SECTION I • Aesthetic Surgery of the Face
5.2
Injectables and resurfacing techniques:
Soft-tissue fillers
Trevor M. Born, Lisa E. Airan, and Daniel Suissa
SYNOPSIS
■ Soft-tissue fillers provide versatile tools in the correction of facial
wrinkles and facial contouring, as well as in the restoration of the
volumetric loss associated with aging.
■ Reversibility is an advantageous property of fillers, allowing
adjustments that may be needed due to technical errors or changes in
the tissues that occur with aging.
■ Inexperienced injectors should always opt for rapidly resorbable fillers
such as hyaluronic acid (HA). This allows for faster resolution of any
technical errors or overinjection. Hyaluronidase can be used to
dissolve the filler.
■ With respect to the treatment of deep folds and tear troughs, it is
important to undercorrect these deformities. This results in a more
natural appearance and leaves room for further correction in the future
if that is desirable. Overcorrection of these areas can result in visible
abnormalities.
■ “Off-label” use of synthetic materials is technically possible but does
carry risk, and discretion should be exercised when using products in
this manner. Additionally, the patient must be informed.
■ Patients often forget their preoperative appearance; pre- and post-
treatment photography as well as highlighting asymmetries prior to
injection are essential.
■ Complications of dermal fillers can be avoided by the use of proper
technique (small aliquots, appropriate depth and quantity of injection,
undercorrection, etc.).
Access the Historical Perspective section online at
Introduction
There has been historical interest in the use of injected
material to modify the contour of skin and underlying soft
tissue. However, effective and safe tools to accomplish such
a goal have become available only in recent decades. The
plastic surgeon now has access to numerous fillers to soften
the stigmata of aging or correct the contour deficits that
occur with many disease processes. In order to use these
fillers optimally, one must understand the nature of each
product.
The goal of this chapter is to present the different classes
of fillers and the indications and techniques for their use.
Particular attention is paid to the correction of the aging face.
Furthermore, we will present possible contraindications and
complications of fillers and how to avoid or treat them. Prior
to mastering the use of soft-tissue fillers, it is important to
understand how wrinkles form.
The pathophysiology of wrinkles
Aging is a complex process, which is the result of both
intrinsic (soft-tissue maturation, skeletal change/atrophy,
and muscular hyperactivity) and extrinsic factors (gravity
and solar damage). As a result, the smooth curvy appearance
of the face is slowly replaced by sharp angles, fine and deep
wrinkles, and abrupt hollows and bulges. The anatomy of
facial aging is thoroughly reviewed in other chapters in this
volume.
With aging, bony changes give rise to a decrease in height
and a moderate widening of the facial skeleton. An increased
orbital volume, caused in part by a lower orbital rim, results
in sunken eyes. This, when combined with an age-related
reduction in maxillary height, leads to a reduced area for the
attachment of midfacial soft tissues. The cheeks descend and
consequently the nasolabial folds become deeper. The upper
lip complex appears bulkier, while tear troughs and perioral
rhytides appear. If teeth are lost, alveolar height decreases and
the chin atrophies. Additionally, the ligamentous attachments
of the soft tissues become lax, which further contributes to the
appearance of furrows and creases.
With age, cell division slows. The epidermis thins out, and
the epidermal–dermal junction becomes flatter. The integrity
of the stratum corneum decreases and the basal cells acquire
more atypia. As a result of these changes, water loss through
Access video lecture content for this chapter online at expertconsult.com
40
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
while for older patients, surgery can be combined with fillers
and other surface treatments to create an optimal result.8,9
Although the number and variety of products available are
impressive, the ideal filler has not yet been found.10–12 The
definition of an ideal filler may be debatable, but there are
certain basic qualities that are agreed upon (Box 5.2.1). Ulti-
mately, even though it is important that worldwide research
and development for the ideal soft-tissue filler continues, a
balance is needed between embracing new products and
ensuring patient safety. In fact, in May 2015, the FDA released
a safety communication entitled Unintentional Injection of Soft
Tissue Filler into Blood Vessels in the Face, which states that:
… unintentional injection of soft tissue fillers into blood vessels
in the face can result in rare, but serious side effects … This can
cause vision impairment, blindness, stroke and damage and/or
death of the skin (necrosis) and underlying facial structures. …
certain injection locations where blood vessel blockage have been
reported more often. These sites include the skin between the
eyebrows and nose (glabella), in and around the nose, forehead,
and around the eyes (periorbital region).13
The statement also goes on to recommend avoiding the injec-
tion of fillers if the level of training and experience is
insufficient.13
the skin is increased, leading to drier, more fragile skin. The
dermis becomes thinner and contains fewer elastic and col-
lagen fibers. Sebaceous glands are less numerous and less
active, which also contributes to skin dryness. All the above
changes lead to a drier, less elastic, more fragile skin that is
more susceptible to gravity and thus wrinkling.
Chronic sun exposure is the most significant environmental
factor impacting skin aging. It is responsible for dyschromia,
lentigines, telangiectasias, and the loss of the youthful pink
hue. Skin texture becomes coarser because the epidermis is
thicker in photoaged skin than in normal skin. Overall colla-
gen amount decreases, except in the superficial dermis where
there is an area of increased collagen production (grenz zone)
representing a chronic inflammatory process known as helio-
dermatitis. Solar elastosis is pathognomonic of photoaged
skin with abundant, degraded, thickened elastic fibers. Lastly,
sun exposure contributes to a reduction in ground substance,
contributing to deeper folds and wrinkles.
Microscopically, all wrinkles appear like thinned breaks in
the dermis. Even though the terms wrinkles, folds, creases,
furrows, and rhytides are often used interchangeably, specific
features can be used to distinguish between different types of
rhytides. Fine wrinkles refer to changes in the texture of the
skin that involve the superficial aspect of the dermis. Mimetic
wrinkles can extend down to the middle level of the dermis
(lines) or down to its full thickness (furrows). These are due
to the repeated folding of the skin secondary to the contrac-
tion of the facial muscles. As a result, they are perpendicular
to the direction of these muscles and occur in locations such
as the glabella, periorbita, forehead, and lips. Dynamic
wrinkles eventually become static, remaining visible even
when the underlying muscle is relaxed.
Folds refer to larger grooves with some level of skin
overlap. These are the result of soft-tissue descent second-
ary to gravity, decreased support, and loss of skin elasticity.
Examples include upper eyelid dermatochalasis, nasolabial
folds, marionette lines, jowls, and horizontal neck lines.
The tear trough is an infraorbital groove that results from
soft-tissue tethering along the arcus marginalis between
bulging orbital fat above and descending deflated soft
tissue below.
The importance of being able to classify wrinkles is central
to being able to direct treatment.1 Superficial lines that course
at the upper level of the dermis are amenable to dermabra-
sion, chemical peels, and lasers. Mimetic wrinkles respond to
muscle inactivation with neuromodulators (Botox, Dysport,
and Xeomin) or myotomy/myectomy but can also be
improved with the concomitant use of fillers. Finally, fillers
are most useful in the treatment of folds, during their early
stages, or as an adjuvant modality to surgery, during their
more advanced stages. To help guide the physician’s treat-
ment and their assessment of improvement, several classifica-
tion systems have appeared over the years. One of these, the
Lemperle classification, is based on wrinkle depth and can be
very helpful (Table 5.2.1).
Classification of fillers
Soft-tissue fillers are an ideal option for patients seeking facial
rejuvenation with minimal downtime. For the young patient
not requiring surgery, these materials offer a viable option,
Table 5.2.1 Biological fillers approved by the Food and Drug
Administration (FDA) in the United States
FDA-approved biological filler
Type
Cymetra
Human dermis
AlloDerm
Human dermal matrix
Dermalogen
Human collagen matrix
Surgisis
Porcine collagen matrix
Restylane/Perlane
Hyaluronic acid (bacterial)
Elevess
Hyaluronic acid (bacterial)
Juvederm
Hyaluronic acid (bacterial)
BOX 5.2.1 Ideal filler characteristics
• Non-toxic
• Biocompatible
• Long-lasting (if not permanent)
• Reversible
• Off the shelf
• Autologous
• Easy to use
• Safe
• Produces positive, natural, discernible change
• Minimal downtime
• Level of placement (could be placed through dermis at
subcutaneous, intramuscular, or periosteal levels)
• Predictable (permanence, bulk, and behavior)
• Performs well as a person ages
• Not discernible by touch/appearance
40.e1
Historical perspective
Historical perspective
The earliest reports of tissue augmentation by subcutaneous
implantation of small adipose grafts appeared over a century
ago with German surgeon Neuber.2 Later, with the discovery
of the syringe, Brunning first injected fat in 1911, but signifi-
cant resorption and fat necrosis depopularized this technique.
It was not until liposuction and the concept of micro fat graft-
ing that the use of lipoaspirate for soft-tissue augmentation
successfully resurfaced.
Concurrent with the initial efforts to graft fat came attempts
to inject other synthetic materials in order to volumize soft
tissue.2,3 In 1899, Robert Gersuny first injected Vaseline, while
later, Eckstein used paraffin to correct fistulas and hernias and
to attain aesthetic soft-tissue augmentation. Serious complica-
tions such as granulomatous inflammatory reactions (paraf-
finomas) and nodule formation, embolization, and migration
were reported early on, yet paraffin kept being used for over
two decades before it was abandoned.
The first reports of the use of silicone date from the end of
World War II in Japan when numerous women had their
breasts injected with non-medical grade silicone.4 Shortly
after, in 1947, Dr. James Barrett Brown first used silicone for
the correction of soft-tissue deficits in the US. Concurrently,
hard and rubber silicone found use in creating alloplastic
implants. Early flawed animal experiments suggested that
injectable silicone was safe, and physicians relied heavily on
this improper information. The popularity of the technique
led to numerous complications such as lump formation,
migration, ulceration, and extrusion. The illicit injection of
non-medical grade silicone continues to this day, even though
the US Food and Drug Administration (FDA) took a more
active role in criminalizing its use in the 1990s. Today, highly
purified medical grade silicone oil (AdatoSil 5000, Silikone
1000) is FDA approved for the treatment of retinal detachment
but not for cosmetic injections. These products can be used
“off label” for soft-tissue augmentation, but the safety data to
back up such practices are unfortunately not available.5,6
In 1981, bovine collagen was the first filler approved by the
FDA for soft-tissue augmentation; it soon became the gold
standard against which all fillers were compared. Its rapid
resorption and allergenic nature led to a series of efforts to
develop a compound that would not cause allergic reactions
and that would last longer. It was not until two decades later
that HA became available for clinical use. HA found multiple
medical uses before it was approved in the USA as a soft-
tissue filler. HA dermal fillers rapidly replaced collagen as the
gold standard in cosmetic soft-tissue augmentation.
The high demand and success of HA products led to an
intense search for products that are similar to HA, did not
cause hypersensitivity reactions, but are longer lasting.7 This
in turn led to a number of newer and longer-lasting products
such as poly-l-lactic acid (PLLA: Sculptra, FDA approval in
2004 for HIV-related facial lipoatrophy; Sculptra Aesthetic,
FDA approval in 2009), calcium hydroxyl apatite (Radiesse,
FDA approval in 2006), and polymethylmethacrylate (PMMA)/
polyacrylamide products such as Bellafill (previously Artefill,
FDA approval in 2006). Today, plastic surgeons have in their
armamentarium numerous safe fillers that can produce
unprecedented aesthetic results, provided that they are used
in an educated/safe manner.
41
Classification of fillers
A newer product, called Harvest PRP (Harvest-Terumo,
Plymouth, MA; FDA approval 2012) offers a cost- and time-
efficient in-office PRP extraction method, which only takes
15 min to process.
Also relatively recent, LAVIV or Azficel-T (Fibrocell Science,
Exton, PA; FDA approval 2011) is approved for the correction
of moderate to deep nasolabial folds. LAVIV is an autologous
cellular product composed of fibroblasts harvested from
postauricular skin.23 The fibroblasts obtained from the skin
biopsy are aseptically cultured and expanded until sufficient
cells for three consecutive injections are obtained. The
treatment sessions are spaced 3–6 weeks apart. Although
the mechanism of action of LAVIV is unclear, a two-point
improvement in the Lemperle classification scale was achieved
in up to 57% of subjects treated. The longevity of this correc-
tion beyond 6 months remains to be shown.24
Biologic fillers
Biologic materials derived from organic sources (humans,
animals, or bacteria) offer the benefits of ready, “off-the-shelf”
availability, but can introduce issues of allergenicity, immuno-
genicity, and transmission of disease.25–29 Biologics provide
only a temporary effect and typically do not correct the
wrinkles or creases completely. The three major types of bio-
logic tissue fillers are acellular soft-tissue matrix, collagen,
and HA products (see Table 5.2.1).
AlloDerm (LifeCell, Branchburg, NJ) is an acellular, struc-
turally intact sheet of human dermal graft that was first used
clinically in the treatment of full-thickness burns. Processed
from prescreened human cadaver skin, the cells responsible
for immunogenicity are removed while the matrix structure
and biochemical components are left intact. The grafted mate-
rial then acts as a template for recipient cell repopulation,
resulting in soft-tissue regeneration. Some of its cosmetic-
related applications include lip augmentation, nasolabial
fold correction, glabellar wrinkle softening, and rhinoplasty
(dorsum and tip), as well as septal perforation, Frey syndrome,
liposuction defect, and scar treatments. Complications include
infection, persistent palpability or lumpiness, and variable
“take” of the grafted material.
Cymetra (LifeCell, Branchburg, NJ) is also a lyophilized
acellular collagen matrix derived from human cadaver dermis,
but in a particulate form. It is FDA-approved for subcutane-
ous injection and is used for lips, nasolabial folds, and deep
wrinkles.
Bovine collagen, marketed as Zyderm and Zyplast (Aller-
gan, Irvine, CA), became available in 1981 and was the first
commercially marketed injectable approved by the FDA for
soft-tissue augmentation; at the time, it was the standard
against which all other fillers were compared. CosmoDerm
and CosmoPlast (Allergan, Irvine, CA) contained human col-
lagen and did not require a pretreatment skin test.30–32 They
are no longer available.
Hyaluronic acid is a glycosaminoglycan common to most
living organisms and is a component of synovial fluid and of
connective tissues of the skin, cartilage, and bone. In human
skin, HA adds bulk and acts as a shock absorber and lubricant.
HA, in its unprocessed molecular configuration, only lasts for
a couple days as it is rapidly degraded and metabolized by
the liver.33 The solution to this problem has been to cross-link
In order to better understand the properties of each product
that is either already available or in the pipeline, fillers can be
classified into the following categories:
■ autologous materials
■ biologic materials
■ synthetic materials.
Autologous fillers
Autologous materials are derived from the patient’s own
tissue.14–17 They therefore come closest to matching the
description of the ideal soft-tissue filler in terms of safety.
However, they are not as convenient to use since they require
a two-step procedure – harvesting of tissue and injection.
Toxicity, allergenicity, immunogenicity, carcinogenicity, and
teratogenicity are not issues, but there can be problems with
donor site scar, infection, migration, inflammatory reactions,
loss of persistence, and unreliable reproducibility. Autologous
fillers include:
■ dermis, fascia, cartilage, superficial musculoaponeurotic
system (SMAS), breast implant capsule
■ fat grafts
■ platelet-rich fibrin matrix (PRFM)
■ platelet-rich plasma (PRP)
■ cultured fibroblasts
■ bone marrow-derived and adipose-derived stem cells.
Dermis and cartilage grafts have a long history of use in
plastic surgery, and with careful handling and placement,
these grafts may have good, long-lasting results. Similarly,
fascial grafts from the fascia lata of the thigh, the temporalis,
and the SMAS can be used. In a good recipient bed, fascia is
permanent and persists through a combination of creeping
replacement by host fibroblasts and continued viability of
fascial fibroblasts.
Fat grafts as free en bloc transfers of tissue lose at least
one-half of their bulk after transplantation, and frequently
develop cysts, calcifications, and necrotic lumps. However,
this is not the case with micro fat grafting in which small
intact packets of fatty tissue are harvested as atraumatically
as possible and injected in tiny amounts along multiple tracts.
This keeps the injected fat cells near a blood supply for
increased survival and integration. The great advantage
of this technique is that the fat that survives is permanent.
The disadvantage is the unpredictability of the survival, the
need for a donor site, and the time required to process the
fat.14–16,18
Selphyl (Aesthetic Factors, Princeton, NJ) is a patented
system that allows the extraction of PRFM from the patient’s
own blood.19,20 This novel technology allows processing of
blood in the office in a three-step process that takes approxi-
mately 20 min. The collected PRFM is then injected into the
patient’s wrinkles. The collection of a 9-cc blood sample
allows the collection of 4 cc of PRFM. The development of
collagen and dermal matrix increases over a period of 3 weeks
and there is early evidence to suggest long-lasting wrinkle
correction (up to 20 months).19,21,22
Possible applications include correction of nasolabial folds,
glabellar lines, and panfacial rejuvenation, as well as acne and
other scar treatments. Selphyl has been cleared for use in the
US (FDA) and Europe (CE mark).
42
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
Table 5.2.2 Biological fillers not approved by the Food and Drug Administration (FDA) in the United States
Non-FDA-approved biological fillers
Type
Country (approval)
R-fine
Hyaluronic acid
Canada, Europe, Asia
Emervel
Hyaluronic acid (cross-linked)
Europe
Hyaluderm
Hyaluronic acid
Europe
Revanesse/ReDexis
Hyaluronic acid (cross-linked)
Canada
MacDermol S/MacDermol R
Hyaluronic acid (avian, cross-linked)
Europe
Varioderm
NASHA
Europe
Amalian
NASHA
Europe
Macrolane
NASHA
Europe
Teosyal
NASHA
Europe, Canada
Zetaderm/Zetavisc
NASHA
Europe, Canada, Russia
HydraFill
NASHA (cross-linked)
Europe
Esthelis/Fortelis/Belotero
NASHA (CMP technology cross-linked)
Europe, Canada, Asia
Puragen
NASHA (DXL technology cross-linked)
Europe
Rolifan/Philoderm/Beautygel/ Esthirase/Coilingel
NASHA (cross-linked)
Europe, Canada, Brazil
HyalSkin
NASHA (BDDE cross-linked)
Europe
BDDE, 1,4-butanediol diglycidyl ether; CMP, cohesive polydensified matrix; DXL, double cross-linked; NASHA, non-animal-stabilized hyaluronic acid.
HAs into more stable compounds with significantly longer
degradation times.34
HA, being extremely hydrophilic, maintains its volume by
binding water from the interstitial fluids around it. In fact, 1 g
of HA can bind an impressive 6 L of water.33 As the HA is
progressively degraded by the surrounding tissues, underly-
ing molecules of HA bind more water and therefore maintain
the initial filling volume. This process is called “isovolumetric
degradation” and it is the reason that HA fillers can maintain
a virtually constant fill volume until the product is almost
completely degraded.33,35
The significant differences between the HA fillers on the
market today include the source of HA, concentration, type
and degree of cross-linking, amount of free unmodified HA
present, and whether the product is monophasic (cohesive
gel) or biphasic (particulate). Another crucial characteristic
is the elastic modulus or G′ (pronounced G prime) of a
gel, which is a measure of its firmness and resistance to
deformation.36
Restylane (Galderma, Lausanne, Switzerland) is a HA soft-
tissue filler that originally received FDA approval in 2003 for
use in the correction of facial wrinkles.7,37–45 It is now mar-
keted as four products differing in the size of the constituent
particles: Restylane, Restylane-L, Restylane Silk, and Perlane.
Hydrelle, previously Elevess (Arnica Therapeutics, Bedford,
MA; FDA approval 2006), is a product that contains higher
concentrations of HA as well as lidocaine and is intended for
medium wrinkles and deeper folds. Prevelle Silk (Mentor,
Santa Barbara, CA; FDA approval 2008) was introduced in
the US in 2008, and it is equivalent to Restylane. In 2006,
Allergan’s Juvederm series of HA fillers received FDA clear-
ance. Juvederm fillers come in various concentrations and
viscosities. In Europe, they are labeled as Juvederm Ultra
2, 3, and 4 and Juvederm Voluma, while in North America
they are marketed as Juvederm Ultra and Juvederm Ultra
Plus and may contain lidocaine (Juvederm XC). In 2013,
Juvederm Voluma XC obtained FDA approval, but Volbella
and Volift are still only available in Canada and Europe at
the time of writing this chapter. These newer HA fillers use a
patented Vycross technology, which incorporates short- and
long-chain HA leading to more efficient cross-linking than
Juvederm Ultra, which only has long-chain HA. Addition
of the short chains of HA permits more cross-links, more
stability, and consequently, a longer lasting filler than the
previous generation. This increased cross-linking also pro-
duces a more viscose gel, and therefore a greater lift capacity
as well.46
Belotero Balance (Merz Aesthetics, Greensboro, NC; FDA
approval 2011) is another of the newer HA fillers available. It
has unique properties that make it softer (lower G′), longer
lasting, and particularly useful for superficial injections of fine
lines. Its low viscosity allows it to spread evenly throughout
the soft tissues, which makes for a soft, smooth fill.47
As discussed above, many of the recent fillers already
contain lidocaine, but alternatively, lidocaine (usually 2%) can
be mixed with most fillers to obtain analgesia during injec-
tion. However, doing this will most probably change the
viscosity of the product, as well as certain of its properties.
There are still a large number of non-FDA-approved biologi-
cal fillers, which are available in the rest of the world.48 These
are mainly HA-based products, with various sources, process-
ing, and cross-linking (Table 5.2.2).
Synthetic fillers
Synthetic materials can offer permanence. Many injectable
and surgically implantable synthetic products have been used
over the years, and many have been condemned for complica-
tions, including granulomas, acute and delayed infections,
migration or displacement, and deformities that can result
from complications or removal of the material. It is with these
products that the difference between the regulatory process
43
Injection technique
Table 5.2.3 Synthetic fillers approved by the Food and Drug
Administration (FDA) in the United States
FDA-approved
synthetic fillers
Type
AdatoSil 5000
Silicone
Silikon 1000
Silicone
Bellafill (Artecoll)
Polymethylmethacrylate (PMMA)
Radiesse
Calcium hydroxyapatite
Sculptra (New-Fill)
Poly-L-lactic acid (PLLA)
Table 5.2.4 Synthetic fillers not approved by the Food and Drug
Administration (FDA) in the United States
Non-FDA
approved
synthetic fillers
Type
Country
(approval)
Bioplastique
Silicone
Europe
Aquamid
Polyacrylamide
Europe, 40 other
countries
Beautical
Polyacrylamide
Europe
Bio-Alcamid
Polyacrylamide
Europe
Outline
Polyacrylamide
Europe
Evolution
Polyacrylamide
Europe
Formacryl
Polyacrylamide
Russia
Argiform
Polyacrylamide
Russia
Bioformacryl
Polyacrylamide
Ukraine
Amazing Gel
Polyacrylamide
Asia
DermaLive/
DermaDeep
Polyacrylamide
France
Metacril
Methylmethacrylate
Brazil
ArteSense
Methylmethacrylate
Europe, Canada,
Asia
Rhegecoll
Methylmethacrylate
Pending
worldwide
Laresse Dermal
Filler
Carboxymethylcellulose/
polyethylene
Europe
Atléan BTCP
Tricalcium phosphate
Europe
Bioinblue
Polyvinyl alcohol
Europe
Reviderm
DEAE Sephadex
Europe, Canada,
Asia
Matridex
DEAE Sephadex
Europe
DEAE, diethylaminoethyl.
in the US and that in the rest of the world is highlighted. The
FDA controls access to the US market and enforces strict
“labeling” practices, which means that the manufacturer must
spell out the exact applications for which the material has
been approved. Synthetic fillers approved by the FDA appear
in Table 5.2.3.
AdatoSil 5000 and Silikone 1000 are silicone gels with
improved viscosity that have been approved by the FDA for
use in treating detached retina. They are not approved for
cosmetic use in the US, and caution is advised with these
products. Historically, injectable silicone products have
tended to harden, migrate, and cause inflammation and skin
necrosis.4,49
Bellafill is a permanent injectable implant consisting of
polished PMMA microspheres suspended in bovine collagen
in a 20 : 80% ratio.50–52 After injection, the collagen is resorbed
and the round, smooth microspheres are encapsulated by host
collagen where they are stabilized and become permanent.
Used in Europe for the past decade as Artecoll, Bellafill was
approved by the FDA in October of 2006.
Radiesse is a mixture of calcium hydroxyapatite (30%) and
polysaccharide gel (70%).52–58 The polysaccharide gel is very
white, which makes Radiesse inappropriate for use in the
dermis. Radiesse is FDA-approved (December 2006) for
nasolabial and labiomental crease correction, and since mid-
2015 it is also FDA approved as a cosmetic filler for the dorsum
of the hand.59 It is reported to last anywhere between 1 and 2
years.
Sculptra (Galderma, Lausanne, Switzerland) is a biocom-
patible, biodegradable material that is composed of PLLA
(poly-l-lactic acid), sodium carboxymethylcellulose, and non-
pyrogenic mannitol. It must be reconstituted with 5–10 mL of
sterile water at least 2 h prior to injection and does not require
a skin test.60,61 Sculptra is hypothesized to induce the produc-
tion of fibroblasts leading to collagen production. Over time
(6–24 months), Sculptra is degraded in the skin to carbon
dioxide and water.62,63
Sculptra has been used in surgical products for more than
20 years as a component of dissolvable sutures. It has also
been safely used outside the US since 1999 in over 30 countries
under the trade name of “New-Fill” for a variety of facial
volume and contour deformities. It was approved by the FDA
in August of 2004 as the only product for the correction
of human immunodeficiency virus (HIV)-associated facial
lipoatrophy and is also approved for cosmetic use in the USA
(Sculptra Aesthetic; FDA approval 2009). It is injected subcu-
taneously in the area of fat loss/volume loss and provides a
gradual and significant increase in volume. It is reported to
last up to 2 years after three consecutive treatment sessions,
approximately 1 month apart.
A large number of other synthetic fillers are available in
various parts of the world and a few are listed in this
chapter48,64 and in Tables 5.2.4 and 5.2.5. It is difficult to
comment on the effectiveness and safety of these products
because very little evidence to support these products is found
in the literature.
Injection technique
Before using injectable fillers, anesthesia of the areas to be
treated should be considered. Nerve blocks, such as mental,
infraorbital, and supraorbital/supratrochlear, work well and
provide analgesia to large areas of the face. Direct infiltration
of the area with lidocaine is another option, but this could lead
to distortion of the anatomic structure to be corrected, and
thus potentially to over- or undercorrection. The inclusion
of epinephrine in the infiltration can potentially decrease
bruising.65
44
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
Table 5.2.5 Filler characteristics
Filler
Category
Composition
Viscosity*
Level of
placement†
Advantages
Disadvantages and
complications
Perlane
Biologic
HA (bacterially derived)
+++
Deep dermis
Long-lasting
Can be used in
deep tissue and
along bone
Minimal reactions
No skin test
More swelling – up to 3–5
days
Juvederm
Ultra Plus
Puragen
Restylane
Biologic
HA (bacterially derived)
++
Superficial
dermis
Long-lasting
Can be used in
deep tissue and
along bone
Minimal reactions
No skin test
More swelling – up to 3–5
days
Juvederm
Ultra
HA (bacterially derived)
HA (bacterially derived)
HA (avian culture-
derived)
Elevess
Hylaform
Restylane
Fine Lines
Biologic
HA (bacterially derived)
+
Dermoepidermal
junction
Great for glabellar
region and fine
lines
Do not use along
bone
Shorter-term longevity than
Restylane or Perlane
Bellafill
(ArteColl)
Synthetic/
biologic
Polymethylmethacrylate
(PMMA) beads
covered with bovine
collagen
+++
Deep dermis or
subcutaneous
Long-lasting in
deep folds and
acne scars
Bumps, which may require
treatment with steroids or
surgery to remove
Risk of granuloma
Collagen reactivity
Requires skin test
Radiesse
Synthetic
Calcium hydroxyapatite
+++
Deep dermis or
subcutaneous
Long-lasting
Can be used in
deep tissue and
along bone
Minimal reactions
No skin test
More swelling – up to 3–5
days
Irregularities (technically
dependent)
Sculptra
Synthetic
Poly-L-lactic acid
(PLLA)
++
Deep dermis or
subcutaneous
Long-lasting
Can be used in
deep tissue and
along bone
Minimal reactions
No skin test
More swelling – up to 3–5
days
Irregularities (technically
dependent)
Inflammatory reactions
Multiple treatments required
HA, hyaluronic acid.
*Viscosity is not measured by most companies in terms of flow: + least thickness, easiest/best flow; ++ in between; +++ most thickness, more difficult flow.
†Level of placement is also dependent on amount/type of desired correction.
The needle used for injection largely depends on the viscos-
ity of the product injected. Less viscous HA products, such as
Restylane Fine Lines, are injected with 30–31 G needles. More
viscous HA products, such as Restylane, Perlane, and Juva-
derm, can be slowly injected through either a small needle
such as a 30 G or a larger 28 G needle with more ease. Radiesse
usually requires a 28 G needle, while Sculptra and Bellafill,
which are among the most viscous products injected, require
at least a 26 G needle. Injection is usually in an anterograde or
retrograde fashion, as the needle is advanced or withdrawn
respectively.
The injection technique can vary from simple linear thread-
ing and the deposition of a small aliquot to more complex
methods such as serial linear threading, radial fanning, cross-
hatching, and serial puncture deposition.66 These techniques
are used in combination depending on the location to be
treated.
The linear threading or tunneling technique involves injec-
tion either intradermally or into the subcutaneous level (Fig.
5.2.1A). Once the needle is inserted, the product is injected in
a retrograde fashion. Linear threading is most commonly
used to correct wrinkles and furrows. However, when deeper
creases are treated, multiple parallel linear threads at different
levels have to be used to accomplish the desired volumetric
augmentation (Fig. 5.2.1C). Examples of where this technique
is commonly used include the glabellar lines, the nasolabial
folds, the lips, and the tear trough, among others.
Radial fanning is a variation of the linear threading tech-
nique (Fig. 5.2.2A). Just before the needle is completely with-
drawn from the skin, it is reinserted in a different direction
45
Injection technique
Fig. 5.2.1 The (A) linear threading or tunneling, (B) droplet or depot, and (C)
parallel linear threading techniques for dermal filler injection.
A
Epidermis
Dermis
Subcutaneous
tissue
B
Epidermis
Dermis
Subcutaneous
tissue
Muscle
Periosteum
Bone
C
Epidermis
Dermis
Subcutaneous
tissue
A
B
Fig. 5.2.2 (A) Radial fanning and (B) cross-hatching techniques of dermal filler
injection.
46
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
then neuromodulators will be very helpful in achieving a
better result and increasing longevity. If neuromodulators are
not used, then the filler may only last for a short period of time.
Caution with neuromodulators should be exercised in patients
with moderate to severe brow ptosis. More commonly, low-
viscosity fillers (i.e., Restylane Fine Lines) are used, and these
are placed at the dermal–epidermal junction using a serial
droplet or linear threading technique (Fig. 5.2.3C).
Eyebrows
The eyebrows may be elevated 1–2 mm by the addition of an
MVHA filler such as Restylane to the deep tissue layer of the
lateral eyebrow. The volume of the temples generally decreases
with age and the placement of approximately 1 cc of HA on
the deep layer can help restore the youthful contour and raise
the eyebrow. Moreover, the surgical removal of the fat of the
upper eyelid is sometimes to such a degree that it results in a
hollow or skeletonized orbital rim. The same hollowing may
be seen in some individuals as a consequence of the aging
process. This cadaveric appearance may be corrected with
placement of HA on the inferior aspect of the supraorbital rim.
This also gives the illusion of raising the eyebrows while
restoring a more youthful appearance to the upper lid and
eyebrow region.
Care must be taken to inject small volumes with each
pass to prevent emboli and injury to the sensory nerves.
The filler is placed at a level that is not mobile. Caution is
necessary in the eyebrow region as the supraorbital and
supratrochlear nerves/vessels emerge here. MVHA fillers
are good deep fillers in this case. HVHAs, such as Perlane,
are a longer-lasting alternative and can be used in a similar
fashion.
Tear troughs
Tear troughs can be corrected with fillers to give a rested and
more youthful appearance. The infraorbital rim hollowing
and the nasojugal groove can be filled by injecting product
deep on the bone and periosteum (Fig. 5.2.4). This ensures that
the product is not palpable or visible, especially with anima-
tion. Various fillers have been used for this purpose, but the
most commonly applied are Restylane, Juvederm, or Perlane.
Other long-term fillers such as Radiesse, Sculptra, and Bellafill
can have a devastating outcome in the case of visible nodular/
granulomatous formation, and should be avoided for this
use.53,70–72
Usually 0.5–1.5 cc of filler is used per side, depending on
the severity of the tear trough and the desired projection of
the malar prominence. The area to be corrected should be
marked before the injection of local anesthetic, and adequate
time should be given to maximize the effect of the epinephrine
and minimize bruising. The filler is applied in a retrograde
fashion using the serial droplet or serial threading technique,
always feeling for the orbital rim with the free hand. Once
injected, the product can be massaged to smoothen its distri-
bution over the bone and the hollow. If swelling and bruising
are noticed immediately after filler injection, pressure and
cold compresses should be applied. In the case of overcorrec-
tion, the product can be massaged down for up to 2–3 weeks.
If the overcorrection persists, the HA filler can be partially
dissolved with hyaluronidase.
and the product is again injected in a retrograde fashion. This
process is repeated multiple times in different directions until
adequate correction is accomplished. This approach is particu-
larly useful in malar augmentation, but it is also used in the
correction of the prejowl sulcus and the nasolabial fold.
Cross-hatching is often used in the correction of large
surface areas such as the marionette lines/prejowl sulcus or
the hollowing of the lower cheek (Fig. 5.2.2B). Two indepen-
dent radial fanning injections oriented perpendicular to each
other constitute also a form of cross-hatching and are com-
monly used in cheek augmentation.
Frequently the needle is inserted deep into the tissue and
an aliquot of product is laid down; this is known as the depot
or droplet technique (Fig. 5.2.1B). Large volumes deposited in
this fashion can lead to palpable nodules and irregularities.
Usually small droplets are deposited in a serial fashion; this
is known as the serial puncture technique. These aliquots
have to be close together to prevent irregularities. If any
irregularities appear they can be managed by massaging. This
technique is frequently used for tear trough correction and in
lip augmentation, but also in the treatment of all other wrinkles
and creases. Experienced injectors often use combinations of
all of these techniques.
Some practitioners recommend the use of blunt-tipped
microcannulas. Many authors describe their experience of
decreased bruising, especially when using a fanning injection
technique.67–69
Indications and applications
There are multiple indications for the use of dermal fillers.
Below is a list of the most common areas of the aging face
usually addressed with injectables. The appropriate types of
fillers for each area, as well as some technical nuances for their
optimal application, are also described. For the purpose of this
discussion, low-viscosity HA (LVHA) fillers refer to Restylane
Fine Lines/Belotero Balance, medium-viscosity HA (MVHA)
fillers refers to Restylane/Juvederm Ultra/Hydrelle, while
high-viscosity HA (HVHA) fillers include Perlane/Juvederm
Ultra Plus.
Glabellar lines
The folds of the glabella are ideally treated in combination
with neuromodulators (botulinum toxin). The glabellar fold
may be a fairly superficial line with a deeper etched compo-
nent that is best treated with Restylane Fine Lines at the
dermal–epidermal junction; the product is placed in a serial
droplet or serial linear threading fashion. The threading can
be parallel or cross-hatched. If the fold is broader, then an
MVHA filler may be used; this is placed at the mid to super-
ficial dermis. Small amounts must be injected to avoid tissue
necrosis. When combined with neuromodulators, the effect
can last from 8 months to much longer. Layering of these
fillers may be needed on occasion. Care should be taken in
the patient with very thin skin as the filler may cause lumps
or bumps.
Forehead lines
The injection technique in this area is similar to that used for
the glabellar lines. If the patient has a very dynamic forehead,
47
Indications and applications
Fig. 5.2.3 Injection of dermal filler into the deep tissue/periosteal level (A), more
superficial into the subcutaneous tissue (B), and into the most superficial
epidermal–dermal junction (C).
A
Epidermis
Dermis
Subcutaneous
tissue
Muscle
Bone
Periosteum
B
Epidermis
Dermis
Subcutaneous
tissue
C
Epidermis
Dermis
Subcutaneous
tissue
Fig. 5.2.4 Tear troughs. (A) This 48-year-old woman presented with significant
tear troughs that made her appear tired. Perlane was placed at the depth of the
periorbital hollow on the bone and on the malar bone to augment cheek projection
and minimize the negative vector. A total volume of 1.1 cc was placed per side; it
was placed mainly in the periorbital hollow, but a smaller amount was placed on
the malar bone to increase cheek projection relative to the globe. (B) The patient is
seen 6 months after treatment.
A
B
Nasolabial folds
The nasolabial folds may be of different shapes, lengths, and
depths. In addition, some patients have pre-existing telangi-
ectasia in this area that can be made worse with injections.
The gradation system, as described by Dr. Lemperle (Table
5.2.6), is useful in evaluating and discussing with patients
their goals.
The amount of change in the average case should be
approximately 50% correction of the depth of the fold (Fig.
5.2.5). Care must be taken not to overfill the fold because this
will give patients an odd appearance when they animate or
smile. Fillers can be used to soften the broader portion of the
fold, which is usually the upper two-thirds down to the lateral
oral commissure. Choices here include all types of fillers.39
MVHAs and collagens can be placed at the level of the mid
to deep dermis. With HVHA fillers such as Perlane, as well as
the semipermanent or permanent fillers (Radiesse, Sculptra,
Bellafill), the product should be placed in the deep subcutane-
ous tissue (see Fig. 5.2.3C).43,70,73,74 The filler is placed at angles
to the fold in order to decrease the risk of intra-arterial facial
artery injection. Layering may be performed to enhance lon-
gevity (see Fig. 5.2.4B). Also, for very deep folds, more viscous
products (Perlane) or permanent/semipermanent products
(Radiesse, Sculptra, Bellafill) may be placed deep under less
viscous fillers such as Restylane and Juvederm. This may
increase longevity of the correction and give a more polished
appearance. If the nasolabial fold has a superficial line etched
into it, this can be softened with Restylane Fine Lines. As with
all repeated injections of HA, the product lasts longer and less
volume of product is needed to achieve the same volume and
contour change. Taping of the fold after the injection for a few
days may help the product bind into place with scar tissue
and can prevent the lateral displacement of the product to the
nasolabial fold when the patient smiles.
48
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
be used in this manner applying the product over bone, into
deep tissue, and in the dermis. Alternatively, more durable
fillers such as HVHAs, Radiesse, Sculptra, or Bellafill can be
used deep, with MVHAs placed more superficial to obtain
further refinement if necessary. This approach leads to a more
durable result. The most appropriate technique for malar
augmentation is the radial fanning technique, with entry
points first lateral and then inferior to the malar prominence
(see Fig. 5.2.4A). Nevertheless, any other technique can prob-
ably yield adequate results. Pressure over the augmented area
should be avoided over the first week post-treatment. When
used appropriately, dermal fillers can replace the use of an
implant for malar augmentation.
Marionette lines
Marionette lines extend from the oral commissure in a down-
ward oblique fashion, giving a sad appearance. Usually there
is a volume deficit medially extending to the level of the
jawline, creating what is known as the prejowl sulcus. There-
fore, correction of the marionette lines is often combined with
correction of the prejowl sulcus. Most fillers available today
can be used for correction of the marionette lines. The prin-
ciples mentioned earlier for other sites apply here too. More
permanent viscous fillers are used for deeper correction, with
less viscous, finer products such as Restylane for more super-
ficial correction.76 The area to be filled is actually triangular,
extending from the marionette line to the lower lateral lip
vermilion to the superolateral aspect of the chin (Fig. 5.2.6).
Usually a radial fanning technique from two independent
injection sites, superior and inferior, can lead to a smooth
correction of the area (see Fig. 5.2.4C). In this dynamic area,
partial to complete correction is possible, but overcorrection
can lead to lumps that are visible or felt intraorally under
the oral mucosa, as well as a strange appearance upon
animation.
Jawline augmentation
In the areas along the jawline (filling the hollow anterior to
the jowl), filler is best placed on the very deep plane on the
bone (ideally beneath the periosteum) or subcutaneously to
allow augmentation of the soft tissues similar to a solid
implant (see Fig. 5.2.3A). HVHAs or MVHAs may be used.
Jawline augmentation is usually combined with marionette/
prejowl sulcus correction. HA is placed in the deepest point
of the hollow. This will correct most of the deformity. Place-
ment of the material in the deep dermis may be required for
complete correction of the jowl deformity.
Panfacial volumetric augmentation
With aging, soft-tissue descent and atrophy make the appear-
ance of hollows and creases more pronounced. Reconstitution
of the overall facial volume, including correction or the tem-
poral hollowing, lifting of the brow, filling of the periorbital
hollowing, and malar, jawline, and perioral enhancement, can
result in a markedly rejuvenated appearance (Figs. 5.2.7 &
5.2.8). This non-surgical facelift can be achieved with HA,
Sculptra, or Radiesse injected in the deep tissues, in combina-
tion with superficial HA injections to obtain more refinement.
Because both Radiesse and Sculptra show a delay in the
appearance of the final result and because multiple
Malar augmentation
Malar augmentation can be achieved with most fillers avail-
able.75 In the case of semipermanent and permanent fillers,
care must be taken for the product to be injected deep in the
tissue (see Fig. 5.2.3A). With HA fillers, the product can be
applied from the deepest layers to the most superficial (see
Fig. 5.2.3A–C). MVHAs such as Juvederm and Restylane can
Table 5.2.6 The Lemperle nasolabial fold classification
Class
Description
0
No wrinkles
1
Just-perceptible wrinkles
2
Shallow wrinkles
3
Moderately deep wrinkles
4
Deep wrinkles, well-defined edges
5
Very deep wrinkles, redundant folds
Fig. 5.2.5 Nasolabial folds and marionette lines. (A) This 64-year-old woman
presented with perioral lines and significant jowls. However, she was not interested
in surgical rejuvenation and wanted just to soften the appearance of her perioral
wrinkles and folds. Approximately 0.4 cc of Restylane was used for each nasolabial
fold and 0.3 cc to address the marionette lines on each side. (B) The patient is
shown 1 month post-treatment.
A
B
49
Indications and applications
Fig. 5.2.6 Technique used (A) for malar augmentation, (B) for marionette lines,
and (C) for nasolabial folds.
A
1st needle
insertion point
2nd needle insertion point
B
2nd
1st
C
2nd
2nd
3rd
1st (0.5” needle)
1st (0.25” needle)
Fig. 5.2.7 Sculptra. (A) Preoperative and (B) 1-year postoperative results after
augmentation to the brow, cheeks, and jawline with three sessions of Sculptra (two
vials per session) in a 51-year-old female. The dilution of each vial of Sculptra
consisted of 7 cc of sterile water and 3 cc of 1% Xylocaine with epinephrine.
A
B
injections may be required, the use of more viscous HA fillers
in the deep tissues may be used instead for an immediate
effect and more predictable results. The advantage of using
Radiesse and Sculptra is that they last for 1 and 2–3 years,
respectively. Alternatively, fat can be used for panfacial
volumetric augmentation, with “finer” fillers such as Restylane
or Restylane Fine Lines used to obtain a more superficial
correction.
Facial lipoatrophy
HVHAs or MVHAs are ideal fillers to soften the appearance
of lipoatrophy associated with antiretroviral therapy for HIV.
Other options include Sculptra, Radiesse, Bellafill, and fat.77,78
The areas that are best treated are the concavities adjacent to
the zygomatic–temporal bone, the zygomatic arch, and less so
for the inframalar hollow. In the temple and adjacent to the
arch, it is important to place the filler deep within or under
the periosteum and take care to inject slowly to be sure of even
placement and to minimize bruising. The product is easily
massaged, but if the massage is too aggressive the entire effect
will be minimized. The idea is not to fill the entire area of
atrophy completely but to soften the contours so that the
wasting does not appear too severe. In the inframalar hollow,
the goal should be to correct one-third to one-half of the
50
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
to their lips at the start. In these patients, just augmenting the
vermilion is enough to produce an excellent result. Often the
left and right sides of the lips differ in length and thickness,
and this must be demonstrated to the patient prior to
augmentation.
The injection process generally starts with augmentation of
the vermilion border of the lip to enhance its definition and
provide increased projection. The philtral columns may also
be augmented with filler placed in the mid dermal level but
care must be taken not to lengthen the upper lip. Palpation of
the tissue as the filler is injected is important. Injection of the
lip proper from the wet–dry junction to the vermilion border
may also be carried out just deep to the mucosa within the
orbicularis oris muscle. If it is placed immediately beneath the
mucosa, it will be seen as a blue color. Placement posterior to
the wet–dry junction along the wet mucosa may enhance the
lip volume as well as the projection. Variation in the place-
ment of the product must be done, depending on the desires
of the patient and the starting shape of the lips.
hollow. Linear threading or a fanning technique may be used,
and a gradual and consistent result can be achieved.
Volumes of 0.5–1.5 cc per area may be used, on average.
This will vary among individuals, depending on their
requested goals. Repeated injections on a 2–4-week basis may
help to contour areas that have a large volume deficiency.
Lips
Contouring of the lips may be accomplished with several kind
of fillers (Fig. 5.2.9A,B).79,80 Ideally, patients have a good shape
Fig. 5.2.8 Fat grafts. (A) Preoperative and (B) 1-year postoperative results after
micro fat grafting to the temples, cheeks, and jawline, and bilateral upper
blepharoplasty in a 50-year-old male.
A
B
Fig. 5.2.9 Lips. (A) This 51-year-old woman requested lip augmentation.
Restylane was injected into the vermilion border and philtral columns to achieve a
narrower appearance. Restylane was injected from the inside of the lip from the
vermilion border to the wet–dry junction. (B) She is shown 3 months after injection
with good persistence of filler.
A
B
51
Indications and applications
Care should be taken to inject small amounts (<0.1 cc) with
each pass and to assess continuously for blanching to avoid
any skin compromise. One of the advantages of using HA
fillers lies in the fact that the product can be dissolved by
injecting hyaluronidase in cases of post-injection blanching;
nitroglycerin paste and warm compresses can also help
prevent or limit skin necrosis in such cases.
Scars and deformities
Many soft-tissue deformities can be corrected with HA fillers
(Restylane/Juvederm), or permanent fillers (Bellafill, fat). The
choice somewhat depends on the depth and extent of the scar.
It is important that the scar tissue be soft and distensible. The
product should not be placed under high pressure as this may
The cupid’s bow becomes wider with age and should be
made narrower. The depth of the mental fold increases with
age and may require softening. Frequently the upper lip is
atrophied above the vermilion border, particularly the lateral
aspects, and restoration is done with MVHA placed at the mid
dermal level to improve volume and projection of the upper
lip. One should use minimal volume in the upper lip above
the vermilion border as any added volume may cause length-
ening of the upper lip. Care must also be taken to limit the
amount of filler placed in the upper lip skin adjacent to the
nasolabial fold because this will result in an awkward anima-
tion of the upper lip and nasolabial fold, particularly during
smiling, and can give the appearance of a “joker-type” upper
lip or create an unusual fold at the lateral edge of the upper
lip.
Patients with long, thin lips and very broad smiles may get
limited results because of tissue tension. Often patients com-
plain that their lips are too thin when they smile. This is a
dynamic change and cannot be corrected with fillers or
implants. Patients with lips that are tight to the dentition or a
class II occlusion should be augmented with conservative
volumes, since irregularities of dentition may be reflected in
the upper lip appearing too prominent or “duck-like”.
Approximate volumes for augmentation of the lips may
range from 0.5–1.0 mL per lip. MVHAs should last for a
period of 4–6 months; however, when it is repeated, the results
may last for 8 to 12 months. Care must be taken in persons
with soft, supple lips that move a lot with animation; these
patients may not respond well to HVHAs, and their lips may
appear too stiff. When injecting HVHAs, one must avoid the
formation of lumps or bumps as they are difficult to massage
out of the tissue. Radiesse and Sculptra should not be used
for lip augmentation due to their high incidence of nodule
formation. Bellafill is an option for permanent augmentation,
but can result in visible nodularity.
If the patient has lip implants, then the filler may be added
around the implant. HA fillers can also be combined with
other tissue fillers. Less viscous HAs may first be injected
along the vermilion border, which provides augmentation of
the white roll. MVHAs may also be placed in areas where
Bellafill has been placed previously after a minimum waiting
period of 2–3 months. Lastly, patients with a history of herpes
should be given prophylaxis because the treatment may cause
a herpetic outbreak and scarring.
Nasal reshaping (off label)
Many fillers have been used in the correction of minor nasal
deformities (Fig. 5.2.10A,B).56,81 More commonly, HA fillers
and calcium hydroxyapatite have been used for non-surgical
rhinoplasty. Radiesse, even though it may provide more
support than HA fillers, can also become visible if placed in
large amounts or too superficially. In general, permanent
fillers have a higher risk of becoming visible or palpable. If a
permanent filler such as Bellafill is to be used, it is probably
preferable to attempt correction with a resorbable filler first.
Injection can be by either serial threading or tunneling tech-
niques. The product should be placed in the subcutaneous
layer, especially in patients with thin skin, to avoid visibility.
Irregularities over the dorsum or the tip can be corrected in
this manner. There are reports of alar skin and nasal tip
necrosis with injection of fillers, especially post-rhinoplasty.
Fig. 5.2.10 Nose. (A) This 30-year-old woman had concerns about the irregular
appearance of her nasal tip cartilage. Restylane was used to fill in the hollows and
shape the tip of her nose. Restylane, 0.4 cc, was used to soften the appearance of
the nasal cartilage. The patient had inquired initially about rhinoplasty with tip
alteration. She had not had previous surgery, and the nasal tip had not changed
other than the irregularity becoming more noticeable with time. The skin at the tip
of the nose was very thin, and any slight surgical irregularity may have been
noticeable; additionally, the skin may have been compromised by an open
rhinoplasty. The new tip contour was achieved under a block with local anesthetic
and 0.4 cc of Restylane. (B) She is seen here 5 months after injection.
A
B
52
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
present from a young age and are a result of animation.
Obliteration can result in an unnatural mask-like appearance.
This should be pointed out to the patient who wants some
folds completely erased.
In patients who are prone to form keloids and hypertrophic
scars, the risk should be stressed to the patient.89 Also, it is
always best to try first with a small amount of filler and
possibly test the product in an inconspicuous area. The pres-
ence of infection, foreign-body reaction, or inflammation is a
contraindication to filler use. If a known allergy to collagen
exists, then the use of Bellafill, which contains collagen, should
not be used.
The use of blood thinners (coumadin, non-steroidal anti-
inflammatories, heparin) or “natural” products with similar
effects (fish oils, vitamin D, garlic), can lead to significant
ecchymoses. The patient should be informed of this fact and
should preferably stop taking such substances several weeks
prior to injection. If that is not possible, dermal fillers can be
used as long as the patient is willing to accept the possible
bruising.
In patients with telangiectasias, it is possible that the injec-
tion of filler will make their appearance and size worse.
However, this is not a strict contraindication and the use of
lasers can help diminish the appearance of these superficial
vascular malformations.
result in tissue necrosis. More than one treatment may be
required for full correction, but often the correction is perma-
nent. Excellent results can be achieved in acne, chickenpox,
and traumatic scars, and these can be long lasting. Simultane-
ous release of the scar with an 18 G needle may improve the
results. The use of Restylane Fine Lines in steroid atrophy is
helpful but may result in incomplete correction. Botox is
helpful in scars located in mobile areas such as the glabella,
forehead, and chin, where the mimetic action may be reduced.
This may increase the longevity of the filler placed.
Hand rejuvenation
Even though the primary use of dermal fillers is in facial
rejuvenation, increasing attention has been paid to their
application in hand rejuvenation (Fig. 5.2.11A,B).82–84 This
soft-tissue augmentation decreases the appearance of veins,
extensor tendons, and bony prominences, which become
pronounced with aging. Multiple fanning subcutaneous injec-
tions can be used, making sure to avoid the vessels, tendons,
and nerves of the dorsal hand. Fat has been shown to be an
excellent autologous filler for this purpose, but its use requires
surgical harvesting. HA fillers and Radiesse (off label) can be
used to plump up the soft tissues over the dorsum of the hand
and up to the level of the metacarpophalangeal joints.
Use and dosage of hyaluronidase
As mentioned in several of the sections above, hyaluronidase
is extremely useful for dissolving HA fillers when there is an
excess, nodule, asymmetry, or migration of the product. In
2005, Vartanian and colleagues conducted a randomized
study that confirmed the efficacy of hyaluronidase for dissolv-
ing Restylane.85 Although the use of hyaluronidase is wide-
spread today, no clear dosing guidelines exist because different
HA fillers respond differently to hyaluronidase.86 Some case
series suggest efficacy with doses of up to 75–150 units of
hyaluronidase, but they also show increased allergic reactions
with higher doses.85 These often dose-related allergic reactions
can present as redness, angioedema, and rarely anaphylactic
shock.87
In a recent review article, Bailey et al. recommend starting
with small doses of 5–15 units per site, with repeated treat-
ment 2 weeks later if needed. This approach should theoreti-
cally minimize the chance of an allergic reaction. The authors
also advocate avoiding treatment of patients with bee-sting
allergies, since there is a risk of cross-reactivity to the hyal-
uronidase. The same is mentioned about patients with allergic
reaction to bovine collagen, unless bovine-based hyaluroni-
dase is avoided.88
Contraindications and considerations
There are not many strict contraindications to the use of
dermal fillers. Probably the most important is unrealistic
patient expectations. The use of fillers is not a substitute for
surgery in cases where tissue descent and skin laxity are
advanced. In such cases, the patient should be advised of the
adjuvant role that fillers can play in relation to the more
dramatic improvement that could be achieved surgically.
Furthermore, some of the creases and folds of the face are
Fig. 5.2.11 Hand. (A) Preoperative and (B) 6-month postoperative results after
injection of 1.3 cc of Radiesse to the left hand in a 60-year-old female.
A
B
53
Complications and their treatment
minimally responsive to local steroid injection, they may
require oral steroid treatment. Allergic reactions can result in
long-term scarring.
With Sculptra and Radiesse, inflammatory nodules or
papules can develop and are usually associated with superfi-
cial injection. Skin discoloration can accompany such super-
ficial nodules. The role of massage is critical in preventing
such inflammatory nodule formation. With Radiesse, compli-
cations occur most often in the lips, where there can be a
10–20% early nodularity rate. If a lump, bump, or irregularity
occurs, it may be treated with a dilute steroid injection and
massage. However, irregularities may require excision if they
persist and do not respond to steroids. Recently, there has
been an interest in the potential implication of biofilms in
some permanent filler nodules. They are thought to present
as nodules with low-grade persistent inflammation that do
not respond to antibiotics or steroid injections, and may
require removal of the filler.101–106
Other early reactions to fillers include sterile abscess and
telangiectasia.107–109 When larger volumes of filler are used at
one time, a sterile abscess may occur that will require drain-
age. This may occur up to 2 weeks after the initial injection.
This is treated with local incision and drainage using an 18 G
needle. Immediate drainage of clear fluid mixed with yellow-
white debris resolves the problem, with rapid resolution of
the symptoms.
Bellafill can result in local granulomatous reactions.90,110,111
The instances reported to date in North America are low
(0.02–1%). There have been more extensive reports of granu-
lomas in Europe (perhaps due to the earlier generations of the
product). These may present as localized bumps, nodules that
are tender to the touch. Giant cells and multinuclear giant
cells are present in the nodules on histologic examination of
the tissue with an accompanying inflammatory response. If
the product is placed too superficial in the dermis, the resul-
tant tissue formation may lead to a white coloring of the skin.
This is similar to the bluish discoloration (Tyndall effect) that
may occur with any of the HA fillers when placed in the
superficial layer of the dermis. If Bellafill is not placed in small
amounts with each pass, nodules can occur. These may be
treated with local excision, massage, or dilute steroid injection
(0.2 mg Kenalog/mL). Stronger Kenalog concentration (up to
40 mg/mL) may be needed to control the inflammation. If
granuloma occurs, treatment options include direct steroid
injection, excision, systemic treatment with oral steroids, or a
combination of these treatments depending on the severity of
the granuloma.90,98,111
The injection of all filling substances may result in a her-
petic outbreak, and patients with a previous history of herpes
simplex outbreak should therefore receive prophylactic treat-
ment with an appropriate antiviral medication.
Soft-tissue necrosis and embolic phenomenon have
been reported, and although rare, they can be extremely
serious.112–115 An algorithm for treatment of post-injection
blanching of any area of the face includes warm compresses,
nitroglycerine, hyaluronidase, aspirin, and heparin, in an
attempt to reverse/minimize such ischemic events. Blindness
is perhaps the most severe of these post-injection ischemic
events and presents as loss of vision and excruciating ocular
pain. Through an extensive review of the literature, Ozturk
and colleagues found 61 cases of vascular occlusion second-
ary to facial fillers other than fat (hyaluronic acid, calcium
The use of lasers does not affect deep fillers such as Radiesse
or Bellafill. This is due to the fact that the product is deep and
the melting point of these compounds is much higher than
the heat generated by the laser. However, the injection of more
superficial HA and collagen fillers should be done at a later
date following laser treatment, if possible.
There are no data to suggest adverse effects of dermal filler
use during pregnancy, breastfeeding, and in patients under 18
years of age. Despite the fact that such side effects are unlikely,
it is prudent to avoid the use of fillers in these groups of
patients.
Viscous and longer-lasting compounds such as Radiesse,
Sculptra, Bellafill, and Perlane/Juvaderm Ultra Plus are
contraindicated for use in the superficial dermis because
of palpable/visible nodule formation. Specifically, Radiesse
should be avoided in the lips since there is a significant per-
centage of early nodule formation (up to 20%).
Because the use of fillers may result in an undesirable
appearance, it is more prudent to use a temporary filler the
first time. If the effect is indeed that anticipated by the patient,
a more permanent correction may be pursued the next time.
Fillers have not been associated with any autoimmune
disease. Moreover, autoimmune and connective tissue dis-
eases such as scleroderma are not a contraindication to the use
of dermal fillers, since wound healing is normal. There is
some evidence to suggest that certain conditions such as
sarcoidosis may predispose to a more pronounced inflamma-
tory reaction (extensive granuloma formation and facial
edema) with Sculptra injection, but it is anecdotal. Similarly,
these products can be used in patients with diabetes, HIV, or
immunosuppression, without a significantly higher incidence
of infection.
Patients with very thin skin have a higher risk of palpabil-
ity or visibility; deep injection of small amounts of filler is
important. Sebaceous skin camouflages irregularities better,
but product can escape through pores and even form
pustules.
Lastly, there have been no reports of adverse reaction with
the layering of different types of fillers. However, it would be
prudent only to inject a second type of filler in the same area
several months after the primary injection. This way, in case
of an adverse reaction, it would be possible to identify which
product is responsible for the adverse reaction.
Complications and their treatment
All fillers have possible side effects. Common complications
that may occur are lumps, bumps, and irregularities; pain;
ecchymoses or hematoma; overcorrection; and asymmetry.
Uncommonly the patient may experience intermittent swell-
ing in the region treated. This usually resolves by 2–6 weeks.
The occasional individual will have massive swelling in
response to the injection and may consider using oral steroids
to alleviate this immediate swelling.90–99
Rarely, individuals may develop erythema of the overlying
skin for the first several weeks. Clinically it does not behave
like an allergy and cellulitis has to be ruled out. A light topical
steroid may be used as an initial treatment. In general, this
reaction resolves without therapy over a short period of time.
HA fillers have an incidence of allergic reaction of approxi-
mately 0.03%.100 If these reactions are unresponsive or
54
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: soft-tissue fillers
Conclusion
The development of numerous fillers has armed the plastic
surgeon with an invaluable tool in the area of minimally
invasive facial rejuvenation. Diagnosis, proper technique, and
choice of fillers are the keys to creating a natural appearance
and avoiding iatrogenic problems.
hydroxylapatite, poly-l-lactic acid, collagen, and dermal
matrix). Twelve of these cases suffered from immediate blind-
ness, and the most common sites of injection leading to visual
complications were the nose (32.8%), the glabella (26.2%), and
the nasolabial fold (26.2%).116
Other review articles seem to suggest that compared to
synthetic fillers, blindness caused by injection of autologous
fat is almost always permanent and has in a few cases been
associated with concomitant cerebral infarction.117–120
1. Lemperle G, Holmes RE, Cohen SR, et al. A classification of facial
wrinkles. Plast Reconstr Surg. 2001;108:1751–1752. The authors offer a
standard classification for the assessment of facial rhytides. This system
is based on wrinkle depth and can be a useful guide in the treatment of
wrinkles, including nasolabial folds.
2. Kontis TC, Rivkin A. The history of injectable facial fillers. Facial
Plast Surg. 2009;25:67–72.
16. Coleman SR. Structural fat grafts: the ideal filler? Clin Plast Surg.
2001;28:111–119. In this article, Coleman first presents micro fat grafts
as an ideal autologous filler. Structural fat grafts have become a unique
tool in permanent soft-tissue augmentation with applications that span
all areas of plastic surgery.
19. Sclafani AP. Platelet-rich fibrin matrix for improvement of deep
nasolabial folds. J Cosmet Dermatol. 2010;9:66–71.
66. Arian LE, Born TM. Nonsurgical lower eyelid lift. Plast Reconstr
Surg. 2005;116:1785–1792. In this publication the authors present for
the first time a means of correcting the tear trough and the infraorbital
rim hollow. They offer a non-surgical alternative to a lower
blepharoplasty by camouflaging the infraorbital fat bulge. This is ideal in
the case of the non-surgical candidate.
77. Sturm LP, Cooter RD, Mutimer KL, et al. A systematic review of
permanent and semipermanent dermal fillers for HIV-associated
facial lipoatrophy. AIDS Patient Care STDS. 2009;23:699–714.
91. Sclafani AP, Fagien S. Treatment of injectable soft tissue filler
complications. Dermatol Surg. 2009;35(suppl 2):1672–1680. Even
though rare, complications of dermal fillers can be devastating. The
authors present a thorough review of all possible complications of dermal
fillers and their causes in order to prevent them. The authors also offer
an algorithm of how to treat such complications once they occur.
108. Sherman RN. Avoiding dermal filler complications. Clin Dermatol.
2009;27:S23–S32.
Access the complete reference list online at
54.e1
References
References
1. Lemperle G, Holmes RE, Cohen SR, et al. A classification of facial
wrinkles. Plast Reconstr Surg. 2001;108:1751–1752. The authors offer a
standard classification for the assessment of facial rhytides. This system
is based on wrinkle depth and can be a useful guide in the treatment of
wrinkles, including nasolabial folds.
2. Kontis TC, Rivkin A. The history of injectable facial fillers. Facial
Plast Surg. 2009;25:67–72.
3. Glicenstein J. The first “fillers”, Vaseline and paraffin. From
miracle to disaster. Ann Chir Plast Esthet. 2007;52:157–161.
4. Allevato MA, Pastorale EP, Zamboni M, et al. Complications
following industrial liquid silicone injection. Int J Dermatol.
1996;35:193–195.
5. Mastruserio DN, Pesqueira MJ, Cobb MW. Severe granulomatous
reaction and facial ulceration occurring after subcutaneous silicone
injection. J Am Acad Dermatol. 1996;34:849–852.
6. Lemperle G, de Fazio S, Nicolau P. ArteFill: a third-generation
permanent dermal filler and tissue stimulator. Clin Plast Surg.
2006;33:551–565.
7. Brandt FS, Cazzaniga A. Hyaluronic acid fillers: Restylane and
Perlane. Facial Plast Surg Clin North Am. 2007;15:63–76.
8. Carruthers JD, Carruthers A. Facial sculpting and tissue
augmentation. Dermatol Surg. 2005;31:1604–1612.
9. Buck DW 2nd, Alam M, Kim JY. Injectable fillers for facial
rejuvenation: a review. J Plast Reconstr Aesthet Surg. 2009;62:11–18.
10. Broder KW, Cohen SR. An overview of permanent and
semipermanent fillers. Plast Reconstr Surg. 2006;118(suppl):7S–
14S.
11. Graivier M, Cohen SR. The semipermanent and permanent
dermal/subdermal fillers supplement. Plast Reconstr Surg.
2006;118(suppl):6S.
12. Rohrich RJ. Semipermanent and permanent dermal/subdermal
fillers supplement. Plast Reconstr Surg. 2006;118(suppl):1S–3S.
13. <
ucm448255.htm>.
14. Chajchir A. Fat injection: long term follow up. Aesthetic Plast Surg.
1996;20:291–296.
15. Coleman SR. Long-term survival of fat transplants: controlled
demonstrations. Aesthetic Plast Surg. 1995;19:421–425.
16. Coleman SR. Structural fat grafts: the ideal filler? Clin Plast Surg.
2001;28:111–119. In this article, Coleman first presents micro fat grafts
as an ideal autologous filler. Structural fat grafts have become a unique
tool in permanent soft-tissue augmentation with applications that span
all areas of plastic surgery.
17. Fagien S. Facial soft-tissue augmentation with injectable
autologous and allogeneic human tissue collagen matrix
(autologen and dermalogen). Plast Reconstr Surg. 2000;105:
362–373.
18. Matsudo P, Toledo L. Experience in injected fat grafting. Aesthetic
Plast Surg. 1988;12:35–38.
19. Sclafani AP. Platelet-rich fibrin matrix for improvement of deep
nasolabial folds. J Cosmet Dermatol. 2010;9:66–71.
20. Sclafani AP. Applications of platelet-rich fibrin matrix in facial
plastic surgery. Facial Plast Surg. 2009;25:270–276.
21. Sclafani AP, McCormick SA. Induction of dermal collagenesis,
angiogenesis, and adipogenesis in human skin by injection of
platelet-richfibrin matrix. Arch Facial Plast Surg. 2012;14:132–136.
22. Sclafani AP, Azzi J. Platelet preparations for use in facial
rejuvenation and wound healing: a critical review of current
literature. Aesthetic Plast Surg. 2015;39:495–505.
23. <>.
24. Smith SR, Munavalli G, Weiss R. A multicenter, double-blind,
placebo-controlled trial of autologous fibroblast therapy for the
treatment of nasolabial fold wrinkles. Dermatol Surg.
2012;38:1234–1243.
25. Achauer B, VanderKam VM, Celikoz B, et al. Augmentation of
facial soft-tissue defects with Alloderm dermal graft. Ann Plast
Surg. 1998;41:503–507.
26. Burres S. Soft-tissue augmentation with Fascian. Clin Plast Surg.
2001;28:101–110.
27. Castor SA, To WC, Papay FA. Lip augmentation with AlloDerm
acellular allogenic dermal graft and fat autograft: a comparison
with autologous fat injection alone. Aesthetic Plast Surg.
1999;23:218–223.
28. Friedman PM, Mafong EA, Kauvar AN, et al. Safety data of
injectable nonanimal stabilized hyaluronic acid gel for soft tissue
augmentation. J Dermatol Surg. 2002;28:491–494.
29. Downie J, Mao Z, Rachel Lo TW, et al. A double-blind, clinical
evaluation of facial augmentation treatments: a comparison of PRI
1, PRI 2, Zyplast and Perlane. J Plast Reconstr Aesthet Surg.
2009;62:1636–1643.
30. Cockerham K, Hsu VJ. Collagen-based dermal fillers: past, present,
future. Facial Plast Surg. 2009;25:106–113.
31. Matarasso SL. Injectable collagens: lost but not forgotten – a
review of products, indications, and injection techniques. Plast
Reconstr Surg. 2007;120(suppl):17S–26S.
32. Bauman L. CosmoDerm/CosmoPlast (human bioengineered
collagen) for the aging face. Facial Plast Surg. 2004;20:125–128.
33. Dyan SH, Bassichis BA. Facial dermal fillers: selection of
appropriate products and techniques. Aesthet Surg J.
2008;28:335–347.
34. Monheit GD, Coleman KM. Hyaluronic acid fillers. Dermatol Ther.
2006;19:141–150.
35. Tezel A, Fredrickson GH. The science of hyaluronic acid dermal
fillers. J Cosmet Laser Ther. 2008;10:35–42.
36. Kablik J, Monheit GD, Yu L, et al. Comparative physical properties
of hyaluronic acid dermal fillers. Dermatol Surg. 2009;35(suppl
1):302–312.
37. Lambros V. Volumizing the brow with hyaluronic acid fillers.
Aesthet Surg J. 2009;29:174–179.
38. 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;13:183–192.
39. Pinsky MA, Thomas JA, Murphy DK, et al. Juvéderm injectable
gel: a multicenter, double-blind, randomized study of safety and
effectiveness. Aesthet Surg J. 2008;28:17–23.
40. Edwards PC, Fantasia JE. Review of long-term adverse effects
associated with the use of chemically-modified animal and
nonanimal source hyaluronic acid dermal fillers. Clin Interv Aging.
2007;2:509–519.
41. Smith KC. Practical use of Juvéderm: early experience. Plast
Reconstr Surg. 2007;120(suppl):67S–73S.
42. Clark CP 3rd. Animal-based hyaluronic acid fillers: scientific and
technical considerations. Plast Reconstr Surg.
2007;120(suppl):27S–32S.
43. Baumann LS, Shamban AT, Lupo MP, et al. Comparison of
smooth-gel hyaluronic acid dermal fillers with cross-linked bovine
collagen: a multicenter, double-masked, randomized, within-
subject study. Dermatol Surg. 2007;33(suppl 2):S128–S135.
44. Monheit GD, Prather CL. Juvéderm: a hyaluronic acid dermal
filler. J Drugs Dermatol. 2007;6:1091–1095.
45. Rohrich RJ, Ghavami A, Crosby MA. The role of hyaluronic acid
fillers (Restylane) in facial cosmetic surgery: review and technical
considerations. Plast Reconstr Surg. 2007;120(suppl):41S–54S.
46. Callan P, Goodman GJ, Carlisle I, et al. Efficacy and safety of a
hyaluronic acid filler in subjects treated for correction of midface
volume deficiency: a 24 month study. Clin Cosmet Investig Dermatol.
2013;6:81–89.
47. Lorenc ZP, Fagien S, Flynn TC, et al. Clinical application and
assessment of Belotero: a roundtable discussion. Plast Reconstr
Surg. 2013;132(suppl 2):69S–76S.
48. The European Aesthetic Guide, Dermal Filler Product Comparison
Chart, Spring. 2009. Available online at: <>.
49. Fagien S, Klein AW. A brief overview and history of temporary
fillers: evolution, advantages, and limitations. Plast Reconstr Surg.
2007;120(suppl):8S–16S.
54.e2
SECTION I
CHAPTER 5.2 • Injectables and resurfacing techniques: Soft-tissue fillers
50. Lemperle G, Gauthier-Hazan N, Lemperle M. PMMA-
microspheres (Artecoll) for long-lasting correction of wrinkles:
refinements and statistical results. Aesthetic Plast Surg.
1998;22:356–365.
51. Lemperle G, Kind P. Biocompatibility of Artecoll. Plast Reconstr
Surg. 1999;103:338–340.
52. Broder KW, Cohen SR. ArteFill: a permanent skin filler. Expert Rev
Med Devices. 2006;3:281–289.
53. Hevia O. A retrospective review of calcium hydroxylapatite for
correction of volume loss in the infraorbital region. Dermatol Surg.
2009;35:1487–1494.
54. Sklar JA, White SM. Radiance FN: a new soft tissue filler. Dermatol
Surg. 2004;30:764–768, discussion 768.
55. Zide B. Radiance: short term experience. Aesthet Surg J.
2003;23:495–499.
56. Siclovan HR, Jomah JA. Injectable calcium hydroxylapatite for
correction of nasal bridge deformities. Aesthetic Plast Surg.
2009;33:544–548.
57. Ahn MS. Calcium hydroxylapatite: Radiesse. Facial Plast Surg Clin
North Am. 2007;15:85–90.
58. Flaharty P. Radiance. Facial Plast Surg. 2004;20:165–169.
59. <
ProductsandMedicalProcedures/DeviceApprovalsandClearances/
Recently-ApprovedDevices/ucm451776.htm>.
60. Lam SM, Azizzadeh B, Graivier M. Injectable poly-L-lactic acid
(Sculptra): technical considerations in soft-tissue contouring. Plast
Reconstr Surg. 2006;118:55S–63S.
61. Vleggaar D. Poly-L-lactic acid: consultation on the injection
techniques. J Eur Acad Dermatol Venereol. 2006;(suppl 1):17–21.
62. Gogolewski S, Jovanovic M, Perren SM, et al. Tissue response and
in vivo degradation of selected polyhydroxyacids: polylactides
(PLA), poly(3-hydroxybutyrate) (PHB), and poly(3-
hydroxybutyrate-co-3-hydroxyvalerate) (PHB/VA). J Biomed Mater
Res. 1993;27:1135–1148.
63. Vleggaar D, Bauer U. Facial enhancement and the European
experience with Sculptra (poly-L-lactic acid). J Drugs Dermatol.
2004;3:542–547.
64. Nácul AM, Nácul AP, Greca de Born A. Bioplastique as a
complement in conventional plastic surgery. Aesthetic Plast Surg.
1998;22:444–450.
65. Funt D, Pavicic T. Dermal fillers in aesthetics: an overview of
adverse events and treatment approaches. Clin Cosmet Investig
Dermatol. 2013;6:295–316.
66. Arian LE, Born TM. Nonsurgical lower eyelid lift. Plast Reconstr
Surg. 2005;116:1785–1792. In this publication the authors present for
the first time a means of correcting the tear trough and the infraorbital
rim hollow. They offer a non-surgical alternative to a lower
blepharoplasty by camouflaging the infraorbital fat bulge. This is ideal in
the case of the non-surgical candidate.
67. Fulton J, Caperton C, Weinkle S, et al. Filler injections with the
blunt-tip microcannula. J Drugs Dermatol. 2012;11:1098–1103.
68. Zeichner JA, Cohen JL. Use of blunt tipped cannulas for soft tissue
fillers. J Drugs Dermatol. 2012;11:70–72.
69. Niamtu J III. Filler injection with micro-cannula instead of needles.
Dermatol Surg. 2009;35:2005–2008.
70. Alam M, Yoo SS. Technique for calcium hydroxylapatite injection
for correction of nasolabial fold depressions. J Am Acad Dermatol.
2007;56:285–289.
71. Biesman B. Caution in the use of soft tissue injectable fillers in the
tear trough region. Aesthet Surg J. 2010;30:269.
72. Goldberg RA. Nonsurgical filling of the periorbital hollows.
Aesthet Surg J. 2006;26:69–71.
73. Bass LS, Smith S, Busso M, et al. Calcium hydroxylapatite
(Radiesse) for treatment of nasolabial folds: long-term safety and
efficacy results. Aesthet Surg J. 2010;30:235–238.
74. Salles AG, Lotierzo PH, Gimenez R, et al. Evaluation of the
poly-L-lactic acid implant for treatment of the nasolabial
fold: 3-year follow-up evaluation. Aesthetic Plast Surg. 2008;32:
753–756.
75. Lowe NJ, Grover R. Injectable hyaluronic acid implant for malar
and mental enhancement. Dermatol Surg. 2006;32:881–885,
discussion 885.
76. Weinkle S. Injection techniques for revolumization of the perioral
region with hyaluronic acid. J Drugs Dermatol. 2010;9:367–371.
77. Sturm LP, Cooter RD, Mutimer KL, et al. A systematic review of
permanent and semipermanent dermal fillers for HIV-associated
facial lipoatrophy. AIDS Patient Care STDS. 2009;23:699–714.
78. Burgess CM, Quiroga RM. Assessment of the safety and efficacy of
poly-L-lactic acid for the treatment of HIV-associated facial
lipoatrophy. J Am Acad Dermatol. 2005;52:233–239.
79. Hoffmann C, Schuller-Petrovic S, Soyer HP, et al. Adverse
reactions after cosmetic lip augmentations with permanent
biologically inert implant materials. J Am Acad Dermatol.
1999;40:100–102.
80. Born T, Airan LE, McGrath MH, et al. Soft tissue fillers in aesthetic
surgery. In: Nahai F, ed. The Art of Aesthetic Surgery. Vol. I. St.
Louis, MO: Quality Medical Publishing; 2005:224–288.
81. Humphrey CD, Arkins JP, Dayan SH. Soft tissue fillers in the nose.
Aesthet Surg J. 2009;29:477–484.
82. Marmur ES, Al Quran H, De Sa Earp AP, et al. A five-patient
satisfaction pilot study of calcium hydroxylapatite injection for
treatment of aging hands. Dermatol Surg. 2009;35:1978–1984.
83. Man J, Rao J, Goldman M. A double-blind, comparative study of
nonanimal-stabilized hyaluronic acid versus human collagen for
tissue augmentation of the dorsal hands. Dermatol Surg.
2008;34:1026–1031.
84. Busso M, Applebaum D. Hand augmentation with Radiesse
(calcium hydroxylapatite). Dermatol Ther. 2007;20:385–387.
85. Vartanian AJ, Frankel AS, Rubin MG. Injected hyaluronidase
reduces Restylane-mediated cutaneous augmentation. Arch Facial
Plast Surg. 2005;7:231–237.
86. Sall I, Férard G. Comparison of the sensitivity of 11 cross-linked
hyaluronic acid gels to bovine testis hyaluronidase. Polym Degrad
Stab. 2007;92:915–919.
87. Brody HJ. Use of hyaluronidase in the treatment of granulomatous
hyaluronic acid reactions or unwanted hyaluronic acid
misplacement. Dermatol Surg. 2005;31:893–897.
88. Bailey SH, Fagien S, Rohrich RJ. Changing role of hyaluronidase in
plastic surgery. Plast Reconstr Surg. 2014;133:127e–132e.
89. Taylor SC, Burgess CM, Callender VD. Safety of nonanimal
stabilized hyaluronic acid dermal fillers in patients with skin of
color: a randomized, evaluator-blinded comparative trial. Dermatol
Surg. 2009;35(suppl 2):1653–1660.
90. Lemperle G, Gauthier-Hazan N, Wolters M, et al. Foreign body
granulomas after all injectable dermal fillers: part 1. Possible
causes. Plast Reconstr Surg. 2009;123:1842–1863.
91. Sclafani AP, Fagien S. Treatment of injectable soft tissue filler
complications. Dermatol Surg. 2009;35(suppl 2):1672–1680. Even
though rare, complications of dermal fillers can be devastating. The
authors present a thorough review of all possible complications of dermal
fillers and their causes in order to prevent them. The authors also offer
an algorithm of how to treat such complications once they occur.
92. Winslow CP. The management of dermal filler complications.
Facial Plast Surg. 2009;25:124–128.
93. Hirsch RJ, Stier M. Complications of soft tissue augmentation. J
Drugs Dermatol. 2008;7:841–845.
94. Cohen JL. Understanding, avoiding, and managing dermal filler
complications. Dermatol Surg. 2008;34(suppl 1):S92–S99.
95. Goldberg DJ. Legal ramifications of off-label filler use. Clin Plast
Surg. 2006;33:597–601.
96. Lemperle G, Duffy DM. Treatment options for dermal filler
complications. Aesthet Surg J. 2006;26:356–364.
97. Narins RS, Jewell M, Rubin M, et al. Clinical conference:
management of rare events following dermal fillers – focal
necrosis and angry red bumps. Dermatol Surg. 2006;32:426–434.
98. Ghislanzoni M, Bianchi F, Barbareschi M, et al. Cutaneous
granulomatous reaction to injectable hyaluronic acid gel. Br J
Dermatol. 2006;154:755–758.
54.e3
References
99. Lowe NJ, Maxwell CA, Patnaik R. Adverse reactions to dermal
fillers: review. Dermatol Surg. 2005;31:1616–1625.
100. Lupton JR, Alster TS. Cutaneous hypersensitivity reaction to
injectable hyaluronic gel. Dermatol Surg. 1998;24:1317–1325.
101. Narins RS, Coleman WP III, Glogau RG. Recommendations and
treatment options for nodules and other filler complications.
Dermatol Surg. 2009;35(suppl 2):1667–1671.
102. Lewis K. Riddle of biofilm resistance. Antimicrob Agents Chemother.
2001;45:999–1007.
103. Rohrich RJ, Monheit G, Nguyen AT, et al. Soft-tissue filler
complications: the important role of biofilms. Plast Reconstr Surg.
2010;125:1250–1256.
104. Bjarnsholt T, Tolker-Nielsen T, Givskov M, et al. Detection of
bacteria by fluorescence in situ hybridization in culture-negative
soft tissue filler lesions. Dermatol Surg. 2009;35(suppl 2):1620–1624.
105. Christensen L. Normal and pathologic tissue reactions to soft
tissue gel fillers. Dermatol Surg. 2007;33(suppl 2):S168–S175.
106. Alhede M, Er Ö, Eickhardt S, et al. Bacterial biofilm formation and
treatment in soft tissue fillers. Pathog Dis. 2014;70:339–346.
107. Shafir R, Amir A, Gur E. Long-term complications of facial
injection with Restylane (injectable hyaluronic acid). Plast Reconstr
Surg. 2000;106:1215–1216.
108. Sherman RN. Avoiding dermal filler complications. Clin Dermatol.
2009;27:S23–S32.
109. Glogau RG, Kane MA. Effect of injection techniques on the rate of
local adverse events in patients implanted with nonanimal
hyaluronic acid gel dermal fillers. Dermatol Surg. 2008;34(suppl
1):S105–S109.
110. Kim KJ, Lee HW, Lee MW, et al. Artecoll granuloma: a rare
adverse reaction induced by microimplant in the treatment of neck
wrinkles. Dermatol Surg. 2004;30:545–547.
111. Lemperle G, Gauthier-Hazan N. Foreign body granulomas after all
injectable dermal fillers: part 2. Treatment options. Plast Reconstr
Surg. 2009;123:1864–1873.
112. Glaich AS, Cohen JL, Goldberg LH. Injection necrosis of the
glabella: protocol for prevention and treatment after use of dermal
fillers. Dermatol Surg. 2006;32:276–281.
113. Hanke CW, Higley HR, Jolivette DM, et al. Abscess formation and
local necrosis after treatment with Zyderm or Zyplast collagen
implant. J Am Acad Dermatol. 1991;25:319–326.
114. Grunebaum LD, Bogdan Allemann I, Dayan S, et al. The risk of
alar necrosis associated with dermal filler injection. Dermatol Surg.
2009;35(suppl 2):1635–1640.
115. Inoue K, Sato K, Matsumoto D, et al. Arterial embolization and
skin necrosis of the nasal ala following injection of dermal fillers.
Plast Reconstr Surg. 2008;121:127e–128e.
116. Ozturk CN, Li Y, Tunk R, et al. Complications following injection
of soft-tissue fillers. Aesthet Surg J. 2013;33:862–877.
117. Sung MS, Kim HG, Woo KI, et al. Ocular ischemia and ischemic
oculomotor nerve palsy after vascular embolization of injectable
calcium hydroxylapatite filler. Ophthal Plast Reconstr Surg.
2010;26:289–291.
118. Lazzeri D, Agostini T, Figus M, et al. Blindness following cosmetic
injections of the face. Plast Reconstr Surg. 2012;129:994–1012.
119. Park SW, Woo SJ, Park KH, et al. Iatrogenic retinal artery occlusion
caused by cosmetic facial filler injections. Am J Ophthalmol.
2012;154:653–662.
120. Roberts SA, Arthurs BP. Severe visual loss and orbital infarction
following periorbital aesthetic poly-L-lactic acid (PLLA) injection.
Ophthal Plast Reconstr Surg. 2012;28:e68–e70.
SECTION I • Aesthetic Surgery of the Face
5.3
Injectables and resurfacing techniques:
Botulinum toxin (BoNT-A)
Michael A. C. Kane
SYNOPSIS
■ When properly administered to appropriately selected individuals,
botulinum toxin type A (BoNT-A) can have a rejuvenating effect on
nearly the entire face and neck.
■ Carefully observing the functional anatomy of each patient is the key to
determining how much BoNT-A to administer and where to place each
injection.
■ In some facial areas, fine control can be achieved by only partially
affecting muscles, causing the neighboring musculature to compensate
for the ensuing weakness.
Access the Historical Perspective section online at
Introduction
There are many components to the process of facial aging.
Thinning of the dermis, elastosis, loss of facial volume, genetic
factors, gravity, skeletal changes, sun damage, and smoking
all play a part in this process. So does facial animation. Certain
rhytids are primarily caused by facial movement. Others are
caused by other factors as well as a component of animation.
Therefore, as long as a wrinkle or unattractive shape is as least
partially caused by muscular action, it can be treated with
botulinum toxin A (BoNT-A); however, how well a specific
unaesthetic area responds to treatment with BoNT-A depends
on how much of the unattractive area is caused by factors
other than animation. For example, a glabellar rhytid that is
almost completely caused by the actions of the corrugators
and procerus muscles in a relatively young patient can be
totally eradicated with BoNT-A. In contrast, vertical lip rhytids
in an elderly woman with thin skin, sun damage, a history of
smoking, and loss of lip volume may only be partially
improved by careful injection of the orbicularis oris muscle,
which contributes to the accordion-like scrunching of the
overlying lip skin.
BoNT-A treatment is currently the most frequently per-
formed cosmetic procedure in the US, and its importance
in aesthetic plastic surgery simply cannot be overstated. In
2008, nearly 3.6 million BoNT-A procedures were performed
in the US. That is more than all liposuction, breast augmen-
tation, rhinoplasty, facelift, and blepharoplasty procedures
combined.1
Although the subject of this chapter is focused on the
manipulation of facial animation, the ability of the overlying
skin to resist these underlying forces that would deform it is
also of paramount importance when discussing rhytids.
Basic science
Pharmacology and pharmacokinetics
Clostridium botulinum is a Gram-positive, anaerobic bacterium
that is known to produce seven serologically distinct types of
toxin, designated A through G, of which type A is the most
potent. Botulinum toxin types A and B are used medically and
are available in the US. The type A toxin is a fully sequenced,
1296 amino acid polypeptide protein consisting of a 100-kDa
heavy chain joined by a disulfide bond to a 50-kDa light
chain.6
In the normally functioning neuromuscular junction, the
propagation of an action potential at the presynaptic neuron
terminal opens voltage-dependent calcium channels. The
influx of extracellular calcium ions causes vesicles containing
acetylcholine to dock and fuse to the presynaptic neuron’s
cell membrane through the action of a 25-kDa soluble
N-ethylmaleimide-sensitive factor attachment protein (SNAP-
25). The released acetylcholine crosses the synaptic cleft,
where it binds with nicotinic receptors at the motor endplate,
opens sodium–potassium ion channels, depolarizes the motor
endplate, and initiates the sequence of events that leads to
contraction of the muscle fiber.7
Access video lecture content for this chapter online at expertconsult.com
55.e1
Historical perspective
Historical perspective
BoNT-A was first used in ophthalmology for the treatment of
strabismus:
■ Injecting BoNT-A into spastic extraocular muscles
provided a non-invasive alternative to surgery.
■ Effectiveness was first established in Rhesus monkeys.2
■ The safety and effectiveness were later demonstrated in
human patients.3
■ The ophthalmic use of BoNT-A soon included treatment
of incapacitating essential blepharospasm:
• Injecting BoNT-A into the orbicularis oculi provided
relief of spasm for an average of 12 weeks.4
■ The use of BoNT-A rapidly expanded into the field of
aesthetic medicine:
• A report describing the cosmetic value of BoNT-A on
glabellar rhytids in 18 patients was published in 1992.5
• Glabellar muscles remain the most commonly injected
muscles for cosmetic reasons; however, BoNT-A has
been used to treat every mimetic muscle of the face with
varying results.
56
SECTION I
CHAPTER 5.3 • Injectables and resurfacing techniques: Botulinum toxin (BoNT-A)
vacuum-dried Clostridium botulinum type A neurotoxin
complex, 0.5 mg of albumin human, and 0.9 mg of
sodium chloride without a preservative.8
■ Botox Cosmetic (onabotulinumtoxinA) for injection
(Allergan Inc., Irvine, CA) is provided in vials
containing 50 U of vacuum-dried Clostridium
botulinum type A neurotoxin complex, 0.25 mg of
albumin human, and 0.45 mg of sodium chloride
without a preservative; or 100 U of vacuum-dried
Clostridium botulinum type A neurotoxin complex,
0.5 mg of albumin human, and 0.9 mg of sodium
chloride without a preservative.9
■ Dysport for injection (abobotulinumtoxinA) (Tercica Inc.,
Brisbane, CA; and Medicis Aesthetics Inc., Scottsdale, AZ)
is supplied in vials containing 500 or 300 U of lyophilized
abobotulinumtoxinA, 125 µg human serum albumin and
2.5 mg lactose.10
■ Xeomin for injection (incobotulinumtoxinA)
(Merz North America, Raleigh, NC) in 50- and
100-unit vials.
Commercial source of BoNT-B
■ Myobloc (rimabotulinumtoxinB) injection (Solstice
Neurosciences Inc., South San Francisco, CA) is provided
in 3.5-mL vials containing 5000 U of botulinum toxin type
B per mL in 0.05% human serum albumin, 0.01 M sodium
succinate, and 0.1 M sodium chloride.11
The BoNT-A in Dysport and Botox are produced by fer-
mentation of the bacterium Clostridium botulinum type A (Hall
Strain), while BoNT-B in Myobloc is produced by fermenta-
tion of the bacterium Clostridium botulinum type B (Bean
strain).12 It is important to note that the potency of each product
is specific to the preparation and assay method utilized, and is
not interchangeable with other preparations of botulinum toxin
products.13,14
While this list is comprehensive at the time of writing, there
are other toxins in clinical trials, which we will have in our
armamentarium. Whether these are injectable or topically
applied (RT001, Revance Therapeutics, Newark, CA), the
strategy for these products remains the same; to identify the
offending muscular segments and relax them to a certain
extent. Dosing regimens with these products will always be
in a state of flux. Good judgment, a critical eye, and an under-
standing of functional anatomy will never go out of style.
Thus, this chapter is adaptable for neurotoxins not yet in use.
New BoNT-A formulations will have different complexing
proteins, different excipients, different complex sizes, differ-
ent pharmacokinetics, and definitely different dosing regi-
mens. The key to evaluating these products will be dissociation.
The basic function of the lone 1296 amino acid chain is the
same.
Cosmetic indications
Botox Cosmetic is indicated for the temporary improvement
in the appearance of moderate to severe glabellar lines
associated with corrugator and/or procerus muscle activ-
ity in adult patients. It is also indicated for the temporary
improvement in the appearance of moderate to severe lateral
canthal lines associated with orbicularis oculi activity in adult
patients.9
Following the administration of botulinum toxin, the heavy
chain binds to the axon terminal, which enables the toxin to
enter the neuron via endocytosis. In the cytoplasm, the pro-
teolytic light chain degrades SNAP-25, thereby preventing
fusion of the acetylcholine-containing vesicle with the cell
membrane, preventing release of acetylcholine. Within a few
days, the affected nerve is incapable of releasing acetylcholine,
resulting in flaccid paralysis of the muscle fiber it innervates.
Type-B botulinum toxin also causes flaccid paralysis but does
so by inhibiting synaptobrevin, a vesicle-associated membrane
protein similar to SNAP-25.7 Unless specified, the remainder
of this chapter concerns botulinum toxin type A.
Recovery begins to occur after several weeks, although the
mechanism for this is not completely understood. Initially,
small neuritic processes grow out of the affected neurons and
establish new functional synapses, which are capable of ace-
tylcholine release; however, these neuritic networks shrink
and disappear as the original neurons regain function. The
initial clinical response to botulinum toxin is usually readily
apparent for 3–4 months, although 6–7 months are often
required for the effects to completely disappear. BoNT-A
begins to display an increased duration of action in most
patients when they undergo treatment on a regular basis.
When used cosmetically, the duration of action of BoNT-B is
significantly less than that of type A, with an effective initial
response of 2–3 months.
Commercial sources of BoNT-A
Several botulinum toxin products are currently available in
the US:
■ Botox (onabotulinumtoxinA) for injection (Allergan Inc.,
Irvine, CA) is supplied in vials containing 100 U of
Key points
• The most important elements for facial rejuvenation with
BoNT-A are functional anatomy, functional anatomy, and
functional anatomy!
• To minimize the risk of a frozen, unnatural appearance, use
the minimally effective dose of BoNT-A.
• Brow elevation depends on the relative weakness of the
brow elevators versus brow depressors.
• The dose of BoNT-A used should be based on the
estimated mass of the muscle being injected, not the depth
of the rhytid.
• Avoiding the use of aspirin and non-steroidal anti-
inflammatory medications will decrease the occurrence and
severity of ecchymosis.
• The lower frontalis muscle has the greatest effect on brow
elevation.
• Threading the injection through the lips gives a more
natural result than the near universal point technique.
• Cooling the skin before injection minimizes discomfort.
• As a general rule, injecting depressors more strongly than
elevators will tend to give a more gentle lift to the area
involved.
• Over-injecting the mentalis can result in a “witch’s chin”
deformity and oral incompetence.
57
Basic science
symptoms consistent with botulinum toxin effects. These may
include asthenia, generalized muscle weakness, diplopia, blurred
vision, ptosis, dysphagia, dysphonia, dysarthria, urinary
incontinence, and breathing difficulties. These symptoms have
been reported hours to weeks after injection. Swallowing and
breathing difficulties can be life threatening and there have been
reports of death. The risk of symptoms is probably greatest in
children treated for spasticity but symptoms can also occur in
adults treated for spasticity and other conditions, particularly in
those patients who have underlying conditions that would
predispose them to these symptoms. In unapproved uses,
including spasticity in children and adults, and in approved
indications, cases of spread of effect have occurred at doses
comparable to those used to treat cervical dystonia and at lower
doses.
Adverse events reported by the manufacturers of BoNT-A
and BoNT-B products include nasopharyngitis, headache,
injection site pain, bleeding, bruising, edema, erythema, infec-
tion, inflammation, sinusitis, ecchymosis and nausea.8–11 Weak-
ness of adjacent muscles may also occur due to spread of
toxin resulting in undesired effects. These types of adverse
events are described in greater detail below. To minimize
bruising, patients should avoid the use of aspirin and non-
steroidal anti-inflammatory medications for 2 weeks prior to
treatment.
Patients have uncommonly developed neutralizing anti-
bodies for BoNT-A following cosmetic use. These events are
more often associated with the use of high doses for neuro-
logic purposes,20,21 although this has been reported following
cosmetic use resulting in treatment failure.22
Dosing
The manufacturer of each BoNT-A product provides recom-
mended dosing for their product, which is limited to the
indicated uses. However, the facial musculature of patients is
highly variable and precludes the use of standardized dosing
for different aesthetic procedures. Gender also presents an
obvious difference, as men typically (but not always) have
larger muscles requiring higher BoNT-A doses compared to
women.
Using Botox for the treatment of glabellar lines as an
example, the manufacturer recommends injecting 8 U in each
corrugator muscle and 4 U in the procerus muscle for a total
dose of 20 U; however, many practitioners inject an average
of 25 U per glabella, while some advocate doses as high as
80 U and upper face doses of nearly 100 U. A median dose of
15 U is used by the author with a dose range of 5–22.5 U.
Consequently, each clinician must gain familiarity with these
products through experience and establish their own optimum
BoNT-A dosing techniques.
These principles were demonstrated during a recent clini-
cal study. Patients were stratified by demographics and ran-
domized to receive a single treatment with different doses of
BoNT-A (Dysport) or placebo.23 Based on procerus/corrugator
muscle mass, women received doses of 50, 60, or 70 U, while
men were treated with 60, 70, or 80 U. Using this variable
dosing technique, 85% of BoNT-A-treated patients were rated
as treatment responders by a blinded evaluator after 30 days
compared with 3% of placebo-treated patients (p < 0.001).
Compared with patients in other studies who received 50 U
to the glabella (the approved, on-label dose), variably dosed
Dysport is indicated for the temporary improvement in the
appearance of moderate to severe glabellar lines associated
with procerus and corrugator muscle activity in adult patients
<65 years of age.10
Xeomin is indicated for the temporary improvement in the
appearance of moderate to severe glabellar lines associated
with corrugator and/or procerus muscle activity in adult
patients.15
Although the approved use of BoNT-A formulations for
cosmetic use is limited to glabellar rhytids and lateral canthal
lines, it is extensively used off label, and the author has used
it to treat every muscle in the face since 1991.
BoNT-B plays a relatively minor role for cosmetic applica-
tions. It has a faster onset of action than BoNT-A, which can
be beneficial, but its cosmetic usefulness is limited by greater
pain on injection due to its low pH and a shorter duration of
action. In isolated instances, it may be considered if a patient
fails to respond to BoNT-A. It may also be useful for full-face
laser resurfacing and lower-face scar revision, as the shorter
duration of action will keep the treated area relatively motion-
less during the early healing phase while avoiding prolonged,
unattractive facial weakness.
The use of BoNT-A and BoNT-B for neurological purposes
has become extensive. Its approved use for the treatment of
cervical dystonia16 has grown to include limb spasticity and
dystonias, hypersecretory syndromes such as sialorrhea,
headache, low back pain,17 and writer’s cramp.18
Warnings and contraindications
The use of products containing botulinum toxin is contrain-
dicated in the presence of infection at the proposed injection
site and in individuals with known hypersensitivity to any
botulinum toxin preparation or to any of the components in
the formulation. The use of BoNT-A is contraindicated in
patients with disorders of neuromuscular transmission, such
as myasthenia gravis or Lambert–Eaton myasthenic syn-
drome. Dysport contains a small amount of lactose and may
contain trace amounts of cow’s milk protein. Dysport should
not be use in patients with a known allergy to cow’s milk
protein.10
BoNT-A products should be used with caution in patients
currently taking drugs known to affect neuromuscular trans-
mission such as neuromuscular blockers, lincosamides,
aminoglycosides, polymyxins, quinidine, magnesium sulfate,
anticholinesterases, or succinylcholine chloride as they may
potentiate the effects of BoNT-A. The safety of administering
botulinum toxin to pregnant women has not been established,
and its use in this population should be avoided.
Adverse effects
In the United States, due to reports received by the Food and
Drug Administration regarding serious systemic adverse
reactions including respiratory compromise and death follow-
ing the use of botulinum toxins types A and B for both
approved and unapproved uses,19 the labeling of all botuli-
num toxin-containing products are required to containing the
following boxed warning:
Postmarketing reports indicate that the effects of all botulinum
toxin products may spread from the area of injection to produce
58
SECTION I
CHAPTER 5.3 • Injectables and resurfacing techniques: Botulinum toxin (BoNT-A)
Patient selection
Decision-making details of selecting
a patient for BoNT-A
The absolute key to becoming a proficient BoNT-A injector
instead of a mere technician is understanding the functional
anatomy of the face. Anatomy textbooks show the location of
different facial muscles and their origins and insertions. While
these texts allow for small and expected anatomic variations,
they cannot prepare the clinician for the overwhelming differ-
ences in functional anatomy between individuals, or even
different sides of the same face. Even though all individuals
have the same mimetic muscles, their smile patterns vary
depending on which muscles dominate within the group.25
Even within a single muscle, different portions of that muscle
can dominate and severely alter animation (Fig. 5.3.1).
Therefore, it is essential that the face of each patient be
carefully analyzed to determine which portions of which
muscles dominate facial activity and cause wrinkles or other
unaesthetic shaping of the face. These are the muscle seg-
ments that benefit from treatment with BoNT-A. The key is to
take the necessary time to analyze the patient’s face and
discern these details. This is especially important in the lower
face, and plastic surgeons should become highly familiar with
these muscles and their possible anatomic variations. Under-
standing how the lower face moves is the key to using BoNT-A
patients tended to have improved efficacy and quicker onset
without increased adverse events.
BoNT-A products are not bioequivalent and cannot be used
interchangeably because of differences in unit potency and
fundamental differences in how these units are measured. A
randomized, double-blind study comparing onabotulinum-
toxinA and incobotulinumtoxinA was performed at a dose of
24 units per glabella and revealed incobotulinumtoxinA to be
non-inferior to onabotulinumtoxinA.24 I believe it is fair to say
that onabotulinumtoxinA and incobotulinumtoxinA have
similar dosing regimens while the units of abobotulinum-
toxinA are quite different.
The indicated dilution volume for the 100-unit vial of Botox
Cosmetic is 2.5 mL and for the 300-unit vial of Dysport is either
2.5 mL or 1.5 mL, both with non-preserved normal saline. In
actual practice, a wide range of volumes are used from 1.0 mL
to 6.0 mL. Most practitioners use preserved saline (off label) for
its weak anesthetic effect (benzyl alcohol is the preservative)
and as a preservative if the vial is stored for a few days between
uses. A recent poll of a consensus group of experts revealed
that nearly all used each vial on more than one patient (also
not according to the label). Smaller volumes allow for more
concentrated dosing with less pain (based on volume of injec-
tion) per dosage point. Larger volumes allow for more injec-
tion points per dosage and thus, perhaps, more control. I have
used 4.0 mL of non-preserved saline for both onabotulinum-
toxinA and incobotulinumtoxinA 100-unit vial since 1991 and
2011 and 3.0 mL of non-preserved saline for Dysport since its
introduction.
Fig. 5.3.1 Facial muscles.
Galea aponeurotica
Procerus
Corrugator supercilii
Nasalis
Zygomaticus minor
Zygomaticus major
Levator anguli oris
Buccinator
Masseter
Orbicularis oris
Frontalis
Orbicularis oculi, pretarsal portion
Orbicularis oculi, preseptal portion
Orbicularis oculi, orbital portion
Levator labii superioris alaeque nasi
Levator labii superioris
Auricularis anterior
Risorius
Depressor septi nasi
Platysma
Depressor anguli oris
Depressor labii inferioris
Mentalis
59
Treatment technique
Forehead
Horizontal forehead rhytids may be relieved by injecting and
weakening the frontalis muscle. Using Botox and Xeomin, the
dosing range for treating the frontalis is about 2.5–20 U,
although most require 3.75–6.25 U. The median dose of
Dysport in this area is 15 U (all total doses). The frontalis has
highly variable functional anatomy, and care must be taken to
not overly denervate the frontalis, which can lead to an overly
smooth, artificial appearance, brow ptosis, and eyelid ptosis
in patients who use the frontalis as an accessory eyelid eleva-
tor. Despite its appearance in most anatomy texts, the frontalis
is usually continuous across the forehead with muscle tissue
present even at the midline.
After the patient has been observed during normal anima-
tion, they are asked to raise and lower their brows repeatedly,
almost to the point of exhaustion. After observing this motion,
the strongest portions of the muscle, not the rhytids, are tar-
geted. The author is unaware of any standard pattern of
injection that produces reproducibly excellent results.
Crow’s feet and lower eyelids
In selected patients, the lateral and inferior orbicularis oculi
can be weakened to diminish the presence of crow’s feet and
lower eyelid rhytids. Patients typically seek treatment for
their crow’s feet once they become visible in repose. Prior to
the availability of BoNT-A, the lateral orbicularis was weak-
ened surgically.28 The convergence of crow’s feet and lower
lid rhytids and the fact that they are both created by the same
muscle lends them to concomitant treatment with BoNT-A.
The classification of crow’s feet patterns is based on the
functional anatomy of this area.29 In patients with the full-fan
pattern, the lateral orbicularis contracts and wrinkles the
overlying skin from the lateral brow to the lower lid/upper
cheek junction. It is important to recognize different patterns
as well as degrees of asymmetry that may occur in individual
patients, and treatment is based on the functional anatomy of
the orbicularis oculi.
Overly aggressive treatment in this area can result in
unpleasant results ranging from the “deer in the headlights”
appearance to cheek ptosis. While most plastic surgeons are
aware that the upper lateral orbicularis oculi is a brow depres-
sor, many fail to realize that the lower lateral portion of the
muscle is an important accessory cheek elevator. If overly
denervated in its lower lateral section, malar flattening as well
as an extra “roll” of skin between the lower lid and cheek can
occur.
Excessive chemodenervation of the orbicularis oculi across
the lower lid can produce several unaesthetic results. In
patients with a relatively lax lower eyelid, frank ectropion or
lower lid retraction may result. In patients with minimal-to-
borderline orbital fat prolapse, weakening the preseptal
orbicularis oculi can exaggerate and hasten the appearance of
fat “bags” of the lower lids. Since this sheet of muscle also
functions as a pump, severe denervation can result in
lymphedema.
These potential problems necessitate that these areas be
injected judiciously. Although there are no standard doses or
dosing patterns, the author uses between 3.75 and 5 U of
Botox and Xeomin or 12.5 U of Dysport per side for most
patients for both crow’s feet and lower lid orbicularis. BoNT-A
to improve nasolabial folds, perioral rhytids, chin dimpling,
marionette lines, and downturned oral commissures. This is
not an area for the novice injector, as a few misplaced units of
BoNT-A is not tolerated nearly as well as they are in the upper
face.26,27
Treatment technique
Treatment with BoNT-A does not need to be an all-or-nothing
phenomenon. A certain amount of toxin will block a certain
number of nerve terminals. Thus, fine control over the amount
of denervation desired is possible. Despite the common use
of the word “paralysis” when discussing the toxin, it is rare
that this is actually the desired effect. Rather, a selective
weakening of the musculature is performed to achieve a
pleasant cosmetic effect.
Glabella
The glabella was the first area to be treated cosmetically with
BoNT-A injections. Similar to other areas of the upper face,
this use of BoNT-A was based on longstanding surgical pro-
cedures. During a bicoronal browlift, it was common to debulk
the glabellar musculature to ease glabellar furrowing and
reduce downward pull on the brow.
Even in a seemingly straightforward area of the face as the
glabella, there is a great deal of variation in functional anatomy.
When most people frown, they primarily bring their brows
together as well as depress them; however, not everyone does
this. Some people primarily frown in a vertical pattern, dra-
matically depressing their brows. When others frown, they
may actually raise their medial brows while moving them
medially, resulting in a quizzical look.
The median dose of BoNT-A used by the author for treating
the corrugators and procerus muscles is 15–17.5 U of Botox
and Xeomin for women and men, respectively, or 50–60 U
of Dysport for women and men, respectively (total dose).
After observing the normal animation of each patient during
the consultation process, the patient is asked to frown and
relax, repeatedly, and then scrunch their nose as if smell-
ing something unpleasant and relax, repeatedly. This allows
gauging as to which sections of which muscles dominate
and which specific areas are to be targeted with BoNT-A
(Fig. 5.3.2).
To inject, the author displaces the forehead and brow
cephalad and then with the non-injecting hand fixes it in
position by placing pressure across the superior orbital rim.
The patient is asked to frown, revealing an indentation in the
skin corresponding to the site where the tail of the corrugator
inserts into the dermis of the skin of the brow in a horizontal
frowner. I begin injecting in this area and progress medially
with small injections to the procerus, which receives little
BoNT-A. The same procedure is repeated across the other
brow, moving from lateral to medial. Most men have signifi-
cantly longer corrugators than women with the tail extending
lateral to the mid-pupillary line. Vertical frowners require
much more BoNT-A to be injected into the medial (dominant)
portions of the corrugators and heavy injection of the pro-
cerus. The author often does not inject the lateral tail of the
corrugators in male patients, reducing feminizing brow
spread and permitting more normal animation.
60
SECTION I
CHAPTER 5.3 • Injectables and resurfacing techniques: Botulinum toxin (BoNT-A)
A
B
C
D
E
F
Fig. 5.3.2 This patient is in her late 40s. She has been injected with BoNT-A by the author for 16 years. It is 2 years since her last injection. She has shown an increasing
duration of action since 3 years after her injections began. (A) Patient is frowning before injection. Due to long-term atrophy, she is not able to sharply fold her skin but has
mild wrinkling, evidence of muscle bulge, and downward pull on her brows and upper eyelids. (B) Frowning after injection of 60 Dysport units to her glabellar complex. Her
fine rhytids are improved, she can no longer depress her lids to fully eclipse her lateral eyelids, and her muscle bulge is diminished. Note she has some recruitment of her
orbicularis, greater on her right – this occasionally happens after muscle atrophy. (C) Patient is raising her brows before injection. She is mildly stronger on her left side.
(D) Raising brows after 20 Dysport units were injected into her frontalis with 11 U in her left frontalis and 9 U in her right frontalis. Her forehead is smoother, yet she is able
to exhibit animation and emotion. Her brow asymmetry is partially corrected. Perfect symmetry is not always the goal. As long as asymmetry is not worsened, most patients
are very pleased with the results, as small asymmetries are often not noticed by the patient prior to injection. (E) Smiling prior to injection. Note the depression of her
lateral brow/upper lid mass. She also has a significant pretarsal orbicularis bulge that she found unsightly. (F) Smiling after 15 Dysport units were injected into her lateral
canthal and lower eyelid area (each side received 15 U). Her crow’s feet are diminished, but very importantly, not removed. No crow’s feet upon smiling is a most unnatural
appearance. Teenagers have crow’s feet when smiling. Her lateral brow is less depressed and her orbicularis roll greatly improved without sacrificing lower lid position.
61
Treatment technique
G
H
I
J
(G) Showing her lower teeth prior to injection. She exhibits very little depressor anguli oris (DAO) activity. The DAO is the quickest muscle of the lower
face to exhibit signs of atrophy in the author’s experience. Note the asymmetry – the DAO is also the most asymmetric muscle in the lower face by the author’s experience.
(H) Contracting the DAO post-7 Dysport units to the left DAO and 3 units to the right. Her asymmetry is improved. Her DAO dimple on her left is also improved and her oral
commissures are raised. (I) Repose before injection. (J) Repose after above injections. Her rhytids are improved and she has a slight lift of the brows with decreased upper
lid heaviness. The uptick in her oral commissures is evident. Remember, this patient had less to gain than average patients due to her long-term muscle atrophy.
Fig. 5.3.2, cont’d
should not be wasted on relatively adynamic sections of the
muscle. To do this, one must recognize that the functional
anatomy of the lateral periorbita varies widely. I inject the
most dynamic area of the muscle first, followed by smaller
injections radiating out from this point. The idea is to create
a gentle gradient of decreased muscle activity and avoid
sharp extremes between total muscle immobility and adjacent
areas of compensatory hypermotility.
Brow elevation
The use of BoNT-A injections to achieve brow elevation was
once considered controversial. Publications in the plastic
surgical and dermatologic press claimed that BoNT-A could
only depress the brows or at best create the illusion of a
browlift by dropping the medial brow; however, the author
routinely uses BoNT-A to easily and reliably lift the brows in
excess of 6 mm. The concept is remarkably easy.
To lift the brows, concentrate on injecting muscle segments
that depress the brows actively and at rest, allowing the brows
to rise. On the other hand, the concept of increasing browlift
by weakening the only muscle that lifts them is not well
understood. The explanation for this seeming paradox is that
the non-weakened sections of frontalis react by increasing
their pull in compensatory fashion. This explains why when
the lateral orbicularis is strongly injected, lower lid rhytids
will increase.
This is not simply an illusion due to smoothing of the skin
laterally but the result of increasing the resting tone of the
non-injected portion of the muscle across the lower lid. This
62
SECTION I
CHAPTER 5.3 • Injectables and resurfacing techniques: Botulinum toxin (BoNT-A)
platysma band becomes apparent and may be grasped
between the thumb and index finger of the non-injecting
hand. The patient is then asked to relax, and the muscle is
injected starting just below the mandibular border and pro-
gressing inferiorly to the point at which the band is visible
during normal animation. The horizontal “necklace” rhytids
can also be very minimally improved by injecting toxin just
above and below them.
Good candidates for the treatment of platysmal bands
with BoNT-A include the following: relatively young (35–45
years) patients with strong bands and minimal skin laxity
are excellent candidates; similarly, patients of any age who
have undergone surgical removal of excess skin and which
have recurrent bands are also good candidates. A smaller
but more frequently seen group includes young patients
following an aggressive fat removal via liposuction in
the neck, who subsequently develop visible platysmal
bands.
also explains why the lateral brows often peak in an unat-
tractive “Mr. Spock” appearance with worsening of lateral
suprabrow rhytids when only the central frontalis is injected
with a high dose of BoNT-A. Weakening portions of the
frontalis causes other portions of the frontalis to compensate
and lift more strongly. To maximize browlift, injecting the
portions of the frontalis not responsible for raising brows
will induce the frontalis responsible for brow elevation to
pull harder. Usually, this means injecting the frontalis more
strongly centrally in the zone above and medial to the
brows. The frontalis lateral to the brows is also injected,
causing the frontalis directly over the brows to lift more
strongly.
There are 11 muscle segments that can depress the medial
brow: the procerus, transverse heads of the corrugator, oblique
heads of the corrugator, depressor supercilii, medial orbicu-
laris oculi, and in some patients, the nasalis muscles. In most
patients, the effect of the nasalis on brow position is negligible;
however, injecting the other medial brow depressors has
occasionally resulted in disappointing brow elevation. With
the other muscle segments completely non-functional, these
patients depress their brows by wrinkling their nasalis.
Subsequent nasalis injection gave the brows additional
elevation.
The lateral brow is depressed by the cephalad portion of
the lateral orbicularis oculi. The dynamic of this action differs
widely among patients, and there is no single point that can
be injected to reliably elevate the lateral brow. Some patients
who do not depress their brows when smiling will not achieve
reliable brow elevation by simply injecting the upper lateral
orbicularis. The key is individualized treatment, based on the
functional anatomy of each patient.
There is no standard BoNT-A injection pattern for brow
elevation. For a more medial brow elevation, denervate the
medial depressors and weaken the frontalis over the lateral
brow, leaving the medial frontalis strong. For a more lateral
elevation, weaken the lateral depressor and the medial fron-
talis. For a peaked and arched brow, weaken the lateral
depressor and leave the frontalis over the junction of the
middle and lateral third of the brow strong. For men, leave a
wider band of frontalis working to raise the brows uniformly,
while keeping them flat, avoiding feminized, peaked brows.
For a unilateral browlift (in addition to the zones not directly
over the brows), weaken the frontalis slightly over the higher
brow, inducing the frontalis over the lower brow to pull
harder.
Neck
Platysmal bands are another area where BoNT-A injections
can yield excellent results.30 The key to evaluating the neck as
a potential site for cosmetic improvement involves determin-
ing the relative contributions of the skin and the platysma to
banding. The best patients have minimal skin excess and rela-
tively strong bands (Fig. 5.3.3). Patients with lax neck skin are
poor candidates for BoNT-A injection because the lax skin will
continue to hang even when the bands are completely
paralyzed.
Using Xeomin and Botox, the dosing range is approximately
15–30 U, with most patients requiring about 17.5 U. The
typical dose of Dysport is about 50 U. By asking the patient
to show their lower teeth with their teeth clenched, the
Fig. 5.3.3 This patient is in her mid-30s and requested neck rejuvenation.
(A) Straining prior to injection. She has minimal excess skin or fat and prominent
platysmal bands. Her platysma is thick on palpation, she has a greater than normal
muscle mass. (B) Straining post-injection of Botox 20 U to her right primary
(medial) band and 7.5 U to her right secondary (lateral) band as well as treatment
of her left platysma.
A
B
63
Treatment technique
range for this muscle is about 3.75–10 U of Xeomin or Botox
with most patients requiring 5 U in total. The usual total dose
of Dysport is about 15–20 U.
Perioral lines
BoNT-A is an excellent adjunct for rejuvenating the lower
face; however, excellent control and familiarity with the drug
is essential before injecting these rewarding but technically
demanding areas of the face (Fig. 5.3.5). Perioral rhytids,
dimpled chin, and downturned oral commissures are all
amenable to improvement by BoNT-A injection. Once again,
fully understanding the functional anatomy of each patient is
the key to achieving reproducibly good results and avoiding
the disastrous consequences of a few misplaced units of
BoNT-A. When first beginning to inject the lower face, lower
doses of BoNT-A and more frequent touch-ups are better than
larger initial doses and severe complications.26,27
The perioral rhytids are a common area of complaint for
many patients. Radially oriented rhytids are caused by intrin-
sic aging of the skin (dermal thinning, sun damage, smoking),
a loss of volume over time, and forced wrinkling of the skin
caused by its densely adherent underlying muscle, the orbi-
cularis oris. The most common rejuvenative procedure for this
area is the injection of fillers. Injecting hyaluronic acid-
containing products into the vermilion and cutaneous lip
improves the rhytids, restores lost volume, and offers imme-
diate results with negligible recovery time; however, BoNT-A
is an effective rejuvenative modality for some patients. First,
there are those who are already undergoing BoNT-A treat-
ment into other areas of the face and wish to also improve
their lip lines. Others want to improve their wrinkles but are
adamant about not increasing the size of their lips for fear of
looking “done”. The third and largest group of patients
receive concomitant BoNT-A and filler injections. The dermal
filler restores volume and fills wrinkles while the BoNT-A
relieves some of the contracting force applied to the skin by
the underlying orbicularis oris.
To judge the relative strength of the sphincter muscle, the
patient is asked to repeatedly purse, then relax, the lips. The
dosing range for Xeomin and Botox is about 2–7 U per lip
(5–15 U for Dysport), although most patients will require only
about 3 U per lip (7.5 U for Dysport). In contrast with other
areas of the face where small, precise doses of BoNT-A are
injected, this area is more broadly injected to achieve a diffuse,
Nasolabial folds
The nasolabial fold is an excellent area for BoNT-A injections
in properly selected patients who have been instructed what
to expect.31,32 The levator labii superioris alaeque nasi is the
muscle primarily responsible for the medial nasolabial fold
and the final 3–4 mm of central upper lip elevation.31 Weaken-
ing this muscle smooths the medial nasolabial fold and
changes the smile pattern of the patient. The three major
smiling patterns were described by Rubin.25 The most common
or “Mona Lisa” smile pattern is dominated by the zygomati-
cus muscle, which elevates the oral commissures to the highest
point of the smile. The “canine smile” is caused by a dominant
levator labii superioris, and the highest part of the smile is the
central upper lip. This pattern occurs in 35% of the popula-
tion, and they are the potential candidates for this procedure.
Since injecting this muscle results in a drop of the central
upper lip when smiling, it converts “canine” smilers into
“Mona Lisa” smilers. Injecting patients with the Mona Lisa
smile results in an exaggerated Mona Lisa smile that most
patients find unattractive.
Patients with “gummy smiles” are basically extreme canine
smile pattern patients (Fig. 5.3.4). This group benefits the most
from BoNT-A injection of the levator labii superioris aleque
nasi. Gummy smilers often smile asymmetrically, requiring
asymmetric injection. They also tend to have deeper medial
nasolabial folds, which are the area of primary improvement
with this technique. The resulting drop of the upper lip hides
the gingiva and results in a more pleasing smile.
The technique for this injection is relatively straightforward
once the patient has been determined to be a suitable candi-
date. Before injection, the patient can be given a preview of
the proposed change: the patient smiles into a mirror held at
eye level. Pushing the upper lip down 3–4 mm with a cotton
applicator stick gives the patient a rough approximation of
the change to be expected to the smile as well as the nasolabial
fold.
During injection, use the index finger of the non-injecting
hand to firmly press against the inferior portion of the nasal
bone where it meets the maxilla. Thus, half of the finger is
falling into the pyriform aperture while the other half lies in
the groove between the nasal bone and maxilla. Then ask the
patient to smile strongly – the levator labii superioris alaeque
nasi can usually be felt just lateral to this groove. It is injected
once on each side, just above the periosteum. The dosing
Fig. 5.3.4 This patient is in her mid-30s
and requested improvement of her gummy
smile. (A) Prior to injection, smiling.
(B) After injection of 750 U of Myobloc
(BoNT-B) to her levator labii superioris
alaeque nasi muscles and 500 U into her
upper orbicularis oris. Note the softening of
her nasolabial folds as well as the lowering
of her central greater than her lateral lower
lip. This illustrates how all toxins can be
used for cosmetic improvement. The
cosmetic use of the currently available
BoNT-B is limited, however, by its increased
pain on injection (lower pH), potential for
greater spread, and decreased duration of
action compared to current BoNT-A
preparations.
A
B
64
SECTION I
CHAPTER 5.3 • Injectables and resurfacing techniques: Botulinum toxin (BoNT-A)
A
B
C
D
E
F
Fig. 5.3.5 This patient complained about the overall appearance of her lower face. The most obvious cause is her mentalis, which is contracted even in repose (see G).
(A) Patient contracting her mentalis prior to injection by pushing her lower lip up. (B) Her mentalis after 5 Botox units were injected across its surface. The irregularities are
greatly improved. (C) Depressing her lower lip reveals her gingival and bilateral rhytids across her labiomental area (her “DAO dimple”; DAO, depressor anguli oris).
(D) Depressing her lower lip after 7.5 Botox units were injected to her DAO muscles symmetrically. She is unable to show her gingival or even the lower half of her
dentition. Her DAO dimples are greatly improved. (E) Patient puckering her lips prior to injection. (F) Puckering her lips after 2 Botox units were injected into each lip. Her
skin puckering is improved but not gone. Threading toxin injections across the lip can improve this appearance.
65
Treatment technique
G
H
I
J
(G) Repose prior to injection. (H) Repose after the above injections. Her chin is less wide and more refined from mentalis injection. Her commissures
are raised and her apparent volume deficit below the commissures is gone, due to relaxation of the DAO. Her lips appear more full and without rhytids from her orbicularis
oris injection. The horizontal width of her mouth appears diminished and the overall shape of the lower face has been improved. (I) Smiling prior to injection. (J) After
injection, the patient exhibits a natural smile. Her lower lip is slightly raised, which helps protect her oral competence and is also more youthful. When injecting many areas
of the lower face simultaneously, the patient can experience a feeling of weakness.
Fig. 5.3.5, cont’d
general weakening of the sphincter muscle. The philtrum is
almost never injected, as it rarely contains strong rhytids.
The addition of normal saline into the syringe containing the
appropriate BoNT-A dose allows more even placement of the
drug.27 The needle is inserted parallel to and a few millimeters
above the vermillion border and the BoNT-A is injected as the
needle is withdrawn. The upper and lower lips can be treated
in the same session. Complications can easily result in this
area and are usually due to over-injection. Excessive weaken-
ing of the upper lip leads to problems, first with plosive
sounds, followed by general speech, and finally oral compe-
tence. Over-injection of the lower lip is more likely to result
in drooling and competence problems. Beware the elderly
patient with severe rhytids and decreased muscle mass.
Slightly weakening the superficial fibers of the orbicularis
oris can help alleviate the overlying rhytids caused by this
sphincter, with or without concomitant filler injection. In 1998,
the author abandoned the more popular injection point
technique and began using the method of threading the injec-
tion a few millimeters above the vermilion border. This results
in a more even appearance and avoids compensatory areas of
hypermotility.
Mentalis
Many patients form an unattractive, dimpled pattern on their
chin during active speech or repose with the lips closed. This
appearance results from contraction of the underlying men-
talis muscle, which is connected to the overlying dermis by
dense fibrous septae. These septae transmit the forces and
contours of the superficial mentalis to the skin. Dimpling and
occasional ridging of the skin in patients with hypertrophy of
the mentalis can result.
Using Botox or Xeomin, the dosing range for the mentalis
is about 2.5–10 U, with most patients requiring 2.5–5 U.
Similar results may be achieved using 7–13 U of Dysport (all
66
SECTION I
CHAPTER 5.3 • Injectables and resurfacing techniques: Botulinum toxin (BoNT-A)
treated with BoNT-A, maintaining brow elevation. Overly
elevated brows can be dropped by aggressively injecting
the frontalis muscle.
■ Chin augmentation: Surgical misadventures leading to
mentalis disinsertion and dimpling of the chin can be
effectively treated with careful injection of the superficial
mentalis.
■ Breast augmentation: Prolonged spasm of the pectoralis
major can be treated by injecting the lower pectoralis
major.
■ Surgery or trauma: Facial nerve injuries can often be
effectively masked by weakening the unaffected muscle
on the other side of the face. For marginal mandibular
nerve injury after facelift, this usually entails injecting the
contralateral depressor anguli oris muscle and possibly
the depressor labii inferioris and mentalis.
Hyperhidrosis
BoNT-A injections have been used for the treatment of
palmar,33 plantar,34 facial,35 and axillary36,37 hyperhidrosis
(excessive sweating). Injections of the soles and palms may be
very painful unless some analgesia is used,38 and care must
be taken not to inject and weaken hand and foot muscles.
Results for this application typically last somewhat longer,
approximately 6 months.
Salivary glands
Large salivary glands can be decreased in size with BoNT-A.
Controversy exists in plastic surgery over the surgical resec-
tion of submandibular glands during face or necklift proce-
dures. The author has been decreasing the apparent size of
submandibular and parotid glands for 20 years with BoNT-A.
Twenty units of Xeomin or Botox are used per parotid gland
(50 U of Dysport). Large submandibular glands are started
with 15 U of Xeomin or Botox (40 U of Dysport), which can
often be tapered with repeat injection as the gland shrinks
down to 5–7.5 U (Xeomin or Botox) or 12.5–15 U of Dysport.
Patients are observed in the office for 30 min after subman-
dibular gland in injection for signs of bleeding into the neck.
Postoperative care
There is wide disagreement regarding postoperative care
during the first 24 h following treatment with BoNT-A. Rec-
ommendations range from no bending for 6 h, to avoiding
airline travel for the first 24 h after treatment, although evi-
dence for these is lacking. Nevertheless, the author believes it
may be beneficial for patients to avoid heavy exertion for
90 min following treatment with BoNT-A. That is approxi-
mately the time most believe it takes for the toxin to bind to
the neuron cell membrane.
Outcomes, prognosis, complications
Potential adverse reactions
Adverse events happen with every procedure and BoNT-A
is no exception. Complications, however, tend to be mild,
doses total). Weakening the mentalis must be done cautiously,
as this muscle raises the chin pad and lower lip and is critical
for oral competence. Care must be taken to inject only the
superficial mentalis, leaving the deep mentalis fully func-
tional. The injection needle is threaded cephalad, parallel to
the skin surface, aiming for the plane between the superficial
muscle and its overlying fascia. It is important to remember
that patients who have an underlying problem with oral
competence can exhibit mentalis hypertrophy from constant
use and present with dimpling. These patients must be
injected with caution and told of the possible risks this treat-
ment entails. Consequently, injection of the mentalis is often
paired with depressor anguli oris injection to maintain the
height of the lower lip.
Depressor anguli oris
The depressor anguli oris is a triangularly shaped muscle that
depresses the oral commissures. This action contributes to the
formation of marionette lines and often creates a distinct
diagonal rhytid below the commissure. Injecting this muscle
with BoNT-A raises the oral commissures and decreases the
show of the lower dentition when smiling. It also helps to
improve marionette lines and the horizontal crease below the
commissure.
Using Xeomin or Botox, the dosing range is about 2.5–10 U,
with most patients requiring 5–7.5 U (10–15 U of Dysport). All
doses are total for both sides. The patient is repeatedly asked
to show their lower teeth with their dentition occluded. This
usually creates a diagonal rhytid below the commissure. Each
muscle is injected twice with the point of the first injection at
the level of the horizontal rhytid. The second injection point
is midway between the first point and the lower border of the
mandible, and in the direction that the muscle pulls the com-
missure when contracting. Most patients pull their commis-
sures down and laterally when contracting; however, some
patients will pull their commissures down and medially. It is
along this axis of motion that the second injection is placed.
Once again, the key to success is to know the functional
anatomy of each patient. Also, care must be taken not to inject
the cephalad portion of this muscle. First, there is very little
muscle activity in the cephalad portion as the muscle tapers
and becomes aponeurotic. Second, the existing muscle (lower
orbicularis oris) does not tolerate concentrated injections lat-
erally, which can easily result in oral incompetence and drool-
ing. When properly injected, the depressor anguli oris is one
of the safest muscles to inject in the lower face. Even if it is
slightly over-injected, it does not lead to oral incompetence
but an actual rising of the lower lip. In fact, patients with oral
competence problems caused by the lower orbicularis oris or
mentalis weakening or a facial nerve injury, may obtain relief
by injecting the depressor anguli oris. Injection of the lower
lip with a viscous hyaluronic acid product at the same time
can also add some static support.
Repair of surgical complications
Many complications from aesthetic surgical procedures can
be effectively treated with BoNT-A:
■ Browlift: Excessive downward muscle pull on the brows
observed during the early postoperative period caused by
incomplete corrugator or procerus resection can be
67
Secondary procedures
BoNT-A and fillers is highly synergistic. They attack unaes-
thetic areas via their different causes, often with outstanding
results. While BoNT-A attacks the underlying mimetic cause,
the filler addresses volume and structural causes of facial and
neck aging.
Laser resurfacing is another procedure that benefits from
treatment with BoNT-A. In many ways, the mechanism is
similar to the improved results seen with BoNT-A and scar
revision. It appears that the relative decrease in motion
improves wound healing and results in less apparent scar
tissue. In addition, it has been apparent that BoNT-A has
several direct dermal effects, which are now being studied.
The author tries to avoid BoNT-A drift into the dermis because,
while it may have a beneficial effect on acne and pore size,
it frequently gives the skin a shiny, plastic, unnatural
appearance.
infrequent, and temporary. Most adverse events related to
treatment arise from proximity spread of the toxin into adja-
cent musculature. Difficulty in assessing muscle mass and
consequent dosing also may play a part as there is no definite
method to measure muscle mass prior to injection.
Ecchymosis and tenderness are common adverse events
that can occur with any percutaneous procedure. The most
frequent adverse events from toxin in the upper face are brow
and lid ptosis. Occasionally, these may be improved with
additional weakening of depressor musculature, leaving the
elevating musculature (frontalis) dominant. Alpha agonist
drops may also help to ameliorate lid ptosis by stimulating
Müller’s muscle.
Lower face complications from BoNT-A administration
include asymmetry, dysphagia, and oral competence issues.
For example, adverse events associated with the treatment of
vertical lip rhytids include eating and drinking difficulties or
difficulty making certain plosive sounds.
Secondary procedures
Treating patients who had the procedure but
desire improved results
The most common secondary procedure associated with
BoNT-A injection is concomitant filler injection. The use of
1. American Society for Aesthetic Plastic Surgery. Cosmetic Surgery
National Data Bank: 2014 Statistics. Online. Available at: http://
aesthetic-plastic-surgery-reports-americans-spent-more-than-12-
billion-in-2014---pro.
2. Scott A, Rosenbaum A, Collins C. Pharmacologic weakening of
extraocular muscles. Invest Ophthalmol Vis Sci. 1973;12:924–927.
3. Scott A. Botulinum toxin injection into extraocular muscles as an
alternative to strabismus surgery. J Pediatr Ophthalmol Strabismus.
1980;17:21–25.
4. Scott A, Kennedy R, Stubbs H. Botulinum A toxin injection as a
treatment for blepharospasm. Arch Ophthalmol. 1985;103:347–350.
5. Carruthers J, Carruthers J. Treatment of glabellar frown lines with
Clostridium botulinum A exotoxin. Dermatol Surg. 1992;18:17–21.
6. Sharma S, Zhou Y, Singh B. Cloning, expression, and purification of
C-terminal quarter of the heavy chain of botulinum neurotoxin type
A. Protein Expr Purif. 2006;45:288–295.
7. Huang W, Foster J, Rogachefsky A. Pharmacology of botulinum
toxin. J Am Acad Dermatol. 2000;43:249–259.
8. Botox® (onabotulinumtoxinA) for injection. Prescribing
Information. Irvine, CA: Allergan, Inc.; 2009.
9. Botox® Cosmetic (onabotulinumtoxinA) for injection. Prescribing
Information. Irvine, CA: Allergan, Inc.; 2014.
10. Dysport™ for injection (abobotulinumtoxinA). Prescribing
Information. Brisbane, CA: Tercica, Inc., and Scottsdale, AZ: Medicis
Aesthetics Inc.; 2014.
11. Myobloc® (rimabotulinumtoxinB) injection. Prescribing
Information. South San Francisco, CA: Solstice Neurosciences Inc.;
2009.
12. Wenzel R, Jones D, Borrego J. Comparing two botulinum toxin type
A formulations using manufacturers’ product summaries. J Clin
Pharm Ther. 2007;32:387–402.
13. Wohlfarth K, Sycha T, Ranoux D, et al. Dose equivalence of two
commercial preparations of botulinum neurotoxin type A: Time for
a reassessment? Curr Med Res Opin. 2009;25:1573–1584.
14. Karsai S, Raulin C. Current evidence on the unit equivalence of
different botulinum neurotoxin A formulations and
recommendations for clinical practice in dermatology. Dermatol
Surg. 2009;35:1–8.
15. Xeomin (incobotulinumtoxinA) for injection. Prescribing
Information. Greensboro, NC: Merz Pharmaceuticals LLC; 2013.
16. Truong D, Duane D, Jankovic J, et al. The efficacy and safety of
botulinum type A toxin (Dysport) in cervical dystonia: results of the
first US randomized double-blind, placebo-controlled study. Mov
Disord. 2005;20:783–791.
17. Ney J, Joseph K. Neurologic uses of botulinum neurotoxin type A.
Neuropsychiatr Dis Treat. 2007;3:785–798.
18. Wissel J, Kabus C, Wenzel R, et al. Botulinum toxin in writer’s
cramp: objective response evaluation in 31 patients. J Neurol
Neurosurg Psychiatry. 1996;61:172–175.
19. Food and Drug Administration. Update of Safety Review of
OnabotulinumtoxinA (marketed as Botox/Botox Cosmetic),
AbobotulinumtoxinA (marketed as Dysport) and
RimabotulinumtoxinB (marketed as Myobloc). Department of
Health and Human Services; 2009 Online. Available at:
<
PostmarketDrugSafetyInformationforPatientsandProviders/
DrugSafetyInformationforHeathcareProfessionals/ucm174959.htm>.
20. Borodic G, Johnson E, Goodnough M, et al. Botulinum toxin
therapy, immunologic resistance, and problems with available
materials. Neurology. 1996;46:26–29.
21. Dressler D, Adib Saberi F. New formulation of Botox: complete
antibody-induced treatment failure in cervical dystonia. J Neurol
Neurosurg Psychiatry. 2007;78:108–109.
Access the complete reference list online at
67.e1
References
References
1. American Society for Aesthetic Plastic Surgery. Cosmetic Surgery
National Data Bank: 2014 Statistics. Online. Available at: http://
aesthetic-plastic-surgery-reports-americans-spent-more-than-12-
billion-in-2014--pro.
2. Scott A, Rosenbaum A, Collins C. Pharmacologic weakening of
extraocular muscles. Invest Ophthalmol Vis Sci. 1973;12:924–927.
3. Scott A. Botulinum toxin injection into extraocular muscles as an
alternative to strabismus surgery. J Pediatr Ophthalmol Strabismus.
1980;17:21–25.
4. Scott A, Kennedy R, Stubbs H. Botulinum A toxin injection as a
treatment for blepharospasm. Arch Ophthalmol. 1985;103:347–350.
5. Carruthers J, Carruthers J. Treatment of glabellar frown lines with
Clostridium botulinum A exotoxin. Dermatol Surg. 1992;18:17–21.
6. Sharma S, Zhou Y, Singh B. Cloning, expression, and purification of
C-terminal quarter of the heavy chain of botulinum neurotoxin type
A. Protein Expr Purif. 2006;45:288–295.
7. Huang W, Foster J, Rogachefsky A. Pharmacology of botulinum
toxin. J Am Acad Dermatol. 2000;43:249–259.
8. Botox® (onabotulinumtoxinA) for injection. Prescribing Information.
Irvine, CA: Allergan, Inc.; 2009.
9. Botox® Cosmetic (onabotulinumtoxinA) for injection. Prescribing
Information. Irvine, CA: Allergan, Inc.; 2014.
10. Dysport™ for injection (abobotulinumtoxinA). Prescribing
Information. Brisbane, CA: Tercica, Inc., and Scottsdale, AZ: Medicis
Aesthetics Inc.; 2014.
11. Myobloc® (rimabotulinumtoxinB) injection. Prescribing Information.
South San Francisco, CA: Solstice Neurosciences Inc.; 2009.
12. Wenzel R, Jones D, Borrego J. Comparing two botulinum toxin type
A formulations using manufacturers’ product summaries. J Clin
Pharm Ther. 2007;32:387–402.
13. Wohlfarth K, Sycha T, Ranoux D, et al. Dose equivalence of two
commercial preparations of botulinum neurotoxin type A: Time for
a reassessment? Curr Med Res Opin. 2009;25:1573–1584.
14. Karsai S, Raulin C. Current evidence on the unit equivalence of
different botulinum neurotoxin A formulations and
recommendations for clinical practice in dermatology. Dermatol
Surg. 2009;35:1–8.
15. Xeomin (incobotulinumtoxinA) for injection. Prescribing Information.
Greensboro, NC: Merz Pharmaceuticals LLC; 2013.
16. Truong D, Duane D, Jankovic J, et al. The efficacy and safety of
botulinum type A toxin (Dysport) in cervical dystonia: results of the
first US randomized double-blind, placebo-controlled study. Mov
Disord. 2005;20:783–791.
17. Ney J, Joseph K. Neurologic uses of botulinum neurotoxin type A.
Neuropsychiatr Dis Treat. 2007;3:785–798.
18. Wissel J, Kabus C, Wenzel R, et al. Botulinum toxin in writer’s
cramp: objective response evaluation in 31 patients. J Neurol
Neurosurg Psychiatry. 1996;61:172–175.
19. Food and Drug Administration. Update of Safety Review of
OnabotulinumtoxinA (marketed as Botox/Botox Cosmetic),
AbobotulinumtoxinA (marketed as Dysport) and RimabotulinumtoxinB
(marketed as Myobloc). Department of Health and Human Services;
2009 Online. Available at: <
DrugSafety/PostmarketDrugSafetyInformationforPatientsand
Providers/DrugSafetyInformationforHeathcareProfessionals/
ucm174959.htm>.
20. Borodic G, Johnson E, Goodnough M, et al. Botulinum toxin
therapy, immunologic resistance, and problems with available
materials. Neurology. 1996;46:26–29.
21. Dressler D, Adib Saberi F. New formulation of Botox: complete
antibody-induced treatment failure in cervical dystonia. J Neurol
Neurosurg Psychiatry. 2007;78:108–109.
22. Borodic G. Botulinum toxin, immunologic considerations with
long-term repeated use, with emphasis on cosmetic applications.
Facial Plast Surg Clin North Am. 2007;15:11–16.
23. Kane M, Brandt F, Rohrich R, et al. Evaluation of variable-dose
treatment with a new U.S. Botulinum Toxin Type A (Dysport) for
correction of moderate to severe glabellar lines: results from a
phase III, randomized, double-blind, placebo-controlled study. Plast
Reconstr Surg. 2009;124:1619–1629.
24. Sattler G, Callander MJ, Grablowitz D, et al. Noninferiority of
incobotulinumtoxinA, free from complexing proteins, compared
with another botulinum toxin type A in the treatment of glabellar
frown lines. Dermatol Surg. 2010;36(suppl 4):2146–2154.
25. Rubin L. The anatomy of a smile: its importance in the treatment of
facial paralysis. Plast Reconstr Surg. 1975;53:384–387.
26. Kane M. Botox injections for lower facial rejuvenation. Oral
Maxillofac Surg Clin North Am. 2005;17:41–49.
27. Kane M. The functional anatomy of the lower face as it applies to
rejuvenation via chemodenervation. Facial Plast Surg. 2005;21:55–64.
28. Aston S. Orbicularis oculi muscle flaps: a technique to reduce
crow’s feet and lateral canthal skin folds. Plast Recostr Surg.
1980;8:679–686.
29. Kane M. Classification of crow’s feet patterns among Caucasian
women: the key to individualizing treatment. Plast Reconstr Surg.
2003;112(suppl):S33–S39.
30. Kane M. Nonsurgical treatment of platysmal bands with injection
of botulinum toxin A. Plast Reconstr Surg. 1999;103:656–663.
31. Pessa J. Improving the acute nasolabial angle and medial nasolabial
fold by levator alae muscle resection. Ann Plast Surg. 1992;29:23–30.
32. Kane M. The effect of botulinum toxin injections on the nasolabial
fold. Plast Reconstr Surg. 2003;112(suppl):S66–S72.
33. Moreau M, Cauhepe C, Magues J, et al. A double-blind,
randomized, comparative study of Dysport® vs. Botox® in primary
palmar hyperhidrosis. Br J Derm. 2003;149:1041–1045.
34. Benohanian A. Treatment of recalcitrant plantar hyperhidrosis with
type-A botulinum toxin injections and aluminum chloride in
salicylic acid gel. Dermatol Online J. 2008;28:5.
35. Glaser D, Hebert A, Pariser D, et al. Facial hyperhidrosis: best
practice recommendations and special considerations. Cutis.
2007;79(5 suppl):29–32.
36. Heckmann M, Ceballos-Baumann A, Plewig G. Botulinum toxin A
for axillary hyperhidrosis (excessive sweating). N Engl J Med.
2001;344:488–493.
37. Heckmann M, Plewig G. Low-dose efficacy of botulinum toxin A
for axillary hyperhidrosis. Arch Dermatol. 2005;141:1255–1259.
38. Richards R. Ethyl chloride spray for sensory relief for botulinum
toxin injections of the hands and feet. J Cutan Med Surg.
2009;13:253–256.
SECTION I • Aesthetic Surgery of the Face
5.4
Injectables and resurfacing techniques:
Laser resurfacing
Steven R. Cohen, Ahmad N. Saad, Tracy Leong, and E. Victor Ross
SYNOPSIS
■ Non-surgical facial rejuvenation relies on matching the presenting skin
pathology to an appropriate intervention that reverses that aspect of
aging.
■ Laser-based interventions rely on precise skin injury based on either
selective photothermolysis, precise deposition of layered heating, or
fractional wounding.
■ Facial rejuvenation procedures that work at the skin surface can be
complemented by neurotoxins and fillers as well as with autogenous
fat grafting with varying degrees of stromal vascular fraction
enrichment.
■ Laser-based therapy can be complemented by deeper heating,
long-pulse skin-tightening procedures (radiofrequency, ultrasound).
■ Fractional lasers achieve their rejuvenative effect with decreased risks
of infection, pigment dyschromia, pain, as well as shorter recovery
times versus their non-fractional counterparts.
■ Vascular dyschromias can be reduced by a wide range of visible light
and near-infrared technologies.
■ Hyperpigmented lesions can be treated by selective photothermolysis,
repeated fractional procedures, or by precise ablative approaches that
confine heating based on short laser–tissue interaction times.
Access the Historical Perspective section online at
Introduction
Laser, chemical peeling, and other energy-based technologies
have increasingly been applied in facial rejuvenation.1 A
logical approach to rejuvenation follows an understanding of
skin anatomy and physiology, as they relate to skin aging.
Any assessment of the face should include the surface, where
sun and aging result in pigment inhomogeneities, wrinkles,
and telangiectasia. Epidermal changes include basilar hyper-
pigmentation, hyperkeratosis, and thinning of the “living”
portion of the epidermis. Another component of skin aging
derives from changes in the dermis, where decreased glycos-
aminoglycans (GAGs), decreased elastin fibers, and changes
in the character of collagen result in fine lines, sallowness, and
eventually in cobblestoning of the skin. Microscopically, the
changes present as solar elastosis. Also, weakened blood
vessels dilate and present as telangiectasia. In some patients,
hyperpigmentation results from both dermal and epidermal
pigment dyschromias. The third component of aging skin
results from bone regression, weakening of connections from
the hypodermis to the surface, and volume loss.1,2
Most energy-based interventions address one or more of
these components of skin aging. Epidermal pigmentation can
be addressed by pigment-specific lasers or laser peels. In the
first case, visible (VIS) light is used to selectively heat the
epidermis. Proper parameter selection allows for preferential
targeting of the hyperpigmented lesion, whereas the normal
background “innocent” bystander skin is unharmed. Tradi-
tional “non-fractional” laser peels, on the other hand, target
water and therefore heat a confluent “slab” of the uppermost
skin. The depths of ablation of heating are determined by
wavelength, power density, fluence, and pulse-width.1
Blood vessels are heated by three broad categories of
devices: (a) visible light technologies (520–600 nm); (b) near-
infrared I (NIR I) technologies (755, 800 nm); and (c) NIR
II (940, 980, 1064 nm). The former is associated with very
strong hemoglobin (HgB) and melanin heating, the second
by moderate HgB and melanin heating, and the third by
moderate HgB heating but relatively weak melanin heating.
Deep heating devices have included laser, halogen lamps,
xenon flash lamps with long wavelength cut-off filters,
radiofrequency (RF), ultrasound (US), and combination
technologies.3
The use of light as a medical treatment has grown consider-
ably since the advent of the medical laser in the 1960s. The
word “laser” is an acronym for the term: light amplification
by stimulated emission of radiation. The device itself consists
of an energy source, a laser medium, and a resonating tube.
The medium can be a gas, liquid, or solid, and this will often
Access video lecture content for this chapter online at expertconsult.com
68.e1
Historical perspective
Historical perspective
Lasers have been used in medicine for several decades. Alex-
ander et al.1 noted that Albert Einstein was the first to describe
the concept behind the laser in the theory of stimulated emis-
sion of radiation in 1917.2 Theodore Maimon developed the
first laser light with use of a ruby crystal in 1960 and shortly
thereafter, lasers were being used in ophthalmology.1 During
the next several years, practitioners in many other medical
fields, including dermatology, otolaryngology, neurosurgery,
and gynecology, incorporated lasers into their practices. Selec-
tive photothermolysis is the theoretical foundation that
allowed the development of lasers designed to target specific
tissues.4,5 According to Alexander et al.,1 the first of these
lasers was the pulsed dye laser, with a wavelength of 577 nm,
one of the absorption peaks of hemoglobin. This device was
applied primarily for vascular lesions. Alexander1 noted that
Leon Goldman, a dermatologist – considered by many to be
the father of laser medicine, pioneered much of the early work
with cutaneous lasers and published his experience in the
treatment of vascular birthmarks with the ruby laser.6–8
The CO2 laser, developed in 1964, was initially a continuous
wave laser. It was designed with a highly focused handpiece
to cut skin.1 Its injury was associated with a bloodless field. It
also appeared to generate less edema, possibly because the
laser-sealed lymphatics.9 Sterling Baker, an ophthalmologist,
is credited with having performed the first laser blepharo-
plasty in 1984.10 The CO2 laser was also used as an ablative
tool for cutaneous lesions, but early lasers had limited control
of energy parameters, leading to frequent thermal injury and
scarring.1
According to Alexander and his co-authors,1 changing the
delivery of laser energy from a continuous to a pulsed mode
was key in the early improvement of the resurfacing laser.
Electronic shutters were developed to interrupt the continu-
ous wave and produce intermittent bursts of laser energy,
known as pulses, thereby decreasing the laser exposure time.
The original pulses were 0.1–1 s in duration, still too long an
exposure time to avoid scar formation unless very low powers
were applied.1 Superpulse lasers were then developed, which
delivered shorter pulse durations (pulse-widths) and higher
power, but still led to an unacceptable incidence of complica-
tions.1 Ultrapulse technology provided an increase in power
seven times that of the superpulse lasers, and the pulse-width
was decreased to less than 1 ms.1 These early advances helped
limit the thermal damage and associated scar formation,
allowing the CO2 laser to be used effectively as a resurfacing
tool. In 1991, Fitzpatrick et al. used this laser to treat actinic
damage of the face and actinic cheilitis and noted improve-
ment in wrinkles.11 These observations led to the use of laser
resurfacing with short-pulsed, high-energy CO2 to treat pho-
todamaged skin and acne scars.1
The introduction of short-duration Er : YAG lasers in the
mid-1990s offered another option for resurfacing, either alone
or in combination with the CO2 laser.1 Most of the initial laser
resurfacing research is credited to dermatologists.12 Laser
resurfacing grew in popularity and gained widespread accep-
tance among aesthetic plastic surgeons. As more problems
with scarring and hypopigmentation were reported, the early
enthusiasm toward ablative CO2 and Er : YAG waned.1
In an effort to expand treatment to all skin types and to
improve safety, reducing the frequency of scarring and loss of
pigmentation, fractional laser resurfacing was introduced by
Reliant technologies in 2003 as a new class of therapy. Frac-
tional photothermolysis has become an important modality in
management of a number of skin conditions and photoaging.
Unlike full-surface flat-beam resurfacing, fractional resurfac-
ing damages specific microtreatment zones within the target
area. It seems that almost any laser wavelength can be frac-
tionated and the initial non-ablative fractional lasers have
been safe and effective for treatment of fine wrinkles, pigmen-
tation, and acne scars.
Deeper rhytids and more extensive solar elastosis have not
responded as well to non-ablative wavelengths and hence,
fractional CO2 and Er : YAG lasers have been developed that
retain much of the safety of non-ablative fractional resurfac-
ing, but push the efficacy closer to non-fractional laser abla-
tion. Since the introduction of the first fractional laser in 2003,
numerous devices delivering fractionated treatment with a
variety of different capabilities have appeared on the market.
More importantly, in the aesthetic arena, where safety is of
paramount importance, fractional laser resurfacing has reso-
nated widely with both patients and physicians alike and has
become a leading trend in minimally invasive cosmetic
surgery.13–15
Another non-ablative technique that has gained popularity
within the last decade is monopolar radiofrequency skin
tightening.16 Developed in the mid-1990s and later approved
for use by the FDA in 2002, monopolar radiofrequency deliv-
ers a controlled radiofrequency pulse to the dermis and sub-
dermis to promote collagen remodeling.16 Inadvertent injury
to the more superficial dermis is avoided through use of a
cryogen spray during application of the energy.16 In 2013,
“injectable” temperature controlled radiofrequency devices
were introduced to the market. These devices provide the
operator with better control of the maximum target tissue
temperature and clinical endpoints. With improved control,
peer-validated parameters can be duplicated, and treatment
more standardized. Ultrasound-based therapies have also
gained popularity. These devices deliver focused depth- and
temperature-controlled ultrasound energy to the dermis, to
stimulate collagen production and rejuvenate the skin.
69
Introduction
be used to name the type of laser (e.g., ruby laser and CO2
laser). The light emitted is composed of photons that travel in
the same direction, making laser light highly directional.
Laser light is monochromatic, which means that all photons
have the same wavelength. By contrast, intense pulsed light
(IPL) consists of many different wavelengths. The specific
wavelength of each laser will determine how the laser beam
interacts with tissue. The light can be reflected by tissue, scat-
tered by the tissue, or transmitted through tissue. The inten-
tion is that the laser light be absorbed by a specific target
tissue (the “chromophore”). The mechanism by which lasers
are used to target specific tissue is called selective photo
thermolysis (photo = light; thermolysis = decomposition by
heat).4
Lasers can be broadly broken into two categories, ablative
and non-ablative. Until recently, ablative (meaning “to
remove”) lasers have been the “gold standard” of care for
wrinkle reduction. The carbon dioxide laser with a wave-
length of 10 600 nm and the Er : YAG (erbium-doped yttrium
aluminum garnet) with a wavelength of 2940 nm are main-
stays of ablative laser treatment. A relative newcomer is
erbium : YSGG (erbium : yttrium–scandium–gallium–garnet)
(at 2790 nm).5 With each of these lasers, an intense burst of
energy is delivered onto the skin. The energy heats water in
the skin and causes both the water and tissues to vaporize.
With each pass of the laser, a controlled depth of skin is
vaporized and/or coagulated. In response to the injury and
subsequent healing, new layers of collagen are produced.
While ablative non-fractional lasers can be very effective and
have a firm place in laser skin rejuvenation, each can be
associated with risks of infection, scarring, hypopigmenta-
tion, and unnatural alterations in the texture and sheen of the
skin. Moreover, complex aftercare is required until the skin is
fully healed. Resolution of erythema may take months.
Non-ablative non-fractional treatments are safer than their
ablative counterparts, but require epidermal cooling, which
may reduce efficacy of the treatment. Generally, small thera-
peutic windows are associated with non-ablative treatments
and, outside of dyschromia reduction with visible light
approaches, only modest cosmetic enhancement is achieved.
The Nd : YAG (neodymium-doped yttrium aluminum garnet)
1320 nm pulsed laser is an example of a non-ablative laser in
wide clinical use. IPL, monopolar radiofrequency skin tight-
ening, light heat energy (LHE), and light emitting diode (LED)
are all examples of non-ablative treatments.1–3
Skin rejuvenation with fractional photothermolysis repre-
sents a newer class of therapy (Fig. 5.4.1). Thousands of
microscopic wounds surrounded by viable tissue permit
rapid healing and are made with a variety of laser wavelengths
and delivery systems. Immediate and delayed therapeutic
results are seen through a combination of epidermal coagula-
tion for surface enhancement and dermal heating for deeper
remodeling. Unlike selective photothermolysis, in which
targets are damaged based on color contrast, fractional pho-
tothermolysis only damages specific zones based on the
pattern of the micro-beams, leaving other zones completely
intact. Fractional laser techniques began with a 1550 nm
wavelength. The concept of a fractional laser can be applied,
however, to almost any wavelength of light and can be used
with both ablative laser resurfacing and non-ablative laser
rejuvenation. With increasingly aggressive densities and
depths of injury, the fractional approach may achieve
Fig. 5.4.1 Conventional (A) versus fractional (B) photothermolysis.
Vascular
lesion
Pigmented
lesion
Conventional selective photothermolysis
A
Vascular
lesion
Pigmented
lesion
Fractional photothermolysis
B
70
SECTION I
CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
Inflammation
Tissue injury leads to parenchymal cell damage and the
extravasation of blood constituents. The blood clot that forms
re-establishes hemostasis and provides a provisional matrix
for cell migration. Vasoactive and inflammatory mediators are
then generated by platelets (platelet-derived growth factor;
PDGF), the coagulation cascade, the activated complement
pathway (C3a and C5a), and injured or activated parenchymal
cells.10 Vasoconstriction begins within seconds of the injury
and lasts 10–15 min and occurs as a result of epinephrine being
released in to the peripheral circulation, stimulation of the
sympathetic nervous system, and release of norepinephrine.
Vasodilatation and capillary leak are mediated by a variety of
factors including leukotrienes, prostaglandins, kinins, hista-
mine, and complement factors C3a and C5a. Leukocyte migra-
tion is stimulated by components of the extracellular matrix
and several inflammatory mediators. Neutrophils cleanse the
wound of foreign particles and bacteria and are then extruded
with the eschar or phagocytosed by macrophages. In response
to specific chemoattractants, monocytes infiltrate the wound
and become activated macrophages that contribute to the
coordination of wound healing. Specifically, angiogenesis,
fibroblast migration and proliferation, collagen production,
and wound contraction are all directed by macrophages.17,18
The wound healing process is regulated, in a large part, by
the ordered production of cytokines that control gene activa-
tion responsible for cellular migration and proliferation and
synthetic activities.17
Proliferation
This phase includes epithelialization, angiogenesis, granula-
tion tissue formation, and collagen deposition. Epithelializa-
tion was discussed above in the previous section. Angiogenesis,
stimulated by tumor necrosis factor alpha (TNF-α), is marked
by endothelial cell migration and capillary formation. The
migration of capillaries into the wound bed is critical for
proper wound healing.17,18 Much of the angiogenesis occurs
during the early phase of wound healing and involves the
sprouting of endothelial cells from post-capillary venules. The
granulation phase and tissue deposition require nutrients
supplied by the capillaries, and failure of this to occur results
in a chronically unhealed wound. The final part of the prolif-
erative phase is granulation tissue formation. Fibroblasts
migrate into the wound site from the surrounding tissue,
become activated, and begin synthesizing collagen and pro-
liferate. PDGF and EGF are the main signals to fibroblasts and
are derived from platelets and macrophages. PDGF expres-
sion by fibroblasts is amplified by autocrine and paracrine
signaling.17,18 Fibroblasts already located in the wound site
(termed “wound fibroblasts”) will begin synthesizing collagen
and transform into myofibroblasts for wound contraction
(induced by macrophage-secreted TGF-β1); they have less
proliferation compared with the fibroblasts coming in from
the wound periphery. In response to PDGF, fibroblasts begin
synthesizing a provisional matrix composed of collagen type
III, glycosaminoglycans, and fibronectin.17
Remodeling
This phase is comprised of both wound contraction and col-
lagen remodeling.
comparable results to non-fractional approaches, without the
associated side effects.4
Fractional photothermolysis was introduced in 2003. It was
cleared by the US Food and Drug Administration (FDA) for
periorbital wrinkles (2004), skin resurfacing (2005), melasma
(2005), pigmented lesions, freckles, age spots (2004), and acne
(2006). Since then, a number of other companies have intro-
duced lasers capable of delivering fractionated light. Herein,
we review the various laser devices available and discuss our
clinical experience with fractional photothermolysis.4,5
Basic science of resurfacing
procedures
Biology of wound healing
The three main stages of wound healing include re-
epithelialization, scar formation, and wound contraction.17
In superficial insults to the skin, the basal layer of epider-
mis is intact and is capable of proliferating and repopulating
the epidermis. This form involves minimal involvement of
the underlying dermis, and thus no scar formation ensues.
Following deeper injuries to skin, wound healing relies on
keratinocytes from the wound edge and skin adnexa to
migrate and proliferate. Collagen within the dermis is affected
and undergoes some change. The migration of keratinocytes
from the wound edge begins within hours of injury and
involves four phases: (1) Mobilization: epithelial cells immedi-
ately adjacent to the wound enlarge, flatten, and detach from
neighboring cells and the basement membrane; (2) Migration:
as marginal cells migrate, the cells immediately behind them
also tend to flatten, break connections, and drift along. The
epithelial stream continues until advancing cells contact cells
from the other side, whereupon motion stops abruptly – a
process called contact inhibition; (3) Proliferation/mitosis: fixed
basal cells away from the wound edge begin mitosis to replace
the migrating cells. The cells that have migrated in turn start
to divide and multiply; (4) Differentiation: once the wound gap
is bridged by advancing cells from the perimeter, normal dif-
ferentiation of basal cells occurs. The stimuli for keratinocyte
migration and proliferation include loss of cell-to-cell contact,
growth factors (epidermal growth factor (EGF), transform-
ing growth factor alpha (TGF-α), keratinocyte growth factor,
transforming growth factor beta (TGF-β)), loss of contact with
normal components of a basement membrane (type IV colla-
gen and laminin), and contact with proteins of the provisional
matrix (fibrin, fibronectin, type I collagen).17,18
The re-epithelialization is facilitated by a moist environ-
ment (the proper dressing), debridement of scabs (fibrin,
dead neutrophils, and other debris), growth factors, and high
concentration of skin adnexa (the face and scalp).17,18
Once contact of keratinocytes occurs and contact inhibition
is achieved, hemidesmosomes re-form, cells become more
basaloid, and cellular proliferation generates a multi-laminated
neo-epidermis that is slightly thinner.17,18
Wound healing that occurs following deeper insults to the
skin (deeper chemical peels) result in the scar formation
pathway of wound healing. The phases of this process include
inflammation, proliferation, and remodeling and are described
below.
71
Basic science of resurfacing procedures
Basic parameters for any procedure using light are power,
time, and spot size, for continuous wave lasers; and for pulsed
lasers, the energy per pulse, pulse duration, spot size, fluence,
and repetition rate.20 All of these parameters should be con-
sidered in characterizing a laser procedure. Energy is mea-
sured in joules (J). The amount of energy delivered per unit
area is the fluence, sometimes called the dose or radiant
exposure, given usually in J/cm2. The rate of energy delivery
is called power, measured in watts (W). One watt is one joule
per second (W = J/s). The power delivered per unit area is
called the irradiance or power density, usually given in W/
cm2. Laser exposure duration (called pulse-width for pulsed
lasers) is the time over which energy is delivered.1
Fluence is equal to the irradiance times the exposure dura-
tion.21 Other important factors are the laser exposure spot size
(which for wavelengths from 400 to 1200 nm greatly affects
intensity inside the skin), whether the incident light is conver-
gent, divergent, or diffuse, and the uniformity of irradiance
over the exposure area (spatial beam profile). The pulse
profile, that is, the character of the pulse shape in time (instan-
taneous power versus time), is another feature that can impact
the tissue response.20–22
Molecular basis of light–tissue interaction (LTI)
In any light–tissue interaction, the thermal or photochemical
effects depend on the local absorbed energy density at the
target. Spatial localization of temperature elevation is possible
when (1) the absorption coefficient of the target exceeds that
of surrounding tissue (selective photothermolysis); (2) when
the “innocent bystander” tissues are cooled so that their peak
temperatures do not exceed some damage threshold22; or (3)
by applying very small (usually <500 µm in diameter) beam-
lets or microbeams (i.e., fractional methods – vide supra).
Localized heating, for example, in telangiectases and lentigi-
nes, follows from the relative excess of HgB and melanin,
respectively, in the lesions versus surrounding skin. In con-
trast, “non-fractional” mid-infrared (MIR) lasers spatially
confine temperature elevation by using heating and cooling
schemes that allow for selective dermal heating.23
Targeting discrete chromophores offers advantages over
targeting tissue water, especially where the ratio of light
absorption between the chromophore and surrounding tissue
is large (i.e., >10).22–24 For example, at least in lighter skinned
patients, targeting dermal HgB can be achieved with minimal
surface cooling. Whereas cooling is desirable, even in these
cases, when the primary indication is analgesia rather than
epidermal protection. Also, the risk of a severe injury to the
skin is lessened, as there is no bulk heating. Lastly, because
temperature elevations are localized, there is often less pain
than with devices targeting ubiquitous tissue water. Thermal
injury is determined by time/temperature combinations.
Protein denaturation is dependent linearly on exposure time
and exponentially on temperature. That is, cell death is more
sensitive to temperature than time.22 Most devices for rejuve-
nation are based on photothermal or “electrothermal” mecha-
nisms, that is, the conversion of light or electrical energy to
heat. More recently, ultrasound devices have been applied to
tighten the skin.25 Two processes govern all interactions of
light with matter: absorption and scattering. The absorption
spectra of major skin chromophores dominate laser–tissue
interactions. If tissues were clear, then only absorption would
Wound contraction is the result of specialized fibroblasts
that express α-actin (myofibroblasts) and their interaction
with cytokines and the extracellular matrix (ECM). During the
second week of healing, fibroblasts assume a myofibroblast
phenotype characterized by large bundles of actin-containing
microfilaments along the cytoplasmic surface of the cell
membrane. Fibroblasts maintain contact with collagen matrix
by integrin receptors.17,18 Contraction requires stimulation by
TGF-β, PDGF and myofibroblast–ECM interaction via integrin
receptors. As myofibroblasts contract, they exert force on the
ECM and subsequently the wound margin. Scar remodeling
predominates after ~21 days. There is no net increase in col-
lagen content despite an increase in tensile strength. Collagen
production continues, although at a slower rate, and there is
an equal rate of collagen breakdown by collagenases. As the
wound matures, disorganized fine collagen fibers are replaced
with thicker fibers arranged parallel to skin stresses. The
percentage of type III collagen gradually decreases, as does
the quantity of water and proteoglycans. The duration of the
maturation process varies depending on how long the wound
remains open.17,18
The edge of migrating epithelium marks transition between
inflammation and fibroproliferation. In the center, where the
wound is open, chronic bacterial invasion provides persistent
stimulus for inflammation. This tissue contains inflammatory
cells, a high concentration of immature vessels, and the com-
ponents of a provisional matrix (collagen type I, fibrin, and
fibronectin).17,18 When the inflammatory response is pro-
longed, this tissue looks like “granulation tissue”. Once epi-
thelium covers the wound, the inflammatory stimulus is
eliminated and fibroblasts predominate. Further behind the
migrating epithelium, there are fewer fibroblasts, indicating a
more mature wound. Epithelial cells appear to be the source
of a stimulus for inflammatory cells to undergo apoptosis.
However, if the inflammatory phase continues longer than
2–3 weeks, then this stimulus may be lost and hypertrophic
scarring may result.
Laser–tissue interactions and
properties of lasers
An understanding of light–tissue and electrical–tissue interac-
tions allows physicians to expand their laser repertoire and
optimize outcomes. Lasers as light sources are useful because
they allow for exquisite control of where and how much one
heats.19 However, tissue reactions are not intrinsically specific
to the heating source. In principle, a large number of non-laser
devices (i.e., intense pulsed light) can be used for heating
skin.19 In many cases, laser is simply a way to convert lamp-
light to a more powerful monochromatic form. With respect
to lasing media, there are diode lasers, solid-state lasers, and
gas lasers.1 An example of a solid-state laser is the erbium : glass
laser. These lasers have a solid rod that is pumped by a flash
lamp. Miniaturized diode lasers have become popular. Some
diode lasers are housed separately from the handpiece and
delivered by fiberoptics. Others are configured with the laser
diodes in the handpiece. Intense pulsed light devices are
increasingly comparable to lasers that emit millisecond (ms)
domain pulses. Absorption spectra of skin chromophores are
broad, and therefore a broadband light source is a logical
approach for certain cosmetic applications.1
72
SECTION I
CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
Biostimulation
Biostimulation (also called low-level laser therapy) belongs to
the group of photochemical interactions. Most biostimulation
studies involve low-power lasers, and this field continues to
be a subject of controversy. Home-use devices that use LEDs
are now available in a wide range of wavelength ranges.
Typical fluences are in the range of 1–10 J/cm2, and normally
there is no acute temperature elevation, nor any clinical
endpoint.1,4
Cooling
Before the addition of surface cooling, fluence thresholds for
efficacy and epidermal damage were often close. Visible light
technologies, (especially green–yellow light sources such as
IPL, potassium titanium oxide phosphate (KTP) laser, and
pulsed dye laser (PDL)) are the wavelength ranges where
epidermal damage is most likely. The epidermis is an innocent
bystander in cutaneous laser applications where the intended
targets, such as hair follicles or blood vessels, are located in
the dermis.1,4
Beyond visible light (green, yellow, and red) sources,
surface cooling also has been employed in NIR and MIR
lasers. With NIR lasers, surface cooling is important, but
not only because of dermal/epidermal junction-derived
epidermal heating. In addition, deep beam penetration may
cause catastrophic bulk heating. With MIR lasers (1.32, 1.45,
and 1.54 µm), the chromophore is water. It follows that
with even very low fluences, surface cooling is imperative.
Without cooling or a fractional design, water’s ubiquitous
nature in the skin causes a laser-induced top-to-bottom injury.
All techniques are susceptible to operator error and device
failure. It follows that as physicians rely more heavily on
cooling devices, any lack of their proper deployment unveils
the dark side of cooling. Fractured sapphire windows,
disabled cryogen spray apparatus, and crimped forced air
chiller tubes have all contributed to unintended epidermal
injury.1,4
Non-ablative facial skin rejuvenation (NSR)
The original concept of NSR was wrinkle reduction by selec-
tive dermal heating.26,27 Deeply penetrating non-fractional
mid-IR lasers coupled with surface cooling were designed to
“bypass” the epidermis. A slab-like dermal injury was created.
Unfortunately, “CO2-like” results were never replicated
because dermal heating was either too deep or too mild.
Superficial severe dermal heating was almost always associ-
ated with epidermal damage. It followed that all of these
devices “bypassed” the solar elastosis ultimately responsible
for most static wrinkles of the face.1,4
The “non-ablative” term has now evolved to include any
electrical-, light-, radiofrequency-, or ultrasound-based inter-
vention with “relative” epidermal preservation.28 In addi-
tion to wrinkle reduction, new outcome measures include
acne scar improvement, telangiectasia resolution, homog-
enization of pigment, pore size reduction, skin tightening
(jowls, neck, and some extrafacial sites), and “improved” skin
tone.26–28
Radiofrequency and ultrasound-based technologies have
recently gained more popularity. RF energy uses the tissue’s
resistance within the skin to transform the radiofrequency
be required to characterize light propagation in skin. However,
the dermis is white because of light scatter (milk is a reason-
able model for the dermis with regard to scattering). Scattering
is responsible for much of the light’s behavior in the skin
(beam dispersion, spot size effects, etc.). The main scattering
wavelengths are between 400 and 1200 nm (those where
tissue water absorption is poor).1
There are three chromophores of interest in skin (water,
blood, and melanin). Water makes up about 65% of the dermis
and lower epidermis. There is some water absorption in the
ultraviolet (UV). Between 400 and 800 nm, water absorption
is quite small (which is consistent with our real world experi-
ence that visible light propagates quite readily through a glass
of water). Beyond 800 nm, there is a small peak at 980 nm,
followed by larger peaks at 1480 and 10 600 nm. The water
maximum is 2940 nm (Er : YAG).1
Selective photothermolysis (SPT)
With the exception of cases where water is heated, rejuvena-
tion of the skin is based on discrete heating by chromophores
of relatively low concentration (i.e., melanin, hemoglobin).
Anderson described the concept of selective photothermolysis
more than 25 years ago.4 He noted that extreme localized
heating achieved with selective photothermolysis relies on (1)
a wavelength that reaches and is preferentially absorbed by
the desired target structures; (2) an exposure duration less
than or equal to the time necessary for cooling of the target
structures; and (3) sufficient energy to damage the target.4 The
heterogeneity of the skin with respect to HgB and melanin
allows for very selective injury in thousands of microscopic
targets.
The thermal relaxation time is the time it takes for a target to
cool to a certain percentage of its peak temperature (after laser
exposure). Larger targets take longer to cool, and therefore
spatial selectivity is preserved with a wider range of pulse
durations. Even so, as a general rule, assuming adequate flu-
ences are applied, longer pulse durations will result in greater
collateral damage. In laser scenarios, we assume instanta-
neous heating of the target, so that τ is usually thought of as
the time for cooling after the pulse.4
Reaction types
Photothermal
Most laser applications rely on heating. Photothermal
approaches depend on the type and degree of heating, from
coagulation to vaporization. There is a range of effects on
tissue based on temperature. Below 43°C, the skin remains
unharmed, even for exposures as long as 20 min. Thus, one
can exceed body temperature by about 5°C without a measur-
able change in the skin. The first change is a conformational
change in the molecular structure. These typically occur at
temperatures from 42–50°C. At higher temperatures, very
short times (seconds or in extreme cases (>100°C) less than
1 ms) can induce cell death.1,4
Photochemical
Photochemical reactions are governed by specific reaction
pathways, and the most common photosensitizer (PS) in skin
is protoporphyrin IX (PpIX). This PS is formed in skin cells by
the pro-drug, aminolevulinic acid (ALA).1,4
73
Diagnosis and clinical evaluation
Diagnosis and clinical evaluation
Adequate evaluation and photographic documentation of the
patient prior to laser treatment is essential.29,30,31 This assess-
ment includes consideration of the severity of actinic damage,
depth and number of rhytides, and need for any additional
resurfacing procedures. The patient with deep rhytides and
excessive facial skin laxity is likely a better candidate for
traditional rhytidectomy. The patient with moderate photo-
damage and medium rhytides may be a more optimal candi-
date for one of the many types of resurfacing procedures.
Some patients may benefit from both procedures because
rhytidectomy typically addresses skin quantity and soft-tissue
malposition, whereas resurfacing addresses skin quality.30,31 It
should be noted, however, that great care should be under-
taken when both rhytidectomy and resurfacing are performed
concurrently. If rhytidectomy is performed, it is recommended
to avoid any resurfacing of the undermined facial skin, as
wound healing issues may ensue.30,31
An important tool of the evaluation of the patient for a
resurfacing procedure is Fitzpatrick’s scale of sun-reactive
skin types. This scale describes patients’ reactions to ultravio-
let radiation and existing degree of pigmentation. Type I
patients always burn and never tan. Type II patients tan only
with difficulty and usually burn. Type III patients tan but
sometimes burn. Type IV patients rarely burn and tan with
ease. Type V patients tan very easily and very rarely burn.
Type VI patients tan very easily and never burn.32 Patients
with lighter skin types can expect to undergo peeling or laser
treatments with minimal concern for abnormal pigment
changes, whereas individuals with darker skin are at higher
risk for unwanted hyperpigmentation or hypopigmentation.32
An often ignored rule is that patients tend to revert to their
constitutive color after resurfacing (unless it is carried out
into thermal energy. This modality can be used for patients
of all skin types, promoting new collagen production and
contraction. Ultrasound-based technologies create “thermal
coagulation points” in the skin, inducing new collagen pro-
duction and skin tightening.
Sadick developed a classification scheme for NSR based on
photodamage type. In his paper, type I photodamage con-
sisted of surface irregularities, of which there were three
subtypes. Type 1a included rosacea and telangiectases; 1b was
comprised of pore size and skin roughness; and type 1c
included pigmentation changes. Type II rejuvenation included
deeper wrinkles and volume loss.28
Fractional resurfacing
Resurfacing with fractional photothermolysis represents a
newer class of therapy (see Fig. 5.4.1). The stratum corneum
is left largely intact as thousands of microscopic wounds sur-
rounded by viable tissue are made with a variety of laser
wavelengths and delivery systems. Immediate and delayed
results are seen through a combination of epidermal coagula-
tion for resurfacing effect and dermal heating for deeper
remodeling.
As mentioned above, fractional laser resurfacing first
became commercially available in 2003.29 The initial fractional
laser uses an erbium-doped fiber to deliver 3000 infrared
(1550 nm) laser pulses per second and targets water as a
chromophore. The original fractionated laser created an array
of microthermal treatment zones (MTZs) measuring 50–150 µm
in densities ranging from 400 to 6400 MTZ/cm2.29 Each MTZ
forms a column of thermally denatured collagen from the
epidermis to mid-dermis. In contrast to non-fractional lasers,
fractional lasers coagulate only a portion of the treated area,
sparing islands of viable epidermis and untreated dermis
that maintain the skin’s barrier function while speeding
re-epithelialization (Fig. 5.4.2).1,29
Fig. 5.4.2 Fractional resurfacing (2940 nm): (A) immediately after treatment, (B) before laser, and (C) 3 months after laser.
A
B
C
74
SECTION I
CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
pigmentation and vascularity is achieved by direct heating of
melanosomes and HgB (either by a single wavelength or flash
lamp).34 While devices targeting HgB/vessels are confined to
pulse-widths (pw) ranging from 0.45 to 100 ms, melanosome
heating is achieved by either Q-switched nanosecond pulses,
or gentler heating with millisecond-domain pulses. For dis-
crete smaller (0.1–0.6 mm) telangiectases, PDL, KTP laser, or
IPL can be applied (Fig. 5.4.3).34 For larger vessels (>1 mm)
and/or darker skin, the Nd : YAG laser is preferred, but care
must be taken to apply the smallest fluence and smallest spot
sufficient for closure. An alternative would be a combination
of 595-nm and 1064-nm sequential pulses that can simultane-
ously address both smaller and larger telangiectases.35
If a patient presents with telangiectases confined to very
small areas, we typically use a small spot size (1–4 mm) and
the long pulsed KTP laser or PDL.1,34 Alternatively, we use
non-purpuric settings with an IPL. The specific type of PDL
very deeply). So, although there is a concern that constitu-
tively dark patients might be at risk for temporary dyspig-
mentation, on a practical level it is the severely photodamaged
type II and III patients that present the greatest challenges in
moderate-depth resurfacing. This group of patients, once
their bronzing is removed by the procedure, tend to remain
“white” after the photodamage is reduced. This can result
in conspicuous lines of demarcation between treated and
untreated areas. Another helpful classification system is the
Glogau33 photodamage scale. Type 1 patients have little wrin-
kling, no keratoses, no scarring, and require no make-up. Type
2 patients have early wrinkling, early actinic changes, minimal
scarring, and require a small amount of make-up. Type 3
patients have wrinkles present at rest, moderate actinic kera-
toses, moderate scarring, and always require make-up. Type
4 patients have severe wrinkling, actinic keratoses, and scar-
ring that even large amounts of make-up does not cover.
A thorough medical history and review of systems should
be completed in concert with the physical examination, as
part of a thorough patient work-up.30,31 Pre-existing cardiac,
hepatic, and renal disease may influence the treatment deci-
sion and choice of chemical peel or alternative resurfacing
method. The use of exogenous estrogens, oral contraceptives,
and other photosensitizing medications have been shown to
predispose patients to unpredictable pigment changes.30,31
Therefore, such agents should be avoided several weeks
before and after treatment. For any procedure that includes
epidermal compromise, the physician should provide antivi-
ral prophylaxis several days before and after the treatment for
those patients with a history of herpes simplex infection.
Prophylaxis will help minimize chances of unwanted viral
reactivation as the re-epithelialization process occurs. It is also
advisable to allow any existing viral-type lesion to heal com-
pletely before proceeding with a resurfacing procedure.30,31
Patient cooperation and compliance with the post-treatment
regimen is required to ensure normal wound healing and to
avoid complications.30,31 It is ill advised to treat patients likely
to be non-compliant or unable to avoid sun exposure because
of occupation. Men are considered less optimal candidates
because of thicker, oilier skin that risks uneven penetration of
the peeling agent or laser. Men are also less likely to be willing
to use camouflage make-up in the event of pigmentary dis-
turbances. Patients with a decreased number of epithelial
appendages from prior radiation treatment or current isotreti-
noin (Accutane) use are also poor candidates because healing
will proceed more slowly and scarring is more likely. Consider
recent use of Accutane an absolute contraindication to medium
and deep peels, or certain types of laser resurfacing. One
should wait at least 6 months after stopping Accutane to allow
sufficient regeneration of epithelial appendages prior to treat-
ment.30,31 For non-ablative treatments, the role of isotretinoin
(Accutane) in wound healing is unclear. Most likely, healing
will proceed unimpeded and no special precautions are neces-
sary. Still, treatments during an actual course of Accutane
should only be undertaken if the benefits outweigh the poten-
tial risks.
Patient selection and treatment
For wavelengths from 520 to 800 nm, the primary absorbers
are hemoglobin and melanin, so that improvement of
Fig. 5.4.3 (A) Pre- and (B) post-KTP (potassium titanium oxide phosphate) laser
treatment (8 J/cm2, 20 ms).
A
B
75
Patient selection and treatment
lentigines, particularly if they are evolving into a seborrheic
keratosis (SK).1,34–37 More exophytic, lighter seborrheic kerato-
ses must be treated with ablative lasers, or as an alternative,
so long as there is at least minimal color contrast. We focus
the Q-switched alexandrite beam to a very small spot (1–2 mm)
and vaporize smaller flatter SKs by repeated pulses (the Q
532-nm laser can be used as well). Sometimes slight bleeding
is observed, but this technique is associated with rapid
healing. Alternatively, the long pulsed diode laser (810 nm) or
long pulsed alexandrite laser can used for some pigmented
seborrheic keratoses.1,17 High fluences must be applied, and in
darker patients one should mask the normal surrounding skin
with a plastic “guard”.37
We also use the long pulse alexandrite laser for pan-facial
rejuvenation, both with and without cooling. With cooling,
both vessels and pigment can be treated; however, only light
skinned patients are appropriate candidates, as the ratio for
melanin : HgB heating is high for 755 nm. For treatment of
exclusively pigmented lesions, no cooling is necessary. Like
the IPL, one must be careful to avoid darker beard areas to
decrease the risk of alopecia.1,34–37
For flash lamp systems, filters placed between the lamp
and skin are configured to optimize heating of specific targets.
In choosing a laser or IPL for pan-facial rejuvenation of the
face or neck, the pulse configuration should achieve maximal
differential heating between the epidermis and the dermal
vessels. Models show that longer pulses (or pulse trains) favor
vessel heating over epidermal heating.1,37
Melasma is a challenging condition to treat with lasers,
most likely due to its dynamic and inflammatory nature
(compared with the static nature of lentigines).39 Ablative
lasers sometimes improve the condition; however, the abla-
tion normally has to be carried out deeply (or very superficially
– just involving the upper epidermis), or PIH may outweigh
any achievement gains. On the other hand, longer pulsed
visible light laser technologies, Q-switched Nd : YAG lasers,
and fractional approaches can sometimes achieve gradual
improvement in melasma, so long as the settings are not too
high.40,41 If the patient presents exclusively with melasma and
no discrete “static” pigmented lesions (i.e., lentigines), we
start with topical hydroquinone and retinoids before consid-
ering interventional therapy. Use of the Q-switched Nd : YAG
laser, treating every 1–2 weeks for approximately eight ses-
sions, often clears some of the pigment; however, there is
a high relapse rate. Also, recently guttate hypomelanosis
has been reported after multiple treatments with Q-switch
Nd : YAG laser.42,43 We have not found Q-switched alexandrite,
Q-switched ruby, or Q-switched 532-nm lasers helpful in
melasma.1,37 In all cases, although there is nice resolution
within 1 week, worsening of the melasma usually follows.
Small nevi can be lightened by repeated Q-switched
Nd : YAG and Q-switched alexandrite laser sessions; we
reserve these treatments for Asian patients with small, dis-
crete, uniformly colored lesions on the face. Long pulsed
alexandrite lasers can be used. Red scars and traumatic tattoos
can be treated by a combination of PDL and Q-switched YAG
laser.1,34–41 Banal-appearing flesh-colored nevi in Caucasians
can be treated by ablative CO2 or Er : YAG lasers. Optimally, a
shave of the lesions is performed to debulk the lesions (at
least one of which should be submitted for pathologic inter-
pretation as a representative sample if all of the lesions are
clinically similar), after which the laser can be used with a
determines the spot size, fluence range, and cooling type, and
pulse-width. Modern PDLs can generate effective fluences
with 10–12 mm spots; moreover, the macropulses (pulse
envelopes) are comprised of 6–8 micropulses, allowing for
greater efficacy without a high risk of purpura. However, the
most popular modern pulsed dye laser requires two passes for
complete rejuvenation, one for treatment of pigmented lesions
(with a dedicated pigmented lesion “compression” handpiece)
or the cooling device disabled, and another for treatment of
vascular lesions.1,34 More recently, the alexandrite laser has
been used for medium-diameter blood vessels. The depth of
penetration permits coagulation of vessels as large as 1–2 mm,
but the high melanin absorption limits its usefulness to lighter
patients unless very aggressive cooling is applied.36
If a lighter patient presents with a few discrete lentigines,
we use the Q-switched alexandrite laser. The endpoint is
frosty whitening. The only exception to our Q-switched
approach for isolated dyschromias is when a patient has a
pressing engagement where “robust” crusting is intolerable.
In these cases, despite the better one-time treatment clearance
with nanosecond pulses, we apply millisecond devices as the
delayed “coffee-ground” crusts tend to be less obvious.1,34,35
On the other hand, in darker skinned groups, we usually
observe some persistence of pigment after Q-switched 532-,
755-, and 694-nm applications. In this scenario, it is sometimes
difficult to determine after a short interval, whether the
pigment represents residual melanin in the treated lesion
or post-inflammatory hyperpigmentation (PIH). As patients
usually report almost complete clearance of the lesions after
3–7 days, we suggest, at least for thinner lentigines, that most
persistent pigmentation is post-inflammatory. We therefore
delay repeat treatments for 8–12 weeks, allowing for at last
partial resolution of any PIH. Unfortunately, this period is
poorly accepted by patients, who, with the exception of exo-
phytic seborrheic keratoses, are disappointed or angry that
the lesions are darker than on initial presentation. Clearing of
PIH can be accelerated by use of creams containing hydroqui-
none, tretinoin, and/or topical steroids of various strengths
and combinations. Pretreatment with these agents might
decrease the risk of PIH. Sun protection is essential. For lighter,
thinner seborrheic keratoses, one can apply multiple 532-nm
nanosecond pulses. For some thicker, darker seborrheic kera-
toses, the long pulsed diode laser or long pulsed alexandrite
can be used to clinical endpoint of graying. Care must be taken
to mask any darker perilesional background skin.1,37 A recent
article suggests that longer pulse visible light technologies are
less likely to cause PIH in darker patients.38 However, for
lighter lentigines or somewhat tanned skin, whether one
applies PDL with compression, IPL, or KTP laser, selective
lesional heating is compromised because there is often insuf-
ficient color contrast. For these so-called “low-contrast”
lesions, the “therapeutic index” is dangerously small.
For diffuse hyperpigmentation (also called actinic bronz-
ing), we apply the long pulsed variable spot KTP laser with
contact cooling as a first choice. This laser enjoys a low rate
of side effects, will not damage the hair bulb (important for
male patients), and the handpiece is light and maneuverable.
When confronted with a combination of darker and lighter
lentigines in Caucasian patients, we use the Q-switched
alexandrite laser for the lighter lentigines first, followed by
pan-facial treatment with IPL or KTP laser in the same session.
We use the pulsed CO2 laser or Er : YAG laser for some lighter
76
SECTION I
CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
Fig. 5.4.4 Acne scar treatment with
1550-nm erbium : glass fractional laser:
(A) before and (B) 6 months after these
treatments.
A
B
small spot (1–2 mm) to vaporize the lesions “flush” with the
surrounding skin. Recurrence is not uncommon; also, even in
cases where flattening has been achieved, surface darkening
can occur. Q-switched alexandrite or ruby laser treatments are
then applied until the pigment remains clear.
Improvement in wrinkles can be performed by primary
heating of vasculature (low-fluence PDL, low-fluence KTP,
or low-fluence 1064 nm). These technologies depend solely
on a cascade effect, i.e., release of inflammatory mediators
after capillary heating for wrinkle reduction. Short pulsed
(0.3–50 ms) low-fluence Nd : YAG lasers have been used for
rejuvenation. The principle is that gentle sequential heating
over a large volume (or either possibly through focal heating
of microvessels) might stimulate new collagen deposition,
tighten skin, reduce inflammation, and even reduce pore
size.44–46 One example is the “Genesis” procedure where
5000–12 000 pulses are painted over the face at 5–7 Hz
with a 5 mm spot at 12–15 J/cm2. The endpoint is localized
transient skin warming just below the pain threshold. No
anesthetic is applied, thus ensuring that the patient will
provide feedback regarding excessive temperatures. A newer
version of this laser includes a real-time temperature feedback
option.47
Improvement in skin can be performed by heating of
dermal tissue water (1.32-, 1.54-, and 1.45-µm devices). These
lasers heat tissue water. It follows that, without surface
cooling, unless very small fluences or microbeams (<0.4 mm)
are applied, a top-to-bottom broad thermal injury is observed.
All of these wavelengths can be made to heat the reticular
dermis with the proper mixture of fluences, repetition rates,
epidermal cooling, and pulse duration.48–51
Acne scars are common and can be improved via non-
ablative techniques. Jacob et al.52 proposed a three-type scar
system: ice pick, rolling, and boxcar. Ice-pick scars are narrow,
deep, sharply demarcated “holes” that extend into the deep
dermis or subcutaneous layer. Rolling scars are usually wider
than 4–5 mm and stem from the tethering of otherwise normal
looking skin. Boxcar scars are depressions with sharply
demarcated vertical edges. Another classification scheme
includes other scar designations, including macular scars
(erythematous, white, or brown), elastolytic scars (like mini-
striae), papular scars, and hypertrophic scars.53
A rational approach considers the microscopic anatomy of
the scar. Rolling scars occur deep in the follicle and are the
end-product of inflammation that causes destruction of the
subcuticular fat. A number of “dedicated” skin-tightening
procedures can be applied (radiofrequency or ultrasound-
based energy). Although sometimes helpful, predictable
improvement is lacking, and the intervention should only be
reserved for rolling scars or others with volume loss (atrophy).
For boxcar scars, fractional technologies should be considered
first (non-ablative or ablative), depending on the patient’s
expectations and tolerance for downtime. The best results are
achieved with high densities (20–30% surface area per treat-
ment) and “deeper” holes.1,28,29
Long pulse and millisecond-domain Nd : YAG devices have
been applied to acne scars.54 The Q-switched Nd : YAG laser
beam is typically delivered at 2–4 J/cm2 with a 4–6 mm spot
and three passes per region. The endpoint is erythema
and occasionally petechiae. The treatments are only mildly
uncomfortable, with the exception of male patients, where
pulses over hair-bearing areas can be more painful. In apply-
ing the longer pulse systems, multiple passes (usually three)
are delivered at 10–50 J/cm2. Endpoints are mild erythema
and edema.54 Care should be taken to avoid black-haired areas
in male patients to avoid potential hair reduction. Fillers
can complement the aforementioned procedures, particularly
when there is marked volume loss associated with rolling-
type scars (Fig. 5.4.4).
First proposed as a means for treating individual AKs,
photodynamic therapy (PDT) is now being used with blue
and red light for “photo” peels. In one configuration, 20%
liquid aminolevulinic acid (ALA) solution is spread lightly
over the skin for 0.5–2 h, after which the entire cosmetic unit
is irradiated with a wide array of light sources (Fig. 5.4.5).
ALA has been shown to enhance the pulsed light responses
for dyschromias and vascular lesions.55 We use ALA in the
following manner: If a patient presents with AKs, telangiec-
tases, and dyschromias, we combine ALA with a pulsed
visible light source followed by 5–10 min of a continuous
wave (CW) red light source. In this scenario, immediately after
an acetone scrub, the solution is applied, and 30 min later, a
5% lidocaine cream is applied. After an additional 30 min, the
pulsed light source is used, immediately followed by the CW
light source. Refrigerated air is applied for anesthesia. We
shorten the ALA application period with numbing cream, as
we have found it accelerates the ALA absorption and enhances
the PDT effect. If the patient presents solely with AKs and few
77
Patient selection and treatment
Fig. 5.4.5 (A,B) Photodynamic therapy with aminolevulinic acid.
A
B
dyschromias and telangiectases (and if the patient desires
insurance coverage for the entire procedure), we apply ALA
(without anesthesia) for 1–2 h, followed by application of red
CW light. Although ALA-PDT has been recommended for
sebaceous hyperplasia,56 we have only found it helpful with
longer incubation times and CW red light.
More recently, the fractional 1927-nm laser has received
FDA clearance for AKs. The laser is used in a multiple-pass
session until about 90% coverage is achieved. With this high-
coverage mode, the entirety of the AK can be eliminated when
the laser is applied in a full-face or segmental-face fashion as
a field therapy. For tinker lesion, pretreatment curettage is
sometimes applied.
Deeper heating long pulse
skin-tightening procedures
Recently, multimodal approaches for treatment of facial aging
have become common practice. It is essential that the operator
of laser devices becomes familiar with other available
technologies to be able to deliver a more comprehensive
approach to the aging face and achieve superior outcomes.
There are a number of deep heating handpieces for skin
tightening. The main approaches include (1) monopolar RF;
(2) bipolar RF; (3) tripolar RF; (4) fractionated RF needles; (5)
xenon flash lamp with rapid repetition rates and filtering that
features 800–1200 nm portion of the output spectrum; (6) deep
heating halogen lamps; and (7) ultrasound. Most deep heating
strategies are based on time/temperature-dependent heating
of collagen, which can produce focal “fractional” fibril damage.
Monopolar radiofrequency uses a controlled radiofre-
quency pulse to selectively heat zones of the lower dermis and
subdermis while avoiding injury to the superficial dermis
through use of a cryogen spray.16 It was approved by the FDA
in 2005 for full-body skin-tightening treatments. Some studies
have revealed high patient satisfaction with the device when
proper technique and patient selection are employed.16 Treat-
ment typically involves between one and three applications
of the radiofrequency to the affected areas, depending on the
severity of the deformity. Pain and downtime are minimal.
Most patients are able to resume all normal activities imme-
diately after treatment. Appropriate patients include those
with mild to moderate rhytids who understand the limita-
tions of the device (Fig. 5.4.6).16
The new generation of “injectable” monoplar RF employs
temperature-controlled radiofrequency by deploying an array
of needles to a prescribed depth in the skin. This device allows
the operator to “inject” the radiofrequency energy while at the
same time regulate the tissue temperature through sensitive
probes and provide a more controlled therapy. One such
device achieves skin tightening by coagulating deeper dermal
zones (2–3 mm deep) by deploying five pairs of needle elec-
trodes into the skin for each “pulse”. Temperatures of about
70°C are sustained for about 4 s, 1–3 mm beneath the skin
surface in the most common application.
Bipolar and tripolar RF technologies are also available and
effectively treat rhytids, skin laxity, acne, vascular and pig-
mented lesions.57–63
Deeper penetration halogen lamps heat the upper 1–2 mm
of the dermis. Pulses typically last 2–6 s and are accompanied
by surface cooling. Xenon flash lamp devices have been
electronically modulated to deliver rapid pulse trains with
surface cooling. Like their halogen counterparts, the goal is
sustained elevation of the dermal temperature. Low cost IR
(temperature) meters are used during treatment to maintain
surface temperatures of 38–41°C. A newly introduced ultra-
sound system (Ultherapy, Ulthera Inc., Mesa, AZ) coagulates
small dermal zones about 3–5 mm deep in the dermis. The
depth is dependent on the transducer configuration. The goal
is brow, cheek, and neck elevation/tightening.
Fractional photothermolysis
A broad array of fractional lasers have appeared on the market
since the introduction of the technology. In general, the critical
determinant for long-term skin resurfacing results is not the
degree of immediate skin tightening, but the production of
new collagen – a biological process that is highly dependent
upon the depth of damage.1,64,65
Fractional lasers penetrate deeply into the skin dermis with
thousands of tiny MTZs, employing a technique called frac-
tional photothermolysis.29,64,65
78
SECTION I
CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
With the newly designed optical zoom hand control system,
physicians can penetrate up to 1.0 mm below the skin surface
with precise dosage control. Deeper penetration provides a
greater catalyst for natural generation of new collagen to
promote self healing and remodeling.29,64,65
After 2–3 years of study, the fractional CO2 was introduced
to the market in December 2007. The Fraxel Re:pair is a frac-
tionally ablative microscopic CO2 laser with a 10 600-nm
wavelength. This laser approaches the efficacy of fully abla-
tive lasers, but with markedly less downtime, less risk of
adverse events and no reports of delayed hypopigmentation.
A single treatment is carried out for most patients, although
the treatment may be repeated 3–6 months later. There are 2–3
days of real downtime with severe erythema and oozing fol-
lowed by marked redness fading to a lighter shade by day 6
or 7. Over the next month, the redness gradually fades. The
primary clinical targets are wrinkle removal, skin tightening,
severe photodamage, acne, and surgical scars. Whereas the
Fraxel Re:store 1500 coagulates the epithelial and dermal
tissue in the microthermal zone of injury, the Re:pair vapor-
izes the tissue centrally, leaving a rim of coagulation necrosis
on the periphery of the injury and produces immediate skin
tightening and wrinkle reduction. As pulse energy is increased,
penetration depth also increases. As density is increased,
more surface area is treated. With experience and carefully
chosen parameters, varying both energy and density, one can
safely treat virtually all skin types. The Re:pair delivers
the deepest injury of any of the non-ablative and ablative
fractional lasers. Although the injury is pronounced,
re-epithelialization occurs within 48 hours.29,64,65
In 2009, the same manufacturer introduced the dual wave-
length fractional laser (Fraxel Dual). This technology boasts
two different wavelengths (1550 nm and 1927 nm). The addi-
tional wavelength enables the operator to better address
pigmentation and dyschromia.
Recently, our group reported our experience with 716
patients who underwent fractional lasers in our center. Frac-
tional lasers were carried out with three different laser
Treating the skin fractionally with patterns of microscopic
laser spots, each of which is 70–100 µm in diameter, results in
a unique wound healing process. This is aided by the fact that
each laser spot (MTZ) is surrounded by healthy tissue. Many
of the stem cells and melanocytes in the papillary dermis
are spared. Fractional wound healing results in both rapid
re-epithelialization of the epidermis as well as collagen
remodeling to depths of 400–700 µm.29,64,65
Clinical studies4,5,9 suggest that 4–6 treatments spaced about
1 week apart produce a gradual remodeling of dermal matrix
components, firming collagen and elastin. A topical anesthetic
and a blue dye were used prior to treatment, which takes
about 60 minutes. Laser treatment itself takes another 45 min.
With the newer lasers, the blue dye is no longer needed.
Side effects are generally minimal. A mild sunburn sensa-
tion occurs for approximately 1 h after the treatment. The skin
has a pinkish tone for 1–3 days (see Fig. 5.4.5). This is a normal
sign of healing. Swelling is minimal. Within 24 h, new epider-
mal skin begins to emerge. This process of skin repair involves
flaking and bronzing. The use of sunscreen throughout the
process is absolutely necessary. Optimal improvement may
take 3–6 months.4,5,9
Fractional laser treatment appears to be effective in reduc-
tion of fine wrinkles; rejuvenation of sun-damaged skin on the
face, neck, chest, shoulders, hands, and arms; reduction of age
spots, blotches, and dyschromia; acne scars; hyperpigmenta-
tion; and in some patients, coarse and deeper wrinkles may
demonstrate considerable improvement.29,64,65
In 2004, fractional laser was introduced to the market
(Fraxel Re:store 1500, Solta Medical, Pleasanton, CA). It is a
1550-nm fractionated erbium : glass laser. This version com-
bines proprietary advancements in optical technology with
medical software offering physicians a treatment option that
penetrates up to 30% deeper than the previous version laser,
delivering consistent dosage control and optimizing lesion
depths. This leap in technology provides patients a safe and
effective, non-invasive treatment option for skin conditions
ranging from mild sun damage to severe acne scarring.29,64,65
Fig. 5.4.6 (A) Pre- and (B) 6 months
post-treatment with monopolar
radiofrequency.
A
B
79
Patient selection and treatment
must be replaced with each treatment and is the only
consumable.29,64,65
The fractional 2940-nm wavelength Er : YAG laser (Harmony
XL, Alma Lasers, Buffalo Grove, IL) that is part of a platform
system that offers multiple applications including 10 distinct
technologies that treat a wide array of problems ranging from
vascular lesions to photoaging. The 2940-nm Er : YAG, micro-
optic lens creates 49 (7 × 7) or 81 (9 × 9) pixel size ablation dots
on the skin with an 11 × 11 mm treatment zone. The spot size
is three times larger than the Fraxel Re:pair and has a fixed
density of 20%. This laser delivers energy to a depth of
20–50 µm when using the fractional handpiece. The pulse
duration is 1, 1.5, or 2 ms. Delivery of the laser is pulsed.
Maximum coverage rate ranges from 98 mm2/s to 121 mm2/s.
The handpiece must be replaced for each treatment. The laser
is touted as providing the patient with the effectiveness of an
ablative approach with the comfort level and convenience of
a non-ablative treatment. The laser can safely be used on the
face, neck, chest, arms and hands.29,64,65
Other available fractional lasers differ based on the spot
sizes, depth of treatment, energy delivered, and mode of
delivery (static vs. dynamic).
One system incorporates two fractional handpieces in the
sane device. The Icon (Cynosure, Chelmsford, MA) platform
combines a 1540-nm and a 2940-nm fractional handpiece.
Both handpieces use a diffractive optic to create a fixed pitch
array of microthermal injuries. Multiple passes are made until
the total density and depth of lesions are achieved for that
particular application.
Another newer device (Halo, Sciton, Palo Alto, CA) applies
a scanning technology that combines 1470-nm (non-ablative)
and 2940-nm ablative wavelengths simultaneously in the
same pass and same handpiece. In this system, the provider
can titrate the degree of ablative and non-ablative fractional
wounds to optimize outcomes in skin rejuvenation and scar
treatments. The platform also incorporates a ratline surface
temperature monitor to reduce the risk of bulk heating of the
skin.
Clinical experience with fractional
resurfacing procedures
Perioral wrinkles (Figs. 5.4.7 & 5.4.8) are most difficult to treat
with all fractional lasers and require 4–6 treatments, 2–4 weeks
wavelengths, depending on the condition(s) treated (wrin-
kling vs. pigmentation issues, etc.) and the patients’ length of
downtime. The fractional 1550/1927 dual wavelength laser
was used in 222 patients; the fractional 1550 laser was used
in 325; and the fractional CO2 laser was used in 169 patients.
Adverse events and complications occurred in 29 of 716
patients (4.05%). Complications were generally minor and all
resolved completely with treatment. Complications occurred
in 1.12% of patients having the fractional 1550/1927, 4.05%
having the fractional 1550, and 3.38% having the fractional
CO2 laser. Complications included minor burns/abrasions in
2 patients, acne outbreaks in 11, rash in 4, herpes outbreak in
3, and prolonged erythema in 2 patients.66
Multiple other ablative and non-ablative
fractional lasers commercially available
The 1440-nm erbium : glass laser (Affirm, Cynosure, Westford,
MA) is non-ablative. It has some unique features that, in
essence, deliver fractionated treatments to the skin surface.
The unique aspect of this laser is the combined apex pulse
(CAP) technology, which employs diffractive elements to
bend the wavelength to treat larger surface areas. The laser
also delivers both high- and low-energy light to the selected
treatment areas, which “fractionates” the treatment. The
CAP array in the 1440-nm Nd : YAG Affirm laser system was
developed to combine both mechanisms in a single treatment,
using high-fluence regions surrounded by low-level heating.
This microthermal rejuvenation approach creates apices of
high-fluence regions for collagen remodeling surrounded by
a collagen-stimulating, low-fluence treatment zone. The CAP
array is a special lens construction that consists of approxi-
mately 1000 diffractive elements affecting more surface area
per single pulse. The high-fluence “apices” create a pattern
of coagulated columns, while the background fluence gently
heats the intervening uncoagulated tissue. Histologically,
the high-fluence CAP columns are limited to approximately
300 µm in depth, constraining treatment to the zone of
superficial photodamage. This combination of mechanisms
is proposed to improve treatment efficacy, while maintaining
the side effects profile of existing methods. The laser light
is delivered via a stamping technology with a spot size of
300 µm, which is five times the spot size relative to repair.
It is delivered with a pulsed technique. The handpiece
Fig. 5.4.7 1550-nm fractional
erbium : glass laser for perioral wrinkles:
(A) before and (B) 6 months after six
treatments.
A
B
80
SECTION I
CHAPTER 5.4 • Injectables and resurfacing techniques: Laser resurfacing
apart, depending on severity of the wrinkles. They are slow
to respond and often require skin fillers. Higher energy is
usually needed (3–4 passes). That said, for deeper perioral
wrinkles, we generally recommend a non-fractional CO2 or
Er : YAG laser (see Fig. 5.4.8). For acne scarring, one must be
patient and allow time for collagen remodeling (see Fig. 5.4.4).
With the 1550 erbium : glass fractional laser, 4–6 treatments,
3–4 weeks apart is usually required. As aggressive as the skin
type allows, higher energy is used.1,29 Analgesic pre-medication
may be needed. Hyperpigmentation is improved as well.
Patients with melasma and dyschromia are pretreated with
hydroquinone. Generally, 4–5 treatments are used, spaced
10–14 days apart. Lower energy is used with more passes.
Good results may be seen in Asian skin, although melasma
may be very difficult to treat and eradicate. Treatment failures
with melasma are not uncommon and may be disappointing.
Realistic expectations must be set with the patient, and patient
education is necessary to insure they understand the limita-
tions of treatment.1,29,64,65
Although infrequent, complications do occur. Post-
inflammatory hyperpigmentation (PIH) can occur and can
take 3–6 months to resolve. It is managed with hydroquinone
and tretinoin (0.05% or 0.10%). We use the Obagi skin care
system consisting of hydroquinone, tretinoin, vitamin C, and
sunscreen. Patients with a history of herpes may experience
an outbreak if not pretreated with Zovirax or a similar medi-
cation. If this history is known, we treat the patient for 48 h
prior to fractional laser therapy.1,29
In our practice prophylactic Valtrex (GlaxoSmithKline,
Research Triangle Park, NC) 500 mg, 1 tablet PO bid, is started
48 h prior to treatment administration in all patients, regard-
less of a history of herpes simplex virus (HSV), at their
pretreatment appointment. Administration of prophylactic
antiviral and antibiotic (Keflex, unless allergy was noted, then
clindamycin is given) medication is given to all CO2 laser
patients regardless of HSV history. Instructions are given to
discontinue all irritating or abrasive products (Retina-A,
glycolic, salicylic, lactic acids, benzol-peroxides, or any facial
cleansing scrubs) 3 weeks prior to treatment and until 6 weeks
post-treatment.
Fig. 5.4.8 Treatment of perioral wrinkles
with fractional CO2 laser: (A) before and
(B) 6 months after a single treatment.
A
B
Over time, the patient can expect lessening of hyperpig-
mentation, then improvement of “crepey” skin tone, followed
by lessening of fine lines and then deep lines. Changes in deep
lines can be a delayed phenomenon and can take months to
occur due to the collagen remodeling process. Significant
tightening of the skin may result as a secondary response and
appears to be cumulative. The tightening is particularly
evident in the nasolabial folds and glabella. Results with the
use of the 1550 erbium : glass fractional laser have been more
consistent than those obtained with other non-ablative
systems. No comparative clinical outcome data for the other
fractional lasers in this class are available, so it is difficult
to assume equivalency, especially if lasers do not penetrate
as deeply or if similar numbers of treatments are not
delivered.1,29,64,65
Patients tolerate the 1550 erbium : glass fractional laser
as well as the other Er : YAG or erbium : glass laser treat-
ments when used with the Zimmer Cooler, Benadryl,
and Tylenol (or similar medications). Men tolerate it less
well than women and lower energy may need to be used.
Women’s skin may be more sensitive around their menstrual
cycle.1,29,64,65
The best response is in solar damaged skin, fine lines, and
“crepey” skin. Very good outcomes may also be seen with
periorbital lines. Using a lower setting and a higher density
(6–8 mJ/cm2; 250 MTZ/cm2) results in a good response.
Fractional photothermolysis can be utilized as an adjunct to
surgery as well, but safety parameters have not been fully
studied. Fractional laser of undermined skin flaps during
facelift is unknown (Fig. 5.4.9).1,29,64,65
In patients undergoing fractional CO2 therapy, our pre-
laser skin care regimen is similar to the less invasive, 1550-nm
erbium : glass fractional laser. Patients are prepped with
topical anesthetic ointment for 1 h prior to the laser. Metal eye
shields are routinely used. Many require an oral pain medica-
tion, and some require nerve blocks to divisions I–III of the
trigeminal nerve for facial anesthesia. Full-face laser takes
around 20 min. The energy and density are selected based on
the patient’s skin type and condition being treated. Lower
energies and densities are used for darker Fitzpatrick skin
81
Patient selection and treatment
Fig. 5.4.10 Before and after ThermiRF
(ThermiAesthetics, LLC, Southlake, TX) & Fraxel.
A
B
Fig. 5.4.9 Fractional CO2 resurfacing done
sequentially – SMAS facelift followed by
fractional CO2 3 months later: (A) before
and (B) 6 months after treatment.
A
B
types and higher energies and densities are used for acne and
deep wrinkles, depending on skin type. In general, lower
energies and densities are used on the neck and chest as
well.1,29,64,65
In the last few years, a multimodal approach for non-
surgical facial rejuvenation has become common practice.
The use of ablative or non-ablative lasers in conjunction
with deeper heating long pulse skin-tightening technolo-
gies (radiofrequency or ultrasound based) provides excel-
lent aesthetic outcomes. In such treatment, lasers provide
photothermolysis that results in the changes addressed
previously in the chapter, while radiofrequency or ultrasound
technologies deliver thermal energy to the deep layers and
promote collagen regeneration, contraction, and skin tightening
(Fig. 5.4.10).
Contraindications
Laser and chemical resurfacing have common contraindica-
tions. These include active bacterial, viral, fungal, or herpetic
