Atlas Phẫu Thuật Thẩm Mỹ (Tập 2) – Atlas of Cosmetic Surgery

13/10/2026 • by Bs CKI Phẫu thuật tạo hình, tái tạo và thẩm mỹ Trương Hoài Anh •

Tập 2 của bộ Atlas Phẫu thuật thẩm mỹ kinh điển, trình bày minh họa sắc nét các thủ thuật tạo hình khuôn mặt và định hình cơ thể. Tài liệu hỗ trợ tra cứu nhanh các bước tiến hành phẫu thuật chuẩn y khoa.


📂 Chuyên mục: Tài liệu thẩm mỹ, Phẫu thuật thẩm mỹ, Giải phẫu học

🏷️ Từ khóa: atlas thẩm mỹ, phẫu thuật thẩm mỹ, tạo hình cơ thể, cosmetic surgery, tạo hình khuôn mặt

Trang: / 556
Trang 1 Trang 2 Trang 3
📖 Xem bản dịch / Nội dung văn bản

SECOND EDITION Atlas of COSMETIC SURGERY Michael S Kaminer, Kenneth A Arndt, Jeffrey S Dover, Thomas E Rohrer, Christopher B Zachary SAUNDERS

Michael Abrishami MD
Department of Surgery,
University of Southern California
Los Angeles, CA, USA
Murad Alam MD MSCI
Chief, Section of Cutaneous and Aesthetic Surgery,
Department of Dermatology, Northwestern University,
Chicago, IL, USA
Macrene Alexiades-Armenakas MD PhD
Assistant Clinical Professor
Dermatology and Laser Surgery, Director of Private Practice
Yale University School of Medicine, Clinical Constructor
New York, NY, USA
Tina S Alster MD
Director
Washington Institute of Dermatologic Laser Surgery
Clinical Professor of Dermatology
Georgetown University Medical Center
Washington, DC, USA
Kenneth A Arndt MD
Clinical Professor, Section of Dermatologic Surgery and
Cutaneous Oncology, Yale Medical School, New Haven, CT;
Adjunct Professor of Medicine (Dermatology) at Dartmouth
Medical School, Hanover, NH; and Clinical Professor of
Dermatology, Harvard Medical School, Boston, MA;
SkinCare Physicians, Inc.,
Chestnut Hill, MA, USA
Sonia Batra MD
SkinCare Physicians, Inc.
Chestnut Hill, MA, USA
Leslie Baumann MD
Assistant Professor of Clinical Dermatology
Department of Dermatology and Cutaneous Surgery
University of Miami Medical School
Cosmetic Center, Cedars Medical Center
Miami, FL, USA
Ken Beer MD
Clinical Instructor in Dermatology
Director, Palm Beach Esthetic Center
University of Miami, Florida, FL, USA
Eric Bernstein MD
Director, Laser Surgery and Cosmetic Dermatology Centers
Marlton, NJ, USA
Ashish C Bhatia MD
Director of Dermatology and Dermatologic Surgery
River North Dermatology and Dermatologic Surgery
Naperville, IL, USA
Brian Biesman MD
Associate Clinical Professor of Opthamology,
The University of Tenessee Health Science Center
Memphis, TN, USA
Melissa A Bogle MD
Director, The Laser and Cosmetic Surgery Center
of Houston, Houston, TX
Clinical Assistant Professor, Department of Dermatology,
The University of Texas MD Anderson Cancer Center,
Houston, TX, USA
Christine M Choi MD
SkinCare Physicians of Chestnut Hill,
Chestnut Hill, MA, USA
Christine Dierickx MD
Director, Laser Clinic,
Boom, Belguim
Lisa Donofrio MD
Associate Clinical Professor, Department of Dermatology,
Yale University School of Medicine,
New Haven, CT, USA
Jeffrey S Dover MD FRCPC FRCP
Associate Clinical Professor of Dermatology,
Yale Medical School, New Haven, CT;
Adjunct Professor of Medicine (Dermatology) at Dartmouth
Medical School, Hanover, NH;
SkinCare Physicians, Inc.;
Chestnut Hill, MA, USA
Timothy C Flynn MD
Clinical Professor
Department of Dermatology
Cary Skin Center
Cary, NC, USA
List of contributors

viii
Wade Foster MD
Chief Resident
Department of Dermatology
University of Alabama at Birmingham
School of Medicine
Alabama, USA
Ted Grossbart PhD
Assistant Clinical Professor in Psychology, Department
of Psychiatry, Harvard Medical School,
Boston, MA, USA
Chris Harmon MD
Clinical Instructor
Department of Dermatology
University of Alabama at Birmingham Medical Center
Birmingham, AL, USA
David Horne MD
SkinCare Physicians, Inc.
Chestnut Hill, MA, USA
Jeff Hsu MD
SkinCare Physicians, Inc.
Chestnut Hill, MA, USA
Carolyn Jacob MD
Associate Clinical Instructor, Department of Dermatology,
Northwestern University Medical School
Chicago, IL, USA
Michael S Kaminer MD
Assistant Clinical Professor of Dermatology,
Section of Dermatologic Surgery and Oncology,
Yale Medical School, New Haven, CT;
Adjunct Associate Professor of Medicine (Dermatology)
at Dartmouth Medical School, Hanover, NH;
SkinCare Physicians, Inc.;
Chestnut Hill, MA, USA
Kristen Kelly MD
Associate Clinical Professor of Dermatology,
University of California
Irvine, CA, USA
Wendy Long MD
SkinCare Physicians, Inc.
Chestnut Hill, MA, USA
Tonya McLeod MD
SkinCare Physicians of Chestnut Hill
Chestnut Hill, MA, USA
Rhonda S Narins MD
Clinical Professor of Dermatology at New York University
Medical Center
New York, NY, USA
Joseph Niamtu MD
Cosmetic Facial Surgery
Richmond, VA, USA
Thomas E Rohrer MD
Clinical Associate Professor of Dermatology,
Boston University School of Medicine,
Boston, MA;
SkinCare Physicians, Inc.;
Chestnut Hill, MA, USA
David Sarwer MD
Department of Psychiatry
University of Pennsylvania
Philadelphia, PA, USA
Diedre A Steinman MD
Chula Vista, CA, USA
Howard Kenneth Steinman MD
Assistant Clinical Professor of Dermatology
Chula Vista, CA , USA
Elizabeth Tanzi MD
Clinical Faculty, Department of Dermatology,
John Hopkins Medical Center
Co-Director
Washington Institute of Dermatologic Laser Surgery
Washington, DC, USA
Rodney L Trytko MD
Anesthesiologist
Deaconess Medical Center
Anesthesia Associates,
Spokane, WA, USA
Walter Unger MD
Clinical Professor and Co-Director
Dermatologic Surgery and Laser Center
University of California, San Francisco
San Francisco, CA, USA
Christopher B Zachary MD
Professor and Chair of the Department of Dermatology,
University of California at Irvine
Irvine, CA, USA
Section 1 List of contributors

The public is constantly bombarded with images of beauty and youth. Conventional wisdom,
backed up by a number of scientific studies, suggests that a very attractive individual is more
likely to get a desirable job than a less attractive one. Beautiful people are perceived by oth­
ers as being more successful financially as well as in their personal life. The media touts the
wonders of cosmetic surgery and especially minimally invasive procedures with perfect results
without risks or downtime. The baby boomers are rapidly aging and are currently in their
prime earning years with significant disposable income. All of these forces make the rapidly
increasing demand for cosmetic surgery services easy to understand.
To meet this seemingly insatiable demand for cosmetic services is a rapidly growing army
of providers eager to satisfy this need. Initially, cosmetic procedures were provided by the
traditional “cosmetic” specialties such as dermatology, plastic surgery, facial plastic surgery
and oculoplastic surgery. However, over the last half-dozen years, the list of providers has
grown from all areas of medicine including family practitioners, anesthesiologists, obstetri­
cians, emergency room doctors, dentists and even vascular surgeons. The development of
minimally invasive procedures has opened up the cosmetic procedure field to allied health
professionals such as registered nurses, nurse practitioners, physician assistants, aestheticians
etc. Many cosmetic practices have incorporated spa-like services into their offerings and many
spas have partnered with physicians, or sometimes without physician involvement, to offer
minimally invasive cosmetic procedures to their spa clients. These “medispas” are rapidly
proliferating in most metropolitan areas and, with some cosmetic procedures such as laser hair
removal, have become the market share leader.
Fortunately for all of the potential cosmetic surgery patients, the procedures available to
cosmetic surgery providers have demonstrated improved efficacy and safety over the last 30
years. In the 1970s cosmetic procedures were primarily surgical in nature such as rhytidec­
tomy, blepharoplasty, punch hair transplantation, dermabrasion and medium to deep chemi­
cal peels. During the 1980s, the first lasers based on the theory of selective photothermolysis
were introduced initially for vascular lesions to be soon followed by lasers for pigmented le­
sions. These lasers allowed very effective treatment with minimal risk of complications and
limited discomfort for the patient. Tumescent liposuction was introduced making liposuction
an office-based procedure performed under local anesthesia with far less blood loss and faster
recovery. Hair transplantation moved away from the punch grafts with the frequent corn row
look toward a far more natural appearance with follicular unit grafting. The 1990s introduced
the golden period of effective and safe laser treatment based on selective photothermolysis
including laser resurfacing, laser hair removal and photorejuvenation.
The current decade is the time of minimally invasive facial rejuvenation with soft tissue
fillers, not only for wrinkle and scar correction, but for facial recontouring to rebuild volume
and soft tissue lost with aging augmented with botulinum toxin injections to reduce dynamic
rhytids. The first new fillers in 20 years were approved by the FDA starting in 2003. Since then
multiple new fillers including CosmoDerm, CosmoPlast, Restylane, Hylaform, Captique, Ju­
vederm, Perlane, Sculptra, Radiesse and ArteFill have been approved for fine wrinkles, deep
wrinkles, scars, and volume restoration, with the correction lasting anywhere from a few
months to many years. This has allowed American physicians to catch up to the Europeans
who have had access to these and other fillers for many years. Laser and light technology has
been joined by radiofrequency and ultrasound energy sources to tighten skin and rejuvenate
the face and body. Fractionated laser energy delivery may enhance photorejuvenation and
Foreword

x
scar correction results while reducing the risk of complications over traditional laser resurfac­
ing. The mainstay of leg vein treatment used to be sclerotherapy and surgery in the operating
room. Now, with endovenous laser or radiofrequency treatment and ambulatory phlebectomy
the abnormal veins can be ablated in an office setting under local tumescent anesthesia. The
cosmetic surgery field is evolving at an ever faster pace with the increasing patient demand,
new technology and more providers entering the field.
New cosmetic surgery providers need to decide which procedures to offer and to learn, and
how to do them in a safe and effective way. Existing cosmetic surgeons need to keep up with
all of the new techniques and refinements in existing ones. The Atlas of Cosmetic Surgery, 2nd Edi­
tion is a complete re-write of the first edition. It addresses cosmetic surgery from a practical
“how to” angle without neglecting the scientific basis for the various procedures described.
The neophyte will find step-by-step, richly illustrated techniques, while the more seasoned
surgeon will be able to refine his own technique by studying how other experts in the field
perform cosmetic procedures, as well as learning new techniques and the latest advances in
existing techniques.
The Atlas of Cosmetic Surgery is called an atlas because it is not a reference text to be put on
a bookshelf and forgotten. It is designed to be kept close to the bedside and accessed daily
for pointers and refinements of technique. I have found that some of most useful educational
experiences for me have been visiting other practices and observing procedures performed by
the experts on their home turf. The DVD accompanying the Atlas gives the reader just such
an opportunity as it contains many of the procedures described in the text being carried out
by the authors themselves in their own offices or surgical suites.
The editors of the Atlas are leaders in the cosmetic surgery field with each one contributing
their own individual style to the book. Dr. Kaminer is a meticulous cosmetic surgeon who loves
to do “real” cosmetic surgery, being an expert in liposuction and various face and neck lifting
procedures. Dr. Dover has been at the forefront of developing clinical laser applications since we
shared a small office at the Wellman Lab at the Massachusetts General Hospital over 20 years
ago. He also has a keen understanding of what true beauty represents and how to achieve it with
his patients. Dr. Arndt was editor of the Archives of Dermatology and chief of dermatology at Beth
Israel Hospital in Boston for many years. He is able to provide a longitudinal perspective to the
cosmetic surgery field and to separate the wheat from the chaff. Dr. Rohrer has been intimately
involved in the development of various non-invasive laser technologies that are in wide use today.
Dr. Zachary is a cosmetic surgeon who thinks outside the box. He constantly questions the status
quo and does it with a liberal dose of his British sense of humor. He is always looking for a better
way to do cosmetic surgery, and has no fear of treading on anyone’s toes as long it is better for the
patient. The editors have contributed liberally of their knowledge to the Atlas and have recruited
a group of world class cosmetic surgery experts to write about their areas of expertise.
In summary, the Atlas of Cosmetic Surgery is a practical cosmetic surgery book describing the
latest effective rejuvenation techniques. It is written by proven experts in the field and should
prove to be a valuable educational resource for both the experienced cosmetic surgeon as well
as a provider just starting out in the cosmetic surgery field.
George J. Hruza, MD
Clinical Associate Professor of Dermatology and Otolaryngology,
St. Louis University, St. Louis, MO
Medical Director, Laser & Dermatologic Surgery Center, Chesterfield, MO, USA

Foreword

Have you ever had one of those “what was I thinking” moments? Well that was exactly the
thought that crossed my mind (umpteen times) when the deadline for this book was fast ap­
proaching, and less than half the chapters had been completed. To make matters worse I was
getting that déjà vu feeling from similar experiences with the first edition of the Atlas of Cosmetic
Surgery in 2002. Indeed, what was I thinking? It is at times like these that many of us need a
little reality check.
One of the many lessons we all learn in medicine is that it isn’t about us, it is about our pa­
tients. No matter how grand your ego, or expansive your intellect, it always comes down to one
common denominator, the patient. The end result is often the ability of physicians to move
beyond what we think is our capacity, to somehow push forwards when fatigued, or frustrated.
We have all spent countless hours awake during medical school, internship and residency. We
have dealt with that frustrating, persistent bleeder during surgery. What choice do we have?
Pushed to the limits, we tend to learn a bit about ourselves. So we must press on, and in many
ways that is what continued to push this book forward: the patient.
A mentor once told me that the real reason to write a book is for one reason and one
reason only (with tongue firmly in cheek): your mother. But after hundreds of hours working
with my colleagues Ken Arndt, Jeff Dover, Tom Rohrer, and Chris Zachary on this project,
it is abundantly clear that there are other valid reasons. The Atlas of Cosmetic Surgery is undeni­
ably about the patient. So much has changed in our field over the past five to ten years that
it can be daunting to keep pace with new developments. Just when your brand new laser is
getting warmed up, it seems a newer, better, faster version is ready to take its place (and make
your investment obsolete). Technological innovations appear almost daily, and hundreds of
physicians with superbly honed skills help us to continually push the envelope of creativity
and technique. To stand still is to rapidly fall behind. This makes it imperative that we share
information, and that it be presented to our colleagues in a non-biased, well thought out, use­
ful format. That is the mission of the Atlas of Cosmetic Surgery, and one that in the end leads to
a broader and hopefully higher level of knowledge and skill in our specialty. In the end, it also
benefits the ultimate end user, our patients.
Our patients simply demand that we continue to innovate, and more importantly than ever
we are held to standards that expect us to do this ethically and humanely. Bravo! So much has
changed since the first edition of the Atlas of Cosmetic Surgery. ­Liposuction is now performed not
only with conventional tumescent technique, but also in combination with minimally invasive
laser technology. Non-surgical skin tightening is a field that didn’t even exist when the first
edition was written. Hyaluronic acid and other fillers have literally exploded onto the mar­
ket. Body dysmorphic disorder has become a front page diagnosis, with physician and public
awareness increasing on an almost daily basis. Fractional resurfacing has revolutionized the
way we treat many of our patients with photoaging.
So there we have it: we need to get smarter, faster, technologically better, and all this in an
internet age where our patients and colleagues can keep a close eye on everything. It is time that
we brought our innovative efforts into the light for everyone to see, and this textbook is simply
one piece of that ever expanding puzzle. It is our intent to “open the books”, so to speak, and we
have tried to make this book the equivalent of a full disclosure discussion on cosmetic surgery.
An addition to this second edition of the Atlas of Cosmetic Surgery is the use of video in the
form of the DVD that comes with the book. In the digital and visual age, we all can learn a
great deal by simply watching and listening to our colleagues. So in addition to reading the
words, where appropriate we have tried to provide visuals to accompany the text. It is our hope
that you will find this visual aide a valuable addition and complement to the printed page.
Preface

xiv
Hopefully, the sharing of information, techniques and insights will allow everyone who
reads this text to become a better physician. That is the goal, and in short that is the reason this
second edition of the Atlas of Cosmetic Surgery was written. Ultimately, it is also what helped get
me past the “what was I thinking” moment. I can’t thank enough the colleagues and friends
who have contributed their time and expertise to this book. They have literally spent hundreds
of hours of their own free time to help advance the knowledge base of the rest of us, which in
essence is the beauty of our field. The selflessness and collegiality of the physicians we all work
with is inspiring, and their efforts are proof that in the end it is all about the patient.
Michael S. Kaminer, MD

Preface

Over 11.7 million Americans underwent a cosmetic surgi­
cal or minimally invasive procedure in 2007. Since 2000, the
number of these procedures has increased by 59%.1 The vast
majority of these procedures consisted of relatively new, mini­
mally invasive, nonsurgical procedures, which have increased
by 81%.1 These numbers, while familiar to many cosmetic
surgeons, are often staggering to other medical profession­
als and lay persons who have little idea of the number of
Americans who turn to medicine to enhance their physical
appearance. The dramatic increase in these numbers likely
reflects an increased acceptance and desirability of improving
appearance by medical means. It also underscores the pre­
mium that is placed on physical appearance in America in
contemporary culture.2
Several factors have likely contributed to the growth in
popularity of cosmetic surgery.3–5 Changes in the medical
and surgical communities, including improvements in safety
and direct-to-consumer marketing, have increased access to
cosmetic surgery and likely contributed to the growth. The
effect of our physical appearance on the way people react to
us in social interactions is another possible influence on the
increasing popularity of cosmetic surgery. A large body of
research indicates that perceived attractiveness often leads to
preferential treatment in a variety of social situations.2,6 The
mass media have long championed cosmetic surgery, perhaps
no more so than during the current era of widely watched
‘reality-based’ television programs such as ‘Dr. 90210.’ These
shows are part of a virtually inescapable bombardment of
mass media ideals of beauty. These medical advances and
mass media coverage serve as a backdrop to the significant
dissatisfaction that most Americans experience with regard to
their physical appearance.7 When all of these factors are con­
sidered, the dramatic growth in cosmetic surgical and mini­
mally invasive treatments is not surprising.
For the majority of patients, the cosmetic surgical expe­
rience is quite positive. Most surgeons are well trained to
­foresee and avoid a wide range of potential medical compli­
cations. By contrast, few surgeons have systematic training in
evaluation of the psychosocial status of a prospective patient,
a skill that is essential to avoiding psychological pitfalls.8
A surgeon can perform a procedure to the highest standards
of medical practice, yet be faced with a frustrating, infuri­
ating, or personally costly outcome. A bitterly dissatisfied
­patient can seriously damage the reputation of a practice. An
unwarranted lawsuit, even if ultimately dismissed, can take a
toll well beyond the legal costs. Self-destructive behaviors can
undo surgical results. At a rare extreme, some procedures
can be part of an unfortunate chain of events that ends in
patient suicide or even homicide with the surgeon as victim.
Cosmetic surgeons and mental health professionals have
long been interested in the psychological aspects of cosmetic
surgery.9,10 In 1990, before the recent growth of cosmetic
medical procedures, Pruzinsky and Edgerton11 suggested that
cosmetic surgery is analogous to psychological interventions.
Since that time, an extensive body of research has investigated
both the psychosocial characteristics of individuals ­interested
in cosmetic surgery, as well as the psychological changes that
occur postoperatively.2–5,12–19 This literature is reviewed
in detail in the recent book Psychological Aspects of ­Reconstructive
and Cosmetic Plastic Surgery: Clinical, Empirical, and Ethical
­Perspectives.20
PREOPERATIVE PSYCHOLOGICAL
EVALUATION OF THE COSMETIC
SURGERY PATIENT
Sarwer has written extensively on the psychological assess­
ment of patients who present for cosmetic surgery.3,4,20,21
In general, surgeons should assess the following three areas:
motivations and expectations, body image dissatisfaction and
body dysmorphic disorder, general psychiatric status and his­
tory. The questions in Appendix A at the end of this chapter
may be useful in assessing these areas. In addition, surgeons
should be observant of patients’ office behavior and they
should be well prepared to provide referrals to mental health
professionals when appropriate. Attending to these areas will
Understanding the Cosmetic
Surgery Patient
David B. Sarwer,
Ted A. Grossbart, and
Alexander W. Baker
C h a p t e r
1
p a r t 1

4
Chapter 1
Evaluation of the cosmetic surgery patient
help to improve care and, perhaps more importantly, reduce
the risk of negative outcomes.
Motivations and expectations
From the very first contact, the surgeon must be listening for
the patient’s motivations for and expectations of cosmetic sur­
gery. Motivations can be categorized as internal (e.g. under­
going the surgery to improve one’s self-esteem) or external
(e.g. undergoing the surgery for some secondary gain, such
as obtaining a promotion or starting a new romantic rela­
tionship).22–25 In some cases, the primary motivation for sur­
gery may not come directly from the patient, but a spouse or
romantic partner. In those cases, who truly defines a successful
result – the patient or the partner? To assess this issue, it may
be useful to start the initial consultation by asking why patients
are interested in surgery at this time.
Postoperative expectations can be grouped into three
­categories: surgical, psychological, and social.22,26 Surgical
expectations address the specific concerns about physical ap­
pearance, both pre- and postoperative. In some cases the pa­
tient and surgeon may not agree on the postoperative result.
When this happens it is important for the surgeon to handle
the situation with care. The patient may simply be dissatisfied,
but they also may be suffering from psychopathology that was
not detected preoperatively. It is not unheard of for these pa­
tients to file suit for damages and, in the most extreme cases,
threaten violence and inflict physical harm on their surgeon.
Psychological expectations include potential improvements in
psychological functioning, such as anticipated changes in self-
esteem after surgery.
Social expectations address the potential social benefits of
cosmetic surgery. Patients are typically considered to be more
physically attractive by others after surgery, but there is no
evidence that cosmetic surgery leads to changes in social or
romantic behavior. Prospective patients need to be reminded
that an improvement in appearance is not likely to result in a
change in the social responses of others. In fact, negative post­
operative reactions from romantic partners, parents, or close
friends may undermine psychosocial outcomes.
In their review of studies investigating psychological out­
comes following cosmetic surgery, Honigman et al.27 found
three studies that suggested that unrealistic expectations are
associated with lower levels of postoperative satisfaction.28–30
In contrast, patients who are internally motivated and who
have realistic expectations may be the most likely to be satis­
fied with their postoperative result.
Body image dissatisfaction and body
dysmorphic disorder
Assessing the degree of preoperative body image dissatisfaction
is an essential part of the preoperative consultation. Some
dissatisfaction is typical among most patients – presumably
those who are pleased with their physical appearance will not
present for cosmetic surgery. Some patients, however, have an
intense preoccupation with aspects of their appearance. It is
as though all the emotional pain of their lives becomes focused
on their bodies. Extreme dissatisfaction like this may suggest
the presence of body dysmorphic disorder (BDD), defined as
a preoccupation with a slight or imagined defect in appear­
ance that leads to significant disruption in daily functioning.31
While BDD is believed to occur in 1–2% of the general popu­
lations, numerous studies have suggested that it occurs in up to
15% of cosmetic surgical and dermatological patients.18,32–35
To further assess for BDD, patients should be asked how
their feelings about their appearance impact their daily func­
tioning. Patients without obvious extreme defects who report
that their appearance concerns prevent them from maintain­
ing employment or relationships, or from engaging in daily ac­
tivities most people would do without a second thought, may
have BDD. It is important to remember, however, that BDD
symptoms fall on a continuum. Severe cases where individu­
als are unable to maintain employment or rarely leave their
homes are relatively easy to recognize. In less severe forms
of the disorder, individuals are able to work and maintain re­
lationships, but their quality of life suffers dramatically. For
example, they avoid various social situations or endure them
with considerable self-consciousness, or they spend substantial
time checking and re-checking their appearance in ­mirrors.
Some patients may unintentionally reveal the extent of their
preoccupation by presenting the surgeon with ­numerous pho­
tographs of models or celebrities who have the feature(s) they
desire. Others may take photographs of ­ themselves and,
­either through crude pencil drawings or elaborate computer
enhancements, attempt to depict the desired changes. These
behaviors should be considered as possible symptoms of BDD.
Patients also should be asked what measures they have taken
to improve their appearance in the past. Approximately 36%
of cosmetic surgery patients report that they have undergone
a previous cosmetic procedure.1 These numbers, ­ however,
likely do not account for other less invasive treatments and
homemade remedies patients may have tried. For example,
among 200 persons with BDD, 71% sought and 60% received
nonpsychiatric medical treatments including cosmetic surgery
and dermatological treatments.36 Unfortunately, greater than
90% of these procedures led to no change or a worsening in
BDD symptoms, suggesting that these patients do not benefit
from cosmetic surgical treatments.36
The cosmetic surgeon may have a difficult time identifying
BDD in patients who present for consultation dissatisfied with
the results of a previous procedure. Similarly, the surgeon faces
a serious conundrum when asked to repair a self-inflicted in­
jury or damage, such as often seen with chronic skin picking.
This latter condition can result from a range of psychological
pictures, with or without a primary skin disorder like acne.
Successful surgical results can be quickly reversed if the skin
picking has not been adequately treated. Cognitive behavio­
ral psychotherapy and psychopharmacologic treatments can
­effectively treat skin picking; hypnosis can be quite helpful as

5
Understanding the cosmetic surgery patient  •  Chapter 1
well.37 Active collaboration between the surgeon, the patient,
and the mental health provider, with the promise of surgery at
a mutually agreed upon level of mastery of the disorder, also
can effectively treat the condition.
Cosmetic surgeons are clearly aware of the presence of
individuals with BDD in their patient population. A survey
of cosmetic surgeons suggested that they believed that 2% of
patients seen for an initial cosmetic consultation suffered from
BDD.38 Eighty percent of surgeons indicated that they had
observed some of the characteristic symptoms of the disorder
in patients.38 The vast majority of surveyed surgeons (84%) re­
ported that they had refused to operate on a patient ­suspected
of having BDD; 64% had scheduled a second consultation;
and 50% had referred patients for a mental health consulta­
tion. Also, 84% of surgeons indicated that they had operated
on a patient whom they believed was appropriate for surgery,
only to realize after the operation that the patient may have
had BDD. Most importantly, of surgeons who had this expe­
rience, 82% reported that the patient had a poor outcome
with regard to BDD symptoms. Approximately 30% of survey
respondents indicated that they had been threatened legally
by a patient that they believed had BDD and approximately
10% reported that they had been threatened both legally and
physically. This finding, coupled with the finding that less than
5% of patients with BDD report improvement in their symp­
toms following nonpsychiatric treatment, suggests that BDD is
a contraindication to cosmetic surgery.
General mental health status
and history
As in any medical consultation, the surgeon should assess a
patient’s mental health status and history. While all of the for­
mal psychiatric diagnoses likely appear in the population of
cosmetic surgery patients, special attention should be paid to
disorders with a body image component, such as BDD and
eating disorders, as well as mood disorders.
Eating disorders
Given the central role of body image in both eating disorders
and cosmetic surgery, patients seeking procedures such as lipo­
suction or breast augmentation also should be screened for
anorexia and bulimia. To help assess for the presence of an
eating disorder, the height and weight of all patients should be
used to calculate body mass index (the patient’s weight [in kil­
ograms] divided by their height [in meters] squared). Patients
with a BMI <20 kg/m2 should be asked about a history of
recent weight fluctuations, ongoing dieting efforts, binge eat­
ing, and purging or other compensatory behaviors. Women
also should be asked about amenorrhea.
Mood disorders
Dissatisfaction with one’s body image also can contribute to a
mood disorder. Identifying irregularities in a patient’s mood,
affect, and overall presentation is the first step in screening for
mood disorders. If the treating physician identifies problems
in these areas, neurovegetative symptoms, including sleep,
­appetite, and concentration, should be assessed. If patients
endorse these symptoms, they should be asked about the
­frequency of crying or irritability, social isolation, feelings of
hopelessness, and the presence of suicidal thoughts.
Within the past several years, several large-scale epidemio­
logical studies have found an unexpected relationship between
cosmetic breast augmentation and suicide.39–43 In one inves­
tigation, breast augmentation candidates were found to have
a higher rate of psychiatric hospitalizations as compared to
those who underwent other cosmetic surgical procedures.40
While our understanding of the relationship between cos­
metic breast augmentation and suicide is still in its infancy,
additional assessment of the symptoms of depression in this
patient population is warranted.44,45
Untreated mood disorders increase dissatisfaction with
many aspects of life – one’s body included. This discontent
may contribute to the motivation for surgery, as patients may
believe that they will feel better about themselves if they look
better and, in turn, feel better about their bodies. ­Underlying
mood disorders also may contribute to lower levels of satis­
faction with the postoperative results. Many of these ­patients
likely would be better served by psychotherapeutic or psy­
chopharmacologic treatment than cosmetic surgery.
In addition to assessing current mental health status, the
treating surgeon should obtain a psychiatric history. This in­
formation should be routinely obtained as part of the patients’
general medical history. If this information is typically col­
lected on a preprinted form completed by the patient before
seeing the surgeon, patients’ responses should be reviewed
during the initial visit. Some patients are reluctant to candidly
report mental health histories, in part out of fear that previ­
ous or ongoing treatment will preclude cosmetic treatment.
When there is suspicion that information is being withheld,
repeating the same questions in different forms can yield the
needed answers.
Nineteen percent of cosmetic surgery patients reported a
mental health history, which was significantly greater than 4%
of noncosmetic plastic surgery patients.46 Furthermore, 18%
of cosmetic surgery patients reported using a psychiatric med­
ication (almost exclusively antidepressant medications) at the
time of their initial consultation, which also was significantly
greater than 5% of noncosmetic surgery patients. Many of
these patients likely received these medications from their
primary care physician and not from a psychiatrist. Clinical
experience, as well as investigations from other surgical
­populations,47 suggests that primary care professionals often
prescribe subtherapeutic dosages of these medications.
Patients with a history of psychopathology who are not
currently engaged in mental health treatment may warrant a
preoperative mental health consultation to further assess their
psychological status. Patients currently in treatment should be
asked if their mental health professional is aware of their
­interest in surgery. Surgeons should contact these professionals

6
Chapter 1
Evaluation of the cosmetic surgery patient
to confirm that the proposed treatment is appropriate at this
time. Patients who have not mentioned their interest in cos­
metic surgery to their mental health provider, or refuse to al­
low the surgeon to contact that person, should be viewed with
caution. While such secretiveness was once commonplace, in
the current environment of greater acceptance of cosmetic
surgery, it may reflect a degree of paranoid thinking suggestive
of psychopathology. These patients warrant a mental health
consultation. Patients who are dissatisfied with their post­
operative result have used their psychiatric history as part of
their legal action against the surgeon, arguing that their psy­
chiatric condition prevented them from fully ­understanding
the procedure and its potential outcomes. These occurrences
underscore the importance of assessing and documenting the
psychiatric status of all patients undergoing cosmetic surgery.
Observing office behavior
Patients’ behavior during their office visits should be observed
closely. A 30-minute to 45-minute consultation is a relatively
brief period of time to assess patients’ psychosocial function­
ing. Patients typically are on their best behavior during their
initial consultation and will often expend a great deal of effort
to present themselves to the surgeon as ‘appropriate’ for sur­
gery. Important psychosocial information may be withheld
if patients believe that it may result in rejection for surgery.
Therefore, every bit of information obtained either during the
consultation, or observed during interactions with the nursing
or office staff, should be used in making a determination of
appropriateness for surgery.
Nursing staff and office assistants, as compared to cosmetic
surgeons, are in unique positions to gather important and
­potentially problematic information about patients. Members
of the office staff often witness different aspects of patients’
behavior during their interactions in the office.48 These
­behaviors can often suggest the presence of psychopathology
that may interfere with the postoperative outcome.
Patients who have difficulty following the office routine
warrant further attention. Those who frequently cancel or
change appointments, ask for appointments outside of office
hours, or who do not wish to talk to anyone other than the
surgeon should be reconsidered for surgery. Patients who raise
concerns among the staff should, at a minimum, be seen for
a second preoperative consultation. If concerns persist, these
patients should be referred to a psychologist or psychiatrist for
a consultation.
Mental health referrals
A trusted mental health professional serving as a consultant is
an essential tool for a successful cosmetic surgery practice. If
the surgeon and/or staff have concerns about the psychologi­
cal status of prospective patients, a referral to a psychologist
or psychiatrist for an evaluation is essential. Given the rela­
tionship between body image dissatisfaction and ­ cosmetic
surgery,9–10 a psychologist or psychiatrist with interest or
expertise in body image may be the ideal consultant. These
mental health professionals often work with other forms of
psychopathology with a body image component, such as
­eating disorders or BDD.
Patients will often react to mental health referrals with
anger and many will frequently refuse to accept the referral.
These patients are probably not good candidates for treat­
ment. Unfortunately, in this current competitive environment,
many patients will ‘doctor shop’ until they eventually find a
physician who will treat them, thereby not receiving the men­
tal healthcare they need. It is important for physicians to make
an effort to identify these individuals because the potential
consequences are serious for both parties. Hopefully, some pa­
tients will hear the concerns of the surgeon they initially con­
sulted and realize that cosmetic treatment is not appropriate
at this time. Therefore, it is important that the surgeon treat
the referral to the psychologist or psychiatrist like any other
referral to a medical professional. This frequently will help
destigmatize the mental health professional to the patient and
make the referral more acceptable. It is important to com­
municate to the patient the reason for the consultation. It may
be useful to say:
Undergoing a cosmetic medical treatment is an important decision. You
are considering making changes to your appearance that are more or less
permanent. These treatments often lead to changes in how you feel about
your appearance – some which may be positive and others that may be
less positive. I think it is important that we both are 100% sure that
this treatment is right for you at this time. Therefore, because I care about
your well-being, I would like you to see a psychologist (psychiatrist) who
often works with us to help us decide if this is the right time.
Such a statement underscores the importance of the
consultation to the patient in a nonthreatening manner and
hopefully prevents the patient from responding with anger or
hostility.
Either based on the information gathered during the initial
consultation or following a consultation with a mental health
professional, surgeons may find themselves in the unusual po­
sition of wanting to say ‘No’ to patients who have requested
treatment. Training in both the medical and mental health
professions, both directly and indirectly, teaches profession­
als to help everyone who seeks treatment. Nevertheless, there
will be patients who ask for the wrong kind of help. Some
will ask for cosmetic surgery when a mental health treatment
is more appropriate. Others may ask for a treatment outside
of the professional’s area of expertise. Still others may sim­
ply rub the professional the wrong way, making an appro­
priate professional relationship difficult. In these cases, the
professional should remember that a cosmetic treatment is
an elective treatment for both parties involved. Patients can
elect to have them; professionals can elect to say no.
If a medical professional elects to say ‘No’ to a proposed
treatment, it should be communicated clearly, with sensitiv­
ity, and in person. The conversation should be thoroughly

7
Understanding the cosmetic surgery patient  •  Chapter 1
­documented in the chart and followed by a letter to the pa­
tient. Professionals who do not deal with these issues directly
and avoid these patients can put themselves at greater risk for
legal action.
Postoperative Management
of Cosmetic Surgery Patients
Several studies have found that cosmetic surgery patients
typically experience improvements in body image following
surgery.14–16 The effects of cosmetic surgery on other areas
of psychological functioning are mixed. Some studies have
found improvements in quality of life and depressive symp­
toms, while others have found no changes in these psychoso­
cial domains. Clearly, additional studies are needed to further
investigate the effects of cosmetic surgery on other areas of
functioning.
While the vast majority of patients report satisfaction with
their postoperative outcomes, on occasion cosmetic surgeons
will encounter dissatisfied patients for whom additional surgi­
cal treatment is not appropriate. Some patients may be dis­
satisfied with what the surgeon considers to be a successful
procedure. In other instances, patients may experience an ex­
acerbation of psychopathology that was not detected preop­
eratively. (These same situations also may occur with patients
who undergo reconstructive procedures.) Patients in both ex­
amples warrant assessment by a psychologist or psychiatrist.
Psychotherapeutic care, rather than additional cosmetic
­procedures, may be the most appropriate treatment for
these individuals.
Summary
Assessment of patients’ psychosocial status is an essential step
in determining their appropriateness for surgery. Patients’
motivations and expectations, physical appearance and body
image concerns, and mental health history and status, all may
be associated with postoperative outcomes. Patients who com­
plain of minimal appearance flaws, suffer from excessive emo­
tional distress, or report skin picking should be evaluated for
BDD. Patients presenting for body procedures, such as lipo­
plasty, abdominoplasty, and breast augmentation, should be
assessed for symptoms of eating disorders. Mood disorders can
distort the perceived need for surgery and set the stage for dis­
satisfaction with the results. Since patients with these disorders
may be more likely to present for surgical rather than mental
health treatment, cosmetic treatment providers are in a unique
position to identify these patients and to provide appropriate
referrals to mental health professionals. Knowing when and
how to say no can provide substantial benefit to the patient,
and save the surgeon and staff from multiple problems.
REFERENCES
  1. American Society of Plastic Surgeons. 2007 National plastic surgery
statistics. Arlington Heights, IL: ASPS; 2008.
  2. Sarwer DB, Magee L. Physical appearance and society. In: Sarwer DB,
Pruzinsky T, Cash TF, et al., eds. Psychological aspects of reconstructive
and cosmetic plastic surgery: empirical, clinical, and ethical issues
Philadelphia: Lippincott, Williams, and Wilkens; 2006:23–36.
  3. Sarwer DB, Crerand CE. Body image and cosmetic medical treatments.
Body Image: Int J Res, 2004; 1:99–111.
  4. Sarwer DB. Psychological assessment of cosmetic surgery patients. In:
Sarwer DB, Pruzinsky T, Cash TF, et al., eds. Psychological aspects
of reconstructive and cosmetic plastic surgery: empirical, clinical, and
ethical issues. Philadelphia: Lippincott, Williams, and Wilkins;
2006 :267–283.
  5. Cash TF. Body image and cosmetic surgery. In: Sarwer DB, Pruzinsky T,
Cash TF, et al., eds. Psychological aspects of reconstructive and
cosmetic plastic surgery: empirical, clinical, and ethical issues.
Philadelphia: Lippincott, Williams, and Wilkens; 2006:37–59.
  6. Etcoff NL. Survival of the prettiest: the science of beauty. New York:
Anchor Books; 1999.
  7. Cash TF, Pruzinsky T. Body Image: A handbook of theory, research,
and clinical practice. New York: Guilford Press; 2002.
  8. Gorney M. Professional and legal considerations in cosmetic surgery.
In: Sarwer DB, Pruzinsky T, Cash TF, et al., eds. Psychological aspects
of reconstructive and cosmetic plastic surgery: empirical, clinical, and
ethical issues. Philadelphia: Lippincott, Williams, and Wilkins;
2006 :315–328.
  9. Crerand CE, Cash TF, Whitaker LA. Cosmetic surgery of the face.
In: Sarwer DB, Pruzinsky T, Cash TF, et al., eds. Psychological aspects
of reconstructive and cosmetic plastic surgery: empirical, clinical, and
ethical issues. Philadelphia: Lippincott, Williams, and Wilkins;
2006 :233–249.
10. Sarwer DB, Didie ER, Gibbons LM. Cosmetic surgery of the body. In:
Sarwer DB, Pruzinsky T, Cash TF, et al., eds. Psychological aspects
of reconstructive and cosmetic plastic surgery: empirical, clinical, and
ethical issues. Philadelphia: Lippincott, Williams, and Wilkins;
2006 :251–266.
11. Pruzinsky T, Edgerton MT. Body image change in cosmetic plastic
surgery. In: Cash TF, Pruzinsky T, eds. Body images: development,
deviance, and change. New York: Guilford Press; 1990 :217–236.
12. Sarwer DB, Magee L, Crerand, CE. Cosmetic surgery and cosmetic
medical treatments. In: Thompson JK, ed. Handbook of eating
disorders and obesity. Hoboken: Wiley; 2004:718–737.
13. Sarwer DB, Wadden TA, Pertschuk MJ, et al. The psychology of
cosmetic surgery: A review and reconceptualization. Clin Psychol Rev
1998; 18:1–22.
14. Cash TF, Duel LA, Perkins LL. Women’s psychosocial outcomes
of breast augmentation with silicone gel-filled implants: a 2-year
prospective study. Plast Reconstr Surg 2002; 109:2112–2121.
15. Bolton MA, Pruzinsky T, Cash TF, et al. Measuring outcomes in plastic
surgery: body image and quality of life in abdominoplasty patients. Plast
Reconstr Surg 2003; 112(2):619–625.
16. Dunofsky M. Psychological characteristics of women who undergo
single and multiple cosmetic surgeries. Ann Plast Surg 1997; 39(3):223–228.
17. Rankin M, Borah GL, Perry AW, et al. Quality-of-life outcomes after
cosmetic surgery. Plast Reconstr Surg 1998; 102(6):2139–2145.
18. Sarwer DB, Wadden TA, Pertschuk MJ, et al. Body image dissatisfaction
and body dysmorphic disorder in 100 cosmetic surgery patients. Plast
Reconstr Surg 1998; 101(6):1644–1649.
19. Sarwer DB, Wadden TA, Whitaker LA. An investigation of changes
in body image following cosmetic surgery. Plast Reconstr Surg 2002;
109:363–369.
20. Sarwer DB, Pruzinsky T, Cash TF, et al. Psychological aspects of
reconstructive and cosmetic plastic surgery: empirical, clinical, and
ethical issues. Philadelphia: Lippincott, Williams, and Wilkins; 2006.
21. Sarwer DB. Psychological considerations in cosmetic surgery. In:
Goldwyn RM, Cohen MI, eds. The unfavorable result in plastic surgery.
3rd edn. Philadelphia: Lippincott, Williams, & Wilkins; 2001.

8
Chapter 1
Evaluation of the cosmetic surgery patient
22. Grossbart TA, Sarwer DB. Cosmetic surgery: Surgical tools –
psychosocial goals. Semin Cutan Med Surg 1999; 18:101–111.
23. Edgerton MT, Knorr NJ. Motivational patterns of patients seeking
cosmetic (aesthetic) surgery. Plast Reconstr Surg 1971; 48:551–557.
24. Goin JM, Goin MK. Changing the body: psychological effects of plastic
surgery. Baltimore, MD: Williams & Wilkins; 1981.
25. Myer E, Jacobson WE, Edgerton MT, et al. Motivational patterns in
patients seeking elective plastic surgery. Psychol Med 1960; 22:193–202.
26. Pruzinsky T. Cosmetic plastic surgery and body image: critical factors in
patient assessment. In: Thompson JK, ed. Body image, eating disorders,
and obesity. Washington, DC: American Psychological Association;
1996:109–127.
27. Honigman R, Phillips KA, Castle DJ. A review of psychological
outcomes for patients seeking cosmetic surgery. Plast Reconstr Surg
2004; 113:1229–1237.
28. Beale S, Lisper H, Palm B. A psychological study of patients seeking
augmentation mammaplasty. Br J Psychol 1980; 136:133–138.
29. Edgerton MT, Meyer E, Jacobson WE. Augmentation mammaplasty:
II. Further surgical and psychiatric evaluation. Plast Reconstr Surg
1961; 27:279–301.
30. Napoleleon A. The presentation of personalities in plastic surgery.
Ann Plast Surg 1993; 31:193–208.
31. Diagnostic and statistical manual of mental disorders: DSM-IV-TR.
4th edn. text revision 2000. Washington, DC: American Psychiatric
Association; 2000:507–510.
32. Crerand CE, Sarwer DB, Magee L, et al. Rate of body dysmorphic
disorder among patients seeking facial plastic surgery. Psychiatr Ann
2004; 34:958–965.
33. Crerand CE, Franklin ME, Sarwer DB. Body dysmorphic disorder and
cosmetic surgery. Plast Reconstr Surg 2006; 118(7):167e–180e.
34. Dufresne RG, Phillips KA, Vittorio CC, et al. A screening questionnaire
for body dysmorphic disorder in a cosmetic dermatologic surgery
practice. Dermatol Surg 2001; 27:457–462.
35. Phillips KA, Dufresne RG, Wilkel C, et al. Rate of body dysmorphic
disorder in dermatology patients. J Am Acad Dermatol 2000;
42:436–441.
36. Crerand CE, Phillips KA, Menard W, et al. Nonpsychiatric medical
treatment of body dysmorphic disorder. Psychosomatics 2005;
46(6):549–555.
37. Grossbart TA, Sherman C. Skin deep: a mind/body program for
healthy skin. New Mexico: Health Press; 1992.
38. Sarwer DB. Awareness and identification of body dysmorphic disorder
by aesthetic surgeons: results of a survey of American Society for
Aesthetic Plastic Surgery members. Aesth Surg J 2002; 22:531–535.
39. Brinton LA, Lubin JH, Burich MC, et al. Mortality among
augmentation mammaplasty patients. Epidemiology 2001; 12:321–326.
40. Jacobsen PH, Holmich LR, McLaughlin JK, et al. Mortality and suicide
among Danish women with cosmetic breast implants. Arch Intern Med
2004; 164:2450–2455.
41. Koot VC, Peeters PH, Granath F, et al. Total and cause specific
mortality among Swedish women with cosmetic breast implants:
A prospective study. Br Med J 2003; 326:527–528.
42. Pukkala E, Kulmala I, Hovi SL, et al. Causes of death among Finnish
women with cosmetic breast implants, 1971–2001. Ann Plast Surg 2003;
51:339–342.
43. Brinton LA, Lubin JH, Murray MC, et al. Mortality rates among
augmentation mammaplasty patients: an update. Epidemiology 2006;
17:162–169.
44. McLaughlin JK, Wise TN, Lipworth L. Increased risk of suicide
among patients with breast implants: do the epidemiologic data support
psychiatric consultation? Psychosomatics 2004; 45:277–280.
45. Sarwer DB, Brown GK, Evans DL. ���������������������������������
Cosmetic breast augmentation and
suicide. Am J Psychiatry 2007; 164:1006–1013.�
46. Sarwer DB, Zanville HA, LaRossa D, et al. Mental health histories
and psychiatric medication usage among persons who sought cosmetic
surgery. Plast Reconstr Surg 2004; 114:1927–1933.
47. Sarwer DB, Cohn NI, Gibbons LM, et al. Psychiatric diagnoses and
psychiatric treatment among bariatric surgery candidates. Obes Surg
2004; 14:1148–1156.
48. Goldwyn RM. Psychological aspects of plastic surgery: A surgeon’s
observations and reflections. In: Sarwer DB, Pruzinsky T, Cash TF,
et al., eds. Psychological aspects of reconstructive and cosmetic plastic
surgery: empirical, clinical, and ethical issues. Philadelphia: Lippincott,
Williams, and Wilkins; 2006:13–21.

9
Understanding the cosmetic surgery patient  •  Chapter 1
Appendix A
QUESTIONS FOR THE PREOPERATIVE
COSMETIC SURGERY PATIENT
Motivations and Expectation
• Why are you interested in surgery now (as compared to 6 months ago)?
• How do you anticipate your life will be different following surgery?
• How do people in your life feel about your getting cosmetic surgery?
Physical Appearance and Body Image
• What is it that you dislike about your appearance?
• How unhappy do you become when you think about your appearance?
• When does the feature bother you the most?
• Do you ever camouflage or hide the feature from others?
• Do you ever feel like you spend too much time thinking about your appearance?
• Do your feelings about your appearance keep you from doing certain activities?
• What other things have you done to improve your appearance?
Psychiatric History and Status
• Have you ever had any significant problems with depression or anxiety?
• Have you ever, or are you currently, under the care of a mental health professional?
• Have you ever taken, or are you currently taking, an antidepressant or other psychiatric medication?
• If yes, who is prescribing this medication?
Permission is granted by Lippincott Williams & Wilkins to copy and distribute this questionnaire for routine patient care only.

COSMETIC PROCEDURES,
THE FACIAL FEEDBACK HYPOTHESIS,
AND EMOTIONS
The cosmetic use of botulinum toxins, soft tissue fillers and
many aesthetic treatments has changed the face of cosmetic
surgery. Ubiquitous, minimally invasive procedures are now
able to alter facial expressions in a manner that eludes detection
by observers. As such, in users, these therapies can modify the
visible manifestations of emotions. It has been suggested that
actors and actresses partaking of botulinum toxin injections
are sacrificing emotional range for the imperative of seem­
ing younger. Novice patients suspect that there is something
to be feared by drugs and procedures so subtle yet powerful,
and it is not uncommon to have a patient willing to undergo a
face-lift but evince concern about botulinum toxin injections.
The cosmetic dermatologist’s answer to the patient fear of
post-treatment concerns has been logic and encouragement.
After all, babies too lack upper face wrinkles and yet are able
to convey their emotional state without ­difficulty.
A deeper analysis suggests that botulinum toxin injections
and simple cosmetic enhancements, far from impairing emo­
tional expression, may actually improve patients’ emotional
states. The induction of positive emotions and reduction of
negative emotions may, in turn, lead to a more positive state
of mind. Using botulinum toxin as the index procedure, the
remainder of this chapter will discuss normal facial expres­
sions and those altered by cosmetic procedures, using the psy­
chological theory known as the ‘facial feedback hypothesis’
to support this assertion. Confirmatory and contradictory
evidence, including both classical psychological testing and
EMG experiments, will be evaluated.
THE FACIAL FEEDBACK HYPOTHESIS
In simplest terms, the facial feedback hypothesis maintains
that expressive behavior can activate or regulate emotions.1,2
As Izard notes, the seeds of this idea are lost in time, with
examples occurring in ancient writings, including the Iliad.
In Shakespeare’s Henry V, soldiers are charged on the eve of
battle to construct fearsome expressions in preparation for
their imminent exertions:
Then imitate the action of the tiger:
Stiffen the sinews, summon up the blood,
Disguise fair nature with hard-favored rage;
Then lend the eye a terrible aspect:
Let it pry through the portage of the head
Like the brass cannon; let the brow o’erwhelm it
As fearfully as doth a galled rock
O’erhand and jutty his confounded base
Swilled with the wild and wasteful ocean
Now set the teeth and stretch the nostril wide
Hold hard the breath and bend up every spirit
To his full height
Act iii, Scene i
In the scientific world, one of the first to mention the feed­
back idea was Charles Darwin. Darwin was startlingly clear
at times, noting that ‘even the simulation of an emotion tends
to arouse it in our minds.’ While he was not always consistent
Understanding Facial
Expression
Murad Alam,
Karen C. Barrett,
Robert M. Hodapp, and
Kenneth A. Arndt
C H A P T E R
2
P A R T 1

12
Chapter 2
Evaluation of the cosmetic surgery patient
and also described emotions as proceeding from a ‘state of
mind,’ he clearly believed that even if not the sole determi­
nant of emotions, expressive behavior had a major role in
control of these emotions:
The free expression by outward signs of an emotion ­intensifies
it. On the other hand, the repression, as far as this is ­possible,
of all outward signs softens our emotions. He who gives
way to violent gestures will increase his rage; he who does
not ­control the signs of fear will experience fear to a greater
degree.3
William James, about two decades later, concurred: ‘Refuse
to express a passion and it dies … If we wish to conquer unde­
sirable emotional tendencies in ourselves, we must assiduously,
and in the first instance, go through the outward movements
of those contrary dispositions which we prefer to cultivate.’4
Other scholars further refined these theories, with Gellhorn5
providing some of the earliest laboratory evidence and
­Tomkins6 some of the first modern formulations of the theory.
Specifically, using curare to relax laboratory animals’ striated
muscles, Gellhorn found a decrease in sympathetic nervous
system and hypothalamic responsiveness which he ascribed to
the therapeutic effects of reduced muscle tone on emotional
tension. Tomkins defined emotions as facial manifestations of
such and awareness of these; in this system, emotions are not
internally generated but rather are what the individual expe­
riences when they realize their face is contorted in a manner
consistent with an emotion. Perhaps the clearest and most
verifiable theoretical statement of the facial feedback hypoth­
esis was offered by Laird,7 who postulated that a subject-blind,
experimenter-created facial expression would induce a similar
emotional experience in the subject.
UPPER FACE MUSCLES AFFECTED
BY BOTULINUM TOXIN INJECTIONS
AND THE EMOTIONS TO WHICH
THEY LIKELY PERTAIN
Before we can assess the evidence supporting or refuting the
facial feedback hypothesis, it is useful to review the primary
upper face muscles responsible for emotional expressions. Then,
to the extent that facial feedback can modify the expressions
created by these muscles, the feedback process may be able to
affect the internal experiences that patients are experiencing.
When botulinum toxin is injected into the upper face, the
primary aesthetic targets are the glabellar rhytides (‘frown’),
horizontal forehead lines (‘look up’), and crow’s feet (‘big
smile’). The muscles of expression most involved at each of
these sites, are, respectively, corrugator supercilii and procerus
(glabella), frontalis (forehead), and orbicularis oculi (crow’s
feet) (Fig. 2-1). The corrugator and procerus seem to be most
associated with negative emotions, given that they are intrinsic
to brow furrowing. With regard to emotional significance,
the corrugator is the best studied of the upper face muscles,
and activation of this muscle, as indicated by EMG, has been
systematically associated with sadness, anger, and fear.8,9 The
frontalis is also involved with negative emotions, including
sadness and fear, but can also be crucial in non-negative emo­
tional expressions, such as surprise, which can appear as rais­
ing of the inner and outer fibers of this muscle.1,10–13 Since the
frontalis is a large muscle, it abuts other muscle groups, and
its actions can be confounded with the contractions of these
and hence with a host of emotional expressions. In general,
to the extent that botulinum toxin reduced the movements of
corrugator, and frontalis (especially the inner aspect), it should
affect the display of negative emotion, and the ­various ­possible
consequences of that, as described below.
In contrast, the orbicularis oculi, which encircle the eyes,
are involved with smiling and, hence, expressions of happi­
ness and joy. A few EMG studies have supported the activa­
tion of the smile muscle (zygomaticus major; see also Fig. 2-1)
in displays of happiness.1,2,6 However, the orbicularis oculi
has proven difficult to assess accurately in EMG studies of
­emotion. Nevertheless, an abundance of research ­investigating
the visible movement of orbicularis oculi has supported its
role in expressions of happiness.
Fig. 2-1  Forehead and brow superficial muscular anatomy,
including frontalis, procerus, corrugator supercilii, orbicularis oculi,
and zygomaticus major. In order from top to bottom, flat muscle
of forehead is frontalis (note lateral and medial, or inner and outer,
fibers); V-shaped muscle above nose is procerus, diagonal muscle
extending medially from nose to periocular area is corrugator super­
cilii, muscle encircling eye is orbicularis oculi (note inner and outer
fibers), and diagonal muscle on cheek from lateral face to perioral
area is zygomaticus major.

13
Understanding facial expression  •  Chapter 2
TESTING FACIAL FEEDBACK
There are two major experimental paradigms for testing the
facial feedback hypothesis. First, investigators can measure
facial expressions in muscular or anatomic terms. Second,
electroencephalographic (EEG) or electromyographic (EMG)
data can be recorded during the appearance of facial expres­
sions. An extensive literature spawned by the emergence of
these techniques has attempted to delineate the phenomena
associated with the hypothesis.
Muscular measurement tends to utilize one of two meas­
urement tools, either the Facial Action Coding System (FACS)
developed by Ekman and Friesen,8,9 or the system developed
by Izard.10 FACS is an anatomically based system that permits
reduction of any facial expression into visually distinguishable
muscular actions through repeated slow-motion viewings of
the video of the expression. Validated across age groups and
cultures, FACS is designed to account for all observed facial
movements, which are represented as either single numeri­
cal FACS codes or a combination of such codes. Manuals
are available that present visual representations of each of
hundreds of basic FACS expressions, as well as ­instructions
on how to recreate these (Figs 2-2–2-6) Reliabilities for FACS
scoring are typically greater than 0.80.14 The Izard scheme,10
the Maximally Descriptive Facial Movement Coding System,
is similar but less exhaustive in that it includes only those facial
movements believed by the author to be relevant to emotion.
Facial electromyography (EMG) measurements register
small electronic potentials generated by contracting muscle
tissue. Surface electrodes are placed over different regions
of the skin, and signals immediately recorded without the
intervention of an observer/recorder.
Fig. 2-2  Fear. Contraction of Action Unit 1 (AU1), which raises the
inner corner of the brow (via inner fibers of the frontalis). See also
Fig. 2-1. (With permission, courtesy of Paul Ekman, from: Ekman P,
Friesen WV, Hager JC. Facial action coding system: the manual
network. Salt Lake City, UT: Information Research Corporation;
2002:466.)
Fig. 2-3  Intense fear. Simultaneous contraction of Action Unit 1
(AU1), which raises the inner corner of the brow (via inner fibers
of the frontalis), and AU4i, which lowers and draws the eyebrows
together (via the procerus and corrugator). The contraction of AU4
is mild rather than intense. The combined effect of AU (1+4i) entails
pulling of the medial portion of the eyebrows upwards and together,
producing of an oblique, triangular shape to the eyebrows, causing
of the skin in the center of the forehead to wrinkle horizontally, and
possibly creating vertical lines, wrinkles, or bunching of the skin
between the brows. See also Fig. 2-1. (With permission, courtesy
of Paul Ekman, from: Ekman P, Friesen WV, Hager JC. Facial action
coding system: the manual network. Salt Lake City, UT: Information
Research Corporation; 2002:470.)

14
Chapter 2
Evaluation of the cosmetic surgery patient
The advantages of EMG are that it is not labor intensive
and can detect extremely slight muscle movements that may
be missed by a human observer. The disadvantages include
the obtrusiveness of the EMG apparatus and the restriction
of its recording selectivity to region specificity rather than
muscle specificity. Conversely, movement scoring techniques
using skilled human intermediaries are unobtrusive to the
­person being rated, but insensitive to very subtle movements
and labor intensive.
FACIAL EXPRESSIONS INITIATE
AND MODULATE EMOTIONS
Of the many experiments performed using the aforemen­
tioned techniques, some are particularly seminal and repre­
sentative. Ekman imbued the study of facial feedback with
laboratory rigor in the 1970s and 1980s, with his efforts
culminating in a widely discussed article in Science.14,15 In
this study, six target emotions, surprise, disgust, sadness, anger,
fear, and happiness, were examined via a ‘directed facial
action task.’15 In each case, a coach provided subjects not with
a global command to make an expression representative of
an emotion but rather a set of precise instructions regarding
which muscles to contract so as to create a facial expression
consistent with a particular emotion. For example, in lieu
of posing anger, subjects were asked to: ‘pull your eyebrows
down and together, raise your upper eyelid and tighten your
lower eyelid, narrow your lips, and press them together.’ Next,
the subjects were asked to relive emotional experiences of a
similar type from the past. Facial behavior was recorded on
Fig. 2-4  Fear/surprise. Contraction of Action Unit 2 (AU2), which
raises the outer corner of the brow (via the outer fibers of the fron­
talis). See also Fig. 2-1. (With permission, courtesy of Paul Ekman
from: Ekman P, Friesen WV, Hager JC. Facial action coding system:
the manual network. Salt Lake City, UT: Information Research
Corporation; 2002:466.)
Fig. 2-5  Genuine Duchenne smile. Simultaneous contraction
of Action Unit 6 (AU6), which circles the eye, narrowing it by pulling
more skin from around the eye (via the outer fibers of the orbicularis
oculi); AU12, which pulls the corners of the lips back and upward
(obliquely) creating a bow-shape to the mouth while deepening
the nasolabial furrow thus pulling it laterally and up; and AU25ii,
which permits parting of the lips, with resulting possible exposure
of the inner mucosal area and teeth and gums. The combined
effect of AU(6+12+25ii) entails the lip corners being pulled up
obliquely, deepening of the nasolabial furrow, appearing of crow’s
feet wrinkles, raising of the infraorbital triangle, and deepening
of the ­infraorbital furrow. (With permission, courtesy of Paul Ekman
from: Ekman P, Friesen WV, Hager JC. Facial action coding system:
the manual network. Salt Lake City, UT: Information Research
­Corporation; 2002:485.)

15
Understanding facial expression  •  Chapter 2
videotape, and involuntary autonomic nervous system param­
eters, including heart rate, left and right hand temperatures,
and skin resistance, were measured throughout. It was found
that similar autonomic responses were elicited when subjects
re-experienced actual emotions from the past and when they
artifactually created the facial experiences consistent with
such emotions. Not only did negative expressions differ from
positive expressions on autonomic parameters regardless of
the method used to create these expressions, but expressions
of particular emotions differed from each other on autonomic
parameters. This study provides some of the initial evidence
in support of the hypothesis that facial expressions, rather
than being merely a manifestation of antecedent internal
emotional states, can alone create the internal and biological
experience of emotions.
Subsequent studies have clarified the role of facial expres­
sions in initiating and modulating emotions. Investigations
have sought to minimize the subjects’ awareness of the emo­
tional meaning of the experimental manipulation to reduce
the likelihood that subjects will consciously or cognitively
experience this emotion. Strack, Martin, and Stepper16 found
that having subjects hold a pen between their teeth (a simu­
lation of smiling) caused them to find cartoons more funny
(Fig. 2-7). Likewise, Larsen, Kasimatis, and Frey17 attached
two golf tees to either side of subjects’ foreheads and asked
subjects to try to move the two tees together (a simulation of
frowning); with the tees closer together, subjects rated unpleas­
ant photographs more negatively (Fig. 2-8). A subtle constraint
was Zajonc’s18,19 attempt to have individuals pronounce
the phoneme ü (simulation of a scowl) or o (simulation of a
relaxed face) for 1 minute. The ü caused a significant increase
in forehead temperature, previously shown to be associated
with negative feelings, and indeed, the participants rated the
o sound as more pleasant than the ü. A more naturalistic study
approximating a real situation required research subjects to
engage in positive or negative facial expressions while smelling
pleasant and unpleasant odors. The subjects’ ratings of the
quality of the odors depended mostly on the odors but were
moderated by the type of face they were making at the time
they smelled them.
Facial mimicry and emotional contagion are two addi­
tional concepts that have been demonstrated empirically.
Lanzetta20–22 was instrumental in exploring the extent of the
latter, which can be loosely described as the process whereby
one persons emotions are transmitted to another, especially
when the ­ transmission occurs in the absence of signifi­
cant conscious awareness. ‘Contagion’23,24 of this type has
Fig. 2-6  Anger. Contraction of Action Unit w4 (AUw4), which lowers
and draws the eyebrows together (using the procerus and corru­
gator) but, unlike AU4i, creates wrinkles between the brows that
are more angular than vertical. See also Fig. 2-1. (With permission,
­courtesy of Paul Ekman from: Ekman P, Friesen WV, Hager JC.
­Facial action coding system: the manual network. Salt Lake City,
UT: Information Research Corporation; 2002:465.)
Fig. 2-7  Subjects asked to hold a pen between their teeth so as
to simulate a grin found a cartoon to be funnier than did subjects
who were not asked to perform this maneuver (Strack, Martin,
and Stepper).

16
Chapter 2
Evaluation of the cosmetic surgery patient
applicability for group cohesion (e.g. smiles can instigate
acceptance, approval, and bonding) and group survival (e.g.
fearful facial displays and vocalizations can alert other group
members to danger). A subtype of emotional contagion,
facial mimicry, entails the elicitation of spontaneous synchro­
nous facial expressions in others in response to particular
facial expressions in the index individual. Such mimicry has
been documented in human infants as early as the first few
days of life.25 In adults, more complex emotions are subject
to transmission in this manner.26 Interestingly, while almost
all facial expressions have some ability to undergo transmis­
sion by mimicry, some are particularly inducers of emotional
expressions. Smiles, in particular, have the ability to propagate
almost irresistibly in observers.27
Smiling was definitively studied by the French neuroanato­
mist Duchenne de Boulogne,28 who wrote in 1962. Remarkably,
his work was not translated into English until 1990 ­although
Darwin’s own writings did allude to Duchenne’s ­ideas. Duch­
enne’s central insight was that the smile of enjoyment could
be distinguished from deliberately produced smiles by consid­
eration of two muscles, the zygomaticus major, which pulls
the lip corners up obliquely, and the orbicularis oculi, which
encircles the eye and pulls skin from the cheek and forehead
towards it:
The first [zygomaticus major] obeys the will but the second
[orbicularis oculi] is only put in play by the sweet emotions
of the soul; the … fake joy, the deceitful laugh, cannot pro­
voke the contraction of this latter muscle. [This muscle] …
does not obey the will; it is only brought into play by a true
feeling … Its inertia in smiling unmasks a false friend.
More recent work has found that most people can volun­
tarily contract the inner part of the orbicularis oculi, the pars
medialis, which is highlighted by tightening and raising of the
lower eyelid; the true smile of enjoyment is thus contingent on
the action of the pars lateralis part of the orbicularis, which
raises the cheeks to produce crow’s feet rhytides and which
few individuals can deliberately move.29,30
Electical measurement of facial
and emotional expression
It has also been shown that the conveyance of emotional
expressions via contagion can be modified by other factors,
including pre-existing cognition and opinions. In one oft-cited
study, subjects were exposed to eight facially expressive vide­
otaped displays of a US president (Reagan). For each trial,
skin conductance and facial muscle activity in the corrugator
supercilii (brow) and zygomaticus major (cheek) were moni­
tored continuously by EMG. Subjects whose prior attitudes
were biased against the president responded with uniformly
negative reactions to all of his emotional displays. Subjects
biased in favor of the president, responded negatively to his
fear/anxiety and anger/threat displays, but positively to his
happiness/reassurance displays. In short, mimicry is enhanced
by pre-existing warm feelings towards the instigator and at least
partly reversed by a negative bias towards this individual.
Even when emotions are not initiated by mimicked facial
expressions, facial expressions can ‘modulate’ the experience
of emotion. Utilizing imagery to create emotions, Hess et al.31
compared the time it took subjects to reach four emotional
states during three conditions. In the ‘Feel’ condition, partici­
pants subjectively experienced an emotion through cognitive
representations of imagery, in the ‘Show’ condition they posed
an expression consistent with an emotion, and in the ‘Feel-and-
Show’ they did both. In this study, which used EMG data as a
marker of when target emotional states were reached, subjects
in the ‘Feel’ condition reached these states more slowly than
those in the ‘Feel-and-Show’ condition. This suggests that
both cognition and internal experience of emotion as well as
facial expressions indicative of the said emotion are relevant
to emotional experience. Similar results were found by Rus­
alova et al.32 in a study of professional Soviet actors trained
to imagine scenes evocative of joy, fear, anger, and sadness.
For these subjects, the pattern of EMG activity was emotion-
specific for all four conditions; moreover, EMG activity was
highest in the spontaneous conditions (feel the emotion and
express it), intermediate in the suppress-­expression condition
(feel the emotion but not express it), and lowest in the condi­
tion where subjects expressed the emotion and suppressed the
feeling.
Overall, a substantial body of work has identified specific
EMG and EEG responses to positive and negative emotion-
evoking stimuli. Feeling bad or unhappy by recalling specific
events or being cued by an external image has been shown
to be associated with an increase in corrugator (brow furrow­
ing; frowning) muscle33,34 and a decrease in right frontal alpha
­activity.35,36 Remembering pleasant events or seeing positive
images is associated with a selective up-regulation of ­zygomatic
Fig. 2-8  Subjects who had two golf tees attached to either side
of their foreheads and were asked to try to move these together so
as to simulate a frown concurrently rated unpleasant photographs
more negatively than subjects who viewed the same photographs
but did not simultaneously attempt the movement (Larsen, Kasimatis,
and Frey).

17
Understanding facial expression  •  Chapter 2
(mouth corner raising; smiling) muscle firing37 and a decline
in left frontal alpha activity.38–40 Others have shown that even
when incident stimuli are processed unconsciously, with the
subject distracted by other sounds, the same EMG and EEG
results are observed. In one study that identified ‘repressors’
as those with self-reported psychological questionnaire scores
indicative of repressive emotional tendencies, experimental
differences on EMG were found between repressors and non­
repressors: Repressors displayed more intense EMG responses
to unconscious versus conscious words.
Neuropsychological and brain imaging studies, including
functional magnetic resonance imaging (MRI) and positron
emission tomography (PET) scans, have localized the gen­
eration of specific facial emotional to particular areas of the
brain. Fearful facial expressions are associated with increased
activation of the left amygdala,41 disgust expressions with both
the basal ganglia and the insula, sad expressions with the left
amygdala and right temporal pole, and angry expressions with
the orbitofrontal and anterior cingulated cortex. ­ Moreover,
elegant experiments have confirmed the surprising finding
that facial affect and facial identity are processed separately
in the brain. Thus, prosopagnosics, patients who have suf­
fered brain damage of the right-occipital temporal cortex and
consequently lose the ability to recognize faces, can respond
emotionally to emotional facial expressions without knowing
who the person is. Similarly and inversely, after injury to the
orbitofrontal cortex and amygdala, patients can identify faces
but cannot recognize or respond to facial expressions.
CONCLUSIONS FROM FACIAL
FEEDBACK STUDIES
The conclusions derived from EMG and EEG investigations
of facial emotional expressions have limitations. On the one
hand, many investigations have reaffirmed the importance
of the corrugator region as a fundamental discriminator of
negative emotional states, including sadness, anger, and fear.
Indeed, this primacy of corrugator supercilii was foreshad­
owed by Darwin, who dubbed it the muscle of ‘disturbance.’
However, the impact of other muscle groups is less clear. The
frontalis, also involved in displays of sadness and fear, with the
inner and outer fibers raised in surprise, has been less exten­
sively studied. Despite the similarity in emotional effect to the
corrugator, the frontalis is difficult to isolate even with precise
placement of electrodes since EMG signals are corrupted by
interference from adjacent muscle groups. Similarly, the orbic­
ularis oculi, shown to be activated in the genuine Duchenne
smile, is less successfully analyzed with regard to its involve­
ment with other positive emotions.
There have also been criticisms of investigations of the
­facial feedback hypothesis that utilize facial expression coding
systems. One concern is that such studies contain cues that lead
participants to behave in certain ways.37 A similar worry is that
instructions regarding facial expressions are silly or embar­
rassing, thus potentially changing emotional responses.42–44
Both these concerns have been largely overcome by more
subtle experiments, with consistent results obtained regard­
ing the induction of positive and negative emotional expres­
sions. It has also been argued that because certain expressions
are difficult for participants to create, negative emotions may
be confounded with difficulty of manipulation. That is, par­
ticipants may like smiling better just because smiling is easier
than frowning. Ekman and others have definitively refuted this
challenge by demonstrating that the degree of effort required
to produce a facial emotional expression is unrelated to the
negative or positive valence of the same.45,46 In general, there
is convincing evidence supporting the ‘dimensional’ model of
the facial feedback hypothesis, in which negative facial expres­
sions beget negative moods and vice versa. The evidence dem­
onstrating the validity of the ‘categorical’ model, the capacity
of specific facial expressions to elicit specific emotions, is less
complete.
CONSIDERATIONS
IN SUBPOPULATIONS
In addition to the general features of the facial feedback
hypothesis and facial expression modulation discussed thus
far, there are many special cases and subpopulations that
have been studied. For one, demographic features such as
age, ­gender, and developmental stage may impact facial emo­
tional expressions. A relatively consistent finding, for instance,
is that when environmental cues are reduced, men have
­better autonomic self-perception than women, and are more
able to detect their own emotionally relevant physiological
changes, such as heartbeat. This suggests that facial feedback
effects would be more notable in men than in women, espe­
cially to the extent that self-awareness enhances noticing of
these effects.47 Among young children, categorizing of facial
expressions of basic emotions at better than chance levels has
been demonstrated in 2-year-olds, but these discriminations
are less ­accurate than those of older children.48 By the age of
10, recognition of facial expressions reaches a level of quality
comparable to that of adults. During the period from 2 to 10,
the developmental pattern of facial expression identification
favors certain emotions, with happiness and sadness catego­
rized sooner than fear and disgust. Errors of classification in
school-age children most commonly confound expressions
of disgust and anger.49,50 Studies of emotions in older age
are limited, but indicate a decrease in emotional expression
that is associated with decreased autonomic nervous system
activity and less social activity in this age group51 Still, up
to and beyond the seventh decade of life, the basic machin­
ery of facial expression remains intact. In contradistinction

18
Chapter 2
Evaluation of the cosmetic surgery patient
to younger women, older women may be more susceptible
to facial feedback as they report more intense emotional
­experiences ­ associated with relived emotional memories.
Between childhood and old age, individuals’ capacities to
maintain positive facial emotional expressions can result in
significantly improved quality of life.52 In one study, women’s
college yearbook pictures were assessed by trained raters for
degree of positive emotion displayed.53 When subjects were
asked to rate the students in these pictures on several person­
ality dimensions, the women with more positive facial expres­
sions were ranked higher and interactions with these women
were predicted to be more rewarding. More startlingly, posi­
tive emotional expressions were good indicators of favorable
outcomes in marriage and personal well-being up to 30 years
later. These results remained when the photographic rep­
resentations were controlled for physical attractiveness and
social desirability.
As noted previously, the coding systems for facial emo­
tional expressions appear to be valid across cultures. The
cross-cultural similarity of facial expressions has been con­
vincingly established by many investigators, most notably
Ekman and his colleagues. Even when examining cultures
as different from a US adult sample as the matrilineal, Mus­
lim, agrarian Minangkabau of West Sumatra, Ekman found
consistency in the autonomic nervous system differences
­between emotions and in the facial expression of these emo­
tions.54 Of course, minor cultural differences in the expres­
sion of emotion are inevitable. For instance, in the US, the
folk wisdom that ‘smile and the world smiles with you, frown
and you frown alone,’ appears close to the truth.55 Over half
of US subjects respond to a smile with a smile, while few
frown in reaction to a frown.
How individuals manage their facial emotional expressions
can color their social judgments and even affect their mental
health. When asked to evaluate the level of fame of several
celebrities, subjects who were concurrently asked to furrow
their brows reported the same celebrities to be less famous.56
How emotional facial expressions can affect cognitively medi­
ated assessments is not well understood, but some hypotheses
have been advanced. Thus, in a series of conditioning experi­
ments, it was found that angry faces have an excitatory effect
whereas happy faces have an inhibitory effect. The effect of
such induced excitation or relaxation on cognition may be
further modified by the individual’s stable internal emotion­
al style. That is, some subjects appear to be inherently less
expressive, and exhibit less intense and less differentiated facial
emotional expressions. Dysphoric persons are an extreme
example, with these less likely to show an expected increase in
zygomatic EMG activity to happy expressions than a control
group.57 Corrugator activity in response to unhappy images
was the same for the dysphoric and normal subsets, and on
occasion the dysphoric patients even reacted to happy stimuli
with corrugator (frown) response. It appears that dysphoric
individuals have an impaired interpersonal reactivity specific
to happy displays.
FACIAL COSMETIC SURGERY
AND THE FACIAL FEEDBACK
HYPOTHESIS
Facial expressions mediate the experience of emotion, but this
influence is not absolute or exclusive. Factors other than facial
emotional expression, including spontaneous autonomic nerv­
ous system states and active cognition, also affect subjective
emotional experience. Still, it is surprising the extent to which
facial expressions of emotions are these emotions. Regardless
of the response, the fact that Ekman58 can pose the query,
‘Can there be emotion without facial expression?’ confirms
the power of the face.
At issue are more than botulinum toxin injections for
cosmetic improvement of the upper face. While such treat­
ments are the most direct means for modifying the muscles
of facial emotional expression, many other cosmetic interven­
tions have a similar effect. To wit, soft-tissue augmentation
materials infused into the nasolabial folds and perioral areas
can alter the smile and grimace, as well expressions of anger
and sadness. Face lifts, and periorificial laser resurfacing, may
have like impacts, in particular blunting lines around the eyes
and mouth, and generally reducing the ability to dynamically
crease facial skin.
Accentuating positive emotions
Based on the available evidence regarding the facial feedback
hypothesis, alterations in facial expressiveness due to the use of
botulinum toxin and other cosmetic agents may increase the
experience of positive emotions in treated individuals. Sev­
eral types of beneficial changes are possible. For one, patients
receiving treatments to the upper face may have more happy
emotions if they have more difficulty constructing frowns. The
relaxation of the corrugator and adjacent muscles may induce
a reduction in anger and other negative emotions. Unpleasant
life episodes will still be felt, but these will not be reinforced
by equally negative facial expressions; as a result, adverse
events may be perceived as a half-full rather than a half-
empty glass.
Given the phenomena of emotional contagion and facial
mimicry, the treated person’s positive facial expressions would
affect the emotional states of others around them (Fig. 2-9).
Friends, relatives, and bystanders would not only see a younger,
less wrinkled face, but also a happier, more positive person, who
would inspire similar emotions in themselves. If many people
in the social orbit of a given target individual have reduced
anger and sadness facial expressions, the cumulative induction
of positive emotions in this person may be ­substantial.
Apart from feeling better and helping others feel better,
treated individuals may also be healthier after botulinum ­toxin
injections. More than psychological health may be ­ameliorated,
with heart rates, autonomic nervous system ­ activation, and

19
Understanding facial expression  •  Chapter 2
other physiological markers of stress decreased in those who
are less able to maintain negative facial emotional expres­
sions.51 Minor reductions in physiological stress, such as those
deriving from moderate alcohol consumption and social sup­
port, have been previously associated with reduction of physi­
cal morbidity; happier emotional expressions after cosmetic
treatments could possibly also have such an inductive effect.
This may not be that far-fetched since it has already been
shown that habitually positive facial expressions can lead to
better life outcomes decades in the future (see yearbook study,
above). Those who do not have an innate tendency to smile
and look agreeable may achieve similar results by erasing a
lifelong frown or grimace with botulinum toxin. As has been
demonstrated, smiling stimulates the world to smile with you.
It is reasonable to suppose that an endless concatenation of
positive interactions initiated by a baseline warm smile in the
bearer would have a magnified additive effect that would lead
to a happier, more hassle-free life.
Curtailing negative emotions
When adverse circumstances necessitate unhappy feelings,
chemically induced forehead wrinkle reduction can at least
diminish the intensity of negative emotions. Sad, painful,
fearful, infuriating, or depressing events can be accompanied
by facial expressions that while similar in valence are at least
attenuated in degree (Fig. 2-10). This may help affected indi­
viduals to better focus on the positive aspects of a mostly bad
outcome. Also, recovery from misery may be more rapid in the
absence of strongly reinforcing negative facial expressions.
Another benefit accruing from the reduction of negative
expressions would be decreased transparency of the indi­
vidual’s emotional state to external observers. Elimination of
crow’s feet, in particular, appears able to alter manifestations
of the ‘Duchenne smile,’ a contortion not amenable to con­
scious manipulation before the advent of botulinum toxin.
Other so-called ‘reliable’ facial expressions may also succumb
to transformation after cosmetic procedures. Deception is
not a primary goal of facial rejuvenation, but in a competi­
tive world in which people are ever more able to control their
own destinies, there is no reason why they should be helpless
to react to stimuli in predetermined ways, with stock facial
expressions.
At times, positive facial expressions would be inappropriate,
and even with therapeutic levels of botulinum toxin, nega­
tive expressions must necessarily be induced. Fortunately, the
toxin-mediated diminution in negative facial expressions does
not preclude successful communication of ­negative emotions.
Botulinum toxin’s effect is not so complete that all of the mus­
cle groups involved in any particular emotion are blocked
from contracting. Moreover, individuals who are ­ exp­osed
to those treated with toxin are not helpless automatons
Patient looks unhappier
More negative emotion
Patient feels angry,
sad, anxious
Others respond less favorably
in social situations
Patient looks happier
More positive emotion
Patient feels better
Others respond more favorably
in social situations
Age
Botulinum toxin
Fig. 2-9  Facial feedback as it may pertain to botulinum toxin therapy and other facial rejuvenation procedures. Chemical manipulation alters
facial expression, reducing frown lines, leaving the face appearing more happy, and less sad or angry. This more positive facial expression
leads to internal emotional experience of happiness in the affected individual. Additionally, the happy expression elicits happier expressions
from bystanders, thus further reinforcing the happy expression and happy emotional state of the index person.

20
Chapter 2
Evaluation of the cosmetic surgery patient
who must always mimic the expressions they see. When the
­subject and the observer exhibit mutual dislike or ­ distrust
(see the experiments regarding responses to politicians’
­expressions),the subject’s expression can elicit an opposite
expression in the viewer. Finally, as demonstrated in the
‘feel-and-show’ condition, whatever the facial expressions, these
are only part of the complete emotional ­experience. Internal
experience of emotion can modify, either by ­ weakening or
strengthening, the emotional significance of external facial
expressions.
One potentially revolutionary use of botulinum toxin may
be to correct maladaptive emotional patterns early in life.
Children and adolescents with dysfunctional, intensely nega­
tive facial expressions that upset others or dissuade potential
friends from approaching may be treated to change these
expressions. In this manner, children may be saved from the
detrimental effects of social isolation. Additionally, treated
children may be less likely have a disproportionate number
of negative interactions with others; once their own negative
expressions are reduced, the process of mimicry may induce
others who do respond to them to be warm and supportive
rather than angry or dismissive.
CONCLUSIONS
Botulinum toxin, facial fillers, resurfacing, and other cosmetic
procedures can change facial emotional expressions. In partic­
ular, botulinum toxin may reduce negative facial expressions
and enhance positive expressions. Benefits may accrue to both
the treated individuals and those with whom these people
interact. While the precise effects of chemical mediators on
emotional expression and emotions themselves are not well
understood, these effects are likely substantial in extent.
In modern society, the emphasis on cognition has left a
peripheral role for emotions, but facial emotional expressions
remain a major route for communication and transaction. As
Lazarus59 has noted, more so even than conscious thought,
‘emotions contain the wisdom of the ages.’ By better under­
standing and modifying the manifestations of our own emo­
tions, we can improve our own life experience and felicitously
influence that of others. Emotions and emotional expressions
contain information, with botulinum toxin facilitating control
of the dissemination of this knowledge and the associated
A
B
C
D
Fig. 2-10  A middle-aged woman with (A) brows knitted and (B) upward gaze before treatment. The same maneuvers, (C) and (D), induce
fewer dynamic creases and less angry and anxious expression 2 weeks after injection of the glabellar and forehead complex with botulinum toxin.

21
Understanding facial expression  •  Chapter 2
moods. Writing more than a century ago, Edgar Allan Poe
understood the ability of facial expressions to guide lives:
When I wish to find out how wise or how stupid or how good
or how wicked is anyone, or what are his thoughts at the
moment, I fashion the expression of my face, as accurately as
possible, in accordance with the expression of his, and then
wait to see what thoughts or sentiments arise in my mind or
heart, as if to match or correspond with the expression. (The
Purloined Letter, 1844)
REFERENCES
  1. Izard CE. Facial expressions and the regulation of emotions. J Person
Soc Psych 1990; 58:487–498.
  2. McIntosh DN. Facial feedback hypotheses: evidence, implications, and
directions. Motivation Emotion 1996; 20:121–147.
  3. Darwin CR. The expression of emotions in man and animals. Chicago:
University of Chicago Press; 1965:365 (original work 1872).
  4. James W. The principles of psychology (vol 2). New York: Dover
Publications; 1950:463 (original work published 1890).
  5. Gellhorn E. The physiological basis of neuromuscular relaxation. Arch
Intern Med 1958; 102;392–399.
  6. Tomkins SS. Affect, imagery, and consciousness (vol. 1). the positive
affects. New York, Springer; 1963.
  7. Laird JD. Self-attribution of emotion: the effects of expressive behavior
on the quality of emotional experience. J Pers Soc Psych 1974; 29:
475–486.
  8. Ekman P. Facial expressions of emotion: an old controversy and new
findings. Phil Trans R Soc Lond B 1992; 335:63–69.
  9. Gladwell M. The naked face. The New Yorker, August 5, 2002:38–49.
10. Ekman P, Friesen WV. Measuring facial movements. Environ Psychol
Nonverb Behav 1976; 1:56–75.
11. Ekman P, Friesen WV. Facial action coding system: a technique for the
measurement of facial movement. Palo Alto, California: Consulting
Psychologists Press; 1978.
12. Izard CE. The maximally discriminative facial movement coding system
(MAX). Newark, DE: Univ. of Delaware, Instructional Resources
Center; 1979.
13. Ekman P, Levenson RW, Friesen WV. Autonomic nervous system
activity distinguishes among emotions. Science 1983; 221:1208–1210.
14. Levenson R, Ekman P, Friesen WV. Voluntary facial action generates
emotion-specific autonomic nervous system activity. Psychophysiology
1990; 27:363–384.
15. Ekman P, Oster H. Facial expression of emotion. Annu Rev Psychol
1979; 30:527–554.
16. Strack R, Martin LL, Stepper S. Inhibiting and facilitating conditions
of facial expressions: a non-obstrusive text of the facial feedback
hypothesis. J Pers Social Psych 1988; 54:768–777.
17. Larsen RJ, Kasimatis M, Frey K. Facilitating the furrowed brow: an
unobstrusive test of the facial feedback hypothesis applied to unpleasant
affect. Cognition Emotion 1992; 6:321–338.
18. Zajonc RB, Murphy ST, Inglehart M. Feeling and facial efference:
implications of the vascular theory of emotions. Psychol Rev 1989;
96:395–416.
19. Zajonc RB, Murphy ST, McIntosh DN. Brain temperature and
subjective emotional experience. In: Lewis M, Haviland JM, eds.
Handbook of emotions. New York: Guilford; 1993:209–220.
20. Lanzetta JT, McHugo GJ. The history and current status of the facial
feedback hypothesis. Psychophysiology 1986; 23:415–416.
21. Lanzetta JT, Englis BG. Expectations of cooperation and competition
and their effects on observers’ vicarious emotional responses. J Pers Soc
Psych 1989; 56:543–554.
22. McHugo GJ, Lanzetta JT, Sullivan DJ, et al. Emotional reactions to
a political leader’s expressive displays. J Pers Soc Psych 1985; 49:
1513–1529.
23. Hatfield E, Cacioppo JT, Rapson RL. Emotional contagion. Cambridge:
Cambridge University Press; 1994.
24. McIntosh DN, Druckman D, Zajonc RB. Socially-induced affect.
In: Druckman D, Bjork RA, eds. Learning, remembering, believing:
enhancing human performance. Washington, DC: National Academy
Press; 1994:251–276, 364–371.
25. Field TM, Woodson R, Greenberg R, et al. Discrimination and imitation
of facial expressions by neonates. Science 1982; 218:179–181.
26. Dimberg U. Facial reactions to facial expressions. Psychophysiology
1982; 19:643–647.
27. Ekman P, Davidson RJ. Voluntary smiling changes regional brain
activity. Psychol Sci 1993; 4:342–345.
28. Duchenne B. The mechanism of human facial expression or an electro-
physiological analysis of the expression of the emotions (translated by
A. Cuthbertson). New York: Cambridge University Press; 1990 (original
work published 1862).
29. Ekman P, Frisen WV, O’Sullivan M. Smiles when lying. J Pers Soc
Psych 1988; 54:414–420.
30. Ekman P, Roper G, Hager JC. Deliberate facial movement. Child
Develop 1980; 51:886–891.
31. Hess U, Kappas A, McHugo GJ, et al. The facilitative effect of facial
expression on the self-generation of emotion. Int J Psychophysiol 1992;
12:251–265.
32. Rusalova MN, Izard CE, Simonov PV. Comparative analysis of mimical
and autonomic components of man’s emotional state. Aviation Space
Environ Med 1975; 46:1132–1134.
33. Cacioppo JT, Martzke JS, Petty RE, et al. Specific forms of facial EMG
response index emotions during an interview: from Darwin to the
continuous flow hypothesis of affect-laden information processing. J Pers
Soc Psych 1988; 54:592–604.
34. Schwartz GE, Fair PL, Slat P, et al. Facial muscle patterning to affective
imagery in depressed and non-depressed subjects. Science 1976;
192:489–491.
35. Davidson RJ, Schwartz CG, Saron E, Bennett J, Goleman DJ. Frontal
versus parietal EEG asymmetry during positive and negative affect.
Psychophysiology 1979;16:202–203.
36. Wexler BE. Dichotic presentation as a method for single hemisphere
stimulation. In: Hugdahl K (ed), Handbook of Dichotic Listening.
London: John Wiley; 1988.
37. Davidson RJ, Fox NA. Asymmetrical brain activity discriminates
between positive and negative affective stimuli in human infants. Science
1981; 38:169–174.
38. Ahern GL, Schwartz GE. Differential lateralization for positive
and negative emotion in the human brain: EEG spectral analysis.
Neuropsychologia 1985; 23:745–755.
39. Fox NA, Davidson RJ. Taste-elicited changes in facial signs of emotion
and the asymmetry of brain electrical activity in human newborns.
Neuropsychologia 1986; 24:417–422.
40. Breiter HC, Etcoff NL, Whalen PJ, Kennedy WA, Rauch SL, Buckner RL,
et al. Response and habituation of the human amygdale during visual
processing of facial expression. Neuron 1996; 17:875–887.
41. Morris JS, Frith CD, Perrett DI, et al. A differential neural response in
the human amygdale to fearful and happy facial expressions. Nature
1996; 383:812–815.
42. Fridlund AJ. Human facial expression: an evolutionary view. New York:
Academic Press; 1994.
43. Ekman P. Facial expressions of emotions: new findings, new questions.
Psychol Sci 1992; 3:34–38.
44. Levenson RW, Ekman P. Difficulty does not account for emotion-
specific heart rate changes in the directed facial action task.
Psychophysiology 2002; 39:397–405.
45. McHugo GJ, Smith CA. The power of faces: a review of John T.
Lanzetta’s research on facial expression and emotion. Motivation
Emotion 1996; 20:85–120.
46. Winton WM. The role of facial response in self-reports of emotion:
a critique of Laird. J Pers Soc Psych 1986; 50:808–812).
47. Pennebaker JW, Roberts T. Towards a his and hers theory of emotion:
gender differences in visceral perception. J Soc Clin Psychol 1992;
11:199–212.

22
Chapter 2
Evaluation of the cosmetic surgery patient
48. Gosselin P, Larocque C. Facial morphology and children’s
categorization of facial expressions of emotions: a comparison between
Asian and Caucasian faces. J Genet Psychol 2000; 161:346–358.
49. Camras LA. Children’s understanding of facial expressions used during
conflict encounters. Child Develop 1980; 51:879–885.
50. Gosselin P, Pelissier D. The effect of intensity on categorizing facial
emotional prototypes in children and adults. Int J Psychol 1996; 31:
225–234.
51. Levenson RW, Cartensen LL, Friesen WV, et al. Emotion, physiology,
and expression in old age. Psychol Aging 1991; 6:28–35.
52. Kleinke CL, Peterson TR, Rutledge TR. Effects of self-generated facial
expressions on mood. J Pers Soc Psych 1998; 74:272–279.
53. Harker L, Keltner D. Expressions of positive emotion in women’s
college yearbook pictures and their relationship to personality and life
outcomes across adulthood. J Pers Soc Psych 2001; 80:112–124.
54. Levenson RW, Ekman P, Heider K, et al. Emotion and autonomic
nervous system activity in the Minankabau of West Sumatra. J Pers Soc
Psych 1992; 62:972–988.
55. Hinsz VB, Tomhave JA. Smile and (half) the world smiles with you,
frown and you frown alone. Pers Soc Psych Bull 1991; 17:586–592.
56. Strack F, Neumann R. Furrowing the brow may undermine perceived
fame: the role of facial feedback in judgments of celebrity. Pers Soc
Psych Bull 2000; 26:762–768.
57. Sloan DM, Bradley MM, Dimoulas E, et al. Looking at facial
expressions: dysphoria and facial EMG. Biol Psychol 2002; 60:79–90.
58. Ekman P. Facial expression and emotion. Am Psychol 1003; 48:
376–379.
59. Lazarus RS. Thoughts on the relations between emotion and cognition.
In: Scherer KS, Ekman P (eds), Approaches to emotion. Hillsdale, NJ:
Lawrence Erlbaum Associates; 1984:247–257.

BACKGROUND AND HISTORY
As a highly visible organ at the environmental interface, the
skin is subjected to both intrinsic and extrinsic factors that
combine to produce an aged appearance as well as diminished
function.1–3 Intrinsic aging, also called chronologic aging,
occurs at a genetically determined rate throughout the body,
and its skin manifestations can be observed in sun-protected
areas of older people. In contrast, extrinsic aging or photo­
aging is a function of environmental influences, the major
insult being chronic solar ultraviolet radiation.
Chronologic aging primarily causes physiologic changes
in the skin. Epidermal turnover, barrier function, sensory
perception, vitamin D production, immunosurveillance,
­thermoregulation, DNA repair capacity, and mechanical
protection are all reduced during the intrinsic aging process.
Consequences of these changes include slower wound heal­
ing, increased risk of irritant dermatitis, skin cancer, and easy
tearing or shearing of skin. Morphologic changes of intrinsic
aging are relatively subtle and consist of laxity, fine wrinkling,
fat redistribution and a variety of benign neoplasms such as
seborrheic keratoses and cherry angiomata.
Photoaging refers to changes in skin that are largely the
result of ultraviolet (UV) radiation. While the majority of UV
exposure is from the sun, other sources include phototherapy,
arc welding, fluorescent light, and tanning beds. Photoaging
has unique features but also exaggerates many of the changes
seen in chronologic aging (Box 3-1).4 Chronic photodamage
accelerates an aged appearance to the skin, as demonstrated
by the contrast between chronically photoexposed skin on the
neck and the area naturally shielded from ultraviolet damage
by the chin and lower face (Fig. 3-1).
Clinically, photoaged skin is characterized by irregular pig­
mentation, roughness, variable atrophy and hyperplasia, fine
and coarse wrinkling, fat redistribution, telangiectases, and a
variety of benign neoplasms (Figs 3-2, 3-3). Skin cancers occur
most commonly on habitually sun-exposed skin, and the risk
correlates closely with severity of photoaging as well as an
individual’s lifelong cumulative sun exposure. The character
of photoaging is also influenced by skin type, with fair-skinned
individuals (skin types I and II) tending to have generally
atrophic and dysplastic changes (Fig. 3-2), and ­darker-skinned
individuals (skin types III through VI) tending to have hyper­
plastic changes, with prominent coarse wrinkling and textural
change (Fig. 3-4).
The changes in the skin that occur with aging are ­largely
preventable by avoiding photoinjury. However, despite the
availability of excellent sunscreens, in our society, many
­younger people enjoy the appearance of a dark tan and ­ignore
Aging and Photoaging
Michael Abrishami,
Sonia Batra, and
Thomas E. Rohrer
C h a p t e r
3
P A R T 1
Key Points
n Photoaging and skin cancer increase with lifelong
UV exposure.
n Clinically apparent photodamage is related to skin
type, with increased susceptibility in fair-skinned
people.
n All-trans retinoic acid partially restores levels of type I
collagen and ameliorates features of photoaging.
n Broad-spectrum sunscreens can protect against
photoaging and skin cancer.
Box 3-1  Clinical features of photoaging
Irregular pigmentation
Purpura
Roughness
Laxity
Diffuse erythema
Fat redistribution
Telangiectasia
Fine wrinkles
Lentigines
Coarse wrinkles

24
Chapter 3
Evaluation of the cosmetic surgery patient
the ramifications of delayed effects of sun exposure on their
skin. Detection of photodamage and pigmentary alteration
can be enhanced with the use of ultraviolet photography
before such changes become clinically pronounced (Fig. 3-5).
Beyond the burden of skin cancer, demand for cosmetic
treatment of wrinkled, mottled, and coarse skin will surely
increase. The following section focuses on the action spectra
and molecular mechanisms of photoaging.
BASIC SCIENCE
Action spectrum
Terrestrial sunlight contains UV radiation (290–400 nm),
visible light (400–700 nm), and infrared radiation (>700 nm).
While visible light and infrared radiation have negligible
effects on skin, UV radiation has significant deleterious effects.
Fig. 3-1  Photoaging exaggerates many of the features of
­intrinsically aged skin, as evidenced the contrast between
­chronically exposed skin on the neck and the area shielded from
sunlight by the chin and lower face.
Fig. 3-2  This woman with skin phototype II had a history of
­blistering sunburns in childhood and lifelong sun exposure in
­Southern California. Photoaging of the skin is evidenced by
atrophy, wrinkling, solar lentigines, and actinic keratoses.
Fig. 3-3  The dorsal hand of the woman in Figure 3-2 displays
­thinning of the epidermis, subcutaneous fat atrophy, texture
­changes, lentigines and prominent actinic keratoses.
Fig. 3-4  Photoaging of the skin in a Hispanic woman with skin
phototype IV. Note the prominent hyperplastic changes, such as
coarse wrinkling and textural change. This woman had a basal cell
carcinoma on the right nasolabial fold.

25
Aging and photoaging  •  Chapter 3
­Ultraviolet radiation is divided into UVC (200–290 nm), the
most energetic UV wavelengths; UVB (290–320 nm), also
called the sunburn spectrum; and UVA (320–400 nm), also
called black (invisible) light or near-UV. UVC is filtered effi­
ciently by the ozone layer. UVB, which constitutes less than
0.5% of terrestrial sunlight, is responsible for most of the
acute and chronic photoinjury to normal skin.
Ultraviolet rays are reflected, scattered, or absorbed during
their passage through the epidermis and upper dermis. The
depth of penetration of UV is directly related to wavelength
such that the most energetic photons of shortest wavelength
are absorbed more superficially while longer UVB ­wavelengths
tend to penetrate into the epidermis where they may be
­absorbed by nucleic acids. Photon absorption by nucleic acids
rapidly declines with increasing wavelength. Therefore, UVA
rays tend to penetrate more deeply in the dermis where they
are scattered and absorbed by cellular chromophores such as
NADH and riboflavin. On average, approximately 10% of
UVB photons and 50% of UVA photons reach the dermis,
a depth of 0.1–0.2 mm. The corollary is that UVB photons
preferentially affect the epidermis, whereas UVA photons
are equally likely to affect molecular targets in the papillary
­dermis.
Action spectra for acute effects of sun exposure, such as
sunburn and tanning, have been determined experimentally
in humans. The spectra are virtually identical, peaking sharply
in the UVB portion of the spectrum at approximately 300 nm
and falling off exponentially with increasing wavelength over
the UVA range. The curves also closely conform to the action
spectrum for formation of DNA photoproducts such as thym­
ine dimers, strongly implicating UV-induced DNA damage
as a primary etiology. More than 90% of human squamous
cell carcinomas contain UVB ‘signature mutations’ in the p53
tumor suppressor protein and transcription factor. ‘Signature
mutations’ are characteristic DNA base substitutions that can
only result from incorrect repair of UV-induced ­pyrimidine
dimers. Further support for UVB’s major role in photo­
carcinogenesis derives from patients with xeroderma pigmen­
tosum (XP), in which inherited mutations in one of several
loci required for repair of DNA photoproducts results in a
greater than thousandfold increase in skin cancer incidence,
with many patients succumbing to metastatic squamous cell
carcinoma or melanoma in the first decades of life. Pure UVA
irradiation is also capable of causing skin cancers in experi­
mental animals, and lifelong UVA irradiation may contribute
to ­human photocarcinogenesis. Whether the UVA contribu­
tion to photocarcinogenesis is proportionate to the UVA con­
tribution to sunburn and suntanning is a subject of debate.
The action spectrum for human photoaging is least well
studied and remains controversial. It is likely that different
components of the photoaged phenotype (e.g. dyspigmen­
tation versus wrinkling) have different action spectra. For
­example, the epidermal changes of surface roughness and
irregular pigmentation that often characterize photoaged
skin appear at a very early age in patients with XP and are
the features for which the condition was named, strongly
suggesting a relationship to UVB-induced DNA damage. In
contrast, patients with XP do not have prominent wrinkling,
a change presumed to result from damage to dermal targets
by the longer wavelengths seen in UVA. Further, because
of its longer wavelength compared with UVB, UVA is less
affected by atmospheric conditions or altitude. In the action
spectrum for dermal photoaging, one must consider that UVA
is approximately twentyfold more abundant in terrestrial sun­
light, penetrates more deeply into the dermis than UVB and
is not filtered by window glass.5 However, it remains unclear
A
B
Fig. 3-5  Photograph (A) is taken in natural
light and is contrasted with the same area
photographed seconds later with ultraviolet
light (B). Diffuse photodamage and epidermal
pigment changes are evident with the aid
of ultraviolet light. This patient had a lentigo
maligna melanoma and basal cell carcinoma
on the opposite cheek.

26
Chapter 3
Evaluation of the cosmetic surgery patient
­whether it is the occasional UVB photon or the more numer­
ous UVA photons reaching the dermis that account for the
cumulative and long-lasting effects on collagen, elastin, and
the vasculature.
Molecular mechanisms
Progressive changes in individual cells within tissues and
organs presumably lead to aging of the organism. The precise
molecular mechanisms of photoaging are unknown. How­
ever, recent studies have provided new insights into molecular
mechanisms of intrinsic and UV-induced cellular aging that
contribute to the photoaging process.
Studies have demonstrated that the lifespan of cells in vitro
is inversely related to the chronologic age of the donor. Nor­
mal human cells have a finite ability to divide, after which
they remain viable but can no longer undergo mitosis, a state
termed senescence.6 For newborn human fibroblasts, the
number of serial divisions prior to senescence is approximately
60, while fibroblasts from adult donors divide approximately
20 times prior to senescence. Furthermore, cells derived from
individuals with premature aging syndromes generally under­
go senescence far sooner than cells from normal age-matched
controls. It is postulated that in normal aging, tissues contain
a growing population of senescent cells. Such cells would no
longer be able to respond to proliferative signals, for example
during wound healing, and would continue to accumulate cel­
lular damage, These observations suggest that the lifespan and
senescence of cells are under the control of a genetic ‘biologic
clock.’
Several studies suggest the ‘biologic clock’ that determines
replicative senescence and aging is telomere length. Telom­
eres are the terminal portion of eukaryotic chromosomes,
and telomere length is known to decrease with advancing
donor age both in cultured cells and in cells harvested ­directly
from tissue. Adequate telomere length is believed critical to
DNA stability, and sufficient telomere shortening triggers cell
growth arrest or apoptosis (programmed cell death), depend­
ing on the cell type. Consequently, transfecting telomer­
ase into ­cultured ­human cells greatly extends their culture
lifespan.
Factors which intrinsically impact the skin are ­compounded
by the effects of UV-induced damage of both nuclear and
mitochondrial DNA. Mutations in genomic DNA presumably
compromise a variety of protein functions, of which the best
studied is cell growth regulation, and damage to ­mitochondrial
DNA impairs cellular respiration and presumably therefore a
wide variety of metabolic functions.
Photoaging also creates histologic changes in the dermal
extracellular matrix (ECM). In photoaged skin, precursors of
both fibrillar type collagen I and III, the major collagenous
constituents of healthy dermis, are significantly reduced. This
reduction is a result of reduced procollagen biosynthesis and
increased enzymatic breakdown via matrix metalloprotein­
ases. The reduction in these collagens has been shown to cor­
relate well with the clinical severity of photoaging.7,8 Of note,
all-trans retinoic acid, a vitamin A derivative, partially restores
levels of type I collagen in the dermis and ameliorates clinical
features of photoaging.9,10
In summary, the molecular mechanisms responsible for
photoaging are those of intrinsic aging, with the superposi­
tion of UV-induced cell damage. Proliferative senescence in
aging skin coupled with UV-induced DNA and ECM damage
likely work synergistically on a molecular level to contribute to
photodamaged skin.
CLINICAL STUDIES
Epidemiology of skin cancer
Squamous cell carcinoma
Incidence of skin cancers appears to be related to photo­
damage (Table 3-1). The relationship is clearest for squamous
cell carcinoma.11 Both recent and lifetime sun exposure have
been shown to be risk factors for squamous cell carcinoma in
humans.12,13 Premalignant actinic keratoses as well as squa­
mous cell carcinomas are reduced by the use of sunscreen.14–16
An Australian study that entailed application of sun ­protection
Table 3-1  Association of common skin cancers with solar radiation
Cancer type
Associated solar radiation pattern
Squamous
cell carcinoma
Recent and lifetime sun exposure. Cumulative ultraviolet exposure is a risk factor, with highest risk on anatomic
sites receiving heavy sun. Same pattern of solar radiation is associated with the incidence of actinic keratoses,
which can also develop into squamous cell carcinomas.
Basal cell
­carcinoma
Relatively small amounts of sun at an early age. Lesions frequently occur on sites of only moderate cumulative
sun exposure.
Melanoma
Childhood sun exposure and recreational (intermittent) exposure. As with basal cell carcinoma, the timing
of ­exposure appears more important than the cumulative dose. Lentigo maligna type frequently does occur
on anatomic sites of maximal cumulative sun exposure.

27
Aging and photoaging  •  Chapter 3
factor (SPF) 17 sunscreen or vehicle to experimental and
control subjects, respectively, confirmed the protective effect
of the active substance.15 After one summer, patients in the
sunscreen group had on average 0.6 fewer actinic keratoses
than when they had begun, while patients in the control group
had one additional keratosis. Squamous cell carcinoma of the
lip is, similarly, less common in women who use lip protection
than women who do not, or in men.17
The incidence of squamous cell carcinoma appears to be
rising in recent decades. The Rochester Epidemiology Project,
a registry that captures virtually all the inhabitants of Olmsted
County, Minnesota, noted a marked rise in the rate of new
squamous cell carcinomas between 1984 and 1986 (incidence:
46.5/100 000, female; 71.2/100 000, male) and 1990 to 1992
(incidence: 125.9/100 000, female; 155.5/100 000, male).18
The magnitude of the difference was significantly greater
than could be explained by demographic shifts or other
­incidental factors.
Similarly, an Australian study looking at people over 13
years of age found that the rates of squamous cell carcino­
ma rose from 166 to 321 per 100 000 from 1985 to 1995, an
increase of 93%.19
Basal cell carcinoma
Basal cell carcinoma, the other primary non-melanoma skin
cancer, accounts for most of the estimated 1.2 million annual
cases of non-melanoma skin cancer in the United States.20
While most of the 2100 annual deaths from non-melanoma
skin cancer are attributable to squamous cell carcinoma, basal
cell carcinoma generate a greater proportion of patient incon­
venience and medical visits. Surprisingly, there is less evidence
to support the efficacy of sunscreen in the prevention of basal
cell carcinoma.11 Unlike squamous cell carcinoma, basal cell
carcinoma often arise on areas receiving only moderate sun
exposure, such as the upper trunk in men and women and the
lower leg in women.21 Retrospective data indicate that basal
cell carcinoma genesis may be linked to episodic ultraviolet
light exposure at an early age.12,13 Interestingly, recent data
suggest that there is an apparent inverse relationship between
the degree of facial wrinkling and the occurrence of facial
basal cell carcinomas.22
Melanoma
Melanoma may be partly caused by sun exposure, but the
relationship is complex. As in the case of basal cell ­carcinoma,
and in contrast to squamous cell carcinoma, the timing of
solar exposure may be more important than the cumulative
dose.11 The exception is lentigo maligna melanoma, a type
that typically evolves on areas of maximum sun exposure.11
In general, the action spectrum for melanoma is not
known.23 Risk does increase with significant childhood expo­
sure to sunlight,11 and a history of sunburns during child­
hood is positively correlated with the likelihood of eventual
­melanoma.24–27 Data from the Nurse’s Health Study demon­
strated that blistering sunburns at ages 15 to 20, but not after
age 30, were associated with a significantly increased risk (rel­
ative risk of 2.2 for greater than five sunburns).28 Migration
studies have also verified that long periods of sun exposure in
childhood are correlated with heightened melanoma risk in
adulthood.29 Outdoor activity and sun during the early years
of life is also associated with development of greater numbers
of melanocytic nevi, a known risk factor for melanoma.30–32
The mechanisms for melanoma risk via childhood exposure
are not well understood. There may be an age-specific con­
stitutional sensitivity to sunlight, or exposure may be more
pervasive because of greater leisure time and less clothing
worn.21 Nonetheless, exposure during childhood to light suf­
ficient to induce burns is a consistent finding in case-control
studies of melanoma.33
Likelihood of melanoma is actually decreased in persons
with occupational exposure to ultraviolet light as adults.34,35
Recreational exposure to sun, conversely, adds to the base­
line risk of melanoma.11,23,36 Since vacationers and outdoor
enthusiasts are only episodically exposed to sunlight whereas
outdoor workers undergo more constant exposure, intermit­
tent exposure may be the relevant risk factor. On the other
hand, cumulative sun exposure appears to influence the likeli­
hood of melanoma, and patients with a history of actinic ker­
atoses and non-melanoma skin cancer are at increased risk.37
Limited evidence exists that sunscreen use prevents
­mela­noma.11 Though intuitively obvious, the proof of a
beneficial effect is difficult to establish due to methodological
constraints.38–41 Study participants have difficulty precisely
­recalling details, such as degree of sun exposure and number of
burns, from the distant past. Moreover, with use of a sunscreen,
a person may stay in the sun for longer periods and accumu­
late greater ultraviolet light exposure because he or she is not
deterred by sunburns. Studies of sunscreen use in melanoma
have yielded conflicting results.27,42–48 A recent meta-analysis
of the available studies demonstrated no significant protective
effect of sunscreen usage in the development of melanoma,
but also no increased risk of developing melanoma.49
Worldwide incidence of melanoma has been rising for
decades, and this trend precedes the ubiquity of sunscreen.50
It has been postulated that the cause may be increased sun-
related leisure activities made possible by growing affluence
in industrialized nations. Annual incidence rates among
fair-skinned populations have increased 3–7% per year dur­
ing the last three decades.21 An examination of population-
based incidence rates for the period 1973 to 1994 using the
US Surveillance, Epidemiology, and End Results tumor reg­
istries indicated an annual increase in incidence of 3.6% and
an increase in 2-year mortality from melanoma.51,52 Absolute
annual mortality rates range from 1 to 3/100 000 for fair-
skinned people in the northern hemisphere to 5 to 10/100 000
in ­Australia and New Zealand.53–55 In the United States, the
American Cancer Society56 estimates that there will be 62 190
new cases of melanoma in 2006, with melanoma (exclud­
ing basal and squamous cell carcinoma) being the fifth most
­common ­cancer in men (5% of all new cancer cases) and sixth

28
Chapter 3
Evaluation of the cosmetic surgery patient
most common cancer in women (4% of new cancer cases).
Five thousand American men and 2890 American women will
die of melanoma in 2006, and the lifetime risks for melanoma
are 1 in 60 and 1 in 80, respectively, for men and women.
Skeptics have wondered to what extent the growing fre­
quency of melanoma is medically significant.50 More frequent
registration of newly found lesions, vigilant monitoring of
melanocytic lesions by patients and physicians, and submis­
sion of numerous nevi for pathologic diagnosis may contrib­
ute to the apparent increased incidence. Overall, however, the
magnitude of the increase suggests that at least part of the
growing number of melanoma is clinically important. Rates
of melanoma remain higher in those who burn only and never
tan,57 thus providing credence to the view that sun exposure is
likely a major causative factor.
Environmental influences
In addition to increased sun exposure, environmental changes
may be contributing to higher rates of photodamage. Impair­
ment of the ozone layer, a natural shield in the stratosphere
that absorbs much of the damaging solar ultraviolet radia­
tion, may be resulting in more harmful light reaching the
earth’s surface 58 When present in adequate quantities, ozone
blocks all UVC, 90% of UVB, especially wavelengths from
290 to 300 nm, and a small amount of UVA.4,59 Unfortu­
nately, in the early 1980s, scientists amassed evidence that
­chlorofluorocarbons (CFCs) and other synthetic agents were
depleting the ozone layer.58 It has been shown that heavily
populated areas now absorb more ultraviolet radiation than
two decades ago.60
Measures have been devised to quantify the significance
of increased ultraviolet light hitting the planet. The radiation
amplification factor (RAF) is the percentage increase in bio­
logically active ultraviolet light seen by individuals that results
from a 1% decrease in the ozone layer at a particular loca­
tion.61 A similar statistic is the amplification factor (AF), the
percentage rise in non-melanoma skin cancer attributable to a
1% decrease in ozone.62 Estimated AF values of 1.7 for basal
cell carcinoma and 3.0 for squamous cell carcinoma, respec­
tively, point to a substantial growth in incidence of these lesions
if there is a sustained decrease in the thickness of the ozone
layer. Additionally, it has been estimated that a 1% decrease in
ozone increases melanoma mortality by 1–2%.63
Variables other than the ozone layer can affect the amount
of sunlight reaching the earth.58 Ultraviolet light intensity is
maximal at high altitudes, where there is less atmosphere to
absorb incoming radiation. For every 1000 feet in increased
altitude there is an increase of 8–10% in UV intensity. Fur­
thermore, with each degree increase in latitude, there is a 3%
increase in UV radiation reaching the earth’s surface.64 Sea­
sonal influences can result in differential sun exposure, with
ultraviolet intensity in the northern hemisphere greatest in
the summer months, when the incident angle of sunlight is
approximately 90 degrees. Thin cloud cover typically blocks
20–40% of sun-related ultraviolet radiation, and window
glass, virtually 100% of UVB but only 50% of UVA.4,65 Sand,
snow, concrete, and water can reflect up to 85% of sunlight,
thus nearly doubling the ambient ultraviolet exposure. Beach­
goers ostensibly protected by an umbrella may therefore be
subject to the equivalent of direct sunlight due to the proxim­
ity of numerous reflective surfaces. About 50% of ultraviolet
radiation can reach skin submerged in shallow water.4
Smoking
Smoking also appears to contribute to the photoaging process.
Histologically, tobacco smoke and UVA may work synergisti­
cally to induce photoaging by inducing matrix metalloprotei­
nase 1 in an additive manner.66 Matrix metalloproteinase 1
breaks down collagen type I, a major collagenous constituent
of healthy dermis, whose reduction correlates with clinical
photoaging. Clinically, a Finnish study showed that blinded
panelists who evaluated smokers estimated their age to be an
average of 2.1 years higher than their actual chronologic age,
whereas non-smokers were estimated as being an average of
0.7 years younger than their actual age ( p<0.05).67
Tanning
UVA is more efficient at inducing tanning, whereas UVB is
more efficient in inducing erythema.68 Immediate pigment
tanning occurs within seconds of UVA exposure and disap­
pears within 2 hours after exposure. Delayed tanning peaks at
72 hours after UVA exposure and is the result of an increase
in melanocytes, melanosomes and the number of melanocytes
transferred to keratinocytes. While UVB-induced delayed tan­
ning has a SPF of 3, UVA induced tanning is not photopro­
tective.69 Of note, a close correlation has been demonstrated
between erythema and DNA damage. Mutations in the p53
gene have been found in 90% of squamous cell carcinomas,
60% of actinic keratosis, and 50% of basal cell carcinomas.70
Even suberythemal doses of UVR have been shown to induce
reactive oxygen species-mediated DNA damage and pyrimi­
dine dimers.71 Of particular concern is evidence demonstrat­
ing the carcinogenic potential of sun beds in humans (i.e.
DNA alterations and p53 expression in the skin).72–79 A recent
study demonstrated that individuals younger than 36 years
old who regularly use an indoor tanning lamp had 8.1 times
greater risk of melanoma (95% confidence interval [CI]:
1.3–49.5) as compared with never-users.80
The evidence linking sun beds with skin cancer has
prompted the American Academy of Dermatology and the
American Medical Association to discourage their use. Fur­
ther, the World Health Organization has recommend that
persons younger than 18 years should not use indoor UV
radiation tanning devices.81 Nonetheless, a recent study found
that the prevalence of sun bed use was 26% in youth aged 15
to 18 years old, and 40% in girls aged 17 to 18.82 Although
regulations restrict youth-targeted advertising of other car­
cinogens such as tobacco, no regulations limit youth-targeted
advertising of indoor UV tanning.83 Surprisingly, as of 2005,

29
Aging and photoaging  •  Chapter 3
only six US states had in place minimum age limits for UV
tanning patrons: Texas, Illinois, Wisconsin, California, North
Carolina, and New Hampshire. Currently, a proposal is being
introduced in the legislature to have the FDA review ­whether
the current labeling on tanning beds provides adequate
information regarding its risks.
Sunscreens
Mitigation of sun-induced photoaging is possible with the
appropriate use of sunscreens; however, rates of use remain
low in the US. In a survey of beachgoers, 70% indicated that
they were there to get or maintain a tan, and during the average
stay of 4 hours, only half applied sunscreen.84 In the United
States, as few as 25% of sunbathers routinely use a sunscreen
product with sun protection factor (SPF) of 15 or greater.85
The National Canadian Survey of Sun Exposure and Protec­
tive Behaviors revealed that 62% of respondents did not wear
sunscreen on the face, and 68% did not use sunscreen on the
rest of their bodies.86 Young adolescents,87 male college stu­
dents,88 and skiers with past experience of sunburns89 have
been shown to utilize sunscreen at low rates. Childhood expo­
sure continues to be significant, but although past burn history
is a determinant of future sunscreen application,87 as few as
one-third of parents adequately protect their children.90
Definition and rationale for use
Sunscreens are topical preparations designed to reduce ­actinic
damage and prevent sunburn.39 Active ingredients within
sunscreens diminish the amount of ultraviolet radiation pen­
etrating the skin, and optimal sunscreens should block both
UVB and UVA (Table 3-2).91 Most commercially distributed
products contain a number of active compounds that collec­
tively impart broad-spectrum protection. Animal evidence
indicates that sunscreens, especially those with high SPF, can
reduce the visible and microscopic stigmata of ­photoaging.11
­Sunlight-induced skin sagging has been demonstrably reduced
in experimental animals after sunscreen application. Reduc­
tion of risk of certain skin cancers (see previous section) may
also accrue from regular use of sunscreens.
A grading system has been devised to measure sunscreen-
derived protection against erythema, primarily UVB induced
since UVB is 1000 times as erythemogenic as UVA.39 SPF is a
ratio of the amount of ultraviolet radiation required to gener­
ate a minimal erythema response, 24 hours after exposure, in
a sunscreen-protected area of the skin to the amount required
to induce the same degree of erythema in unprotected skin.
Importantly, measurement of sunscreen’s exclusion of UVA is
less standardized than that of UVB, and there is concern that
biologically significant amounts of UVA are able to pierce
even so-called broad-spectrum preparations.11
Historically, sunscreens were classified as physical or chemi­
cal types.39 In view of the active chemical properties of the
sunblocks previously referred to as physical (e.g. titanium
­dioxide, zinc oxide), the preferred terms are now inorganic and
organic compounds.39 Organic compounds in sunscreens may
be primarily useful against UVA or UVB. The major classes
of organic agents available are PABA and its esters (UVB;
e.g. octyl dimethyl PABA), salicylates (UVB; e.g. octyl sali­
cylate), cinnamates (UVB; e.g. 2-ethylhexyl p-methoxycinna­
mate; UVB/UVA; e.g. octocrylene), anthranilates (UVA; e.g.
methyl anthranilate), benzophenones (UVA; e.g. oxybenzone),
dibenzoylmethanes (UVA; e.g. avobenzone, or Parsol 1789),
and benzylidene camphors (UVA; e.g. terephthalylidene
dicamphor sulfonic acid, or Mexoryl SX). The major classes
of inorganic agents are zinc oxide and titanium oxide. Both
provide broad-spectrum protection although they tend to be
more opaque than the inorganic blockers. Users of sunscreen
should be aware that the polarity and pH of a particular com­
bination of solvents and active compounds can influence the
absorption maxima of a given sunscreen;92 in other words,
not all sunscreens with similar compositions are equally
Table 3-2  Active ingredients of sunscreens
Organic sunscreens
Inorganic Sunscreens
Class
Examples
PABA and its esters
Octyl dimethyl PABA (UVB)
Zinc oxide
Salicylates
Octyl salicylate (UVB)
Titanium dioxide
Cinnamates
2-ethylhexyl p-methoxycinnamate (UVB)
­octocrylene (2-ethylhexyl-2-cyano-3,
3-diphenyl-acrylate) (UVB/UVA)
Anthranilates
Methyl anthranilate (UVA)
Benzophenones
Oxybenzone (UVA)
Dibenzoylmethanes
Avobenzone (butyl methoxydibenzoylmethane
[Parsol 1789]) (UVA)
Benzylidene camphors
Terephthalylidene dicamphor sulfonic acid
(Mexoryl SX) (UVA)

30
Chapter 3
Evaluation of the cosmetic surgery patient
­protective. The ability of a sunscreen product to maintain its
effectiveness, especially when exposed to water, is a desirable
feature.
Method of application
To benefit from sunscreens to the full extent of their SPF
labeling, users must apply them in a prescribed manner.11 In
the United States, SPF values are determined on the basis of
testing at 2 mg/cm2, and in Europe the hypothetical delivery
is defined as 1.5 mg/cm2. If less than these amounts is used,
the corresponding sun protection will be diminished.93,94 Sur­
vey data suggest that actual usage of sunscreen is far below
recommended amounts, with layering usually in the range
0.5–1 mg/cm2, effectively lowering the SPF.95 While the evi­
dence indicates that few people use sunscreen correctly, regu­
latory authorities have not required manufacturers to correct
displayed SPF values to reflect this reality. Public health mes­
sages impressing the need for adequate thickness layering of
sunscreen also remain rare.
Use in vulnerable populations
Sunscreen use in special populations has been investigated.
Among the elderly, few are likely to develop skin cancers or
visible photodamage from current sun exposure, yet sunscreen
may be useful to prevent acute burns.11 The active elderly, who
engage in outdoor sports and have a significant life expectancy,
may benefit from more deliberate sunscreen use comparable
to that in younger adults. Older patients treated for actinic
keratoses or non-melanoma skin cancers can become exceed­
ingly anxious about future sun exposure. Such patients should
be reassured that major lifestyle changes are not required for
health maintenance.
Some recommend that sunscreen should not be applied to
children younger than 6 months.39 The theoretical concern is
that infants may be unable to metabolize the chemicals within
these preparations.96 Until babies are able to move independ­
ently, they may be best sheltered from the sun by strict sun
avoidance and clothing. The Australian Cancer Society, in
concert with the Australasian College of Dermatologists, has
recommended that sunscreen be used on babies when physical
protection, such as apparel, is inadequate.97 In its policy state­
ment regarding ultraviolet light-related hazards to children,
the American Academy of Pediatrics98 states that in infants
it may be reasonable to apply sunscreen to small, otherwise
poorly protected areas, such as the face and the back of the
hands.
Microbiologic and histologic benefits
Suberythemal doses of UVB can induce immunosuppression,
and sunlight has been observed to suppress resistance to infec­
tion.99 In an Italian study, 100 minutes of solar exposure at
midday resulted in clinically notable reduction in resistance to
infection with Listeria monocytogenes.100 Use of sunscreens may
decrease ultraviolet light-induced immunosuppression.101–105
Occurrence of ultraviolet-induced herpes labialis has been
shown to be prevented by judicious use of lip balm containing
sunscreen.106
Sunscreens also reduce histologic signs of photodamage.
Skin biopsies have verified that regular application of an SPF
30 sunscreen over a period of 24 months results in a signifi­
cant decrease in solar elastosis compared with control sites.107
Combined UVA- and UVB-blocking preparations are believed
to be most effective in minimizing histologic photoeffects.
Safety
Habitual use of sunscreens appears to be safe. Repeated appli­
cations by millions in the United States alone has not resulted
in reports of serious ill effects. Photoallergic contact dermati­
tis has been seen with sunscreen use, but allergy to the active
ingredients is rare.11,39 Irritant reactions are far more likely
than allergy.108 Other side effects include accidental migration
or spreading of sunscreen to the eyes, which can cause irrita­
tion, redness, or tearing.5
The photochemistry of sunscreens has been partially eluci­
dated. The protective process entails the reflection or absorp­
tion of ultraviolet radiation by sunscreen molecules that must
then re-enter a ground state by dissipating this energy.39 Stored
energy is likely dissipated via fluorescence, phosphorescence,
self-quenching, and heat generation.109 Some speculate that
the associated photochemical reactions may create reactive
oxygen species and other photoproducts that may subsequent­
ly react with cellular proteins, RNA, or DNA. While this has
never been shown to occur in a medically significant manner,
additional research may help confirm the long-term safety of
sunscreens.109,110
Other photoprotective strategies
Clothing and apparel
In some patients, sunscreen use may be inadequate. Sun­
screens may be avoided because they are perceived as unat­
tractive, uncomfortable, messy, or expensive.111 Alternatively,
for some fair-skinned individuals, even diligent sunscreen use
may not provide sufficient protection. Both these groups may
benefit from wearing clothing that filters sunlight effectively.
Transmission of ultraviolet radiation through fabric is quanti­
tated by the ultraviolet protection factor (UPF), which can be
determined experimentally for any piece of cloth.112 Weave,
weight, color, and stretch contribute to the UPF, and a higher
UPF is more effective.113,114 SPF rises with mass and weight,
yet the relationship is not linear. Closely knit/densely woven
fabrics are associated with higher SPF, and dyeing fabrics
tends to greatly enhance their sun-blocking properties.111,115
Moisture can diminish the SPF of clothing. For instance, the
average T-shirt has an SPF of 15 when dry, but merely SPF 5
when wet.116 Maximally protective clothing may have an SPF
as high as 36.
In addition to clothing, other devices may be used to reduce
sun exposure, particularly to the upper body. A hat with a

31
Aging and photoaging  •  Chapter 3
7–10 cm brim can reduce head and neck ultraviolet exposure
by as much as 70%, equivalent to an SPF of 3 to 4.115 Hats
and caps with partial or less wide brims are less effective at sun
protection and may provide adequate coverage for only part
of the face.117 Eye protection has recently been recognized
as a vital component of a complete sun protection regimen.
Melanoma of the uveal tract, the most common primary
intraocular neoplasm in adults, is associated with a tendency to
sunburn and with intense exposure to ultraviolet radiation.118
The American Academy of Ophthalmology states that excess
exposure of the eyes to ultraviolet radiation can cause painful
burns of the cornea and that long-term exposure to ultraviolet
radiation may increase the incidence of cataracts, pterygium,
and possibly macular degeneration.119 Sunglasses can effec­
tively protect the eye and eyelids, with larger, curved glasses
extending this coverage to the lateral periocular area. Since
no uniform labeling system currently exists for the protective
efficacy of sunglasses, patients should read package descrip­
tions carefully before purchase.
Behavioral change
Various other protective behaviors can further reduce photo­
damage sustained from sunlight and artificial sources of ultra­
violet radiation. Avoiding the sun during the midday hours,
when incident solar radiation is at its peak, can greatly reduce
cumulative exposure 39 Similarly, parents of schoolchildren
should modify the scheduling of team sports or outdoor school
functions to earlier or later day hours. At the urging of pro­
fessional medical organizations, media outlets have in recent
decades begun to broadcast messages encouraging photopro­
tection. Soundbites that have been loudly propagated include
the observation that a tan is a response to injury rather than
a healthy change in appearance;39 that people obtain up to
80% of their lifetime sun exposure before age 18;119 that skin
cancer can be prevented by sun avoidance, and is curable
if detected early;24 and that cosmetically undesirable photo­
aging can result from unprotected tanning.
Public policy
Policy makers have also become more animated in address­
ing issues related to photodamage. Thus, the American Acad­
emy of Dermatology and the Centers for Disease Control
and Prevention Consensus Conference have adopted a set
of ­ guidelines for appropriate sun protection (Box 3-2).120
Recommendations include limiting exposure to ultraviolet
light, especially between 10 a.m. and 4 p.m.; wearing protec­
tive clothing and sunglasses; using sunscreen with SPF of at
least 15 in combination with SPF lip balms; avoiding artifi­
cial tanning devices; and encouraging children to practice the
shadow rule, which notes the importance of seeking shade at
times when ultraviolet exposure is high, as indicated by one’s
shadow being shorter than oneself.
Box 3-2  Guidelines for appropriate sun protection
Behavior
Limit exposure to ultraviolet radiation, especially between 10 a.m. and 4 p.m.
Seek shelter in shaded areas if outdoors for a prolonged period.
Avoid artificial tanning devices.
Modify daily sun protection measures based on the local UV index reading.
Conduct self-examinations for melanoma based on the ABCD rule.
Apparel
Wear protective clothing that is colored, closely knit, and dry. Use hats with 10 cm brims.
Cover the eyes with wrap-around sunglasses that completely block ultraviolet light.
Sunscreen
Apply sunscreen with SPF of at least 15 to all exposed body surfaces every day.
Substitute more protective sunscreen when in bright light or during long exposures.
Include the daily application of lip balm with SPF protection.
Select broad-spectrum sunscreen products including UVB and UVA blocking agents.
Children
Protect infants from sun exposure, and use protective ­garments when outdoors.
If necessary for adequate protection, apply sunscreen to infants younger than 6 months.
Encourage children to follow the ‘shadow rule.’
Provide children with sun-safe play areas.
Model appropriate behaviors for children to imitate.

32
Chapter 3
Evaluation of the cosmetic surgery patient
At present, shade is often difficult to find in schoolyards,
where the competing need to construct sports fields results
in areas bereft of trees.121 Wide umbrellas can provide per­
sonal shade, but their use is often impractical, particularly for
­active children.119 Slowing and eventually correcting the loss
of ozone in the stratosphere is an even greater public policy
challenge. Until this is accomplished, the public must be made
aware of impending increases in solar radiation. In 1994, the
National Weather Service, in cooperation with the US Envi­
ronmental Protection Agency and the Centers for Disease
Control and Prevention, initiated the ‘UV index’ for 58 cities
(Table 3-3).121 This index rates the intensity of ultraviolet light
reaching the surface at a particular location and time. Satel­
lite measurements of total ozone are used in the computation
of the UV indices. Ratings range from very high (10+: fair-
skinned persons may burn in less than 5 minutes), to high (7–
9: burn in 10 minutes), moderate (5–6: burn in 15 ­minutes),
low (3–4: burn in 20 minutes), and very low (0–2: burn in
greater than 1 hour). More effective patient education may
result in reduced rates of photodamage in the future. It has
been suggested that inculcation regarding the harmful effects
of sunlight should begin as early as age 3.24 Messages should
be tailored to children’s ages and levels of sophistication, and
authorities agree that parents can contribute by modeling
responsible photoprotective behaviors.
Sunlight and vitamin D
Vitamin D is a hormone that is made naturally in the
skin. The precursor to vitamin D exists in the skin as
7-­dehydrocholesterol, which is converted to previtamin D3
when exposed to solar ultraviolet B (UVB) radiation of 290–
315 nm wavelength. Previtamin D3 undergoes thermal isomer­
ization to form vitamin D3. Once formed, vitamin D3 enters the
circulation and is bound to the vitamin D-binding protein.122
In addition to being recognized as vital to the prevention
of osteoporosis, there has been recent evidence linking
vitamin D deficiency to colon,123 breast,124,125 ovarian,126 and
prostate127 cancer. Vitamin D inadequacy has been reported
in approximately 36% of otherwise healthy young adults.128
Given this information, controversy has recently emerged
regarding the health effects of sunlight exposure. In particular,
there has been concern that UVB-absorbing sunscreens may
interfere with vitamin D synthesis in human skin. The data
suggest that this concern is unfounded. In one study, when
SPF 17 sunscreen was applied continuously during one sum­
mer, there was no marked alteration in vitamin D levels.129
A double-blind, randomized, placebo-controlled trial that
lasted 7 months also did not detect any decrease in mean
levels of vitamin D and its precursors in patients using sun­
screens.129 Even intensive sun protection practiced by xero­
derma pigmentosum patients over a 6-year period was not
associated with abnormal vitamin D levels.130 When consid­
ering the risk of developing skin cancer secondary to excessive
sun exposure, vitamin D may best be obtained by eating a diet
rich in fortified foods and possibly judicious ­supplementation.
­Additionally, a range of sun exposure based on skin type
might be indicated: from 5 min a day three times a week for
light-skinned individuals to 10 min a day three times a week
for darker-skinned individuals.131
Chemoprevention
Sporn defined cancer chemoprevention in 1976 as the use of
natural, synthetic, or biologic chemical agents to reverse, sup­
press, or prevent carcinogenic progression.132 While cancer
chemoprevention is an appealing topic, to date, the evidence
in skin cancer has been mixed.133 Trials in both the primary
prevention and adjuvant settings have shown no benefit for
either beta carotene or selenium.134–136
Cyclooxygenase (COX) inhibitors and statins are two
promising area for chemoprevention research. Most tissues
Table 3-3  UV Index exposure categories
Numerical index
Word index
Recommendations
10+
Very high
Very high risk of harm from unprotected sun exposure. Fair-skinned persons
may burn in less than 5 minutes. Outdoor workers and vacationers at especially
high risk.
7–9
High
High risk of harm from unprotected sun exposure. Fair-skinned persons may burn
in less than 10 minutes.
5–6
Moderate
Moderate risk of harm from unprotected sun exposure. Fair-skinned persons may
burn in less than 15 minutes.
3–4
Low
Low risk of harm from unprotected sun exposure. Fair-skinned persons may burn
in less than 20 minutes.
0–2
Minimal
Minimal danger from the sun’s ultraviolet radiation for the average person. Most
people can stay in the sun for up to 1 hour during the hours of peak sun strength,
10 a.m. to 4 p.m., without burning. People with very sensitive skin and infants
should always be protected from prolonged sun exposure.

33
Aging and photoaging  •  Chapter 3
express COX-1 constitutively whereas COX-2 is inducible,
and increased levels are seen with inflammation and in many
types of cancer.137–140 Immunohistochemical analysis suggests
that squamous cell carcinomas (SCCs) are significantly more
likely to be COX-2 positive (p<0.01) than normal skin.141 In
addition, a retrospective examination in 83 white subjects
found that COX inhibitor users had significantly lower rates
of melanoma outcome measures (odds ratio 0.08; 95% con­
fidence interval 0.01–0.77; p=0.03).142 Limited studies look­
ing at statins have found similar results. For example, a study
of 6605 individuals demonstrated a significantly decreased
incidence of new melanomas in the lovastatin arm compared
with the placebo arm (27/3301 versus 14/3304; p=0.04).143
The majority of the data on chemoprevention and skin
cancer comes from the retinoid literature. Retinoids (vitamin
A and its analogs) are modulators of differentiation and pro­
liferation of epithelial cells. They have the capacity to regu­
late gene expression through transduction signal modulation
mediated by nuclear retinoid receptors. Studies elucidating
the role of systemic retinoids in chemoprevention have had
mixed results. For example, the Southwest Skin Cancer Pre­
vention Study Group treated 525 patients with at least four
prior non-melanoma skin cancer with daily retinol, isotretin­
oin, or placebo for 3 years and found no beneficial chemopre­
ventive effect from either retinol or isotretinoin.144 Similarly,
the Isotretinoin-Basal Cell Carcinoma Prevention Trial, which
treated 981 patients with two or more biopsy-proven basal cell
carcinomas (BCCs) within 5 years of enrollment with daily
low-dose isotretinoin (10 mg) or placebo for 3 years, found that
isotretinoin did not prevent BCC.145
On the other hand, several trials have shown clear benefit
of retinoids in preventing progression of actinic keratosis (AK)
or the development of SCCs. In particular, the Skin Cancer
Prevention-Actinic Keratosis trial randomized 2297 subjects
at moderate risk to oral retinol (25 000 IU/day) or placebo for
up to 5 years and found that it prevented SCC (p=0.04) but
not BCC.146 Similarly, patients with xeroderma pigmentosum
have been shown to benefit from retinoid therapy. Kraemer
et al. found that patients with XP who were treated with oral
isotretinoin for 2 years had a 63% average risk reduction,
although the positive effect tapered once therapy was discon­
tinued (p=0.007).147 Similar results have been seen in renal
transplants patients using oral retinoids.148 Finally, in a paired
analysis of patients with psoriasis treated with psoralen-UVA,
which compared each patient’s own tumor experience while
using and not using retinoids, retinoid use was associated with
a 30% reduction in SCC incidence (p=0.002).149
In conclusion, while a variety of agents hold future promise
in skin cancer chemoprevention, retinoids appear to be the
most effective at this time. Retinoids are more beneficial in
patients with earlier stages of premalignancy than in patients
with resected or overt malignancies. The studies done in
patients with xeroderma pigmentosum and renal transplants
suggest that retinoids have a preventive role in the develop­
ment of squamous cell carcinomas.
DISCUSSION
Anyone exposed to sufficient sunlight will develop photoaging.
For fair-skinned people, the extent of this damage will be pro­
portionately greater, as will the likelihood of sun-induced skin
cancer. Unfortunately, even the most strident public declara­
tions by dermatologists may have limited impact on changing
behaviors. While the attractiveness of a ‘healthy tan’ is imme­
diately apparent, the adverse effects are delayed and often
perceived as hypothetical. Changes in behavior may thus be
more effectively induced by itemizing not only the horrors
of cancer but in addition the deleterious cosmetic effects of
premature photoaging. Physical beauty is associated with high
self-esteem, social success, and career advancement. If people
are convinced that any short-term gains from sun exposure
will be vastly outweighed by a protracted period of impaired
physical appearance, they may be reluctant to expose them­
selves to excessive sunlight.
REFERENCES
  1. Gilchrest BA, ed. Photodamage. Cambridge, Mass: Blackwell Science,
1995.
  2. Gilchrest BA, Bohr VA, eds. The Role of DNA Damage and Repair
in Cell Aging. New York: Elsevier Scientific, 2001 :255.
  3. Yaar M, Gilchrest BA. Aging of the skin. In: Freedberg IM, Eisen AZ,
Wolff K, et al., eds. Fitzpatrick’s dermatology in general medicine, 5th
edn. New York: McGraw-Hill; 1999 :1697–1706.
  4. Kaminer MS. Photodamage: magnitude of the problem. In: Gilchrest
BA, ed. Photodamage. Cambridge, Mass: Blackwell Science, 1995.
  5. Kullavanijaya P, Lim H. Photoprotection. J Am Acad Dermatol June
2005; 52:937.
  6. Linskens MH, Harley CB, West MD, et al. Replicative senescence and
cell death. Science 1995; 267(5194):17.
  7. Fisher GJ, Wang ZQ, et al. Pathophysiology of premature skin aging
induced by UV light. N Engl J Med 1997; 337:1419–1428.
  8. Griffiths CEM, Russman AN, et al. Reduced type I and type III
procollagens in photodamaged adult human skin. J Invest Dermatol
1995; 105:285–290.
  9. Talwar HS, Griffiths CEM, et al. Restoration of collagen formation
in photodamaged human skin by tretinoin. N Engl J Med 1993;
329:530–535.
10. Watson R, Griffiths CEM. Pathogenic aspects of cutaneous
photoaging. J Cosmetic Dermatol 2005; 4:230–236.
11. McLean DI, Gallagher R. Sunscreens: use and misuse. Dermatol Clin
1998; 16:219–226.
12. Gallagher RP, Hill GB, Badjik CD. Sunlight exposure, pigmentary
factors, and risks of nonmelanoma skin cancer, part I: basal cell
carcinoma. Arch Dermatol 1995; 131:164–169.
13. Rosso S, Zanetti R, Martinez C. The multicentre south European
study ‘Hellos,’ part II: different sun exposure patterns in the etiology
of basal cell and squamous cell carcinomas of the skin. Br J Cancer
1996; 73:1447–1454.
14. Naylor MF, Boyd A, Smith DW. High sun protection factor sunscreens
in the suppression of actinic neoplasia. Arch Dermatol 1995; 131:
170–175.
15. Thompson SC, Jolley D, Marks R. Reduction of solar keratoses by
regular sunscreen use. N Engl J Med 1993; 329:1147–1151.
16. Miyagi T, Bhutto AM, Nonaka S. The effects of sunscreens in UVB
erythema and Langerhans’ cell depression. J Dermatol 1994; 21:
645–651.

34
Chapter 3
Evaluation of the cosmetic surgery patient
17. Pogoda JM, Preston MS. Solar radiation, lip protection, and lip cancer
risk in Los Angeles County women. Cancer Causes Control 1996;
7:458–463.
18. Gray DT, Suman VJ, Su WPD, et al. Trends in the population-based
incidence of squamous cell carcinoma of the skin first diagnosed
between 1984 and 1992. Arch Dermatol 1997; 133:735–740.
19. Staples M, Marks R, Giles G. Trends in the incidence of non-
melanocytic skin cancer treated in Australia 1985–1995: are primary
prevention programs starting to have an effect? Int J Cancer 1998;
78:144–148.
20. Chuang T-Y, Reizner GT, Elpem DJ, et al. Squamous cell carcinoma
in Kauai, Hawaii. Int J Dermatol 1995; 34:393–397.
21. Marks R. Epidemiology of melanoma. Clin Exp Dermatol 2000;
25:459–463.
22. Brooke RCC, Newbold SA. Discordance between facial wrinkling and
the presence of basal cell carcinoma. Arch Dermatol 2001; 137:
751–754.
23. Weinstock MA, Lim HW, DeLeo V, et al. Tanning, tanning booths, and
melanoma: risky or protective? J Am Acad Dermatol 1999; 41:84–87.
24. Lim HW, Bergfeld W. Prevention strategies. J Am Acad Dermatol
1999; 41:95–96.
25. Zanetti R, Franceschi S, Rosso S, et al. Cutaneous melanoma and
sunburns in childhood in a southern European population. Eur J
Cancer 1992; 28A:1172–1176.
26. Cross RD, Holly EA, Ahn DK. Cutaneous melanoma in women, part V:
characteristics of those who tan and those who burn when exposed to
summer sun. Epidemiology 1995; 6:538–543.
27. Holly EA, Aston DA, Cross RD, et al. Cutaneous melanoma in
women, part I: exposure to sunlight, ability to tan, and other risk
factors related to ultraviolet light. Am J Epidemiol 1995; 141:923–933.
28. Weinstock MA, Colditz GA, Willett WC. Nonfamilial cutaneous
melanoma incidence in women associated with sun exposure before
20 years of age. Pediatrics 1989; 84:199–204.
29. Khlat M, Vail A, Parkin M, et al. Mortality from melanoma in
migrants to Australia: variation by age at arrival and duration of stay.
Am J Epidemiol 1992; 135:1103–1113.
30. Harrison SL, MacLennan R, Speare R, et al. Sun exposure and
melanocytic nevi in young Australian children. Lancet 1994;
344:1529–1532.
31. Green A, Siskind V, Hansen ME, et al. Melanocytic nevi in school­
children in Queensland. J Am Acad Dermatol 1989; 20:1054–1060.
32. Fritschi L, McHenry P, Green A, et al. Nevi in schoolchildren in
Scotland and Australia. Br J Dermatol 1994; 130:599–603.
33. Autier P, Dore JF. Influence of sun exposures during childhood and
during adulthood in melanoma risk. Int J Cancer 1998; 77:533–537.
34. Elwood JM, Gallagher RP, Hill GB. Cutaneous melanoma in relation
to intermittent and constant sun exposure – the Western Canada
Melanoma Study. Int J Cancer 1985; 35:427–433.
35. Gallagher RP, Elwood JM, Yang CP. Is chronic sunlight important in
accounting for increases in melanoma incidence? Int J Cancer 1989;
44:813–815.
36. Elwood JM. Melanoma and sun exposure: contrasts between
intermittent and constant exposure. World J Surg 1992; 16:157–166.
37. Green AC, O’Rourke MG. Cutaneous malignant melanoma in
association with other skin cancers. J Nat Cancer Inst 1985; 74:977–980.
38. Holly EA, Kelly JW, Ahn DK. Risk of cutaneous melanoma by
number of melanocytic nevi and correlation of nevi by anatomic
site. In: Gallagher RP, Elwood JM, eds. Epidemiological aspects of
cutaneous malignant melanoma Boston: Kluwer Academic; 1994:
159–172.
39. Rosen CF. Photoprotection. Semin Cutan Med Surg 1999; 18:
307–314.
40. Rosen CF. Unanswered questions on the use of sunscreens. J Am Acad
Dermatol 1999; 41:87–93.
41. Osterlind A, Tucker MA, Stone BJ. The Danish case-control study
of cutaneous malignant melanoma, part II: importance of UV-light
exposure. Int J Cancer 1988; 42:319–324.
42. Westerdahl J, Olsson H, Masback A. Is the use of sunscreens a risk
factor for malignant melanoma? Melanoma Res 1995; 5:59–65.
43. Beitner H, Norell SE, Ringborg U. Malignant melanoma: aetiological
importance of individual pigmentation and sun exposure. Br J
Dermatol 1990; 122:43–51.
44. Klepp O, Magnus K. Some environmental and bodily characteristics
of melanoma patients: a case-control study. Int J Cancer 1979; 23:
482–486.
45. Autier P, Dore J-F, Schifflers E. Melanoma and use of sunscreens: an
EORTC case-control study in Germany, Belgium and France. Int J
Cancer 1995; 61:749–755.
46. Graham S, Marshall J, Haughey B. An inquiry into the epidemiology
of melanoma. Am J Epidemiol 1985; 122:606–619.
47. Rodenas JM, Delgado-Rodriguez M, Herranz M. Sun exposure,
pigmentary traits, and risk of cutaneous malignant melanoma: a case-
control study in a Mediterranean population: an analysis separating
histogenetic types. Cancer Causes Control 1996; 7:275–283.
48. Holman CDJ, Armstrong BK. Cutaneous malignant melanoma
and indicators of total accumulated exposure to the sun: an analysis
separating histogenetic types. J Natl Cancer Inst 1984; 73:75.
49. Huncharek M, Kupelnick B. Use of topical sunscreens and the risk of
malignant melanoma: a meta-analysis of 9067 patients from 11 case-
control studies. Am J Public Health 2002; 92:1173–1177.
50. Rivers JK. Increased incidence of melanoma: real or epiphenomenon.
J Am Acad Dermatol 1999; 41:93–95.
51. Dennis LK. Analysis of the melanoma epidemic, both apparent and
real: data from the 1973 through 1994 Surveillance, Epidemiology,
and End Results Program Registry. Arch Dermatol 1999; 135:
275–280.
52. Surveillance, Epidemiology and End Results (SEER) Program
Public Use CD-ROM (1973–1994). Bethesda, Md: National Cancer
Institute, Division of Cancer Prevention and Control, Surveillance
Program, Cancer Statistics Branch, May 1997. Based on August 1996
submission.
53. Armstrong BK, Kricker A. Cutaneous melanoma. Cancer Surveys:
Trends Cancer Incidence 1994; 19:219–239.
54. Dennis LK, White E, Lee JAH. Recent cohort trends in malignant
melanoma by anatomic site in the United States. Cancer Causes
Control 1993; 4:93–100.
55. Giles G, Thursfield V. Trends in skin cancer in Australia. Cancer
Forum 1996; 20:188–191.
56.  Cancer Facts and Figures 2006. Report of the
American Cancer Society; pp. 3, 10, 19.
57. Evans RD, Kopf AW, Lew RA. Risk factors for the development of
malignant melanoma, part I: review of case-control studies. J Dermatol
Surg Oncol 1988; 14:393–406.
58. Rubenstein R, Hufford D, Downham T II, et al. The health impact of
solar radiation and prevention strategies: report of the Environment
Council, American Academy of Dermatology, part I: A. Stratospheric
ozone depletion: major or minor health risk? J Am Acad Dermatol
1999; 41:82–84.
59. Coldiron BM. Thinning of the ozone layer: facts and consequences.
J Am Acad Dermatol 1992; 27:653–662.
60. Herman JR, Bhatia PK, Ziemke J, et al. UV-B increases (1979–1992)
from decreases in total ozone. Geophysical Res Lett 1996; 23:2117–
2120.
61. Madronich S, de Gruijl FR. Stratospheric ozone depletion between
1979 and 1992: implications for biologically active ultraviolet-B
radiation and non-melanoma skin cancer incidence. Photochem
Photobiol 1994; 59:541–546.
62. Scotto J, Fears TR, Fraumeni JF Jr. Incidence of nonmelanoma skin
cancer in the United States. National Cancer Institute, National
Institutes of Health, Public Health Service, US Department of Health
and Human Services, Bethesda, Md. NIH Publication No. 83-2433.
April 1983.
63. Kripke ML, Pitcher H, et al. Potential carcinogenic impact of
stratospheric ozone depletion. J Environ Sci Health 1989; 7:53–74.
64. Rigel DS, Rigel EG, et al. Effects of altitude and latitude on ambient
UVB radiation. J Am Acad Dermatol 1999; 40:114–116.
65. Taylor CR, Stern RS, Leyden JJ. Photoaging, photodamage and
photoprotection. J Am Acad Dermatol 1990; 22:1–15.

35
Aging and photoaging  •  Chapter 3
66. Yin L, Morita A, Tsuji T. Skin aging induced by ultraviolet exposure
and tobacco smoking: evidence from epidemiological and molecular
studies. Photodermatol Photoimmunol Photomed 2001; 17(4):178–183.
67. Raitio A, Kontinen J. Comparison of clinical and computerized image
analyses in the assessment of skin ageing in smokers and non-smokers.
Acta Derm Venereol. 2004; 84(6):422–427.
68. Moyal D, Fourtanier A. Acute and chronic effects of UV on skin. In:
Rigel DS, Weiss RA, Lim HW, et al., eds. Photoaging. New York:
Marcel Dekker; 2004 :15–32.
69. Honigsmann H. Erythema and pigmentation. Protodermatol
Photoimmunol Photomed 2002; 18:75–81.
70. DeBuys HV, Levy SB, et al. Modern approaches to photoprotection.
Dermatol Clin 2000; 18:577–590.
71. Van Weelden H, van der Putte SC, et al. UUVA-induced tumors in
pigmented hairless mice and the carcinogenic risks of tanning with
UVA. Arch Dermatol Res 1990; 282:289–294.
72. Whitmore S, Morison W, Potten C, et al. Tanning salon exposure and
molecular alterations. J Am Acad Dermatol 2001; 44:775–780.
73. Adam SA, Sheaves JK, Wright NH, et al. A case-control study of
the possible association between oral contraceptives and malignant
melanoma. Br J Cancer 1981; 44:45–50.
74. Autier P, Joarlette M, Lejeune F, et al. Cutaneous malignant
melanoma and exposure to sunlamps and sunbeds: a descriptive study
in Belgium. Melanoma Res 1991; 1:69–74.
75. Swerdlow AJ, English JSC, MacKie RM, et al. Fluorescent lights,
ultraviolet lamps, and risk of cutaneous melanoma. Br Med J 1988;
297:647–650.
76. Walter SD, Marrett LD, From L, et al. The association of cutaneous
malignant melanoma with the use of sunbeds and sunlamps. Am J
Epidemiol 1990; 131:232–243.
77. Autier P, Dore J-F, Lejeune F, et al. Cutaneous malignant melanoma
and exposure to sunlamps or sunbeds: an EORTC multicenter case-
control study in Belgium, France, and Germany. EORTC Melanoma
Cooperative Group. Int J Cancer 1994; 58:809–813.
78. Westerdahl J, Olsson H, Masback A, et al. Use of sunbeds or sunlamps
and malignant melanoma in southern Sweden. Am J Epidemiol 1994;
140:691–699.
79. Swerdlow AJ, Weinstock MA. Do tanning lamps cause melanoma? An
epidemiologic assessment. J Am Acad Dermatol 1998; 38:89–98.
80. Westerdahl J, Ingvar C, Masback A, et al. Risk of cutaneous malignant
melanoma in relation to use of sunbeds: further evidence for UV-A
carcinogenecity. Br J Cancer 2000; 82:1593–1599.
81. Hartl G. The World Health Organization recommends that no person
under 18 should use a sun bed. World Health Organization Web site.
Available at:
np07/en/.
82. Cokkinides VE, Weinstock MA, et al. Use of indoor tanning sunlamps
by US youth, ages 11–18 years, and by their parent or guardian care­
givers: prevalence and correlates. Pediatrics 2002; 109(6):1124–1130.
83. Francis SO, Burkhardt DH, Dellavalle RP. A banner year for new US
youth access tanning regulations. Arch Dermatol 2005; 141:524–525.
84. Zitser BS, Shah AN, Adams ML. A survey of sunbathing practices on
three Connecticut state beaches. Conn Med 1996; 60:591–594.
85. Koh HK, Bak SM, Geller AC. Sunbathing habits and sunscreen use
among white adults. Am J Public Health 1997; 87:1214–1217.
86. Shovellev JA, Lovato CY, Peters L. Canadian National Survey on
sun exposure and protective behaviors: adults at leisure. Cancer Prev
Control 1998; 2:111–116.
87. Zinman R, Schwartz S, Gordon K. Predictors of sunscreen use in
childhood. Arch Pediatr Adolesc Med 1995; 149:804–807.
88. Vail-Smith K, Felts WM. Sunbathing: college students’ knowledge,
attitudes, and perceptions of risks. J Am Coll Health 1993; 42:21–26.
89. Leinweber C, Campbell HS. High risk sports – spring skiing and
sunburns. Presented at the Third Symposium on the Epidemiology
of Melanoma and Non-melanocytic Skin Cancer; May 27–28, 1996;
Vancouver.
90. Bourke JF, Graham-Brown RAC. Protection of children against
sunburn: a survey of parental practice in Leicester. Br J Dermatol
1995; 133:264–266.
91. Gilchrest BA. A review of skin ageing and its medical therapy. Br J
Dermatol 1996; 135:867–875.
92. Shaath NA. The chemistry of sunscreens. In: Lowe NJ, Shaath NA,
Pathak MA, eds. Sunscreens: development, evaluation and regulatory
aspects, 2nd edn. New York: Dekker; 1997 :313–351.
93. Wulf H-C, Stender I-M, Lock-Andersen J. Sunscreens used at the
beach do not protect against erythema: a new definition of SPF is
proposed. Photodermatol Photoimmunol Photomed 1997; 13:129–132.
94. Stenberg C, Larko O. Sunscreen application and its importance for the
sun protection factor. Arch Dermatol 1985; 121:1400–1402.
95. Bech-Thomsen N, Wulf H. Sunbathers’ application of sunscreens
probably inadequate to obtain the sunprotective factor assigned to the
preparation. Photodermatol Photoimmunol Photomed 1992; 9:242–244.
96. Notice of proposed rule-making on sunscreen drug products for over-
the-counter human use: tentative final monograph. Federal Register.
May 12, 1993; 58:28241.
97. Australian Cancer Society. Policy statement: babies and sunscreen.
Sydney, Australia: Australian Cancer Society, 1998.
98. American Academy of Pediatrics, Committee on Environmental
Health. Policy statement: ultraviolet light: a hazard to children.
Pediatrics 1999; 104:328–333.
99. Walker SI, Young AR. Sunscreens offer the same UVB protection
factors for inflammation and immunosuppression in the mouse. J Invest
Dermatol 1997; 108:133–138.
100. Garssen J, Goettsch W, deGruijl F. Risk assessment of UVB effects
on resistance to infectious diseases. Photochem Photobiol 1996; 64:
269–294.
101. Ho KKL, Halliday GM, Barnetson R. Sunscreens protect epidermal
Langerhans cells and thy-1+ cells but not local contact sensitization
from the effects of ultraviolet light. J Invest Dermatol 1992; 98:720–
724.
102. Reeve VE, Boehm-Wilcox C, Bosnic M, et al. Differential
photoimmunoprotection by sunscreen ingredients is unrelated to
epidermal cis urocanic acid formation in hairless mice. J Invest
Dermatol 1994; 103:801–806.
103. Whitmore SE, Morison WL. Prevention of UVB-induced
immunosuppression in humans by a high sunprotective factor
sunscreen. Arch Dermatol 1995; 131:1128–1133.
104. Wolf P, Donawho CK, Kripke ML. Analysis of the protective effect of
different sunscreens on ultraviolet radiation-induced heat and systemic
suppression of contact hypersensitivity and inflammatory responses in
mice. J Invest Dermatol 1993; 100:254–259.
105. Lavker RM. Cutaneous aging: chronologic versus photoaging. In:
Gilchrest BA, ed. Photodamage. Cambridge, Mass: Blackwell Science;
1995:123–135.
106. Kricker A, Armstrong BK, English DR. Does intermittent sun
exposure cause basal cell carcinoma? A case-control study in Western
Australia. Int J Cancer 1995; 60:489–494.
107. Boyd AS, Naylor M, Cameron GS, et al. The effects of chronic
sunscreen on the histologic changes of dermatoheliosis. J Am Acad
Dermatol 1995; 33:941–946.
108. Foley P, Nixon R, Marks R. The frequency of reactions to sunscreens:
results of a longitudinal population-based study on the regular use of
sunscreens in Australia. Br J Dermatol 1993; 128:512–518.
109. Martincigh BS, Allen JM, Allen SK. Sunscreens: the molecules and
their photochemistry. In: Gasparro FP, ed. Sunscreen photobiology.
Berlin: Springer-Verlag; 1997 :11–45.
110. Knowland J, McHugh PJ, Dunford R. The photochemical potential
of some sunscreens to damage DNA. In: Gasparro FP, ed. Sunscreen
photobiology. Berlin: Springer-Verlag; 1997:47–61.
111. Davis S, Capjack L, Kerr N, et al. Clothing as protection from
ultraviolet radiation: which fabric is most effective. Int J Dermatol
1997; 36:374–379.
112. Ravishankar J, Diffey B. Laboratory testing of UV transmission
through fabrics may underestimate protection. Photodermatol
Photoimmunol Photomed 1997; 13:202–203.
113. Pailthorpe M. Apparel textiles and sun protection: a marketing
opportunity or a quality control nightmare? Mutation Res 1998;
422:175–183.

36
Chapter 3
Evaluation of the cosmetic surgery patient
114. Gies PH, Roy CR, Toomey S. Protection against solar ultraviolet
radiation. Mutation Res 1998; 422:15–22.
115. Marks R, Fraser P. Ozone depletion and human health: fact or
fiction? In: Burgdorf WHC, Katz SI, eds. Dermatology: progress and
perspectives. New York: Parthenon Publishing; 1993:111–114.
116. Jevtic AP. The sun protective effect of clothing, including beachwear.
Australas J Dermatol 1990; 31:5–7.
117. Diffey BL, Cheeseman J. Sun protection with hats. Br J Dermatol
1992; 127:10–12.
118. Holly EA, Aston DA, Char DH, et al. Uveal melanoma in relation to
ultraviolet light exposure and host factors. Cancer Res 1990; 50:5773–
5777.
119. Miller AJ, Gordon S, Gross P, et al. Prevention: public messages. J Am
Acad Dermatol 1999; 41:96–99.
120. Goldsmith L, Koh HK, Bewerse B, et al. Proceedings from the national
conference to develop a national skin cancer agenda: American
Academy of Dermatology and Centers for Disease Control and
Prevention, April 8–10, 1995. J Am Acad Dermatol 1996; 34:822–823.
121. Long CS, Miller AJ, Lee HT, et al. Ultraviolet Index forecast issued
by the National Weather Service. Bull Am Metereol Soc 1996; 64:
792–799.
122. Holick MF, MacLaughlin JA, Clark MB, et al. Photosynthesis of
previtamin D3 in human skin and the physiologic consequences.
Science 1980; 210(4466):203–205.
123. Garland C, Garland F. Do sunlight and vitamin D reduce the
likelihood of colon cancer? Int J Epidemiol 1980; 9: 227–231.
124. Gorham E, Garland C, Garland F. Acid haze air pollution and breast
and colon cancer in 20 Canadian cities. Can J Public Health 1989; 80:
96–100.
125. Garland F, Garland C, Gorham E, et al. Geographic variation in
breast cancer mortality in the United States: a hypothesis involving
exposure to solar radiation. Prev Med 1990; 19:614–622.
126. Lefkowitz ES, Garland CF. Sunlight, vitamin D, and ovarian cancer
mortality rates in US women. Int J Epidemiol 1994; 23(6):1133–1136.
127. Schwartz GG, Hulka BS. Is vitamin D deficiency a risk factor for
prostate cancer? (Hypothesis). Anticancer Res 1990; 10(5A):1307–
1311.
128. Holick MF. High prevalence of vitamin D inadequacy and
implications for health. Mayo Clin Proc 2006; 81(3):353–373.
129. Marks R, Foley PA, Jolley D. The effect of regular sunscreen use on
vitamin D levels in an Australian population. Arch Dermatol 1995;
131:415–421.
130. Sollitto RB, Kraemer KH, DiGiovanna JJ. Normal vitamin D
levels can be maintained despite rigorous photoprotection: six years
experience with xeroderma pigmentosum. J Am Acad Dermatol 1997;
37:942–947.
131. Berwick M, Kesler D. Ultraviolet radiation exposure, vitamin D, and
cancer. Photochem Photobiol 2005; 81(6):1261–1266.
132. Sporn MB. Approaches to prevention of epithelial cancer during the
preneoplastic period. Cancer Res 1976; 36:2699–2702.
133. Tsao AS, Kim ES Hong WK. Chemoprevention of cancer. Cancer J
Clin 2004; 54:150–180.
134. Greenberg ER, Baron JA, Stukel TA, et al. A clinical trial of beta
carotene to prevent basal-cell and squamous-cell cancers of the skin.
The Skin Cancer Prevention Study Group. N Engl J Med 1990;
323:789–795.
135. Clark LC, Combs GF Jr, Turnbull BW, et al. Effects of selenium
supplementation for cancer prevention in patients with carcinoma
of the skin. A randomized controlled trial. Nutritional Prevention of
Cancer Study Group. JAMA 1996; 276:1957–1963.
136. Green A, Williams G, Neale R, et al. Daily sunscreen application
and betacarotene supplementation in prevention of basal-cell and
squamous-cell carcinomas of the skin: a randomised controlled trial.
Lancet 1999; 354:723–729.
137. Kutchera W, Jones DA, Matsunami N, et al. Prostaglandin H synthase
2 is expressed abnormally in human colon cancer: evidence for
atranscriptional effect. Proc Natl Acad Sci USA 1996; 93:4816–4820.
138. Eberhart CE, Coffey RJ, Radhika A, et al. Up-regulation of
cyclooxygenase 2 gene expression in human colorectal adenomas and
adenocarcinomas. Gastroenterology 1994; 107:1183–1188.
139. Ristimaki A, Honkanen N, Jankala H, et al. Expression of
cyclooxygenase-2 in human gastric carcinoma. Cancer Res 1997;
57:1276–1280.
140. Hida T, Yatabe Y, Achiwa H, et al. Increased expression of
cyclooxygenase 2 occurs frequently in human lung cancers, specifically
in adenocarcinomas. Cancer Res 1998; 58:3761–3764.
141. Nijsten T, Colpaert CG, Vermeulen PB, et al. Cyclooxygenase-2
expression and angiogenesis in squamous cell carcinoma of the skin
and its precursors: a paired immunohistochemical study of 35 cases.
Br J Dermatol 2004; 151(4):837.
142. Ramirez CC, et al. Use of COX inhibitors and risk of melanoma in
high risk patients. Dermatol Surg. 2005; 31:748–752.
143. Downs JR, Clearfield M, Weis S et al. Primary prevention of acute
coronary events with lovastatin in men and women with average
cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas
Coronary Atherosclerosis Prevention Study. JAMA 1998; 279:1615–
1622.
144. Moon TE, Levine N, Cartmel B, et al. Effect of retinol in preventing
squamous cell skin cancer in moderate-risk subjects: a randomized,
double-blind, controlled trial. Southwest Skin Cancer Prevention Study
Group. Cancer Epidemiol Biomarkers Prev 1997; 6:949–956.
145. Tangrea JA, Edwards BK, Taylor PR, et al. Long-term therapy
with low-dose isotretinoin for prevention of basal cell carcinoma: a
multicenter clinical trial. Isotretinoin-Basal Cell Carcinoma Study
Group. J Natl Cancer Inst 1992; 84:328–332.
146. Levine N, et al. Trial of retinol and isotretinoin in skin cancer
prevention: a randomized, double blind, controlled trial. Southwest
Skin Cancer Prevention Study Group. Cancer Epidemiol Biomarkers
Prev 1997; 6:957–961.
147. Kraemer KH, DiGiovanna JJ, Moshell AN, et al. Prevention of skin
cancer in xeroderma pigmentosum with the use of oral isotretinoin.
N Engl J Med 1988; 318:1633–1637.
148. Bavinck JN, Tieben LM, Van der Woude FJ, et al. Prevention of skin
cancer and reduction of keratotic skin lesions during acitretin
therapy in renal transplant recipients: a double-blind, placebo-controlled
study. J Clin Oncol 1995; 13(8):1933–1938.
149. Nijsten TE, Stern RS. Oral retinoid use reduces cutaneous squamous
cell carcinoma risk in patients with psoriasis treated with psoralen-
UVA: a nested cohort study. J Am Acad Dermatol 2003; 49:644–650.

HISTORY
Aging is an inevitable process that can affect ones concept of
self-image and interaction with the outside world. While differ­
ent individuals do not necessarily age in the same fashion or at
the same rate, there is a fundamental pattern and sequence to
changes in facial appearance through the various stages of life.1
Over the last 30 years, there has been an increase in the
number of available cosmetic procedures which help to main­
tain a youthful appearance or reverse undesirable changes as­
sociated with aging.2 This is the result of an aging population
with higher discretionary income, dramatic developments in
minimally invasive rejuvenation techniques, and dissemina­
tion of information about available options. The media have
increasingly commented on and influenced public opinion on
cosmetic procedures. It is not unusual for the evening news to
air public interest or health segment stories on the newest and
latest techniques for rejuvenation. An appearance on Oprah
can generate thousands of calls to offices relating to a particu­
lar procedure.
Television make-over shows have also popularized new
techniques, increased the public’s understanding of surgical
and anatomic principles, and increased patient awareness of
available options.3 Thirty years ago cosmetic surgery was not
openly discussed, and patients who did desire an improvement
in appearance were forced to undergo conventional surgical
procedures, with sometimes lengthy recovery times as their
only option. Today, patients have access to a variety of non­
invasive procedures with zero or minimal recovery procedures
that they can easily incorporate into their busy schedules as
part of their general upkeep and grooming.
For centuries, an impression of good health has been in­
tricately linked with beauty, and beauty is the embodiment
of youth.4–7 This is true even more so in current society.
Studies have shown that individuals perceived as attractive
receive preferential treatment in education, employment,
medical care, and legal proceedings.6,8 What motivates
someone to seek out cosmetic procedures varies from per­
son to person. Motivations may be related to employment
and a desire to feel competitive in one’s field, or they may
be more personal, such as the desire to please a spouse or
improve one’s sense of well-being. In careers involving
intense interpersonal interaction such as sales, politics,
business, acting, or television, a person’s appearance is sig­
nificant. Attractive individuals earn more than those with
an average appearance, and individuals with below-average
looks garner the lowest hourly wages.9
An equally valid motivation is a personal desire to look
younger in persons who are aging. Physical appearance is
linked to body image, self-esteem, confidence, and psycho­
logical well-being.3,10 Repeated expressions can produce
hyperfunctional facial lines which can make a person look
tired, angry, or unapproachable, causing anxiety and inaccu­
rate communication of emotions during social interaction.6
Aging skin itself has also been associated with increased levels of
anxiety during interpersonal interactions.11 Older individuals
Evaluation of the Aging Face
Melissa A. Bogle,
Kenneth A. Arndt,  
Jeffrey S. Dover,
and Michael S. Kaminer
C h a p t e r
4
Key Points
Major elements of facial aging
n Chronic damage from ultraviolet light (telangiecta­
sias, dyspigmentation, rough texture);
n Dynamic rhytides from hyperfunctional facial
muscles;
n Loss of subcutaneous fat;
n Remodeling of underlying bone and cartilaginous
structures;
n Gravitational changes from loss of elasticity.
p a r t 1

38
Chapter 4
Evaluation of the cosmetic surgery patient
who maintain a more youthful appearance tend to be healthier,
live longer, and have a more positive outlook on life.12
SCIENCE
The two broad components of aging which contribute to
changes in facial appearance are intrinsic and extrinsic aging.13
Intrinsic, or biologic aging is due primarily to hereditary fac­
tors.2 Because genetic influences are programmed at a cellu­
lar level, they are essentially uncontrollable given our current
understanding and ability (or lack thereof) to modify cellular
events.14 Certain races and hereditary backgrounds tend to
age more slowly than others, mostly due to genetically based
skin coloring and the protection that it affords from ultraviolet
radiation. Intrinsic aging is not a homogeneous process and
appears to evolve with periods of acceleration and decelera­
tion at different times in a person’s life.
Extrinsic aging is influenced by a person’s exposure to the
elements and lifestyle habits, making it somewhat more con­
trollable than intrinsic aging.2 The chief extrinsic contributors
to facial aging are ultraviolet exposure and smoking, although
health habits such as sleep, diet, muscle activity, and exercise
also play a role.2,15 Temperature extremes, wind, and ultra­
violet radiation take a particularly harsh toll on facial skin be­
cause it is almost continuously exposed to the environment
over a person’s lifetime.
When one examines histologic samples of sun-­damaged
skin in contrast to non-sun-damaged skin, sun-dam­
aged skin reveals a markedly thickened and disorganized
epidermis with dyskeratotic changes.13 Chronic stimula­
tion of epidermal melanocytes causes them to become
enlarged, more numerous, and found in higher levels of
the epidermis. This appears as dyschromia, focal hyper­
pigmentation, lentigines, and keratoses. The extrinsically
aged dermal–epidermal junction (DEJ) contains a stretch
of densely packed collagen with little or no elastic content
and a flattening of the rete ridges, making it fragile and
susceptible to injury from shearing forces.2,16 Beneath the
DEJ there is a broad zone containing tangled masses of
elastotic material intermixed among degenerated collagen
fibrils. This change, known as solar elastosis, is responsible
for many of the changes in dermal architecture associated
with photoaging, seen as wrinkling and uneven texture.
Aged skin cells also have a reduction in metabolic activity and
subsequently have a decreased ability to synthesize collagen, poor
wound healing, and altered biomechanical function.17 Skin is less
distensible, less resilient, and prone to fine wrinkling, textural ab­
normalities, and laxity.18 Decreased collagen and elastic fibers in
the dermis with a decreased water content lead to a thinning of
the dermis.19 In women, skin thickness reaches maximum at age
35, and in men, it reaches maximum at age 45.20 Both sexes have
a gradual decline thereafter.20
STUDIES
If one examines faces over time, there are characteristic mor­
phologic changes that occur with aging. Across cultures, youth­
ful features include a high, arched brow, well-defined cheek
mass, sharp jaw line, and rounded, full lips with a detailed
Cupid’s bow and sharp demarcation of the vermilion. With
age, inevitable changes occur in facial morphology and skin
quality including fat atrophy, sagging, wrinkles, dyspigmenta­
tion, fine telangiectasias, and irregular texture.
The Glogau classification system attempts to classify the
severity of photodamage by grading the degree of epidermal
and dermal changes on a four-point scale.21 Category I en­
compasses those with minimal sun damage, category II in­
cludes those with mild wrinkling and early laxity, category III
includes those with moderate wrinkling and depression of the
cheek fat pads, and category IV is reserved for those with
severe laxity and extensive rhytides.21
Without sun protection, the first signs of damage can ap­
pear in childhood or the early teens as innocuous-appearing
lentigines sprinkled over the face or shoulders. The skin and
facial morphology are, however, typically smooth and plump
with well-defined features.
Individuals in their twenties may begin to develop fine
lines which become more noticeable as they approach their
thirties. Fine wrinkling generally appears first in the upper
face with subtle lines over the lateral and inferior periorbital
areas. Facial expression habits play a role in the development
of early rhytides. Individuals prone to squinting may develop
lines around the lateral periorbital area (crow’s feet) due to
the underlying action of the orbicularis oculi muscle, and
lines around the inferior periorbital area may be accentuated
by the zygomaticus muscle in the cheek. Vertical glabellar
lines may result from contraction of the corrugator supercilii
muscles, and transverse rhytides at the nasal root may result
from contraction of the procerus muscle (Fig. 4-1).
As a person enters the thirties, horizontal forehead rhytides
develop due to contraction of the frontalis muscle. There is
gradual ptosis of soft tissue in the forehead, leading to descent
of the lateral portion of the eyebrows and increased hooding
in the upper eyelid. The frontalis muscle eventually develops
a perpetually contracted state in an attempt to overcome this
ptosis, leading to deeper, fixed forehead lines.22 Increased skin
laxity and weakening of the orbital septum frequently appears
in the mid to late thirties, contributing to excess skin of the
upper eyelids and bulging of the intraorbital fat pads of both
the upper and lower eyelids.
Changes in the lower portion of the face first begin to ap­
pear in the late twenties and early thirties. There is a natural
groove at the superior aspect of the nasolabial folds which
represents the point at which the zygomaticus major and
risorius muscles interdigitate and insert into the dermis.22 The
zygomaticus major and risorius muscles are two in a group

39
Evaluation of the aging face  •  Chapter 4
of six muscles, collectively known as the quadratus labii supe­
rioris, which control the upper mouth. The groove that they
shape is present even in very young faces. In the late twenties
and early thirties, the groove begins to elongate and deepen,
becoming the first signs of a nasolabial fold.
Young faces have a well-defined cheek mass composed pri­
marily of fat within fine facial septae.23 With age, facia-retaining
ligaments weaken to varying degrees, causing the cheek to suc­
cumb to the effects of gravity. The result of this is that individu­
als in their late forties and older have a paucity of soft tissue in
the infraorbital region and accentuated nasolabial folds due to
an anterior and inferior projection of the cheek mass.24,25
There is a gradual weakening of the superficial muscular
aponeurotic system (SMAS) beginning in the late thirties and
early forties, causing further ptosis of the lateral and mid-face
regions.2 Along with these changes comes an accumulation
of submandibular and submental fat, sagging of the sub­
mandibular gland, and weakening of the platysma muscle, all
of which obscure the smooth contour of a youthful-appearing
jaw line and a sharp cervicomental angle.
In the aging face, redistribution and loss of subcutaneous fat
is a significant contributor to flat, hollow contours, particularly
in the infraorbital regions, cheeks, and around the mouth. Areas
prone to wasting include the buccal fat pads, malar fat pads,
perioral fat, chin, temporal fossa, and periorbital area (Fig. 4-2).
Individuals in their fifties may begin to see bony absorp­
tion of the maxilla and mandible, enlarging the pre-jowl
­sulcus and enhancing the appearance of the jowls. Soft tissue
changes in mid-life also contribute to alterations in the ap­
pearance of the nose. The connection between the upper and
lower lateral cartilages and the support mechanisms of the tip
and interdomal ligaments slowly weaken.26 The nasal tip ro­
tates downward and the entire nose actually becomes longer.1
Nasal changes are often visually accentuated by the vertical
shortening of the maxilla and mandible.
Also at this time, fine vertical rhytides may become ­visible
around the lips due to the underlying action of the ­orbicularis
oris muscle. Smokers and those who purse their lips habitu­
ally can see these changes as early as their mid to late ­thirties.
The aged upper lip has a tendency to lengthen and descend
vertically and there is a generalized loss of fullness and sup­
port throughout the entire structure. The Cupid’s bow and
philtrum flatten with age and the smooth, rolled ridge of
collagen at the vermilion border becomes nondistinct. In
advanced age, exaggeration of age-related changes occurs.
Figures 4-3 and 4-4 show a progression of a male and
female face over time. The first photos are of the individuals
in their twenties, showing well-defined features with ample fa­
cial fat, superiorly placed cheek masses, smooth skin, and full
lips. The second photos are of the pair in their early thirties.
Both have begun to have a loss of facial fat and cheek fullness,
with deepening of the nasolabial folds, thinning of the lips and
Fig. 4-1  Illustration of the muscles of facial expression. Dynamic
lines that become more permanent with age run perpendicular to
the vector of contraction.
Temporal fossa
fat pad
Malar fat pad
Buccal fat
pad
Perioral fat
pad
Chin and jaw
line fat
Periorbital fat
Fig. 4-2  Illustration of the distribution of facial fat. The buccal fat
pads, malar fat pads, perioral, chin, jaw line, temporal fossa, and
perioral fat all give roundness and shape to a youthful-appearing face.

40
Chapter 4
Evaluation of the cosmetic surgery patient
A
B
C
D
Fig. 4-3  Progression of a female’s face through her twenties, thirties, forties, and sixties.
a slight hooding of the upper eyelid. The third photo shows
the couple in their forties, with increased loss of facial fat,
ptosis of the cheek masses, dulling of the cervicomandibu­
lar angle, and dynamic lines on the forehead, glabella, and
periocular region. The last photos are of the individuals in
their late sixties, showing exaggeration of age-related changes,
including hyperfunctional lines, lipoatrophy, ptosis, thinning
of the lips, and alterations in bony structure.
DISCUSSION
The first step in evaluating a candidate for cosmetic procedures
is to determine the patient’s motivation for correction and what
the ultimate goal is. This is important because it can have a
significant impact on the patient’s satisfaction after treatment.

41
Evaluation of the aging face  •  Chapter 4
B
A
C
D
Fig. 4-4  Progression of a male’s face through his twenties, thirties, forties, and sixties.

42
Chapter 4
Evaluation of the cosmetic surgery patient
In general, patients who are undergoing a procedure to please
someone else or who seek out unnecessary procedures due to
perceived flaws will have a higher likelihood of dissatisfaction
post-procedure. Patients with unrealistic expectations may be
disappointed if the result falls short of their ideal, even if a signifi­
cant improvement is made. Certain psychopathologic syndromes,
such as body dysmorphic disorder, hypomania, and adjustment
disorder, may predispose individuals to have a distorted percep­
tion of their appearance or to have unrealistic treatment goals.27
The great majority of patients seeking treatment for their aging
appearance, however, are emotionally healthy and do not have a
serious contributing psychopathology.27
The consultation is also a good time to question the patient
about health and lifestyle habits which may be contributing
to extrinsic aging. For example, the patient should be asked
about smoking, alcohol, use of sunscreens, tanning habits, and
involvement in hobbies with excessive sun exposure such as
golf, tennis, or boating.
Likewise, it is important to pay close attention to what fea­
tures are bothersome to the patient. What the physician sees and
what the patient sees are often not the same issue. If the physician
addresses what he or she perceives to be problematic, but does
not address the patient’s primary concern, it can lead to disap­
pointment and misgivings on both sides of the relationship. For
example, if a woman with severe acne scarring on the cheeks and
prominent nasolabial folds comes in complaining mainly of her
nasolabial folds, a series of nonablative laser treatments which
diminishes her scars almost completely may still leave her upset
because what she really wanted was correction of her nasolabial
folds. The physician would have been much better offering her a
facial filler, and then addressing the scarring at a future follow-up
after a trusting relationship had been established.
After a picture of the patient’s goals, motivation, and life­
style is complete, a comprehensive physical examination of
the face is performed. Careful attention should be paid to the
quality of the skin (texture, rhytides, telangiectasias, dyschro­
mia), muscle or movement-related furrows, quality and posi­
tion of subcutaneous fat, and degree of laxity. A well-trained
eye will be able to hone in on intricate facial changes asso­
ciated with aging and develop a plan for facial rejuvenation
which will give the greatest benefit with the least risk.
Goals in the management of the aging face include elements
of surface repair, restoration and enhancement. When forming a
framework of therapeutic options, it is easy for a physician to get
into the habit of offering one or two favorite treatments which
may or may not suit all patients equally well. It is essential to
look at each patient individually, including what kind of upkeep
they are willing to tolerate. For example, the first treatment many
physicians would consider for improving nasolabial folds is a soft
tissue filler such as those containing hyaluronic acid. However,
patients have to return approximately every 6 months for retreat­
ment. For patients unwilling or unable to tolerate such a sched­
ule, it may be a better option to offer a more permanent filler
such as fat or silicone microinjections, or to go another direction
entirely such as infrared or radiofrequency skin tightening.
A skilled physician should be able to attack a problem
from many different angles, depending on his or her available
resources and what is the best fit for the individual patient.
A variety of treatments and procedures should be discussed
with the patient, outlining the risks, side effects, costs, invasive­
ness, recovery time, and anticipated outcomes.
Laser or light therapy, chemical peels, and microdermabra­
sion can be used to improve the skin’s tone, color, and texture.
Prominent telangiectasias can be treated with visible light
lasers such as the pulsed dye laser, KTP laser, or intense pulsed
light. Lentigines can be treated with lasers that target melanin.
Fair-skinned patients with a mix of telangiectasias and patchy,
irregular pigmentation are good candidates for intense pulsed
light treatments.
Uneven skin texture, rhytides and scarring can be improved
with a myriad of methods for nonablative rejuvenation.
Infrared lasers (1064  nm, 1320  nm, 1450  nm, and 1540  nm),
low-energy plasma regeneration, fractional photothermo­
lysis, visible light lasers (yellow, green), narrow-band light
sources (light emitting diodes), broad-band light sources
(intense pulsed light), and radiofrequency devices can all be
considered.28–30
Ablative resurfacing is still the gold standard for the treat­
ment of deep wrinkles and severe solar elastosis. The carbon
• It is important to understand the patient’s
goals and motivations for seeking cosmetic
improvement.
• Listen to the patient and focus primarily on his
or her concerns.
• Examine the face as a comprehensive unit with
an eye for age-related changes.
• Individualize treatment plans to the lifestyle and
means of each particular patient.
• Remember Glogau’s four Rs: Relax (muscle
related wrinkles), Refill (fat atrophy and volume
loss), Redrape (sagging, lax skin), and Resur­
face (texture, color and tone).
Pearls
• Patients who are undergoing a procedure
to please someone else, or who seek out
unnecessary procedures for perceived flaws,
will have a higher likelihood of dissatisfaction.
• Patients with unrealistic expectations may be
disappointed if the result falls short of their ideal,
even if a significant improvement is made.
• Avoid treating issues that bother you if they
are not an issue for the patient; this will end in
disappointment and misgivings on both sides
of the relationship.
• Failing to appreciate underlying anatomic
defects behind the signs of aging can lead
to erroneous procedures and inferior results.
Pitfalls

43
Evaluation of the aging face  •  Chapter 4
dioxide (CO2) and variable pulsed Er:YAG lasers have excellent
results in terms of heat-induced tissue tightening and improve­
ment of texture, pigment, and rhytides.31 Plasma regeneration
at high energies, or a series of fractional photothermolysis
treatments, can also be considered.31
Dynamic rhytides in the aging face are best treated with
botulinum toxin to decrease underlying muscle contraction.
Injection into the lateral brow area can raise the eyebrow and
compensate for brow ptosis and upper lid laxity. Dynamic
lines are most noticeable around the eyes, forehead, and gla­
bella. Botulinum toxin can also be injected into muscles in the
lower face and neck to improve a variety of conditions such
as perioral lines, a down-turned mouth, and prominent neck
folds or platysmal bands.
Facial fillers can be used to plump up lines and folds, scars,
and defects due to fat wasting in the aging face. There are two
broad categories of fillers including micro- and macro-fillers.­
Which type of filler to use depends on the size and depth of
the defect. Micro-fillers include products such as collagen
and hyaluronic acid, and are best suited for filling fine lines
or ­localized areas such as the lips, scars, or superficial dermal
folds. Macro-fillers, such as fat, are better suited for large-volume
correction such as the cheeks, resculpting the jaw line and
pre-jowl sulcus, or for diffuse facial volume correction. Either
type of filler works well in the nasolabial folds, corners of the
mouth, and marionette lines.
Volume restoration is an extremely important concept in
minimally invasive facial restoration. Many patients are not
aware of the lipoatrophy that occurs with aging and are in­
stead focused on the concept of excess skin. They may think
that they need a face-lift, when a face-lift would simply pull
the skin taught against bony facial contours, giving a gaunt,
skeletal appearance. The goal in volume restoration is to re­
store the rounded contours and convexities of a youthful face
with fat repositioning or augmentation. Autologous fat trans­
fer provides a safe, long-term method of volume restoration,
although other injectable fillers such as hyaluronic acid, col­
lagen and microdroplet silicone can be considered.
Another approach to shaping and lifting sagging fat is
radiofrequency or infrared skin tightening. These procedures
work particularly well in the mid-face and along the jaw line,
but can also be used on the eyelids, neck, and forehead.
Restoration of aging lips is an art form of its own. The phy­
sician should carefully take note of what changes have taken
place in the patient’s natural contour. Ideally, filler substances
can be used to enhance the fullness of the body of the lip,
paying careful attention to mimic natural contours such as the
Cupid’s bow, as well as to enhance the vermilion border and
restore a flattened philtrum.
Patients desiring at-home maintenance for facial rejuvena­
tion can be prescribed a myriad of different products to de­
crease pigmentation, reduce the appearance of fine lines, and
improve skin texture. These include topical retinoids, alpha-
hydroxy acids (such as glycolic acid), antioxidants, sunscreens,
hydroquinone and others.13,32,33
REFERENCES
  1. Pessa JE. An algorithm of facial aging. Plast Reconstr Surg 2000;
106:479–488.
  2. Fedok FG. The aging face. Facial Plast Surg 1996; 12:107–115.
  3. Mendelson BC. Cosmetic surgery of the aging face. Aust Fam Physician
1992; 21:907–919.
  4. Graham JA, Kligman AM. Physical attractiveness, cosmetic use and self-
perception in the elderly. Int J Cosmet Sci 1985; 7:85–97.
  5. Kligman AM, Graham JA. The psychology of appearance in the elderly.
Dermatol Clin 1986; 4:501–507.
  6. Cox SE, Finn JC. Social implications of hyperdynamic facial lines and
patient satisfaction outcomes. Int Ophthalmol Clin 2005; 45:13–24.
  7. Alam M, Dover JS. On beauty: evolution, psychosocial considerations,
and surgical enhancement. Arch Derm 2001; 137:795–807.
  8. Etcoff N. Survival of the prettiest. The science of beauty. New York:
Random House; 1999.
  9. Hamermesh DS, Biddle JE. Beauty and the labor market. Am Econ Rev
1994; 84:1174–1194.
10. Prusinsky T. Psychological factors in cosmetic plastic surgery: recent
developments in patient care. Plast Surg Nurs 1993; 13:64–70.
11. Gupta MA, Schork NJ, Ellis CN. Psychosocial correlates of the
treatment of photodamaged skin with topical retinoic acid.
A prospective controlled study. J Am Acad Dermatol 1994; 30:969–972.
12. Kligman AM. Psychological aspects of skin disorders in the elderly.
Cutis 1989; 43:498–501.
13. Roenigk HH Jr. Treatment of the aging face. Dermatol Clin 1995;
13:245–261.
14. Yaar M, Gilchrest BA. Cellular and molecular mechanisms of cutaneous
aging. Dermatol Surg Oncol 1990; 16:915–922.
15. Taylor CR, Stern RS, Leyden JJ, et al. Photoaging, photodamage, and
photoprotection. J Am Acad Dermatol 1990; 22:1–15.
16. Kligman AM, Baker TJ, Gordon HL. Long-term histologic follow-up of
phenol face peels. Plast Recontr Surg 1985; 75:652–659.
17. Bailey AJ, Robins SP, Balin G. Biological significance of the
intermolecular crosslinks of collagen. Nature 1974; 251:105–109.
18. Daly CH, Odland GF. Age-related changes in the mechanical properties
of human skin. J Invest Dermatol 1979; 73:84–87.
19. Miyahara T, Murai A, Tanaka T, et al. Age-related differences in
human skin collagen. J Gerontol 1982; 37:651–655.
20. Leveque JL, Corcuff P, de Rigal J, et al. In vivo studies of the evaluation
of physical properties of the human skin with age. Int J Dermatol 1984;
23:322–329.
21. Glogau RG. Chemical peeling and aging skin. Arch Dermatol 1994;
2:30–35.
22. Ellis DA, Ward DK. The aging face. J Otolaryngol 1986; 15:217–223.
23. Rubin LR, Mishriki Y, Lee G. Anatomy of the nasolabial fold: the
keystone of the smiling mechanism. Plast Reconstr Surg 1995; 83:1–10.
24. Hamra ST. Repositioning the orbicularis oculi muscle in the composite
rhytidectomy. Plast Reconstr Surg 1992; 90:14–22.
25. Yousif NJ. Changes of the mid-face with age. Clin Plast Surg 1995;
22:213–226.
26. Janeke JB, Wright WK. Studies on the support of the nasal tip. Arch
Otolaryngol 1971; 93:458–464.
27. Gupta MG. The aging face: a psychocutaneous perspective. Facial Plast
Surg 1995; 11:86–90.
28. Hirsch RJ, Dayan SH. Nonablative resurfacing. Facial Plast Surg 2004;
20:57–61.
29. Weiss RA, McDaniel DH, Geronemus RG, et al. Clinical experience
with light-emitting diode (LED) photomodulation. Dermatol Surg 2005;
31:1199–1205.
30. Geronemus RG. Fractional photothermolysis: current and future
applications. Lasers Surg Med 2006; 38:169–176.
31. Papadavid E, Katsambas A. Lasers for facial rejuvenation: a review. Int J
Dermatol 2003; 42:480–487.
32. Lauker RM. Topical therapy of aging skin. J Ger Dermatol 1994; 2:20–23.
33. Goldfarb MT, Ellis CN, Voorhees JJ. Topical tretinoin: its use in daily
practice to reverse photoaging. Br J Dermatol 1990; 122:87–91.

HISTORY
Photography has seen tremendous improvements in the last
decade. While instant photography, such as with Polaroid
cameras, increased the convenience of using photographs for
medical documentation, this technology remained relatively
expensive. This cost was attributed not to the cost of the cam­
era, but mostly to the cost of the film. Today, digital cameras
produce instant images with superior quality at a fraction of
the cost of instant photography.
There are several reasons to keep photographic records
of the cosmetic patient. Pictures can provide surgical site or
injection site documentation, before-and-after comparisons,
and long-term patient monitoring. Furthermore, the images
may play an important role in defense against medicolegal
allegations.
While advances in technology continue to debut at a rapid
rate, fundamental principles often remain unchanged. The
­science behind photography, like medicine and cosmetics,
­relies on basic rules and standards. Although major inno­
vations do occur, most of the advances in technology focus
on minor improvements and tweaks of existing technology.
Whether it is a digital camera with more megapixels, or an
injectable filler that lasts longer, one can easily see the under­
lying principles that inspire such advances. Fortunately, since
photography is based on a set of standard principles, skills
with one camera will often translate easily to next-­generation
­cameras. An ­ understanding of cosmetic surgery photog­
raphy fundamentals will empower physicians to take rich
­photographs in both their personal and professional lives.
This chapter mentions several products as examples of
technology as it exists at the time of writing. As technology
progresses, there may be better equipment options that will
make obsolete any recommendations made here.
Imaging
Ashish C. Bhatia,
Matthew A. Molenda,
Michael P. Heffernan, and
Doug Roach
C H A P T E R
5
n The goal of medical and surgical photography
is to take consistent and reproducible photographs
that accurately represent the subject matter. The
best way to achieve this goal is by ­controlling
the environment as much as possible. Keeping
the lighting, the distance from the subject to the
­camera, and the camera settings all constant
will vastly improve the reproducibility of medical
­photographs.
n Cosmetic surgery can benefit greatly from the
­advances in photography over the past few
years. Digital technology has enabled physicians
to enhance patient care and record-keeping with
a more practical and versatile tool than ever
before.
n �����Photography, whether digital or film, has several
roles in the practice of cosmetic surgery. These
­include the precise documentation of cosmetic
sites, before-and-after photos, and the ability to
monitor subtle changes over time.
n �����Photography provides invaluable visual aids to the
education of peers and trainees.
n �����Photographs of patients who underwent similar
procedures for similar conditions can help set
realistic expectations for the prospective
cosmetic patient as long as there is good
judgment in selecting photographs on the part
of the cosmetic surgeon.
Key Points
P A R T 1

46
Chapter 5
Evaluation of the cosmetic surgery patient
SCIENCE
Photography equipment
• Photography captures information about the light that enters
the camera and strikes the film or electronic sensor.
• Portability, image quality, memory capacity, durability,
ergonomics, and other subjective factors should be consid­
ered when choosing photographic equipment for a medical
practice.
The universal goal of all photography is to capture and record
light that reflects off a subject and strikes a light-sensitive
image sensor. The image sensor can be film or digital. A lens
helps bend (focus) the light waves to strike the image sensor
more precisely. Accurate focus, in conjunction with regula­
tion of the amount and color of light striking the sensor, will
­produce sharp, true-to-life photographs. Since 35 mm film
photography employs very similar principles to digital SLR
photography, and since film photography costs significantly
more to use and is being used less frequently with time, this
chapter will focus on digital photography.
Single lens reflex versus compact
­cameras
Single lens reflex (SLR) cameras have internal mirrors that
reflect light to the viewfinder so that the camera operator can
preview the qualities of the picture. When a picture is taken,
this mirror system flips out of the way to expose the light-
sensitive image sensor. The moving parts within SLR cameras
make them inherently bulky. Additionally, in order to reach
the camera’s full potential, SLR camera owners typically
find it necessary to purchase additional attachments such as
lenses, flashes, and filters. In contrast, ‘point and shoot’ com­
pact cameras are smaller, less expensive, easier to use, and all-
inclusive (lens and flash built in) (Fig. 5-1). Although the ­quality
of photos taken by compact cameras continues to improve,
many professional photographers value the customizability
and manual controls offered by SLRs.
Control is particularly important in medical and cosmetic
photography to produce consistent images. However, these
manual controls require a more advanced knowledge of ­several
principles in photography. Automated photography is more
widely used because it relies on a computer within the camera
to make decisions on exposure, white balance, and other set­
tings which affect the quality of the final image. While there is
no question that automated modes in modern SLR and com­
pact cameras can produce excellent results, the inconsisten­
cies in settings made by cameras in automatic mode result in
images that may be difficult to compare. In ­cosmetic derma­
tology, monitoring and documenting both subtle and drastic
changes over time is vital for publishing, research, education,
and medicolegal reasons. If the photographs have inconsistent
exposure, color tone, or a host of other variables, it makes it
difficult to draw legitimate conclusions from before-and-after
images. Since SLR cameras allow for control of many more
settings than compact cameras, they are the better choice for
capturing images with reproducible settings.
Lenses
Another important benefit of SLR cameras is the ability to
change lenses. The lens interchange system allows the attach­
ment of a variety of lenses, increasing the versatility of
the camera. For instance, a macro lens can be attached for
extreme close-up photography, and can be quickly switched
out to a lens that allows the camera to attach to a microscope
for capturing photomicrographs.
There are specific lenses for specific tasks, so it is beneficial
to have a general familiarity of the types of lenses best suited
for office photography. If the goal is to capture full-body pho­
tographs, a wide-angle lens is necessary unless there is signifi­
cant space in the examination room to back away from the
subject before snapping the photograph. A normal or short
telephoto lens may be more appropriate for photographing
A
B
Fig. 5-1  (A, B) Digital compact camera (on left) versus a digital
SLR camera (on right). Note the difference in size. The SLR camera
may even be bulkier if an auxiliary flash is used. (Images courtesy
of Derm.md [)

47
Imaging  •  Chapter 5
a single section of the body such as the face. A good lens for
portrait photography is around 100 mm. This range will give
the most accurate portrayal of the facial features. Wider angle
lenses tend to make objects in the foreground appear larger,
while telephoto lenses tend to compress objects in the fore­
ground. For even smaller objects, such as a lesion or scar, a
macro lens will keep a close-up photograph properly focused.
Many dual-function lenses are available on the market allow­
ing macro imaging and relatively wide-angle functionality in
a single lens.
If multiple different lenses are used in the office setting, be
sure to take note of which lens was used for each patient/view.
Using different lenses can distort perspective, and perhaps even
give the illusion of improvement. For example, using a wide-
angle lens to photograph a face before a rhinoplasty could
make the nose appear wider and larger than its actual size.
Using a standard lens after the surgery could make the photo­
graphic improvement better than the actual improvement.
By taking note of which lens was used, consistent ­follow-up
pictures can be taken, thereby avoiding ­accidental misrepre­
sentation of results. Obviously, if different lenses were used
to purposefully exaggerate improvement, this would be an
­unethical practice.
Zoom
Lenses with zoom functionality are capable of changing
the field of view while the camera itself remains stationary.
Most compact cameras on the market today have basic zoom
capabilities. However, it is important to note the difference
between optical and digital zoom (Fig. 5-2). Optical zoom
keeps the image quality consistent because it relies upon optics
to produce a close-up image. On the other hand, a digitally
zoomed image is produced by discarding information from
the periphery of the image and enlarging the center of the
image to simulate results from a zoom lens. This results in an
image with lower resolution than the original image. Compact
cameras are usually limited in their optical zoom capabilities
and include digital zoom in their specifications to market an
overall higher zoom capability. SLR cameras, in contrast, rely
solely on the optics of interchangeable lenses for zoom func­
tionality allowing zoom without image degradation.
Macro or ‘close-up’ lenses
Close-up photography is important when dealing with dis­
crete lesions or small areas in cosmetic dermatology. The best
type of lens for this type of photograph is a macro lens. An
SLR macro lens is the most reliable and reproducible tool
to produce quality close-up photographs. Look for a macro
lens with a 1:1 or 1:2 subject to film reproduction ratio and
a focal length of 60–100  mm. The suggested reproduction
ratios ensure the images are captured at ‘life size’ or ‘one-half
life size,’ respectively. The suggested focal length ensures an
adequate working distance between the camera operator and
the patient, thereby preventing an uncomfortable invasion of
the subject’s personal space (Fig. 5-3).
Flash
The lighting in the office or surgical suite varies throughout
the day based upon several factors. These include light from
open doors, windows, variations in bulbs, and the intensity
and angle of the sun. To achieve the most consistent light­
ing during clinical photography, flash photography is rec­
ommended. While flashless photography may be adequate
for documentation of treatment sites, it leaves much to be
desired in terms of proper exposure, color balance, and
image consistency. Furthermore, a flash helps ensure an
adequate depth of field and relatively quick shutter speeds.
Reasonably good results can be obtained by using the stand­
ard flash that comes integrated on most modern cameras.
However, built-in flashes typically have weak output to pre­
serve camera battery life. The use of an auxiliary flash unit
can produce an even more consistent and professional image,
especially when there are greater working distances between
the subject and camera. If purchasing an auxiliary flash, look
for one with a guide number (GN) of 80 or higher (at ISO
100) to be sure it emits light intense enough to achieve good
results.
A variety of auxiliary flash options exist today. Choosing
the proper type depends upon the type of photography to
be performed. For example, a ring flash is one type of flash
that is commonly used in medical and, in particular, dental
photography. This type of flash mounts to the front of the lens
Fig. 5-2  Optical zoom versus digital zoom. Note the fine detail
present when a photograph is taken with optical zoom and lost
when a photograph is taken with digital zoom. This image is a
­simulation. (Image courtesy of Derm.md [)

hacklink satın al mumu模拟器 雷电模拟器 向日葵 giftcardmall/mygift giftcardmall balance mygift giftcardmall matbet matbet giriş Casibom Casibom Giriş Adresi Casibom Casibom Casibom Güncel Giriş Casibom Deneme Bonusu Veren Siteler Deneme Bonusu Veren Siteler Deneme Bonusu Veren Siteler Deneme Bonusu Veren Siteler Deneme Bonusu Veren Siteler Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Fixbet Fixbet Güncel Giriş Fixbet Betgaranti Betgaranti Güncel Adres Betgaranti Fixbet Fixbet Güncel Giriş Fixbet Fim İzle Fim İzle Giriş Fim İzle Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Grandpashabet Grandpashabet Güncel Giriş Grandpashabet Fim İzle Fim İzle Güncel Adres Fim İzle jojobet jojobet giriş jojobet jojobet giriş jojobet jojobet giriş Casibom Casibom Giriş Adresi Casibom Casibom Casibom Güncel Adres Casibom Casibom Casibom Giriş Adresi Casibom Casibom Casibom Giriş Casibom Turk İfsa Turk İfsa Güncel Giriş Turk İfsa Canlı Maç Canlı Maç İzle Canlı Maç Porno İzle Porno İzle Güncel Adres Porno İzle Turk İfsa Turk İfsa Güncel Giriş Turk İfsa Porno İzle Porno İzle Güncel Adres Porno İzle Jojobet Jojobet Giriş Jojobet Canlı Maç Canlı Maç İzle Canlı Maç Deneme Bonusu Film İzle Deneme Bonusu Veren Siteler Deneme Bonusu Türkçe Dublaj Film İzle Film İzle Deneme Bonusu Deneme Bonusu Giriş Deneme Bonusu Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Casibom Casibom Resmi Adres Casibom Casibom Güncel Adres Casibom Casibom Güncel Adres Casibom Casibom Resmi Adres Casibom Casibom Giriş Adresi perabet perabet giriş holiganbet holiganbet giriş Casibom Lesfillmercom Casibom Lesfillmercom Giriş Casibom Casibom Güncel Giriş Casibom Casibom Güncel Giriş Casibom Tevfikmuratyildirimcom Casibom Gerbergirlcom Casibom Gerbergirlcom Güncel Giriş Casibom Tevfikmuratyildirimcom Casibom Tevfikmuratyildirimcom Casibom Spcelectriccontrolcom Casibom Casibom Resmi Adres Casibom Casibom Giriş Adresi jojobet jojobet giriş jojobet jojobet giriş marsbahis marsbahis giriş jojobet jojobet giriş jojobet jojobet giriş jojobet jojobet giriş Casibom Casibom Giriş Casibom Casibom Giriş Adresi Casibom Casibom Giriş Adresi Casibom Casibom Giriş Casibom Casibom Güncel Giriş vaycasino vaycasino giriş vaycasino güncel giriş vaycasino vaycasino giriş vaycasino güncel giriş matbet matbet giriş matbet güncel giriş vaycasino vaycasino güncel giriş vaycasino giriş matbet matbet giriş pusulabet pusulabet giriş pusulabet pusulabet güncel giriş pusulabet giriş matbet matbet güncel giriş matbet giriş Casibom Casibom Resmi Adres Casibom Casibom Güncel Giriş Casibom Casibom Giriş Adresi Casibom Casibom Resmi Adres pusulabet pusulabet giriş pusulabet güncel giriş Fixbet Fixbet Güncel Giriş Salvobet Salvobet Giriş Salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom Turk Porno Turk Porno Giriş Turk Porno casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom casibom Casibom Casibom Giriş Adresi Casibom salvobet salvobet salvobet salvobet salvobet casibom casibom casibom casibom Casibom Casibom Resmi Adres Casibom Casibom Giriş Adresi casibom casibom jojobet izmir escort izmir buca escort buca escort jojobet casibom holiganbet holiganbet giriş jojobet holiganbet holiganbet giriş jojobet jojobet jojobet jojobet giriş jojobet güncel giriş izmir escort izmir buca escort buca escort izmir escort bayan salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet salvobet marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis marsbahis Deneme Bonusu Veren Siteler Deneme Bonusu Veren Siteler Giriş Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Deneme Bonusu Veren Giriş Deneme Bonusu Veren salvobet salvobet salvobet salvobet Casibom betgaranti betgaranti betgaranti matbet matbet giriş matbet matbet giriş Casibom Casibom Salvobet jojobet Salvobet Salvobet Salvobet Casibom Casibom Casibom Güncel Adres Casibom Güncel Giriş Marsbahis Marsbahis Marsbahis bahsegel Fixbet Fixbet Güncel Adres Grandpashabet Grandpashabet Giriş Grandpashabet Grandpashabet Güncel Giriş 1xbet 1xbet Resmi Adres Casibom Casibom Giriş Marsbahis Marsbahis Marsbahis Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Siteler Casibom Casibom Resmi Adres Casibom Casibom Resmi Adres Casibom Casibom Resmi Adres Grandpashabet Grandpashabet Güncel Adres Grandpashabet Grandpashabet Giriş Adresi jojobet jojobet giriş jojobet güncel giriş vaycasino vaycasino giriş vaycasino güncel giriş jojobet jojobet giriş jojobet güncel giriş Deneme Bonusu Deneme Bonusu Veren Siteler Listesi Grandpashabet Grandpashabet Giriş Grandpashabet Grandpashabet Grandpashabet Resmi Adres Grandpashabet Grandpashabet Güncel Giriş Grandpashabet Grandpashabet Güncel Adres Grandpashabet Grandpashabet Güncel Giriş Grandpashabet Grandpashabet Güncel Giriş Grandpashabet Grandpashabet Giriş Adresi Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Siteler grandpashabet grandpashabet grandpashabet Grandpashabet Grandpashabet Resmi Adres Grandpashabet Grandpashabet Resmi Adres Deneme Bonusu Deneme Bonusu Veren Siteler Grandpashabet Grandpashabet Giriş Adresi Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Siteler vaycasino vaycasino giriş Casibom Casibom Giriş www.giftcards.com Marsbahis Casibom Casibom Casibom Casibom Casibom Grandpashabet Grandpashabet Giriş Marsbahis Marsbahis Marsbahis Marsbahis Grandpashabet Grandpashabet Resmi Adres Casibom Fixbet Fixbet Giriş Casibom Deneme Bonusu Deneme Bonusu Veren Siteler Holiganbet Holiganbet Güncel Adres Nevşehir escort Kapadokya escort Nevşehir escort bayan nevşehir eskort escort nevşehir Casibom Casibom Giriş Adresi Kapadokya esc Casibom Casibom Resmi Adres Matbet Matbet Matbet Güncel Adres Pusulabet Pusulabet Giriş Adresi Deneme Bonusu Deneme Bonusu Veren Siteler Deneme Bonusu Deneme Bonusu Veren Siteler Trabzon escort escort trabzon Trabzon escort bayan Deneme Bonusu Deneme Bonusu Veren Siteler grandpashabet casibom grandpashabet casibom güncel giriş casibom