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Herausgeber: John Wiley & Sons
Kategorie: Fachliteratur
Sprache: Englisch

Beschreibung

Back for a new edition, Zoe Draelos' outstanding resource to cosmetic dermatology again provides a highly-illustrated, clinical guide to the full range of cosmetic skin treatments.

Bringing together experts from research, industry, surgery and practice, it is structured in four distinct parts for easy navigation by the busy clinician:

Basic Concepts - giving an overview of the physiology pertinent to cosmetic dermatology and the delivery systems by which treatments can take effect;
Hygiene Products - evaluating cleansing and moisturising products;
Adornment - looking at aesthetic techniques such as cosmetics, nail protheses and hair treatment;
Antiaging - ie, injectables, resurfacing and skin contouring techniques, and the rapidly growing area of Cosmeceuticals.

With over 300 high-quality images and key summary boxes throughout, this new edition incorporates the newest procedural innovations in this rapidly developing field. Perfect for all dermatologists, especially those specialising in cosmetic dermatology and whether hospital-based or in private practice, it provides the complete cosmetic regimen for your patients and will be an indispensable tool to consult over and over again.

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Cosmetic Dermatology

Products and Procedures

Edited by

Zoe Diana Draelos MD

Consulting Professor Department of Dermatology Duke University School of Medicine Durham, North Carolina USA

Second Edition

Registered office: John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

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All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by health science practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.

Library of Congress Cataloging-in-Publication Data

Cosmetic dermatology (Draelos) Cosmetic dermatology : products and procedures / edited by Zoe Diana Draelos.—Second edition. p. ; cm. Includes bibliographical references and index. ISBN 978-1-118-65558-0 (cloth) I. Draelos, Zoe Kececioglu, editor. II. Title. [DNLM: 1. Cosmetics. 2. Dermatologic Agents. 3. Cosmetic Techniques. 4. Dermatologic Surgical Procedures. 5. Skin Care—methods. QV 60] RL87 646.7′2—dc23

2015030110

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover images: background © Getty Images/Ian Hooton/SPL; middle © Getty Images/Renee Keith

Contributors

Foreword

Preface

PART I Basic Concepts

Section 1: Skin Physiology Pertinent to Cosmetic Dermatology

CHAPTER 1 Epidermal Barrier

Introduction

Structural components of the epidermal barrier

Functions of epidermal barrier

Regulation of barrier homeostasis

Methods for studying barrier structure and function

Relevance of skin barrier to cosmetic product development

Summary and future trends

References

CHAPTER 2 Photoaging

Introduction

Definition

Physiology

Molecular mechanisms of photoaging

Ethnic skin: photoaging

Prevention

Failure of prevention: immunosuppression

Conclusions

References

CHAPTER 3 Pigmentation and Skin of Color

Introduction

Melanocytes

Dyspigmentation

Natural sun protective factor in skin of color

Skin of color

Hair

References

CHAPTER 4 Sensitive Skin and the Somatosensory System

Introduction

Peripheral nervous system

The central projections

Conclusions

References

CHAPTER 5 Novel, Compelling, Non-invasive Techniques for Evaluating Cosmetic Products

Introduction

Commonly used non-invasive bioinstrumentation methods in cosmetic studies

Use of digital photography as a non-invasive technique for assessing skin features

Review of terminology in clinical photography

Use of raking light optical profilometry (RLOP) to detect improvements in periocular fine lines and wrinkles

A non-invasive method for assessing the antioxidant protection of topical formulations in humans

Use of image analysis for assessing a variety of skin conditions

Emerging technology for skin imaging and assessment

Conclusions

References

CHAPTER 6 Contact Dermatitis and Topical Agents

Introduction

Pathophysiology and clinical presentation

Common irritants and allergen groups

Specific cosmetic products

Diagnosis

Treatment

Conclusions

References

Section 2 Delivery of Cosmetic Skin Actives

CHAPTER 7 Percutaneous Delivery of Cosmetic Actives to the Skin

Introduction

The basics

Vehicle effect

Penetration enhancers

Penetration enhancement vectors

Devices for penetration enhancement

In vitro

and

in vivo

delivery assessment

Conclusions and future trends

References

CHAPTER 8 Creams and Ointments

Definitions of creams (and lotions) and ointments

Composition of a cream and an ointment

Ointments

References

PART II Hygiene Products

Section 1 Cleansers

CHAPTER 9 Bar Cleansers

Introduction

Impact of cleansing bars on skin structure and function

Studies comparing mildness properties of soap and syndet cleansing bars

Practical implications of mild cleansing for patients with common skin disease

The future of cleansing bars

Conclusions

References

CHAPTER 10 Personal Cleansers: Body Washes

Background

Types of body wash

Major formula components of body washes

In-use performance considerations for body washes

Who will benefit from using body washes?

Conclusions

References

CHAPTER 11 Facial Cleansers and Cleansing Cloths

A brief history of facial cleansing

How facial cleansers work

Types of facial cleanser

Guide to selecting facial cleansers

Summary

References

CHAPTER 12 Hand Cleansers and Sanitizers

Introduction

Hand microbiota

Hand hygiene guidelines

Hand Hygiene Techniques and Compliance

Antimicrobial handwash and hand sanitizer formulations

Efficacy of antimicrobial handwashes and hand sanitizers

Effectiveness of antimicrobial hand washes and hand sanitizers in institutional and community settings

Handwash and hand sanitizer safety

Future directions

References

CHAPTER 13 Shampoos for Normal Scalp Hygiene and Dandruff

Definition

Introduction

Product and formulation technology overview

Unique attributes of scalp care products

Advantages and disadvantages of the use of therapeutic shampoos

Effective use of products (see Table 13.5)

Benefits of use of scalp care shampoos

Summary

References

Section 2 Moisturizers

CHAPTER 14 Facial Moisturizers

Introduction

Dry facial skin

Facial moisturization

Facial moisturizer formulation

Moisturizer ingredients and function

Facial moisturizer testing

Use of facial moisturizers in common inflammatory dermatoses

Conclusions

References

CHAPTER 15 Hand and Foot Moisturizers

Introduction

Moisturization needs of the hand and foot

Moisturizing formulations and technologies

Natural moisturizing factors

Ultrastructural effects

Clinical demonstrations of product efficacy of sodium lactate and urea formulations

The future: Next-generation moisturizers

Conclusions

References

CHAPTER 16 Sunless Tanning Products

Introduction

Sunless tanning products

Formulation challenges

Delivery vehicles

Regulatory considerations

Product attributes

Trends in sunless tanning

Conclusions

References

CHAPTER 17 Sunscreens

Introduction

Regulatory status of sunscreens

Development of sunscreens

Criteria and methods for evaluating the efficacy of sunscreen products

Conclusions

References

Section 3 Personal Care Products

CHAPTER 18 Antiperspirants and Deodorants

Introduction

Physiology

Chemistry and formulation of antiperspirants

Delivery systems

Dermatologic concerns

Strengths and weakness of antiperspirants

Conclusions

References

CHAPTER 19 Blade Shaving

Introduction

Hair biology basics

Shaving and the razor explored

Summary

References

PART III Adornment

Section 1 Colored Facial Cosmetics

CHAPTER 20 Facial Foundation

Introduction

Complexion makeup – an ancient practice

Formulation diversity

Compact foundations

Facial foundation application

Emphasis on quality, safety and confirmed performance

Conclusions and prospects

References

CHAPTER 21 Camouflage Techniques

Introduction

Definitions

Camouflage makeup application procedures

Other camouflage therapies

Medical indications for camouflage makeup

Beginning a camouflage clinic

The camouflage therapist

Camouflage makeup and quality of life

Conclusions

References

CHAPTER 22 Lips and Lipsticks

Introduction

Lip anatomy

Lipsticks

Conclusions

References

CHAPTER 23 Eye Cosmetics

Definition

Eye cosmetic history

Eyelash physiology

Mascara

Eyebrows

Eyeshadow

Eyeliners

Product application

Safety and regulatory considerations for eye area cosmetics

The future of eye cosmetics

References

Note

Section 2 Nail Cosmetics

CHAPTER 24 Nail Physiology and Grooming

Introduction: Nail physiology

Physical properties of nails

Nail grooming principles

Conclusions

References

List of Tables

Chapter 1

Table 1.1

Table 1.2

Table 1.3

Table 1.4

Chapter 4

Table 4.1

Chapter 5

Table 5.1

Table 5.2

Table 5.3

Chapter 6

Table 6.1

Table 6.2

Chapter 7

Table 7.1

Table 7.2

Table 7.3

Chapter 8

Table 8.1

Table 8.2

Table 8.3

Table 8.4

Table 8.5

Chapter 11

Table 11.1

Chapter 12

Table 12.1

Table 12.2

Table 12.3

Chapter 13

Table 13.1

Table 13.2

Table 13.3

Table 13.4

Table 13.5

Chapter 14

Table 14.1

Chapter 15

Table 15.1

Table 15.2

Table 15.3

Table 15.4

Chapter 16

Table 16.1

Table 16.2

Chapter 17

Table 17.1

Table 17.2

Table 17.3

Table 17.4

Table 17.5

Chapter 19

Table 19.1

Chapter 20

Table 20.1

Chapter 22

Table 22.1

Table 22.2

Table 22.3

Table 22.4

Chapter 23

Table 23.1

Table 23.2

Chapter 24

Table 24.1

Table 24.2

Table 24.3

Chapter 25

Table 25.1

Table 25.2

Table 25.3

Chapter 26

Table 26.1

Table 26.2

Chapter 27

Table 27.1

Table 27.2

Table 27.3

Chapter 28

Table 28.1

Table 28.2

Table 28.3

Chapter 29

Table 29.1

Table 29.2

Table 29.3

Chapter 30

Table 30.1

Table 30.2

Chapter 31

Table 31.1

Table 31.2

Table 31.3

Table 31.4

Chapter 32

Table 32.1

Table 32.2

Table 32.3

Table 32.4

Table 32.5

Table 32.6

Chapter 33

Table 33.1

Table 33.2

Chapter 34

Table 34.1

Table 34.2

Table 34.3

Chapter 35

Table 35.1

Table 35.2

Chapter 37

Table 37.1

Table 37.2

Table 37.3

Table 37.4

Table 37.5

Table 37.6

Chapter 38

Table 38.1

Table 38.2

Chapter 39

Table 39.1

Chapter 40

Table 40.1

Table 40.2

Table 40.3

Chapter 41

Table 41.1

Chapter 43

Table 43.1

Chapter 45

Table 45.1

Table 45.2

Table 45.3

Table 45.4

Chapter 46

Table 46.1

Table 46.2

Table 46.3

Table 46.4

Table 46.5

Table 46.6

Chapter 47

Table 47.1

Chapter 48

Table 48.1

Table 48.2

Table 48.3

Table 48.4

Chapter 49

Table 49.1

Table 49.2

Chapter 50

Table 50.1

Table 50.2

Table 50.3

Chapter 51

Table 51.1

Chapter 53

Table 53.1

Table 53.2

Table 53.3

Chapter 54

Table 54.1

Table 54.2

Table 54.3

Chapter 55

Table 55.1

Table 55.2

Chapter 56

Table 56.1

Table 56.2

Chapter 57

Table 57.1

Chapter 58

Table 58.1

Table 58.2

Table 58.3

Table 58.4

Table 58.5

Chapter 59

Table 59.1

Table 59.2

List of Illustrations

Chapter 1

Figure 1.1

Diagram of the epidermis indicating the different layers of the epidermis and other structural components of the epidermal barrier.

Chapter 2

Figure 2.1

Ultraviolet light interacts with different skin cells at different depths. More specifically, energy from UVB rays is mostly absorbed by the epidermis and affects epidermal cells such as the keratinocytes. Energy from UVA rays affects both epidermal keratinocytes and the deeper dermal fibroblasts. AP-1, activator protein 1; NF-κB, nuclear factor κB; MMP, matrix metalloproteinase; mtDNA, mitochondrial DNA; ROS, reactive oxygen species. (Source: Berneburg

et al

., 2000 [30]. Reproduced with permission of John Wiley & Sons.)

Figure 2.2

The regulation of procollagen production: the TGF-β/Smad signaling pathway. AP-1, activator protein 1; TβR, TGF-β receptor; TGF-β, transforming growth factor β. (Source: Kang

et al.

, 2001 [3]. Reproduced with permission of Elsevier.)

Figure 2.3

Model depicting the acute and chronic effects of UV irradiation on skin angiogenesis and extracellular matrix (ECM) degradation in human skin. MMP, matrix metalloproteinase; TSP, thrombospondin-1 (ECM protein; inhibitor of angiogenesis in epithelial tissues); VEGF, vascular endothelial growth factor. (Source: Chung & Eun, 2007 [17]. Reproduced with permission of John Wiley & Sons.)

Figure 2.4

Model depicting the effect of topical retinoids on photoaged human skin. ECM, extracellular matrix; MMP, matrix metalloproteinase; VEGF, vascular endothelial growth factor. (Source: Chung and Eun, 2007 [17]. Reproduced with permission of John Wiley & Sons.)

Chapter 3

Figure 3.1

Morphologic signs of aging. (Source: Halder, 2006 [55]. Adapted with permission of Taylor & Francis.)

Figure 3.2

The spectrum of curliness in human hair. (Source: Loussouarn

et al

., 2007 [

Int J Dermatol

46 (Suppl 1), 2, 3, 4, 5, 6.] Reproduced with permission of John Wiley & Sons.)

Figure 3.3

K38 hair keratin distribution in hair follicles. K38 pattern in (a) straight, (b) wavy, and (c) curly hair longitudinal sections. K38 pattern in (d) straight and (e) curly hair cross-sections. (Source: Thibaut

et al

., 2007 [

]. Reproduced with permission of John Wiley & Sons.)

Chapter 4

Figure 4.1

A cross-sectional perspective of (a) glabrous and (b) hairy skin. (Source: R.T. Verrillo, artist. Reproduced with permission.)

Figure 4.2

The four types of low threshold mechanoreceptors in human glabrous skin are depicted. The four panels in the center show the nerve firing responses to a ramp and hold indentation and the frequency of occurrence (%) and putative morphologic correlate. The black dots in the left panel show the receptive fields of type I (top) and type II (bottom) afferents. The right panel shows the average density of type I (top) and type II (bottom) afferents with darker area depicting higher densities. (Source: Westling, 1986 [29]. Reproduced with permission.)

Figure 4.3

Resting discharge of a C cold fiber at room temperature [11]. (a) The resting discharge is suppressed by warming of the receptive field (RF) from 31°C to 35°C. (b) From a holding temperature of 35°C, at which the unit is silent, activity is initiated by cooling the RF to 31°C. (Time bar: 5 s.)

Figure 4.4

(a) Outline of the somatosensory pathways from the digit tip to primary somatosensory cortex, via the dorsal column nuclei and the thalamus. (b) Penfield’s somatosensory homunculus. Note the relative overrepresentation of the hands and lips, and the relative underrepresentation of the trunk and arms.

Figure 4.5

Cortical areas subserving somatosensation. Primary somatosensory cortex is located in the posterior bank of the central sulcus and the posterior gyrus and comprises areas 2, 1, 3a and 3b, secondary somatosensory cortex is located in the upper bank of the lateral sulcus with two further somatosensory regions in the posterior parietal cortex, areas 5 and 7b.

Chapter 5

Figure 5.1

An example of a Stephens & Associates, Inc. photographic studio. The studio is equipped for taking photographs using standard lighting, parallel and polarized lighting, cross polarized lighting and raking light.

Figure 5.2

An example of raking light photography technique accentuating cellulite condition on the back of the thighs. (a) Standard light; (b) raking light.

Figure 5.3

Examples of a parallel-polarized lighting technique (a) and cross-polarized lighting technique (b).

Figure 5.4

Before and after UV reflectance photographs of a subject treated with a skin lightening product. (a) Ultraviolet reflectance at baseline. (b) Ultraviolet reflectance at 12 weeks.

Figure 5.5

Ultraviolet fluorescence technique.

Figure 5.6

Before and after photographs using Raking Light Optical Profilometry. Top row: Digital photographs from a trial of a subject before (a) and 8 weeks after (b) treatment. Note the improvement in the appearance of wrinkling under the eye. Bottom row: Photographs shows wrinkles and fine lines highlighted in red after SWIRL analysis. (c) Baseline. (d) Eight weeks after. The area of interest (AOIs) were + located in each digital image by using anatomic landmarks as anchors.

Figure 5.7

Pattern of UV responses for a site treated with an antioxidant and a site treated with a vehicle control.

Figure 5.8

An example of images captured using SiaScope.

Figure 5.9

An example of images taken using VivoSight.

Chapter 7

Figure 7.1

Possible pathways for a penetrant to cross the skin barrier. (1) Across the intact horny layer; (2) through the hair follicles with the associated sebaceous glands; or (3) via the sweat glands. (Source: Daniels R. Strategies for skin penetration enhancement.

Skin Care Forum

, www.scf-online.com.)

Figure 7.2

Cumulative amount of indomethicin (initial loading 0.5% w/v) per unit area, permeating through excised rat skin when released from PNBCA nanocapsule dispersion in pH 7.4 phosphate buffer, PNBCA nanocapsule dispersion in Pluronic F-127 gel and 25% w/w Pluronic F-127 gel. Each value is the mean ± SE of four determinations. (Source: Miyazaki

et al

., 2003 [

J Pharm Pharmaceut Sci

6, 238–45]. Creative Common license (Attribution-ShareAlike) License.)

Figure 7.3

Solid microneedles fabricated out of silicon, polymer, and metal, imaged by scanning electron microscopy. (a) Silicon microneedle (150 μm tall) from a 400-needle array etched out of a silicon substrate. (b) Section of an array containing 160 000 silicon microneedles (25 μm tall). (c) Metal microneedle (120 μm tall) from a 400-needle array made by electrodepositing onto a polymeric mold. (d–f) Biodegradable polymer microneedles with beveled tips from 100-needle arrays made by filling polymeric molds. (d) Flat-bevel tip made of polylactic acid (400 μm tall). (e) Curved-bevel tip made of polyglycolic acid (600 μm tall). (f) Curved-bevel tip with a groove etched along the full length of the needle made of polyglycolic acid (400 μm tall). (Source: McAllister

et al

., 2003 [

Proc Natl Acad Sci USA

100,

13755–60]. Reproduced with permission.)

Figure 7.4

The Franz diffusion chamber.

Figure 7.5

The microdialysis apparatus for the evaluation of penetration through the human skin barrier. (Source: Schnetz & Fartasch, 2001 [

Eur J Pharm Sci

12, 165–74]. Reproduced with permission of Elsevier.)

Chapter 8

Figure 8.1

Different emulsion types.

Chapter 9

Figure 9.1

Dollar segmentation of U.S. cleanser market shows that bars continue to command significant share. Bars in the U.S. alone have a total value of $1.6billion of which syndet bars are the majority share. (2013 data.)

Figure 9.2

Schematic representation of the molecular structures of soap (sodium alkyl carboxylate) and syndet (sodium acyl isethionate) showing the difference in head group structure and size.

Figure 9.3

Swelling of the stratum corneum in different pH buffer solutions. (a) Optical coherence tomography (OCT) images of ex vivo skin treated with different buffer solutions. The arrows show the position and thickness of the stratum corneum. (b) The bar chart provides a graphic representation of the same difference.

Figure 9.4

Environmental scanning electron micrographs (ESEM) and transmission electron micrographs (TEM) images of human skin washed with water, soap, and a syndet bar (9 repeat washes). Water washed and mild syndet bar washed skin shows well-preserved lipids and plumped (hydrated) corneocytes. By contrast, images of harsh soap-washed skin show significant removal of lipids and damage to proteins.

Figure 9.5

Visual dryness change observed in a forearm controlled application test (FCAT) using two commercially available syndet Bars at pH 5.5 based compared to neutral pH syndet bar. Bars at pH 5.5 cause more dryness than the one at pH 7.0.

Figure 9.6

Visual dryness change observed in a forearm controlled application test (FCAT) using two syndet bars identical in surfactant composition and differing only in pH. The pH 5.5 bars appears to cause more dryness than the one at pH 7.0.

Figure 9.7

Binding of anionic surfactant, sodium lauroyl isethionate, increases with decrease in pH from neutral pH region. Binding shows a minimum around the neutral pH region. Increase in binding with decrease in pH in the acidic region is thought to be due to increase in the number of positive sites and reduction in the negative sites. IEP (isoelectric point of keratin is around pH 5)

Figure 9.8

Harsh cleansing leads to loss of lipids leaving skin more vulnerable to irritation, decreased barrier function and further damage to future washing episodes.

Figure 9.9

Skin changes after 5 days of twice daily washing with soaps and syndet using the forearm controlled application test (FCAT) method. (a) Transepidermal water loss rate and (b) Visual dryness are significantly lower for syndet bar as compared to regular soaps

Figure 9.10

Changes in skin mechanical properties (stiffness) after 5 days of twice daily washing with soap and syndet using the FCAT method. Soap washing induced a progressive increase in stratum corneum stiffness as measured using a linear skin rheometer whereas the syndet bar did not induce stiffness.

Figure 9.11

Skin dryness induced by soap and syndet bars in a 5-day controlled arm wash test compared to dryness induced by 2–7 days of normal use once daily for facial cleansing. Arm wash test carried out on the same subjects as the 7-day facial wash test. Most soap users were unable to continue soap use for a full week. Most syndet users were able to complete a full week of daily face washing – dryness scores are based on assessments made on day 7 for the whole panel.

Figure 9.12

Use of a syndet bar instead of a soap bar reduced severity of skin ashiness on arms and legs while visual dryness significantly improved on forearms and elbows.

Figure 9.13

Use of a syndet bar instead of a soap bar reduced clinically assess appearance of photodamaged facial skin, with significant effects on texture, clarity brightness and tone.

Figure 9.14

Changes in dermatologist and patient assessment of skin condition after 4 weeks’ daily use of syndet cleansing bars by adult and child (7–15 years) patients with atopic dermatitis (AD). A total of 25 patients used bar A and 25 used bar B. The patients were patients with chronic AD stabilized using a variety of treatment regimens which they continued during the trial. The bars were similar in composition with the same acyl isethionate synthetic surfactant system and different ratios of emollients.

Figure 9.15

Dermatologist assessed changes in skin condition of patients with mild to moderate acne or mild to moderate rosacea after 4 weeks’ use of soap or syndet bar for daily cleansing. In the acne study were 50 patients using topical benzamycin or benzamycin plus differin. In the rosacea study were 70 patients using topical metronidazole. The syndet bar was acyl isethionate synthetic surfactant and the soap bar was a standard 80/20 soap.

Chapter 10

Figure 10.1

Expert dryness scores after 7 days of once-daily washing with marketed body wash products. The results show marked differences in the products’ abilities to provide a dry skin improvement (i.e. a skin moisturization benefit).

Figure 10.2

Scanning electron microscope (SEM) photomicrographs of skin flakes adhering to tape strips taken from subjects’ legs before (a) and after (b) using a petrolatum-depositing body wash for 3 weeks. Baseline samples show numerous large, thick, dry skin flakes; endpoint samples show fewer and thinner flakes.

Figure 10.3

Responses to psychosocial questions answered by African-American subjects before and after using a syndet bar or petrolatum-depositing body wash for 4 weeks. Items were rated on a +3 (strongly agree) to −3 (strongly disagree) scale. Ratings were not significantly different at baseline (P ≥ 0.48); endpoint ratings given by subjects assigned to use the body wash were significantly better than those given by subjects assigned to use the syndet bar (P < 0.01).

Chapter 11

Figure 11.1

One of the main cleansing ritual preferences: no substrate/substrate and lathering/non-lathering.

Figure 11.2

Products for the removal of excess sebaceous oil.

Figure 11.3

Products for the removal of dirt and makeup.

Figure 11.4

Products for the removal of dry, dead skin cells.

Figure 11.5

Products for patients for whom dry skin is a key complaint.

Chapter 12

Figure 12.1

The common microbiota of the hand.

Figure 12.2

Effects of different hand sanitizer formulations on greasy soil.

Chapter 13

Figure 13.1

(A) Image of normal scalp skin. (B) Dandruff scalp image showing adherent white flakes. (C) Seborrheic dermatitis with more evidence of sebum yellowing on flakes and underlying erythema.

Figure 13.2

Representation of the shampoo segments, differentiating cosmetic from therapeutic shampoos and their key attributes. The category of cosmetically optimized therapeutics achieves therapeutic benefits without diminishing esthetic attributes.

Figure 13.3

(a) Conceptual representation of the zone of inhibition of fungal growth surrounding ZPT particles and the importance of spatial distribution of particles to achieve uniformity of coverage. (b) ZPT can dissociate into component pyrithione (PT) and zinc (Zn) which reduces the presence of the intact bioactive species. The addition of zinc carbonate alters this equilibrium to maintain ZPT in its bioactive intact form.

Figure 13.4

Electron micrograph of a unique form of ZPT, optimized for size and morphology to maximize the efficiency of surface coverage.

Chapter 14

Figure 14.1

Skin surface hydration and transepidermal water loss (TEWL) and SciCon ratio.

Chapter 15

Figure 15.1

Freeze–fracture scanning electron micrographs of the stratum corneum of skin treated with a vehicle lotion (a) or the vehicle lotion containing 10% urea and sodium lactate (b).

Figure 15.2

Stratum corneum urea content before application, after 2 weeks of daily use, and 3 days after discontinuing application of an oil-in-water emulsion containing 5% urea and 2.5% sodium lactate.

Figure 15.3

Improvement in hand eczema (top) and xerosis (bottom) after 4 weeks of daily usage (right) of a hand cream containing 5% urea and sodium lactate.

Figure 15.4

Improvement in diabetic foot skin after 6 weeks of daily usage of a foot cream containing 10% urea and 5% sodium lactate. Pretreatment photos (left) of two different subjects (top and bottom) and their corresponding week 6 photos (right).

Figure 15.5

Immunohistochemical localization of the AQP3 protein in keratinocyte monolayers stained with a rabbit antihuman AQP3 antibody. Background control (left), untreated control (center), treatment with 3% enhanced glycerol derivative for 48 hours (right).

Figure 15.6

In vivo

study of 23 volunteers with dry skin. Transepidermal water loss (TEWL) measurement after the following treatments: vehicle; vehicle with 6.5% glycerol; and vehicle with 6.5% glycerol and 5% enhanced glycerol derivative (EGD).

Chapter 16

Figure 16.1

Chemical structure of dihydroxyacetone (DHA).

Chapter 18

Figure 18.1

Underarm sweat gland mechanism.

Figure 18.2

Cross-section of skin and sweat glands.

Figure 18.3

Sweat metabolism cycle.

Figure 18.4

Antiperspirant formula matrix delivery systems.

Chapter 19

Figure 19.1

Optical micrographs of hair cross-sections taken from the beard (a) and scalp (b) area of the same subject. Beard fibers have a greater cross-sectional area and more cuticle layers than scalp hair [3]. Magnification 915×.

Figure 19.2

A scanning electron micrograph of a replica of an area of cheek on a male face. The topography of the skin is highly variable and combined with the presence of hairs this creates a very irregular terrain over which an incredibly sharp blade traverses.

Figure 19.3

Cross-section of a double-edge razor showing exposure geometry.

Figure 19.4

Model of multiple blade razors and skin management: five blade razors with lower inter-blade distance (a) distribute the shaving force more evenly onto the skin than fewer blades with a larger inter-blade span (b), thus reducing the height of the skin bulges between the blades for a more comfortable shave.

Figure 19.5

The key components of a razor and their functions.

Figure 19.6

Illustration showing computer modeling of the stress in skin caused by hair cutting force. Finer blades (a) cut with less force versus thicker blades (b). This results in reduced stress in the surrounding skin [12].

Figure 19.7

Effect of hydration time on force required to cut (beard) hair. The most significant reduction occurs over the first 2 minutes.

Chapter 20

Figure 20.1

Diversity of textures: from fluid emulsion to paste dispersion.

Figure 20.2

The four iron oxides used in foundations.

Figure 20.3

Shape variety of fillers (a

–

c).

Figure 20.4

(a) The color of the forehead was measured using a spectroradiometer inside a Chromasphere™. (b) The volunteer placed her face into the Chromasphere. A standardized camera was used to acquire pictures of the face. (c) A spectroradiometer measured the reflectance of forehead in the visible field 400–700 nm every 4 nm. The recorded spectrum was expressed in the CIE 1976 standard colorimetric space L*C*h D65/10 ° where each color is described through three coordinates that reflect perception by human eye. h, Hue angle (angular coordinate); C*, chroma (radius coordinate); L*, lightness (

axis).

Figure 20.5

The worldwide skin color space depicted in (h, L*) and split in six groups of skin tones that reflect the color diversity.

Chapter 21

Figure 21.1

Ideal corrective makeup: a compromise between coverage and cosmetic qualities. After Sylvie Guichard, L'Oréal Research.

Figure 21.2

Camouflage makeup technique. (a) Warm the product on the back of the hand. (b) Apply over the imperfection to be covered. (c) Blend in round the edges.

Figure 21.3

Perioribital hyperpigmentation: (a) before and (b) after camouflage.

Figure 21.4

Vitiligo: (a) (i & ii) before and (b) (i & ii) after camouflage.

Figure 21.5

Melasma: (a) before and (b) after camouflage.

Figure 21.6

Vascular malformation: (a) (i & ii) before and (b) (i & ii) after camouflage.

Figure 21.7

Telangiectasia: (a) before and (b) after camouflage.

Figure 21.8

Acne: (a) before and (b) after camouflage.

Chapter 22

Figure 22.1

Lip histology.

Chapter 23

Figure 23.1

Eyelash SEM images. The eyelash tapers to a fine tip. The cross section may be circular or elliptical (A), and the surface is composed of overlapping cuticle cells (B).

Figure 23.2

Twisted wire brush mascara applicators.

Figure 23.3

Molded mascara applicator with precisely engineered parallel bristles.

Figure 23.4

Various molded mascara applicator designs showing the wide range of possibilities that are possible with this versatile applicator type.

Figure 23.5

The impact of eye cosmetics on eye beauty.

Figure 23.6

SEM images of mascara film morphology. Rough mascara film of a long wearing waterproof mascara that lasts a day (a), and microscopically smooth continuous mascara film of a semi-permanent mascara that lasts multiple days (b).

Chapter 24

Figure 24.1

Nail unit with lines indicating important structures.

Figure 24.2

Diagram of the nail unit.

Figure 24.3

Paronychia.

Figure 24.4

(a & b) Onycholysis.

Figure 24.5

(a–c) Brittle nails.

Figure 24.6

Onychoschizia, distal lamallar peeling of the nail plate.

Figure 24.7

(a) Manicure; (b–d) Pedicure.

Figure 24.8

Psoriasis: salmon patch oil drop discoloration.

Figure 24.9

Onychomycosis.

Figure 24.10

Yellow staining from nail polish.

Figure 24.11

Allergic contact dermatitis from nail cosmetics. (a) On the eyelid. (b) On periungal skin caused by acrylates.

Figure 24.12

(a & b) Keratin granulations.

Figure 24.13

Infection caused by

Pseudomonas

Chapter 25

Figure 25.1

Lacquered nails. (Source: OPI Products, Inc., Los Angeles, CA. Reproduced with permission.)

Figure 25.2

Painting a nail. (Source: OPI Products, Inc., Los Angeles, CA. Reproduced with permission.)

Figure 25.3

Be careful with the cuticle. (Source: OPI Products, Inc., Los Angeles, CA. Reproduced with permission.)

Figure 25.4

Infected nail. (Source: Nails Magazine. Reproduced with permission.).

Figure 25.5

Dermatitis on the finger. (Source: Nails Magazine. Reproduced with permission.).

Figure 25.6

Nail lacquer. (Source: OPI Products, Inc., Los Angeles, CA. Reproduced with permission.)

Figure 25.7

Brittle nail. (Source: Nails Magazine. Reproduced with permission.)

Figure 25.8

Formaldehyde versus methylene glycol. Reproduced by permission of OPI Products, Inc.

Figure 25.9

Tosylamide formaldehyde resin. Reproduced by permission of OPI Products, Inc.

Figure 25.10

UV curing lamp. (Source: OPI Products, Inc., Los Angeles, CA. Reproduced with permission.)

Figure 25.11

Polish remover in action. (Source: OPI Products, Inc., Los Angeles, CA. Reproduced with permission.)

Chapter 26

Figure 26.1

The use of custom-blended colored powders with methacrylate monomers to “illusion sculpt” and extend the apparent length of a short nail bed while also correcting a habitually splitting nail plate. (Source: Creative Nail Design, Inc., Vista, CA, USA. Reproduced with permission.)

Figure 26.2

Chemical structure differences between methacrylates and acrylates.

Figure 26.3

Equipment used to create liquid and powder artificial nails. 1, Nail scrub brush; 2, Dappen dishes containing liquid and powder; 3, Mylar nail form; 4, Abrasive files; 5, Nail enhancement application brush; 6, ABS preformed nail tips; 7, Plastic-backed cotton pad; 8, Nitrile gloves; 9, N-95 dust mask. (Source: Paul Rollins Photography, Inc. Geyserville, CA, USA.)

Figure 26.4

Traditional fluorescent-style UV nail lamp (Source: Paul Rollins Photography, Inc. Geyserville, CA, USA.)

Figure 26.5

Newer LED-style UV nail lamp (Source: Paul Rollins Photography, Inc. Geyserville, CA, USA.)

Figure 26.6

Materials needed to apply nail wraps. 1, Abrasive file for nail preparation and final shaping; 2, Scissors for cutting fabric; 3, Block buffer for high-shining; 4, Cyanoacrylates; 5, Spray-on catalyst; 6, Silk fabric; 7, Pusher to gently remove skin from the nail plate. (Source: Paul Rollins Photography, Inc. Geyserville, CA, USA.)

Figure 26.7

Surface nail damage caused by improper removal of nail coatings; 1. Peeling, 2. Aggressive scraping, 3. Aggressive filing and scraping, 4. Residual nail coating left on the nail plate when removal time is improperly shortened. (Source: Doug Schoon, Schoon Scientific, Dana Point, CA, USA.)

Figure 26.8

Example of an adverse skin reaction caused by repeated contact to the skin. (Source: Paul Rollins Photography, Inc. Geyserville, CA, USA.)

Figure 26.9

Example of a nail infection growing underneath an artificial nail. (Source: Paul Rollins Photography, Inc., Geyserville, CA, USA.)

Chapter 27

Figure 27.1

(a) Horizontal section of a 4 mm scalp biopsy specimen demonstrating follicular units containing 1, 2, 3, or 5 anagen follicles. (b) Vertical section of a 4-mm scalp punch biopsy specimen from a normal, healthy Caucasian female in her early twenties.

Figure 27.2

Schematic presentation of the complex pattern of hair keratin expression in the human hair follicle. (Source: Langbein, 2007 [2]. Reproduced with permission of Nature Publishing.)

Chapter 28

Figure 28.1

Hair cross-section showing color penetration after semi-permanent dyeing.

Figure 28.2

Hair cross-section showing color penetration after demi-permanent dyeing.

Figure 28.3

Hair cross-section showing color penetration after permanent dyeing.

Figure 28.4

Longitudinal section of hair fiber showing melanin distribution across the cortex.

Figure 28.5

Some typical oxidative dye precursors (top) and couplers (bottom).

Figure 28.6

The three main steps in oxidative dye formation (here with p-phenylenediamine and m-phenylenediamine).

Figure 28.7

Change in surface hydrophobicity before (a) and after (b) bleaching.

Chapter 29

Figure 29.1

(a) The fracture plane of a hair fiber clearly shows the composite of a fibrillar core with flattened cuticle cell coating (SEM ×1420). (b) Just emerging hair: 1, scalp surface; 2, cuticle pattern of hair fiber surface; 3, interior of the hair with cortical cells; 4, medullary cells; 5, cell membrane.

Figure 29.2

The intact cuticle pattern of the hair fiber near the scalp (SEM ×800).

Figure 29.3

The worn cuticle-free split end of hair (SEM ×800).

Figure 29.4

Coiled (alfa-helical) and amorphous molecules of hair proteins are cross-linked by disulfide bonds inside the cortical cells. Helical proteins are stabilized by hydrogen bonds.

Figure 29.5

Chemical formula of the amino acid “cystine”.

Figure 29.6

Chemical reaction formulas 0–2.

Figure 29.7

(a) Sulfur bridges between the proteins are closed. (b) Part of the sulfur bridges are being cleaved, proteins shift, take on the form. (c) Sulfur bridges are being rebuilt at a different site, neutralizer fixes the new shape.

Figure 29.8

(a) Shampooed hair is wound on curlers while still moist. Bending strain is applied to the protein chains. (b) Perm-wave lotion 1 is applied to the hair and cleaves part of the sulfur bridges by the reducing (thioglycolic acid) and the alkalizing agent. Hair is softened, proteins creep and adjust to the shape of the curler. (c) Neutralizing process: an acid neutralizer (peroxide) rebuilds the sulfur bridges at different sites and the new shape is permanent.

Figure 29.9

Hair, properly wound, fixed on rollers, and wetted by the perming lotion (a) delivers perfect locks (b).

Figure 29.10

The curtain-like structure of a hair surface indicates heavy perming damage.

Figure 29.11

A bleach applied immediately after a perming treatment chips off the cuticle as a whole (SEM ×700).

Chapter 30

Figure 30.1

Hair classification types to differentiate the degree of curl in hair.

Scheme 30.1

Scheme 30.2

Scheme 30.3

Figure 30.2

Scanning electron micrograph images of hair fibers under different treatment conditions, (a) virgin; (b) after relaxer rinse only; (c) after neutralization; (d) after conditioning.

Figure 30.3

Combing profiles of curly and straightened hair.

Chapter 31

Figure 31.1

Styling aids can provide improved appearance of hair volume and smoothness. (a) Frizzy unruly hair dried without styling aids. (b) Frizzy unruly hair smoothed with application of styling aids. (c) Fine/thin hair dried without styling aids. (d) Fine/thin hair volumized through the application of styling aids.

Figure 31.2

Mechanisms to stabilize hair structure and shape via keratin chain interactions. (Source: Umbach, 2004 [7]. Reproduced with permission of John Wiley & Sons.)

Figure 31.3

Curl retention with and without addition of spray in high humidity (85% relative humidity. (Source: Wella, 2001 [8]. Reproduced with permission of Pocter & Gamble.)

Figure 31.4

The broad range of modern styling aid forms and chemistries.

Figure 31.5

Hairspray bond – spot weld.

Figure 31.6

Comparison of African (a), Caucasian (b), and Asian (c) hair structure.

Chapter 33

Figure 33.1

Skin inflammation pathway.

Figure 33.2

Proposed mechanism for curcumin inhibition of inflammatory signaling pathways.

Figure 33.3

Anti-inflammatory properties of antioxidants. (a) Inhibition of the inflammatory mediator prostaglandin E 2 (PGE-2) in human keratinocytes by antioxidants. (b) Inhibition of four important skin inflammatory mediators by luteolin and vitamin C.

Figure 33.4

Glucocorticoid and immunomodulator inhibition of inflammatory pathways. (a) Mechanism of glucocorticoid inhibition of the NF-κB driven inflammation pathway. (b) Diagram of calcineurin and NFAT activation and inhibition by tacrolimus/pimecrolimus.

Figure 33.5

Inhibition of UVR induced erythema by post-irradiation topical application of phenolic antioxidant, 4-propyl guaiacol. Photograph taken 6 hours after UVB irradiation with 3 MED.

Chapter 34

Figure 34.1

Phenylalanine, one of the 20 proteinogenic amino acids. The “side chain” which is characteristic of each amino acid (here a phenyl group) is shown in the box.

Figure 34.2

Glutathione (γ-glutamyl-cysteinyl-glycine).

Figure 34.3

The matrikine concept: A tissue protein (e.g. collagen, elastin, fibronectin) is broken into fragments by enzymatic hydrolysis, either during normal tissue renewal, or as a consequence of induced damages (free radicals, burning, mechanical wound). The breaking up of the protein does not occur randomly, nor sequentially from one or the other end; various pieces of amino acid strings are generated, which when small enough, are readily available to act as “messengers” in the surrounding tissue, and will act as chemoattractants, transport aids, and stimulants to trigger neosynthesis of the necessary tissue molecules to renew/repair the three-dimensional structure.

Figure 34.4

A Dermascan C (Cortex) echograph equipped with a 50 MHz frequency probe was used to obtain images approximately 6 mm wide and 3 mm thick with a resolution of 25 × 60 μm. A sequence of 100 successive images was recorded over 4 cm. Five representative images were extracted and analysed by image analysis. The SLEB is traced accurately over a width of 5.5 mm allowing its depth (in μm) and density (in Grey Scale Levels or GSL) to be calculated automatically.

Figure 34.5

Hair follicles in survival medium, incubated 14 days; (a & b) control; (c & d) 5 p.p.m. Biot-GHK.

Figure 34.6

Expression lines on the front before and after treating a panelist with the Pal-KM(O

)K peptide for two months.

Figure 34.7

demonstration of the improvement of skin firmness after using the Ac-Tyr-Arg-hexadecylester dipeptide for one month. A weight is attached to the jowl and the skin extension is quantified. Left: before; right: after one month.

Figure 34.8

Scanning electron microscope (SEM) pictures of skin treated with an occlusive patch for 2 hours; (a) control cream pH 7; (b) cream with AHA to pH 3.5; (c) cream with 2% proteolytic enzyme solution (10 proteolytic units/mL).

Chapter 35

Figure 35.1

Healing and remodeling of skin damaged by the effect of intrinsic aging, extrinsic aging, wound or laser procedures. (Source: Mehta & Fitzpatrick, 2007 [2]. Reproduced with permission of John Wiley & Sons.)

Figure 35.2

Histology of skin before (a) and after 3 months of TNS Recovery Complex (b) showing increase in grenz-zone collagen and epidermal thickness after treatment [11].

Figure 35.3

Photograph of periorbital and upper cheek area before (a) and after 6 months of TNS Recovery Complex (b) showing reduction in wrinkles and fine lines after treatment [12].

Figure 35.4

Human skin model for determining biological activity of growth factor containing products [18].

Chapter 36

Figure 36.1

Biochemical pathways from dietary provitamins A to biological responses. Abbreviations: ARAT, acyl-coenzyme A:retinol acyltransferase; BCO, β-carotene-15,15’-monooxygenase; CAR, β-carotene; CYP26, cytochrome P450 26; LRAT, lecithin:retinol acyltransferase; oxoRA, all-

trans

-4-oxoretinoic acid; oxoRAL, all-

trans

-4-oxoretinal; oxoROL, all-

trans

-4-oxoretinol; RA, all-

trans

-retinoic acid; RA-Glu, all-

trans

-retinoyl-β-D-glucuronide; RAL, all-

trans

-retinaldehyde; RALDH, retinal dehydrogenase; RE, retinyl esters; REH, retinyl ester hydrolase; RoDH, retinol dehydrogenase; ROL, all-

trans

-retinol; ROL-Glu, all-

trans

-retinyl- β-D-glucuronide; UGT, UDP-glucuronosyl transferase.

Figure 36.2

Molecular structures. The molecular structures of therapeutic (A) and cosmeceutical (B) retinoids are indicated. Notes: (1) “R” in retinyl esters represents an acyl radical; (2) 4-oxoretinoids are indicated, because they have been shown to have a “soft” retinoid action [11]; however, to our knowledge, they haven’t yet been added in topical formulations; (3) OGG is not a retinoid, but, as mentioned in the text, is a potential cosmeceutical retinoid partner.

Chapter 37

Figure 37.1

Conversion of retinyl ester into trans-retinoic acid in the skin.

Figure 37.2

Topical retinyl propionate (RP) reduces the appearance of fine lines/wrinkles. 0.2% retinyl propionate in a stable skin care emulsion system was applied twice daily for 12 weeks. Images were taken at baseline, and weeks 4, 8, and 12.

Figure 37.3

Niacinamide as precursor to energy co-factors: nicotinamide adenine dinucleotide (NAD), nicotinamide adenine dinucleotide phosphate (NADP), and their reduced forms NADH and NADPH.

Figure 37.4

Topical niacinamide reduces hyperpigmented spots.

Chapter 38

Figure 38.1

Maltobionic acid, a bionic acid.

Figure 38.2

Reduction of advanced glycation end-products (AGEs) by targeting specific steps in the Maillard reaction.

Figure 38.3

Percent inhibition of non-enzymatic glycation by maltobionic acid *p < 0.05.

Figure 38.4

Inhibition of matrix metalloproteinase (MMP) activity by maltobionic acid

in vitro.

Figure 38.5

Histologic staining for acid mucopolysaccharides/glycosaminoglycans (GAGs): ×400. (a) Specimen shows staining of untreated control forearm skin. (b) Specimen shows staining following topical application of 8% maltobionic acid cream (pH 3.8) for 12 weeks. Increased density of blue colloidal iron stain demonstrates an increase in GAGs. (Source: Green & Briden, 2009 [11]. Reproduced with permission of Elsevier.)

Figure 38.6

Hyperkeratotic feet treated once nightly with a cream containing an AHA/PHA/bionic acid blend (20% total) for 3 weeks. (a) Before treatment. (b) After treatment.

Figure 38.7

Periocular wrinkling is reduced on this 49-year-old female following twice daily application of 8% maltobionic acid cream (pH 3.8) for 12 weeks. (a) Before treatment. (b) After treatment.

Figure 38.8

Improvement in acne and superficial acne scarring following application of five glycolic acid peels (35%, 50%, 50%, 50%, 70%) with use of adjunctive home care products containing AHAs, PHAs, bionic acids and other benefit ingredients.

Figure 38.9

Improvement in periocular rhytides in a rosacea patient following application of four glycolic acid peels (35%, 50%, 70%, 70%) with use of adjunctive home care products containing AHAs, PHAs, bionic acids and other benefit ingredients.

Figure 38.10

Improvement in post-inflammatory hyperpigmentation in an eczema patient following application of two glycolic acid peels (35%, 50%) with use of adjunctive PHA-containing home care products (cleanser, day cream SPF 15 and night cream) in conjunction with a 2% hydroquinone + PHA/bionic acid cream applied to areas of hyperpigmentation and a topical corticosteroid applied to eczema lesions.

Chapter 40

Figure 40.1

Relevant musculature of the upper face. (Source: Sommer B, Sattler G, eds. (2001)

Botulinum Toxin in Aesthetic Medicine

. Blackwell Science, Boston, MA. Reproduced with permission of John Wiley & Sons.)

Figure 40.2

Horizontal forehead lines before (a) and after (b) Botox injection.

Figure 40.3

Glabellar frown lines before (a) and after (b) Botox injection.

Figure 40.4

“Crow’s feet” before (a) and after (b) Botox injection.

Figure 40.5

The lateral bow lift can be obtained by injection into the superolateral fibers of the orbicularis oculi muscle. This technique relaxes the specific aspect of the orbicularis oculi that is pulling the lateral brow downward. (Source: Sommer B, Sattler G, eds. (2001)

Botulinum Toxin in Aesthetic Medicine

. Blackwell Science, Boston, MA. Reproduced with permission of John Wiley & Sons.)

Figure 40.6

Treatment of a downturned smile is accomplished by injection into the posterior fibers of the depressor anguli oris (DAO) muscles. (Source: Sommer B, Sattler G, eds. (2001)

Botulinum Toxin in Aesthetic Medicine.

Blackwell Science, Boston, MA. Reproduced with permission of John Wiley & Sons.)

Chapter 42

Figure 42.1

Calcium hydroxylapatite microspheres, 25–45 μm in diameter. (Source: BioForm Medical, San Mateo CA. Reproduced with permission.)

Figure 42.2

Gradual dissolution of microspheres. (Source: BioForm Medical, San Mateo CA. Reproduced with permission.)

Figure 42.3

(a) Light microscopic section at 1 month post-injection showing microspherules at the dermal subcuticular junction and a slight increase in histiocytes (arrows). (Illustration courtesy of Drs. David J. Goldberg and Ellen Marmur.) (b) Electron microscopic section at 6 months showing both an intact microspherule and one undergoing a histiocytic derived catabolic process into smaller particles of calcium (black particles). The phosphate ions are not seen because they are dissolved in the processing of tissue for electron microscopy analysis. (Source: David J. Goldberg and Ellen Marmur. Reproduced with permission.)

Figure 42.4

Preinjection (a) and post-injection (b) of 2.6 mL CaHA.

Figure 42.5

Preinjection (a) and immediately post-injection (b) of 2.6 mL CaHA.

Figure 42.6

Radiesse mixed with lidocaine, using a female–female connector.

Figure 42.7

Preinjection (a) and post-injection (b) of CaHA into the hand.

Chapter 43

Figure 43.1

Platelet-rich plasma kit from Regen Lab containing three vacuum tubes, using a thixotropic gel for cell separation and sodium citrate as an anticoagulant.

Chapter 44

Figure 44.1

Serial puncture and fanning techniques. (a) Fan technique. (b) Cross-hatching technique.

Figure 44.2

(a) Before and after Sculptra injections: this is the result of three sessions, each with one bottle of Sculptra. This is typical of a three bottle correction with excellent volume restoration of the cheek area. The correction was durable for more than 18 months. (b) This is the result of three bottles initially with an excellent response that lasted for several years.

Chapter 45

Figure 45.1

White frost seen with a trichloroacetic acid (TCA) peel indicating epidermal protein coagulation. The intensity of the frost corresponds with the peel depth.

Figure 45.2

White discoloration of the skin seen during a salicylic acid peel caused by evaporation of the vehicle and precipitation of salicylate on the skin.

Figure 45.3

(

a) Typical tray set-up for a salicylic acid peel. (b) Excess peel solution is removed from sponge prior to application.

Figure 45.4

Standard peel procedure for a salicylic acid peel. (a) Face is degreased with acetone; (b) peel solution is applied; (c) erythema and white precipitate form on skin; (d) patient rinses face with water.

Figure 45.5

(a) Pre-peel; (b) immediately post-peel; (c) 24 hours after a salicylic acid peel.

Chapter 46

Figure 46.1

Standard setup for Jessner’s and trichloracetic acid (TCA) combination peel. The standard setup includes a facial cleanser such as Septisol, acetone, Jessner’s solution, 35% TCA, cotton-tipped applicators, 2 × 2 inch and 4 × 4 inch gauze pads, and cool-water soaks for patient comfort.

Figure 46.2

Frosting observed immediately after combined Jessner’s and TCA peel. Typical opaque white frosting with mild erythema observed 2 minutes after TCA application.

Figure 46.3

Sequential exfoliation, granulation, and re-epithelialization after Jessner’s and TCA combination medium depth peel. (a) Postoperative day 1: inflammation with edema, erythema; (b) day 2: early epidermal separation with hyperpigmentation; (c, d) day 3 morning; and (e, f) day 3 afternoon: dermal inflammation with granulation tissue and early re-epithelialization; (g, h) days 5 and 6, respectively: full desquamation with regeneration of new epidermis and beginning dermal remodeling.

Figure 46.4

Jessner’s TCA peel performed for photoaging skin and actinic keratoses. (a) Preoperative; (b) 5 weeks postoperative; (c) 10 weeks postoperative.

Figure 46.5

Jessner’s 35% TCA peel for actinic keratoses. (a & b) Preoperative diffuse actinic keratoses and seborrheic keratoses; (c & d) 9 months postoperative.

Chapter 47

Figure 47.1

(a) Two passes of CO

laser at 7 J/cm

leaves approximately 70 μm of residual thermal necrosis. (b) Two passes of Er:YAG laser at 10 J/cm

results in removal of approximately 50 μm of this necrotic tissue. (Source: Carcamo & Goldman, 2006; Skin resurfacing with ablative lasers. In: Goldman MP, ed.

Cutaneous and Cosmetic Laser Surgery

. London: Mosby-Elsevier. Reproduced with permission.)

Figure 47.2

Combination UltraPulse CO

(UPCO

) and Er:YAG laser (patient’s right side) showing improvement equal to left side treated with UPCO

alone. (a) Before treatment; (b) immediately after treatment; (c) 7 days after laser resurfacing; (d) 3 weeks after laser resurfacing; (e) 2 months after resurfacing. (Source: Carcamo & Goldman, 2006; Skin resurfacing with ablative lasers. In: Goldman MP, ed.

Cutaneous and Cosmetic Laser Surgery

. London: Mosby-Elsevier. Reproduced with permission.)

Figure 47.3

Histology of Active FX laser impulse at 100 mJ.

Figure 47.4

Histology of Deep FX laser impulse at 17.5 mJ. Zones of ablation are created, leaving bridges of intact tissue to aid in regeneration. Lateral and vertical coagulation stimulate a tissue regeneration response between the ablated columns.

Figure 47.5

Forty-year-old female treated with Active FX fractionated CO

laser with a 1.3 mm diameter spot size, density 2, 100 mJ: (a) before; (b) two months after treatment.

Figure 47.6

Forty-year-old female (same as in Figure 47.5) treated with Deep FX at 17.5 mJ density 1, one pass 3 months after Active FX treatment as above. (a) Immediately before; (b) immediately after treatment; (c) 1 day after treatment; (d) 2 days after treatment; (e) 2 months after treatment.

Figure 47.7

Fifty-one-year-old women treated with Deep FX at 15 mJ, density 1, one pass in the periorbital and perioral area followed by Active FX to the entire face at 100 mJ, density 2, one pass. Before and 2 months after treatment.

Figure 47.8

52-year-old female treated with Active and Deep FX (A) before treatment (B) immediately after treatment (C) 1 day after treatment (D) 2 days after treatment (E)3 days after treatment (F) 1 week after treatment.

Figure 47.9

63-year-old female (A) before treatment (B) 4 months after Fraxel Re:Pair full face and neck, UPCO

/Erbium periorbital/periocular, VBeam and topical Sculptra applied with Alma. (Source: Dr. Richard Fitzpatrick. Reproduced with permission.)

Figure 47.10

Patient treated with the SLIM E30 Mixto SX fractionated CO

laser. (a) Before treatment; (b) 1 day after treatment; (c) 3 days; (d) 7 days; (e) 2 weeks; (f) 8 weeks. (Source: Dr. Jeffery Hsu. Reproduced with permission.)

Figure 47.11

The Controlled Chaos Technology minimizes thermal damage by spacing each beam further apart to reduce the collateral thermal effect of the laser beams.

Figure 47.12

The 120 μm beam size has a deep penetration depth (up to 2.4 mm).

Figure 47.13

(a) Before treatment; (b) 1 day after treatment; (c) 2 days; (d) 3 days; (e) 4 days; (f) 5 days; (g) 1 week; (h) 4 weeks.

Figure 47.14

Diagrammatic representation of non-specific thermal damage by controlling the pulse width of the Sciton Er:YAG laser. (Source: Sciton, Inc., Palo Alto, CA. Reproduced with permission.)

Figure 47.15

Patient treated with the Sciton Profractional at 150 μm, 1.9%. (a) Before; (b) 4 weeks after treatment. (Source: Dr. Michael Gold. Reproduced with permission.)

Figure 47.16

Patient treated with the Sciton Profractional-XC at 100 μm, 11%, two passes. (a) Before treatment; (b) 4 weeks after three treatments. (Source: Dr. Kent Remington. Reproduced with permission.)

Figure 47.17

Patient treated with the Palomar fractionated 2940 nm Er:YAG laser 6 mm diameter spot, 300 μm depth, 120 μm crater diameter, 40–60% coverage. (a) Before treatment; (b) immediately after treatment; (c) 3 months after treatment. (Source: Dr. E. Vic Ross. Reproduced with permission.)

Chapter 49

Figure 49.1

Dermabrasion after partial thickness Mohs layer on the nose (a) Male patient with a partial thickness defect after 1 stage of Mohs micrographic surgery for the removal of basal cell carcinoma (b) Immediately after spot dermabrasion to blend the surgical defect with the surrounding skin (c) 2 weeks after Mohs and dermabrasion.

Figure 49.2

Dermabrasion of scar on the nose after Mohs surgery and reconstruction (a) Female patient with a scar on the right nasal sidewall and lateral tip 6 weeks after Mohs surgery and flap reconstruction. (b) Immediately after dermabrasion to multiple cosmetic subunits of the nose. Feathering the border of the dermabraded area (arrows) helps to minimize the color differences between the treated and untreated areas. (c) 2 weeks after dermabrasion with significant improvement in the appearance and texture of the scar.

Figure 49.3

Dermabrasion of acne scars (a) African-American male with severe acne scarring prior to dermabrasion. (b) Immediate postoperative appearance of the treated area. (c) Appearance 4 weeks after dermabrasion.

Figure 49.4

Technical considerations (a) Proper grasp of the hand engine. (b) Clockwise rotation (against the angle of the rotating bristles) of the wire brush results in removal of a thicker plane of tissue with each pass than counter-clockwise rotation (with the angle of the bristles) (c) The treatment stroke. After the wire brush comes in contact with the skin (1), it is pulled across the treatment area in in a unidirectional fashion perpendicular to the direction of the rotating wire brush (2). Following completion of the treatment stroke, the wire brush is lifted from the skin surface (3), and in an arciform fashion (4–5) is moved to a new area.

Chapter 50

Figure 50.1

(a) Pretreatment of the right axillary area with coarse hair. (b) Only fine hair exists after 3 months after five treatments with a 1064 nm Nd:YAG laser.

Figure 50.2

(a) Pretreatment of the upper lip area. (b) Seven weeks after two treatments with intense pulsed light (IPL) system.

Figure 50.3

Blister formation 3 days after treatment with IPL system.

Chapter 51

Figure 51.1

Subcutaneous atrophy from unipolar radiofrequency using old protocol with high fluencies.

Figure 51.2

(a) Pre-Thermage and Fraxel laser. (b) Post-Thermage and Fraxel laser.

Chapter 52

Figure 52.1

Smoothing of the skin seen after eight treatments over 4 weeks of Gentlewaves

photomodulation (Gentlewaves, Inc., Charlotte, NC, USA) (a) Before treatments. (b) Eight weeks after baseline. Reduction in wrinkles, pigmentation and improvement of texture are noted.

Figure 52.2

Gentlewaves LED photomodulation device. Array of LEDs.

Figure 52.3

(a) Before shows flare of eczema following withdrawal of all therapy. (b) Atopic eczema after three treatments with Gentlewave LED photomodulation. The after image (b) shows effects of reduction of inflammation by LED photomodulation within 10 days.

Chapter 53

Figure 53.1

A 2-L liposuction canister filled with liposuction aspirate.

Figure 53.2

Blanching of skin visible after infusion of tumescent anesthesia with tumescent local anesthesia (TLA) technique.

Figure 53.3

Lower abdomen, anterior view: (a) pretreatment; (b) post-treatment.

Figure 53.4

Lower abdomen and hips liposuction, lateral view: (a) pretreatment; (b) post-treatment.

Figure 53.5

Lower abdomen, hips, and lateral thigh liposuction, lateral view: (a) pretreatment; (b) post-treatment.

Figure 53.6

Arm, anterior view: (a) pretreatment; (b) post-treatment.

Figure 53.7

Neck, lateral view: (a) pretreatment; (b) post-treatment.

Figure 53.8

Neck liposuction markings: (a) anterior view; (b) lateral view.

Figure 53.9

Adverse complication of liposuction: skin dimpling and scarring in medial thighs after overly aggressive liposuction procedure.

Chapter 54

Figure 54.1

The youthful neck with a cervicomental angle of 100 °. The facial and Frankfurt plane are shown with glabella, subnasale, and chin in alignment.

Figure 54.2

Marginal mandibular branch of the facial nerve and other relevant anatomy.

Figure 54.3

Grasping and tucking the submental fat to demonstrate expected results of submental liposuction without upward posterior retraction seen in rhytidectomy.

Figure 54.4

Preoperative markings.

Figure 54.5

Operative position with chin extended. Three of the five entry sites are denoted with circles and typical fanning pattern shown.

Figure 54.6