Michel Goldberg

Editor

Understanding
Dental Caries
From Pathogenesis to
Prevention and Therapy

123
Understanding Dental Caries
Michel Goldberg
Editor

Understanding Dental
Caries
From Pathogenesis to Prevention
and Therapy
Editor
Michel Goldberg
UMR-S 1124
INSERM
Paris
France

ISBN 978-3-319-30550-9 ISBN 978-3-319-30552-3 (eBook)

DOI 10.1007/978-3-319-30552-3

Library of Congress Control Number: 2016941182

© Springer International Publishing Switzerland 2016

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Preface

Dental and periodontal diseases are two major public health pathologies.
Teeth injuries include enamel and dentin carious lesions and periodontal dis-
orders. Carious lesions are the most widespread dental pathologies. They
may be limited to simple occlusal fissures or located solely in the proximal
aspect, or they expand to complex class II and/or cervical lesions.
In the United States, over 50 % of 5–9-year-old children have at least one
cavity and/or one restoration of decayed teeth [(D) and/or filled (F)]. That
proportion increases to 78 % among 17-year-old children. The World Health
Organization (WHO) estimation of global DMFT [decayed, missing, filled
teeth] for 12-year-old children has reported that in the 188 countries included
in their database, on a global basis, about 240 millions of teeth are injured in
this age group [Bagramian RA, Garcia-Godoy F, Volpe AR. The global
increase in dental caries. A pending public health crisis. Am J Dent 2009; 22:
3–8]. These evaluations underline the significance of dental caries and its cor-
relation with dental practice. In contrast, severe periodontitis was limited to
only 5–20 % of the adult population.
Younger and older patients are the targets of dental carious decay, well
recognized as a major health problem in most industrialized countries, affect-
ing 60–90 % of school-aged children and the vast majority of adults (Petersen
et al., The global burden of oral diseases and risks to oral health. Bulletin of
the WHO 2005; 83: 661–669). Patients with three DMFT constitute 51 % of
the patients at the age of 12, while the other patients displayed higher values.
Therefore, most dental practitioners are implicated in their everyday practice
by the treatment of dental caries.
Clearly, this implies also that carious lesion is more than likely the most
prominent pathology of the mouth, and the importance of carious lesions is
fundamental both for patients and for dental practitioners. This underlines
also the significance of understanding dental caries, their pathogenesis, pre-
vention, and subsequent therapies.
The present book focuses most exclusively on the carious lesion, going
from the initial pathogenesis of the lesion, mild enamel alteration, to deep
dentin lesions, which appear as a major pathology with pulpal irreversible
incidences. The therapies and prevention of the enamel decay are analyzed in
the first part of this book.
After a brief description concentrating on the structure and epidemiology
of the diverse forms of enamel alterations, carious lesions are reported. We
describe successively enamel softening and analyze the etching pattern of

v
vi Preface

acidic effects on enamel. Doing so, we moved from the superficial etching to
the initial enamel carious lesion. Bacterial films and acidic biofilms of the
dental plaque lead to the formation of active and/or inactive lesions. The
methods used for an accurate diagnosis of the carious lesion were improved
during the past few years, and a specific chapter concludes the first part of the
book, by reporting new diagnostic methods.
Another group of chapters is devoted to the carious dentin and to active or
inactive lesions, superficial or deep, reaching the dental pulp and/or located
exclusively in the cervical region. How the patient brush and eliminate the
dental plaque is another topic. Which toothpastes are used, the evolution,
and/or the stabilization of the lesion are factors involved in the carious pro-
gression. Eventually, non-carious cervical lesions may regenerate, and it is
well documented that some cervical pathology remineralize spontaneously.
In addition, we note that 8–13 % among adult patients are affected by the
increasing problem of dental erosions.
Finally, new trends in resin infiltrations of the initial lesion, minimal inva-
sive therapies aiming to stabilize the carious lesion, and strategies devised to
prevent the expansion of the lesion are control and preventive measures
restraining the broad field of cariology.
Fluoride is considered to be the main tool of carious prevention. At some
high doses, it induces pathologic fluorosis, but if added in minimal quantity
in controlled assays, different forms of fluoride prevents the evolution of cari-
ous lesions, contributing to remineralization of the initial lesion or to their
stabilization. Other preventive therapies have been elaborate, and we focused
on the differences that appear between prevention and minimal restorative
dentistry.
The different chapters of this book were written as requested by different
researchers and clinicians recognized to be the best in their specific domain.
We wish sincerely to acknowledge their outstanding contributions, and I wish
to thank them warmly for what they did for the dental community.

Paris, France Michel Goldberg

January 2016
Contents

Part I The Carious Enamel

1 Understanding Dental Caries – from Pathogenesis
to Prevention and Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Nigel Pitts
2 Enamel Softening (Dental Erosion) . . . . . . . . . . . . . . . . . . . . . . . 11
Michel Goldberg
3 Enamel Etching . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Michel Goldberg
4 The Early Enamel Carious Lesion . . . . . . . . . . . . . . . . . . . . . . . 29
Michel Goldberg
5 Dental Biofilms in Health and Disease . . . . . . . . . . . . . . . . . . . . 41
P.D. Marsh
6 New Caries Diagnostic Methods . . . . . . . . . . . . . . . . . . . . . . . . . 53
Klaus W. Neuhaus and Adrian Lussi
7 From the Initial Carious Lesion of Enamel to the Early
Development of Coronal Dentin Carious Lesion . . . . . . . . . . . . 63
Michel Goldberg

Part II The Carious Dentin

8 The Dentinoenamel Junction . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
Michel Goldberg
9 Superficial and Deep Carious Lesions . . . . . . . . . . . . . . . . . . . . 85
Michel Goldberg
10 Cervical Sclerotic Dentin: Resin Bonding . . . . . . . . . . . . . . . . . 97
Franklin R. Tay, Manar Abu Nawareg,
Dalia Abuelenain, and David H. Pashley
11 The Pulp Reaction Beneath the Carious Lesion. . . . . . . . . . . . . 127
Michel Goldberg

vii
viii Contents

Part III Cervical Erosions

12 Ultrastructure of the Enamel-Cementum Junction . . . . . . . . . . 153
Michel Goldberg
13 Cervical Erosions: Morphology and Restoration of Cervical
Erosions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
Wolfgang H. Arnold
14 Cervical Regeneration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
Michel Goldberg

Part IV Fluoride
15 Fluoride . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
Pam Denbesten, Robert Faller, and Yukiko Nakano

Part V Invasive and Non-invasive Therapies

16 Brushing, Toothpastes, Salivation, and Remineralization . . . . 187
Robert Faller and Agnes Bloch-Zupan
17 Resin Infiltration Treatment for Caries Lesions . . . . . . . . . . . . 199
Colin Robinson
18 Minimally Invasive Therapy: Keeping Treated
Teeth Functional for Life . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Jo E. Frencken and Soraya C. Leal
19 Invasive and Noninvasive Therapies . . . . . . . . . . . . . . . . . . . . . . 233
Sophie Doméjean, Michèle Muller-Bolla,
and John D.B. Featherstone
 Part I
The Carious Enamel
 Understanding Dental
Caries – from Pathogenesis
1
to Prevention and Therapy

Nigel Pitts

Abstract
This chapter provides an overview demonstrating the pivotal importance
of understanding the caries process in enamel (and then, for a subset of
lesions which ever progress, beyond that, into the dentine) if we are to best
prevent and control dental caries over the life course in both patients and
populations. There is a need also to understand the complexities and
opportunities in the detection, assessment and diagnostic steps in order to
inform decision-making and effective, personalised care planning. Modern
caries care, provided at the right times on the basis of caries risk, should
ensure that the disease is controlled and that tooth structure is preserved
whenever possible.

1.1 The Carious Enamel tal caries over the life course in both patients and
populations. It sets the scene for the detail that
1–1 Dental caries: structure, diagnosis, which follows in subsequent chapters. Aside from
treatment is appropriate. appreciating the science around enamel structure
which underpins caries prevention and control,
there is also a need also to understand the com-
1.2 Introduction plexities and opportunities in the detection,
assessment and diagnostic steps employed by cli-
This chapter provides an overview demonstrating nicians examining their patients. Rather than just
the pivotal importance of understanding the car- finding “holes to fill”, dentists of today need to
ies process in enamel (and then, for a subset of carefully assess tooth sites and assess both lesion
lesions which ever progress, beyond that, into the severity and activity. This is in order to inform
dentine) if we are to best prevent and control den- their decision-making in selecting from an ever-
widening choice of preventive and minimally
invasive care options. The goal is to achieve
effective, personalised and risk-based care plan-
N. Pitts ning with a long-term perspective. Modern caries
Dental Innovation and Translation Centre, care, provided at the right times on the basis of
Kings College London Dental Institute, London, UK
e-mail: nigel.pitts@kcl.ac.uk caries risk, should ensure caries is controlled and

© Springer International Publishing Switzerland 2016 3

M. Goldberg (ed.), Understanding Dental Caries, DOI 10.1007/978-3-319-30552-3_1
4 N. Pitts

that tooth structure is preserved whenever possi- “surface zone” of the initial caries lesion.
ble. The era of “automatic” decisions to restore Preserving this zone has tremendous clinical
all lesions detected should now be past, but value in maintaining the potential to arrest and
change can be frustratingly slow in many coun- reverse lesions.
tries and systems.

1.4 Diagnosis
1.3 Structure
The evidence-based consensus statements from
One important element of understanding the the ICW-CCT, a major international consensus
healthy structure of enamel as well as carious workshop on caries clinical trials (Pitts and
enamel is to appreciate the long-term clinical Stamm 2004), clearly differentiated three impor-
value of the sound tissue. In terms of coping with tant and different elements and terms related to
a lifetime of thermal, chemical and physical chal- caries diagnosis. These were caries: detection,
lenges in a hostile wet environment, tooth enamel assessment and diagnosis.
is still superior in its physical properties to any of Detection is concerned with the clinical deci-
the currently available artificial alternatives. This sion as to whether a tissue is classified as sound
reality underpins the guiding philosophy to pro- or carious (and may record degrees of caries
tect and preserve as much natural tooth structure severity, which can be staged), assessment char-
and specifically enamel as possible. Even though acterises the behaviour of a lesion (i.e. is this
we have at our disposal the clinical technology to lesion active now or is it arrested), and finally
cut enamel very rapidly and efficiently, this diagnosis represents the human summation by
should only be done as a last resort (Pitts 2004a, the clinician of all information available (from
b; Ismail et al 2013). clinical visual and radiographic assessments as
The following series of chapters describe and well as from any other special tests which may be
illustrate the unique, highly organised structure employed) to decide the disease status of a par-
of the enamel, the hardest mineralised tissue in ticular tooth surface (Pitts and Stamm 2004;
the human body. This varies from the important Longbottom et al 2009).
superficial aprismatic surface enamel, which The wide variation in the way in which the ter-
matures for a period following eruption into the minology around caries diagnosis was used in the
oral environment, to the deeper bulk of the pris- literature, and specifically the ambiguity associ-
matic enamel – which is comprised of prismatic ated with many of the different criteria used and
enamel (carbonated hydroxyapatite) and inter- reporting for caries clinical trials and research,
prismatic enamel. gave rise after this meeting to the creation in
Knowledge of the sound structure is important 2002 of a harmonised system built, on integrating
in understanding the differing initial mechanisms the best evidence. This is the “ICDAS”, an
of the caries process (producing net sub-surface International Caries Detection and Assessment
demineralisation after long alternating periods of System (www.icdas.org/). This system was
de- and remineralisation) as opposed to the direct developed to facilitate caries epidemiology,
surface loss of tissue which is associated with research and appropriate clinical management
erosive tooth wear. In caries, there is a critical (Pitts 2004a, b; Ismail et al 2007) and has been
interplay between the superficial structure of the developed over the years into a number of
enamel and the covering complex biofilm which, approved options. The system has also been
when cariogenic, can shift ecologically to pro- incorporated into a number of international con-
duce and retain a low pH at the tooth surface (see ventions and recommendations from bodies such
Chapter I-4- by Phil Marsh). It is this interplay as the FDI World Dental Federation (Fisher and
and the periods of repeated de- and remineralisa- Glick 2012) and the American Dental Association
tion that give rise to the macroscopically intact (ADA 2015).
1 Understanding Dental Caries – from Pathogenesis to Prevention and Therapy 5

The ICDAS criteria were built around the evi- ies most effectively in their patients when
dence relating the clinical visual appearance of assessed for caries risk. It should be further
the enamel (and dentine) to the histological appreciated that there are a range of other method
extent of the lesion within the tooth tissue. and technologies which have been developed to
Critically, the very first clinical visual changes in act diagnostic aids to clinicians. These are con-
the enamel can only be seen when the tooth is sidered in a forthcoming chapter (Chapter I-5- by
clean and has been dried with compressed air, Neuhaus and Lussi, 2016).
ideally for 5 s. White spot lesions visible only In terms of assessing enamel caries, the depth
when dry extend less far into the enamel than of penetration through the enamel is an important
those visible when the enamel is wet with saliva, consideration. This information helps determine
due to changes in the refractive index masking what kind of treatments and care strategies may
the initial lesion. In the latter case, the lesion may be required and are appropriate for each lesion. It
extend across the full thickness of the enamel, also helps in the monitoring of lesion develop-
and defence reaction changes may be visible in ment and, conversely, in establishing the degree
the underlying dentine. It is therefore important of success obtained when seeking to stop further
to examine teeth which are clean and dry and to progression of a lesion. The so-called diagnostic
use sharp eyes, rather than sharp probes (which threshold (or cut point) at which caries is recog-
have been found many years ago to cause iatro- nised as disease has dramatic affects at both the
genic damage whilst not contributing signifi- individual patient level and at the population
cantly more diagnostic information than health level (Selwitz et al. 2007). There is a need
visual-alone examination). for more clarity and consistency on this issue,
Whilst clinical examination is the foundation both internationally and across dental “silos”.
for assessing caries, for teeth in anatomical con- Caries activity information is prized highly by
tact, there remain fundamental limitations in both clinicians and researchers, but despite this
assessing approximal caries and also in under- there are evidence gaps and surprisingly few sys-
standing the depth of penetration of some occlu- tems currently available to help dentists with this
sal lesions. For these reasons dental radiography, type of caries assessment task (ICDAS website;
and particularly the bitewing projection, has Pitts 2011). New systems, such as using biolumi-
become ubiquitous in many countries as part of a nescence in order to identify increases in free cal-
routine examination. The use of radiography in cium associated with actively demineralising
addition to clinical visual examination provides lesions, show promise for future clinical
the most comprehensive clinical picture of caries practice.
status (Pitts and Kidd 1992a; b).
Although there have been some debates and
concerns about using ionising radiation too fre- 1.5 Which Treatment Is
quently in low caries populations (particularly in Appropriate (When)
Scandinavia), the evidence supporting the use
and clinical utility of properly timed radiographs The importance (and for many years the neglect
for planning both preventive and operative care of) considering the decision-making process in
remains. The International Caries Detection and treatment planning has come to the fore over the
Assessment System (ICDAS), which classifies last decade. Rather than simple no-drill vs. drill
carious lesions, has been developed into a com- (binary decisions), clinicians today have to con-
prehensive International Caries Classification sider a wide range of factors at the population,
and Management System (ICCMS™). This patient, tooth and service levels.
includes methods for staging of the caries pro- The context for making treatment decisions in
cess which combines the findings from both caries care is also changing. Factors which are
radiographic and visual examinations (Pitts and operating in the background include international
Ekstrand 2013). This helps dentists manage car- agreements to phase down the use of dental
6 N. Pitts

amalgam on environmental grounds and to phase build the International Caries Classification and
up prevention (United Nations Environment Management System, ICCMSTM. This is a health
Programme 2013), as well as the widespread outcomes focused system that aims to maintain
desire for preventive interventions to link oral health and preserve tooth structure, by using a
and systemic health improvements with the so- simple form of the ICDAS caries severity and
called NCDs. A current example is a systematic activity classification model in order to derive an
re-examination of evidence around the role of appropriate, personalised, preventively based,
sugar in caries and the desire to link caries risk-adjusted and tooth-preserving management
improvements to those in diabetes, obesity and plan for each patient (Pitts NB et al. on behalf of
heart disease (Moynihan and Skelly 2014). This the participating authors of the International
has led to new WHO Guidelines on Sugar Intake Caries Classification and Management System
for Adults and Children (World Health (ICCMSTM) Implementation Workshop, 2013).
Organisation 2015). An international consensus workshop held at
A further influence on decision-making is an Kings College London in 2013 laid the ground-
increasing awareness of the need to try to reduce work for the incremental development of this
health inequalities in caries (Pitts et al. 2011a, b) guide for practitioners and educators. The guide
and, therefore, to consider caries risk by popula- is available in a number of formats and languages,
tion subgroups. These various threads have led to including a short quick reference guide, from the
a renewed interest in international public health ICDAS website ((www.icdas.org/). The relation-
advocacy for caries prevention and control, ships between ICDAS, ICCMS and the more
through groupings such as the Alliance for a recent Global Collaboratory for Caries
Cavity-Free Future (www.allianceforacavity- Management – GCCM are shown in Fig. 1.1.
freefuture.org/), and also a parallel push for The best evidence for deciding which treat-
social movements in caries prevention which ment is appropriate and when has been assem-
links with public/private collaborations bled by a group of 75 international academics
(Bonecker et al. 2012). and practitioners in a cyclical format with four
There has been a focus in recent years on main elements which together lead to beneficial
achieving consensus on exactly what a graduat- patient outcomes (see Fig. 1.2). These elements
ing dentist should know about caries. The ele- are:
ments across pathogenesis, prevention and
therapy are key parts of this knowledge and skill 1. HISTORY – which provides a patient-level
set. Europe has led the way with a core cariology caries risk assessment
curriculum which was built by research and edu- 2. CLASSIFICATION – caries staging and
cation organisations working together to build activity assessment
consensus (Schulte et al. 2011). This process also 3. DECISION-MAKING – both synthesis and
generated specific guidance on caries risk assess- diagnoses
ment, diagnosis and the synthesis of all informa- 4. MANAGEMENT – personalised caries pre-
tion into a care plan (Pitts et al. 2011a, b) which vention, control and tooth-preserving opera-
established that nonoperative and surgical treat- tive care
ments should be deemed to have equal “value”,
but the surgical treatment should only be used as Leading to OUTCOMES assessed in the
a last resort. This European resource material has domains of health maintenance, disease control,
been debated, fine-tuned and localised in a range patient-centred quality metrics and wider impacts
of territories including Colombia (Martignon on systems and society.
et al. 2014), Malaysia and most recently the USA Important features of the ICCMSTM are that it
(Fontana et al. 2016). is risk based. For some years there have been
Since 2010 the ICDAS Foundation (a regis- groups advocating the CAMBRA philosophy
tered charity) has been working internationally to (Caries Management by Risk Assessment), and
1 Understanding Dental Caries – from Pathogenesis to Prevention and Therapy 7

Fig. 1.1 Interrelationships

and definitions of ICDAS
and ICCMS and GCCM

ICCMSTM
Comprehensive Assessment &
Personalised Caries Care Plan
CLASSIFICATION
Caries Staging & Activity
Assessment

DECISION
HISTORY
MAKING
Patient-level
Synthesis
Caries Risk
and
Assessment
Diagnoses

MANAGEMENT
Personalised Caries
Prevention, Control &
Risk-based
Recall interval
Tooth Preserving
with monitor and Operative Care
review

Health
Disease control
maintenance
OUTCOMES
Wider impacts of Patient-centred
ICCMSTM quality metrics

Fig. 1.2 ICCMS™: Overview of the comprehensive assessment and personalised caries care plan
8 N. Pitts

ICCMSTM

Comprehensive Assessment &

Personalised Caries Care Plan
CLASSIFICATION Staged Caries
Caries Staging & Activity Severity and
Assessment with Activity
Information
Intraoral Assessments

DECISION
HISTORY
MAKING
Patient-level
Caries risk Synthesis
Caries Risk and and
Assessment likelihood
Matrix Diagnoses

Risk-based
Recall interval MANAGEMENT
with monitor Personalised Caries
and review
Prevention, Control &
Tooth Preserving
Operative Care

Tooth Sound
Preserving (Preventing The Key
Operative Care New Caries) Components of
of Lesions Non-
Operative Care
the Clinical Caries
of Lesions Management
(Control) Element of care

RISK MANAGEMENT

Fig. 1.3 ICCMS™ – Detail showing the key components of the clinical caries management element of care

in terms of planning appropriate recall strategies

References
for patients, the UK National Health Service’s
National Institute for Clinical Excellence (NICE) Alliance for a Cavity Free Future – ACFF. http://www.
convened a guideline development group to look allianceforacavityfreefuture.org/.
at the evidence in this area. They recommended Bonecker M, Pucca GA, Bella Costa P, Pitts NB. A social
that for dental recall, the interval between rou- movement to reduce caries prevalence in the world.
Braz Oral Res. 2012;26(6):491–2 (São Paulo).
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and risk based (NICE 2004). For caries manage- and management: the FDI World Dental Federation
ment this means monitoring and review is Caries Matrix. JADA. 2012;143:546–51.
required. Fontana M, et al. Development of a core curriculum in
cariology for US Dental Schools. J Am Dental Educ
Figure 1.3 shows the key components of the Assoc. 2016 (in press).
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These are all underpinned by risk management Pitts NB. The International Caries Detection and
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 Enamel Softening (Dental Erosion)
2
Michel Goldberg

Abstract
For many years, most of the published reports of enamel softening dealt
with consequences of acid or chelator etching. It occurs without bacterial
involvement. The 2–5 nm thick outer enamel surface layer is mainly con-
cerned. Limited crystallite dissolution is due to abrasion, attrition, abfrac-
tion, or erosion. More than likely, enamel dissolution is due to acidic
demineralization. At early stages, it is a reversible process. Preventive
strategies include dietary counseling, stimulation of salivary flow, optimi-
zation of fluoride regimens, modification of erosive beverages, and ade-
quate oral hygiene measures.

2.1 Introductory Remarks Dental enamel is the most highly mineralized

structure of the skeleton. The percentage of inor-
For many years, most of the published reports ganic components of enamel is greater than in bone
were dealing with three well-identified enamel- and dentin. It is the actual target of specifically
induced pathologies, which have been specifi- defined aggressions directed toward the enamel
cally studied and compared. They included three structure. Due to the presence of an outer apris-
groups of major studies studying enamel soften- matic layer, dental erosions, attritions, abfractions,
ing getting worse and becoming a more severe and abrasion became the most prominent lesions
acid or chelator etching and ultimately being during the past decades. Such phenomena are obvi-
converted into carious lesions. The etio- ously in continuity with enamel softening. After an
pathologic complexity of the early enamel lesions acid attack, or following the action of chelators, the
was increased, whereas a parallel decreased of presence of a prismatic enamel layer is determinant
carious lesions was noted. for an etching pattern, beneath the dental plaque,
which is responsible for the progression of carious
lesions within enamel. The cascade of enamel
decays leads from one type of superficial alteration
M. Goldberg to more severe deterioration.
University Paris Descartes, Sorbonne, Paris Cité The comparison between the three enamel
and INSERM UMR-S1124, 45 rue des Saints Pères, alterations provides a better understanding of the
Cedex 06, 75270 Paris, France
e-mail: mgoldod@gmail.com carious process, the specific topic of this book.

© Springer International Publishing Switzerland 2016 11

M. Goldberg (ed.), Understanding Dental Caries, DOI 10.1007/978-3-319-30552-3_2
12 M. Goldberg

Hence, analysis of enamel softening opens gates tion affecting a screw-like structure, due to the
on enamel etching and shed lights on the early presence of defective Burger vectors) or at the lat-
stages of the enamel carious lesion. eral border and eventually at the edge of the crys-
tallite. This outer screw dislocation occurs at the
edge of the crystallite. The prism sheath (organic
2.2 Dental Erosion extracellular matrix) and the prism core are dis-
solved, leaving apparent a honeycomb structure
Tooth wear or dental erosive lesion involves mul- mostly identifiable after acid etching. Differences
tifactorial causes. There is an interplay between in the behavioral, biological, and chemical factors
chemical, biological, and behavioral factors. may contribute to explain why some individuals
Erosion as a pathology entity results from the display more erosion than others.
chemical loss of dental hard tissue by an acid, If the acidic impact persists (e.g., longer peri-
without bacterial involvement. Attrition (physi- ods of interaction and/or increased concentra-
cal wear through tooth-tooth contact) and abra- tions), further dissolution of the enamel occurs.
sion (physical wear produced by the interaction The dissolution becomes irreversible and leads to
between a tooth surface and another material) are a severe alteration associated with a reduction of
two other well-recognized factors. Dental erosion enamel thickness.
is exclusively a surface phenomenon, whereas in The erosion may be also dietary or result from
contrast, the initial carious lesion implicates both chronic regurgitation. Soft drinks have an erosive
surface and subsurface modifications. potential. The effects of soft drinks on enamel can
Erosion is due to structural feature of the be evaluated by measuring the amount of calcium
tooth, physiological properties of saliva, and or phosphate ions released by enamel. There was
intrinsic and extrinsic acidic sources (Lussi et al. no significant correlation between the % SMHC
2011). The critical pH below which enamel dis- (percentage of superficial microhardness changes)
solves is about 5.5. Erosion starts by initial soft- and the other variables tested for a number of
ening of the enamel surface, followed by a loss of drinks leading to enamel surface softening. The
volume with a softened layer persisting at the pH seems to have more influence on the erosive
surface of the remaining tissue. Exposure to acids potential of these drinks. Increased protective and
combined with insufficient salivary flow results defensive factors can restore or prevent loss of
in enhanced dissolution. Enamel tends to dis- calcium and phosphate from enamel.
solve more slowly than dentin. Tooth brushing, citric acid, or orange juice
During the initial stage of dental erosion, the may remove the superficial part of the softened
loss of tooth hard tissue affects up to 80 % of the enamel (Figs. 2.1a, 2.2, and 2.4a). The thickness
adults and ~ 50 % of the children (more recent of the softened layer varied between 254 and
evaluations indicate a prevalence of erosion as 323 nm, depending on the acid used and its con-
high as 68 %). Enamel dissolution is due to acidic centration. In any case, it is obvious that soft
demineralization. At these early stages, it is a drink consumption increases the potential for
reversible process. Soft drink consumption of enamel erosion.
acidic food and drinks is correlated with the Remineralization agents induced reduced car-
decrease of milk consumption, and in addition, ies and appropriately promote subsurface depos-
this points at calcium deficiency. its. Acid neutralization may be obtained by
buffering components of the diet. In addition to
an early diagnosis of dental erosion, the detection
2.3 Crystallite Dissolution of isolated factors like sports drinks may be
implicated in multifactorial erosions. The signifi-
Hydrogen ions or chelating agents begin their del- cance of the mechanisms involved constitutes
eterious effects by dissolving enamel crystal, prerequisites, which are mandatory to initiate
either in the center of crystallites (central dissolu- preventive and therapeutic measures.
2 Enamel Softening (Dental Erosion) 13

Aprismatic outer enamel Prismatic enamel

IP

a b

Fig. 2.1 Rat’s molar enamel. (a) Normal aprismatic face, enamel displays a prismatic structure, where prisms
outer enamel/hydroxyapatite crystals are parallel, forming (P) (or rods) alternate with interprismatic enamel (IP)
a continuous palisade-like structure. (b) Beneath the sur- (interrod enamel)

2.3.1 Four Types of Physical 3. Abfraction is located mainly in the cemento-

and Chemical Dental Erosions enamel region where microfractures occur
Have Been Reported (also defined as fatigue wear). Wedge-shaped
defects are related to abfractions or wedge-
Imfeld (1996a, b) has defined different types of shaped non-carious cervical lesions. Analyses
tissue losses. According to Ganss (2006), each that demonstrate theoretical stress concentra-
type of alteration bears its own specificity. tion at the cervical areas of the teeth have not
yet been actually proven. However, there are
1. Abrasion is located on the incisal or occlusal some strong arguments favoring this possibil-
surfaces and depends on the abrasiveness of ity. The non-carious stress-induced cervical
the individual diet. The most abrasive agents lesion or abfractions are observed in the buc-
are toothpaste, as shown by clinical data and cal surface at the cemento-enamel junction of
in vitro studies. Both patient factors and mate- the teeth, with prevalence ranging in humans
rial factors influence the prevalence of from 27 to 85 % (Sarode and Sarode 2013)
abrasion. 4. Erosion results from the action of acids or
2. Attrition results from the action of the antago- chelators acting on plaque-free tooth surfaces.
nistic teeth. It has also been named demastica- The loss of tooth structure is due to acid dis-
tion. It is a mixture of abrasion and attrition. solution without involvement of bacteria.
14 M. Goldberg

Aprismatic
outer enamel

Prismatic
enamel

Fig. 2.2 Human enamel. The surface outer enamel layer looks laminated. This is not the case for the prismatic enamel
located underneath

Regurgitated gastric acids or extrinsic compo- with enlarged inter-crystallite spaces. With
nents (soft drinks, acidic fruits) may act as effects that are time dependent and concentration
extrinsic agents. Erosion is related to enamel dependent, the 5–15 μm thick aprismatic layer
surface softening. Repeated direct removal of disappears gradually; and consequently the over-
a softened enamel layer favors more rapid all enamel thickness is reduced. The 3–5 μm pris-
demineralization and tissue loss (Figs. 2.3b matic enamel, which is now exposed by the
and 2.4b). erosion, displays a scalloped profile with numer-
ous indentations and a drastic calcium and phos-
phate loss that is important near the new surface.
2.3.2 Structure and Chemistry The loss is gradually reduced until it reaches the
of Dental Erosion original enamel level. The inner prismatic enamel
is not altered, and both the enamel shape and
Table 2.1 thickness are undamaged.
Structurally, the outer layer of enamel (apris- The thickness of the softened outermost
matic zone) consists of parallel crystals forming enamel and dentin layers is estimated to be
a palisade-like structure (Figs. 2.1a and 2.3b). 2–5 μm. Citric acid erosion caused a mean sub-
The free ending of the crystals, located beneath a stance loss of 16.0 μm (SD ± 2.5 μm).
glycoprotein structure, which is controlled by the Remineralization of re-hardened enamel is appar-
dental plaque, melts in response to the acidic ently similar to the original structure (Feagin
extracellular gel or displays corroded extremities et al. 1969).
2 Enamel Softening (Dental Erosion) 15

a b

Fig. 2.3 (a) The outer enamel layer displays some interruptions or defects after softening. (b) The surface of corroded
enamel displays structural alterations at the tip of crystallites and, at some locations, between crystallites

Fig. 2.4 (a) At the

surface, crystallite
endings look irregular
with a scalloped profile.
(b) There is a gradual
100
mineral increase after b
80
the mineral loss due to V
the softening agent in in % 60
the outer enamel surface. 40
The percentage of 20
mineral reaches a surface softened enamel
0
“normal” value at 50 μm 0 50 100 150
under the enamel surface d in µm
16 M. Goldberg

Table 2.1 Composition percentage in enamel and dentine of the western population. In such case, the ero-
Enamel Dentine sion is mostly palatal, due to reflux disease,
percent by percent by regurgitation, anorexia, bulimia, and rumination
Component volume volume
(Eisenburger 2009).
Carbonated 85 47
Micro- and nanoindentations, indentation
hydroxyapatite
Water 12 20
length, and surface hardness measurements,
Protein and lipid 3 33 according to Knoop or Vickers, have identified
See references by: Curzon and Featherstone (1983); De
rhomboid indentation of about 30–40 μm length.
Carvalho Sales-Peres et al. (2007); Featherstone and Lussi They have been recorded immediately and are
(2006); and Lussi and Jaeggi (2008) not time dependent. Surface profilometry allows
determining by scanning electron microscopy the
The mineral part of teeth is a calcium-deficient tendency of the stylus to penetrate the fragile
carbonated hydroxyapatite. Substitutions in the outer layer. Altogether, other methods such as
crystal lattice render the mineral phase more acid SEM and ESEM, surface hardness measure-
soluble. The direct attack by hydrogen ion com- ments, surface profilometry, iodide permeability
bines with the carbonate and phosphate release of test, atomic force microscopy, nanoindentations,
the crystal surface, leading to direct surface etch- and ultrasonic measurement of enamel thickness
ing. The citrate ion can also form complex with may provide insights on the effects of acid solu-
the calcium removed from the crystal surface. tions on enamel softening and the subsequent
The substitutions in the mineral crystal lattice erosion (Fig. 2.4b).
disturb the structure. The carbonate content of Preventive strategies of patients suffering
“sound” enamel is approximately 3 %, while in from erosion include dietary counseling, stimula-
dentine it is 5–6 %. Therefore the mineral is even tion of salivary flow, optimization of fluoride
more acid soluble in dentine. Crystals in dentine regimens, modification of erosive beverages, and
are smaller than in enamel; consequently the dis- adequate oral hygiene measures (Magalhaes
solution process needs shorter periods of time in et al. 2009).
dentine compared with enamel.
Chemical factors explain erosive attack.
Addition of calcium and phosphate salts to ero- References
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