Skin Rejuvenation

Options for both the cosmetic surgeon offering and patients seeking treatment for cutaneous aging have expanded greatly in recent years and continue to grow. Increasingly sophisticated aesthetic patients are seeking procedures to rejuvenate in record numbers but many are unwilling to tolerate a large amount of downtime. In expert hands, deeply ablative laser resurfacing has a long history of dramatic results for the treatment of cutaneous aging. Over the last decade, there have been a growing number of reports of modalities targeting the more superficial skin structure. Such modalities offer more modest results without the downtime associated with more aggressively ablative procedures. These resurfacing techniques include the use of mechanical, chemical, and thermal forces.

Keywords: superficial skin resurfacing, erbium:YAG laser, chemical peels, alpha-hydroxy acid, jessner’s peel, TCA peel, thermage, coblation, microdermabrasion, nonablative laser resurfacing, intense pulsed light, Nd:YAG laser, salicylic acids, aging, skin

ANATOMY OF THE SKIN

The approach to superficial resurfacing of the skin necessitates a thorough understanding of the skin’s distinct anatomy and histology. The epidermis is the most superficial layer of the skin and provides a critical barrier of protection. The principal building block of the epidermis is a keratinocyte. The epidermis is comprised of four distinct layers: the cornified, granular, spinous, and basal layers. The cornified layer is the most superficial and provides significant protection to the skin. It is formed from flattened, enucleate keratinocytes and compacted keratin granules. It varies in thickness with the eyelid being the thinnest and the palms and soles the thickest. The next granular cell layer, contains keratinocytes and lamellar bodies which contribute to the cornification of the skin. The spinous layer contains keratinocytes, as well as a variety of immunologic cells. The basal layer, the deepest layer of the epidermis, contains basal cells, whose duplicative effort replaces the cells of the superficial layers every two weeks. The basal layer also contains melanin producing melanocytes, which provide pigmentation in the skin.

The dermis has the important function of thermoregulation and supports the vascular network to supply the avascular epidermis with nutrients. The dermis is subdivided into two zones, a papillary dermis and a reticular layer. The dermis contains mostly fibroblasts which are responsible for secreting collagen, elastin, and the viscous ground substance that gives support and elasticity of the skin. Also present are immune cells that are involved in defense against foreign invaders passing through the epidermis.

There are two main types of collagen in the dermis. Type I collagen, constituting 80% of dermal collagen, imparts tensile strength to the dermis. Type III collagen, comprising 15% of dermal collagen, anchors the epidermis to the dermis. Papillary dermis is primarily made of Type III collagen with a small amount of Type I collagen and fibronectin. Reticular dermis is primarily made of Type I collagen with Type III collagen and fibronectin serving adjunct roles. (1) Elastic fibers constitute approximately 3% of the dermis, and provide the skin elasticity and resilience.

HISTOPATHOLOGY

After the age of 28, the first signs of skin aging begin to appear. (2) Intrinsically aged skin results in atrophy of skin components. Although aged skin is thin with reduced elastic capacity, if there has been minimal sun exposure clinically, aged skin is smooth and unblemished. Collagen production and cross linking of the distinct collagen bundles is decreased. Dermal elastic fibers are fewer, thicker, and less functional. Decreasing production of sebum that accompanies maturation of the skin explains the frequent finding of xerosis in mature patients.

Environmental factors, such as sun exposure and smoking greatly accelerate these changes. (3) Dermatoheliosis, also known as actinically damaged or photoaged skin, is morphologically and histologically distinct from intrinsically, non-solar exposed aged skin. Photoaged skin clinically presents as deep rhytides, uneven pigmentation and mottling, and in its most severe form, a thickened texture reminiscent of leather. Most cutaneous damage secondary to ultraviolet irradiation is to the dermal connective tissues, in large measure by increasing important matrix metalloproteinases responsible for the orderly destruction of collagen fibers, which in turn keeps in check total production (4)

Characteristic dermal findings of actinically damaged skin include haphazard arrangement of collagen and elastin fibers, degradation of collagen, breakdown in elastic fibers known as elastosis, excess dermal melanosomes, telangiectasias, and precancerous lesions known as actinic keratosis.(5)

CUTANEOUS RESURFACING

Skin resurfacing by the cosmetic surgeon is a process that causes a controlled injury to skin, and then stimulates a wound healing response. In response to injury, fibroblasts in the papillary dermis increase production of type I and type III procollagen, as well as transforming growth factor beta-1. The collagen increase in turns thickens the dermis which enhances the tensile strength of the skin and yields the clinical appearance of rejuvenation.

Skin resurfacing is most commonly classified based on the depth of injury. Superficial wounding extends to the stratum granulosum or papillary dermis. Medium-depth wounding results from extension into the upper reticular dermis. Deep wounding extends into the midreticular dermis. If the resurfacing technique is limited to superficial injury to the epidermis and very superficial papillary dermis, healing will generally occur without scarring. If the injury extends deep into reticular dermis beyond adnexal structures scarring is the likely result. (6)

Invasive treatments for the treatment of solar damaged skin and facial rhytids include ablative laser resurfacing with carbon dioxide and erbium laser wavelengths, dermabrasion, and deep chemical peeling agents. Ablative resurfacing achieves the outcome of rejuvenation via the destruction of the outermost, and thus most photodamaged layers of the skin. The subsequent laying down of newly formed collagen and a tightened skin appearance follows this removal. (7) Recently, multiple studies have been reported regarding the use of non-ablative techniques for skin rejuvenation. In this article, we review options we can offer patients for skin rejuvenation.

The term resurfacing encompasses many arenas. This spectrum includes retinoids and other topical preparations, varied depths of chemical peeling, dermabrasion and microdermabrasion, ablative and nonablative resurfacing, and one of the newest technologies, radiofrequency coblation. Retinoids are known to reverse photodamage, increase epidermal turnover and the production of dermal collagen and elastin. Importantly, they have been shown to stimulate neoangiogenesis, an effect which can often be seen in the early period of titration. For those patients who cannot tolerate retinoids, retinols are an option. Retinols are vitamin A aldehydes and they penetrate the skin very well. They are converted into small amounts of tretinoin but are tolerated with significantly less irritation.

CHEMICAL PEELING

Chemical peels are the application of chemical agents which damage skin in a controlled manner. These agents can be subdivided into very superficial peels, which remove the stratum corneum, and superficial peels which remove the entire epidermis. Superficial peels require repetitive peeling sessions to optimize results. The limiting therapeutic factor of superficial peels is its depth, and dermal pigmentation, particularly evident in cases of severe dermatoheliosis and melasma, will not be improved despite repeated application.

Since the days of ancient Egypt, when it was rumored that Cleopatra used the debris of the bottom of wine barrels for facial rejuvenation, people have been using chemoexfoliation methods to rejuvenate skin. The original chemoexfoliant was lactic acid, an active ingredient of sour milk that was used topically by the nobles as part of an ancient skin rejuvenation regimen. In the Middle Ages, old wine with tartaric acid as its active ingredient was used for the same purpose. Today, these historical chemoexfoliants are known to contain alpha hydroxy acids, which are the active ingredients responsible for the skin exfoliation.

Modern day chemical peeling originally was promoted by dermatologists, such as P.G. Unna, who first described the properties of salicylic acid, resorcinol, phenol, and trichloroacetic acid (TCA). Slowly, the early practitioners of chemical peels began to develop other peeling agents for varying depths of penetration. In the 1960s, Baker and Gordon developed a deep peeling agent, which was able to smooth deeper furrows, especially around the mouth. From the 1980s to the present, an explosion has occurred in the mass of research on this subject, with the elucidation of many different types of peels, each for a specific range of problems. (8)

The chemical peel produces a controlled partial thickness injury to the skin. Following the insult to the skin, a wound healing process ensues that can regenerate epidermis from surrounding epithelium and adnexal structures which leads to the development of new dermal connective tissue. The result is an improved clinical appearance of the skin, with fewer rhytids and decreased pigmentary dyschromia.

To understand the peeling process, there are a few key concepts. The concentration and pH of a peeling agent determine the effectiveness of a given peeling agent. Generally the greater the concentration is the more potent the chemical agent. However, concentration may vary based on the method of dilution. The strongest method is a dilution of a saturated solution. The weakest method is grams of acid crystal mixed to 100 cc of water. {The weight to weight method and the weight to volume method are intermediate in determining the concentration of the peeling agent}. The pH is also important in determining the effectiveness of the peeling agent. This occurs when the free acid component is biologically active, i.e. when the pH is close to the pKA.

Chemical peeling is classified by the depth of penetration of the peeling achieved. (9) [Table 1] The process of healing involves coagulation and inflammation and is followed by re-epithelialization, granulation tissue formation, angiogenesis, and a prolonged period of collagen remodeling. It is this remodeling that accounts for the continuing appearance of clinical improvement in the months following the peel procedure. A useful grading system for pre-treatment classification is the Glogau system. (10) [Table 2] Peel depth can be modulated in response to the individual patient’s classification.

Application of most peeling agents is similar. Prior to application the skin to be treated is first defatted with acetone or rubbing alcohol. The clinical endpoint is a brisk erythema. Since most chemical peels are lipophobic this facilitates greater depth and promotes even distribution of the peel. The peel is applied to subunits of the face with gauze or a cotton tip applicator. To provide a consistent effect it is important to apply the chemical peel evenly and prevent pooling of the agent on the face. The peel is blended with untreated skin by feathering it at the edges.

ALPHA HYDROXY ACIDS

Alpha hydroxy acids have been used for thousands of years to improve the appearance of the face. Chemically, alpha hydroxy acids are organic carboxylic acids with a hydroxyl group at the alpha position. Alpha hydroxy acids are known to normalize keratinization by diminishing corneocyte adhesion in the granular cell layer; this in turn promotes improved cell turnover. Commonly used AHA derive from fruit and dairy products, such as glycolic acid from sugar cane, lactic acid from fermented milk, citric acid from fruits, tartaric acid from grapes, and malic acid from apples. With its particular affinity for the skin, glycolic acid is the most commonly used.

The efficacy and penetrating depths of assorted AHA preparations are greatly dependant on their concentration, the vehicle, and the pH. Brands available for OTC use are set at 3-10% concentrations and induce a slow exfoliation over several weeks. This strength can also be used as a pre-treatment for a higher concentration peel or another resurfacing modality. Higher strengths may be used by supervised estheticians (8-30%) for light peels. The highest strengths (40-70%) are available for dermatologists and cosmetic surgeons for in- office peels.

The cautions are intuitive. The surgeon must take care to note the expiration date as the peel will lose effective potency with time. Solutions with a pH below 2 that contain only free glycolic acid have the potential to induce crusting and necrosis. These products can be buffered with an addition of sodium bicarbonate or sodium hydroxide resulting in a higher pH and a weaker acid. This is independent of the concentration used. The desquamative and proliferation-stimulating effects of lactic acid are very pH and concentration dependent, suggesting the “free acid” concentration is the active moiety. (11)

Standard strength of professional grade alpha hydroxy acid peels is 50% or higher. Alpha hydroxy peels differ from other peels in that they are time dependent. The time to peel is dependent on both the concentration and the pH of the peel. Higher concentrations and lower pH require shorter peeling periods. Following placement of an alpha hydroxy acid preparation the skin becomes erythematous. A frost is not desirable in an alpha hydroxy peel because it denotes penetration depth into the dermis. (12) The alpha hydroxy acid peel requires neutralization with cold water or a basic solution. Mild stinging and erythema will typically disappear after an hour. The subsequent exfoliation will take place over a few days with re-epithelization in about a week. Multiple treatments may be required for the desired result, but should be spaced at least three weeks to allow the epidermis to recover. (13)

Complications of AHA peels are mild and temporary when the peel is performed by trained professionals using standard techniques. Care is taken to be certain the eyes are protected and that the patient has no known allergies to any of the peel’s ingredients. Standard of care is for prescription retinoid users to cease use of the agent for 2- 3 days prior to a superficial peel so as to not cause excess irritation. Patients are susceptible to post inflammatory skin pigmentation and require UVA and UVB protection both pre and post peel. (14)

Deeper than intended peeling may occur if neutralization is not performed within the correct window. In our experience, we have also seen increased erythema and inflammation surrounding peeled areas over sites recently augmented with bovine collagen implants. We either avoid these areas with peeling or defer placement of filler agents for a two week period prior to peeling.

JESSNER’S PEEL

A Jessner’s peel is a combination of salicylic acid 14%, lactic acid 14%, and resorcinol 14% in alcohol. It is considered a mild peeling agent. Its ability to disrupt the barrier function of the epidermis is utilized as an ideal primer for TCA peels. This allows TCA peels to penetrate safely and evenly. Jessner’s solution peeling action is through intense keratolysis. Alone, Jessner’s is an easy to use peeling agent without timing restriction. Skin sloughing occurs within 2 to 4 days with subsequent epidermal regrowth. (15)

TCA

Trichloroacetic acid (TCA) typically is used as a superficial-intermediate-to-deep peeling agent in concentrations ranging from 20-50%. TCA (10-35%) has been used for many years and is safe in use at lower concentrations. At higher concentrations, such as 50% and above, TCA has a tendency to scar and is less manageable than other agents used for superficial peels. (16)

TCA is a keratocoagulant that produces a frost or whitening of the skin, which is dependent on the concentration used. Level I frosting, defined as erythema with streaky whitening of the face, is the endpoint for superficial resurfacing. Level II frosting is defined as white coated frosting with patches of erythema showing through. Level III frosting, which is associated with penetration through the papillary dermis, is a solid white enamel frost with minimal visible erythema. Level III frosting must be reserved for areas of severe actinic damage. (17)

TCA’s peeling mechanism of action at lower concentration is through protein precipitation. Vigorous rubbing of the agent, as compared to blotting, yields a deeper penetration. This technique is not time dependent, and the agent does not require neutralization. During the procedure, if frosting is not uniform, reapplication may be performed until frosting of a desired plateau is reached. Once completed, skin sloughing will proceed for several days, and re-epithelialization is complete within 10-14 days. Patient discomfort is controlled with oral pain medications.

The results of TCA peels of superficial depths are mild reversal of some fine wrinkles and improvement in dyspigmentation. The results may not be that which is achieved by TCA 35% Jessner’s combination but the recovery period and risk is also less. (18)

SALICYLIC ACID

Beta hydroxy acids (BHA), also known as salicylic acids, are not AHA’s but chemically defined as having an organic carboxylic acid with a hydroxyl group at the beta position. BHA’s have more of a predilection for sebum containing cells and is lipid soluble, therefore, it is an excellent peeling agent for comedonal acne. Another benefit of salicylic acid is that it does not need to be neutralized. After applying BHA to the skin, salt is formation on the skin is seen. (19)

Results of salicylic acid seem to provide a safe, mild rejuvenation to skin. A study by Grimes PE, et al. looked at concentrations of salicylic acid between 20-30% in Fitzpatrick skin types V and VI. (20) They concluded that 88% of patients described a moderate to significant improvement in acne, oily skin, textural changes, melasma, and post-inflammatory pigmentation. Minimal side effects occurred in 16% of patients.

Klingman D, et al. Also demonstrated that beta-hydroxy acids at 30% concentration were efficacious in photoaged skin. (21) They found reduction in fine lines, surface roughness, and pigment spots

Adverse effects, usually only found with high-dose oral ingestion, include headache, nausea, and ringing of the ears, each of which may be resolved with a few glasses of water and rest. These have never been reported with a peel procedure. Cutaneous side effects are minimal and can include erythema and mild irritation to the salt formation on the skin. (22)

DERMABRASION

Dermabrasion is an older technique that removes the epidermis and upper dermis by use of an abrasive wheel driven by a high-speed engine. This mechanical removal yields a mid-dermal wound. Healing is achieved via reepithelialization and repigmentation from the residual adnexae. Areas with diminished numbers of adnexal structures, such as keloids and hypertrophic scars, respond poorly to mechanical dermabrasion as these adnexae are not present. (23) Dermabrasion is used with less frequency since the advent of laser resurfacing but still offers an excellent option in the treatment of deep acne scars.

MICRODERMABRASION

Microdermabrasion originated in Italy in 1985 by Marini and Lo Brutto who reported both gross and histologic improvement in treated skin. (24) Its ease of performance and lack of downtime has made it a patient favorite in the United States. Clinically, it is mechanical debridement of the most superficial layers of epidermis. It commonly involves the use of a closed-loop, negative pressure system with debriding aluminum oxide crystals to ablate the superficial layers of the epidermis. Some systems use sodium chloride which is a positive pressure system. (25)

Quality and purity can vary substantially amongst the crystals. The substance most often used is aluminum oxide. It is usually preferred because of its hardness, inertness, and superior abrasion qualities. Alternative crystal mediums are also available and range from bicarbonate sodium to salt. Advantages of bicarbonate sodium crystals are their purity and that it dissolves in water during clean up, leaving no gritty residue. A disadvantage is that it’s softer than aluminum oxide and requires more passes.

Performance of a microdermabrasion treatment is technically simple. No preoperative anesthesia or antibiotics are necessary. The handpiece has a vacuum that draws in the skin as the handpiece is passed over the area to be resurfaced. Depth of abrasion is controlled by pressure of the crystals being propulsed, pressure of the handpiece and speed of the pass. The face will typically require two passes, with the second pass perpendicular to the first one. Vertical passes only are advisable for the neck area.

Historically, the assumption on microdermabrasion was that repetitive intraepidermal injury has the ability to gradually improve photodamaged skin by stimulating fibroblast activity and new collagen deposition in the dermis. (26) A recent study from Freedman et al suggests that microdermabrasion may indeed yield greater histologic improvement then previously realized, (27)with treated patients showing histological evidence of thickening of the epidermis and dermis, flattening of the rete pegs, vascular ectasia, and perivascular inflammation, and newly deposited collagen and elastic fibers as compared to control subjects. A study by Shim et al. Demonstrated a statistical significant improvement in roughness, mottled pigmentation, and overall improvement in skin appearance in a small number of patients. (28)

LASER RESURFACING-ABLATIVE

When performed by an experienced practitioner, ablative laser skin resurfacing yields often dramatic and reproducible improvement in the appearance of photoaged skin. It does so by reducing solar-induced dyspigmentation, rhytids, and improving allover skin tone. (29) Histologically these changes correlate with architectural normalization of the epidermis and the formation of a dermal repair zone comprised of parallel collagen arrays. (30) The two principal lasers used are the CO2 and Er:YAG systems with similar mechanisms: ablation of photodamaged skin, thermal collagen contraction, and stimulation of immediate and delayed collagen remodeling.

Resurfacing requires an understanding of laser biophysics and its’ interaction with skin. Laser is an acronym for light amplification by stimulated emission of radiation. The therapeutic action of light energy is the product of characteristics distinct to laser light and resultant laser-tissue interactions. Laser light is monochromatic, in other words, the emitted light is of a single wavelength. At specific wavelengths, specific absorption of light energy by a pigmented target can occur. Another property is coherence, both in time and space, analogous to a marching band in step. A third property is collimation, which is the emission of a powerful beam of light in a parallel manner which permits its focus into very small spot sizes which permits precise tissue destruction. (31)

Lasers have several vital characteristics which influence its ultimate effects in tissue. The fluency, power density, and frequency each function to adapt the effect of laser light on tissue. Tissue ablation occurs when the tissue is heated to its boiling point. Depending on the absorbance of the host target tissue, the laser may cause unintended damage to the surrounding tissue. This can be measured with the tissue relaxation time. When the time of laser delivery is greater than the tissue relaxation time, unintended damage to the surrounding tissues will result. When the energy level is above the critical value for the particular tissue and delivered in less than the thermal relaxation time for that particular tissue, tissue is ablated with minimal heat conduction to the surrounded tissues. (32) The understanding of this principle of selective photothermolysis changed the face of laser resurfacing and brought a new era in the treatment of photoaging.

The CO2 laser emits infrared light with a 10,600 nm wavelength absorbed by intracellular and extracellular water. After this energy is absorbed, water is immediately converted into steam with charring of tissue and minimization of collateral tissue damage. (33) Pulsed systems provide the further advantage of minimizing damage to adjacent tissue. (34) In trained hands, impressive results are safely achieved in the treatment of severe photoaging. The major limiting factor for this procedure is the extended duration of recovery, with pronounced erythema for 3-6 months. Additionally, significant postoperative complications such as oozing, bleeding, and infection can occur. (35) Also of great concern is the risk of delayed permanent hypopigmentation seen in up to 20% of patients when multiple-pass carbon dioxide resurfacing is performed. (36,37)

The demand for less aggressive resurfacing modalities led to the development of the short-pulsed erbium yttrium-aluminum-garnet (Er:YAG) laser. The Er:YAG laser, with a wavelength of 2940 nm, produces laser irradiation in the near infrared portion of the electromagnetic spectrum. This wavelength corresponds to a main peak of water absorption, one that is much more (10-15 times) efficiently absorbed by superficial (densely water containing) tissues and the Er:YAG arrived on the scene to great enthusiasm as practitioners hoped for a comparable clinical result to CO2 with more rapid wound healing. However, Er:YAG resurfacing has since been shown to yield less apparent clinical improvement for rhytids than CO2 at equivalent depths of treatment. (38) This is because the Er:YAG system produces only about 5-20 microns of thermal damage per pass, as opposed to the 50-125 microns of thermal damage seen with each CO2 pass.

Short pulsed erbium treatment can be adjusted to go superficially mimicking the benefit of a MD or it can go deeper with multiple stacked passes mimicking the benefits of CO2. Short pulsed erbium is best utilized as a superficial treatment at the limits of the dermis.

CO2 systems produce a significant amount of thermal effect which acts as a “heat sink” for the next laser pass yielding increased damaged collagen and leading to an increase in new collagen production. (39) Additionally, the Er:YAG system offers the laser surgeon poor intraoperative hemostasis, unlike the excellent hemostasis provided by CO2. Recently, modulated (short-and-long-pulsed) Er:YAG systems have been introduced to facilitate deeper ablation of tissue and improve intraoperative hemostasis. (40,41) Indications favoring use of a short pulsed Er:YAG system are mild to moderate photoaging, superficial dyspigmentation, and patients with darker skin phototypes. (42) The modulated systems offer results between that of CO2 and short-pulsed Er:YAG systems.

Er:YAG systems yield photomechanical benefits while the CO2 laser utilities a photothermal effect. The lack of a photothermal effect for the Er:YAG laser means that heat does not dissipate deeper into the surrounding tissues. There are fewer complications of severe thermal damage with the Er:YAG laser. However, this also translates to less collagen shrinkage with the Er:YAG laser versus the CO2 laser. (43) Er;YAG resurfacing though may soon reemerge as a middle ground option, providing patients with an moderate improvement in skin texture and tone, beyond that which is achieved with microdermabrasion and superficial treatments yet without the associated downtime of the deeper reaching modalities. (Figure 1)

LASER RESURFACING-NON-ABLATIVE

The devices available for nonablative photorejuvenation can be split into two primary categories: visible light devices 532 nm (green) and 585 nm (yellow) light best suited to treat pigmentary and vascular lesions. These wavelengths are strongly absorbed by oxyhemoglobin and melanin in the epidermis and superficial dermis. Mid-infrared wavelength devices at 980 nm, 1320 nm, 1450 nm, and 1540 nm are coupled with cooling mechanisms that serve to protect the epidermis while simultaneously stimulating direct collagen remodeling in the dermis. These mid-infrared wavelengths are absorbed primarily in water (intra- and extra-cellular) and can uniformly heat tissue independent of skin type. (44)

While using a pulsed dye laser for treatment of vascular periocular lesions, it was noted that there was a decrease in the clinical appearance of rhytids. (45) Histologic improvement of dermal collagen was also noted after treatment with the pulsed dye laser. Using these findings, Zelickson et al evaluated the use of a 585 nm pulsed dye laser in the treatment of facial rhytids and reported improvement. (46) The Zelickson report suggests that there also is potential efficacy with lower fluences than used in the trial and less associated purpura, the endpoint that patients find least cosmetically acceptable.

The first system specifically designed for the purpose of nonablative resurfacing was a 1320-nm neodymium:yttrium-aluminum-garnet (YAG) laser (Cool Touch, Cool Touch Corp, Roseville, CA). The goal of this system, similar to that of the previously described systems, is improvement of rhytids without the creation of an open wound. The 1320-nm wavelength is advantageous in its high scattering coefficient. Thus, the laser irradiation scatters throughout the treated dermis after nonspecific absorption by dermal water. Studies have reported that this system is able to produce thermal stimulation of dermal fibroblasts within the papillary and mid-reticular dermis while concomitantly cooling the epidermis to protect it from undesired thermal injury. (47)

Histologically, there is replacement of the irregular collagen bands with organized new collagen fibrils. (48) In a 1999 study, Kelly et al reported the use of the 1320 nm wavelength Nd:YAG laser for the treatment of facial rhytids. They reported statistically significant findings at 12 weeks. (49) In another study of similar technology, Goldberg et al reported clinical improvement in eight of the ten patients in the study. (50) The Cooltouch was modified and reintroduced as the Cooltouch II which delivers energy densities up to 24 J/cm2 with a 10 mm spot handpiece. The laser handpiece has three roles: delivery of the laser pulse, application of a thermal spray for cryogen cooling, and a sensor for the assessment of skin temperature at the surface.

Recently, Ross et al described the Smoothbeam1450-nm diode laser system that was also shown to be modestly effective for the nonablative treatment of photoaged skin. The 1450-nm wavelength is extremely well absorbed by water. 16 patients (14 periorbital, 2 perioral) with rhytids were treated with split face treatments; half with four visits three weeks apart with the 1450 nm laser device and the contralateral side with cryogen cooling alone. The laser utilizes spray cryogen cooling to protect the epidermis and permit selective dermal heating. The authors reported mild to moderate improvement in twelve to sixteen patients on the treated side. (51)

The long pulse 1064 –nm laser with its low scattering coefficient and weak absorption by water and melanin has also been shown to improve the appearance of coarse wrinkles, fine lines and to reduce skin laxity. Following seven treatment sessions spaced over fourteen weeks patients’ subjectively graded improvements in their skin’s appearance mirrored masked physician observers recognized improvements in the same categories. This data reached statistical significance. (52)

Intense pulsed light, a non-laser light source, can be delivered at a variety of wavelengths (590 to 1200 nm.) Filters permit the inclusion and exclusion of given wavelengths.(53) With blockage of shorter wavelengths, deeper wavelengths can be absorbed in the dermis and yield non-ablative dermal remodeling. (54) Goldberg reported on five patients who underwent four sessions of intense pulsed light source therapy and from whom pre- and six month post-treatment biopsies were obtained. Their results indicated histological evidence of new upper papillary dermal collagen formation. (55) The IPL has particular utility for the treatment of dyschromias and mottling. (56)

THERMAL RESURFACING

Thermal resurfacing, also referred to as cold ablation (“coblation”) or radiofrequency ablation is essentially removal of the outer layer of skin via bipolar electrical current. It is a descendent of the bipolar systems originally used in orthopedics to resurface joint cartilage. While lasers rely on heat to remove tissue, coblation disrupts molecular bonds at a cellular level via the movement of ions and free electrons, which strike the bonds and disrupt them. (57)

The coblation procedure begins with application of povidine iodine to the skin. Local anesthetic may then be applied. Lastly, saline gel is placed over all of the areas to be treated. This gel is essential because the coblation device will energize particles in the saline gel, which will consequently strike tissues and disrupt tissues via their movement. (58)

Coblation can also use a saline solution. Isotonic saline is then passed over the stylet while the stylet remains in constant contact with the skin. Three bipolar strips separated by one mm are situated at the end of a stylet. Ions within the isotonic saline are energized by the bipolar frequency and form a “plasma” of charged ions able to break down molecular bonds within the tissue and cause separation of the epidermal-dermal junction. The plasma is theorized to form a plasma shield, decreasing both the energy reaching the target tissue and reducing the collateral tissue damage. (59) Skin is aggressively precooled and cooled during electrical current production in order to protect the epidermis and dermis. (60)

Topical and PO pain relief is given prior to the procedure, for deeper treatments a local anesthetic field blocks are performed. Antiviral and antibiotic prophylaxis are given to all patients because the layer of necrotic cobalted debris which will slough off after the treatment is a potential bacterial culture medium. (61)

Coblation injury is reported to be in between that of CO2 laser resurfacing and Er:YAG laser resurfacing. If the voltage is reduced so that the saline is not transformed into plasma, small vessels can be coagulated creating a bloodless field. However, some authors have reported some bleeding with over-aggressive wiping of skin, especially in those patients with prominent extant telangiectasias at the time of treatment. Ablation may be effective in some scar revision. It is probably less effective reduction in rhytids than CO2 or Er:YAG lasers. (62) Coblation also appears to have less erythema than laser resurfacing. Grekin reported less pronounced erythema, and resolution within two months. (63) Coblation seems to offer potential as a superficial resurfacing device. Due to the limited studies on thermal resurfacing, the ideal parameters of the device are not yet known.

CONTRAINDICATIONS TO RESURFACING

Given the significant potential morbidity following cutaneous resurfacing procedures, all candidates must receive and extensive preoperative treatment evaluation. Patients must be screened for their ability to tolerate the necessary recuperation and unpleasant cosmetic period immediately following the procedure. Preoperative medical evaluation should include a complete medical history and any medication allergies. Patients with active cutaneous infections must be excluded from therapy.

Patients should be asked about any history of poor scarring or keloid development, allergic tendencies, connective tissue disorders, or a history of oral herpes simplex virus. Recent literature suggests that patients with a recent history of Accutane (Isotretinoin) ingestion are at an increased risk for keloid development, consequently, these patients should not be treated for 12 months after completion of the course of therapy. (64)

In expert hands, complications are minimal. The exception is poor technique. (65) The great majority of complications occur during the post-operative reepithelialization process. There are differing opinions on the prophylaxis of herpes infections. (66,67) We routinely prophylax for all erbium Yag and carbon dioxide laser procedures as well as TCA chemical peels, regardless of history. Seven percent of patients developing a herpes infection post laser resurfacing do not report any history of herpes labialis. (Figure 2) By contrast, superficial chemical peels limited to the epidermis and superficial dermis that do not result in deepitheliazation are not routinely prophylaxed. (68)

A prior history of resurfacing or surgical procedures is another important possible contraindication. Some authors list prior blepharoplasty or face lift within the last 2 months as a relative contraindication to resurfacing due to the increased risk of scarring and temporary altered blood supply post-operatively. However, there is documented evidence of successful outcomes in patients who have had resurfacing done simultaneously with facelifts. Nontheless, caution is warranted when resurfacing an area with vascular compromise secondary to a recent procedure. Additionally, patients who have had prior skin muscle flap lower eyelid blepharoplasty through a subciliary approach may have reduced lower lid laxity secondary to weakened orbicularis muscular support. Skin contraction and further compromise to lower lid support following medium depth resurfacing of thin lower eyelid skin can occur placing the patient at particular risk for ectropion.

Other pertinent historical facts includes allergic or hypersensitivity reactions to topical anesthetics, petrolatum or lanolin. Although rare allergies to these agents can be problematic since they are routinely used in superficial and deeper resurfacing protocol and can lead to extension of the dermal injury. Also patients with recurrent facial candidal and/or adenexal infections require precautionary measures prior to a superficial resurfacing procedure and they may be relatively contraindicated for a deeper treatment.

CONCLUSION

Best results for all rejuvenating modalities lie in the joint hands of the cosmetic surgeon and the patient. The absolute need for pretreatment education and post treatment care cannot be overemphasized. Additionally, other adjunctive efforts such as judicious use of botulinum toxin and the use of filler substances can optimize results. Ultimately it is a combination of the surgeon’s skill and the patient’s compliance with instruction that determines the overall result. Setting realistic expectations for patients is an absolute imperative and will serve to maximize patient satisfaction.

Table I CHEMICAL PEEL CLASSIFICATION

Adapted from Matarasso SL, Glogau RG. Chemical face peels. Dermatol Clin 1991;9(1):131-5

Table II GLOGAU CLASSIFICATION OF PHOTOAGING

Adapted from Glogau RG. Aesthetic and anatomic analysis of the aging skin. Semin Cutan Med Surg 1996;15(3):134-8.

REFERENCES

1. Gilchrest BA. Skin and aging process. Boca Raton, FL: CRC Press, 1984:1, 120.

2. Gilchrest BA. Cellular and molecular changes in aging skin. J Geriatr Dermatol 1994;2:3-6.

3. Hurley HH. Skin in senescience: a summation. J Geriatr Dermatol 1993;1:55-61.

4. Lavker RM. Topical therapy of aging skin. J Geriatr Dermatol 1994;2:20-23.

5. Lavker RM, Kligman AM. Chronic heliodermatitis: a morphologic evaluation of chronic actinic dermal damage with emphasis on the role of mast cells. J Invest Dermatol 1988;90(3):325-330.

6. Glogau RM. Chemical peeling and aging skin. J Geriatr Dermatol 1994;2:30-35.

7. Kauvar ANB, Geronemus RG: Histology of Laser Resurfacing. Derm Clinics 1997;15(3) 459-467.

8. Ridge JM, Siegle RJ, Zuckerman J. Use of alpha hydroxyl acids in the therapy of photoaged skin. J Amer Acad Dermatol 1990;23:932.

9. Matarasso SL, Glogau RG. Chemical face peels. Dermatol Clin 1991;9(1):131-50.

10. Glogau RG. Aesthetic and anatomic analysis of the aging skin. Semin Cutan Med Surg 1996;15(3):134-8.

11. Thueson DO, Chan EK, et al. The roles of pH and concentration in lactic acid-induced stimulation of epidermal turnover. Dermatol Surg 1998;24(6):641-5.

2. Van Scott E. Alpha hydroxyl acids. Procedures for use in clinical practice. Cutis 1989;43:222-228.

13. Tung RC, Bergfeld WF, Vidimos AT, Remzi BK. Alpha-Hydroxy acid-based cosmetic procedures. Guidelines for patient management. Am J Dermatol 2000;1(2):81-8.

4. Tsai TF, Bowman PH, et al. Effects of glycolic acid on light-induced skin pigmentation in Asian and caucasian subjects. J Am Acad Dermatol 2000;43(2, pt. 1):238-43.

5. Monheit GD. Advances in chemical peeling. Facial Plastic Surg Clin N Amer 1994;2:5-9.

6. Brody HJ. Variations and comparisons in medium strength chemical peeling. J Dermatol Surg Oncol 1989;15:953-963.

7. Rubin M. Manual of chemical peels. Philadelphia: Lippincott, 1995

8. Monheit GD. The Jessner’s – TCA peel. Dermatol Clin 1995;13:277-283.

9. Leveque JL, Corcuff P, Rougier A, Pierard GE. Mechanism of action of a lipophilic salicylic acid derivative on normal skin. Eur J Dermatol 2002;12(4):XXXV-XXXVIII.

20. Grimes PE. The safety and efficacy of salicylic acid chemical peels in darker racial-ethnic groups. Dermatol Surg 1999;25(1):18-22.

21. . Kligman D, Kligman AM. Salicylic acid peels for the treatment of photoaging. Dermatol Surg 1998;24(3):325-8.

22. Smith W. Hydroxy acids and skin aging. Soap Cosmet Chem Spec 1993;9:55-56.

23. Roenigk H. Dermabrasion:Rejuvenation and scar revision, in Roenigk RH (ed): Surgical Dermatology. London, Martin Dunitz, 1993 509-516.

24. Hopping S. The Power Peel: Its Emergence and Future in Cosmetic Surgery. Int J Cosmet Surg 1999;6:98-100.

25. Freedman BM, Rueda-Pedraza E, Waddell SP. The epidermal and dermal changes associated with microdermabrasion. Dermatol Surg 2001;27(12):1031-3; discussion 1033-4.

26. Rubin MG, Greenbaum SS. Histologic effects of aluminum oxide microdermabrasion on facial skin. J Aesthetic Dermatol 2000;1:237-9

27. Freedman BM, Rueda-Pedraza E, Waddell SP. The epidermal and dermal changes associated with microdermabrasion. Dermatol Surg 2001;27(12):1031-3; discussion 1033-4.

28. Shim EK, Barnette D, Hughes K, et al. Microdermabrasion: A Clinical Histopathologic Study. Dermatol Surg 2001;27:524-9.

29. Hruza GJ, Dover JS: Laser skin resurfacing. Arch Dermatol 1996;132:451-455

30. Ross EV, McKinley JR, Anderson RR. Why does carbon dioxide laser resurfacing work? Arch Dermatol 1999;135:444-454

31. Hirsch RJ, Anderson RR. Principles of Laser-Skin Interactions. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology Elsevier Science London

32. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983;220:524-527

33. Garden JM: Dermatologic laser surgery. J Derm Surg Onc 1990;16:156-168.

34. Anderson RR, Parrish JA: Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science. 1983;220:524-527

35. Pappadivid E, Katsambas A. Lasers for facial rejuvenation: a review. Int J Dermatol 2003;42(6):480-7.

36. Goldberg DJ. Er:YAG resurfacing: what is its role? Aesthetic Surgery J 1998;18:255-260

37. Alster TS, Hirsch RJ. Single pass CO2 laser skin resurfacing of light and dark skin: extended experience with 52 patients. J Cosmet Laser Ther 2003;5:39-42.

38. Khatri KA, Ross V, Grevelink JM, Margo MM, Anderson RR. Comparison of erbium:YAG and carbon dioxide lasers in resurfacing of facial rhytids. Arch Derm 1999;135:391-397.

39. Alster TS: Cutaneous resurfacing with CO2 and erbium: YAG lasers: preoperative, intraoperative, and postoperative considerations. Plast Reconstr Surg 1999;103(2):619-32; discussion 633-4.

40. Alster TS: Cutaneous resurfacing with Er:YAG lasers. Dermatol Surg 2000;26(1):73-5.

4. Zachary CB: Modulating the Er:YAG laser. Lasers Surg Med 2000; 26(2):223-6.

42. Alster TS: Cutaneous resurfacing with CO2 and erbium: YAG lasers: preoperative, intraoperative, and postoperative considerations. Plast Reconstr Surg 1999;103(2): 619-32; discussion 633-4.

43. Bass LS. Erbium:YAG laser skin resurfacing: preliminary clinical evaluation. Ann Plastic Surg 1998;40:328-334.

44. Pham RT. Nonablative laser resurfacing. Facial Plastic Surgery Clinics of North America. 2001;9(2):303-10, ix.

45. S. Dayan, AJ Vartanian, Menaker G. NonAblative laser resurfacing using a long pulse 1064-nm Nd:YAG laser. Arch Facial Plas Surg. 2003; 5:310-315.

46. Zelickson BD, Kilmer SL, Bernstein E, et al: Pulsed dye laser therapy for sun damaged skin. Lasers Surg Med 1999;25(3): 229-36.

47. Lask GL, Lee PK, Seyfadeh M, et al. Nonablative laser treatment of facial rhytids. SPIE Proc 1997;2970:338-349.

48. Nelson JS, Millner TE, Dave D, et al: Clinical study of non-ablative laser treatment of facial rhytides. Lasers Surg Med 1998;17 (suppl 9): 150.

49. Kelly KM. Nelson JS. Lask GP. Geronemus RG. Bernstein LJ. Cryogen spray cooling in combination with nonablative laser treatment of facial rhytides. Archives of Dermatology 1999; 135(6):691-4.

50. Goldberg DJ: Non-ablative subsurface remodeling: clinical and histologic evaluation of a 1320-nm Nd:YAG laser. J Cutan Laser Ther 1999;1(3): 153-7.

51. Ross EV, Hardaway C, Barnette D, Keel D, Paithankar DY. Non-ablative skin remodeling with a 1450nm laser. Proceedings of the 20th annual meeting of the World Congress of Dermatology. Paris, France

53. Goldberg DJ, Cutler KB. Non-ablative treatment of rhytids with intense pulsed light. Lasers Surg Med 2000;26(2):186-200.

54. Bitter PJ. Noninvasive rejuvenation of photoaged skin using serial, full face intense pulsed light treatments. Dermatol Surg 2000;26:835-843.

55. Goldberg DJ. New collagen formation after dermal remodeling with an intense pulsed light source. J Cut Laser Ther 2000;2:59-61.

56. Goldberg DJ: Nonablative resurfacing. Clin Plast Surg 2000; 27(2): 287-92, xi.

57. Bornick DP. Coblation:An emerging technology and new technique for soft-tissue surgery. Plastic & Reconstructive Surgery 2001:107(2):615.

58. Burns RL, Carruthers A, Langtry JA, Trotter MJ, West TB, Alster TS. Electrosurgical skin resurfacing: a new bipolar instrument. Dermatol Surg 1999:25(7):586.

59. Sherk HH, Black JD, Prodoehl JA, et al. The effects of lasers and electrosurgical devices on human menicsal tissue. Clinical Orthoped & Relat Research 1995(310):14-20.

60. Grekin RC, Tope WD, Yarborough JM, et al. Electrosurgcial resurfacing: a prospective multicenter study of efficacy and safety. Archive Dermatol 2000;136(11):1309-1316.

6. Alster TS. Electrosurgical ablation: A new mode of cutaneous resurfacing. Plastic & Reconstructive Surgery 2001;107(7):1894.

62. Hirsch RJ, Lewis AB. Treatment of acne scarring. Semin Cutan Med Surg. 2001; 20(3):190-8.

63. Grekin RC, Tope WD, Yarborough JM, et al. Electrosurgcial resurfacing: a prospective multicenter study of efficacy and safety. Archive Dermatol 2000;136(11):1309-1316.

64. Katz BE, Mac Farlane DF..Atypical facial scarring after isotretinoin therapy in a patient with previous dermabrasion. J Am Acad Dermatol 1994;30(5 Pt 2):852-3.

65. Horton S, Alster TS. Preoperative and postoperative considerations for carbon dioxide laser resurfacing. Cutis 1999;64:399-405.

66. Walia S, Alster TS. Cutaneous CO2 resurfacing infection rate with and without prophylactic antibiotics. Dermatol Surg 1999;25:857-61.

67. Nanni CA, Alster TS. Complications of carbon dioxide resurfacing. Dermatol Surg 1998;24:315-320.

68. Manuskiatti W, Fitzpatrick RE, Goldman MP, Krejci-Papa, N., Prophylactic antibiotics in patients undergoing laser resurfacing of the skin. J AMer Acad Dermatol 1999;40:77-84.