Sunteți pe pagina 1din 22

Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

A cosmetic approach to cutaneous defects


Christopher B. Harmon, MD*, Michael L. Hadley, MD
Department of Dermatology, University of Alabama at Birmingham, 1919 7th Avenue South, SDB-76, Birmingham, AL 35294-0007, USA

The pursuit of youth and beauty has undergone a resurgence of interest, as evidenced by the increased number of people making visits to providers of cosmetic procedures [1]. As a result of medical advances and economic development, there has been an unprecedented 25 years of added life expectancy to the average American over the past century. There also has been a distinct increase in the proportion of elderly persons, with one in eight Americans (12.6%) being age 65 or older currently, a number that is expected to be one in ve (20.3%) by 2030 [2]. Concurrently there have been many exciting advances in the arena of facial rejuvenation, from a multiplicity of lasers to new-llers to botulinum toxin, cosmeceuticals, and many other innovations that complement the existing array of tried-and-true techniques. With a surge of interest in facial rejuvenation from an expanded aging population, it is incumbent for cosmetic surgeons to be familiar with these innovations to better inform and tailor treatment for their patients.

Aging Skin aging is a complex and dynamic process that results from the interplay of extrinsic and intrinsic factors. Extrinsic factors are environmental inuences that lead to premature aging, such as exposure to smoking, chemicals, eects of gravity, and, most notably, sunlight. Intrinsic aging is largely genetically determined. Although separation of extrinsic from intrinsic aging is articial, it is useful from an academic viewpoint in helping to dene the factors that play a role in aging. Exposure to ultraviolet (UV) radiation from the sun is the primary environmental factor that leads to premature aging or photoaging. Photoaging is the cumulative aect of sun exposure on skin, and it preferentially aects persons with lighter skin color. The characteristic features of photoaging include rough texture, ne and coarse wrinkles, yellow or sallow color, and mottled pigmentation [3]. A primary mechanism whereby photoaging occurs is through UV-generated reactive oxygen species [4]. Once generated, these reactive oxygen species have been shown to initiate a cascade of molecular events that lead to the production of collagen-degrading enzymes while simultaneously inhibiting the enzymes responsible for new collagen synthesis. Skin pigment has been shown to play an important role in providing protection from collagen degradation. Persons with lighter skin have been shown to have an increased production of collagen-degrading enzymes when exposed to UV irradiation as compared with persons with darker skin types [5]. This protection occurs because of the broad UV absorption that melanin provides in attenuating UV penetration, which accounts for the observations that photoaging is less severe in persons with darker pigments. The net effect of sunlight is crippling on the molecular machinery responsible for maintaining the structural integrity of proteins that give strength and resiliency to skin, which is especially true in persons with lighter skin [5].

* Corresponding author. Dermatology Associates, 2100 16th Avenue South, Suite 202, Birmingham, AL 35205, USA. E-mail address: charmon887@pol.net (C.B. Harmon). 1061-3315/04/$ - see front matter 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.cxom.2003.10.008

142

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

Intrinsic aging is dened as the role that genetics plays relative to chronologic age. Changes caused by intrinsic aging include alteration of skeletal mass and proportion, atrophy and redistribution of subcutaneous fat, increased laxity of the underlying fascia and musculature, and epidermal thinning or atrophy. A recent study by Guinot et al [6] showed that intrinsic aging, presumably genetic in character, seems to play a much larger role than previously suspected. In the study, a cohort of 361 white women (age range, 1880 years) was studied in an effort to help dene how skin characteristics associated with aging related to chronologic aging. To study this association, a skin age score based on 24 skin characteristics (eg, pigmentation, milia, comedos, wrinkles, and sagging) was established. An analysis also was performed to determine whether certain lifestyle habits and other physical factors could account for the discrepancies between chronologic age and the skin age score. Predictably, effects of skin phototype, body mass index, menopausal status, degree of lifetime sun exposure, and years of cigarette smoking were seen to correlate positively with age. These factors only accounted for 10% of the discrepancies, however. More importantly, the changes used in the skin age score (eg, wrinkles and sagging) seemed to represent intrinsic aging rather than changes expected from photodamage or other extrinsic factors. Preoperative consultation One of the most important steps in appropriately tailoring treatment for a patient lies in the initial assessment and preoperative consultation. The skin of the face is supported by bone and cartilage intervened by layers of subcutaneous fat, muscle, and fascia. In assessing the senescent face, it is important to realize that any of these structural layers may be aected dierentially. For instance, a patient may have a preponderance of skin redundancy and facial sagging best treated with a facelift. Alternatively, a patient may present with many of the sequelae of photoaging, including ne lines and dyschromia that is treatable with laser resurfacing or a medium depth chemical peel. Often a patient presents with senescent sequelae of all facial structures. Most important is the consideration of a patients own desires regarding guidance of appropriate therapy. Although a patient may be a good candidate for a facelift or other more aggressive procedure, the cosmetic surgeon should place the patients interests rst in prescribing a remedy with an acceptable risk-benet prole. Increasingly many patients are unwilling to undergo the increased risk and downtime associated with a bigger procedure, preferring instead a quicker lunch time procedure. Once a physician has assessed a patient and discussed his or her needs, a treatment plan can be devised that best incorporates goals and expectations. Skin changes and assessment As part of the preoperative consultation, an objective skin assessment is critical. A useful method for assessing skin-related photoaging was developed by Monheit and Fulton [7]. The system combines age-related textural and lesional changes into a numerical scale (Table 1). Skin textural changes include dynamic wrinkles, static wrinkles, ne lines, leathered or parchmentlike appearance, pebbling, and pore size. Lesional changes associated with aging include lentigines, telangiectasias, actinic keratoses, senile comedones, and skin cancers. The system provides the clinician with an easy method to assess simply and systematically the degree of photoaging and help guide possible treatment options. Skin changes can be treated in various ways that range from simple topical agents for mild symptoms of early photodamage to medium-depth chemical peels for more pronounced lentigines and ne wrinkles to ablative resurfacing for more pronounced rhagades. In general, it has been shown that regarding more pronounced photoaging, ecacy and longevity of improvement tend to be inversely proportional to wounding depth [8]. Facial structure Assessment of facial structure is another centerpiece of the preoperative consultation. Aging produces many structural changes. A useful method for analyzing these changes divides the face into thirds.

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162 Table 1 Index of photoaging Texture changes Wrinkles: dynamic (% of potential lines) Wrinkles: photoaging (% of potential lines) Cross-hatched lines: ne lines (% of potential lines) Sallow color and dyschromia Leathery appearance Crinkly (thin and parchment-like) Pebbly (deep whitish nodules) (% of face) Pore number and size Lesions Freckles: mottled skin 1 (number present) \ 10 Lentignes (dark/irregular) and 2 SKs (size) \ 5 mm Telangiectasias: erythema ush 1 (number present) \5 AKs and SKs 2 (number present) \5 Skin cancers 2 (number present, now or by history)1 ca Senile comedones 1 (in cheekbone area) \5 Total Score 2 \ 25 4 \ 10 mm 2 \ 10 4 \ 10 4 2 ca 2 \ 10 1 \ 25% 1 \ 25% 1 \ 10% 1 Dull 1 1 2 \ 25% 2 \ 25% 2 \ 50% 2 \ 50% 2 \ 20% 2 Yellow 2 2 4 \ 50% 4 \ 50% Points 3 \ 75% 3 \ 75% 3 \ 40% 3 Brown 3 3 6 \ 75% 6 \ 75% Points 3 \ 50 6 \ 15 mm 3 \ 15 6 \ 15 6 3 ca 3 \ 20 4 \ 100 8 \ 20 mm 4 [ 15 8 [ 15 8 [ 4 ca 4 [ 20 4 \ 100% 4 \ 100% 4 \ 60% 4 Black 4 4 8 \ 100% 8 \ 100% Score Score

143

Corresponding Rejuvenation Program Score 16 711 1216 17 or more Needs Skin care program with tretinoin, glycolic acid peels Same plus Jessners peel; pigmented lesion laser or vascular laser Same plus medium peel-Jessners + trichloroacetic acid peel; skin llers or Botox Same plus laser resurfacing

Abbreviations: AK, actinic keratosis; Ca, cancer; SK, seborrheic keratosis.

Upper face Ptosis of the brow is a characteristic change in the aging face [9]. In men, the ideal brow is at or just above the supraorbital rim, whereas in women the brow should be well above the rim. Dermatochalasis describes the redundancy of the upper and lower eyelid skin with time. The orbital septum that serves to compartmentalize intra- and extraorbital fat becomes stretched and inelastic, which leads to fat pad herniations and results in the clinical appearance of baggy eyelids. Sometime the bagginess impairs visual elds. Other changes include static rhytides arranged perpendicularly to the underlying muscles. They occur on the forehead and glabella and radiate from the lateral canthus (crows feet). With time, atrophy of the temporal fat pad leads to a hollowing of this region. Middle face The nose undergoes multiple changes with aging [10]. The cartilaginous support of the lower third of the nose weakens and broadens, which results in tip ptosis. Sebaceous glands of the nose tend to become more prominent. In rosacea, sebaceous gland hypertrophy may result in disguring rhinophyma. The buccal fat pad tends to atrophy with time, which imparts increased laxity to the midface and a sunken-in appearance. This sinking in also can accentuate the malar

144

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

eminences. Other changes include loss of dentition and resorption of bone, which is especially true of alveolar and mandibular bone. Bony resorption combined with fat atrophy and increased laxity of skin and underlying fascia leads to drooping of the mid and lower face. Clinically this results in accentuated nasolabial folds and prominent jowls. Lower face and neck The formation of jowls from the relative excess of skin and loss of underlying support serves to blunt the delineation between the jawline, chin, and neck. The cervicomental anglethe angle formed between the neck and chin (ideally is approximately 90 )increases with age [11]. The turkey gobbler deformity refers to the protrusion of fat between the chin and hyoid bone that results from excess fat and separation of the paired platysmal muscles. Other age-related changes of the lower face and neck include development of perioral rhytids, drooping of the oral commissurae, and attening of the lips. Platysmal banding is another change found frequently on the senescent neck. Structural changes can be handled with surgical and nonsurgical techniques. In addressing the upper third of the face, there are some useful techniques. Simple dynamic wrinkles of the forehead and crows feet can be handled with botulinum toxin. Brow ptosis, dermatochalasis, and orbital fat pad herniation can be treated surgically with a brow lift or a lid blepharoplasty. Treatment of the middle third of the face includes midface lift for facial drooping, cheek implants for increased malar prominence, and rhinoplasty nasal tip ptosis. Techniques for rejuvenating the lower third of the face include use of various llers for lips and nasolabial folds, face-lift procedures for facial sagging, liposuction, and platysmal muscle tightening for neck fullness. Often the physician encounters multiple age-related changes of facial structures that range from skin to deeper facial structures. Treatment of these changes often is best achieved with a multidisciplinary approach. When expertise from various disciplines is combined, optimum results and patient satisfaction are more likely to occur.

Medical therapy in facial rejuvenation Skin care The rst line of intervention by the physician is educating the patient regarding causes of aging, including providing information on how avoiding sun, smoking, and other environmental factors helps to prevent premature aging. The selection of an appropriate skin regimen also can help to slow down premature aging. A comprehensive skin care program includes sunscreen, topical retinoids, and, when needed, bleaching agents. Various cosmeceuticals, such as alpha hydroxy acids and antioxidants, also may play a secondary role in facial rejuvenation. Photoprotection Exposure to UV light has been implicated in premature aging [12]. UV light can be divided into UVA (320400 nm) and B (UVB) (290320 nm). UVB only composes 10% of total UV radiation at its peak between 10:00 AM and 3:00 PM yet is most responsible for burning [13]. UVA penetrates more deeply, is responsible for tanning, and tends to be more constant throughout the day compared with UVB. Until recently UVA was believed to be less harmful; however, it has been shown that UVA accelerates the aging process by causing collagen degeneration [12]. UVA also has been shown to produce many other harmful effects to DNA, such as thymine dimer formation, cross linking, and strand breakage [1416]. UVA also inhibits the Langerhans cells of the skin, which perform a vital immunoprotective role in protection from potential neoplasms [17]. Thymine dimers have been implicated in increased mutation rates and development of skin cancers [16]. Recent studies have shown that regular use of broad-spectrum sunscreens is effective in preventing UV-induced DNA damaging thymine dimerization. Even skipping 1 day

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

145

of sunscreen application resulted in statistically signicant increase in thymine dimer formation [18]. In addition to avoiding the peak UVB hours of 10:00 AM to 3:00 PM, regular use of sunscreen is also important. Many sunscreens provide ample protection against the burning effects of UVB but only deliver partial protection against UVA [13]. Sunscreens are divided into two major categories: physical blockers and chemical blockers. Chemical blockers work by absorbing specic wavelengths of light, especially UVB light, thus sparing the skin from the potential damaging affects of UV light. Many chemical blockers contain benzene rings, which absorb the UV energy. Some of the chemical blockers include oxybenzone, para-aminobenzoic acid, and octyl methoxycinnamate. Physical blockers, unlike chemical blockers, reect and scatter rather than absorb UV light. Physical blockers block UVA and UVB rays. The physical blockers include zinc oxide and titanium dioxide. Traditionally the physical blockers were pasty and cosmetically inelegant; however, newer transparent micronized formulations (Z-Cote, BASF, Mount Olive, New Jersey) have alleviated this problem, which makes them more appealing. Adequate application of sunscreen is critical. Current Food and Drug Administration (FDA) guidelines recommend 2 mg/cm2 [19]. To achieve this amount, one half to one teaspoon is necessary for the face and each arm, 2 teaspoons for the upper body, and 30 mL for the entire body. Although it is true that a sunscreen with SPF-15 blocks 93% of the suns rays and SPF-30 only increases this to 97%, if only half the recommended amount of an SPF-15 sunscreen is applied or is perspired away (a situation that occurs more commonly than not), the SPF falls exponentially to 5 [19]. Sunscreens must be reapplied every 2 hours, particularly during swimming or perspiration-producing activities. To enhance absorption by the stratum corneum, application of sunscreens must occur 30 minutes before going outside.

Retinoids Retinoids are a group of naturally or synthetically derived molecules related to vitamin A and include retinol, retinal, retinaldehyde, retinoic acid (tretinoin and isotretinion), adapalene, and tazarotene. Retinoids have been shown to act on specic retinoic acid receptors, which in turn interact with DNA sequences of the promoter regions of target genes. This interaction aects transcription of genes that regulate a broad range of epidermal and dermal eects [20]. Notable among these eects is that of tretinoin on photodamaged skin. In photodamaged skin, topically applied tretinoin has been shown to have dramatic improvements on ne lines, texture, and skin discolorations in at least four double-blind, placebo-controlled studies [21 24]. These earliest changes of improvement with tretinoin are tactile smoothening, which occurs within the rst week [25]. This change correlates histologically with the compaction of the stratum corneum and an increase in epidermal hyaluronic acid. Hyaluronic acid is a glycosaminoglycan, which is hydroscopic (1000 fold its own weight). The smoothening of the skin is believed to be caused by the compacting of the stratum corneum combined with increased hydration, which is provided by the abundance of hyaluronic acid. In contrast, wrinkle effacement occurs much laterat approximately 3 to 4 months [26]. Effects on deeper wrinkles are believed to occur via affects on collagen synthesis. Collagen in photoaged skin almost doubled after 10 to 12 months of treatment with topical tretinoin therapy compared with placebo [27]. Topical tretinoin is successful in treating liver spots associated with photodamage [28]. In addition to repairing existing photodamage, retinoids are helpful in preventing photodamage. Tretinoin has been shown to inhibit UV induction of matrix metalloproteinases when applied before UV exposure. These matrix metalloproteinases have been shown to degrade collagen types I and III when exposed to UV light [12]. By inhibiting these UV-inducible enzymes with tretinoin, less dermal damage (eg, wrinkling) is believed to occur. FDA-approved therapies specically approved for treatment of skin aging include tretinoin 0.05% or 0.02% retinoic acid and newly introduced tazarotene 0.1%. Tazarotene is a newer generation retinoid that recently was shown to be ecacious in treating photodamage during a 24-week, multicenter, double-blind, randomized, vehicle control study followed by a 28-week, open-label extension that involved 563 patients [29]. In a similarly designed head-to-head study of 173 patients that compared tretinoin 0.05% and tazarotene 0.1%, preliminary data showed

146

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

tazarotene to be more efcacious for improving global photodamage scores compared to tretinoin [30]. Tolerability was equivalent for both. In starting any regimen with a retinoid, it is important to initiate therapy gradually to avoid some of the side eects of retinoid dermatitis, including redness, dryness, peeling, and burning. A popular regimen includes applying the agent every other night after cleansing with a non-soap cleanser and applying only a pea-size amount to cover the entire face. As a patient becomes tolerant and the side eects dissipate, the frequency of application is increased to every night. Use of a gentle moisturizer also is helpful in mitigating some of the retinoid side eects as warranted. Bleaching agents Various bleaching agents available for treatment of hyperpigmentation secondary to photodamage, including hydroquinones, azelaic acid, and kojic acid. Perhaps the most commonly used and best studied agent is hydroquinone. Hydroquinone inhibits tyrosinase, an enzyme responsible for converting dopa to melanin. Various hydroquinone formulations and strengths have been concocted. A common formulation combines hydroquinones with glycolic acid [31]. Another popular formula is Kligmans formula of 5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone [32]. Azelaic acid and kojic acid also inhibit tyrosinase. Twenty percent azelaic acid was found to be similar to 4% hydroquinone in the treatment of melasma [33]. Kojic acid (used extensively in Japan) has been shown to be effective in treating melasma. A study that compared combinations of glycolic acid with either hydroquinones or kojic acid found both to be effective in treating melasma [34]. Kojic acid has been implicated as a signicant source of contact allergy in Japan, where it is found in many cosmetics [35]. It should be emphasized that the eects of bleaching agents can be reversed easily with even slight sun exposure, which underscores the need to continue sun avoidance and daily sunscreen use. Alpha hydroxy acids Alpha hydroxy acids have achieved widespread use over the past decade in the treatment of photoaging. Alpha hydroxy acids are weak organic acids and are structurally distinguished by having a hydroxyl group attached to the alpha position of the acid. Two commonly used alpha hydroxy acids include glycolic and lactic acid. Alpha hydroxy acids in lower concentrations and with higher pH (\ 20% and [ 3.0) are commonly used in skin care products, whereas acids with higher concentrations and lower pH ([ 20% and \ 3.0) are used as peeling agents. Alpha hydroxy acids have multiple mechanisms of action, many of which are still being worked out. Some of these mechanisms are as follows: (1) Diminished corneocyte adhesion above the granular layer, which results in exfoliation. The histologic correlation demonstrates an initial thinning of the stratum corneum, but with time there is a return to near normal levels [36,37]. (2) An increase in dermal collagen and glycosaminoglycan production [38,39]. (3) Improvement of hyperpigmentation [40,41]. Several important studies have documented the eects of alpha hydroxy acids on photoaged skin. A double-blind, placebo vehicle-controlled study of 75 patients who used 5% glycolic acid over 3 months demonstrated statistically signicant improvement in markers of photoaging, including general skin texture and discoloration. Reduction of ne wrinkles, however, was not statistically signicant [41]. In another similarly designed 22-week study that involved 74 patients, researchers demonstrated that either 8% lactic or glycolic acid demonstrated signicant improvements of some markers of photoaging, including skin roughness, mottled hyperpigmentation, sallow appearance, and overall appearance. There was no signicant reduction of ne wrinkles [40]. Other studies have correlated these clinical observations with histologic, ultrastructural, and molecular studies [38,39]. Notable in these studies was the demonstration of increased epidermal (54.7%) and dermal (9.4%) hyaluronic acid after using 20% glycolic acid daily over 3 months. Hyaluronic acid is a glycosaminoglycan that plays a critical role in epidermal and dermal hydration, and it binds up to 1000 times its weight in water. This increased hydration affects skin hydration, appearance, and functionality [38].

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

147

Several factors must be considered in the practical uses of alpha hydroxy acids, including pH, pKa, concentration, vehicle, duration of exposure, and patient skin type. There have been various claims by manufacturers concerning the ecacy of buering, neutralization, and esterication of alpha hydroxy acids. In evaluating these claims, it is important for the clinician to understand that alpha hydroxy acids derive their ecacy from their ability to donate a proton or form a free acid. As a rule, alpha hydroxy acids are more eective in generating a free acid at a low pH, with the optimum formation of free acid occurring at a pH equal with the pKa (acid dissociation constant) of the alpha hydroxy acid. The pKa of trichloroacetic acid is 0.5; the pKa of glycolic and lactic acid is 3.8. Acid concentrations do not have as much eect on pH as one would expect. For example, a 50% glycolic solution has a pH of 1.2, whereas a 5% glycolic solution has a pH of 1.7 [42]. It is important to choose an appropriate vehicle when using an alpha hydroxy acid. Solutions or gels are generally best for oily skin; ointments or creams are best for dry skin; lotions are used for normal skin. Duration of contact becomes important when using alpha hydroxy acids as peeling agents (concentrations generally more than 20% with pH \ 3.0) but is generally not as important for concentrations and pH when using them for daily skin care products. The FDA has mandated that the concentration of alpha hydroxy acids in cosmetics cannot exceed 10% or have a pH less than 3.5 [43]. Trained cosmetologists can use glycolic or lactic acid in concentrations up to 30% with a pH more than 3.0. Physicians can use products that are even stronger (higher concentration and lower pH) as peeling agents, if desired. Various clinical strategies may be used when prescribing an alpha hydroxy acid in a daily skin care regimen. Generally an alpha hydroxy acid should be used once a day, and frequency should increase to twice daily after 2 weeks if tolerated. Concentrations of 8% to 12% work for most skin types; however, sensitive skin may require concentrations of 4%. The alpha hydroxy acid can be in either a cleanser or moisturizer format, with a vehicle appropriate for the patients skin. The combination of retinoic acid at night and an alpha hydroxy acid is a popular regimen and seems more benecial than either agent alone. Currently no studies have validated this approach. Caution should be used when starting a patient on such a regimen, because retinoic acid can potentiate the depth of penetration by the alpha hydroxy acid, with possible resultant irritation. Antioxidants and hormones UV-generated reactive oxygen species are believed to play a principal role in photoaging. There has been a surge of interest in antioxidants and their potential role as rejuvenators in retarding reactive oxygen species. Two popular antioxidant agents are vitamins C and E. Vitamin Cascorbic acidhas been shown to be a potent scavenger of free radicals while regenerating vitamin E [44]. Ten percent ascorbic acid also was effective in a porcine model in reducing the effects of UV light by decreasing sunburn cells [45]. In another study of 10 human subjects, sites that were pretreated with ascorbic acid showed reduced erythema after exposure to UVB radiation [46]. One problem with vitamin C is its volatility. It is easily inactivated and oxidized with exposure to sunlight. Many formulations that contain vitamin C have been produced; however, there has been little research on the efcacy of these products [47]. Vitamin E is another naturally occurring lipid-soluble antioxidant that has become a popular ingredient in many cosmeceuticals. Although there have been various claims regarding its role in reducing UV-mediated skin damage [48,49], to date no double-blind, placebo-controlled studies have been performed on human skin to support the effectiveness of these agents over time. Estrogen has been shown to play a central role in maintenance of collagen in women. Skin collagen has been shown to decline 30% over the rst 10 postmenopausal years in women; this loss was decreased with estrogen replacement [50,51]. Dunn et al [52] showed that estrogen replacement improved dry skin and wrinkling. Surgical treatments for facial rejuvenation Botulinum toxin Botulinum toxin has revolutionized the cosmetic approach for facial rejuvenation and is currently the most frequently used aesthetic treatment in the United States, with more than 1.1

148

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

million botulinum toxin injections performed last year [1]. Botulinum toxin A (BTX-A) was rst used by Scott [53] to treat strabismus; subsequently its use was expanded to various conditions characterized by muscle spasticity. Cosmetic use of BTX-A for treatment of glabellar rhytides was rst systematically reported by Carruthers and Carruthers in 1992 [54]. Glabellar rhytides, like other dynamic rhytides (forehead and crows feet), form perpendicular to the underlying musculature. Since Carruthers original publication, an increasing number of studies have documented its use for various off-label conditions, including crows feet [55], forehead lines [56], and brow position [5759]. There are seven dierent strains of botulinum toxinA to Gand of these, two strains have been used for cosmetic use: BTX-A (Botox, Allergan, Irvine, California) and BTX-B (Myobloc, Elan Pharmaceuticals, Dublin, Ireland). Cosmetic experience has been the greatest with BTX-A (Botox), the most potent serotype [60]. With the recent introduction of BTX-B (Myobloc), increasingly more studies have documented its efcacy in treating hyperfunctional facial lines [61 63]. Dysport, another type of BTX-A currently used in Europe and South America, is anticipated to be introduced to the United States soon. Different botulinum strains bind different presynaptic receptors of striated muscle neuromuscular junctions. The net effect for all strains is inhibition of the release of acetylcholine into the neuromuscular junction, thereby decreasing muscle contraction [60]. The onset of paralysis occurs approximately 1 to 2 days after injection, with maximal effect seen in 7 to 14 days and muscle recovery occurring in 3 to 6 months [64]. The degree and longevity of paralysis are noted to occur in a dose-dependent manner [65]. The use of BTX-A for treatment of upper facial wrinkles is well established [66,67]. Glabellar lines form in response to contraction of the glabellar complex. The relevant musculature of the glabellar complex includes the corrugator supercilii, procerus, orbicularis oculi, and depressor supercilii [68]. Technique and dosage for injection of the glabellar complex must be tailored to the individual. Often, 25 U can be used in a woman as a starting dose, whereas this dose is increased to 35 U in a man. In persons noted to have larger muscles or deeper lines, however, this dose may be increased to 50 U [65]. Injection sites can vary. Carruthers and Carruthers [69] advocate a pattern (Fig. 1). A critical landmark in making these injections is the orbital rim. It is important that all injections are above the orbital rim versus the eyebrow. When injecting the midpupillary line, care should be taken to stay 1 cm superior to this bony landmark. The overall incidence of eyelid ptosis is estimated at 5.4% and is believed to be technique dependent [67]. Blepharoptosis is the result of diffusion of BTX-A through the orbital septum, where it affects the upper eyelid levator muscle. Management of this complication with apraclonidine drops 0.5% (Iopidine, Alcon, Fort Worth, Texas) until the ptosis resolves (generally 2-4 weeks) is helpful [70]. Crows feet, formed by the of contraction of the lateral bers of the orbicularis oculi muscle, are also successfully managed with botulinum toxin [69,70]. A suggested technique injects 10 to 15 U BTX-A per side, which is delivered to either two or three sites. It is important to stay 1 cm lateral to the orbital rim when injecting. Having the patient squint can help in localizing the muscle. Unlike on the forehead and glabella, injections should be supercial (because of the supercial nature of the underlying muscle) and create a bleb directly under the skin, which helps to avoid hitting underlying blood vessels and causing bruising. Other important applications of BTX-A include treating forehead rhytides and producing a browlift. Horizontal forehead rhytides, formed by the contraction of the frontalis muscle, have been treated successfully with BTX-A [71,72]. Evaluation for brow ptosis is an important consideration before injecting the forehead. Brow position is determined in part by the underlying musculature. Brow elevation occurs with frontalis contraction and depression occurs via the action of the brow depressors, including the glabellar complex centrally and superiorlateral portions of the orbicularis oculi laterally. Older individuals, especially men, compensate for brow ptosis by using the frontalis muscle. Injection of the forehead in these individuals may result in profound brow ptosis. Once brow ptosis has been ruled out, a suggested technique uses 15 to 35 U distributed in four to six injection sites across the mid to upper forehead, taking care to stay at least 2.5 cm above the orbital rim. Several recent studies have showed medial and lateral browlifts by injecting the brow depressors [5759,73]. Some authors inject brow depressors when treating forehead rhytides to help avoid brow ptosis [71]. Other important reasons for esthetic application for BTX-A on the mid and lower face include treatment of hypertrophic orbicularis, bunny lines of the upper nasalis, nasal are,

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

149

Fig. 1. Patient with vertical glabellar rhytides produced at maximal frown before (A) and 30 days after (B) treatment with BTX-A. X denotes location of injection sites.

vertical lip rhytides, facial asymmetry, marionette lines, peau dorange chin, upper gum show, horizontal neck lines, and vertical platysmal bands [74]. Most of the complications associated with botulinum toxin are few, temporary, and anecdotal when used in a cosmetic setting. The lethal dose for BTX-A40 U/kg (2800 U for a 70-kg individual)is much more than used for esthetic purposes, which is generally less than 50 U [75]. Localized reactions of pain, edema, ecchymosis, and headache are generally short lived and related to the injection rather than a true allergic reaction to botulinum toxin [76]. Brow and eyelid ptosis are infrequent and can be avoided largely with proper technique and patient selection. Other exclusion criteria for use of botulinum toxin include pregnancy, active breast feeding, hypersensitivity to ingredients (albumin), neuromuscular disease, and medications that can potentiate the effects of botulinum toxin. These medications include aminoglycosides, penicillamine, quinine, and calcium channel blockers [76]. Filler substances The use of autologous, semisynthetic, and synthetic llers for soft-tissue augmentation represents an important treatment option in facial rejuvenation. These agents can be used for

150

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

correction of wrinkles, depressed scars, grooves, and improvement of facial contours. Over the past 10 years there has been much activity, with more than 30 new lling agents introduced [77]. This discussion focuses on some of the more established and promising agents. Autologous materials Autologous fat transplantation has been performed for more than 100 years [78]. The advantage of this technique is its appeal to patients who prefer to avoid the injection of a foreign substance. The disadvantage is the requirement of a separate procedure to harvest and prepare the fat. Controversy regarding longevity [79,80] and preparation of fat still exists [81]. Another autologous substance is dermal graft. Dermal grafts for scar revision, lip augmentation, and facial contouring has been performed successfully for years [82]. Dermal grafts are harvested from separate sites, such as old, less visible surgical scars or a retroauricular location, by excising the material and then de-epithelializing the epidermis. The graft is parceled and placed as needed. Bovine collagen Regarded as the gold standard of lling substances, the most commonly used lling substance is bovine-derived collagen (xenogenic) (Zyderm and Zyplast, Inamed, Santa Barbara, California) [83]. Experience with bovine collagen dates back to 1977, with FDA approval for Zyderm I, Zyderm II, and Zyplast occurring in 1981,1983, and 1985, respectively. Bovine collagen is harvested from a protected herd of cattle. It is pepsin digested to remove the more antigenic teleopeptides and nally is suspended in phosphate-buffered saline with 0.3% lidocaine. Zyderm I has a collagen concentration of 35 mg/mL, and Zyderm II has a concentration of 65 mg/mL. Zyplast has undergone cross-linkage with treatment by glutaraldehyde, which makes it more resistant to proteolytic degradation. Skin testing for potential allergic reactions is mandatory before injecting collagen. Approximately 3% of patients tested exhibit a localized hypersensitivity; 70% of these reactions manifest in the rst 48 to 72 hours [83]. Approximately 3% of patients who have negative results on their rst skin test have positive results with a second test [84]. It is recommended that two skin tests be performed. The rst skin test is performed on the volar forearm and should be read at 4 weeks, with some authors recommending an additional reading at 72 hours. The second test should be administered at 4 weeks and read 2 weeks later. Some clinicians perform this test on the contralateral arm [84], whereas others recommend performing the test near the hairline [85]. Although double testing does not eliminate positive reactions, it decreases the incidence and eliminates more severe reactions [86]. Zyderm I and II are designed for injection into the supercial papillary dermis for treatment of ne rhytides. Of the two products, Zyderm I is more forgiving, easier to inject (due to less viscosity), and less likely to cause beading if injected too supercially [83]. Zyplast was developed to correct deeper defects by placement into the midreticular dermis. All forms of collagen are temporary and require periodic maintenance (ie, every 3 to 6 months) [83]. Zyderm I and II typically are injected into ne rhytides located on the forehead, glabella, and perioral region and distensible acne scars. Uses for Zyplast include correction of deeper rhytides, marionette lines, and nasolabial folds and lip enhancement along the vermilion border (Fig. 2). Although botulinum toxin can produce impressive results for dynamic wrinkles, the same is not necessarily true for static wrinkles. Static wrinkles form in response to a combination of repetitive contractions from underlying musculature and the eects of extrinisic factors, such as photoaging (Fig. 3). Although botulinum toxin may ease these wrinkles, the only way to completely hide them is with a lling substance or ablative resurfacing. A combination approach of botulinum toxin with ller or resurfacing often can be used to produce gratifying results [87,88]. While achieving an outstanding safety record in more than 1 million patients, adverse events rarely occur [89]. Local bruising, herpetic reactivation, and bacterial infections can occur. Supercial necrosis, especially on the glabella, also has been reported, which has led to the recommendation of not injecting Zyplast in this area [90]. Occasional granulomatous allergic reactions may lead to erythematous papules, linear streaks, and, rarely, abscesses, which can be managed with topical and intralesional steroids. The claim that collagen is associated with connective tissue disease has not been supported by retrospective studies [91].

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

151

Fig. 2. Nasolabial folds before (A) and 30 days after (B) treatment with Zyplast.

152

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

Human-derived collagen The newest llers to receive approval from the FDA are CosmoDerm and CosmoPlast, which are manufactured by Inamed (Santa Barbara, California), the same company that produces Zyderm and Zyplast [92]. CosmoDerm and CosmoPlast contain collagen puried from human broblast cell culture. The cell line used for collagen production is qualied by extensive testing for viruses, retroviruses, and sterility. Because these products are human derived, skin testing is not required. Like Zyderm I and II, CosmoDerm is marketed in two concentrations and is indicated for correction of soft-tissue deformities, such as wrinkles and acne scars, and is intended for injection into the supercial papillary dermis [92]. CosmoPlast, like Zyplast, is treated with glutaraldehyde for cross-linking. It is indicated for correction of similar defects and is intended for injection into the mid to deep dermis. The added convenience of not having to perform a skin test is offset by the increased cost of these products. Hyaluronic acid products Perhaps the most anticipated newcomers on the horizon are the hyaluronic acid products. Hyaluronic acid is a glycosaminoglycan biopolymer that occurs naturally in the intercellular matrix of all species, which obviates the need for skin testing. The hydroscopic nature of

Fig. 3. Patient treated in same manner as patient in Fig. 2 before (A) and 30 days after (B) treatment with BTX-A. This photograph illustrates that despite treatment, persistent vertical glabellar rhytides respond to other modalities, including ller or resurfacing procedure.

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

153

hyaluronic acid aids in volumizing and dermal hydration. Restylane (Q-Med, Surrey, United Kingdom) is a hyaluronic acid ller produced by bacterial fermentation used for augmentation in Europe. A recent study of 158 patients treated with restylane for various anatomic locations, including glabella, oral commissural folds, nasolabial folds, and lips, found 80.4% of treated patients with moderate to marked improvement at 8 months based on photographic tests [93]. Histologic conrmation performed on 5 of these patients veried that the material was still present at 8 months [93]. Another hyaluronic acid ller, hylaform, which is derived from rooster combs, is also anticipated to perform similarly. Synthetic llers Artecoll is an injectable soft-tissue ller that is composed of 75% collagen and 25% polymethylmethacrylate microspheres (nonsilicone, carbon-based polymers). Artecolls manufacturer claims that the injectible is permanent, because the microspheres do not absorb into the body but become encapsulated after 2 to 4 months [77]. Artecoll recently received FDA approval with the provisions that a post-approval study for safety over 5 years be conducted, contraindications for lip augmentation be noted, mandatory physician training be provided, and an educational brochure be given to patients [94]. There have been reports of foreign body granulomas after implantation with artecoll [95,96]. Although the promise of a permanent ller is tempting, this must be balanced by the fact that once placed, it becomes difcult (if not impossible) to remove without great morbidity to the patient.

Laser and other treatments for facial telangiectasis and dyspigmentation There are various devices for the treatment of facial telangiectases and dyspigmentation, which is seen as the red, mottled look of photoaged skin. The intense pulsed light device, which emits a broad spectrum of 515 to 1200 nm, has been shown to be eective in the treatment of these conditions. In a recent retrospective review by Weiss et al [97], 80 randomly selected patients treated with an intense pulsed light device were shown to have persistent improvement 4 years after their last treatment based on features of telangiectases, blotchy pigmentation, and textural smoothness. Specically, 60% of persons with telangiectases and 64% with dyspigmentation (including solar lentigines) were noted to have improvement of more than 50%, and 40% noted more than a 50% improvement in smoothness (Fig. 4) [97]. Poikiloderma on the neck also has been treated successfully with the intense pulsed light device [98]. Other vascular lasers that target the chromophore oxyhemoglobin include the 532-nm potassium titany-phosphate (KTP), 595-nm pulse dye, 755-nm alexandrite, 800-nm diode, and the 1064-nm Nd:YAG. The most commonly encountered pigmented lesion in photoaging is the solar lentigo. The chromophore in solar lentigines is melanin. Melanin also can be treated successfully with some of the vascular lasers, including the 532-nm KTP, 595-nm pulse dye, 694-nm ruby, 755-nm alexandrite, 800-nm diode, and the 1064-nm Nd:YAG. As a general rule in selecting a laser, the longer wavelength penetrates deeper, which makes it effective for deeper targets, and the shorter wavelengths are better suited for more supercial targets.

Ablative resurfacing: chemical peels, lasers, dermabrasion All ablative resurfacing techniqueschemical, laser, dermabrasioncan be used to treat the surface irregularities of photodamage (Fig. 5). These techniques work on the premise of controlled depth injury of the skin, with subsequent wound healing. Generally there is a linear relationship, with depth of injury and resultant tissue remodeling, and an inverse relationship for subsequent healing. Wounding is divided into three levels of tissue injury: supercial depth (0.06 mm), which includes wounds from the stratum corneum to the papillary dermis; medium depth (0.50.6 mm), which includes wounds from papillary to upper reticular dermis; deep depth (0.610.8 mm), which includes wounds to the midreticular dermis.

154

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

Fig. 4. (A) Patient with prominent telangiectases before treatment with intense pulsed light. (B) After one treatment, patient shows remarkable improvement.

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

155

Certain preoperative considerations and postoperative complications are equally relevant to all types of ablative resurfacing by means of laser or abrasive. The risk of pigmentary alteration is of paramount importance. Four to 6 weeks after surgery, almost all patients experience a transient postinammatory hyperpigmentation on the malar prominence and forehead. This discoloration reliably fades with the use of topical hydroquinone preparations (4%8%) used from postoperative week 4 to week 12. A much lower percentage of patients (20%30%) develops permanent hypopigmentation that is believed to be the result of irreversible damage to the melanocytes. In these patients the treated areas become lighter than the untreated areas 12 to 18 months after surgery. This change is permanent and inuences most surgeons to perform fullface treatments so that any transition zone is camouaged by the shadow beneath the mandible. Partial treatments around the mouth and eyes may yield a noticeable raccoon-like mask or ring of pallor around the mouth. Patients with types III and IV skin experience the most unpredictable repigmentation. A loss of pigment is much more noticeable in darker skin types. Strict sun avoidance during the 6 to 8 weeks after surgery is critical in preventing uneven repigmentation. All patients who undergo ablative resurfacing should be given antiviral prophylaxis to prevent further scarring from postoperative herpetic ares. A dose of 500 mg valacyclovir taken twice a day for 10 to 14 days prevents new epithelial cells from becoming infected. Any increased pain or supercial ulcerations that develop 7 to 10 days after resurfacing should be treated presumptively with zoster doses of antiviral medications (1 g valacyclovir three times a day). Bacterial and yeast infections are much less likely, can produce painful, non-healing eruptions, and warrant appropriate cultures. The time required for postoperative re-epithelialization has decreased with the development of semipermeable dressing (Vigilon, second skin, Bard, Murray Hill, New Jersey), which provides a plan of critical humidity for the migration of epithelial cells. These dressings not only reduce healing time and postoperative erythema but also decrease burning and stinging after surgery. Dressings are secured with elastic netting and should be changed daily by the nursing sta for 3 to 5 days. Scarring can occur with any resurfacing treatment, ablative or nonablative. The deeper the resurfacing treatment, the greater the chance of scarring. Consequently, deep ablative procedures for deep defects are more likely to produce scarring than supercial resurfacing. Fortunately, the thick, oily skin in which acne scars occur tolerates much deeper corrective resurfacing than the thinner skin of the eyelids. The skin over the bony prominences of the forehead, mandible, and malar prominence has a propensity for hypertrophic scarring. Scars usually begin as areas of persisting erythema that initially can be treated with high-potency topical steroids or steroid-impregnated tape (urandrenalide tape). Palpable lesions should be treated with intralesional triamcinolone acetonide injections (540 mg/cc concentration) every 2 to 4 weeks until they resolve. The ash lamp pulsed dye laser is also helpful in reducing erythematous or hypertrophic scars by targeting the dilated vessels and reducing the vascular component of the inammatory phase of wound healing. Ablative lasers Through a concept known as selective photothermolysis, specic wavelengths of laser-produced energy create thermal injury in targeted tissue components, known as chromophores. If the pulse duration of delivered energy is less than the thermal relaxation time of the tissue (1 millisecond for skin), the targeted tissue is allowed to cool by 50%, which reduces unwanted collateral damage to surrounding tissue. Beyond pulse duration, computerized scanning devices regulate the delivery of laser energy to the skin surface in a controlled manner. Er:YAG (erbium: yttrium aluminum garnet) and CO2 lasers use these principles to ablate the epidermis and dermis supercially. These devices are able to control the depth of ablation reproducibly and precisely by adjusting the parameters of power (J/cm2), spot size, degree of pattern overlap, and number of laser passes. Compared with CO2 lasers (wavelength 10,600 nm), erbium lasers (2940 nm wavelength) have ten times greater afnity for the intracellular water chromophore of the epidermal and dermal cells. Because such a high percentage of energy is absorbed by the water chromophore, there is much less thermal injury with erbium lasers than with CO2 lasers. The erbium laser is well suited

156

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

Fig. 5. Patient with moderate photoaging before (A) treatment with CO2 and 30 days after (B) ablative resurfacing.

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

157

for resurfacing the thin skin around the eyes or nonfacial sites. With a complete lack of thermal injury, however, there is less collagen ber contraction to produce skin tightening and less hemostasis for deep resurfacing. The zone of thermal necrosis is greater with CO2 laser therapy. This thermal injury produces a zone of tissue necrosis (70100 C) around which is a zone of collagen denaturation (3770 C). This outer zone of thermal injury is believed to produce thermal contraction in skin tightening. The CO2 laser is ideally suited for heavy rhytides and undulated stretchable acne scars. Coherent ultra pulse laser with a computer pattern generator typically is used with the following parameters: power, 60 W; uence, 300 mJ; pattern shape, 3; pattern size, 9; overlap density, 5 to 6. These settings completely remove the epidermis in a single pass and visibly shrink and tighten the dermis upon the second pass. The third pass is sometimes helpful over heavily scarred areas of the midcheek. Once the yellow chamois of the dermis is noticed, the maximum number of safe passes has been performed. After each pass, saline-soaked gauze is used to remove the epidermal and dermal debris. After manual debridement, some surgeons prefer to sculpt remaining dermal irregularities and remove the remaining layer of thermal necrosis with the erbium laser. This process is believed to produce a smoother contour and promote wound healing by removing the remaining coagulum. Others surgeons have found that dermabrasion of the CO2 laser-treated surface similarly sculpts persisting blemishes and removes the coagulum of thermal necrosis. Blended or modulated CO2/erbium systems potentially offer the best properties of each laser: decoagulation and tissue tightening of the CO2 laser and reduced thermal necrosis and rapid wound healing of the erbium laser. Three systems are currently available: (1) Derma-K by Lumenis (New York, New York); (2) Contour by Sciton (Palo Alto, California); and (3) C03 by Cynosure (Chelmsford, Massachusetts). Side-by-side comparisons of these systems to purely CO2 lasers have yielded almost as dramatic effects on skin resurfacing, with fewer risks for hypopigmentation and slow healing.

Dermabrasion Mechanical ablative resurfacing can be achieved with a wire brush or diamond fraise driven by a hand-held electrical or pneumatic engine. For some surgeons, manual dermabrasion is also accomplished with wet/dry sandpaper wrapped around a syringe barrel or securely held around a folded piece of gauze. Typically, wire brush or coarse diamond fraise dermabrasion is ideally suited for xed or rigid scars and defects that do not dissipate upon stretching of the skin. Chickenpox scars, sharp-shouldered ice pick acne scars, and some deep rhytides are best resurfaced by sculpting and recontouring with mechanical dermabrasion. Similarly, the thick nodules or cobblestone pattern of severe solar elastosis is best treated with dermabrasion. By producing microlacerations in the papillary-reticular dermal junction, the wire brush allows nonthermal deep resurfacing with rapid healing and less persistent erythema than the thermal injury of multiple CO2 laser passes. Unfortunately, manual dermabrasion is much more technique dependent. With prociency, a consistent depth of injury can be reproduced to achieve dramatic improvement in scars. Some skin conditions, such as extensive full-face acne scars or bulbous rhinophyma, are best treated with a combination of laser and dermabrasive resurfacing. Most patients with numerous acne scars have some defects that are undulated and stretchable and other scars that are rigid and sharp shouldered. Both types of defects are best addressed by combination resurfacing, in which the CO2 laser is used to tighten the stretchable scars and is followed immediately by dermabrasion of the remaining rigid, ice pick scars (especially midcheek, chin, and glabella). Similarly, the large nodules of rhinophyma are frequently debulked with dermabrasion or a wire loop followed by CO2 laser recontouring of the alar rim. The symmetric tissue tightening produced by the CO2 laser reshapes the nasal tip and alar rim to give a natural-looking contour rather than a chiseled or carved appearance. A history of deep recurrent cysts or sinus tracts can produce sharp-shouldered crevices but are best surgically excised, subsized, or punch grafted before resurfacing. In these staged multimodality treatments, it is best to wait 6 to 8 weeks after the initial surgical excision before

158

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

resurfacing the revised scars. Many defects that extend into the deep dermis or the subcutaneous tissue can be addressed only by full-thickness excisional surgery, whereas surface irregularities are improved by ablative resurfacing. Chemical peels Various chemicals may be applied to the face and result in predictable levels of penetration. Treatment of photodamage is one of the main indications for use of a chemical peel. Several factors aect the depth of a peel, including type and concentration of chemical used, number of applications, duration of contact, pretreatment with a degreasing agent, concomitant use of retinoids or alpha hydroxy acids, anatomic location, pressure of application, and skin type. With experience, these variables become easier to account for, leading to the achievement of an optimal result. Supercial peeling agents Some common supercial peeling agents include alpha hydroxy acids (glycolic and lactic), beta hydroxy acids (salicylic), trichloroacetic acid 10% to 30%, and Jessners solution (combination of resorcinol, lactic, and salicylic acids). Supercial chemical peel indications include mild photodamage, lentigines, and mild acne. Supercial chemical peels also can be used in a repetitive manner when dealing with epidermal melasma or concern for hyperpigmentation, especially in darker skin types. Medium depth Medium depth chemical peeling agents include 50% trichloroacetic acid applied singly or combinations of 35% trichloroacetic acid in conjunction with solid CO2, Jessners solution, or 70% glycolic acid. Fifty percent trichloroacetic acid has fallen out of favor because complications such as scarring are more likely to occur. The most popular medium depth chemical peel is the Jessners solution/35% trichloroacetic acid combination (Monheit peel), which has proved to be equally effective as 50% trichloroacetic acid without the risks of scarring [99]. Indications for medium depth chemical peeling are moderate photodamage, pigmentary dyschromias (eg, melasma, solar lentigines), and actinic keratoses and as a blending agent for other resurfacing procedures. Medium depth chemical peels generally require 1 week of healing as the supercial skin sloughs off. Post-peel erythema usually lasts an additional few weeks. Deep chemical peeling The principal agent used for deep chemical peeling is the Baker-Gordon peel. This peel contains phenol, water, hexachlorophene, and croton oil. Although eective, this peel is not without its shortcomings. In addition to the increased risk for permanent hypopigmentation, there has been recent concern about the toxicity of croton oil. Croton oil is known to have cardiovascular and liver toxicity. Its role as a carcinogen also has been questioned [100]. For these reasons, laser resurfacing and dermabrasion are preferred alternatives. Nonablative rejuvenation Nonablative rejuvenation has emerged over the past few years as a potential new method of facial rejuvenation. Nonablative rejuvenation refers to the ability of a laser or light energy source to inict thermal damage selectively on the underlying dermis without disruption of the overlying epidermis. Many of these devices cool the overlying epidermis to protect the skin from the emitted energy. This is accomplished by a cooled hand-piece or dynamic cryogen device that delivers a cool spray. Some of these devices include the 585-nm pulsed dye laser, 1064-nm Qswitched Nd:YAG laser, 1320-nm long pulsed Nd:YAG laser, 1450-nm diode, 1540-nm erbium:glass laser, and the broadband light source or intense pulsed light device, which emits a continuous spectrum of 515 to 1200 nm. Selective thermal injury of chromophores, including hemoglobin, water-containing tissue (collagen), and melanin, is believed to induce neocollagenesis [101]. The prospect of dermal remodeling without the morbidity of traditional ablative surgery is attractive. Although many recent studies have documented the efcacy of these

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

159

devices in improvement of wrinkles [102105], the effect seems to be mild [106]. Two recent systematic reviews of the literature on nonablative rejuvenation have pointed out the difculty in drawing any denitive conclusions about its effectiveness for dermal remodeling [107,108]. A new technology that uses radiofrequency waves as the energy source for nonablative tissue tightening recently was developed. Like other nonablative modalities, simultaneous cooling is used to help protect the overlying epidermis from burning. In contrast to traditional nonablative laser and intense pulsed light devices, which use light, the radiofrequency device (Thermage, Hayward, California) uses radiowaves to generate heat in dermal tissue. In a small study of 15 patients, 14 showed some improvement of nasolabial folds, cheek contour, and mandibular and marionette lines [109]. Nonablative rejuvenation, with its minimal downtime, is a new and evolving modality that may produce more dramatic results. Currently this modality is not nearly as eective as traditional ablative techniques. Summary The options available to cosmetic surgeons for the treatment of the aging face are expanding at a rapid pace. Although any one modality may help, often a combination of approaches provides the most dramatic results. Whereas some of these techniques represent renements of old tools, others represent entirely new modalities (Box 1). To tailor the most effective treatment plan appropriately, the limitations and strengths of these various tools must be understood by the patient and physician. During the preoperative consultation, assessment of a patients expectations is critical when suggesting a treatment plan. By performing an assessment, the physician and patient can experience increased satisfaction because more optimal results are achieved. Box 1. Fine wrinkling Topical retinoids Alpha hydroxyl acids Nonablative resurfacing Chemical peels Laser resurfacing Dermabrasion Moderate to severe wrinkling Chemical peels Laser resurfacing Dermabrasion Face- and brow-lift Dynamic wrinkles Fillers Botulinum toxin Hyperpigmentation Topical hydroquinone Topical retinoids Alpha hydroxyl acids Chemical peels Intense pulsed light Laser targeting melanin (eg, ruby, Nd:YAG) Telangiectases Intense pulsed light Laser-targeting oxyhemoglobin (eg, pulse dye, diode)

160

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

References
[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] American Society of Plastic Surgeons. Cosmetic procedures top $7 billion in 2002. Cosmetic Surgery Times 2003;4. Arndt KA, Travers RL. The demographics of aging in the United States. Arch Dermatol 2002;138:14278. Kligman AM. Early destructive effects of sunlight on human skin. JAMA 1969;10:237780. Kang S, Fisher GJ, Voorhees JJ. Photoaging: pathogenesis, prevention, and treatment. Clin Geriatr Med 2001;17: 64359. Fisher JJ, et al. Mechanisms of photoaging and chronological skin aging. Arch Dermatol 2002;138:146270. Guinot C, et al. Relative contribution of intrinsic vs. extrinsic factors to skin aging as determined by a validated skin age score. Arch Dermatol 2002;138:145460. Monheit GD, Fulton J. Presented at the American Academy of Dermatology. New Orleans, March 25, 1999. Stegman SJ. A comparative histologic study of the effects of three peeling agents and dermabrasion on normal and sun-damaged skin. Aesthet Plast Surg 1982;6:1235. Gonzalez-Ulloa M, Flores ES. Senility of the face: basic study to understand its causes and effects. Plast Reconstr Surg 1965;36:23946. Patterson CN. The aging nose: characteristics and correction. Otolaryngol Clin North Am 1980;13:27588. Dmytryshyn J. Cervico-mandibular and cervico-mental angle problems: its clinical signicance. Facial Plast Surg 1987;4:18596. Fisher GJ, Wang Z, Datta SC, et al. Pathophysiology of premature skin aging induced by ultraviolet light. N Engl J Med 1997;337(20):141928. Rapaport MJ, Rapaport V. Preventive and therapeutic approaches to short- and long-term sun damaged skin. Clin Dermatol 1998;16:42939. Moriwaki S, Rav S, Tarone RE, et al. The effect of donor age on the processing of UV-damaged DNA by cultured human cells: reduced DNA repair capacity and increased DNA mutability. Mutat Res 1996;364:11723. Grossman L. Epidemiology of ultraviolet-DNA repair capacity and human cancer. Environ Health Perspect 1997; 105:92730. Alcalay J, Freeman SE, Goldberg, et al. Excision repair of pyrimidine dimmers induced by simulated solar radiation in the skin of patients with basal cell carcinoma. J Invest Dermatol 1990;95:5069. Kripke ML. Carcinogenesis: ultraviolet radiation. In: Freedbery IM, Eisen AZ, Wolff K, et al, editors. Fitpatricks dermatology in general medicine. New York: McGraw-Hill; 1999. p. 46572. Mahroos MA, Yaar M, Phillips TJ, et al. Effect of sunscreen application on UV-induced thymine dimmers. Arch Dermatol 2002;138:144085. Naylor M, Gasparro F. What you and your patients should know about sunscreens. Skin and Aging 1998;6:4450. Katsambas AD, Katoulis AC. Topical retinoids in the treatment of aging of the skin. In: Mallia C, Vitto JJ, editors. RheumaDerm. New York: Kluwer Academic/Plenum Publishers; 1999. p. 44782. Lever L, Kumar P, Marks R. Topical retinoic acid for treatment of solar damage. Br J Dermatol 1990;122:918. Leyden JJ, Grove GL, Grove MJ, et al. Treatment of photodamaged facial skin with topical tretinoin. J Am Acad Dermatol 1989;21:63844. Weiss JS, Ellis CN, Headington JT, et al. Topical tretinoin improves photoaged skin: a double-blind vehiclecontrolled study. JAMA 1998;259:52732. Sendagorta E, Lesiewicz J, Armstrong RB. Topical isotretinoin for photodamaged skin. J Am Acad Dermatol 1992;27:S158. Bhawan J, Gonzalex-Serva A, Nehal K, et al. Effects of tretinoin on photodamaged skin: a histologic study. Arch Dermatol 1991;127:66672. Ellis CN, Weiss JS, Hamilton TA, et al. Sustained improvement with prolonged topical tretinoin (retinoic acid) for photoaged skin. J Am Acad Dermatol 1990;23:62937. Grifths CEM, Russman AN, Majmudar G, et al. Restoration of collagen formation in photodamaged human skin by tretinoin (retinoic acid). N Engl J Med 1993;329:5305. Rafal ES, Grifths CEM, Ditre CM, et al. Topical tretinoin (retinoic acid) treatment for liver spots associated with photodamage. N Engl J Med 1992;326:36874. Phillips TJ, et al. Efcacy of 0.1% tazarotene cream for the treatment of photodamage: a 12-month multicenter, randomized trial. Arch Dermatol 2002;138:148693. AAD. Tazarotene cream superior to tretinoin treating photodamaged skin: doctors guide global edition. Available at: http://www.pslgroup.com/dg/22ed36.htm. Accessed June 26, 2003. Gladstone HB, Nguyen BA, Williams BS, et al. Efcacy of hydroquinone cream (USP4%) used alone or in combination with salicylic acid peels in improving photodamage on the neck and upper chest. Dermatol Surg 2000; 26(4):3337. Kligman AM. A new formula for depigmentating human skin. Arch Dermatol 1975;111:40. Balina LM, Graupe K. The treatment of melasma: 20% azelaic acid versus 4% hydroquinone cream. Pharmacol Ther 1991;30:893. Fulton DL, Moloney SJ, Troy WR, et al. A new stabilized ascorbic acid solution: percutaneous absorption and effect on relative collagen synthesis. J Cutan Aging Cosmetic Dermatol 1998;1:115. Nakagawa M, Kawai K, Kawai K. Contact allergy to kojic acid in skin care products. Contact Dermatitis 1995; 32:9. Van Scott EJ, Yu RJ. Control of keratinization with a-hydroxy acids and related compounds. Arch Dermatol 1974;110:58690.

[32] [33] [34] [35] [36]

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

161

[37] Van Scott EJ, Yu RJ. Hyperkeratinization, corneocyte cohesion and alpha hydroxyl acids. J Am Acad Dermatol 1984;11:86779. [38] Bernstein EF, Lee J, Brown DB, et al. Glycolic acid treatment increased type I collagen mRNA and hyaluronic acid content of human skin. Dermatol Surg 2001;27:42933. [39] Ditre CM, Grifn TD, Murphy GF, et al. Effects of a-hydroxy acids on photoaged skin: a pilot clinical, histologic, and ultrastructural study. J Am Acad Dermatol 1996;34(2):18795. [40] Stiller MJ, Bartolone J, Stern R, et al. Topical 8% glycolic acid and 8% L-lactic acid creams for the treatment of photodamaged skin: a double-blind vehicle-controlled clinical trial. Arch Dermatol 1996;132:6316. [41] Thibault PK, Wlodarczyk J, Wenck A. A double-blind randomized clinical trial on the effectiveness of a daily glycolic acid 5% formulation in the treatment of photoaging. Dermatol Surg 1998;24:5738. [42] Clark CP. Alpha hydroxyl acids in skin care. Clin Plast Surg 1996;23:4956. [43] Kurtzweil P. Alpha hydroxyl acids for skin care. FDA Consumer 1998;32:30. [44] Kagan V, Witt E, Goldman R, et al. Ultraviolet light-induced generation of vitamin E radicals and their recycling: a possible photosensitizing effect of vitamin E in skin. Free Radic Res Comm 1992;16:5164. [45] Darr D, Combs S, Dunston S, et al. Topical vitamin C protects porcine skin from ultraviolet radiation-induced damaged. Br J Dermatol 1992;127:24753. [46] Murray J, Darr D, Reich J, et al. Topical vitamin C treatment reduces ultraviolet B radiation-induced erythema in human skin. J Invest Dermatol 1991;96:587. [47] Kligman D. Cosmeceuticals. Dermatol Clin 2000;18(4):60915. [48] Dreher F, Denig N, Gabard B, et al. Effect of topical antioxidants on UV-induced erythema formation when administered after exposure. Dermatology 1998;198:525. [49] Eberlein-Konig B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-a-tocopherol (vitamin E). J Am Acad Dermatol 1998;38:458. [50] Brincat M, Moniz CF, Kabalan S, et al. Decline in skin collagen content and metacarpal index after the menopause and its prevention with sex hormone replacement. Br J Obstet Gynaecol 1987;94:1269. [51] Cala Alsinis J. Benets of hormone replacement therapy: overview and update. Int J Fertil Womens Med 1997; 42(Suppl 2):32946. [52] Dunn LB, Damesyn M, Moore AA, et al. Does estrogen prevent skin aging? Arch Dermatol 1997;133:33942. [53] Scott AB. Botulinum toxin injection into extraocular muscles as an alternate to strabismus surgery. Ophthalmology 1980;87:10449. [54] Carruthers JDA, Carruthers JA. Treatment of glabellar frown lines with C. botulinum-A exotoxin. J Dermatol Surg Oncol 1992;18:1721. [55] Carruthers A, Carruthers J. History of the cosmetic use of botulinum A exotoxin. Dermatol Surg 1998;24(11): 116870. [56] Carruthers A, Carruthers J. A prospective, double-blind, randomized, parallel-group, dose-ranging study of botulinum toxin type A in female subjects with horizontal forehead rhytides. Dermatol Surg 2003;29(5):4617. [57] Huang W, Rogachefsky AS, Foster JA. Browlift with botulinum toxin. Dermatol Surg 2000;26:5560. [58] Ahn MS, Catten M, Maas CS. Temporal brow lift using botulinum toxin. A. Plast Reconstr Surg 2000;105(3): 11369. [59] Matarasso A, Deva AK, et al. Botulinum toxin. Plast Reconstr Surg 2002;109(3):11917. [60] Huang W, Foster JA, Rogachefsky AS. Pharmacology of botulinum toxin. J Am Acad Dermatol 2000;43(2): 24959. [61] Baumann L, Black L. Botulinum toxin type B (myobloc). Dermatol Surg 2003;29(5):496500. [62] Sadick NS. Prospective open-label study of botulinum toxin type B (myobloc) at doses of 2,400 and 3,000 U for the treatment of glabellar wrinkles. Dermatol Surg 2003;29(5):5017. [63] Baumann L, Slezinger A, Vujevich J, et al. A double-blinded, randomized, placebo-controlled pilot study of the safety and efcacy of myobloc (botulinum toxin type B) puried neurotoxin complex for the treatment of crows feet: a double-blinded, placebo-controlled trial. Dermatol Surg 2003;29(5):50815. [64] Carruthers A, Carruthers J. Botulinum A exotoxin. In: Narins RS, editor. Cosmetic surgery: an interdisciplinary approach. New York: Marcel Dekker; 2001. p. 33353. [65] Hankins CL, Strimling R, Rogers GS. Botulinum A exotoxin for glabellar wrinkles: dose and response. Dermatol Surg 1998;24:11813. [66] Carruthers A, Carruthers J. Botulinum toxin type A: history and current cosmetic use in the upper face. Semin Cutan Med Surg 2001;20(2):714. [67] Carruthers A, Lowe NJ, Menter MA, et al. A multicenter, double-blind, randomized, placebo-controlled study of the efcacy and safety of botulinum toxin type A in the treatment of glabellar lines. J Am Acad Dermatol 2002; 46(6):8409. [68] Wieder JM, Moy RL. Understanding botulinum toxin: surgical anatomy of the frown, forehead, and periocular region. Dermatol Surg 1998;24(11):11724. [69] Carruthers A, Carruthers J. Clinical indications and injection technique for the cosmetic use of botulinum A exotoxin. Dermatol Surg 1998;24(11):118994. [70] Edelstein C, Shorr N, Jacobs J, et al. Oculoplastic experience with the cosmetic use of botulinum A exotoxin. Dermatol Surg 1998;24(11):120812. [71] Carruthers A, Carruthers J, Cohen J. A prospective, double-blind, randomized, parallel-group, dose-ranging study of botulinum toxin type A in female subjects with horizontal forehead rhytides. Dermatol Surg 1998;24(11):4617. [72] Keen M, Blitzer A, Aviv J, et al. Botulinum toxin A for hyperkinetic facial lines: results of a double-blind, placebocontrolled study. Plast Reconstr Surg 1994;94:9409.

162

C.B. Harmon, M.L. Hadley / Atlas Oral Maxillofacial Surg Clin N Am 12 (2004) 141162

[73] Huilgol S, Carruthers A, Carruthers J. The adjunctive use of botulinum toxin. Dermatol Surg 1999;25:3736. [74] Carruthers J, Carruthers A. Aesthetic botulinum A toxin in the mid and lower face and neck. Dermatol Surg 2003; 29(5):46876. [75] Arnon SS, Schechter R, Inglesby TV, et al., for the Working Group on Civilian Biodefense. Botulinum toxin as a biological weapon: medical and public heath management. JAMA 2001;285:105970. [76] Klein AW. Complications, adverse reactions, and insights with the use of botulinum toxin. Dermatol Surg 2003; 29(5):54956. [77] Klein AW. New lling substances on the horizon. In: Narins RS, editor. Cosmetic surgery: an interdisciplinary approach. New York: Marcel Dekker; 2001. p. 31331. [78] Skouge JW, Ratner D. Autologous fat transplantation. In: Coleman WP, Hanke CW, Alt CW, Asken S, editors. Cosmetic surgery of the skin. St. Louis: Mosby; 1997. p. 20616. [79] Nguyen A, Pasyk KA, Bouvier TN, et al. Comparative study of survival of autologous adipose tissue taken and transplanted by different techniques. Plast Reconstr Surg 1990;85(3):37886. [80] Ersek RA. Transplantation of puried autologous fat: a 3-year follow-up is disappointing. Plast Reconstr Surg 1991;87:219. [81] Rubin A, Hoefin SM. Fat purication: survival of the ttest [correspondence and brief communications]. Plast Reconstr Surg 2002;109(4):14634. [82] Swinehart JM. Dermal grafting. Dermatol Clin 2001;19(3):50922. [83] Klein AW. Filling substances: collagen. In: Narins RS, editor. Cosmetic surgery: an interdisciplinary approach. New York: Marcel Dekker; 2001. p. 193220. [84] Elson ML. The role of skin testing in the use of collagen injectable materials. J Dermatol Surg Oncol 1989;15(3):3013. [85] Klein AW. In favor of double testing. J Dermatol Surg Oncol 1989;15(3):263. [86] Elson ML. Soft tissue augmentation. Dermatol Surg 1995;21:401500. [87] Carruthers J, Carruthers A, Maberley D. Deep resting glabellar rhytides respond to BTX-A and Hylan, B. Dermatol Surg 2003;29(5):53944. [88] Fagien S. Extended use of botulinum toxin A in facial aesthetic surgery. Aesthet Surg J 1998;18:215. [89] Drake I, Dinehart SM, Farmer ER, et al. Guidelines of care for soft tissue augmentation: fat transplantation. J Am Acad Dermatol 1996;34:6907. [90] Bailin PL, Bailin MD. Collagen implantation: clinical applications and lesion selection. J Dermatol Surg Oncol 1988;14(Suppl 1):49. [91] McCoy JP, Waldinger TP, Cohen KA, et al. Connective tissue diseases and bovine collagen implants. J Am Acad Dermatol 1987;16:3158. [92] Department of Health and Human Services. CosmoDerm 1, human-based collagen, CosmoDerm 2, human-based collagen, CosmoPlast human-based collagen. Available at: http://www.fda.gov/cdrh/pdf/P800022S050a.pdf. Accessed June 26, 2003. [93] Duranti F, Salti G, Bovani B, et al. Injectable hyaluronic acid gel for soft tissue augmentation: a clinical and histological study. Dermatol Surg 1998;24:131725. [94] Anonymous. Summary. Presented at the General and Plastic Surgery Devices Panel Meeting. Gaithersburg, MD, February 28, 2003. [95] Requena C, Izquierdo MJ, Navarro M, et al. Adverse reactions to injectable aesthetic microimplants. Am J Dermatopathol 2001;23(3):197202. [96] Rudolph CM, Soyer HP, Schuller-Petrovic S, et al. Foreign body granulomas due to injectable aesthetic microimplants. Am J Surg Pathol 1999;23(1):1137. [97] Weiss RA, Weiss MA, Beasley KL. Rejuvenation of photoaged skin: 5 years results with intense pulsed light of the face, neck, and chest. Dermatol Surg 2002;28:11159. [98] Weiss RA, Goldman MP, Weiss MA. Treatment of poikiloderma of Civatte with an intense pulsed light source. Dermatol Surg 2000;26:8237. [99] Monheit GD. The Jessners + TCA peel: a medium depth chemical peel. J Dermatol Surg Oncol 1989;15:94550. [100] Bertolini T. Is the phenol-croton oil peel safe? Correspondence and brief communications. Plast Reconstr Surg 2002;110(2):7157. [101] Nelson JS, Majaaron B, Kelly KM. What is nonablative photorejuvenation of human skin? Semin Cutan Med Surg 2002;21(4):23850. [102] Zelickson BD, Kilmer SL, Bernstein E, et al. Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999;25:22936. [103] Fournier N, Dahan S, Barneon G, et al. Nonablative remodeling: clinical, histologic, ultrasound, imaging, and prolometric evaluation of a 1540 nm ER:glass laser. Dermatol Surg 2001;27:799806. [104] Goldberg DJ. Full-face nonablative dermal remodeling with a 1320 nm Nd:YAG laser. Dermatol Surg 2000;26: 9158. [105] Bitter PH. Noninvasive rejuvenation of photodamaged skin using serial, full-face intense pulsed light treatments. Dermatol Surg 2000;26:83542. [106] Goldberg D, Tan M, Sarradet MD, et al. Nonablative dermal remodeling with a 585-nm, 350-usec, ashlamp pulsed dye laser: clinical and ultrastructural analysis. Dermatol Surg 2003;29:1614. [107] Leffell DJ. Clinical efcacy of devices for nonablative photorejuvenation. Arch Dermatol 2002;138:15038. [108] Ang P, Barlow RJ. Nonablative laser resurfacing: a systematic review of the literature. Clin Exp Dermatol 2002;27: 6305. [109] Ruiz-Esparza J, Gomez, JB. The medical face lift: a noninvasive, nonsurgical approach to tissue tightening in facial skin nonablative radio frequency. Dermatol Surg 2003;29(4):32532; discussion 332.

S-ar putea să vă placă și