Introduction

With the advancement of laser and non-laser light sources, the focus of skin rejuvenation is optimizing efficacy while minimizing recovery times. The gold standard for rejuvenation, at least for fine wrinkles, has been ablative modalities. Although ablative tools can achieve predictable cosmetic enhancement, the risks of scarring, infection, dyspigmentation, and prolonged recovery time make these modalities less attractive. Patients increasingly try to balance efficacy of skin rejuvenation within the context of downtime. Non-ablative skin rejuvenation normally mitigates the need for advanced anesthesia and can often be performed with only topical anesthesia. Thus, non-ablative modalities have enjoyed a greater role in skin rejuvenation.

A clear definition of non-ablative skin rejuvenation is important as the term is sometimes used haphazardly. In its most pure form, non-ablative rejuvenation improves skin quality without physical removal or vaporization of the skin. Ablative modalities, via vaporization, remove a portion, or all, of the epidermis and sometimes may remove parts of the dermis. This chapter focuses exclusively on non-fractional methods of non-ablative skin rejuvenation.

The dermis (and / or deeper epidermis) can be selectively damaged by two basic approaches:

Treatment of photodamage can be divided into various categories, and treatment protocols are based on a logical approach founded on the laser–tissue interactions delineated above. The goal should be to maximize skin rejuvenation, from reducing telangiectasias and lentigines to enhancing dermal remodeling.

The laser and non-laser systems used for non-ablative rejuvenation are a heterogeneous group of devices that emit wavelengths in the visible (400–760 nm), near-infrared (760–1400 nm), or mid-infrared (1.4–3 µm) ranges, radiofrequency (RF) devices, intense pulsed light (IPL) devices, as well as light-emitting diode (LED) devices (Box 5.1). Each of these modalities can induce dermal remodeling, as well as target other components, without epidermal ablation. Most investigators believe that photothermal heating of the dermis: (1) increases collagen production by fibroblasts and (2) induces dermal matrix remodeling by altering glycosaminoglycans as well as other components of the dermal matrix. Others believe that the laser / light interaction with molecular cellular components alters the cellular function of enzymes as well as cellular structural components. Altering the different components of cells, from enzymes to cellular wall constituents to nucleic acids, may then alter the environment and productivity of a given cell.

Photodynamic therapy (PDT) with aminolevulinic acid (ALA) has been show to augment the effects of laser or other light sources. Multiple laser and light sources have been used for photoactivation of protoporphyrin IX, leading to improved skin rejuvenation (Fig. 5.1).

Figure 5.1 Protoporphyrin IX absorption: due to the multiple absorption peaks of protoporphyrin IX, multiple lasers and light sources can be used to augment the effects following application of porphyrin precursors to the skin.

Non-ablative skin rejuvenation is commonly used to reverse photoaging in the dermis. This damage is directly correlated with the patient’s age and extent of ultraviolet exposure. Ultraviolet B (UVB) light alters nucleic acids as it interacts with epidermal keratinocytes, inducing cellular atypia. Over time, longer-wavelength ultraviolet A (UVA) light causes increases in oxygen radical formation, inducing alterations in the normal homeostasis of vessel formation, apoptosis, pigment generation by melanocytes, immune cell dysregulation, cytokine dysregulation, alteration of dermal matrix composition, and disruption in the transcription, translation, and replication of the cellular genetic code. Histological changes that accompany the clinical findings of photoaging include an atrophic epidermis, loss of the rete pattern, elastic fiber clumping in the papillary dermis, haphazard and reduced collagen production, and increased vasculature. These UV-induced changes correlate with the clinical appearance of photoaged skin, including skin laxity, atrophy and fragility, increased rhytid formation, telangiectasia, and alteration in the overall color, texture, and consistency of the skin. Thus the goal of rejuvenation is to replace damaged epidermal or dermal constituents with more robust, newly created ones. Physicians attempt to alter the quality of the keratinocytes and the pigment production of melanocytes, two key components of epidermal photodamage. Dermal photodamage rejuvenation typically has concentrated on improving the quality and inhibiting the degeneration of fibroblasts. Studies have shown an increase in antioxidant capacity and collagen synthesis after millisecond and nanosecond 532 nm and 1064 nm laser irradiation in fibroblast cell cultures.

Richard Glogau, MD developed a classification scale to chart the progression of clinical photoaging (Table 5.1). One can follow a patient from an early age, with relatively strong homogeneity of skin coloration and minimal wrinkles, to a more aged patient, with wrinkles at rest and a more heterogeneous skin coloration.

As one would expect, treating a Glogau grade I patient with current non-ablative modalities will achieve a higher percentage of photoaging correction versus more severely photodamaged patients. While ablative skin rejuvenation may achieve superior restoration of normal skin structures, especially for the Glogau grade III or IV patient (see Table 5.1), the downtime and potential risks are prohibitive for many patients. Nevertheless, as non-ablative technologies evolve, restoration of young, healthy skin with diminished risks and negligible recovery times is increasingly possible. The remainder of the chapter will focus on patient selection for non-ablative skin rejuvenation and discussion of the different devices.

Patient selection

Patient selection for non-ablative skin rejuvenation begins with an assessment of the degree and type of photoaging (see Table 5.1). The ideal patient is Glogau grade II or III with mild to moderate photodamage. Non-ablative therapies initiate new collagen formation (collagen I and collagen III) and might be appropriate in a Glogau grade I patient to prevent photodamage progression. Alternatively, a patient and / or a physician expecting dramatic change following a non-ablative rejuvenation procedure in a Glogau grade IV patient may be disappointed.

Sadick divides patients in a different manner, where cosmetic deficiencies are based on the histological location of solar damage. His selection process takes into account epidermal (type I) damage (Fig. 5.2) and dermal / subcutaneous (type II) damage (Fig. 5.3), and subsequently treatment is tailored to laser selectivity of the damage.

Figure 5.2 (A–C):Type I photoaging indications.

Republished with permission. Sadick NS 2003 Update on non-ablative light therapy for rejuvenation: a review. Lasers in Surgery and Medicine 32:120-128.

Figure 5.3 Type II Photoaging indications.

Republished with permission. Sadick NS 2003 Update on non-ablative light therapy for rejuvenation: a review. Lasers in Surgery and Medicine 32:120-128.

Another important factor in patient selection is the patient’s Fitzpatrick skin type. Fitzpatrick IV, V, and VI skin types may not be optimal candidates for particular non-ablative rejuvenation modalities that selectively heat melanin. The most common adverse result for non-ablative rejuvenation in darker skin patients is hyperpigmentation, a condition that usually resolves after 4–8 weeks (but can persist longer in some circumstances) with appropriate application of suppressors of melanin synthesis. Mid-infrared lasers, which minimize direct melanin targeting, can be used in patients with darker skin types. However, higher fluences in these patients may result in thermal damage and bulk heating, which can also result in dyspigmentation. Non-cryogen cooling devices can minimize bulk heating, whereas cooling devices that employ cryogen spray may induce pigmentary alterations similar to liquid nitrogen. See Chapter 10 for a detailed discussion of laser and non-laser light sources for the treatment of darker skin types.

Beyond skin type and amount of photodamage, there are some patients who might be excluded from non-ablative lasers and light sources based on medical criteria (Box 5.2). Oral retinoid use, recent rejuvenation procedures, infection, and active dermatitides are reasons to consider deferring a non-ablative rejuvenation procedure. Most likely oral retinoids will not affect the outcome, but no controlled study has investigated their effect on non-ablative skin resurfacing. Many texts advocate waiting a period of 6–12 months, most likely representing an extrapolation from ablative resurfacing wait times. Some cutaneous laser experts have used non-ablative devices 1 month following retinoid use without adverse outcomes.

Physicians must also consider the wavelength of the device. For example, devices that utilize visible light (i.e. LED devices, etc.) may exacerbate a phototoxicity / photosensitivity or a systemic condition that is photosensitive, like cutaneous lupus (although in a recent study only 7% of SLE patients reacted to visible light) (Fig. 5.4). On the other hand, some lasers may confer a protective quality. There is increasing evidence that IPL can activate fibroblasts as well as confer protection from future UV-induced skin damage.

Figure 5.4 Photosensitivity reaction following photodynamic therapy. The patient is shown 6 days after photodynamic therapy. Reaction resolved after 3 weeks.

Fillers and neurotoxins most likely are not affected by non-ablative modalities and can be administered in the same session. However, the non-ablative resurfacing should be performed last. This order will minimize the risk of neurotoxin diffusion, which should cease by 1 hour after the injection, and will reduce the possibility of edema obscuring endpoints in optimal filler placement.

Visible light and near-infrared / vascular lasers (Table 5.2)

Visible light lasers and near-infrared lasers are commonly used to treat vascular and pigmented lesions. Treatment of vascular lesions with visible light lasers can achieve histological correction of dyspigmentation, overall skin texture, dermal matrix abnormalities, and solar elastosis. Clinical improvement of solar lentigines, scars, including keloids and hypertrophic scars, and photoaging have all been observed. Orringer et al have reported increases in type I procollagen messenger RNA and subsequent dermal matrix remodeling following one treatment with a pulsed dye laser. Whether this is secondary to thermal alterations of cellular milieu or to vascular-injury-induced cytokines, the result is dermal remodeling, reversal of photoaging, and partial rhytid correction.