fibrils, senescent fibroblasts, loss of function of glycosaminoglycans, and alterations in the cutaneous microvasculature.¹⁶

Box 1-2 Histologic Effects of Photoaging

• A thickened, more basket-woven stratum corneum

• A thinner, more atrophic epidermis

• Epidermal atypia

• Irregular melanin dispersion in the epidermis

• Decreased glycosaminoglycans in the dermis

• Abnormal-appearing elastic fibers in the dermis

Contributing to exogenous skin aging is the decrease in skin functions that occur with age: decreases in cell replacement, injury response barrier function, sensory perception, immune and vascular responsiveness, thermoregulation, sweat production, sebum production, and vitamin D production.⁵