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Acne Scars
Classification and Treatment

Edited by
Antonella Tosti
Maria Pia De Padova
Kenneth R Beer
Acne Scars
 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: Classification 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
Acne Scars
Classification and Treatment

Edited by

Antonella Tosti, MD
Department of Dermatology
University of Bologna
Bologna
Italy

Maria Pia De Padova, MD

Department of Dermatology
Nigrisoli Private Hospital
Bologna
Italy

Kenneth R Beer, MD
Palm Beach Esthetic Center
West Palm Beach, Florida
USA
© 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 Office: 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: 9781841846873
Orders
Informa Healthcare
Sheepen Place
Colchester
Essex CO3 3LP
UK
Telephone: +44 (0)20 7017 5540
Email: [email protected]

Typeset by C&M Digitals (P) Ltd, Chennai, India

Printed and bound in Great Britain by MPG Books Ltd, Bodmin, Cornwall, UK
Contents

List of Contributors vii

1 Classification of acne scars: A review with clinical and ultrasound correlation 1

Giuseppe Micali, Lidia Francesconi, Beatrice Nardone, and Francesco Lacarrubba

2 Pathophysiology of acne scars 8

Stefano Veraldi and Mauro Barbareschi

3 Hypertrophic and keloidal scars 11

Maria Miteva and Paolo Romanelli

4 Topical therapy for acne scarring 20

James Q Del Rosso and Grace K Kim

5 Superficial peeling 27
Maria Pia De Padova and Antonella Tosti

6 Medium depth and deep peeling 34

Marina Landau

7 Dermabrasion for acne scars 42

Christopher B Harmon and Jens J Thiele

8 Fillers and fat transfer for treatment of acne scarring 49

Timothy Corcoran Flynn and Derek Jones

9 Needling 57
Gabriella Fabbrocini, Nunzio Fardella, and Ambra Monfrecola

10 Fractional photothermolysis for acne scars 67

Kenneth R Beer

11 Nonablative and ablative devices for the treatment of acne scars 72

Vic A Narurkar

12 Surgical techniques: Excision, grafting, punch techniques and subcision 76

Megan Pirigyi and Murad Alam

13 Camouflage: Clinical importance of corrective cover cosmetic (Camouflage)

and quality-of-life outcome in the management of patients with acne scarring
and/or post-inflammatory hyperpigmentation 87
Aurora Tedeschi and Lee E West


 contents
14 Acne scars in Asian patients 90
Evangeline B Handog, Ma Juliet E Macarayo, and Ma Teresita G Gabriel

15 Acne scarring and patients of African descent 98

Ravneet R Kaur, Saba M Ali, and Amy J McMichael

16 Treatment algorithm for acne scars 110

†
Daniele Innocenzi and Ilaria Proietti

Index 127


List of contributors

Murad Alam Timothy Corcoran Flynn

Department of Dermatology Cary Skin Center
Northwestern University Cary, North Carolina
Chicago, Illinois, USA and Department of Dermatology
University of North Carolina
Saba M Ali Chapel Hill, North Carolina, USA
Department of Dermatology
Wake Forest University School of Medicine Lidia Francesconi
Winston-Salem, North Carolina, USA Dermatology Clinic
University of Catania
Mauro Barbareschi Catania, Italy
Institute of Dermatological Sciences, University of
Milan Ma Teresita G Gabriel
IRCCS Foundation Research Institute for Tropical Medicine
and Ospedale Maggiore Policlinico, Mangiagalli and Department of Health
Regina Elena Metro Manila, Philippines
Milan, Italy
Evangeline B Handog
Kenneth R Beer Research Institute for Tropical Medicine
Palm Beach Esthetic Center Department of Health
West Palm Beach, Florida, USA and Department of Dermatology
Asian Hospital and Medical Center
James Q Del Rosso Metro Manila, Philippines
Mohave Skin & Cancer Clinics
Las Vegas, Nevada USA Christopher B Harmon
Valley Hospital Medical Center Surgical Dermatology Group
Las Vegas, Nevada USA Birmingham, Alabama, USA

Maria Pia De Padova Daniele Innocenzi

†

Department of Dermatology Department of Dermatology

Nigrisoli Private Hospital University of Rome I
Bologna, Italy Rome, Italy

Gabriella Fabbrocini Ravneet R Kaur

Department of Dermatology Department of Dermatology
University of Naples Wake Forest University School of Medicine
Naples, Italy Winston-Salem, North Carolina, USA

Nunzio Fardella Grace K Kim

Department of Dermatology Mohave Skin & Cancer Clinics
University of Naples Las Vegas, Nevada USA
Naples, Italy


 list of contributors
Francesco Lacarrubba Megan Pirigyi
Dermatology Clinic Department of Dermatology
University of Catania Northwestern University
Catania, Italy Chicago, Illinois, USA

Marina Landau Ilaria Proietti

Department of Dermatology Department of Dermatology
Wolfson Medical Center University of Rome I
Holon, Israel Rome, Italy

Ma Juliet E Macarayo Paolo Romanelli

Angeles University Foundation Medical Center Department of Dermatology and Cutaneous Surgery
Angeles City, Pampanga, Philippines University of Miami Miller School of Medicine
Miami, Florida, USA
Amy J McMichael
Department of Dermatology Aurora Tedeschi
Wake Forest University School of Medicine Department of Dermatology
Winston-Salem, North Carolina, USA University of Catania
Catania
Giuseppe Micali Italy
Dermatology Clinic
University of Catania Jens J Thiele
Catania, Italy Dermatology Specialists, Inc.
Oceanside, California, USA
Maria Miteva
Department of Dermatology and Cutaneous Suurgery Antonella Tosti
University of Miami Miller School of Medicine Department of Dermatology
Miami, Florida, USA University of Bologna
Bologna, Italy
Ambra Monfrecola
Department of Dermatology Stefano Veraldi
University of Naples Institute of Dermatological Sciences
Naples, Italy University of Milan
and IRCCS Foundation
Beatrice Nardone Ospedale Maggiore Policlinico,
Dermatology Clinic Mangiagalli and Regina Elena
University of Catania Milan, Italy
Catania, Italy
Lee E West
Vic A Narurkar Pharmacy Department
Bay Area Laser Institute Northwestern Memorial Hospital
and California Pacific Medical Center Chicago
San Francisco, California and
and Department of Dermatology Department of Dermatology
University of California at Davis School of Medicine Northwestern University
Davis, California, USA Chicago, Illinois, USA


1 Classification of acne scars: A review with clinical
and ultrasound correlation
Giuseppe Micali, Lidia Francesconi, Beatrice Nardone, and Francesco Lacarrubba

introduction Other clinical entities included in this classification are hyper-

Scar is defined as ‘‘the fibrous tissue that replaces normal trophic scars, keloidal scars, and sinus tracts.(8) Both hypertro-
tissue destroyed by injury or disease’’.(1) Causes of acne scar phic and keloidal scars result from an abnormal excessive tissue
formation can be broadly categorized as either the result repair: clinically, hypertrophic scars are raised within the lim-
of increased tissue formation or, more commonly, loss or its of primary excision, whereas keloidal scars transgress this
damage of local tissue.(2) boundary and may show prolonged and continuous growth.
Clinical manifestations of acne scars as well as severity of (9) Sinus tracts may appear as grouped open comedones his-
scarring are generally related to the degree of inflammatory tologically showing a number of interconnecting keratinized
reaction, to tissue damage, and to time lapsed since the onset channels.(7)
of tissue inflammation.(3, 4) There have been attempts to Another classification is that proposed by Kadunc et al.(3)
classify acne scars in order to standardize severity assess- Based on clinical appearance and relationship to surrounding
ments and treatment modalities.(3, 4) However, consensus skin, acne scars are classified in this system as elevated, dystro-
concerning acne scar nomenclature and classification is still phic, or depressed. Other parameters include shape, consis-
lacking.(3) tency, colour, and distensibility. This classification system may
also serve to assess the efficacy of various therapeutic options
based on acne scars types.(3) Kadunc’s classification is sum-
clinical classifications marized in Table 1.1.
In 1987 Ellis et al. proposed an acne scar classification system Goodman et al. proposed a qualitative grading system that
and utilized the descriptive terms ice pick, crater, undulation, differentiates four grades according to scar severity (Table
tunnel, shallow-type, and hypertrophic scars.(5) Langdon, in 1.2): Grade I corresponds to macular involvement (includ-
1999, distinguished three types of acne scars: Type 1, shallow ing erythematous, hyperpigmented, or hypopigmented scars),
scars that are small in diameter; Type 2, ice pick scars; and Type whereas Grades II, III, and IV correspond to mild, moderate,
3, distensible scars.(6) Lately, Goodman et al. proposed that and severe atrophic and hypertrophic lesions, respectively. (10)
atrophic acne scars may be divided into superficial macular, Interestingly, the authors consider lesion severity also accord-
deeper dermal, perifollicular scarring, and fat atrophy based on ing to visibility at a social distance (> 50 cm). Moreover, since
pathophysiologic features.(7) patients may present various types of acne scars at numer-
One classification system frequently used in clinical prac- ous anatomic sites (i.e., one cheek, the neck, the chest, and so
tice for acne scars is based on both clinical and histological on; these single areas are defined by the authors as “cosmetic
features.(8) Acne scars are classified into three basic types units”), scars are further subdivided into four grades of sever-
depending on width, depth, and 3-dimensional architecture: ity by anatomic sites involved, and the localized disease (up to
three involved areas) is classified as A (focal, 1 cosmetic unit
•• Icepick scars: narrow (diameter < 2 mm), deep, sharply involvement) or B (discrete, 2–3 cosmetic units), whereas the
marginated and depressed tracks that extend vertically to involvement of more cosmetic units is classified as generalized
the deep dermis or subcutaneous tissue. disease, previously described in Table 1.2.
•• Boxcar scars: round to oval depressions with sharply The same authors subsequently, suggested a quantita-
demarcated vertical edges. They are wider at the sur- tive numeric grading system based on lesion counting (1–10,
face than icepick scars and do not taper to a point at 11–20, >20), scar type (atrophic, macular, boxcar, hypertrophic,
the base. These scars may be shallow (0.1–0.5 mm) or keloidal), and severity (mild, moderate, severe). Final scoring
deep (≥ 0.5 mm) and the diameter may vary from 1.5 depends on the addition of points assigned to each respective
to 4.0 mm. category and reflects disease severity, ranging from a minimum
•• Rolling scars: occur from dermal tethering of other- of 0 to a maximum of 84 (Table 1.3).(11)
wise relatively normal-appearing skin and are usually Finally, Dreno et al. first proposed the ECLA scale (echelle
wider than 4 to 5 mm in diameter. An abnormal fibrous d’evaluation clinique des lesions d’acne) (12), followed by
anchoring of the dermis to the subcutis leads to superfi- the ECCA grading scale (echelle d’evaluation clinique des
cial shadowing and to a rolling or undulating appearance cicatrices d’acne) (4). According to this scoring system,
of the overlying skin. morphological aspects of lesions define the type of scars as


 acne scars
Table 1.1 Kadunc’s morphologic classification of acne scars.

Scars Types Clinical Description

1. Elevated
1a. Hypertrophic Hypertrophic lesions raised above the skin surface and limited to the original injured area
1b. Keloidal Usually found in patients with genetic predisposition; their dimensions exceed the initial injured tissue
1c. Papular Soft elevations, like anetodermas, frequently observed on the trunk and chin area
1d. Bridges Fibrous strings over healthy skin
2. Dystrophic Irregular or star-like scar shapes with a white and atrophic floor
3. Depressed
3a.1. Distensible retractions Scars attached only by their central area after skin distension
3a.2. Distensible undulations (valleys) Lesion that do not completely disappear after skin distension
3b.1. Nondistensible superficial Shallow, dish-like defects
3b.2. Nondistensible medium Crater like, with a scar base that is relatively smooth and has normal color and texture and wide diameter
3b.3. Nondistensible deep Narrow and fibrotic scars, ice-pick or pitted scars with sharp shoulders perpendicular to the skin
surface that may appear as epithelial invaginations sometimes reaching the subcutaneous layer
3b.4. Tunnels Two or more ice-pick scars connected by epithelialized tracts

Source: Kadunc BV et al. (3).

Table 1.2 Goodman’s qualitative global scarring grading system.

Grade Level of Disease Clinical Features Examples of Scars

1 Macular disease Erythematous, hyper- or hypo-pigmented flat marks visible to patient or Erythematous, hyper- or
observer irrespective of distance hypo-pigmented flat marks
2 Mild disease Mild atrophy or hypertrophy that may not be obvious at social distances of Mild rolling, small soft papular
50 cm or greater and may be covered adequately by makeup or the normal
shadow of shaved beard hair in males or normal body hair if extrafacial
3 Moderate disease Moderate atrophic or hypertrophic scarring that is obvious at social distances More significant rolling, shallow
of 50 cm or greater and is not covered easily by makeup or the normal shadow ‘‘box car,’’ mild to moderate
of shaved beard hair in males or body hair if extrafacial, but is still able to be hypertrophic or papular scars
flattened by manual stretching of the skin
4 Severe disease Severe atrophic or hypertrophic scarring that is obvious at social distances of Punched out atrophic (deep ‘‘box
50 cm or greater and is not covered easily by makeup or the normal shadow car’’), ‘‘ice pick’’, bridges and tunnels,
of shaved beard hair in males or body hair (if extrafacial) and is not able to be gross atrophy, dystrophic scars,
flattened by manual stretching of the skin significant hypertrophy or keloid

Source: Goodman GJ et al. (10).

follows: atrophic scars (V-shaped, U-shaped and M-shaped), clinical and ultrasound correlations
superficial elastolysis, hypertrophic inflammatory scars (<2
years since onset), and keloid-hypertrophic scars (>2 years Methods
since onset). Each scar type is associated with a quantitative Ultrasound imaging is a noninvasive technique that uses
score (0, 1, 2, 3 depending on the number of lesions) multi- various acoustic properties of biologic tissues. Typically, echo
plied by a weighting factor that varies according to severity, signals are represented in one-dimensional diagrams (A-mode)
evolution, and morphological aspect. The final global score or two-dimensional images (B-mode).
is directly correlated with clinical severity and ranges from Ultrasound of the skin is best performed by equipment
0 to 540 depending on the type and number of acne scars using frequencies of > 20 MHz. Using B-mode imaging,
(Table 1.4). normal skin typically shows an epidermal entrance echo, the

 classification of acne scars: a review with clinical and ultrasound correlation
Table 1.3 Goodman’s quantitative global acne scarring grading system.

Number of Lesions Number of Lesions Number of Lesions

Grade or Type 1 (1–10) 2 (11–20) 3 (>20)

A) Milder scarring (1 point each) 1 point 2 points 3 points

Macular erythematous or pigmented
Mildly atrophic dish-like
B) Moderate scarring (2 points each) 2 points 4 points 6 points
Moderately atrophic, dish like
Punched out with shallow bases small scars (<5 mm)
Shallow but broad atrophic areas
C) Severe scarring (3 points each) 3 points 6 points 9 points
Punched out with deep but normal bases, small scars (<5 mm)
Punched out with deep abnormal bases, small scars (<5 mm)
Linear or troughed dermal scarring
Deep, broad atrophic areas
D) Hyperplastic
Papular scars 2 points 4 points 6 points
Keloidal/hypertrophic scars Area < 5 mm Area 5–20 cm2 Area > 20 cm2
6 points 12 points 18 points

Source: Goodman GJ et al. (11).

Table 1.4 ECCA grading scale.

Weighting Grading
Description Factor (a) Semiquantitative Score (b) (a × b)

V-shaped atrophic scars, diameter of less than 2 mm, and punctiform 15 0 = no scar /______/
1 = a few scars
2 = limited number of scars
3 = many scars
U-shaped atrophic scars, diameter of 2–4 mm, with sheer edges 20 0 = no scar /______/
1 = a few scars
2 = limited number of scars
3 = many scars
M-shaped atrophic scars, diameter of more than 4 mm, superficial and with 25 0 = no scar /______/
irregular surface 1 = a few scars
2 = limited number of scars
3 = many scars
Superficial elastolysis 30 0 = no scar /______/
1 = a few scars
2 = limited number of scars
3 = many scars
Subgrading 1 /______/
Hypertrophic inflammatory scars, scars of less than 2 years of age 40 0 = no scar /______/
1 = a few scars
2 = limited number of scars
3 = many scars
Keloid scars and hypertrophic scars that are more than 2 years of age 50 0 = no scar /______/
1 = a few scars
2 = limited number of scars
3 = many scars
Subgrading 2 /______/
Global Score (Subgrading 1 + 2) /______/

Source: Dreno B et al. (4).


 acne scars
dermal layer, and the subcutaneous layer. This technique offers a vertical extension that reaches a depth correspond-
a wide range of possibilities in clinical and experimental der- ing to the deep dermis (Figure 1.1a–1.1b).
matology. It is used for the evaluation of skin tumour thick-
ness (e.g., basal-cell carcinoma, melanoma). Areas of research
may include scleroderma, psoriasis, and aged and photoaged
skin. Moreover, it provides an objective measurement of skin
thickness and has been utilized to assess thickness of hypertro- b) Boxcar scars (n = 5) uniformly present with a sharp
phic scars before and after treatment.(13) demarcated U-shaped appearance and are characterized
A preliminary study was preformed in a series of by a superficial diameter usually ranging from 2 to 4 mm
patients (N = 20) affected by various types of acne scars and a vertical extension that reaches a depth correspond-
in order to determine whether a correlation exists between ing to the superficial or deep dermis (Figure 1.2a–1.2b).
clinical appearance of selected scar parameters (thickness,
width, depth) with ultrasound examination. Cross-sectional c) Rolling scars (n = 5) uniformly appear as large (up to 5
B-mode scans were obtained using a 22-MHz ultrasound mm) poorly demarcated depressions of the skin; these
system (EasyScan Echo®, Business Enterprise, Trapani, Italy) scars are very superficial, sometimes hardly visible, with
that allowed examination of skin sections of 12 mm in width a vertical extension that is limited to a depth correspond-
and 8 mm in depth. ing to the epidermal thickness (Figure 1.3a–1.3b).

Results •• Hypertrophic and keloidal scars (n = 5) uniformly

•• Atrophic scars appear as invaginations of the skin in appear as dome-shaped, localized increase of skin thick-
which all skin layers are normally represented: ness (Figure 4a–4b; 5a–5b); the dermis usually is less
a) Icepick scars (n = 5) uniformly have a sharp, demar- echogenic than normal skin; in most cases, with the 22
cated V-shaped appearance and are characterized by a MHz probe, keloidal scars may not be entirely visualized
narrow diameter at the surface (usually < 2 mm) and because of their large size.

(a) (b)

Figure 1.1 Icepick scar:

clinical and ultrasound
appearance.


 classification of acne scars: a review with clinical and ultrasound correlation

(a) (b)

Figure 1.2 Boxcar scar:

clinical and ultrasound
appearance.

(a) (b)

Figure 1.3 Rolling scar:

clinical and ultrasound
appearance.


 acne scars

(a) (a)

(b) (b)

Figure 1.4 Hypertrophic scar: clinical and ultrasound appearance. Figure 1.5 Keloidal scar: clinical and ultrasound appearance.

conclusions references
There is a lack of consensus in the literature regarding acne 1. “Scar.” The American Heritage® Stedman’s Medical
scar nomenclature and classification. A major problem is rep- Dictionary. Houghton Mifflin Company. 10 Feb. 2009.
resented by the pleomorphic appearance of scars that may Available from: http://dictionary.reference.com/browse/
cause variable interpretation at clinical examination. A stan- scar.
dard method for evaluation of scar depth represents an unmet 2. Rivera AE. Acne scarring: a review and current treatment
need and is essential for therapeutic and prognostic purposes. modalities. J Am Acad Dermatol 2008; 59: 659–76.
Ultrasound examination provides simple and reproducible 3. Kadunc BV, Trindade de Almeida AD. Surgical treatment
quantitative parameters, representing a promising tool for a of facial acne scars based on morphologic classification: a
more accurate evaluation and classification of acne scars. Brazilian experience. Dermatol Surg 2003; 29: 1200–9.


 classification of acne scars: a review with clinical and ultrasound correlation
4. Dreno B, Khammari A, Orain N et al. ECCA grading scale: 10. Goodman GJ, Baron JA. Postacne scarring: a qualitative
an original validated acne scar grading scale for clinical global scarring grading system. Dermatol Surg 2006; 32:
practice in dermatology. Dermatology 2007; 214: 46–51. 1458–66.
5. Ellis DA, Michell MJ. Surgical treatment of acne scarring: 11. Goodman GJ, Baron JA. Postacne scarring–a quantitative
non-linear scar revision. J Otolaryngol 1987; 16: 2116–9. global scarring grading system. J Cosmet Dermatol 2006;
6. Langdon RC. Regarding dermabrasion for acne scars 5: 48–52.
[letter]. Dermatol Surg 1999; 25: 919–20. 12. Dreno B, Bodokh I, Chivot M et al. ECLA grading: a sys-
7. Goodman GJ. Postacne scarring: a review of its pathophys- tem of acne classification for every day dermatological
iology and treatment. Dermatol Surg 2000; 26: 857–71. practice. Ann Dermatol Venereol 1999; 126: 136–41.
8. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classifi- 13. Lacarrubba F, Patania L, Perrotta R et al. An open-label
cation system and review of treatment options. J Am Acad pilot study to evaluate the efficacy and tolerability of a
Dermatol 2001; 45: 109–17. silicone gel in the treatment of hypertrophic scars using
9. Jemec GB, Jemec B. Acne: treatment of scars. Clin Dermatol clinical and ultrasound assessments. J Dermatol Treat
2004; 22: 434–8. 2008; 19: 50–3.


2 Pathophysiology of acne scars
Stefano Veraldi and Mauro Barbareschi

introduction which explains the relative facility of abnormal scar develop-

Scars can affect a high percentage of patients with acne and can ment in an inflammatory disease like acne.(2–5)
occur early. Two features in scar development are important:
(a) its severity, and (b) the delay before an adequate treatment. the evolution of inflammatory lesion to
It is, therefore, important to inform patients with inflamma- scar development
tory acne (from papular-pustular to nodular-cystic) that they Acne scar begins when noninflammatory comedone evolves
have a high risk of scar development.(1) into an inflammatory lesion that ruptures through the weakened
Dermoepidermal wound is characterized by a cascade of infrainfundibular section of the follicle. Perifollicular abscess
events that culminate in scar development at the site of tissue is the result of such a rupture. This will be repaired without
damage. Morphology of scars varies among patients: This vari- scarring in 7 to 10 days. Cells grow from the epidermis and
ability depends on intrinsic and extrinsic factors, resulting in appendageal structures to circumscribe the inflammatory reac-
the development of a normal or a pathologic scar. tion. If this is complete, there is resolution of the lesion with no
Inspite of the knowledge gathered via research so far, exact sequelae. Sometimes, however, the encapsulation is incomplete
mechanisms of damaged tissue healing remain poorly under- and further rupture occurs. The result may be the development
stood, particularly about pathological scars. of fistulous tracts. Clinical appearance consists of a group of
open comedones with a number of interconnecting keratinized
physiological wound healing and channels. Ice-pick scars represent an example of this evolution:
scar development Histopathological picture is characterized by reticulate tunnels
Physiological wound-healing progresses through three overlap- lined by hyperplastic epithelium. Often there are remnants of
ping phases: inflammation, proliferation, and maturation. inflammation even in old scars of this type.
The starting phase (inflammation) begins at the time of der- Other types of outcome depend on the extent and depth
mal damage, when the activation of the coagulation cascade of inflammation. When inflammation is deep, it will extend
causes release of cytokines that stimulate chemotaxis of neu- beyond the environment of the hair follicle into the subcutane-
trophils and macrophages into the wound. ous tissue, along vascular channels and around sweat glands.
After 48 to 72 hours, the healing process passes from the The consequence is the destruction of subcutaneous fat and the
inflammation phase into the proliferation phase, which lasts development of deep scars.
3 to 6 weeks. Fibroblasts are recruited into the wound in order
to synthesize the scaffold of reparative tissue: the extracellular atrophic acne scars
matrix (ECM). Granulation tissue is made by procollagen, elas- In acne, atrophic scars are much more common than hyper-
tin, proteoglycans, and hyaluronic acid. A particular popula- trophic scars. They most commonly involve the dermis, but can
tion of fibroblasts called myofibroblasts that synthesize actin also involve the underlying fat. The phases of healing include
filaments are responsible for wound contraction. inflammation (in the infrainfundibular region of the pilose-
Once the wound is healed, the immature scar passes into the baceous structure), granulation tissue formation with fibro-
final maturation phase, which may last a few months. ECM is plasia and neovascularization, wound contracture, and tissue
progressively degraded and immature Type III collagen of early remodelling.(6)
wound becomes finally mature Type I collagen. Enzymatic activity and inflammatory mediators also destroy
The balance of synthesis and degradation of scar compo- the deeper structures.
nents shifts into a downregulation of healing, to allow the final
scar to reach maximum organization and strength. Types of atrophic acne scars
This multistep process is regulated by several molecules, The depth and the extent of inflammation will determine the
including epidermal growth factor (EGF), basic fibroblast degree of scar severity.
growth factor (bFGF), transforming growth factor-β (TGF-β), If only epidermis and superficial dermis are involved, scars
mitogen-activated protein kinases (MAPs), and metalloprotei- may appear as macules that may be either erythematous or
nases (MMPs). hyperchromic. This postinflammatory hyperpigmentation is
Molecules that link these regulatory signals and the three more frequent, diffuse, and severe in patients with dark skin:
phases of healing are only partially understood. In such a com- With sunlight avoidance, its duration ranges between 3 months
plicated system, vulnerabilities are not a remote possibility, and 18 to 24 months. When middermis is involved, recurrent


 pathophysiology of acne scars
ruptures of follicles ensue and fistulae can occur. In such cir- in subjects with dark skin is well known. Keloids are usually
cumstances, excision of the entire pilosebaceous apparatus may observed in individuals between 10 and 30 years of age.(17)
be necessary. Fibroblasts involved in keloid development are different,
If deep dermis is affected, sharp-walled or ice-pick scars are according to the phenotypical point of view, from those pres-
produced. ent in normal scars, and also if patients predisposed to keloid
If more extensive dermal damage occurs, broad scars can formation do not always develop abnormal scars.
develop, like rolling or boxcar scars. Sometimes, after a normal initial evolution, some scars may
At the trunk, follicular or perifollicular acne inflammation become keloidal.(18) Keloid fibroblasts present an increased
induces the development of hypopigmented scars.(7) number of growth factor receptors and respond more quickly
to growth factors, like platelet-derived growth factor (PDGF)
Hypertrophyc acne scars and TGF-β that can upregulate these cells.(19) TGF-β is over-
In acne, the development of hypertrophic scars is uncommon. produced by keloid tissue and poorly regulated through normal
In our clinical experience, these scars occur especially in male signalling processes. A loss of feedback control during collagen
patients who suffered from severe varieties of papular-pustular and ECM production was demonstrated in keloid tissue.(20)
or nodular acne, especially on the shoulders and back. Decreased synthesis of molecules that promote matrix break-
down and collagen organization may also explain the lack of scar
differences between hypertrophic scars regression observed in keloids. Abnormal epithelial–mesenchy-
and keloids mal interactions, persistence of fetal wound–healing pathways,
The terms hypertrophic scar and keloid are often used inter- altered immune functions, failure of apoptosis, tissue hypoxia,
changeably. Although there are some clinical similarities between and oxygen-free radical generation have also been suggested as
hypertrophic scars and keloids, there are many biochemical, causal factors of keloid growth.(21, 22)
physiopathological, and clinical differences that support the fact
that these entities are distinct. references
Hypertrophic scars can appear everywhere; they are raised, 1. Layton AM, Henderson CA, Cunliffe WJ. A clinical evalua-
with a smooth surface, pink to red in colour, and rarely accom- tion of acne scarring and its incidence. Clin Exp Dermatol
panied by pruritus. Furthermore, hypertrophic scars do not 1994; 19: 303–8.
extend beyond the margins of the original tissue damage. 2. Niessen FB, Spauwen PH, Schalkwijk J, Kon M. On the
Hypertrophic scars evolve in a limited period of time: It is lon- nature of hypertrophic scars and keloids: a review. Plast
ger in comparison with normal scars, but its duration is less Reconstr Surg 1999; 104: 1435–58.
than a year. 3. Pearson G, Robinson F, Beers Gibson T et al. Mitogen-
Areas where keloids more frequently occur are the ears, activated protein (MAP) kinase pathways: regulation and
upper portion of the chest, shoulders, arms, and the upper physiological functions. Endocr Rev 2001; 22: 153–83.
portion of the back. This suggests the existence of local popu- 4. Fujiwara M, Muragaki Y, Ooshima A. Keloid-derived
lations of abnormal cells or tissue local factors that stimulate fibroblasts show increased secretion of factors involved in
keloid development. The growth of keloids continues indefi- collagen turnover and depend on matrix metalloprotei-
nitely, without a quiescent or regressive phase (8, 9); more- nase for migration. Br J Dermatol 2005; 153: 295–300.
over, they extend to surrounding normal tissue, and pruritus 5. Tsujita-Kyutoku M, Uehara N, Matsuoka Y et al. Compar-
is frequent. Some authors consider keloids a variety of benign ison of transforming growth factor-beta/Smad signaling
fibrous tumour. between normal dermal fibroblasts and fibroblasts derived
From the histopathological point of view, hypertrophic scars from central and peripheral areas of keloid lesions. In Vivo
mainly contain Type III collagen: its fibers are thick and oriented 2005; 19: 959–63.
parallel to the epidermal surface; furthermore, myofibroblasts 6. Knutson DD. Ultrastructural observations in acne vulgaris:
are numerous Keloids are composed by disorganized Type I and the normal sebaceous follicle and acne lesions. J Invest
III collagen bundles, with a low number of myofibroblasts. The Dermatol 1974; 62: 288–307.
collagen pattern is abnormally thick, with irregular branched 7. Wilson BB, Dent CH, Cooper PH. Papular acne scars.
septal collagen bands.(10–12) Both lesions demonstrate over- A common cutaneous finding. Arch Dermatol 1990; 126:
production of multiple fibroblast proteins, suggesting either 797–800.
pathological persistence of healing signals or a failure of the 8. Su CW, Alizadeh K, Boddie A, Lee RC. The problem scar.
appropriate downregulation of healing cells.(13, 14) Clin Plast Surg 1998; 25: 451–65.
9. Burd A, Huang L. Hypertrophic response and keloid
pathophysiology of keloids diathesis: two very different forms of scar. Plast Reconstr
The idea of a generic predisposition to keloid development Surg 2005; 116: 150e–7e.
has long been suggested; furthermore, affected patients often 10. Editorial. Elastic tissue and hypertrophic scars. Burns
report a positive family history.(15, 16) A racial predisposition 1976; 3: 407.


 acne scars
11. Ehrlich HP, Desmoulière A, Diegelmann RF et al. Morpho- single versus multiple site scars. Br J Plast Surg 2005;
logical and immunochemical differences between keloid 58: 28–37.
and hypertrophic scar. Am J Pathol 1994; 145: 105–13. 17. Lane JE, Waller JL, Davis LS. Relationship between age of
12. Blackburn WR, Cosman B. Histologic basis of keloid and ear piercing and keloid formation. Pediatrics 2005; 115:
hypertrophic scar differentiation. Clinicopathologic cor- 1312–4.
relation. Arch Pathol 1966; 82: 65–71. 18. Muir IF. On the nature of keloid and hypertrophic scars.
13. Younai S, Nichter LS, Wellisz T et al. Modulation of Br J Plast Surg 1990; 43: 61–9.
collagen synthesis by transforming growth factor-beta 19. Haisa M, Okochi H, Grotendorst GR. Elevated levels of
in keloid and hypertrophic scar fibroblasts. Ann Plast Surg PDGF alpha receptors in keloid fibroblasts contribute to
1994; 33: 148–51. an enhanced response to PDGF. J Invest Dermatol 1994;
14. Bettinger DA, Yager DR, Diegelmann RF, Cohen IK. 103: 560–3.
The effect of TGF-beta on keloid fibroblast prolifera- 20. Diegelmann RF, Cohen IK, McCoy BJ. Growth kinetics
tion and collagen synthesis. Plast Reconstr Surg 1996; and collagen synthesis of normal skin, normal scar and
98: 827–33. keloid fibroblasts in vitro. J Cell Physiol 1979; 98: 341–6.
15. Bayat A, Walter JM, Bock O et al. Genetic susceptibility to 21. Kazeem AA. The immunological aspects of keloid tumor
keloid disease: mutation screening of the TGFbeta3 gene. formation. J Surg Oncol 1988; 38: 16–8.
Br J Plast Surg 2005; 58: 914–21. 22. Cobbold CA. The role of nitric oxide in the formation of
16. Bayat A, Arscott G, Ollier WE, McGrouther DA, keloid and hypertrophic lesions. Med Hypotheses 2001;
Ferguson MW. Keloid disease: clinical relevance of 57: 497–502.


3 Hypertrophic and keloidal scars
Maria Miteva and Paolo Romanelli

acne scars—general notes further to the formation of the whorls, nodules, and scar
The Merriam Webster’s dictionary defines the word scar as contractures characteristic of hypertrophic scars.
“a mark left on the skin or other tissue after a wound, burn, pus- Acne scarring is a consequence of the damage that occurs
tule, lesion has healed; cicatrix.” However, additional meanings in and around the pilosebaceous follicle during inflamma-
stand for “a marring or disfiguring mark” as well as for “lasting tion. However, the precise mechanisms and factors that govern
mental or emotional effects of suffering or anguish.” According the initiation and exacerbation of inflammation are not fully
to Koo et al., the psychological effects due to acne and acne scar- known. In a study of 185 patients with severe-grade acne on
ring may lead to emotional debilitation, embarrassment, poor the face, chest, and back, Layton et al. showed that 95% of both
self-esteem, frustration, and social isolation.(1) Although these sexes developed facial scarring to some degree.(4) The truncal
effects are difficult to quantify in patient terms, scarring that region of male patients revealed significantly more total HS and
results from tissue damage and inflammation is a significant KS than the same area of female patients. In this study HS and
issue that requires attention and will be expanded herein with KS were most commonly seen in males and 85% of the patients
main focus on hypertrophic and keloidal scars (HS, KS). affected had been previously noted to have nodular acne, and
Epidermal damage per se results in transient erythema and/ in the remaining 15%, only superficial inflammatory lesions
or pigmentary disturbances such as postinflammatory hyper- had been appreciated. The sites of KS formation, in agreement
pigmentation, whereas dermal damage is more long lasting and with previous observations, were more commonly involving
accounts for decrease and increase of tissue. Tissue damage the back, shoulder, and chest, as well as the angle of the jaw.
from acne inflammation can lead to permanent skin-texture Furthermore, untreated acne lesions up to 3 years between ini-
changes and fibrosis, thus resulting in scar formation. Scars tial onset and sufficient treatment regardless of sex or location
normally proceed through the specific phases of the wound- were an important factor in determining resultant scarring.
healing cascade: inflammation, granulation, and remodeling. After this period, the degree of scarring did not increase signifi-
However, even normal scars that have accomplished the healing cantly; the reason for that is still obscure.
process successfully achieve only 80% of previous skin strength. Evidence suggests that acne is not a homogenous disease and
(2) Substantial amount of molecular and cellular data have that patients may generate different type of immune response
been generated in an effort to understand the process of wound since both Th1 and Th2 cytokine profiles have been found in
contraction and scar contracture formation. Basically, after established inflamed lesions from acne patients. Whether this
completing the inflammatory and granulation phases, wound difference contributes to the predisposition of some patients
closure requires generation of proper contractile forces to close to scar was investigated in a study done by Holland et al.(5)
the wound. It has been shown that myofibroblasts appear to be Immunohistochemical methods were used to determine the
intrinsically linked to the development of hypertrophic scars. cell-mediated immune response in developing and resolving
(3) Migration of fibroblasts into and through the extracellular inflamed lesions by examining the prevalence and activation
matrix during the initial phase of wound healing is a fundamen- states of lymphocyte subsets, macrophages, and endothelial
tal component of wound contraction. During this migration, cells, the major components of this response, present in two
the pulling of collagen fibrils into a streamlined pattern, and groups of patients with the same degree of inflamed acne but
the associated production of collagenase, may facilitate a more differing in their propensity to scar. The authors found out that
normal arrangement of collagen. Once the wound has been the cellular infiltrate was large and active with a greater non-
repopulated and the chemotactic gradient that has been estab- specific response (few memory T cells) and subsided in resolu-
lished by inflammatory cells is decreased, fibroblast migration tion in early lesions of patients who were not prone to scarring
will cease. It is at this point that myofibroblasts appear and play (NS). In contrast, a predominantly specific immune response
a key role in the production of hypertrophic scars.(3) Hence, was present in prone to scarring (S) patients—the infiltrate was
one of the pivotal differences between wounds that proceed to initially smaller and ineffective, but the number of CD4+ T cells
normal scar (compared with those that develop hypertrophic in the infiltrate remained increased and activated in resolving
scars) and scar contractures may be the lack and/or late induc- lesions. In addition, significant levels of angiogenesis also per-
tion of myofibroblast apoptotic cell death (see below for further sisted, thus facilitating a prolonged inflammatory response.
details). The combined contribution of fibroblasts and myofi- However, the majority of CD4+ T cells were skin-homing
broblasts to abnormal extracellular matrix protein production memory effector cells, with the absence of unclassified cells,
results in an excessive and rigid scar. The isometric application suggesting that S patients are more susceptible to the causative
of contractile forces by myofibroblasts probably contributes antigens. The authors concluded that in S patients there is a

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