The Aging Face

This chapter provides a comprehensive discussion of facial aging. It is important that the reader also note that specific anatomic aging changes are also discussed in individual chapters within this text.

“Aging is a privilege denied to many,” Dr. Niamtu often tells patients who are unhappy with their aging. However, what is not denied to the cosmetic surgeon is dealing with this patient population daily. Perhaps equally important is how the patient is “handling” their aging. A 60-year-old patient who wants to look 30 is unreasonable, while a 60-year-old patient who wants to look as good as they can for 60, is very reasonable. A big part in a surgeon having favorable outcomes is picking the right patients. Cosmetic facial surgery has become very popular in our culture, and body dysmorphic disorder (BDD) is very prevalent. A normal and balanced cosmetic surgery patient can be a pleasure to work with. However, a patient with BDD can be a nightmare both clinically and legally. This type of patient cannot accept aging, and their entire psyche revolves around narcissism and pathologic body image and well-being. Acquiring the ability to avoid this type of patient is a true skill.

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, to no avail. Aging can be accelerated by both intrinsic and extrinsic factors, and it cannot be stopped or reversed, but its effects can be mitigated.

Despite being a universal process, a complete knowledge of facial aging continues to elude us. The evolution of numerous theories and anatomic observations have continually increased our understanding of the morphologic aging process.

Lambros recently broadened the visual understanding of facial aging with his comprehensive 54-year three-dimensional population study. Building on our shared registration of changes over time, his landmark-based three-dimensional comparative image analysis revealed sex-independent spatial changes, including narrowing of the eyelid aperture, retrusion of the nasal alae into the cheek with thinning of the upper lip unit accentuating the nasolabial crease, and gradual definition of the jowl fat pad over time ( Fig. 2.1 ). Changes do not occur solely along the surface planes of the face, but at right angles, speaking to the multidimensionality of facial aging.

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Comparative image transitions of the average young and old male face showing the spatial changes of narrowing of the eyelid aperture, retrusion of nasal alae into the cheek with a thinning upper lip unit accentuating the nasolabial crease, and demarcation of the jowl fat pad.

Reprinted with permission from Val Lambros, MD.

It is imperative that cosmetic surgeons fully understand the pathophysiology of aging. Accounting for these changes and educating patients about aging helps them appreciate the process and basis for rejuvenation. Most textbook descriptions of facial aging are very mechanical and relate to loss of volume and support. Although these are important factors to recognize in aging reversal through cosmetic surgery, various other intrinsic factors also play a role in aging.

As most cosmetic facial surgery patients are female, the nuances 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 the thighs, abdomen, hip, buttocks, face, and neck. Add the effects 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, which are less frequently discussed in volume loss but are probably moderate contributors. Skeletal muscles can undergo 50% atrophy with aging, and osteoporosis plays a key role in bone resorption, as the majority of women in their fifth decade are osteoporotic. Osteoporotic changes also occur in males and contribute to facial skeletal and dental resorption in both sexes. As the facial skeleton shrinks, even more soft tissue support is lost ( Fig. 2.2 ). Bone in the aging face is more prone to resorption in specific areas such as the orbital rims, maxilla and piriform regions, and anterior mandibular and pre-jowl regions ( Fig. 2.3 ). In addition, ligamentous attachments from bone to soft tissue tether the overlying soft tissue and contribute to hollowing when bone loss drags down the soft tissue anatomy.

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Osseous resorption accounts for many aging changes. Common regions of bony atrophy (arrows) cause loss of support for overlying soft tissue anatomy.

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Images showing soft tissue volume loss and descent secondary, in part, to underlying bony atrophic aging changes.

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

As with 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. It is universally agreed, however, that aging is a gradual process of structural weakening, and its clinical effects begin in the third decade and progress throughout an individual’s lifetime. Aging can be described as a process of deflation similar in the transition from a grape to a raisin ( Fig. 2.4 ).

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The youthful grape transforming to an aging raisin symbolizes skin aging and volume loss over time. Both intrinsic and extrinsic changes affect aging. Note that the grape is drinking water and using sun protection, while the raisin is smoking, drinking alcohol, and not using sun protection.

Babies and toddlers have full rounded faces with full convex contours. This is, in part, from the small skeleton supporting the generous fat compartments in infancy. 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, which produce hereditary but predictable and distinguishable facial changes. Middle age brings the onset of aging changes that progress until death (see later). The cycle of aging is such that infants have large orbits and smaller maxillae, which make their midfacial characteristics resemble an aged person. As the midfacial skeleton grows, the infant takes on the midface of youth. Continued aging produces widening of the orbits with simultaneous maxillary and piriform resorption, which makes the aged person resemble an infant. This is truly the cycle of life. Although some parts of the facial skeleton resorb with age, some areas such as the mandible enlarge, underlining the multifactorial and dynamic changes that contribute to the aging facial skeleton.

The youthful face is tapered like an upside-down egg because of the distinct volume and tight tissue retention ( Fig. 2.5 ). The aging face is more of a reverse taper, similar to a right-side-up egg, because of the descent of volume and fat compartment changes (see Fig. 2.5 ).

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A young, youthful face is tapered toward the jawline, similar to an upside-down egg (top) . An 80-year-old patient with a squared-off lower face similar to a right-side-up egg (bottom) .

Aging changes are not only caused by volume loss and support changes but are also caused by intrinsic and extrinsic factors ( Box 2.1 ).

It is interesting that biologic aging can sometimes exceed chronologic aging, and we all know 45-year-olds who look 60 years old or the inverse. Fig. 2.6 shows a career truck driver with obvious accelerated actinic damage on the driver’s side that is exposed to more sun and wind. Fig. 2.7 shows a 65-year-old female with both hereditary and acquired aging (intrinsic and extrinsic). Lifestyle and hereditary factors are significant contributors to the aging equation. Some aging factors are controllable, while 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. These aging changes are shown with supporting images in the various procedure chapters. An excellent description of cutaneous aging is presented in Chapter 12 .

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Unilateral advance skin actinic damage is shown on a career truck driver whose left side faced the window.

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A 65-year-old female patient with advanced skin aging, likely from sun damage and genetic predisposition.

In a previous text published by Niamtu, Tom Faerber contributed to a section on facial aging that details a study in which he obtained CT scans on his 9-year-old daughter, 42-year-old wife, and 75-year-old mother-in-law to compare aging changes. Particularly notable is that the youthful face is convex, while the aging face is concave as a result of fat atrophy, muscle atrophy, gravitational changes, and ptotic changes ( Figs. 2.8–2.10 ). A pattern of muscle atrophy was demonstrated in the masseter and buccinators muscles in the oldest family member. The parotid gland maintained its volume, whereas 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 concavities in the regions that develop with age, as evidenced in the progressive CT scans. This evidence-based data show facial aging transformations from convex to concave. Although osseous volume loss is a big component of midfacial aging, some studies show that osseous volume increases in the lower face.

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CT scan showing the facial anatomy of a 9-year-old female patient.

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CT scan showing the facial anatomy of a 42-year-old female patient.

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CT scan showing the facial anatomy of a 75-year-old female patient.

Once thought to be a continuous structure anatomically, Rohrich and Pessa revealed that the subcutaneous fat of the face is highly compartmentalized with vascularized fibrous septal boundaries separating individual facial fat compartments ( Figs. 2.11 and 2.12 ).

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Commonly observed sequence of facial fat compartment deflation in facial aging.

Reprinted with permission from Dr. Rod Rohrich and PRS Global Open forum.

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Rohrich and Pessa injected methylene blue dye into cadaveric specimens, allowing dye diffusion to delineate the natural septal boundaries of the facial fat compartments. The unique broad expanse of the lateral temporal cheek compartment was highlighted in this manner (arrow) .

From Rohrich, R. J., & Pessa, J. E. (2007). The fat compartments of the face: anatomy and clinical implications for cosmetic surgery. Plast Reconstr Surg,. 119:2219–2227; discussion 2228.

The nasolabial fat and jowl fat are separate distinct compartments. The periorbital fat is divided into superior, inferior, and lateral compartments. The malar fat is divided into the medial, middle, and a larger lateral temporal-cheek fat spanning the height of the face from the cervical subcutaneous fat to the lateral-most compartment of the forehead. The forehead similarly has three compartments with the central, middle, and lateral temporal-cheek fat. Some compartments, such as the periorbital and malar fat pads, tend to deflate earlier in middle age, while others deflate later in life. In the youthful face, the transition between these subcutaneous compartments is smooth, whereas variable deflation among compartments in the aging face render distinguishable abrupt contour changes. This volumetric understanding of facial aging continues to elicit interest and influence the techniques employed in facial rejuvenation today.

Regional Facial Aging

The most logical means of addressing facial aging and rejuvenation is to start at the top and work downward in an orderly progression during the consultation and discuss the diagnosis and treatment of each unit.

Skin

The most plentiful facial tissue is skin. It serves as the canvas of the face, revealing the deflation and atrophic changes of the various underlying components. Like the exposed hands, it rarely gets respite from the ravaging effects of the environment. Extrinsic factors such as sun exposure, stress, and smoking can accelerate the effects of aging.

Contributing to exogenous skin aging is the decrease in skin functions that occur with age. These changes include decreases in cell replacement, injury response, barrier function, sensory perception, immune and vascular responsiveness, thermoregulation, sweat production, sebum production, and vitamin D production. As normal regulatory pathways become dysfunctional with age, both the rejuvenation and healing processes of the skin are impaired. Recent studies have pointed to dysfunction of the hypoxia-inducible factor (HIF)-1α regulatory pathway as a primary contributor to the decline of both processes. The dermis is thicker on the areas of the face that are less mobile (e.g., forehead and nose) and thinner on the areas of the face with increased movement (e.g., lower eyelids).

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

However, studies of monozygotic twins have highlighted the importance of external factors on the aging of the skin. Originally researched by Dr. Darrick Antell, studies on identical twins have shown the effect of personal lifestyle choices and habits, with smoking and sun exposure attributing the greatest degree of discordance in visible aging between genetically identical twins ( Fig. 2.13 ).

Smoking-associated differences are usually seen in the middle and lower thirds of the face, with fewer attributable differences seen in the upper face. However, photodamage, the aging changes of the skin from chronic ultraviolet (UV) light exposure, is more pervasive and affects all areas of chronic exposure. Cumulative photodamage can be seen in almost every patient by comparing the sun-exposed and sun-protected areas of skin. The most obvious clinical cutaneous aging changes include markedly increased skin roughness, mottled hyperpigmentation, loss of elasticity, wrinkling, and sallowness.

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

Histologically, the effects of skin photoaging include epidermal thickening, keratinocyte atypia, loss of polarity, and increased melanogenesis ( Box 2.2 and Fig. 2.14 ). A fragmented and disorganized dermal fibrillar network is present and forms amorphous groups. Collagenous changes occur in the appearance of fragmented collagen fibrils, senescent fibroblasts, loss of function of glycosaminoglycans, and alterations in cutaneous microvasculature.

Box 2.2

Pathologic changes of photodamaged skin

• Thickened more basket-woven stratum corneum

• Thinner more atrophic epidermis

• Epidermal atypia

• Irregular melanin dispersion in the epidermis

• Decreased glycosaminoglycans in the dermis

• Abnormal-appearing elastic fibers in the dermis

Upper Facial Aging

Hair

Aging in the scalp manifests as the pigment changes of graying, thinning, hair shaft fragility, pattern baldness, and recession. These changes are largely genetically controlled and less at the mercy of the environment compared with the skin. Additionally, “hair aging” is less of an indicator of age, as some 20-year-olds lose their hair, while some 70-year-olds have a full head of thick hair.

The aging scalp is now surgically treated by hair transplantation, with various follicular graft-size harvest techniques available. Robot-assisted transplantation has further streamlined the process and enables more aesthetic donor site harvesting of the occipital scalp. The medical treatment of hair loss, although still in its infancy, continues to evolve and may overcome surgical treatments in the lifetime of many readers of this text.

Minoxidil is a popular topical alopecia treatment drug that produces vasodilation of the hair follicle. Patients taking this drug for blood pressure developed increased hair growth as a side effect, and the US Food and Drug Administration (FDA) eventually approved it for pattern baldness in men and women. Mounting studies and historic experience suggest that higher concentrations of topical minoxidil may enhance efficacy, with both 2% and 5% topical formulations available and well tolerated by both men and women. Finasteride is a medication taken in tablet form that was originally used to treat benign prostatic hypertrophy. It is a 5-alpha (5α)-reductase inhibitor, which blocks the conversion of testosterone to dihydrotestosterone, the latter being toxic to hair. This drug is FDA approved for male pattern baldness only and causes birth defects if taken in pregnancy. Bimatoprost (Latisse, Allergan Inc., Irvine, CA) is a glaucoma medication that has been scientifically shown to make eyelashes thicker, darker, and longer, with its application for hair growth outside the eyelash region under review. Early results from phase 2 trials show similar efficacy to minoxidil, with more robust evidence showing it to be an effective adjunctive topical therapy for treating autoimmune mediated alopecia areata. There is also emerging discourse that platelet-rich plasma (PRP) can lead to renewed hair growth and may be particularly well suited for patients with diffuse hair thinning. PRP as a hair-loss treatment modality entails withdrawing a patient’s own blood, processing it to collect only the enriched cells from the platelet-rich plasma, and injecting it directly into the scalp. Although promising, further research is necessary to confirm whether PRP is truly effective as the present nascent studies are limited by small sample size, technique variations, and differing employed protocols among practitioners.

Forehead and Brow

Younger people have smooth foreheads. Photodamage with the resultant skin changes, tissue ptosis, osseous changes, and gravity contribute to brow and forehead changes.

Although some people, even in youth, never have elevated or arched brows, many do. Most youthful females have brows that arch at the junction of the central and lateral brow (which corresponds to the lateral pupillary limbus). The youthful male brow lies at or slightly above the superior orbital rim. Aging changes coupled with atrophic changes in the brow fat and upper periorbital complex cause the brows to descend in many people. This manifests as lateral hooding and/or generalized ptosis, which gives the appearance of smaller eyes ( Fig. 2.15 ). In severe cases, the eyebrow sits on the lashes. A ptotic brow associated with upper periorbital changes produces a sad and tired appearance. As a result, many females go through their waking hours subconsciously raising their brows, which further compounds the problem of flexed muscles and brow skin wrinkling. Any surgeon who performs browlift surgery can attest to the difficulty of getting some females to relax their brow for a preoperative photograph, or when looking in a mirror.

The treatment for brow and forehead ptosis is endoscopic or open brow techniques. Unfortunately, many patients who are candidates for a browlift end up with blepharoplasty. This can worsen the aging sign by further pulling down the brow. The correct diagnosis of brow and forehead ptosis is paramount in aesthetic rejuvenation. For fair and accurate diagnosis, surgeons who perform blepharoplasty but not browlifts have an ethical responsibility to refer potential browlift patients for consultation with a surgeon experienced in this technique.

The frontalis is the only elevator of the brow and is opposed by numerous depressor muscles, including the procerus, corrugator supercili, orbicularis, and depressor supercili. Wrinkles in the skin run 90 degrees to the underlying muscles, so continual flexing of the frontalis muscles creates horizontal forehead rhytids. Popular parlance refers to vertical glabellar rhytids with two furrows as an 11 and those with three furrows as a 111 . Treatment of glabellar rhytids includes injectable neuromodulators, injectable fillers, radiofrequency nerve ablation, laser skin resurfacing, and muscle disruption with a concomitant browlift.

Upper Eyelids

The upper eyelids are inseparable from brow and forehead aging, as the ptotic brow enhances upper-lid skin redundancy. The upper-eyelid skin is extremely thin, and aging and photodamage lead to redundant and crinkly looking skin, which is known as dermatochalasis . As a result of weakening of the orbital septum, the upper periorbital fat protrudes and produces aged contours. In some patients, the lacrimal gland becomes ptotic and can obstruct the upper-eyelid sulcus. Laxity in the orbicularis retaining ligaments in both the upper and lower eyelids also contributes to this process. The youthful eyelid consists of a slight upward slope from medial to lateral, and weakening of lateral canthal support produces a downward slant of the eyes. Fig. 2.16 shows upper and lower eyelid aging changes. The continual flexing of the orbicularis oculi muscle causes lateral canthal lines (crow’s feet wrinkles), which also contribute to upper facial aging. The skin wrinkles are horizontal to the circular underlying muscle. Treatment of upper-eyelid aging includes blepharoplasty, skin resurfacing, and brow and forehead lifting.