Minimally Invasive Treatments and Procedures for Ageing Skin

    80. CHAPTER 80 Minimally Invasive Treatments and Procedures for Ageing Skin N.J. Lowe Cranley Clinic, London, UK and UCLA School of Medicine, L...
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    80.

CHAPTER 80

Minimally Invasive Treatments and Procedures for Ageing Skin N.J. Lowe Cranley Clinic, London, UK and UCLA School of Medicine, Los Angeles, CA, USA

Types of skin ageing, 80.1

Volume replacement by fillers, 80.4

Intrinsic ageing, 80.1

Botulinum toxins—their use in controlling facial lines,

Extrinsic ageing, 80.2 Prevention of skin and facial ageing, 80.3 Skin rejuvenation procedures, 80.4

80.7

cosmetic indications, 80.10 Radiofrequency, 80.13

Chemical peels for improvement of facial ageing,

Combination minimally invasive treatment, 80.14

80.9

Introduction Over the last century there has been a dramatic increase in the ageing population in most developed countries. For example, it is expected that one in five Americans will be aged 65 years or older by the year 2030 (source 2000 USA census), a trend similar to that in most developed countries. Increased social pressure to look younger has led to great demand for effective cosmetic treatments for skin and facial rejuvenation. In particular, there has been an increase in what have been termed non-invasive and minimallyinvasive cosmetic treatments, that is treatments that avoid surgery and involve surface skin treatment such as lasers or peels, or a variety of injections [1]. Currently, most of those seeking these treatments are women, but an increasing number of men are considering rejuvenation treatments, and it is important for the practising dermatologist to be aware of the treatment options.

Types of skin ageing Skin ageing has historically been divided into intrinsic ageing [2], which will occur in all skin, whether or not exposed to external ageing factors, and extrinsic ageing, which is accelerated skin ageing due to external influences such as smoking and sun exposure [3].

Intrinsic ageing There are numerous factors that contribute to intrinsic ageing, including oxidative phosphorylation that generates destructive ‘superoxides’, which are thought to damage mitochondrial DNA and lead to progressive cell and tissue senescence [2]. Other factors Rook’s Textbook of Dermatology, 8th edition. Edited by DA Burns, SM Breathnach, NH Cox and CEM Griffiths. © 2009 Blackwell Publishing, ISBN: 978-1-4051-6169-5.

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Intense pulsed light and laser treatment—selection for

that can prematurely age skin intrinsically are inflammatory skin diseases, for example inflammatory acne which can lead to dermal injury and subsequent scarring. Collagen comprises up to 80% of the dry weight of ageing skin, and it is type 1 collagen, which comprises 70% of the total collagen content, whose larger diameter fibres provide the mechanical and stretch integrity of the skin. Type 3 collagen, which has narrow fibres, is also important. The quality and functionality of collagen substantially decreases with time [4]. The dermis is a connective tissue matrix of collagen housed in an elastin network. As part of the intrinsic ageing process there is a reduction of fibroblast activity in the dermis, and a decline in the ability of these cells to synthesize collagen and elastin con­ tributes to loss of elasticity and wrinkles. In combination with the decline in collagen synthesis there is altered expression of matrix metalloproteinases (MMP), which mediate collagen breakdown. As a result, intrinsic ageing and dermal thinning occurs; dermal collagen, elastin and glycosaminoglycans are all altered during the ageing process [5]. Skin collagen fibres do not appear to shrink with age, but the balance of their intermolecular cross-links changes, with an increase in cross-linking resulting in a stiffening of the skin. Ageing is also associated with a decrease in proteoglycan content, resulting in a reduction of the tensile strength of the skin. The elastic fibres show a progressive change, and there is evidence that elastin gene expression declines with age [5]. Accompanying these changes is a reduction of skin microvasculature, a reduction in activity but not in numbers of sebaceous glands, and a reduction of subdermal fat leading to skin laxity and change of facial profile (Fig. 80.1). Hyaluronic acid and other glycosaminoglycans decline during the intrinsic ageing process; a 50-year-old is estimated to have half the hyaluronic acid level of a youth. As an accompaniment to the dermal changes of intrinsic ageing, the epidermis becomes thinner, with a reduction in thickness of 10 to 50% between the ages of 30

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80.    Chapter 80: Minimally Invasive Treatments and Procedures for Ageing Skin Table 80.1  Some features of intrinsic skin ageing. Component

Function

Change with age

Fibroblasts

Synthesis and degradation of extracellular matrix (ECM)

Collagen

ECM component Dermal support

Elastin

ECM component Elasticity of skin UV protection—barrier and mechanical protection Cell signalling Melanin carrier Melanogenesis for UV radiation protection Endogenous free radical ‘quencher’ Antigen presentation

Decrease in number Decline in growth factor response Reduced synthesis of ‘new’ and decreased degradation of existing collagen Reduced microfibril content Elastin fragmentation Less proliferation and differentiation Reduced barrier function

Keratinocytes

Melanocytes

Langerhans’ cells

Fig. 80.1  Signs of intrinsic ageing—the patient shows brow ptosis, loss of cheek volume and malar ptosis, hollowness in the lower face, atrophic lips and marionette lines.

and 80. Mitotic activity of keratinocytes is reduced, and the epidermal transit time is increased. The orderly maturation of the epidermis becomes irregular. The corneocytes become less adherent and this produces a clinical appearance of roughness and scale. There is a flattening of the dermal–epidermal interface by as much as 35%, with increased skin fragility [4]. Table 80.1 summarizes some of the changes of intrinsic ageing.

Extrinsic ageing Extrinsic ageing, whose principal cause is ultraviolet radiation, results in changes in areas exposed to the environment such as the face, neck and dorsal hands. UVB (290–320 nm) penetrates to the lower epidermis, whereas UVA (320–400 nm) penetrates into the dermis and may be more responsible for some of the clinical changes associated with photoageing. Other factors that contribute to facial and skin ageing include repetitive facial expressions, leading to dynamic lines and rhytides. Gravity accelerates facial skin ageing, and this factor becomes more evident in the 30s when skin elasticity starts to decline [1]. Cigarette smoking also contributes to some of the characteristic changes of skin ‘coarseness’ and colour, or sallowness, which can be recognized in many who smoke 10 cigarettes or more daily for 10 years [6]. Signs of extrinsically aged skin include fine and coarse rhytides, macular and diffuse pigmentation, solar lentigines, increase in surface roughness, telangiectasiae, sallowness, loss of skin tone

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Decline in melanocyte number and life span

Reduction in number and morphological abnormalities

and solar keratoses, basal and squamous cell carcinomas, and melanoma—particularly superficial variants such as lentigo maligna. Structural changes that occur during extrinsic ageing include deficiency of collagen types 1, 3 and 7, which include the anchoring fibres and fibrillin in the papillary dermis. Fibrillin is thought to be one of the key structural support components. There is usually a decline in connective tissue support for dermal blood vessels, leading to vascular dilatation and the clinical appearance of telangiectasia [6]. A primary cause of UVA skin damage is oxidative damage mediated by a variety of reactive oxygen species [7]. It has been estimated that 50% of UV-induced damage results from the generation of these reactive oxygen species. Unlike intrinsic skin ageing, where collagen production declines, collagen synthesis is increased during UV radiation. There is a decrease in pro-collagen, which is absent 24 hours after exposure to sunlight. Increased production of matrix metalloproteinases, such as collagenase and gelatinase, results in collagen and dermal extracellular matrix degradation. The total collagen content of chronically sun-damaged skin is reported to be 20% less than non-solar exposed skin. Ultraviolet exposure also leads to changes in the structural organization and function of elastic tissues. Photodamage results in abnormally thickened, tangled and disintegrated elastic fibres, which form an amorphous mass [6]. It has been shown that small fluences of repetitive UVA radiation can produce abnormal pigment and vascular damage after 12 weeks of twice-weekly radiation [8]. UV radiation creates a favourable environment for angiogenesis and dermal blood vessel fragility. UVA radiation also damages DNA, cell membranes and proteins, leading to cell ageing and an increased risk of skin cancer. The changes of facial ageing are summarized in Table 80.2 and shown in Figs 80.1 & 80.2.

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Prevention of skin and facial ageing    80. Table 80.2  Some clinical effects of intrinsic and extrinsic facial ageing (see also Figs 80.1 and 80.2). Greater visibility of bony landmarks Increased rhytides Hollowing of the cheek and perioral area Deepening nasolabial folds Descent of facial fat pads Brow ptosis Upper eyelid laxity Infraorbital laxity and fat herniation Atrophy of lips Descent of the corners of the mouth Ptosis of the nasal tip Lower face and neck sagging and laxity Surface photodamage—lentigo, telangiectasia, solar comedones, rhytides Solar keratoses and skin cancers

Fig. 80.2  Signs of extrinsic ageing—surface photodamage, loss of volume, lentigo, sagging, dynamic rhyrid, atrophy of lips and solar elastosis.

References 1 Lowe NJ. Introduction. In: Lowe NJ, Carruthers A, Carruthers J et al., eds. Textbook of Facial Rejuventation. London: Informa Health Care, 2002: 1–2. 2 Gilchrest BA. Overview of skin aging. J Cutan Ageing Cosmet Dermatol 1988; 1: 1–3. 3 Kligman AM, Kligman LH. Photoaging. In: Fitzpatrick TB, Eisen AZ, Wolff K et al., eds. Dermatology in General Medicine. New York: McGraw-Hill, 1993: 2972–9. 4 Koehler MJ, Konig K, Elsner P et al. In vivo assessment of human skin aging by multiphoton laser scanning tomography. Opt Lett 2006; 31: 2879–81. 5 Tzaphlidou M. The role of collagen and elastin in aged skin. An image processing approach. Micron 2004; 35: 173–7. 6 McCullough JL, Kelly KM. Prevention and treatment of skin aging. Ann NY Acad Sci 2006; 1067: 323–31. 7 Runger TM, Kappes UP. Mechanisms of mutation formation with long wave ultraviolet light (UVA). Photodermatol Photo 2008; 24: 2–10. 8 Lowe NJ, Meyers DP, Wieder JM et al. Low doses of repetitive ultraviolet A induce morphologic changes in human skin. J Invest Dermatol 1995; 105: 739–43.

Prevention of skin and facial ageing Topical protection is the primary means of prevention of photodamage and should be a part of routine skin care. The first sunscreen was developed in 1928, and combined benzylsalicylate and

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benzylcinnamate [1]. Details of sunscreens and photoprotection are discussed in Chapter 29. In order to be effective a sunscreen must be both a UVB and UVA filter or reflector. The concept of sun protection factor (SPF) as an assay for protection is well established [2,3]. The methods of evaluating protection by sunscreens against UVA continue to be debated, but guidelines have been established in the UK using an in vitro UVA assay [4].

Topical treatments Photoprotection and topical treatments should be a key part of any antiageing programme. Tretinoin has been shown to be effective for improvement of both photodamaged and intrinsically aged skin [5]. It is a non-selective retinoic acid that increases epidermal thickness, promotes dermal collagen production and reduces its degradation, and inhibits UV-induced matrix metalloproteinases [6]. Other retinoids shown to produce objective clinical and histological changes include retinal, retinaldehyde and retinyl esters [7]. An important part of any topical retinoid treatment protocol is to control retinoid-induced skin irritancy while maintaining retinoid-induced skin rejuvenation. Choice of frequency of treatment and adequate skin moisturization are key variables. A range of non-prescription topical products have been claimed to possess some activity against skin ageing changes. These agents have been called cosmeceuticals, as they are not regulated as medicines by the Food and Drug Administration (FDA) in the USA, or the Medicines and Healthcare Products Regulatory Agency (MHRA) in the UK. Accurate assessment of their efficacy is often difficult because of limited available data. A recent study of the effects of retinol on intrinsically aged forearm skin has been presented as further evidence of the rejuvenation potential of topical retinoids for ageing skin, increased dermal matrix protein synthesis and glycosaminoglycan induction being noted in this study [8]. A variety of antioxidants have been incorporated in the formulation of some topical products. There is evidence that they are capable of reducing some photodamage, with a reduction of erythema and other markers of UV damage such as sunburn cell accumulation. Some topical vitamin C analogues have been shown to regulate collagen and tissue inhibitors of matrix metallopro­ teinase [9]. Other antioxidants employed include botanical agents, such as extracts of grape seed, pomegranate, green tea and raspberry [10]. It appears that polyphenol and isoflavone are also ingredients that may be effective for photoprotection. Coenzyme Q-10, which is a component of a mitochondrial electron transport chain acting as an antioxidant in the skin, has also been used as a protective antioxidant in cosmeceutical topical products [11]. A variety of synthetic plant derivatives such as N6furfuryladenine, and ferulic acid have also been employed in some cosmetic preparations because of their in vitro cell protective properties [12]. Further research is required to confirm the degree of in vivo human activity of these agents in different formulations for photoprotection and repair of ageing skin.

Oestrogen Oral oestrogen use in females is associated with a statistically significant decline in the risk of skin wrinkling, but interestingly

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80.    Chapter 80: Minimally Invasive Treatments and Procedures for Ageing Skin

not in atrophy [13]. These clinical changes are due to an increase in skin collagen content. Topical progesterone is associated with increased skin elasticity in pre- and postmenopausal women, suggesting a possible value for improving some aspects of ageing skin in women [14]. References 1 Shaath NA. Evolution of modern sunscreen chemicals. In: Lowe NJ, Shaath N, Pattack M, eds. Sunscreens, Development, Evaluation and Regulatory Aspects, 2nd edn. New York: Marcel Dekker, 1997: 3–33. 2 Food and Drug Agency. Sunscreen products for over the counter use: tentative final monograph. Federal Register (USA) 1993; 58: 28194–302. 3 European Cosmetic Toiletry and Perfumery Association. Colipa sun protection factor test method. Official Journal of the European Union L 151, 23/06/1993. 4 Diffey BL, Robson JA. A new substrate to measure sunscreen protection factors throughout the ultraviolet spectrum. J Soc Cosmet Chem 1989; 40: 127–33. 5 Kligman AM, Grove GL, Hirose R et al. Topical tretinoin for photoaged skin. J Am Acad Dermatol 1986; 15: 836–59. 6 Griffiths CEM, Finkel J, Tranfalgia MC et al. An in vitro experimental model for effects of topical retinoic acid in human skin. Br J Dermatol 1988; 129: 389–94. 7 Connor MJ, Ashton RE, Lowe NJ. A comparative study of the induction of epidermal hyperplasia by natural and synthetic retinoids. J Pharmacol Exp Ther 1986; 237: 31–5. 8 Kafi R, Kwak S, Shumacher WE et al. Improvement of naturally aged skin with vitamin A (retinol). Arch Dermatol 2007; 143: 606–12. 9 Pinnell SR, Murad S, Darr D. Induction of collagen synthesis by ascorbic acid. A possible mechanism. Arch Dermatol 1987; 123: 1684–6. 10 Katiyar SK, Ahmad N, Mukhtar H. Green tea and skin. Arch Dermatol 2000; 136: 989–94. 11 Hoppe Y, Bergemann J, Diembeck W et al. Coenzyme Q10, a cutaneous antioxidant and energizer. Biofactors 1999; 9: 371–8. 12 Lin FH, Lin JY, Gupta JD et al. Ferulic acid stabilizes a solution of vitamins C and E and doubles its photoprotection of skin. J Inv Derm 2005; 125: 826–32. 13 Sator PG, Sator MO, Schmidt JB et al. A prospective, randomized, double blind, placebo controlled study on the influence of hormone replacement therapy on skin ageing in post menopausal women. Climacteric 2007; 10: 320–34. 14 Holzer G, Riegler E, Honigsmann H et al. Effects and side-effects of 2% progesterone cream on the skin of peri-and post-menopausal women: results from a double-blind, vehicle-controlled, randomized study. Br J Dermatol 2005; 153: 626–34.

Skin rejuvenation procedures There are now many non-invasive or minimally invasive treatments for skin rejuvenation. The remainder of this chapter will discuss some of the more commonly accepted options (Table 80.3).

Volume replacement by fillers Volume replacement using a variety of dermal fillers is designed to address the subcutaneous atrophy and facial hollows that often accompany ageing. A number of soft-tissue fillers are now employed, ranging from non-biodegradable, which may be permanent, to more transient, biodegradable fillers [1]. It is important to know that these fillers have different risks of adverse events [2], which are related to the skill of the injector and the intrinsic properties of the filler [2–4].

Categories of dermal fillers Fillers can be categorized according to their source: • Autogeneic, e.g. fat, autologous plasma, autologous collagen • Allogeneic, e.g. human cadaver tissue, human fibroblast cell culture

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Table 80.3  Some treatment options for facial rejuvenation. Objective

Treatment options

Superficial rejuvenation

Topical antiageing creams Superficial peels Microdermabrasion Intense pulsed light Non-ablative facial Rejuvenation (lasers) Laser and fractional resurfacing Botulinum toxin type A injections Fillers

Dermal remodelling

Muscle relaxation Soft tissue augmentation Volume replacement Deeper rejuvenation

Fractional resurfacing—carbon dioxide fraxel Carbon dioxide lasers Medium peels Deep peels

• Xenogeneic, e.g. collagen, usually derived from bovine or porcine sources; hyaluronic acid products derived from animal sources or the results of bacterial fermentation • Synthetic products, e.g. silicone, polymethyl methacrylate, hydroxyapatite, carboxy cellulose, poly-l-lactic acid, polyacrylamide.

Specific dermal fillers Xenogeneic bovine collagen has been used for over 20 years, and results can last from 3 to 12 months, depending on the choice of bovine collagen [5]. The duration depends on the site and type of injection selected. Because of a risk of delayed cutaneous allergic reactions with bovine collagen it is advised that double skin testing is carried out, as it has been estimated that approximately 3% of injected patients will develop delayed nodular reactions [2,6], including necrotic reactions [7]. Products developed over the last 10 years include a variety of hyaluronic acid derivatives. In some parts of the world there is little regulatory requirement for testing of these new fillers before they are used on patients. The original hyaluronic acid filler was derived from rooster combs [7], but this has now been largely superseded by materials produced by bacterial fermentation and stabilization using proprietary processes [8]. The duration of benefits from hyaluronic acids fillers for correction of nasolabial folds is usually between 6 and 12 months, but it is less when used for lip augmentation [9] (Figs 80.3 & 80.4). The duration of benefit in an individual will depend on several factors, including formulation of the hyaluronic acid filler, depth of injection and laxity of skin injected. Side effects include immediate oedema, haematoma, delayed allergic reactions, nodules, vascular occlusion and infections, including, rarely, atypical mycobacteria [2,3]. There are still occasional delayed reactions to these fillers, leading to inflammatory nodule formation, although their frequency has declined significantly over the past 5 years [2,10]. Other volume replacements that give immediate filling include calcium hydroxyapatite, which is useful as deep injections for

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Skin rejuvenation procedures    80.

Fig. 80.3  Lip augmentation: before (a) and (b) after 1 cc of hyaluronic acid filler.

(a)

(b)

Fig. 80.4  Before (a) and (b) following 0.75 cc of hyaluronic acid filler to the nasolabial folds.

(a)

(b)

volume replacement of cheeks and deep nasolabial folds [11]. Another group of injectables that increase the collagen matrix, ground substance and dermal elastic formation by stimulating dermal fibroblast activity include poly-l-lactic acid (PLLA). This is injected as a dilute suspension which dissolves within the dermis and subcutaneous levels, inducing fibroplasia and increasing dermal and subcutaneous thickness. Originally, PLLA was used to improve the facial lipodystrophy often associated with earlier types of antiretroviral therapy [12]. It was subsequently shown to be effective for correcting facial volume loss in the ageing face and for atrophic scars. The main side effect is nodule formation, most commonly in perioral and periorbital areas, and these are therefore areas which should be avoided with PLLA [12]. It is most useful for nasolabial folds and mid-cheek sites [13]. PLLA has also been used for atrophic scar improvement [14].

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Another recent approach has been to use allogeneic humanderived fibroblasts from a single source of neonatal tissue; this procedure is in the early stages of research and development [15]. Safety phase studies have shown increased dermal and epidermal thickness, and no toxicity. Further studies are proceeding. An autologous filler that has been used for many years is fat, harvested from the patient and processed with filtration plus cleansing, or simply reinjected. A debate as to the efficacy of these different methods of fat replacement injections continues. One problem is variable duration of benefit, and it has been suggested that this is site specific, with the cheek area having the best retention of injectable fat [16]. Post-injection oedema and bruising is temporary but can last several weeks [16]. One study suggested that fresh autologous fat transfer has good viability compared with refrigerated or frozen fat storage and later injection [17].

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80.    Chapter 80: Minimally Invasive Treatments and Procedures for Ageing Skin Table 80.4  Adverse reactions to dermal fillers. Early adverse events (occurring up to several days post-treatment)

Delayed adverse events (occurring from weeks to years post-treatment)

Injection site reactions:   erythema   oedema   pain/tenderness   bruising   pruritus Infection:   erythema   oedema   pain/tenderness   pustules   nodules   abscesses Hypersensitivity:   erythema   oedema   pain/tenderness Lumps caused by maldistribution Discoloration:   erythema   hypochromia   hyperpigmentation Local tissue necrosis caused by vascular occlusion

Infection (e.g. atypical mycobacterial):   erythema   oedema   pain/tenderness   nodules   systemic responses to infection Granulomatous inflammation:   varying from subclinical histological changes to disfiguring nodules Migration of filler Hypersensitivity:   aseptic abscess Persistent hyperpigmentation Persistent scarring

Fat is best used for deeper volume replacement of the face or localized areas of fat atrophy [16].

Adverse reactions (Table 80.4) Adverse reactions to fillers can be described in terms of: • Clinical seriousness • Aesthetic relevance • Immediate versus delayed onset • Causality: expected procedure related events; events related to improper technique; reactions to the product. Reactions can be attributed to the procedure itself, procedural technique and the agent injected. Some of these reactions are preventable, whereas others are inevitable; most are mild and transient. Improving product formulations, altering the concen­ tration of product injected or changing injection technique can dramatically reduce the incidence of adverse reactions. Since its reformulation in mid-1999, the biologically engineered hyaluronic acid filler, Restylane, elicits less than one allergic reaction in 1600 treatments. There are over 85 different hyaluronic acid fillers currently available in Europe. Skin reactions with PLLA (New Fill/Sculptra) are considerably less likely if a greater dilution and deeper injection technique are employed. References 1 Murray CA, Zloty D, Warshawski L. The evolution of soft tissue fillers in clinical practice. Dermatol Clin 2005; 23: 343–53. 2 Lowe NJ, Maxwell CA, Patnaike R. Adverse reactions to dermal fillers: review. Dermatol Surg 2005; 31: 1616–25. 3 Andre P, Lowe NJ, Parc A et al. Adverse reactions to dermal fillers: a review of European Experiences. J Cosmet Laser Ther 2005; 7: 171–6.

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4 Christensen L, Breiting V, Janssen M et al. Adverse reactions to injectable soft tissue permanent fillers. Aesthetic Plast Surg 2005; 29: 34–48. 5 Cooperman LS, Mackinnon V, Bechler G, Pharriss BB. Injectable collagen: a six year investigation. Aesthetic Plast Surg 1985; 9: 145–51. 6 DeLustro F, Smith ST, Sundsmo J et al. Reaction to injectable collagen: results in animal models and clinical use. Plast Reconstr Surg 1987; 79: 581–92. 7 Hanke CW, Higley HH, Jolivette DJ et al. Abscess formation and necrosis after treatment with Zyderm and Zyplaso collagen implant. J Am Acad Dermatol 1991; 25: 319–26. 8 Duranti F, Salti G, Bovani B. Injectable hyaluronic acid gel for soft tissue augmentation. A clinical and histological study. Dermatol Surg 1998; 24: 1317–25. 9 Manna F, Dentini M, Desideri P et al. Comparative chemical evaluation of two commercially available derivatives of hyaluronic acid (hylaform from rooster combs and restylane from streptococcus) used for soft tissue augmentation. J Eur Acad Dermatol Venereol 1999; 13: 183–92. 10 Lowe NJ, Maxwell CA, Lowe P et al. Hyaluronic acid skin fillers: adverse reactions and skin testing. J Am Acad Dermatol 2001; 45: 930–3. 11 Alam M, Yoo SS. Technique for calcium hydroxylapatite injection for correction of nasolabial fold depressions. J Am Acad Dermatol 2007; 56: 285–9. 12 Valantin MA, Aubron-Olivier C, Ghosn J et al. Polylactic acid (New-Fill) to correct facial lipatrophy in HIV-infected patients: results of the open-label study VEGA. AIDS 2003; 17: 2471–7. 13 Lowe NJ. Appropriate use of poly-l-lactic acid and clinical considerations. J Eur Acad Dermatol Venereol 2006; 20: 2–6. 14 Beer K. A single center, open-label study on the use of injectable poly-l-lactic acid for the treatment of moderate to severe scarring from acne or varicella. Dermatol Surg 2007; 33 (Suppl. 2): S159–67. 15 Lowe NJ, Lowe PL, Patuaik R, St Clair Roberts J. A phase 1 study of 1CX-Rhy, a suspension of allogeneic human dermal fibroblasts. J Invest Dermatol 2007; 127: Abstract. 254. 16 Donofrio LM. Panfacial volume restoration with fat. Dermatol Surg 2005; 31: 1496–505. 17 Lidagoster MI, Cinelli PB, Levee EM, Sian CS. Comparison of autologous fat transfer in fresh, refrigerated, and frozen specimens: an animal model. Ann Plast Surg 2000; 44: 512–5.

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Skin rejuvenation procedures    80. Table 80.5  Available botulinum neurotoxins. Product

Toxin type

Toxin mol wt (kDa)

pH

Approved in Europe and USA for cosmetic use

Approved for hyperhidrosis in UK, Europe, USA

Approved for medical indications (dystonia, blepharospasm etc.) in Europe

Botox Dysport Xeomin Neuronox Myobloc/Neurobloc

A A A A B

900 500–900 150 Unknown 300–500

~7 ~7 ~7 6.8 ~5.6

Yes No No No No

Yes No No No No

Yes Yes Yes No Yes

Botulinum toxins—their use in controlling facial lines The first medical use of botulinum neurotoxin was described by Dr Alan Scott during the 1970s when he used a botulinum toxin type A (BTX-A) for reducing over-activity of selected periocular muscles in patients with strabismus [1–3]. Following this observation botulinum neurotoxins have been increasingly studied for a wide variety of therapeutic and aesthetic uses. Double-blind controlled studies of BTX-A for reduction of upper facial lines in the USA have shown benefit of approximately 4 months’ duration [4,5]. These initial observations were followed by double-blind, placebo-controlled studies of several hundred patients performed in the USA, which demonstrated that BTX-A was safe and effective for reducing the severity of glabellar lines (lower forehead vertical frown lines) [6,7]. Significant improvement was observed as early as a few days after treatment, and the mean duration of improvement was in excess of 4 months using appropriate doses of BTX-A, which were initially 20 units for lower forehead frown lines. Several other studies confirm that BTX-A is also effective for lateral periorbital lines, often known as ‘crow’s feet’ [8] and also rhytides of the infraorbital area [9]. There are two main serotypes of botulinum toxins used clinic­ ally—the most commonly used being botulinum toxin type A (BTX-A) (Table 80.5). Type B botulinum toxin (BTX-B) has a much shorter duration of effect than BTX-A, but is occasionally used if therapeutic resistance is observed to BTX-A. Other clinical studies have confirmed that both type A and type B botulinum toxins are effective at reducing facial lines [10], as well as excessive sweating in areas such as the axillae [11,12]. BTX-A treatment for axillary hyperhidrosis has been approved by the MHRA in the UK, and regulatory agencies in numerous other countries including the FDA in the USA. The mode of action of BTX-A is by rapid inhibition of acetylcholine release at the neuromuscular junction. As a result, BTX-A causes localized, reversible muscle relaxation [1], and because some facial lines result from repetitive contraction of underlying muscles this produces a reduction of facial lines [4,5,7,8]. The mode of action against hyperhidrosis (which is covered in more detail in Chapter 44) is again the result of inhibition of release of acetylcholine, which is one of the neurotransmitters for emotional, non-thermoregulatory sweating [11,12]. The sites of injection used to improve facial lines, and therefore some signs of facial ageing, are most commonly: upper face—horizontal forehead lines, vertical forehead lines, supraorbital lines,

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periorbital (crow’s feet) lines, infraorbital lines, paranasal lines; lower face—perioral lines, vertical rhytides above the upper lip and turning down of the angles of the mouth (melomental folds) [13]. Vertical neck bands produced by platysmal muscle activity can also be reduced by the use of BTX-A [14]. Two different commercial types of BTX-A have been available in Europe since the 1990s. They are produced by different bacteria, with differing fermentation and purification processes, and have different potency and diffusion. Dilution and dosing have been investigated, and estimated conversion ratios of one type of BTXA to the other have been proposed [15,16]. Side effects from BTX-A are local at doses used for aesthetic indications, for example bruising and brow and/or eyelid ptosis. They are usually the result of inexpert injection of BTX-A—for example, injection of too high a dose of BTX-A into the lower lateral forehead may result in both brow and upper eyelid ptosis. Injection too low in the infraorbital area may result in upper lip and lower facial weakness. Facial asymmetry may occur. These side effects are usually temporary, but can be of understandable concern to patients [17]. The physician injecting BTX-A should be trained to try to avoid these problems. Other side effects are extremely uncommon. A rare problem is that of resistance to BTX-A, the mechanism of which is unknown, but may involve antibodies blocking the uptake or action of BTX-A.

Combination treatments with BTX-A Combination treatments are selected for appropriate patients to rejuvenate the ageing face [17]. An example of a combination treatment is administration of BTX-A prior to use of either resurfacing lasers [18] (Fig. 80.5) or fractionated rejuvenation lasers (p. 80.11). The BTX-A is ideally delivered at least 1 week prior to the laser; this enables the hyperactive muscle action to be diminished thereby reducing the facial lines. In addition, as one theory of skin rejuvenation with these laser systems is the stimulation of neocollagenesis, it is likely that a less folded skin following BTX-A leads to more uniform neocollagenesis. The effects of combined BTX-A injections and lasers have been confirmed as being superior to placebo injections and laser alone [18]. Another situation where combination treatments are useful is the use of BTX-A and dermal fillers in problems such as deep vertical lower forehead lines. Here, BTX-A alone will improve, but not clear, the deep furrows that are present in some patients. The

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80.    Chapter 80: Minimally Invasive Treatments and Procedures for Ageing Skin

(a)

(a)

(b)

(b)

use of BTX-A plus temporary filler can give a more prolonged effect than using the filler alone [19]. In a similar mechanism, the use of BTX-A to the upper lip area together with filler in the upper lip can provide adjunctive benefit in the correction of upper lip lines. Dermal fillers and BTX-A can also be combined in lower facial areas, where the BTX-A is injected into areas such as depressor angulae oris and mentalis muscles and the filler is injected into melomental folds. Figure 80.6 shows the effect of BTX-A injected in the periorbital area, thereby reducing the intensity of the periorbital rhytides.

References 1 Scott AB. Development of botulinum toxin therapy. Dermatol Clin 2004; 22: 131–3. 2 Scott AB, Rosenbaum A, Collins CC. Pharmacologic weakening of extraocular muscles. Invest Ophthalmol 1973; 12: 924–7. 3 Scott AB. Botulinum toxin injection into extraocular muscles as an alternative to strabismus surgery. Ophthalmology 1980; 87: 1044–9. 4 Keen M, Blitzer A, Aviv J et al. Botulinum toxin A for hyperkinetic facial lines: results of a double-blind, placebo-controlled study. Plast Reconstr Surg 1994; 94: 94–9. 5 Lowe NJ, Maxwell A, Harper H. Botulinum A exotoxin for glabellar folds: a double-blind, placebo-controlled study with an electromyographic injection technique. J Am Acad Dermatol 1996; 35: 569–72. 6 Carruthers JA, Lowe NJ, Menter MA et al. for the BOTOX Glabellar Lines I Study Group. A multicenter, double-blind, randomized, placebo-controlled study of the efficacy and safety of botulinum toxin type A in the treatment of glabellar lines. J Am Acad Dermatol 2002; 46: 840–9.

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Fig. 80.5  (a) Pre-treatment shows photodamage, with solar lentigo and dynamic rhytides (crow’s feet). (b) Post-treatment with botulinum toxin A to crow’s feet, plus ultrapulsed carbon dioxide laser resurfacing full face.

Fig. 80.6  Reduction of lateral periorbital lines (crow’s feet) after injection of BTX-A into the lateral orbicularis oculi muscle; (a) pre-treatment; (b) post-injection. 7 Carruthers JD, Lowe NJ, Menter MA et al. for the BOTOX Glabellar Lines II Study Group. Double-blind, placebo-controlled study of the safety and efficacy of Botulinum toxin type A for patients with glabellar lines. Plast Reconstruc Surg 2003; 112: 1089–98. 8 Lowe NJ, Ascher B, Heckmann M et al. for the Botox Facial Aesthetics Study Team. Double-blind, randomized, placebo-controlled, dose-response study of the safety and efficacy of botulinum toxin type A in subjects with crow’s feet. Dermatol Surg 2005; 31: 257–62. 9 Flynn TC, Carruthers JA, Carruthers JA, Clark RE II. Botulinum A toxin (BOTOX) in the lower eyelid: dose-finding study. Dermatol Surg 2003; 29: 943–50. 10 Lowe NJ, Yamauchi PS, Lask GP et al. Botulinum toxin types A and B for brow furrows: preliminary experiences with type B toxin dosing. J Cosmet Laser Ther 2002; 4: 15–8. 11 Lowe NJ, Campanati A, Bodokh J et al. The place of botulinum toxin type A in the treatment of focal hyperhidrosis. Br J Dermatol 2004; 151: 1115–22. 12 Heckmann M, Plewig H, for the Hyperhidrosis Study Group. Low-dose efficacy of botulinum toxin A for axillary hyperhidrosis: a randomized, side-by-side, open-label study. Arch Dermatol 2005; 141: 1255–9. 13 Lowe NJ. Introduction. In: Lowe NJ, Carruthers A, Carruthers J et al., eds. Textbook of Facial Rejuvenation. London: Informa Health Care, 2002: 1–2. 14 Matarasso A, Matarasso SL, Brandt FS, Bellman B. Botulinum A exotoxin for the management of platysma bands. Plast Reconstr Surg 1999; 103: 645–52. 15 Ascher B, Zakine B, Kestemont P et al. A multicenter, randomized, double-blind, placebo-controlled study of efficacy and safety of 3 doses of botulinum toxin A in the treatment of glabellar lines. J Am Acad Dermatol 2004; 51: 223– 33. 16 Lowe P, Patnaik R, Lowe N. Comparison of two formulations of botulinum toxin type A for the treatment of glabellar lines: a double-blind randomized study. J Am Acad Dermatol 2006; 55: 975–80. 17 Lowe NJ. When and how to combine treatments. In: Lowe NJ, Carruthers A, Carruthers J et al., eds. Textbook of Facial Rejuvenation. London: Informa Health Care, 2002: 322–5.

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Skin rejuvenation procedures    80. 18 Yamauchi P, Lask GL, Lowe NJ. Botulinum toxin type A gives adjunctive benefit to periorbital laser resurfacing. J Cosmet Laser Ther 2004; 6: 145–8. 19 Carruthers J, Carruthers A, Maberley D. Deep resting glabellar rhytides respond to BTX-A and hylan B. Dermatol Surg 2003; 29: 539–44.

Every practitioner using peels in their practice should become trained and familiar with the particular peel they will be using.

Chemical peels for improvement of facial ageing

The density of appendigeal structures, such as pilosebaceous glands, will also govern the safety and healing of the skin following deeper chemical peels. An area such as the face, which has a much higher density of pilosebaceous structures, generally responds in a more predictable way to chemical peels than the neck, chest and limbs. Superficial peels should only be used in areas where there are minimal sebaceous appendages, that is most areas other than the face. Medium-depth peels can be used on the face, but care should be exercised in using them on other parts of the body. Because of the relatively low density of skin appendigeal structures, impaired healing can occur in these non-facial areas, resulting in an increased risk of scarring and pigmentary changes.

Chemical peels have been used for many years for skin surface rejuvenation, and treating irregular pigmentation and superficial scars [1]. A limiting factor is the depth of penetration of the different chemicals used for skin peeling. Another important factor is the toxicity of the chemical, for example phenol or 50% trichloroacetic acid are considerably more toxic to the skin than 50% buffered glycolic acid peels [2,3]. Even in expert hands there are some patients who will have undesirable results from chemical peels. These may include changes in pigmentation, for example hypopigmentation, which can be permanent, and hyperpigmentation, which can be long-lasting, and may be permanent and scarring. More superficial peels, for example glycolic acid, lactic acid [3] and Jessner’s peels, will accelerate epidermal shedding, but other more aggressive peels can chemically destroy epidermis and progressive layers of the dermis by protein coagulation and cell lysis. The main classification of peels is usually based on the expected depth and severity of the peel—a commonly used classification being superficial peels, medium-depth peels and deep peels [2–4]. Examples of the peeling agents leading to different severities of peel are listed in Table 80.6. The nature of the chemical influences the depth of peel; for example, lactic acid is usually a very superficial peeling agent and 50% trichloroacetic acid (TCA) is a much deeper peeling agent [2,3]. Another factor that affects the peel is skin preparation with topical retinoids, which is felt to increase the uniformity of the peel. It alters the stratum corneum barrier, and enhances the pene­ tration of some peeling agents by altering epidermal and stratum corneum morphology. It is possible to change a superficial-depth glycolic acid peel into a medium-depth peel by altering the percutaneous penetration characteristics of the skin with agents such as tretinoin and other peeling agents applied prior to the final peel [5,6]. Superficial peels include a combination of resorcinol, lactic acid and salicylic acid, known as Jessner’s peel. This is useful for abnormal superficial pigment, fine rhytides and very superficial scars. It can be reapplied numerous times over the treatment session [7].

Site dependence

Skin phototype and chemical peels Skin phototype (Table 80.7) is of key importance in chemical peel selection. Because of the risks of facial pigmentation disorders following the peels it is important that skin phototypes III and above are treated with peels that are not likely to result in hypopigmentation [7]. Patients with skin phototype III and above will always have some hyperpigmentation following peels. This is usually transient, but often requires pre- and post-treatment therapy with tretinoin 0.25% or 0.5% creams for 6 weeks prior to the peel, often together with skin lightening preparations such as hydroquinone. Post-peel treatment with these agents is usually begun after complete re-epithelialization and stabilized erythema, several weeks after the peel. This post-peel treatment may reduce the degree of hyperpigmentation [4] (Fig. 80.7). The superficial chemical peels remain valuable for treating milder skin ageing problems and as adjunctive treatments in diseases such as acne. The medium-depth and deeper chemical peels have now largely been replaced by laser skin rejuvenation, as described below in this chapter. There is some agreement that lasers lead to a more controlled impact on the skin and are not dependent on the vagaries of chemical peeling, for example variations of percutaneous penetration and toxicity that can lead to variable results. These problems are much less with modern lasers such as fractionated lasers (Lowe, N.J. personal observations).

Table 80.6  Different depths of chemical peels. Level

Histology

Peel

Superficial

Destruction of epidermis alone

10–25% TCA Glycolic acid 50–70% Jessner’s solution TCA 35% Jessner’s solution Glycolic acid + 35% TCA Baker’s phenol/TCA 50%

Medium

Destruction of epidermis plus papillary dermis

Deep

Destruction of reticular dermis

Table 80.7  Fitzpatrick’s classification of skin phototypes. Skin type

Colour

Reaction to sun

I II III IV V VI

Very white or freckled White White to olive Brown Dark brown Black

Always burns Usually burns Sometimes burns Rarely burns Very rarely burns Never burns

TCA, trichloroacetic acid.

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References 1 Stegman SJ. A comparative histologic study of the effects of three peeling agents and dermabrasion on normal and sundamaged skin. Aesthetic Plastic Surg 1982; 6: 123–35. 2 Brody HJ. Variations and comparisons in medium-depth chemical peeling. J Dermatol Surg 1989; 15: 953–63. 3 Van Scott EJ, Yu RJ. Alpha hydroxyl acids: procedures for use in clinical practice. Cutis 1989; 43: 222–8. 4 Brody HJ. Trichloroacetic acid application in chemical peeling. Operative techniques. Plast Reconstr Surg 1995; 2: 127–8. 5 Bhawan J, Palto MJ, Lee L et al. Reversible histologic effects of tretinoin on photodamaged skin. J Geriat Dermatol 1995; 3: 62–7. 6 Coleman WP 3rd, Futrell JM. The glycolic acid trichloroacetic acid peel. J Dermatol Surg Oncol 1994; 20: 76–80. 7 Lawrence NL, Cox SE, Brody HJ. Treatment of melasma with Jessner’s solution versus glycolic acid: a comparison of clinical efficacy and evaluation of the predictive ability of Wood’s light examination. J Am Acad Dermatol 1997; 36: 589–93.

Intense pulsed light and laser treatment— selection for cosmetic indications Selection of intense pulsed light (IPL) and lasers will depend on the nature of the clinical lesion to be treated. Table 80.8 summarizes some of the more frequent clinical lesions to be treated and the selection of the type of laser and light source to be used. The reader is also referred to Chapter 78 for further information on lasers and light sources.

Intense pulsed light system Intense pulsed light (IPL) sources give a non-coherent emission rather than the coherent specific single wavelength of a laser [1]. Most IPL systems emit a spectrum between 500 and 1200 nm, with a variety of cut-off filters designed to reduce selectively lower visible wavelengths, for example below 515 nm or below 560 nm. This lower wavelength selectivity allows for selection of different treatment indications. For vascular problems, for example telangiectasia and haemangiomas [1], wavelengths down to 500 nm are used, whereas skin pigmentary problems such as lentigo will best respond to wavelengths down to 560 nm. Poikiloderma of Civatte

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Fig. 80.7  (a) Pre-treatment and (b) posttreatment with a combined tretinoin, hydroquinone and hydrocortisone skin ‘lightening cream’, four glycolic peels and broad-spectrum daily sunscreen.

Table 80.8  IPL and laser treatment of clinical problems. Clinical problem

Type of laser

Vascular lesions Telangiectasia Haemangiomas/port-wine stains Cambell de Morgan angiomas Benign pigmented lesions Lentigo, melanosis, melasma Tattoos

Pulsed-dye usually 585–595 nm Copper bromide KTP IPL Q-switched, ruby, alexandrite, neodynium : YAG, IPL Q-switched Ruby, alexandrite Neodynium : YAG Carbon dioxide lasers Erbium YAG lasers Fractional lasers Long pulsed ruby, alexandrite, neodynium : YAG, IPL

Ageing skin, rhytides, laxity Seborrhoeic keratoses Hirsutes (pigmented hair)

has also been treated with IPL. Care has to be taken to obtain a uniform improvement [2].

Skin surface cooling for cosmetic IPL and laser procedures Surface skin cooling has provided significant safety advantages for some laser and IPL systems. The concept is that by cooling the skin surface it is possible to reduce undesirable thermal injury to the epidermis by the IPL or laser, thus diminishing the risk of hypopigmentation and scarring (see Chapter 78). There are three main types of tissue cooling: 1 Cold air convection, which is directed on to the area prior to and during treatment 2 Contact cooling, where the laser or light tip itself is cooled and thereby cools the skin surface 3 Cryogen spray cooling, where a frozen gas is sprayed on to the skin just prior to, and with some lasers during, the delivery of the laser light [3].

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Skin rejuvenation procedures    80.11

Another benefit of the use of cooling is that higher laser and IPL fluences can be used, enabling otherwise more resistant lesions, for example high blood-flow telangiectasia or vascular haemangiomas, to respond. Cooling also has another important effect of reducing the discomfort associated with treatment. It is important, however, to avoid cold injury from the cooling device. Cryogen freeze injury has been seen (Lowe, N.J. personal observations), particularly in skin phototypes III and darker from cryogen-cooled hair removal lasers.

Lasers for skin ageing problems These may be grouped into treatment of vascular, pigmented or skin surface irregularities, that is superficial rhytides, and deeper problems of skin laxity, deeper rhytides and scars.

Vascular changes associated with skin ageing Telangiectasiae on the cheeks, nose and other light-exposed areas are vascular abnormalities commonly associated with skin ageing. In addition, poikiloderma of Civatte, particularly affecting the lateral face and neck, is a superficial abnormality that is probably the result of repetitive ultraviolet injury together with, in some patients, phototoxic or photoallergic reactions to fragrances. Choice of lasers for these vascular problems includes vascular pulsed dye lasers are (usually between 585 and 595 nm), alexandrite (755 nm), Nd : YAG lasers (1064 nm), copper bromide lasers and potassium titanyl phosphate (KTP) lasers. The initial development of these lasers resulted from knowledge of the action spectrum responsible for laser vascular injury [4]. Electrocautery is sometimes used for solitary telangiectasia. One of the problems with electrocautery is a higher risk of recurrence of the lesion and/or atrophic scarring compared with pulsed-dye lasers. However, electrocautery does not give the transient purpura associated with pulsed-dye lasers. Intense pulsed light (IPL) sources with selective wavelength cut-offs down to 500 nm and 550 nm are also used with benefit in these vascular conditions [1,2]. An important guideline when treating a large area with any of these laser or light systems is to perform a test treatment on a small, preferably non-visible part of the skin, to ensure the correct choice of laser and laser parameters. This is particularly important before treating large areas of skin, for example poikiloderma on the neck or extensive telangiectasiae on the cheek. It is possible to get irregular ‘patchy’ improvement that requires numerous further treatment sessions to become more uniform and acceptable. Some darker skin phototypes, for example phototype III and darker, may elicit long-term and occasionally permanent hyperpigmentation following light and laser therapy. If too aggressive an IPL or laser treatment is selected, skin blistering with subsequent scarring and hypopigmentation is possible [5]. Benign pigmented skin lesions associated with ageing The most common type of benign pigmented skin lesion associated with photoageing is the solar lentigo. These usually respond well to a variety of lasers and pulsed light sources. The original observations on laser treatment by Goldman used a ruby laser for tattoos and pigmented lesions [6].

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Naevus of Ota persists into old age and responds well to a variety of Q-switched pigment lasers [7]. Melasma shows an extremely variable response to all lights and laser treatments—indeed to most treatment intervention [7]. The reasons remain to be determined, but possibly involve continued endogenous or exogenous hormonal stimulation of melanogenesis [8]. Lasers for benign pigmented lesions include Q-switched ruby (605 nm), alexandrite (755 nm), Nd : YAG (532 and 1064 nm) and Q-switched KTP (532 nm) [7–9]. Frequently, patients with photodamage will exhibit a combination of facial telangiectasia, plus lentigo and diffuse facial melanosis which can be treated with IPL sources. One advantage of an IPL system is that because of its broad spectrum of visible wavelengths both these types of photodamage may respond to the IPL [5,10]. Pigmented and non-pigmented seborrhoeic keratoses will respond well to laser ablation with either carbon dioxide or Er : YAG lasers. These can give a more accurate lesion vaporization than cryotherapy, and in some patients may be less likely to result in hypopigmented areas.

Lasers for surface skin changes The first laser to be used successfully for photodamage treatment by ‘skin resurfacing’ was a pulsed carbon dioxide laser [11]. The carbon dioxide laser emits a wavelength of 10 600 nm and is absorbed by tissue water content. It penetrates up to 30 mm into previously non-treated skin; once absorbed, further penetration is limited by the reduced tissue water content. Various other types of carbon dioxide laser have been developed, including scanned devices. The concept of ultrapulsing [12,13] is to give a uniform treatment area from the laser that produces skin surface vaporization but rapid re-epithelialization from undamaged hair follicles and other adnexal structures. There is a rejuvenation of the damaged skin surface. In addition, it has been shown that with ultrapulse carbon dioxide lasers there is a degree of dermal tightening which may continue for up to 1 year after treatment [14]. This tissue tightening may be the result of either a delayed wound healing response following the laser or neocollagenesis resulting from release of cytokines and other dermal growth factor stimuli [15–17]. Other carbon dioxide devices have used scanning systems rather than ultrapulsed systems to control skin injury [18]. Another skin resurfacing laser, which has greater affinity for water absorption compared to the carbon dioxide device, is the Er : YAG laser, emitting a wavelength of 2940 nm [19,20]. It is highly absorbed by skin water, but has a relatively low penetrance of 3 to 5 mm. Ultrapulse carbon dioxide lasers are more effective than conventional Er : YAG lasers [21]. In addition, because they do not produce as much haemostasis as the carbon dioxide laser there tends to be a greater degree of bleeding during treatment [21]. Some newer Er : YAG lasers have variable pulse duration so that they act in a manner similar to the carbon dioxide laser (Lowe, N.J. unpublished observations).

Fractional laser skin rejuvenation Newer developments in skin rejuvenation by lasers have been the use of the fractional laser delivery systems [22]. Fractional

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photothermolysis (FP) is a relatively new technology that creates microscopic zones or columns of thermal damage surrounded by healthy tissue, in contrast to layers of thermal vaporization from the ultrapulse carbon dioxide and Erbium : YAG lasers. The first FP laser device was introduced in 2003, as an erbium-doped fibre laser emitting at 1550 nm [22,23]. The microscopic thermal treatment zones vary in depth depending on the energy settings of the laser. As they are surrounded by an area of untreated skin this acts as a reservoir of keratinocytes for rapid repair of the treated areas of skin. Success has been reported with facial rhytides, photodamaged skin and scarring [23–25]. Initially, this system used a surface-applied blue dye to act as an optical activator of the laser [23]. The latest Fraxel laser system employs a motion detector whereby the laser is triggered by motion across the skin. This can be described as a ‘rolling’ FP laser system. The efficacy of FP with the 1550 nm laser, mentioned above, has been reported in a number of studies [23–25]. Results are encouraging for the improvement of surface photodamage, solar lentigo, diffuse facial melanosis, fine rhytides and atrophic facial scars (Figs 80.8–80.10). Another advantage of this laser is that it can be used (at appropriate settings) on areas other than the face, for example the neck, chest and limbs (Fig. 80.11). This is because with fractionated laser delivery, there are remaining areas of non-treated skin which lead to rapid re-epithelialization and reduced scar risk [22]. With previous lasers, for example

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Fig. 80.8  (a) Pre-treatment, showing mild ageing neck changes with horizontal lines and skin folding; (b) after three fractional laser treatments.

Fig. 80.9  Periorbital ageing and skin laxity (a) before and (b) after five Fraxel laser treatments.

ultrapulse carbon dioxide and Erbium : YAG, there was complete epidermal and dermal photothermolysis and a significant risk in non-facial areas of compromised, delayed healing with scarring risk due to the relative paucity of adnexal structures. A very recent development is a fractionated delivery carbon dioxide laser. A variety of other ‘pseudo-fractionated’ and ‘stamp’ fractionated systems have been developed including systems using several wavelengths between 532 and 10 600 nm. These all have their own proponents, but as yet there is a lack of data to enable comparison with the rolling FP system.

Skin preparation and post-treatment care for laser rejuvenation Pre-treatment preparation and post-treatment care of the skin are important, particularly in the management of pigmented and photodamaged skin. Pre-treatment with topical retinoids and, where pigmentation is a problem, additional depigmenting agents such as hydroquinone or combinations thereof, may help to enhance healing and reduce post-laser hyperpigmentation [14]. In addition, it is important to enquire about the occurrence of herpes simplex on the area to be treated, and prophylactic oral aciclovir 400 mg b.d. 1 day prior to and 7 days following laser treatment may be employed [26]. Post-laser care involves the use of topical emollients, as well as treatment of any possible post-laser acne relapses and folliculitis.

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Skin rejuvenation procedures    80.13

Fig. 80.10  Forehead melasma, (a) before and (b) after four Fraxel laser treatments.

(a)

After initial healing—usually 1–2 weeks—the patient should be encouraged to use daily photoprotection with a sunscreen, topical antioxidants and, if necessary, depigmenting agents. Maintenance treatment can include topical retinoids, for example tretinoin 0.025% cream may be used nightly as tolerated.

Non-laser skin surface rejuvenation A recent development is a ‘plasma’ skin rejuvenation system, using high surface energy generated with nitrogen gas released at high velocity. This ‘plasma’ system is currently being evaluated as an alternative to laser skin rejuvenation [27]. References 1 Shroeter CA, Newmann HA. An intense light source. The photoderm VLflashlamp as a new treatment possibility for vascular skin lesions. Dermatol Surg 1998; 24: 743–8. 2 Weiss RA, Goldman MP, Weiss MA. Treatment of poikiloderma of Civatte with an intense pulsed light source. Dermatol Surg 2000; 26: 823–8. 3 Chang CJ, Nelson JS. Cryogen spray cooling and higher fluence pulsed dye laser treatment improve port wine stain clearance while minimizing epidermal damage. Dermatol Surg 1999; 25: 767–72. 4 Tan OT, Murray S, Kurban AK. Action spectrum of vascular specific injury using pulsed irradiation. J Invest Dermatol 1989; 92: 868–71. 5 Ross EV, Smirnov M, Pankratov M, Altshuler G. Intense pulsed light and laser treatment of facial telangiectasias and dyspigmentation: some theoretical and practical comparisons. Dermatol Surg 2005; 31: 1188–98. 6 Goldman L, Blaney DJ, Kindel DJ Jr et al. Pathology of the effect of the laser beam on the skin. Nature 1963; 197: 912–14. 7 Lowe NJ, Wieder JM, Sawcer D et al. Naevus of Ota: treatment with high energy fluences of the Q-switched ruby laser. J Am Acad Dermatol 1993; 29: 997–1101. 8 Nelson JS, Applebaum J. Treatment of superficial cutaneous pigmented lesions by melanin-specific selective photothermolyis using a Q-switched ruby laser. Ann Plast Surg 1992; 29: 231–7. 9 Anderson RR, Margolis RJ, Watanabe S et al. Selective photothermolysis of cutaneous pigmentation by Q-switched Nd : YAG laser pulses at 1064, 532 and 535 nm. J Invest Dermatol 1989; 93: 28–32. 10 Goldman MP, Weiss RA, Weiss MA. Intense pulsed light as a nonablative approach to photoaging. J Dermatol Surg 2005; 31: 1179–87. 11 David LM, Lask GP, Glassberg E et al. Laser abrasion for cosmetic and therapeutic treatment of facial actinic damage. Cutis 1989; 43: 583–7. 12 Fitzpatrick RE, Ruiz-Esparza J, Goldman MP. The depth of thermal necrosis using the CO2 laser: a comparison of the superpulsed mode and the conventional mode. J Dermatol Surg Oncol 1991; 17: 340–4.

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13 Fitzpatrick RE, Goldman MP. Advances in carbon dioxide laser surgery. Clin Dermatol 1995; 13: 35–47. 14 Lowe NJ, Lask G, Griffin ME et al. Skin resurfacing with the Ultrapulse carbon dioxide laser. Observations on 100 patients. Dermatol Surg 1995; 21: 1025–9. 15 Fitzpatrick RE, Tope WD, Goldman MP, Satur NM. Pulsed carbon dioxide laser, trichloroacetic acid, Baker-Gordon phenol, and dermabrasion: a comparative clinical and histologic study in a porcine model. Arch Dermatol 1996; 132; 469–71. 16 Hruza G. Skin resurfacing with lasers. Clin Dermatol 1995; 3: 38–41. 17 Waldorf HA, Kauvar A, Geronemus RG. Skin resurfacing of fine to deep rhytides using a char-free carbon dioxide laser in 47 patients. Dermatol Surg 1995; 21: 940–6. 18 Lask G, Keller G, Lowe N, Gormley D. Laser skin resurfacing with the SilkTouch flashscanner for facial rhytides. Dermatol Surg 1995; 21: 1021–4. 19 Kaufmann R, Hibst R. Pulsed erbium : YAG laser ablation in cutaneous surgery. Lasers Surg Med 1996; 19: 324–30. 20 Hibst R, Stock K, Kaufmann R. Ablation and controlled heating of skin with the Er : YAG laser. Lasers Surg Med 1997; 9 (Suppl.): 40 (Abstract). 21 Khatri K, Russ V, Grevelink I et al. Comparison of erbium : YAG and CO2 lasers in wrinkle removal. Lasers Surg Med 1997; 9 (Suppl.): 37 (Abstract). 22 Mannstein D, Herron GS, Sink RF et al. Fractional photothermolysis: a new concept for cutaneous remodelling using microscopic patterns of thermal injury. Lasers Surg Med 2004; 34: 426–38. 23 Laubach HJ, Tannous Z, Anderson RR, Manstein D. Skin responses to fractional photothermolysis. Lasers Surg Med 2006; 38: 142–9. 24 Geronemus RG. Fractional photothermolysis; current and future applications. Lasers Surg Med 2006; 38: 169–76. 25 Glaich AS, Rahman Z, Goldberg LH, Friedman PM. Fractional resurfacing for the treatment of hypopigmented scars: a pilot study. J Dermatol Surg 2007; 33: 289–94. 26 Lowe NJ, Lowe PL, Yamauchi P, Lask GL. Laser skin resurfacing. In: Lowe NJ, Carruthers A, Carruthers J et al. Textbook of Facial Rejuvenation. London: Informa Health Care, 2002: 123–38. 27 Bogle MA, Arndt KA, Dover JS. Evaluation of plasma skin regeneration technology in low-energy full-facial rejuvenation. Arch Dermatol 2007; 143: 168–74.

Radiofrequency Radiofrequency has been developed as a treatment to promote skin and facial tightening. The results to date are mixed. Appro­ priate patient selection is critical, with early facial laxity subjects more likely to respond than older patients. Monopolar radiofrequency skin tightening was first approved by the US FDA in 2002 as a facial treatment. More recently, it has gained approval for treatment of selected body areas [1,2]. The concept is that a controlled radiofrequency pulse selectively heats

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zones of the dermis and deeper tissue, while a proprietary cooling surface system protects against injury to the epidermis and upper dermis. Initial investigations showed some degree of improvement in selected patients, but in general the first treatment algorithms were unpredictable. Subsequently, this monopolar radiofrequency system has become more consistent and the algorithm is now to use multiple passes over the same area, with moderate energy settings, to give greater consistency. A recent retrospective study showed that 54% of patients observed skin tightening 6 months after treatment, and 26% showed an immediate tightening. This was with the original treatment algorithm. However, with the multiple pass moderate energy treatment algorithm 87% were reported as observing immediate tightening and 92% noted skin tightening 6 months after treatment [2]. In the author’s opinion one of the most important factors in the use of monopolar radiofrequency is patient selection. Patients who are candidates for facelift surgery are clearly not candidates for radiofrequency facial skin tightening. Conversely, patients who have early laxity of forehead, as well as lower facial and neck skin, may be improved using these treatments. Other forms of radiofrequency treatment include bipolar radiofrequency, which is sometimes combined in some instruments with intense pulsed light. One of the problems with these other systems is that there has been little consistent research.

Fig. 80.11  Before (a) and after (b) combining Botulinum toxin A (upper face), deep volume filler (upper cheeks), hyaluronic acid filler (lips) and Fraxel CO2 repair laser (whole face).

Combination minimally invasive treatment The idea of combining several different non- or minimally invasive treatments is a relatively recent concept for facial rejuvenation. See Figure 80.11 for an example of a combination of minimally invasive treatment. Examples of such combinations include: 1 Topical agents, e.g. sunscreens, tretinoin cream, glycolic acid peels and BTX-A 2 BTX-A to forehead and crow’s feet; filler to mid and lower face; Fraxel laser to face and neck 3 Fraxel laser to neck plus BTX-A to platysmal band. These combinations are selected for appropriate indications and patterns of ageing [3,4]. References 1 Fitzpatrick R, Geronemus R, Goldberg D et al. Multicentre study of non-invasive radiofrequency for periorbital tissue tightening. Lasers Surg Med 2003; 33: 232–42. 2 Dover JS, Zelickson B. Results of a survey of 5700 patient monopolar radiofrequency skin tightening treatments: assessment of a low-energy multiple-pass technique leading to a clinical endpoint algorithm. Dermatol Surg 2007; 33: 900–7. 3 Lowe NJ. Introduction. In: Lowe NJ, Carruthers A, Carruthers J et al., eds. Textbook of Facial Rejuventation. Informa Health Care, 2002: 1–2. 4 Lowe P, Patnaik R, Lowe N. Comparison of two formulations of botulinum toxin type A for the treatment of glabellar lines: a double-blind randomized study. J Am Acad Dermatol 2006; 55: 975–80.

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