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www.informahealthcare.com
Telephone House, 69-77 Paul Street, London EC2A 4LQ, UK
52 Vanderbilt Avenue, New York, NY 10017, USA
About the book
Dermatoscopy has increasingly been taken up in dermatology practice
as a non-invasive technique for the diferential diagnosis of pigmented
skin lesions. However, there are further uses for dermatoscopy in several
dermatologic conditions in terms of diagnosis, prognostic evaluation,
and monitoring response to treatment. There is also the technique
of videodermatoscopy – employing the use of digital systems that
ensure high magnifcations – in addition to the dermatoscopy that
conventionally refers to manual devices.
This book aims to advance knowledge of these extended clinical
applications for enhanced visualization and digital imaging using manual
dermatoscopy or videodermatoscopy, beyond the usual indication
of cutaneous pigmented lesions. This will serve as an important yet
relatively simple aid to a dermatologist’s daily ofce practice.
Contents
Introduction * Equipment * Scabies and Pediculosis: Biologic Cycle
and Diagnosis * Videodermatoscopy and Scabies * Videodermatoscopy
and Pediculosis * Therapy of Scabies and Pediculosis: Potential and
Pitfalls * Therapeutic Monitoring of Parasitoses with Videodermatoscopy
* Tungiasis * Hair Loss * Nail Diseases * Psoriasis: Vascular Pattern
under Videodermatoscopy Observation * Psoriasis: Histopathological
Correlations * Palmo-plantar Psoriasis * Psoriatic Balanitis * Scalp Psoriasis
* Clear Cell Acanthoma * HPV Infections * Venular Malformations
(Port Wine Stain Type) * Bowen’s Disease * Pyogenic Granuloma * Lichen
Ruber Planus * Urticaria and Urticarial Vasculitis * Disorders of Collagen
Tissues * Rosacea * Molluscum Contagiosum * Sebaceous Hyperplasia
* Pigmented Purpuric Dermatoses * Actinic Porokeratosis
* Xantomatous Lesions * Dermatoscopy in Cosmetic Applications
About the editors
Giuseppe Micali, MD, is Professor and Chairman at the Department
of Dermatology, AOU Policlinico-Vittorio Emanuele, Catania, Italy
Francesco Lacarrubba, MD, is Researcher at the Department
of Dermatology, AOU Policlinico-Vittorio Emanuele, Catania, Italy
Dermatoscopy
in Clinical Practice
Edited by
Giuseppe Micali
Francesco Lacarrubba
Dermatology
Beyond Pigmented Lesions
Dermatoscopy in Clinical Practice
Series in Dermatological Treatment
Published in association with the Journal of Dermatological Treatment
Series editors: Steven R Feldman and Peter van de Kerkhof
1 Robert Baran, Roderick Hay, Eckhart Haneke, Antonella Tosti
Onychomycosis, second edition, ISBN 9780415385794
2 Ronald Marks,
Facial Skin Disorders, ISBN 9781841842103
3 Sakari Reitamo, Thomas Luger, Martin Steinhoff
Textbook of Atopic Dermatitis, ISBN 9781841842462
4 Calum Lyon, Amanda J Smith
Abdominal Stomas and their Skin Disorders, Second Edition, ISBN 9781841844312
5 Leonard Goldberg
Atlas of Flaps of the Face, ISBN 9781853177262
6 Antonella Tosti, Maria Pia De Padova, Kenneth R Beer
Acne Scars: Classifcation and Treatment, ISBN 9781841846873
7 Bertrand Richert, Nilton di Chiacchio, Eckart Haneke
Nail Surgery, ISBN 9780415472333
8 Giuseppe Micali, Francesco Lacarrubba
Dermatoscopy in Clinical Practice: Beyond Pigmented Lesions, ISBN 9780415468732
Dermatoscopy in Clinical Practice
Beyond Pigmented Lesions
Edited by
Giuseppe Micali, MD
Professor and Chairman
Department of Dermatology
AOU Policlinico-Vittorio Emanuele
Catania, Italy
and
Francesco Lacarrubba, MD
Researcher
Department of Dermatology
AOU Policlinico-Vittorio Emanuele
Catania, Italy
© 2010 Informa UK Ltd
First published in 2010 by Informa Healthcare, Telephone House, 69-77 Paul Street, London EC2A 4LQ. Informa Healthcare is a trading division of
Informa UK Ltd. Registered Offce: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954.
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, without the prior permission of the publisher or in accordance with the provisions of the Copyright,
Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham
Court Road, London W1P 0LP.
Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to
acknowledge in subsequent reprints or editions any omissions brought to our attention.
A CIP record for this book is available from the British Library.
Library of Congress Cataloging-in-Publication Data
Data available on application
ISBN-13: 9780415468732
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Email: CSDhealthcarebooks@informa.com
Typeset by C&M Digitals (P) Ltd, Chennai, India
Printed and bound in Great Britain by MPG Books, Bodmin, Cornwall, UK

Contents
List of Contributors vii
1 Introduction 1
Giuseppe Micali and Francesco Lacarrubba
2 Equipment 2
Pietro Rubegni, Marco Burroni, Niccolò Nami, and Michele Fimiani
3 Parasitoses
3.1 Scabies and pediculosis: Biologic cycle and diagnosis 7
Ani L Tajirian and Robert A Schwartz
3.2 Videodermatoscopy and scabies 11
Francesco Lacarrubba, Nella Pulvirenti, and Giuseppe Micali
3.3 Videodermatoscopy and pediculosis 16
Giuseppe Micali, Marianna Umana, and Francesco Lacarrubba
3.4 Therapy of scabies and pediculosis: Potential and pitfalls 20
Lee E West, Beatrice Nardone, and Dennis P West
3.5 Therapeutic monitoring of parasitoses with videodermatoscopy 25
Giuseppe Micali, Aurora Tedeschi, and Francesco Lacarrubba
3.6 Tungiasis 29
Elvira Moscarella, Renato Bakos, and Giuseppe Argenziano
4 Hair loss 31
Antonella Tosti and Bruna Duque Estrada
5 Nail diseases 45
Antonella Tosti, Bianca Maria Piraccini, and Débora Cadore de Farias
6 Diseases characterized by altered vascular pattern
6.1 Psoriasis
6.1A Vascular pattern under videodermatoscopy observation 52
Giorgio Filosa, Rossella De Angelis, and Leonardo Bugatti
6.1B Histopathological correlations 57

Daniele Innocenzi, Maria Concetta Potenza, and Ilaria Proietti
6.1C Palmoplantar psoriasis 61
Francesco Lacarrubba, Maria Letizia Musumeci, and Giuseppe Micali

contents
6.1D Psoriatic balanitis 64
Giuseppe Micali, Maria Rita Nasca, and Francesco Lacarrubba
6.1E Scalp psoriasis 67
Paolo Rosina
6.2 Clear cell acanthoma 70
Francesco Lacarrubba, Orazia D’Agata, Federica Dall’Oglio, and Giuseppe Micali
6.3 HPV infections 73
Pompeo Donofrio and Maria Grazia Francia
6.4 Venular malformations (port wine stain type) 75
Francisco Vázquez-López
6.5 Bowen’s disease 82
Leonardo Bugatti, Giorgio Filosa, and Alessandra Filosa
6.6 Pyogenic granuloma 86
Pedro Zaballos Diego
7 Miscellanea
7.1 Lichen ruber planus 90
Francisco Vázquez-López
7.2 Urticaria and urticarial vasculitis 96
Francisco Vázquez-López
7.3 Disorders of collagen tissues 100
Paolo Rosina
7.4 Rosacea 103
Paolo Rosina
7.5 Molluscum contagiosum 106
Pedro Zaballos Diego
7.6 Sebaceous hyperplasia 109
Pedro Zaballos Diego
7.7 Pigmented purpuric dermatoses 112
Pedro Zaballos Diego
7.8 Actinic porokeratosis 115
Pedro Zaballos Diego
7.9 Xanthomatous lesions 118
Filomena Mandato, Maurizio Biagioli, and Pietro Rubegni
8 Dermatoscopy in cosmetic applications 121
Warren Wallo
Index 127

List of contributors
Giuseppe Argenziano
Department of Dermatology
Second University of Naples
Naples, Italy
Renato Bakos
Department of Dermatology
Universidade Federal do Rio Grande do Sul
Porte Alegre, Brazil
Maurizio Biagioli
Section of Dermatology
Department of Clinical Medicine and Immunological
Science
University of Siena
Siena, Italy
Leonardo Bugatti
Dermatology Unit
Augusto Murri Hospital
Jesi, Italy
Marco Burroni
Section of Dermatology
Department of Clinical Medicine and Immunological
Science
University of Siena
Siena, Italy
Débora Cadore de Farias
Department of Dermatology
Santa Casa de São Paulo Hospital
São Paulo, Brazil
Maria Concetta Potenza
Department of Dermatology - Polo Pontino
University of Rome “Sapienza”
Rome, Italy
Orazia D’Agata
Department of Dermatology
University of Catania
Catania
Italy
Federica Dall’Oglio
Department of Dermatology
University of Catania
Catania, Italy
Rossella De Angelis
Rheumatology Unit
Department of Molecular Pathology and Innovative
Therapy
Polytechnic University of the Marche
Ancona, Italy
Pedro Zaballos Diego
Dermatology Department
Hospital Sant Pau i Santa Tecla
Tarragona, Spain
Pompeo Donofrio
Section of Dermatology
Department of Systemic Pathology
Genito-Dermatologic Ambulatory Unit
University of Naples Federico II
Naples, Italy
Bruna Duque Estrada
Instituto de Dermatologia Prof. Rubem David Azulay
Rio de Janeiro, Brazil
Alessandra Filosa
Dermatology Unit
Augusto Murri Hospital
Jesi, Italy

lst of contrbutors
Giorgio Filosa
Dermatology Unit
Augusto Murri Hospital
Jesi, Italy
Michele Fimiani
Section of Dermatology
Department of Clinical Medicine and Immunological
Science
University of Siena
Siena, Italy
Maria Grazia Francia
Section of Dermatology
Department of Systemic Pathology
University of Naples Federico II
Naples, Italy

Daniele Innocenzi
Department of Dermatology - Polo Pontino
University of Rome “Sapienza”
Rome, Italy
Tragically deceased 2009
Francesco Lacarrubba
Department of Dermatology
A.O.U. Policlinico-Vittorio Emanuele
Catania, Italy
Filomena Mandato
Section of Dermatology
Department of Clinical Medicine and Immunological
Science
University of Siena
Siena, Italy
Giuseppe Micali
Department of Dermatology
A.O.U. Policlinico-Vittorio Emanuele
Catania, Italy
Elvira Moscarella
Department of Dermatology
Second University of Naples
Naples, Italy
Maria Letizia Musumeci
Department of Dermatology
University of Catania
Catania
Italy
Niccolò Nami
Section of Dermatology
Department of Clinical Medicine and Immunological
Science
University of Siena
Siena, Italy
Beatrice Nardone
Department of Dermatology
University of Catania
Catania
Italy
Maria Rita Nasca
Department of Dermatology
University of Catania
Catania
Italy
Bianca Maria Piraccini
Department of Dermatology
University of Bologna
Bologna, Italy
Ilaria Proietti
Department of Dermatology - Polo Pontino
University of Rome “Sapienza”
Rome, Italy
Nella Pulvirenti
Department of Dermatology
University of Catania
Catania
Italy
Paolo Rosina
Section of Dermatology and Venereology
Department of Biomedical and Surgical Sciences
University of Verona
Verona, Italy

lst of contrbutors
Pietro Rubegni
Section of Dermatology
Department of Clinical Medicine and Immunological
Science
University of Siena
Siena, Italy
Robert A Schwartz
Department of Dermatology
New Jersey Medical School
Newark, New Jersey, USA
Ani L Tajirian
Department of Dermatology
New Jersey Medical School
Newark, New Jersey, USA
Aurora Tedeschi
Department of Dermatology
University of Catania
Catania
Italy
Antonella Tosti
Department of Dermatology
University of Bologna
Bologna, Italy
Marianna Umana
Department of Dermatology
University of Catania
Catania
Italy
Francisco Vázquez-López
Department of Dermatology
Hospital Universitario Central de Asturias
Oviedo, Asturias, Spain
Warren Wallo
Johnson & Johnson Consumer Companies, Inc.
Skillman, New Jersey, USA
Dennis P West
Department of Dermatology
The Feinberg School of Medicine
Northwestern University
Chicago, Illinois, USA
Lee E West
Department of Pharmacy
Northwestern Memorial Hospital
Chicago, Illinois, USA
We dedicate this book to the memory of Daniele Innocenzi, an extraordinary and outstanding
dermatologist and friend

 Introduction
Giuseppe Micali and Francesco Lacarrubba
Dermatoscopy (D) - also called “dermoscopy” or “incident light
microscopy” - is a non-invasive technique that allows a rapid
and magnified in vivo observation of the skin with the visual-
ization of morphologic features invisible to the naked eye. It
may be performed with manual devices that do not require any
computer “assistance” and allow magnifications up to X20, or
with digital systems requiring a video camera equipped with
optic fibers and lenses that ensure magnifications of up to
X1000; in the latter instance the term videodermatoscopy (VD)
is more usual. The images obtained are visualized on a monitor
and stored on a personal computer, in order to process them
and compare any possible changes over time. In many ways,
VD represents the evolution of D. In this book the term “der-
matoscopy” will be referred to the use of manual devices and
“videodermatoscopy” to the use of digital systems operating at
high magnifications.
Both D and VD are widely used in the differential diagnosis
of pigmented skin lesions, usually through the technique called
epiluminescence microscopy, which involves the application of
a liquid (oil, alcohol, or water) to the skin to eliminate light
reflection; recently, new systems utilizing polarized light may
achieve similar results without the need for liquids. However,
apart from their most common use for the differential diagno-
sis of pigmented skin lesions, it has been demonstrated that
D/VD have expanded applications in dermatology. Alternative
applications of D/VD include inflammatory dis eases, parasi-
toses, hair and nails abnormalities, and a large vari ety of other
dermatologic conditions as well as cosmetology. Importantly,
for many of these disorders the use of high magnifications is
needed for research as well as for clinical purpose. Depending
on the skin disorder, D/VD may be useful for differen tial
diagnosis, prognostic evaluation, and monitoring response to
treatment. Moreover, the capability to capture digital images is
perfectly suited to teledermatology - the “store-and-forward”
technique that allows exchange of opinions between derma-
tologists - and might be useful when on-site D/VD services are
not available.
The aim of this book is to advance knowledge of enhanced
visualization/digital imaging using D or VD beyond the tradi-
tional indication of pigmented lesions of the skin. In particular,
the book focuses on those con ditions in which the techniques
are more useful, describing the clinical and histopathologi-
cal correlations associated with the procedure. The book has
plenty of images that will be useful in the daily clinical prac tice
of a dermatologist, who should thus be encouraged to utilize
D/VD in the routine evaluation of skin diseases. The book will
serve as an important yet relatively simple aid in daily office
practice.

 Equipment
Pietro Rubegni, Marco Burroni, Niccolò Nami, and Michele Fimiani
introduction
The optical dermoscope is an instrument containing a light
source that enables skin structures invisible to the naked eye to be
seen. A medium such as ultrasound gel or Vaseline oil is applied
to the skin to make the stratum corneum transparent, while the
objective of the dermoscope is placed against the skin surface.
The instrument makes it possible to observe a vast new range
of dermatological signs. Dermoscopy is currently used in rou­
tine dermatology. The various specialist courses held in recent
years have led to the definition of new methods for improving
the diagnosis of neoplastic and other skin disorders.
VidEodErmoscopy
Analogue Videodermoscopy
Between 1980 and 1990, advances in video technology led to
the development of instruments that displayed dermoscopic
images on a screen.(1) The first videodermoscope had a tele­
camera with video resolution connected to an optical dermo­
scope and a television screen with video recorders to record
examinations. However, during this period, the dermoscopic
examination using these equipment produced only low­quality
images, which is due to the low resolution of the first­genera­
tion video cameras, and other cumbersome documentation and
data­saving procedures; for example, the maximum television
resolution is 768 x 576 pixel for the European PAL broadcast
system and less for the American NTSC, where pixel is the basic
image unit; analogue video recorders of the 1980s often had less
than 400 horizontal lines. Low quality and technical limitations
prevented the widespread use of videodermoscopy.(2)
Digital Videodermoscopy
Between 1990 and 2000, computerized instruments for digitizing
images from telecameras connected to videodermoscopes became
common. Digital dermoscopic images can be obtained by conver­
sion from video telecameras connected to digital cards or by use of
high­resolution digital telecameras or digital cameras coupled with
special dermoscopy adaptors. Computerized systems proved more
practical for managing examinations because they offered the pos­
sibility of saving personal and private data of patients, together
with digital images of pigmented skin lesions (Figure 2.1).(2, 3)
In the case of video telecameras, the signal acquisition
peripheral required a charge­coupled device (3CCD) or sen­
sor for the red, green, and blue bands, in order to keep image
quality high during sampling.(1, 4) Digital telecameras have
better quality for the equivalent video characteristics because
they do not require any conversion. They can have a USB (usu­
ally amateur grade) or Firewire (professional grade, faster and
better quality) interface. Much higher resolution is possible
with digital telecameras than is possible with analogue video
telecameras and this has clear diagnostic advantages, as digital
dermoscopy systems of this type can reach a picture resolution
of 1280 x 1,024 pixels, with images observed in vivo at 15 to
25 photograms per second on computer screens (Figure 2.2).
Digital cameras provide exceptionally high resolutions (up
to 3,000 x 2,000 are common) but have the disadvantage of
not providing full resolution images in vivo but only after the
images have been saved.
Figure 2.1 Instrument for digital dermoscopy.
Figure 2.2 “Real­time” digital dermoscopy analyzer.

equipment
The two types of digital instruments are, therefore, designed
for different users. Clinicians who use video or digital telecameras
(usually specialist centers) carry out many examinations to diag­
nose melanoma or inflammatory skin diseases and observe many
lesions by digital technology. Digital cameras are largely used to
document lesions first observed by traditional dermoscopy.(5)
It is commonly thought that a higher number of pixels
implies better quality images; this is untrue, even if resolution is
the imaging system’s ability to reproduce details. Image quality
is important for early diagnosis of melanoma and depends on
factors such as the optical system of the instrument, illumina­
tion, type of instrument, and resolution.(6) Digital dermoscopy
images generally have resolutions between 768 x 576 and 1,600
x 1,200 pixel; lower resolution compromises diagnosis and
higher resolution is unnecessary (Figure 2.3). The definition
of magnification is only valid for integrated instruments with
always the same screens. Field of view is a preferable param­
eter. Dermoscopy optical systems generally enable a horizontal
“field of view” between 2 mm and 3 cm. Overall magnification
M of digital dermoscopes is calculated as the ratio of screen
diagonal D to field of view diagonal d: M = D/d.
Illumination must be homogeneous and sufficiently strong
while incident intensity should be modified by the lens dia­
phragm rather than by varying electrical potential so as to
keep the color of the study area constant. Reddish or saturated
images are due to low­quality equipment or failure of white
balancing during chromatic calibration.
Contact, noncontact, and polarized dermoscopy
Today there are many types of dermoscopes. Contact incident light
dermoscopes use a glass window placed in contact with the skin, illu­
minated at an angle of about 30 to 45 degrees so as to eliminate direct
Figure 2.3 A: Image at 512 x 384 pixel resolution (42.8 KB). B: The same image at 1,024 x 768 pixel resolution (326 KB).
(A) (B)
Figure 2.4 Dermoimage software for image storage (Ergon srl, Strada Massetana Romana 50/A 53,100 Siena, e­mail: dermoim­
age@ergonsrl.it).

rubegni,burroni,nami,andfimiani
reflection, and a magnifying lens system.(7) A liquid fills the space
between the skin and the glass, rendering the skin translucent and
revealing subcutaneous patterns invisible to the naked eye.(8, 9)
Two polarizing filters can be added to this simple optical
system, one before the telecamera sensor and one on the light
source, so as to eliminate light reflected by cross­polarization.
Light reflected from the skin surface maintaining the polariza­
tion of the light source is eliminated by the polarizer in front of
the sensor; this enables skin patterns to be observed to a greater
depth. Polarization makes it possible to dispense with the glass
window in contact with the skin. This has the advantage of
avoiding transmission of infections and ischemia caused by
pressure of the window on the skin.(8)
data storagE
Digital telecameras and photocameras are now used by all medical
centers, especially dermatology clinics, to acquire skin images.(10,
11) Initially these instruments were used nonroutinely by enthu­
siasts, but soon the need emerged to develop software to store the
data acquired. Such software enables images to be saved and stored
in clinical records together with personal, confidential, and multi­
media data.(12) Some examples for dermatologists are Imagestore
for Healthcare, Mirror Software, and Dermo-Image (Table 2.1). Only
Dermo-Image (Figure 2.4) and Imagestore for Healthcare include a
preset, updatable index of dermatological disorders ready to imple­
ment.(13) The latter enables overlay of multiple images and fade
between them, using the compare feature, and includes retrieval of
digital images by diagnosis, treatment, and anatomical site. Mirror
Software was developed specifically for medical professionals; the
basic management functions of storing, retrieving, viewing, and
printing images were all designed with the workflow of a medical
practice in mind. The loop tool allows practitioners to critically
examine skin features to target problem areas. Images can be trans­
ferred to other programs like Word and Power Point. The software
includes classification by pathology, patient, or examination, and
an advanced image retrieval system based on personalized crite­
ria. Imagestore for Healthcare, Mirror, and Dermo-Image have these
features and also enable comparison of two or more digital images.
This function is useful for assessing results of treatment and evolu­
tion of lesions.(13)
softwarE for objEctiVE assEssmEnt and
assistEd diagnosis
Many research groups have worked on image processing and
numerical assessment of image features for diagnostic purposes
Table 2.1 Selected Commercially Available Database Software for Dermatological Digital Image Management.
Software/contact
Specificallyfor
dermatology
(preset updatable
index and tags)
Specific tags for
image retrieval
Image
modification
tool
Confidentiality
with username
and password
protection
Network
compatible
with image
sharing via the
Internet
History
import
option Cost
Mirror software, product
information available at
www.canfieldsci.com/
Imaging_Products_
Imaging.asp
No Yes Only in the
$2,500 or
over version
Yes Yes No $825 ($2,500
with DPS tools)
Imagestore for healthcare,
product information
available at www
.ttlsoftware.com
Yes Yes Yes Securely access
images from
any Internet­
connected PC
Yes No not available
Dermo­Image, product
information available
atwww.dermoimage.com
Yes Yes Yes Powerful and
flexible permission
system
Yes Yes $900
Figure 2.5 Images can be stored and analyzed using DB­Mips
System; Biomips Engineering, S.R.L., Siena, Italy), with com­
puterized instrument providing a visual database and objective
evaluations of pigmented skin lesions.

equipment
rEfErEncEs
1. Gutenev A, Skladnev VN, Varvel D. Acquisition­time
image quality control in digital dermatoscopy of skin
lesions. Comput Med Imaging Graph 2001; 25(6): 495–9.
2. Schindewolf T, Schiffner R, Stolz W et al. Evaluation of
different image acquisition techniques for a computer
vision system in the diagnosis of malignant melanoma.
J Am Acad Dermatol 1994; 31(1): 33–41.
3. Elbaum M. Computer­aided melanoma diagnosis. Der­
matol Clin 2002; 20(4): 735–47.
4. Sheeler I, Koczan P, Wallage W, de Lusignan S. Low­cost
three­channel video for assessment of the clinical consul­
tation. Inform Prim Care 2007; 15(1): 25–31.
5. Ratner D, Thomas CO, Bickers D. The uses of digital photogra­
phy in dermatology. J Am Acad Dermatol 1999; 41: 749–56.
6. Levy JL, Trelles MA, Levy A, Besson R. Photography in der­
matology: comparison between slides and digital imaging.
J Cosmet Dermatol 2003; 2: 131–4.
7. Benvenuto­Andrade C, Dusza SW, Agero AL et al. Differ­
ences between polarized light dermoscopy and immersion
contact dermoscopy for the evaluation of skin lesions.
Arch Dermatol 2007; 143(3): 329–38.
8. Wang SQ, Dusza SW, Scope A et al. Differences in der­
moscopic images from nonpolarized dermoscope and
polarized dermoscope influence the diagnostic accuracy
and confidence level: a pilot study. Dermatol Surg 2008;
34(10): 1389–95.
9. Pan Y, Gareau DS, Scope A et al. Polarized and nonpolar­
ized dermoscopy: the explanation for the observed differ­
ences. Arch Dermatol 2008; 144(6): 828–9.
10. Scheinfeld NS, Flanigan K, Moshiyakhov M, Weinberg JM.
Trends in the use of cameras and computer technology
Table 2.2 Instruments for Digital Dermoscopy Analysis.
instrument web site Light source magnification camera board software
DB­Mips www.skinlesions.net Halogen, 3,200 K,
150 W
X16 to 25, global 3CCD,
750 lines
768 X 576 lines,
RBG sync, 16 M
colors
Medical records processing,
two statistical classifiers (neural
network, similarity)
Molemax II www.derma.co.at Circular
polarized
X30 fixed 1CCD Not reported Medical record db image
processing, statistical classifier
(diagnostic algorithms)
Videocap www.dsmedigroup.it Halogen, 3,200 K,
150 W
X10, X25, X50,
X100, X200,
X400, X500,
X700
1CCD PCI multiinput,
16 M colors
Medical records, db images,
measurements
Dermogenius www.dermogenious.com Not reported Fixed 1CCD or
3CCD
Not reported Medical records processing,
statistical classifier (diagnostic
algorithms)
Microderm www.visiomed.de Not reported Variable but not
reported
3CCD Not reported Medical records processing,
statistical classifier (neural
network)
Solarscan www.polartechnics.com.av Halogen X10 1CCD or
3CCD
Not reported Medical record processing,
statistical classifier
in the last few years (Table 2.2). The process generally consists
in detecting the borders of the skin area to assess, identifying
the object(s) to examine, and evaluating a number of variables
to differentiate various diagnostic situations (Figure 2.5). Many
recent studies have been concerned with objective computer­
ized analysis of digital images acquired by dermoscopy.(14–16)
In the case of pigmented skin lesions, this has involved iden­
tification of variables such as circularity, maximum diameter,
symmetry, and internal clusters of color, for objective evalua­
tion of all possible types.(15) The new path taken by research­
ers envisages definition of new, unambiguous, reproducible
variables. Objective evaluation also offers the opportunity of
using assisted diagnosis systems to provide diagnostic sugges­
tions.(17, 18) On the basis of morphochromatic characteristics
of lesions, it is possible to build a classifier that can evaluate the
statistical probability of malignancy with the aid of a special
thesaurus.
These instruments have also been used in trichology and aes­
thetics with interesting results. Sensitive tools have been devel­
oped to monitor hair loss and treatment responses. Recently, the
Tricho-scan was launched as a method combining epilumines­
cence microscopy with automatic digital image analysis.(19)
The diagnostic validity and significance of new numerical vari­
ables obtained by digital dermoscopy analysis can be useful to der­
matologists but only when there has been scientific validation.
concLusions
The continuing evolution of digital imaging has led to the obso­
lescence of costly video equipment and the introduction of new
digital cameras and telecameras that offer greater chromatic and
spatial quality. Through this technology, dermatologists are dis­
covering new horizons for research, teaching, and health care.

rubegni,burroni,nami,andfimiani
among dermatologists in New York City 2001–2002.
Dermatol Surg 2003; 29: 822–5.
11. Graschew G, Roelofs TA, Rakowsky S et al. New trends in
the virtualization of hospitals––tools for global e­Health.
Stud Health Technol Inform 2006; 121: 168–75.
12. Starr JC. Integrating digital image management software
for improved patient care and optimal practice manage­
ment. Dermatol Surg 2006; 32: 834–40.
13. Rubegni P, Nami N, Tataranno D, Fimiani M. Gestione
delle immagini digitali. Un software dedicato per la ges­
tione dell’archivio elettronico. Hi Tech Dermo(Italy) 2008;
3(3): 43–9.
14. Pressley ZM, Foster JK, Kolm P et al. Digital image analy­
sis: a reliable tool in the quantitative evaluation of cuta­
neous lesions and beyond. Arch Dermatol 2007; 143(10):
1331–3.
15. Rubegni P, Burroni M, Andreassi A, Fimiani M. The role
of dermoscopy and digital dermoscopy analysis in the
diagnosis of pigmented skin lesions. Arch Dermatol 2005;
141: 1444–6.
16. Rubegni P, Burroni M, Sbano P, Andreassi L. Digital der­
moscopy analysis and internet­based program for dis­
crimination of pigmented skin lesion dermoscopic images.
Br J Dermatol 2005; 152(2): 395–6.
17. Perrinaud A, Gaide O, French LE et al. Can automated der­
moscopy image analysis instruments provide added ben­
efit for the dermatologist? A study comparing the results
of three systems. Br J Dermatol; 157(5): 926–33.
18. Piccolo D, Ferrari A, Peris K et al. Dermoscopic diagnosis
by a trained clinician vs. a clinician with minimal dermos­
copy training vs. computer­aided diagnosis of 341 pig­
mented skin lesions: a comparative study. Br J Dermatol
2002; 147(3): 481–6.
19. Hoffmann R, Van Neste D. Recent findings with com­
puterized methods for scalp hair growth measurements.
J Invest Dermatol Symp Proc 2005; 10(3): 285–8.

3.1 Scabies and pediculosis: Biologic cycle and diagnosis
Ani L Tajirian and Robert A Schwartz
SCABIES
Introduction
Scabies is a common ectoparasite infection. It is caused by
the mite Sarcoptes scabiei variety hominis. Sarcoptes is derived
from the Greek work “sarx” (flesh) and “koptein” (to smile
or cute) and the Latin word “scabere” (to scratch).(1) It is
endemic worldwide, particularly in impoverished commu-
nities. Epidemics may be be evident during famine and war.
Infestations occur when the scabies mite burrows into the skin,
invading the host epidermis. The disease process is mediated
through an inflammatory and allergy-like reaction to mite
products, leading to intense pruritus.
Scabies Mite/ Biologic Cycle
S. scabiei is part of the arachnid family. The nymph and adult
stages have four pairs of legs; the larvae possess three. Adult
females are between 0.3 to 0.5 mm in length and are bigger
compared to males, the small males reaching a size between
0.21 to 0.29 mm.(2) The adult male can be distinguished from
the female by its smaller size, darker color, and the presence
of stalked pulvilli on leg 4, as leg 4 in the female adult ends
in long setae.(3) The mites can crawl up to 2.5 cm per minute on
warm skin and live for approximately 30 days.(4–7) S. sca-
biei can survive outside of the host for 24 to 36 hours.(8–10)
The scabies mite cannot penetrate deeper than the stratum
corneum because oxygen delivery is by diffusion through
the body surface. Mating occurs on the skin surface; males
die shortly thereafter. Females then dig tunnel-like burrows
in the stratum corneum using their mandibles. They lay
approximately 2 to 3 eggs daily. During her lifetime, a female
mite will lay 60 to 90 eggs and usually does not leave the bur-
row. Larvae hatch at 2 to 4 days, become a protonymph after
3 to 4 days, develop into a tritonymph after 2 to 5 days, and after
an additional 5 to 6 days, evolve into sexually mature males or
females. Skin entry can occur at any time and occurs in less than
30 minutes through secretion of enzymes that digest the skin,
which is then consumed by the mite as a nutrient. An infested
host contains approximately 10 to 15 adult female mites on his
or her body at any given time; patients with crusted scabies,
however, can have millions of mites on their skin surface.
Epidemiology
Scabies is most prevalent and endemic in tropical regions. In
industrialized nations, scabies is usually observed in sporadic
individual cases and institutional outbreaks. Past research
estimates suggested that globally scabies might infect about
300 million by the end of the 20th century. Prevalence of sca-
bies is not gender specific, as it can attack both sexes. Ethnic
differences are most likely related to socioeconomic conditions,
overpopulation, and behavioral factors rather than race. Risk
factors include poverty, poor nutrition, homelessness, demen-
tia, and poor hygiene.(11–13) Outbreaks frequently occur in
institutions such as hospitals, nursing homes, prisons, and
elementary schools.
Transmission
Transmission of scabies is by direct skin-to-skin contact, which
occurs through close personal contact, sexual or otherwise, or
indirectly through fomites. Incidence and prevalence is higher
in children and sexually active individuals. Among adults,
sexual contact is the most common means of transmission.
Shaking hands and use of common objects is usually not suf-
ficiently long for transmission, as it can take up to 15 to 20 min-
utes for transmission to occur. Scabies is not easily transmitted
by clothing and bed sheets.
Clinical Features/Pathogenesis
The pathognomonic sign of scabies is the burrow (Figure 3.1),
which represents the tunnel that a female mite excavates while
laying eggs. Nocturnal pruritus and erythematous papules
also form the basis of diagnosis. Burrows are white serpigi-
nous lines in the upper dermis ranging from 1 to 10 mm in
length and are typically located on the interdigital spaces of the
hand, the flexure surface of the wrist, elbows, genitalia, axillae,
umbilicus, belt line, elbows, nipples, buttocks, and penile shaft.
Scabies mites prefer regions with a relatively high temperature
and thin stratum corneum. The back is rarely involved. Head
and neck are usually spared with the exception of infants and
the immunocompromized, in which case, the scalp and face
may also be affected. Cutaneous lesions are usually symmetri-
cal. In men, the penis and scrotum are often involved, whereas
in women, the areola, nipples, and genital area are commonly
affected. The intense pruritus is most severe at night and is
exacerbated by a hot shower or bath. The severe pruritus and
papulovesicles result from a delayed type-IV hypersensitivity
reaction to the mite, its saliva, eggs, or excrements (scybala). In
first-time infections, it usually takes the host’s immune system
2 to 6 weeks to become sensitized to the mite and its excre-
ments; however, upon reinfestation, it usually takes a few days
to develop symptoms. The immune response, washing, and
scratching are reasons why immunocompetent hosts harbor
only 11 to 12 buried female mites despite regular deposition
of eggs.(2) With intense personal hygiene, the number can be
lower (often called scabies of the cleanly) without a decrease in
pruritus.(14) In immunocompromized patients, the mites can
replicate uncontrollably, thus resulting in millions found on

tajirianandschwartz
the body. Even after successful treatment, pruritus and papules
can persist for 2 to 4 weeks; this is often referred to as “post-
scabietic pruritus” and is a manifestation of the delayed-type
immune reaction.
Scabies may be evident atypically in infants, the elderly,
and the immunocompromized, and is often misdiagnosed.
Infantile scabies usually affects the axillae, head, face, diaper
area, and occasionally, the palms and soles, and is seen with
with vesicles, pustules, and nodules.(15, 16) Secondary bacte-
rial infection by group A streptococci or Staphylococcus aureus
commonly occurs in the lesions, particularly in hands and feet
of young children, and should be treated first. Nodular scabies
is a clinical variant occurring in about 7% of scabies cases. It is
composed of extremely pruritic reddish-brown nodules 2 to
20 mm in size present on the male genitalia, buttocks, groin,
and axillary region. The nodules represent an intense hyper-
sensitivity reaction to mite products, can persist for weeks
after treatment, and often require treatment with corticoster-
oid injections.(1)
Crusted scabies or Norwegian scabies is another variant.
It is found most commonly in HIV patients, the elderly, or
other immunosuppressed individuals. However, about 40%
of patients have no identifiable risk factor, suggesting the
possibility of a genetic predisposition.(17) It is evident as a
hyperkeratotic dermatitis resembling psoriasis and distrib-
uted most prominently over the elbows, knees, hands, and feet.
Approximately half of affected patients do not report pruritus.
(17, 18) Crusted scabies is much more infectious, as the mite
burden can total over 1 million.
Diagnosis
Scabies is usually diagnosed through skin scraping. The burrow
should be unroofed using an oil-covered scalpel blade. The oil
helps the scraped material adhere to the blade. The contents are
then brought onto a slide with a coverslip and examined under
the microscope on low power for the presence of adult mites,
eggs, and/or feces. Scrapings should preferably be from a fresh,
nonexcoriated burrow in the interdigital areas of the hand.
Often, repeated scrapings are needed because the sensitivity is
quite low. Burrows can also be visualized using the burrow ink
test in which burrows will absorb the ink from a marker and
become apparent. Videodermatoscopy is another technique for
diagnosing scabies, especially in children, using magnifications
up to 600 times.(19–21)
Differential Diagnosis
All diseases causing pruritus and papules should be considered,
unless skin burrows are clearly seen on examination. The dif-
ferential diagnosis is extensive and includes atopic dermatitis,
neurodermatitis, animal scabies (whose mites cannot complete
the life cycle on human hosts because they cannot burrow),
papular urticaria, folliculitis, dermatitis herpetiformis, prurigo
nodularis, and bites from mosquitoes, fleas, bed bugs, chiggers,
or other mites.(22–28)
PEDICULOSIS
HEAD LICE
Introduction/Epidemiology
Head lice or pediculosis capitis, caused by Pediculus humanus
capitis, is a common health problem that has plagued mankind
for thousands of years. In the United States, pediculosis capitis
affects about 6 to 12 million people every year.(1, 16, 25, 29)
Infestation occurs most commonly in children, with a peak inci-
dence between 5 and 13 years of age. It is found worldwide with-
out predilection for a particular age, sex, race, or socioeconomic
class. Girls are twice as likely as boys to have head lice because
of their longer hair and sharing of brushes and hair accessories.
(30) Head lice is rare in African Americans due to the anatomy
of their hair shaft, which is more oval, making it harder to be
grasped.(23, 31)
Pathogenesis
Pediculus humanus capitis is a host-specific arthropod that
belongs to the order Anoplura. It measures approximately the
size of a sesame seed (2–3 mm) and is grayish-white in color. It
is wingless, has narrow sucking mouthparts concealed within
the head, short antennae, and three pairs of clawed legs for hair
grasping. The louse moves by grasping hairs and is incapable
of flying or jumping. It feeds by piercing the skin of the host
with its mouthparts and sucking blood every 4 to 6 hours. The
female louse lives approximately 30 days and lays about 5 to 10
eggs a day on hair shafts. Eggs, also known as nits, are 0.8 mm
in length and are laid within 1 to 2 mm of the scalp surface for
warmth. The nits are firmly glued to the individual hairs by
a proteinaceous matrix and are difficult to remove. Head lice
can survive for up to 3 days off the host; nits can live for 10 days
away from their host.
Figure 3.1 The burrow, pathognomonic sign of scabies.

scabiesandpediculosis:biologiccycleanddiagnosis
Clinical Features
Pruritus of the scalp is the primary symptom; a number of patients
are asymptomatic yet considered carriers. Pruritus may not be seen
with the first lice infestation, as it takes 1 to 2 months to develop
sensitivity.(31) In repeat infestations, pruritus develops within the
first 24 to 48 hours. Nits are often found in the occipital scalp and
postauricular portions of the head and are easier to identify than
adult lice. Transmission occurs through direct head-to-head con-
tact for an extended period of time.
Diagnosis
The diagnosis is established by identification of viable nits or
an adult louse on the scalp. Visual inspection without comb-
ing is difficult, as head lice avoid light and crawl quickly. Louse
combs are useful tools, as they increase the chance of finding
live lice fourfold over direct visual examination.(32, 33) Viable
eggs are tan to brown in color, and hatched eggs are clear to
white. Recognition can be facilitated through the use of a mag-
nifying glass. Wood’s lamp examination reveals a yellow-green
fluorescence of the lice and their nits. Dermoscopy is also a
possible aid in diagnosis.(34–36)
Dead eggs can remain affixed to the hair shafts as long as
6 months and can lead to a false-positive diagnosis of an active
infestation, as it may be difficult to distinguish between viable
and empty eggs.
Differential Diagnosis
The differential diagnosis for scalp pruritus includes seborrheic
dermatitis and psoriasis; however, the presence of nits or lice is
diagnostic. Nits can be confused with debris on the hair shaft
left by hair spray, with dandruff or with accumulated flakes of
seborrheic dermatitis. Hair casts may also closely resemble nits
stuck to hair shafts and can be noticed by a parent, teacher, or
school nurse, who mistakes them for nits.(29) In contrast to
nits, they are freely moveable along the hair shaft.
CRAB LICE
Introduction/ Epidemiology
Crab lice or pediculosis pubis infestation is spread as a sexually
transmitted disease. It is slightly more prevalent in men probably
due to their increased amount of coarse body hair. It can be seen in
all ethnic groups though it is less common in people whose families
originated in China, Japan, or Korea, or those with minimal pubic
hair. The highest prevalence is in men who are sexually active with
other men. It is most common in men in the age group of 15 to 40
years, those engaging more in sexual activities during this period.
Crab lice may be more common in the winter months.(37)
Pathogenesis
Infestation with crab lice is caused by Phthirus pubis which is
approximately 0.8 to 1.2 mm in length. It has a shorter body
than head lice and resembles microscopic crabs. Phthirus pubis
have serrated edges on their anterior claws that allow them
increased traction and mobility on the entire body.(38) Females
lay up to 3 eggs a day with an incubation period of 7 to 10 days.
The adult crab louse can live up to 2 weeks on the host and
about 36 hours outside of the host.
Clinical Features
Crab lice commonly affect pubic (Figure 3.2), axillary, chest hair,
and more rarely eyelashes, and are evident as with pruritus of the
pubic area. The eggs may be visible to the naked eye as 0.5 mm
brown-opalescent ovals. Macula caerulea is a characteristic finding
with infestation. They are asymptomatic bluish-gray macules on
the trunk and thighs caused by bites of the crab louse. Underwear
can also sometimes be stained with small drops of blood. As crab
lice are transmitted sexually, patients with pediculosis pubis should
be investigated for other sexually transmitted diseases including
HIV, syphilis, scabies, gonorrhea, chlamydia, herpes, warts, and
trichomoniasis. Approximately 30% of patients with crab lice will
have a concurrent sexually transmitted disease.(29) Evidence of
P. pubis in a child may occasionally reflect sexual abuse.
Diagnosis
The identification of crab lice and their nits with the naked eye
or a magnifying glass is diagnostic. However, sometimes the
number of living lice can be small and diagnosis can be aided
by the use of dermoscopy.(36)
Differential Diagnosis
Nits on the pubic hair can be misdiagnosed for white piedra
or trichomycosis pubis.(39, 40) If extensive excoriations are
present, scabies or contact dermatitis should be considered.
REfEREnCES
1. Hengge UR, Currie BJ, Jager G, Lupi O, Schwartz RA. Sca-
bies: a ubiquitous neglected skin disease. Lancet Infect Dis
2006; 6: 769–79.
Figure 3.2 Crab lice (circles) of the pubic region.
1
tajirianandschwartz
2. Burgess I. Sarcoptes scabiei and scabies. Adv Parasitol
1994; 33: 235–92.
3. Walton SF, Currie BJ. Problems in diagnosing scabies, a
global disease in human and animal populations. Clin
Microbiol Rev 2007; 20: 268–79.
4. Sterling GB, Janniger CK, Kihiczak G, Schwartz RA, Fox
MD. Scabies. Am Fam Physician 1992; 46: 1237–41.
5. Haag ML, Brozena SJ, Fenske NA. Attack of the scabies:
what to do when an outbreak occurs. Geriatrics 1993; 48:
45–6.
6. Hogan DJ, Schachner L, Tanglertsampan C. Diagnosis and
treatment of childhood scabies and pediculosis. Pediatr
Clin North Am 1991; 38: 941–57.
7. Molinaro MJ, Schwartz RA, Janniger CK. Scabies. Cutis
1995; 56: 317–21.
8. Arlian LG, Runyan RA, Achar S, Estes SA. Survival and
infectivity of Sarcoptes scabiei var. canis and var. hominis.
J Am Acad Dermatol 1984; 11: 210–5.
9. Arlian LG, Vyszenski-Moher DL, Pole MJ. Survival of
adults and development stages of Sarcoptes scabiei var.
canis when off the host. Exp Appl Acarol 1989; 6: 181–7.
10. Heukelbach J, Feldmeier H. Scabies. Lancet 2006; 367:
1767–74.
11. Walton SF, McBroom J, Mathews JD, Kemp DJ, Currie BJ.
Crusted scabies: a molecular analysis of Sarcoptes scabiei
variety hominis populations from patients with repeated
infestations. Clin Infect Dis 1999; 29: 1226–30.
12. Badiaga S, Menard A, Tissot Dupont H et al. Prevalence
of skin infections in sheltered homeless. Eur J Dermatol
2005; 15: 382–6.
13. Tsutsumi M, Nishiura H, Kobayashi T. Dementia-specific
risks of scabies: retrospective epidemiologic analysis of
an unveiled nosocomial outbreak in Japan from 1989–90.
BMC Infect Dis 2005; 5: 85.
14. Sunderkotter C, Mayser P, Folster-Holst R et al. Scabies.
J Dtsch Dermatol Ges 2007; 5: 424–30.
15. Janniger CK, Micali G, Hengge U et al. Scabies. eMedicine
Pediatrics [journal serial online]. 2009. Available at http://
emedicine.medscape.com/article/911033-overview
16. Wozniacka A, Hawro T, Schwartz RA. Bullous scabies: a
diagnostic challenge. Cutis 2008; 350–2.
17. Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies:
clinical and immunological findings in seventy-eight patients
and a review of the literature. J Infect 2005; 50: 375–81.
18. O’Donnell BF, O’Loughlin S, Powell FC. Management of
crusted scabies. Int J Dermatol 1990; 29: 258–66.
19. Micali G, Lacarrubba F, Tedeschi A. Videodermatoscopy
enhances the ability to monitor efficacy of scabies treat-
ment and allows optimal timing of drug application. J Eur
Acad Dermatol Venereol 2004; 18: 153–4.
20. Lacarrubba F, Musumeci ML, Caltabiano R et al. High-
magnification videodermatoscopy: a new noninvasive dia-
gnostic tool for scabies in children. Pediatr Dermatol
2001; 18: 439–41.
21. Micali G, Lacarrubba F, Lo Guzzo G. Scraping versus vide-
odermatoscopy for the diagnosis of scabies: a comparative
study. Acta Derm Venereol 1999; 79: 396.
22. Stibich AS, Schwartz RA. Papular urticaria. Cutis 2001; 68:
89–91.
23. Steen CJ, Carbonaro PA, Schwartz RA. Arthropods in der-
matology. J Am Acad Dermatol 2004; 50: 819–42.
24. Thomas I, Kihiczak GG, Schwartz RA. Bedbug bites: a
review. Int J Dermatol 2004; 43: 430–3.
25. Nutanson I, Steen C, Schwartz RA. Pediculosis corporis: an
ancient itch. Acta Dermatovenerol Croat 2007; 15: 33–8.
26. Vaidya DC, Schwartz RA. Prurigo nodularis: a benign der-
matosis derived from a persistent pruritus. Acta Derma-
tovenerol Croat 2008; 16: 38–44.
27. Schwartz RA. Papular urticaria. eMedicine Dermatology
[Journal serial online]. 2009. http://emedicine.medscape.
com/article/1051461-overview
28. Schwartz RA. Bedbug bites. eMedicine Dermatology [jour-
nal serial online]. 2009. Available at: http://emedicine.med-
scape.com/article/1088931-overview
29. Ko CJ, Elston DM. Pediculosis. J Am Acad Dermatol 2004;
50: 1–12.
30. Burgess I. The life of a head louse. Nurs Times 2002; 98:
54.
31. Frankowski BL, Weiner LB. Head lice. Pediatrics 2002; 110:
638–43.
32. Mumcuoglu KY, Friger M, Ioffe-Uspensky I, Ben-Ishai F,
Miller J. Louse comb versus direct visual examination for
the diagnosis of head louse infestations. Pediatr Dermatol
2001; 18: 9–12.
33. De Maeseneer J, Blokland I, Willems S, Vander Stichele
R, Meersschaut F. Wet combing versus traditional scalp
inspection to detect head lice in schoolchildren: observa-
tional study. BMJ 2000; 321: 1187–8.
34. Bakos RM, Bakos L. Dermoscopy for diagnosis of pedicu-
losis capitis. J Am Acad Dermatol 2007; 57: 727–8.
35. Di Stefani A, Hofmann-Wellenhof R, Zalaudek I. Dermos-
copy for diagnosis and treatment monitoring of pediculo-
sis capitis. J Am Acad Dermatol 2006; 54: 909–11.
36. Chuh A, Lee A, Wong W, Ooi C, Zawar V. Diagnosis of
Pediculosis pubis: a novel application of digital epilumi-
nescence dermatoscopy. J Eur Acad Dermatol Venereol
2007; 21: 837–8.
37. Mimouni D, Ankol OE, Gdalevich M et al. Seasonality
trends of pediculosis capitis and phthirus pubis in a young
adult population: follow-up of 20 years. J Eur Acad Der-
matol Venereol 2002; 16: 257–9.
38. Burkhart CG , Burkhart CN. Oral ivermectin for Phthirus
pubis. J Am Acad Dermatol 2004; 51: 1037.
39. Schwartz RA, Altman R: Piedra. eMedicine Dermatology
[Journal serial online]. 2009. http://emedicine.medscape.
com/article/1092330-overview
40. Schwartz RA. Superficial fungal infections. Lancet 2004;
364: 1173–82.

3.2 Videodermatoscopy and scabies
Francesco Lacarrubba, Nella Pulvirenti, and Giuseppe Micali
The standard technique for the diagnosis of scabies involves
identification of the mite, eggs, or excreta by microscopic exam-
ination of scales obtained by skin scraping, but this method may
cause discomfort and fear, especially in younger patients. As
the results generally depend on the scraped areas, repeated tests
are sometimes necessary for a conclusive diagnosis. For these
reasons, scraping is not well accepted by patients, who may
not cooperate, or even decline the examination. Follow-up
tests, useful to assess recovery from therapy or to rule out
persisting pruritus due to use of irritant topical agents, are
troublesome, and patients may refuse further scraping, con-
sidering it a useless “torture.” Moreover, handling and pro-
cessing scrapings rapidly and effectively in the office is not
always straightforward.(1–2)
In 1992 Kreusch (3) suggested the use of epiluminescence
microscopy in diagnosing scabies, as this technique allows the
inspection of the skin surface down to the superficial dermis.
The first study was performed by Argenziano et al., which, using
the epiluminescence microscopy technique at X40 magnifica-
tion, made a repetitive finding, a small dark brown triangular
structure located at the end of a subtle linear segment in 93% of
70 patients affected by scabies; together, both structures resem-
bled a jet with contrail.(4–5) On microscopic examination, the
jet-shaped triangular structure corresponded to the pigmented
anterior part of the mite (mouth parts and two anterior pairs of
legs); the contrail-shaped segment was thought to be the bur-
row of the mite along with its eggs and fecal pellets.(4–5)
In 2000, we conducted at our institution a comparative
study (6) of scraping versus high magnification videoderma-
toscopy (VD) in 38 patients suspected of being infested with
scabies (patients were in the age range between 1 month and
81 years). VD was performed using a Video Microscope System
Hi-Scope KH-2,200 [Hirox Co. Ltd., Tokyo, Japan], allowing
the skin observation at magnifications ranging from X4 up to
X1,000. Both scraping and VD examinations were carried out in
each patient by two independent operators, and exchange of infor-
mation was not allowed. The use of VD allowed a detailed inspec-
tion of the skin with rapid identification of burrows, mites, feces,
and eggs in 16 out of 38 patients and, in most cases, it was pos-
sible to observe the mites moving inside the burrows. Microscopic
examination of the scales obtained by skin scraping gave similar
results. Interestingly, two cases were positive only by scraping
and this fact was probably due to impetiginization that ham-
pered VD examination (Figure 3.3); conversely, the two other
cases, characterized by minimal lesions, were found positive
only at VD (Figure 3.4).(6) On the basis of these results, we
conducted a large-scale study in children in which VD was the
only diagnostic tool.(1) A total of 100 young patients (43 boys
and 57 girls, aged between 1 month and 16 years) suspected to
be affected by scabies were enrolled in the study. Patient exami-
nation was first performed using a relatively low magnifica-
tion (about X100), and suspicious lesions (i.e. burrows) were
analyzed at higher magnification (up to X600). No use of oil
or slide on the skin was necessary as image resolution was of
good quality. VD allowed a detailed inspection of the skin in
all patients. Diagnosis of scabies was established in 62 out of
Figure 3.3 A case of impetiginized scabies in which VD exami-
nation may be hampered and may give false-negative result.
Figure 3.4 A case of scabies with minimal lesions in which
traditional skin-scraping may give false-negative result.
2
lacarrubba,pulvirenti,andmicali
Figure 3.5 Burrow at VD observation: The roundish body of
Sarcoptes scabiei (circle) may be observed at one end of the
burrow (X100).
Figure 3.6 Burrow at VD observation: Sarcoptes scabiei may be
observed at the end of the burrow (X200).
Figure 3.7 Sarcoptes scabiei at VD observation (X500): the
roundish body is translucent, whereas the anterior part of the
mite (head and anterior legs) is pigmented (arrow).
Figure 3.8 Eggs (ovular and translucent) and feces (roundish
and white) of Sarcoptes scabiei at VD observation (X500).
100 patients and was based on identification of mites, eggs and
feces. None of the 38 negative patients showed signs of infesta-
tion at a 2-week follow-up examination. The study showed that
high magnification VD is very effective and sensitive, especially
in cases with not specific clinical features, allowing clear detec-
tion of some details (e.g., mites in migration, eggs, and feces)
usually not appreciable at lower magnifications.(1)
The effectiveness of dermoscopy both at low and high mag-
nification in diagnosing scabies has been confirmed by several
other studies.(2, 7–12)
A study comparing the dermoscopic diagnosis of scabies
using a pocket, handheld dermoscope and allowing 10X mag-
nification with traditional skin scraping in 238 patients has
shown that dermoscopy achieves comparable high diagnostic
sensitivity values as scraping (91% vs. 90%, respectively).
Under 10X magnification, after paraffin oil application on the
glass plate of the dermatoscope, Sarcoptes scabiei appears as a
characteristic triangular shape, resembling a circumflex accent
(e.g., in French letter ‘‘ô’’) that corresponds to head and front
legs of the mite.(11)
Dermoscopy affords several advantages compared to tradi-
tional skin scraping. First, it is not invasive and it is well accepted
by the patients, especially by children and those more sensitive
patients who may have had repeated negative results at skin
scraping, as it does not cause physical or psychological discom-
fort. It is easy and quick to perform, allowing inspection of the
entire skin surface usually within few minutes and is significantly
less time consuming than ex vivo microscopic examination.(1, 5)
3
videodermatoscopyandscabies
It is useful for nontraumatic screening of family members who
might refuse skin scraping being asymptomatic. Moreover, being
noninvasive, this technique minimizes the risk of accidental
infections from blood-transmissible agents such as HIV or HCV.
Finally, dermoscopy has demonstrated to be useful in diagnosing
scabies through the technique of teledermatology. In one study,
this approach, which involves sharing digital pictures by captur-
ing dermoscopic images at the remote site and reviewing them
later at the host site, appeared to be a relatively cost-effective
means of providing this service from a distance when on-site
dermatology services is not available.(13)
An important issue to address is which magnification gives
the best performance, considering also that most systems come
equipped with lenses up to X1,000. We recommend the use of
VD wherever possible, as it allows a detailed inspection of the skin
with rapid and clear detection of the diagnostic features of scabies,
such as burrows at magnifications ranging from X40 to X100, and
mites, eggs, or feces at higher magnifications (up to X600) (Figure
3.5–3.8). Using these magnifications, false-negative results are
rare and there is no chance of false-positive results, as the images
obtained are unequivocal: The round, translucent body of the mite
(invisible at low magnifications) is clearly visible and it is always
possible to visualize the other anatomical structures of the mite,
that is, its legs (anterior and posterior) and rostrum; in most cases,
it is also possible to detect the mite moving inside the burrows.
(6–7) Finally, the use of oil and slides is messy and time consuming
and is unnecessary at high magnification, as it does not enhance
image quality.
Figure 3.9a Burrow at low-magnification VD observation: The
“circumflex accent” that corresponds to head and front legs of
mite structure may be observed (arrow) (X20).
Figure 3.9b The same burrow at X40 magnification: The “jet
with contrail” structure is more evident.
Figure 3.9c The same burrow at X400 magnification: both the
mite (on the left) and the eggs (on the right) are clearly evident.
Figure3.9d The same eggs at X600 magnification.

lacarrubba,pulvirenti,andmicali
VD is particularly useful for posttherapeutic follow-up, show-
ing the possible presence of viable mites and thus reducing the risk,
in cases of unsuccessful therapy, of persistence and diffusion of the
infestation.(1, 14) Again, patients are more willing to undergo
posttherapeutic VD examination rather than skin scraping.
In our experience, however, the use of low magnifications
(X10–X40) may have some limitations, and one of them is that
it does not always allow, especially to nonexperienced opera-
tors, a clear differentiation between the “circumflex accent”
(or the “jet-shaped” structure) and minor excoriations and/or
splinters (that may frequently occur in scabies due to repeated
scratching). In addition, low magnifications do not facilitate
visualization of eggs and feces, which are quite often the only
diagnostic clues available to suspect the presence of mites.
Another limitation is that mite viability cannot be assessed
at these magnifications; therefore, posttherapeutic monitoring
cannot be performed. Finally, the use of hand-held dermo-
scope, as recently suggested, may be troublesome when used in
hairy body areas, where a clear visualization of the skin may be
hampered. In addition, the use of hand-held dermatoscopy in
or around the genital region may cause embarrassment because
of close contact between dermoscopist’s head and patient’s skin
surface.(11) In conclusion, considering the possible risk of
false-negative and/or false-positive results, the use of hand-held
dermoscopy might be limited to those cases in which no VD
facilities are available or to a preliminary screening of suspect
lesions before skin scraping is carried out.(11)
The importance of the use of high magnifications may be
better understood by viewing the same lesion at different mag-
nifications (Figure 3.9–3.10).
Finally, when we use the dermoscope or the videoderma-
toscope in diagnosing scabies, the possibility of indirect con-
tamination of the patients through the instrument might be
considered, as mites survive in the outside environment (away
from the host) for up to 72 hours; therefore, disinfection of the
device after each examination is recommended.(11)
REFERENCES
1. Lacarrubba F, Musumeci ML, Caltabiano R et al. High-
magnification videodermatoscopy: a new noninvasive diag-
nostic tool for scabies in children. Ped Dermatol 2001; 18:
439–41.
2. Neynaber S, Wolff H. Diagnosis of scabies with dermos-
copy. CMAJ 2008; 178: 1540–1.
3. Kreusch J. Incident light microscopy: reflection on micros-
copy of the living skin. Int J Dermatol 1992; 31: 618–20.
4. Argenziano G, Fabbrocini G, Delfino M. Epilumines-
cence microscopy. A new approach to in vivo detection of
Sarcoptes scabiei. Arch Dermatol 1997; 133: 751–3.
5. Zalaudek I, Giacomel J, Cabo H et al. Entodermoscopy: a
new tool for diagnosing skin infections and infestations.
Dermatology 2008; 216: 14–23.
6. Micali G, Lacarrubba F, Lo Guzzo G. Scraping versus vid-
eodermatoscopy for the diagnosis of scabies: a compara-
tive study (Letter). Acta Derm Venereol 2000; 79: 396.
7. Brunetti B, Vitiello A, Delfino S, Sammarco E. Findings in
vivo of Sarcoptes scabiei with incident light microscopy.
Eur J Dermatol 1998; 8: 266–7.
8. Bauer J, Blum A, Sönnichsen K et al. Nodular scabies
detected by computed dermatoscopy. Dermatology 2001;
203(2): 190–1.
9. Prins C, Stucki L, French L, Saurat JH, Braun RP. Dermos-
copy for the in vivo detection of sarcoptes scabiei. Derma-
tology 2004; 208(3): 241–3.
10. Fox GN, Usatine RP. Itching and rash in a boy and his
grandmother. J Fam Pract 2006; 55: 679–84.
Figure 3.10b The same mite at X500 magnification is easily
recognizable.
Figure 3.10a Sarcoptes scabiei (arrow) out of the burrow at
low-magnification VD observation: The “circumflex accent” is
hardly visible (X20).

videodermatoscopyandscabies
11. Dupuy A, Dehen L, Bourrat E et al. Accuracy of standard
dermoscopy for diagnosing scabies. J Am Acad Dermatol
2007; 56: 53–62.
12. Ishii N. Executive committee of guideline for the diagno-
sis. Guideline for the diagnosis and treatment of scabies in
Japan (2nd edition). J Dermatol 2008; 35: 378–93.
13. Weinstock MA, Kempton SA. Case report: teledermatol-
ogy and epiluminescence microscopy for the diagnosis of
scabies. Cutis 2000; 66: 61–2.
14. Lacarrubba F, Micali G. Parasitoses of the scalp. In: Tosti A,
(ed). Dermoscopy of Hair and Scalp Disorders: Pathological
and Clinical Correlation. Informa Healthcare Ltd, UK, 2007.

3.3 Videodermatoscopy and pediculosis
Giuseppe Micali, Marianna Umana, and Francesco Lacarrubba
Pediculosis caPitis
Pediculosis capitis (head lice) is a worldwide infestation due to
Pediculus humanus capitis (Figure 3.11), a blood-sucking insect
and specific human parasite, which affects predominantly
children aged between 4 and 14 years. It causes itching and,
occasionally, secondary bacterial infections resulting from
scratching with an associated local retroauricular adenopathy.
Generally, the diagnosis of pediculosis capitis is clinical,
as both mites and their nits may be detectable with close-up
examination; however, search of the mite is time consuming
and, because the head louse moves quickly and avoids light, it
is often not visible.(1) Therefore, the diagnosis is traditionally
based on a combination of scalp itching, eventually accompa-
nied by local bite reactions and/or cervical lymphadenopathy
and the presence of nits.(1) Sometimes nits may be over-
looked and nits containing vital nymphs can be difficult to
differentiate from empty nits and so-called pseudo nits, such
as hair casts, debris of hair spray or gel, or scales from sebor-
rheic dermatitis.(1)
In 2003, we described the use of videodermatoscopy (VD) in
pediculosis.(2) In case of infestation, VD unequivocally shows
the presence of the nits fixed to the hair shaft (Figure 3.12),
allowing a rapid differentiation from scales of different origin
(pseudo nits) that appear as amorphous, whitish structures (3)
(Figure 3.13). Moreover, VD allows a more detailed identifica-
tion of full versus empty nits, where the full nits, which contain
nymphs and indicate a potential active infestation, appear like
ovoid, brown structures with a convex extremity (Figure 3.14a),
whereas the empty nits, which may persist after the recovery,
are translucent and typically show a plane and fissured free
ending (Figure 3.14b).(1, 3) The differentiation between vital
and empty nits provides useful information about therapeu-
tic response. Furthermore, VD does not require hair pulling;
therefore, a large scalp area can be investigated without discom-
fort to the patient.
With a little patience, it is also possible to detect the lice.
In this case VD allows an in vivo evaluation of the move-
ments and physiology of lice (Figure 3.15) and may be
Figure 3.11 VD observation of Pediculus humanus capitis on
a glass slide (X80).
Figure 3.12 Nit fixed to the hair shaft (X80).
Figure 3.13 A scale of seborrheic dermatitis (pseudo nit) appear-
ing as an amorphous, whitish structure (X80).

videodermatoscopyandpediculosis
useful to evaluate the pediculocidal activity of different topical
products.(4)
In conclusion VD can be used as an easy, safe, and reliable diag-
nostic tool in head lice infestation and the procedure can rapidly
confirm the diagnosis in some puzzling cases where parasites and
nits may be not easily identified. Other authors have reported
obtaining similar results by a contact, hand-held dermatoscope
both in vivo and nipping and placing hairs, presenting nits on the
adherent side of a piece of transparent adhesive tape.(1, 5)
Phthiriasis Pubis
The same technique of VD may be extended to diagnosing
phthiriasis pubis (crab lice).(2, 6) Phthirus pubis infests mainly
the hair of the pubic and inguinal region, rarely those of axillae,
chest, and limbs. In children, the edges of scalp hair and eyelashes
Figure 3.14a Full nits, which contain nymphs, appear like
ovoid, brown structures with a convex extremity (X100).
Figure 3.14b Empty nits are translucent and typically show a
plane and fissured free ending (X100).
Figure 3.15 Pediculus humanus “in action” in the hair shafts (X80).
Figure 3.16 Phthirus pubis firmly attached to the pubic hairs (X80).
Figure 3.17 Phthirus pubis at VD observation (X80).

micali,umana,andlacarrubba
(phthiriasis palpebrarum) are the most common site of infesta-
tion because of the lack of terminal hairs on most body regions.
In the majority of cases the diagnosis of pubic lice is clinical
and there is no need for further investigation. VD clearly shows
the presence of the crab lice firmly attached to the pubic hairs
(Figure 3.16–3.17). In most cases, it is possible to recognize the
parasite sucking the blood. Moreover, as observed in pedicu-
losis capitis, VD allows a more detailed identification of full
versus empty nits (Figure 3.18).
In case of phthiriasis palpebrarum, the lice are sometimes
difficult to identify because of their semitransparency and deep
burrowing in the lid margin, so the infestation may exist for a
long time before being recognized (7) and generally misdiag-
nosed with atopic dermatitis or allergic conjunctivitis. In these
cases, VD can rapidly clarify any doubt by revealing the pres-
ence of lice and/or nits (Figure 3.19–3.20).
Finally, VD examination may enhance patient compliance
to therapy both in head and crab lice, by clearly showing on
the VD monitor their presence, persistence, or resolution of the
infestation (6).
reFereNces
1. Di Stefani A, Hofmann-Wellenhof R, Zalaudek I.
Dermoscopy for diagnosis and treatment monitoring
of pediculosis capitis. J Am Acad Dermatol 2006; 54:
909–11.
2. Micali G, Lacarrubba F. Possible applications of videoder-
matoscopy beyond pigmented lesions. Int J Dermatol 2003;
42: 430–3.
3. Zalaudek I, Giacomel J, Cabo H et al. Entodermoscopy: a
new tool for diagnosing skin infections and infestations.
Dermatology 2008; 216: 14–23.
Figure 3.18 Full nit of Phthirus pubis (X60). Figure 3.19 Phthiriasis palpebrarum. Insert: VD observation of
lice and nits (X80).
(a) (b)
Figure 3.20a–b Nits of the eyelashes (a) versus scales of atopic dermatitis (b) at VD observation (X50).

videodermatoscopyandpediculosis
4. Lacarrubba F, Nardone B, Milani M, Botta G, Micali G.
Head lice: ex vivo videodermatoscopy evaluation of the
pediculocidal activity of two different topical products. G
Ital Dermatol Venereol 2006; 141: 233–5.
5. Bakos RM, Bakos L. Dermoscopy for diagnosis of pediculo-
sis capitis. J Am Acad Dermatol 2007; 57: 727–8.
6. Chuh A, Lee A, Wong W, Ooi C, Zawar V. Diagnosis of
Pediculosis pubis: a novel application of digital epilumines-
cence dermatoscopy. J Eur Acad Dermatol Venereol 2007;
21: 837–8.
7. Yoon KC, Park HY, Seo MS, Park YG. Mechanical treatment of
phthiriasis palpebrarum. Korean J Ophthalmol 2003; 17: 71–3.

3.4 Therapy of scabies and pediculosis: Potential and pitfalls
Lee E West, Beatrice Nardone, and Dennis P West
InTroducTIon
A great pitfall for scabies and pediculosis therapeutic studies
to date is that primary and secondary study outcomes are indi-
rectly assessed (presence or absence of live parasites, including
eggs, determined by gross clinical inspection) and data time-
points are nonstandardized (highly variable) relative to time of
therapeutic application. Certainly, kill times and kill rates are
rarely determined or reported. Indeed, meta-analyses of ran-
domized, controlled clinical trials for these parasitoses are scarce
and, by nature, analyses are based on highly variable assessment
methodology and data collection, followed by highly variable
interpretation and reporting.(1, 2)
Utilization of high-resolution, high-magnification video-
dermatoscopy (VD) in establishing highly definitive and pre-
cise quantitative data products used in the treatment of scabies
and pediculosis provides enormous advantages in the quest to
establish reproducible quantitative methodology for efficacy
studies in these parasitoses.(3–6)
Unfortunately, determination of the risk–benefit ratio for
reported treatments does not involve uniform or precise meth-
odology such as VD and, as a result, subjective weighing of lit-
erature reports is used to determine efficacy, and, subsequently,
benefit–risk categorization. Clearly, standard methods such as
VD allow for uniform data and, ultimately, uniform compari-
son and categorization of efficacy.
Considering these significant limitations in efficacy stud-
ies to date for both scabies and pediculosis, the following
overview provides insight into the topical and systemic
pharmacologic and nonpharmacologic approaches to treat-
ment that are reported to be used in the clinical management
of such infestations. See Table 3.1 for a combined subjective
and objective relative assessment of efficacy and safety to
provide a current guide to risk–benefit ratio as categorized
for selected agents reported to be used in scabies and/or
pediculosis.
PedIculosIs
A high percentage of cases of head lice are treated without
medical supervision and with products that may be prone to
overuse, leading to increased risk of developing resistance to
such products. Resistance to virtually all topical products for
treatment of pediculosis, including permethrin, pyrethrins,
malathion monotherapy, and lindane, has been reported.(7–9)
While treatment failure may be due to resistance in some cases,
noncompliance or underuse of medication should always
be considered. Whether changing treatment product or
applying further doses, the importance of consultation and
patient education should be emphasized.(10) Some causes
of treatment failure may be related to misdiagnosis or
reinfestation.
Usually an initial treatment is followed by a second applica-
tion after 7 to 10 days to ensure that any hatching nymphs are
destroyed. Spread of head lice is by transfer of live lice only; nits
or nit cases will not cause infestations.(11)
scabIes
It is important to treat close physical contacts, even if asymp-
tomatic, as well as the infested patient, to minimize the risk of
reinfestation. Topical and systemic agents are quite effective in
killing and eradicating the parasite. Pruritus may increase and
persist for up to 2 weeks after successful treatment due to con-
tinuing reactivity to substances released from the dying mites.
Patients need to be reassured that itching is not always indica-
tive of infestation after treatment. Pruritus lasting longer than
2 weeks after treatment may indicate treatment failure or resis-
tance. Generally, a repeat treatment 7 days after the initial treat-
ment is given to ensure that hatching larvae are destroyed. New
lesions present after 4 weeks may indicate treatment failure or
reinfestation.(12)
Bed linens and towels should be washed after treatment and
areas of frequent body contact such as carpets, chairs, and sofas
should be vacuumed.(13) The vacuum-cleaner bag should be
removed immediately after vacuuming, sealed in a plastic bag,
and discarded. The use of insecticides on inanimate objects,
such as furniture, has not been proven to be of benefit.
PhysIcal removal—PedIculosIs
Nit Combs
Wet combing “bug busting” is a procedure that involves comb-
ing wet hair with a fine-tooth comb every 3 to 4 days for at least
2 weeks to physically remove live lice and nits. Wetness of hair is
important because water slows the motility of lice, making it eas-
ier for removal.(14) Removed lice can then be placed on adhesive
paper. Studies that compared bug busting with malathion mono-
therapy found malathion to be twice as effective.(15) While this
method is labor intensive and poses recurrent infestation issues,
the advantages of low cost and unlimited repetition with no side
effects may warrant further investigation.(16)
While combs and other devices may help remove lice and
nits, treatment is considered more thorough. Fine tooth combs
designed to effectively remove nits and may be used with hair
conditioner or active agent.(17)
Shaving the head is not recommended since this can cause
significant and long-lasting emotional trauma as well as
embarrassment.

therapyofscabiesandpediculosis:potentialandpitfalls
ToPIcal TreaTmenT
Benzyl Alcohol—Pediculosis
Topical lotion, containing benzyl alcohol (5%), is a nonneuro-
toxic pediculocide that acts to fix the spiracles of the louse in an
open position, thus permitting blockage and asphyxiation. Note
that unlike benzyl alcohol, some so-called asphyxiator products
only temporarily stun the spiracles in an open position, thus
allowing the louse to quickly recover and continue infestation.
Complete treatment consists of two 10-minute applications
(hair saturation followed by rinsing) 1 week apart.
Benzyl Benzoate—Scabies and Pediculosis
Benzyl benzoate, a long-standing scabicide and pediculocide,
is known to partially biotransform to benzyl alcohol. Benzyl
benzoate is available in various topical dosage forms for use in
scabies and pediculosis at concentrations as high as 35%. It is
widely used in some countries, but in a study compared to oral
ivermectin, it showed inferior efficacy to ivermectin.(18) The
mechanism of action is unknown.
Carbaryl—Pediculosis
This topical agent functions similarly to malathion by binding
to the same acetylcholinesterase enzyme site to cause respira-
tory paralysis in the louse. Unfortunately, even though tox-
icity of this compound is specific to the louse (and not the
human host) in the topical concentration being used (0.5%),
this agent is reported to be mutagenic and may or may not
prove to be carcinogenic, thus limiting its utility in pediatric
populations.(19)
Crotamiton—Scabies and Pediculosis
Marketed as a 10% topical cream for pruritus, this agent has
been reported to be effective in scabies and has limited report-
ing of effectiveness in pediculosis. Crotamiton is relatively
nontoxic to the human host and the mechanism of action is
unknown.(20) Although relatively safe for use in children, it is
not recommended for use in pregnant or lactating women.
Dimethicone—Pediculosis
Similar to other agents that interfere with the respiratory sys-
tem (interrupted oxygen supply), topical dimethicone (up to
92% concentration) has shown efficacy and yet is considered
safe to the human host, including children and pregnant or
lactating women.(21, 22)
Ivermectin—Scabies and Pediculosis
Although topical ivermectin was reported as beneficial in the
treatment of pediculosis over a decade ago, (23) it is just now
undergoing US trials.
Lindane—Scabies and Pediculosis
Lindane is used as a second-line therapy. Package sizes are lim-
ited to the amount necessary for treatment of one person in an
effort to prevent overuse. The use of lindane has been banned
Table 3.1 Combined Subjective and Objective Relative Assessment
of Reported Efficacy and Safety to Provide a Risk–Benefit
Ratio Category for Selected Agents Used in Scabies and/or
Pediculosis.
agent condition benefit:risk
Benzyl alcohol
Topical
Pediculosis 1
Dimethicone
Topical
Pediculosis 1
Ivermectin
Topical
Pediculosis 1
Ivermectin
Systemic
Scabies and pediculosis 1
Malathion/terpineols
combination therapy
(United States)
Topical
Scabies and pediculosis 1
Permethrin
Topical
scabies & pediculosis 1
Benzyl benzoate
Topical
Scabies and pediculosis 2
Cotrimoxazole
(trimethoprim/
sulfamethoxazole)
Systemic
Pediculosis 2
Crotamiton
Topical
Scabies and pediculosis 2
Lindane
Topical
Scabies and pediculosis 2
Malathion Monotherapy
(UK)
Scabies and pediculosis 2
Petrolatum/Mineral Oil/
Vegetable (eg; Olive) Oils
Topical
Pediculosis 2
Pyrethrins/Piperonyl
Butoxide
Topical
Pediculosis 2
Sulfur
Topical
Scabies 2
Albendazole
Systemic
Pediculosis 3
Carbaryl
Topical
Pediculosis 3
Citronella
Topical
Pediculosis 3
Levamisole
Systemic
Pediculosis 3
Butter/Margarine/
Mayonnaise
Topical
Pediculosis na
Kerosene/Gasoline/
Petroleum Distillates
Topical
Pediculosis na
1=benefit:risk balanced.
2=benefit:risk decreased.
3=benefit:risk marginal.
na=benefit:risk not acceptable.

west,nardone,andwest
in the state of California and some countries, due to potential
toxicity to the human host.(24)
Although there are advantages to using lindane, including
its utility as a pediculicide and ovicide, disadvantages are also
many, including percutaneous absorption that may result in
neurotoxicity. Lindane is not for use in patients with seizure
and other neurologic disorders or in those with known, low-
ered seizure threshold. Lindane persists in fatty tissues and in
the environment over very prolonged periods. Use with caution
for patients weighing less than 50 kg. Lindane is categorized as
U.S. FDA Pregnancy Category C.
Malathion—Scabies and Pediculosis
Malathion in combination with terpineols may be a useful
approach to treatment because it has very little reported resis-
tance. However, malathion as monotherapy (not in combina-
tion with terpineols) has a relatively high rate of resistance.
There are advantages to using the malathion/terpineols com-
bination: It is highly effective, functions as both a pediculicide
and ovicide, and may have residual therapeutic effects.
Disadvantages include an unpleasant odor and that it is
not indicated for use in children under 6 years of age in some
countries. There are emerging resistance data for malathion
monotherapy.
Permethrin—Scabies and Pediculosis
Permethrin is used widely for treatment of head lice in a 1%
cream-rinse formulation, and permethrin cream at 5% is used
widely for scabies.
Advantages include low toxicity to the human host, ability
to function as both a pediculicide and ovicide, and it may have
residual therapeutic effect.
Disadvantages are that there are emerging resistance data
and it is messy to use on hairy areas.
Pyrethrins—Pediculosis
Pyrethrins are available in combination with piperonyl butox-
ide to increase efficacy.
This agent functions as a pediculicide but not as an ovicide.
Disadvantages also include no residual activity, irritant and/
or allergic contact dermatitis potential, and it may produce
systemic toxicity.(25)
oTher ToPIcals—scabIes
Topical corticosteroids may be used for pruritus that may occur
for up to 2 weeks after successful therapy for scabies. If second-
ary skin infections develop, topical or systemic antibiotics may
be necessary.
naTural ProducTs
Acetic Acid (Vinegar)/Formic Acid—Pediculosis
Diluted vinegar or formic acid can be used as a hair rinse to aid
in the removal of nits.(26)
Citronella—Pediculosis
Topical citronella has been reported to be more effective than
vehicle but otherwise scarce published information exists about
safety of topical use and potential for irritant effect.(27)
Sulfur—Scabies
Precipitated sulfur at 6% in petrolatum ointment is used
an extemporaneously compounded topical agent for scabies
treatment.(28)
Advantages of using sulfur include its relatively low cost,
relatively low potential for toxicity, suitability to treat infants
younger than 2 months of age (except premature infants), and
it is safe for use in pregnant and lactating women.
Disadvantages are that it must be applied for at least three
consecutive overnights, and the ointment is messy with an objec-
tionable odor and is capable of staining clothing and bedding.
Petrolatum
Occlusive products such as petrolatum (petroleum jelly) have been
reported as home remedies that are liberally applied to the entire
scalp at night, occluded with a shower cap, then washed out daily
for several days, and the lice removed by combing. Lice are poten-
tially suffocated or slowed down, and then physically removed
by combing, as it will take several washings to remove the petrola-
tum.(11) The ongoing hair grooming connected with daily sham-
pooing may, in effect, account for lice removal.(29)
Tea Tree Oil—Pediculosis
An herbal shampoo containing extract of paw paw, thymol, and
tea tree oil has reported to be effective in treatment of head lice
infestations.(30)
Disadvantages are that tea tree oil may cause allergic contact
dermatitis and formulations are nonstandardized (unregulated
and unknown amounts of tea tree oil due to variation in purity).
alTernaTIve unProven remedIes
Butter/Margarine/Mayonnaise—Pediculosis
Remedies such as mayonnaise, softened margarine, or butter
have been reported to be used, but these are not proven to be
efficacious, as these are also bacterial-growth media. A disad-
vantage includes risk of serious and/or life-threatening infec-
tion, including septicemia.
Kerosene/Gasoline/Petroleum Distillates—Pediculosis
Treatment with kerosene or gasoline and other petroleum
distillate products is extremely dangerous as a fire hazard and
potential inhalant and should never be used. Disadvantages are
serious risk of physical harm and systemic toxicity
sysTemIc TreaTmenT
Albendazole
Albendazole as an oral agent has been shown to be effective
against head lice. Advantages include simple therapy and
3
therapyofscabiesandpediculosis:potentialandpitfalls
enhanced compliance. It is apparently not synergistic with
permethrin for pediculosis.(31)
Ivermectin—Scabies and Pediculosis
Ivermectin as a single, oral dose of 200 mcg/kg is effective in
destroying lice but not nits. A second dose after 7 to 10 days is
needed to kill hatching nymphs. Oral ivermectin has also been
used for the treatment of recalcitrant pediculosis.
Oral ivermectin is also reported to be beneficial in cases of
HIV-infected patients and in outbreaks occurring in institu-
tionalized patients and hospitals.(32) Because the serum half-
life of ivermectin is about 16 hours, the 7-day repeat dose may
not always be necessary. In HIV patients, however, it may be
necessary to dose a second time at 14 days.(33)
Advantages include high patient compliance with simple
dosing and low toxicity potential. Pruritus usually resolves rela-
tively quickly within 48 hours.
Disadvantages are that it is not ovicidal and not intended for
children under 5 years of age or who weigh less than 15 kg.
Cotrimoxazole (trimethoprim/
sulfamethoxazole)—Pediculosis
Oral TMP-SMX may be combined with topical permethrin to
enhance efficacy of topical permethrin.(34) Although this ther-
apy may be used for resistant infestations or treatment failures,
it should not be used in sulfonamide-allergic patients, consid-
ering its serious systemic side effects.
Indomethacin—Pediculosis
Indomethacin is known to decrease cellular glutathione-5-
transferase, and because resistance of lice to pyrethrins and
permethrin may be related to the parasite’s decreased ability to
detoxify the pesticides by conjugation with reduced glutathione,
this area of interest has led to reporting the use of “enhancing”
or “optimizing” agents such as indomethacin in the treatment
of resistant pediculosis.(35)
Levamisole
Levamisole has been examined in an open-label study as a daily
oral dose of 3.5 mg/kg once daily for 10 days.(36) Disadvantages
include the potential for systemic side effects and the lack of
randomized control trials to establish efficacy.
conclusIons
In general, the incidence of scabies and pediculosis is not
decreasing (perhaps partly due to improved reporting) while
evidence and patterns of increased resistance are well docu-
mented. Patients, as well as parents, are increasingly frustrated
with the lack of efficacy of several topical products and alterna-
tive home remedies and are concerned about repeated exposure
to agents that may produce toxicity. Moreover, increased use
and widespread beliefs that alternative agents pose less hazard
than proven treatments has lead to even greater perception that
resistance to treatment exists even when proven therapies may
not yet have been utilized.
For pediculosis, the topical agent of choice may be related
more to geographic location and economic considerations
than other factors such as toxicity and ease of use. In the United
States, the malathion/terpineols combination product, though
it produces objectionable odor and is difficult to use, is highly
efficacious as one of the first-line agents with minimal toxicity
concerns (no reported human toxicity for the topical concen-
tration used) and no proven resistance. Other first-line topical
agents that are both safe and effective include agents such as
benzyl alcohol and dimethicone.
Unchecked scabies infestations in patients with normal
immune status will usually cause extreme discomfort from pru-
ritus, possible secondary bacterial infection from excoriations,
and will be more likely to spread to other persons.
Geographic area, toxicity, and economic status are some of
the factors key to measuring the prevalence of scabies. Until
quantifiable and precise data on organism kill times and kill
rates are generated, analyzed, and reported, particularly using
videodermatoscopy technology, we can rely only on indirect
measurements of efficacy for agents used in the treatment of
scabies and pediculosis.
references
1. Hu S, Bigby M. Treating scabies: results from an updated
Cochrane review. Arch Dermatol 2008; 144(12): 1638–40.
2. Burkhart CN, Burkhart CG. Recommendation to stan-
dardize pediculicidal and ovicidal testing for head lice
(Anoplura: Pediculidae). J Med Entomol 2001; 38(2):
127–9.
3. Micali G, Lacarrubba F, Tedeschi A. Videodermatoscopy
enhances the ability to monitor efficacy of scabies treat-
ment and allows optimal timing of drug application. J Eur
Acad Dermatol Venereol 2004; 18(2): 153–4.
4. Lacarrubba F, Musumeci ML, Caltabiano R et al. High-
magnification videodermatoscopy: a new noninvasive dia g-
nostic tool for scabies in children. Pediatr Dermatol 2001;
18(5): 439–41.
5. Micali G, Lacarrubba F. Possible applications of video-
dermatoscopy beyond pigmented lesions. Int J Dermatol
2003; 42(6): 430–3.
6. Lacarrubba F, Nardone B, Milani M, Botta G, Micali G.
Head lice: ex vivo videodermatoscopy evaluation of the
pediculocidal activity of two different topical products. G
Ital Dermatol Venereol 2006; 141: 233–6.
7. Burkhart CG, Burkhart CN. Clinical evidence of lice resis-
tance to over-the-counter products. J Cutan Med Surg
2000; 4: 199–201.
8. Pollack RJ, Kiszewski A, Armstrong P et al. Differential per-
methrin susceptibility of head lice sampled in the United
States and Borneo. Arch Pediatr Adolesc Med 1999; 153:
969–73.
4
west,nardone,andwest
9. Downs AM, Stafford KA, Harvey I et al. Evidence for dou-
ble resistance to permethrin and malathion in head lice.
Br J Dermatol 1999; 141: 508–11.
10. Chosidow O. Scabies and Pediculosis. Lancet 2000; 355:
819–26.
11. Frankowski BL, Weiner LB. Head lice. Pediatrics 2002; 110:
638–43.
12. Orkin M, Maibach HI. Scabies treatment: current consid-
erations. Curr Prob Dermatol 1996; 24: 151–6.
13. Elston DM. Controversies concerning the treatment of
lice and scabies. J Am Acad Dermatol 2002; 46: 794–6.
14. Ko CJ, Elston DM. Pediculosis. J Am Acad Dermatol 2004;
50: 1–12.
15. Roberts RJ, Casey D, Morgan DA et al. Comparison of wet
combing with malathion for treatment of head lice in the
UK: a pragmatic randomized controlled trial. Lancet 2000;
356: 540–4.
16. Lapeere H, Vander Stichele RH, Naeyaert JM. Evidence
in the treatment of head lice: drowning in a swamp of
reviews. Clin Infect Dis 2003; 37: 1580–2.
17. Speare R, Canyon DV, Cahill C, Thomas G. Comparative
efficacy of two nit combs in removing head lice (Pediculus
humanus var. capitis) and their eggs. Int J Dermatol 2007;
46(12): 1275–8.
18. Glaziou P, Cartel JL, Alzieu P et al. Comparison of iver-
mectin and benzyl benzoate for treatment of scabies. Trop
Med Parasitol 1993; 44(4): 331–2.
19. Grover IS, Ladhar SS, Randhawa SK. Carbaryl-A selective
genotoxicant. Environ Pollut 1989; 58(4): 313–23.
20. Ishii N. Executive committee of guideline for the diag-
nosis. Guideline for the diagnosis and treatment of sca-
bies in Japan (second edition). J Dermatol 2008; 35(6):
378–93.
21. Heukelbach J, Pilger D, Oliveira FA et al. A highly
efficacious pediculicide based on dimeticone: random-
ized observer blinded comparative trial. BMC Infect Dis;
8: 115.
22. Burgess IF, Lee PN, Matlock G. Randomised, controlled,
assessor blind trial comparing 4% dimeticone lotion with
0.5% malathion liquid for head louse infestation. PLoS
One 2007; 2(11): e1127.
23. Youssef MY, Sadaka HA, Eissa MM, el-Ariny AF. Topical
application of ivermectin for human ectoparasites. Am J
Trop Med Hyg 1995; 53(6): 652–3.
24. California Safety Code Section 111246. Sherman Food,
Drug, and Cosmetic Law, Division 104, Part 5, California
Health and Safety Code Section 111246, www.dhs.ca.gov/
fdb/local/PDF/Sherman_2007.PDF, accessed 09-23-09.
25. Hammond K, Leikin JB. Topical pyrethrin toxicity lead-
ing to acute-onset stuttering in a toddler. Am J Ther 2008;
15(4): 323–4.
26. De Felice J, Rumsfield J, Bernstein JE et al. Clinical evalua-
tion of an after-pediculicide nit removal system. Int J Der-
matol 1989; 28: 468–70.
27. Mumcuoglu KY, Magdassi S, Miller J et al. Repellency of
citronella for head lice: double-blind randomized trial of
efficacy and safety. Isr Med Assoc J 2004; 6(12): 756–9.
28. Pruksachatkunakorn C, Damrongsak M, Sinthupuan S.
Sulfur for scabies outbreaks in orphanages.Pediatr Der-
matol 2002; 19(5): 448–53.
29. Schachner LA. Treatment resistant head lice: alternative ther-
apeutic approaches. Pediatr Dermatol 1997; 14(5): 409–10.
30. McCage CM, Ward SM, Paling CA et al. Development of
a paw paw herbal shampoo for the removal of head lice.
Phytomedicine 2002; 98: 743–8.
31. Akisu C, Delibas SB, Aksoy U. Albendazole: single or com-
bination therapy with permethrin against pediculosis
capitis. Pediatr Dermatol 2006; 23(2): 179–82.
32. Buffet M, Dupin N. Current treatments for scabies.
Fundam Clin Pharmacol 2003; 17: 217–25.
33. Fawcett RS. Ivermectin use in scabies. Am Fam Physician
2003; 68: 1089–92.
34. Hipolito RB, Mallorca FG, Zuniga-Macaraig ZO. Head lice
infestation: single drug versus combination therapy with
one percent permethrin and trimethoprim/sulfamethox-
azole. Pediatrics 2001; 107: E30.
35. Namazi MR. The potential utility of indomethacin in
enhancing the pediculocidal activity of permethrin, pyre-
thrins, and DDT. Med Hypotheses 2008; 71(4): 607–8.
36. Namazi MR. Levamisole: a safe and economical weapon
against pediculosis. Int J Dermatol 2001; 40(4): 292–4.
Erratum in: Int J Dermatol 2001; 40(12): 794.

3. Therapeutic monitoring of parasitoses with videodermatoscopy
Giuseppe Micali, Aurora Tedeschi, and Francesco Lacarrubba
Previous studies demonstrated that videodermatoscopy (VD)
is a very effective and sensitive diagnostic tool for some cutane-
ous parasitoses, in particular scabies and pediculosis.(1–3) An
important advantage of VD is its high compliance, as it does
not cause pain or physical discomfort. For these reasons, VD
seems to be a useful technique for evaluation of response to
therapy, especially in those cases in which itch persists after
treatment or patient compliance is doubtful.
Based on these considerations, some studies have been car-
ried out to evaluate VD ability to monitor efficacy of scabies
and pediculosis treatment and whether VD allows determina-
tion of the optimal timing of drug application.
SCABIES
The first study (4) to assess the use of epiluminescence

light
microscopy (ELM) for monitoring antiscabietic therapy was
performed in 2001.

The authors examined the mite’s mor-
phological changes in vivo, the temporal progression of these
changes, and their effectiveness

as criteria for treatment.

A total of 20 patients affected by scabies were observed,
7 patients received 12 mg of ivermectin as a single dose, and
13 patients were treated

with lindane or benzyl benzoate for
3 days.

ELM was performed using X8.25 and X20.8 magnifica-
tion. Before treatment, the average number of adult female mites
on

both hands and feet of all patients was 8.2. Epimeres

(chitin-
ous internal structures attached to legs), anterior outline,

eating
tools, and both pairs of forelegs and hind legs of Sarcoptes sca-
biei were observed.

One week after treatment, the average num-
ber of adult female

mites had dropped to 5.0. After 2 weeks, the

mites began to degrade, and their outlines disappeared gradu-
ally;

however, epimeres were even more distinct now, especially
in

children. A granular hem was noticed in some cases. After
3 weeks, structures had progressively broken down or were

miss-
ing. Statistically, no differences were found between

patients
treated orally and those treated locally. After 4 weeks,

there
were no visible remains.

The authors suggested the decrease in
number of mites might have resulted from both scratching

and
the renewal process of the corneal layer itself. Once the mite
was dead it

was slowly promoted upward under a progressively
thinning cover; this explained why the durable chitinous epim-
eres became even

more distinct with time. The progressive

deg-
radation of its other, less durable components and its gradually

disappearing outline suggested that the mite had degraded
rather

than simply been scratched away. Probably, the granular
hem

was a product of catabolism resulting from treatment.(4)
In our experience, (5) we evaluated a group of patients
affected by scabies undergoing topical treatment with a thermo-
labile foam of pyrethrins (0,165%) synergized with piperonyl
butoxide (1,65%), to determine whether VD would enhance
monitoring of the clinical response to treatment and whether
VD would indicate the optimal timing of drug application. A
total of 20 patients (12 males, 8 females; aged between 1 and
65 years) who were affected by scabies (diagnosis confirmed
by VD) and were treatment naïve were included in the study.
The foam was applied to the entire body, once at bedtime for
two consecutive days. In order to detect treatment response,
VD evaluation of two selected skin areas for each patient was
performed at baseline, and after 12, 24, 36, and 48 hours. VD
examination was performed with a Video Microscope System
Hi-Scope KH-2,200 (Hirox Co. Ltd., Tokyo, Japan) equipped
with a zoom lens that allows skin observation with incidental
light at magnifications ranging from X20 to X600. At 48 hours,
skin scraping of the selected areas followed by microscopic
observation was performed. In all patients, VD showed mite
migration within burrows at 12 hours. At 24 hours, there was
no evidence of active mite migration; at that timepoint most
patients reported that itching symptoms had subsided. At 48
hours, the mites were generally no longer appreciable and an
amorphous material, probably resulting from mite decompo-
sition, was generally detectable at one end of an empty bur-
row (Figure 3.21–3.22). At this time, skin scraping followed
by microscopic observation showed only mite remnants in all
patients. None of the 20 patients showed evidence of infesta-
tion at a 2-week follow-up. VD confirmed that the foam was
effective in the management of scabies, killing the mites at
about 24 hours, when their immobilization could be estab-
lished. At 48 hours, shrinkage and breakdown of the mite with
formation of an amorphous material was observed. At that
time, microscopic examination following skin scraping con-
firmed that this material was composed of mite remnants. In
this study, the use of high magnification (up to X600) allowed
to recognize early the death of mites.
In another single-arm multicenter study (6) including
adults and children from 3 months of age with proven scabies,
5% permethrin cream formulation was tested. In this study,
the evaluation of efficacy was performed with the stereo epi-
luminescence microscope of Kreusch (Fa. Wolfgang Kocher
Feinmechanik, Mössingen, Germany, or a comparable device
of another manufacturer) or with a video microscope with X20
to X60 magnification.
In conclusion, VD enhances the monitoring of clinical
response to treatment (4) and allows determination of the
optimal timing of drug application. This may be particularly
important in minimizing the risk of overtreatment, reduc-
ing the potential for side effects, and enhancing patient
compliance.

micali,tedeschi,andlacarrubba
PEDICULOSIS
Pediculosis is a very frequent parasitosis usually treated with
topical compounds with insecticidal activity (pyrethrin, per-
methrin, and malathion) or with so-called natural products with
mechanical action (e.g., essential oil) or with systemic drugs,
such as antibiotics (trimetroprim) or ivermectin.(7) However,
for many of these products, data about their real therapeutic
efficacy or rapidity of action are not readily available. Moreover,
evaluation methods have been based on very simplistic criteria
(i.e. clinical examination before and after treatment).
VD can be used as a diagnostic tool in head and pubic lice
infestation: It permits an easy identification of parasite and nits
when these are not visible to the naked eye.(8) The differentia-
tion between vital and empty nits provides useful information
about therapeutic response.
An in vivo study (8) was performed by mean of a noncontact
hand-held dermoscope (Dermlite; 3gen, LLC). An 8-year-old
boy affected by pediculus capitis was treated with permethrin
(1%) according to established protocols. One week after the first
treatment cycle, dermoscopic follow-up still revealed the pres-
ence of dark-brown eggs containing nymphs, and two additional
therapeutic cycles were performed. At the last visit, 3 weeks after
diagnosis, no nits were observed and treatment was discontin-
ued. In this case, the dermoscopic examination allowed a safe
and reliable differentiation of eggs containing nymphs from the
empty cases of hatched louses and also from amorphous pseudo
nits. The characteristic dermoscopic features let the authors not
only establish a rapid diagnosis but were also useful for the treat-
ment monitoring because vital eggs were still present after the
first treatment cycle. Therefore, in vivo dermoscopy may replace
the more time consuming ex vivo microscopic examination of
the affected hairs in the daily routine.(8)
In our experience, VD allowed the therapeutic monitoring
with mercurial ointment in a case of phthiriasis palpebrarum.
Figure 3.21a–b VD evaluation showing the presence of Sarcoptes scabiei (arrows) at baseline (X100).
(a) (b)
Figure 3.22a–b After 48 hours of treatment the mites were no longer appreciable (X100).
(a) (b)

therapeuticmonitoringofparasitoseswithvideodermatoscopy
After 5 days of treatment, VD showed the persistence of few full
nits not visible to naked eye (Figure 3.23a–3.23b).
VD permits an in vivo evaluation of the movements and
physiology of lice and eggs. Isolation of an adult parasite allows
to observe through VD the louse and to prove its viability in
ex vivo conditions (by means of a Petri’s capsule). Through the
isolation of Pediculus humanus capitis (that cannot be reared
in laboratory conditions) and through VD evaluation, it is also
possible to assess the efficacy and rapidity in pediculocidal
activity of topical pediculocides.
In 2006 we performed a study (9) using VD to assess
the pediculocidal efficacy and rapidity of action of two
different medications indicated in the treatment of head lice.
A formulation of synergized pyrethrin in thermophobic foam
(Milice®; Mipharm) was compared to a coconut and aniseed
oil–based spray, with a mechanical action obtained by suffoca-
tion (Paranix®; Chefaro). Ten experiments were performed on
the same number of adults’ specimens of Pediculus humanus
capitis obtained from three subjects with head lice infestation,
using a fine-tooth comb. Each louse was placed in a Petri’s
capsule with gauze on the bottom in order to improve the VD
visualization. VD examination was performed using a Video
Microscope System Hirox Hi-Scope KH-2,200 equipped with
lenses allowing magnifications ranging from X20 to X600. An
initial observation by VD of 180-second duration was per-
formed to evaluate movements and peristaltic intestinal activity
(that is visible in transparency) as an indicator of lice viability.
After this time, a minimal quantity of pyrethrin thermophobic
foam was applied on five parasites and the oil-based spray was
applied on another batch of 5 parasites. The activity of parasites
were then observed and recorded for 120 minutes. In the case
of pyrethrin thermophobic foam product, in all the tests per-
formed, the absence of movements of lice was observed within
10 seconds from the contact with the product; the absence of
peristalsis was noted within 60 seconds, which was interpreted as
mite death. With the essential oil-based product the lice was alive
after a continuous observation of 120 minutes after the applica-
tion of the medication (the product’s package showed the time
for optimal product activity to be around 15 minutes).
Recently, we performed another similar preliminary study
with a topical compound that acts through a mechanical action
of “choking” of the mite within few minutes (Figure 3.24).
In conclusion, VD is indeed a valid research tool for evaluat-
ing the efficacy and the time of action taken by topical agents/
pediculocides to act while treating.(8–10) A further and future
use of VD could be measured by studying possible lice resis-
tance to commonly used substances with pediculocidal activity,
Figure 3.23a–b Phthiriasis palpebrarum. A: lice and nits at VD observation (X60). B: VD evaluation after 5 days treatment with
mercurial ointment: persistence of few full nits not visible to naked eye (X60).
(a) (b)
Figure 3.24 VD examination of an adult specimen of Pediculus
humanus treated with the application of a topical compound
that acts through a mechanical action of “choking” (X80).

micali,tedeschi,andlacarrubba
in order to contribute to the identification of alternative and
appropriate therapeutic options.
REFERENCES
1. Argenziano G, Fabbrocini G, Delfino M. Epiluminescence
microscopy. A new approach to in vivo detection of Sar-
coptes scabiei. Arch Dermatol 1997; 133: 751–3.
2. Micali G, Lacarrubba F, Lo Guzzo G. Scraping versus vid-
eodermatoscopy for the diagnosis of scabies: a compara-
tive study. Acta Derm Venereol 2000; 79: 396.
3. Lacarrubba F, Musumeci ML, Caltabiano R et al. High-
magnification videodermatoscopy: a new noninvasive diag-
nostic tool for scabies in children. Pediatr Dermatol 2001;
18: 439–41.
4. Haas N, Sterry W. The use of ELM to monitor the success of
antiscabietic treatment. Arch Dermatol 2001; 137: 1656–7.
5. Micali G, Lacarrubba F, Tedeschi A. Videodermatos-
copy enhances the ability to monitor efficacy of scabies
treatment and allows optimal timing of drug application.
J Eur Acad Dermatol 2004; 18: 153–4.
6. Hamm H, Beiteke U, Höger PH et al. Treatment of scabies
with 5% permethrin cream: results of a German multi-
center study. J Dtsch Dermatol Ges 2006; 4(5): 407–13.
7. Dodd CS. Interventions for treating headlice. Cochrane
Database Syst Rev 2001; 2: CDOO1165.
8. Di Stefani A, Hofmann-Wellenhof R, Zalaudek I. Der-
moscopy for diagnosis and treatment monitoring of
pediculosis capitis. J Am Acad Dermatol 2006; 54(5):
909–11.
9. Lacarrubba F, Nardone B, Milani M, Botta G, Micali G.
Head lice: ex vivo videodermatoscopy evaluation of the
pediculocidal activity of two different topical products.
G Ital Dermatol Venereol 2006; 141: 233–5.
10. Zalaudek I, Giacomel J, Cabo H et al. Entodermoscopy:
a new tool for diagnosing skin infections and infestations.
Dermatology 2008; 216(1): 14–23.

3.6 Tungiasis
Elvira Moscarella, Renato Bakos, and Giuseppe Argenziano
Tungiasis is an ectoparasitic disease caused by the flea Tunga
penetrans, which is endemic in some parts of South and Central
America, Africa, Asia, and the Caribbean. Data on tungiasis
prevalence are variable and are not always available, especially
for African states. Tungiasis is reported to be very frequent in
Trinidad with prevalence varying from 15.7% to 31.4%.(1, 2) A
surveillance performed in communities of lower socioeconomic
status of northeast Brazil has demonstrated prevalence rates of
up to 54.5% among the residents of such areas.(3) In a recent
study conducted in a rural community in Lagos, the prevalence
was 45.2%.(4) Only one autochthon case has been reported in
Europe (5) where all reports are about imported cases in which
the disease was contracted after traveling in endemic areas.
Tunga penetrans is a sand flea that infests the skin of humans
and can have various animals (pigs, cows, cats, dogs, and rats)
serving as usual reservoirs.(6, 7) The disease is usually acquired
by walking barefoot in humid sand contaminated by the flea.
Therefore, the feet are the preferred site of penetration. The
flea is not able to jump high, even so, ectopic lesions have been
reported in almost all parts of the body and are associated with
high infestation grades and young age.(8)
Both male and female flea may penetrate the skin, but after
copulation, the male dies, whereas the female remains into the
skin completing her vital cycle that lasts about 4 to 6 weeks. The
flea penetrates the skin with the head of the exoskeleton, creating a
cavity that reaches the superficial dermis where it is nourished by
the blood of the dermal vascular plexus. After penetration into the
skin, the female starts producing eggs and enlarging her body from
1 mm to about 1 cm in diameter. Eggs and feces are eliminated
through a small opening in the epidermis and then the flea dies in
the cavity. The natural history of the disease has been divided into
5 phases (9): (1) penetration, (2) hypertrophy, (3) the white halo
phase, (4) inoculation, and (5) rest of the fleas in the host’s cutis.
The diagnosis is essentially clinical in endemic areas. It typi-
cally presents multiple, confluent, roundish papules or nodules
located on the feet. The lesions are white-gray-yellowish in
color and exhibit a small, central, brown opening. Penetration
of the flea is asymptomatic or may be followed by an itching
sensation. Only when the parasite enlarges its diameter an
inflammatory process causes pain to the host (10), sometimes
reported as very intense and debilitating.
In nonendemic areas, the lesion is usually single and can be
easily misdiagnosed and confused with several other diseases
like viral warts, foreign body reaction, fungal and bacterial
infections, tumors, myiasis, and vasculitis.
Early diagnosis and correct therapy are crucial to avoid
frequent complications that may be caused by bacterial super-
infections.(11)
Nowadays, traveling-associated dermatoses are more fre-
quently seen by physicians that may not be very familiar to
them.(12) In this scenario, dermoscopy can facilitate the early
diagnosis of tungiasis, thus leading to the correct treatment that
consists of complete surgical excision of the lesion (Figures 3.25
and 3.26). Mechanical removal, curettage, and cryotherapy may
also be considered.
Histopathologic examination reveals hyperkeratosis and
acanthosis of the epidermis. The flea is located between the
epidermis and the superficial dermis, embedded in a pseudo-
cystic cavity that presents a small opening through which eggs
and feces are expelled. An inflammatory perilesional infiltrate
is also present that is constituted by lymphocytes, neutrophils,
and eosinophils.
Bauer et al. (13, 14) first described the dermoscopic aspects
of tungiasis, identifying the dark spot as a pigmented ring with
a central pore. This corresponds to the pigmented chitin sur-
rounding the posterior opening of the flea exoskeleton. Di
Stefani et al. (15) found a dermoscopic grey-blue blotch, which
they inferred to be related to developing eggs. The direct iden-
tification of eggs by dermoscopy has been described by Cabrera
et al.(16) Reaching the dermis by sequential and careful shav-
ing of the epidermis and gently compressing the edges of the
wound, a jelly-like bag will emerge, which is visible as a bag full
of eggs during dermoscopy. Bakos et al. (17) recently described
a further dermoscopic feature defined as “whitish chains.” They
visualized using dermoscopy the presence of whitish structures
Figure 3.25 On dermoscopy, the lesion appears as a white to light
brown yellowish papule with a central brownish opening. The
opening corresponds to the posterior part of the flea’s exoskele-
ton. Gray-blue blotches, sometimes shaped as a comma, can also
be seen and may represent the intestinal part of the flea (X10).
3
moscarella,bakos,andargenziano
in a chain-like distribution perfectly matching in vivo with the
jelly bag described by Cabrera.
Dermoscopy can also allow a rapid differential diagnosis
(18) with plantar warts and pigmented melanocytic lesions (a
case of Tunga penetrans simulating acral melanoma has been
described)(6). In viral warts, the diagnosis is based on the pres-
ence of a verrucous, yellowish unstructured area exhibiting a
variable number of irregularly distributed, red, brown, or black
dots or linear streaks caused by chronic high vascular pressure
at plantar sites. Pigmented acral melanoma can also be easily
differentiated for the presence of specific dermoscopic features
such as the parallel ridge pattern.
REFERENCES
1. Chadee DD. Distribution patterns of tunga penetrans
within a community in Trinidad, West Indies. Trop Med
Hyg 1994; 97: 167–70.
2. Chadee DD. Tungiasis among five communities in south
western Trinidad, West Indies. Ann Trop Med Parassitol
1998; 92: 107–13.
3. Heukelbach J, Costa AML, Wilckle T, Mencke N, Feldmeier
H. The animal reservoir of tunga penetrans in severely
affected communities of north est Brazil. Med Vet Ento-
mol 2004; 18: 329–35.
4. Ugnomoiko US, Ofoezie IE, Heukelbach J. Tungiasis: high
prevalence, parasite load, and morbidity in a rural com-
munity in Lagos State, Nigeria. Int J Dermatol 2007; 46:
475–81.
5. Veraldi S, Carrera C, Schianchi R. Tungiasis had reached
Europe. Dermatology 2000; 201: 382.
6. Franck S, Feldmeier H, Heukelbach J. Tungiasis: more than
an exotic nuisance. Travel Med Infect Dis 2003; 1: 159–66.
7. Kimpel S, Mehlhorn H, Heukelbach J, Feldmeier H,
Mencke N. Field trial of the efficacy of a combination
of imidacloprid and permetrin against Tunga penetrans
(sand flea, jigger flea) in dogs in Brazil. Parassitol Res
2005; 97: S113–S119.
8. Heukelbach J, Wicke T, Eisele M, feldmeier H. Ectopic local-
ization of tungiasis. Am J Trop Med Hyg 2002; 67: 214–6.
9. Eisele M, Heukelbach J, Van Marck E et al. Investigations
on the biology, epidemiology, pathology and control of
Tunga penetrans in Brazil: I. Natural history of tungiasis
in man. Parasitol Res 2003; 9(2): 87–99.
10. Van Bruskirk C, Burd EM, Lee M. A painful, drainig black lesion
on the right heel. Tungiasis. Clin Infect Dis 2006; 43: 65–6.
11. Feldmeier H, Heukelbach J, Eisele M et al. Bacterial super-
infection in human tungiasis. Trop Med Int Health 2002;
7: 559–64.
12. Caumes E, Carriere J, Guermonprez G et al. Dermatosis
associated with travel to tropical countries: a prospective
study of the diagnosis and manaagment of 269 patients
presenting to a tropical disease unit. Clin Infect Dis 1995;
20: 542–8.
13. Bauer J, Forschner A, Garbe C, Rocken M. Dermoscopy of
tungiasis. Arch Dermatol 2004; 140 (6): 761–3.
14. Bauer J, Forschner A, Garbe C, Rocken M. Variability of
dermoscopic features of tungiasis. Arch Dermatol 2005;
141 (5): 643–4.
15. Di Stefani A, Rudolph CM, Hofmann-Wellwnohf R,
Mullegger RR. An additional dermoscopic feature of tun-
giasis. Arch Dermatol 2005; 141 (8): 1045–6.
16. Cabrera R, Daza F. Tungiasis: eggs seen with dermoscopy.
Br J Dermatol. 2008; 158 (3): 635–6.
17. Bakos RM, Bakos L. “Whitish chains”: a remarkable in
vivo dermoscopic finding of tungiasis. B J Dermatol 2008,
159: 991–2.
18. Zalaudek I, Giacomel J, Cabo H et al. Entodermoscopy: a
new tool for diagnosing skin infections and infestations.
Dermatology 2008; 216 (1): 14–23.
Figure 3.26 Another image of tungiasis seen by dermoscopy,
showing comma-like gray-blue blotches, together with whitish
structures forming a chain-like structure and expelled eggs (X10).
,I
a Hair loss
Antonella Tosti and Bruna Duque Estrada
In the last few years, dermoscopy has been increasingly used
in the evaluation of patients with hair loss. We believe that this
technique is a very important tool, as it not only improves diag-
nostic accuracy of hair and scalp disorders but also provides
clues for better understanding the pathogenesis of some condi-
tions. This diagnostic method has provided new clinical signs
for recognizing hair diseases and enhanced features previously
seen with the naked eye.
For scalp examination, dermatologists may use a manual der-
moscope (x10 magnification) or a videodermoscope equipped with
various lenses (from x20 to x1,000 magnification). Both epilu-
minescent and nonepiluminescent modes are employed, and
alcohol or thermal water can be used as interface solutions.
Dermoscopy findings in hair and scalp disorders include
follicular and interfollicular patterns, as well as hair shaft’s
characteristics (Table 4.1).
Normal Scalp
Examination of the normal scalp shows a diffuse white color
and often simple fine red loops, which represent capillary loops
in the dermal papilla.(1) Follicular units contain 2 to 3 terminal
hairs and 1 or 2 vellus hairs inside (Figure 4.1).
In dark-skinned individuals (phototypes V and VI), a perifol-
licular pigmented network (honeycomb pattern) is well appreci-
ated. The network consists of hyperchromic lines that represent
melanocytes in the rete ridge system in contrast with hypochro-
mic areas formed by fewer melanocytes localized in the supra-
papillary epidermis.(1) Small, white dots regularly distributed
among follicular units are also appreciated (Figure 4.2).
Particles of dirt, dust, loose fibers, and other small particu-
late debris, which we defined as dirty dots, may be appreciated
in children aged between 1 and 12 years (Figure 4.3 and 4.4).
These particles are most prominent in the vertex scalp and dis-
appear immediately after shampooing, but reappear as soon
as 24 hours after shampooing. Dirty dots disappear at puberty
when sebaceous excretion possibly prevents deposition of envi-
ronmental particles on the scalp.(2)
Table 1 Videodermoscopic Patterns Seen in Normal and Patho-
logical Scalp.
Interfollicular patterns:
Vascular patterns
Simple red loops
Twisted red loops
Arborizing red lines
Red dots
Pigment pattern: honeycomb pigmented network
Blue-grey dots
Brown halo (peripilar sign)
White dots
Dirty dots
Follicular patterns:
Yellow dots
Keratotic plugs
Black dots (cadaverized hairs)
Figure 4.1 Normal scalp of a Caucasian patient. Note the dif-
fuse white color of the scalp and the follicular units containing
1 to 3 terminal hairs (x20).
Figure 4.2 Scalp dermoscopy of a dark-skinned patient. Note the
honeycomb pigmented network around the follicular units (x20).
,:
1os1i \xn vs1v\n\
aNdrogeNetic alopecia
Androgenetic alopecia (AGA) is the most common form of hair
loss, affecting up to 80% of men and 50% of women. Patients
typically present with progressive thinning and shortening of
hair in androgen-dependent scalp regions including frontal,
temporal, and vertex areas.
Dermoscopic Features
Hair Diameter Diversity
In general, scalp examination in AGA should be taken in an
area delineated at the cross between nose line and ear implan-
tation line.
The progressive miniaturization of hair with visualization
of hairs with different calibers are enhanced by dermoscopic
examination.(3) A hair diameter diversity of >20% is diagnos-
tic of androgenetic alopecia and is significantly correlated to
follicle miniaturization by histological analysis (Figure 4.5).
(4) Using this parameter, Lacharrière proposed a severity scale
based on dermoscopic findings as diameter-diversity and hair-
density scores.(4)
Videodermoscopy allows measurement and monitoring of hair
shaft thickness in androgenetic alopecia, and thus may also help
in calculating the terminal to vellus hair ratio.(3, 5) Under higher
magnifications on videodermoscopy, it is possible to identify and
count vellus hairs (with less than 0.03 mm in width).(4, 5)
It is worthwhile to note that follicular ostia in AGA show pre-
dominance of single hairs, instead of 2 to 4 hair shafts observed
in normal subjects (Figure 4.6).(5)
Figure 4.3 Particles of dust, powder and debris can be seen as
dirty dots in scalp dermoscopy of this Caucasian patient (x20).
Figure 4.4 Small dirty dots are observed in scalp dermoscopy
of this African-American child (x20).
Figure 4.5 A variability in the hair shaft diameter of more than
20% of hair shafts is diagnostic of androgenetic alopecia (x20).
Figure 4.6 A variability of the hair shaft diameter is well observed, as
well as many follicular units compound of single hair shafts (x20).
,,
u\iv ioss
Empty follicular ostia are often seen. They are expression of
the kenogen phase of the hair cycle, which corresponds to the
interval between extrusion of the telogen hair and emergence
of a new anagen hair. Kenogen frequency and duration are
greater in men and women with androgenetic alopecia than in
controls and an increased number of kenogen follicles has been
associated with the progression of female AGA.(6)
In women with longstanding AGA, dermoscopy often shows
small areas of follicular loss (focal atrichia) (Figure 4.7 and 4.8).
Peripilar signs
The presence of a brown halo at the follicular ostium is mostly
found in patients with high hair density and this finding have been
related to superficial perifollicular lymphocytic infiltrates in early
androgenetic alopecia of male and females (Figure 4.5).(7)
Secondary Signs
In patients with advanced androgenetic alopecia, yellow dots
can be observed.(1) These dots represent distention of the
affected follicular infundibulum with keratinous material and
sebum. Thinning of the hair shafts leads to decrease on sebum
drainage and thus to distention of the infundibular portion of
the hair follicle.
A honeycomb-like pigmented network is found in scalp
areas that are sun exposed with progression of baldness. This
pigmentation is well appreciated when comparing parietal scalp
affected with AGA, and unaffected occipital scalp of patients
with phototypes I to IV.
alopecia areata
Alopecia areata is an autoimmune, nonscarring form of alo-
pecia. A wide range of clinical presentations can occur, from
single patch of alopecia to complete loss of scalp hair (alopecia
totalis) or the entire body (alopecia universalis). The disease
affects most commonly scalp hairs, but it may also involve eye-
brows, eyelashes, beard, pubic, axilary, and all body hairs.
Dermoscopic Features
Yellow Dots
The presence of yellow dots is a characteristic finding in alo-
pecia areata. This pattern is characterized by a distinctive array
of yellow to yellow-red, round, and polycyclic dots that vary
in size and correspond to the dilated follicular openings with
or without hairs shafts (Figure 4.9).(1, 8, 9) The dots are best
visualized under epiluminescent dermoscopy, although the
nonepiluminescent mode provides a better view of their pro-
tuberant and greasy aspect. Degreasing the affected area with
acetone results in diminished dot sizes.(1) Dry dermoscopy
(dermoscopy without immersion gel) has also been reported as
a useful technique in diagnosis and follow-up of patients with
alopecia areata. With this method, one can see more clearly a
Figure 4.7 Patient presenting long lasting AGA with diffuse
pattern.
Figure 4.8 Dermoscopy of the patient with long lasting AGA
demonstrates focal atrichia with absence of follicular ostia (x40).
Figure 4.9 Yellow-red, round, and polycyclic dots correspond
to the dilated follicular ostia without hairs shafts (x20).
,a
1os1i \xn vs1v\n\
keratotic plaque with multiple depressed follicular ostia.(10) It
has been suggested that this depressed pattern may correspond
to abnormal hair follicles containing incompletely differenti-
ated hair shafts, the so called nanogen hairs, which cannot be
morphologically categorized as anagen, catagen, or telogen
hairs.(10)
The frequency of observation of yellow dots in Asian patients
has been shown to be lower than that reported in Caucasians.
(1, 9) We have also observed a lower incidence of yellow dots in
patients with phototypes V and VI, possibly because the yellow-
ish color of Asian patients and the presence of the pigmented
network in black patients makes it more difficult to perceive the
yellow dots (Figure 4.10).
Figure 4.10 An African-American patient with alopecia areata in
which the yellow dots are difficult to visualize. Vellus hairs and
short broken hairs are also observed inside the plaque (x20).
Figure 4.13 Exclamation mark hairs are characterized by a dis-
tal and wide tip in comparison with the proximal portion of
the shaft (x20).
Figure 4.11 Cadaverized hairs, as black dots, short broken
hairs, and exclamation mark hairs are observed inside an active
plaque of alopecia areata (x20).
Figure 4.12 Black dots are observed inside the yellow dots and rep-
resent cadaverized hairs that are broken before scalp emergence
(x70).
Dystrophic Hairs
Dystrophic hair shafts are well appreciated by dermoscopy even at
lower magnification (X 20). In active alopecia areata, the anagen
arrest causes hair shafts to fracture before their emergence from
the scalp: these cadaverized hairs appear as black dots at der-
moscopy (Figures 4.11 and 4.12).(1, 5, 9) Growing of the broken
shafts leads to formation of exclamation mark hairs, which are
characterized by a distal, irregular, fractured tip that is wider than
the proximal portion of the shaft (Figure 4.13). Monilethrix-like
changes are observed due to variation in the caliber of the hair
shaft as the result of intermittent inflammatory process affecting
the hair bulb (Figure 4.14). A variable degree of hair shaft hypop-
igmentation is sometimes the unique mark of alopecia areata.
,-
u\iv ioss
Short regrowing, miniaturized, and vellus hairs (shorter
than 10 mm) are also a common feature observed in both acute
and chronic alopecia areata. These hairs represent miniaturized
nanogen hairs that are not able to prolong their anagen phase
and undergo continuous recycling (Figure 4.15).(11)
Recently, statistical analysis made by Inui et al. demonstrated
that for diagnosis of alopecia areata, yellow dots and short vel-
lus hairs were the most sensitive markers. Black dots, excla-
mation-mark hairs, and broken hairs were the most specific
markers. The presence of black dots, exclamation-mark hairs,
and vellus hairs indicate disease activity. Black dots, yellow dots,
and clustered short vellus hairs correlated with the severity of
disease.(9)
Figure 4.14 The variation in the caliber of the hair shaft, as the
result of intermittent inflammatory process affecting the hair
bulb, composes the monilethrix-like hair shaft (x20).
Figure 4.15 Short vellus hairs, with less than 10mm length,
inside a plaque of alopecia areata are found in both acute and
chronic diseases (x20).
Figure 4.16 Alopecia areata incognita. A female patient with
acute and severe thinning of the hair. Clinical aspect is difficult to
differentiate from androgenetic alopecia and telogen effluvium.
alopecia areata iNcogNita
Alopecia areata incognita was first described by Rebora in
1987; it is characterized by acute onset of diffuse shedding
of telogen hairs in the absence of typical patches (Figure
4.16).(12) Patients often concern about severe thinning in
a few months. Differential diagnosis with androgenetic alo-
pecia and telogen effluvium is often difficult, and dermos-
copy has proved to be an important tool in this challenging
diagnosis.
Dermoscopic Features
Yellow Dots
Using the epiluminescent mode, scalp demonstrates diffuse,
round, and polycyclic yellow dots, with varied size and uniform
distribution. The dots are evident within the follicular ostium
with and without hair shafts and affects about 70% of the
follicles (Figure 4.17).(13)
Scalp biopsies show that the yellow dots correspond to
dilated infundibula filed with cornified cells and sebaceous
material.
Short regrowing hairs
Short, miniaturized, and tapered hairs (2–4 mm long) are a
characteristic dermoscopic feature of alopecia areata incognita.
The association of yellow dots with a large number of short
regrowing hairs is very suggestive of alopecia areata incognita
,o
1os1i \xn vs1v\n\
(Figure 4.17). Inui et al. reported the usefulness of dry dermos-
copy (dermoscopy without immersion gel) in detecting tiny
hairs in a patient with diffuse alopecia in which differential
diagnosis with androgenetic alopecia and telogen effluvium is
often difficult.(10)
Histopathology reveals high percentages of telogen hairs
and/or miniaturized hairs. The typical peribulbar lympho-
cytic infiltrate may not be present. The pathological diagnosis
is suggested by the presence of a subtle lymphocytic infiltrate
around miniaturized follicles in the papillary dermis that cor-
relates with the short regrowing hairs observed on dermos-
copy.(13)
Dystrophic Hairs
Exclamation mark hairs and cadaverized hairs are not common
in our experience (Figure 4.18).(13)
tricHotilomaNia
Trichotilomania is a compulsive disorder in which individuals
pull out hair, from scalp or any other body area, resulting in
alopecic patches. It is relatively more common in children.
On physical exam, irregular patches of hair loss, with typical
bizarre borders are observed. Inside the plaques, short broken
hairs with variable lengths are evident.
Dermoscopy is useful to diagnose the disease and to show
patients the signs of plucking who do not admit their habit of
pulling out hairs.
Figure 4.18 Alopecia areata incognita. Note the absence of the
typical plaque and the presence of dystrophic and short broken
hairs in a diffuse distribution (x20).
Figure 4.19 Trichotilomania. Broken hair shafts at different
lengths are frequent findings. Despite its similarity with alope-
cia areata, exclamation mark hairs are not observed in tricho-
tilomania (x40).
Figure 4.20 An African-American patient with the characteris-
tic longitudinal splitting of the shafts in trichotilomania (x30).
Figure 4.17 Alopecia areata incognita. Yellow dots are observed
within the follicular ostium of both empty and hair-bearing
follicles. Short regrowing hairs are also a characteristic feature
of this subtype of alopecia areata (x40).
,,
u\iv ioss
Dermoscopic findings
Short coiled hairs are distributed along the alopecic area with
broken hair shafts with different lengths. These findings are
considered evidence of plucking at different times. Longitudinal
splitting of the hair shafts are also well appreciated in many
cases (Figure 4.19 and 4.20).
coNgeNital triaNgular alopecia
Congenital triangular alopecia usually presents in children in
the age between 3 and 6 years as a triangular or oval patch
of alopecia most frequently localized in the frontotemporal
hairline. Other scalp regions may occasionally be affected.
The triangular or lance-shaped alopecic area contains vellus
hairs and has a typical stable course. The condition may be
bilateral.
Dermoscopy is helpful in the diagnosis when the triangu-
lar alopecia has an atypical location.(14) Dermoscopy of the
patch shows normal follicular openings and numerous vellus
hairs surrounded by normal terminal hairs in the adjacent scalp
(Figure 4.21).
ScarriNg alopecia
Cicatricial alopecias include a group of hair disorders that cause
permanent destruction of the hair follicles. Cicatricial alopecias
are the most challenging hair diseases for differential diagnosis
and treatment.
Causes of cicatricial alopecias are categorized as primary or
secondary. Primary cicatricial alopecias specifically target the
hair follicle and results in its destruction. In secondary scar-
ring, alopecias the hair follicle destruction is secondary to dif-
fuse scarring of the dermis.(15)
Differential diagnosis of cicatricial alopecias requires a scalp
biopsy. Dermoscopy has shown to be useful to find appropriate
sites to take biopsies, as well as to provide new information
about the diseases.
Dermoscopic Features
In all types of cicatricial alopecias, scalp examination reveals a
variable degree of absence of follicular ostia. This feature is more
appreciated in patients with dark skin (phototypes V and VI) and
patients with long-standing alopecia, which develops the pig-
mented network secondary to sun exposure in the affected area.
licHeN plaNopilariS
Lichen planopilaris (LPP) is the most common cause of cicatri-
cial alopecia and most frequently middle-aged women. Patients
present with scalp itching and tenderness. Scalp examination
shows irregular patches of hair loss, which become conflu-
ent, affecting most frequently the pariental and vertex regions.
The disease has a progressive course and severe alopecia may
develop in some patients.
Dermoscopic Features
Dermoscopy reveals absence of follicular openings and the
presence of characteristic perifollicular scales (peripilar casts)
at the periphery of the patch. As scaling becomes more promi-
nent, follicular plugging may be observed (Figure 4.22).
Perifollicular erythema characterized by the presence of
arborizing vessels around the follicular ostia is also observed
(Figure 4.23).
The pigmented network is still well appreciated inside the
LPP plaques of dark-skinned individuals. As interfollicular epi-
dermis is commonly unaffected by the inflammatory process
in LPP, we believe that this sign may help in differentiating this
type of alopecia from other scarring alopecias, such as discoid
lupus erythematosus of the scalp (Figure 4.24).
Figure 4.21 Congenital Triagular alopecia. Dermoscopy shows
many vellus hairs and normal follicular ostia. Terminal hairs of
the normal scalp are well appreciated around the plaque (x20).
Figure 4.22 Lichen Planopilaris. Dermoscopy shows the typical
perifollicular casts and areas with absence of follicular open-
ings (x20).
,8
1os1i \xn vs1v\n\
In frontal fibrosing alopecia, a clinical variant of lichen
planopilaris, the most prominent dermoscopic findings are loss
of follicular openings, peripilar scale, and peripilar erythema
(Figure 4.28).
diScoid lupuS erytHematoSuS
Discoid lupus erythematosus (DLE) of the scalp is character-
ized by single or multiple alopecic patches. Affected scalp shows
erythema, scaling, follicular plugging, atrophy, and telangiecta-
sias. Despite the fact that it is considered as part of the group of
cicatricial alopecias, DLE often shows hair regrowth if promptly
treated. In this way, early diagnosis is important for patients’
prognosis.
Figure 4.24 Dermoscopy of a dark-skinned patient with LPP. The
pigmented network and the white dots regularly distributed among
are much more appreciated inside the alopecic plaque (x20).
Figure 4.25 Liche planopilaris in an African-American patient.
The regular distribution of the white dots is well appreciated,
especially in comparison to the round and wider white holes
that represent the follicular ostia (x10).
Figure 4.26 Blue-grey dots are appreciated in LPP, representing
pigmentar incontinence inside the lesion (x20).
Figure 4.23 Lichen Planopilaris. Arborizing vessels are respon-
sible for the perifollicular erythema observed in these patients.
The absence of follicular ostia is also evident (x20).
Kossard observed white pale dots in a dark-skinned patient
(Figure 4.25).(16)
Blue-grey dots may be found in some patients, especially those
with dark skin (Figure 4.26). A peculiar pattern of round perifol-
licular blue-grey dots—“target pattern”—may be observed in
some dark patients with LPP (Figure 4.27). Histopathologically,
these dots are caused by loose melanin, fine melanin particles,
or melanin “dust” in melanophages or free-floating in the deep
papillary or reticular dermis. The target pattern is associated with
the presence of melophages predominantly around hair follicles,
sparing interfollicular epidermis.
Usually, LPP spares some terminal hair follicles inside the
alopecic patches.
,o
u\iv ioss
Dermoscopic features
Scalp atrophy is represented by a diffuse white color of the scalp
(Figure 4.29). This pattern is well appreciated in dark-skinned
patients, who loose the normally seen pigmented network
within the lesion. Indeed, the honeycomb pigmented network
might be seen at the periphery of the plaque of DLE.
Arborizing and tortuous vessels are the most common vas-
cular patterns seen inside DLE plaques (Figure 4.29). Some
patients also present peculiar red to pink-red, round, and poly-
cyclic dots that are uniform in size and regularly distributed
around follicular openings (Figure 4.30).
Hyperkeratotic follicular pluggings are observed in the
follicles around the patches.
Blue-grey dots may be observed, with a diffuse and speckled
pattern of distribution along the patch (Figures 4.29 and 4.31).
These dots represent pigmentar incontinence in the papillary
dermis of follicular and interfollicular epidermis. We believe
that the different patterns of blue-grey dots described may be a
novel and interesting feature to help dermoscopic differentia-
tion between DLE and LPP.(17)
FolliculitiS decalvaNS
Folliculitis decalvans (FD) is a neutrophilic variant of cica-
tricial alopecias, which accounts for approximately 11% of
all primary cicatricial alopecias.(18) FD usually starts with
follicular papules and pustules on the vertex and/or occipital
area of the scalp, followed by intense inflammatory reaction
and development of an indurated and boggy scarring patch.
Multiple hair tufts are often found emerging from a common,
Figure 4.27 Dark-skinned patient with LPP in which the
blue-grey dots formed a peculiar “target-pattern” around the
follicular units (x10).
Figure 4.29 In discoid lupus erythematosus of the scalp, a white
plaque is well appreciated in the active border, associated with
tortuous vessels, pigmentary (x40).
Figure 4.30 Polycyclic red dots distributed around follicular
openings are observed inside a DLE lesion of the scalp together
with arborizing vessels (x20).
Figure 4.28 Frontal fibrosing alopecia. Dermoscopic features
are the same observed in classic LPP, as perifollicular scale and
erythema (x10).
ao
1os1i \xn vs1v\n\
dilated, follicular opening. Purulent discharge can be observed
if pressure is applied to the perifollicular area. S. aureus can be
isolated from FD lesions and seems to play an important role
in the inflammatory process.
Dermoscopic Findings
Marked diffuse scalp erythema and absence of follicular units
are characteristic of FD (Figure 4.32). Dermoscopy also shows
severe scaling and crusting, which can be prominent around
follicular units.
Pustular lesions are also evident.
The intense inflammatory process is best seen in x50 or higher mag-
nification. Multiple-coiled, dilated capillary loops, similar to those
observed in psoriasis, and arborizing red lines are typical findings
seen all over the affected scalp (Figures 4.33, 4.34, 4.35).(1)
Tufted folliculitis, with several hair shafts emerging from the
scalp, is often seen in advanced cases (Figure 4.36).
dermoScopy iN tHe diFFereNtial diagNoSiS
oF alopecia oF tHe Scalp margiN
In patients who present with alopecia of the scalp margin, der-
moscopy can be very useful, as the differential diagnosis between
traction, alopecia areata, or frontal fibrosing alopecia extending
to the temporal regions may be difficult. A new entity described
as cicatricial, marginal alopecia (19) should also be considered
in the differential diagnosis.
Dermoscopic Features
Alopecia areata affecting the scalp margin include ophiasis and
sisaipho subtypes. The most relevant dermoscopic findings, as
Figure 4.32 Absence of follicular units, diffuse erythema and
arborizing vessels in a patient with FD (x40).
Figure 4.34 Pustular lesion inside a plaque of FD (x20).
Figure 4.33 Neovascularization is a typical feature of FD, which
is observed as multiple coiled capillary loops and arborzing red
lines in the scalp (x20).
Figure 4.31 Pigmentar incontinence represented by blue-grey
dots in a speckled pattern inside the DLE plaque (x20).
aI
u\iv ioss
Figure 4.35 Tufted folliculitis is frequently observed in chronic
FD. It is characterized by the emergency of many hair shafts
from the same ostium (x40).
Figure 4.36 A female patient with alopecia in the scalp margin
due to alopecia areata – sisaipho subtype.
Figure 4.38 Recession of the frontotemporal hairline and alope-
cia of the eyebrows in a patient with frontal fibrosing alopecia.
Figure 4.37 Dermoscopy of the previous patient shows the
characteristic features of AA: yellow dots, dystrophic hairs and
vellus hairs (x20).
hairs, as well as white dots. Sometimes, fractured hair shafts are
seen as a sign of severe traction (Figures 4.40 and 4.41).
A distinctive pattern of alopecia has been recently described
by Goldberg as cicatricial marginal alopecia.(19) Around
40% of them had no history of traction hair styling.

Patients
discussed previously, are yellow dots, dystrophic hairs, and vel-
lus hairs (Figure 4.36 and 4.37).(1, 3, 5, 8, 9)
Frontal fibrosing alopecia, a variant of lichen planopilaris, is
characterized by frontotemporal hair recession, eyebrow loss,
and histopathology identical to lichen planopilaris (Figure
4.38). Dermoscopy shows absence of follicular openings, peri-
follicular scale, and a variable degree of perifollicular erythema
(Figure 4.28).(20)
The periphery of the scalp is the site of predilection of trac-
tion alopecia. Usually the disease affects the frontal, tempo-
ral, and vertex scalp (Figure 4.39). Patients present history of
hairdressing associated with traction of hair scalp for many
years, which include use of elastic bands, plaits, or extensions.
Dermoscopy of alopecic patches highlights several miniaturized
a:
1os1i \xn vs1v\n\
Figure 4.40 Dermoscopy of traction alopecia demonstrates
miniaturized hairs inside the patch, and also the pigmented
network and white dots seen in dark-skinned patients (x20).
Figure 4.41 Traction alopecia. A black dot represents a fracture
of the shaft due to severe traction (x20).
Figure 4.42 Cicatricial marginal alopecia. A Caucasian patient
presenting hair loss in the marginal scalp – occipital margin.
Figure 4.39 Traction alopecia of the frontotemporal hairline in
an African-American patient with some remaining vellus hairs
in the frontal portion of the alopecic area.
present hair loss limited to the periphery of the scalp, includ-
ing frontal, temporal, and occipital margins. Dermoscopy
demonstrated low hair density and loss of follicular ostia
in all cases. Remaining hairs show reduced diameter of the
shafts. Perifollicular hyperkeratosis, abnormal scalp ves-
sels, or signs of traction alopecia are not observed (Figures
4.42–4.45).
As described by Goldberg (19), histological features dem-
onstrate a reduced number of hair follicles with the absence
of terminal anagen hairs, few vellus hair follicles, and normal
and intact sebaceous glands. Inflammatory infiltrates are typi-
cally absent. Replacement of hair follicles by columns of fibrous
tissue (fibrous tracts) are appreciated at the hypodermis.
a,
u\iv ioss
Figure 4.43 Dermoscopy of cicatricial marginal alopecia dem-
onstrates loss of follicular ostia and reduced number of shafts
per follicular units (x40).
Figure 4.45 Cicatricial marginal alopecia. Dermoscopy also
shows perifollicular erythema as arborizing vessels (x20).
Figure 4.44 Cicatricial marginal alopecia. The hair loss in the
frontotemporal region resembles frontal fibrosing alopecia.
very helpful to evaluate response to treatment. Comparison of
dermoscopic photographs can be made by marking the scalp
areas that are analyzed during treatment. When possible, a small
nevus can be chosen as reference in order to avoid tattooing.
In androgenetic alopecia, measurement of hair shaft diameter
and evaluating the hair diameter diversity allows a significant com-
parison. In diseases that present dermoscopic signs of active lesions,
such as alopecia areata and discoid lupus of the scalp, response to
treatment can be better assessed by using videodermoscope.
The phototricogram is a noninvasive technique that allows the
in vivo study of the physiology of the hair cycle and the quantifica-
tion of the amount of the effluvium. Thanks to the advent of the
computer-assisted image analysis, today the technique has been
improved. This method permits an accurate distinction between
anagen and telogen hairs and avoids the technical problem of clas-
sic trichogram.(21) It also evaluates total hair density, an important
index of the degree of the effluvium. The most important advantage
of phototrichogram is that it is possible to repeat the examination
on the same area of the scalp on a monthly basis, in order that each
hair strand can be identified and followed across the various phases
of the hair cycle. In this way, a virtual map of the anagen and telogen
hairs of the scalp can de drawn. This allows the study of the hair
cycle and the changes linked to therapies and aging. With the classic
trichogram, however, these studies are not possible.
reFereNceS
1. Ross EK, Vincenzi C, Tosti A. Videodermoscopy in the
evaluation of hair and scalp disorders. J Am Acad Derma-
tol 2006; 55: 799–806.
2. Fu J, Starace M, Tosti. A dirty dots: a new dermoscopic
finding in healthy children. Arch Dermatol 2009; 145:
596–7.
tHerapeutic moNitoriNg oF Hair loSS witH
videodermatoScopy
The combination of special software programs and videoder-
moscope has offered new tools for monitoring treatment of
hair and scalp disorders. Macrophotographs of the scalp are
aa
1os1i \xn vs1v\n\
3. Lacarrubba F, Dall’Oglio F, Nasca MR, Micali G.
Videodermatoscopy enhances diagnostic capability in
some forms of hair loss. Am J Clin Dermatol 2004; 5:
205–8.
4. de Lacharrière O, Deloche C, Misciali C et al. Hair diam-
eter diversity: a clinical sign reflecting the follicle minia-
turization. Arch Dermatol 2001; 137: 641–6.
5. Rudnika L, Olzewska M, Rakowska A et al. Trichoscopy: a
new method for diagnosis of hair loss. J Drugs Dermatol
2008; 7(7): 651–4.
6. Guarrera M, Rebora A. Kenogen in female androgenetic
alopecia. A longitudinal study. Dermatol 2005; 210(1):
18–20.
7. Deloche C, de Lacharriere O, Misciali C et al. Histologi-
cal features of peripilar signs associated with androgenic
alopecia. Arch Dermatol Res 2004; 295: 422–8.
8. Ben Hassines M, Crickx B, Descamps V. Vidéomicroscopie
au cours de la pelade. Ann Dermatol Vemerol 2007; 34:
35–8.
9. Inui S, Nakajima T, Nakagawa K et al. Clinical significance
of dermoscopy in alopecia areata: analysis of 300 cases. Int
J Dermatol 2008; 47: 688–93.
10. Inui S, Nakajima T, Itami S. Dry dermoscopy in clini-
cal treatment of alopecia areata. J Dermatol 2007; 34:
635–9.
11. Whiting DA. Histopathologic features of alopecia areata.
Arch Dermatol 2003; 139: 1555–9.
12. Rebora A. Alopecia areata incognita: a hypothesis. Derma-
tologica 1897; 174: 214–8.
13. Tosti A, Whiting D, Iorizzo M. The role of scalp dermos-
copy in the diagnosis of alopecia areata incognita. J Am
Acad Dermatol 2008; 59: 64–7.
14. Iorizzo M, Pazzaglia M, Starace M et al. Videodermoscopy:
a useful tool for diagnosing congenital triangular alopecia.
Pediatr Dermatol 2008; 25(6): 652–4.
15. McElwee KJ. Etiology of cicatricial alopecias: a basic sci-
ence point of view. Dermatol Ther 2008; 21: 212–20.
16. Kossard S, Zagarella S. Spotted cicatricial alopecia in dark
skin. A dermoscopic clue to fibrous tracts. Australas J Der-
matol 1993; 34(2): 49–51.
17. Duque-Estrada B, Tamler C, Pereira FBC, Barcaui CB,
Sodré CT. Dermoscopic patterns of cicatricial alopecia
due to Discoid Lupus Erythematosus and Lichen Plano-
pilaris. An Bras Dermatol. In press.
18. Otberg N, Kang H, Alzolibani AA et al. Folliculitis decal-
vans. Dermatol Ther 2008; 21: 238–44.
19. Goldberg LJ. Cicatricial marginal alopecia: is it all trac-
tion? Brit J Dermatol 2009 ; 160(1): 62–8.
20. Inui S, Nakajima T, Shono F et al. Dermocscopic findings
in frontal fibrosing alopecia: report of four cases. Int J
Dermatol 2008; 47: 796–9.
21. D’Amico D,Vaccaro M, Guarnieri F et al. Phototricho-
gram using videomicroscopy: a useful technique in the
evaluation of scalp hair. Eur J Dermatol 2001; 11(1): 17–20.

 Nail diseases
Antonella Tosti, Bianca Maria Piraccini, and Débora Cadore de Farias
The application of dermoscopy in the evaluation of nail dis-
orders is still new and the real benefits of this technique in the
diagnosis of nail conditions are not known. In particular, there
are not evidence-based data showing that the use of dermos-
copy may decrease the necessity of nail biopsies.
As dermoscopy is becoming widely accepted and used in the
medical community, there is now the need to standardize the
dermoscopic findings observed in the nails in order to share
information in this field.
The dermoscopic examination can be performed on the
following:
Nail plate
Hyponychium
Distal edge of the nail plate
Proximal nail fold
Nail bed (directly) and matrix (intraoperative dermoscopy)
Nail plate dermoscopy
On the nail plate, gel immersion (ultrasound gel or cosmetic
gel) is required because of the convex shape of the nail. This
gel will fill the gap between the convex nail surface and the
hand-held or videodermoscopy device. An exception would
be the examination of nail plate surface for abnormali-
ties, where it is better to use mineral oil, water, or alcohol
solution.
Examination is usually made with a magnification of 10×
with a hand-held dermoscope, but digital videodermoscopic
systems provide higher magnifications, and therefore, better
information.(1)
Nail plate dermoscopy has been mainly utilized for evalua-
tion of nail pigmentation.
Diagnosis and follow-up of other nail diseases can also pos-
sibly benefit from the use of dermoscopy, as it may detect sub-
clinical nail plate surface abnormalities, visualize progression
of onychomychosis, show abnormalities in the nail bed ves-
sels, and possibly be helpful in the diagnosis of nonpigmented
tumors of the nail.
Dermoscopy of the hyponychium
Examination of the hyponychium can be performed using
mineral oil, gel, water, or alcohol solution. Polarized devices
that do not require the application of immersion fluids can also
be utilized in this area.
The simple architecture of the hyponychium capillary net-
work makes capillary loops in this anatomic area appear as
regular red dots because of their perpendicular arrangement
to the skin (each red dot observed represents the top of one
loop).
Use of dermoscopy in the hyponychium can detect the
following:
1. Micro-Hutchinson’s sign: pigmentation of the periun-
gual tissues that could not be seen with the naked eye.
This may be important for early diagnosis of subungual
melanoma.
2. Vascular abnormality: increase/decrease of the vessel num-
ber, abnormalities in the vessel shape, and distribution.
Dermoscopy of the distal edge of the nail plate
Originally described by Braun et al. in 2006, it is useful to
localize the pigment within the nail plate.(2) This is impor-
tant for understanding the site of melanin production, as pig-
mentation in the ventral nail plate indicates that the lesion is
localized in the distal nail matrix, whereas pigmentation in
the dorsal nail plate indicates that the lesion is localized in
the proximal nail matrix. Distal-edge dermoscopy can then
be used as a preoperative tool to select the anatomical site of
excision.
It is also useful to confirm the clinical diagnosis of
onychomatricoma.
Dermoscopy of the proximal nail fold
Examination of the proximal nail fold can be performed using
mineral oil, gel, water, or alcohol solution. Polarized devices can
also be utilized in this area.
Proximal nail-fold dermoscopy is very important in the
diagnosis and follow-up of connective-tissue disorders. It
can also be useful to evaluate pigmentation of the periungual
tissues.
Intraoperative dermoscopy
It is better to use polarized devices that do not require the
application of immersion fluids; this allows examination with
no direct contact, maintaining aseptic conditions.
The main problem of nail plate dermoscopy in the evalua-
tion of nail pigmentation is that we do not examine the site of
melanin production but just the site of melanin deposition.
Hirata et al. suggested intraoperative, polarized, light der-
moscopic examination of the nail bed and matrix for better
evaluation of pigmented lesions.(3, 4) Intraoperative dermos-
copy visualizes the site of melanin production and can also help
the surgeons to select the surgical margins, as it visualizes even

tosti,piraccini,anddefarias
small pigmented foci. However, this is an invasive procedure
that cannot be used routinely.
PSORIASIS
The clinical and dermoscopic features of nail psoriasis depend
on which parts of the nail apparatus are affected by the disease.
Nail matrix psoriasis produces nail plate surface abnormalities
such as pitting and nail crumbling. Nail bed psoriasis causes
onycholysis, salmon patches, splinter hemorrhages, and nail
bed hyperkeratosis. Dermoscopy can better visualize nail plate
and nail bed abnormalities and detect vascular changes that are
indicative of the disease.
Nail plate dermoscopy
A magnification power of 40X to 70X is utilized to better visu-
alize nail plate and nail bed abnormalities. High magnification
permits to detect subclinical signs that can be very helpful for
a definitive diagnosis of nail psoriasis in doubtful cases.
Dermoscopy Findings: (Figure 5.1)
Pits: irregular in shape and size, present a peripheral •
white border;
Salmon patches: red-to-orange patches of nail bed dis- •
coloration that are irregular in size and shape;
Onycholysis: The area can be homogeneously white or •
present multiple, thin, longitudinal, white striae. Dermo-
scopy often permits to visualize the presence of a “sub-
clinical” erythematous border as a patchy red-to-orange
discoloration of the nail bed surrounding the white ony-
cholytic area. This finding is quite specific for a diagnosis
of nail psoriasis
Splinter hemorrhages: brown, purple-to-black spots •
arranged in a longitudinal fashion. These are due to pin-
point bleeding in the longitudinally arranged nail bed
capillaries and successive incorporation of the blood in
the ventral nail plate. Splinter hemorrhages are not neces-
sarily an indicator of psoriasis, as they commonly occur in
onychomychosis, contact dermatitis, and traumatic nail
disorders as well.
Dilation and tortuosity of the capillary of the distal nail •
bed is also commonly observed in psoriasis.
Hyponychium dermoscopy
In psoriasis, dermoscopic examination of hyponychium
shows dilated, tortuous, and elongated capillaries with an
irregular distribution (Figure 5.2). Capillary density is posi-
tively correlated with disease severity. A magnification power
of 40X is best for visualizing and counting the abnormal
capillaries.(5)
A dermoscopic examination of the hyponychium is in our
experience the best tool for confirming the diagnosis of pso-
riasis in patients with simple onycholysis or mild nail bed
hyperkeratosis.
Proximal nail-fold dermoscopy
Nail-fold dermoscopy is useful to evaluate severity of psoriasis,
as it reflects the degree of microvascular changes.(6)
Nail-fold capillaries present both quantitative and morpho-
logical abnormalities.
Zarik et al. (1982) reported a significantly shorter mean capillary
loop length in psoriasis patients as compared to controls.(7)
Bhushan et al. (2000) showed that the number of capillar-
ies in the nail fold was significantly reduced in psoriasis when
Figure 5.1 Nail plate dermoscopy in psoriasis. Dermoscopy
shows onycholysis characterized by a homogeneously white
area with multiple, thin, longitudinal white striae. Pits irregular
in shape and size are filled by gel and show a peripheral white
border. Also note patchy, orange discoloration of the nail bed,
splinter hemorrhages, and dilaltion and tortuosity of the capil-
laries in the distal nail bed (x20).
Figure 5.2 Hyponychium dermoscopy in psoriasis. Dermoscopy
shows increased capillary density with dilated, tortuous, and
elongated capillaries, with an irregular distribution (x20).

naildiseases
compared to normal controls. Capillaries in psoriasis also
presented a decreased diameter of the arterial limb.(8)
Brittle Nails
Brittle nails are a common complaint characterized by weak fragile
nails that split, flake, and crumble. Nail fragility may be a conse-
quence of factors that alter the nail plate production and/or factors
that damage the already keratinized nail plate. In the latter case,
environmental and occupational conditions that reduce the water
content of the nail plate have an important additional role.
Nail plate dermoscopy
The nail plate presents irregular longitudinal fissures and
grooves that often appear pigmented due to deposition of
exogenous particles. The distal nail margin is often white due
to scaling and exfoliation (Figure 5.3).
Dermoscopy may be used to score severity of fissuring and
exfoliation and evaluate improvement with treatment.
COllAgeN TISSue DISORDeRS
Morphological changes in the nail-fold capillaries confirm
the diagnosis of autoimmune connective tissue diseases, and
severity in the capillary changes is related with systemic disease
activity.
Nail-fold capillaroscopy is, therefore, useful both as a diag-
nostic tool and as a predictor of disease progression.(9)
Magnifications of 30X to 50X are usually utilized.
Nail-fold dermoscopy
In normal conditions, the microvascular pattern is charac-
terized by a regular array of microvessels with large intra- or
inter-individual variability. However, capillary loss and giant
capillaries are not seen in normal pattern.(10)
The scleroderma pattern is characterized by the presence of
giant capillaries and microhemorrhages in early stages and loss
of capillaries with avascular areas in late stages.(10, 11)
The dermatomyositis pattern is often similar to the sclero-
derma pattern. Two or more of the following findings in at least
two nail folds are considered consistent for dermatomyositis:
enlargement of capillary loops, loss of capillaries, disorganiza-
tion of the normal distribution of capillaries, bushy capillaries,
twisted enlarged capillaries, and capillary hemorrhages.(12, 13)
In systemic lupus erythematosus (SLE), capillary density is
normal, but capillaries are tortuous, elongated, and dilated.(14)
ONyCHOmyCHOSIS
Onychomycosis refers to the invasion of the nail plate by
dermatophytes, yeasts, or nondermatophytic moulds.
Different clinical patterns of infection depend on the way
and the extent to which fungi colonize the nail:
- In distal subungual onychomycosis (DSO), the most com-
mon type, fungi reach the nail from the hyponychium and
colonize the nail bed;
- In proximal subungual onychomycosis (PSO), fungi pen-
etrate the nail matrix via the proximal nail fold and colonize
the deep portion of proximal nail plate;
- In white superficial onychomycosis (WSO), fungi are local-
ized on the nail plate surface;
Some fungi can produce melanin and cause longitudinal mel-
anonychia. These include certain moulds: S. dimidiatum, A.
alternata, Wangiella dermatitidis, and Microascus cirrosus (syn.
M.desmosporus), and Trichophyton rubrum var. nigricans.
Nail plate dermoscopy
In distal subungual onychomychosis, dermoscopy is useful to
better delimitate proximal progression of the infection and
detect subclinical streaks (Figure 5.4).
In white superficial onychomychosis, the nail plate pres-
ents irregular, white-to-yellowish patches of different size and
shape. The surface of these areas is opaque with superficial and
peripheral scaling. At high magnification (50X to 70X) it is
possible to detect subclinical spotted lesions.
In onychomycosis due to fungi that produce melanin, der-
moscopy reveals a homogenous, brown-to-black, pigmented
band that is devoid of visible melanin inclusions, and thus
helps to correctly identify hyperchromia of nonmelanocytic
origin.(15)
SubuNguAl HemATHOmA
Subungual hematomas are common nail bed injuries caused
by trauma to the fingers or toes. The affected nail shows a
patchy or diffuse pigmentation that migrates distally with nail
growth.
Hemathoma does not exclude malignancy as patients
with melanoma of the nail unit may experience spontaneous
bleeding.
Figure 5.3 Brittle nails. Nail plate dermoscopy shows irregular
longitudinal fissures and grooves. The pigmentation is due to
deposition of exogenous particles (x20).

tosti,piraccini,anddefarias
Nail plate dermoscopy
Blood deposition appears as a dark band or an irregularly shaped
purple to brown–black area. It is typical to see round, dark-red
spots at the periphery and a “filamentous” distal end (Figure 5.5).
NAIl TumORS
OnichOmatrichOma
Onychomatrichoma is a benign tumor of the nail matrix that
develops within the nail plate. The nail is thickened and presents
an increased lateral overcurvature. The nail plate overlying the
tumor shows a yellow discoloration and multiple splinter hem-
orrhages.(16) This tumor can occur both in fingernails and toe-
nails and has no sex prevalence.(17)
Nail plate dermoscopy
The nail plate shows longitudinal white lines that correspond to
the channels that contain the tumor projections. The proximal
part of the tumor shows purple-to-brown splinter hemorrhages.
Distal edge of the nail plate dermoscopy
Dermoscopy of the distal edge of the nail plate is pathogno-
monic, as would show small woodworm-like cavities within the
nail plate.
OnichOpapillOma
Onychopapilloma is clinically characterized by longitudinal
erythronychia, which, in some patients, is associated with hem-
orrhagic longitudinal lines.(18)
The distal portion of the nail bed presents a keratinized
expansion that often produces a fissure in the distal nail plate.
Nail plate dermoscopy
The nail plate presents a homogeneous, pale red, longitudinal
band extending from the proximal nail fold to the distal edge. The
proximal border of the band has a characteristic convex shape
and its distal part may appear white because of onycholysis.
The band may contain one or more longitudinal, dark
red-to-black streaks that correspond to splinter hemorrhages
(Figure 5.6). The distal nail plate usually presents longitudinal
splitting and a wedge-shaped notch.
Distal edge of the nail plate dermoscopy
Shows the small subungual keratotic mass that often contains
hemorrhagic vessels (Figure 5.7).
pyOgenic granulOma
Pyogenic granuloma is a common, acquired, benign vascular
lesion. It usually presents as a solitary, rapidly growing, papule
that bleeds easily after minor trauma. It occurs more often on
Figure 5.4 Onychomycosis. Nail plate dermoscopy shows the
white–yellow streaks and is useful to establish degree of proxi-
mal progression (x20).
Figure 5.5 Hemathoma. Nail plate dermoscopy shows an irreg-
ular area, purple to brown in color, with round, red spots at the
periphery and a “filamentous” distal end (x20).
Figure 5.6 Onychopapilloma. Nail plate dermoscopy shows a
pale red longitudinal band extending from the proximal nail
fold to the distal edge. The band contains a longitudinal, dark-
brown stria (x20).

naildiseases
the fingers, where it may have a periungual or a subungual loca-
tion. Pyogenic granuloma of the toes may be subungual.
Differential diagnosis of solitary lesions should always take
in account amelanotic melanoma.
The dermoscopic examination of the lesion shows a reddish
homogeneous area that often presents a white collarette at the
periphery. White lines similar to a double rail may intersect
older lesions. Ulceration and hemorrhagic crusts are typically
seen in longstanding lesions.(19)
Warts
Warts are the most common benign tumor of the nail unit and
occur more frequently in children and young adults as well as
in patients who are immunocompromized.(20)
Dermoscopy shows black dots corresponding to vessels
within the keratotic lesion.
glOmus tumOr
Glomus tumor is a rare benign tumor that characteristically
causes severe pain and increases in severity, which tempera-
ture changes and pressure. The lesion may be barely visible
as a red violaceous patch in the nail bed. Other clinical signs
include erythronychia, distal onycholysis, and an increase in the
Lovibond’s angle.(21)
Nail plate dermoscopy
It is useful to detect subclinical lesions that are seen as a reddish
irregular area of variable size that may contain teleangiectasic
vessels (Figure 5.8).
melanOnychia
The term melanonychia describes the presence of melanin
in the nail plate. Most commonly, melanonychia appears as
a longitudinal, brown-to-black band of nail pigmentation,
longitudinal melanonychia (LM). Pigmented lesions in the nail
bed usually do not cause LM and are viewed through the nail as
grayish-brown or black spots.
Nail pigmentation may be caused by melanocytic activation
or by benign or malignant melanocyte hyperplasia. Melanonychia
is the first symptom of nail melanoma in most cases.
melanocyte activation
Causes of nail matrix melanocyte activation include drugs and
postinflammatory, traumatic, systemic, and neoplastic nail dis-
orders. Transverse melanonychia is always due to melanocytic
activation.
melanocyte hyperplasia
Melanocytic hyperplasia is defined as an increase in the num-
ber of nail matrix melanocytes. Benign melanocytic hyperplasia
can be subdivided into lentigo when nests are absent or nevus
when at least one nest is present.
Malignant melanocytic hyperplasia includes in situ and
invasive melanoma of the nail apparatus.
nail matrix nevi
Nevi can be congenital or acquired. The nail presents one or
more longitudinal pigmented bands varying in size from few
millimeters to the whole nail width and light brown to black
in color.
melanoma
Clinical presentation depends on the site of origin, whether
pigmented or not.
Nail matrix melanoma: usually causes a band of longitudinal
melanonychia.(22, 23) The nail plate may present a fissure or
a split corresponding to the band, indicating compression or
destruction of the nail matrix epithelium by the melanoma.
Figure 5.7 Onychopapilloma. Dermoscopy of the distal edge of
the nail plate shows a keratotic nail bed expansion with some
brown tiny spots that correspond to hemorrhages (x20).
Figure 5.8 Glomous tumor. Nail plate dermoscopy of shows an
irregular reddish area with longitudinal filamentous projections
(x20).

tosti,piraccini,anddefarias
Nail bed melanoma: causes a pigmented or a nonpigmented
(25% to 30% of cases) subungual nodule. Nail bed ulceration
and bleeding occur when the tumor grows.
Although nail plate dermoscopy has been proposed as an effec-
tive tool to help the clinician in the differential diagnosis of nail
pigmentation, experience in this field is still very limited and speci-
ficity and sensitivity of the technique have not been validated.(24)
Nail plate dermoscopy
The following dermoscopic patterns have been reported using nail
plate dermoscopy in melanonychia of different etiology.(1, 25–27)
Bands with a grayish background are indicative of melano-
cyte activation. The color of these bands vary from light to dark
gray and the band often contains thin, gray, regular, longitudi-
nal, parallel lines (Figure 5.9).
In traumatic melanocyte activation, tiny dark red-to-brown
spots caused by splinter hemorrhages may also be seen.
Bands with a brown background are indicative of melanocyte
hyperplasia . These bands vary in color from light brown to black.
(A) Bands due to nail matrix nevi usually have sharply delim-
ited lateral borders and contain thin, regular, longitudinal
parallel lines that are brown or black in color. In children,
black DOTS similar to those described in skin melano-
cytic lesions are frequently observed (Figure 5.10).
(B) Bands due to nail matrix melanoma have blurred lateral
margin and contain longitudinal lines of different thickness
and color with disruption of parallelism (Figure 5.11).
Distal edge of the nail plate dermoscopy
With this technique, we can identify whether the lesion is local-
ized in the proximal or in the distal matrix. A pigmentation of
the ventral nail plate originates from the distal matrix and a
pigmentation of the dorsal nail plate originates from proximal
nail matrix.
Hyponychium and proximal nail-fold dermoscopy
Micro-Hutchinson’s sign: periungual pigmentation, not detected
with naked eye, but detected with the dermoscopy. It is an
extension of brown–black pigmentation from the matrix and
nail bed to the surrounding tissues and represents the radial
growth phase of subungual melanoma (Figure 5.12).
The presence of micro-Hutchinson’s sign is very indicative
but not exclusive of melanoma, as congenital nevi often involve
the nail folds and the hyponychium.
Very dark bands are often associated with pigmentation of
the cuticle due to the fact that the dark pigmentation on the nail
plate is visible through the transparent nail fold. This is referred
as pseudo Hutchinson’s sign and is not a sign of malignancy.
Figura 5.9 Drug-induced melanocyte activation. Nail plate
dermoscopy shows a grayish background with thin, gray, regu-
lar, longitudinal, parallel lines (x20).
Figure 5.10 Nevus. Nail plate dermoscopy shows a brown band
with regular, longitudinal, parallel lines (x20).
Figure 5.11 Melanoma. Nail plate dermoscopy shows a dark-
brown band with irregular longitudinal lines. Note irregulari-
ties in thickness, spacing, and color (x20).

naildiseases
Nail bed and matrix dermoscopy
Intraoperative dermoscopy permits direct visualization of the
melanocytic lesion. In melanocyte activation, intraoperative der-
moscopy reveals gray lines. In melanocyte hyperplasia, it shows
brown lines that are regular and associated with globules in nevi
but irregular in melanoma (Hirata unpublished).
reFereNCes
1. Thomas L, Dalle S. Dermoscopy provides useful informa-
tion for the management of melanonychia striata. Derma-
tol Ther 2007; 20: 3–10.
2. Braun RP, Baran R, Saurat JH, Thomas L. Surgical Pearl:
dermoscopy of the free edge of the nail to determine the
level of nail plate pigmentation and the location of its
probable origin in the proximal or distal nail matrix. J Am
Acad Dermatol 2006; 55: 512–3.
3. Hirata SH, Yamada S, Almeida FA et al. Dermoscopy of the
nail bed and matrix to assess melanonychia striata. J Am
Acad Dermatol 2005; 53: 884–6.
4. Hirata SH, Yamada S, Almeida FA et al. Dermoscopic
examination of the nail bed and matrix. Int J Dermatol
2006; 45: 28–30.
5. Iorizzo M, Dahdah M, Vincenti C, Tosti A. Videodermos-
copy of the hyponychium in nail bed psoriasis. J Am Acad
Dermatol 2008; 58: 714–5.
6. Ohtsuka T, Yamakage A, Miyachi Y. Statistical definition
of nailfold capillary pattern in patients with psoriasis. Int
J Dermatol 1994; 33: 779–82.
7. Zaric D, Clemmensen OJ, Worm AM, Stahl D. Capillary
microscopy of the nail fold in patients with psoriasis and
psoriatic arthritis. Dermatologica 1982; 164: 10–4.
8. Bhushan M, Moore T, Herrick AL, Griffiths CEM. Nailfold
video capillaroscopy in psoriasis. Br J Dermatol 2000; 142:
1171–6.
9. Blockmans D, Beyens G, Verhaeghe R. Predictive value of
nailfold capillaroscopy in the diagnosis of connective tis-
sue diseases. Clin Rheumatol 1996; 15: 148–53.
10. Cutolo M, Sulli A, Secchi ME, Paolino S, Pizzorni C. Nail-
fold capillaroscopy is useful for the diagnosis and follow-
up of autoimmune rheumatic diseases. A future tool for
the analysis of microvascular heart involvement? Rheu-
matology 2006; 45: 43–6.
11. Cutolo M, Matucci Cerinic M. Nailfold capillaroscopy
and classification criteria for systemic sclerosis. Clin Exp
Rheumatol 2007; 25: 663–5.
12. Bergman R, Sharony L, Schapira D et al. The handheld
dermatoscope as a nail-fold capillaroscopic instrument.
Arch Dermatol 2003; 139: 1027–30.
13. Klyscz T, Bogenschutz O, Junger M, Rassner G. Microan-
giopathic changes and functional disorders of nail fold cap-
illaries in dermatomyositis. Hautarzt 1996; 47: 289–93.
14. Keberle M, Tony HP, Jahns R et al. Assessment of micro-
vascular changes in Raynaud’s phenomenon and con-
nective tissue disease using colour Doppler ultrasound.
Rheumatology 2000; 39:1206–13.
15. Braun RP, Baran R, Le Gal FA et al. Diagnosis and manage-
ment of nail pigmentations. J Am Acad Dermatol 2007;
56: 835–47.
16. Faylor J, Baran R, Perrin CH et al. Onychomatricoma with
misleading features. Acta Dermatol Venereol 2000; 80: 370–2.
17. Piraccini BM, Antonucci A, Rech G et al. Onychomatri-
coma: first description in a Child. Pediatr Dermatol 2007;
24: 46–8.
18. Baran R, Perrin C. Longitudinal erythronychia with distal
subungual keratosis: onychopapilloma of the nail bed and
Bowen’s disease. Br J Dermatol 2000; 143: 132–5.
19. Zaballos P, Llambrich A, Cuellar F, Puig S, Malvehy J. Dermoscopy
of pyogenic granuloma. Br J Dermatol 2006; 154: 1108–11.
20. Tosti A, Piraccini BM. Warts of the nail unit: surgical and
nonsurgical approaches. Dermatol Surg 2001: 27: 235–9.
21. Dominguez Cherit J, Chanussot Deprez C, Maria Sarti
H et al. Nail unit tumors: a study of 234 patients in the
dermatology department of the ‘‘Dr Manuel Gea Gonza-
lez’’ general hospital in Mexico City. Dermatol Surg 2008;
34:1363–71.
22. Kato T, Suetake T, Sugiyama Y et al. Epidemiology and
prognosis of subungual melanoma in 34 Japanese patients.
Br J Dermatol 1996; 134: 383–7.
23. Thai KE, Young R, Sinclair RD. Nail apparatus melanoma.
Australas J Dermatol 2001; 42: 71–81.
24. Tosti A, Piraccini BM, Farias DC. Dealing with melanony-
chia. Semin Cutan Med Surg 2009; 28(1): 49–54.
25. Ronger S, Touzet S, Ligeron C et al. Dermatoscopic examina-
tion of nail pigmentation. Arch Dermatol 2002; 138: 1327–33.
26. Andre J, Lateur N. Pigmented nail disorders. Dermatol
Clin 2006; 24: 329–39.
27. Lateur N, Andre J. Melanonychia diagnosis and treatment.
Dermatol Ther 2002; 15: 131–41.
Figure 5.12 Melanoma. Dermoscopy of the hyponychium shows
the micro-Hutchinson’s sign (x20).

6.1aVascular pattern under videodermatoscopy observation
Giorgio Filosa, Rossella De Angelis, and Leonardo Bugatti
Definition of Psoriasis
Psoriasis is a papulosquamous disease with variable morphol-
ogy, distribution, severity, and course (1), affecting about 1.5%
of the Caucasian population.(2) Psoriatic lesions are sharply
demarcated, red in color, and slightly raised, with silver-
whitish scales.(2) The microscopic alterations of psoriatic
plaques include infiltration of immune cells in the dermis and
epidermis, dilatation, and increase in the number of blood ves-
sels in the upper dermis, and extremely thickened epidermis
with keratinocyte differentiation.(2)
The immune system plays an important role in the pathogen-
esis of psoriasis, and there is strong evidence that activated T cells
make the first move in the inflammatory reaction. Recently made
discoveries regarding T cell populations, dendritic cells, mac-
rophages, keratinocyte signal transduction, and novel cytokines,
including interleukin (IL)-22, IL-23, and IL-20, suggest that the
pathogenesis of psoriasis consists of distinct subsequent stages
in which different cell types have a governing role.(2)
angiogenesis anD Psoriasis
The microvasculature is of pathologic relevance to psoria-
sis and excessive dermal angiogenesis is a characteristic fea-
ture. Until now, it is still a matter of debate whether the early
changes in psoriasis are referred to the epidermis or to the vas-
culature. There is evidence that epidermal hyperplasia cannot
occur without vascular proliferation, which is represented as
an abnormal growth of endothelial cells in the microvessels
around the perilesional skin.(3) Also, the existence of dilata-
tion and increased tortuosity of dermal capillary loops before
dermal hyperplasia is demonstrated.(4) The starting event of
psoriasis seems to be the initial vasodilatation that is accom-
panied by exudates of inflammatory cells and serum in the
papilla.(4) Nevertheless, some authors have provided evidence
that keratinocyte-derived proangiogenic cytokines such as IL-1
and vascular endothelial growth factor (VEGF) are increased in
psoriatic epidermis.(5, 6) Furthermore, the fact that epidermal
changes may initiate lesions is substantiated by the observation
that even nonlesional psoriatic skin showed an enhanced pro-
duction of cytokines and appeared to be primed for leukocyte
adherence.(7)
There is considerable support about the role of TNF-α
in expansion of the dermal microvasculature in psoriasis.
(5, 8–11) TNF-α is recognized in raising the expression of
adhesion molecules and vascular cell adhesion molecules on
keratinocytes (11) and in inducing the VEGF production,
which stimulates endothelial mitogenic activity in the skin.
(5) The exhibition of adhesion molecules and chemokines
results in the enrolment of additional inflammatory cells
to the plaque. The recruited cells can then produce further
TNF-α and γ-interferon, potentially amplifying local inflam-
mation and keratinocyte proliferation.(11)
During plaque formation, the superficial papillary micro-
vessels undergo elongation, thus widening and tortuosity.
These blood vessels must, therefore, play an important but
probably secondary role in the pathogenesis of clinical lesions
in psoriasis.(12)
ViDeoDermatoscoPy anD
ViDeocaPillaroscoPy in Psoriasis
The cutaneous microcirculation is organized as two horizon-
tal plexuses. One is situated 1.5 mm below the skin surface
and the other at the dermal–subcutaneous junction and con-
nected by ascending arterioles and descending venules. From
the upper layer, arterial capillaries rise to form the dermal
capillary loops that represent the nutritive component of the
skin circulation.(13)
In psoriasis, the overall organization of the dermal micro-
circulation is the same as in normal skin. However, it displays
many anatomical and physiological changes, mainly described
in the intrapapillary portion of the loops. Each papilla contin-
ues to be served by a single capillary, but the limbs are twisted
along their major axis.(12) The outside endothelial diameters
of the loops are also wider (6–17 μm) than the correspond-
ing segments in normal skin (3.5–6 μm).(12) The papillary
microvessel changes are homogeneously distributed through-
out clinical lesions.(12)
A comprehensive evaluation of the cutaneous microvascular
structure is possible using different tools, including videocapillaros-
copy (VCP) and/or high magnification videodermatoscopy (VD).
VD is a noninvasive technique, which consists of in vivo skin
observation with a video camera that allows magnifications
ranging from x4 to x1,000.(14) Visibility of vessels strongly
depends on the method of examination. The glass plate of a
videodermatoscope is placed carefully upon the skin, to reach
a minimal compression of capillaries, which is then easily visual-
ized. The application of a conspicuous amount of high-viscosity
gel is advisable and appropriate.
VCP is a widely used method to study the morphology and
dynamics of microcirculation, by means of a computerized video
microscope, equipped with optic contact probes and magnifica-
tions ranging between x50 and x500. A drop of cedar oil is gener-
ally used to improve capillary visibility.
An appropriate knowledge of the vascular pattern in normal
skin is a prerequisite for recognizing the psoriasis microvessels,
which appear different in shape and morphology. In normal
skin observed by VD, vessels come out as tiny red dots, regularly

vascularpatternundervideodermatoscopyobservation
dispersed over the skin surface (15); in glabrous skin, these red
dots are aligned along the crests of the ridges. The upper dermal
plexus is visible as a coarse network of broader vessels.(15) Under
VCP observation, especially after x100 and x200 magnification,
capillary loops appear with the major axis running perpendic-
ular to the skin surface, and are, therefore, characterized by a
comma-like appearance inside the dermal papilla (Figure 6.1).
The normal capillaroscopic picture differs according to the body
areas: in some districts, such as the dorsum of the hand, and not
all of the capillaries run perpendicular to the skin surface, and
visibility is not limited to the apical portion; in the forehead; for
example, all capillaries run parallel to the skin surface, with a net-
work appearance. The evidence of the deep venular subpapillary
plexus depends on the skin transparency.
Vascular Patterns in Psoriasis
A few studies in the past have described some dermoscopic fea-
tures of psoriasis as a homogeneous arrangement of vascular
structures (Figure 6.2) (16, 17), and systematic effort to identify
the dermoscopic features of the psoriatic microvasculature are
only recently available.(4, 18)
A latest study including 300 lesions from 255 patients with
solitary, red, scaly patches or plaque features tried to describe
the most significant morphologic findings seen on VD, in order
to formulate a diagnostic model based on these characteristics.
For psoriasis, the significant features identified were a homo-
geneous vascular pattern, red dots, and light-red background,
yielding a diagnostic probability of 99% if all three features
were present.(18) Red dots were seen in all examples of psoria-
sis studied (Figure 6.3). The presence of arborizing vessels was
the most valuable negative feature in differentiating psoriasis
from basal-cell carcinoma and intraepidermal carcinoma.(18)
In hair and scalp disorders, the observation of twisted loops in
both psoriasis and psoriasis-like forms of seborrheic dermatitis
reflect true overlap disease, as captured by the term sebopso-
riasis.(19)
The capillaroscopic picture of plaque psoriasis has been
extensively described in literature (10, 20–22), reporting that
examination of the untreated psoriatic skin shows many uni-
formly arranged tortuous and dilated capillaries, appearing as
“bushy,” with a highly distinctive pattern (Figure 6.4, Figure
6.5). Moreover, the VCP technique allows the obtaining of
additional information about distribution, morphology, and
density of capillaries in the psoriatic plaques. Corresponding to
the perilesional skin, capillary loops show a parallel course with
respect to the skin surface and with a lengthened apex directed
toward the marginal zone of the lesion (10) (Figure 6.6). The
number of capillary loops per area unit seems to increase in
perilesional skin compared to lesional skin (42.8 ± 4.05 vs.
29.73 ± 3.53).(12) A minimal shift of the probe from the per-
ilesional to normal-appearing skin allows the visualization of
capillary loops that gradually become perpendicular.
These studies lead to the recognition of a critical pathoge-
netic role of angiogenesis in sustaining and spreading out of
the psoriasis lesions.
theraPy monitoring
There are a number of studies that report morphological modi-
fications and loop changes after local and systemic treatments,
which goes to show that the role of VD and VCP in psoriasis for
in vivo therapy monitoring is a subject pursued with growing
interest.(17, 20, 23, 24)
VD may help in revealing that the overuse of topical steroids
results in the appearance of clinically imperceptible but der-
moscopically evident “red lines” (“linear telangiectasias”) in
the treated plaques/skin adjacent (p < 0.03), before the atrophy
becomes permanent.(17)
VD evaluation at the fingernail hyponichium (between x20
and x70) in patients with nail-bed psoriasis after a 3-month
Figure 6.1 Videocapillaroscopy, x 200 magnification. Normal
skin: “comma-like” appearance of the capillary loops.
Figure 6.2 Videodermatoscopy, x70 magnification. Psoriatic
skin: “bushy” capillaries.

filosa,angelis,andbugatti
dimension of the capillaries (p = 0.0005).(23) Modification
of the capillaroscopic aspects took place in a progressive
manner in all the patients and according to the length of the
therapy.(23)
Investigation of microcirculation by capillaroscopy in
psoriatic skin after biologic therapies had brought to light
considerable information about the role of angiogenesis.
A single infusion of infliximab induced significant morpho-
logical changes to the capillary loops in psoriatic lesions, which
appeared less tortuous and dilated, showing an evident reduc-
tion in shape and size (25) (Figure 6.7, Figure 6.8). The num-
ber of “bushy” loops was manifestly reduced, which suggests
Figure 6.3 Videodermatoscopy, x50 magnification. Psoriatic
skin: red dots aligned along the dermatoglyphics.
Figure 6.5 Videocapillaroscopy, x200 magnification. Psoriatic
skin showing many uniformly arranged dilated capillaries.
Figure 6.6 Videocapillaroscopy, x200 magnification. Psoriatic
perilesional skin: capillary loops show a parallel course, with
respect to the skin surface, with a lengthened apex directed
toward the marginal zone of the lesion.
Figure 6.4 Videocapillaroscopy, x200 magnification. Psoriatic
skin showing many uniformly arranged tortuous.
course of calcipotriol treatment showed a significant decrease
in the number of capillaries, especially for patients with lichen
planus.(24) By means of a VD with x200 magnification, the
grossly dilated and tortuous aspect of the untreated psoriatic
capillaries appeared to be reduced in five patients after the
application of tacalcitol ointment 4 µg/g, with a marked sim-
plification of the coiling of the capillary ball occurring after
3 weeks in 2 cases.(20)
A 3-month treatment course with cyclosporine (4 mg/
kg/day) produced a statistical reduction in microcirculatoy
alterations, as assessed by digital capillaroscopy (x300 magni-
fication), and in 70% of the subjects treated, especially in the

vascularpatternundervideodermatoscopyobservation
that infliximab may achieve its results, in part by targeting the
angiogenetic properties of TNF-α
As comprehensive studies are required to further establish
the modalities of action of TNF-α blockers in reducing psori-
atic lesions (25, 26), both VD and VCP represent reproducible
techniques that may allow an easy and accurate assessment of
microvascular modifications of the psoriatic skin after topic
and systemic therapies.
references
1. Langley RG, Krueger GG, Griffiths CE. Psoriasis: epidemi-
ology. Clinical features and quality of life. Ann Rheum Dis
2005; 64(Suppl 2): 18–23.
2. Sabat R, Philipp S, Höflich C et al. Immunopathogenesis
of psoriasis. Exp Dermatol 2007; 16: 779–98.
3. Folkmann J. Angiogenesis in cancer, vascular, rheumatoid
and other diseases. Nat Med 1995; 1: 27–31.
4. Creamer JD, Barker JNWN. Vascular proliferation and
angiogenic factors in psoriasis. Clin Exp Dermatol 1995;
20: 6–9.
5. Detmar M, Brown LF, Claffey KP et al. Overexpression of
vascular permeability factor/vascular endothelial growth
factor and its receptors in psoriasis. J Exp Med 1994; 180:
1141–6.
6. Debets R, Hegmans JPJJ, Troost RJJ et al. Enhanced produc-
tion of biologically active interleukin-1α and interleukin-1α
by psoriatic epidermal cells ex vivo: evidence of increased
cytosolic interleukin-1α levels and facilitated interleukin-1
release. Eur J Immunol 1995; 25: 1624–30.
7. Prens EP, Debets R. Reply to the letter of Li et al. J Am Acad
Dermatol 1996; 1020–1.
8. Creamer D, Allen MH, Sousa A et al. Localization of
endothelial proliferation and microvascular expansion in
active plaque psoriasis. Br J Dermatol 1997; 136: 859–65.
9. Ettehadi P, Greaves W, Wallach D et al. Elevated tumor
necrosis factor-alpha (TNF-α) biological activity in pso-
riatic skin lesions. Clin Exp Immunol 1994; 96: 146–51.
10. De Angelis R, Bugatti L, Del Medico P et al. Videocapilla-
roscopic findings in the microcirculation of the psoriatic
plaque. Dermatology 2002; 204: 236–9.
11. Krueger JG. The immunologic basis for the treatment of
psoriasis with new biologic agents. J Am Acad Dermatol
2002; 46: 1–23.
12. Hern S, Mortimer PS. In vivo quantification of microves-
sels in clinically uninvolved psoriatic skin and in normal
skin. Br J Dermatol 2007; 156: 1224–9.
13. Braverman IM. The cutaneous microcirculation. J Invest
Derm Symp Proc 2000; 5: 3–9.
14. Micali G, Nardone B, Scuderi A, Lacarrubba F. Videoder-
matoscopy enhances the diagnostic capability of palmar
and/or plantar psoriasis. Am J Clin Dermatol 2008; 9:
119–22.
15. Kreusch JF. Vascular patterns in skin tumors. Clin Derma-
tol 2002; 20: 248–54.
16. Vasquez-Lopez F, Manjon-Haces JA, Maldonado-Seral
C et al. Dermoscopic features of plaque psoriasis and
lichen planus: new observation. Dermatology 2003; 207:
151–6.
17. Vasquez-Lopez F, Marghoob AA. Dermoscopic assessment
of long-term topical therapies with potent steroids in
chronic psoriasis. J Am Acad Dermatol 2004; 51: 811–3.
18. Pan Y, Chamberlain AJ, Bailey M et al. Dermatoscopy aids
in the diagnosis of the solitary red scaly patch or plaque-
features distinguishing superficial basal cell carcinoma,
intraepidermal carcinoma and psoriasis. J Am Acad Der-
matol 2008; 59: 268–74.
19. Ross EK, Vincenzi C, Tosti A. Videodermoscopy in the
evaluation of hair and scalp disorders. J Am Acad Derma-
tol 2006; 55: 799–806.
Figure 6.7 Videocapillaroscopy, x200 magnification. Untreated
psoriatic skin.
Figure 6.8 Videocapillaroscopy, x200 magnification. The num-
ber of “bushy” loops are manifestly reduced, after infliximab
treatment.
6
filosa,angelis,andbugatti
20. Strumia R, Altieri E, Romani I et al. Tacalcitol in psoriasis:
a video-microscopy study. Acta Derm Venereol (Stock)
1994; Suppl 186; 85–7.
21. Fuga GC, Marmo W, Acierno F et al. Cutaneous microcircu-
lation in psoriasis. A videocapillaroscopic morphofunctional
study. Acta Derm Venereol (Stock) 1994; Suppl 186: 138.
22. Okada N, Nakatani S, Ozawa K et al. Video macroscopic
study of psoriasis. J Am Acad Dermatol 1991; 25: 1077–8.
23. Stinco G, Lautieri S, Valente F, Patrone P. Cutaneous
vascular alterations in psoriatic patients treated with
cyclosporine. Acta Derm Venereol 2007; 87: 152–4.
24. Iorizzo M, Dahadah M, Vincenzi C, Tosti A. Videodermos-
copy of the hyponychium in nail bed psoriasis. J Am Acad
Dermatol 2008; 58: 714–5.
25. De Angelis R, Gasparini S, Bugatti L, Filosa G. Early vid-
eocapillaroscopic changes of the psoriatic skin after anti-
tumour necrosis factor-alpha treatment. Dermatology
2005; 210: 241–3.
26. Nickoloff BJ, Nestle FO. Recent insights into the immu-
nopathogenesis of psoriasis provide new therapeutic
opportunities. J Clin Invest 2004; 113: 1664–75.

6.1b Histopathological correlations

Daniele Innocenzi, Maria Concetta Potenza, and Ilaria Proietti
IntroductIon
Psoriasis is a common, chronic, relapsing, inflammatory, and
hyperproliferative skin disorder with genetic predisposition and
multifactorial pathogenesis.(1) There is not a typical clinical
and histological picture of psoriasis, and there is no standard
treatment available.(2) The classical presentation of this skin
disorder is plaques psoriasis, and, as this form is usually easy to
identify, histopathologic examination is generally not required.
In this case, the diagnosis is made on clinical grounds by a “visu-
ally literate” clinician.(3) However, all dermatologists recog-
nize the difficulty in identifying the disease in many instances,
especially when the appearance is not typical. Psoriasis is the
prototype of a group of cutaneous disorders (psoriasiform der-
matitis) that show psoriasiform epidermal hyperplasia, defined
as regular elongation of the rete ridges with preservation of the
rete ridge–dermal papillae pattern.(4) Other histologic clues
to the diagnosis of psoriasis include more dilated and tortu-
ous papillary blood vessels, neutrophils within the epidermis
associated with spongiosis (spongiform pustules), neutrophils
beneath the cornified layer (subcorneal pustules), neutrophils
within the cornified and parakeratotic horn, hypogranulosis,
and more keratinocytic mitotic figures above the basal-cell
layer.(5–6)
Plaques PsorIasIs
In its classical presentation (plaques psoriasis), the disease is
characterized by well-circumscribed, reddish, and scaly pap-
ules and plaques typically located on elbows, knees, scalp, and
other cutaneous sites.(2) Psoriasis is characterized by abnormal
keratinocytic proliferation resulting in thickening of epidermis
(producing well-circumscribed clinical plaques) and stratum
corneum (producing scales).(7)
As compared with normal skin, psoriatic lesions show
up to 27 times the mitotic activity, a 12-fold decrease in the
cell-cycle time of basal and suprabasal keratinocytes, and a
greater than 7-fold increase in the epidermis turnover time
(7 days in psoriatic skin vs. 56 days in normal skin). There
is also an increase in the apoptotic rate, in concert with a
reduction of bcl-2 (an antiapoptotic protein) expression in
basal cells. In psoriatic skin, basal keratinocytes maintain
expression of K5 and K14 (the keratins typical of basal kera-
tinocytes in normal skin), whereas K1 and K10 (the keratins
typical of suprabasal cells in normal skin) are replaced by
socalled hyperproliferation-associated keratins, K6 and K16,
in addition to K17.(8)
We must also consider the “histodynamic” of the psoriatic
plaque. Psoriasis shows lesions with different clinicopathological
aspect according to the moment in which the lesion is taken.
Clinically, in the psoriatic plaque, we can observe essentially
three phases:
A nonspecific • initial phase characterized by the presence
of erythematous edematous plaques, in rapid evolution
toward the other phases.
The intermediate or • steady-state phase (divided in
early and late steady state), which, for us, is the most
interesting because this is the moment when we visit the
patients.
Figure 6.9 Clinical and histological features of the initial phase.

innocenzi,potenza,andproietti
The final erythematodesquamative phase • (phase of reso-
lution) is usually observed after successful treatments
and representing the phase of progressive resolution and
clearing.
These different clinical aspects can coexist in the same patient
because, psoriasis plaques not always show synchronous devel-
opment. Clinical polymorphism correspond to different and
specific histological stages.
The • initial phase, clinically characterized by erithema-
tous and edematous lesions, is aspecific, fleeting, and
quickly slips toward following steps. The earliest changes
can be nonspecific, with a preponderance of dermal
changes, including a sparse, superficial, and perivascular
T-lymphocytic infiltrate (Figure 6.9).
This • intermediate phase, a well-developed plaque phase,
can be divided from an histopathological point of view
in.
Early steady-state phase, • which clinically corresponds
to plaque elevation, is characterized by acanthosis with
regular elongation of the rete ridges, thickening in their
lower portion, thinning of the suprapapillary epidermis
with occasional presence of small spongiform pustules,
pallor of the upper layers of the epidermis, diminished
to absent granular layer, confluent parakeratosis, and
presence of Munro microabscesses (Figure 6.10). It is
possible to find elongation and edema of the dermal
papillae and dilated and tortuous capillaries. It is still
not entirely clear what causes these changes in plaque
skin. One possibility is that in psoriasis the dermal
microvessels may receive a specific trigger/stimulus.
There are now a considerable evidences indicating that
angiogenesis plays a role in triggering the microcircu-
latory changes in psoriatic skin.(9, 10) Elongation and
tortuosity of the dermal papillary vessels are not, how-
ever, exclusive to psoriasis. Also, an increase in capil-
lary width may be seen in other skin conditions such as
port wine stains, eczema, lichen planus, and dermatitis
herpetiformis.(11) The striking difference in psoriasis is
that the papillary vessel changes are dramatic and uni-
formly distributed throughout clinical lesions.(9) The
combination of superficial dermal capillaries and over-
lying suprapapillary epidermal thinning is responsible
for the erythematous appearance of psoriatic lesion and
the Auspitz sign (pinpoint bleeding points on removal
of the scale). This stage corresponds to the increase in
number of dwarf handles or bush vases at videoderma-
toscopy (Figure 6.11).
Figure 6.10 Clinical and histological features of the early steady-state phase.
Figure 6.11 Videodermatoscopy of dwarf handles and bush
vases in a psoriatic plaque at early steady-state phase (X200).

histopathologicalcorrelations
Late steady-state phase • clinically corresponds to fully
developed clinical plaques because it shows marked epi-
dermal hyperplasia. This phase is histologically charac-
terized by club-shaped thickening of the lower rete pegs
with coalescence of these in some areas. Lesions show
silvery scales as result of the ortokeratosis of corneus and
an intact granular layer with parakeratosis. Exocytosis
of inflammatory cells is usually mild, and there is some
thickening of the suprapapillary plates and fine fibrillary
collagen (Figure 6.12). This stage relates to the presence
of white-silvery images on a red background during vid-
eodermatoscopy (Figure 6.13).
The • phase of resolution corresponds to resolving or
treated plaques of psoriasis (Figure 6.14). It initially
shows progressive reduction in the presence of neutro-
phils within the stratum corneum and parakeratosis,
with reformation of the granular zone and orthokera-
tosis. The epidermal hyperplastic changes resolve later.
Figure 6.12 Clinical and histological features of the late steady state.
Figure 6.13 Videodermatoscopy of a psoriatic plaque at late
steady stage (X200).
Figure 6.14 Clinical and histological features of the resolution phase.
6
innocenzi,potenza,andproietti
There may be residual, mild, superficial, dermal fibrosis
with persistence of papillary dermal capillary dilatation
and tortuosity as the only histopathologic clues to this
disease. The clinical resolution of lesions is associated
with the abnormal-to-normal return of plaques’ micro-
vessels.(12) As the plaques regress, they often start to clear
in the center, with a persistent marginal activity at the
borders, which confers an annular or polycyclic appear-
ance. Hypopigmentation is usually associated with clear-
ing (psoriatic leukoderma).
These different aspects of the psoriatic plaque correspond to
different biochemical events that occurs in the psoriatic lesion.
For that reason we understand that making a correct diagnosis
and deciding the appropriate treatment for different patients
is not so easy; in order to better chose the therapy, it would be
really helpful to understand how the single plaque responds to
the treatment depending on its histopathological phase.
reFerences
1. Gudjonsson JE, Elder JT. Psoriasis: epidemiology Clin
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2. Naldi L, Gambini D. The clinical spectrum of psoriasis.
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8. Leigh IM, Navsaria H, Purkis PE et al. Keratins (K16 and
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9. Creamer D, Allen MH, Sousa A, Poston R, Barker JN.
Localization of endothelial proliferation and microvas-
cular expansion in active plaque psoriasis. Br J Dermatol
1997; 136(6): 859–65.
10. Bacharach-Buhles M, el Gammal S, Panz B, Altmeyer P.
In psoriasis the epidermis, including the subepidermal
vascular plexus, grows downwards into the dermis. Br J
Dermatol 1997; 136(1): 97–101.
11. Braverman IM. The role of blood vessels and lymphatics
in cutaneous inflammatory processes: an overview. Br J
Dermatol 1983; 109(25):89–98.
12. Hern S, Mortimer PS. In vivo quantification of microves-
sels in clinically uninvolved psoriatic skin and in normal
skin. Br J Dermatol 2007; 156(6): 1224–9.

.c Palmoplantar psoriasis
Francesco Lacarrubba, Maria Letizia Musumeci, and Giuseppe Micali
The diagnosis of palmar and/or plantar psoriasis is usually
uncomplicated, especially when typical anatomic sites are
involved. However, in cases with only palmar and/or plantar
involvement, it may be troublesome, often requiring skin biopsy
with histopathological evaluation. Differential diagnosis includes
eczematous dermatitis (allergic, irritative), tinea manuum/
pedis, lichen planus, porokeratosis, pityriasis rubra pilaris, ker-
atodermas, mycosis fungoides, epidermolysis bullosa, syphilis,
scabies, and drug reactions.
Videotermatoscopy (VD) may be helpful to address the diagno-
sis of palmoplantar psoriasis in the presence of no readily apparent
diagnostic features through the evaluation of superficial vascular
structures. VD examination must be performed with the epilumi-
nescence technique, carefully avoiding vessels blanching and apply-
ing to the skin the least possible pressure with the contact plate.
In normal palmoplantar skin surface, VD examination at
X100 to X200 magnification shows the presence of capillary
loops linearly arranged along the furrows of dermatoglyphics
(Figure 6.15A–6.15B). In palmoplantar psoriasis, the evalua-
tion of the vascular structure by VD shows dilated and tortuous
capillaries, homogeneously appearing as “bushy” (1–4) and lin-
early arranged along the furrows of dermatoglyphics (Figure
6.16A–6.16D). A major limitation in this anatomical site, which
may interfere with a reliable VD evaluation, is represented by the
frequent presence of excessive hyperkeratosis that may hamper
vascular structure analysis; in such cases, VD examination might
be performed in residual erythematous areas or after application
of keratolytic products (such as 30%–50% urea) for 3 to 4 days.
The efficacy of VD in recognizing palmoplantar psoriasis has
been demonstrated in a series of patients affected by palmar and/
or plantar dermatoses with no otherwise specific diagnostic fea-
tures.(5) A total of 32 subjects (12 males and 20 females; mean
age = 50 years, age range between 20 and 72 years) were enrolled
in an open study. Inclusion criteria were the presence of clinically
nonspecific, active, and untreated palmar and/or plantar, ery-
thematous, scaly lesions with no other skin involvement. Exclusion
criteria were past medical history positive for psoriasis or eczema,
pustular psoriasis, presence of comorbid disorders potentially
altering microcirculation (diabetes), use of vasodilator drugs, pres-
ence of excessively hyperkeratotic lesions, use of systemic and/or
topical drugs within 4 and 2 weeks of study entry, respectively.
Twenty-two cases presented with palmar lesions only, 7 with plantar
involvement; and 3 patients had palmar/plantar localization. A
video microscope system, Hi-Scope KH-2,200 [Hirox Co., Tokyo,
Japan], equipped with a zoom lens, was used for vascular pattern
evaluation that was performed under standard environmental
conditions (temperature, humidity). An average of three fields for
each lesion was examined with two magnifications, X50 and X200,
after covering each field with immersion oil in order to avoid light
reflection and thus allowing a good visualization of vascular struc-
tures. After VD examination, a skin biopsy from the affected areas
was taken from each patient for H&E stain. At the end of the study,
VD was able to identify the cases of palmoplantar psoriasis, as later
confirmed by histopathological examination, showing in all exam-
ined fields at low magnification (X50) the presence of pinpoint-like
capillaries linearly arranged along the furrows of dermatoglyphics;
Figure 6.15A–6.15B VD examination of normal palmar skin surface: presence of capillary loops arranged linearly along the
furrows of dermatoglyphics at X100 (A) and X200 (B) magnifications.
(A) (B)

lacarrubba,musumeci,andmicali
(A)
(B)
(C)
(D)
Figure 6.16A–6.16D Plantar psoriasis. A: clinical aspect. B:
VD examination shows at X50 magnification the presence of
pinpoint-like capillaries arranged linearly along the furrows of
dermatoglyphics. C: at X200 magnification, the same capillar-
ies appear dilated and tortuous, with a “bushy” aspect. Insert:
normal capillaries at the same magnification (X200). D: bushy
capillaries at X400 magnification.
at X200 magnification, the same capillaries appeared dilated and
tortuous, with a bushy, homogeneous aspect (Figure 6.17A–6.17B).
In the other cases, the diagnosis of psoriasis was excluded; in fact,
in some of these patients, VD showed no relevant features at X50
magnification and a normal capillary pattern at X200 magnifica-
tion (Figure 6.18A–6.18B), and in the remaining patients it showed
the presence of pinpoint-like capillaries at X50 magnification but
did not show bushy capillaries at X200 magnification. In these two

palmoplantarpsoriasis
last groups, histopathology showed a pattern consistent with a
diagnosis of eczematous dermatitis.
In conclusion, analysis of superficial vascular pattern by VD
represents a promising noninvasive diagnostic tool in palmar
and/or plantar localization of psoriasis. For capillary pattern
evaluation the use of both low (50X) and high (200X) magnifica-
tions is recommended as, in our experience in some subjects, low
magnification identified a pinpoint-like vascular pattern that did
not correspond to bushy capillaries at higher magnification.
REFERENCES
1. De Angelis R, Bugatti L, Del Medico P, Nicolini M, Filosa G.
Videocapillaroscopic findings in the microcirculation of the
psoriatic plaque. Dermatology 2002; 204: 236–9.
2. Okada N, Nakatani S, Ozawa K, Sato K, Yoshikawa K. Video
macroscopic study of psoriasis. J Am Acad Dermatol 1991;
25: 1077–8.
3. Bull RH, Bates DO, Mortimer PS. Intravital video-capillar-
oscopy for the study of the microcirculation in psoriasis. Br
J Dermatol 1992; 126: 436–45.
4. Hern S, Stanton AWB, Mellor RH et al. In vivo quantifi-
cation of the structural abnormalities in psoriatic micro-
vessels before and after pulsed dye laser treatment. Br J
Dermatol 2005; 152: 505–11.
5. Micali G, Nardone B, Scuderi A, Lacarrubba F. Video-
dermatoscopy enhances the diagnostic capability of pal-
mar and/or plantar psoriasis. Am J Clin Dermatol 2008; 9:
119–22.
Figure 6.17A–6.17B A: palmar dermatosis with no specific
clinical features. B: VD examination showing at X200 magnifi-
cation the presence of “bushy” capillaries, suggesting a diagno-
sis of psoriasis, later confirmed by histopathology.
(A)
(B)
Figure 6.18A–6.18B A: palmar dermatosis with no specific
clinical features: B: VD examination showing at X200 magni-
fication normal capillaries. In this case, a diagnosis of psoriasis
was excluded.
(A)
(B)

.1dPsoriatic balanitis
Giuseppe Micali, Maria Rita Nasca, and Francesco Lacarrubba
The term balanitis defines an inflammation of glans penis
that may be caused by a wide range of conditions including
infectious, neoplastic, and inflammatory dermatoses, and
among these, candidiasis, contact dermatitis, erythroplasia of
Queyrat, lichen sclerosus, lichen planus, Zoon’s balanitis, and
psoriasis.
Psoriatic balanitis is clinically characterized by erithematous,
nonscaling plaques most commonly located proximally on the
glans and under the prepuce.(1) In general, genital psoriasis is
part of a more generalized cutaneous disorder. However, in case
of exclusive penile involvement, the correct diagnosis may be
troublesome, and several investigations, including skin biopsy,
are often necessary.(2)
Videodermatoscopic (VD) examination of glans in healthy
subjects shows at X100 magnification the presence of normal
capillary loops (Figure 6.19).
Similarly to cutaneous lesions of psoriasis (3–6), VD evalu-
ation of psoriasis of the glans shows dilated and tortuous
capillaries homogeneously appearing as “bushy.” In this site,
however, due to the absence of scales, the visualization of vas-
cular structures is easy.
We examined by VD a series of patients affected by psori-
atic balanitis in order to establish whether this technique may
be able, by evaluating the superficial vascular pattern, to pro-
vide additional information useful to address the diagnosis
beyond standard clinical observation.(7) Six subjects (mean
age 49.1 years, age ranging between 41 and 70 years) were
enrolled in an open study. Inclusion criteria were the presence
Figure 6.19 VD examination of normal glans penis: presence
of normal capillary loops (X100).
of biopsy-proven psoriatic balanitis and no other skin involve-
ment. Exclusion criteria were the presence of comorbid dis-
orders and the use of systemic and/or topical medications for
4 and 2 weeks, respectively. VD was performed using a video
microscope system, Hi-Scope KH-2,200 [Hirox Co. Ltd., Tokyo,
Japan], allowing the observation at incident light of skin magni-
fications ranging from X20 up to X600. In order to evaluate the
vascular pattern, VD examination (X100-X400) was performed
Figure 6.20 (continued)
(A) (B)

psoriaticbalanitis
Figure 6.20 Psoriatic balanitis––A: clinical aspect. B: VD examination showing dilated and tortuous capillaries, with a “bushy”
aspect (X100). Insert: normal capillaries at the same magnification (X100). C: the same “bushy” capillaries at X200. D: “bushy”
capillaries at higher magnification (X400).
(C) (D)
Figure 6.21–6.22 Psoriatic balanitis––A: clinical aspect. B: VD examination showing dilated and tortuous capillaries, with a
“bushy” aspect (X200).
(A)
(C)
(B)
(D)

micali,nasca,andlacarrubba
after covering each field with immersion oil to eliminate light
reflection and achieve optimal visualization of capillaries. In
addition, six cases of nonpsoriatic balanitis, histologically or
microbiologically proven (2 lichen planus, 1 lichen sclerosus,
1 Zoon’s balanitis and 2 candidiasis) were also evaluated by VD.
At the end of the study, VD showed in all subjects affected by
psoriatic balanitis a uniform pattern consisting of dilated and
tortuous capillaries with a typical bushy, homogenous aspect in
all examined fields (Figure 6.20–6.22). This pattern histologi-
cally corresponded to dilated, elongated, and tortuous capillary
loops in the papillary dermis. In the six cases of nonpsoriatic
balanitis, no bushy pattern was observed, and the presence of
dilated, linear, and irregularly distributed capillaries, without
any peculiar aspect, was evident (Figure 6.23).
In conclusion, VD seems to hold promise as a tool that can
potentially improve the clinical diagnosis of psoriatic balanitis
through the evaluation of superficial vascular structures, thus
avoiding skin biopsy. This might be particularly useful in those
cases in which psoriatic lesions located in typical body areas or
elsewhere in the body are missing. It should be remarked that
VD examination must be performed with the epiluminescence
technique and that particular care is needed while applying the
contact to the skin with a minimal pressure in order to avoid
vessels blanching.
Figure 6.23 Lichen ruber planus––A: clinical aspect. B: VD examination showing a not specific vascular pattern with dilated, lin-
ear, irregularly distributed capillaries (X200).
(A) (B)
REFERENCES
1. Buechner SA. Common skin disorders of the penis. BJU Int
2002; 9: 498–506.
2. Palamaras I, Hamill M, Sethi G, Wilkinson D, Lamba H.
The usefulness of a diagnostic biopsy clinic in a genitouri-
nary medicine setting: recent experience and a review of the
literature. J Eur Acad Dermatol Venereol 2006; 20: 905–10.
3. De Angelis R, Bugatti L, Del Medico P, Nicolini M, Filosa
G. Videocapillaroscopic findings in the microcirculation of
the psoriatic plaque. Dermatology 2002;204:236–9.
4. Bull RH, Bates DO, Mortimer PS. Intravital video-capilla-
roscopy for the study of the microcirculation in psoriasis.
Br J Dermatol 1992; 91: 343–5.
5. Rosina P, Zamperetti MR, Giovannini A, Girolomoni G.
Videocapillaroscopy in the differential diagnosis between
psoriasis and seborrheic dermatitis of the scalp. Dermatology
2007; 214: 21–4.
6. Micali G, Nardone B, Scuderi A, Lacarrubba F. Video-
dermatoscopy enhances the diagnostic capability of pal-
mar and/or plantar psoriasis. Am J Clin Dermatol 2008; 9:
119–22.
7. Lacarrubba F, Nasca MR, Micali G. Videodermatoscopy
enhances diagnostic capability in psoriatic balanitis. J Am
Acad Dermatol, in press.

.1e Scalp psoriasis
Paolo Rosina
Videocapillaroscopy (VCP) allows morphological and func-
tional analysis of microcirculation at all cutaneous sites, includ-
ing the scalp. Psoriasis capillary changes determine a specific
vascular pattern: capillaries are enlarged, elongated, and tortu-
ous and look like a bush or clew.(1–4) This pattern is already
visible with hand-held dermatoscope (Figure 6.24) but are bet-
ter valuable with a greater magnification using videodermatos-
copy or videocapillaroscopy (Figure 6.25).
Psoriasis and seborrheic dermatitis can be difficult to dif-
ferentiate, especially when lesions are confined to the scalp.
The lesions of seborrheic dermatitis may closely resemble
clinically those of psoriasis. Their distribution is generally dif-
ferent, but when lesions are confined to the scalp and are long
standing, even histology may hardly differentiate the two con-
ditions. Distinction of seborrheic dermatitis from psoriasis is
obviously relevant for the long-term prognosis, but it may be
particularly important in patients with arthritis symptoms.
In fact, the presence of skin psoriasis is the most relevant
criteria for the diagnosis of psoriatic arthritis, and deciding
whether erythematous scaly plaques on the scalp are psoriasis
or seborrheic dermatitis may change the interpretation of the
rheumatic symptoms. An important difference between pso-
riasis and seborrheic dermatitis could be the microvascula-
ture changes, which are constantly present and characteristic
in psoriasis.(5, 6)
In a recent study we employed videocapillaroscopy (VCP)
to compare capillary morphology, distribution, and density
in psoriasis and seborrheic dermatitis of the scalp to use for
differential diagnosis.(1) VCP was performed using an optical
probe (Videocap 200
R
DS Medica, Milano, Italy) on histology-
confirmed scalp lesions of 30 patients with chronic plaque pso-
riasis, 30 patients with seborrheic dermatitis, and 30 healthy
subjects.
Scalp psoriasis presented a homogeneous pattern with tor-
tuous and dilated capillaries (appearing as bushes or clews)
and a completely disarranged microangioarchitecture (Figure
6.26). The capillary loops have identical “bushy” morphology
Figure 6.24 Tortuous capillary loops visible with hand-held
dermatoscope (x10).
Figure 6.25 Videocapillaroscopic appearance of capillary loops
in lesional scalp psoriasis (x100).
Figure 6.26 Homogeneous psoriatic pattern with tortuous and
dilated capillaries (appearing as bushes or clews) and a com-
pletely disarranged microangioarchitecture (x100).

rosina
in all scalp locations (Figure 6.27). In contrast, scalp sebor-
rheic dermatitis presented a multiform pattern, with mildly
tortuous capillaries and only isolated bushy, and mildly dilated
capillaries (Figure 6.28 and 6.29), with a conserved, local micro-
angioarchitecture similar to healthy scalp skin (Figure 6.30).
The diameter of capillary bush of scalp psoriasis is much greater
than in scalp affected by seborrheic dermatitis or normal scalp
skin of healthy subjects. In seborrheic dermatitis, mean diam-
eter of capillary bush was similar to that of the scalp of healthy
subjects. Capillary loop density was similar in all conditions.
Normal looking skin of patients with both dermatitis did not
show significant changes compared to normal skin of healthy
subjects.
Figure 6.27 Capillary loops with “bushy” morphology in pso-
riasis (x200).
Figure 6.29 Mildly tortuous capillaries and only isolated
“bushy” in seborrheic dermatitis (x200).
Figure 6.30 Normal scalp skin of healthy subject (x100). Figure 6.28 Lesional scalp seborrheic dermatitis with a con-
served local microangioarchitecture similar to healthy scalp
skin (x100).
In conclusion, VCP demonstrated that psoriasis exhibit homo -
geneously tortuous and dilated capillaries, confirming previous
findings, and it could be a useful and noninvasive method for
differentiating psoriasis and seborrheic dermatitis, especially
when the scalp is the only site affected.
RefeRences
1. Rosina P, Zamperetti MR, Giovannini A, Girolomoni G.
Videocapillaroscopy in the differential diagnosis between
psoriasis and seborrheic dermatitis of the scalp. Dermatology
2007; 214: 21–4.
2. Hern S, Mortimer PS. Visualization of dermal blood
vessels––capillaroscopy. Clin Exp Dermatol 1999; 24: 473–8.

scalppsoriasis
3. De Angelis R, Bugatti L, Del Medico P. Videocapillaroscopic
findings in the microcirculation of the psoriatic plaque.
Dermatology 2002; 204: 236–9.
4. Braverman IM, Yen A. Ultrastucture of the capillary loops
in the dermal papillae of psoriasis. J Invest Dermatol 1977;
68: 53–60.
5. Braun-Falco O, Heilgermeir GP, Lincke-Plewig H. Histo -
patho logical differential diagnosis of psoriasis vulgaris and
seborrheic eczema of the scalp. Hautarzt 1979; 30: 478–83.
6. Hern S, Stanton AWB, Mellor RH et al. In vivo quantification of
the structural abnormalities in psoriatic microvessels before and
after pulsed dye laser treatment. Br J Dermatol 2005; 152: 505–11.

6.2 Clear cell acanthoma
Francesco Lacarrubba, Orazia D’Agata, Federica Dall’Oglio, and Giuseppe Micali
Clear cell acanthoma (CCA) is a usually solitary benign epi-
dermal tumor first described by Degos in 1962.(1) The mean
age of onset is about 52 years, with equal frequency in men and
women.(2–5) It clinically appears as a dome-shaped, sharply
circumscribed, reddish papule, variable in size from 5 to 20
mm; a peripheral scaling collarette is characteristic, but not
always present (Figure 6.31–6.32). CCA occurs frequently on
the lower extremities, but other anatomic sites (trunk, upper
extremities) have been reported. Multiple lesions (from 2 up
to 400) are rarely encountered; the rate between solitary and
multiple CCA is estimated to be 1:9–1:15.(2–6) Ichthyosis
and varicose veins are the most frequent associated findings.
The etiology is not well understood; although some authors
suggest that the lesion may represent a benign epithelial neo-
plasm, others consider the disease as a localized reactive inflam-
matory dermatosis (pseudotumor).(2–5)
The differential diagnosis of single and/or multiple CCA
includes several conditions, such as histiocytomas, seborrheic
keratoses, basal-cell carcinomas, pyogenic granulomas, syrin-
gomas, hidradenomas, leiomyomas, fibromas, perifolliculomas,
disseminated granuloma annulare, lichen planus, and sarcoidosis.
The diagnosis of CCA is usually confirmed by histologic exam-
ination, showing in the epidermis acanthosis, papillomatosis,
and a sharply demarcated epidermal proliferation of keratino-
cytes with a clear and slightly larger cytoplasm and a positive
PAS stain. In the superficial dermis, enlarged capillaries in the
papillae are evident.
In 2001, Blum et al. reported a single case of CCA and
first described a characteristic dermoscopic vascular pattern
at X20 magnification, consisting of “partly homogeneous,
symmetrically or bunch-like arranged, pinpoint-like capillar-
ies”.(7) Histo pathologically this pattern corresponded to dilated,
tortuous capillaries within markedly elongated dermal papillae.
Although the authors stated that a similar pattern could also
be seen in psoriatic plaques, after removal of the scales, and
considering that both entities possessed similar histopathologic
features, they concluded that the dermatoscopic examination
might anyway be of help to differentiate CCA from other skin
tumours.(7)
Successively, Bugatti et al. reported six cases of CCA charac-
terized by this psoriasis-like vascular findings on dermatoscopy (8); Figure 6.31 Multiple CCAs of the legs (arrows).
Figure 6.32 Close-up clinical view of a CCA: reddish, sharply
circumscribed papule with a peripheral scaling collarette.

clearcellacanthoma
they observed that the dotted vessels were regularly distributed in
a reticular array; moreover, they detected the presence of a squa-
mous surface with translucid collarette as an additional charac-
teristic dermatoscopic finding. The authors concluded that the
psoriasis-like pattern of CCA would appear to provide further
evidence of a neoangiogenetic inflammatory process rather than
a neoplastic one for CCA formation.(8)
Zalaudek et al. stated that dermoscopic features of CCA are
different from those of psoriasis (9) as, in their experience, in
CCA the dotted vessels are linearly arranged as pearls on a line,
whereas in psoriasis they are homogeneously and regularly
distributed throughout the entire lesion. Therefore, in their
opinion, these pearl-like vessels represent a peculiar dermo-
scopic pattern of CCA.(9)
In the same year, we studied the videodermatoscopic pat-
tern of multiple CCAs in a single patient (10), with all of them
showing the same pattern: symmetrical and homogeneous
pinpoint-like vascular structures throughout the entire lesion.
The pearl-like vessels disposition, at least in a portion of each
lesion, was always present (Figure 6.33–6.34), whereas the
presence of a net-like pattern was a frequent but not constant
finding (Figure 6.35–6.36). At higher magnification (X200),
each vascular structure appeared to have a bush-like aspect
(Figure 6.37).
Figure 6.33 VD examination of CCA: presence of symmetrical,
homogeneous pinpoint-like vascular structures with a pearl-
like disposition (X30).
Figure 6.35 VD examination of CCA: presence of symmetrical,
homogeneous pinpoint-like vascular structures arranged in a
net-like pattern (X30).
Figure 6.36 VD examination of CCA: presence of symmetrical,
homogeneous pinpoint-like vascular structures arranged in a
net-like pattern (X30).
Figure 6.34 VD examination of CCA: presence of symmetrical,
homogeneous pinpoint-like vascular structures with a pearl-like
disposition (X30).
2
lacarrubba,d'agata,dall'oglioandmicali
Figure 6.37 A detail at high-magnification depicting the bush-
like aspect of pinpoint-like capillaries in CCA (X200).
Figure 6.38 The VD pattern of CCA corresponds to the histo-
logical aspect of regularly elongated rete ridges and enlarged
capillaries in the dermal papillae.
The VD pattern of CCA corresponds to the histologic
aspect of regularly elongated rete ridges and enlarged capil-
laries in the dermal papillae (Figure 6.38). For this reason, the
dermatoscopic pattern of CCA resembles that of psoriasis and,
possibly, of other psoriasiform disorders (such as pityriasis
rubra pilaris and some variants of contact dermatitis) char-
acterized by epidermal proliferation and dermal capillaries
dilation, thus implying the need for additional diagnostic
criteria. Differential diagnosis from psoriasis is particularly
relevant in the case of multiple CCAs. Other cutaneous con-
ditions, such as warts, actinic, and seborrhoeic keratoses;
Bowen’s disease, squamous cell carcinoma; hypopigmented
Spitz nevus; melanoma; and melanoma metastasis may some-
times show pinpoint-like vessels. In these instances, however,
a correct evaluation of anamnestic and clinical features, along
with additional dermatoscopic features, will help to address
the correct diagnosis.
In conclusion, VD may improve the clinical diagnosis of sin-
gle or multiple CCAs, ruling out clinically similar disorders that
do not show the same features of CCA.
REFERENCES
1. Degos R, Delort J, Civatte J, Baptista P. Tumeur épider-
mique d’aspect particulier: acanthome à cellules claires.
Ann Dermatol Syphiligr 1962; 89: 361–71.
2. Trau H, Fisher BK, Schewach-Millet M. Multiple clear cell
acanthomas. Arch Dermatol 1980; 116: 433–4.
3. Bonnetblanc JM, Delrous JL, Catanzano G, Licout A,
Roux J. Multiple clear cell acanthoma. Arch Dermatol
1981; 117: 1.
4. Innocenzi D, Barduagni F, Cerio R, Wolter M. Dissemi-
nated eruptive clear cell acanthoma: a case report with
review of the literature. Clin Exp Dermatol 1994; 19:
249–53.
5. Wilde JL, Meffert JJ, McCollough ML. Polypoid clear cell
acanthoma of the scalp. Cutis 2001; 67: 149–51.
6. Burg G, Wursch TH, Fah J, Elsner P. Eruptive hamar-
tomatous clear-cell acanthomas. Dermatology 1994; 189:
437–9.
7. Blum A, Metzler G, Bauer J, Rassner G, Garbe C. The
dermatoscopic pattern of clear cell acanthoma resembles
psoriasis vulgaris. Dermatology 2001; 203: 50–2.
8. Bugatti L, Filosa G, Broganelli P, Tomasini C. Psoriasis-like
dermoscopic pattern of clear cell acanthoma. J Eur Acad
Dermatol Venereol 2003; 17: 452–5.
9. Zalaudek I, Hofmann-Wellenhof R, Argenziano G. Der-
moscopy of clear-cell acanthoma differs from dermoscopy
of psoriasis. Dermatology 2003; 207: 428.
10. Lacarrubba F, de Pasquale R, Micali G. Videodermatos-
copy improves the clinical diagnostic accuracy of multiple
clear cell acanthoma. Eur J Dermatol 2003; 13: 596–8.

6. HPV infections
Pompeo Donofrio and Maria Grazia Francia
Human papillomaviruses (HPV) are DNA viruses that infect
basal epithelial (cutaneous or mucosal) cells. There is interna-
tional consensus that “high-risk” genotypes, including geno-
types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 and 66, can
lead to cervical cancer and are associated with other mucosal
anogenital and head and neck cancers.(1) Infections with other
genotypes, termed “low-risk,” can cause benign or low-grade
cervical tissue changes and genital warts (condylomata acumi-
nata), which are growths of cervix, vagina, vulva and anus in
women and penis, scrotum and anus in men.(1) Early HPV
infection may be accompanied by mild changes of the epithe-
lium that are detectable only using virological and/or cytological
techniques, allowing an early treatment. HPV genital infection
is considered to be the most prevalent sexually transmitted dis-
ease in the US and Europe, affecting 1–2 percent of the sexually
active population between 15 and 49 years of age.(1)
Genital HPV infection is primarily transmitted by genital
skin-to-skin contact, usually but not necessarily during sexual
intercourse. HPV infection can occur at any age and has been
reported in healthy young children.
Dermatoscopy of the genital region may be called as peno-
vulvoscopy. This technique allows the recognition of some
morphological patterns that can be observed in both physi-
ological or pathological conditions of the genital area. Digital
peno-vulvoscope allows enlargement of images with the use of
special algorithms, defined “digital filters” or curves of color,
in order to improve the visibility of the vascular pattern of
the genital area, not provided by the natural contrast present
in other cutaneous districts due to its notable vascularization.
(2) Particular optics provided polarized light, allowing to avoid
improper chromatic variations toward the red, typical of the
genital mucosa.
The vascular pattern that may be observed in external ano-
genital warts has a dotted aspect that can be defined as “mosaic
like” (Figure 6.39). This pattern in progress of HPV infec-
tion is probably due to the local production of nitric oxide
from the papillomaviruses, with consequent vasodilatation of
the capillary handles. Such pattern, which may be observed
at X10–X40 magnification (Figure 6.40), is constituted by
short capillary handles perpendicular to the cutaneous sur-
face (Figure 6.41) that dermoscopically appear as sting red in
color and elegantly distributed.(2) The mosaic-like vascular
pattern may be frequently observed in the apparently unaf-
fected perilesional area (Figure 6.42), where, in the following
weeks, the onset of new lesions may be observed (subclinical
infection).(3)
Figure 6.39 Anogenital warts: The vascular pattern that may
observed assumes a punctiform aspect that can be defined as
“mosaic like” in appearance (X20).
Figure 6.40 Anogenital warts: punctiform vascular pattern at
X40 magnification (X20).
Differential Diagnosis
Pearly Papules
In the male patients, the pearly papules located in the glans
crown represent a frequent, but not pathological, condition.
(4) They present at X20 magnification a characteristic vascu-
lar pattern: The handle that serves every single papilla origi-
nates from the base, reaches the apex of the papilla, and then
refolds again toward the base, showing a hairpin-like appear-
ance (Figure 6.43).

donofrioandfrancia
Fordyce spots
These physiological formations may commonly be observed
on the skin of the penis and on the prepuce and are consid-
ered isolated sebaceous glands not connected to follicles. In
women, they are frequently seen on the labia minora. Clinically
Figure 6.41 The dotted pattern is constituted by short capillary
handles perpendicular to the cutaneous surface, which dermo-
scopically appear sting red in color and elegantly distributed
(X20).
Figure 6.42 Anogenital warts: the vascular “mosaic-like” pat-
tern is frequently observed also in the perilesional areas (X40).
Figure 6.43 Vascular hairpin pattern in pearly papules (X20).
they appear as yellowish reliefs of the diameter of 1–2 mm.
At peno-vulvoscopy observation, they show a characteristic,
vascular, “garland-like” appearance, whose “bows” seemed
to wind the yellowish lobules of the spots without crossing
them. In every case, these ectopic glands do not require any
treatment.
references
1. Ljubojevic´ S, Lipozencic´ J, Grgec DL et al. Human papil-
loma virus associated with genital infection. Coll Antropol
2008; 32(3): 989–97.
2. Micheletti L, Bogliatto F, Lynch PJ. Vulvoscopy: review of a
diagnostic approach requiring clarification. J Reprod Med
2008; 53(3): 179–82.
3. Bleeker MC, Hogewoning CJ, Voorhorst FJ et al. HPV-
associated flat penile lesions in men of a non-STD hospital
population: less frequent and smaller in size than in male
sexual partners of women with CIN. Int J Cancer 2005;
113(1): 36–41.
4. Hogewoning CJ, Bleeker MC, van den Brule AJ et al. Pearly
penile papules: still no reason for uneasiness. J Am Acad
Dermatol 2003; 49(1): 50–4.

6.4 Venular malformations (port wine stain type)
Francisco Vázquez-López
The value of dermoscopy for further evaluating venular malfor-
mations (VM) has been proposed.(1) Venular malformations
(or capillary vascular malformations) are congenital, low-flow,
vascular abnormalities of the dermal capillaries. VM affect
0.3%–0,5% of newborns with equal prevalence in male and
female patients. They may have a genetic basis, tend to be pres-
ent at birth, and grow with age. VM are initially flat and smooth
(macular) but nodules may develop with time. The color varies
from pink, red, to deep purple. VM may be part of syndromes
such as Sturge-Weber and Klippel-Trenaunay. Very rarely, VM
may present late onset in adolescents and adults, usually caused
by trauma. VM are characterized by ectatic vessels with flat-
tened endothelium, most of them situated in the papillary der-
mis and upper part of the reticular dermis, but may be located
deeper. The origin of VM is unclear, possibly being a result of
vascular channel developmental defects or segmental deficiency
of autonomic inervation of postcapillary venules.(2, 3)
VM are being classified according to their color and loca-
tion. In addition, the recent introduction of noninvasive image
techniques such as dermoscopy or videodermoscopy has allowed
the analysis of the capillary composition, that is, the type of
the capillary involved (4–8) (Figures 6.44–6.57), which may
be related to prognosis. By means of these devices, a better
understanding of the morphology of the vessels involved can
be obtained in daily practice, and rapidly, without the risk of
injury to the patient and without additional cost, revealing
significant vascular structures hidden in the standard visual
inspection. By means of dermoscopy, the vessels are visualized
Figure 6.44 Clinical view of a flat, partially treated, long-stand-
ing venular malformation (VM) of the forehead.
Figure 6.45 Dermoscopy of this VM reveals a superficial pattern of
VM, showing scattered type 1 ectatic vessels (red, rounded vessels)
with a variable size (original magnification: X10). This pattern
has been related to the superficial capillary loops of the papillae.
Round vessels may be pinpointed or globular according to their
size. Largest structures are similar to “red lagoons”.
Figure 6.46 Dermoscopy of VM showing type 1, round capillar-
ies in greater number. The contrast with the surrounding normal
skin is well evident. Some authors describe this pattern as a better
response to laser therapy. The main prognostic factors are the depth
and diameter of capillaries of VM (original magnification: X10).
because of the red blood cells filling and passing through them.
Therefore, it is important to avoid excessive pressure on the
lesion when performing this procedure, which causes occlusion
6
vzquez-lpez
Figure 6.47 Dermoscopy of VM showing numerous type 1
round vessels, disclosing a variable size (dotted, globular, and
similar to lagoons) (original magnification: X10).
Figure 6.48 Clinical view of a VM located on the thigh.
Figure 6.49 Dermoscopy of the former lesion reveals a type 2 vas-
cular pattern, devoid of round type 1 vessels. Tortuous, thin, linear
vessels configured in an irregular network are demonstrated. Type 2
linear vessels are thought to correspond to the subepidermal, hori-
zontal, vascular plexus of the dermis (original magnification: X10).
Figure 6.50 Dermoscopy of the border of same lesion (higher
degree of magnification), where the contrast between VM vessels
and the surrounding normal skin can be better appreciated. Type
1 round vessels are not seen.
and lack of visualization of the vessels if nonpolarized dermos-
copy is applied or when taking dermoscopic photographs with
skin contact.
Several authors (1, 4, 7) have described two types of ves-
sels in VM with videodermoscopy: type 1 (superficial papil-
lary vessels) and type 2 (deeper subpapillary vessels). Mixed
and undefined vascular patterns can also be observed. Digital
videodermoscopy allows a higher magnification of vessels
involved and the ability to record and compare the digital
images, but similar structures can also be revealed with stere-
omicroscope (4) and pocket dermoscope.(6) Type I vessels are
seen as red and sharp structures having a round to oval shape
and a variable size (termed as dotted, pinpointed, or globu-
lar, according to their size) (Figures 6.44–6.47). They have
been correlated to ectatic capillary loops of the papillae.(5)
In contrast, type 2 subpapillary vessels are seen as red, linear
structures, showing a variable tortuosity, thickness, and sharp-
ness and forming irregular networks (Figures 6.48–6.56). Type
2 linear vessels have been correlated to the horizontal subepi-
dermal vascular plexus.(5) In addition a gray-whitish veil has
also been reported related to the deeper vessels of the lower
reticular dermis.(4) According to videodermoscopy, VM have
been predominantly classified into type 1 (superficial) or type
2 (deep) patterns (Figures 6.44–6.50). In addition, mixed and
undefined patterns (5, 7) can also be observed (Figures 6.51–
6.58). Nevertheless, a clear correlation between dermoscopic

venularmalformations
Figure 6.51 Clinical view of a VM located on the leg.
Figure 6.52 Dermoscopy of this lesion revealed not only a pre-
dominantly type 2 vascular pattern (linear vessels) but also
scattered, well-defined, dotted, type 1 vessels (X10).
Figure 6.53 Dermoscopy of the same lesion, with a higher degree
of magnification after applying digital zoom to the attached
camera. Round, dotted vessels are easily demonstrated in con-
junction to linear vessels.
and histological observations has not been found by some
authors.(4) A correlation between these patterns and anatom-
ical location has been reported. VM located in the dermatome
V3, neck, and trunk showed mainly a type 1 pattern, whereas
lesions located on dermatome V2 and extremities showed
mainly a type 2 or a mixed pattern.(5) Round vessels, either
as an isolated finding or in a mixed pattern, have been found
in most VM in some studies.(4) Round vessels of VM may
appear quite small and as tiny dots (especially in children)
or large, globular structures. The largest globules, previously
described as “red lagoons,” are characteristic of hemangiomas.
Lagoons or lacunae appear small, deeply red in color, sharply
demarcated, varying in size, as oval to round structures and
appear either as tightly clustered or as loosely scattered. They
may or may not be located within round- to oval-shaped red
patches. Lagoons of hemangiomas are secondary to both pro-
liferation and ectasia of the vessels involved, whereas round
vessels of vascular malformations represent only a vascular
dilatation devoid of proliferation (Figures 6.59–6.64).
Dermoscopy offers, therefore, new clinical insights into
VM. Interestingly, it has been proposed that these findings
may have a prognostic significance.(1, 4, 5) The current stan-
dard treatment of VM is the pulsed-dye laser, although a com-
plete lightening of the lesion is rare. Dermoscopic findings
in VM may help to predict the outcome of the therapy. The
response of VM to laser treatment is believed to be dependent
on several factors, which may be related to partial damage
of some vessels, persistence of lesions, or neovascularization
after therapy.
1. Therapy of VM and clinical data (color, location, size of
VM, age of patients).(9–11)
- The color of VM (pink, red, purple) has been found
to be predictive of response to treatment, with purple
and red lesions tending to respond better than the
pink ones.
- Location: Certain sites for VM respond better to
laser treatment. Lesions on the distal extremities and
medial face tend to do less well than lesions on the
lateral face or trunk. As regards the dermatomal dis-
tribution of VM, those involving V2 respond less well
than those located on V1 and V3.
2. Therapy of VM and histological data: depth and diam-
eter of the capillaries of VM.(12, 13)
A number of studies have established the importance of capil-
lary depth and diameter in determining the response of VM to
laser treatments. It seems that the response of an untreated VM
to laser treatment will be dependent on the range of depths and

vzquez-lpez
Figure 6.55 Dermoscopy (low magnification) revealed herein a
mixed pattern with linear, tortuous, short, and arboriform vessels,
and also round, globular vessels (original magnification: X10).
Figure 6.56 Dermoscopy of the same lesion with a higher
degree of magnification. Tortuous linear vessels and globular
vessels are demonstrated herein, despite the previous therapy.
Figure 6.57 Long-standing VM of the face, partially masked by
a cosmetic camouflage, and partially treated with electrodes-
sication. At this phase, lesions may become darker, violaceous,
thicker, and may develop blebs, in contrast with the patient of
the Figure 6.44.
diameters of capillaries comprising the lesion. Deeper vessels
with a small diameter are those responding less well.
3. Therapy of VM and dermoscopic data.
Dermoscopic data provide information related to the mor-
phology of the vessels involved, which has been related to their
depth. The presence of type 2 vessels (1, 5, 7) and gray-whitish
veil (4) has been related to deeper vessels and with less response
to the treatment; meanwhile type 1 round vessels were related
to superficial vessels, and hence, a better response to therapy.
A clear correlation between dermoscopic and histological
observations has not been found by all authors (4), who found
the presence of a gray-whitish veil hiding the inferior structures
as the most significant feature related to prognosis. Recently,
a videomicroscope that is capable of determining morphol-
ogy, depth, and diameter of capillaries (depth-measuring
videomicroscope, DMV) has been developed and applied for
evaluating VM (8). This tool is similar to a traditional video
microscope, but it facilitates better visualization of vessel
depth and diameter in the dermis. This device allows indi-
vidual capillaries to be imaged and their depth and diameter
to be calculated.
Figure 6.54 Clinical view of a VM located on the cheek. The
lesion has been previously treated with laser. Blanched areas are
well evident.

venularmalformations
Figure 6.59 Clinical image showing a patient with a prominent
midline “salmon patch” VM of the neck, which are classified
separately from lateral Port Wine stains.
Figure 6.60 Dermoscopy of this lesion revealed a homoge-
neous, type 1, globular vascular patterns, devoid of linear ves-
sels (original magnification: X10). Perifollicular areas seem to
be uninvolved. Perifollicular white halos are an unspecific and
peculiar dermoscopic finding, which may be observed in both
melanocytic and nonmelanocytic skin lesions.(15)
Figure 6.61 Dermoscopy of an acquired hemangioma. Hema-
ngiomas are characterized by lagoons or lacunae, which are red
to blue-red or blue-black to maroon in color, appear round to
oval in shape, and as sharp structures, either tightly clustered
or loosely scattered throughout the lesion (original magnifica-
tion: X10). Lagoons are a result of the proliferation of dilated
venules, whereas VM present only vascular ectasia.
According to the results obtained with this device (8) and also
according to the previous histological results (12, 13), it seems
that the small, deeply located vessels are more resistant to the
laser treatment and tend to remain uncoagulated. The outcome
of VM therapy will most likely depend on the depth and size of
the deeper vessels. Deep vessels may be revealed only after clear-
ing the superficially located type 1 capillaries by four or five dye
laser treatments, which previously obscured them.(8)
As regards correlations between these different clinical, his-
tological, and dermoscopic parameters of VM, a controversy
exists between different studies; however, only a few authors
corroborate the correlations between these parameters, (5)
Figure 6.58 Dermoscopy of the former lesion revealed an unde-
fined pattern, with a deep purplish background; red lagoons;
and a delicate, whitish network (original magnification: X10).
while most others are of the impression that such correlations
might not be possible.(8, 9)
4. Other factors (8, 9, 14)
It must be taken into account that other factors may play a role
in the response of VM to laser treatment, in addition to capillary

vzquez-lpez
depth and diameter or the dermoscopic vessel type, such as the
flow through these capillaries, and the amount of competing chro-
mophores within the skin, such as melanin or the thickness of the
skin.
In sum, dermoscopy and videodermoscopy serve to further
evaluate VM on a non-invasive basis. In conjunction with the
clinical examination, this device improves the understanding
of the morphology of the vessels involved, which may have a
prognostic significance. It can be applied in most settings,
without additional cost for demonstrating significant vascular
structures that are hidden in the standard visual inspection;
for some authors, these vascular structures (round type 1 and
Figure 6.63 Clinical view of a patient with a mixed vascular
malformation on the arm with prominent, deep component,
which is different from venular malformations.
Figure 6.64 Dermoscopy of this lesion reveals tightly clustered,
red, globular vessels and blue lagoons (original magnification:
X10). These structures are related to the vessel ectasia and not
to vascular proliferation.
linear type 2 vessels), are related to the depth of the vessels
involved.(1,5,7)
In addition, videodermoscopy is also helpful in deciding
more accurately when to end the treatment because it objec-
tively shows when a VM becomes resistant to further treat-
ments (persistence of small and deep vessels). It is also helpful
for demonstrating this to patients and their parents by means
of an objective image.
Moreover, it has been speculated that videomicroscopy
may facilitate in the future the development of newer pulsed-
dye lasers to treat VM more efficiently, as pulse duration and
wavelength could be matched to measured vessel diameter and
depth, respectively.
REFERENCES
1. Motley RJ, Lanigan SW, Katugampola GA. Videomicros-
copy predicts outcome in treatment of port-wine stains.
Arch Dermatol 1997; 133: 921–2.
2. Meghan FS, Glick SA, Hirsch RJ. Laser treatment of pedi-
atric vascular lesions: Port wine stains and hemangiomas.
J Am Acad Dermatol 2008; 58: 261–85.
3. Garzon MC, Huang JT, Enjolras O, Frieden IJ. Vascular
malformations: Part I. J Am Acad Dermatol 2007; 56:
353–70.
4. Procaccini EM, Argenziano G, Staibano S, Ferrara G,
Monfrecola G. Epiluminescence microscopy for port-wine
stains: pretreatment evaluation. Dermatology 2001; 203:
329–32.
5. Eubanks LE, McBurney EI. Videomicroscopy of port-wine
stains: correlation of location and depth of lesion. J Am
Acad Dermatol 2003; 48: 984–5.
Figure 6.62 Dermoscopy of acquired angioma serpiginosum
revealing multiple, scattered, sharp lagoons (original magnifi-
cation: X10).

venularmalformations
6. Vázquez-López F, Manjón-Haces JA, Vázquez-López AC,
Pérez-Oliva N. The hand-held dermatoscope improves
the clinical evaluation of port-wine stains. J Am Acad Der-
matol 2003; 48: 984–5.
7. Sevila A, Nagore E, Botella-Estrada R et al. Videomicros-
copy of venular malformations (port-wine stain type):
prediction of response to pulsed dye laser. Pediatr Derma-
tol 2004; 21: 589–96.
8. Sivarajan V, Mackay IR The depth measuring videomicro-
scope (DMV): a non-invasive tool for the assessment of
capillary vascular malformations. Lasers Surg Med 2004;
34: 193–7.
9. Sivarajan V, MacKay IR. The relationship between loca-
tion, color, and vessel structure within capillary vascular
malformations. Ann Plast Surg 2004; 53(4): 378–81.
10. Renfro L, Geronemus RG. Anatomical differences of port-
wine stains in response to treatment with the pulsed dye
laser. Arch Dermatol 1993; 129(2): 182–8.
11. Nguyen CM, Yohn JJ, Huff C et al. Facial port wine stains
in childhood: prediction of the rate of improvement as
a function of the age of the patient, size and location of
the port wine stain and the number of treatments with
the pulsed dye (585 nm) laser. Br J Dermatol 1998; 138:
821–5.
12. Onizuka K, Tsuneda K, Shibata Y, Ito M, Sekine I. Efficacy
of flashlamp-pumped pulsed dye laser therapy for port
wine stains: clinical assessment and histopathological
characteristics. Br J Plast Surg 1995; 48: 271–9.
13. Fiskerstrand EJ, Svaasand LO, Kopstad G et al. Laser treat-
ment of port wine stains: therapeutic outcome in relation
to morphological parameters. Br J Dermatol 1996; 134:
1039–43.
14. Nagore E, Requena C, Sevila A et al. Thickness of healthy
and affected skin of children with port wine stains: poten-
tial repercussions on response to pulsed dye laser treat-
ment. Dermatol Surg 2004; 30: 1457–61.
15. Vázquez-López F, Más-Vidal A, Sánchez-Martín J, Pérez-
Oliva N, Argenziano G. Perifollicular white halo: a dermo-
scopic subpattern of melanocytic and non melanocytic
skin lesions. Arch Dermatol (in press).

6.5 Bowen’s disease
Leonardo Bugatti, Giorgio Filosa, and Alessandra Filosa
Bowen’s disease (BD) is an intraepidermal (in situ) squamous-
cell carcinoma clinically presenting as a slowly enlarging
sharply demarcated erythematous plaque with a crusting and
scaling surface (Figure 6.65a). Resemblance with psoriasis or
dermatitis classically leads to a delay in the correct diagnosis.
It predominantly affects older female patients, and in about
three-quarters of the cases, it is located on the lower limbs.
Lesions are usually solitary but may be multiple in 10%–20% of
patients. Unusual sites or variants include pigmented, subun-
gual/periungual, palmar, genital, perineal, and verrucous BD.
Most studies suggest a risk of tumoral progression to be about
3%–5% for classic BD.
Reported relevant etiological factors are irradiation (solar,
photochemiotherapy, radiotherapy), long-term arsenic expo-
sure, immunosuppression, and oncogenic HPV (mainly 16, 18
subtypes). Development of ulceration is usually a sign of invasive
carcinoma. Histopathologically, BD is characterized by acanthotic
epidermis with elongation and thickening of rete ridges, with
convoluted and dilated papillary vessels. Throughout the epider-
mis, the cells lie in complete disorder, resulting in a “windblown
appearance.” Many cells are highly atypical, showing large hyper-
chromatic nuclei with conspicuous nucleoli and abundant cyto-
plasm. Another common feature is the presence of occasional,
individually atypical, keratinized cells (Figure 6.65b). The border
between epidermis and dermis appears sharp and the basement
membrane remains intact. The upper dermis shows a moderate
amount of chronic inflammatory infiltrate, which sometimes
adopts a lichenoid distribution.
Several dermoscopic features of BD have been described
(Table 6.1). The most peculiar and common findings for this
tumor seem to be multicomponent global pattern (90%–
100%), atypical vascular structures (86.6%–100%) and scaly
surface (64.2–90%).(1, 2)
The presence of vascular structures on the surface of the
tumor is consisting mainly of dotted vessels (50%) irregularly
distributed in clusters, but linear, arborizing, bushy, and hairpin-
like vessels can also be found (Figure 6.66, 6.67). Dotted vessels
histopathologically correlate with dilated tortuous capillaries of
middle reticular dermis progressing to the top of the papillae.
Higher magnification can disclose a distinctive type of vascular
structures, namely, “glomerular vessels,” characterized by highly
convoluted tortuous capillaries mimicking the glomerular appa-
ratus of the kidney (Figure 6.68). Some authors prefer to keep
dotted vessels as distinct from glomerular vessels, as the latter are
usually larger in size, often looped, and regularly arranged in a
patchy distribution (Figure 6.69a, 6.69b).(2, 3) Glomerular mor-
phology has also been described for severe venous stasis.(4)
Table 6.1 Dermoscopic Features of Bowen’s Disease.
• Multicomponent global pattern
• Atypical vascular structures (dotted/glomerular)
• Scaly surface
• Pseudonetwork
• Irregular, structureless, diffuse pigmentation
• Patchy distribution of small, brown globules
• Focal/multifocal hypopigmentation
• Blue-whitish veil
• Peppering/white areas
• Hemorrhages
Figure 6.65 (a) Sharply demarcated erythemato-desquamative plaque. (b) Epidermal acanthosis with a number of highly atypical
keratinocytes often with features of dyskeratosis (ematoxylin-eosin, at x100 magnification).
(a) (b)

bowen

sdisease
A variety of peculiar vascular structures can be recognized
under dermoscopic examination, and though not specific, they
have a diagnostic significance.(5) Atypical (or polymorphous)
vascular pattern has been described as red structures irregularly
distributed outside areas of regression in melanocytic lesions,
showing three features: (i) linear, irregular vessels; (ii) dotted or
pinpoint, regularly shaped vessels; and( iii) milky red globules.
(6, 7) Kreusch has given a thorough morphological illustration
of the vascular component of skin tumors and has suggested
an algorithm for the diagnosis based on dermoscopic vascular
patterns.(8) The recognition of distinctive vascular structures
enhances the diagnostic range of dermoscopy, especially when
the classic pigmented structures are lacking.(9)
It can be speculated that vascular morphology is consis-
tent with a process of tumoral neoangiogenesis in BD. Video-
capillaroscopic studies might better describe the vascular
structures involved in BD and other cutaneous neoplasias.
Figure 6.66 Brownish pseudonetwork, dotted and linear vascu-
lar structures (original magnification, x10).
Figure 6.68 Multicomponent global pattern, irregular diffuse
structureless pigmentation, dotted (glomerular) vascular pat-
tern, and scaly surface (original magnification, x10).
Figure 6.67 Dotted vascular structures, scaly surface, hemor-
rhages (original magnification, x10).
Figure 6.69 (a) Dotted vascular structures and multifocal
hypo pigmentation (original magnification, x10). (b) Magnified
detail of Figure 6.69a. Tortuous capillaries with glomerular,
hairpin, bushy morphology.
(a)
(b)

bugatti,filosa,andfilosa
Figure 6.70 Dotted vascular structures, scaly surface, hemor-
rhages (original magnification, x10).
Figure 6.71 Scaly surface, irregular diffuse pigmentation, and
patchy distribution of globules (original magnification, x10).
Figure 6.72 Pseudonetwork and irregular, structureless diffuse
pigmentation (original magnification, x10).
dermopathologic examination. The false atypical pigmented
network may be created by the thickening of the rete ridges due
to deposits of melanin within the tumoral cells in the dermal
papillae.(12)
Dotted vessels can commonly be found in melanocytic
tumors, sometimes of seborrheic keratoses and other skin dis-
eases, such as psoriasis, warts, clear-cell acanthoma, and der-
matofibroma. In most cases of psoriasis, red-dotted globules are
homogenously distributed over the entire surface, whereas dotted
vessels in warts are distinctive for a pale halo of keratinization.
(13) Dotted vessels in clear-cell acanthoma are often arranged
uniformly like pearls in a line with a psoriasiform appearance.
(14) In dermatofibromas, dotted vessels may be either centrally
located or diffuse throughout the lesion, together with other
accompanying features, such as globular structures, scar-
like white patch, and peripheral fine network.(15) Dotted
vessels are reported to be a frequent finding in amelanotic
melanoma, especially in early thin lesions. In this case, the
concurrence of a white to pinkish veil and a small amount
of residual, light-brown pigmentation may contribute to the
diagnosis.(16–18)
Dermoscopy has also been proposed as a valuable tool for mon-
itoring of nonsurgical treatment of BD, where the disappearance
of vascular structures may indicate adequate treatment.(12)
In conclusion, multicomponent global pattern, vascular
component (dotted vessels or “glomerular” subtype morphol-
ogy) and scaly surface represent valuable dermoscopic clues
to the diagnosis of BD. However, further studies are needed to
assess the specificity and sensitivity of these dermoscopical cri-
teria in differentiating BD from other pigmented and nonpig-
mented skin tumors.(1, 2, 19)
references
1. Bugatti L, Filosa G, De Angelis R. Dermoscopic observa-
tion of Bowen’s disease. J Eur Acad Dermatol Venereol
2004; 18: 572–4.
The degree of scaling may vary according to different fac-
tors, such as body location, environmental conditions, topical
pretreatment, and type of lubricant used to minimize surface
reflection. The greater thickness of the corneal layer in acral
skin gives rise to heavier scaling. (Figure 6.70) (10)
BD is generally scarcely pigmented, although pigmented
structures can be detected, especially in the unusual form of
heavily pigmented BD, such as the presence of pseudonet-
work (10–35.7%), irregular structureless diffuse pigmentation
(64.2–80%), and small brown globules (64.2–90%).(1, 2) The
pigmented globules are usually smaller than those associated
with melanocytic lesions and follow a regular patchy distribu-
tion over the lesion (Figure 6.71). In heavily pigmented BD
pseudonetwork or reticular pigmentation, sometimes simulat-
ing atypical network, can be the main dermoscopic criterion
lacking other, well-expressed, standard criteria (Figure 6.72).
(11) This should bring to the prompt removal of the lesion for
5
bowen

sdisease
2. Zalaudek I, G.Argenziano, B.Leinweber et al. Der-
moscopy of Bowen’s disease. Br J Dermatol 2004; 150:
1112–6.
3. Zalaudek I, Di Stefani A, Argenziano G. The specific der-
moscopic criteria of Bowen’s disease JEADV 2006; 20:
341–62.
4. Vaquez-Lopez F, Kreusch J, Marghoob AA. Dermoscopic
semiology: further insights into vascular features by screen-
ing a large spectrum of nontumoral skin lesions. Br J Derma-
tol 2004; 150: 226–31.
5. Kreusch J, Koch F. Characterization of vascular patterns in
skin tumors by incident light microscopy. Hautartz 1996;
47: 264–72.
6. Stolz W, Landthaler M, Falco OB et al. Color Atlas of
Dermatoscopy 2nd ed. Oxford: Blackwell Publishing;
2002.
7. Argenziano G, Fabbroncini G, Carli P et al. Clinical and
dermoscopic criteria for the preoperative evaluation of
cutaneous melanoma thickness. J Am Acad Dermatol
1999; 40: 61–8.
8. Kreusch JF. Vascular patterns in skin tumors. Clin Derma-
tol 2002; 20: 248–54.
9. Argenziano G, Zalaudek I, Corona R et al. Vascular struc-
tures in skin tumors. A dermoscopy study. Arch Dermatol
2004; 140: 1485–9.
10. Bugatti L, Filosa G, De Angelis R. The specific dermo-
scopical criteria of Bowen’s disease. J Eur Acad Dermatol
Venereol 2007; 21: 700–1.
11. Stante M, De Giorgi V, Massi D et al. Pigmented Bowen’s
disease mimicking cutaneous melanoma: clinical and der-
moscopic aspects. Dermatol Surg 2004; 30: 541–4.
12. Hu C, Chiu H, CHEN G et al. Dermoscopy as a diagnostic
and follow-up tool for pigmented Bowen’s disease on acral
region. Dermatol Surg 2008; 34: 1248–53.
13. Vasquez-Lopez F, Kreuscj J, Marghoob AA. Dermoscopic
semiology: further insights into vascular features by
screening a large spectrum of nontumoral skin lesions Br
J Dermatol 2004; 150: 226–31.
14. Bugatti L, Filosa G, Broganelli P, Tomasini C. Psoriasis-like
dermoscopic pattern of clear cell acanthoma. J Eur Acad
Dermatol Venereol 2003; 17: 452–5.
15. Zaballos P, Puig S, Llambrich A, Malvehy J. Dermoscopy
of dermatofibromas: a prospective morphological study
of 412 cases. Arch Dermatol 2008; 144: 75–83.
16. Pizzichetta MA, Talamini R, Stanganelli I et al. Amelanotic/
hypomelanotic melanoma: clinical and dermoscopic fea-
tures. Br J Dermatol 2004; 150: 1117–24.
17. Bono A, Maurichi A, Moglia D et al. Clinical and derma-
toscopic diagnosis of early amelanotic melanoma. Mela-
noma Res 2001; 11: 491–4.
18. Zalaudek I, Argenziano G, Kerl H et al. Amelanotic/
Hypomelanotic melanoma––is dermatoscopy useful for
diagnosis? J Dtsch Dermatol Ges 2003; 1: 369–73.
19. J. Hernández-Gil J, Fernández-Pugnaire MA, Serrano-
Falcón C et al. Clinical and dermoscopic features of pigmented
Bowen disease. Actas Dermosifiliogr 2008; 99: 419–27.

. Pyogenic granuloma
Pedro Zaballos Diego
PYOGENIC GRANULOMA
Pyogenic granuloma is a relatively common, benign, vascular lesion
of the skin and mucous membranes whose exact cause is unknown.
This misnamed entity is neither infectious nor granulomatous and,
therefore, some authors prefer the term lobular capillary heman-
gioma to describe these lesions because of the histologic findings.
Pyogenic granuloma is relatively common and it is especially fre-
quent in children and young adults.(1–3) It represents 0.5% of all
skin nodules in children.(4) The typical lesion appears as a pap-
ule or polyp with a glistening surface, which bleeds easily. Sites of
predilection include the gingiva, lips, mucosa of the nose, face, and
extremities (mainly the fingers). Pyogenic granuloma with satellito-
sis, a subcutaneous subtype, a intravenous subtype, and a dissemi-
nated variant have been described in literature. The gingival lesion
developed during pregnancy termed epulis gravidorum is consid-
ered a variant of this tumor. A few reports of lesions developing in
a preexisting nevus flammeus or spider angioma exist. The exact
etiopathogenesis of this condition is unknown. It has been thought
to be a reactive, hyperproliferative, vascular response to a variety of
stimuli, such as infective organisms, penetrating injury, hormonal
factors, and retinoid therapy. Pyogenic granulomas usually develop
at the site of a preexisting injury, where they evolve rapidly over a
period of weeks to a maximun size and then shrink in a fibroma that
can regress within a few months. The histopathologic findings in all
variants of pyogenic granuloma are similar. Early lesions resemble
granulation tissue, that is, numerous capillaries and venules with
plump endothelial cells arrayed radially toward the skin surface
(usually eroded, ulcerated, and covered with scabs) amidst an
edematous stroma containing a mixed inflammatory infiltrate. The
matured polypoid lesion exhibits a fibromyxoid stroma separating
the lesion into a lobular pattern. Each lobule is composed of aggre-
gations of capillaries and venules with plump endothelial cells. In
this stage, reepithelialization of the surface and a peripheral col-
larette of hyperplastic adnexal epithelium may be noted, with less
inflammatory infiltrates present and disappearance of edema of the
stroma. Older lesions tend to organize and partly fibrose and, in
time, pyogenic granuloma resolves into fibroma.(1–4)
Although the clinical diagnosis of pyogenic granuloma is rather
easy, in some instances the differentiation from other benign and
malignant tumors, such as amelanotic melanoma, is difficult to
determine. In 38 % of one case series (5), the clinical diagnosis of
pyogenic granuloma proved to be wrong. Misdiagnosis documented
in medical literature include keratoacanthoma, squamous-cell car-
cinoma, basal-cell carcinoma, inflamed seborrhoeic keratosis, com-
mon warts, melanocytic nevus, Spitz nevus, amelanotic melanoma,
metastasic carcinoma, Kaposi´s Sarcoma, and true hemangiomas
among others.(1–6)
Dermoscopy may be helpful in the recognition of pyogenic
granulomas.(7, 8) The results of one study where 13 pyogenic
granulomas were collected and evaluated reveal that a reddish
homogeneous area surrounded by a white collarette is the most
frequent dermoscopic finding in pyogenic granulomas (Figures
6.73–6.75 and 6.77).(7) This pattern was identified in 84.6% of
Figure 6.73 The characteristic dermoscopic pattern of pyogenic
granuloma is made up of a reddish homogeneous area surrounded
by a white collarette. We can also observe superficial scales and
“white rail” bands (instead of lines) that intersect the lesion (X10).
Figure 6.74 Another characteristic pyogenic granuloma with a
reddish homogeneous area surrounded by a white collarette.
We can also see scales and ulceration (X10).

pyogenicgranuloma
Figure 6.75 Figure shows the characteristic dermoscopic pat-
tern in a pyogenic granuloma located on a upper lip (X10).
pyogenic granulomas of the study. Other dermoscopic struc-
tures that were found were “white rail” lines (Figures 6.73 and
6.76) that intersect the lesion in 30.7% of cases and ulceration in
46.1% of pyogenic granulomas (Figures 6.74 and 6.76). The his-
topathologic correlation of the reddish homogeneous area may
be attributed to the presence of numerous small capillaries or
proliferating vessels that are set in a myxoid stroma of pyogenic
granulomas. The white collarette corresponds to the hyper-
plastic adnexal epithelium that partially or totally embraces
the lesion at the periphery of most pyogenic granulomas. The
white lines similar to a double rail that intersect the lesion in
some pyogenic granulomas may correspond histologically
to the fibrous septa that surround the capillary tufts or lob-
ules in more advanced cases. Finally, pyogenic granulomas
are frequently eroded and crusted and may bleed very easily.
This feature may explain the hemorrhagic crusts or ulceration
that we can observe in some cases of pyogenic granulomas.
Occasionally, we can observe different vascular structures like
Figure 6.76 Pyogenic granuloma that shows a reddish homoge-
neous area and “white rail” lines that intersect the lesion. This is
a pediculated lesion, and, in these cases, it is difficult to see the
white collarette on polarized contact dermoscopy. We can also
see a scale in the left part of the lesion and an area of ulceration
in the upper part (X10).
Figure 6.78 An atypical dermoscopic image of pyogenic granu-
loma with a central area of ulceration and polymorphous/atyp-
ical vessels (linear irregular, hairpin, and glomerular vessels).
The lesion should be excised in order not to misdiagnose an
amelanotic melanoma (X10).
Figure 6.77 Figure shows the characteristic pattern of pyogenic
granuloma (a reddish homogeneous area surrounded by a
white collarette), but there are several vascular structures. In
these cases, it is important to remove the lesions in order not to
misdiagnose an amelanotic melanoma (X10).

zaballos
dotted vessels, telangiectasias, glomerular vessels, hairpin ves-
sels, linear-irregular vessels, and polymorphous/atypical vessels
(Figures 6.77 and 6.78). In our opinion, all cases of pyogenic
granulomas with vascular structures should be excised in order
not to misdiagnose an amelanotic melanoma.
Dermoscopic differential diagnosis between pyogenic granuloma
and other vascular lesions, such as angiomas and angiokeratomas,
and other pigmented lesions, such as basal-cell carcinoma, Spitz
nevus, and amelanotic melanoma, should be considered.(7, 9)
Regarding other vascular lesions, the dermoscopic hallmark of
most hemangiomas is the presence of red lacunas, which are char-
acterized by well-demarcated, round to oval, red or reddish-blue
areas and correspond histopathologically to dilated, blood-filled
vessels in the papillary dermis. Lacunas commonly vary in size
and color within a given lesion and may be either tightly clustered
or loosely scattered throughout.(10) They are often located on a
background of a red, red-bluish, or red-whitish homogeneous
area. In a recent study, 6 dermoscopic structures were observed
in at least 50% of the solitary angiokeratomas (11): dark lacu-
nas (93.8%), whitish veil (90.6%), erythema (68.8%), peripheral
erythema (53.1%), red lacunas (53.1%), and hemorrhagic crusts
(53.1%). The structure “dark lacunas” is the most frequent dermo-
scopic finding in solitary angiokeratomas and represents the most
valuable criteria for correctly diagnosing this vascular tumor with
a sensitivity of 93.8% and a specificity of 99.1%.(11) “Dark lacu-
nas,” like red lacunas, also represent dilated vascular spaces in the
upper dermis and their dark violaceous, blue, or black color cor-
responds to vascular spaces that are partially or completely throm-
bosed. It is important to note that the pattern composed of “dark
lacunas plus whitish veil” was determined to be the most com-
mon pattern in solitary angiokeratomas. Another vascular tumor
whose dermoscopic image has been described in the literature is
targetoid hemosiderotic hemangioma.(12, 13) Although patients
usually describe cyclic changes and, therefore, the dermoscopic
appearance is changing, most cases show a pattern composed of a
central area with reddish or dark lacunas surrounded by a reddish,
violaceous, or brownish homogeneous pigmentation.
Nodular basal-cell carcinoma and amelanotic melanoma
may be also included in the differential diagnosis of a reddish
tumor. The dermoscopic criteria for basal-cell carcinoma (14)
include lack of features of a melanocytic lesion and the pres-
ence of at least one of the following criteria: large gray-blue
ovoid nests, multiple blue-gray globules, maple leaf–like areas,
spoke-wheel areas, arborizing telangiectasias, and ulceration.
When these tumors are ulcerated they may resemble pyo-
genic granulomas because ulceration has been also described
in 46.1% of pyogenic granulomas in one study.(7) However,
none of the other specific dermoscopic criteria of basal-cell
carcinoma has been described in pyogenic granulomas and the
peripheral white collarette is not a characteristic of basal-cell
carcinomas. Regarding amelanotic melanoma, in a recent study
(15), the most positive predictors of amelanotic and hypomel-
anotic melanoma were multiple blue-gray dots, irregularly
shaped depigmentation, brown dots or globules irregular in
size or distribution, 5 to 6 colors, predominant central vessels,
red-blue color, and peripheral, light-brown, structureless areas
of more than 10% of the area of the lesion. Although Menzies
et al. did not include any pyogenic granuloma in their study,
all these features were significant, positive predictors of mela-
noma, compared with benign melanocytic lesions and nonmel-
anocytic lesions of the study. As for vascular features, the most
predictive for melanoma were central vessels, hairpin vessels,
milky red–pink areas, more than 1 shade of pink, a combina-
tion of dotted and linear irregular vessels, and linear, irregular
vessels as the predominant vessel type. Milky red-pink areas
are defined as larger areas than globules of fuzzy or unfocused
milky-red color usually corresponding to an elevated part of
the lesion.(16) It is important to note that, in some pyogenic
granulomas, the “white rail” lines that intersect the lesion in
30.7% of cases (7) could divide the total reddish homogeneous
area in structures similar to milky red–pink areas. Moreover,
occasionally, we have found several vascular structures (dot-
ted vessels, telangiectasias, glomerular vessels, hairpin vessels,
linear-irregular vessels, and polymorphous/atypical vessels) in
some pyogenic granulomas. However, none of the 105 amel-
anotic and hypomelanotic melanomas of the study of Menzies
et al.(16) showed a peripheral white collarette. In our opinion,
according to this study, all cases of reddish tumor with charac-
teristic dermoscopic structures of pyogenic granulomas (a total
reddish homogeneous area surrounded by a white collarette),
including those with more than one shade of pink and/or vas-
cular structures (mostly having predominantly central vessels,
milky red pink areas not surrounded by white-rail lines and
Figure 6.79 Figure shows a dermoscopic image of an amelan-
otic melanoma previously diagnosed clinically as a pyogenic
granuloma. Under dermoscopy, we can observe polymorphous/
atypical vessels, irregularly shaped depigmentation (white lines
and structures), brown dots or globules irregular in size and
distribution, and light-brown, structureless areas of more than
10% of the area of the lesion (X10).

pyogenicgranuloma
polymorphous/atypical vessels), should be excised in order not
to misdiagnose an amelanotic melanoma (Figure 7.69).
REFERENCES
1. Mooney MA, Janninger CK. Pyogenic granuloma. Cutis
1995; 55: 133–6.
2. Pagliai KA, Cohen BA. Pyogenic granuloma in children.
Pediatric Dermatology 2004; 21: 10–3.
3. Requena L, Sangueza OP. Cutaneous vascular prolifera-
tion. Part II. Hyperplasias and benign neoplasms. J Am
Acad Dermatol 1997; 37: 887–919.
4. Grimalt R, Caputo R. Symmetric pyogenic granuloma.
J Am Acad Dermatol 1993; 29: 652.
5. Rowe L. Granuloma pyogenicum. AMA Arch Dermatol
1958; 78: 341–7.
6. Elmets CA, Ceilley RI. Amelanotic melanoma as a pyo-
genic granuloma. Cutis 1980; 25: 164–7.
7. Zaballos P, Llambrich A, Cuellar F, Puig S, Malvehy J. Der-
moscopic findings in pyogenic granuloma. Br J Dermatol
2006; 154: 1108–11.
8. Zaballos P, Salsench E, Puig S, Malvehy J. Dermoscopy of
pyogenic granulomas. Arch Dermatol 2007; 143: 824.
9. Wolf IH. Dermoscopic Diagnosis of Vascular lesions. Clin
Dermatol 2002; 20: 273–5.
10. Argenziano G, Soyer HP, Chimenti S et al. Dermos-
copy of pigmented skin lesions: results of a consensus
meeting via the Internet. J Am Acad Dermatol 2003; 48:
679–93.
11. Zaballos P, Daufí C, Puig S et al. Dermoscopy of solitary
angiokeratoma: a morphological study. Arch Dermatol
2007; 143: 318–25.
12. Sahin MT, Demir MA, Gunduz K, Ozturkcan S, Türel-
Ermertcan A. Targetoid haemosiderotic haemangioma:
dermoscopic monitoring of three cases and review of the
literatura. Clin Exp Dermatol 2005; 30: 672–6.
13. Morales-Callaghan AM, Martinez-Garcia G, Aragoneses-
Fraile H, Miranda-Romero A. Targetoid hemosiderotic
hemangioma: clinical and dermoscopical findings. J Eur
Acad Dermatol Venereol 2007; 21: 267–9.
14. Menzies SW, Westerhoff K, Rabinovitz H et al. Surface
microscopy of pigmented basal cell carcinoma. Arch Der-
matol 2000; 136: 1012–6.
15. Menzies SW, Kreusch J, Byth K et al. Dermoscopic evalu-
ation of amelanotic and hypomelanotic melanoma. Arch
Dermatol 2008; 144: 1120–7.
16. Argenziano G, Zalaudek I, Corona R et al. Vascular struc-
tures in skin tumors. A dermoscopy study. Arch Dermatol
2004; 140: 1485–9.

7.1 Lichen ruber planus
Francisco Vázquez-López
Lichen planus is a subacute or chronic dermatosis character-
ized by violaceous papules that may coalesce into plaques.
Postinflammatory hyperpigmentation may appear, being trou-
blesome for the patients if it is long standing. Histologically,
active papules of lichen planus show (a) hyperkeratosis, (b)
focal hypergranulosis, (c) irregular acanthosis, (d) damage to
the basal cell layer, and (e) band-like dermal infiltrate in close
approximation to the epidermis.(1)
The surface of lichen planus lesions shows clinically pathog-
nomonic white lines or dots in a variable configuration
(Wickham striae, WS), which recall those observed in the oral
mucosa. The histological correlate of WS is a compact orthok-
eratosis above the zones of wedge-shaped hypergranulosis and
acanthosis, centered around acrosyringia and acrotrichia.(1, 2)
Wickham striae cannot always be recognized in the standard
visual inspection.
They are rendered more evident by painting the lesions with
oil and by examining them with a magnifying lens. The use of
dermoscopy improves and facilitates this maneuver, allowing an
easier and rapid recognition of WS in clinical practice. Therefore,
dermoscopy improves the clinical diagnosis of lichen ruber
planus in patients with active lesions.(3–5) Dermoscopy also
serves for monitoring the evolution of LP lesions and for evalu-
ating the type of postinflammatory hyperpigmentation, which
may present a prognostic significance.(6) The usual precautions
must be taken in order to prevent nosocomial infections if con-
tact, nonpolarized dermoscopy is performed on eroded lesions.
By means of dermoscopy, the vessels are visualized because of the
red blood cells fulfilling and passing through them. Therefore, it
is also important to avoid excessive pressure on the lesion when
performing this procedure, which may cause blanching and lack
of visualization of the vessels if nonpolarized dermoscopy is
applied or when taking photographs with skin contact.
DERMOSCOPIC APPEARANCE AND EVOLUTION OF
THE LESIONS OF LICHEN PLANUS
1. Initial LP lesions (round, pink papules): Initial pap-
ules of LP show round, small Wickham Striae (WS)
with a central yellow-brown dot. WS are visualized as
pearly whitish, opaque structures. WS can be observed
with both polarized and nonpolarized dermoscopes.
Polarized dermoscopes allows for better recognition
of deeper structures (vasculature, dermal pigment,
fibrosis) but for worse recognition of the superficial
layers of the epidermis. Structures such as the milia
cysts of seborrheic keratoses and the blue-white veil
associated with orthokeratosis may be harder to
Figure 7.1 Clinical view of a patient with active, well-developed,
violaceous papules and plaques of lichen ruber planus located
on the arms.
Figure 7.2 Dermoscopy with low magnification of the same
patient. A polygonal network of pathognomonic, white, Wickham
Striae surrounded by red capillaries is shown in active LP
lesions. Vascular structures are seen because they are filled with
red cells (original magnification: X10). In order to prevent their
occlusion it is important to avoid an excessive pressure over the
lesions if nonpolarized dermoscopy is performed.
appreciate with this device.(7) In LP lesions, polarized
dermoscopes serve for accurately demonstrating WS,
specially of its contour, but WS appear less uniform,
with variations in the intensity of the color, which gives
1
lichenruberplanus
Figure 7.4 Dermoscopy of active LP lesions (digitally zoomed
images). WS can be revealed with both polarized and nonpolar-
ized dermoscopes. In LP lesions, polarized dermoscopes serve
for accurately demonstrating WS, but they appear speckled-
like, less uniform, showing variations in the intensity of the
color. With nonpolarized dermoscopes WS appear more uni-
form, compact, and pearly whitish.
Figure 7.5 Dermoscopy of LP papules (digitally zoomed images).
The WS presents herein thin projections of the border (“comb-
like” appearance), intermingled with well-defined radial capillar-
ies. These are the most characteristic vascular finding of LP, but
round vessels (globular/dots) can also be seen.
Figure 7.6 Dermoscopy of LP lesions showing radial, lin-
ear capillaries. Round vessels can also appear but are less
characteristic (original magnification: X10).
Figure 7.3 Dermoscopy of active LP lesions (digitally zoomed
images). The Wickham Striae contours show broad ramifications,
which become a reticular configuration in the largest lesion. WS
are surrounded by radial capillaries. The magnification of the der-
moscopic images obtained with Dermlite Foto can be increased by
means of the digital zoom of the attached camera.
a more speckled and “unfocused-like” appearance. With
nonpolarized dermoscopes WS appear more focused,
compact, and uniformly pearly whitish. In addition to
the WS, peripheral capillaries become progressively
more evident in LP lesions. The initial yellow-brown
area of some LP papules could correspond to vacuolar
alterations of basal keratinocytes and to spongiosis in
the spinous zone.(1)
2. Mature LP lesions (violaceous papules or plaques)
(Figures 7.1–7.8). Mature LP lesions remain isolated or
become confluent in reticular networks. WS become
polymorphic and show projections of the border, which
are visualized as thin spikes (“comb-like” projections)
or as broad arboriform ramifications. In this phase,
the central yellow-brown area disappears and promi-
nent peripheral linear, radial capillaries surround the WS

vzquez-lpez
Figure 7.7 Clinical view of an active lichen planus plaque. Figure 7.9 Clinical view of long-standing annular LP of the
axillary region.
contour, intermingled with the projections of the border.
Less characteristic round vessels can also be seen. Several
types of pearly white WS can be recognized:
(a) Round WS
(b) Linear WS
(c) Arboriform WS
(d) Reticular WS
(e) Annular WS
3. Evolved LP lesions: These lesions show WS with decreas-
ing, less prominent peripheral vessels. Pigmented structures
begin to appear surrounding the WS contour. Long-standing
lesions show pigmented structures, with or without WS
devoid of capillaries, according to their duration and the
intensity of the inflammatory process.
4. Annular lichen ruber planus. This type of configuration
appears most commonly in the groin and axillary area.
Dermoscopy of the active border shows WS, capillar-
ies, or pigmented structures according to their duration
(Figures 7.9, 7.10).
5. Hypertrophic lichen planus appear as thickened, hyperk-
eratotic plaques on anterior legs. These lesions may show
under dermoscopy comedo-like structures filled with
yellow plugs or round corneal structures (“corn pearls”)
in addition to WS and vascular findings (Figure 7.11).
Figure 7.8 Dermoscopy of this plaque revealed round and linear
WS configured in a well-developed white, polygonal network,
most prominent in the periphery, and outlined by radial capillaries.
Some WS show yellow-brown areas (original magnification: X10).
Figure 7.10 Dermoscopy (high degree of digital zoom magni-
fication) reveals herein a granular pigment deposition in the
border of the previous annular LP lesion.

lichenruberplanus
Figure 7.12 Dermoscopy of long-standing pigmented LP lesions,
revealing granular pigment outlining the contour of polygonal
WS (original magnification: X10). Nonatrophic ashy or brown
LP macules may present with dermoscopy a homogeneous,
structureless, light-brown pattern, or a granular pigmentation.
This last pattern seems to persist longer and corresponds to pig-
ment-laden dermal melanophages.
Figures 7.14 Higher magnification of this lesion. The “ashy-holes”
and a “sewing machine-like” distribution of pigment granules are
well evident.
Figures 7.13 Dermoscopy of pigmented LP lesions. Granular pig-
ment consists of fine or coarse, grey-blue or brown round dots or
globules. They outline the WS contour in recognizable patterns,
such as the “ashy-holes,” showing granules clustered into round
“holes” surrounded by round WS. A striking “sewing machine-like”
regular distribution of clusters of pigment outlining the WS contour
can also be recognized. Pigment granules first surround the WS and
finally are an isolated finding (original magnification: X10).
Figure 7.11 Dermoscopy of long-standing LP plaque (high degree
of digital zoom), showing “corn pearls.” Comedo-like structures
filled with yellow plugs or round, yellow corneal structures (corn
pearls) can appear within some LP lesions over time.
6. Postinflammatory hyperpigmentation of LP (ashy der-
matosis, lichen planus pigmentosus, dyscromic and pig-
mented actinic lichen planus, and lichen planus with
hyperpigmentation). Discolorations related to LP may
present a long evolution, which is disturbing for patients.
Different dermoscopic patterns of nonatrophic, macular,
pigmented LP may be related to prognosis (6) (Figures
7.12–7.17).
Ashy or brown macules secondary to lichen planus may
present with dermoscopy: (a) Homogeneous, structureless, light-
brown areas devoid of granularity. This type of pigmentation
seems to present a shorter course. (b) Granular pigmentation,
which corresponds to pigment-laden dermal melanophages.
This pattern seems to persist longer when large amounts
of granules are present. Granular pigment consists of fine or
coarse, gray-blue or brown, clustered, round dots or globules,

vzquez-lpez
Figure 7.15 Clinical view of ashy dermatosis related to lichen
planus.
FIgure 7.16 Dermoscopy of the same ashy LP lesions. Pigment
granules are located herein within homogeneous brown discol-
orations (original magnification: X10).
Figure 7.17 Coarse and fine gray-blue and brown globules are
better visualized in the previous lesion by increasing the mag-
nification with zoom (Dermlite Foto).
Figure 7.18 Dermoscopy of a psoriatic plaque (original mag-
nification: X10), revealing multiple, uniformly sized and dis-
tributed rounded vessels (dots/globules). The color of the
surrounding background may vary from pink to deep red.
Figure 7.19 Dermoscopy of plaque psoriasis (center of the
lesion). A high degree of digital zoom reveals that these appar-
ently rounded vessels are indeed convoluted, “coiled” curvilin-
ear capillaries.
within or without light-brown discolorations. They outline the
WS contour in recognizable patterns such as follows:
(a) “Ashy-holes”. Pigment granules are seen in greater
amounts in rounded, depressed areas that appear cen-
trally within some rounded WS.
(b) “Sewing machine” pigment distribution. The clusters
of pigment granules outline the WS contour in a strik-
ing regular distribution.
Plaque psoriasis (PP) and lichen planus (LP) are well dif-
ferentiated clinically. Nevertheless, dermoscopy may be helpful

lichenruberplanus
for discriminating between them in special instances, such as in
atypical patients or when LP coexist with PP.(3, 8) As described
above, LP is characterized by a network of whitish striae, which
are always absent in plaque psoriasis. In contrast, PP shows
multiple, uniformly sized and distributed round vessels (globu-
lar/dotted), surrounded by a colored background (pink to red)
(9–10) (Figure 7.18). Nevertheless, by increasing the degree of
magnification (stereomicroscope, video microscope) they are
really seen as curvilinear, twisted, or convoluted vessels (Figures
7.19–7.20). The subpapillary horizontal vascular plexus is not
seen with any magnification, being hidden by the epidermal
hyperplasia, unless an atrophy secondary to topical steroid treat-
ment develops.(11)
In sum, dermoscopy, in conjunction with clinical examina-
tion, is a very useful and low-cost tool for diagnosing LP in
most settings. It improves the recognition of pathognomonic
structures (Wickham striae) and allows the recognition of dif-
ferent patterns of postinflammatory pigmentation likely related
to prognosis. In addition, dermoscopy may be used herein for
investigative and teaching purposes.
REFERENCES
1. Ragaz A, Ackerman AB. Evolution, maturation, and
regression of lesions of lichen planus. New observations
and correlations of clinical and histologic findings. Am J
Dermatopathol 1981; 3: 5–25.
2. Rivers JK, Jackson R, Orizaba M. Who was Wickham and
what are his striae? Int J Dermatol 1986; 25: 611–3.
3. Vázquez-López F, Alvarez-Cuesta C, Hidalgo-García Y,
Pérez-Oliva N. The handheld dermatoscope improves the
recognition of Wickham striae and capillaries in Lichen
planus lesions. Arch Dermatol 2001; 137: 1376.
4. Vázquez-López F, Manjón-Haces JA, Maldonado-Seral C
et al. Dermoscopic features of plaque psoriasis and lichen
planus: new observations. Dermatology 2003; 207: 151–6.
5. Vázquez-López F, Gómez-Díez S, Sánchez J, Pérez-Oliva
N. Dermoscopy of active lichen planus. Arch Dermatol
2007; 143: 1092.
6. Vázquez-López F, Maldonado-Seral C, López-Escobar M,
Pérez-Oliva N. Dermoscopy of pigmented lichen planus
lesions. Clin Exp Dermatol 2003; 28: 554–5.
7. Pan Y, Gareau DS, Scope A et al. Polarized and nonpolar-
ized dermoscopy: the explanation for the observed differ-
ences. Arch Dermatol 2008; 144: 82–9.
8. Zalaudek I, Argenziano G. Dermoscopy subpatterns
of inflammatory skin disorders. Arch Dermatol 2006;
142: 808.
9. Vazquez-López F, Marghoob A, Kreusch J. Other uses of
dermoscopy. In: Marghoob AA, Braun RP, Kopf AW, eds.
Atlas of Dermoscopy. London, Taylor & Francis, 2005:
299–306.
10. Vázquez-López F, Zaballos P, Fueyo-Casado A, Sánchez-
Martín J. A dermoscopy subpattern of plaque-type psoria-
sis: red globular rings. Arch Dermatol 2007; 143: 1612.
11. Vázquez-López F, Marghoob AA. Dermoscopic assess-
ment of long-term topical therapies with potent steroids in
chronic psoriasis. J Am Acad Dermatol 2004; 51: 811–3.
Figure 7.20 Dermoscopy of plaque psoriasis (periphery of the
lesion). The capillary loops are less coiled at the margins of the
plaques (high degree of digital zoom).

7.2 Urticaria and urticarial vasculitis
Francisco Vázquez-López
Dermoscopy may be of great help for the study of common urti-
caria and similar disorders, such as urticarial vasculitis and may
be used for differentiating between them on a noninvasive basis
in most settings. The usual precautions must be taken in order to
prevent nosocomial infections if contact, nonpolarized dermos-
copy is performed or when taking photographs with skin contact.
Recognition of vascular structures is fundamental for evaluating
lesions of urticaria. Vessels are visualized because of the red blood
cells fulfilling and passing through them. Therefore, it is impor-
tant to avoid excessive pressure on the lesion when performing
this procedure, which may cause occlusion and lack of visual-
ization of the vessels, if nonpolarized dermoscopy is applied or
when taking contact photographs.
Common urticaria (CU) is characterized by the acute or
chronic appearance of transient, recurrent wheals. Histologically,
urticaria is characterized by dermal or subcutaneous edema
and a sparse or dense perivascular lymphocytic infiltrate, inter-
mingled with neutrophils and eosinophils.(1, 2) Dermoscopy
of CU serves to reveal the transiently dilated superficial dermal
capillaries of the lesions (3) (Figures 7.21–7.26).
Urticaria vasculitis (UV) presents episodes of urticaria often
associated with arthralgia and abdominal pain and rarely with
glomerulonephritis. The individual lesions tend to persist lon-
ger than common wheals (1–3 days). They may reveal faint
purpura and resolve with residual discoloration. The degree of
clinical purpura in UV is variable. Purpuric areas may be mini-
mal and unapparent by means of the standard visual inspec-
tion, requiring biopsy for diagnosis. Dermoscopy serves herein
Figure 7.21 Clinical appearance of transient lesions (wheals) of
common urticaria (CU) in a patient with vitiligo.
Figure 7.22 Polarized dermoscopy (low magnification) of a
wheal (CU), disclosing a well-circumscribed, oval area, with a
red network of linear vessels (original magnification: X10).
Figure 7.23 Dermoscopy with greater magnification, disclosing
an irregular red network of linear vessels, which corresponds to
transiently dilated, horizontally oriented dermal capillaries.
for improving their recognition, as a first-line screening tool
(4, 5) (Figures 7.27–7.30). Histologically, UV disclose fibrinoid
deposits in the vessels walls, nuclear dust, neutrophilic infil-
trates, and slight-to-moderate extravasation of erythrocytes.
For differentiating between CU and UV lesions, nuclear dust
and dermal hemorrhage have been considered the most specific
differential criteria for UV.(1, 2)
7
urticariaandurticarialvasculitis
Common urticaria and urticarial vasculitis clinically overlap,
and biopsy is required for differentiation between them. This dis-
crimination is important because UV may be a cutaneous mani-
festation of an underlying connective tissue disease. Dermoscopy,
in conjunction with history and clinical examination, may be
very useful for discriminating between them in daily practice.
Dermoscopic differentiation between CU and UV requires the
knowledge of both vascular and purpuric structures.(3–5)
Dermoscopic vascular findings observed at standard mag-
nification (x10 fold) may be seen as round (vertically oriented
papillary vessels) or as linear structures (horizontal subpapillary
vessels). Round vessels may be dotted/punctate/pinpointed, or
globular according to their size, although this differentiation
may be difficult to make. Linear vessels may appear as simple or
as arboriform structures, with a defined or a blurred contour,
and may form networks (Figures 7.22–7.24).
Dermoscopic purpuric structures may be mainly of two
types:
(a) Homogeneous, structureless purpura. It is observed
in noninflammatory forms of dermal hemorrhage
(vessel-wall dysfunction or trauma; degeneration of the
supporting stroma; coagulation-fibrinolytic disorders,
infective organisms) (e.g., senile purpura) (Figure 7.31)
(b) Round purpuric dots/globules (PG), derived from
perivascular hemorrhage. PG are associated with diverse
purpuric inflammatory processes (pigmented purpu-
ric dermatoses, arthropods reactions, viral and drugs
reactions, leucocytoclastic vasculitis, infective organ-
isms) (Figure 7.32). Purpuric globules are blurred and
appear within a purpuric background and later within
orange-brown patches. The color of the background
surrounds PG but may obscure them if it is prominent
or when tissue necrosis appears.
(c) Other purpuric patterns that may be recognized include
purpuric/black dots of subcorneal purpura and hemor-
rhagic crusts.
Under dermoscopy, the lesions of common urticaria (CU)
reveal a process of transient vasodilatation of dermal capillaries,
without presenting other structures. According to the previous
basic semiology, the wheals of CU disclose under dermoscopy a
red, reticular network of linear vessels (Figures 7.21–7.26). This
Figure 7.24 Dermoscopy of the same lesion after increasing the
degree of magnification. The magnification of the dermoscopic
images obtained with Dermlite Foto can be increased by
means of the digital zoom of the attached camera, although
with reduction of the image quality if it is excessive.
Figure 7.25 A peripheral red network of linear vessels surrounding
a central negative area are shown in a CU lesion. The vessels were
obscured by a prominent edema (original magnification: X10).
Figure 7.26 Dermoscopy of a CU lesion, showing a red network of
linear vessels. In addition, sharp, red, round vessels can be recog-
nized along their course. This vascular finding must be differenti-
ated from true purpuric structures (original magnification: X10).

vzquez-lpez
dermoscopic pattern corresponds histologically with ectatic
subpapillary vessels, horizontally oriented. Linear vessels may
be associated with dotted vessels (Figure 7.26). Red lines may
surround structureless, negative areas devoid of vascular find-
ings in some lesions (Figure 7.25), representing areas where
vessels have been obscured by a prominent edema (negative
areas). Purpuric structures are not observed in CU, and red
lines disappear after making a pressure on the lesion.
In contrast to CU, lesions of UV characteristically show
more or less prominent and numerous blurred, round purpu-
ric structures or globules (PG). PG may appear or not appear
Figure 7.28 Polarized dermoscopy of a lesion of UV revealing
blurred purpuric globules (PG). Lesions of UV with slight hemor-
rhage may also show a surrounding linear network of vessels (orig-
inal magnification: X10). These PG may be clinically unapparent.
Figure 7.30 Dermoscopy of the previous lesion. Purpuric glob-
ules within purpuric patches: They can be demonstrated by
using dermoscopy with low magnification and also in a clinical
basis (original magnification: X10).
Figure 7.29 Clinical image of a patient with urticarial vasculi-
tis. Lesions consist of pruriginous, raised, urticariform plaques,
but showing well-evident, numerous pethechiae. In this case,
the degree of dermal hemorrhage is so severe that it is clinically
evident even without dermoscopy.
within purpuric or orange-brown patches (Figures 7.27–7.30).
Recognition of PG allows easy differentiation with CU. In addi-
tion to purpuric dots/globules, lesions of UV with slight hem-
orrhage may reveal linear vessels (Figure 7.28). These purpuric
structures correspond histologically with the presence of vas-
culitis and are associated with perivascular extravasation and
degradation of red blood cells. The degree of dermal hemor-
rhage in UV lesions is variable. Dermoscopy may be of great
value for the screening of lesions with minimal purpuric areas
Figure 7.27 Clinical picture of a patient with urticarial vasculitis
(UV). The lesions do not show clinically purpuric areas, but UV
may be suspected after screening with dermoscopy.

urticariaandurticarialvasculitis
Figure 7.31 Dermoscopy of a noninflammatory form of pur-
pura. A homogeneous, structureless purpuric patch devoid of
other findings is shown (original magnification: X10).
(Figures 7.27, 7.28), although purpura can be clinically evident
in some severe cases (Figures 7.29, 7.30).
Dermoscopic red lines and purpuric globules are not
specific to urticaria and urticarial vasculitis, respectively.
However, their recognition will help in discriminating between
them, with the presence of PG in urticaria lesions being
indicative of an underlying vasculitis. These structures are eas-
ily recognizable even by nonexpert observers and after mini-
mal training. Dermoscopic purpuric structures of UV must
be differentiated only from round vessels, which are occasion-
ally present in CU (Figure 7.26), and from crusted erosions
rarely seen in CU. Round vessels are red, well demarcated, and
are located along linear vessels, whereas the purpuric globules
are blurred, irregular, and not related to the vessels. In addi-
tion, the ectatic vessels of CU disappear after making a pres-
sure on the lesion while purpuric structures of UV lesions do
not blanch.
In sum, dermoscopy, in conjunction with history and stan-
dard clinical examination, may serve as a first-line screening
tool for discriminating between common urticaria and urti-
caria vasculitis on a noninvasive and low-cost basis in daily
practice. This discrimination is based on an unspecific feature
(purpuric globules) but which is rendered highly specific for
UV when both diseases are confronted.
REFERENCES
1. Ackerman AB. Histologic diagnosis of inflammatory skin
diseases. Baltimore: Williams and Wilkins; 1997.
2. Peteiro C, Toribio J. Incidence of leukocytoclastic vasculi-
tis in chronic idiopathic urticaria. Study of 100 cases. Am J
Dermatopathol 1989; 11: 528–33.
3. Vázquez-López F, Kreusch J, Marghoob AA. Dermoscopic
semiology: further insights into vascular features by screen-
ing a large spectrum of nontumoral skin lesions. Br J
Dermatol 2004; 150: 226–31.
4. Vázquez-López F, Maldonado-Seral C, Soler-Sánchez T,
Perez-Oliva N, Marghoob AA. Surface microscopy for dis-
criminating between common urticaria and urticarial vas-
culitis. Rheumatology 2003; 42: 1079–82.
5. Vazquez-López F, Marghoob A, Kreusch J. Other uses of der-
moscopy. In: Marghoob AA, Braun RP, Kopf AW, eds. Atlas of
Dermoscopy. London, Taylor & Francis, 2005: 299–306.
Figure 7.32 Dermoscopy of inflammatory purpura. A lesion of
leucocytoclastic vasculitis is shown, disclosing multiple, numer-
ous, blurred, purpuric globules. Some of them are located within
yellow-brown patches (original magnification: X10).

7.3 Disorders of collagen tissues
Paolo Rosina
In normal conditions or in primary Raynaud’s phenom-
enon (RP), the normal nailfold videocapillaroscopic (VCP)
pattern shows a regular disposition of the capillary loops
along the nail-bed (Figure 7.33). By contrast, in subjects
suffering from secondary RP, one or more alterations in the
VCP findings (architectural disorganization, enlarged loops,
giant capillaries, microhemorrhages, reduction of capillary
density, angiogenesis, avascular areas, etc.) should suggest a
connective tissue disease (Figure 7.34 and 7.35).
Figure 7.33 Regular disposition of the capillary loops along the
nail bed (x100).
Figure 7.35 Irregular capillaries distribution with few giant capil-
laries and avascular area in scleroderma “late” pattern (x100).
Figure 7.34 Videocapillaroscopic appearance of giant capillary
loop (x200).
Figure 7.36 Giant capillary and hemorrhage visible with hand-
held dermatoscope (x10).
Patients initially diagnosed as having primary RP may shift
to secondary during the follow-up. VCP analysis twice a year
can early detect the transition to a secondary form in patients
showing at the beginning a normal pattern or not-specific nail-
fold capillary abnormalities.(1)
In patients affected by systemic sclerosis (SSc), the most
typical nail-fold VCP pattern of microangiopathy, the so-
called scleroderma pattern (SP), is commonly observed.
It is characterized by irregularly enlarged capillaries, giant

disordersofcollagentissues
disorganization, and ramified capillaries are typical abnor-
malities of late SP.(2)
Nail-fold VC helps to staging the patient affected by SSc
and provides prognostic information. In fact, scleroderma pat-
terns are related to disease subset and disease severity, affecting
different sites as peripheral circulation, skin, heart, and lung.
Scleroderma patients with late VC pattern show an increased
risk to have an active disease and to be affected by a moder-
ate/severe skin or visceral involvement, compared with patients
with early and active patterns.(3)
The VC features observed in dermatomyositis and in undif-
ferentiated connective tissue disease are generally reported as
being of the “scleroderma-like pattern.”
Nail-fold capillary microscopy can be performed with
various optical instruments such as videocapillaroscope,
Figure 7.38 Tortuous and “bushy” capillaries in discoid lupus
erythematosus visible with hand-held dermatoscope (x10).
Figure 7.39 Completely disarranged microangioarchitecture
with loss of capillaries and marked angiogenesis in discoid
lupus erythematosus (x200).
Figure 7.40 Vessel tortuosity with partial respect of normal
reticular pattern in subacute lupus erythematosus (x200).
Figure 7.37 Giant capillary and hemorrhage visible with video-
capillaroscope (x100).
capillaries (capillary diameter >50 micron of both arteriolar
and venular branches), microbleedings, reduced capillary
number with avascular areas, capillary architecture disorga-
nization, as well as ramified capillaries. The giant capillary
is pathognomonic of the scleroderma pattern. Three distinct
NVC patterns of microangiopathy have been described in
SSc patients: “early,” “active,” and “late,” which do not nor-
mally coexist at the same time. Early SP is characterized by
irregularly enlarged capillaries, a few giant capillaries and
hemorrhages; capillary architecture is almost regular without
significant loss of capillaries. In the active pattern frequent
giant capillaries and hemorrhages may be observed and mild
loss of capillaries and capillary architecture disorganization
with a few ramified capillaries. Severe loss of capillaries with
few giant capillaries, avascular areas, capillary architecture

rosina
videodermatoscope, stereomicroscope, ophthalmoscope, and
also hand-held dermatoscope.(4) The simplest and most direct
way to carry out an approximate evaluation of skin microcircu-
lation conditions is the hand-held dermatoscope (Figure 7.36).
It is relatively easy to recognize certain features of microvascu-
lar involvement in systemic sclerosis (giant capillaries, microb-
ledding, etc.), although sensitivity is limited by the low level of
magnification possible (Figure 7.37).
In cutaneous discoid lupus erythematous, tortuous and
irregular “bushy” capillaries are already visible with hand-held
dermatoscope (Figure 7.38), but in advanced lesions, a completely
disarranged microangioarchitecture with loss of capillaries (avas-
cular areas) and marked angiogenesis are better observed with
VC (Figure 7.39). In subacute lupus erythematosus, polygon
irregularities and vessel tortuosity with partial respect of normal
reticular pattern are observed (Figure 7.40). This vascular pattern
can be used in differential diagnosis when cutaneous manifesta-
tion of lupus erythematosus clinically resemble psoriasis.
RefeRences
1. Cutolo M, Grassi W, Matucci Cerinic M. Raynaud’s fenom-
enon and the role of capillaroscopy. Arthritis Rheum 2003;
48: 3023–30.
2. Cutolo M, Pizzorni C, Sulli A. Capillaroscopy. Best Pract
Res Clin Rheumatol 2005; 19: 437–52.
3. Caramaschi P, Canestrini S, Martinelli N et al. Scleroderma
patients nailfold videocapillaroscopic patterns are associ-
ated with disease subset and disease severity. Rheumatology
2007; 46: 1566–9.
4. Bergman R, Sharony L, Schapira D, Nahir MA, Balbir-
Gurman A. The handheld dermatoscope as a nail-fold capil-
laroscopic instrument. Arch Dermatol 2003; 139: 1027–30.

7.4 Rosacea
Paolo Rosina
Rosacea is a common dermatosis affecting 10% to 20% of the
middle-aged population, especially among fair-skinned sub-
jects. Rosacea primarily involves the cutaneous microcircula-
tion of the central part of the face. Several etiologic factors and
pathogenetic mechanisms have been proposed. Age and expo-
sure to environmental factors, in particular ultraviolet light,
are probably causing initial dermal modification in susceptible
individuals.
There is a general agreement that rosacea is primarily a vas-
cular disorder characterized by persistent small-vessel dilatation
and angiogenesis, increased vascular permeability and vascu-
lar hyperreactivity which results in flushing, teleangiectases,
papules pustules, and phyma.(1, 2)
The National Rosacea Society Expert Committee has pro-
posed a classification and staging of rosacea defining four
subtypes (erythematotelangiectatic, papulopustular, phy-
matous, and ocular) and one variant (granulomatous rosa-
cea) and a grading system based on clinical score.(3) There
are currently no objective measures or laboratory tests for
assessing and monitoring the severity of rosacea, which rests
only on clinical judgment. Some studies on rosacea have
considered skin-color changes as a surrogate measurement
of vessel changes. The majority of the trials evaluating ery-
thema and teleangiectasia have utilized subjective methods of
color measurement and vessel changes. The development of
instrumental techniques is obviously important for a more
reproducible disease assessment and may allow a more rigor-
ous comparisons between studies, especially on drug efficacy.
Figure 7.41 Videocapillaroscopic images of normal facial skin
(x100).
Figure 7.42 Reddish background in erythematotelangiectatic
rosacea (x100).
(4, 5) Capillaroscopy is widely used on nail-fold region to
diagnose and monitor rheumatologic diseases and has been
considered superior to indirect technique (e.g., laser Doppler)
for the clinical investigation of cutaneous microcirculation in
various skin disease.(6)
We used the videocapillaroscopic technique to evaluate
qualitative and quantitative microvessels alterations of facial
rosacea and compared them with those of seborrheic derma-
titis.(1) Our results indicate that videocapillaroscopy may rep-
resent a valid adjunctive method in the early identification and
measurement of erythematotelangiectatic rosacea.
Figure 7.43 Larger polygons with thickened vessel walls in
rosacea (x100).
4
rosina
Thirty patients with erythematoteleangiectatic rosacea were
compared with 30 age- and sex-matched patients with facial
seborrheic dermatitis and 30 healthy control subjects, using
an optical probe (Videocap 200R DS Medica, Milano, Italy)
at x100 and x200 magnifications. Parameters analyzed on the
cheek area were background color and morphological (poly-
gons irregularity, vessel tortuosity, neoangiogenesis) and quan-
titative parameters (polygon perimeter, mean diameter of
teleangiectases and vessels).
A regular polygonal net represents the normal distribution
of the cutaneous microcirculation on the cheek, with capillary
loops projected at the inner and outer part of the polygons
(Figure 7.41).
Patients with rosacea showed a reddish background due
to the extended vessel dilatation of the subpapillary plexus
Figure 7.44 Neoangiogenesis and polygonal net in rosacea (x100).
Figure 7.45 Teleangiectases and larger Rosacea vessel in rosacea
(x200).
Figure 7.46 Marked polygon irregularities and pink back-
ground in seborrheic dermatitis (x100).
(Figure 7.42). In contrast, healthy subjects and patients with
seborrheic dermatitis displayed a pink background.
Characteristic alterations of skin vessels were observed in
facial rosacea, with a pattern distinct from that of facial sebor-
rheic dermatitis. In particular, rosacea showed neoangiogenesis
and significantly larger polygons with thickened vessel walls
(Figure 7.43 and 7.44), more prominent teleangiectases, and
larger mean vessel diameter (Figure 7.45), compared to sebor-
rheic dermatitis. Seborrheic dermatitis displayed more polygon
irregularities and vessel tortuosity (Figure 7.46 and 7.47).
For all the morphological and quantitative parameters inves-
tigated, no substantial differences were noted between male
and female patients. In some subjects videocapillaroscopy was
repeated at least twice, with an interval of 48 hours between
the first and the second videocapillaroscopic examination.
Figure 7.47 Vessel tortuosity in seborrheic dermatitis (x100).

rosacea
Erythema was slightly changing, but vessel characteristics did
not change significantly from day 1 of the treatment, in single
individuals.
In contrast, no alterations were found in the nail-fold
region, suggesting that rosacea specifically affects the facial
microvasculature.
In conclusion, facial rosacea was found to present charac-
teristic alterations of skin vessels, with a pattern distinct from
that of facial seborrheic dermatitis. In particular, neoangio-
genesis, larger polygons, more prominent teleangiectases, and
larger vessels diameter was observed only in rosacea, whereas
seborrheic dermatitis displayed polygon irregularities and
vessel tortuosity.
Videocapillaroscopy is a noninvasive and easily repeat-
able technique that can disclose specific and measurable vessel
alterations and may represent a valid adjunctive method in the
early diagnosis and measurement of erythematotelangiectatic
rosacea.
RefeRences
1. Rosina P, Zamperetti MR, Giovannini A, Chieregato
C, Girolomoni G. Videocapillaroscopic alterations in
erythematotelangiectatic rosacea. J Am Acad Dermatol
2006; 54: 100–4.
2. Crawford GH, Pelle MT, James WD. Rosacea: I. Etiology,
pathogenesis, and subtype classification. J Am Acad Dermatol
2004; 51: 327–41.
3. Wilkin J, Dahl M, Detmar M et al. Standard classification
of rosacea: report of the National Rosacea Society Expert
Committee on the classification and staging of rosacea.
J Am Acad Dermatol 2004; 50: 907–12.
4. Bamford JTM, Gessert CE, Renier CM. Measurement of the
severity of rosacea. J Am Acad 2004; 51: 697–703.
5. Carpentier PH. New techniques for clinical assessment of
the peripheral microcirculation. Drugs 1999; 58: 17–22.
6. Hern S, Mortimer PS. Visualization of dermal blood vessels—
capillaroscopy. Clin Exp Dermatol 1999; 24: 473–8.

7.5 Molluscum contagiosum
Pedro Zaballos Diego
MOLLUSCUM CONTAGIOSUM
Molluscum contagiosum (MC) is a disease caused by a pox-
virus of the Molluscipox virus genus that produces a cutane-
ous, mucosal, benign, self-limited papular eruption of multiple,
umbilicated, cutaneous tumors. It was first described and later
assigned its name by Bateman in the beginning of the nineteenth
century. Though generally thought to infect only humans,
case reports of the virus occurring in other animals have been
published. There are four main subtypes of molluscum con-
tagiosum virus (MCV): MCV I, MCV II, MCV III, and MCV
IV. There is no apparent relationship between viral subtype,
morphology, or anatomical distribution. However, there
appears to be marked geographical variation in the distribu-
tion of subtypes. This disease is transmitted primarily through
direct skin contact with an infected individual. Fomites and
sexual transmission have been suggested as another source of
infection. The MCV can be found worldwide with a higher
distribution in tropical areas and has a higher incidence in chil-
dren, sexually active adults, and those who are immunodefi-
cient. The average incubation time is between 2 and 7 weeks
with a range extending to 6 months. Clinically, MC produces
a papular eruption of multiple umbilicated lesions (Figures
7.48 and 7.49). The morphology of an individual lesion is a
dome-shaped papule, flesh colored or pearly, with an umbili-
cated center. Lesions vary in size from 1 to 10 mm, although
occasionally giant lesions are seen. The papules may become
inflamed spontaneously or after trauma and present atypically
in size, shape, and color. The lesions are often grouped in small
Figure 7.48 Clinical image of a typical case of molluscum con-
tagiosum in a child.
Figure 7.49 Molluscum contagiosum on a face of an adult.
Figure 7.50 Figure shows the typical pattern of molluscum
contagiosum (central, poliglobular, white-yellowish amorphous
structure and peripheral crown of vessels) (X10).
areas but may also become widely disseminated. Any cutane-
ous surface may be involved, but favored sites include the axil-
lae, the antecubital and popliteal fossae, and the crural folds
in children. Autoinoculation is common. MC in adults affects
the groin, genital area, thighs, and lower abdomen and is often
acquired sexually. Histologically, MC exhibits epidermal hyper-
plasia producing a crater filled with huge, up to 35 microns,
eosinophilic to basophilic intracytoplasmatic inclusions that
7
molluscumcontagiosum
are called molluscum bodies or Henderson–Patterson bodies.
MC is a self-limited disease, which, left untreated, will eventu-
ally resolve itself in immunocompetent hosts but may be pro-
tracted in atopic and immunocompromised individuals. Most
of the common treatments consist of various means to trauma-
tize the lesions. Antiviral and immune-modulating treatments
have recently been added to the options.(1–5)
The clinical diagnosis of MC is usually easy, mainly in pedi-
atric patients, because they are normally quite characteristic in
appearance. However, MC may be occasionally confused with
other tumors, particularly those found in adulthood.(6) In these
cases, dermoscopy discloses additional information to improve
our diagnosis.(6–10) Dermoscopically, MC displays a character-
istic pattern composed of the presence of a poliglobular white-
yellowish amorphous structure in the center of the lesions with a
surrounding crown of linear, fine, and sometimes blurred vessels,
some of them branching, which do not usually cross the center
of the lobules (Figures 7.50–7.53).(6–10) In some cases, we can
also observe curvilinear vessels that form a peripheral, reddish,
ring-like structure that encircle the poliglobular, white-yellowish
structures, and, in more rare cases, we can see arborizing vessels
(Figure 7.54), comma vessels, red globules, and dotted vessels.
A central pore or umbilication could be an additional feature
in some cases. The histopathological correlation of central,
Figure 7.51 Another typical dermoscopic image of molluscum
contagiosum (X10).
Figure 7.53 Figure shows two pearly, waxy, dome-shaped papules located on the nose of a 76-year-old man that were clinically
diagnosed as basal-cell carcinomas. However, the dermoscopic image of both lesions shows the characteristic pattern of mollus-
cum contagiosum (a central, poliglobular, white-yellowish, amorphous structure and a peripheral crown of vessels) (X10).
Figure 7.52 Figure shows central, poliglobular, white-yellowish,
amorphous structure surrounded by a peripheral crown of ves-
sels with reddish globules and areas of erythema (X10).

zaballos
aggregated, white-yellowish globules could be the lobulated,
endophytic epidermal hyperplasia with intracytoplasmic inclu-
sion bodies, also known as molluscum or Henderson–Paterson
bodies. The crown of vessels or “red corona” corresponds histo-
pathologically to dilated vessels in the dermis and is characteristic
of MC. Vazquez-Lopez et al. (8) evaluated and classified the der-
moscopic vascular structures seen in 33 nontumoral dermatoses
and found this vascular structure in 10 of 15 patients with MC.
However, these crown vessels are not solely limited to MC, we can
also find these vascular structures in sebaceous hyperplasia.(11)
However, the recognition of this pattern (a central, poliglobular,
white-yellowish, amorphous structure and a peripheral crown of
vessels) is very helpful in the clinical diagnosis of MC, above all
in adulthood, and allows us to differentiate these disease from
Figure 7.54 Atypical case of molluscum contagiosum. Dermoscopic
image shows isolated, peripheral, white-yellowish globules (aster-
isks) and arborizing vessels throughout the lesion (X10).
many other skin lesions with high confidence. Zaballos et al. (7)
published an atypical case of a 67-year-old woman with two
5-mm, pearly, waxy, dome-shaped papules of 7-month duration,
one located on the thorax and the other on the back, which were
clinically diagnosed as basal-cell carcinomas and, dermoscopi-
cally, as MC because they presented this characteristic pattern.
REFERENCES
1. Diven DG. An overview of poxviruses. J Am Acad Derma-
tol 2001; 44: 1–14.
2. Brown ST, Nalley JF, Kraus SJ. Molluscum contagiosum.
Sex Transm Dis 1981; 8: 227–34.
3. Hanson D, Diven DG. Molluscum contagiosum. Dermatol
Online J 2003; 9: 2.
4. Gottlieb SL, Myskowki PL. Molluscum contagiosum. Int J
Dermatol 1994; 33: 453–61.
5. Valentine CL, Diven DG, Treatment modalities for mol-
luscum contagiosum. Dermatol Ther 2000; 13: 285–9.
6. Morales A, Puig S, Zaballos P, Malvehy J. Dermoscopy of
Molluscum contagiosum. Arch Dermatol 2005; 141: 1644.
7. Zaballos P, Ara M, Puig S, Malvehy J. Dermoscopy of mol-
luscum contagiosum: a useful tool for clinical diagnosis
in adulthood. J Eur Acad Dermatol Venereol 2006; 20:
482–3.
8. Vázquez-López F, Kreusch J, Marghoob AA. Dermoscopic
semiology: further insights into vascular features by screen-
ing a large spectrum of nontumoral skin lesions. Br J Der-
matol 2004; 150: 226–31.
9. Zalaudek I, Argenziano G, Di Stefani A et al. Dermoscopy
in general dermatology. Dermatology 2006; 212: 7–18.
10. Zalaudek I, Giacomel J, Cabo H et al. Entodermoscopy:
a new tool for diagnosing skin infections and infestations.
Dermatology 2008; 216: 14–23.
11. Zaballos P, Ara M, Puig S, Malvehy J. Dermoscopy of seba-
ceous hyperplasia. Arch Dermatol 2005; 141: 808.

7.6 Sebaceous hyperplasia
Pedro Zaballos Diego
SEBACEOUS HYPERPLASIA
Sebaceous hyperplasia is the most common proliferative abnor-
mality of the sebaceous glands. It most often presents on the face
of older adults, particularly males. The forehead and cheeks are
predominantly affected and occasionally diffuse facial involve-
ment occurs. Other less common sites include the mouth, nose,
upper arms, chest, areola, penis, and vulva. Sebaceous hyperpla-
sia lesions begin to appear in the fifth or sixth decade of person´s
life and continue to appear into later life. However, premature or
familial cases have been reported in which younger individuals
are affected with multiple lesions, suggesting a genetic predispo-
sition. Lesions may occur individually, in groups, or as a sheet
of papules. The classic appearance of sebaceous hyperplasia on
physical examination reveals whitish-yellow or skin-colored,
normally umbilicated, papules that are soft and vary in size from
2 to 9 mm. Rarely reported variants have included a giant form,
a linear or zosteriform arrangement, a diffuse form, and a famil-
ial form. Juxtaclavicular beaded lines are an additional vari-
ant characterized by closely placed papules arranged in parallel
rows. Sebaceous hyperplasia significantly increases in transplant
patients, particularly males following heart and renal trans-
plantation, and this may be related to therapy with cyclosporin
A. Sebaceous hyperplasia has been reported in association with
internal malignancy in the setting of Muir–Torre syndrome but
alone does not signify a predisposition to cancer or represent a
sign of Muir–Torre syndrome. Sebaceous hyperplasia has no
direct association with malignant degeneration and is not a cause
of morbidity, except perhaps related to cosmesis and, therefore,
is often found incidentally upon examination. Clinically, the
primary entities that must be included in the differential diag-
nosis of sebaceous hyperplasia are basal-cell carcinoma, fibrous
papule of the face, milia, molluscum contagiosum, and other
adnexal tumors.(1, 2) Sebaceous hyperplasia is frequently clini-
cally misdiagnosed as basal-cell carcinoma.(3) Some papules
Figure 7.55 Typical dermoscopic image of sebaceous hyper-
plasia with aggregated white-yellowish globules in the center
of the lesion (“cumulus sign”) with surrounding crown of ves-
sels. We can also observe brownish globular structures with
ring-like appearance in the center of the lesion (X10).
Figure 7.56 Characteristic dermoscopic image of sebaceous
hyperplasia (X10).
Figure 7.57 Another dermoscopic image of sebaceous hyper-
plasia (X10).

zaballos
structures in 100% of the sebaceous hyperplasias of their studies.
These aggregated yellowish globules are not limited solely to seba-
ceous hyperplasia and may also be seen in some molluscum con-
tagiosum, nevus sebaceous of Jadassohn, and sebaceous adenoma.
(7–9) Sometimes, the ostium of the gland is visible as a small crater
or umbilication in the center of these yellowish structures. Oztas
et al. (5) named the association of the central umbilication sur-
rounded by cumulus sign as “Bonbon Toffee sign” and found this
pattern in 80% of sebaceous hyperplasias (Figures 7.58 and 7.59).
Regarding vascular structures that we can find at the periphery of
sebaceous hyperplasias, the most common ones are the “crown
vessels” (Figures 7.55–7.60).(3–7) These vascular structures have
been defined as groups of orderly, bending, scarcely branching
may be associated with characteristics similar to this malignant
tumor, such as telangiectasia, and dermoscopy may be useful as a
noninvasive tool to distinguish between nodular basal-cell carci-
noma and sebaceous hyperplasia, reducing unnecessary surgery.
Dermoscopically, sebaceous hyperplasia shows a pattern com-
posed of the presence of aggregated white-yellowish globules
in the center of the lesions with a surrounding crown of vessels
(Figures 7.55–7.61).(3–7) The central aggregated white-yellowish
structures or globules, showing a sharp difference from surround-
ing skin, were defined by Bryden et al. (3) as “cumulus sign,” a
descriptive sign, because these structures resemble the cumulus
clouds and correspond histopathologically to hyperplastic seba-
ceous glands. Bryden et al. (3) and Oztas et al. (5) observed these
Figure 7.58 “Bonbon Toffee sign” is the association of a central
umbilication surrounded by cumulus sign. We can also see a periph-
eral crown of vessels, characteristic of this tumor (X10).
Figure 7.59 Another sebaceous hyperplasia with the “Bonbon
Toffee sign” (central umbilication surrounded by aggregated white-
yellowish globules) and peripheral crown of vessels (X10).
Figure 7.60 Large sebaceous hyperplasia. Figure shows aggregated
white-yellowish globules and groups of orderly, bending, scarcely
branching vessels located throughout the lesion (X10).
Figure 7.61 Figure shows the characteristic dermoscopic pat-
tern of a sebaceous hyperplasia located on the penis (X10).

sebaceoushyperplasia
vessels located along the border of the lesion.(10) These vessels
may extend toward the center but do not usually cross it. They are
very common in sebaceous hyperplasias, but we can find these ves-
sels in some lesions of molluscum contagiosum. Argenziano et al.
(10) found crown vessels in 83.3% of sebaceous hyperplasias, and
Oztas et al. (5) found crown vessels in 86.7% of cases. Other vascu-
lar structures that we can observe are arborizing vessels in 16.7%
of cases according to Argenziano et al.(10) Sebaceous hyperplasia
is frequently clinically misdiagnosed as basal-cell carcinoma and
arborizing telangiectasias are among the characteristic criteria of
this tumor. However, none of the other specific criteria of BCC
(11) (blue globules; large, blue-gray, ovoid nests; leaf-like areas;
spoke-wheel structures; and ulceration) have beeen found in seba-
ceous hyperplasias, and aggegrated white-yellowish globules are
not typical in BCC. Brown dots and globules, some of them with
ring-like appearance and milia-like cysts, are less common features
that we can see in few sebaceous hyperplasias.
REFERENCES
1. Lazar AJF, McKee PH. Tumors and related lesions of the
sebaceous glands. In: McKee PH, Calonje E, Granter SR eds.
Pathology of the Skin with Clinical Correlations. China:
Elsevier Mosby; 2005.
2. Simpson NB, Cunliffe WJ. Disorders of the sebaceous
glands. In: Burns T, Breathnach S, Cox N, Griffiths C
eds. Rook´s Textbook of Dermatology. Oxford: Blackwell
Publishing Ltd; 2004.
3. Bryden AM, Dawe RS, Fleming C. Dermatoscopic features
of benign sebaceous proliferation. Clin Exp Dermatol 2004;
29: 676–7.
4. Zaballos P, Ara M, Puig S, Malvehy J. Dermoscopy of seba-
ceous hyperplasia. Arch Dermatol 2005; 141: 808.
5. Oztas P, Polat M, Oztas M, Alli N, Ustun H. Bonbon
toffee sign: a new dermatoscopic feature for sebaceous
hyperplasia. J Eur Acad Dermatol Venereol 2008; 22:
1200–2.
6. Zalaudek I, Argenziano G, Di Stefani A et al. Dermoscopy
in general dermatology. Dermatology 2006; 212: 7–18.
7. Kim NH, Zell DS, Kolm I, Oliviero M, Rabinovitz HS. The
dermoscopic differential diagnosis of yellow lobularlike
structures. Arch Dermatol 2008; 144: 962.
8. Morales A, Puig S, Zaballos P, Malvehy J. Dermoscopy
of Molluscum contagiosum. Arch Dermatol 2005; 141:
1644.
9. Zaballos P, Ara M, Puig S, Malvehy J. Dermoscopy of mol-
luscum contagiosum: a useful tool for clinical diagnosis
in adulthood. J Eur Acad Dermatol Venereol 2006; 20:
482–3.
10. Argenziano G, Zalaudek I, Corona R et al. Vascular struc-
tures in skin tumors: a dermoscopy study. Arch Dermatol
2004; 140: 1485–9.
11. Menzies SW, Westerhoff K, Rabinovitz H et al. Surface
microscopy of pigmented basal cell carcinoma. Arch
Dermatol 2000; 136: 1012–6.

7.7 Pigmented purpuric dermatoses
Pedro Zaballos Diego
PIGMENTED PURPURIC DERMATOSES
Pigmented purpuric dermatoses (PPD), also called purpura sim-
plex or chronic capillaritis, is the generic term for a variety of
chronic conditions characterized by orange/brown pigmentation
(due to hemosiderin deposition likened to cayenne pepper), inter-
spersed with fine-point purpura (due to extravasated red blood
cells).(1–3) PPD typically occurs on the lower limbs (Figures
7.62–7.68) in a symmetrical distribution and often shows a
benign and self-limited, although chronic, course. The etiology of
PPD is unknown. Gravidity and increased venous pressure are
Figure 7.62 Characteristic dermoscopic image of PPD
(Schamberg´s disease). Pattern composed of irregular, round to
oval, red dots, globules, and patches, with a red-brownish or
red-coppery, diffuse, homogeneous pigmentation in the back-
ground (X10).
Figure 7.63 Another characteristic area in the same patient
where we can also find vascular structures (X10).
Figure 7.64 A more advanced stage of pigmented purpuric der-
matosis (Schamberg´s disease) where the red-brownish patches
predominate (X10).
Figure 7.65 Figure shows the presence of irregular, round to
oval, red dots, globules, and patches, with a red-brownish or
red-coppery, diffuse, homogeneous pigmentation in the back-
ground in a case of a pigmented, purpuric, lichenoid dermato-
sis of Gougerot and Blum. In the image, we can also observe a
network of brownish to gray interconnected lines (X10).

pigmentedpurpuricdermatoses
Figure 7.66 Figure shows the presence of round to oval, red dots
and globules and scales, with a red-brownish or red-coppery,
diffuse, homogeneous pigmentation in the background in a case
of Eczematoid-like purpura of Doucas and Kapetanakis (X10).
Figure 7.67 Presence of round to oval, red dots, globules, and
patches, with a scanty, red-brownish, diffuse, homogeneous
pigmentation in the background in a case of Majocchi´s disease
(X10).
Figure 7.68 Figure shows the characteristic dermoscopic pat-
tern of PPD (lichen aureus) with irregular, round to oval, red
dots, globules, and patches, with a red-brownish or red-coppery,
diffuse, homogeneous pigmentation in the background. In the
image we can also observe a network of brownish to gray inter-
connected lines, mainly in the upper part of the lesion (X10).
important localizing factors in many cases and triggering factors
such as drugs, chemical ingestions, food additives, infections, or
underlying hematologic/internal diseases have been described.(1–3)
PPD have traditionally been divided into five clinical entities: pro-
gressive, pigmented, purpuric dermatosis or Schamberg´s disease;
purpura annularis telangiectodes or Majocchi´s disease; pigmented,
purpuric, lichenoid dermatosis of Gougerot and Blum; eczema-
toid-like purpura of Doucas and Kapetanakis; and lichen aureus.
(1–3) Schamberg´s disease (Figures 7.62–7.64) is characterized
by usually asymptomatic, chronic, and persistent purpura and
petechiae with conspicuous pigmentation located predominantly
on the lower limbs. In Majocchi´s disease (Figure 7.67), the lesions
tend to be reddish annular macules located on the lower limbs
and associated with telangiectases. Patients with pigmented, pur-
puric, lichenoid dermatosis of Gougerot and Blum (Figure 7.65)
developed lichenoid papules in addition to purpuric lesions,
most often on the legs. Eczematoid-like purpura of Doucas and
Kapetanakis (Figure 7.66) or itching purpura has many similari-
ties to Schamberg´s disease but is generally more extensive, devel-
ops more rapidly, and is characterized by a persistent, intense itch.
Finally, lichen aureus (Figure 7.68) is a localized variant of PPD
that is characterized by the appearance of sudden-onset, limited
lichenoid papules in association with purpuric lesions, located
commonly on the lower limbs, and occasionally on the trunk and
the face. There are other more unusual presentations that include
the itching purpura of Loewenthal, linear, granulomatous, quad-
rantic, transitory, and familial forms.(1–3)
All these disorders may show overlapping clinical and histolog-
ical features. Indeed, under dermoscopic examination, all forms
of PPD show similar findings.(4–6) The dermoscopic pattern
associated with PPD is the presence of irregular, round to oval, red
dots, globules, and patches, with a red-brownish or red-coppery,
diffuse, homogeneous pigmentation in the background (Figures
7.62–7.68). The histopathological correlation of the red-brownish
or red-coppery background may be the presence of the dermal
infiltrate of lymphocytes and histiocytes, extravasated red blood
cells, and hemosiderin-laden macrophages. The irregular red
dots, globules, and patches, which were not blanched by compres-
sion, can also correspond histologically to the extravasation of red

zaballos
blood cells and to the increased number of blood vessels, some
of which are dilated and swollen. In some cases, some gray dots
and a network of brownish to gray interconnected lines (Figures
7.65 and 7.68) can be observed that correlate histopathologically
to hemosiderin-laden macrophages (gray dots) and the presence
of hyperpigmentation of the basal-cell layer and incontinentia
pigmenti in the upper dermis (network-like structure) related
to some lichenoid infiltrates. This characteristic pattern of PPD
could be useful to distinguish them from other diseases such as
angioma serpiginosum and venous stasis dermatitis. Numerous
small, relatively well-demarcated, round to oval red lacunas with-
out the brownish background were determined with dermoscopy
in angioma serpiginosum (7–9), and the presence of glomerular
vessels and a scaly surface is the characteristic pattern of venous
stasis dermatitis.(10, 11) However, this is not a pathognomonic
pattern and the presence of red dots, globules, and patches, with a
red-brownish pigmentation in the background is not solely lim-
ited to PPD, as we can find a similar pattern in other diseases also.
Vázquez-López et al. found a pattern composed of purpuric or
reddish dots and globules in a patchy, orange-brown background
in two cases of urticaria vasculitis (12) and also described a simi-
lar pattern composed of reddish or brownish globules in diffuse
brownish areas in some cases of pigmented lichen planus.(13)
REFERENCES
1. Cox NH, Piette WW. Purpura and microvascular occlu-
sion. In: Burns T, Breathnach S, Cox N, Griffiths C eds.
Rook´s Textbook of Dermatology. Oxford: Blackwell
Publishing Ltd; 2004.
2. Superficial and deep perivascular inflammatory derma-
toses. In: McKee PH, Calonje E, Granter SR eds. Pathol-
ogy of the Skin with Clinical Correlations. China: Elsevier
Mosby; 2005.
3. Sardana K, Sarkar R, Sehgal VN. Pigmented purpuric der-
matoses: an overview. Int J Dermatol 2004; 43: 482–8.
4. Zaballos P, Puig S, Malvehy J. Dermoscopy of pigmented
purpuric dermatoses (lichen aureus): a useful tool for
clinical diagnosis. Arch Dermatol 2004; 140(10): 1290–1.
5. Zalaudek I, Ferrara G, Brongo S, Giorgio CM, Argenziano
G. Atypical clinical presentation of pigmented purpuric
dermatosis. J Dtsch Dermatol Ges 2006; 4: 138–40.
6. Zalaudek I, Argenziano G, Di Stefani A et al. Dermoscopy
in general dermatology. Dermatology 2006; 212: 7–18.
7. Ohnishi T, Nagayama T, Morita T et al. Angioma serpigi-
nosum: a report of 2 cases identified using epilumines-
cence microscopy. Arch Dermatol 1999; 135: 1366–8.
8. Kalisiak MS, Haber RM. Angioma serpiginosum with lin-
ear distribution: case report and review of the literatura.
J Cutan Med Surg 2008; 12: 180–3.
9. Ilknur T, Fetil E, Akarsu S et al. Angioma serpiginosum:
dermoscopy for diagnosis, pulsed dye laser for treatment.
J Dermatol 2006; 33: 252–5.
10. Zaballos P, Salsench E, Puig S, Malvehy J. Dermoscopy
of venous stasis dermatitis. Arch Dermatol 2006; 142:
1526.
11. Vázquez-López F, Kreusch J, Marghoob AA. Dermo-
scopic semiology: further insights into vascular features
by screening a large spectrum of nontumoral skin lesions.
Br J Dermatol 2004; 150: 226–31.
12. Vázquez-López F, Fueyo A, Sánchez-Martín J, Pérez-
Oliva N. Dermoscopy for the screening of common
urticaria and urticaria vasculitis. Arch Dermatol 2008;
144: 568.
13. Vázquez-López F, Maldonado-Seral C, López-Escobar M,
N Pérez-Oliva. Dermoscopy of pigmented lichen planus
lesions. Clin Exp Dermatol 2003; 28: 554–64.

7.8 Actinic porokeratosis
Pedro Zaballos Diego
ACTINIC POROKERATOSIS
Porokeratosis is a clonal disorder of keratinization clini-
cally characterized by sharply demarcated, atrophic, annular
lesions with a distinct keratotic edge corresponding histologi-
cally to the presence of the cornoid lamella, a column of par-
akeratotic cells extending through the stratum corneum. The
patophysiology of this disease is due to a clonal hyperprolif-
eration of atypical keratinocytes that leads to the formation
of the cornoid lamella, which expands peripherally and forms
the raised boundary between abnormal and normal keratino-
cytes. Several risk factors for the development of porokeratosis
have been identified; these factors include genetic inheritance,
ultraviolet radiation, and immunosuppression. The formation
of squamous or basal-cell carcinomas has been reported in all
forms of porokeratosis, although the degree of premalignant
potential is controversial. Five clinical variants of porokera-
tosis are recognized: classic porokeratosis of Mibelli, dissemi-
nated superficial actinic porokeratosis (DSAP), porokeratosis
palmaris et plantaris disseminata, linear porokeratosis, and
punctate porokeratosis.(1–3)
DSAP is the most common presentation, with lots of lesions
of up to 10 mm, predominantly in sun-exposed sites in middle-
aged individuals in their third or fourth decade of life, especially
those with sun-sensitive skin. DSAP is 3 times as likely to develop
in women than in men. The tendency to develop these lesions
is inherited as an autosomical dominant. Multiple, annular,
keratotic lesions that develop predominantly on the extensor
surfaces of the legs and the arms characterize DSAP. The lesion
begins as a 1–3 mm conical papule, reddish or brownish in color,
which contains a keratotic plug that expands to a sharp, slightly
raised, keratotic ring, producing a plaque of 10 mm or more. The
skin within the ring is usually somewhat atrophic and mildly
reddened or hyperpigmented. In a few cases, the center of the
area becomes inflamed, covered by thick hyperkeratosis, or even
Figure 7.69 Typical dermoscopic image of actinic porokeratosis with
a peripheral “white track” that demarcates a central, red-whitish,
homogeneous area with dotted vessels and scales (X10).
Figure 7.70 Figure shows a peripheral white-brownish track
and a central, whitish, homogeneous area. We can also observe
peripheral vascular structures in some areas (X10).
Figure 7.71 Figure shows a peripheral white track and a central,
whitish, homogeneous area, with dotted vessels, red globules,
and a delicate pigment network (X10).

zaballos
and corresponds histopathologically to the cornoid lamella.
Although nonpathognomonic, the cornoid lamella is the most his-
topathologic, distinctive feature of the various types of porokera-
tosis and consists of a thin column of tightly packed parakeratotic
cells within a keratin-filled epidermal invagination. The papillary
dermis beneath the cornoid lamella contains a moderately dense,
lymphocytic infiltrate and dilated capillaries. Therefore, we can
observe brownish pigmentation on the inner side of the white track
and a peripheral vascularization. Liquefactive degeneration of the
basal layer of the epithelium is sometimes present and occasionally
provokes melanophagia, and, in these cases, we can observe some
blue-gray coarse granules. White track demarcates a central, light-
whitish, homogeneous area with different kind of vessels (red dots
and globules, linear-irregular vessels, or telangiectasias) (Figures
ulcerated and crusted. They are usually asymptomatic, but they
may itch slightly. The lesions of DSAP are easily mistaken for
actinic keratoses, with which they may coexist, and psoriasis.
There is a nonactinic form of disseminated, superficial porokera-
tosis after organ transplantation, renal failure, HIV infection, or
in association with other causes of immunosuppression that may
have a generalized distribution of identical lesions, sparing the
palms and the soles.(1–3)
Dermoscopically, porokeratosis reveals a whitish annular struc-
ture called “white track” located at the periphery of the lesion, with
a brownish pigmentation on the inner side and with a double white
track in some areas (Figures 7.69–7.75).(4–7) The color of this
annular structure could be yellowish or light brown in rare cases.
This single or double white track is characteristic of porokeratosis
Figure 7.72 Another example of actinic porokeratosis with a
peripheral white track and a central area with dotted vessels and
red globules (X10).
Figure 7.73 Figure shows a peripheral white track with different
kind of vessels (X10).
Figure 7.74 Figure shows a peripheral white track with a central
scaly surface (X10).
Figure 7.75 In this case of actinic porokeratosis, the epithelium
toward the center was acanthotic and because of that we can
observe a verrucous surface in the center of the lesion (X10).
7
actinicporokeratosis
2. Shumack SP, Commens CA. Disseminated superficial
actinic porokeratosis: a clinical study. J Am Acad Dermatol
1989; 20: 1015–22.
3. Sasson M, Krain AD. Porokeratosis and cutaneous malig-
nancy. A review. Dermatol Surg 1996; 22: 339–42.
4. Delfino M, Argenziano G, Nino M. Dermoscopy for the
diagnosis of porokeratosis. J Eur Acad Dermatol Venereol
2004; 18: 194–5.
5. Zaballos P, Puig S, Malvehy J. Dermoscopy of dissemi-
nated superficial actinic porokeratosis. Arch Dermatol
2004; 140(11): 1410.
6. Panasiti V, Rossi M, Curzio M, Bruni F, Calvieri S. Dis-
seminated superficial actinic porokeratosis diagnosed by
dermoscopy. Int J Dermatol 2008; 47: 308–10.
7. Vargas-Laguna E, Nagore E, Alfaro A et al. Monitoring the
evolution of a localized type of porokeratosis using [der-
matoscopy]. Actas Dermosifiliogr 2006; 97: 77–8.
8. Zalaudek I, Giacomel J, Argenziano G et al. Dermoscopy
of facial nonpigmented actinic keratosis. Br J Dermatol
2006; 155: 951–6.
9. Peris K, Micantonio T, Piccolo D, Fargnoli MC. Dermo-
scopic features of actinic keratosis. J Dtsch Dermatol Ges
2007; 5: 970–6.
10. Vázquez-López F, Manjón-Haces JA, Maldonado-Seral C
et al. Dermoscopic features of plaque psoriasis and lichen
planus: new observations. Dermatology 2003; 207: 151–6.
11. Zalaudek I, Argenziano G, Di Stefani A et al. Dermoscopy
in general dermatology. Dermatology 2006; 212: 7–18.
7.69–7.73) that are more easily observed because of the presence
of atrophic epithelium in the center of the porokeratosis.(4–7)
The epithelium toward the center may be of normal thickness or
even acanthotic and because of this we can observe, in less com-
mon cases, an intense white homogeneous area or even a verru-
cous surface (Figures 7.74 and 7.75) . Other uncommon structures
that we can see in the center of the porokeratosis are delicate pig-
ment network or brown globules, some of them with a ring-like
appearance. The lesions of DSAP are possibly mistaken for actinic
keratoses, with which they may coexist, and psoriasis. Four essen-
tial dermoscopic features were observed in nonpigmented actinic
keratosis that combined to produce the “strawberry pattern”:
(a) erythema, revealing a marked, pink-to-red “pseudonetwork”
surrounding the hair follicles; (b) white-to-yellow surface scale;
(c) fine, linear-wavy vessels surrounding the hair follicles; and
(d) hair follicle openings filled with yellowish keratotic plugs and/
or surrounded by a white halo.(8, 9) Although all the actinic kera-
tosis of the study were located on the face, none of the lesions
showed the characteristic peripheral “white track” of DSAP. The
dermoscopic pattern associated with psoriasis is composed of
multiple, uniformly sized, and distributed dotted vessels or red
globules, together with a central surface scale.(10, 11)
REFERENCES
1. Judge MR, Malean WHI, Munro CS. Disorders of kera-
tinization. In: Burns T, Breathnach S, Cox N, Griffiths C
eds. Rook´s Textbook of Dermatology. Oxford: Blackwell
Publishing Ltd; 2004.

7.9 Xanthomatous lesions
Filomena Mandato, Maurizio Biagioli, and Pietro Rubegni
Xanthomatous lesions of the skin manifest as typically yellowish,
sometimes tending to orange or blue, macules (flat xanthomas),
papules (eruptive xanthomas), nodules (tuberous xanthomas),
or tendon infiltrations (tendon xanthomas).(1) Their histol-
ogy is characterized by accumulation of xanthomatous cells
(macrophages) containing lipids responsible for their color.
Sometimes they are idiopathic, but they are more commonly
encountered in patients with internal diseases, especially with
high cardiovascular risk.(2) As xanthomatous lesions often indi-
cate the concomitance of secondary or acquired hyperlipidemia,
these patients should undergo analysis of lipid profile. In other
cases, fortunately rare, a syndrome is involved (Table 7.1).(3–6)
Xanthomization indicates a gradual process of accumula-
tion of lipids in tumoral lesions such as histiocytomas (Figure
7.76) or inflammatory sequelae such as lipid necrobiosis,
foreign body reaction, histiocytosis X, erythema elevatum
diutinum, and leprosy scars.
Xanthelasms––These are the most frequent xantheloma-
tous lesions (Figure 7.77). They manifest as yellowish papules,
usually arranged symmetrically at the internal canthus of the
eye, on the upper eyelids, and sometimes on the lower ones.
If untreated, they may join up to form plaques that need to be
removed to avoid ectropion.(7–8)
Tuberous xantoma––These lesions are hard, yellowish,
slowly evolving nodules, often surrounded by an erythema-
tous halo. They are generally located symmetrically in pressure
regions (elbows, knees, and ankles).
Eruptive papular xantoma––These are small, inflamma-
tory-like papules that erupt on elbows or knees and are some-
times itchy. Initially red, the papules veer to yellowish and may
unite to form tuberous/eruptive xanthomas.(9)
Palmar, striated xanthochromia––This skin disease pres-
ent with yellowish, infiltrative maculopapules in the digital and
palmar folds. It is a pathognomonic sign of hereditary dysbeta-
lipoproteinemia, usually responsive to fibrates treatment and a
diet low in fats and carbohydrates.
Diffuse, flat, normolipidemic xanthomas––These large,
yellowish, papular plaques with well-defined borders occur
Table 7.1 Syndromes Associated with Skin Xanthomas.
Syndrome Clinical symptoms and signs
Necrobiotic xanthoma Purplish inflammatory plaques and
nodules with a xanthomatous central area
(chest and periorbital), associated with
paraproteinemia in 80% of cases, may
be associated with other hematological
disorders but nondyslipidemia.
Montgomery
disseminated xanthoma
Papular xanthomas of the skin (neck, folds,
periorbital, and perioral) and mucosa
(pharynx, larynx) associated with diabetes
insipidus in 30% of cases.
Cerebrotendinous
xanthomatosis
Rare autosomal dominant hereditary
disease characterized by xanthelasmas,
tendon xanthomas, and tuberous
xanthomas. Young patients also have mental
retardation, progressive spasticity, cataracts,
and high cardiovascular risk. The disorder is
caused by diffuse deposition of cholesterol
and cholestanol.
Figure 7.76 Solitary rethiculohistiocytoma. Dermoscopy reveals
branched and linear vessels predominantly at the periphery of
the lesion on an orange-yellow background (X10).
9
xanthomatouslesions
on the face, trunk, neck, elbows, and folds (10–11) (Figure
7.78). They are not associated with dyslipidemia and may be
idiopathic.
Juvenile xanthogranuloma––This is the most frequent
non-Langerhans histiocytosis and consists of hard, yellow to
orange papule or nodule with clear borders, usually on the face
or neck (Figure 7.79).(12–13) It is more frequent in children
but possible also in adults. It may be isolated or eruptive and
micro- (0.2–0.5 cm) or macro- (1–3 cm) nodular.
DermoSCopiC aSpeCtS of XanthomatouS
leSionS
Xanthomatous lesions show similar patterns under the dermo-
scope (Figure 7.76–7.79).(14) There is always a yellowish back-
ground that may veer from pale yellow to orange (sunset color).
Figure 7.77 Xanthelasma. Dermoscopy reveals only yellow
background (X10).
Figure 7.78 Diffuse, flat, normolipidemic xanthomas. Dermoscopic
examination shows only pale yellow deposits (X10).
Figure 7.79 Juvenile xanthogranuolma. The dermoscopic
pattern is characterized by orange-yellow background with
“clouds” of paler yellow deposits. Moreover, branched and
linear vessels running from the periphery to the center of the
lesions are present (X10).

mandato,biagioli,andrubegni
Most contain randomly disposed linear and branched vessels.
(15) A word of warning: during dermoscopic examination,
undue pressure of the dermoscope on the skin may limit blood
flow to the lesion and prevent observation of the vascular com-
ponent.(16–17) Apart from these two features, xanthomas have
no other dermoscopic characteristics, though some lesions may
show other details. For example, brownish globules and dots
of hemosiderin, detected by the pathology lab, were recently
observed in reticulohistiocytoma. The same authors also pro-
posed dermoscopic analysis of a xanthomized dermofibroma
revealing peripheral delicate pigment network that is usually
seen in typical dermatofibromas, corresponding to hyperplastic
epidermis with basal hyperpigmentation.(18)
referenCeS
1. De Schaetzen V, Richert B, De La Brassinne M. Les xan-
thomes. Rev Med Liege 2004; 59: 46–50.
2. Crook M. Xanthelasma and cardiovascular risk. Int J Clin
Pract 2008; 62: 178–9.
3. Fernández-Herrera J, Pedraz J. Necrobiotic xanthogranu-
loma. Semin Cutan Med Surg 2007; 26: 108–13.
4. Shah KC, Poonnoose SI, George R, Jacob M, Rajshekhar V.
Necrobiotic xanthogranuloma with cutaneous and cere-
bral manifestations. Case report and review of the litera-
ture. J Neurosurg 2004; 100: 1111–4.
5. Kumakiri M, Sudoh M, Miura Y. Xanthoma disseminatum.
Report of a case, with histological and ultrastructural stud-
ies of skin lesions. J Am Acad Dermatol 1981; 4: 291–9.
6. Romero JO, Callejón JR, Alonso G. Cerebrotendinous
xanthomatosis. Neurologia 2008; 23: 530–1.
7. Rohrich RJ, Janis JE, Pownell PH. Xanthelasma palpe-
brarum: a review and current management principles.
Plast Reconstr Surg 2002; 110: 1310–4.
8. Singla A. Normolipemic papular xanthoma with xan-
thelasma. Dermatol Online J 2006; 12(3): 19.
9. Merola JF, Mengden SJ, Soldano A, Rosenman K. Eruptive
xanthomas. Dermatol Online J 2008; 14: 10.
10. Breier F, Zelger B, Reiter H, Gschnait F, Zelger BW. Papular
xanthoma: a clinicopathological study of 10 cases. J Cutan
Pathol 2002; 29: 200–6.
11. Caputo R, Passoni E, Cavicchini S. Papular xanthoma
associated with angiokeratoma of Fordyce: considerations
on the nosography of this rare non-Langerhans cell histio-
cytoxanthomatosis. Dermatology 2003; 206: 165–8.
12. Shoo BA, Shinkai K, McCalmont TH, Fox LP. Xanthogran-
ulomas associated with hematologic malignancy in adult-
hood. J Am Acad Dermatol 2008; 59: 488–93.
13. Satter EK, Gendernalik SB, Galeckas KJ. Diffuse xan-
thogranulomatous dermatitis and systemic Langerhans
cell histiocytosis: a novel case that demonstrates bridg-
ing between the non-Langerhans cell histiocytosis and
Langerhans cell histiocytosis. J Am Acad Dermatol 2008;
60: 841–8.
14. Cavicchini S, Tourlaki A, Tanzi C, Alessi E. Dermoscopy
of solitary yellow lesions in adults. Arch Dermatol 2008;
144: 1412.
15. Palmer A, Bowling J. Dermoscopic appearance of juvenile
xanthogranuloma. Dermatology 2007; 215: 256–9.
16. Rubegni P, Mandato F, Fimiani M. Juvenile Xanthogranu-
loma: dermoscopic pattern. Dermatology 2008; 218: 380.
17. Rubegni P, Mandato F, Mourmouras V, Miracco C,
Fimiani M. Xanthomatous papule in a child. Clin Exp
Dermatol, paper in press.
18. Zaballos P, Puig S, Llambrich A, Malvehy J. Dermoscopy
of dermatofibromas: a prospective morphological study
of 412 cases. Arch Dermatol 2008; 144: 75–83.

8 Dermatoscopy in cosmetic applications
Warren Wallo
Dermatoscopy can be a great visual help in monitoring skin
changes during treatment. Accuracy and reproducibility in
positioning of skin sites over time can be achieved through
documentation of skin landmarks. Color, resolution, lighting,
and magnification standards should be recorded to assure pre-
cision and reproducibility of measurements.(1)
Figure 8.1 Xerotic skin on the lower leg, before (A) and after 14 days’ treatment (B) with oatmeal-containing moisturizer. Imaging
shows dramatic visual improvements in skin textural properties, including dryness and flaking after 2 weeks, using the oatmeal-
containing skin-protectant lotion (100x) (from reference 2, by permission of Johnson & Johnson Consumer Companies, Inc.
(J&JCCI); J.Nebus).
(A) (B)
(B)
Figure 8.2 (Continued)
(A)

wallo
(D) (C)
Figure 8.2 Dermatoscopy is valuable when studying moisturization in skin of color: (A, D) baseline, (B, E) Day 1, and (C, F) Day
14, in two patients (A-C and D-F). Images show visible improvements in the appearance of skin ash and scale in skin of color
patients, as well as visible improvements in skin textural lines as early as Day 1. There was continued visible improvement in skin
ash at Day 14 (20x) (from reference 3, by permission of J&JCCI; G. Smith).
(E) (F)

videodermatoscopyincosmeticapplications
Figure 8.3 The appearance of ashy skin (A, baseline) was greatly improved after treatment with a regimen consisting of twice daily
topical application of an oatmeal-containing moisturizer and an exfoliating scrub containing oatmeal used on a weekly basis by
an African-American female (B, 1 day; C, 7 days; D, 14 days). The presence of a hypopigmented mark can be useful in locating
the exact positioning for subsequent imaging. The exact same hair follicles can also be located, and the growth of hairs can be a
compelling indication of the reproducibility of this technique (20x). (from reference 5, by permission of J&JCCI; G. Smith)
(C) (D)
(A) (B)
Xerosis anD ashy skin
In dry skin (xerosis), the corneocytes are disorderly arranged and
their borders project above the surface, producing a visually dull
appearance. By using the dermatoscope in cross-polarization,
we enhance the visualization of the lifted coenocytes’ edges and
skin flakes, which will appear white. This technique can be used
to view at high magnification the improvement in skin dryness.
After moisturization, the skin appears smoother and the white
flakes disappear.(2) (Figure 8.1)
In skin of color, the presence of fine scaliness (ash) and flakes
is more apparent because of its contrast with darker skin.(1)
Clinical studies have used digital dermatoscopy to monitor the
improvement of ashy skin in darker skin types after applica-
tions of an oatmeal-containing moisturizer. Dermatoglyphics
and dryness were visibly less apparent as early as Day 1 and
continued to improved at Day 14.(3) (Figures 8.2 and 8.3)
Postinflammatory HyPerPigmentation (PiH)
Skin inflammation alters the activity of melanocytes and may lead to
pigmented macules and patches lasting long after the inflammation
is gone (postinflammatory hyperpigmentation). Because melano-
somes in dark skin can produce large quantities of melanin, PIH is

wallo
(A) (B)
Figure 8.4 Documenting postinflammatory hyperpigmenta-
tion (PIH) over time with dermatoscopy: (A) baseline, (B) 4
weeks, and (C) 8 weeks. With careful attention to detail, PIH
marks, on the lower legs of African-American females, were
followed over time, as seen in this patient. The value of der-
matoscopy is clearly demonstrated for assessing changes in
pigmentation and documenting changes over time and with
treatment (Captured at 12x / further cropped and enlarged
for publication by 5x (therefore overall mag 60x)) (from ref-
erence 5, by permission of J&JCCI; G. Smith).
(C)
most prevalent in darker skin types, and it is the cause of significant
complaints by patients, especially with acne and pseudofolliculitis
barbae (PFB).(4) Dermatoscopy, in cross-polarization mode, can be
used to beautifully document the changes in melanin pigmentation
over time and with treatment.(5) (Figure 8.4)
PseuDofolliculitis BarBae (PfB)
PFB is an inflammatory condition frequently affecting people
of darker skin color with tightly coiled hair. The cause of PFB
is usually the penetration of shaved hair into adjacent skin.
(6) The outcome is often the formation of an inflammatory
papule at the site of the in-grown hair, followed by postinflam-
matory hyperpigmentation. Dermatoscopy in cross-polarization
mode is extremely helpful in identifying the extrafollicular skin
penetration of hair and in treatment follow-up.(5) (Figure 8.5)
Dermatoscopy has also been used in the clinical practice to show
patients the in-growing of hair corresponding to individual
papules and to enhance compliance in treatment.(7)

videodermatoscopyincosmeticapplications
tricHostasis
Trichostasis spinulosa is a follicular condition in which pores
retain fascicles of hair embedded in sebaceous material. This is
more prominent on the centrofacial region of adult and older
individuals and appears as dark pores.(8) Owing to the clear
contrast between the dark-brown, clogged follicles and the
surrounding skin color, videodermatoscopy and epilumines-
cence have been used to investigate the removal of trichostatic
impactions with the use of pore strips.(9)
acne lesions
Acne consists of noninflammatory (comedones) and inflam-
matory lesions (papules, pustules, and nodules). In mild acne,
patients are often concerned with the appearance and evolu-
tion of individual papules and pustules. They often purchase
Figure 8.5 Dermatoscopy of facial acne on African-American males with pseudofolliculitis barbae (PFB). Dermatoscopy was used
to illustrate (A) (20X) normal skin, and various examples of the spectrum of PFB symptoms, including (B) (20X) cheek area with
skin dryness around follicle; (C) (100X) site of recurring PFB; and (D) (100X) PFB lesion with extrafollicular penetration (from
reference 5, by permission of J&JCCI; J. Woodruff).
(A) (B)
(C) (D)
acne-spot treatments to selectively target those lesions. The abil-
ity to accurately capture images of individual lesions is, there-
fore, important to study their evolution with treatment. Several
studies have used digital dermatoscopy to demonstrate the effi-
cacy of topical formulations to quickly improve papules and
pustules in acne.(10) (Figure 8.6).
conclusion
Dermatoscopy represents an extremely valuable tool to monitor
skin conditions under magnification and standardized lighting
settings. The ability of epiluminescence to visualize subsurface
pigment has enabled researchers to detect details not appreciated
by the naked eye. Furthermore, digitization of images has allowed
the archiving of images and dramatically helped dermatologists
in the monitoring of lesions and skin treatments.

wallo
6. Garcia-Zuazaga J. Pseudofolliculitis barbae: review and update
on new treatment modalities. Mil Med 2003; 168: 561–4.
7. Chuh A, Zawar V. Epiluminescence dermatoscopy enhanced
patient compliance and achieved treatment success in
pseudofolliculitis barbae. Australas J Dermatol 2006; 47:
60–2.
8. Pagnoni A, Kligman AM, el Gammal S, Stoudemayer T.
Determination of density of follicles on various regions of
the face by cyanoacrylate biopsy: correlation with sebum
output. Br J Dermatol 1994; 131: 862–5.
9. Pagnoni A, Kligman AM, Stoudemayer T. Extraction
of follicular horny impactions of the face by polymers.
Efficacy and safety of a cosmetic pore-cleansing strip
(Biore’). J Dermatol Treat 1999; 10: 47–52.
10. Coret C, Chantalat J, Miller D, Kurtz E. Fast-acting treatment
of mild to moderate acne lesions by a novel 2% salicylic acid
microgel complex. J Am Acad Dermatol 2006; 54: AB18.
Figure 8.6 Dermatoscopy of a target acne lesion before and
after treatment with a 2% salicylic acid product: (A) baseline,
(B) 8 hours, and (C) 24 hours. Acne target lesions can be fol-
lowed using dermatoscopy, offering the opportunity to observe
and measure changes in size and redness over time (12X) (from
reference 10, by permission of J&JCCI; D. Miller).
references
1. Wallo W, Smith G, Luedtke M, Kurtz ES. Micro-imaging
of skin with innovating methodology: Valuable for Skin of
color. Poster presented at: 62nd AAD Meeting; February
6–11, Washington, DC, 2004: P278.
2. Nebus J, Wallo W, Kurtz E. Alleviating itchy, extra dry
skin with an oatmeal, skin protectant lotion. J Am Acad
Dermatol 2006; 54: AB53.
3. Nebus JA, Smith G, Kurtz ES, Wallo W. Alleviating dry,
ashen skin in patients with skin of color. Poster presented
at: 62nd AAD Meeting; February 6–11, Washington, DC,
2004: P294.
4. Baumann L, Rodriguez D, Taylor SC, Wu J. Natural
considerations for skin of color. Cutis 2006; 78: 2–19.
5. Wallo W, Woodruff J, Smith G, Kurtz ES. Documentation of
cutaneous conditions important in skin of color with innovative
imaging approaches. J Am Acad Dermatol 2005; 52: 89.
(A) (B)
Baseline
8 hours
(C)
24 hours

Index
acetic acid 22
acne lesions 125
actinic keratosis 117
actinic porokeratosis 115–17
albendazole 22–3
alopecia areata 33–5, 40
dystrophic hair 34–5
yellow dots 33–4
alopecia areata incognita
dystrophic hairs 36
short regrowing hairs 35–6
yellow dots 35
amelanotic melanoma 88
analogue videodermoscopy 2
androgenetic alopecia (AGA) 43
hair diameter diversity 32–3
peripilar signs 33
secondary signs 33
angiogenesis and psoriasis 52
anogenital warts 73
ashy skin 123
Auspitz sign 58
balanitis 64
benzyl alcohol 21
benzyl benzoate 21
Bowen’s disease
dermoscopic features of 82, 83
detection of 84
brittle nails 47
butter/margarine/mayonnaise 22
capillaroscopy 103
carbaryl 21
chronic capillaritis 112
cicatricial alopecias 37
citronella 22
clear cell acanthoma (CCA)
definition 70
dermoscopic features of 71
diagnosis of 70
videodermatoscopy of 72
collagen tissues, disorders of 100–2
common urticaria (CU) 96, 97–8, 99
congenital triangular alopecia 37
contact incident light dermoscope 3–4
cosmetic applications, videodermatoscopy in 121–2, 126
acne lesions 125
postinflammatory hyperpigmentation (PIH) 123–4
pseudofolliculitis Barbae (PFB) 124
trichostasis spinulosa 125
xerosis and ashy skin 123
cotrimoxazole 23
crab lice 9, 17–18
crotamiton 21
crusted scabies see Norwegian scabies
cyclosporine 54
data storage 4
dermatological digital image management, database software
for 4
dermatomyositis 47
dermatoscopy 1, 2
alopecia 40–2
scabies 12–13
alopecia areata see alopecia areata
alopecia areata incognita see alopecia areata incognita
androgenetic alopecia (AGA) 32–3
cicatricial alopecias 37
congenital triangular alopecia 37
discoid lupus erythematosus (DLE) 39
folliculitis decalvans (FD) 40
lichen planopilaris (LPP) 37–8
trichotilomania 37
xanthomatous lesions 119–20
pyogenic granuloma 48–9
tungiasis 29–30
venular malformations 75–6, 77
warts 49
Dermo-Image 4
dermoscopy see dermatoscopy
diffuse, flat, normolipidemic xanthomas 118–19
digital dermoscopy analysis, instruments for 5
digital videodermoscopy 2–3
dimethicone 21
discoid lupus erythematosus (DLE) 38–9, 102
Page references in italics refer to tables.

index
disseminated superficial actinic porokeratosis
(DSAP) 115–16, 117
distal subungual onychomycosis (DSO) 47
epidermal hyperplasia 52
epiluminescence microscopy 1, 11, 25
epimeres 25
epulis gravidorum 86
eruptive papular xantoma 118
erythematotelangiectatic rosacea 103, 104
folliculitis decalvans (FD) 39–40
frontal fibrosing alopecia 41
glomus tumor 49
hair loss
alopecia areata 33–5
alopecia areata incognita 35–6
androgenetic alopecia (AGA) 32–3
congenital triangular alopecia 37
dermoscopy in the differential diagnosis of alopecia 40–3
discoid lupus erythematosus (dle) 38–9
folliculitis decalvans (fd) 39–40
lichen planopilaris (lpp) 37–8
normal scalp 31–2
scarring alopecia 37
therapeutic monitoring of hair loss with
videodermatoscopy 43
trichotilomania 36–7
head lice
clinical features 8
diagnosis of 9, 16
differential diagnosis 9
epidemiology 8
pathogenesis 8
videodermatoscopy 16–17
hemangiomas 88
Henderson–Paterson bodies 106–7, 108
human papillomaviruses (HPV) 73–4
definition 73
differential diagnosis
Fordyce spots 74
pearly papules 73–4
hypomelanotic melanoma 88
hyponychium dermoscopy 45, 46
Imagestore for Healthcare 4
indomethacin 23
infantile scabies 8
ivermectin 21, 23
juvenile xanthogranuloma 119
kerosene/gasoline/petroleum distillates 22
lacunas 88
levamisole 23
lichen aureus 113
lichen planopilaris (LPP) 37–8
lichen planus
annular lichen ruber planus 92
definition 90
evolved LP lesions 92
hypertrophic lichen planus 92
initial LP lesions 90–1
mature LP lseions 91–2
postinflammatory hyperpigmentation
of LP 93–5
lindane 21–2
lobular capillary hemangioma 86
Majocchi’s disease 113
malathion 22
melanocyte activation 50
melanocytic hyperplasia 49, 50, 51
melanonychia 49
distal edge of the nail plate dermoscopy 50
hyponychium and proximal nail-fold dermoscopy 50
intraoperative dermoscopy 52
melanocyte activation 49
melanocytic hyperplasia 49–50
nail plate dermoscopy of 50
Micro-Hutchinson’s sign 45, 50
Mirror Software 4
molluscipox virus 106
molluscum bodies 106–7, 108
molluscum contagiosum (MC) 106–8
clinical diagnosis of 107
epidermal hyperplasia 106–7
molluscum contagiosum virus (MCV) 106
Muir–Torre syndrome 109
nail bed melanoma 50
nail disease 45
brittle nails 47
dermoscopic examination 45
dermoscopy of hyponychium 45
distal edge of the nail plate,
dermoscopy of 45
intraoperative dermoscopy 45–6
melanonychia 49–51
nail plate dermoscopy 45
nail tumors 48
glomus tumor 49
onychomatrichoma 48
onychopapilloma 48

index
pyogenic granuloma 48–9
warts 49
onychomycosis 47
proximal nail fold dermoscopy 45
psoriasis 46
subungual hemathoma 47–8
nail matrix melanoma 49
nail matrix nevi 49
nail matrix psoriasis 46
nail plate dermoscopy 45
brittle nails and 47
glomus tumor and 49
onychomatrichoma and 48
onychomycosis and 47
onychopapilloma and 48
psoriasis and 46
subungual hematomas and 48
nail tumors 48
glomus tumor 49
onychomatrichoma 48
onychopapilloma 48
pyogenic granuloma 48–9
warts 49
National Rosacea Society Expert Committee 103
nits 9, 16
nonpsoriatic balanitis 66
Norwegian scabies 8
onychomatrichoma 48
onychomycosis 47
onychopapilloma 48
optical dermoscope 2
oral ivermectin 23
palmar, striated xanthochromia 118
palmoplantar psoriasis 61–3
pediculosis
crab lice 9
head lice 8–9
therapeutic monitoring with videodermatoscopy 25–6
videodermatoscopy 16–18
pediculosis capitis see head lice
pediculosis pubis infestation see crab lice
Pediculus humanus capitis 8, 16
peno-vulvoscopy 73, 74
perifollicular erythema 37
permethrin 22
petrolatum (petroleum jelly) 22
phototricogram 43
Phthirus pubis 17
pigmented purpuric dermatoses (PPD) 112–14
clinical entities of 113
dermoscopic examination of 113–14
occurrence of 112
plaque psoriasis 53, 67, 94–5
phases of 57–8
stages of clinical polymorphism 58–60
early steady-state phase 58
initial phase 58
intermediate phase 58
late steady-state phase 59
phase of resolution 59–60
porokeratosis
clinical variants of 115–16
dermoscopic features of 116
risk factors of 115
postinflammatory hyperpigmentation (PIH) 123–4
proximal nail-fold dermoscopy 45, 46
proximal subungual onychomycosis (PSO) 47
pseudofolliculitis barbae (PFB) 124
psoriasis 46
angiogenesis and 52
definition 52, 57
histopathological correlations of 57–60
palmoplantar 61–3
psoriatic balanitis 64–6
scalp 67–8
therapy monitoring 53–5
vascular patterns in 53
videocapillaroscopy in 52
videodermatoscopy in 52–3
see also plaque psoriasis
psoriatic balanitis 64–6
Pthirus pubis 9
pubic lice 18, 25
purpura simplex 112
pyogenic granuloma 48–9, 89
clinical diagnosis of 86
dermoscopy in recognition of 86–7
with vascular structures 87–8
pyrethrins 22
Raynaud’s phenomenon (RP) 100
rosacea 103–5
symptoms of 104
videocapillaroscopic technique and 103
Sarcoptes scabiei 7, 25
scabies 7
biologic cycle 7
clinical features 7–8
dermoscopic diagnosis of 12
diagnosis 8
differential diagnosis 8
epidemiology 7
therapeutic monitoring with videodermatoscopy 26–8
transmission 7
videodermatoscopy and 11–14

index
scalp atrophy 39
scalp pruritus 9
scalp psoriasis 67–8
scarring alopecia 37
Schamberg’s disease 113
scleroderma 47
scleroderma pattern (SP) 100–1
scraping versus high magnification videodermatoscopy (VD)
11–12
sebaceous hyperplasia
appearance of 109
dermoscopic features of 110
diagnosing 109–10
vascular structures 110–11
seborrheic dermatitis 9, 16, 53, 67, 68, 103, 104, 105
softwares for assessment and diagnosis 4–5
subacute lupus erythematosus 102
subungual hematomas 47–8
sulfur 22
systemic lupus erythematosus (SLE) 47
systemic sclerosis (SSc) 100, 101
tea tree oil 22
teledermatology 1, 13
therapeutic monitoring of parasitoses with
videodermatoscopy
scabies 25–6
pediculosis 26–8
therapy of scabies and pediculosis 20
alternative unproven remedies 22
natural products 22
nit combs 20
pediculosis 20
scabies 20
systemic treatment 22–3
topical treatment 21–2
TNF-α 52, 55
topical corticosteroids 22
Tricho-scan 5
trichostasis spinulosa 125
trichotilomania 36–7
tuberous xantoma 118
tunga penetrans 29
tungiasis 29–30
urticaria 96
urticarial vasculitis (UV) 96
dermoscopic purpuric structures, types of 97–8
lesions of 99
vascular endothelial growth factor (VEGF) 52
venular malformations 75–80
clinical data and therapy of 78
definition 75
dermoscopic data and therapy of 78–80
dermoscopy of 75–6, 77, 80
histological data and therapy of 78
vessels in 76–7
videocapillaroscopy
collagen tissues and 100
in psoriasis 52–3
scalp psoriasis and 67
videodermatoscopy (VD) 1, 2, 14, 20
analogue 2
clear cell acanthoma (CCA) 72
contact, noncontact and polarized 3–4
cosmetic applications 121–6
digital 2–3
palmoplantar psoriasis 61–3
pediculosis and 16–18
pediculosis capitis 16–17
phthiriasis pubis 17–18
psoriasis 52–3
psoriatic balanitis 64–5
scabies 8
therapeutic monitoring of hair loss with 43
venular malformations 76–7, 80
videodermoscopy see videodermatoscopy
white superficial onychomycosis (WSO) 47
Wickham striae 90, 91, 92, 95
xanthelasms 118
xanthomatous lesions 118–20
xanthomization 118
xerosis 123
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www.informahealthcare.com
Telephone House, 69-77 Paul Street, London EC2A 4LQ, UK
52 Vanderbilt Avenue, New York, NY 10017, USA
About the book
Dermatoscopy has increasingly been taken up in dermatology practice
as a non-invasive technique for the diferential diagnosis of pigmented
skin lesions. However, there are further uses for dermatoscopy in several
dermatologic conditions in terms of diagnosis, prognostic evaluation,
and monitoring response to treatment. There is also the technique
of videodermatoscopy – employing the use of digital systems that
ensure high magnifcations – in addition to the dermatoscopy that
conventionally refers to manual devices.
This book aims to advance knowledge of these extended clinical
applications for enhanced visualization and digital imaging using manual
dermatoscopy or videodermatoscopy, beyond the usual indication
of cutaneous pigmented lesions. This will serve as an important yet
relatively simple aid to a dermatologist’s daily ofce practice.
Contents
Introduction * Equipment * Scabies and Pediculosis: Biologic Cycle
and Diagnosis * Videodermatoscopy and Scabies * Videodermatoscopy
and Pediculosis * Therapy of Scabies and Pediculosis: Potential and
Pitfalls * Therapeutic Monitoring of Parasitoses with Videodermatoscopy
* Tungiasis * Hair Loss * Nail Diseases * Psoriasis: Vascular Pattern
under Videodermatoscopy Observation * Psoriasis: Histopathological
Correlations * Palmo-plantar Psoriasis * Psoriatic Balanitis * Scalp Psoriasis
* Clear Cell Acanthoma * HPV Infections * Venular Malformations
(Port Wine Stain Type) * Bowen’s Disease * Pyogenic Granuloma * Lichen
Ruber Planus * Urticaria and Urticarial Vasculitis * Disorders of Collagen
Tissues * Rosacea * Molluscum Contagiosum * Sebaceous Hyperplasia
* Pigmented Purpuric Dermatoses * Actinic Porokeratosis
* Xantomatous Lesions * Dermatoscopy in Cosmetic Applications
About the editors
Giuseppe Micali, MD, is Professor and Chairman at the Department
of Dermatology, AOU Policlinico-Vittorio Emanuele, Catania, Italy
Francesco Lacarrubba, MD, is Researcher at the Department
of Dermatology, AOU Policlinico-Vittorio Emanuele, Catania, Italy
Dermatoscopy
in Clinical Practice
Edited by
Giuseppe Micali
Francesco Lacarrubba
Dermatology
Beyond Pigmented Lesions

Dermatoscopy in Clinical Practice

Series in Dermatological Treatment Published in association with the Journal of Dermatological Treatment Series editors: Steven R Feldman and Peter van de Kerkhof

1 2 3 4 5 6 7 8

Robert Baran, Roderick Hay, Eckhart Haneke, Antonella Tosti Onychomycosis, second edition, ISBN 9780415385794 Ronald Marks, Facial Skin Disorders, ISBN 9781841842103 Sakari Reitamo, Thomas Luger, Martin Steinhoff Textbook of Atopic Dermatitis, ISBN 9781841842462 Calum Lyon, Amanda J Smith Abdominal Stomas and their Skin Disorders, Second Edition, ISBN 9781841844312 Leonard Goldberg Atlas of Flaps of the Face, ISBN 9781853177262 Antonella Tosti, Maria Pia De Padova, Kenneth R Beer Acne Scars: Classification and Treatment, ISBN 9781841846873 Bertrand Richert, Nilton di Chiacchio, Eckart Haneke Nail Surgery, ISBN 9780415472333 Giuseppe Micali, Francesco Lacarrubba Dermatoscopy in Clinical Practice: Beyond Pigmented Lesions, ISBN 9780415468732

Dermatoscopy in Clinical Practice Beyond Pigmented Lesions Edited by Giuseppe Micali. Italy and Francesco Lacarrubba. MD Researcher Department of Dermatology AOU Policlinico-Vittorio Emanuele Catania. Italy . MD Professor and Chairman Department of Dermatology AOU Policlinico-Vittorio Emanuele Catania.

electronic. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-13: 9780415468732 Orders Informa Healthcare Sheepen Place Colchester Essex CO3 3LP UK Telephone: +44 (0)20 7017 5540 Email: CSDhealthcarebooks@informa. UK . Bodmin. stored in a retrieval system. photocopying. London W1T 3JH. Registered Office: 37/41 Mortimer Street. Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency. Cornwall. No part of this publication may be reproduced. recording. Informa Healthcare is a trading division of Informa UK Ltd. A CIP record for this book is available from the British Library. 90 Tottenham Court Road. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication.com Typeset by C&M Digitals (P) Ltd. or transmitted. mechanical. Chennai. India Printed and bound in Great Britain by MPG Books. All rights reserved. without the prior permission of the publisher or in accordance with the provisions of the Copyright. Registered in England and Wales number 1072954. London EC2A 4LQ. in any form or by any means. we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. or otherwise. 69-77 Paul Street. London W1P 0LP.© 2010 Informa UK Ltd First published in 2010 by Informa Healthcare. Telephone House.

and Ilaria Proietti 6.3 Videodermatoscopy and pediculosis Giuseppe Micali. Renato Bakos. Nella Pulvirenti. Bianca Maria Piraccini. and Dennis P West 3. and Débora Cadore de Farias Diseases characterized by altered vascular pattern 6.1 Scabies and pediculosis: Biologic cycle and diagnosis Ani L Tajirian and Robert A Schwartz 3. Marianna Umana. Rossella De Angelis.Contents List of Contributors 1 Introduction Giuseppe Micali and Francesco Lacarrubba Equipment Pietro Rubegni. Beatrice Nardone. and Giuseppe Micali 3. and Francesco Lacarrubba 3. Marco Burroni.2 Videodermatoscopy and scabies Francesco Lacarrubba. and Michele Fimiani Parasitoses 3. Niccolò Nami.1 Psoriasis 6. Aurora Tedeschi.1B Histopathological correlations † Daniele Innocenzi. and Giuseppe Micali vii 1 2 2 3 7 11 16 20 25 29 31 5 45 6 52 57 61  . and Francesco Lacarrubba 3. Maria Concetta Potenza. and Giuseppe Argenziano 4 Hair loss Antonella Tosti and Bruna Duque Estrada Nail diseases Antonella Tosti.6 Tungiasis Elvira Moscarella.1C Palmoplantar psoriasis Francesco Lacarrubba.4 Therapy of scabies and pediculosis: Potential and pitfalls Lee E West. Maria Letizia Musumeci. and Leonardo Bugatti 6.5 Therapeutic monitoring of parasitoses with videodermatoscopy Giuseppe Micali.1A Vascular pattern under videodermatoscopy observation Giorgio Filosa.

and Giuseppe Micali 6.4 Rosacea Paolo Rosina 7.8 Actinic porokeratosis Pedro Zaballos Diego 7.4 Venular malformations (port wine stain type) Francisco Vázquez-López 6.2 Urticaria and urticarial vasculitis Francisco Vázquez-López 7.6 Sebaceous hyperplasia Pedro Zaballos Diego 7.contents 6.7 Pigmented purpuric dermatoses Pedro Zaballos Diego 7.3 HPV infections Pompeo Donofrio and Maria Grazia Francia 6.5 Bowen’s disease Leonardo Bugatti.5 Molluscum contagiosum Pedro Zaballos Diego 7.1E Scalp psoriasis Paolo Rosina 6.2 Clear cell acanthoma Francesco Lacarrubba. Federica Dall’Oglio.1 Lichen ruber planus Francisco Vázquez-López 7. Maurizio Biagioli. Orazia D’Agata. Maria Rita Nasca.1D Psoriatic balanitis Giuseppe Micali. and Pietro Rubegni 8 Dermatoscopy in cosmetic applications Warren Wallo 64 67 70 73 75 82 86 90 96 100 103 106 109 112 115 118 121 Index 127  .3 Disorders of collagen tissues Paolo Rosina 7. and Francesco Lacarrubba 6. Giorgio Filosa.9 Xanthomatous lesions Filomena Mandato. and Alessandra Filosa 6.6 Pyogenic granuloma Pedro Zaballos Diego 7 Miscellanea 7.

Italy Bruna Duque Estrada Instituto de Dermatologia Prof. Spain Pompeo Donofrio Section of Dermatology Department of Systemic Pathology Genito-Dermatologic Ambulatory Unit University of Naples Federico II Naples. Brazil Maria Concetta Potenza Department of Dermatology . Brazil Maurizio Biagioli Section of Dermatology Department of Clinical Medicine and Immunological Science University of Siena Siena. Italy Orazia D’Agata Department of Dermatology University of Catania Catania Italy Federica Dall’Oglio Department of Dermatology University of Catania Catania.Polo Pontino University of Rome “Sapienza” Rome. Brazil Alessandra Filosa Dermatology Unit Augusto Murri Hospital Jesi. Italy Débora Cadore de Farias Department of Dermatology Santa Casa de São Paulo Hospital São Paulo. Italy Leonardo Bugatti Dermatology Unit Augusto Murri Hospital Jesi. Rubem David Azulay Rio de Janeiro. Italy  .List of contributors Giuseppe Argenziano Department of Dermatology Second University of Naples Naples. Italy Renato Bakos Department of Dermatology Universidade Federal do Rio Grande do Sul Porte Alegre. Italy Marco Burroni Section of Dermatology Department of Clinical Medicine and Immunological Science University of Siena Siena. Italy Rossella De Angelis Rheumatology Unit Department of Molecular Pathology and Innovative Therapy Polytechnic University of the Marche Ancona. Italy Pedro Zaballos Diego Dermatology Department Hospital Sant Pau i Santa Tecla Tarragona.

Italy Elvira Moscarella Department of Dermatology Second University of Naples Naples. Italy Ilaria Proietti Department of Dermatology . Italy Giuseppe Micali Department of Dermatology A.U. Italy Maria Grazia Francia Section of Dermatology Department of Systemic Pathology University of Naples Federico II Naples. Italy Beatrice Nardone Department of Dermatology University of Catania Catania Italy Maria Rita Nasca Department of Dermatology University of Catania Catania Italy Bianca Maria Piraccini Department of Dermatology University of Bologna Bologna. Italy Tragically deceased 2009 † Maria Letizia Musumeci Department of Dermatology University of Catania Catania Italy Niccolò Nami Section of Dermatology Department of Clinical Medicine and Immunological Science University of Siena Siena.O. Italy Daniele Innocenzi Department of Dermatology . Italy Francesco Lacarrubba Department of Dermatology A. Italy Filomena Mandato Section of Dermatology Department of Clinical Medicine and Immunological Science University of Siena Siena. Italy  . Policlinico-Vittorio Emanuele Catania.O. Italy Michele Fimiani Section of Dermatology Department of Clinical Medicine and Immunological Science University of Siena Siena.Polo Pontino University of Rome “Sapienza” Rome.lst of contrbutors Giorgio Filosa Dermatology Unit Augusto Murri Hospital Jesi.Polo Pontino University of Rome “Sapienza” Rome.U. Policlinico-Vittorio Emanuele Catania. Italy Nella Pulvirenti Department of Dermatology University of Catania Catania Italy Paolo Rosina Section of Dermatology and Venereology Department of Biomedical and Surgical Sciences University of Verona Verona.

Asturias. New Jersey.lst of contrbutors Pietro Rubegni Section of Dermatology Department of Clinical Medicine and Immunological Science University of Siena Siena. USA Ani L Tajirian Department of Dermatology New Jersey Medical School Newark. Italy Marianna Umana Department of Dermatology University of Catania Catania Italy Francisco Vázquez-López Department of Dermatology Hospital Universitario Central de Asturias Oviedo. Italy Robert A Schwartz Department of Dermatology New Jersey Medical School Newark. Illinois. USA Dennis P West Department of Dermatology The Feinberg School of Medicine Northwestern University Chicago. Illinois. Spain Warren Wallo Johnson & Johnson Consumer Companies. Inc. New Jersey. USA Lee E West Department of Pharmacy Northwestern Memorial Hospital Chicago. New Jersey. USA Aurora Tedeschi Department of Dermatology University of Catania Catania Italy Antonella Tosti Department of Dermatology University of Bologna Bologna. USA  . Skillman.

We dedicate this book to the memory of Daniele Innocenzi. an extraordinary and outstanding dermatologist and friend .

VD represents the evolution of D. in the latter instance the term videodermatoscopy (VD) is more usual. usually through the technique called epiluminescence microscopy. the capability to capture digital images is perfectly suited to teledermatology . recently.the “store-and-forward” technique that allows exchange of opinions between dermatologists . and a large variety of other dermatologic conditions as well as cosmetology. Introduction Giuseppe Micali and Francesco Lacarrubba D/VD have expanded applications in dermatology. The images obtained are visualized on a monitor and stored on a personal computer. Dermatoscopy (D) . In this book the term “dermatoscopy” will be referred to the use of manual devices and “videodermatoscopy” to the use of digital systems operating at high magnifications. new systems utilizing polarized light may achieve similar results without the need for liquids. Moreover. In particular.also called “dermoscopy” or “incident light microscopy” .is a non-invasive technique that allows a rapid and magnified in vivo observation of the skin with the visualization of morphologic features invisible to the naked eye. or water) to the skin to eliminate light reflection. describing the clinical and histopathological correlations associated with the procedure.and might be useful when on-site D/VD services are not available. who should thus be encouraged to utilize D/VD in the routine evaluation of skin diseases. hair and nails abnormalities. The book has plenty of images that will be useful in the daily clinical practice of a dermatologist. Importantly. It may be performed with manual devices that do not require any computer “assistance” and allow magnifications up to X20. or with digital systems requiring a video camera equipped with optic fibers and lenses that ensure magnifications of up to X1000. and monitoring response to treatment. Depending on the skin disorder. the book focuses on those conditions in which the techniques are more useful. In many ways. The aim of this book is to advance knowledge of enhanced visualization/digital imaging using D or VD beyond the traditional indication of pigmented lesions of the skin. which involves the application of a liquid (oil. D/VD may be useful for differential diagnosis. prognostic evaluation. Alternative applications of D/VD include inflammatory diseases. in order to process them and compare any possible changes over time. it has been demonstrated that  . for many of these disorders the use of high magnifications is needed for research as well as for clinical purpose. However. parasitoses. Both D and VD are widely used in the differential diagnosis of pigmented skin lesions. apart from their most common use for the differential diagnosis of pigmented skin lesions. alcohol. The book will serve as an important yet relatively simple aid in daily office practice.

Dermoscopy is currently used in rou­ tine dermatology. Much higher resolution is possible with digital telecameras than is possible with analogue video telecameras and this has clear diagnostic advantages. while the objective of the dermoscope is placed against the skin surface. as digital dermoscopy systems of this type can reach a picture resolution of 1280 x 1.  .000 x 2.2 “Real­time” digital dermoscopy analyzer. the dermoscopic examination using these equipment produced only low­quality images. The instrument makes it possible to observe a vast new range of dermatological signs. where pixel is the basic image unit.(2. 4) Digital telecameras have better quality for the equivalent video characteristics because they do not require any conversion. computerized instruments for digitizing images from telecameras connected to videodermoscopes became common.2). Marco Burroni. Niccolò Nami.1 Instrument for digital dermoscopy.(2) Digital Videodermoscopy Between 1990 and 2000. for example. Digital dermoscopic images can be obtained by conver­ sion from video telecameras connected to digital cards or by use of high­resolution digital telecameras or digital cameras coupled with special dermoscopy adaptors. and other cumbersome documentation and data­saving procedures. Equipment Pietro Rubegni. They can have a USB (usu­ ally amateur grade) or Firewire (professional grade. Digital cameras provide exceptionally high resolutions (up to 3.024 pixels. which is due to the low resolution of the first­genera­ tion video cameras. A medium such as ultrasound gel or Vaseline oil is applied to the skin to make the stratum corneum transparent. faster and Figure 2. the signal acquisition peripheral required a charge­coupled device (3CCD) or sen­ sor for the red. 3) In the case of video telecameras. in order to keep image quality high during sampling.000 are common) but have the disadvantage of not providing full resolution images in vivo but only after the images have been saved. advances in video technology led to the development of instruments that displayed dermoscopic images on a screen.(1. Computerized systems proved more practical for managing examinations because they offered the pos­ sibility of saving personal and private data of patients. The various specialist courses held in recent years have led to the definition of new methods for improving the diagnosis of neoplastic and other skin disorders. VidEodErmoscopy Analogue Videodermoscopy Between 1980 and 1990. together with digital images of pigmented skin lesions (Figure 2. with images observed in vivo at 15 to 25 photograms per second on computer screens (Figure 2. and Michele Fimiani introduction The optical dermoscope is an instrument containing a light source that enables skin structures invisible to the naked eye to be seen.1). analogue video recorders of the 1980s often had less than 400 horizontal lines. Low quality and technical limitations prevented the widespread use of videodermoscopy. Figure 2. green. the maximum television resolution is 768 x 576 pixel for the European PAL broadcast system and less for the American NTSC. and blue bands. better quality) interface. during this period.(1) The first videodermoscope had a tele­ camera with video resolution connected to an optical dermo­ scope and a television screen with video recorders to record examinations. However.

The two types of digital instruments are.(5) It is commonly thought that a higher number of pixels implies better quality images. lower resolution compromises diagnosis and higher resolution is unnecessary (Figure 2. Contact incident light dermoscopes use a glass window placed in contact with the skin. B: The same image at 1.equipment (A) (B) Figure 2. therefore. Overall magnification M of digital dermoscopes is calculated as the ratio of screen diagonal D to field of view diagonal d: M = D/d. Reddish or saturated images are due to low­quality equipment or failure of white balancing during chromatic calibration. Image quality is important for early diagnosis of melanoma and depends on factors such as the optical system of the instrument.3 A: Image at 512 x 384 pixel resolution (42.(6) Digital dermoscopy images generally have resolutions between 768 x 576 and 1. e­mail: dermoim­ age@ergonsrl.024 x 768 pixel resolution (326 KB). and polarized dermoscopy Today there are many types of dermoscopes. Figure 2. Illumination must be homogeneous and sufficiently strong while incident intensity should be modified by the lens dia­ phragm rather than by varying electrical potential so as to keep the color of the study area constant.100 Siena. illu­ minated at an angle of about 30 to 45 degrees so as to eliminate direct  .600 x 1. Strada Massetana Romana 50/A 53. Dermoscopy optical systems generally enable a horizontal “field of view” between 2 mm and 3 cm.200 pixel. Contact. designed for different users. Clinicians who use video or digital telecameras (usually specialist centers) carry out many examinations to diag­ nose melanoma or inflammatory skin diseases and observe many lesions by digital technology. illumina­ tion. Digital cameras are largely used to document lesions first observed by traditional dermoscopy. and resolution.3). type of instrument. this is untrue. noncontact.8 KB).it). even if resolution is the imaging system’s ability to reproduce details. The definition of magnification is only valid for integrated instruments with always the same screens. Field of view is a preferable param­ eter.4 Dermoimage software for image storage (Ergon srl.

500 or over version Confidentiality with username and password protection Yes Network compatible with image History sharing via the import Internet option Cost Yes No $825 ($2.ttlsoftware. and multi­ media data. Light reflected from the skin surface maintaining the polariza­ tion of the light source is eliminated by the polarizer in front of the sensor. Biomips Engineering. updatable index of dermatological disorders ready to imple­ ment. and Dermo-Image have these features and also enable comparison of two or more digital images. Only Dermo-Image (Figure 2. this enables skin patterns to be observed to a greater depth. reflection. Such software enables images to be saved and stored in clinical records together with personal.(10. confidential. with com­ puterized instrument providing a visual database and objective evaluations of pigmented skin lesions.(13) The latter enables overlay of multiple images and fade between them. Siena. and fimiani Table 2.(12) Some examples for dermatologists are Imagestore for Healthcare. The loop tool allows practitioners to critically examine skin features to target problem areas.5 Images can be stored and analyzed using DB­Mips System.(13) softwarE for objEctiVE assEssmEnt and assistEd diagnosis Many research groups have worked on image processing and numerical assessment of image features for diagnostic purposes Figure 2. nami. product information available atwww.L. product information available at www. The software includes classification by pathology. burroni. but soon the need emerged to develop software to store the data acquired. one before the telecamera sensor and one on the light source.com Dermo­Image. and an advanced image retrieval system based on personalized crite­ ria. and printing images were all designed with the workflow of a medical practice in mind.canfieldsci. 11) Initially these instruments were used nonroutinely by enthu­ siasts.1). Imagestore for Healthcare.4) and Imagestore for Healthcare include a preset. This has the advantage of  .1 Selected Commercially Available Database Software for Dermatological Digital Image Management.asp Imagestore for healthcare. and includes retrieval of digital images by diagnosis.500 with DPS tools) Software/contact Mirror software. rendering the skin translucent and revealing subcutaneous patterns invisible to the naked eye. Mirror. Specificallyfor dermatology Image (preset updatable Specific tags for modification index and tags) image retrieval tool No Yes Only in the $2.rubegni. This function is useful for assessing results of treatment and evolu­ tion of lesions. using the compare feature. and anatomical site. Polarization makes it possible to dispense with the glass window in contact with the skin. viewing. especially dermatology clinics. patient. Images can be trans­ ferred to other programs like Word and Power Point..(7) A liquid fills the space between the skin and the glass.com Yes Yes Yes Securely access images from any Internet­ connected PC Yes No not available Yes Yes Yes Powerful and Yes flexible permission system Yes $900 avoiding transmission of infections and ischemia caused by pressure of the window on the skin. Italy).(8. Mirror Software. retrieving.R. and Dermo-Image (Table 2. product information available at www .(8) data storagE Digital telecameras and photocameras are now used by all medical centers. the basic management functions of storing. and a magnifying lens system. to acquire skin images. treatment.com/ Imaging_Products_ Imaging. or examination. 9) Two polarizing filters can be added to this simple optical system.dermoimage. Mirror Software was developed specifically for medical professionals. S. so as to eliminate light reflected by cross­polarization.

Flanigan K. Evaluation of different image acquisition techniques for a computer vision system in the diagnosis of malignant melanoma. Dusza SW. 143(3): 329–38.200 K. Weinberg JM. 144(6): 828–9. Thomas CO. global 3CCD. 25(6): 495–9. J Cosmet Dermatol 2003. instrument DB­Mips web site www.dsmedigroup. Acquisition­time image quality control in digital dermatoscopy of skin lesions. 16 M colors Circular X30 fixed 1CCD Not reported polarized Halogen.com 1CCD or Not reported 3CCD 3CCD Not reported Microderm www. statistical classifier (neural network) Medical record processing. Skladnev VN.(19) The diagnostic validity and significance of new numerical vari­ ables obtained by digital dermoscopy analysis can be useful to der­ matologists but only when there has been scientific validation. Bickers D. Low­cost three­channel video for assessment of the clinical consul­ tation. 150 W X100. 3. two statistical classifiers (neural network. The process generally consists in detecting the borders of the skin area to assess. Many recent studies have been concerned with objective computer­ ized analysis of digital images acquired by dermoscopy.2 Instruments for Digital Dermoscopy Analysis. Levy JL.(14–16) In the case of pigmented skin lesions. Gareau DS. 18) On the basis of morphochromatic characteristics of lesions. Objective evaluation also offers the opportunity of using assisted diagnosis systems to provide diagnostic sugges­ tions. Levy A. X10.dermogenious. Recently. 34(10): 1389–95. Wallage W. this has involved iden­ tification of variables such as circularity.visiomed.at Halogen.co. Wang SQ. 150 W 750 lines RBG sync. X16 to 25. 8. rEfErEncEs 1. Trelles MA. Scheinfeld NS. Moshiyakhov M.de Not reported Variable but not reported X10 Solarscan www. and evaluating a number of variables to differentiate various diagnostic situations (Figure 2. Pan Y.it Medical records processing. Photography in der­ matology: comparison between slides and digital imaging. Polarized and nonpolar­ ized dermoscopy: the explanation for the observed differ­ ences.(17. X50. 31(1): 33–41. Schiffner R. 7. Arch Dermatol 2007. 6. Comput Med Imaging Graph 2001. 4. and health care. X200. it is possible to build a classifier that can evaluate the statistical probability of malignancy with the aid of a special thesaurus. Computer­aided melanoma diagnosis. 5. Differences in der­ moscopic images from nonpolarized dermoscope and polarized dermoscope influence the diagnostic accuracy and confidence level: a pilot study. Benvenuto­Andrade C. J Am Acad Dermatol 1999. dermatologists are dis­ covering new horizons for research. teaching. Arch Dermatol 2008.skinlesions.com. 2: 131–4. maximum diameter. statistical classifier in the last few years (Table 2. Dermatol Surg 2008. Sheeler I. concLusions The continuing evolution of digital imaging has led to the obso­ lescence of costly video equipment and the introduction of new digital cameras and telecameras that offer greater chromatic and spatial quality. Besson R.5). Sensitive tools have been devel­ oped to monitor hair loss and treatment responses. reproducible variables. 768 X 576 lines. X500. X400. Elbaum M. statistical classifier (diagnostic algorithms) Medical records processing. 16 M colors measurements Dermogenius www. Inform Prim Care 2007. Scope A et al. Varvel D.polartechnics. Dusza SW. 15(1): 25–31. 3. 2. Stolz W et al. the Tricho-scan was launched as a method combining epilumines­ cence microscopy with automatic digital image analysis. Scope A et al. Der­ matol Clin 2002.200 K. Gutenev A. Koczan P. statistical classifier (diagnostic algorithms) PCI multiinput. Differ­ ences between polarized light dermoscopy and immersion contact dermoscopy for the evaluation of skin lesions. 41: 749–56. identifying the object(s) to examine.derma. Schindewolf T. Through this technology. for objective evalua­ tion of all possible types.2). X25. X700 Not reported Fixed 1CCD Videocap www. 20(4): 735–47.(15) The new path taken by research­ ers envisages definition of new.av Halogen 1CCD or Not reported 3CCD Medical records processing. 9.net Light source magnification camera board software Molemax II www. similarity) Medical record db image processing. 10. Agero AL et al. Medical records. Ratner D.equipment Table 2. 3. Trends in the use of cameras and computer technology  . symmetry. db images. de Lusignan S. The uses of digital photogra­ phy in dermatology. J Am Acad Dermatol 1994. unambiguous. and internal clusters of color. These instruments have also been used in trichology and aes­ thetics with interesting results.

Arch Dermatol 2007. 29: 822–5. Sbano P. Fimiani M. 10(3): 285–8. Br J Dermatol. Gestione delle immagini digitali. 147(3): 481–6. Rubegni P. Andreassi A. 16. Tataranno D. Can automated der­ moscopy image analysis instruments provide added ben­ efit for the dermatologist? A study comparing the results of three systems. 13. Roelofs TA. Andreassi L. burroni. Hoffmann R. Piccolo D. Starr JC. Van Neste D. 11. New trends in the virtualization of hospitals––tools for global e­Health. Digital image analy­ sis: a reliable tool in the quantitative evaluation of cuta­ neous lesions and beyond. Graschew G. Stud Health Technol Inform 2006. Kolm P et al. Burroni M. 141: 1444–6. Peris K et al. 12. 18. 143(10): 1331–3. Br J Dermatol 2002. 157(5): 926–33. Foster JK. Recent findings with com­ puterized methods for scalp hair growth measurements. Un software dedicato per la ges­ tione dell’archivio elettronico. French LE et al. Ferrari A. 17. 15. Hi Tech Dermo(Italy) 2008. Fimiani M. Dermatol Surg 2003. Nami N. Arch Dermatol 2005. Rakowsky S et al. Dermoscopic diagnosis by a trained clinician vs. 32: 834–40. The role of dermoscopy and digital dermoscopy analysis in the diagnosis of pigmented skin lesions. 19. Rubegni P. 152(2): 395–6. J Invest Dermatol Symp Proc 2005. 14. Br J Dermatol 2005. computer­aided diagnosis of 341 pig­ mented skin lesions: a comparative study. Burroni M. Gaide O.  . Perrinaud A. a clinician with minimal dermos­ copy training vs. Digital der­ moscopy analysis and internet­based program for dis­ crimination of pigmented skin lesion dermoscopic images. Dermatol Surg 2006. Integrating digital image management software for improved patient care and optimal practice manage­ ment. and fimiani among dermatologists in New York City 2001–2002. 121: 168–75. nami. Rubegni P. Pressley ZM. 3(3): 43–9.rubegni.

Adult females are between 0. and behavioral factors rather than race.1 SCABIES Scabies and pediculosis: Biologic cycle and diagnosis Ani L Tajirian and Robert A Schwartz differences are most likely related to socioeconomic conditions. the larvae possess three. belt line. washing.1).(8–10) The scabies mite cannot penetrate deeper than the stratum corneum because oxygen delivery is by diffusion through the body surface. Head and neck are usually spared with the exception of infants and the immunocompromized. which is then consumed by the mite as a nutrient. elbows. homelessness. Epidemics may be be evident during famine and war. Burrows are white serpiginous lines in the upper dermis ranging from 1 to 10 mm in length and are typically located on the interdigital spaces of the hand. Females then dig tunnel-like burrows in the stratum corneum using their mandibles. eggs. the small males reaching a size between 0. During her lifetime.(2) With intense personal hygiene. nipples. Among adults. dementia. however. and genital area are commonly affected. sexual or otherwise. They lay approximately 2 to 3 eggs daily. upon reinfestation. develop into a tritonymph after 2 to 5 days. In men.(3) The mites can crawl up to 2. the scalp and face may also be affected. In industrialized nations. Epidemiology Scabies is most prevalent and endemic in tropical regions. Ethnic  . evolve into sexually mature males or females. Scabies Mite/ Biologic Cycle S. In first-time infections. Transmission Transmission of scabies is by direct skin-to-skin contact.3. Risk factors include poverty. poor nutrition. and penile shaft. males die shortly thereafter. and poor hygiene. can have millions of mites on their skin surface. however. Shaking hands and use of common objects is usually not sufficiently long for transmission.(11–13) Outbreaks frequently occur in institutions such as hospitals. Cutaneous lesions are usually symmetrical. axillae. The disease process is mediated through an inflammatory and allergy-like reaction to mite products.5 cm per minute on warm skin and live for approximately 30 days. or indirectly through fomites. a female mite will lay 60 to 90 eggs and usually does not leave the burrow. leading to intense pruritus. An infested host contains approximately 10 to 15 adult female mites on his or her body at any given time. umbilicus. which represents the tunnel that a female mite excavates while laying eggs. scabiei can survive outside of the host for 24 to 36 hours. and scratching are reasons why immunocompetent hosts harbor only 11 to 12 buried female mites despite regular deposition of eggs.5 mm in length and are bigger compared to males.(4–7) S. it usually takes a few days to develop symptoms. Scabies mites prefer regions with a relatively high temperature and thin stratum corneum. It is caused by the mite Sarcoptes scabiei variety hominis.3 to 0. in which case. which occurs through close personal contact. Infestations occur when the scabies mite burrows into the skin. genitalia. The nymph and adult stages have four pairs of legs. Past research estimates suggested that globally scabies might infect about 300 million by the end of the 20th century. scabies is usually observed in sporadic individual cases and institutional outbreaks. invading the host epidermis. whereas in women. Mating occurs on the skin surface. or excrements (scybala). The back is rarely involved. scabiei is part of the arachnid family. sexual contact is the most common means of transmission. and elementary schools. its saliva. prisons. the mites can replicate uncontrollably.(14) In immunocompromized patients.21 to 0. Larvae hatch at 2 to 4 days. as it can attack both sexes. and the presence of stalked pulvilli on leg 4. as it can take up to 15 to 20 minutes for transmission to occur. Prevalence of scabies is not gender specific. nipples. The intense pruritus is most severe at night and is exacerbated by a hot shower or bath. The immune response.(2) The adult male can be distinguished from the female by its smaller size. Clinical Features/Pathogenesis The pathognomonic sign of scabies is the burrow (Figure 3.29 mm. the areola. Incidence and prevalence is higher in children and sexually active individuals. patients with crusted scabies. Skin entry can occur at any time and occurs in less than 30 minutes through secretion of enzymes that digest the skin. overpopulation. particularly in impoverished communities. Scabies is not easily transmitted by clothing and bed sheets. buttocks. become a protonymph after 3 to 4 days. the number can be lower (often called scabies of the cleanly) without a decrease in pruritus. nursing homes. thus resulting in millions found on Introduction Scabies is a common ectoparasite infection.(1) It is endemic worldwide. elbows. darker color. the penis and scrotum are often involved. The severe pruritus and papulovesicles result from a delayed type-IV hypersensitivity reaction to the mite. Nocturnal pruritus and erythematous papules also form the basis of diagnosis. and after an additional 5 to 6 days. the flexure surface of the wrist. Sarcoptes is derived from the Greek work “sarx” (flesh) and “koptein” (to smile or cute) and the Latin word “scabere” (to scratch). as leg 4 in the female adult ends in long setae. it usually takes the host’s immune system 2 to 6 weeks to become sensitized to the mite and its excrements.

diaper area.(15.(1) Crusted scabies or Norwegian scabies is another variant. eggs. The nodules represent an intense hypersensitivity reaction to mite products. are 0. Diagnosis Scabies is usually diagnosed through skin scraping. (17. dermatitis herpetiformis. is a common health problem that has plagued mankind for thousands of years. Scrapings should preferably be from a fresh. folliculitis. Nodular scabies is a clinical variant occurring in about 7% of scabies cases. knees. The contents are then brought onto a slide with a coverslip and examined under  . Eggs. and should be treated first. 29) Infestation occurs most commonly in children. pruritus and papules can persist for 2 to 4 weeks. sex. 31) Pathogenesis Pediculus humanus capitis is a host-specific arthropod that belongs to the order Anoplura. pediculosis capitis affects about 6 to 12 million people every year. or other immunosuppressed individuals.(22–28) PEDICULOSIS HEAD LICE Introduction/Epidemiology Head lice or pediculosis capitis. 16) Secondary bacterial infection by group A streptococci or Staphylococcus aureus commonly occurs in the lesions.(17) It is evident as a hyperkeratotic dermatitis resembling psoriasis and distributed most prominently over the elbows. pathognomonic sign of scabies. and nodules. repeated scrapings are needed because the sensitivity is quite low. about 40% of patients have no identifiable risk factor. 16. also known as nits. fleas. buttocks. Videodermatoscopy is another technique for diagnosing scabies. and is seen with with vesicles. suggesting the possibility of a genetic predisposition. this is often referred to as “postscabietic pruritus” and is a manifestation of the delayed-type immune reaction. It measures approximately the size of a sesame seed (2–3 mm) and is grayish-white in color. can persist for weeks after treatment. and bites from mosquitoes. (30) Head lice is rare in African Americans due to the anatomy of their hair shaft. nonexcoriated burrow in the interdigital areas of the hand. unless skin burrows are clearly seen on examination. It feeds by piercing the skin of the host with its mouthparts and sucking blood every 4 to 6 hours. head. pustules. Girls are twice as likely as boys to have head lice because of their longer hair and sharing of brushes and hair accessories. using magnifications up to 600 times. which is more oval. Often. papular urticaria. caused by Pediculus humanus capitis. Scabies may be evident atypically in infants. prurigo nodularis. It is found worldwide without predilection for a particular age. or socioeconomic class. It is composed of extremely pruritic reddish-brown nodules 2 to 20 mm in size present on the male genitalia. The female louse lives approximately 30 days and lays about 5 to 10 eggs a day on hair shafts. and the immunocompromized. Burrows can also be visualized using the burrow ink test in which burrows will absorb the ink from a marker and become apparent.1 The burrow. the elderly.(23.tajirian and schwartz the microscope on low power for the presence of adult mites. and occasionally. and three pairs of clawed legs for hair grasping. the elderly. and axillary region. especially in children. particularly in hands and feet of young children. or other mites. Head lice can survive for up to 3 days off the host. The burrow should be unroofed using an oil-covered scalpel blade. making it harder to be grasped. the body. hands. and often require treatment with corticosteroid injections. Approximately half of affected patients do not report pruritus. short antennae. In the United States. as the mite burden can total over 1 million. The oil helps the scraped material adhere to the blade. groin. It is wingless. Even after successful treatment. the palms and soles.8 mm in length and are laid within 1 to 2 mm of the scalp surface for warmth. It is found most commonly in HIV patients. chiggers. face. 25. has narrow sucking mouthparts concealed within the head.(1. The louse moves by grasping hairs and is incapable of flying or jumping. The differential diagnosis is extensive and includes atopic dermatitis. and/or feces. However. and is often misdiagnosed. race. nits can live for 10 days away from their host.(19–21) Differential Diagnosis All diseases causing pruritus and papules should be considered. and feet. Infantile scabies usually affects the axillae. 18) Crusted scabies is much more infectious. neurodermatitis. Figure 3. bed bugs. with a peak incidence between 5 and 13 years of age. animal scabies (whose mites cannot complete the life cycle on human hosts because they cannot burrow). The nits are firmly glued to the individual hairs by a proteinaceous matrix and are difficult to remove.

as it may be difficult to distinguish between viable and empty eggs. Lupi O. Dermoscopy is also a possible aid in diagnosis.2 mm in length.(34–36) Dead eggs can remain affixed to the hair shafts as long as 6 months and can lead to a false-positive diagnosis of an active infestation. Differential Diagnosis The differential diagnosis for scalp pruritus includes seborrheic dermatitis and psoriasis. and trichomoniasis. Schwartz RA.2 Crab lice (circles) of the pubic region. The eggs may be visible to the naked eye as 0.8 to 1. as head lice avoid light and crawl quickly. chlamydia. patients with pediculosis pubis should be investigated for other sexually transmitted diseases including HIV. Diagnosis The identification of crab lice and their nits with the naked eye or a magnifying glass is diagnostic. Nits are often found in the occipital scalp and postauricular portions of the head and are easier to identify than adult lice. Crab lice may be more common in the winter months.5 mm brown-opalescent ovals. Nits can be confused with debris on the hair shaft left by hair spray. warts.scabies and pediculosis: biologic cycle and diagnosis Clinical Features Pruritus of the scalp is the primary symptom. Diagnosis The diagnosis is established by identification of viable nits or an adult louse on the scalp. Transmission occurs through direct head-to-head contact for an extended period of time.  . REfEREnCES 1. Approximately 30% of patients with crab lice will have a concurrent sexually transmitted disease. CRAB LICE Introduction/ Epidemiology Crab lice or pediculosis pubis infestation is spread as a sexually transmitted disease. and are evident as with pruritus of the pubic area. The highest prevalence is in men who are sexually active with other men. or Korea. Phthirus pubis have serrated edges on their anterior claws that allow them increased traction and mobility on the entire body. sometimes the number of living lice can be small and diagnosis can be aided by the use of dermoscopy. It has a shorter body than head lice and resembles microscopic crabs. Hair casts may also closely resemble nits stuck to hair shafts and can be noticed by a parent. and more rarely eyelashes. The adult crab louse can live up to 2 weeks on the host and about 36 hours outside of the host. as it takes 1 to 2 months to develop sensitivity. they are freely moveable along the hair shaft. Pruritus may not be seen with the first lice infestation. Underwear can also sometimes be stained with small drops of blood. or those with minimal pubic hair. Clinical Features Crab lice commonly affect pubic (Figure 3. Recognition can be facilitated through the use of a magnifying glass. who mistakes them for nits. or school nurse.(32. Louse combs are useful tools. syphilis. They are asymptomatic bluish-gray macules on the trunk and thighs caused by bites of the crab louse.(29) Evidence of P. 6: 769–79. Scabies: a ubiquitous neglected skin disease. a number of patients are asymptomatic yet considered carriers. Visual inspection without combing is difficult. herpes. Macula caerulea is a characteristic finding with infestation.(31) In repeat infestations. with dandruff or with accumulated flakes of seborrheic dermatitis. axillary. Japan. as they increase the chance of finding live lice fourfold over direct visual examination. scabies. Currie BJ.(37) Pathogenesis Infestation with crab lice is caused by Phthirus pubis which is approximately 0. however. Hengge UR.(36) Differential Diagnosis Nits on the pubic hair can be misdiagnosed for white piedra or trichomycosis pubis. Wood’s lamp examination reveals a yellow-green fluorescence of the lice and their nits. gonorrhea. It can be seen in all ethnic groups though it is less common in people whose families originated in China.(38) Females Figure 3. It is most common in men in the age group of 15 to 40 years. scabies or contact dermatitis should be considered. 33) Viable eggs are tan to brown in color. 40) If extensive excoriations are present. pubis in a child may occasionally reflect sexual abuse. chest hair. Jager G. those engaging more in sexual activities during this period. As crab lice are transmitted sexually. lay up to 3 eggs a day with an incubation period of 7 to 10 days.2). and hatched eggs are clear to white. However. pruritus develops within the first 24 to 48 hours.(29) In contrast to nits. teacher. It is slightly more prevalent in men probably due to their increased amount of coarse body hair.(39. Lancet Infect Dis 2006. the presence of nits or lice is diagnostic.

Schachner L. BMJ 2000. Willems S. 34. J Am Acad Dermatol 2007. 51: 1037. Mathews JD. Janniger CK. Crusted scabies: a molecular analysis of Sarcoptes scabiei variety hominis populations from patients with repeated infestations. Available at http:// emedicine. 36. Tissot Dupont H et al. Ko CJ. Int J Dermatol 2004. Schwartz RA. O’Donnell BF. eMedicine Pediatrics [journal serial online]. Arlian LG. 13. Attack of the scabies: what to do when an outbreak occurs. Burgess I. Am Fam Physician 1992. Walton SF. 32. Wet combing versus traditional scalp inspection to detect head lice in schoolchildren: observational study. 20. Folster-Holst R et al. Badiaga S. Tanglertsampan C. Mayser P. Blokland I. Hofmann-Wellenhof R. Lacarrubba F. Nishiura H. Diagnosis and treatment of childhood scabies and pediculosis. 16: 38–44. 38: 941–57. Zalaudek I. Lee A. J Am Acad Dermatol 2004. J Eur Acad Dermatol Venereol 2002. 9. 2009. 48: 45–6. Bedbug bites. Lacarrubba F. hominis. 35. Schwartz RA.medscape. Scabies. 23. 16: 257–9. 5: 424–30. 15. Lancet 2006. Nurs Times 2002. 15: 382–6. Steen C. 29: 1226–30. Seasonality trends of pediculosis capitis and phthirus pubis in a young adult population: follow-up of 20 years. Kobayashi T. 30.tajirian and schwartz 2. http://emedicine. Scabies.medscape. 33: 235–92. Heukelbach J. 38. http://emedicine. Dementia-specific risks of scabies: retrospective epidemiologic analysis of an unveiled nosocomial outbreak in Japan from 1989–90. Janniger CK. 54: 909–11. Louse comb versus direct visual examination for the diagnosis of head louse infestations. Currie BJ. 7. Di Stefani A. 18: 9–12. Survival and infectivity of Sarcoptes scabiei var. O’Loughlin S. Cutis 2008. 57: 727–8. Pediatrics 2002. Int J Dermatol 1990. Lacarrubba F. Survival of adults and development stages of Sarcoptes scabiei var. De Maeseneer J. Dermoscopy for diagnosis and treatment monitoring of pediculosis capitis. 2009. Dermoscopy for diagnosis of pediculosis capitis. 17. Eur J Dermatol 2005. J Infect 2005. J Eur Acad Dermatol Venereol 2007. com/article/1092330-overview 40. Pediculosis corporis: an ancient itch. Schwartz RA. Nutanson I. Pediatr Clin North Am 1991. Powell FC. Janniger CK. Acta Dermatovenerol Croat 2007. Steen CJ. Bullous scabies: a diagnostic challenge. Musumeci ML. 21. J Eur Acad Dermatol Venereol 2004.medscape. J Am Acad Dermatol 2004. Sterling GB. 5: 85. 31. 4. Caltabiano R et al. 56: 317–21. Meersschaut F. 46: 1237–41. Achar S. Prevalence of skin infections in sheltered homeless. Bakos RM. Highmagnification videodermatoscopy: a new noninvasive diagnostic tool for scabies in children. Estes SA. Runyan RA. Friger M. Carbonaro PA. 18: 439–41. 10. Micali G. J Am Acad Dermatol 1984. canis and var. 1 . 79: 396. 350–2. Walton SF. Ben-Ishai F. Haag ML. com/article/1051461-overview 28. Papular urticaria. Micali G. 11: 210–5. Management of crusted scabies. Schwartz RA. Vaidya DC. McBroom J. eMedicine Dermatology [Journal serial online]. Currie BJ. Weiner LB.medscape. Schwartz RA. Pole MJ. 22. 50: 375–81. Available at: http://emedicine. Tedeschi A. 12. 6: 181–7. a global disease in human and animal populations. Papular urticaria. Bakos L. Cutis 1995. 29: 258–66. 25. Bedbug bites: a review. Scabies. Scraping versus videodermatoscopy for the diagnosis of scabies: a comparative study. Feldmeier H. Schwartz RA. Elston DM. Kihiczak GG. 20: 268–79. 3. 364: 1173–82. Hawro T. Schwartz RA. eMedicine Dermatology [journal serial online]. 50: 819–42. 110: 638–43. Sarcoptes scabiei and scabies. The life of a head louse. 15: 33–8. 2009. 37. Brozena SJ. Problems in diagnosing scabies. 11. Acta Derm Venereol 1999. Arlian LG. Burkhart CN. 6. Miller J. Crusted scabies: clinical and immunological findings in seventy-eight patients and a review of the literature. Burgess I. Kihiczak G. Fox MD. Prurigo nodularis: a benign dermatosis derived from a persistent pruritus. Schwartz RA. eMedicine Dermatology [Journal serial online]. Gdalevich M et al. Vander Stichele R. Scabies. Sunderkotter C. Mimouni D. Tsutsumi M. Wozniacka A. Roberts LJ. Pediculosis. Huffam SE. Chuh A. Thomas I. Schwartz RA. 367: 1767–74. Pediatr Dermatol 2001. 21: 837–8. Schwartz RA. Wong W. Scabies. J Am Acad Dermatol 2004. 98: 54. 14. Adv Parasitol 1994.com/article/1088931-overview 29. 26. 68: 89–91. 8. 33. Arthropods in dermatology. Altman R: Piedra. Kemp DJ. BMC Infect Dis 2005. Oral ivermectin for Phthirus pubis. Acta Dermatovenerol Croat 2008. J Dtsch Dermatol Ges 2007. Lo Guzzo G. 2009. Mumcuoglu KY. Videodermatoscopy enhances the ability to monitor efficacy of scabies treatment and allows optimal timing of drug application. Clin Microbiol Rev 2007. Walton SF. Burkhart CG . Hogan DJ. Cutis 2001. Exp Appl Acarol 1989. 50: 1–12. Molinaro MJ. 321: 1187–8. Ioffe-Uspensky I. Pediatr Dermatol 2001.com/article/911033-overview 16. Superficial fungal infections. Zawar V. Hengge U et al. 43: 430–3. Lancet 2004. Geriatrics 1993. 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the contrail-shaped segment was thought to be the burrow of the mite along with its eggs and fecal pellets. For these reasons. or even decline the examination.3). Follow-up tests. mites.3.. especially in younger patients. and exchange of information was not allowed. the two other cases.(1–2) In 1992 Kreusch (3) suggested the use of epiluminescence microscopy in diagnosing scabies. aged between 1 month and 16 years) suspected to be affected by scabies were enrolled in the study.e.(6) On the basis of these results. and suspicious lesions (i. Interestingly. The first study was performed by Argenziano et al. a small dark brown triangular structure located at the end of a subtle linear segment in 93% of 70 patients affected by scabies. which. As the results generally depend on the scraped areas. No use of oil or slide on the skin was necessary as image resolution was of good quality. useful to assess recovery from therapy or to rule out persisting pruritus due to use of irritant topical agents. in most cases.” Moreover. Tokyo. conversely. eggs.4 A case of scabies with minimal lesions in which traditional skin-scraping may give false-negative result. allowing the skin observation at magnifications ranging from X4 up to X1. two cases were positive only by scraping and this fact was probably due to impetiginization that hampered VD examination (Figure 3.(4–5) In 2000.200 [Hirox Co.2 Videodermatoscopy and scabies Francesco Lacarrubba.000. Figure 3. repeated tests are sometimes necessary for a conclusive diagnosis. were found positive only at VD (Figure 3. who may not cooperate. and 57 girls. Nella Pulvirenti. are troublesome. Patient examination was first performed using a relatively low magnification (about X100).3 A case of impetiginized scabies in which VD examination may be hampered and may give false-negative result. handling and processing scrapings rapidly and effectively in the office is not always straightforward. Japan]. VD was performed using a Video Microscope System Hi-Scope KH-2. both structures resembled a jet with contrail. VD allowed a detailed inspection of the skin in all patients. characterized by minimal lesions. it was possible to observe the mites moving inside the burrows. Microscopic examination of the scales obtained by skin scraping gave similar results. The use of VD allowed a detailed inspection of the skin with rapid identification of burrows. considering it a useless “torture. using the epiluminescence microscopy technique at X40 magnification. made a repetitive finding. and eggs in 16 out of 38 patients and.4). scraping is not well accepted by patients. feces. as this technique allows the inspection of the skin surface down to the superficial dermis.(1) A total of 100 young patients (43 boys Figure 3.(4–5) On microscopic examination. Both scraping and VD examinations were carried out in each patient by two independent operators. we conducted a large-scale study in children in which VD was the only diagnostic tool. Ltd. but this method may cause discomfort and fear. or excreta by microscopic examination of scales obtained by skin scraping. together. we conducted at our institution a comparative study (6) of scraping versus high magnification videodermatoscopy (VD) in 38 patients suspected of being infested with scabies (patients were in the age range between 1 month and 81 years). burrows) were analyzed at higher magnification (up to X600). and patients may refuse further scraping. Diagnosis of scabies was established in 62 out of  . the jet-shaped triangular structure corresponded to the pigmented anterior part of the mite (mouth parts and two anterior pairs of legs).. and Giuseppe Micali The standard technique for the diagnosis of scabies involves identification of the mite.

.(2. as it does not cause physical or psychological discomfort. Figure 3. resembling a circumflex accent (e.7 Sarcoptes scabiei at VD observation (X500): the roundish body is translucent. mites in migration. especially by children and those more sensitive patients who may have had repeated negative results at skin scraping. especially in cases with not specific clinical features. eggs and feces. It is easy and quick to perform.. in French letter ‘‘ô’’) that corresponds to head and front legs of the mite.5 Burrow at VD observation: The roundish body of Sarcoptes scabiei (circle) may be observed at one end of the burrow (X100). and feces) usually not appreciable at lower magnifications.lacarrubba. it is not invasive and it is well accepted by the patients. 7–12) A study comparing the dermoscopic diagnosis of scabies using a pocket. Sarcoptes scabiei appears as a characteristic triangular shape. 90%. handheld dermoscope and allowing 10X magnification with traditional skin scraping in 238 patients has shown that dermoscopy achieves comparable high diagnostic Figure 3. pulvirenti.(1) The effectiveness of dermoscopy both at low and high magnification in diagnosing scabies has been confirmed by several other studies. First. 100 patients and was based on identification of mites.(11) Dermoscopy affords several advantages compared to traditional skin scraping. sensitivity values as scraping (91% vs. after paraffin oil application on the glass plate of the dermatoscope.g.(1. None of the 38 negative patients showed signs of infestation at a 2-week follow-up examination. 5) 2 .6 Burrow at VD observation: Sarcoptes scabiei may be observed at the end of the burrow (X200). allowing clear detection of some details (e. allowing inspection of the entire skin surface usually within few minutes and is significantly less time consuming than ex vivo microscopic examination. and micali Figure 3. eggs. The study showed that high magnification VD is very effective and sensitive.g.8 Eggs (ovular and translucent) and feces (roundish and white) of Sarcoptes scabiei at VD observation (X500). whereas the anterior part of the mite (head and anterior legs) is pigmented (arrow). Figure 3. Under 10X magnification. respectively).

It is useful for nontraumatic screening of family members who might refuse skin scraping being asymptomatic. We recommend the use of Figure3. 3 . which involves sharing digital pictures by capturing dermoscopic images at the remote site and reviewing them later at the host site. as the images obtained are unequivocal: The round. dermoscopy has demonstrated to be useful in diagnosing scabies through the technique of teledermatology. that is. this approach.9a Burrow at low-magnification VD observation: The “circumflex accent” that corresponds to head and front legs of mite structure may be observed (arrow) (X20). Figure 3. In one study. being noninvasive. Using these magnifications. appeared to be a relatively cost-effective means of providing this service from a distance when on-site dermatology services is not available. VD wherever possible. such as burrows at magnifications ranging from X40 to X100. false-negative results are rare and there is no chance of false-positive results.9c The same burrow at X400 magnification: both the mite (on the left) and the eggs (on the right) are clearly evident. and mites.9b The same burrow at X40 magnification: The “jet with contrail” structure is more evident. the use of oil and slides is messy and time consuming and is unnecessary at high magnification. Moreover. this technique minimizes the risk of accidental infections from blood-transmissible agents such as HIV or HCV.videodermatoscopy and scabies Figure 3. as it does not enhance image quality.5–3. or feces at higher magnifications (up to X600) (Figure 3. as it allows a detailed inspection of the skin with rapid and clear detection of the diagnostic features of scabies. its legs (anterior and posterior) and rostrum. it is also possible to detect the mite moving inside the burrows. Finally.8).000.9d The same eggs at X600 magnification. considering also that most systems come equipped with lenses up to X1. Figure 3.(13) An important issue to address is which magnification gives the best performance. (6–7) Finally. in most cases. eggs. translucent body of the mite (invisible at low magnifications) is clearly visible and it is always possible to visualize the other anatomical structures of the mite.

lacarrubba. and micali Figure 3. 178: 1540–1. however.(11) In conclusion. the use of hand-held dermoscope.(11) The importance of the use of high magnifications may be better understood by viewing the same lesion at different magnifications (Figure 3.(1. CMAJ 2008. Stucki L. patients are more willing to undergo posttherapeutic VD examination rather than skin scraping. J Fam Pract 2006. Vitiello A. Acta Derm Venereol 2000. posttherapeutic monitoring cannot be performed. Lacarrubba F. Diagnosis of scabies with dermoscopy. and one of them is that it does not always allow. especially to nonexperienced operators. Delfino S. therefore. 8. 208(3): 241–3. 55: 679–84. In addition. Dermatology 2004. Blum A. 31: 618–20. Another limitation is that mite viability cannot be assessed at these magnifications. considering the possible risk of false-negative and/or false-positive results. Eur J Dermatol 1998. in cases of unsuccessful therapy. Neynaber S. 216: 14–23. In addition. 133: 751–3.10b The same mite at X500 magnification is easily recognizable. A new approach to in vivo detection of Sarcoptes scabiei. 2. Musumeci ML. Fabbrocini G. Nodular scabies detected by computed dermatoscopy. as mites survive in the outside environment (away from the host) for up to 72 hours. low magnifications do not facilitate visualization of eggs and feces. Caltabiano R et al. Entodermoscopy: a new tool for diagnosing skin infections and infestations. Dermatology 2001. Itching and rash in a boy and his grandmother. the possibility of indirect contamination of the patients through the instrument might be Figure 3. Findings in vivo of Sarcoptes scabiei with incident light microscopy. considered. Cabo H et al. Int J Dermatol 1992. Wolff H. Dermatology 2008. Arch Dermatol 1997. disinfection of the device after each examination is recommended. 14) Again. Delfino M.  . showing the possible presence of viable mites and thus reducing the risk. Epiluminescence microscopy. 4. In our experience. the use of low magnifications (X10–X40) may have some limitations. Kreusch J. where a clear visualization of the skin may be hampered. Finally. 9. as recently suggested. when we use the dermoscope or the videodermatoscope in diagnosing scabies. the use of hand-held dermoscopy might be limited to those cases in which no VD facilities are available or to a preliminary screening of suspect lesions before skin scraping is carried out. Highmagnification videodermatoscopy: a new noninvasive diagnostic tool for scabies in children. the use of hand-held dermatoscopy in or around the genital region may cause embarrassment because of close contact between dermoscopist’s head and patient’s skin surface. 6. Argenziano G. 5. Lacarrubba F. Zalaudek I. 8: 266–7. Brunetti B.9–3. Finally. Dermoscopy for the in vivo detection of sarcoptes scabiei. Giacomel J. Prins C. 7.10a Sarcoptes scabiei (arrow) out of the burrow at low-magnification VD observation: The “circumflex accent” is hardly visible (X20). Usatine RP. Micali G. VD is particularly useful for posttherapeutic follow-up. therefore. may be troublesome when used in hairy body areas. 10. Sönnichsen K et al. Fox GN. Bauer J. 79: 396. 18: 439–41. Ped Dermatol 2001. of persistence and diffusion of the infestation. Saurat JH. Incident light microscopy: reflection on microscopy of the living skin. Scraping versus videodermatoscopy for the diagnosis of scabies: a comparative study (Letter). French L. Sammarco E. 3. pulvirenti. Lo Guzzo G.(11) REFERENCES 1. 203(2): 190–1. Braun RP. which are quite often the only diagnostic clues available to suspect the presence of mites. a clear differentiation between the “circumflex accent” (or the “jet-shaped” structure) and minor excoriations and/or splinters (that may frequently occur in scabies due to repeated scratching).10).

Kempton SA.  . J Dermatol 2008. Accuracy of standard dermoscopy for diagnosing scabies. 14. Dermoscopy of Hair and Scalp Disorders: Pathological and Clinical Correlation. 13. Cutis 2000. Dupuy A. J Am Acad Dermatol 2007. 66: 61–2. Case report: teledermatology and epiluminescence microscopy for the diagnosis of scabies. Micali G. Lacarrubba F. (ed).videodermatoscopy and scabies 11. Bourrat E et al. Weinstock MA. 12. Dehen L. 2007. 56: 53–62. Executive committee of guideline for the diagnosis. 35: 378–93. In: Tosti A. Ishii N. Informa Healthcare Ltd. UK. Parasitoses of the scalp. Guideline for the diagnosis and treatment of scabies in Japan (2nd edition).

15) and may be Figure 3. Furthermore. occasionally.12 Nit fixed to the hair shaft (X80). where the full nits.13). With a little patience. which contain nymphs and indicate a potential active infestation. Marianna Umana. a large scalp area can be investigated without discomfort to the patient. which affects predominantly children aged between 4 and 14 years.14a). we described the use of videodermatoscopy (VD) in pediculosis. or scales from seborrheic dermatitis.3. Moreover. as both mites and their nits may be detectable with close-up examination. VD unequivocally shows the presence of the nits fixed to the hair shaft (Figure 3. Giuseppe Micali. however.(1) In 2003.12). and Francesco Lacarrubba Figure 3. the diagnosis is traditionally based on a combination of scalp itching.11). allowing a rapid differentiation from scales of different origin (pseudo nits) that appear as amorphous. whitish structure (X80).14b). VD does not require hair pulling.3 Videodermatoscopy and pediculosis Pediculosis caPitis Pediculosis capitis (head lice) is a worldwide infestation due to Pediculus humanus capitis (Figure 3. therefore. are translucent and typically show a plane and fissured free ending (Figure 3. eventually accompanied by local bite reactions and/or cervical lymphadenopathy and the presence of nits. whereas the empty nits. secondary bacterial infections resulting from scratching with an associated local retroauricular adenopathy.(1) Therefore.13 A scale of seborrheic dermatitis (pseudo nit) appearing as an amorphous.11 VD observation of Pediculus humanus capitis on a glass slide (X80). it is often not visible. It causes itching and.(1) Sometimes nits may be overlooked and nits containing vital nymphs can be difficult to differentiate from empty nits and so-called pseudo nits. whitish structures (3) (Figure 3. In this case VD allows an in vivo evaluation of the movements and physiology of lice (Figure 3. 3) The differentiation between vital and empty nits provides useful information about therapeutic response. because the head louse moves quickly and avoids light. it is also possible to detect the lice. debris of hair spray or gel. search of the mite is time consuming and. a blood-sucking insect and specific human parasite. the diagnosis of pediculosis capitis is clinical. appear like ovoid.(2) In case of infestation. VD allows a more detailed identification of full versus empty nits. such as hair casts. which may persist after the recovery.(1. brown structures with a convex extremity (Figure 3.  . Generally. Figure 3.

5) Phthiriasis Pubis The same technique of VD may be extended to diagnosing phthiriasis pubis (crab lice).15 Pediculus humanus “in action” in the hair shafts (X80). Other authors have reported obtaining similar results by a contact. chest. the edges of scalp hair and eyelashes Figure 3. Figure 3. and limbs.16 Phthirus pubis firmly attached to the pubic hairs (X80). safe. and reliable diagnostic tool in head lice infestation and the procedure can rapidly confirm the diagnosis in some puzzling cases where parasites and nits may be not easily identified. useful to evaluate the pediculocidal activity of different topical products. hand-held dermatoscope both in vivo and nipping and placing hairs. brown structures with a convex extremity (X100).(2. Figure 3.14a Full nits. In children.(1. which contain nymphs. appear like ovoid.  .17 Phthirus pubis at VD observation (X80). Figure 3. 6) Phthirus pubis infests mainly the hair of the pubic and inguinal region.14b Empty nits are translucent and typically show a plane and fissured free ending (X100). rarely those of axillae.(4) In conclusion VD can be used as an easy. presenting nits on the adherent side of a piece of transparent adhesive tape.videodermatoscopy and pediculosis Figure 3.

Int J Dermatol 2003. 2. 42: 430–3. VD allows a more detailed identification of full versus empty nits (Figure 3. Entodermoscopy: a new tool for diagnosing skin infections and infestations. Finally. VD clearly shows the presence of the crab lice firmly attached to the pubic hairs (Figure 3. Di Stefani A. In these cases. Insert: VD observation of lice and nits (X80). Possible applications of videodermatoscopy beyond pigmented lesions. Cabo H et al.17).18). so the infestation may exist for a long time before being recognized (7) and generally misdiagnosed with atopic dermatitis or allergic conjunctivitis.16–3. VD examination may enhance patient compliance to therapy both in head and crab lice.18 Full nit of Phthirus pubis (X60). Moreover. J Am Acad Dermatol 2006. 216: 14–23. Dermatology 2008.20). by clearly showing on the VD monitor their presence. 54: 909–11. 3. In case of phthiriasis palpebrarum. Lacarrubba F. Figure 3. Zalaudek I. or resolution of the infestation (6). it is possible to recognize the parasite sucking the blood. Hofmann-Wellenhof R.20a–b Nits of the eyelashes (a) versus scales of atopic dermatitis (b) at VD observation (X50). Giacomel J.19–3. In most cases. the lice are sometimes difficult to identify because of their semitransparency and deep burrowing in the lid margin. Micali G. (b) (a) Figure 3.  . In the majority of cases the diagnosis of pubic lice is clinical and there is no need for further investigation. VD can rapidly clarify any doubt by revealing the presence of lice and/or nits (Figure 3.micali. persistence. reFereNces 1. (phthiriasis palpebrarum) are the most common site of infestation because of the lack of terminal hairs on most body regions. and lacarrubba Figure 3. as observed in pediculosis capitis.19 Phthiriasis palpebrarum. Dermoscopy for diagnosis and treatment monitoring of pediculosis capitis. Zalaudek I. umana.

Ooi C. Mechanical treatment of phthiriasis palpebrarum.  . Park YG. Zawar V. Nardone B. Bakos RM. 7. Wong W. Yoon KC. 141: 233–5. Bakos L. Park HY. J Am Acad Dermatol 2007. Dermoscopy for diagnosis of pediculosis capitis. 21: 837–8. Diagnosis of Pediculosis pubis: a novel application of digital epiluminescence dermatoscopy. 17: 71–3. Chuh A. Lacarrubba F. Head lice: ex vivo videodermatoscopy evaluation of the pediculocidal activity of two different topical products. Lee A. Seo MS. Milani M.videodermatoscopy and pediculosis 4. Botta G. J Eur Acad Dermatol Venereol 2007. Micali G. 6. 5. Korean J Ophthalmol 2003. G Ital Dermatol Venereol 2006. 57: 727–8.

benefit–risk categorization. leading to increased risk of developing resistance to such products.(17) Shaving the head is not recommended since this can cause significant and long-lasting emotional trauma as well as embarrassment. See Table 3. the following overview provides insight into the topical and systemic pharmacologic and nonpharmacologic approaches to treatment that are reported to be used in the clinical management of such infestations.(3–6) Unfortunately. sealed in a plastic bag. even if asymptomatic. has been reported. has not been proven to be of benefit. including permethrin.(10) Some causes of treatment failure may be related to misdiagnosis or reinfestation. Topical and systemic agents are quite effective in killing and eradicating the parasite. subjective weighing of literature reports is used to determine efficacy. and. Resistance to virtually all topical products for treatment of pediculosis. noncompliance or underuse of medication should always be considered.3. and lindane. including eggs. high-magnification videodermatoscopy (VD) in establishing highly definitive and precise quantitative data products used in the treatment of scabies and pediculosis provides enormous advantages in the quest to establish reproducible quantitative methodology for efficacy studies in these parasitoses.(7–9) While treatment failure may be due to resistance in some cases. making it easier for removal.1 for a combined subjective and objective relative assessment of efficacy and safety to provide a current guide to risk–benefit ratio as categorized for selected agents reported to be used in scabies and/or pediculosis.(12) Bed linens and towels should be washed after treatment and areas of frequent body contact such as carpets.(15) While this method is labor intensive and poses recurrent infestation issues. Beatrice Nardone. such as furniture. Patients need to be reassured that itching is not always indicative of infestation after treatment. a repeat treatment 7 days after the initial treatment is given to ensure that hatching larvae are destroyed.4 Therapy of scabies and pediculosis: Potential and pitfalls Lee E West. the advantages of low cost and unlimited repetition with no side effects may warrant further investigation. analyses are based on highly variable assessment methodology and data collection. chairs. Considering these significant limitations in efficacy studies to date for both scabies and pediculosis. kill times and kill rates are rarely determined or reported. The use of insecticides on inanimate objects. uniform comparison and categorization of efficacy. PhysIcal removal—PedIculosIs Nit Combs Wet combing “bug busting” is a procedure that involves combing wet hair with a fine-tooth comb every 3 to 4 days for at least 2 weeks to physically remove live lice and nits. 2) Utilization of high-resolution. subsequently. and sofas should be vacuumed. pyrethrins. by nature. ultimately.(11) scabIes It is important to treat close physical contacts. Studies that compared bug busting with malathion monotherapy found malathion to be twice as effective. New lesions present after 4 weeks may indicate treatment failure or reinfestation.(1. and discarded. Usually an initial treatment is followed by a second application after 7 to 10 days to ensure that any hatching nymphs are destroyed. malathion monotherapy. Spread of head lice is by transfer of live lice only. and Dennis P West InTroducTIon A great pitfall for scabies and pediculosis therapeutic studies to date is that primary and secondary study outcomes are indirectly assessed (presence or absence of live parasites. Fine tooth combs designed to effectively remove nits and may be used with hair conditioner or active agent.(13) The vacuum-cleaner bag should be removed immediately after vacuuming. Wetness of hair is important because water slows the motility of lice. Pruritus lasting longer than 2 weeks after treatment may indicate treatment failure or resistance.(14) Removed lice can then be placed on adhesive paper.  . determination of the risk–benefit ratio for reported treatments does not involve uniform or precise methodology such as VD and. PedIculosIs A high percentage of cases of head lice are treated without medical supervision and with products that may be prone to overuse. as well as the infested patient. Generally. Clearly. determined by gross clinical inspection) and data timepoints are nonstandardized (highly variable) relative to time of therapeutic application. standard methods such as VD allow for uniform data and. to minimize the risk of reinfestation. the importance of consultation and patient education should be emphasized. meta-analyses of randomized. treatment is considered more thorough.(16) While combs and other devices may help remove lice and nits. Whether changing treatment product or applying further doses. Pruritus may increase and persist for up to 2 weeks after successful treatment due to continuing reactivity to substances released from the dying mites. nits or nit cases will not cause infestations. Indeed. as a result. followed by highly variable interpretation and reporting. controlled clinical trials for these parasitoses are scarce and. Certainly.

therapy of scabies and pediculosis: potential and pitfalls
Table 3.1 Combined Subjective and Objective Relative Assessment of Reported Efficacy and Safety to Provide a Risk–Benefit Ratio Category for Selected Agents Used in Scabies and/or Pediculosis.
agent Benzyl alcohol Topical Dimethicone Topical Ivermectin Topical Ivermectin Systemic Malathion/terpineols combination therapy (United States) Topical Permethrin Topical Benzyl benzoate Topical Cotrimoxazole (trimethoprim/ sulfamethoxazole) Systemic Crotamiton Topical Lindane Topical Malathion Monotherapy (UK) Petrolatum/Mineral Oil/ Vegetable (eg; Olive) Oils Topical Pyrethrins/Piperonyl Butoxide Topical Sulfur Topical Albendazole Systemic Carbaryl Topical Citronella Topical Levamisole Systemic Butter/Margarine/ Mayonnaise Topical Kerosene/Gasoline/ Petroleum Distillates Topical condition Pediculosis Pediculosis Pediculosis Scabies and pediculosis Scabies and pediculosis benefit:risk 1 1 1 1 1

ToPIcal TreaTmenT Benzyl Alcohol—Pediculosis Topical lotion, containing benzyl alcohol (5%), is a nonneurotoxic pediculocide that acts to fix the spiracles of the louse in an open position, thus permitting blockage and asphyxiation. Note that unlike benzyl alcohol, some so-called asphyxiator products only temporarily stun the spiracles in an open position, thus allowing the louse to quickly recover and continue infestation. Complete treatment consists of two 10-minute applications (hair saturation followed by rinsing) 1 week apart. Benzyl Benzoate—Scabies and Pediculosis Benzyl benzoate, a long-standing scabicide and pediculocide, is known to partially biotransform to benzyl alcohol. Benzyl benzoate is available in various topical dosage forms for use in scabies and pediculosis at concentrations as high as 35%. It is widely used in some countries, but in a study compared to oral ivermectin, it showed inferior efficacy to ivermectin.(18) The mechanism of action is unknown. Carbaryl—Pediculosis This topical agent functions similarly to malathion by binding to the same acetylcholinesterase enzyme site to cause respiratory paralysis in the louse. Unfortunately, even though toxicity of this compound is specific to the louse (and not the human host) in the topical concentration being used (0.5%), this agent is reported to be mutagenic and may or may not prove to be carcinogenic, thus limiting its utility in pediatric populations.(19) Crotamiton—Scabies and Pediculosis Marketed as a 10% topical cream for pruritus, this agent has been reported to be effective in scabies and has limited reporting of effectiveness in pediculosis. Crotamiton is relatively nontoxic to the human host and the mechanism of action is unknown.(20) Although relatively safe for use in children, it is not recommended for use in pregnant or lactating women. Dimethicone—Pediculosis Similar to other agents that interfere with the respiratory system (interrupted oxygen supply), topical dimethicone (up to 92% concentration) has shown efficacy and yet is considered safe to the human host, including children and pregnant or lactating women.(21, 22) Ivermectin—Scabies and Pediculosis Although topical ivermectin was reported as beneficial in the treatment of pediculosis over a decade ago, (23) it is just now undergoing US trials. Lindane—Scabies and Pediculosis Lindane is used as a second-line therapy. Package sizes are limited to the amount necessary for treatment of one person in an effort to prevent overuse. The use of lindane has been banned

scabies & pediculosis Scabies and pediculosis Pediculosis

1 2 2

Scabies and pediculosis Scabies and pediculosis Scabies and pediculosis Pediculosis

2 2 2 2

Pediculosis

2

Scabies Pediculosis Pediculosis Pediculosis Pediculosis Pediculosis

2 3 3 3 3 na

Pediculosis

na

1=benefit:risk balanced. 2=benefit:risk decreased. 3=benefit:risk marginal. na=benefit:risk not acceptable.



west, nardone, and west
in the state of California and some countries, due to potential toxicity to the human host.(24) Although there are advantages to using lindane, including its utility as a pediculicide and ovicide, disadvantages are also many, including percutaneous absorption that may result in neurotoxicity. Lindane is not for use in patients with seizure and other neurologic disorders or in those with known, lowered seizure threshold. Lindane persists in fatty tissues and in the environment over very prolonged periods. Use with caution for patients weighing less than 50 kg. Lindane is categorized as U.S. FDA Pregnancy Category C. Malathion—Scabies and Pediculosis Malathion in combination with terpineols may be a useful approach to treatment because it has very little reported resistance. However, malathion as monotherapy (not in combination with terpineols) has a relatively high rate of resistance. There are advantages to using the malathion/terpineols combination: It is highly effective, functions as both a pediculicide and ovicide, and may have residual therapeutic effects. Disadvantages include an unpleasant odor and that it is not indicated for use in children under 6 years of age in some countries. There are emerging resistance data for malathion monotherapy. Permethrin—Scabies and Pediculosis Permethrin is used widely for treatment of head lice in a 1% cream-rinse formulation, and permethrin cream at 5% is used widely for scabies. Advantages include low toxicity to the human host, ability to function as both a pediculicide and ovicide, and it may have residual therapeutic effect. Disadvantages are that there are emerging resistance data and it is messy to use on hairy areas. Pyrethrins—Pediculosis Pyrethrins are available in combination with piperonyl butoxide to increase efficacy. This agent functions as a pediculicide but not as an ovicide. Disadvantages also include no residual activity, irritant and/ or allergic contact dermatitis potential, and it may produce systemic toxicity.(25) oTher ToPIcals—scabIes Topical corticosteroids may be used for pruritus that may occur for up to 2 weeks after successful therapy for scabies. If secondary skin infections develop, topical or systemic antibiotics may be necessary. naTural ProducTs Acetic Acid (Vinegar)/Formic Acid—Pediculosis Diluted vinegar or formic acid can be used as a hair rinse to aid in the removal of nits.(26) Citronella—Pediculosis Topical citronella has been reported to be more effective than vehicle but otherwise scarce published information exists about safety of topical use and potential for irritant effect.(27) Sulfur—Scabies Precipitated sulfur at 6% in petrolatum ointment is used an extemporaneously compounded topical agent for scabies treatment.(28) Advantages of using sulfur include its relatively low cost, relatively low potential for toxicity, suitability to treat infants younger than 2 months of age (except premature infants), and it is safe for use in pregnant and lactating women. Disadvantages are that it must be applied for at least three consecutive overnights, and the ointment is messy with an objectionable odor and is capable of staining clothing and bedding. Petrolatum Occlusive products such as petrolatum (petroleum jelly) have been reported as home remedies that are liberally applied to the entire scalp at night, occluded with a shower cap, then washed out daily for several days, and the lice removed by combing. Lice are potentially suffocated or slowed down, and then physically removed by combing, as it will take several washings to remove the petrolatum.(11) The ongoing hair grooming connected with daily shampooing may, in effect, account for lice removal.(29) Tea Tree Oil—Pediculosis An herbal shampoo containing extract of paw paw, thymol, and tea tree oil has reported to be effective in treatment of head lice infestations.(30) Disadvantages are that tea tree oil may cause allergic contact dermatitis and formulations are nonstandardized (unregulated and unknown amounts of tea tree oil due to variation in purity). alTernaTIve unProven remedIes Butter/Margarine/Mayonnaise—Pediculosis Remedies such as mayonnaise, softened margarine, or butter have been reported to be used, but these are not proven to be efficacious, as these are also bacterial-growth media. A disadvantage includes risk of serious and/or life-threatening infection, including septicemia. Kerosene/Gasoline/Petroleum Distillates—Pediculosis Treatment with kerosene or gasoline and other petroleum distillate products is extremely dangerous as a fire hazard and potential inhalant and should never be used. Disadvantages are serious risk of physical harm and systemic toxicity sysTemIc TreaTmenT Albendazole Albendazole as an oral agent has been shown to be effective against head lice. Advantages include simple therapy and



therapy of scabies and pediculosis: potential and pitfalls
enhanced compliance. It is apparently not synergistic with permethrin for pediculosis.(31) Ivermectin—Scabies and Pediculosis Ivermectin as a single, oral dose of 200 mcg/kg is effective in destroying lice but not nits. A second dose after 7 to 10 days is needed to kill hatching nymphs. Oral ivermectin has also been used for the treatment of recalcitrant pediculosis. Oral ivermectin is also reported to be beneficial in cases of HIV-infected patients and in outbreaks occurring in institutionalized patients and hospitals.(32) Because the serum halflife of ivermectin is about 16 hours, the 7-day repeat dose may not always be necessary. In HIV patients, however, it may be necessary to dose a second time at 14 days.(33) Advantages include high patient compliance with simple dosing and low toxicity potential. Pruritus usually resolves relatively quickly within 48 hours. Disadvantages are that it is not ovicidal and not intended for children under 5 years of age or who weigh less than 15 kg. Cotrimoxazole (trimethoprim/ sulfamethoxazole)—Pediculosis Oral TMP-SMX may be combined with topical permethrin to enhance efficacy of topical permethrin.(34) Although this therapy may be used for resistant infestations or treatment failures, it should not be used in sulfonamide-allergic patients, considering its serious systemic side effects. Indomethacin—Pediculosis Indomethacin is known to decrease cellular glutathione-5transferase, and because resistance of lice to pyrethrins and permethrin may be related to the parasite’s decreased ability to detoxify the pesticides by conjugation with reduced glutathione, this area of interest has led to reporting the use of “enhancing” or “optimizing” agents such as indomethacin in the treatment of resistant pediculosis.(35) Levamisole Levamisole has been examined in an open-label study as a daily oral dose of 3.5 mg/kg once daily for 10 days.(36) Disadvantages include the potential for systemic side effects and the lack of randomized control trials to establish efficacy. conclusIons In general, the incidence of scabies and pediculosis is not decreasing (perhaps partly due to improved reporting) while evidence and patterns of increased resistance are well documented. Patients, as well as parents, are increasingly frustrated with the lack of efficacy of several topical products and alternative home remedies and are concerned about repeated exposure to agents that may produce toxicity. Moreover, increased use and widespread beliefs that alternative agents pose less hazard than proven treatments has lead to even greater perception that resistance to treatment exists even when proven therapies may not yet have been utilized. For pediculosis, the topical agent of choice may be related more to geographic location and economic considerations than other factors such as toxicity and ease of use. In the United States, the malathion/terpineols combination product, though it produces objectionable odor and is difficult to use, is highly efficacious as one of the first-line agents with minimal toxicity concerns (no reported human toxicity for the topical concentration used) and no proven resistance. Other first-line topical agents that are both safe and effective include agents such as benzyl alcohol and dimethicone. Unchecked scabies infestations in patients with normal immune status will usually cause extreme discomfort from pruritus, possible secondary bacterial infection from excoriations, and will be more likely to spread to other persons. Geographic area, toxicity, and economic status are some of the factors key to measuring the prevalence of scabies. Until quantifiable and precise data on organism kill times and kill rates are generated, analyzed, and reported, particularly using videodermatoscopy technology, we can rely only on indirect measurements of efficacy for agents used in the treatment of scabies and pediculosis. references 1. Hu S, Bigby M. Treating scabies: results from an updated Cochrane review. Arch Dermatol 2008; 144(12): 1638–40. 2. Burkhart CN, Burkhart CG. Recommendation to standardize pediculicidal and ovicidal testing for head lice (Anoplura: Pediculidae). J Med Entomol 2001; 38(2): 127–9. 3. Micali G, Lacarrubba F, Tedeschi A. Videodermatoscopy enhances the ability to monitor efficacy of scabies treatment and allows optimal timing of drug application. J Eur Acad Dermatol Venereol 2004; 18(2): 153–4. 4. Lacarrubba F, Musumeci ML, Caltabiano R et al. Highmagnification videodermatoscopy: a new noninvasive diagnostic tool for scabies in children. Pediatr Dermatol 2001; 18(5): 439–41. 5. Micali G, Lacarrubba F. Possible applications of videodermatoscopy beyond pigmented lesions. Int J Dermatol 2003; 42(6): 430–3. 6. Lacarrubba F, Nardone B, Milani M, Botta G, Micali G. Head lice: ex vivo videodermatoscopy evaluation of the pediculocidal activity of two different topical products. G Ital Dermatol Venereol 2006; 141: 233–6. 7. Burkhart CG, Burkhart CN. Clinical evidence of lice resistance to over-the-counter products. J Cutan Med Surg 2000; 4: 199–201. 8. Pollack RJ, Kiszewski A, Armstrong P et al. Differential permethrin susceptibility of head lice sampled in the United States and Borneo. Arch Pediatr Adolesc Med 1999; 153: 969–73.

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Fundam Clin Pharmacol 2003. Hammond K. Int J Dermatol 2001. 40(12): 794. and west 9. J Am Acad Dermatol 2002. California Safety Code Section 111246. Randhawa SK. 8: 115. and DDT. 36. 107: E30. Guideline for the diagnosis and treatment of scabies in Japan (second edition). 19. Alzieu P et al. Int J Dermatol 1989. Elston DM. Heukelbach J.PDF. Phytomedicine 2002. 28. 19(5): 448–53. nardone. The potential utility of indomethacin in enhancing the pediculocidal activity of permethrin. www. Pilger D. Ko CJ. Lancet 2000. Vander Stichele RH. Eissa MM. Comparison of ivermectin and benzyl benzoate for treatment of scabies. Thomas G. Treatment resistant head lice: alternative therapeutic approaches. Lee PN. Med Hypotheses 2008. Hipolito RB. 15(4): 323–4. Naeyaert JM. Executive committee of guideline for the diagnosis. Sulfur for scabies outbreaks in orphanages. Speare R. 16. Repellency of citronella for head lice: double-blind randomized trial of efficacy and safety. 58(4): 313–23. 33. 24: 151–6. 14(5): 409–10. Head lice. and Cosmetic Law. Delibas SB. 12. Topical application of ivermectin for human ectoparasites. Environ Pollut 1989. Maibach HI. Pediatr Dermatol 1997. 21. Division 104. 17. Matlock G. Casey D. Pruksachatkunakorn C. Controversies concerning the treatment of lice and scabies. 29. PLoS One 2007. el-Ariny AF. 68: 1089–92. Elston DM. 17: 217–25. Youssef MY. Morgan DA et al. 34. Grover IS. Comparison of wet combing with malathion for treatment of head lice in the UK: a pragmatic randomized controlled trial. Aksoy U. Schachner LA.5% malathion liquid for head louse infestation. Evidence in the treatment of head lice: drowning in a swamp of reviews. BMC Infect Dis.Pediatr Dermatol 2002. 26. 11. Glaziou P. Harvey I et al. 18. pyrethrins. 356: 540–4. Leikin JB. Drug. Mallorca FG. Pediatr Dermatol 2006. 32. Rumsfield J. California Health and Safety Code Section 111246. A highly efficacious pediculicide based on dimeticone: randomized observer blinded comparative trial. Oliveira FA et al. Am Fam Physician 2003. Namazi MR. Ishii N. 30. 13.gov/ fdb/local/PDF/Sherman_2007.west. Fawcett RS. Frankowski BL. 31. 2(11): e1127. Current treatments for scabies. capitis) and their eggs. Development of a paw paw herbal shampoo for the removal of head lice. Scabies treatment: current considerations. Evidence for double resistance to permethrin and malathion in head lice. 35(6): 378–93. Roberts RJ. Orkin M. 20. assessor blind trial comparing 4% dimeticone lotion with 0. Erratum in: Int J Dermatol 2001. 23(2): 179–82. 10. Buffet M. accessed 09-23-09. J Dermatol 2008. J Am Acad Dermatol 2004. 24. Isr Med Assoc J 2004. Canyon DV. 355: 819–26. 27. 50: 1–12. Albendazole: single or combination therapy with permethrin against pediculosis capitis. Int J Dermatol 2007. Lapeere H. Comparative efficacy of two nit combs in removing head lice (Pediculus humanus var. 53(6): 652–3. Dupin N. Topical pyrethrin toxicity leading to acute-onset stuttering in a toddler. Miller J et al. Bernstein JE et al. De Felice J. Burgess IF. Sherman Food. 44(4): 331–2. Head lice infestation: single drug versus combination therapy with one percent permethrin and trimethoprim/sulfamethoxazole. Magdassi S. 37: 1580–2. Ivermectin use in scabies. 40(4): 292–4. Cahill C. 110: 638–43. 6(12): 756–9. McCage CM. 22. Pediatrics 2002. Part 5. Stafford KA. Zuniga-Macaraig ZO. controlled. 4 . 71(4): 607–8. Ward SM. 14. Clinical evaluation of an after-pediculicide nit removal system. Carbaryl-A selective genotoxicant. Mumcuoglu KY. Clin Infect Dis 2003. 35. Akisu C. Namazi MR. Am J Ther 2008. Ladhar SS. Levamisole: a safe and economical weapon against pediculosis. 28: 468–70. Pediatrics 2001. Randomised. 141: 508–11. Pediculosis.ca. Chosidow O. Sinthupuan S. Cartel JL. Am J Trop Med Hyg 1995. Damrongsak M. Trop Med Parasitol 1993. Downs AM. Scabies and Pediculosis. 23. Paling CA et al. 25. Curr Prob Dermatol 1996.dhs. Sadaka HA. 98: 743–8. Lancet 2000. 15. Br J Dermatol 1999. 46(12): 1275–8. 46: 794–6. Weiner LB.

. there were no visible remains.2. epimeres were even more distinct now. Statistically. Epimeres (chitinous internal structures attached to legs). A total of 20 patients affected by scabies were observed. no differences were found between patients treated orally and those treated locally.3. however. the mites began to degrade. In this study. A total of 20 patients (12 males. VD confirmed that the foam was effective in the management of scabies. Tokyo. and enhancing patient compliance.22).165%) synergized with piperonyl butoxide (1. killing the mites at about 24 hours. At 48 hours. 8 females. less durable components and its gradually disappearing outline suggested that the mite had degraded rather than simply been scratched away. 24. In conclusion.8 magnification. skin scraping of the selected areas followed by microscopic observation was performed. at that timepoint most patients reported that itching symptoms had subsided.0. once at bedtime for two consecutive days. Ltd. 36. None of the 20 patients showed evidence of infestation at a 2-week follow-up. In this study. and 48 hours. probably resulting from mite decomposition. The authors examined the mite’s morphological changes in vivo. and their outlines disappeared gradually. or a comparable device of another manufacturer) or with a video microscope with X20 to X60 magnification. After 3 weeks. 7 patients received 12 mg of ivermectin as a single dose. (5) we evaluated a group of patients affected by scabies undergoing topical treatment with a thermolabile foam of pyrethrins (0. This may be particularly important in minimizing the risk of overtreatment. The authors suggested the decrease in number of mites might have resulted from both scratching and the renewal process of the corneal layer itself. Before treatment. The progressive degradation of its other. For these reasons. some studies have been carried out to evaluate VD ability to monitor efficacy of scabies and pediculosis treatment and whether VD allows determination of the optimal timing of drug application. Aurora Tedeschi. the evaluation of efficacy was performed with the stereo epiluminescence microscope of Kreusch (Fa. After 2 weeks.25 and X20. there was no evidence of active mite migration. Probably. and Francesco Lacarrubba Previous studies demonstrated that videodermatoscopy (VD) is a very effective and sensitive diagnostic tool for some cutaneous parasitoses. and after 12. Japan) equipped with a zoom lens that allows skin observation with incidental light at magnifications ranging from X20 to X600. the average number of adult female mites on both hands and feet of all patients was 8. SCABIES The first study (4) to assess the use of epiluminescence light microscopy (ELM) for monitoring antiscabietic therapy was performed in 2001. and their effectiveness as criteria for treatment. the temporal progression of these changes. In order to detect treatment response. the granular hem was a product of catabolism resulting from treatment. to determine whether VD would enhance monitoring of the clinical response to treatment and whether VD would indicate the optimal timing of drug application. structures had progressively broken down or were missing. the use of high magnification (up to X600) allowed to recognize early the death of mites. when their immobilization could be established. was generally detectable at one end of an empty burrow (Figure 3. reducing the potential for side effects. In all patients. At that time. Wolfgang Kocher Feinmechanik.65%). VD seems to be a useful technique for evaluation of response to therapy. A granular hem was noticed in some cases. One week after treatment. VD examination was performed with a Video Microscope System Hi-Scope KH-2. Therapeutic monitoring of parasitoses with videodermatoscopy Giuseppe Micali. Once the mite was dead it was slowly promoted upward under a progressively thinning cover. The foam was applied to the entire body. At 48 hours. At 48 hours. At 24 hours. microscopic examination following skin scraping confirmed that this material was composed of mite remnants. 5% permethrin cream formulation was tested. VD enhances the monitoring of clinical response to treatment (4) and allows determination of the optimal timing of drug application. Germany. aged between 1 and 65 years) who were affected by scabies (diagnosis confirmed by VD) and were treatment naïve were included in the study.21–3. ELM was performed using X8. the average number of adult female mites had dropped to 5.  . and both pairs of forelegs and hind legs of Sarcoptes scabiei were observed. At this time. and 13 patients were treated with lindane or benzyl benzoate for 3 days. in particular scabies and pediculosis. as it does not cause pain or physical discomfort.(4) In our experience. especially in children.(1–3) An important advantage of VD is its high compliance. especially in those cases in which itch persists after treatment or patient compliance is doubtful. shrinkage and breakdown of the mite with formation of an amorphous material was observed. VD showed mite migration within burrows at 12 hours. this explained why the durable chitinous epimeres became even more distinct with time.200 (Hirox Co. Based on these considerations. anterior outline. VD evaluation of two selected skin areas for each patient was performed at baseline. In another single-arm multicenter study (6) including adults and children from 3 months of age with proven scabies. After 4 weeks. eating tools. skin scraping followed by microscopic observation showed only mite remnants in all patients. the mites were generally no longer appreciable and an amorphous material. Mössingen.

such as antibiotics (trimetroprim) or ivermectin. for many of these products.(8) The differentiation between vital and empty nits provides useful information about therapeutic response. Moreover. At the last visit. LLC). dermoscopic follow-up still revealed the presence of dark-brown eggs containing nymphs. An in vivo study (8) was performed by mean of a noncontact hand-held dermoscope (Dermlite. essential oil) or with systemic drugs.(8) In our experience. evaluation methods have been based on very simplistic criteria (i. permethrin. and malathion) or with so-called natural products with mechanical action (e. and lacarrubba (a) (b) Figure 3. An 8-year-old boy affected by pediculus capitis was treated with permethrin (1%) according to established protocols.22a–b After 48 hours of treatment the mites were no longer appreciable (X100).  . (a) (b) Figure 3.. in vivo dermoscopy may replace the more time consuming ex vivo microscopic examination of the affected hairs in the daily routine. VD can be used as a diagnostic tool in head and pubic lice infestation: It permits an easy identification of parasite and nits when these are not visible to the naked eye. VD allowed the therapeutic monitoring with mercurial ointment in a case of phthiriasis palpebrarum.e. In this case. clinical examination before and after treatment). Therefore. and two additional therapeutic cycles were performed.g. PEDICULOSIS Pediculosis is a very frequent parasitosis usually treated with topical compounds with insecticidal activity (pyrethrin. 3gen. data about their real therapeutic efficacy or rapidity of action are not readily available.micali. 3 weeks after diagnosis.(7) However. no nits were observed and treatment was discontinued. the dermoscopic examination allowed a safe and reliable differentiation of eggs containing nymphs from the empty cases of hatched louses and also from amorphous pseudo nits. The characteristic dermoscopic features let the authors not only establish a rapid diagnosis but were also useful for the treatment monitoring because vital eggs were still present after the first treatment cycle. tedeschi. One week after the first treatment cycle.21a–b VD evaluation showing the presence of Sarcoptes scabiei (arrows) at baseline (X100).

With the essential oil-based product the lice was alive after a continuous observation of 120 minutes after the application of the medication (the product’s package showed the time for optimal product activity to be around 15 minutes). Isolation of an adult parasite allows to observe through VD the louse and to prove its viability in ex vivo conditions (by means of a Petri’s capsule). with a mechanical action obtained by suffocation (Paranix®. Mipharm) was compared to a coconut and aniseed oil–based spray. which was interpreted as mite death. VD examination was performed using a Video Microscope System Hirox Hi-Scope KH-2.  . The activity of parasites were then observed and recorded for 120 minutes. A formulation of synergized pyrethrin in thermophobic foam (Milice®.23b). the absence of movements of lice was observed within 10 seconds from the contact with the product. Chefaro). a minimal quantity of pyrethrin thermophobic foam was applied on five parasites and the oil-based spray was applied on another batch of 5 parasites. in all the tests performed. VD permits an in vivo evaluation of the movements and physiology of lice and eggs. we performed another similar preliminary study with a topical compound that acts through a mechanical action of “choking” of the mite within few minutes (Figure 3. Recently. VD showed the persistence of few full nits not visible to naked eye (Figure 3. B: VD evaluation after 5 days treatment with mercurial ointment: persistence of few full nits not visible to naked eye (X60). Figure 3. A: lice and nits at VD observation (X60).therapeutic monitoring of parasitoses with videodermatoscopy (a) (b) Figure 3.200 equipped with lenses allowing magnifications ranging from X20 to X600. Each louse was placed in a Petri’s capsule with gauze on the bottom in order to improve the VD visualization. Ten experiments were performed on the same number of adults’ specimens of Pediculus humanus capitis obtained from three subjects with head lice infestation.23a–b Phthiriasis palpebrarum.24 VD examination of an adult specimen of Pediculus humanus treated with the application of a topical compound that acts through a mechanical action of “choking” (X80). After this time. In conclusion.23a–3. it is also possible to assess the efficacy and rapidity in pediculocidal activity of topical pediculocides. VD is indeed a valid research tool for evaluating the efficacy and the time of action taken by topical agents/ pediculocides to act while treating. After 5 days of treatment. using a fine-tooth comb. In 2006 we performed a study (9) using VD to assess the pediculocidal efficacy and rapidity of action of two different medications indicated in the treatment of head lice.24).(8–10) A further and future use of VD could be measured by studying possible lice resistance to commonly used substances with pediculocidal activity. Through the isolation of Pediculus humanus capitis (that cannot be reared in laboratory conditions) and through VD evaluation. In the case of pyrethrin thermophobic foam product. the absence of peristalsis was noted within 60 seconds. An initial observation by VD of 180-second duration was performed to evaluate movements and peristaltic intestinal activity (that is visible in transparency) as an indicator of lice viability.

Videodermatoscopy enhances the ability to monitor efficacy of scabies treatment and allows optimal timing of drug application. 5. Beiteke U. 6. 2. tedeschi. 10. Hamm H. 9. 4. 7. Micali G. Giacomel J. The use of ELM to monitor the success of antiscabietic treatment. and lacarrubba in order to contribute to the identification of alternative and appropriate therapeutic options. J Eur Acad Dermatol 2004. REFERENCES 1. Dodd CS. Botta G. Musumeci ML. Scraping versus videodermatoscopy for the diagnosis of scabies: a comparative study. Haas N. Cabo H et al. Fabbrocini G. 133: 751–3. J Dtsch Dermatol Ges 2006. Delfino M. Lacarrubba F. Interventions for treating headlice. 18: 439–41. Arch Dermatol 1997. Epiluminescence microscopy. Milani M. Di Stefani A. Zalaudek I. Cochrane Database Syst Rev 2001. Micali G. Dermoscopy for diagnosis and treatment monitoring of pediculosis capitis. 3. J Am Acad Dermatol 2006. Hofmann-Wellenhof R. Höger PH et al. Treatment of scabies with 5% permethrin cream: results of a German multicenter study. Zalaudek I. Entodermoscopy: a new tool for diagnosing skin infections and infestations. 54(5): 909–11. Head lice: ex vivo videodermatoscopy evaluation of the pediculocidal activity of two different topical products. 137: 1656–7. 8.micali. Tedeschi A. Arch Dermatol 2001. A new approach to in vivo detection of Sarcoptes scabiei. Argenziano G. 18: 153–4. Lacarrubba F. 79: 396. Acta Derm Venereol 2000. Micali G. Nardone B. Pediatr Dermatol 2001. Caltabiano R et al. 2: CDOO1165. Dermatology 2008. Lacarrubba F. Lacarrubba F. G Ital Dermatol Venereol 2006. 141: 233–5.  . 4(5): 407–13. Lo Guzzo G. Highmagnification videodermatoscopy: a new noninvasive diagnostic tool for scabies in children. 216(1): 14–23. Sterry W.

brown opening.2%. The direct identification of eggs by dermoscopy has been described by Cabrera et al. but after copulation. The flea is located between the epidermis and the superficial dermis. sometimes shaped as a comma. and Giuseppe Argenziano Nowadays. Gray-blue blotches. creating a cavity that reaches the superficial dermis where it is nourished by the blood of the dermal vascular plexus. traveling-associated dermatoses are more frequently seen by physicians that may not be very familiar to them. dogs. especially for African states. foreign body reaction. (17) recently described a further dermoscopic feature defined as “whitish chains. fungal and bacterial infections. and (5) rest of the fleas in the host’s cutis.25 and 3. the female starts producing eggs and enlarging her body from 1 mm to about 1 cm in diameter. After penetration into the skin.(3) In a recent study conducted in a rural community in Lagos. (2) hypertrophy. The diagnosis is essentially clinical in endemic areas. It typically presents multiple. which they inferred to be related to developing eggs.3. and vasculitis. whereas the female remains into the skin completing her vital cycle that lasts about 4 to 6 weeks.(12) In this scenario. (4) inoculation. An inflammatory perilesional infiltrate is also present that is constituted by lymphocytes. (3) the white halo phase. embedded in a pseudocystic cavity that presents a small opening through which eggs and feces are expelled. Bakos et al. Penetration of the flea is asymptomatic or may be followed by an itching sensation. Only when the parasite enlarges its diameter an inflammatory process causes pain to the host (10). dermoscopy can facilitate the early diagnosis of tungiasis. The flea is not able to jump high. ectopic lesions have been reported in almost all parts of the body and are associated with high infestation grades and young age.6 Tungiasis Elvira Moscarella. 14) first described the dermoscopic aspects of tungiasis. Histopathologic examination reveals hyperkeratosis and acanthosis of the epidermis. Early diagnosis and correct therapy are crucial to avoid frequent complications that may be caused by bacterial superinfections. can also be seen and may represent the intestinal part of the flea (X10).(6.” They visualized using dermoscopy the presence of whitish structures Tungiasis is an ectoparasitic disease caused by the flea Tunga penetrans. neutrophils. This corresponds to the pigmented chitin surrounding the posterior opening of the flea exoskeleton. cats. central. tumors. The lesions are white-gray-yellowish in color and exhibit a small. Therefore. and the Caribbean. The flea penetrates the skin with the head of the exoskeleton. even so. the male dies. curettage.(16) Reaching the dermis by sequential and careful shaving of the epidermis and gently compressing the edges of the wound. Africa. and eosinophils. myiasis. the lesion is usually single and can be easily misdiagnosed and confused with several other diseases like viral warts. In nonendemic areas. Bauer et al. 2) A surveillance performed in communities of lower socioeconomic status of northeast Brazil has demonstrated prevalence rates of up to 54. Eggs and feces are eliminated through a small opening in the epidermis and then the flea dies in the cavity. (13. confluent. which is endemic in some parts of South and Central America. Asia. the feet are the preferred site of penetration.26).5% among the residents of such areas. Mechanical removal. thus leading to the correct treatment that consists of complete surgical excision of the lesion (Figures 3. (15) found a dermoscopic grey-blue blotch. a jelly-like bag will emerge.(4) Only one autochthon case has been reported in Europe (5) where all reports are about imported cases in which the disease was contracted after traveling in endemic areas. Data on tungiasis prevalence are variable and are not always available.4%. roundish papules or nodules located on the feet. and rats) serving as usual reservoirs. Di Stefani et al. The opening corresponds to the posterior part of the flea’s exoskeleton.25 On dermoscopy. the prevalence was 45. The natural history of the disease has been divided into 5 phases (9): (1) penetration. 7) The disease is usually acquired by walking barefoot in humid sand contaminated by the flea.(11) Figure 3. cows.(1. sometimes reported as very intense and debilitating. Renato Bakos.  .7% to 31. Tungiasis is reported to be very frequent in Trinidad with prevalence varying from 15. Tunga penetrans is a sand flea that infests the skin of humans and can have various animals (pigs. and cryotherapy may also be considered.(8) Both male and female flea may penetrate the skin. which is visible as a bag full of eggs during dermoscopy. identifying the dark spot as a pigmented ring with a central pore. the lesion appears as a white to light brown yellowish papule with a central brownish opening.

8. Arch Dermatol 2004. yellowish unstructured area exhibiting a variable number of irregularly distributed. Caumes E. 92: 107–13. Bacterial superinfection in human tungiasis. Chadee DD. Tungiasis among five communities in south western Trinidad. 12. 46: 475–81. 6. B J Dermatol 2008. Eisele M. 5. Costa AML. Med Vet Entomol 2004. and morbidity in a rural community in Lagos State. Heukelbach J. Garbe C. Heukelbach J. Daza F. 20: 542–8. Forschner A. 159: 991–2. 9. Mehlhorn H. 18. Variability of dermoscopic features of tungiasis. Rocken M. 67: 214–6. Tungiasis: eggs seen with dermoscopy. Feldmeier H. West Indies. red. Br J Dermatol. 7: 559–64. Arch Dermatol 2005. 141 (5): 643–4. Arch Dermatol 2005. 97: S113–S119. Rocken M. showing comma-like gray-blue blotches. 140 (6): 761–3. Trop Med Int Health 2002. Feldmeier H. Heukelbach J. 201: 382. Van Bruskirk C. Am J Trop Med Hyg 2002. Guermonprez G et al.26 Another image of tungiasis seen by dermoscopy. 18: 329–35. Dermatosis associated with travel to tropical countries: a prospective study of the diagnosis and manaagment of 269 patients presenting to a tropical disease unit. REFERENCES 1. Cabo H et al. Feldmeier H. Wicke T. Heukelbach J. Trop Med Hyg 1994. Dermoscopy can also allow a rapid differential diagnosis (18) with plantar warts and pigmented melanocytic lesions (a case of Tunga penetrans simulating acral melanoma has been described)(6). Clin Infect Dis 2006. Clin Infect Dis 1995. Dermatology 2008. Schianchi R. Mencke N. bakos. Heukelbach J. Carriere J. and argenziano 4. 158 (3): 635–6. jigger flea) in dogs in Brazil. Wilckle T. 16. drainig black lesion on the right heel. In viral warts. Ann Trop Med Parassitol 1998. 1: 159–66. Tungiasis. Nigeria. 2008. Garbe C. Franck S. Zalaudek I. Parasitol Res 2003. together with whitish structures forming a chain-like structure and expelled eggs (X10). Rudolph CM. or black dots or linear streaks caused by chronic high vascular pressure at plantar sites. Mullegger RR. Pigmented acral melanoma can also be easily differentiated for the presence of specific dermoscopic features such as the parallel ridge pattern. Carrera C. 2. 216 (1): 14–23. Burd EM. Natural history of tungiasis in man. Tungiasis: more than an exotic nuisance. “Whitish chains”: a remarkable in vivo dermoscopic finding of tungiasis. 141 (8): 1045–6. 10. Bakos L. Tungiasis had reached Europe. Kimpel S. Forschner A. Distribution patterns of tunga penetrans within a community in Trinidad. Hofmann-Wellwnohf R. pathology and control of Tunga penetrans in Brazil: I. 3. parasite load. Chadee DD. Eisele M et al. 97: 167–70. 14. Tungiasis: high prevalence. West Indies.moscarella. An additional dermoscopic feature of tungiasis. Entodermoscopy: a new tool for diagnosing skin infections and infestations. Bauer J. in a chain-like distribution perfectly matching in vivo with the jelly bag described by Cabrera. Mencke N. Ofoezie IE. Bakos RM. Lee M. Travel Med Infect Dis 2003. Parassitol Res 2005. 15. 13. 3 . The animal reservoir of tunga penetrans in severely affected communities of north est Brazil. Heukelbach J. Giacomel J. Figure 3. Ugnomoiko US. Feldmeier H. feldmeier H. 11. brown. Cabrera R. Ectopic localization of tungiasis. A painful. Field trial of the efficacy of a combination of imidacloprid and permetrin against Tunga penetrans (sand flea. Dermoscopy of tungiasis. epidemiology. the diagnosis is based on the presence of a verrucous. 43: 65–6. Heukelbach J. 7. 17. 9(2): 87–99. Eisele M. Investigations on the biology. Di Stefani A. Int J Dermatol 2007. Bauer J. Veraldi S. Van Marck E et al. Dermatology 2000.

Interfollicular patterns: Vascular patterns Simple red loops Twisted red loops Arborizing red lines Red dots Pigment pattern: honeycomb pigmented network Blue-grey dots Brown halo (peripilar sign) White dots Dirty dots Follicular patterns: Yellow dots Keratotic plugs Black dots (cadaverized hairs) Figure 4. The network consists of hyperchromic lines that represent melanocytes in the rete ridge system in contrast with hypochromic areas formed by fewer melanocytes localized in the suprapapillary epidermis. Dirty dots disappear at puberty when sebaceous excretion possibly prevents deposition of environmental particles on the scalp. Table 1 Videodermoscopic Patterns Seen in Normal and Pathological Scalp.(1) Small.4 Hair loss Antonella Tosti and Bruna Duque Estrada In the last few years. Figure 4. Both epiluminescent and nonepiluminescent modes are employed. which we defined as dirty dots. dermatologists may use a manual dermoscope (x10 magnification) or a videodermoscope equipped with various lenses (from x20 to x1.000 magnification). dust.(2)  . and other small particulate debris. may be appreciated in children aged between 1 and 12 years (Figure 4. Dermoscopy findings in hair and scalp disorders include follicular and interfollicular patterns. This diagnostic method has provided new clinical signs for recognizing hair diseases and enhanced features previously seen with the naked eye. dermoscopy has been increasingly used in the evaluation of patients with hair loss.4).1 Normal scalp of a Caucasian patient. Note the honeycomb pigmented network around the follicular units (x20). white dots regularly distributed among follicular units are also appreciated (Figure 4.1). For scalp examination. which represent capillary loops in the dermal papilla. Note the diffuse white color of the scalp and the follicular units containing 1 to 3 terminal hairs (x20). Particles of dirt.3 and 4. a perifollicular pigmented network (honeycomb pattern) is well appreciated. In dark-skinned individuals (phototypes V and VI).2). and alcohol or thermal water can be used as interface solutions. These particles are most prominent in the vertex scalp and disappear immediately after shampooing.1). Normal Scalp Examination of the normal scalp shows a diffuse white color and often simple fine red loops. We believe that this technique is a very important tool. as well as hair shaft’s characteristics (Table 4.(1) Follicular units contain 2 to 3 terminal hairs and 1 or 2 vellus hairs inside (Figure 4. loose fibers.2 Scalp dermoscopy of a dark-skinned patient. but reappear as soon as 24 hours after shampooing. as it not only improves diagnostic accuracy of hair and scalp disorders but also provides clues for better understanding the pathogenesis of some conditions.

The progressive miniaturization of hair with visualization of hairs with different calibers are enhanced by dermoscopic Figure 4. it is possible to identify and count vellus hairs (with less than 0. Patients typically present with progressive thinning and shortening of hair in androgen-dependent scalp regions including frontal.5 A variability in the hair shaft diameter of more than 20% of hair shafts is diagnostic of androgenetic alopecia (x20).6).(5)  . 5) It is worthwhile to note that follicular ostia in AGA show predominance of single hairs. and thus may also help in calculating the terminal to vellus hair ratio. scalp examination in AGA should be taken in an area delineated at the cross between nose line and ear implantation line. (4) Using this parameter. affecting up to 80% of men and 50% of women.6 A variability of the hair shaft diameter is well observed. powder and debris can be seen as dirty dots in scalp dermoscopy of this Caucasian patient (x20).4 Small dirty dots are observed in scalp dermoscopy of this African-American child (x20). instead of 2 to 4 hair shafts observed in normal subjects (Figure 4. Lacharrière proposed a severity scale based on dermoscopic findings as diameter-diversity and hairdensity scores.(4. Figure 4. 5) Under higher magnifications on videodermoscopy. examination. as well as many follicular units compound of single hair shafts (x20).(4) Videodermoscopy allows measurement and monitoring of hair shaft thickness in androgenetic alopecia.3 Particles of dust.(3.tosti and estrada Figure 4. temporal.03 mm in width).(3) A hair diameter diversity of >20% is diagnostic of androgenetic alopecia and is significantly correlated to follicle miniaturization by histological analysis (Figure 4. and vertex areas. Dermoscopic Features Hair Diameter Diversity In general. aNdrogeNetic alopecia Androgenetic alopecia (AGA) is the most common form of hair loss. Figure 4.5).

beard. dermoscopy often shows small areas of follicular loss (focal atrichia) (Figure 4. and unaffected occipital scalp of patients with phototypes I to IV. alopecia areata Alopecia areata is an autoimmune. Dermoscopic Features Yellow Dots The presence of yellow dots is a characteristic finding in alopecia areata. nonscarring form of alopecia. 9) The dots are best visualized under epiluminescent dermoscopy. yellow dots can be observed. and all body hairs. but it may also involve eyebrows.8).(1. 8. and polycyclic dots that vary in size and correspond to the dilated follicular openings with or without hairs shafts (Figure 4. Empty follicular ostia are often seen.9). A honeycomb-like pigmented network is found in scalp areas that are sun exposed with progression of baldness.8 Dermoscopy of the patient with long lasting AGA demonstrates focal atrichia with absence of follicular ostia (x40). Kenogen frequency and duration are greater in men and women with androgenetic alopecia than in controls and an increased number of kenogen follicles has been associated with the progression of female AGA. Figure 4.(7) Figure 4. Thinning of the hair shafts leads to decrease on sebum drainage and thus to distention of the infundibular portion of the hair follicle. This pigmentation is well appreciated when comparing parietal scalp affected with AGA.9 Yellow-red. A wide range of clinical presentations can occur.7 Patient presenting long lasting AGA with diffuse pattern. eyelashes. Degreasing the affected area with acetone results in diminished dot sizes. which corresponds to the interval between extrusion of the telogen hair and emergence of a new anagen hair. and polycyclic dots correspond to the dilated follicular ostia without hairs shafts (x20). round. With this method. round. from single patch of alopecia to complete loss of scalp hair (alopecia totalis) or the entire body (alopecia universalis).5). They are expression of the kenogen phase of the hair cycle. The disease affects most commonly scalp hairs. Peripilar signs The presence of a brown halo at the follicular ostium is mostly found in patients with high hair density and this finding have been related to superficial perifollicular lymphocytic infiltrates in early androgenetic alopecia of male and females (Figure 4.7 and 4.  .(6) In women with longstanding AGA. axilary. one can see more clearly a Figure 4. This pattern is characterized by a distinctive array of yellow to yellow-red.(1) Dry dermoscopy (dermoscopy without immersion gel) has also been reported as a useful technique in diagnosis and follow-up of patients with alopecia areata. although the nonepiluminescent mode provides a better view of their protuberant and greasy aspect.(1) These dots represent distention of the affected follicular infundibulum with keratinous material and sebum. pubic.hair loss Secondary Signs In patients with advanced androgenetic alopecia.

(1.tosti and estrada Figure 4.10).11 and 4. or telogen hairs. irregular. Monilethrix-like changes are observed due to variation in the caliber of the hair shaft as the result of intermittent inflammatory process affecting the hair bulb (Figure 4.12). Vellus hairs and short broken hairs are also observed inside the plaque (x20).14). (1.11 Cadaverized hairs. 9) We have also observed a lower incidence of yellow dots in patients with phototypes V and VI. as black dots. 9) Growing of the broken shafts leads to formation of exclamation mark hairs. which cannot be morphologically categorized as anagen. keratotic plaque with multiple depressed follicular ostia. catagen. In active alopecia areata.(10) It has been suggested that this depressed pattern may correspond to abnormal hair follicles containing incompletely differentiated hair shafts. the anagen arrest causes hair shafts to fracture before their emergence from the scalp: these cadaverized hairs appear as black dots at dermoscopy (Figures 4. A variable degree of hair shaft hypopigmentation is sometimes the unique mark of alopecia areata. Figure 4.(10) The frequency of observation of yellow dots in Asian patients has been shown to be lower than that reported in Caucasians.12 Black dots are observed inside the yellow dots and represent cadaverized hairs that are broken before scalp emergence (x70). possibly because the yellowish color of Asian patients and the presence of the pigmented network in black patients makes it more difficult to perceive the yellow dots (Figure 4. Figure 4. Dystrophic Hairs Dystrophic hair shafts are well appreciated by dermoscopy even at lower magnification (X 20).13 Exclamation mark hairs are characterized by a distal and wide tip in comparison with the proximal portion of the shaft (x20). the so called nanogen hairs.13). Figure 4. short broken hairs. fractured tip that is wider than the proximal portion of the shaft (Figure 4.10 An African-American patient with alopecia areata in which the yellow dots are difficult to visualize. and exclamation mark hairs are observed inside an active plaque of alopecia areata (x20). 5. 4 . which are characterized by a distal.

and tapered hairs (2–4 mm long) are a characteristic dermoscopic feature of alopecia areata incognita. round. statistical analysis made by Inui et al.(13) Scalp biopsies show that the yellow dots correspond to dilated infundibula filed with cornified cells and sebaceous material. and broken hairs were the most specific markers.(12) Patients often concern about severe thinning in a few months.16).(9) Dermoscopic Features Yellow Dots Using the epiluminescent mode. exclamation-mark hairs. and dermoscopy has proved to be an important tool in this challenging diagnosis. inside a plaque of alopecia areata are found in both acute and chronic diseases (x20). exclamation-mark hairs. scalp demonstrates diffuse. yellow dots and short vellus hairs were the most sensitive markers. alopecia areata iNcogNita Alopecia areata incognita was first described by Rebora in 1987.15). with less than 10mm length. and clustered short vellus hairs correlated with the severity of disease. as the result of intermittent inflammatory process affecting the hair bulb. A female patient with acute and severe thinning of the hair. Black dots. yellow dots. Figure 4. Differential diagnosis with androgenetic alopecia and telogen effluvium is often difficult. demonstrated that for diagnosis of alopecia areata.(11) Recently. miniaturized. and vellus hairs indicate disease activity. and polycyclic yellow dots. The presence of black dots. Short regrowing hairs Short. Clinical aspect is difficult to differentiate from androgenetic alopecia and telogen effluvium.14 The variation in the caliber of the hair shaft. and vellus hairs (shorter than 10 mm) are also a common feature observed in both acute and chronic alopecia areata. The association of yellow dots with a large number of short regrowing hairs is very suggestive of alopecia areata incognita  .15 Short vellus hairs. miniaturized. it is characterized by acute onset of diffuse shedding of telogen hairs in the absence of typical patches (Figure 4. These hairs represent miniaturized nanogen hairs that are not able to prolong their anagen phase and undergo continuous recycling (Figure 4.hair loss Figure 4. Figure 4. composes the monilethrix-like hair shaft (x20). The dots are evident within the follicular ostium with and without hair shafts and affects about 70% of the follicles (Figure 4. with varied size and uniform distribution.17). Black dots. Short regrowing.16 Alopecia areata incognita.

Yellow dots are observed within the follicular ostium of both empty and hair-bearing follicles. resulting in alopecic patches. Inside the plaques. exclamation mark hairs are not observed in trichotilomania (x40). The typical peribulbar lymphocytic infiltrate may not be present. short broken hairs with variable lengths are evident. Inui et al.18).17 Alopecia areata incognita.  . (Figure 4. Dermoscopy is useful to diagnose the disease and to show patients the signs of plucking who do not admit their habit of pulling out hairs. Short regrowing hairs are also a characteristic feature of this subtype of alopecia areata (x40). with typical bizarre borders are observed. reported the usefulness of dry dermoscopy (dermoscopy without immersion gel) in detecting tiny hairs in a patient with diffuse alopecia in which differential diagnosis with androgenetic alopecia and telogen effluvium is often difficult. Broken hair shafts at different lengths are frequent findings. Figure 4.18 Alopecia areata incognita. Dystrophic Hairs Exclamation mark hairs and cadaverized hairs are not common in our experience (Figure 4. Figure 4.tosti and estrada Figure 4. from scalp or any other body area. Note the absence of the typical plaque and the presence of dystrophic and short broken hairs in a diffuse distribution (x20). It is relatively more common in children. Despite its similarity with alopecia areata. irregular patches of hair loss. The pathological diagnosis is suggested by the presence of a subtle lymphocytic infiltrate around miniaturized follicles in the papillary dermis that correlates with the short regrowing hairs observed on dermoscopy.(13) Figure 4.(10) Histopathology reveals high percentages of telogen hairs and/or miniaturized hairs. On physical exam.17).19 Trichotilomania.(13) tricHotilomaNia Trichotilomania is a compulsive disorder in which individuals pull out hair.20 An African-American patient with the characteristic longitudinal splitting of the shafts in trichotilomania (x30).

Other scalp regions may occasionally be affected. These findings are considered evidence of plucking at different times. Dermoscopy shows many vellus hairs and normal follicular ostia.22 Lichen Planopilaris. Primary cicatricial alopecias specifically target the hair follicle and results in its destruction. As interfollicular epidermis is commonly unaffected by the inflammatory process in LPP.(15) Differential diagnosis of cicatricial alopecias requires a scalp biopsy.23). Causes of cicatricial alopecias are categorized as primary or secondary. affecting most frequently the pariental and vertex regions. The condition may be bilateral. Scalp examination shows irregular patches of hair loss. Cicatricial alopecias are the most challenging hair diseases for differential diagnosis and treatment.21). we believe that this sign may help in differentiating this type of alopecia from other scarring alopecias.hair loss Figure 4. Dermoscopic findings Short coiled hairs are distributed along the alopecic area with broken hair shafts with different lengths. This feature is more appreciated in patients with dark skin (phototypes V and VI) and patients with long-standing alopecia. which become confluent. In secondary scarring. Patients present with scalp itching and tenderness. sites to take biopsies.24). Dermoscopy shows the typical perifollicular casts and areas with absence of follicular openings (x20). as well as to provide new information about the diseases. Dermoscopy has shown to be useful to find appropriate Figure 4. alopecias the hair follicle destruction is secondary to diffuse scarring of the dermis. The disease has a progressive course and severe alopecia may develop in some patients. follicular plugging may be observed (Figure 4.21 Congenital Triagular alopecia. Dermoscopy is helpful in the diagnosis when the triangular alopecia has an atypical location. Dermoscopic Features Dermoscopy reveals absence of follicular openings and the presence of characteristic perifollicular scales (peripilar casts) at the periphery of the patch. such as discoid lupus erythematosus of the scalp (Figure 4.22). licHeN plaNopilariS Lichen planopilaris (LPP) is the most common cause of cicatricial alopecia and most frequently middle-aged women. which develops the pigmented network secondary to sun exposure in the affected area. Terminal hairs of the normal scalp are well appreciated around the plaque (x20). As scaling becomes more prominent.(14) Dermoscopy of the patch shows normal follicular openings and numerous vellus hairs surrounded by normal terminal hairs in the adjacent scalp (Figure 4. The pigmented network is still well appreciated inside the LPP plaques of dark-skinned individuals.19 and 4. Perifollicular erythema characterized by the presence of arborizing vessels around the follicular ostia is also observed (Figure 4. scalp examination reveals a variable degree of absence of follicular ostia. ScarriNg alopecia Cicatricial alopecias include a group of hair disorders that cause permanent destruction of the hair follicles.20). coNgeNital triaNgular alopecia Congenital triangular alopecia usually presents in children in the age between 3 and 6 years as a triangular or oval patch of alopecia most frequently localized in the frontotemporal hairline. Dermoscopic Features In all types of cicatricial alopecias. The triangular or lance-shaped alopecic area contains vellus hairs and has a typical stable course.  . Longitudinal splitting of the hair shafts are also well appreciated in many cases (Figure 4.

28).27). representing pigmentar incontinence inside the lesion (x20).(16) Blue-grey dots may be found in some patients. especially those with dark skin (Figure 4. The target pattern is associated with the presence of melophages predominantly around hair follicles. a clinical variant of lichen planopilaris. sparing interfollicular epidermis. Histopathologically. Figure 4. early diagnosis is important for patients’ prognosis. The absence of follicular ostia is also evident (x20). Figure 4. In this way. these dots are caused by loose melanin. Figure 4. Despite the fact that it is considered as part of the group of cicatricial alopecias. atrophy. diScoid lupuS erytHematoSuS Discoid lupus erythematosus (DLE) of the scalp is characterized by single or multiple alopecic patches. fine melanin particles.tosti and estrada Figure 4. LPP spares some terminal hair follicles inside the alopecic patches. The regular distribution of the white dots is well appreciated. Usually. and telangiectasias. A peculiar pattern of round perifollicular blue-grey dots—“target pattern”—may be observed in some dark patients with LPP (Figure 4. peripilar scale. scaling.25 Liche planopilaris in an African-American patient. and peripilar erythema (Figure 4. Kossard observed white pale dots in a dark-skinned patient (Figure 4. or melanin “dust” in melanophages or free-floating in the deep papillary or reticular dermis. DLE often shows hair regrowth if promptly treated. especially in comparison to the round and wider white holes that represent the follicular ostia (x10).26 Blue-grey dots are appreciated in LPP. In frontal fibrosing alopecia. follicular plugging. Affected scalp shows erythema. The pigmented network and the white dots regularly distributed among are much more appreciated inside the alopecic plaque (x20).  . the most prominent dermoscopic findings are loss of follicular openings.25).26).24 Dermoscopy of a dark-skinned patient with LPP. Arborizing vessels are responsible for the perifollicular erythema observed in these patients.23 Lichen Planopilaris.

Hyperkeratotic follicular pluggings are observed in the follicles around the patches.29 and 4. Figure 4. Multiple hair tufts are often found emerging from a common.(18) FD usually starts with follicular papules and pustules on the vertex and/or occipital area of the scalp. Arborizing and tortuous vessels are the most common vascular patterns seen inside DLE plaques (Figure 4.29). Dermoscopic features Scalp atrophy is represented by a diffuse white color of the scalp (Figure 4. Some patients also present peculiar red to pink-red. Blue-grey dots may be observed. round. This pattern is well appreciated in dark-skinned patients. Figure 4. Indeed. pigmentary (x40). a white plaque is well appreciated in the active border. associated with tortuous vessels.29). which accounts for approximately 11% of all primary cicatricial alopecias. the honeycomb pigmented network might be seen at the periphery of the plaque of DLE. followed by intense inflammatory reaction and development of an indurated and boggy scarring patch. with a diffuse and speckled pattern of distribution along the patch (Figures 4.(17) FolliculitiS decalvaNS Folliculitis decalvans (FD) is a neutrophilic variant of cicatricial alopecias.30). We believe that the different patterns of blue-grey dots described may be a novel and interesting feature to help dermoscopic differentiation between DLE and LPP.hair loss Figure 4.28 Frontal fibrosing alopecia. as perifollicular scale and erythema (x10).27 Dark-skinned patient with LPP in which the blue-grey dots formed a peculiar “target-pattern” around the follicular units (x10). who loose the normally seen pigmented network within the lesion.30 Polycyclic red dots distributed around follicular openings are observed inside a DLE lesion of the scalp together with arborizing vessels (x20). These dots represent pigmentar incontinence in the papillary dermis of follicular and interfollicular epidermis.  . Figure 4. and polycyclic dots that are uniform in size and regularly distributed around follicular openings (Figure 4.29 In discoid lupus erythematosus of the scalp. Dermoscopic features are the same observed in classic LPP.31).

as the differential diagnosis between traction. 4.34 Pustular lesion inside a plaque of FD (x20).(1) Figure 4. alopecia areata. and arborizing red lines are typical findings seen all over the affected scalp (Figures 4.31 Pigmentar incontinence represented by blue-grey dots in a speckled pattern inside the DLE plaque (x20).36).32 Absence of follicular units. Dermoscopic Findings Marked diffuse scalp erythema and absence of follicular units are characteristic of FD (Figure 4. dilated capillary loops. 4.34. is often seen in advanced cases (Figure 4. marginal alopecia (19) should also be considered in the differential diagnosis. dermoscopy can be very useful. similar to those observed in psoriasis. Tufted folliculitis. The most relevant dermoscopic findings.33.33 Neovascularization is a typical feature of FD. The intense inflammatory process is best seen in x50 or higher magnification. Multiple-coiled.35). Figure 4. or frontal fibrosing alopecia extending to the temporal regions may be difficult. S. dermoScopy iN tHe diFFereNtial diagNoSiS oF alopecia oF tHe Scalp margiN In patients who present with alopecia of the scalp margin. Figure 4. A new entity described as cicatricial.tosti and estrada Figure 4. dilated. diffuse erythema and arborizing vessels in a patient with FD (x40). which can be prominent around follicular units. with several hair shafts emerging from the scalp. aureus can be isolated from FD lesions and seems to play an important role in the inflammatory process. Pustular lesions are also evident. Purulent discharge can be observed if pressure is applied to the perifollicular area. which is observed as multiple coiled capillary loops and arborzing red lines in the scalp (x20). follicular opening. Dermoscopic Features Alopecia areata affecting the scalp margin include ophiasis and sisaipho subtypes.32). as 4 . Dermoscopy also shows severe scaling and crusting.

fractured hair shafts are seen as a sign of severe traction (Figures 4. Usually the disease affects the frontal. 9) Frontal fibrosing alopecia. Figure 4. as well as white dots. It is characterized by the emergency of many hair shafts from the same ostium (x40).38). 5. and a variable degree of perifollicular erythema (Figure 4.37 Dermoscopy of the previous patient shows the characteristic features of AA: yellow dots. 8.41).38 Recession of the frontotemporal hairline and alopecia of the eyebrows in a patient with frontal fibrosing alopecia. and histopathology identical to lichen planopilaris (Figure 4.28).35 Tufted folliculitis is frequently observed in chronic FD. eyebrow loss. A distinctive pattern of alopecia has been recently described by Goldberg as cicatricial marginal alopecia. Dermoscopy of alopecic patches highlights several miniaturized Figure 4. perifollicular scale. temporal. Figure 4. plaits.40 and 4. Sometimes. are yellow dots.(1. and vertex scalp (Figure 4.(20) The periphery of the scalp is the site of predilection of traction alopecia. Patients present history of hairdressing associated with traction of hair scalp for many years. Patients 4 . and vellus hairs (Figure 4. dystrophic hairs and vellus hairs (x20).39). or extensions. 3.hair loss Figure 4.36 A female patient with alopecia in the scalp margin due to alopecia areata – sisaipho subtype. hairs. is characterized by frontotemporal hair recession. dystrophic hairs. Dermoscopy shows absence of follicular openings. which include use of elastic bands.(19) Around 40% of them had no history of traction hair styling. discussed previously.36 and 4. a variant of lichen planopilaris.37).

42–4. A Caucasian patient presenting hair loss in the marginal scalp – occipital margin. abnormal scalp vessels. Figure 4. histological features demonstrate a reduced number of hair follicles with the absence of terminal anagen hairs. A black dot represents a fracture of the shaft due to severe traction (x20). few vellus hair follicles. Perifollicular hyperkeratosis.40 Dermoscopy of traction alopecia demonstrates miniaturized hairs inside the patch. temporal.42 Cicatricial marginal alopecia. including frontal.39 Traction alopecia of the frontotemporal hairline in an African-American patient with some remaining vellus hairs in the frontal portion of the alopecic area. and normal and intact sebaceous glands. 4 . Figure 4.45). Replacement of hair follicles by columns of fibrous tissue (fibrous tracts) are appreciated at the hypodermis. Inflammatory infiltrates are typically absent.tosti and estrada Figure 4. Remaining hairs show reduced diameter of the shafts.41 Traction alopecia. Dermoscopy demonstrated low hair density and loss of follicular ostia in all cases. or signs of traction alopecia are not observed (Figures 4. As described by Goldberg (19). and also the pigmented network and white dots seen in dark-skinned patients (x20). and occipital margins. present hair loss limited to the periphery of the scalp. Figure 4.

response to treatment can be better assessed by using videodermoscope. Comparison of dermoscopic photographs can be made by marking the scalp areas that are analyzed during treatment. This method permits an accurate distinction between anagen and telogen hairs and avoids the technical problem of classic trichogram. Tosti. these studies are not possible. Vincenzi C. This allows the study of the hair cycle and the changes linked to therapies and aging. In this way.hair loss Figure 4. With the classic trichogram. The hair loss in the frontotemporal region resembles frontal fibrosing alopecia. The most important advantage of phototrichogram is that it is possible to repeat the examination on the same area of the scalp on a monthly basis. Tosti A. Thanks to the advent of the computer-assisted image analysis. The phototricogram is a noninvasive technique that allows the in vivo study of the physiology of the hair cycle and the quantification of the amount of the effluvium. in order that each hair strand can be identified and followed across the various phases of the hair cycle. In androgenetic alopecia. Figure 4. 145: 596–7. Starace M. 55: 799–806.43 Dermoscopy of cicatricial marginal alopecia demonstrates loss of follicular ostia and reduced number of shafts per follicular units (x40). Ross EK. however. Dermoscopy also shows perifollicular erythema as arborizing vessels (x20).44 Cicatricial marginal alopecia. such as alopecia areata and discoid lupus of the scalp. a small nevus can be chosen as reference in order to avoid tattooing. 2. When possible. reFereNceS 1. measurement of hair shaft diameter and evaluating the hair diameter diversity allows a significant comparison. A dirty dots: a new dermoscopic finding in healthy children. Fu J.(21) It also evaluates total hair density.45 Cicatricial marginal alopecia. 4 . Macrophotographs of the scalp are very helpful to evaluate response to treatment. J Am Acad Dermatol 2006. Videodermoscopy in the evaluation of hair and scalp disorders. In diseases that present dermoscopic signs of active lesions. tHerapeutic moNitoriNg oF Hair loSS witH videodermatoScopy The combination of special software programs and videodermoscope has offered new tools for monitoring treatment of hair and scalp disorders. a virtual map of the anagen and telogen hairs of the scalp can de drawn. today the technique has been improved. Arch Dermatol 2009. Figure 4. an important index of the degree of the effluvium.

Arch Dermatol Res 2004. 34(2): 49–51. Kenogen in female androgenetic alopecia. Otberg N. Pazzaglia M. 19. 14. The role of scalp dermoscopy in the diagnosis of alopecia areata incognita. Rebora A. Vidéomicroscopie au cours de la pelade. Folliculitis decalvans. Micali G.tosti and estrada 3. Int J Dermatol 2008. Rakowska A et al. Misciali C et al. Ben Hassines M. Histopathologic features of alopecia areata. J Drugs Dermatol 2008. Pediatr Dermatol 2008. 9. Sodré CT. Iorizzo M. 13. McElwee KJ. 139: 1555–9. Whiting D. Pereira FBC. Zagarella S. 15. Dermoscopic patterns of cicatricial alopecia due to Discoid Lupus Erythematosus and Lichen Planopilaris. 7(7): 651–4. Shono F et al. Whiting DA. Descamps V. Inui S. 4. 47: 688–93. Hair diameter diversity: a clinical sign reflecting the follicle miniaturization. 7. Dall’Oglio F. Arch Dermatol 2003. Olzewska M. Misciali C et al. 10. 20. 21: 212–20. Kossard S. Starace M et al. 21. 295: 422–8. Tosti A. 47: 796–9. Dermatol 2005. Cicatricial marginal alopecia: is it all traction? Brit J Dermatol 2009 . Etiology of cicatricial alopecias: a basic science point of view. Dermatol Ther 2008. Dermatol Ther 2008. 137: 641–6. 160(1): 62–8.Vaccaro M. Arch Dermatol 2001. Australas J Dermatol 1993. Goldberg LJ. Lacarrubba F. Kang H. Inui S. Nakagawa K et al. 174: 214–8. 16. J Dermatol 2007. Alzolibani AA et al. 21: 238–44. Nasca MR. Alopecia areata incognita: a hypothesis. Videodermatoscopy enhances diagnostic capability in some forms of hair loss. Trichoscopy: a new method for diagnosis of hair loss. 17. 59: 64–7. Int J Dermatol 2008. de Lacharriere O. 34: 635–9. Dermocscopic findings in frontal fibrosing alopecia: report of four cases. 5. Tamler C. Inui S. de Lacharrière O. 11(1): 17–20. Clinical significance of dermoscopy in alopecia areata: analysis of 300 cases. Rebora A. An Bras Dermatol. Itami S. A dermoscopic clue to fibrous tracts. 25(6): 652–4. 5: 205–8. Deloche C. Rudnika L. 44 . J Am Acad Dermatol 2008. Phototrichogram using videomicroscopy: a useful technique in the evaluation of scalp hair. Crickx B. Histological features of peripilar signs associated with androgenic alopecia. Ann Dermatol Vemerol 2007. 8. Eur J Dermatol 2001. Guarrera M. 210(1): 18–20. 11. Nakajima T. A longitudinal study. Spotted cicatricial alopecia in dark skin. Dry dermoscopy in clinical treatment of alopecia areata. D’Amico D. 12. Nakajima T. Am J Clin Dermatol 2004. Videodermoscopy: a useful tool for diagnosing congenital triangular alopecia. Deloche C. 18. 34: 35–8. 6. Nakajima T. Iorizzo M. Barcaui CB. Guarnieri F et al. In press. Duque-Estrada B. Dermatologica 1897.

Intraoperative dermoscopy It is better to use polarized devices that do not require the application of immersion fluids. Proximal nail-fold dermoscopy is very important in the diagnosis and follow-up of connective-tissue disorders. visualize progression of onychomychosis. water. polarized. Hirata et al. Micro-Hutchinson’s sign: pigmentation of the periungual tissues that could not be seen with the naked eye.(3. Distal-edge dermoscopy can then be used as a preoperative tool to select the anatomical site of excision. show abnormalities in the nail bed vessels. Use of dermoscopy in the hyponychium can detect the following: 1. as it may detect subclinical nail plate surface abnormalities. It can also be useful to evaluate pigmentation of the periungual tissues. Dermoscopy of the hyponychium Examination of the hyponychium can be performed using mineral oil. water. abnormalities in the vessel shape. Vascular abnormality: increase/decrease of the vessel number. better information. Dermoscopy of the proximal nail fold Examination of the proximal nail fold can be performed using mineral oil. This may be important for early diagnosis of subungual melanoma.(2) This is important for understanding the site of melanin production. Nail diseases Antonella Tosti. and distribution. Diagnosis and follow-up of other nail diseases can also possibly benefit from the use of dermoscopy. but digital videodermoscopic systems provide higher magnifications. gel. as pigmentation in the ventral nail plate indicates that the lesion is localized in the distal nail matrix.(1) Nail plate dermoscopy has been mainly utilized for evaluation of nail pigmentation. Polarized devices that do not require the application of immersion fluids can also be utilized in this area. or alcohol solution. there are not evidence-based data showing that the use of dermoscopy may decrease the necessity of nail biopsies. It is also useful to confirm the clinical diagnosis of onychomatricoma. or alcohol solution. gel. 2. Bianca Maria Piraccini. it is useful to localize the pigment within the nail plate. As dermoscopy is becoming widely accepted and used in the medical community. and Débora Cadore de Farias regular red dots because of their perpendicular arrangement to the skin (each red dot observed represents the top of one loop). whereas pigmentation in the dorsal nail plate indicates that the lesion is localized in the proximal nail matrix. where it is better to use mineral oil. or alcohol solution. This gel will fill the gap between the convex nail surface and the hand-held or videodermoscopy device. An exception would be the examination of nail plate surface for abnormalities. In particular. maintaining aseptic conditions. Examination is usually made with a magnification of 10× with a hand-held dermoscope. The main problem of nail plate dermoscopy in the evaluation of nail pigmentation is that we do not examine the site of melanin production but just the site of melanin deposition. in 2006. 4) Intraoperative dermoscopy visualizes the site of melanin production and can also help the surgeons to select the surgical margins. this allows examination with no direct contact. Dermoscopy of the distal edge of the nail plate Originally described by Braun et al. Polarized devices can also be utilized in this area. light dermoscopic examination of the nail bed and matrix for better evaluation of pigmented lesions. gel immersion (ultrasound gel or cosmetic gel) is required because of the convex shape of the nail. there is now the need to standardize the dermoscopic findings observed in the nails in order to share information in this field. and therefore. as it visualizes even The application of dermoscopy in the evaluation of nail disorders is still new and the real benefits of this technique in the diagnosis of nail conditions are not known. The dermoscopic examination can be performed on the following: Nail plate Hyponychium Distal edge of the nail plate Proximal nail fold Nail bed (directly) and matrix (intraoperative dermoscopy) Nail plate dermoscopy On the nail plate. and possibly be helpful in the diagnosis of nonpigmented tumors of the nail. suggested intraoperative. The simple architecture of the hyponychium capillary network makes capillary loops in this anatomic area appear as  . water.

1) • Pits: irregular in shape and size. tortuous. this is an invasive procedure that cannot be used routinely. Also note patchy. and traumatic nail disorders as well. Figure 5.tosti. longitudinal. Zarik et al. Dermoscopy often permits to visualize the presence of a “subclinical” erythematous border as a patchy red-to-orange discoloration of the nail bed surrounding the white onycholytic area. Dermoscopy shows onycholysis characterized by a homogeneously white area with multiple. as they commonly occur in onychomychosis. and elongated capillaries. (2000) showed that the number of capillaries in the nail fold was significantly reduced in psoriasis when  . longitudinal white striae. Splinter hemorrhages are not necessarily an indicator of psoriasis. orange discoloration of the nail bed. Hyponychium dermoscopy In psoriasis. Nail bed psoriasis causes onycholysis. Pits irregular in shape and size are filled by gel and show a peripheral white border. A magnification power of 40X is best for visualizing and counting the abnormal capillaries. and nail bed hyperkeratosis.2 Hyponychium dermoscopy in psoriasis. present a peripheral white border. Figure 5. thin. splinter hemorrhages. • Onycholysis: The area can be homogeneously white or present multiple. Nail plate dermoscopy A magnification power of 40X to 70X is utilized to better visualize nail plate and nail bed abnormalities. splinter hemorrhages. salmon patches. High magnification permits to detect subclinical signs that can be very helpful for a definitive diagnosis of nail psoriasis in doubtful cases. dermoscopic examination of hyponychium shows dilated. as it reflects the degree of microvascular changes.(7) Bhushan et al. and de farias small pigmented foci. Dermoscopy can better visualize nail plate and nail bed abnormalities and detect vascular changes that are indicative of the disease.2). Dermoscopy Findings: (Figure 5.(5) A dermoscopic examination of the hyponychium is in our experience the best tool for confirming the diagnosis of psoriasis in patients with simple onycholysis or mild nail bed hyperkeratosis. Capillary density is positively correlated with disease severity. Dermoscopy shows increased capillary density with dilated. This finding is quite specific for a diagnosis of nail psoriasis • Splinter hemorrhages: brown. and elongated capillaries with an irregular distribution (Figure 5. with an irregular distribution (x20). piraccini. These are due to pinpoint bleeding in the longitudinally arranged nail bed capillaries and successive incorporation of the blood in the ventral nail plate. purple-to-black spots arranged in a longitudinal fashion. • Dilation and tortuosity of the capillary of the distal nail bed is also commonly observed in psoriasis. tortuous. white striae.1 Nail plate dermoscopy in psoriasis. (1982) reported a significantly shorter mean capillary loop length in psoriasis patients as compared to controls.(6) Nail-fold capillaries present both quantitative and morphological abnormalities. Nail matrix psoriasis produces nail plate surface abnormalities such as pitting and nail crumbling. • Salmon patches: red-to-orange patches of nail bed discoloration that are irregular in size and shape. and dilaltion and tortuosity of the capillaries in the distal nail bed (x20). However. thin. Proximal nail-fold dermoscopy Nail-fold dermoscopy is useful to evaluate severity of psoriasis. contact dermatitis. PSORIASIS The clinical and dermoscopic features of nail psoriasis depend on which parts of the nail apparatus are affected by the disease.

bushy capillaries. COllAgeN TISSue DISORDeRS Morphological changes in the nail-fold capillaries confirm the diagnosis of autoimmune connective tissue diseases. Nail-fold capillaroscopy is. but capillaries are tortuous. Dermoscopy may be used to score severity of fissuring and exfoliation and evaluate improvement with treatment. Capillaries in psoriasis also presented a decreased diameter of the arterial limb. yeasts. dermoscopy is useful to better delimitate proximal progression of the infection and detect subclinical streaks (Figure 5.(15) SubuNguAl HemATHOmA Subungual hematomas are common nail bed injuries caused by trauma to the fingers or toes. In onychomycosis due to fungi that produce melanin.In white superficial onychomycosis (WSO). In white superficial onychomychosis. capillary loss and giant capillaries are not seen in normal pattern. and crumble. disorganization of the normal distribution of capillaries. and dilated. Nail fragility may be a consequence of factors that alter the nail plate production and/or factors that damage the already keratinized nail plate. The surface of these areas is opaque with superficial and peripheral scaling. and capillary hemorrhages. These include certain moulds: S. The affected nail shows a patchy or diffuse pigmentation that migrates distally with nail growth. . pigmented band that is devoid of visible melanin inclusions. capillary density is normal. the most common type. Two or more of the following findings in at least two nail folds are considered consistent for dermatomyositis: enlargement of capillary loops. The pigmentation is due to deposition of exogenous particles (x20). Wangiella dermatitidis. Some fungi can produce melanin and cause longitudinal melanonychia.nail diseases The scleroderma pattern is characterized by the presence of giant capillaries and microhemorrhages in early stages and loss of capillaries with avascular areas in late stages.or inter-individual variability. nigricans. Nail-fold dermoscopy In normal conditions.3). fungi reach the nail from the hyponychium and colonize the nail bed. compared to normal controls. flake.(12. fungi penetrate the nail matrix via the proximal nail fold and colonize the deep portion of proximal nail plate. loss of capillaries.(10. and Microascus cirrosus (syn.(8) Brittle Nails Brittle nails are a common complaint characterized by weak fragile nails that split. brown-to-black. At high magnification (50X to 70X) it is possible to detect subclinical spotted lesions. M. elongated. useful both as a diagnostic tool and as a predictor of disease progression. environmental and occupational conditions that reduce the water content of the nail plate have an important additional role.(9) Magnifications of 30X to 50X are usually utilized.(14) ONyCHOmyCHOSIS Onychomycosis refers to the invasion of the nail plate by dermatophytes. 13) In systemic lupus erythematosus (SLE).(10)  . therefore. Figure 5.desmosporus). Different clinical patterns of infection depend on the way and the extent to which fungi colonize the nail: . dimidiatum. and thus helps to correctly identify hyperchromia of nonmelanocytic origin. the microvascular pattern is characterized by a regular array of microvessels with large intra. Nail plate dermoscopy shows irregular longitudinal fissures and grooves.In distal subungual onychomycosis (DSO).4). The distal nail margin is often white due to scaling and exfoliation (Figure 5. or nondermatophytic moulds. However. alternata. In the latter case. and severity in the capillary changes is related with systemic disease activity. twisted enlarged capillaries. Nail plate dermoscopy In distal subungual onychomychosis. fungi are localized on the nail plate surface. A.3 Brittle nails. dermoscopy reveals a homogenous. Hemathoma does not exclude malignancy as patients with melanoma of the nail unit may experience spontaneous bleeding. white-to-yellowish patches of different size and shape. . Nail plate dermoscopy The nail plate presents irregular longitudinal fissures and grooves that often appear pigmented due to deposition of exogenous particles.In proximal subungual onychomycosis (PSO). the nail plate presents irregular. and Trichophyton rubrum var. 11) The dermatomyositis pattern is often similar to the scleroderma pattern.

Nail plate dermoscopy The nail plate shows longitudinal white lines that correspond to the channels that contain the tumor projections.(17) Nail plate dermoscopy The nail plate presents a homogeneous.6). The distal nail plate usually presents longitudinal splitting and a wedge-shaped notch. pyOgenic granulOma Pyogenic granuloma is a common. OnichOpapillOma Onychopapilloma is clinically characterized by longitudinal erythronychia. It occurs more often on  . which. as would show small woodworm-like cavities within the nail plate. papule that bleeds easily after minor trauma. Nail plate dermoscopy Blood deposition appears as a dark band or an irregularly shaped purple to brown–black area. The nail is thickened and presents an increased lateral overcurvature. red spots at the periphery and a “filamentous” distal end (x20). in some patients. It is typical to see round. Distal edge of the nail plate dermoscopy Dermoscopy of the distal edge of the nail plate is pathognomonic.tosti.6 Onychopapilloma. with round. Nail plate dermoscopy shows a pale red longitudinal band extending from the proximal nail fold to the distal edge. darkbrown stria (x20). It usually presents as a solitary. dark-red spots at the periphery and a “filamentous” distal end (Figure 5. The proximal border of the band has a characteristic convex shape and its distal part may appear white because of onycholysis. The band contains a longitudinal. The band may contain one or more longitudinal.5).(16) This tumor can occur both in fingernails and toenails and has no sex prevalence. Figure 5. acquired. dark red-to-black streaks that correspond to splinter hemorrhages (Figure 5. benign vascular lesion. purple to brown in color.(18) The distal portion of the nail bed presents a keratinized expansion that often produces a fissure in the distal nail plate. Distal edge of the nail plate dermoscopy Shows the small subungual keratotic mass that often contains hemorrhagic vessels (Figure 5. is associated with hemorrhagic longitudinal lines.5 Hemathoma. rapidly growing.4 Onychomycosis. pale red. Nail plate dermoscopy shows an irregular area. Nail plate dermoscopy shows the white–yellow streaks and is useful to establish degree of proximal progression (x20). longitudinal band extending from the proximal nail fold to the distal edge. Figure 5. The nail plate overlying the tumor shows a yellow discoloration and multiple splinter hemorrhages. NAIl TumORS OnichOmatrichOma Onychomatrichoma is a benign tumor of the nail matrix that develops within the nail plate.7). The proximal part of the tumor shows purple-to-brown splinter hemorrhages. and de farias Figure 5. piraccini.

8).nail diseases Figure 5.(22. systemic. 23) The nail plate may present a fissure or a split corresponding to the band.(20) Dermoscopy shows black dots corresponding to vessels within the keratotic lesion.  . The lesion may be barely visible as a red violaceous patch in the nail bed. The dermoscopic examination of the lesion shows a reddish homogeneous area that often presents a white collarette at the periphery. Pyogenic granuloma of the toes may be subungual.(21) Nail plate dermoscopy It is useful to detect subclinical lesions that are seen as a reddish irregular area of variable size that may contain teleangiectasic vessels (Figure 5. Malignant melanocytic hyperplasia includes in situ and invasive melanoma of the nail apparatus.(19) Warts Warts are the most common benign tumor of the nail unit and occur more frequently in children and young adults as well as in patients who are immunocompromized.7 Onychopapilloma. nail matrix nevi Nevi can be congenital or acquired. melanoma Clinical presentation depends on the site of origin. White lines similar to a double rail may intersect older lesions. Differential diagnosis of solitary lesions should always take in account amelanotic melanoma. and an increase in the Lovibond’s angle. Other clinical signs include erythronychia. Benign melanocytic hyperplasia can be subdivided into lentigo when nests are absent or nevus when at least one nest is present. Dermoscopy of the distal edge of the nail plate shows a keratotic nail bed expansion with some brown tiny spots that correspond to hemorrhages (x20). brown-to-black band of nail pigmentation. the fingers. Nail plate dermoscopy of shows an irregular reddish area with longitudinal filamentous projections (x20). melanocyte hyperplasia Melanocytic hyperplasia is defined as an increase in the number of nail matrix melanocytes. whether pigmented or not. The nail presents one or more longitudinal pigmented bands varying in size from few millimeters to the whole nail width and light brown to black in color. which temperature changes and pressure. Pigmented lesions in the nail bed usually do not cause LM and are viewed through the nail as grayish-brown or black spots. traumatic. Nail matrix melanoma: usually causes a band of longitudinal melanonychia. Melanonychia is the first symptom of nail melanoma in most cases. and neoplastic nail disorders. distal onycholysis. indicating compression or destruction of the nail matrix epithelium by the melanoma. Nail pigmentation may be caused by melanocytic activation or by benign or malignant melanocyte hyperplasia. longitudinal melanonychia (LM). glOmus tumOr Glomus tumor is a rare benign tumor that characteristically causes severe pain and increases in severity. melanocyte activation Causes of nail matrix melanocyte activation include drugs and postinflammatory. melanOnychia The term melanonychia describes the presence of melanin in the nail plate. melanonychia appears as a longitudinal. Ulceration and hemorrhagic crusts are typically seen in longstanding lesions. where it may have a periungual or a subungual location.8 Glomous tumor. Transverse melanonychia is always due to melanocytic activation. Figure 5. Most commonly.

11). regular. we can identify whether the lesion is localized in the proximal or in the distal matrix. regular.tosti. parallel lines (Figure 5.10 Nevus. Figure 5. as congenital nevi often involve the nail folds and the hyponychium. In children.(1. longitudinal. The presence of micro-Hutchinson’s sign is very indicative but not exclusive of melanoma. and de farias Figura 5. Nail bed ulceration and bleeding occur when the tumor grows. A pigmentation of the ventral nail plate originates from the distal matrix and a pigmentation of the dorsal nail plate originates from proximal nail matrix. but detected with the dermoscopy. Nail bed melanoma: causes a pigmented or a nonpigmented (25% to 30% of cases) subungual nodule. It is an extension of brown–black pigmentation from the matrix and nail bed to the surrounding tissues and represents the radial growth phase of subungual melanoma (Figure 5. This is referred as pseudo Hutchinson’s sign and is not a sign of malignancy. (A) Bands due to nail matrix nevi usually have sharply delimited lateral borders and contain thin. Nail plate dermoscopy shows a darkbrown band with irregular longitudinal lines.12). Very dark bands are often associated with pigmentation of the cuticle due to the fact that the dark pigmentation on the nail plate is visible through the transparent nail fold. Bands due to nail matrix melanoma have blurred lateral margin and contain longitudinal lines of different thickness and color with disruption of parallelism (Figure 5. not detected with naked eye. parallel lines (x20). longitudinal. Distal edge of the nail plate dermoscopy With this technique. Bands with a brown background are indicative of melanocyte hyperplasia . 25–27) Bands with a grayish background are indicative of melanocyte activation.9 Drug-induced melanocyte activation. tiny dark red-to-brown spots caused by splinter hemorrhages may also be seen. Nail plate dermoscopy shows a grayish background with thin. experience in this field is still very limited and specificity and sensitivity of the technique have not been validated. longitudinal. Although nail plate dermoscopy has been proposed as an effective tool to help the clinician in the differential diagnosis of nail pigmentation. Nail plate dermoscopy shows a brown band with regular. and color (x20). piraccini. In traumatic melanocyte activation.9).  . longitudinal parallel lines that are brown or black in color. gray. parallel lines (x20). gray. (B) Figure 5. Hyponychium and proximal nail-fold dermoscopy Micro-Hutchinson’s sign: periungual pigmentation. spacing. The color of these bands vary from light to dark gray and the band often contains thin. Note irregularities in thickness.10). black DOTS similar to those described in skin melanocytic lesions are frequently observed (Figure 5.(24) Nail plate dermoscopy The following dermoscopic patterns have been reported using nail plate dermoscopy in melanonychia of different etiology. regular. These bands vary in color from light brown to black.11 Melanoma.

Antonucci A. In melanocyte activation. intraoperative dermoscopy reveals gray lines. Griffiths CEM. Schapira D et al. Acta Dermatol Venereol 2000. Dermoscopy provides useful information for the management of melanonychia striata. Hautarzt 1996. Farias DC. Figure 5. Saurat JH. Puig S. 11. Baran R. 18. Beyens G. Semin Cutan Med Surg 2009. Dermatol Clin 2006. Lateur N. 4. 142: 1171–6. In melanocyte hyperplasia. Braun RP. Zaballos P. 16. Pediatr Dermatol 2007. Baran R. Sinclair RD. J Am Acad Dermatol 2005. Andre J. Piraccini BM. Hirata SH. 139: 1027–30. Lateur N. Dermoscopy of pyogenic granuloma. Paolino S. Br J Dermatol 2006. Surgical Pearl: dermoscopy of the free edge of the nail to determine the level of nail plate pigmentation and the location of its probable origin in the proximal or distal nail matrix. Andre J. 15: 148–53. Yamakage A. Epidemiology and prognosis of subungual melanoma in 34 Japanese patients. 22.nail diseases 9. Sulli A. Nailfold capillaroscopy is useful for the diagnosis and followup of autoimmune rheumatic diseases. J Am Acad Dermatol 2007. 19. Dermoscopy of the hyponychium shows the micro-Hutchinson’s sign (x20). 53: 884–6. Perrin C. Dermatol Ther 2007. Piraccini BM. Arch Dermatol 2002. Br J Dermatol 2000. 15. 33: 779–82. 164: 10–4. Cutolo M. 42: 71–81. Diagnosis and management of nail pigmentations. 20: 3–10. Dermatol Surg 2008. Vincenti C. Blockmans D. Matucci Cerinic M. Dominguez Cherit J. 55: 512–3. Dermoscopy of the nail bed and matrix to assess melanonychia striata. Cuellar F. 27. Nail unit tumors: a study of 234 patients in the dermatology department of the ‘‘Dr Manuel Gea Gonzalez’’ general hospital in Mexico City. Chanussot Deprez C. Dermatol Surg 2001: 27: 235–9. Zaric D. Worm AM. Assessment of microvascular changes in Raynaud’s phenomenon and connective tissue disease using colour Doppler ultrasound. Kato T. Moore T. 5. Tony HP. 138: 1327–33. Warts of the nail unit: surgical and nonsurgical approaches. Dermatologica 1982. Br J Dermatol 2000. Nail bed and matrix dermoscopy Intraoperative dermoscopy permits direct visualization of the melanocytic lesion. Hirata SH. Touzet S. 134: 383–7. Verhaeghe R. Pizzorni C. 24: 46–8. Bergman R. Miyachi Y. Sharony L. Yamada S. Clemmensen OJ. Junger M. Rassner G.  . Ronger S. Almeida FA et al. Melanonychia diagnosis and treatment. 25. Bhushan M. Predictive value of nailfold capillaroscopy in the diagnosis of connective tissue diseases. 24: 329–39. Onychomatricoma with misleading features. Keberle M. Dahdah M. Dermatoscopic examination of nail pigmentation. Perrin CH et al. Jahns R et al. Thomas L. 3. Capillary microscopy of the nail fold in patients with psoriasis and psoriatic arthritis. Faylor J. 154: 1108–11. Sugiyama Y et al. Suetake T.12 Melanoma. 80: 370–2. 2. Braun RP. 23. Young R. 17. 10. Dermatol Ther 2002. A future tool for the analysis of microvascular heart involvement? Rheumatology 2006. The handheld dermatoscope as a nail-fold capillaroscopic instrument. Microangiopathic changes and functional disorders of nail fold capillaries in dermatomyositis. 39:1206–13. Le Gal FA et al. Cutolo M. Iorizzo M. 143: 132–5. 14. Malvehy J. Australas J Dermatol 2001. Statistical definition of nailfold capillary pattern in patients with psoriasis. Rheumatology 2000. Bogenschutz O. 21. Tosti A. Nailfold video capillaroscopy in psoriasis. Stahl D. 8. Videodermoscopy of the hyponychium in nail bed psoriasis. Secchi ME. Pigmented nail disorders. Almeida FA et al. it shows brown lines that are regular and associated with globules in nevi but irregular in melanoma (Hirata unpublished). Clin Rheumatol 1996. Nailfold capillaroscopy and classification criteria for systemic sclerosis. Ligeron C et al. reFereNCes 1. 56: 835–47. Onychomatricoma: first description in a Child. 7. 28(1): 49–54. J Am Acad Dermatol 2008. 15: 131–41. Nail apparatus melanoma. Longitudinal erythronychia with distal subungual keratosis: onychopapilloma of the nail bed and Bowen’s disease. Dermoscopic examination of the nail bed and matrix. 12. 58: 714–5. 45: 43–6. Piraccini BM. Arch Dermatol 2003. Thai KE. Rech G et al. Herrick AL. 6. Baran R. Llambrich A. 20. 13. Tosti A. Baran R. Tosti A. Klyscz T. Dalle S. Br J Dermatol 1996. Ohtsuka T. 24. 25: 663–5. 47: 289–93. Dealing with melanonychia. 45: 28–30. Yamada S. Clin Exp Rheumatol 2007. Maria Sarti H et al. Thomas L. J Am Acad Dermatol 2006. 34:1363–71. Int J Dermatol 1994. Int J Dermatol 2006. 26.

(7) There is considerable support about the role of TNF-α in expansion of the dermal microvasculature in psoriasis. macrophages. the superficial papillary microvessels undergo elongation. by means of a computerized video microscope.(2) The immune system plays an important role in the pathogenesis of psoriasis. regularly  . the fact that epidermal changes may initiate lesions is substantiated by the observation that even nonlesional psoriatic skin showed an enhanced production of cytokines and appeared to be primed for leukocyte adherence. The application of a conspicuous amount of high-viscosity gel is advisable and appropriate. From the upper layer. suggest that the pathogenesis of psoriasis consists of distinct subsequent stages in which different cell types have a governing role. and novel cytokines. and course (1).5 mm below the skin surface and the other at the dermal–subcutaneous junction and connected by ascending arterioles and descending venules. and IL-20. including interleukin (IL)-22.5–6 μm).5% of the Caucasian population. which is then easily visualized. Recently made discoveries regarding T cell populations.(12) A comprehensive evaluation of the cutaneous microvascular structure is possible using different tools. keratinocyte signal transduction.(14) Visibility of vessels strongly depends on the method of examination. (5. Each papilla continues to be served by a single capillary.(11) During plaque formation. severity. which stimulates endothelial mitogenic activity in the skin. the existence of dilatation and increased tortuosity of dermal capillary loops before dermal hyperplasia is demonstrated. A drop of cedar oil is generally used to improve capillary visibility. There is evidence that epidermal hyperplasia cannot occur without vascular proliferation. mainly described in the intrapapillary portion of the loops. and slightly raised.1a Vascular pattern under videodermatoscopy observation Giorgio Filosa. dendritic cells. which appear different in shape and morphology. but the limbs are twisted along their major axis. Rossella De Angelis. Until now.(13) In psoriasis. One is situated 1.(4) Nevertheless. it displays many anatomical and physiological changes. with silverwhitish scales.(4) The starting event of psoriasis seems to be the initial vasodilatation that is accompanied by exudates of inflammatory cells and serum in the papilla. potentially amplifying local inflammation and keratinocyte proliferation. red in color.(12) ViDeoDermatoscoPy anD ViDeocaPillaroscoPy in Psoriasis The cutaneous microcirculation is organized as two horizontal plexuses. dilatation.(2) The microscopic alterations of psoriatic plaques include infiltration of immune cells in the dermis and epidermis.000. These blood vessels must. which consists of in vivo skin observation with a video camera that allows magnifications ranging from x4 to x1. and there is strong evidence that activated T cells make the first move in the inflammatory reaction.(2) angiogenesis anD Psoriasis The microvasculature is of pathologic relevance to psoriasis and excessive dermal angiogenesis is a characteristic feature. which is represented as an abnormal growth of endothelial cells in the microvessels around the perilesional skin. to reach a minimal compression of capillaries.(12) The papillary microvessel changes are homogeneously distributed throughout clinical lesions. distribution. 8–11) TNF-α is recognized in raising the expression of adhesion molecules and vascular cell adhesion molecules on keratinocytes (11) and in inducing the VEGF production. An appropriate knowledge of the vascular pattern in normal skin is a prerequisite for recognizing the psoriasis microvessels.(5.(2) Psoriatic lesions are sharply demarcated. and Leonardo Bugatti Definition of Psoriasis Psoriasis is a papulosquamous disease with variable morphology. some authors have provided evidence that keratinocyte-derived proangiogenic cytokines such as IL-1 and vascular endothelial growth factor (VEGF) are increased in psoriatic epidermis. play an important but probably secondary role in the pathogenesis of clinical lesions in psoriasis. VD is a noninvasive technique. (5) The exhibition of adhesion molecules and chemokines results in the enrolment of additional inflammatory cells to the plaque. and extremely thickened epidermis with keratinocyte differentiation. arterial capillaries rise to form the dermal capillary loops that represent the nutritive component of the skin circulation. equipped with optic contact probes and magnifications ranging between x50 and x500. However. In normal skin observed by VD. therefore.(3) Also. The recruited cells can then produce further TNF-α and γ-interferon. 6) Furthermore.(12) The outside endothelial diameters of the loops are also wider (6–17 μm) than the corresponding segments in normal skin (3. including videocapillaroscopy (VCP) and/or high magnification videodermatoscopy (VD).6. and increase in the number of blood vessels in the upper dermis. IL-23. The glass plate of a videodermatoscope is placed carefully upon the skin. affecting about 1. vessels come out as tiny red dots. VCP is a widely used method to study the morphology and dynamics of microcirculation. the overall organization of the dermal microcirculation is the same as in normal skin. it is still a matter of debate whether the early changes in psoriasis are referred to the epidermis or to the vasculature. thus widening and tortuosity.

53).2 Videodermatoscopy. therefore. before the atrophy becomes permanent. 17).  . The evidence of the deep venular subpapillary plexus depends on the skin transparency. x 200 magnification.1).” with a highly distinctive pattern (Figure 6. and density of capillaries in the psoriatic plaques.(18) Red dots were seen in all examples of psoriasis studied (Figure 6. scaly patches or plaque features tried to describe the most significant morphologic findings seen on VD. red. these red dots are aligned along the crests of the ridges. Moreover. The presence of arborizing vessels was the most valuable negative feature in differentiating psoriasis from basal-cell carcinoma and intraepidermal carcinoma.(18) In hair and scalp disorders.03).(17. morphology. and systematic effort to identify the dermoscopic features of the psoriatic microvasculature are only recently available.05 vs. appearing as “bushy. red dots. which goes to show that the role of VD and VCP in psoriasis for in vivo therapy monitoring is a subject pursued with growing interest. Figure 6. and not all of the capillaries run perpendicular to the skin surface. Corresponding to the perilesional skin. reporting that examination of the untreated psoriatic skin shows many uniformly arranged tortuous and dilated capillaries. such as the dorsum of the hand. dispersed over the skin surface (15).3). the observation of twisted loops in both psoriasis and psoriasis-like forms of seborrheic dermatitis reflect true overlap disease. theraPy monitoring There are a number of studies that report morphological modifications and loop changes after local and systemic treatments. the VCP technique allows the obtaining of additional information about distribution. all capillaries run parallel to the skin surface. The number of capillary loops per area unit seems to increase in perilesional skin compared to lesional skin (42.8 ± 4.(4.(19) The capillaroscopic picture of plaque psoriasis has been extensively described in literature (10.vascular pattern under videodermatoscopy observation Vascular Patterns in Psoriasis A few studies in the past have described some dermoscopic features of psoriasis as a homogeneous arrangement of vascular structures (Figure 6. 20–22).2) (16. for example. 18) A latest study including 300 lesions from 255 patients with solitary.1 Videocapillaroscopy. Psoriatic skin: “bushy” capillaries. Normal skin: “comma-like” appearance of the capillary loops. as captured by the term sebopsoriasis.4.(15) Under VCP observation. the significant features identified were a homogeneous vascular pattern. and visibility is not limited to the apical portion. x70 magnification. in glabrous skin. yielding a diagnostic probability of 99% if all three features were present.5). capillary loops appear with the major axis running perpendicular to the skin surface.6). Figure 6. and are.(12) A minimal shift of the probe from the perilesional to normal-appearing skin allows the visualization of capillary loops that gradually become perpendicular. For psoriasis. 24) VD may help in revealing that the overuse of topical steroids results in the appearance of clinically imperceptible but dermoscopically evident “red lines” (“linear telangiectasias”) in the treated plaques/skin adjacent (p < 0. These studies lead to the recognition of a critical pathogenetic role of angiogenesis in sustaining and spreading out of the psoriasis lesions. The normal capillaroscopic picture differs according to the body areas: in some districts. especially after x100 and x200 magnification. The upper dermal plexus is visible as a coarse network of broader vessels. with a network appearance. in order to formulate a diagnostic model based on these characteristics. in the forehead. 20. characterized by a comma-like appearance inside the dermal papilla (Figure 6. capillary loops show a parallel course with respect to the skin surface and with a lengthened apex directed toward the marginal zone of the lesion (10) (Figure 6.73 ± 3. and light-red background. 23. 29.(17) VD evaluation at the fingernail hyponichium (between x20 and x70) in patients with nail-bed psoriasis after a 3-month Figure 6.

filosa.8).(23) Investigation of microcirculation by capillaroscopy in psoriatic skin after biologic therapies had brought to light considerable information about the role of angiogenesis. Psoriatic perilesional skin: capillary loops show a parallel course. angelis.(20) A 3-month treatment course with cyclosporine (4 mg/ kg/day) produced a statistical reduction in microcirculatoy alterations. and in 70% of the subjects treated.4 Videocapillaroscopy. especially in the Figure 6.0005). and bugatti Figure 6.3 Videodermatoscopy.5 Videocapillaroscopy. x50 magnification. especially for patients with lichen planus.(24) By means of a VD with x200 magnification. which appeared less tortuous and dilated. x200 magnification. A single infusion of infliximab induced significant morphological changes to the capillary loops in psoriatic lesions. x200 magnification. Psoriatic skin: red dots aligned along the dermatoglyphics. Figure 6. course of calcipotriol treatment showed a significant decrease in the number of capillaries. x200 magnification.(23) Modification of the capillaroscopic aspects took place in a progressive manner in all the patients and according to the length of the therapy. which suggests  .7.6 Videocapillaroscopy. dimension of the capillaries (p = 0. the grossly dilated and tortuous aspect of the untreated psoriatic capillaries appeared to be reduced in five patients after the application of tacalcitol ointment 4 µg/g. Figure 6. with a lengthened apex directed toward the marginal zone of the lesion. with a marked simplification of the coiling of the capillary ball occurring after 3 weeks in 2 cases. The number of “bushy” loops was manifestly reduced. Figure 6. Psoriatic skin showing many uniformly arranged dilated capillaries. with respect to the skin surface. as assessed by digital capillaroscopy (x300 magnification). showing an evident reduction in shape and size (25) (Figure 6. Psoriatic skin showing many uniformly arranged tortuous.

Clinical features and quality of life. Immunopathogenesis of psoriasis. 15. Debets R. 207: 151–6. Folkmann J. Hegmans JPJJ. Griffiths CE. 51: 811–3. intraepidermal carcinoma and psoriasis.  . Krueger GG. The immunologic basis for the treatment of psoriasis with new biologic agents. Vascular proliferation and angiogenic factors in psoriasis. Barker JNWN. Kreusch JF. Vincenzi C. 14.8 Videocapillaroscopy. 17. Manjon-Haces JA. Nat Med 1995. Elevated tumor necrosis factor-alpha (TNF-α) biological activity in psoriatic skin lesions. 204: 236–9. Br J Dermatol 2007. 16: 779–98. 136: 859–65. Clin Exp Immunol 1994. Dermoscopic features of plaque psoriasis and lichen planus: new observation. J Am Acad Dermatol 2002. Exp Dermatol 2007. Overexpression of vascular permeability factor/vascular endothelial growth factor and its receptors in psoriasis. Scuderi A. Detmar M. Psoriasis: epidemiology. The cutaneous microcirculation. Brown LF. 9. J Invest Derm Symp Proc 2000. 7. Vascular patterns in skin tumors. Am J Clin Dermatol 2008. Del Medico P et al. Pan Y. 59: 268–74. Creamer D. 13. Figure 6. Maldonado-Seral C et al. Br J Dermatol 1997. Marghoob AA. De Angelis R. Videodermoscopy in the evaluation of hair and scalp disorders. J Am Acad Dermatol 2006. Figure 6.7 Videocapillaroscopy. J Am Acad Dermatol 1996. J Am Acad Dermatol 2004. that infliximab may achieve its results. Höflich C et al. 20: 6–9. 10. Enhanced production of biologically active interleukin-1α and interleukin-1α by psoriatic epidermal cells ex vivo: evidence of increased cytosolic interleukin-1α levels and facilitated interleukin-1 release. 19. 18. Hern S. 6. 26). references 1. 96: 146–51. 25: 1624–30. after infliximab treatment. Ross EK. Philipp S. vascular. x200 magnification. Krueger JG. Reply to the letter of Li et al. 64(Suppl 2): 18–23. Sousa A et al. Vasquez-Lopez F. The number of “bushy” loops are manifestly reduced. 16. J Am Acad Dermatol 2008. 156: 1224–9. Wallach D et al. Claffey KP et al. in part by targeting the angiogenetic properties of TNF-α As comprehensive studies are required to further establish the modalities of action of TNF-α blockers in reducing psoriatic lesions (25. Langley RG. Eur J Immunol 1995. Troost RJJ et al. Tosti A. 1: 27–31. Dermatology 2003. Ettehadi P. 8. 180: 1141–6. Localization of endothelial proliferation and microvascular expansion in active plaque psoriasis. Allen MH. Sabat R. Dermoscopic assessment of long-term topical therapies with potent steroids in chronic psoriasis. Videocapillaroscopic findings in the microcirculation of the psoriatic plaque. Clin Dermatol 2002.vascular pattern under videodermatoscopy observation 3. Prens EP. 55: 799–806. 1020–1. 20: 248–54. Videodermatoscopy enhances the diagnostic capability of palmar and/or plantar psoriasis. Creamer JD. Vasquez-Lopez F. Dermatoscopy aids in the diagnosis of the solitary red scaly patch or plaquefeatures distinguishing superficial basal cell carcinoma. 4. Untreated psoriatic skin. Angiogenesis in cancer. Micali G. 5. Ann Rheum Dis 2005. x200 magnification. both VD and VCP represent reproducible techniques that may allow an easy and accurate assessment of microvascular modifications of the psoriatic skin after topic and systemic therapies. 5: 3–9. 11. Chamberlain AJ. Clin Exp Dermatol 1995. Debets R. J Exp Med 1994. Bugatti L. Mortimer PS. Lacarrubba F. 2. 9: 119–22. rheumatoid and other diseases. Braverman IM. 12. Bailey M et al. In vivo quantification of microvessels in clinically uninvolved psoriatic skin and in normal skin. Dermatology 2002. Greaves W. 46: 1–23. Nardone B.

Nakatani S. Acta Derm Venereol (Stock) 1994. Lautieri S. Stinco G. 25: 1077–8. Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. Altieri E. 87: 152–4. Bugatti L. 210: 241–3. 113: 1664–75. J Am Acad Dermatol 2008. Suppl 186: 138. 6 . Gasparini S. 25. Ozawa K et al. 24. and bugatti 20. J Am Acad Dermatol 1991. Iorizzo M. angelis. Nestle FO. Cutaneous vascular alterations in psoriatic patients treated with cyclosporine. 21. Videodermoscopy of the hyponychium in nail bed psoriasis. Okada N. Nickoloff BJ. Cutaneous microcirculation in psoriasis. Early videocapillaroscopic changes of the psoriatic skin after antitumour necrosis factor-alpha treatment. Dermatology 2005. J Clin Invest 2004. Strumia R. 85–7. De Angelis R. 23. Fuga GC. Romani I et al.filosa. Video macroscopic study of psoriasis. Acta Derm Venereol (Stock) 1994. Marmo W. Vincenzi C. Patrone P. A videocapillaroscopic morphofunctional study. Valente F. Acierno F et al. Dahadah M. Filosa G. Acta Derm Venereol 2007. 22. Tacalcitol in psoriasis: a video-microscopy study. Tosti A. 58: 714–5. Suppl 186. 26.

in addition to K17. relapsing. and hyperproliferative skin disorder with genetic predisposition and multifactorial pathogenesis. • The intermediate or steady-state phase (divided in early and late steady state). histopathologic examination is generally not required. neutrophils within the cornified and parakeratotic horn.(4) Other histologic clues to the diagnosis of psoriasis include more dilated and tortuous papillary blood vessels.1b Histopathological correlations † Daniele Innocenzi. scalp.9 Clinical and histological features of the initial phase. neutrophils beneath the cornified layer (subcorneal pustules). inflammatory. all dermatologists recognize the difficulty in identifying the disease in many instances. for us. In this case. Clinically. is the most interesting because this is the moment when we visit the patients. and.(3) However. K6 and K16. in rapid evolution toward the other phases. reddish. Maria Concetta Potenza. knees.(2) The classical presentation of this skin disorder is plaques psoriasis. hypogranulosis. and more keratinocytic mitotic figures above the basal-cell layer. chronic. IntroductIon Psoriasis is a common. the diagnosis is made on clinical grounds by a “visually literate” clinician. In psoriatic skin. neutrophils within the epidermis associated with spongiosis (spongiform pustules).(1) There is not a typical clinical and histological picture of psoriasis. and Ilaria Proietti keratinocytic proliferation resulting in thickening of epidermis (producing well-circumscribed clinical plaques) and stratum corneum (producing scales). in the psoriatic plaque. as this form is usually easy to identify.(2) Psoriasis is characterized by abnormal Figure 6. basal keratinocytes maintain expression of K5 and K14 (the keratins typical of basal keratinocytes in normal skin). which. and scaly papules and plaques typically located on elbows. and other cutaneous sites. There is also an increase in the apoptotic rate.6. Psoriasis shows lesions with different clinicopathological aspect according to the moment in which the lesion is taken. Psoriasis is the prototype of a group of cutaneous disorders (psoriasiform dermatitis) that show psoriasiform epidermal hyperplasia. we can observe essentially three phases: • A nonspecific initial phase characterized by the presence of erythematous edematous plaques.  . especially when the appearance is not typical. and there is no standard treatment available. 56 days in normal skin).(7) As compared with normal skin.(8) We must also consider the “histodynamic” of the psoriatic plaque. whereas K1 and K10 (the keratins typical of suprabasal cells in normal skin) are replaced by socalled hyperproliferation-associated keratins. the disease is characterized by well-circumscribed. psoriatic lesions show up to 27 times the mitotic activity. in concert with a reduction of bcl-2 (an antiapoptotic protein) expression in basal cells. a 12-fold decrease in the cell-cycle time of basal and suprabasal keratinocytes.(5–6) Plaques PsorIasIs In its classical presentation (plaques psoriasis). and a greater than 7-fold increase in the epidermis turnover time (7 days in psoriatic skin vs. defined as regular elongation of the rete ridges with preservation of the rete ridge–dermal papillae pattern.

One possibility is that in psoriasis the dermal microvessels may receive a specific trigger/stimulus. however. superficial.11). thinning of the suprapapillary epidermis with occasional presence of small spongiform pustules. is characterized by acanthosis with regular elongation of the rete ridges. Also. potenza. is aspecific. an increase in capillary width may be seen in other skin conditions such as port wine stains. exclusive to psoriasis. thickening in their lower portion.10). eczema.10 Clinical and histological features of the early steady-state phase. psoriasis plaques not always show synchronous development. These different clinical aspects can coexist in the same patient because. • The final erythematodesquamative phase (phase of resolution) is usually observed after successful treatments and representing the phase of progressive resolution and clearing. including a sparse.11 Videodermatoscopy of dwarf handles and bush vases in a psoriatic plaque at early steady-state phase (X200). which clinically corresponds to plaque elevation. fleeting. confluent parakeratosis.(11) The striking difference in psoriasis is that the papillary vessel changes are dramatic and uniformly distributed throughout clinical lesions. and quickly slips toward following steps. and dermatitis herpetiformis. 10) Elongation and Figure 6. can be divided from an histopathological point of view in.innocenzi. and proietti Figure 6. lichen planus.9). with a preponderance of dermal changes.(9. diminished to absent granular layer. • Early steady-state phase. clinically characterized by erithematous and edematous lesions. • The initial phase. and perivascular T-lymphocytic infiltrate (Figure 6. There are now a considerable evidences indicating that angiogenesis plays a role in triggering the microcirculatory changes in psoriatic skin. The earliest changes can be nonspecific.  . a well-developed plaque phase. and presence of Munro microabscesses (Figure 6. Clinical polymorphism correspond to different and specific histological stages. • This intermediate phase. It is possible to find elongation and edema of the dermal papillae and dilated and tortuous capillaries. This stage corresponds to the increase in number of dwarf handles or bush vases at videodermatoscopy (Figure 6. tortuosity of the dermal papillary vessels are not. pallor of the upper layers of the epidermis. It is still not entirely clear what causes these changes in plaque skin.(9) The combination of superficial dermal capillaries and overlying suprapapillary epidermal thinning is responsible for the erythematous appearance of psoriatic lesion and the Auspitz sign (pinpoint bleeding points on removal of the scale).

Lesions show silvery scales as result of the ortokeratosis of corneus and an intact granular layer with parakeratosis.14 Clinical and histological features of the resolution phase. Exocytosis of inflammatory cells is usually mild. This phase is histologically characterized by club-shaped thickening of the lower rete pegs with coalescence of these in some areas. with reformation of the granular zone and orthokeratosis. It initially shows progressive reduction in the presence of neutrophils within the stratum corneum and parakeratosis.13).13 Videodermatoscopy of a psoriatic plaque at late steady stage (X200).histopathological correlations Figure 6. Figure 6.  .12 Clinical and histological features of the late steady state.14). Figure 6. and there is some thickening of the suprapapillary plates and fine fibrillary collagen (Figure 6. • Late steady-state phase clinically corresponds to fully developed clinical plaques because it shows marked epidermal hyperplasia. This stage relates to the presence of white-silvery images on a red background during videodermatoscopy (Figure 6.12). • The phase of resolution corresponds to resolving or treated plaques of psoriasis (Figure 6. The epidermal hyperplastic changes resolve later.

Am J Dermatopathol 1979. The histopathologic spectrum of psoriasis. Br J Dermatol 1983. New observations and correlation of clinical and histologic findings. Gambini D. dermal fibrosis with persistence of papillary dermal capillary dilatation and tortuosity as the only histopathologic clues to this disease. 1: 199–214.Clin Dermatol 2007. in order to better chose the therapy. 136(6): 859–65. Cox AJ. Arch Pathol 1967. with a persistent marginal activity at the borders. Burgoon Jr CF. The importance of being visually literate. The clinical spectrum of psoriasis. Evolution. 2. In vivo quantification of microvessels in clinically uninvolved psoriatic skin and in normal skin. Ragaz A. Panz B. 111: 632–6. they often start to clear in the center. reFerences 1. Keratins (K16 and K17) as markers of keratinocyte hyperproliferation in psoriasis in vivo and in vitro. 6 . These different aspects of the psoriatic plaque correspond to different biochemical events that occurs in the psoriatic lesion. Gordon M. Murphy M. Navsaria H. Br J Dermatol 2007. 8. Histopathology and histochemistry of psoriasis: II. Br J Dermatol 1997. Br J Dermatol 1995. Arch Dermatol 1972. including the subepidermal vascular plexus. 136(1): 97–101. 6. Ackerman AB. Kerr P. 109(25):89–98. Allen MH. The role of blood vessels and lymphatics in cutaneous inflammatory processes: an overview. Purkis PE et al. mild. 84: 443–50. superficial. Altmeyer P. 25(6): 510–8. it would be really helpful to understand how the single plaque responds to the treatment depending on its histopathological phase. which confers an annular or polycyclic appearance. and regression of lesions of psoriasis. 25(6): 524–8. Histological variations in lesions of psoriasis. Mortimer PS. Naldi L. Localization of endothelial proliferation and microvascular expansion in active plaque psoriasis. Observations on the art and science of making a morphological diagnosis in dermatology. Gudjonsson JE. maturation. Clin Dermatol 2007. Psoriasis: epidemiology Clin Dermatol 2007. Elder JT. Br J Dermatol 1997. Grant-Kels JM.(12) As the plaques regress. potenza. Hern S. Watson W. 7. el Gammal S. 9. 5. Creamer D. 133: 501–11. Hypopigmentation is usually associated with clearing (psoriatic leukoderma). 106: 503–6. Braverman IM. 3. Dynamics of lesions during treatment. Jackson R. 12. 156(6): 1224–9. 25(6): 535–46. grows downwards into the dermis. and proietti There may be residual.innocenzi. Bacharach-Buhles M. 11. In psoriasis the epidermis. Johnson WC. Leigh IM. Sousa A. The clinical resolution of lesions is associated with the abnormal-to-normal return of plaques’ microvessels. For that reason we understand that making a correct diagnosis and deciding the appropriate treatment for different patients is not so easy. Barker JN. Arch Dermatol 1975. 10. 4. Poston R.

Inclusion criteria were the presence of clinically nonspecific. scaly lesions with no other skin involvement. epidermolysis bullosa. 7 with plantar involvement. scabies. A major limitation in this anatomical site. VD was able to identify the cases of palmoplantar psoriasis. lichen planus. An average of three fields for each lesion was examined with two magnifications.15B VD examination of normal palmar skin surface: presence of capillary loops arranged linearly along the furrows of dermatoglyphics at X100 (A) and X200 (B) magnifications. VD examination might be performed in residual erythematous areas or after application of keratolytic products (such as 30%–50% urea) for 3 to 4 days. (A) (B) Figure 6. Differential diagnosis includes eczematous dermatitis (allergic. At the end of the study. which may interfere with a reliable VD evaluation. especially when typical anatomic sites are involved. Hi-Scope KH-2. respectively. as later confirmed by histopathological examination. X50 and X200.  . after covering each field with immersion oil in order to avoid light reflection and thus allowing a good visualization of vascular structures. Videotermatoscopy (VD) may be helpful to address the diagnosis of palmoplantar psoriasis in the presence of no readily apparent diagnostic features through the evaluation of superficial vascular structures.16D). in such cases. porokeratosis. The diagnosis of palmar and/or plantar psoriasis is usually uncomplicated. However. Maria Letizia Musumeci. irritative). homogeneously appearing as “bushy” (1–4) and linearly arranged along the furrows of dermatoglyphics (Figure 6. Tokyo. mycosis fungoides. equipped with a zoom lens. VD examination at X100 to X200 magnification shows the presence of capillary loops linearly arranged along the furrows of dermatoglyphics (Figure 6. age range between 20 and 72 years) were enrolled in an open study.15B). was used for vascular pattern evaluation that was performed under standard environmental conditions (temperature. and 3 patients had palmar/plantar localization. and untreated palmar and/or plantar. often requiring skin biopsy with histopathological evaluation. tinea manuum/ pedis. and Giuseppe Micali The efficacy of VD in recognizing palmoplantar psoriasis has been demonstrated in a series of patients affected by palmar and/ or plantar dermatoses with no otherwise specific diagnostic features. Twenty-two cases presented with palmar lesions only. carefully avoiding vessels blanching and applying to the skin the least possible pressure with the contact plate.16A–6. a skin biopsy from the affected areas was taken from each patient for H&E stain. showing in all examined fields at low magnification (X50) the presence of pinpoint-like capillaries linearly arranged along the furrows of dermatoglyphics. erythematous.(5) A total of 32 subjects (12 males and 20 females. presence of comorbid disorders potentially altering microcirculation (diabetes). After VD examination.. Exclusion criteria were past medical history positive for psoriasis or eczema.200 [Hirox Co. VD examination must be performed with the epiluminescence technique. Japan]. is represented by the frequent presence of excessive hyperkeratosis that may hamper vascular structure analysis. active.15A–6.c Palmoplantar psoriasis Francesco Lacarrubba. pityriasis rubra pilaris. In palmoplantar psoriasis. mean age = 50 years.15A–6. humidity). the evaluation of the vascular structure by VD shows dilated and tortuous capillaries. in cases with only palmar and/or plantar involvement.. use of vasodilator drugs. syphilis. In normal palmoplantar skin surface. presence of excessively hyperkeratotic lesions. use of systemic and/or topical drugs within 4 and 2 weeks of study entry. A video microscope system. keratodermas. it may be troublesome. and drug reactions. pustular psoriasis.

and micali (A) (C) (D) (B) Figure 6. C: at X200 magnification.lacarrubba. In these two  .17B). D: bushy capillaries at X400 magnification. A: clinical aspect. in fact. the same capillaries appeared dilated and tortuous. the same capillaries appear dilated and tortuous.16D Plantar psoriasis. at X200 magnification. musumeci.17A–6. In the other cases.18A–6. with a “bushy” aspect. B: VD examination shows at X50 magnification the presence of pinpoint-like capillaries arranged linearly along the furrows of dermatoglyphics. homogeneous aspect (Figure 6. VD showed no relevant features at X50 magnification and a normal capillary pattern at X200 magnification (Figure 6.16A–6. Insert: normal capillaries at the same magnification (X200).18B). the diagnosis of psoriasis was excluded. with a bushy. and in the remaining patients it showed the presence of pinpoint-like capillaries at X50 magnification but did not show bushy capillaries at X200 magnification. in some of these patients.

later confirmed by histopathology. In vivo quantification of the structural abnormalities in psoriatic microvessels before and after pulsed dye laser treatment. Br J Dermatol 2005. Videodermatoscopy enhances the diagnostic capability of palmar and/or plantar psoriasis. Bates DO. 152: 505–11. Nardone B. a diagnosis of psoriasis was excluded. Bugatti L. Figure 6. Dermatology 2002. Hern S. 2. Scuderi A.17A–6.18A–6. Intravital video-capillaroscopy for the study of the microcirculation in psoriasis. For capillary pattern evaluation the use of both low (50X) and high (200X) magnifications is recommended as. Nicolini M. B: VD examination showing at X200 magnification the presence of “bushy” capillaries. Videocapillaroscopic findings in the microcirculation of the psoriatic plaque. Yoshikawa K. 204: 236–9. Filosa G. analysis of superficial vascular pattern by VD represents a promising noninvasive diagnostic tool in palmar and/or plantar localization of psoriasis. 5. Bull RH. In conclusion. low magnification identified a pinpoint-like vascular pattern that did not correspond to bushy capillaries at higher magnification. Del Medico P. De Angelis R.palmoplantar psoriasis (A) (A) (B) (B) Figure 6. Br J Dermatol 1992. 3. suggesting a diagnosis of psoriasis. Am J Clin Dermatol 2008. In this case. in our experience in some subjects. 126: 436–45.17B A: palmar dermatosis with no specific clinical features. Sato K.  . Mellor RH et al. histopathology showed a pattern consistent with a diagnosis of eczematous dermatitis. J Am Acad Dermatol 1991. REFERENCES 1. 9: 119–22. Lacarrubba F. last groups. 25: 1077–8. Micali G. Stanton AWB. Video macroscopic study of psoriasis. Mortimer PS. 4. Ozawa K.18B A: palmar dermatosis with no specific clinical features: B: VD examination showing at X200 magnification normal capillaries. Okada N. Nakatani S.

Japan]. nonscaling plaques most commonly located proximally on the glans and under the prepuce. erythroplasia of Queyrat. genital psoriasis is part of a more generalized cutaneous disorder.. VD examination (X100-X400) was performed (B) Figure 6. by evaluating the superficial vascular pattern. are often necessary. age ranging between 41 and 70 years) were enrolled in an open study.” In this site.. candidiasis.200 [Hirox Co. and several investigations. and Francesco Lacarrubba The term balanitis defines an inflammation of glans penis that may be caused by a wide range of conditions including infectious. Tokyo. Hi-Scope KH-2. Similarly to cutaneous lesions of psoriasis (3–6). Ltd. However. and among these. respectively.(7) Six subjects (mean age 49.19).(1) In general.1d Psoriatic balanitis Giuseppe Micali. In order to evaluate the vascular pattern. including skin biopsy. in case of exclusive penile involvement. We examined by VD a series of patients affected by psoriatic balanitis in order to establish whether this technique may be able. Exclusion criteria were the presence of comorbid disorders and the use of systemic and/or topical medications for 4 and 2 weeks. lichen sclerosus. to provide additional information useful to address the diagnosis beyond standard clinical observation. lichen planus. however. the correct diagnosis may be troublesome. due to the absence of scales.20 (continued)  . Inclusion criteria were the presence (A) Figure 6. the visualization of vascular structures is easy. neoplastic. Psoriatic balanitis is clinically characterized by erithematous. Maria Rita Nasca. allowing the observation at incident light of skin magnifications ranging from X20 up to X600. and psoriasis. VD evaluation of psoriasis of the glans shows dilated and tortuous capillaries homogeneously appearing as “bushy. VD was performed using a video microscope system. Zoon’s balanitis.1 years.(2) Videodermatoscopic (VD) examination of glans in healthy subjects shows at X100 magnification the presence of normal capillary loops (Figure 6. and inflammatory dermatoses. contact dermatitis. of biopsy-proven psoriatic balanitis and no other skin involvement.19 VD examination of normal glans penis: presence of normal capillary loops (X100).

Insert: normal capillaries at the same magnification (X100). with a “bushy” aspect (X200). B: VD examination showing dilated and tortuous capillaries. (A) (B) (C) (D) Figure 6.20 Psoriatic balanitis––A: clinical aspect.psoriatic balanitis (C) (D) Figure 6. C: the same “bushy” capillaries at X200. B: VD examination showing dilated and tortuous capillaries. with a “bushy” aspect (X100).21–6.22 Psoriatic balanitis––A: clinical aspect.  . D: “bushy” capillaries at higher magnification (X400).

Bugatti L. Palamaras I. six cases of nonpsoriatic balanitis. and irregularly distributed capillaries. linear.23). VD seems to hold promise as a tool that can potentially improve the clinical diagnosis of psoriatic balanitis through the evaluation of superficial vascular structures. In the six cases of nonpsoriatic balanitis.  . irregularly distributed capillaries (X200).204:236–9. no bushy pattern was observed. It should be remarked that VD examination must be performed with the epiluminescence technique and that particular care is needed while applying the contact to the skin with a minimal pressure in order to avoid vessels blanching. Hamill M. linear. Rosina P. Lamba H. in press. Lacarrubba F. Br J Dermatol 1992. Common skin disorders of the penis. Videodermatoscopy enhances diagnostic capability in psoriatic balanitis. Sethi G. B: VD examination showing a not specific vascular pattern with dilated. 9: 498–506.23 Lichen ruber planus––A: clinical aspect. histologically or microbiologically proven (2 lichen planus. Am J Clin Dermatol 2008. 20: 905–10. without any peculiar aspect. BJU Int 2002. Nardone B. Videodermatoscopy enhances the diagnostic capability of palmar and/or plantar psoriasis. Micali G. Girolomoni G. and lacarrubba (A) (B) Figure 6. Nicolini M. Zamperetti MR. Del Medico P. 3. This pattern histologically corresponded to dilated. and the presence of dilated. 4. REFERENCES 1. Dermatology 2007. Lacarrubba F. J Eur Acad Dermatol Venereol 2006. Dermatology 2002. De Angelis R. thus avoiding skin biopsy. elongated. 91: 343–5. was evident (Figure 6. and tortuous capillary loops in the papillary dermis. At the end of the study. Intravital video-capillaroscopy for the study of the microcirculation in psoriasis. Scuderi A. Videocapillaroscopy in the differential diagnosis between psoriasis and seborrheic dermatitis of the scalp. Nasca MR. This might be particularly useful in those cases in which psoriatic lesions located in typical body areas or elsewhere in the body are missing.22).micali. 6. homogenous aspect in all examined fields (Figure 6. Bull RH. J Am Acad Dermatol. VD showed in all subjects affected by psoriatic balanitis a uniform pattern consisting of dilated and tortuous capillaries with a typical bushy. Videocapillaroscopic findings in the microcirculation of the psoriatic plaque. nasca. Bates DO. 1 lichen sclerosus. In addition. 1 Zoon’s balanitis and 2 candidiasis) were also evaluated by VD. In conclusion. 9: 119–22. Wilkinson D. The usefulness of a diagnostic biopsy clinic in a genitourinary medicine setting: recent experience and a review of the literature. Buechner SA.20–6. 2. Mortimer PS. 7. Giovannini A. after covering each field with immersion oil to eliminate light reflection and achieve optimal visualization of capillaries. 214: 21–4. Micali G. 5. Filosa G.

(5. Psoriasis capillary changes determine a specific vascular pattern: capillaries are enlarged. the presence of skin psoriasis is the most relevant criteria for the diagnosis of psoriatic arthritis. In fact. elongated. and deciding whether erythematous scaly plaques on the scalp are psoriasis or seborrheic dermatitis may change the interpretation of the rheumatic symptoms.25). The capillary loops have identical “bushy” morphology Figure 6.1e Scalp psoriasis Paolo Rosina Videocapillaroscopy (VCP) allows morphological and functional analysis of microcirculation at all cutaneous sites. especially when lesions are confined to the scalp. even histology may hardly differentiate the two conditions. An important difference between psoriasis and seborrheic dermatitis could be the microvasculature changes. and tortuous and look like a bush or clew.26).24) but are better valuable with a greater magnification using videodermatoscopy or videocapillaroscopy (Figure 6.25 Videocapillaroscopic appearance of capillary loops in lesional scalp psoriasis (x100). and density in psoriasis and seborrheic dermatitis of the scalp to use for differential diagnosis.26 Homogeneous psoriatic pattern with tortuous and dilated capillaries (appearing as bushes or clews) and a completely disarranged microangioarchitecture (x100).(1) VCP was performed using an optical probe (Videocap 200R DS Medica. including the scalp. 6) In a recent study we employed videocapillaroscopy (VCP) to compare capillary morphology. Distinction of seborrheic dermatitis from psoriasis is obviously relevant for the long-term prognosis. but when lesions are confined to the scalp and are long standing.. Their distribution is generally different. Figure 6. Figure 6. which are constantly present and characteristic in psoriasis. but it may be particularly important in patients with arthritis symptoms. Milano. distribution. Scalp psoriasis presented a homogeneous pattern with tortuous and dilated capillaries (appearing as bushes or clews) and a completely disarranged microangioarchitecture (Figure 6.(1–4) This pattern is already visible with hand-held dermatoscope (Figure 6. and 30 healthy subjects. Italy) on histologyconfirmed scalp lesions of 30 patients with chronic plaque psoriasis.  . The lesions of seborrheic dermatitis may closely resemble clinically those of psoriasis.24 Tortuous capillary loops visible with hand-held dermatoscope (x10). Psoriasis and seborrheic dermatitis can be difficult to differentiate. 30 patients with seborrheic dermatitis.

and mildly dilated capillaries (Figure 6. RefeRences 1. Figure 6. with mildly tortuous capillaries and only isolated bushy.29 Mildly tortuous capillaries and only isolated “bushy” in seborrheic dermatitis (x200). Capillary loop density was similar in all conditions.28 and 6. 24: 473–8. In contrast. Zamperetti MR.27 Capillary loops with “bushy” morphology in psoriasis (x200).  . Giovannini A. Dermatology 2007. In seborrheic dermatitis. with a conserved.28 Lesional scalp seborrheic dermatitis with a conserved local microangioarchitecture similar to healthy scalp skin (x100). Visualization of dermal blood vessels––capillaroscopy. Figure 6. In conclusion. Rosina P. Girolomoni G. in all scalp locations (Figure 6. Normal looking skin of patients with both dermatitis did not show significant changes compared to normal skin of healthy subjects.rosina Figure 6. Hern S. Videocapillaroscopy in the differential diagnosis between psoriasis and seborrheic dermatitis of the scalp. and it could be a useful and noninvasive method for differentiating psoriasis and seborrheic dermatitis. scalp seborrheic dermatitis presented a multiform pattern.29).30 Normal scalp skin of healthy subject (x100). Clin Exp Dermatol 1999. confirming previous findings. especially when the scalp is the only site affected. 2. mean diameter of capillary bush was similar to that of the scalp of healthy subjects. Figure 6. 214: 21–4.27). VCP demonstrated that psoriasis exhibit homogeneously tortuous and dilated capillaries. local microangioarchitecture similar to healthy scalp skin (Figure 6. The diameter of capillary bush of scalp psoriasis is much greater than in scalp affected by seborrheic dermatitis or normal scalp skin of healthy subjects. Mortimer PS.30).

6. 68: 53–60. Heilgermeir GP. J Invest Dermatol 1977. Br J Dermatol 2005. 5. Bugatti L. Histopathological differential diagnosis of psoriasis vulgaris and seborrheic eczema of the scalp. 30: 478–83. 204: 236–9. Ultrastucture of the capillary loops in the dermal papillae of psoriasis. In vivo quantification of the structural abnormalities in psoriatic microvessels before and after pulsed dye laser treatment. De Angelis R. 4. Hautarzt 1979. Del Medico P. Dermatology 2002. Hern S. Braverman IM. Videocapillaroscopic findings in the microcirculation of the psoriatic plaque. Yen A. Lincke-Plewig H.scalp psoriasis 3. 152: 505–11.  . Braun-Falco O. Stanton AWB. Mellor RH et al.

tortuous capillaries within markedly elongated dermal papillae. symmetrically or bunch-like arranged. disseminated granuloma annulare.31 Multiple CCAs of the legs (arrows). reddish papule. perifolliculomas.32). The diagnosis of CCA is usually confirmed by histologic examination. pyogenic granulomas.2 Clear cell acanthoma Francesco Lacarrubba. but not always present (Figure 6. and sarcoidosis. Bugatti et al. Orazia D’Agata. upper extremities) have been reported. reported six cases of CCA characterized by this psoriasis-like vascular findings on dermatoscopy (8). seborrheic keratoses. they concluded that the dermatoscopic examination might anyway be of help to differentiate CCA from other skin tumours. and Giuseppe Micali Clear cell acanthoma (CCA) is a usually solitary benign epidermal tumor first described by Degos in 1962. showing in the epidermis acanthosis. sharply circumscribed. enlarged capillaries in the papillae are evident. and considering that both entities possessed similar histopathologic features. Figure 6. Although the authors stated that a similar pattern could also be seen in psoriatic plaques. sharply circumscribed papule with a peripheral scaling collarette. fibromas. a peripheral scaling collarette is characteristic. reported a single case of CCA and first described a characteristic dermoscopic vascular pattern at X20 magnification.(2–5) It clinically appears as a dome-shaped. In the superficial dermis.(2–5) The differential diagnosis of single and/or multiple CCA includes several conditions. leiomyomas.6. and a sharply demarcated epidermal proliferation of keratinocytes with a clear and slightly larger cytoplasm and a positive PAS stain. CCA occurs frequently on the lower extremities.(1) The mean age of onset is about 52 years. lichen planus.31–6.32 Close-up clinical view of a CCA: reddish. suggest that the lesion may represent a benign epithelial neoplasm. The etiology is not well understood.  . the rate between solitary and multiple CCA is estimated to be 1:9–1:15. Federica Dall’Oglio. In 2001.(2–6) Ichthyosis and varicose veins are the most frequent associated findings. consisting of “partly homogeneous. syringomas. papillomatosis. although some authors Figure 6.(7) Successively. with equal frequency in men and women. such as histiocytomas. pinpoint-like capillaries”. after removal of the scales. Multiple lesions (from 2 up to 400) are rarely encountered. basal-cell carcinomas. Blum et al. but other anatomic sites (trunk.(7) Histopathologically this pattern corresponded to dilated. others consider the disease as a localized reactive inflammatory dermatosis (pseudotumor). variable in size from 5 to 20 mm. hidradenomas.

(8) Zalaudek et al.(9) In the same year. homogeneous pinpoint-like vascular structures with a pearllike disposition (X30). each vascular structure appeared to have a bush-like aspect (Figure 6. The pearl-like vessels disposition. at least in a portion of each lesion.33 VD examination of CCA: presence of symmetrical. was always present (Figure 6.34 VD examination of CCA: presence of symmetrical. in CCA the dotted vessels are linearly arranged as pearls on a line. homogeneous pinpoint-like vascular structures arranged in a net-like pattern (X30). Figure 6.clear cell acanthoma Figure 6. whereas the presence of a net-like pattern was a frequent but not constant finding (Figure 6. homogeneous pinpoint-like vascular structures arranged in a net-like pattern (X30). in their experience. At higher magnification (X200). these pearl-like vessels represent a peculiar dermoscopic pattern of CCA. we studied the videodermatoscopic pattern of multiple CCAs in a single patient (10).34). in their Figure 6. with all of them showing the same pattern: symmetrical and homogeneous pinpoint-like vascular structures throughout the entire lesion. moreover. homogeneous pinpoint-like vascular structures with a pearl-like disposition (X30). Therefore.35 VD examination of CCA: presence of symmetrical.33–6.  . whereas in psoriasis they are homogeneously and regularly distributed throughout the entire lesion. they detected the presence of a squamous surface with translucid collarette as an additional characteristic dermatoscopic finding. opinion. The authors concluded that the psoriasis-like pattern of CCA would appear to provide further evidence of a neoangiogenetic inflammatory process rather than a neoplastic one for CCA formation.36 VD examination of CCA: presence of symmetrical.36).37).35–6. Figure 6. they observed that the dotted vessels were regularly distributed in a reticular array. stated that dermoscopic features of CCA are different from those of psoriasis (9) as.

McCollough ML. Filosa G. dall'oglio and micali rubra pilaris and some variants of contact dermatitis) characterized by epidermal proliferation and dermal capillaries dilation. Licout A. Civatte J. and seborrhoeic keratoses. Multiple clear cell acanthomas. along with additional dermatoscopic features. hypopigmented Spitz nevus. will help to address the correct diagnosis. Differential diagnosis from psoriasis is particularly relevant in the case of multiple CCAs. For this reason. 5. 89: 361–71. 8. REFERENCES 1. Schewach-Millet M. the dermatoscopic pattern of CCA resembles that of psoriasis and. Wilde JL. 67: 149–51. Videodermatoscopy improves the clinical diagnostic accuracy of multiple clear cell acanthoma. VD may improve the clinical diagnosis of single or multiple CCAs. possibly. 9. 17: 452–5. Metzler G. 3. Cutis 2001. Bugatti L. Dermatology 2001. Psoriasis-like dermoscopic pattern of clear cell acanthoma. Tumeur épidermique d’aspect particulier: acanthome à cellules claires. 10. Dermatology 2003. Innocenzi D. Delort J. Figure 6. Arch Dermatol 1980. Barduagni F. Figure 6. 19: 249–53. Eruptive hamartomatous clear-cell acanthomas. a correct evaluation of anamnestic and clinical features. 207: 428. Ann Dermatol Syphiligr 1962. Wolter M. 203: 50–2. Bauer J. de Pasquale R. 6. In conclusion. Trau H. 7. Degos R. Rassner G. Disseminated eruptive clear cell acanthoma: a case report with review of the literature. 117: 1. however. Burg G. Delrous JL. Other cutaneous conditions. Hofmann-Wellenhof R. of other psoriasiform disorders (such as pityriasis 2 .lacarrubba. Elsner P. The dermatoscopic pattern of clear cell acanthoma resembles psoriasis vulgaris. 189: 437–9. Cerio R. The VD pattern of CCA corresponds to the histologic aspect of regularly elongated rete ridges and enlarged capillaries in the dermal papillae (Figure 6. Polypoid clear cell acanthoma of the scalp. d'agata. Zalaudek I. Wursch TH. Roux J. Arch Dermatol 1981. Bowen’s disease. Meffert JJ. Catanzano G. Blum A. Argenziano G. Baptista P. J Eur Acad Dermatol Venereol 2003. such as warts. Lacarrubba F. Garbe C. Clin Exp Dermatol 1994. Tomasini C. Fah J. and melanoma metastasis may sometimes show pinpoint-like vessels. ruling out clinically similar disorders that do not show the same features of CCA. Eur J Dermatol 2003. thus implying the need for additional diagnostic criteria. 4.38). 116: 433–4.38 The VD pattern of CCA corresponds to the histological aspect of regularly elongated rete ridges and enlarged capillaries in the dermal papillae. Dermatology 1994. In these instances. actinic. Fisher BK. Bonnetblanc JM. 2. Micali G. Dermoscopy of clear-cell acanthoma differs from dermoscopy of psoriasis. Multiple clear cell acanthoma. melanoma. 13: 596–8. Broganelli P. squamous cell carcinoma.37 A detail at high-magnification depicting the bushlike aspect of pinpoint-like capillaries in CCA (X200).

with consequent vasodilatation of the capillary handles.  . HPV infection can occur at any age and has been reported in healthy young children. 59 and 66. termed “low-risk. The vascular pattern that may be observed in external anogenital warts has a dotted aspect that can be defined as “mosaic like” (Figure 6. 56. including genotypes 16. scrotum and anus in men. but not pathological. 51. 52. affecting 1–2 percent of the sexually active population between 15 and 49 years of age. Digital peno-vulvoscope allows enlargement of images with the use of special algorithms. There is international consensus that “high-risk” genotypes. 39. 31. typical of the genital mucosa. (4) They present at X20 magnification a characteristic vascular pattern: The handle that serves every single papilla originates from the base. 18.(2) The mosaic-like vascular pattern may be frequently observed in the apparently unaffected perilesional area (Figure 6. not provided by the natural contrast present in other cutaneous districts due to its notable vascularization. which may be observed at X10–X40 magnification (Figure 6.(3) Figure 6.(1) Infections with other genotypes. 45. in order to improve the visibility of the vascular pattern of the genital area. This technique allows the recognition of some morphological patterns that can be observed in both physiological or pathological conditions of the genital area. vulva and anus in women and penis.41) that dermoscopically appear as sting red in color and elegantly distributed.40). vagina.43). HPV infections Pompeo Donofrio and Maria Grazia Francia Human papillomaviruses (HPV) are DNA viruses that infect basal epithelial (cutaneous or mucosal) cells. 35. reaches the apex of the papilla. showing a hairpin-like appearance (Figure 6. allowing an early treatment. condition.(1) Genital HPV infection is primarily transmitted by genital skin-to-skin contact. 58. and then refolds again toward the base. where. (2) Particular optics provided polarized light. allowing to avoid improper chromatic variations toward the red. Such pattern. This pattern in progress of HPV infection is probably due to the local production of nitric oxide from the papillomaviruses.40 Anogenital warts: punctiform vascular pattern at X40 magnification (X20). Dermatoscopy of the genital region may be called as penovulvoscopy.39 Anogenital warts: The vascular pattern that may observed assumes a punctiform aspect that can be defined as “mosaic like” in appearance (X20).6.” can cause benign or low-grade cervical tissue changes and genital warts (condylomata acuminata). is constituted by short capillary handles perpendicular to the cutaneous surface (Figure 6. Differential Diagnosis Pearly Papules In the male patients.(1) Early HPV infection may be accompanied by mild changes of the epithelium that are detectable only using virological and/or cytological techniques.39). can lead to cervical cancer and are associated with other mucosal anogenital and head and neck cancers. which are growths of cervix. 33. Figure 6. the onset of new lesions may be observed (subclinical infection). the pearly papules located in the glans crown represent a frequent. defined “digital filters” or curves of color. usually but not necessarily during sexual intercourse.42). in the following weeks. HPV genital infection is considered to be the most prevalent sexually transmitted disease in the US and Europe.

Coll Antropol 2008. J Reprod Med 2008. van den Brule AJ et al. they appear as yellowish reliefs of the diameter of 1–2 mm. Hogewoning CJ. Ljubojevic S. these ectopic glands do not require any treatment. Fordyce spots These physiological formations may commonly be observed on the skin of the penis and on the prepuce and are considered isolated sebaceous glands not connected to follicles. vascular. Micheletti L. Int J Cancer 2005. they are frequently seen on the labia minora. references 1. Bleeker MC. Bleeker MC. Human papil´ ´ loma virus associated with genital infection. 53(3): 179–82. Figure 6. 49(1): 50–4. J Am Acad Dermatol 2003. Bogliatto F. 3. 4. Hogewoning CJ. Lynch PJ. In every case. Pearly penile papules: still no reason for uneasiness.donofrio and francia Figure 6. In women. they show a characteristic. At peno-vulvoscopy observation. Clinically  . Lipozencic J.42 Anogenital warts: the vascular “mosaic-like” pattern is frequently observed also in the perilesional areas (X40). 32(3): 989–97.43 Vascular hairpin pattern in pearly papules (X20). Grgec DL et al. HPVassociated flat penile lesions in men of a non-STD hospital population: less frequent and smaller in size than in male sexual partners of women with CIN. whose “bows” seemed to wind the yellowish lobules of the spots without crossing them. Figure 6. 113(1): 36–41. which dermoscopically appear sting red in color and elegantly distributed (X20). Vulvoscopy: review of a diagnostic approach requiring clarification. Voorhorst FJ et al.41 The dotted pattern is constituted by short capillary handles perpendicular to the cutaneous surface. 2. “garland-like” appearance.

5% of newborns with equal prevalence in male and female patients. 3) VM are being classified according to their color and location. This pattern has been related to the superficial capillary loops of the papillae. and grow with age. low-flow. By means of these devices. The origin of VM is unclear. long-standing venular malformation (VM) of the forehead. rounded vessels) with a variable size (original magnification: X10). without the risk of injury to the patient and without additional cost. red. the vessels are visualized because of the red blood cells filling and passing through them. the recent introduction of noninvasive image techniques such as dermoscopy or videodermoscopy has allowed the analysis of the capillary composition.45 Dermoscopy of this VM reveals a superficial pattern of VM. round capillaries in greater number. partially treated. Therefore. VM are characterized by ectatic vessels with flattened endothelium. the type of the capillary involved (4–8) (Figures 6. possibly being a result of vascular channel developmental defects or segmental deficiency of autonomic inervation of postcapillary venules. The main prognostic factors are the depth and diameter of capillaries of VM (original magnification: X10).44–6. They may have a genetic basis. By means of dermoscopy. VM may present late onset in adolescents and adults.  . but may be located deeper. In addition. Figure 6. Figure 6. it is important to avoid excessive pressure on the lesion when performing this procedure. to deep purple. tend to be present at birth. showing scattered type 1 ectatic vessels (red. Largest structures are similar to “red lagoons”. VM are initially flat and smooth (macular) but nodules may develop with time. and rapidly. that is. VM affect 0. usually caused by trauma. which causes occlusion Figure 6.57). most of them situated in the papillary dermis and upper part of the reticular dermis. revealing significant vascular structures hidden in the standard visual inspection. a better understanding of the morphology of the vessels involved can be obtained in daily practice. VM may be part of syndromes such as Sturge-Weber and Klippel-Trenaunay. The contrast with the surrounding normal skin is well evident.44 Clinical view of a flat.46 Dermoscopy of VM showing type 1. The color varies from pink.6.4 Venular malformations (port wine stain type) Francisco Vázquez-López The value of dermoscopy for further evaluating venular malformations (VM) has been proposed. Very rarely.(2. which may be related to prognosis. Some authors describe this pattern as a better response to laser therapy. Round vessels may be pinpointed or globular according to their size.3%–0.(1) Venular malformations (or capillary vascular malformations) are congenital. vascular abnormalities of the dermal capillaries.

disclosing a variable size (dotted. In addition. VM have been predominantly classified into type 1 (superficial) or type 2 (deep) patterns (Figures 6.44–6. thickness. Figure 6. 4.58).vzquez-lpez Figure 6. where the contrast between VM vessels and the surrounding normal skin can be better appreciated. and similar to lagoons) (original magnification: X10). Several authors (1. showing a variable tortuosity.48–6. Tortuous.49 Dermoscopy of the former lesion reveals a type 2 vascular pattern.51– 6. Type 1 round vessels are not seen. type 2 subpapillary vessels are seen as red.(5) In addition a gray-whitish veil has also been reported related to the deeper vessels of the lower reticular dermis.(4) According to videodermoscopy. vascular plexus of the dermis (original magnification: X10).50 Dermoscopy of the border of same lesion (higher degree of magnification).48 Clinical view of a VM located on the thigh. linear vessels configured in an irregular network are demonstrated. or globular. according to their size) (Figures 6. Mixed and undefined vascular patterns can also be observed. In contrast. 7) have described two types of vessels in VM with videodermoscopy: type 1 (superficial papillary vessels) and type 2 (deeper subpapillary vessels).56).50). horizontal. Digital videodermoscopy allows a higher magnification of vessels involved and the ability to record and compare the digital images. and lack of visualization of the vessels if nonpolarized dermoscopy is applied or when taking dermoscopic photographs with skin contact. mixed and undefined patterns (5.44–6.47). but similar structures can also be revealed with stereomicroscope (4) and pocket dermoscope.(5) Figure 6. 7) can also be observed (Figures 6. linear structures. and sharpness and forming irregular networks (Figures 6. Type 2 linear vessels have been correlated to the horizontal subepidermal vascular plexus. globular. pinpointed. a clear correlation between dermoscopic 6 . Nevertheless. Figure 6. devoid of round type 1 vessels. They have been correlated to ectatic capillary loops of the papillae.(6) Type I vessels are seen as red and sharp structures having a round to oval shape and a variable size (termed as dotted. thin.47 Dermoscopy of VM showing numerous type 1 round vessels. Type 2 linear vessels are thought to correspond to the subepidermal.

as oval to round structures and appear either as tightly clustered or as loosely scattered. either as an isolated finding or in a mixed pattern.to oval-shaped red patches.(1. As regards the dermatomal distribution of VM.(5) Round vessels.(4) A correlation between these patterns and anatomical location has been reported.(4) Round vessels of VM may appear quite small and as tiny dots (especially in children) or large. Round. 5) The current standard treatment of VM is the pulsed-dye laser. 1. those involving V2 respond less well than those located on V1 and V3. VM located in the dermatome V3. with purple and red lesions tending to respond better than the pink ones. Figure 6. Interestingly. They may or may not be located within round.52 Dermoscopy of this lesion revealed not only a predominantly type 2 vascular pattern (linear vessels) but also scattered.53 Dermoscopy of the same lesion. Lagoons of hemangiomas are secondary to both proliferation and ectasia of the vessels involved. size of VM. well-defined. 13) A number of studies have established the importance of capillary depth and diameter in determining the response of VM to laser treatments. previously described as “red lagoons. 4. or neovascularization after therapy. The response of VM to laser treatment is believed to be dependent on several factors. It seems that the response of an untreated VM to laser treatment will be dependent on the range of depths and Figure 6.(12. have been found in most VM in some studies. and histological observations has not been found by some authors. sharply demarcated. whereas lesions located on dermatome V2 and extremities showed mainly a type 2 or a mixed pattern. Lagoons or lacunae appear small. although a complete lightening of the lesion is rare. .Location: Certain sites for VM respond better to laser treatment.64).51 Clinical view of a VM located on the leg. The largest globules. globular structures. type 1 vessels (X10). deeply red in color. Lesions on the distal extremities and medial face tend to do less well than lesions on the lateral face or trunk. purple) has been found to be predictive of response to treatment. dotted. Therapy of VM and clinical data (color. therefore. it has been proposed that these findings may have a prognostic significance. new clinical insights into VM. location. whereas round  . dotted vessels are easily demonstrated in conjunction to linear vessels.59–6. Dermoscopic findings in VM may help to predict the outcome of the therapy. Therapy of VM and histological data: depth and diameter of the capillaries of VM. Dermoscopy offers.(9–11) . and trunk showed mainly a type 1 pattern. age of patients). neck. which may be related to partial damage of some vessels. persistence of lesions. with a higher degree of magnification after applying digital zoom to the attached camera.” are characteristic of hemangiomas. red. vessels of vascular malformations represent only a vascular dilatation devoid of proliferation (Figures 6. 2. varying in size.venular malformations Figure 6.The color of VM (pink.

a better response to therapy. globular vessels (original magnification: X10). who found the presence of a gray-whitish veil hiding the inferior structures as the most significant feature related to prognosis.57 Long-standing VM of the face. This device allows individual capillaries to be imaged and their depth and diameter to be calculated. At this phase.56 Dermoscopy of the same lesion with a higher degree of magnification. Deeper vessels with a small diameter are those responding less well. meanwhile type 1 round vessels were related to superficial vessels. Figure 6. and diameter of capillaries (depth-measuring videomicroscope. and also round. tortuous. 7) and gray-whitish veil (4) has been related to deeper vessels and with less response to the treatment. 5. Blanched areas are well evident. 3. Recently. which has been related to their depth. short. DMV) has been developed and applied for evaluating VM (8). lesions may become darker. and may develop blebs. in contrast with the patient of the Figure 6. and partially treated with electrodessication.44. and arboriform vessels. thicker. a videomicroscope that is capable of determining morphology. but it facilitates better visualization of vessel depth and diameter in the dermis. and hence. Figure 6. diameters of capillaries comprising the lesion.vzquez-lpez Figure 6.55 Dermoscopy (low magnification) revealed herein a mixed pattern with linear. A clear correlation between dermoscopic and histological  . Figure 6. observations has not been found by all authors (4). Dermoscopic data provide information related to the morphology of the vessels involved. This tool is similar to a traditional video microscope.54 Clinical view of a VM located on the cheek. violaceous. The presence of type 2 vessels (1. The lesion has been previously treated with laser. despite the previous therapy. Tortuous linear vessels and globular vessels are demonstrated herein. partially masked by a cosmetic camouflage. depth. Therapy of VM and dermoscopic data.

appear round to oval in shape. 14) It must be taken into account that other factors may play a role in the response of VM to laser treatment. whitish network (original magnification: X10). it seems that the small. Figure 6. which previously obscured them. histological. which are red to blue-red or blue-black to maroon in color. The outcome of VM therapy will most likely depend on the depth and size of the deeper vessels. globular vascular patterns.venular malformations Figure 6. Other factors (8. which may be observed in both melanocytic and nonmelanocytic skin lesions. a controversy exists between different studies. while most others are of the impression that such correlations might not be possible. and dermoscopic parameters of VM. Perifollicular areas seem to be uninvolved. Hemangiomas are characterized by lagoons or lacunae. (5) Figure 6. 9. however. According to the results obtained with this device (8) and also according to the previous histological results (12. Deep vessels may be revealed only after clearing the superficially located type 1 capillaries by four or five dye laser treatments. and a delicate. red lagoons. only a few authors corroborate the correlations between these parameters. type 1. in addition to capillary  .(8) As regards correlations between these different clinical.(8. deeply located vessels are more resistant to the laser treatment and tend to remain uncoagulated. devoid of linear vessels (original magnification: X10). with a deep purplish background. Perifollicular white halos are an unspecific and peculiar dermoscopic finding.60 Dermoscopy of this lesion revealed a homogeneous. and as sharp structures.59 Clinical image showing a patient with a prominent midline “salmon patch” VM of the neck. 9) 4. Lagoons are a result of the proliferation of dilated venules. 13). whereas VM present only vascular ectasia.61 Dermoscopy of an acquired hemangioma. either tightly clustered or loosely scattered throughout the lesion (original magnification: X10).58 Dermoscopy of the former lesion revealed an undefined pattern. which are classified separately from lateral Port Wine stains.(15) Figure 6.

deep component. Frieden IJ. red. 58: 261–85. J Am Acad Dermatol 2003. such as the flow through these capillaries. and the amount of competing chromophores within the skin. Argenziano G. Garzon MC.vzquez-lpez Figure 6. videodermoscopy is also helpful in deciding more accurately when to end the treatment because it objectively shows when a VM becomes resistant to further treatments (persistence of small and deep vessels). such as melanin or the thickness of the skin.  . globular vessels and blue lagoons (original magnification: X10). Motley RJ. Figure 6. 3. Procaccini EM. 133: 921–2. respectively.7) In addition. In conjunction with the clinical examination. which is different from venular malformations.63 Clinical view of a patient with a mixed vascular malformation on the arm with prominent.62 Dermoscopy of acquired angioma serpiginosum revealing multiple. dermoscopy and videodermoscopy serve to further evaluate VM on a non-invasive basis. Dermatology 2001.64 Dermoscopy of this lesion reveals tightly clustered. It can be applied in most settings.5. Laser treatment of pediatric vascular lesions: Port wine stains and hemangiomas. 5. are related to the depth of the vessels involved. It is also helpful for demonstrating this to patients and their parents by means of an objective image. scattered. sharp lagoons (original magnification: X10). These structures are related to the vessel ectasia and not to vascular proliferation. J Am Acad Dermatol 2007. Moreover. Enjolras O. Figure 6. Huang JT. McBurney EI. as pulse duration and wavelength could be matched to measured vessel diameter and depth. without additional cost for demonstrating significant vascular structures that are hidden in the standard visual inspection. 4. which may have a prognostic significance. these vascular structures (round type 1 and REFERENCES 1. Glick SA. Staibano S. Hirsch RJ.(1. Ferrara G. this device improves the understanding of the morphology of the vessels involved. Videomicroscopy predicts outcome in treatment of port-wine stains. for some authors. Monfrecola G. Vascular malformations: Part I. Arch Dermatol 1997. Meghan FS. 56: 353–70. it has been speculated that videomicroscopy may facilitate in the future the development of newer pulseddye lasers to treat VM more efficiently. Eubanks LE. In sum. 203: 329–32. Videomicroscopy of port-wine stains: correlation of location and depth of lesion. 48: 984–5. 2. Lanigan SW. Epiluminescence microscopy for port-wine stains: pretreatment evaluation. depth and diameter or the dermoscopic vessel type. linear type 2 vessels). J Am Acad Dermatol 2008. Katugampola GA.

Huff C et al. The relationship between location. Nagore E. 7. Nagore E. Sivarajan V.venular malformations 6. Tsuneda K. Videomicroscopy of venular malformations (port-wine stain type): prediction of response to pulsed dye laser. Svaasand LO. Vázquez-López F. Vázquez-López F. 129(2): 182–8. J Am Acad Dermatol 2003. 13. Fiskerstrand EJ. Sevila A et al. Mackay IR The depth measuring videomicroscope (DMV): a non-invasive tool for the assessment of capillary vascular malformations. 14. Sivarajan V. Br J Plast Surg 1995. Facial port wine stains in childhood: prediction of the rate of improvement as a function of the age of the patient. Sánchez-Martín J. Onizuka K. 53(4): 378–81. Br J Dermatol 1996. Efficacy of flashlamp-pumped pulsed dye laser therapy for port wine stains: clinical assessment and histopathological characteristics. and vessel structure within capillary vascular malformations. 138: 821–5. Ann Plast Surg 2004. Shibata Y. color. Arch Dermatol (in press). Vázquez-López AC. Manjón-Haces JA. 12. Br J Dermatol 1998. Renfro L. Pediatr Dermatol 2004. Geronemus RG. Sevila A. Pérez-Oliva N. The hand-held dermatoscope improves the clinical evaluation of port-wine stains. 11. Lasers Surg Med 2004. 8. Dermatol Surg 2004. 34: 193–7. 21: 589–96. 48: 984–5.  . MacKay IR. size and location of the port wine stain and the number of treatments with the pulsed dye (585 nm) laser. Argenziano G. 9. Perifollicular white halo: a dermoscopic subpattern of melanocytic and non melanocytic skin lesions. 15. Yohn JJ. Anatomical differences of portwine stains in response to treatment with the pulsed dye laser. Kopstad G et al. 30: 1457–61. Nguyen CM. Thickness of healthy and affected skin of children with port wine stains: potential repercussions on response to pulsed dye laser treatment. Sekine I. 10. Ito M. 134: 1039–43. Arch Dermatol 1993. Laser treatment of port wine stains: therapeutic outcome in relation to morphological parameters. 48: 271–9. PérezOliva N. Requena C. Botella-Estrada R et al. Más-Vidal A.

69b). Throughout the epidermis. The upper dermis shows a moderate amount of chronic inflammatory infiltrate. and verrucous BD. immunosuppression. and Alessandra Filosa Table 6.” characterized by highly convoluted tortuous capillaries mimicking the glomerular apparatus of the kidney (Figure 6. • Multicomponent global pattern • Atypical vascular structures (dotted/glomerular) • Scaly surface • Pseudonetwork • Irregular. The most peculiar and common findings for this (a) tumor seem to be multicomponent global pattern (90%– 100%). arborizing.1 Dermoscopic Features of Bowen’s Disease. subungual/periungual.(1. atypical vascular structures (86. Most studies suggest a risk of tumoral progression to be about 3%–5% for classic BD. photochemiotherapy. with convoluted and dilated papillary vessels.6. the cells lie in complete disorder. diffuse pigmentation • Patchy distribution of small. 3) Glomerular morphology has also been described for severe venous stasis. and hairpinlike vessels can also be found (Figure 6. Some authors prefer to keep dotted vessels as distinct from glomerular vessels. keratinized cells (Figure 6.5 Bowen’s disease Leonardo Bugatti. as the latter are usually larger in size. radiotherapy).1).6%–100%) and scaly surface (64. Giorgio Filosa. The border between epidermis and dermis appears sharp and the basement membrane remains intact. 18 subtypes). Another common feature is the presence of occasional.66. individually atypical. namely. bushy. Unusual sites or variants include pigmented.67). which sometimes adopts a lichenoid distribution. brown globules • Focal/multifocal hypopigmentation • Blue-whitish veil • Peppering/white areas • Hemorrhages Bowen’s disease (BD) is an intraepidermal (in situ) squamouscell carcinoma clinically presenting as a slowly enlarging sharply demarcated erythematous plaque with a crusting and scaling surface (Figure 6. Dotted vessels histopathologically correlate with dilated tortuous capillaries of middle reticular dermis progressing to the top of the papillae. (b) Epidermal acanthosis with a number of highly atypical keratinocytes often with features of dyskeratosis (ematoxylin-eosin. Lesions are usually solitary but may be multiple in 10%–20% of patients. Higher magnification can disclose a distinctive type of vascular structures. BD is characterized by acanthotic epidermis with elongation and thickening of rete ridges. 6. It predominantly affects older female patients. Histopathologically. palmar. it is located on the lower limbs. Resemblance with psoriasis or dermatitis classically leads to a delay in the correct diagnosis. but linear.” Many cells are highly atypical. and in about three-quarters of the cases. often looped.69a. Development of ulceration is usually a sign of invasive carcinoma.(4) (b) Figure 6. 6. genital. perineal.(2. Several dermoscopic features of BD have been described (Table 6. resulting in a “windblown appearance.2–90%). structureless. showing large hyperchromatic nuclei with conspicuous nucleoli and abundant cytoplasm. at x100 magnification).65b).65 (a) Sharply demarcated erythemato-desquamative plaque. Reported relevant etiological factors are irradiation (solar. “glomerular vessels. 2) The presence of vascular structures on the surface of the tumor is consisting mainly of dotted vessels (50%) irregularly distributed in clusters. long-term arsenic exposure.65a). and regularly arranged in a patchy distribution (Figure 6.  .68). and oncogenic HPV (mainly 16.

(6.  .66 Brownish pseudonetwork. (ii) dotted or pinpoint. x10). 7) Kreusch has given a thorough morphological illustration of the vascular component of skin tumors and has suggested an algorithm for the diagnosis based on dermoscopic vascular patterns. dotted (glomerular) vascular pattern. scaly surface. A variety of peculiar vascular structures can be recognized under dermoscopic examination. Tortuous capillaries with glomerular.68 Multicomponent global pattern.(8) The recognition of distinctive vascular structures enhances the diagnostic range of dermoscopy.69 (a) Dotted vascular structures and multifocal hypopigmentation (original magnification. showing three features: (i) linear. irregular vessels. x10). and( iii) milky red globules. (b) Figure 6. Figure 6.67 Dotted vascular structures. x10). hemorrhages (original magnification.69a. and scaly surface (original magnification.(9) It can be speculated that vascular morphology is consistent with a process of tumoral neoangiogenesis in BD. Videocapillaroscopic studies might better describe the vascular structures involved in BD and other cutaneous neoplasias. they have a diagnostic significance. Figure 6.bowens disease (a) Figure 6. and though not specific. regularly shaped vessels. x10). bushy morphology. (b) Magnified detail of Figure 6.(5) Atypical (or polymorphous) vascular pattern has been described as red structures irregularly distributed outside areas of regression in melanocytic lesions. especially when the classic pigmented structures are lacking. dotted and linear vascular structures (original magnification. hairpin. irregular diffuse structureless pigmentation.

red-dotted globules are homogenously distributed over the entire surface.bugatti. multicomponent global pattern.(1. such as globular structures. (14) In dermatofibromas. In this case.(12) In conclusion.72 Pseudonetwork and irregular. such as body location. filosa.71 Scaly surface. whereas dotted vessels in warts are distinctive for a pale halo of keratinization. 2. x10).70 Dotted vascular structures. (13) Dotted vessels in clear-cell acanthoma are often arranged uniformly like pearls in a line with a psoriasiform appearance. Figure 6. structureless diffuse pigmentation (original magnification. clear-cell acanthoma. The degree of scaling may vary according to different factors. and dermatofibroma. The false atypical pigmented network may be created by the thickening of the rete ridges due to deposits of melanin within the tumoral cells in the dermal papillae. De Angelis R. irregular diffuse pigmentation. where the disappearance of vascular structures may indicate adequate treatment. Bugatti L. and peripheral fine network. and filosa Figure 6. vascular component (dotted vessels or “glomerular” subtype morphology) and scaly surface represent valuable dermoscopic clues to the diagnosis of BD. 18: 572–4. 19) references 1. The greater thickness of the corneal layer in acral skin gives rise to heavier scaling.2–80%). further studies are needed to assess the specificity and sensitivity of these dermoscopical criteria in differentiating BD from other pigmented and nonpigmented skin tumors. and small brown globules (64. although pigmented structures can be detected. hemorrhages (original magnification. warts. (Figure 6. environmental conditions. irregular structureless diffuse pigmentation (64. Filosa G. In most cases of psoriasis. such as the presence of pseudonetwork (10–35. together with other accompanying features. x10).71). the concurrence of a white to pinkish veil and a small amount of residual. (11) This should bring to the prompt removal of the lesion for  .(12) Dotted vessels can commonly be found in melanocytic tumors.(1. J Eur Acad Dermatol Venereol 2004. such as psoriasis.2–90%). light-brown pigmentation may contribute to the diagnosis. dotted vessels may be either centrally located or diffuse throughout the lesion. In heavily pigmented BD pseudonetwork or reticular pigmentation.(15) Dotted vessels are reported to be a frequent finding in amelanotic melanoma. especially in early thin lesions.7%). standard criteria (Figure 6. x10). Dermoscopic observation of Bowen’s disease. scaly surface. especially in the unusual form of heavily pigmented BD. sometimes of seborrheic keratoses and other skin diseases.(16–18) Dermoscopy has also been proposed as a valuable tool for monitoring of nonsurgical treatment of BD. and patchy distribution of globules (original magnification. well-expressed. Figure 6. However. can be the main dermoscopic criterion lacking other.72).70) (10) BD is generally scarcely pigmented. dermopathologic examination. 2) The pigmented globules are usually smaller than those associated with melanocytic lesions and follow a regular patchy distribution over the lesion (Figure 6. topical pretreatment. sometimes simulating atypical network. and type of lubricant used to minimize surface reflection. scarlike white patch.

1: 369–73. 6. Argenziano G. Stanganelli I et al. 21: 700–1. Clinical and dermoscopic criteria for the preoperative evaluation of cutaneous melanoma thickness. Argenziano G. Filosa G. Stante M. Vascular structures in skin tumors. The specific dermoscopic criteria of Bowen’s disease JEADV 2006. Hu C. 30: 541–4. Color Atlas of Dermatoscopy 2nd ed. 11. Br J Dermatol 2004. Marghoob AA. Arch Dermatol 2008. Pizzichetta MA. 16. Amelanotic/ Hypomelanotic melanoma––is dermatoscopy useful for diagnosis? J Dtsch Dermatol Ges 2003. SerranoFalcón C et al. 99: 419–27. 19. Zalaudek I. De Angelis R. Kreusch JF. 13. 3. J. 10. 20: 341–62. A dermoscopy study. Hautartz 1996. 20: 248–54. Vasquez-Lopez F. The specific dermoscopical criteria of Bowen’s disease. 18. Broganelli P. Dermoscopy as a diagnostic and follow-up tool for pigmented Bowen’s disease on acral region. 15. Bono A. Massi D et al. Kreusch J. 4. Dermoscopy of dermatofibromas: a prospective morphological study of 412 cases. 8. Bugatti L. 150: 1117–24. Argenziano G. Stolz W. Malvehy J. 17: 452–5. Br J Dermatol 2004. 150: 1112–6. 11: 491–4. 34: 1248–53. 140: 1485–9. 2002. Corona R et al. Amelanotic/ hypomelanotic melanoma: clinical and dermoscopic features. Clinical and dermatoscopic diagnosis of early amelanotic melanoma. De Giorgi V. Tomasini C. Oxford: Blackwell Publishing. Zalaudek I. Hernández-Gil J. B. Koch F. Landthaler M.bowens disease 2. 17.Leinweber et al. G. Llambrich A. Zalaudek I. 5. 150: 226–31. J Am Acad Dermatol 1999. Characterization of vascular patterns in skin tumors by incident light microscopy. Psoriasis-like dermoscopic pattern of clear cell acanthoma. Dermatol Surg 2008. 7. Kerl H et al. Melanoma Res 2001. Zalaudek I. Clin Dermatol 2002. Br J Dermatol 2004. Moglia D et al. Marghoob AA. Talamini R. 47: 264–72. Dermoscopic semiology: further insights into vascular features by screening a large spectrum of nontumoral skin lesions Br J Dermatol 2004. 40: 61–8. Vaquez-Lopez F. Kreuscj J. Dermoscopic semiology: further insights into vascular features by screening a large spectrum of nontumoral skin lesions. 12. J Eur Acad Dermatol Venereol 2007. Carli P et al. 14. Zaballos P. 144: 75–83. Pigmented Bowen’s disease mimicking cutaneous melanoma: clinical and dermoscopic aspects. Maurichi A. Clinical and dermoscopic features of pigmented Bowen disease. Bugatti L. 9. Dermatol Surg 2004. 150: 226–31. Di Stefani A. CHEN G et al. 5 . Vascular patterns in skin tumors. Kreusch J. Argenziano G. Chiu H. Fabbroncini G. Puig S. Arch Dermatol 2004. Fernández-Pugnaire MA. Actas Dermosifiliogr 2008. J Eur Acad Dermatol Venereol 2003.Argenziano. Falco OB et al. Dermoscopy of Bowen’s disease. Filosa G.

lips. Misdiagnosis documented in medical literature include keratoacanthoma. Pyogenic granuloma Pedro Zaballos Diego PYOGENIC GRANULOMA Pyogenic granuloma is a relatively common.6% of Figure 6. metastasic carcinoma. A few reports of lesions developing in a preexisting nevus flammeus or spider angioma exist. face. basal-cell carcinoma.77). and retinoid therapy. hyperproliferative. mucosa of the nose. such as infective organisms. 8) The results of one study where 13 pyogenic granulomas were collected and evaluated reveal that a reddish homogeneous area surrounded by a white collarette is the most frequent dermoscopic finding in pyogenic granulomas (Figures 6. squamous-cell carcinoma. the clinical diagnosis of pyogenic granuloma proved to be wrong. amelanotic melanoma. some authors prefer the term lobular capillary hemangioma to describe these lesions because of the histologic findings.(1–4) Although the clinical diagnosis of pyogenic granuloma is rather easy. common warts. In this stage. is difficult to determine. melanocytic nevus.(7) This pattern was identified in 84. therefore. We can also see scales and ulceration (X10). vascular lesion of the skin and mucous membranes whose exact cause is unknown. It has been thought to be a reactive. such as amelanotic melanoma. which bleeds easily. This misnamed entity is neither infectious nor granulomatous and. pyogenic granuloma resolves into fibroma. Sites of predilection include the gingiva. a subcutaneous subtype.(1–3) It represents 0. and true hemangiomas among others. in some instances the differentiation from other benign and malignant tumors. ulcerated. with less inflammatory infiltrates present and disappearance of edema of the stroma. The gingival lesion developed during pregnancy termed epulis gravidorum is considered a variant of this tumor. Each lobule is composed of aggregations of capillaries and venules with plump endothelial cells. Kaposi´s Sarcoma.(4) The typical lesion appears as a papule or polyp with a glistening surface. Spitz nevus.(7. numerous capillaries and venules with plump endothelial cells arrayed radially toward the skin surface (usually eroded. a intravenous subtype. in time. The exact etiopathogenesis of this condition is unknown.. Pyogenic granuloma with satellitosis. Pyogenic granuloma is relatively common and it is especially frequent in children and young adults.73–6. and extremities (mainly the fingers). hormonal factors. inflamed seborrhoeic keratosis.(1–6) Dermoscopy may be helpful in the recognition of pyogenic granulomas. We can also observe superficial scales and “white rail” bands (instead of lines) that intersect the lesion (X10). reepithelialization of the surface and a peripheral collarette of hyperplastic adnexal epithelium may be noted. In 38 % of one case series (5). The histopathologic findings in all variants of pyogenic granuloma are similar.74 Another characteristic pyogenic granuloma with a reddish homogeneous area surrounded by a white collarette. benign. where they evolve rapidly over a period of weeks to a maximun size and then shrink in a fibroma that can regress within a few months. penetrating injury.73 The characteristic dermoscopic pattern of pyogenic granuloma is made up of a reddish homogeneous area surrounded by a white collarette. Early lesions resemble granulation tissue. that is.  . and a disseminated variant have been described in literature. Older lesions tend to organize and partly fibrose and. Figure 6.75 and 6. vascular response to a variety of stimuli.5% of all skin nodules in children. The matured polypoid lesion exhibits a fibromyxoid stroma separating the lesion into a lobular pattern. Pyogenic granulomas usually develop at the site of a preexisting injury. and covered with scabs) amidst an edematous stroma containing a mixed inflammatory infiltrate.

we can observe different vascular structures like  . it is important to remove the lesions in order not to misdiagnose an amelanotic melanoma (X10). pyogenic granulomas of the study. In these cases.76 Pyogenic granuloma that shows a reddish homogeneous area and “white rail” lines that intersect the lesion. The lesion should be excised in order not to misdiagnose an amelanotic melanoma (X10). pyogenic granulomas are frequently eroded and crusted and may bleed very easily. This is a pediculated lesion.7% of cases and ulceration in 46. Figure 6.74 and 6. Figure 6. Finally. Other dermoscopic structures that were found were “white rail” lines (Figures 6.77 Figure shows the characteristic pattern of pyogenic granuloma (a reddish homogeneous area surrounded by a white collarette).76). and glomerular vessels). Occasionally.pyogenic granuloma Figure 6. it is difficult to see the white collarette on polarized contact dermoscopy. and. We can also see a scale in the left part of the lesion and an area of ulceration in the upper part (X10). hairpin. The white collarette corresponds to the hyperplastic adnexal epithelium that partially or totally embraces the lesion at the periphery of most pyogenic granulomas.73 and 6. The histopathologic correlation of the reddish homogeneous area may be attributed to the presence of numerous small capillaries or proliferating vessels that are set in a myxoid stroma of pyogenic granulomas. This feature may explain the hemorrhagic crusts or ulceration that we can observe in some cases of pyogenic granulomas. but there are several vascular structures.78 An atypical dermoscopic image of pyogenic granuloma with a central area of ulceration and polymorphous/atypical vessels (linear irregular.76) that intersect the lesion in 30. The Figure 6.1% of pyogenic granulomas (Figures 6. white lines similar to a double rail that intersect the lesion in some pyogenic granulomas may correspond histologically to the fibrous septa that surround the capillary tufts or lobules in more advanced cases. in these cases.75 Figure shows the characteristic dermoscopic pattern in a pyogenic granuloma located on a upper lip (X10).

(10) They are often located on a background of a red. should be considered. whitish veil (90. Although Menzies et al.1%). and hemorrhagic crusts (53. dotted vessels. irregular vessels as the predominant vessel type. we have found several vascular structures (dotted vessels. structureless areas of more than 10% of the area of the lesion (X10). 13) Although patients usually describe cyclic changes and. more than 1 shade of pink. all cases of pyogenic granulomas with vascular structures should be excised in order not to misdiagnose an amelanotic melanoma. such as angiomas and angiokeratomas. In a recent study. or black color corresponds to vascular spaces that are partially or completely thrombosed. the dermoscopic hallmark of most hemangiomas is the presence of red lacunas. the dermoscopic appearance is changing. brown dots or globules irregular in size and distribution. the most predictive for melanoma were central vessels. hairpin vessels.(7. irregularly shaped depigmentation (white lines and structures). violaceous. or red-whitish homogeneous area. occasionally. according to this study. Another vascular tumor whose dermoscopic image has been described in the literature is targetoid hemosiderotic hemangioma. the “white rail” lines that intersect the lesion in 30. and polymorphous/atypical vessels (Figures 6.8% and a specificity of 99. linear-irregular vessels. maple leaf–like areas. The dermoscopic criteria for basal-cell carcinoma (14) include lack of features of a melanocytic lesion and the presence of at least one of the following criteria: large gray-blue ovoid nests. It is important to note that the pattern composed of “dark  . blue. glomerular vessels. and light-brown. 5 to 6 colors. Milky red-pink areas are defined as larger areas than globules of fuzzy or unfocused milky-red color usually corresponding to an elevated part of the lesion. Under dermoscopy.8%). also represent dilated vascular spaces in the upper dermis and their dark violaceous. hairpin vessels. in some pyogenic granulomas. milky red pink areas not surrounded by white-rail lines and Figure 6. all these features were significant. we can observe polymorphous/ atypical vessels. which are characterized by well-demarcated. a combination of dotted and linear irregular vessels.6%). blood-filled vessels in the papillary dermis. Spitz nevus. 9) Regarding other vascular lesions.(16) showed a peripheral white collarette.78). red or reddish-blue areas and correspond histopathologically to dilated. positive predictors of melanoma. the most positive predictors of amelanotic and hypomelanotic melanoma were multiple blue-gray dots. Regarding amelanotic melanoma. arborizing telangiectasias. Nodular basal-cell carcinoma and amelanotic melanoma may be also included in the differential diagnosis of a reddish tumor.1%. 6 dermoscopic structures were observed in at least 50% of the solitary angiokeratomas (11): dark lacunas (93. glomerular vessels.8%). therefore. none of the 105 amelanotic and hypomelanotic melanomas of the study of Menzies et al.7% of cases (7) could divide the total reddish homogeneous area in structures similar to milky red–pink areas. As for vascular features. In our opinion.(11) “Dark lacunas. light-brown.1%). compared with benign melanocytic lesions and nonmelanocytic lesions of the study. multiple blue-gray globules. and linear. However. milky red–pink areas.1%). telangiectasias. predominant central vessels.77 and 6. red-bluish. and other pigmented lesions. In our opinion. red lacunas (53. and polymorphous/atypical vessels) in some pyogenic granulomas. red-blue color. irregularly shaped depigmentation.(7) However. Moreover.1% of pyogenic granulomas in one study. hairpin vessels. all cases of reddish tumor with characteristic dermoscopic structures of pyogenic granulomas (a total reddish homogeneous area surrounded by a white collarette).(16) It is important to note that.79 Figure shows a dermoscopic image of an amelanotic melanoma previously diagnosed clinically as a pyogenic granuloma. and ulceration.zaballos lacunas plus whitish veil” was determined to be the most common pattern in solitary angiokeratomas. The structure “dark lacunas” is the most frequent dermoscopic finding in solitary angiokeratomas and represents the most valuable criteria for correctly diagnosing this vascular tumor with a sensitivity of 93.” like red lacunas. and amelanotic melanoma. brown dots or globules irregular in size or distribution. spoke-wheel areas. Lacunas commonly vary in size and color within a given lesion and may be either tightly clustered or loosely scattered throughout. none of the other specific dermoscopic criteria of basal-cell carcinoma has been described in pyogenic granulomas and the peripheral white collarette is not a characteristic of basal-cell carcinomas. structureless areas of more than 10% of the area of the lesion. most cases show a pattern composed of a central area with reddish or dark lacunas surrounded by a reddish. such as basal-cell carcinoma. telangiectasias. peripheral erythema (53. in a recent study (15).(12. round to oval. or brownish homogeneous pigmentation. linear-irregular vessels. did not include any pyogenic granuloma in their study. erythema (68. including those with more than one shade of pink and/or vascular structures (mostly having predominantly central vessels. and peripheral. Dermoscopic differential diagnosis between pyogenic granuloma and other vascular lesions. When these tumors are ulcerated they may resemble pyogenic granulomas because ulceration has been also described in 46.

pyogenic granuloma
polymorphous/atypical vessels), should be excised in order not to misdiagnose an amelanotic melanoma (Figure 7.69). REFERENCES 1. Mooney MA, Janninger CK. Pyogenic granuloma. Cutis 1995; 55: 133–6. 2. Pagliai KA, Cohen BA. Pyogenic granuloma in children. Pediatric Dermatology 2004; 21: 10–3. 3. Requena L, Sangueza OP. Cutaneous vascular proliferation. Part II. Hyperplasias and benign neoplasms. J Am Acad Dermatol 1997; 37: 887–919. 4. Grimalt R, Caputo R. Symmetric pyogenic granuloma. J Am Acad Dermatol 1993; 29: 652. 5. Rowe L. Granuloma pyogenicum. AMA Arch Dermatol 1958; 78: 341–7. 6. Elmets CA, Ceilley RI. Amelanotic melanoma as a pyogenic granuloma. Cutis 1980; 25: 164–7. 7. Zaballos P, Llambrich A, Cuellar F, Puig S, Malvehy J. Dermoscopic findings in pyogenic granuloma. Br J Dermatol 2006; 154: 1108–11. 8. Zaballos P, Salsench E, Puig S, Malvehy J. Dermoscopy of pyogenic granulomas. Arch Dermatol 2007; 143: 824. 9. Wolf IH. Dermoscopic Diagnosis of Vascular lesions. Clin Dermatol 2002; 20: 273–5. 10. Argenziano G, Soyer HP, Chimenti S et al. Dermoscopy of pigmented skin lesions: results of a consensus meeting via the Internet. J Am Acad Dermatol 2003; 48: 679–93. 11. Zaballos P, Daufí C, Puig S et al. Dermoscopy of solitary angiokeratoma: a morphological study. Arch Dermatol 2007; 143: 318–25. 12. Sahin MT, Demir MA, Gunduz K, Ozturkcan S, TürelErmertcan A. Targetoid haemosiderotic haemangioma: dermoscopic monitoring of three cases and review of the literatura. Clin Exp Dermatol 2005; 30: 672–6. 13. Morales-Callaghan AM, Martinez-Garcia G, AragonesesFraile H, Miranda-Romero A. Targetoid hemosiderotic hemangioma: clinical and dermoscopical findings. J Eur Acad Dermatol Venereol 2007; 21: 267–9. 14. Menzies SW, Westerhoff K, Rabinovitz H et al. Surface microscopy of pigmented basal cell carcinoma. Arch Dermatol 2000; 136: 1012–6. 15. Menzies SW, Kreusch J, Byth K et al. Dermoscopic evaluation of amelanotic and hypomelanotic melanoma. Arch Dermatol 2008; 144: 1120–7. 16. Argenziano G, Zalaudek I, Corona R et al. Vascular structures in skin tumors. A dermoscopy study. Arch Dermatol 2004; 140: 1485–9.



7.1

Lichen ruber planus Francisco Vázquez-López

Lichen planus is a subacute or chronic dermatosis characterized by violaceous papules that may coalesce into plaques. Postinflammatory hyperpigmentation may appear, being troublesome for the patients if it is long standing. Histologically, active papules of lichen planus show (a) hyperkeratosis, (b) focal hypergranulosis, (c) irregular acanthosis, (d) damage to the basal cell layer, and (e) band-like dermal infiltrate in close approximation to the epidermis.(1) The surface of lichen planus lesions shows clinically pathognomonic white lines or dots in a variable configuration (Wickham striae, WS), which recall those observed in the oral mucosa. The histological correlate of WS is a compact orthokeratosis above the zones of wedge-shaped hypergranulosis and acanthosis, centered around acrosyringia and acrotrichia.(1, 2) Wickham striae cannot always be recognized in the standard visual inspection. They are rendered more evident by painting the lesions with oil and by examining them with a magnifying lens. The use of dermoscopy improves and facilitates this maneuver, allowing an easier and rapid recognition of WS in clinical practice. Therefore, dermoscopy improves the clinical diagnosis of lichen ruber planus in patients with active lesions.(3–5) Dermoscopy also serves for monitoring the evolution of LP lesions and for evaluating the type of postinflammatory hyperpigmentation, which may present a prognostic significance.(6) The usual precautions must be taken in order to prevent nosocomial infections if contact, nonpolarized dermoscopy is performed on eroded lesions. By means of dermoscopy, the vessels are visualized because of the red blood cells fulfilling and passing through them. Therefore, it is also important to avoid excessive pressure on the lesion when performing this procedure, which may cause blanching and lack of visualization of the vessels if nonpolarized dermoscopy is applied or when taking photographs with skin contact. DERMOSCOPIC APPEARANCE AND EVOLUTION OF THE LESIONS OF LICHEN PLANUS 1. Initial LP lesions (round, pink papules): Initial papules of LP show round, small Wickham Striae (WS) with a central yellow-brown dot. WS are visualized as pearly whitish, opaque structures. WS can be observed with both polarized and nonpolarized dermoscopes. Polarized dermoscopes allows for better recognition of deeper structures (vasculature, dermal pigment, fibrosis) but for worse recognition of the superficial layers of the epidermis. Structures such as the milia cysts of seborrheic keratoses and the blue-white veil associated with orthokeratosis may be harder to

Figure 7.1 Clinical view of a patient with active, well-developed, violaceous papules and plaques of lichen ruber planus located on the arms.

Figure 7.2 Dermoscopy with low magnification of the same patient. A polygonal network of pathognomonic, white, Wickham Striae surrounded by red capillaries is shown in active LP lesions. Vascular structures are seen because they are filled with red cells (original magnification: X10). In order to prevent their occlusion it is important to avoid an excessive pressure over the lesions if nonpolarized dermoscopy is performed. appreciate with this device.(7) In LP lesions, polarized dermoscopes serve for accurately demonstrating WS, specially of its contour, but WS appear less uniform, with variations in the intensity of the color, which gives

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lichen ruber planus

Figure 7.3 Dermoscopy of active LP lesions (digitally zoomed images). The Wickham Striae contours show broad ramifications, which become a reticular configuration in the largest lesion. WS are surrounded by radial capillaries. The magnification of the dermoscopic images obtained with Dermlite Foto can be increased by means of the digital zoom of the attached camera.

Figure 7.5 Dermoscopy of LP papules (digitally zoomed images). The WS presents herein thin projections of the border (“comblike” appearance), intermingled with well-defined radial capillaries. These are the most characteristic vascular finding of LP, but round vessels (globular/dots) can also be seen.

Figure 7.4 Dermoscopy of active LP lesions (digitally zoomed images). WS can be revealed with both polarized and nonpolarized dermoscopes. In LP lesions, polarized dermoscopes serve for accurately demonstrating WS, but they appear speckledlike, less uniform, showing variations in the intensity of the color. With nonpolarized dermoscopes WS appear more uniform, compact, and pearly whitish. a more speckled and “unfocused-like” appearance. With nonpolarized dermoscopes WS appear more focused, compact, and uniformly pearly whitish. In addition to the WS, peripheral capillaries become progressively more evident in LP lesions. The initial yellow-brown area of some LP papules could correspond to vacuolar

Figure 7.6 Dermoscopy of LP lesions showing radial, linear capillaries. Round vessels can also appear but are less characteristic (original magnification: X10).

alterations of basal keratinocytes and to spongiosis in the spinous zone.(1) 2. Mature LP lesions (violaceous papules or plaques) (Figures 7.1–7.8). Mature LP lesions remain isolated or become confluent in reticular networks. WS become polymorphic and show projections of the border, which are visualized as thin spikes (“comb-like” projections) or as broad arboriform ramifications. In this phase, the central yellow-brown area disappears and prominent peripheral linear, radial capillaries surround the WS

1

vzquez-lpez

Figure 7.7 Clinical view of an active lichen planus plaque.

Figure 7.9 Clinical view of long-standing annular LP of the axillary region.

Figure 7.8 Dermoscopy of this plaque revealed round and linear WS configured in a well-developed white, polygonal network, most prominent in the periphery, and outlined by radial capillaries. Some WS show yellow-brown areas (original magnification: X10). contour, intermingled with the projections of the border. Less characteristic round vessels can also be seen. Several types of pearly white WS can be recognized: (a) (b) (c) (d) (e) Round WS Linear WS Arboriform WS Reticular WS Annular WS

Figure 7.10 Dermoscopy (high degree of digital zoom magnification) reveals herein a granular pigment deposition in the border of the previous annular LP lesion.

3. Evolved LP lesions: These lesions show WS with decreasing, less prominent peripheral vessels. Pigmented structures begin to appear surrounding the WS contour. Long-standing

lesions show pigmented structures, with or without WS devoid of capillaries, according to their duration and the intensity of the inflammatory process. 4. Annular lichen ruber planus. This type of configuration appears most commonly in the groin and axillary area. Dermoscopy of the active border shows WS, capillaries, or pigmented structures according to their duration (Figures 7.9, 7.10). 5. Hypertrophic lichen planus appear as thickened, hyperkeratotic plaques on anterior legs. These lesions may show under dermoscopy comedo-like structures filled with yellow plugs or round corneal structures (“corn pearls”) in addition to WS and vascular findings (Figure 7.11).



lichen ruber planus

Figure 7.11 Dermoscopy of long-standing LP plaque (high degree of digital zoom), showing “corn pearls.” Comedo-like structures filled with yellow plugs or round, yellow corneal structures (corn pearls) can appear within some LP lesions over time.

Figures 7.13 Dermoscopy of pigmented LP lesions. Granular pigment consists of fine or coarse, grey-blue or brown round dots or globules. They outline the WS contour in recognizable patterns, such as the “ashy-holes,” showing granules clustered into round “holes” surrounded by round WS. A striking “sewing machine-like” regular distribution of clusters of pigment outlining the WS contour can also be recognized. Pigment granules first surround the WS and finally are an isolated finding (original magnification: X10).

Figure 7.12 Dermoscopy of long-standing pigmented LP lesions, revealing granular pigment outlining the contour of polygonal WS (original magnification: X10). Nonatrophic ashy or brown LP macules may present with dermoscopy a homogeneous, structureless, light-brown pattern, or a granular pigmentation. This last pattern seems to persist longer and corresponds to pigment-laden dermal melanophages. 6. Postinflammatory hyperpigmentation of LP (ashy dermatosis, lichen planus pigmentosus, dyscromic and pigmented actinic lichen planus, and lichen planus with hyperpigmentation). Discolorations related to LP may present a long evolution, which is disturbing for patients. Different dermoscopic patterns of nonatrophic, macular, pigmented LP may be related to prognosis (6) (Figures 7.12–7.17).

Figures 7.14 Higher magnification of this lesion. The “ashy-holes” and a “sewing machine-like” distribution of pigment granules are well evident. Ashy or brown macules secondary to lichen planus may present with dermoscopy: (a) Homogeneous, structureless, lightbrown areas devoid of granularity. This type of pigmentation seems to present a shorter course. (b) Granular pigmentation, which corresponds to pigment-laden dermal melanophages. This pattern seems to persist longer when large amounts of granules are present. Granular pigment consists of fine or coarse, gray-blue or brown, clustered, round dots or globules,



17 Coarse and fine gray-blue and brown globules are better visualized in the previous lesion by increasing the magnification with zoom (Dermlite Foto). dermoscopy may be helpful Figure 7. uniformly sized and distributed rounded vessels (dots/globules). within or without light-brown discolorations.vzquez-lpez Figure 7. Plaque psoriasis (PP) and lichen planus (LP) are well differentiated clinically. FIgure 7.16 Dermoscopy of the same ashy LP lesions.19 Dermoscopy of plaque psoriasis (center of the lesion). A high degree of digital zoom reveals that these apparently rounded vessels are indeed convoluted. Pigment granules are seen in greater amounts in rounded. depressed areas that appear centrally within some rounded WS. (b) “Sewing machine” pigment distribution.15 Clinical view of ashy dermatosis related to lichen planus. The clusters of pigment granules outline the WS contour in a striking regular distribution. Nevertheless. They outline the WS contour in recognizable patterns such as follows: (a) “Ashy-holes”. Figure 7. revealing multiple. “coiled” curvilinear capillaries. The color of the surrounding background may vary from pink to deep red. Pigment granules are located herein within homogeneous brown discolorations (original magnification: X10).  . Figure 7.18 Dermoscopy of a psoriatic plaque (original magnification: X10).

London. or convoluted vessels (Figures 7. Pérez-Oliva N. In addition. Dermoscopy subpatterns of inflammatory skin disorders. Scope A et al. Am J Dermatopathol 1981. Nevertheless. Clin Exp Dermatol 2003. Braun RP. 207: 151–6. 3. The subpapillary horizontal vascular plexus is not seen with any magnification. dermoscopy may be used herein for investigative and teaching purposes. 25: 611–3. Vázquez-López F. Sánchez J. Figure 7. Gareau DS. López-Escobar M. Arch Dermatol 2001. in conjunction with clinical examination. Polarized and nonpolarized dermoscopy: the explanation for the observed differences. and regression of lesions of lichen planus. Vázquez-López F. Dermatology 2003. surrounded by a colored background (pink to red) (9–10) (Figure 7. Vázquez-López F. being hidden by the epidermal hyperplasia. The handheld dermatoscope improves the recognition of Wickham striae and capillaries in Lichen planus lesions. Alvarez-Cuesta C. Dermoscopic features of plaque psoriasis and lichen planus: new observations. Rivers JK. Who was Wickham and what are his striae? Int J Dermatol 1986. J Am Acad Dermatol 2004. Arch Dermatol 2007. Kreusch J. Hidalgo-García Y. Dermoscopy of pigmented lichen planus lesions. Jackson R. 5. Zalaudek I.20). 142: 808. REFERENCES 1. such as in atypical patients or when LP coexist with PP. video microscope) they are really seen as curvilinear. eds. 144: 82–9. Atlas of Dermoscopy. twisted. 3: 5–25. Vázquez-López F. Gómez-Díez S. 11. is a very useful and low-cost tool for diagnosing LP in most settings. Evolution. LP is characterized by a network of whitish striae. Marghoob A. Arch Dermatol 2007. 7. Pérez-Oliva N. Manjón-Haces JA. Arch Dermatol 2006. The capillary loops are less coiled at the margins of the plaques (high degree of digital zoom). Vázquez-López F. uniformly sized and distributed round vessels (globular/dotted).(3. Vazquez-López F. which are always absent in plaque psoriasis. Arch Dermatol 2008. 4.18). 51: 811–3. Ackerman AB. 2005: 299–306. Kopf AW. for discriminating between them in special instances. New observations and correlations of clinical and histologic findings. Dermoscopic assessment of long-term topical therapies with potent steroids in chronic psoriasis. Argenziano G. 8) As described above. 10. Maldonado-Seral C et al. 2. maturation. It improves the recognition of pathognomonic structures (Wickham striae) and allows the recognition of different patterns of postinflammatory pigmentation likely related  . Ragaz A. Pérez-Oliva N. Marghoob AA. 8.20 Dermoscopy of plaque psoriasis (periphery of the lesion). 28: 554–5. PP shows multiple. dermoscopy. Pan Y. Other uses of dermoscopy. 6. Taylor & Francis.(11) In sum. Dermoscopy of active lichen planus. 9. SánchezMartín J. 143: 1612. A dermoscopy subpattern of plaque-type psoriasis: red globular rings. 143: 1092. Fueyo-Casado A.lichen ruber planus to prognosis. In contrast. by increasing the degree of magnification (stereomicroscope. unless an atrophy secondary to topical steroid treatment develops. 137: 1376.19–7. Orizaba M. Vázquez-López F. Maldonado-Seral C. Zaballos P. In: Marghoob AA.

UV disclose fibrinoid deposits in the vessels walls. 2) Figure 7.30). Purpuric areas may be minimal and unapparent by means of the standard visual inspection.  . nuclear dust and dermal hemorrhage have been considered the most specific differential criteria for UV. which corresponds to transiently dilated. intermingled with neutrophils and eosinophils. For differentiating between CU and UV lesions. Histologically.22 Polarized dermoscopy (low magnification) of a wheal (CU). neutrophilic infiltrates. Histologically. The degree of clinical purpura in UV is variable.21 Clinical appearance of transient lesions (wheals) of common urticaria (CU) in a patient with vitiligo. 2) Dermoscopy of CU serves to reveal the transiently dilated superficial dermal capillaries of the lesions (3) (Figures 7. with a red network of linear vessels (original magnification: X10). oval area. requiring biopsy for diagnosis. 5) (Figures 7.27–7. which may cause occlusion and lack of visualization of the vessels.2 Urticaria and urticarial vasculitis Francisco Vázquez-López Dermoscopy may be of great help for the study of common urticaria and similar disorders. for improving their recognition.(1. disclosing an irregular red network of linear vessels. Therefore. Vessels are visualized because of the red blood cells fulfilling and passing through them.(1. horizontally oriented dermal capillaries.7. Figure 7. The usual precautions must be taken in order to prevent nosocomial infections if contact. urticaria is characterized by dermal or subcutaneous edema and a sparse or dense perivascular lymphocytic infiltrate. recurrent wheals.21–7.26). Recognition of vascular structures is fundamental for evaluating lesions of urticaria. such as urticarial vasculitis and may be used for differentiating between them on a noninvasive basis in most settings. The individual lesions tend to persist longer than common wheals (1–3 days). Urticaria vasculitis (UV) presents episodes of urticaria often associated with arthralgia and abdominal pain and rarely with glomerulonephritis. Common urticaria (CU) is characterized by the acute or chronic appearance of transient.23 Dermoscopy with greater magnification. disclosing a well-circumscribed. and slight-to-moderate extravasation of erythrocytes. it is important to avoid excessive pressure on the lesion when performing this procedure. nonpolarized dermoscopy is performed or when taking photographs with skin contact. as a first-line screening tool (4. nuclear dust. if nonpolarized dermoscopy is applied or when taking contact photographs. They may reveal faint purpura and resolve with residual discoloration. Dermoscopy serves herein Figure 7.

Figure 7. Dermoscopy.g. showing a red network of linear vessels. the wheals of CU disclose under dermoscopy a red. This Figure 7. It is observed in noninflammatory forms of dermal hemorrhage (vessel-wall dysfunction or trauma. Under dermoscopy. round vessels can be recognized along their course. infective organisms) (e. Purpuric globules are blurred and appear within a purpuric background and later within orange-brown patches.urticaria and urticarial vasculitis Figure 7.22–7. PG are associated with diverse purpuric inflammatory processes (pigmented purpuric dermatoses. The vessels were obscured by a prominent edema (original magnification: X10). According to the previous basic semiology. degeneration of the supporting stroma. although with reduction of the image quality if it is excessive.32). although this differentiation may be difficult to make. vessels).(3–5) Dermoscopic vascular findings observed at standard magnification (x10 fold) may be seen as round (vertically oriented papillary vessels) or as linear structures (horizontal subpapillary 7 . This vascular finding must be differentiated from true purpuric structures (original magnification: X10). with a defined or a blurred contour. derived from perivascular hemorrhage. This discrimination is important because UV may be a cutaneous manifestation of an underlying connective tissue disease. coagulation-fibrinolytic disorders. leucocytoclastic vasculitis. the lesions of common urticaria (CU) reveal a process of transient vasodilatation of dermal capillaries.21–7.26). structureless purpura. viral and drugs reactions. may be very useful for discriminating between them in daily practice. or globular according to their size. Dermoscopic purpuric structures may be mainly of two types: (a) Homogeneous.24). arthropods reactions. Linear vessels may appear as simple or as arboriform structures. red.24 Dermoscopy of the same lesion after increasing the degree of magnification.25 A peripheral red network of linear vessels surrounding a central negative area are shown in a CU lesion. The color of the background surrounds PG but may obscure them if it is prominent or when tissue necrosis appears.. infective organisms) (Figure 7. reticular network of linear vessels (Figures 7.31) (b) Round purpuric dots/globules (PG). Dermoscopic differentiation between CU and UV requires the knowledge of both vascular and purpuric structures. The magnification of the dermoscopic images obtained with Dermlite Foto can be increased by means of the digital zoom of the attached camera. and may form networks (Figures 7.26 Dermoscopy of a CU lesion. and biopsy is required for differentiation between them. senile purpura) (Figure 7. In addition. Common urticaria and urticarial vasculitis clinically overlap. sharp. without presenting other structures. Round vessels may be dotted/punctate/pinpointed. in conjunction with history and clinical examination. (c) Other purpuric patterns that may be recognized include purpuric/black dots of subcorneal purpura and hemorrhagic crusts.

Linear vessels may be associated with dotted vessels (Figure 7. These purpuric structures correspond histologically with the presence of vasculitis and are associated with perivascular extravasation and degradation of red blood cells. lesions of UV with slight hemorrhage may reveal linear vessels (Figure 7. but showing well-evident. The lesions do not show clinically purpuric areas. Purpuric structures are not observed in CU. The degree of dermal hemorrhage in UV lesions is variable.29 Clinical image of a patient with urticarial vasculitis.27–7. lesions of UV characteristically show more or less prominent and numerous blurred. horizontally oriented.30 Dermoscopy of the previous lesion. These PG may be clinically unapparent. representing areas where vessels have been obscured by a prominent edema (negative areas).28 Polarized dermoscopy of a lesion of UV revealing blurred purpuric globules (PG). dermoscopic pattern corresponds histologically with ectatic subpapillary vessels.vzquez-lpez Figure 7. Figure 7. Lesions of UV with slight hemorrhage may also show a surrounding linear network of vessels (original magnification: X10). Lesions consist of pruriginous.30). raised. PG may appear or not appear Figure 7. In this case.26). but UV may be suspected after screening with dermoscopy. numerous pethechiae. Figure 7. urticariform plaques. Dermoscopy may be of great value for the screening of lesions with minimal purpuric areas  .25). and red lines disappear after making a pressure on the lesion. the degree of dermal hemorrhage is so severe that it is clinically evident even without dermoscopy.27 Clinical picture of a patient with urticarial vasculitis (UV). negative areas devoid of vascular findings in some lesions (Figure 7.28). In addition to purpuric dots/globules. Recognition of PG allows easy differentiation with CU. within purpuric or orange-brown patches (Figures 7. Red lines may surround structureless. round purpuric structures or globules (PG). Purpuric globules within purpuric patches: They can be demonstrated by using dermoscopy with low magnification and also in a clinical basis (original magnification: X10). In contrast to CU.

Braun RP. 4. Baltimore: Williams and Wilkins. blurred.26). 42: 1079–82. Peteiro C. In addition. in conjunction with history and standard clinical examination.29.28). Figure 7. 5. Vázquez-López F.30). Am J Dermatopathol 1989. may serve as a first-line screening tool for discriminating between common urticaria and urticaria vasculitis on a noninvasive and low-cost basis in daily practice. Marghoob AA. Surface microscopy for discriminating between common urticaria and urticarial vasculitis.urticaria and urticarial vasculitis Figure 7. Incidence of leukocytoclastic vasculitis in chronic idiopathic urticaria. 11: 528–33.27. Br J Dermatol 2004. Some of them are located within yellow-brown patches (original magnification: X10). disclosing multiple. Histologic diagnosis of inflammatory skin diseases. 1997.31 Dermoscopy of a noninflammatory form of purpura. respectively. eds. Kopf AW. REFERENCES 1. dermoscopy. Rheumatology 2003. However. Dermoscopic red lines and purpuric globules are not specific to urticaria and urticarial vasculitis. This discrimination is based on an unspecific feature (purpuric globules) but which is rendered highly specific for UV when both diseases are confronted. 2. Soler-Sánchez T. In sum. irregular. although purpura can be clinically evident in some severe cases (Figures 7. Kreusch J. which are occasionally present in CU (Figure 7. Study of 100 cases. structureless purpuric patch devoid of other findings is shown (original magnification: X10). Dermoscopic purpuric structures of UV must be differentiated only from round vessels. purpuric globules. London. Round vessels are red. Marghoob AA.32 Dermoscopy of inflammatory purpura.  . 3. Atlas of Dermoscopy. (Figures 7. Other uses of dermoscopy. Ackerman AB. 150: 226–31. Maldonado-Seral C. 2005: 299–306. the ectatic vessels of CU disappear after making a pressure on the lesion while purpuric structures of UV lesions do not blanch. their recognition will help in discriminating between them. Dermoscopic semiology: further insights into vascular features by screening a large spectrum of nontumoral skin lesions. In: Marghoob AA. Vazquez-López F. Taylor & Francis. Perez-Oliva N. with the presence of PG in urticaria lesions being indicative of an underlying vasculitis. A homogeneous. Vázquez-López F. A lesion of leucocytoclastic vasculitis is shown. numerous. 7. well demarcated. Kreusch J. Toribio J. 7. whereas the purpuric globules are blurred. Marghoob A. These structures are easily recognizable even by nonexpert observers and after minimal training. and not related to the vessels. and from crusted erosions rarely seen in CU. and are located along linear vessels.

33). one or more alterations in the VCP findings (architectural disorganization.36 Giant capillary and hemorrhage visible with handheld dermatoscope (x10). the socalled scleroderma pattern (SP).34 and 7.) should suggest a connective tissue disease (Figure 7. enlarged loops. VCP analysis twice a year can early detect the transition to a secondary form in patients showing at the beginning a normal pattern or not-specific nailfold capillary abnormalities. the most typical nail-fold VCP pattern of microangiopathy. It is characterized by irregularly enlarged capillaries. giant capillaries. Figure 7. is commonly observed.35). By contrast. giant Figure 7. reduction of capillary density. in subjects suffering from secondary RP. avascular areas. Figure 7. angiogenesis.(1) In patients affected by systemic sclerosis (SSc).3 Disorders of collagen tissues Paolo Rosina In normal conditions or in primary Raynaud’s phenomenon (RP).34 Videocapillaroscopic appearance of giant capillary loop (x200). Patients initially diagnosed as having primary RP may shift to secondary during the follow-up.  . etc. the normal nailfold videocapillaroscopic (VCP) pattern shows a regular disposition of the capillary loops along the nail-bed (Figure 7.33 Regular disposition of the capillary loops along the nail bed (x100).7.35 Irregular capillaries distribution with few giant capillaries and avascular area in scleroderma “late” pattern (x100). Figure 7. microhemorrhages.

Three distinct NVC patterns of microangiopathy have been described in SSc patients: “early. capillary architecture is almost regular without significant loss of capillaries.” “active. The giant capillary is pathognomonic of the scleroderma pattern. Scleroderma patients with late VC pattern show an increased risk to have an active disease and to be affected by a moderate/severe skin or visceral involvement. Figure 7. as well as ramified capillaries. compared with patients with early and active patterns.” Nail-fold capillary microscopy can be performed with various optical instruments such as videocapillaroscope. and ramified capillaries are typical abnormalities of late SP. capillaries (capillary diameter >50 micron of both arteriolar and venular branches). In fact. heart. Early SP is characterized by irregularly enlarged capillaries.38 Tortuous and “bushy” capillaries in discoid lupus erythematosus visible with hand-held dermatoscope (x10).” and “late. microbleedings. scleroderma patterns are related to disease subset and disease severity.40 Vessel tortuosity with partial respect of normal reticular pattern in subacute lupus erythematosus (x200).37 Giant capillary and hemorrhage visible with videocapillaroscope (x100). skin. disorganization.” which do not normally coexist at the same time.(2) Nail-fold VC helps to staging the patient affected by SSc and provides prognostic information. a few giant capillaries and hemorrhages. capillary architecture Figure 7.(3) The VC features observed in dermatomyositis and in undifferentiated connective tissue disease are generally reported as being of the “scleroderma-like pattern. In the active pattern frequent giant capillaries and hemorrhages may be observed and mild loss of capillaries and capillary architecture disorganization with a few ramified capillaries.disorders of collagen tissues Figure 7. avascular areas.  . Severe loss of capillaries with few giant capillaries. capillary architecture disorganization. reduced capillary number with avascular areas. and lung.39 Completely disarranged microangioarchitecture with loss of capillaries and marked angiogenesis in discoid lupus erythematosus (x200). affecting different sites as peripheral circulation. Figure 7.

Schapira D. Best Pract Res Clin Rheumatol 2005. 2. microbledding. 46: 1566–9. polygon irregularities and vessel tortuosity with partial respect of normal reticular pattern are observed (Figure 7. Capillaroscopy. Grassi W. In subacute lupus erythematosus. and also hand-held dermatoscope. stereomicroscope. It is relatively easy to recognize certain features of microvascular involvement in systemic sclerosis (giant capillaries.). Scleroderma patients nailfold videocapillaroscopic patterns are associated with disease subset and disease severity. Pizzorni C. Rheumatology 2007. tortuous and irregular “bushy” capillaries are already visible with hand-held dermatoscope (Figure 7. Raynaud’s fenomenon and the role of capillaroscopy. etc.37). 48: 3023–30. 3. a completely disarranged microangioarchitecture with loss of capillaries (avascular areas) and marked angiogenesis are better observed with VC (Figure 7.rosina videodermatoscope. Cutolo M. Arthritis Rheum 2003.36). Cutolo M. Matucci Cerinic M. Sharony L.(4) The simplest and most direct way to carry out an approximate evaluation of skin microcirculation conditions is the hand-held dermatoscope (Figure 7. Caramaschi P. Sulli A. The handheld dermatoscope as a nail-fold capillaroscopic instrument. Arch Dermatol 2003. Canestrini S. In cutaneous discoid lupus erythematous. Bergman R. BalbirGurman A. 19: 437–52. RefeRences 1. Martinelli N et al. 139: 1027–30. 4.  .40). ophthalmoscope. Nahir MA.39). but in advanced lesions.38). This vascular pattern can be used in differential diagnosis when cutaneous manifestation of lupus erythematosus clinically resemble psoriasis. although sensitivity is limited by the low level of magnification possible (Figure 7.

papules pustules. Figure 7. The majority of the trials evaluating erythema and teleangiectasia have utilized subjective methods of color measurement and vessel changes.41 Videocapillaroscopic images of normal facial skin (x100). and ocular) and one variant (granulomatous rosacea) and a grading system based on clinical score.(1. Rosacea primarily involves the cutaneous microcirculation of the central part of the face. in particular ultraviolet light. increased vascular permeability and vascular hyperreactivity which results in flushing.(6) We used the videocapillaroscopic technique to evaluate qualitative and quantitative microvessels alterations of facial rosacea and compared them with those of seborrheic dermatitis.(1) Our results indicate that videocapillaroscopy may represent a valid adjunctive method in the early identification and measurement of erythematotelangiectatic rosacea.4 Rosacea Paolo Rosina Rosacea is a common dermatosis affecting 10% to 20% of the middle-aged population. teleangiectases. especially on drug efficacy.7. Age and exposure to environmental factors. phymatous.  . The development of instrumental techniques is obviously important for a more reproducible disease assessment and may allow a more rigorous comparisons between studies. are probably causing initial dermal modification in susceptible individuals.43 Larger polygons with thickened vessel walls in rosacea (x100). Figure 7.g. Some studies on rosacea have considered skin-color changes as a surrogate measurement of vessel changes.(3) There are currently no objective measures or laboratory tests for assessing and monitoring the severity of rosacea. which rests only on clinical judgment.42 Reddish background in erythematotelangiectatic rosacea (x100). papulopustular.. laser Doppler) for the clinical investigation of cutaneous microcirculation in various skin disease. especially among fair-skinned subjects. (4. 5) Capillaroscopy is widely used on nail-fold region to diagnose and monitor rheumatologic diseases and has been considered superior to indirect technique (e. Several etiologic factors and pathogenetic mechanisms have been proposed. There is a general agreement that rosacea is primarily a vascular disorder characterized by persistent small-vessel dilatation and angiogenesis. and phyma. 2) The National Rosacea Society Expert Committee has proposed a classification and staging of rosacea defining four subtypes (erythematotelangiectatic. Figure 7.

more prominent teleangiectases. Figure 7. with an interval of 48 hours between the first and the second videocapillaroscopic examination.45). using an optical probe (Videocap 200R DS Medica. with capillary loops projected at the inner and outer part of the polygons (Figure 7. Characteristic alterations of skin vessels were observed in facial rosacea. Italy) at x100 and x200 magnifications. with a pattern distinct from that of facial seborrheic dermatitis. rosacea showed neoangiogenesis and significantly larger polygons with thickened vessel walls (Figure 7.46 Marked polygon irregularities and pink background in seborrheic dermatitis (x100).41). Figure 7. For all the morphological and quantitative parameters investigated.42). no substantial differences were noted between male and female patients. A regular polygonal net represents the normal distribution of the cutaneous microcirculation on the cheek.44). In some subjects videocapillaroscopy was repeated at least twice.rosina Figure 7. compared to seborrheic dermatitis.46 and 7. Patients with rosacea showed a reddish background due to the extended vessel dilatation of the subpapillary plexus Figure 7.45 Teleangiectases and larger Rosacea vessel in rosacea (x200). (Figure 7.47 Vessel tortuosity in seborrheic dermatitis (x100). In particular. neoangiogenesis) and quantitative parameters (polygon perimeter.43 and 7. Parameters analyzed on the cheek area were background color and morphological (polygons irregularity. Thirty patients with erythematoteleangiectatic rosacea were compared with 30 age. Milano. Seborrheic dermatitis displayed more polygon irregularities and vessel tortuosity (Figure 7. and larger mean vessel diameter (Figure 7. mean diameter of teleangiectases and vessels).and sex-matched patients with facial seborrheic dermatitis and 30 healthy control subjects. vessel tortuosity. healthy subjects and patients with seborrheic dermatitis displayed a pink background.44 Neoangiogenesis and polygonal net in rosacea (x100). In contrast.47). 4 .

pathogenesis. Giovannini A. Rosacea: I. Hern S. Etiology. 54: 100–4. RefeRences 1. Mortimer PS. New techniques for clinical assessment of the peripheral microcirculation. Videocapillaroscopic alterations in erythematotelangiectatic rosacea. Girolomoni G. and larger vessels diameter was observed only in rosacea. more prominent teleangiectases. Renier CM. Measurement of the severity of rosacea. suggesting that rosacea specifically affects the facial microvasculature. whereas seborrheic dermatitis displayed polygon irregularities and vessel tortuosity. in single individuals. Pelle MT. no alterations were found in the nail-fold region. In particular. Dahl M. 50: 907–12.  . Bamford JTM. with a pattern distinct from that of facial seborrheic dermatitis. Gessert CE. J Am Acad Dermatol 2004. neoangiogenesis. James WD. facial rosacea was found to present characteristic alterations of skin vessels. Visualization of dermal blood vessels— capillaroscopy. larger polygons. 51: 697–703. 5. and subtype classification. Videocapillaroscopy is a noninvasive and easily repeatable technique that can disclose specific and measurable vessel alterations and may represent a valid adjunctive method in the early diagnosis and measurement of erythematotelangiectatic rosacea. 58: 17–22. Clin Exp Dermatol 1999. Detmar M et al. Crawford GH. Wilkin J. J Am Acad Dermatol 2006. 6. 24: 473–8. Zamperetti MR. J Am Acad 2004. In contrast. 3. Standard classification of rosacea: report of the National Rosacea Society Expert Committee on the classification and staging of rosacea. 2. 4.rosacea Erythema was slightly changing. 51: 327–41. J Am Acad Dermatol 2004. Drugs 1999. In conclusion. Chieregato C. Carpentier PH. but vessel characteristics did not change significantly from day 1 of the treatment. Rosina P.

Figure 7. mucosal. poliglobular. Autoinoculation is common. The average incubation time is between 2 and 7 weeks with a range extending to 6 months. MCV II. and color. with an umbilicated center. Histologically.50 Figure shows the typical pattern of molluscum contagiosum (central. and the crural folds in children. shape. and MCV IV. Though generally thought to infect only humans.48 Clinical image of a typical case of molluscum contagiosum in a child.5 Molluscum contagiosum Pedro Zaballos Diego MOLLUSCUM CONTAGIOSUM Molluscum contagiosum (MC) is a disease caused by a poxvirus of the Molluscipox virus genus that produces a cutaneous. thighs. MCV III. or anatomical distribution. umbilicated. The MCV can be found worldwide with a higher distribution in tropical areas and has a higher incidence in children. Clinically. up to 35 microns. but favored sites include the axillae. Fomites and sexual transmission have been suggested as another source of infection. The papules may become inflamed spontaneously or after trauma and present atypically in size. There are four main subtypes of molluscum contagiosum virus (MCV): MCV I. MC exhibits epidermal hyperplasia producing a crater filled with huge.48 and 7.  . and those who are immunodeficient. there appears to be marked geographical variation in the distribution of subtypes. eosinophilic to basophilic intracytoplasmatic inclusions that Figure 7. flesh colored or pearly. cutaneous tumors. although occasionally giant lesions are seen. self-limited papular eruption of multiple. morphology.49 Molluscum contagiosum on a face of an adult.7. the antecubital and popliteal fossae. MC in adults affects the groin. Any cutaneous surface may be involved. This disease is transmitted primarily through direct skin contact with an infected individual. The morphology of an individual lesion is a dome-shaped papule. The lesions are often grouped in small Figure 7. and lower abdomen and is often acquired sexually. genital area. benign. white-yellowish amorphous structure and peripheral crown of vessels) (X10). sexually active adults. It was first described and later assigned its name by Bateman in the beginning of the nineteenth century.49). areas but may also become widely disseminated. case reports of the virus occurring in other animals have been published. Lesions vary in size from 1 to 10 mm. However. MC produces a papular eruption of multiple umbilicated lesions (Figures 7. There is no apparent relationship between viral subtype.

MC may be occasionally confused with other tumors. in more rare cases.53). Figure 7. amorphous structure surrounded by a peripheral crown of vessels with reddish globules and areas of erythema (X10).50–7.(6–10) In some cases. MC is a self-limited disease. will eventually resolve itself in immunocompetent hosts but may be protracted in atopic and immunocompromised individuals.52 Figure shows central.(1–5) The clinical diagnosis of MC is usually easy. white-yellowish structures. particularly those found in adulthood. white-yellowish. poliglobular. and dotted vessels. left untreated. white-yellowish. red globules. ring-like structure that encircle the poliglobular. mainly in pediatric patients.(6–10) Dermoscopically. dermoscopy discloses additional information to improve our diagnosis. amorphous structure and a peripheral crown of vessels) (X10). However. and sometimes blurred vessels.51 Another typical dermoscopic image of molluscum contagiosum (X10). Antiviral and immune-modulating treatments have recently been added to the options. dome-shaped papules located on the nose of a 76-year-old man that were clinically diagnosed as basal-cell carcinomas. are called molluscum bodies or Henderson–Patterson bodies. the dermoscopic image of both lesions shows the characteristic pattern of molluscum contagiosum (a central. A central pore or umbilication could be an additional feature in some cases. However. we can see arborizing vessels (Figure 7. which do not usually cross the center of the lobules (Figures 7.53 Figure shows two pearly. Most of the common treatments consist of various means to traumatize the lesions. MC displays a characteristic pattern composed of the presence of a poliglobular whiteyellowish amorphous structure in the center of the lesions with a surrounding crown of linear.(6) In these cases. comma vessels. because they are normally quite characteristic in appearance. and.molluscum contagiosum Figure 7. fine. Figure 7. 7 . which. The histopathological correlation of central. poliglobular.54). we can also observe curvilinear vessels that form a peripheral. some of them branching. waxy. reddish.

The crown of vessels or “red corona” corresponds histopathologically to dilated vessels in the dermis and is characteristic of MC. and allows us to differentiate these disease from  . Valentine CL. 5. REFERENCES 1. peripheral.zaballos many other skin lesions with high confidence. Molluscum contagiosum. 9: 2. Puig S. Treatment modalities for molluscum contagiosum. J Am Acad Dermatol 2001. Giacomel J. 7. one located on the thorax and the other on the back. Dermoscopic semiology: further insights into vascular features by screening a large spectrum of nontumoral skin lesions. Zalaudek I. Hanson D. Dermoscopic image shows isolated. Diven DG. Dermatol Online J 2003. Brown ST. 8: 227–34. Cabo H et al. However. Kreusch J. Di Stefani A et al. Malvehy J. J Eur Acad Dermatol Venereol 2006. 3. white-yellowish globules could be the lobulated. Ara M. Puig S.(11) However. Diven DG. Entodermoscopy: a new tool for diagnosing skin infections and infestations. pearly. Morales A. the recognition of this pattern (a central. as MC because they presented this characteristic pattern. Arch Dermatol 2005. Zaballos P.54 Atypical case of molluscum contagiosum. 20: 482–3. aggregated. Int J Dermatol 1994. dermoscopically. 8. poliglobular. Sex Transm Dis 1981. Arch Dermatol 2005. 141: 1644. endophytic epidermal hyperplasia with intracytoplasmic inclusion bodies. Molluscum contagiosum. white-yellowish globules (asterisks) and arborizing vessels throughout the lesion (X10). we can also find these vascular structures in sebaceous hyperplasia. Dermatol Ther 2000. Dermatology 2008. white-yellowish. Malvehy J. 216: 14–23. Molluscum contagiosum. Argenziano G. (8) evaluated and classified the dermoscopic vascular structures seen in 33 nontumoral dermatoses and found this vascular structure in 10 of 15 patients with MC. Zaballos P. which were clinically diagnosed as basal-cell carcinomas and. 44: 1–14. Malvehy J. Puig S. 141: 808. Dermatology 2006. Ara M. Zalaudek I. 11. waxy. (7) published an atypical case of a 67-year-old woman with two 5-mm. dome-shaped papules of 7-month duration. Diven DG. 6. Marghoob AA. Dermoscopy of molluscum contagiosum: a useful tool for clinical diagnosis in adulthood. Zaballos P. 13: 285–9. 10. Vázquez-López F. also known as molluscum or Henderson–Paterson bodies. 33: 453–61. Figure 7. Vazquez-Lopez et al. 2. amorphous structure and a peripheral crown of vessels) is very helpful in the clinical diagnosis of MC. Myskowki PL. Dermoscopy in general dermatology. Gottlieb SL. Zaballos et al. Br J Dermatol 2004. Dermoscopy of sebaceous hyperplasia. 4. above all in adulthood. these crown vessels are not solely limited to MC. 150: 226–31. 9. Dermoscopy of Molluscum contagiosum. Kraus SJ. An overview of poxviruses. Nalley JF. 212: 7–18.

the primary entities that must be included in the differential diagnosis of sebaceous hyperplasia are basal-cell carcinoma. Other less common sites include the mouth. except perhaps related to cosmesis and. areola. fibrous papule of the face. a linear or zosteriform arrangement.(3) Some papules Figure 7. Figure 7. in groups. and other adnexal tumors. upper arms. and a familial form. premature or familial cases have been reported in which younger individuals are affected with multiple lesions. particularly males. nose. Lesions may occur individually. Sebaceous hyperplasia has been reported in association with internal malignancy in the setting of Muir–Torre syndrome but alone does not signify a predisposition to cancer or represent a Figure 7. Rarely reported variants have included a giant form. Juxtaclavicular beaded lines are an additional variant characterized by closely placed papules arranged in parallel rows. Sebaceous hyperplasia significantly increases in transplant patients. molluscum contagiosum.(1. chest. The classic appearance of sebaceous hyperplasia on physical examination reveals whitish-yellow or skin-colored. sign of Muir–Torre syndrome. particularly males following heart and renal transplantation.55 Typical dermoscopic image of sebaceous hyperplasia with aggregated white-yellowish globules in the center of the lesion (“cumulus sign”) with surrounding crown of vessels. papules that are soft and vary in size from 2 to 9 mm.7. penis.56 Characteristic dermoscopic image of sebaceous hyperplasia (X10). Sebaceous hyperplasia lesions begin to appear in the fifth or sixth decade of person´s life and continue to appear into later life. milia.57 Another dermoscopic image of sebaceous hyperplasia (X10). Sebaceous hyperplasia has no direct association with malignant degeneration and is not a cause of morbidity. Clinically. is often found incidentally upon examination. and this may be related to therapy with cyclosporin A. It most often presents on the face of older adults. The forehead and cheeks are predominantly affected and occasionally diffuse facial involvement occurs. suggesting a genetic predisposition.  . or as a sheet of papules. therefore. However.6 Sebaceous hyperplasia Pedro Zaballos Diego SEBACEOUS HYPERPLASIA Sebaceous hyperplasia is the most common proliferative abnormality of the sebaceous glands. normally umbilicated. We can also observe brownish globular structures with ring-like appearance in the center of the lesion (X10). 2) Sebaceous hyperplasia is frequently clinically misdiagnosed as basal-cell carcinoma. and vulva. a diffuse form.

such as telangiectasia.60). (3) as “cumulus sign. scarcely branching  .58 and 7. scarcely branching vessels located throughout the lesion (X10).(3–7) These vascular structures have been defined as groups of orderly. (7–9) Sometimes.61).55–7. and sebaceous adenoma. structures in 100% of the sebaceous hyperplasias of their studies. sebaceous hyperplasia shows a pattern composed of the presence of aggregated white-yellowish globules in the center of the lesions with a surrounding crown of vessels (Figures 7.” a descriptive sign. These aggregated yellowish globules are not limited solely to sebaceous hyperplasia and may also be seen in some molluscum contagiosum. Oztas et al. bending. Figure 7. reducing unnecessary surgery. (5) named the association of the central umbilication surrounded by cumulus sign as “Bonbon Toffee sign” and found this pattern in 80% of sebaceous hyperplasias (Figures 7. Regarding vascular structures that we can find at the periphery of sebaceous hyperplasias. Figure 7.(3–7) The central aggregated white-yellowish structures or globules. We can also see a peripheral crown of vessels.61 Figure shows the characteristic dermoscopic pattern of a sebaceous hyperplasia located on the penis (X10). nevus sebaceous of Jadassohn. because these structures resemble the cumulus clouds and correspond histopathologically to hyperplastic sebaceous glands. Dermoscopically. Bryden et al.55–7. may be associated with characteristics similar to this malignant tumor.59 Another sebaceous hyperplasia with the “Bonbon Toffee sign” (central umbilication surrounded by aggregated whiteyellowish globules) and peripheral crown of vessels (X10). (5) observed these Figure 7. bending. the ostium of the gland is visible as a small crater or umbilication in the center of these yellowish structures. and dermoscopy may be useful as a noninvasive tool to distinguish between nodular basal-cell carcinoma and sebaceous hyperplasia. the most common ones are the “crown vessels” (Figures 7. were defined by Bryden et al.60 Large sebaceous hyperplasia. Figure shows aggregated white-yellowish globules and groups of orderly. (3) and Oztas et al.zaballos Figure 7. showing a sharp difference from surrounding skin. characteristic of this tumor (X10).59).58 “Bonbon Toffee sign” is the association of a central umbilication surrounded by cumulus sign.

and ulceration) have beeen found in sebaceous hyperplasias. Dermatoscopic features of benign sebaceous proliferation. Malvehy J. Lazar AJF. Griffiths C eds. Oxford: Blackwell Publishing Ltd. J Eur Acad Dermatol Venereol 2008. Dermoscopy in general dermatology. 2004. Kim NH. and aggegrated white-yellowish globules are not typical in BCC.(10) Sebaceous hyperplasia is frequently clinically misdiagnosed as basal-cell carcinoma and arborizing telangiectasias are among the characteristic criteria of this tumor. Bonbon toffee sign: a new dermatoscopic feature for sebaceous hyperplasia. Arch Dermatol 2005. 141: 1644. and Oztas et al. large. 20: 482–3. Malvehy J. Argenziano et al. Ara M. Ustun H. (5) found crown vessels in 86. Zell DS. Other vascular structures that we can observe are arborizing vessels in 16.  . Zalaudek I. Surface microscopy of pigmented basal cell carcinoma. Disorders of the sebaceous glands. Westerhoff K. Oliviero M. Kolm I. 7. Dermoscopy of sebaceous hyperplasia. 22: 1200–2. Puig S. Argenziano G. Malvehy J. blue-gray. Dermoscopy of molluscum contagiosum: a useful tool for clinical diagnosis in adulthood. none of the other specific criteria of BCC (11) (blue globules. Simpson NB. Dawe RS. Arch Dermatol 2000. but we can find these vessels in some lesions of molluscum contagiosum. Rook´s Textbook of Dermatology. some of them with ring-like appearance and milia-like cysts. leaf-like areas.3% of sebaceous hyperplasias. Dermatology 2006. Tumors and related lesions of the sebaceous glands. Zaballos P. Rabinovitz HS. Dermoscopy of Molluscum contagiosum. Arch Dermatol 2004. Menzies SW. Alli N. Oztas P. They are very common in sebaceous hyperplasias. Polat M. McKee PH. spoke-wheel structures.7% of cases according to Argenziano et al. Argenziano G. 144: 962. REFERENCES 1. Granter SR eds. 136: 1012–6. 6. Vascular structures in skin tumors: a dermoscopy study. 2. Zaballos P. Cunliffe WJ. Arch Dermatol 2008. (10) found crown vessels in 83. Ara M.sebaceous hyperplasia vessels located along the border of the lesion. However. Puig S. 212: 7–18. Pathology of the Skin with Clinical Correlations. In: McKee PH. 4. 5. China: Elsevier Mosby. Corona R et al. Breathnach S. The dermoscopic differential diagnosis of yellow lobularlike structures. are less common features that we can see in few sebaceous hyperplasias. Bryden AM. Rabinovitz H et al. Fleming C. Cox N. Arch Dermatol 2005. Brown dots and globules. In: Burns T. 9. Zalaudek I. Zaballos P. 140: 1485–9. Clin Exp Dermatol 2004. 10. 29: 676–7. 2005. Calonje E. Oztas M. 11.7% of cases. Morales A. Puig S. J Eur Acad Dermatol Venereol 2006. Di Stefani A et al. 3.(10) These vessels may extend toward the center but do not usually cross it. 141: 808. 8. ovoid nests.

65 Figure shows the presence of irregular. homogeneous pigmentation in the background (X10).62–7. cells). is the generic term for a variety of chronic conditions characterized by orange/brown pigmentation (due to hemosiderin deposition likened to cayenne pepper). homogeneous pigmentation in the background in a case of a pigmented.62 Characteristic dermoscopic image of PPD (Schamberg´s disease). diffuse. globules. although chronic.64 A more advanced stage of pigmented purpuric dermatosis (Schamberg´s disease) where the red-brownish patches predominate (X10). Pattern composed of irregular. lichenoid dermatosis of Gougerot and Blum. round to oval.63 Another characteristic area in the same patient where we can also find vascular structures (X10). diffuse. with a red-brownish or red-coppery.7 Pigmented purpuric dermatoses Pedro Zaballos Diego PIGMENTED PURPURIC DERMATOSES Pigmented purpuric dermatoses (PPD).  . and patches. round to oval. Figure 7.(1–3) PPD typically occurs on the lower limbs (Figures 7. Gravidity and increased venous pressure are Figure 7. globules. red dots. Figure 7. red dots.68) in a symmetrical distribution and often shows a benign and self-limited.7. and patches. interspersed with fine-point purpura (due to extravasated red blood Figure 7. we can also observe a network of brownish to gray interconnected lines (X10). also called purpura simplex or chronic capillaritis. with a red-brownish or red-coppery. In the image. The etiology of PPD is unknown. purpuric. course.

red dots.(1–3) PPD have traditionally been divided into five clinical entities: progressive. homogeneous pigmentation in the background. and familial forms. red dots.(4–6) The dermoscopic pattern associated with PPD is the presence of irregular. and is characterized by a persistent. and persistent purpura and petechiae with conspicuous pigmentation located predominantly on the lower limbs. globules. homogeneous pigmentation in the background (Figures 7.67 Presence of round to oval. Figure 7. can also correspond histologically to the extravasation of red  . pigmented. quadrantic. red dots. Patients with pigmented. round to oval. linear. important localizing factors in many cases and triggering factors such as drugs. lichen aureus (Figure 7. diffuse.64) is characterized by usually asymptomatic. the lesions tend to be reddish annular macules located on the lower limbs and associated with telangiectases. and patches. globules. transitory. extravasated red blood cells. diffuse. intense itch. lichenoid dermatosis of Gougerot and Blum. under dermoscopic examination. globules. homogeneous pigmentation in the background in a case of Majocchi´s disease (X10).67). In Majocchi´s disease (Figure 7. and patches.62–7.66) or itching purpura has many similarities to Schamberg´s disease but is generally more extensive. develops more rapidly. diffuse.(1–3) All these disorders may show overlapping clinical and histological features. most often on the legs. and patches. with a red-brownish or red-coppery. chemical ingestions. pigmented.68) is a localized variant of PPD that is characterized by the appearance of sudden-onset. homogeneous pigmentation in the background in a case of Eczematoid-like purpura of Doucas and Kapetanakis (X10).62–7. Indeed. There are other more unusual presentations that include the itching purpura of Loewenthal. with a scanty. located commonly on the lower limbs. round to oval. all forms of PPD show similar findings.pigmented purpuric dermatoses Figure 7. which were not blanched by compression. The irregular red dots. In the image we can also observe a network of brownish to gray interconnected lines. infections. red-brownish.65) developed lichenoid papules in addition to purpuric lesions. with a red-brownish or red-coppery. limited lichenoid papules in association with purpuric lesions. diffuse. food additives. red dots and globules and scales. Finally. or underlying hematologic/internal diseases have been described. globules. chronic. Eczematoid-like purpura of Doucas and Kapetanakis (Figure 7. purpuric. Figure 7. and lichen aureus. and hemosiderin-laden macrophages.68 Figure shows the characteristic dermoscopic pattern of PPD (lichen aureus) with irregular.68). granulomatous. purpuric dermatosis or Schamberg´s disease. lichenoid dermatosis of Gougerot and Blum (Figure 7. mainly in the upper part of the lesion (X10). purpura annularis telangiectodes or Majocchi´s disease. (1–3) Schamberg´s disease (Figures 7. and patches.66 Figure shows the presence of round to oval. purpuric. eczematoid-like purpura of Doucas and Kapetanakis. The histopathological correlation of the red-brownish or red-coppery background may be the presence of the dermal infiltrate of lymphocytes and histiocytes. with a red-brownish or red-coppery. and occasionally on the trunk and the face.

Fueyo A. 135: 1366–8. globules. Ferrara G. 33: 252–5. Dermatology 2006. Dermoscopy in general dermatology. J Cutan Med Surg 2008. 4: 138–40. Argenziano G. Dermoscopic semiology: further insights into vascular features by screening a large spectrum of nontumoral skin lesions. Numerous small. Rook´s Textbook of Dermatology. Sehgal VN. Purpura and microvascular occlusion. Morita T et al. Vázquez-López F. some of which are dilated and swollen.65 and 7. Ilknur T. Dermoscopy of pigmented purpuric dermatoses (lichen aureus): a useful tool for clinical diagnosis. Oxford: Blackwell Publishing Ltd. 7. This characteristic pattern of PPD could be useful to distinguish them from other diseases such as angioma serpiginosum and venous stasis dermatitis. Angioma serpiginosum: dermoscopy for diagnosis. 150: 226–31. Angioma serpiginosum with linear distribution: case report and review of the literatura. round to oval red lacunas without the brownish background were determined with dermoscopy in angioma serpiginosum (7–9). Atypical clinical presentation of pigmented purpuric dermatosis. Clin Exp Dermatol 2003. Zalaudek I. Vázquez-López et al. 10.68) can be observed that correlate histopathologically to hemosiderin-laden macrophages (gray dots) and the presence of hyperpigmentation of the basal-cell layer and incontinentia pigmenti in the upper dermis (network-like structure) related to some lichenoid infiltrates. 11. some gray dots and a network of brownish to gray interconnected lines (Figures 7. Nagayama T. Cox N. Pigmented purpuric dermatoses: an overview. Vázquez-López F. Puig S.zaballos blood cells and to the increased number of blood vessels. as we can find a similar pattern in other diseases also. Malvehy J.(13) REFERENCES 1. 13. orange-brown background in two cases of urticaria vasculitis (12) and also described a similar pattern composed of reddish or brownish globules in diffuse brownish areas in some cases of pigmented lichen planus. 142: 1526. Dermoscopy of venous stasis dermatitis. Pathology of the Skin with Clinical Correlations. Dermoscopy of pigmented lichen planus lesions. Fetil E. 6. J Dtsch Dermatol Ges 2006. PérezOliva N. 28: 554–64. Piette WW. Zalaudek I. Arch Dermatol 1999. Angioma serpiginosum: a report of 2 cases identified using epiluminescence microscopy. and the presence of glomerular vessels and a scaly surface is the characteristic pattern of venous stasis dermatitis. Akarsu S et al. Ohnishi T.(10. Sarkar R. Calonje E. 2004.  . 144: 568. Br J Dermatol 2004. 12. 2005. Salsench E. Argenziano G. and patches. Kalisiak MS. In some cases. 11) However. with a red-brownish pigmentation in the background is not solely limited to PPD. Arch Dermatol 2004. found a pattern composed of purpuric or reddish dots and globules in a patchy. 12: 180–3. relatively well-demarcated. Breathnach S. Arch Dermatol 2006. 212: 7–18. Sánchez-Martín J. Maldonado-Seral C. Malvehy J. Di Stefani A et al. 4. J Dermatol 2006. Puig S. Dermoscopy for the screening of common urticaria and urticaria vasculitis. N Pérez-Oliva. 43: 482–8. Giorgio CM. In: McKee PH. Sardana K. Arch Dermatol 2008. Cox NH. 2. Superficial and deep perivascular inflammatory dermatoses. 140(10): 1290–1. Granter SR eds. Brongo S. Griffiths C eds. Haber RM. Marghoob AA. pulsed dye laser for treatment. China: Elsevier Mosby. In: Burns T. 5. Zaballos P. Vázquez-López F. Int J Dermatol 2004. this is not a pathognomonic pattern and the presence of red dots. 3. Kreusch J. López-Escobar M. 9. 8. Zaballos P.

or even Figure 7. annular. We can also observe peripheral vascular structures in some areas (X10). predominantly in sun-exposed sites in middleaged individuals in their third or fourth decade of life. The skin within the ring is usually somewhat atrophic and mildly reddened or hyperpigmented. reddish or brownish in color. the center of the area becomes inflamed. Multiple. Five clinical variants of porokeratosis are recognized: classic porokeratosis of Mibelli. porokeratosis palmaris et plantaris disseminata. and immunosuppression. Several risk factors for the development of porokeratosis have been identified.70 Figure shows a peripheral white-brownish track and a central. The formation of squamous or basal-cell carcinomas has been reported in all forms of porokeratosis. with lots of lesions of up to 10 mm. red-whitish. atrophic. covered by thick hyperkeratosis. keratotic lesions that develop predominantly on the extensor Figure 7. although the degree of premalignant potential is controversial.(1–3) DSAP is the most common presentation. The patophysiology of this disease is due to a clonal hyperproliferation of atypical keratinocytes that leads to the formation of the cornoid lamella. which contains a keratotic plug that expands to a sharp.69 Typical dermoscopic image of actinic porokeratosis with a peripheral “white track” that demarcates a central. a column of parakeratotic cells extending through the stratum corneum. and punctate porokeratosis. these factors include genetic inheritance.  . surfaces of the legs and the arms characterize DSAP. which expands peripherally and forms the raised boundary between abnormal and normal keratinocytes. with dotted vessels. disseminated superficial actinic porokeratosis (DSAP). keratotic ring. slightly raised.71 Figure shows a peripheral white track and a central. and a delicate pigment network (X10). whitish. whitish. red globules. homogeneous area with dotted vessels and scales (X10). DSAP is 3 times as likely to develop in women than in men. The tendency to develop these lesions is inherited as an autosomical dominant. ultraviolet radiation. In a few cases. annular lesions with a distinct keratotic edge corresponding histologically to the presence of the cornoid lamella. homogeneous area. producing a plaque of 10 mm or more.8 Actinic porokeratosis Pedro Zaballos Diego ACTINIC POROKERATOSIS Porokeratosis is a clonal disorder of keratinization clinically characterized by sharply demarcated. linear porokeratosis. Figure 7. The lesion begins as a 1–3 mm conical papule. especially those with sun-sensitive skin. homogeneous area.7.

ulcerated and crusted.73 Figure shows a peripheral white track with different kind of vessels (X10). Liquefactive degeneration of the basal layer of the epithelium is sometimes present and occasionally provokes melanophagia. Therefore. linear-irregular vessels. the epithelium toward the center was acanthotic and because of that we can observe a verrucous surface in the center of the lesion (X10). sparing the palms and the soles. The lesions of DSAP are easily mistaken for actinic keratoses. White track demarcates a central. but they may itch slightly. lymphocytic infiltrate and dilated capillaries.75). with a brownish pigmentation on the inner side and with a double white track in some areas (Figures 7. This single or double white track is characteristic of porokeratosis Figure 7. with which they may coexist. Although nonpathognomonic. HIV infection. superficial porokeratosis after organ transplantation. renal failure. the cornoid lamella is the most histopathologic. we can observe some blue-gray coarse granules. There is a nonactinic form of disseminated. lightwhitish. distinctive feature of the various types of porokeratosis and consists of a thin column of tightly packed parakeratotic cells within a keratin-filled epidermal invagination.69–7. in these cases. The papillary dermis beneath the cornoid lamella contains a moderately dense. Figure 7.72 Another example of actinic porokeratosis with a peripheral white track and a central area with dotted vessels and red globules (X10). Figure 7. or in association with other causes of immunosuppression that may have a generalized distribution of identical lesions.zaballos Figure 7. and corresponds histopathologically to the cornoid lamella. or telangiectasias) (Figures  .75 In this case of actinic porokeratosis. and psoriasis. we can observe brownish pigmentation on the inner side of the white track and a peripheral vascularization.(1–3) Dermoscopically. porokeratosis reveals a whitish annular structure called “white track” located at the periphery of the lesion. They are usually asymptomatic. and.(4–7) The color of this annular structure could be yellowish or light brown in rare cases.74 Figure shows a peripheral white track with a central scaly surface (X10). homogeneous area with different kind of vessels (red dots and globules.

47: 308–10. an intense white homogeneous area or even a verrucous surface (Figures 7. Argenziano G et al. with which they may coexist. Commens CA.(8.75) . Br J Dermatol 2006. Maldonado-Seral C et al. Micantonio T. 97: 77–8. Breathnach S. Dermoscopy for the diagnosis of porokeratosis. linear-wavy vessels surrounding the hair follicles. Dermoscopy of disseminated superficial actinic porokeratosis. Other uncommon structures that we can see in the center of the porokeratosis are delicate pigment network or brown globules. Dermoscopic features of actinic keratosis. uniformly sized. (c) fine. 2004. 207: 151–6.69–7.(10. 212: 7–18.(4–7) The epithelium toward the center may be of normal thickness or even acanthotic and because of this we can observe. 2. Dermatol Surg 1996. Rook´s Textbook of Dermatology.74 and 7. Disseminated superficial actinic porokeratosis: a clinical study. Nino M. Argenziano G. Nagore E. Malvehy J. Krain AD. Giacomel J. Calvieri S. Dermatology 2003. and distributed dotted vessels or red globules. Griffiths C eds. 22: 339–42. Four essential dermoscopic features were observed in nonpigmented actinic keratosis that combined to produce the “strawberry pattern”: (a) erythema. A review. Disseminated superficial actinic porokeratosis diagnosed by dermoscopy. Dermatology 2006. Sasson M. together with a central surface scale. J Eur Acad Dermatol Venereol 2004. Actas Dermosifiliogr 2006. 20: 1015–22. Dermoscopy in general dermatology. Munro CS. J Am Acad Dermatol 1989. 155: 951–6. 11. 11) REFERENCES 1. Zalaudek I. Peris K. Dermoscopic features of plaque psoriasis and lichen planus: new observations. (b) white-to-yellow surface scale. Shumack SP. Rossi M.73) that are more easily observed because of the presence of atrophic epithelium in the center of the porokeratosis. Di Stefani A et al. Dermoscopy of facial nonpigmented actinic keratosis. Cox N. Monitoring the evolution of a localized type of porokeratosis using [dermatoscopy]. The lesions of DSAP are possibly mistaken for actinic keratoses. Zaballos P. 5: 970–6. In: Burns T.actinic porokeratosis 7. Porokeratosis and cutaneous malignancy. Puig S. Fargnoli MC. Int J Dermatol 2008. 9) Although all the actinic keratosis of the study were located on the face. 140(11): 1410. 3. Vázquez-López F. Alfaro A et al. 8. Delfino M. Bruni F. 7. and psoriasis. 4. J Dtsch Dermatol Ges 2007. 9. Argenziano G. 18: 194–5. Malean WHI. Zalaudek I. Curzio M. pink-to-red “pseudonetwork” surrounding the hair follicles. Piccolo D. 10. Oxford: Blackwell Publishing Ltd. 7 . in less common cases. Manjón-Haces JA. Panasiti V. Disorders of keratinization. none of the lesions showed the characteristic peripheral “white track” of DSAP. and (d) hair follicle openings filled with yellowish keratotic plugs and/ or surrounded by a white halo. some of them with a ring-like appearance. Vargas-Laguna E. Judge MR. 5. 6. revealing a marked. Arch Dermatol 2004. The dermoscopic pattern associated with psoriasis is composed of multiple.

and leprosy scars. the papules veer to yellowish and may unite to form tuberous/eruptive xanthomas. histiocytosis X. Diffuse. sometimes tending to orange or blue.(7–8) Tuberous xantoma––These lesions are hard. but they are more commonly encountered in patients with internal diseases.7.(9) Palmar. Figure 7.77). papular plaques with well-defined borders occur  . flat. They manifest as yellowish papules. these patients should undergo analysis of lipid profile. Xanthelasms––These are the most frequent xanthelomatous lesions (Figure 7.76 Solitary rethiculohistiocytoma. foreign body reaction. Dermoscopy reveals branched and linear vessels predominantly at the periphery of the lesion on an orange-yellow background (X10). they may join up to form plaques that need to be removed to avoid ectropion. papules (eruptive xanthomas). tendon xanthomas. slowly evolving nodules. and perioral) and mucosa (pharynx. larynx) associated with diabetes insipidus in 30% of cases. yellowish. Cerebrotendinous Rare autosomal dominant hereditary xanthomatosis disease characterized by xanthelasmas.(3–6) Xanthomization indicates a gradual process of accumulation of lipids in tumoral lesions such as histiocytomas (Figure 7. and sometimes on the lower ones. The disorder is caused by diffuse deposition of cholesterol and cholestanol. knees. a syndrome is involved (Table 7. or tendon infiltrations (tendon xanthomas). and Pietro Rubegni Xanthomatous lesions of the skin manifest as typically yellowish. infiltrative maculopapules in the digital and palmar folds. Eruptive papular xantoma––These are small. They are generally located symmetrically in pressure regions (elbows.(1) Their histology is characterized by accumulation of xanthomatous cells (macrophages) containing lipids responsible for their color.76) or inflammatory sequelae such as lipid necrobiosis. progressive spasticity. Syndrome Necrobiotic xanthoma Clinical symptoms and signs Purplish inflammatory plaques and nodules with a xanthomatous central area (chest and periorbital). yellowish.1 Syndromes Associated with Skin Xanthomas. disseminated xanthoma periorbital. If untreated. Young patients also have mental retardation. macules (flat xanthomas). fortunately rare. striated xanthochromia––This skin disease present with yellowish. Maurizio Biagioli. especially with high cardiovascular risk. usually responsive to fibrates treatment and a diet low in fats and carbohydrates. and high cardiovascular risk. Sometimes they are idiopathic. inflammatory-like papules that erupt on elbows or knees and are sometimes itchy. folds. on the upper eyelids. and tuberous xanthomas. Initially red. erythema elevatum diutinum. cataracts. often surrounded by an erythematous halo. It is a pathognomonic sign of hereditary dysbetalipoproteinemia. normolipidemic xanthomas––These large. usually arranged symmetrically at the internal canthus of the eye. associated with paraproteinemia in 80% of cases. Montgomery Papular xanthomas of the skin (neck. In other cases.9 Xanthomatous lesions Filomena Mandato. Table 7. nodules (tuberous xanthomas). and ankles). may be associated with other hematological disorders but nondyslipidemia.(2) As xanthomatous lesions often indicate the concomitance of secondary or acquired hyperlipidemia.1).

9 .(14) There is always a yellowish background that may veer from pale yellow to orange (sunset color). yellow to orange papule or nodule with clear borders.78 Diffuse. Dermoscopy reveals only yellow background (X10). The dermoscopic pattern is characterized by orange-yellow background with “clouds” of paler yellow deposits. branched and linear vessels running from the periphery to the center of the lesions are present (X10).77 Xanthelasma. They are not associated with dyslipidemia and may be idiopathic. on the face. trunk.79).5 cm) or macro.78).flat.79 Juvenile xanthogranuolma. Moreover. Figure 7. Figure 7. usually on the face or neck (Figure 7.(1–3 cm) nodular. Juvenile xanthogranuloma––This is the most frequent non-Langerhans histiocytosis and consists of hard.76–7. DermoSCopiC aSpeCtS of XanthomatouS leSionS Xanthomatous lesions show similar patterns under the dermoscope (Figure 7. It may be isolated or eruptive and micro.79).(12–13) It is more frequent in children but possible also in adults.Dermoscopic examination shows only pale yellow deposits (X10).xanthomatous lesions Figure 7. and folds (10–11) (Figure 7.normolipidemicxanthomas. neck.2–0. elbows.(0.

Rajshekhar V. Dermatology 2003. Dermatology 2007. 62: 178–9. Pownell PH. Jacob M. Zelger B. George R. For example. and rubegni Most contain randomly disposed linear and branched vessels. Rohrich RJ. Normolipemic papular xanthoma with xanthelasma. 7. Pedraz J. Crook M. 12(3): 19. Necrobiotic xanthogranuloma with cutaneous and cerebral manifestations. (15) A word of warning: during dermoscopic examination. Xanthelasma and cardiovascular risk. Dermoscopy of dermatofibromas: a prospective morphological study of 412 cases. Shinkai K. 11. Callejón JR. were recently observed in reticulohistiocytoma. Plast Reconstr Surg 2002. Fimiani M. 14. Merola JF. Arch Dermatol 2008. Tanzi C. 100: 1111–4. Cavicchini S. Xanthogranulomas associated with hematologic malignancy in adulthood. Kumakiri M.(16–17) Apart from these two features. Papular xanthoma: a clinicopathological study of 10 cases. Miura Y. xanthomas have no other dermoscopic characteristics. Fernández-Herrera J. Breier F. Malvehy J. with histological and ultrastructural studies of skin lesions. 59: 46–50. 59: 488–93. Soldano A. Dermoscopy of solitary yellow lesions in adults. 110: 1310–4. J Cutan Pathol 2002. Zelger BW. Int J Clin Pract 2008. De Schaetzen V. Fox LP. Fimiani M. Report of a case. Neurologia 2008. 29: 200–6. 206: 165–8. corresponding to hyperplastic epidermis with basal hyperpigmentation. Alonso G. 2. Papular xanthoma associated with angiokeratoma of Fordyce: considerations on the nosography of this rare non-Langerhans cell histiocytoxanthomatosis. The same authors also proposed dermoscopic analysis of a xanthomized dermofibroma revealing peripheral delicate pigment network that is usually seen in typical dermatofibromas. McCalmont TH. Gschnait F. 16. 10. De La Brassinne M. Puig S. 218: 380. 5. Satter EK. 15. Reiter H. 3. Dermoscopic appearance of juvenile xanthogranuloma. J Neurosurg 2004. Juvenile Xanthogranuloma: dermoscopic pattern. Semin Cutan Med Surg 2007. 14: 10. J Am Acad Dermatol 1981. undue pressure of the dermoscope on the skin may limit blood flow to the lesion and prevent observation of the vascular component. though some lesions may show other details. Rubegni P. Shoo BA.  . Singla A. detected by the pathology lab. Richert B. Llambrich A. Dermatol Online J 2008. Palmer A. biagioli. Cerebrotendinous xanthomatosis. 26: 108–13. Xanthomatous papule in a child. 9. 8. Gendernalik SB. Dermatol Online J 2006. 144: 75–83. Shah KC. J Am Acad Dermatol 2008. paper in press. Rubegni P. Eruptive xanthomas. Necrobiotic xanthogranuloma. brownish globules and dots of hemosiderin. 13. 23: 530–1. Clin Exp Dermatol. Cavicchini S. Romero JO. Zaballos P. Alessi E. Mourmouras V. 18. Xanthoma disseminatum. 215: 256–9. Rosenman K. 4. 12. Poonnoose SI. 6. 60: 841–8. Caputo R. Passoni E. Rev Med Liege 2004.(18) referenCeS 1. Tourlaki A. Mengden SJ. Miracco C. 17. Arch Dermatol 2008. Sudoh M. Les xanthomes. 144: 1412. Case report and review of the literature. Mandato F. Galeckas KJ. J Am Acad Dermatol 2008. Dermatology 2008.mandato. 4: 291–9. Xanthelasma palpebrarum: a review and current management principles. Janis JE. Diffuse xanthogranulomatous dermatitis and systemic Langerhans cell histiocytosis: a novel case that demonstrates bridging between the non-Langerhans cell histiocytosis and Langerhans cell histiocytosis. Bowling J. Mandato F.

(A) (B) Figure 8. Imaging shows dramatic visual improvements in skin textural properties. Color. using the oatmealcontaining skin-protectant lotion (100x) (from reference 2.(1) (B) Dermatoscopy can be a great visual help in monitoring skin changes during treatment. before (A) and after 14 days’ treatment (B) with oatmeal-containing moisturizer. and magnification standards should be recorded to assure precision and reproducibility of measurements. (J&JCCI). by permission of Johnson & Johnson Consumer Companies. lighting. Inc. Accuracy and reproducibility in positioning of skin sites over time can be achieved through (A) Figure 8.8 Dermatoscopy in cosmetic applications Warren Wallo documentation of skin landmarks.2 (Continued)  . resolution.1 Xerotic skin on the lower leg. J.Nebus). including dryness and flaking after 2 weeks.

as well as visible improvements in skin textural lines as early as Day 1. (B. in two patients (A-C and D-F). F) Day 14. Smith).2 Dermatoscopy is valuable when studying moisturization in skin of color: (A. by permission of J&JCCI. and (C. Images show visible improvements in the appearance of skin ash and scale in skin of color patients. There was continued visible improvement in skin ash at Day 14 (20x) (from reference 3.wallo (C) (D) (E) (F) Figure 8. G. E) Day 1.  . D) baseline.

by permission of J&JCCI. the presence of fine scaliness (ash) and flakes is more apparent because of its contrast with darker skin.(3) (Figures 8.1) In skin of color.(2) (Figure 8. (from reference 5. Smith) Xerosis anD ashy skin In dry skin (xerosis).2 and 8. and the growth of hairs can be a compelling indication of the reproducibility of this technique (20x). PIH is  . the corneocytes are disorderly arranged and their borders project above the surface. The exact same hair follicles can also be located.3) Postinflammatory HyPerPigmentation (PiH) Skin inflammation alters the activity of melanocytes and may lead to pigmented macules and patches lasting long after the inflammation is gone (postinflammatory hyperpigmentation). 14 days). the skin appears smoother and the white flakes disappear. D.3 The appearance of ashy skin (A. After moisturization. This technique can be used to view at high magnification the improvement in skin dryness. C. producing a visually dull appearance. By using the dermatoscope in cross-polarization. The presence of a hypopigmented mark can be useful in locating the exact positioning for subsequent imaging. we enhance the visualization of the lifted coenocytes’ edges and skin flakes. Because melanosomes in dark skin can produce large quantities of melanin.(1) Clinical studies have used digital dermatoscopy to monitor the improvement of ashy skin in darker skin types after applications of an oatmeal-containing moisturizer. 1 day. 7 days. G. which will appear white. baseline) was greatly improved after treatment with a regimen consisting of twice daily topical application of an oatmeal-containing moisturizer and an exfoliating scrub containing oatmeal used on a weekly basis by an African-American female (B. Dermatoglyphics and dryness were visibly less apparent as early as Day 1 and continued to improved at Day 14.videodermatoscopy in cosmetic applications (A) (B) (C) (D) Figure 8.

The value of dermatoscopy is clearly demonstrated for assessing changes in pigmentation and documenting changes over time and with treatment (Captured at 12x / further cropped and enlarged for publication by 5x (therefore overall mag 60x)) (from reference 5.(5) (Figure 8. in cross-polarization mode. The cause of PFB is usually the penetration of shaved hair into adjacent skin. especially with acne and pseudofolliculitis barbae (PFB). and (C) 8 weeks. G. PIH marks. by permission of J&JCCI.wallo (A) (B) (C) Figure 8.(7)  . as seen in this patient.4 Documenting postinflammatory hyperpigmentation (PIH) over time with dermatoscopy: (A) baseline. With careful attention to detail. (6) The outcome is often the formation of an inflammatory papule at the site of the in-grown hair. and it is the cause of significant complaints by patients. Smith). most prevalent in darker skin types. (B) 4 weeks. were followed over time. Dermatoscopy in cross-polarization mode is extremely helpful in identifying the extrafollicular skin penetration of hair and in treatment follow-up.4) PseuDofolliculitis BarBae (PfB) PFB is an inflammatory condition frequently affecting people of darker skin color with tightly coiled hair. can be used to beautifully document the changes in melanin pigmentation over time and with treatment.5) Dermatoscopy has also been used in the clinical practice to show patients the in-growing of hair corresponding to individual papules and to enhance compliance in treatment. on the lower legs of African-American females.(5) (Figure 8. followed by postinflammatory hyperpigmentation.(4) Dermatoscopy.

Dermatoscopy was used to illustrate (A) (20X) normal skin. tricHostasis Trichostasis spinulosa is a follicular condition in which pores retain fascicles of hair embedded in sebaceous material. This is more prominent on the centrofacial region of adult and older individuals and appears as dark pores.5 Dermatoscopy of facial acne on African-American males with pseudofolliculitis barbae (PFB). patients are often concerned with the appearance and evolution of individual papules and pustules. In mild acne. conclusion Dermatoscopy represents an extremely valuable tool to monitor skin conditions under magnification and standardized lighting settings. clogged follicles and the surrounding skin color. Several studies have used digital dermatoscopy to demonstrate the efficacy of topical formulations to quickly improve papules and pustules in acne. Furthermore. (C) (100X) site of recurring PFB. therefore. The ability to accurately capture images of individual lesions is. videodermatoscopy and epiluminescence have been used to investigate the removal of trichostatic impactions with the use of pore strips.(10) (Figure 8.(8) Owing to the clear contrast between the dark-brown. J.(9) acne lesions Acne consists of noninflammatory (comedones) and inflammatory lesions (papules. Woodruff). by permission of J&JCCI. The ability of epiluminescence to visualize subsurface pigment has enabled researchers to detect details not appreciated by the naked eye. pustules. and (D) (100X) PFB lesion with extrafollicular penetration (from reference 5. including (B) (20X) cheek area with skin dryness around follicle.videodermatoscopy in cosmetic applications (A) (B) (C) (D) Figure 8.  . and various examples of the spectrum of PFB symptoms. and nodules). digitization of images has allowed the archiving of images and dramatically helped dermatologists in the monitoring of lesions and skin treatments.6). They often purchase acne-spot treatments to selectively target those lesions. important to study their evolution with treatment.

Kurtz E. Nebus JA. Epiluminescence dermatoscopy enhanced patient compliance and achieved treatment success in pseudofolliculitis barbae.  . Washington. (B) 8 hours. Luedtke M. Chantalat J. Smith G. J Am Acad Dermatol 2006. 4. Poster presented at: 62nd AAD Meeting. el Gammal S. 8. Woodruff J. Kligman AM. Wallo W. Nebus J. DC. Wu J. Acne target lesions can be followed using dermatoscopy. D. Micro-imaging of skin with innovating methodology: Valuable for Skin of color. Kurtz ES. Kurtz ES. February 6–11. J Dermatol Treat 1999. ashen skin in patients with skin of color. Natural considerations for skin of color. skin protectant lotion. by permission of J&JCCI. references 1. J Am Acad Dermatol 2006. Poster presented at: 62nd AAD Meeting. extra dry skin with an oatmeal. 168: 561–4. Wallo W. Cutis 2006. DC. Miller). 2004: P278. 47: 60–2. Wallo W. offering the opportunity to observe and measure changes in size and redness over time (12X) (from reference 10. Pseudofolliculitis barbae: review and update on new treatment modalities.6 Dermatoscopy of a target acne lesion before and after treatment with a 2% salicylic acid product: (A) baseline. Stoudemayer T. Chuh A. Efficacy and safety of a cosmetic pore-cleansing strip (Biore’). Smith G. Pagnoni A. 7. Determination of density of follicles on various regions of the face by cyanoacrylate biopsy: correlation with sebum output. J Am Acad Dermatol 2005. Miller D. Rodriguez D. Kurtz E. Alleviating dry.wallo (A) (B) Baseline (C) 8 hours 24 hours Figure 8. 54: AB18. and (C) 24 hours. Kurtz ES. Documentation of cutaneous conditions important in skin of color with innovative imaging approaches. 6. Extraction of follicular horny impactions of the face by polymers. Baumann L. 5. Australas J Dermatol 2006. 10. February 6–11. 52: 89. Alleviating itchy. Fast-acting treatment of mild to moderate acne lesions by a novel 2% salicylic acid microgel complex. 131: 862–5. 10: 47–52. 78: 2–19. Coret C. Br J Dermatol 1994. 54: AB53. Washington. Zawar V. Garcia-Zuazaga J. Wallo W. 2004: P294. 3. Taylor SC. Mil Med 2003. Pagnoni A. 2. Stoudemayer T. Kligman AM. 9. Smith G.

disorders of 100–2 common urticaria (CU) 96. 17–18 crotamiton 21 crusted scabies see Norwegian scabies cyclosporine 54 data storage 4 dermatological digital image management. instruments for 5 digital videodermoscopy 2–3 dimethicone 21 discoid lupus erythematosus (DLE) 38–9. normolipidemic xanthomas 118–19 digital dermoscopy analysis. videodermatoscopy in 121–2. 102  . 83 detection of 84 brittle nails 47 butter/margarine/mayonnaise 22 capillaroscopy 103 carbaryl 21 chronic capillaritis 112 cicatricial alopecias 37 citronella 22 clear cell acanthoma (CCA) definition 70 dermoscopic features of 71 diagnosis of 70 videodermatoscopy of 72 collagen tissues. 40 dystrophic hair 34–5 yellow dots 33–4 alopecia areata incognita dystrophic hairs 36 short regrowing hairs 35–6 yellow dots 35 amelanotic melanoma 88 analogue videodermoscopy 2 androgenetic alopecia (AGA) 43 hair diameter diversity 32–3 peripilar signs 33 secondary signs 33 angiogenesis and psoriasis 52 anogenital warts 73 ashy skin 123 Auspitz sign 58 balanitis 64 benzyl alcohol 21 benzyl benzoate 21 Bowen’s disease dermoscopic features of 82. 97–8. 77 warts 49 Dermo-Image 4 dermoscopy see dermatoscopy diffuse.Index Page references in italics refer to tables. 2 alopecia 40–2 scabies 12–13 alopecia areata see alopecia areata alopecia areata incognita see alopecia areata incognita androgenetic alopecia (AGA) 32–3 cicatricial alopecias 37 congenital triangular alopecia 37 discoid lupus erythematosus (DLE) 39 folliculitis decalvans (FD) 40 lichen planopilaris (LPP) 37–8 trichotilomania 37 xanthomatous lesions 119–20 pyogenic granuloma 48–9 tungiasis 29–30 venular malformations 75–6. flat. database software for 4 dermatomyositis 47 dermatoscopy 1. 99 congenital triangular alopecia 37 contact incident light dermoscope 3–4 cosmetic applications. acetic acid 22 acne lesions 125 actinic keratosis 117 actinic porokeratosis 115–17 albendazole 22–3 alopecia areata 33–5. 126 acne lesions 125 postinflammatory hyperpigmentation (PIH) 123–4 pseudofolliculitis Barbae (PFB) 124 trichostasis spinulosa 125 xerosis and ashy skin 123 cotrimoxazole 23 crab lice 9.

50 Mirror Software 4 molluscipox virus 106 molluscum bodies 106–7. 108 molluscum contagiosum (MC) 106–8 clinical diagnosis of 107 epidermal hyperplasia 106–7 molluscum contagiosum virus (MCV) 106 Muir–Torre syndrome 109 nail bed melanoma 50 nail disease 45 brittle nails 47 dermoscopic examination 45 dermoscopy of hyponychium 45 distal edge of the nail plate.index disseminated superficial actinic porokeratosis (DSAP) 115–16. 50. 11. 51 melanonychia 49 distal edge of the nail plate dermoscopy 50 hyponychium and proximal nail-fold dermoscopy 50 intraoperative dermoscopy 52 melanocyte activation 49 melanocytic hyperplasia 49–50 nail plate dermoscopy of 50 Micro-Hutchinson’s sign 45. 25 epimeres 25 epulis gravidorum 86 eruptive papular xantoma 118 erythematotelangiectatic rosacea 103. 117 distal subungual onychomycosis (DSO) 47 epidermal hyperplasia 52 epiluminescence microscopy 1. 16 differential diagnosis 9 epidemiology 8 pathogenesis 8 videodermatoscopy 16–17 hemangiomas 88 Henderson–Paterson bodies 106–7. 23 juvenile xanthogranuloma 119 kerosene/gasoline/petroleum distillates 22 lacunas 88 levamisole 23 lichen aureus 113 lichen planopilaris (LPP) 37–8 lichen planus annular lichen ruber planus 92 definition 90 evolved LP lesions 92 hypertrophic lichen planus 92 initial LP lesions 90–1 mature LP lseions 91–2 postinflammatory hyperpigmentation of LP 93–5 lindane 21–2 lobular capillary hemangioma 86 Majocchi’s disease 113 malathion 22 melanocyte activation 50 melanocytic hyperplasia 49. dermoscopy of 45 intraoperative dermoscopy 45–6 melanonychia 49–51 nail plate dermoscopy 45 nail tumors 48 glomus tumor 49 onychomatrichoma 48 onychopapilloma 48  . 108 human papillomaviruses (HPV) 73–4 definition 73 differential diagnosis Fordyce spots 74 pearly papules 73–4 hypomelanotic melanoma 88 hyponychium dermoscopy 45. 46 Imagestore for Healthcare 4 indomethacin 23 infantile scabies 8 ivermectin 21. 104 folliculitis decalvans (FD) 39–40 frontal fibrosing alopecia 41 glomus tumor 49 hair loss alopecia areata 33–5 alopecia areata incognita 35–6 androgenetic alopecia (AGA) 32–3 congenital triangular alopecia 37 dermoscopy in the differential diagnosis of alopecia 40–3 discoid lupus erythematosus (dle) 38–9 folliculitis decalvans (fd) 39–40 lichen planopilaris (lpp) 37–8 normal scalp 31–2 scarring alopecia 37 therapeutic monitoring of hair loss with videodermatoscopy 43 trichotilomania 36–7 head lice clinical features 8 diagnosis of 9.

89 clinical diagnosis of 86 dermoscopy in recognition of 86–7 with vascular structures 87–8 pyrethrins 22 Raynaud’s phenomenon (RP) 100 rosacea 103–5 symptoms of 104 videocapillaroscopic technique and 103 Sarcoptes scabiei 7. 25 scabies 7 biologic cycle 7 clinical features 7–8 dermoscopic diagnosis of 12 diagnosis 8 differential diagnosis 8 epidemiology 7 therapeutic monitoring with videodermatoscopy 26–8 transmission 7 videodermatoscopy and 11–14  . 57 histopathological correlations of 57–60 palmoplantar 61–3 psoriatic balanitis 64–6 scalp 67–8 therapy monitoring 53–5 vascular patterns in 53 videocapillaroscopy in 52 videodermatoscopy in 52–3 see also plaque psoriasis psoriatic balanitis 64–6 Pthirus pubis 9 pubic lice 18. 94–5 phases of 57–8 stages of clinical polymorphism 58–60 early steady-state phase 58 initial phase 58 intermediate phase 58 late steady-state phase 59 phase of resolution 59–60 porokeratosis clinical variants of 115–16 dermoscopic features of 116 risk factors of 115 postinflammatory hyperpigmentation (PIH) 123–4 proximal nail-fold dermoscopy 45. 16 peno-vulvoscopy 73. 46 proximal subungual onychomycosis (PSO) 47 pseudofolliculitis barbae (PFB) 124 psoriasis 46 angiogenesis and 52 definition 52. 25 purpura simplex 112 pyogenic granuloma 48–9. 74 perifollicular erythema 37 permethrin 22 petrolatum (petroleum jelly) 22 phototricogram 43 Phthirus pubis 17 pigmented purpuric dermatoses (PPD) 112–14 clinical entities of 113 dermoscopic examination of 113–14 occurrence of 112 plaque psoriasis 53.index pyogenic granuloma 48–9 warts 49 onychomycosis 47 proximal nail fold dermoscopy 45 psoriasis 46 subungual hemathoma 47–8 nail matrix melanoma 49 nail matrix nevi 49 nail matrix psoriasis 46 nail plate dermoscopy 45 brittle nails and 47 glomus tumor and 49 onychomatrichoma and 48 onychomycosis and 47 onychopapilloma and 48 psoriasis and 46 subungual hematomas and 48 nail tumors 48 glomus tumor 49 onychomatrichoma 48 onychopapilloma 48 pyogenic granuloma 48–9 warts 49 National Rosacea Society Expert Committee 103 nits 9. striated xanthochromia 118 palmoplantar psoriasis 61–3 pediculosis crab lice 9 head lice 8–9 therapeutic monitoring with videodermatoscopy 25–6 videodermatoscopy 16–18 pediculosis capitis see head lice pediculosis pubis infestation see crab lice Pediculus humanus capitis 8. 67. 16 nonpsoriatic balanitis 66 Norwegian scabies 8 onychomatrichoma 48 onychomycosis 47 onychopapilloma 48 optical dermoscope 2 oral ivermectin 23 palmar.

92. 91.index scalp atrophy 39 scalp pruritus 9 scalp psoriasis 67–8 scarring alopecia 37 Schamberg’s disease 113 scleroderma 47 scleroderma pattern (SP) 100–1 scraping versus high magnification videodermatoscopy (VD) 11–12 sebaceous hyperplasia appearance of 109 dermoscopic features of 110 diagnosing 109–10 vascular structures 110–11 seborrheic dermatitis 9. 20 analogue 2 clear cell acanthoma (CCA) 72 contact. 77. 95 xanthelasms 118 xanthomatous lesions 118–20 xanthomization 118 xerosis 123  . 53. 80 videodermoscopy see videodermatoscopy white superficial onychomycosis (WSO) 47 Wickham striae 90. 103. 101 tea tree oil 22 teledermatology 1. 16. types of 97–8 lesions of 99 vascular endothelial growth factor (VEGF) 52 venular malformations 75–80 clinical data and therapy of 78 definition 75 dermoscopic data and therapy of 78–80 dermoscopy of 75–6. 14. 55 topical corticosteroids 22 Tricho-scan 5 trichostasis spinulosa 125 trichotilomania 36–7 tuberous xantoma 118 tunga penetrans 29 tungiasis 29–30 urticaria 96 urticarial vasculitis (UV) 96 dermoscopic purpuric structures. 67. 68. 80 histological data and therapy of 78 vessels in 76–7 videocapillaroscopy collagen tissues and 100 in psoriasis 52–3 scalp psoriasis and 67 videodermatoscopy (VD) 1. 2. 105 softwares for assessment and diagnosis 4–5 subacute lupus erythematosus 102 subungual hematomas 47–8 sulfur 22 systemic lupus erythematosus (SLE) 47 systemic sclerosis (SSc) 100. 104. 13 therapeutic monitoring of parasitoses with videodermatoscopy scabies 25–6 pediculosis 26–8 therapy of scabies and pediculosis 20 alternative unproven remedies 22 natural products 22 nit combs 20 pediculosis 20 scabies 20 systemic treatment 22–3 topical treatment 21–2 TNF-α 52. noncontact and polarized 3–4 cosmetic applications 121–6 digital 2–3 palmoplantar psoriasis 61–3 pediculosis and 16–18 pediculosis capitis 16–17 phthiriasis pubis 17–18 psoriasis 52–3 psoriatic balanitis 64–5 scabies 8 therapeutic monitoring of hair loss with 43 venular malformations 76–7.

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beyond the usual indication of cutaneous pigmented lesions. UK 52 Vanderbilt Avenue. USA www. MD. is Researcher at the Department of Dermatology. is Professor and Chairman at the Department of Dermatology.Dermatology About the book Dermatoscopy has increasingly been taken up in dermatology practice as a non-invasive technique for the differential diagnosis of pigmented skin lesions. Italy Telephone House. There is also the technique of videodermatoscopy – employing the use of digital systems that ensure high magnifications – in addition to the dermatoscopy that conventionally refers to manual devices. MD. However. and monitoring response to treatment. Catania.com . 69-77 Paul Street.informahealthcare. NY 10017. Italy Francesco Lacarrubba. This will serve as an important yet relatively simple aid to a dermatologist’s daily office practice. New York. there are further uses for dermatoscopy in several dermatologic conditions in terms of diagnosis. Catania. prognostic evaluation. Contents Introduction * Equipment * Scabies and Pediculosis: Biologic Cycle and Diagnosis * Videodermatoscopy and Scabies * Videodermatoscopy and Pediculosis * Therapy of Scabies and Pediculosis: Potential and Pitfalls * Therapeutic Monitoring of Parasitoses with Videodermatoscopy * Tungiasis * Hair Loss * Nail Diseases * Psoriasis: Vascular Pattern under Videodermatoscopy Observation * Psoriasis: Histopathological Correlations * Palmo-plantar Psoriasis * Psoriatic Balanitis * Scalp Psoriasis * Clear Cell Acanthoma * HPV Infections * Venular Malformations (Port Wine Stain Type) * Bowen’s Disease * Pyogenic Granuloma * Lichen Ruber Planus * Urticaria and Urticarial Vasculitis * Disorders of Collagen Tissues * Rosacea * Molluscum Contagiosum * Sebaceous Hyperplasia * Pigmented Purpuric Dermatoses * Actinic Porokeratosis * Xantomatous Lesions * Dermatoscopy in Cosmetic Applications About the editors Giuseppe Micali. London EC2A 4LQ. AOU Policlinico-Vittorio Emanuele. AOU Policlinico-Vittorio Emanuele. This book aims to advance knowledge of these extended clinical applications for enhanced visualization and digital imaging using manual dermatoscopy or videodermatoscopy.

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