Textbooks in Contemporary Dentistry

Nikolaos Kotsanos
Haim Sarnat
Kitae Park Editors

Pediatric
Dentistry
Textbooks in Contemporary Dentistry
This textbook series presents the most recent advances in all fields of dentistry, with the aim of bridging the
gap between basic science and clinical practice. It will equip readers with an excellent knowledge of how to
provide optimal care reflecting current understanding and utilizing the latest materials and techniques. Each
volume is written by internationally respected experts in the field who ensure that information is conveyed in
a concise, consistent, and readily intelligible manner with the aid of a wealth of informative illustrations.
Textbooks in Contemporary Dentistry will be especially valuable for advanced students, practitioners in the
early stages of their career, and university instructors.

More information about this series at http://www.­springer.­com/series/14362

Nikolaos Kotsanos • Haim Sarnat • Kitae Park
Editors

Pediatric Dentistry
Editors
Nikolaos Kotsanos Haim Sarnat
Department of Paediatric Dentistry Department of Pediatric Dentistry, School
Aristotle University of Thessaloniki of Dental Medicine
Thessaloniki Tel Aviv University
Greece Tel Aviv
Israel
Kitae Park
Institute of Oral Health Science
Samsung Medical Center, School of Medicine
Sungkyunkwan University
Seoul
Korea (Republic of)

Originally published by Fylatos Publishing, Thessaloniki, 2015

ISSN 2524-4612     ISSN 2524-4620 (electronic)

Textbooks in Contemporary Dentistry
ISBN 978-3-030-78002-9    ISBN 978-3-030-78003-6 (eBook)
https://doi.org/10.1007/978-3-030-78003-6

© Springer Nature Switzerland AG 2015, 2022

1th edition: © Fylatos Publishing, Thessaloniki 2015

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 V

Contents

1 Pediatric Dentistry: Past, Present, and Future . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Nikolaos Kotsanos, Haim Sarnat, and Kitae Park

2  hild Cognitive Development: Building Positive Attitudes

C
toward Dentists and Oral Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Trilby Coolidge, Jacqueline P. Spector, and Jaap Verkamp

3 Pediatric Body Growth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

Panagiota Triantafyllou and Stephanie Roberts

4 Child Dental Fear, Communication and Cooperation . . . . . . . . . . . . . . . . . . . . . . . . 37

Trilby Coolidge and Nikolaos Kotsanos

5 Behavior Guidance and Communicative Management . . . . . . . . . . . . . . . . . . . . . 61

Travis Nelson and Nikolaos Kotsanos

6 Examination, Diagnosis, and Treatment Plan Implementation . . . . . . . . . . . . . 79

Stergios Arizos, Johan K. M. Aps, and Konstantinos N. Arapostathis

7 Local Anesthesia in Pediatric Dentistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111

Konstantinos N. Arapostathis and Jean-Louis Sixou

8  harmacologic Behavior Management (Sedation – General

P
Anesthesia) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Dimitrios Velonis, Dimitrios Emmanouil, and Keira P. Mason

9 Growth of the Craniofacial Complex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155

Fernando Pugliese, Anastasios A. Zafeiriadis, and Mark G. Hans

10 Tooth Eruption, Shedding, Extraction and Related Surgical Issues . . . . . . . . 177

Aristidis Arhakis, Ola B. Al-Batayneh, and Hubertus van Waes

11 Orthodontic Knowledge and Practice for the Pediatric Dentist . . . . . . . . . . . . 207

Kitae Park, Anastasios A. Zafeiriadis, and Nikolaos Kotsanos

12 Dental Caries Prevention in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . 247

Nikolaos Kotsanos, Rosalyn Sulyanto, and Man Wai Ng

13 Restoration of Carious Hard Dental Tissues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281

Nikolaos Kotsanos and Ferranti Wong

14 Pulp Therapy in Pediatric Dentistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315

Aristidis Arhakis, Elisabetta Cotti, and Nikolaos Kotsanos

15 Periodontal Diseases in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . 347

Aikaterini-Elisavet Doufexi and Frank Nichols

16 Dentoalveolar Trauma of Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . 363

Cecilia Bourguignon, Aristidis Arhakis, Asgeir Sigurdsson,
and Nikolaos Kotsanos
VI Contents

17 Developmental Defects of the Teeth and Their Hard Tissues . . . . . . . . . . . . . . . 415

Nikolaos Kotsanos, Petros Papagerakis, Haim Sarnat,
and Agnès Bloch-­Zupan

18 Tooth Wear in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465

Nikolaos Kotsanos and Dowen Birkhed

19 Temporomandibular Disorders in Children and Adolescents . . . . . . . . . . . . . . . 475

Linda Van den Berghe and Louis Simoen

20 Oral Lesions in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 485

Stephen Porter and Alexandros Kolokotronis

21 The Young Dental Patient with Systemic Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515

Aristidis Arhakis and Nikolaos Kotsanos

22  isabilities, Neuropsychiatric Disorders, and Syndromes in Childhood

D
and Adolescence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 527
Nikolaos Kotsanos, Luc A. M. Marks, Konstantinos N. Arapostathis, and Kazumi
Kubota

23 Child-Centred Dentistry: Engaging and Protecting Children . . . . . . . . . . . . . . . 553

Zoe Marshman and Helen Rodd

Supplementary Information
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565
 VII

Contributors

Ola B. Al-Batayneh Preventive Dentistry Department, Jordan University of Science and

Technology, Irbid, Jordan
olabt@just.edu.jo

Johan K. M. Aps School of Oral Hygiene, Artevelde University of Applied Sciences, Ghent,
Belgium
Department of Pneumology, Free University Brussels, Brussels, Belgium
Opinident BV, Marke, Belgium

Konstantinos N. Arapostathis Department of Paediatric Dentistry, School of Dentistry,

Aristotle University of Thessaloniki, Thessaloniki, Greece
koarap@dent.auth.gr

Aristidis Arhakis Department of Paediatric Dentistry, School of Dentistry, Aristotle

University of Thessaloniki, Thessaloniki, Greece
arhakis@dent.auth.gr

Stergios Arizos Department of Paediatric Dentistry, School of Dentistry, Aristotle University

of Thessaloniki, Thessaloniki, Greece
starizos@otenet.gr

Linda Van Den Berghe Ghent University, Faculty of Medicine and Health Sciences, Oral
Health Sciences, Department of Special Care in Dentistry, University Hospital, Ghent,
Belgium
Linda.VanDenBerghe@UGent.be

Dowen Birkhed Former: Department of Cariology, Göteborg University, Gothenburg,

Sweden

Agnès Bloch-Zupan Faculté de Chirurgie Dentaire, University of Strasbourg, Strasbourg,

France
agnes.bloch-zupan@unistra.fr

Cecilia Bourguignon Private Practice in Endodontics and Dental Traumatology in Paris,

Paris, France

Trilby Coolidge Oral Health Sciences, University of Washington, Seattle, WA, USA
tcoolidg@uw.edu

Elisabetta Cotti Department of Conservative Dentistry and Endodontics, University of

Cagliari, Cagliari, Italy

Aikaterini-Elisavet Doufexi Department of Preventive Dentistry, Periodontology and Implant

Biology, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece
doufexi@dent.auth.gr
VIII Contributors

Dimitrios Emmanouil Department of Paediatric Dentistry, School of Dentistry, National and

Kapodistrian University, Athens, Greece
emmand@dent.uoa.gr

Mark G. Hans Department of Orthodontics, Case Western Reserve University, School of

Dental Medicine, Cleveland, OH, USA
mgh4@case.edu

Alexandros Kolokotronis School of Dentistry, Aristotle University, Thessaloniki, Greece

alkoloko@dent.auth.gr

Nikolaos Kotsanos Department of Paediatric Dentistry, School of Dentistry, Aristotle Uni-

versity of Thessaloniki, Thessaloniki, Greece
kotsanos@dent.auth.gr

Kazumi Kubota Department of Special Needs Dentistry, Division of Hygiene and Oral Health,
School of Dentistry Showa University, Tokyo, Japan
kubotan@dent.showa-u.ac.jp

Luc A. M. Marks Center for Dentistry and Oral Hygiene – UMCG, University of Groningen,
Groningen, The Netherlands
l.a.m.marks@umcg.nl

Zoe Marshman Unit of Oral Health, Dentistry and Society, School of Clinical Dentistry,
University of Sheffield, Sheffield, UK
z.marshman@sheffield.ac.uk

Keira P. Mason Department of Anaesthesia, Harvard Medical School, Boston, MA, USA
Keira.Mason@childrens.harvard.edu

Travis Nelson Department of Pediatric Dentistry, University of Washington, Seattle,

WA, USA
tmnelson@uw.edu

Man Wai Ng Boston Children’s Hospital, Boston, MA, USA

Manwai.ng@childrens.harvard.edu

Frank Nichols Division of Periodontology, Department of Oral Health and Diagnostic

Sciences, University of Connecticut School of Dental Medicine, Farmington, CT, USA
nichols@uchc.edu

Petros Papagerakis College of Dentistry, University of Saskatchewan, Saskatoon, Canada

petros.papagerakis@usask.ca

Kitae Park Institute of Oral Health Science, Samsung Medical Center, School of Medicine,
Sungkyunkwan University, Seoul, Korea (Republic of)
park2426@skku.edu

Stephen Porter UCL Eastman dental Institute, University College, London, UK

s.porter@ucl.ac.uk

Fernando Pugliese Department of Orthodontics, Case Western Reserve University, School of

Dental Medicine, Cleveland, OH, USA
fdp10@case.edu
 IX
Contributors

Stephanie Roberts Attending in Endocrinology, Boston Children’s Hospital, Boston, MA,

USA
Stephanie.Roberts@childrens.harvard.edu

Helen Rodd Unit of Oral Health, Dentistry and Society, School of Clinical Dentistry,
University of Sheffield, Sheffield, UK
h.d.rodd@sheffield.ac.uk

Haim Sarnat Department of Pediatric Dentistry, School of Dental Medicine, Tel Aviv
University, Tel Aviv, Israel
sarnatha@tauex.tau.ac.il

Asgeir Sigurdsson New York University College of Dentistry, New York, NY, USA
asgeir.sigurdsson@nyu.edu

Louis Simoen Ghent University, Faculty of Medicine and Health Sciences, Oral Health
Sciences, Department of Special Care in Dentistry, University Hospital, Ghent, Belgium
louis.simoen@ugent.be

Jean-Louis Sixou Department: Paediatric Dentistry, Faculty of Dentistry, University of

Rennes 1, Rennes, France
jean-louis.sixou@univ-rennes1.fr

Jacqueline P. Spector Oral Health Sciences and Psychology, University of Washington,

Seattle, WA, USA
jpick@uw.edu; jpick@u.washington.edu

Rosalyn Sulyanto Harvard School of Dental Medicine, Boston Children’s Hospital, Boston,
MA, USA
rosalyn.sulyanto@childrens.harvard.edu

Panagiota Triantafyllou Scientific collaborator in Pediatric Endocrinology, Department of

Pediatrics, Aristotle University of Thessaloniki, Thessaloniki, Greece
ptriantafyllou@auth.gr

Dimitrios Velonis Pediatric Dentist, Oral Medicine Specialist, Pediatric Laser Dentistry,
Larisa, Greece

Jaap Verkamp Clinic for Paediatric Dentistry, Kindertand, Amsterdam, Netherlands

admin@Kindertand.nl

Hubertus Van Waes Clinic of Orthodontics and Peadiatric Dentistry Center for Dental
Medicine, University of Zurich, Zurich, Switzerland
Hubertus.vanwaes@zzm.uzh.ch

Ferranti Wong Barts and the London School of Medicine and Dentistry, Queen Mary
University of London, London, UK
f.s.l.wong@qmul.ac.uk

Anastasios A. Zafeiriadis Department of Orthodontics, School of Dentistry, Aristotle

University of Thessaloniki, Thessaloniki, Greece
tzafeir@dent.auth.gr
 1 1

Pediatric Dentistry: Past,

Present, and Future
Nikolaos Kotsanos, Haim Sarnat, and Kitae Park

Contents

1.1 Brief Historical Overview – 2

1.2 Child Oral Health. Inequalities and the Dental Services – 4

1.2.1 Trends in Pediatric Dentistry in the Future – 6

1.3 Addressing Children’s Rights – 6

1.4 Breadth of Knowledge in Pediatric Dentistry – 7

References – 9

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_1
 2 N. Kotsanos et al.

1.1 Brief Historical Overview

1
Meeting the oral among other health needs, in a humane
manner, and successfully preventing oral disease of chil-
dren and adolescents, including those with disabilities, is
a right for the youth. It is also a measure of a high stan-
dard of living and is seen nowadays in many societies
across the globe while it remains a goal for many others.
Its fulfillment has taken long efforts of dental educating
and planning pediatric dental services, and the pioneer-
ing attempts to set the foundation for today’s level of
care should be acknowledged.
The first organized child dental treatment efforts
seem to have started at the end of the eighteenth cen-
tury in New York and Paris by private practitioners’ ini-
tiatives. Examination of 5- to 12-year-old children was
recorded in 1850 in Belgium, and, on the other side of
the Atlantic, the Baltimore College of Dentistry in 1840
and the Harvard School of Dental Medicine in 1867 ..      Fig. 1.1 A dental surgery of the second quarter of the twentieth
century. Museum items
were founded. Thus, over time, dental education moved
from a largely proprietary to science-based education
housed within the university and/or academic health
center structure [1]. In the early 1900s Europe, follow-
ing the publication of the first epidemiological studies in
children recording massive caries rates, the first school-­
based dental care was established in Strasbourg by the
Danish dentist E. Jessen, and this model for child oral
care was then followed in several countries, particularly
in Scandinavia, focused at that time on the permanent
teeth only [2].
At the same time, dental clinics were established
in order to provide free care to impoverished children
by philanthropists, Forsyth in Boston and Eastman in
Rochester at US East coast. In the second quarter of the ..      Fig. 1.2 Orthodontic treatment with bands bearing brackets at
twentieth century, the first books devoted to “pedodon- the third quarter of the twentieth century
tics” were published, and new such departments estab-
lished in US dental schools (. Fig. 1.1), which, beyond
theoretical courses, included clinical training. Thus, by ative, in maintaining carious primary teeth or the space
the end of World War II, pediatric dentistry was already from their premature loss. As for available restorative
a separate discipline. materials, the approach could not be primarily aesthetic
Before then, local anesthesia was neither standard- at a time that only few children had access or happily
ized nor as efficient as nowadays. Behavior management accepted orthodontic treatment (. Fig. 1.2).
and guidance was during the third quarter of the twen- Preventive dentistry and its teaching acquired its
tieth century progressively based on knowledge and decisive role in that third quarter of the twentieth cen-
principles of child psychology, when the concomitant tury [4], mainly connected to oral hygiene measures for
evolution of the latter allowed for it. The progress of dental decay. Artificial fluoridation of drinking water
dental science and research and the emphasis on psycho- was established in some countries, starting with the
logical and behavioral aspects have had a great impact in USA, and the global spread of the use of fluoridated
changing the image of dentistry for children and adults toothpaste significantly reduced caries in children. This
alike. The development of post graduate programs had was at first in industrialized countries, where fluoride
centered in a more total patient care approach in pediat- toothpaste consumption has come to be today around
ric dentistry [3]. The dental treatment was mainly restor- 300 ml per person (three normal size tubes). The effec-
Pediatric Dentistry: Past, Present, and Future
tiveness of brushing in dental and gingival health has
since been connected with a healthy mouth and a bright
smile in modern culture (. Fig. 1.3).
The acid etching of enamel, which was first described
in 1955, was a further breakthrough. It proved to be the
decisive technology for the continuous improvement of
composite resins. Mainly these were the aesthetic restor-
ative materials contributing to a more conservative
approach in restoring carious teeth including sealing
vulnerable fissures for caries reduction. Thus, the end of
..      Fig. 1.3 The bright smile reflects health and communication in
modern societies
..      Fig. 1.4 Logos of world leading pediatric dentistry bodies
3 1
the twentieth century saw a shift from mainly restorative
to preventive, cosmetic, and orthodontic procedures in
children and adolescents [5, 6], which continues to date.
Overview
Milestones of pediatric dentistry in the twentieth century
(from beginning to end):
1. Epidemiological recording of dental caries docu-
ments extent.
2. Pediatric dentistry textbooks get published.
3. Effective formulated local anesthesia is introduced.
4. Postgraduate pediatric dentistry programs are
developed.
5. Communicative behavior management is widely
taught.
6. Topical fluorides prevail and major caries decrease
is evidenced in children.
7. Etching the enamel boosts fissure sealing and com-
posite as restorative.
8. The rights of the child concept are adopted.
The American Academy of Pediatric Dentistry was
founded as early as 1947 and affected the academic and
professional developments in other parts of the world.
Two decades later, the International Association of Pae-
diatric Dentistry was established in 1969 [7], and after
another two decades, the European and the Austral-
asian Academies were founded in 1990 for the better
coordination of the already existing national pediatric
dental societies in those continents. Their major con-
tributions are the political influence and advocacy for
child oral health as well as the issuing of guidelines for
improved and evidence-based dental care for children
(. Fig. 1.4). Throughout the second half of the twen-
tieth century, pediatric dentistry was increasingly recog-
nized as a specialty of dentistry in many countries and
this trend continues to date.
 4 N. Kotsanos et al.

1.2  hild Oral Health. Inequalities

C caries experience among 35- to 45-year-old and 65- to
1 and the Dental Services 74-year-old groups was still on the rise [13]. At about
the same period with China, i.e., 1992–2016, a decline
Dental caries is the most common chronic disease in started showing in 2–5- and 11–15-year-olds in India [14]
childhood [8]. For about 2/3 of the twentieth century, it (. Fig. 1.6). Other reports however find caries levels to
posed a physical as well as a social problem for children be relatively low in many emerging Asian countries, even
and adults in the industrialized countries. Implementing though, for the most part, carious and periodontal needs
preventive programs achieved some caries reduction in remain there largely unmet [16]. Notwithstanding the
the child population after that time. For example, the diversity of dental caries reports in the various parts of
mean dmfs (sum of decayed, missing, and filled primary Africa, caries does not seem to be among the prime fac-
tooth surfaces) of 4-year-olds in southern Sweden was tors influencing oral health-related quality of life [17].
reduced from 8 to 2 between 1967 and 1980 [9]. At the Regarding restorative needs, a decrease of multi-­
same trend, 70% of the Danish 5-year-olds in 1998 were surface cavities, endodontic treatment needs, and place-
caries-free, while the mean DMFS (same index for per- ment of preformed metal crowns in primary teeth has
manent teeth) of 12-year-olds was reduced to 1.5 [10]. been noted in university pediatric dentistry clinics of
Similar reductions had been observed in the USA in the countries showing significant caries decline. Though
1970s. The average DMFS of children aged 5–17 years these are still widely performed there today, the most
decreased from 7.1 to 4.8 with a dramatic decrease in the frequent recipients are those socioeconomically worse
number of extracted first permanent molars [11]. It was and minorities like immigrants [18–20]. Before, caries
remarkable that this trend was irrespective of systemic indices were high because dental caries, by affecting the
ways of fluoride use (. Fig. 1.5). majority of children in the early and mid-twentieth cen-
In other parts of the world this improvement came tury, was considered a disease of modernization; there
somewhat delayed. In Italy, for example, a report for was a higher prevalence in developed countries and in
preschool children showed caries decline in the last individuals with higher socioeconomic status. In the
decade of the past century [12]. In China this seemed late twentieth and the twenty-first century, this pattern
to occur in the first decade of the current century, while of caries prevalence and severity changed in developing

..      Fig. 1.5 Tooth decay Tooth Decay Trends in Fluoridated and Non-Fluoridated
(DMFT) trends of 12-year-olds Countries
in fluoridated and non-fluori- WHO data on DMFT in 12 year olds*
dated countries. (Accessed at
7 https://fluoridealert.­org/ Ice
lan
studies/caries01) d
8 Ne
wZ
eal
an Ital
d y
Non-Fiuoridated**
Decayed, Missing of Filled Teeth (DMFT)

Jap Fluoridated
6 an

Aus
t rali
a

4
Belgium
United Sta Irela
nd
tes
2

1970 1980 1990 2000 2010

Years 1970 through 2010
* World Health Organization (WHO). Collaborating Centre for Education, Training, and Research in Oral
Health, Malmö University, Sweden, http://www.mah.se/CAPP/ (accessed June 10, 2012).

** No water or salt fluoridation.

Pediatric Dentistry: Past, Present, and Future
5 1
..      Fig. 1.6 The changing DMFT
pattern of caries incidence in 5
12-year-olds in developed and Developed countries All countries Developing countries
developing countries during the
last two decades of the twentieth
century and beyond [15] 4

0
1980 1981 1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002

and developed countries; low income, low education lev-

els, and lower classes of occupations have been consis-
tently related to high caries risk [21–25]. To effectively
combat this established discriminative caries pattern,
contemporary research and clinical efforts are directed
toward reliably targeting high-risk children, i.e., with
active disease before being symptomatic. Interventions
that begin early and combine multiple strategies hold
greatest potential [26].
Within this frame, refugee populations except for
being subject to worse physical, mental, and social
health outcomes experience difficulties accessing health
services in their new country [27]. Further, in most low-
and middle-income countries, oral health-care demands
are beyond the capacities of their health-care systems,
..      Fig. 1.7 Contemporary orthodontic treatment with tooth-­
while in the private sector there may be an uneven dis-
colored material. (Courtesy of Dr. Manoukakis)
tribution of dental services in the expense of rural areas
[28]. Despite being largely preventable, oral diseases are
still a major public health problem in child populations of periodontal disease and anomalies of occlusion.
in many parts of the world [29]. The idealization of smile aesthetics nowadays, which
Special needs children have, or are at risk, for chronic ­promotes images of healthy teeth and gums, helps the
physical, developmental, behavioral, or emotional con- adoption of good oral hygiene habits (. Fig. 1.3).
ditions, which can impact on their oral health and usu- Consequently, it is very likely that the gingival health
ally require increased and/or special services for dental has improved [32]. Regarding orthodontics, it seems
and periodontal disease. Studies of special care needs now attractive, considering the large increase of accep-
children show much higher prevalence of caries com- tance and frequency of children under orthodontic
pared to children in the general population. In two stud- treatment (. Fig. 1.7). While it has a positive impact
ies reporting on disabled children in Kuwait and children on the oral health-related quality of life of adolescents
with autism in South Africa, the teeth most affected [33], treatment requirements – compliance to treatment,
were the first permanent molars and their periodontal long duration, costs – pose a burden to many population
and restorative needs were mostly unmet [30, 31]. groups.
Although there is little longitudinal data on the his- Dental auxiliary personnel were introduced several
tory of oral diseases/conditions other than caries, there decades ago in industrialized countries for various rea-
has been some progress in the prevalence and treatment sons including the reduction of costs, which are higher
 6 N. Kotsanos et al.
for dental education than any other health profession.
1 One such example was in Australia’s health-care system
in the mid-1960s, in trying to address the then difficult-­
to-­meet treatment needs for child dental disease. Today,
oral health therapists and hygienists comprise one quar-
ter of the dental workforce providing fissure sealants,
restorations and primary tooth extractions, oral health
instruction, fluoride applications, scale and cleans,
and some periodontal services [34]. Thus, much of the
less complex dental treatment needs are not provided
by dentists themselves, and this, along with the caries
decline, means that their involvement with restorative
procedures has decreased significantly.
Lastly, upcoming social changes bring about other
issues. As many families nowadays have limited free
time, either because both parents are occupied at work or
because they escort children in several organized extra-
curricular activities (. Fig. 1.8), they become more selec-
tive in search of high-quality services for their children.
Even though restorative procedures show reduction, the
emphasis on quality and the increase in preventive, cos-
metic, and orthodontic services compensate for it.
Τhe recent pandemic of airborne Covid-19 with
even asymptomatic carriers spreading the disease has
challenged dentistry among other health professions.
Concerns regarding dentists’ and patients’ safety dur-
ing the outbreaks limited dental care to emergencies
compromising preventive appointments. Among other
impacts [35], the aerosols produced in several dental
procedures imposed a higher level of protection than
before, necessitating the use of FFP2/FFP3 masks and
other protective gear. The production of successful vac-
cines has somewhat eased fears for dental visits, but
the risk of similar viral future threats calls for constant
alertness.
..      Fig. 1.8 Appointment delays with families of limited free time
1.2.1  rends in Pediatric Dentistry
T
in the Future
Future trends for the practice of pediatric dentistry
based on research advances may include the following:
1. Predominance of prevention of dental caries by early
identifying high caries risk, informing and engaging
parents, promoting oral health care at home, use of
fluoride and other prevention technologies, applica-
tion of fissure sealants, and establishment of efficient
recall system.
2. Increased intervention in orthodontic anomalies and
smile aesthetics, which already are of high interest
among parents and children.
3. Improved accessibility and dental care for people
with disabilities, alongside with extending the dental
neglect concept to them.
4. Increased use of new technology dental equipment
(e.g., evolution of laser devices [36], sophisticated
electronic anesthesia techniques that increase effi-
ciency and acceptance by children, etc.).
5. Therapeutic approaches based on the principles of
preventive dentistry including minimally invasive
operative approaches lead to painless and often
pleasant dental procedures for children. This
improved dentist’s image will further reduce phobic
young adults.
6. Exclusive use of tooth-colored materials with ever-
improving bonding and with emphasis on safety
(lack of toxicity), while these principles increasingly
apply to preformed crowns.
7. Molecular biology and engineering bring potential
applications in the dental practice with regeneration
of dental tissue by the stem cell technology.
8. Better understanding the microbiome of the human
body and its environment will allow development of
preventive health measures for oral and general
health.
1.3 Addressing Children’s Rights
A growing body of evidence leads to the view that chil-
dren’s development, following the social transformation
of childhood in modern societies, is influenced both by
family and by the social and cultural norms of society.
Thus, children’s health, development, achievements, and
social attainments have come to require the interest,
guidance, and protection of both families and society
[37].
In the United Nations Convention on the Rights of
the Child [38], the term “child” refers to anyone under
the age of 18. It was signed on November 20, 1989 and
is commemorated on this date as world’s children’s day,
Pediatric Dentistry: Past, Present, and Future
and it is the most widely ratified human rights treaty
(about 200 countries currently). Its purpose is to defend
children’s rights and protect them from exploitation
­ failure of parent or guardian to seek and follow through
phenomena, violence, and abuse. Oral health is not spe-
cifically mentioned but is nevertheless implied under
general health and wellbeing. The reference to health
rights in articles 23–25 briefly includes:
7 1
cause for suspecting neglect. The American Academy of
Pediatric Dentistry defines dental neglect as “the willful
with treatment necessary to ensure a level of oral heath
essential for adequate function and freedom from pain
and infection” [42].

55 No child is deprived of the right of access to highest

Overview
attainable standard of health.
In general, a contemporary practicing dentist should:
55 The child receives periodic review of the treatment.
55 Embrace risk assessment tools being prevention-­
55 Disabled children have effective access to and receive
minded
health-care and rehabilitation services.
55 Utilize changing technology for improved patient
care
On the other hand, article 22 states these health rights
55 Appreciate evidence-based advances in biomedical
also apply to children with refugee state, further to those
and behavioral sciences
for protection and humanitarian assistance. Undergrad-
55 Be willing to interact professionally with other
uate pediatric dentistry programs in most schools con-
health-care providers
tain some clinical training on patients with disabilities.
55 Be committed to ethics both in treatment choices
One of postgraduate orientations in pediatric dentistry
and electronic patient record use
is the training at competency level of oral care of these
individuals at least up until early adulthood.
Recognizing the need to prevent severe early child-
hood caries, which remains a very frequent cause of 1.4  readth of Knowledge in Pediatric
B
oral inflammation and pain in many population groups,
Dentistry
impacts on child’s quality of life [39]. The first dental
visit has been set to be when the first tooth erupts and
Guiding and caring each child to stay orally healthy is
not later than the child’s first birthday [40]. This is for
a serious responsibility and has an educating influence
informing and educating parents on proper child tooth
for her/his psychological maturation. If done effectively,
care because the above severe disease undermines the
it earns the trust of the parents, is rewarded with great
rights of the children, affecting not only their physical
satisfaction, and promotes good oral health in the long
but also their psychological health. The definition of
run. To adequately train the new dentists for this task
health by the WHO includes the general state of the indi-
(. Fig. 1.9), the discipline of pediatric dentistry needs
vidual, which includes avoiding dental fear and anxiety.
to draw and transfer knowledge from other non-dental
Informed consent of the parent and perhaps the
disciplines, primarily from the fields of medicine and
patient is another issue. It is the legal instrument that
child psychology, so that they acquire:
protects the right of the patient – defended by the par-
ent or legal guardian in case of a minor – to a repres-
sive approach and treatment without her/his approval.
While this is in a positive direction for children’s’ rights,
with particularly skeptical and difficult-to-convince par-
ents, dentists may be more prone to sedation techniques
for treating more challenging young dental patients,
cooperation-­wise. This poses the risk of moving to more
defensive pediatric dentistry approaches.
It is important for all health-care providers (includ-
ing dental providers) to be knowledgeable and alert
about signs and symptoms of child abuse and neglect
and to know how to respond [41]. Physical abuse, sex-
ual abuse, bite marks, bullying, and human trafficking
all constitute abuse issues. All findings when there is
reasonable suspicion of abuse should be reported for
further investigation. The dentist should also look for
adequate clothing and general and oral hygiene. Poor ..      Fig. 1.9 University dental school setting for pediatric dentistry
diet and lack of medical and dental care should be clinical training (prior to the covid-19 era)
 8 N. Kotsanos et al.

1. Good dental knowledge, in prevention of oral dis- 55 Support training programs, advising accreditation
1 eases, restoring dental cavities, wear and various boards, and sponsoring programs to enhance success
defects, pulp treatment, dental materials, oral sur- throughout their career
gery, preventive orthodontics, and certain principles 55 Be competitive in pursuing and advancing collabora-
of prosthetic dentistry tive research
2. Basic knowledge of pediatrics, anesthesiology, gen-
eral medicine and oral pathology, growth and devel- Engagement with pediatric dentistry ascribes the prac-
opment, as well as nutrition ticing dentist with an additional important social role
3. Knowledge of mental, emotional development, and as an educator, trainer, and protector of the vulnerable
child psychological issues, because each child groups, often in collaboration with the pediatrician and
requires different management, depending on age, many other clinicians and scientists. Along with prog-
maturity, and other physical abilities ress in recognizing children’s rights, this is still important
because access to care remains a serious public health
It is apparent, however, that the dentist has an obliga- problem, even in population sections of industrialized
tion to recognize the limits of his/her knowledge either countries. This role includes:
in dental/medical or in the behavior management
skills. In cases where the patient’s needs exceed those 55 Dynamic interventions for impoverished, neglected,
limits, the dentist must refer the patient to a special- or abused children
ist pediatric dentist. Moreover, the level of dental care 55 Undertaking interventions on preventing of dental
provided to the child should be of quality that can be caries, which remains a plague for certain groups of
­certified. Dental care and treatment options should unprivileged child populations, by individual or col-
not be empirical or even based only on expert opin- laborative voluntary activities (. Fig. 1.10)
ion. Today it is evidence-based as far as possible, which 55 Counseling parents and children on obesity, an epi-
means knowledge that comes from randomized control demic of our time, discussing healthy eating habits
trials, systematic reviews, and meta-analyses. Research and regular exercise
today is deemed to fill the gaps in the documentation
of knowledge in pediatric dentistry, as in other fields
of medicine.
Pediatric dentistry has widely expanded its content,
due to the recognition of the importance of child oral
health and its effect on normal physical and psychologi-
cal development. Its effective practice requires the pedi-
atric dentist to collaborate with various other pediatric
specialties. The extensive level of education in pediatric
dentistry is not possible to be integrated in undergradu-
ate dental programs and it is taught in postgraduate spe-
cialization programs. These, according to the principles
of international bodies of pediatric dentistry [43–45],
aim to specialize the trainee in all aspects in order to be
able to:

55 Care of all the oral needs of infants, children, and

adolescents, including the medically compromised
and the young people with disabilities
55 Search for continuous improvement of his/her
knowledge by continuing clinical education and
acquire adequate teaching ability for disseminating
this knowledge
55 Participate in interdisciplinary groups for the caring
of children with special needs, e.g., the craniofacial
anomalies
55 Use the authority and expertise to advocate for ..      Fig. 1.10 Voluntary outreach service to underprivileged children
patient safety, improved outcomes, and intelligent as a joint action of local pediatric dental society members working
regulatory oversight on a company-sponsored caravan transformed to a dental surgery
Pediatric Dentistry: Past, Present, and Future
9 1
References 21. Armfield JM. Socioeconomic inequalities in child oral health:
a comparison of discrete and composite area-­based measures. J
Public Health Dent. 2007;67(2):119–25.
1. DePaola DP. The evolution of dental education as a profession,
22. Traebert J, Guimarães Ldo A, Durante EZ, Serratine AC. Low
1936–2011, and the role of the journal of dental education. J
maternal schooling and severity of dental caries in Brazilian pre-
Dent Educ. 2012;76(1):14–27.
school children. Oral Health Prev Dent. 2009;7(1):39–45.
2. Poulsen S, Koch G. Pediatric oral health care: the perspectives,
23. Christensen LB, Twetman S, Sundby A. Oral health in chil-
Ch 1. Ιn: Pediatric dentistry; a clinical approach. 2nd edn, Koch
dren and adolescents with different socio-cultural and socio-
G and Poulsen S (eds), Wiley-Blackwell, Chichester 2009.
economic backgrounds. Acta Odontol Scand. 2010;68(1):34–42.
3. Casamassimo PS. The practical importance of pediatric den-
https://doi.org/10.3109/00016350903301712.
tistry, Ch. 1. In: Casamassimo PS, Fields Jr HW, McTigue DJ,
24. Ferro R, Cecchin C, Besostri A, Olivieri A, Stellini E, Mazzo-
Nowak AJ, editors. Pediatric dentistry; infancy through adoles-
leni S. Social differences in tooth decay occurrence in a sample
cence. 5th ed. St Louis: Elsevier; 2013.
of children aged 3 to 5 in north-east Italy. Community Dent
4. Gerbert B. Planned change and the future of the dental educa-
Health. 2010;27(3):163–6.
tion system. J Dent Educ. 1986;50(10):585–93.
25. Marcenes W, Kassebaum NJ, Bernabé E, Flaxman A, Naghavi
5. Association of Pedodontic Diplomats. Survey of orthodontic
M, Lopez A, et al. Global burden of oral conditions in 1990–
services provided by pedodontists. Pediatr Dent. 1983;5:204–6.
2010: a systematic analysis. J Dent Res. 2013;92:592–7.
6. Christensen GJ. The future of dental practice. J Dent Educ.
26. Edelstein BL, Hirsch G, Frosh M, Kumar J. Reducing early
1986;50:114–8.
childhood caries in a Medicaid population: a systems model
7. Gelbier S. History of the International Association of Paediatric
analysis. J Am Dent Assoc. 2015;146(4):224–32. https://doi.
Dentistry. Part 3: Samuel D. Harris and some early pressures for
org/10.1016/j.adaj.2014.12.024.
international developments. Int J Paediatr Dent. 1995;5:123–5.
27. Riggs E, Rajan S, Casey S, Kilpatrick N. Refugee child oral
8. Oral health in America: a report of the Surgeon General. J Calif
health. Oral Dis. 2017;23:292–9. https://doi.org/10.1111/
Dent Assoc. 2000;28(9):685–95.
odi.12530.
9. Stecksen-Blicks C, Borssen E. Dental caries, sugar-eating habits
28. Saliba NA, Moimaz SA, Garbin CA, Diniz DG. Dentistry in
and tooth-brushing in 4-year-old children 1967-1997 in the city
Brazil: its history and current trends. J Dent Educ. 2009;73(2):
of Umea, Sweden. Caries Res. 1999;33:409–14.
225–31.
10. Holm AK, Poulsen S. Oral health in children and adolescents.
29. Watt RG, Mathur MR, Aida J, Bönecker M, Venturelli R,
Ch 2. In: Koch G, Poulsen S, editors. Pediatric dentistry; a clini-
Gansky SA. Oral health disparities in children: a canary in the
cal approach. Copenhagen: Munksgaard; 2001.
coalmine? Pediatr Clin N Am. 2018;65(5):965–79. https://doi.
11. National caries program. National Institute of Dental Research:
org/10.1016/j.pcl.2018.05.006.
The national dental caries prevalence survey: The prevalence of
30. Shyama M, Al-Mutawa SA, Morris RE, Sugathan T, Honkala
dental caries in the United States. US department of Health and
E. Dental caries experience of disabled children and young
Human Services, NIH Publication No 82–2245, Dec. 1981.
adults in Kuwait. Community Dent Health. 2001;18(3):181–6.
12. Ferro R, Besostri A, Olivieri A. Survey of caries experience in
31. Naidoo M, Singh S. The Oral health status of children with
3- to 5-year-old children in Northeast Italy in 2011 and its trend
autism Spectrum disorder in KwaZulu-Nata, South Africa.
1984-2011. Oral Health Prev Dent. 2017;15(5):475–81. https://
BMC Oral Health. 2018;18(1):165. https://doi.org/10.1186/
doi.org/10.3290/j.ohpd.a38976.
s12903-­018-­0632-­1.
13. Liu J, Zhang SS, Zheng SG, Xu T, Si Y. Oral health status and oral
32. Dye BA, Tan S, Smith V, Lewis BG, Barker LK, Thornton-
health care model in China. Chin J Dent Res. 2016;19(4):207–15.
Evans G, et al. Trends in oral health status: United States, 1988-
https://doi.org/10.3290/j.cjdr.a37145.
1994 and 1999-2004. Vital Health Stat. 2007;11(248):1–92.
14. Mehta A. Trends in dental caries in Indian children for the
33. Ferrando-Magraner E, García-Sanz V, Bellot-­Arcís C, Mon-
past 25 years. Indian J Dent Res. 2018;29(3):323–8. https://doi.
tiel-Company JM, Almerich-Silla JM, Paredes-­ Gallardo
org/10.4103/ijdr.IJDR_615_17.
V. Oral health-related quality of life of adolescents after orth-
15. Petersen PE (2003) The World Oral Health Report 2003. www.
odontic treatment. A systematic review. J Clin Exp Dent.
sciencedirect.com/topics/medicine-and-dentistry/dmft-index.
2019;11(2):e194–202. https://doi.org/10.4317/jced.55527.
Accessed on 21/14/2020.
34. Teusner DN, Satur J, Gardner SP, Amarasena N, Brennan
16. Saekel R. Comparison of oral health status in Asia: results for
DS. Variations in Australian dental therapy practice by practi-
eight emerging and five high income countries or regions and
tioner and workplace characteristics. Int Dent J. 2018;68(4):235–
implications. Chin J Dent Res. 2016;19(4):191–206. https://doi.
44. https://doi.org/10.1111/idj.12382.
org/10.3290/j.cjdr.a37144.
35. Campagnaro R, Collet GO, Andrade MP, Salles JPDSL, Calvo
17. Malele-Kolisa Y, Yengopal V, Igumbor J, Nqcobo CB, Rale-
Fracasso ML, et al. COVID-19 pandemic and pediatric dentistry:
phenya TRD. Systematic review of factors influencing oral
fear, eating habits and parent’s oral health perceptions. Child
health-related quality of life in children in Africa. Afr J
Youth Serv Rev. 2020;118:105469. https://doi.org/10.1016/j.
Prim Health Care Fam Med. 2019;11(1):e1–e12. https://doi.
childyouth.2020.105469.
org/10.4102/phcfm.v11i1.1943.
36. American Academy of Pediatric Dentistry. Policy on the use
18. Waldman HB. Are minority children getting their fair share of
of lasers for pediatric dental patients. Pediatr Dent. 2017;39(6):
dental services? ASDC J Dent Child. 1990;57(5):380–4.
93–5.
19. Blen M, Narendran S, Jones K. Dental caries in children
37. Children’s Health, The Nation’s Wealth. Assessing and improv-
under age three attending a university clinic. Pediatr Dent.
ing child health. National Research Council; Institute of Medi-
1999;21(4):261–4.
cine. Washington, DC: National Academies Press (US); 2004.
20. Ferrazzano GF, Cantile T, Sangianantoni G, Ingenito A, Rengo
https://doi.org/10.17226/10886.
S, Alcidi B, et al. Oral health status and Unmet Restorative
38. Convention on the rights of the child. At: https://www.unicef.
Treatment Needs (UTN) in disadvantaged migrant and not
org/sites/default/files/2019-04/UN-Convention-Rights-Child-
migrant children in Italy. Eur J Paediatr Dent. 2019;20(1):10–4.
text.pdf
https://doi.org/10.23804/ejpd.2019.20.01.02.
 10 N. Kotsanos et al.
39. Chen KJ, Gao SS, Duangthip D, Lo ECM, Chu CH. Prevalence
1 of early childhood caries among 5-year-old children: a system-
atic review. J Investig Clin Dent. 2019;10(1):e12376. https://doi.
org/10.1111/jicd.12376.
40. American Academy of Pediatric Dentistry. Periodicity of exami-
nation, preventive dental services, anticipatory guidance/coun-
seling, and oral treatment for infants, children, and adolescents.
Reference manual 2018/19, 40 (No. 6); 194–204.
41. American Academy of Pediatric Dentistry. Oral and dental
aspects of child abuse and neglect. Reference manual 2018/19,
40 (No. 6); 243–9.
42. American Academy of Pediatric Dentistry. Definition of dental
neglect. Reference manual 2018/19, 40 (No. 6);13.
43. European Academy of Paediatric Dentistry. Curriculum guidelines
for education and training in paediatric dentistry. At: www.eapd.
eu/uploads/files/Curriculum%20guidelines%20for%20Educa-
tion%20and%20Training%20in%20Paediatric%20Dentistry.pdf.
44. Australasian Academy of Paediatric Dentistry. Mission and
vision. At: www.aapd.org.au/viewStory/Mission-and-Vision.
45. American Academy of Pediatric Dentistry. Residency programs.
At: https://www.aapd.org/resources/member/residentresources/
residency-programs/.
 11 2

Child Cognitive Development:

Building Positive Attitudes
toward Dentists and Oral
Health
Trilby Coolidge, Jacqueline P. Spector, and Jaap Verkamp

Contents

2.1  he Dentist’s Long-Term Goal for Pediatric Patients

T
and an Introduction to Piaget’s Stages of Cognitive
Development – 12
2.1.1 S ensorimotor Stage – 12
2.1.2 Preoperational Stage – 15
2.1.3 Concrete Operational Stage – 17
2.1.4 Formal Operational Thought – 18

2.2  sing Memory Principles to Help Prevent the

U
Development of Fear – 20

2.3 Tailoring Oral Messages to the Individual Patient – 21

References – 22

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_2
 12 T. Coolidge et al.
2.1  he Dentist’s Long-Term Goal
T ..      Table 2.1 Stages of cognitive development of the child
for Pediatric Patients and an
Introduction to Piaget’s Stages
2 of Cognitive Development
Helping children develop positive attitudes about den-
tists and oral health is an effective strategy to ensure that
these patients continue to have positive attitudes about
dentists and oral health throughout their lives. This
long-term goal involves developing a relationship with
the child and his/her parents that fosters trust, as well
as providing those dental services that result in promot-
ing oral health in keeping children healthy throughout
their childhood. In our opinion, many of the difficulties
dentists encounter while trying to provide dental care to
young children are a result of focusing on the short-term
goal of completing a particular dental procedure, rather
than keeping this long-term goal in mind. A strong
background in child cognitive development will pro-
vide clinicians with tools helpful for accomplishing both
short- and long-term goals when working with children.
The Swiss psychologist Jean Piaget studied the
development of children’s thought processes for nearly
50 years (. Fig. 2.1). It became apparent to Piaget that
children are not simply “little” versions of adults whose
knowledge gradually increases. Rather, while their brains
go through processes of biological maturation which are
genetically influenced, children’s experiences interact
..      Fig. 2.1 Jean Piaget (1896–1980), Swiss philosopher and psy-
chologist
according to Piaget [2]
Birth to
2 years
2–6 years 6–11 years 11+ years
Senso- Preopera- Concrete Formal operational
rimotor tional operational (hypothetical/
abstract thinking)
with that physical maturation and result in the devel-
opment of cognitive abilities, i.e., interaction between
genetic and environmental features [1], and result in
qualitatively different ways of thinking or behaving as
they develop.
These new ways can be identified as occurring at
distinct times, or stages, during a child’s development.
This concept alone will serve the pediatric dentist well.
Piaget’s stage model of cognitive development provides
clinicians with the structure with which to understand
the thought processes of pediatric patients. Piaget stated
that children go through four different stages of cognitive
development (. Table 2.1) [2].
An understanding of Piaget’s model provides the cli-
nician about what behaviors to expect from children of
different ages and, important for that long-term goal,
how to help create positive schemata – mental represen-
tations – about dentists, dental visits, and good home
oral health behaviors.
2.1.1 Sensorimotor Stage
Case Study
You enter the operatory to find a new patient,
15-month-old Sally, and her mother. It’s Sally’s first
visit to a dentist. Your assistant had seated Sally in a
pediatric dental chair, and her mother is sitting on a
regular chair beside her, holding restless Sally’s hand.
Sally is holding a chain that has several large plas-
tic toy keys strung on it and is putting one or two
keys into her mouth and then pulling them out again.
After greeting her mother, you sit in your dental chair
and scoot over to Sally. As you get closer, you smile
and say “Hi, Sally.” She freezes, looks at you, closes
her eyes and turns her head away, and starts to cry.
The plastic keys fall out of her mouth. You turn on
the overhead exam light and focus it on Sally’s mouth,
move in between her and her mother, and use a den-
tal mirror to do a quick exam. Sally kicks harder and
cries more loudly, moving her head back and forth.
Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health
..      Fig. 2.2 Piaget’s early sensorimotor stage
The sensorimotor stage begins at birth and lasts until
approximately the child’s second birthday. Children are
born with reflexes (e.g., sucking), can see and hear, and
explore and learn about their worlds through their senses
and their ability to move (. Fig. 2.2). This means that
they understand their world through what they can sense
and physically interact with. One frequent way of learn-
ing about objects during this stage is to put them in one’s
mouth. Other ways to learn about objects and the world
around include looking and handling things with one’s fin-
gers. Some fascinating research has demonstrated that new-
borns can mimic adults who are sticking out their tongues
or making other facial gestures, indicating that mimicry is
another method of sensorimotor exploration [3].
Especially during the first year of life, the sensorimo-
tor child does not have a fully developed, individuated
sense of self. That is, she does not consider herself to
be a completely separate person from her caregivers.
This is why physical contact with caregivers is soothing,
while physical separation from them can be stressful. In
addition, children of this age are only concerned with
what they can sense in the present moment. The clini-
cian needs to remember how a child thinks at this stage:
“out of sight, out of mind.”
Piaget believed that children begin to construct
­schemata or concepts – ideas about how the world works –
during this stage. Schemata are mental representations
about the world and include different kinds of objects,
individuals, actions, descriptors or properties, and abstrac-
tions [4]. For example, parents point out a dog and say:
“Look, honey, see the doggie!” Eventually, the child points
to a different dog and says: “Doggie!” It seems that the
child has learned that certain objects are “doggies.” In
Piaget’s terms, the child has used assimilation to apply
the “doggie” schema to a new object. However, it is not
uncommon for children to point to a different animal (say,
a cat) and say “Doggie!” From the adult’s point of view,
the child is incorrect to assign a cat to the concept of “dog-
gie.” The parent may say, “No, honey, that is a kitty,” and
provide some information about why the object is a cat
and not a dog. This starts the process of developing a new
13 2
schema (“kitty”). It also further refines the child’s schema
for “doggie.” According to Piaget, the child has accommo-
dated the “doggie” schema to include the new information.
The general processes of assimilation and accommo-
dation are facilitated by the child’s growing understand-
ing of what constitutes a prototypical example of the
schema. For example, the child learns that the prototypic
zebra has white and black stripes, while the prototypic
horse does not. In various cultures, prototypic men and
women may wear different clothes and/or have differ-
ent hairstyles. Similarly, although they are both objects
which one can shelter inside of, prototypic houses differ
from prototypic tree forts.
This raises the issue of what a prototypic dentist is
like. For some adults, the prototypic dentist is someone
wearing a white coat who helps people have good oral
health. For other adults, the dentist is someone frighten-
ing who causes pain inside one’s mouth. Dentists and
parents can each work to influence the child to develop
a positive prototypic schema for dentists. The pediat-
ric dentist and the parents can help the child learn the
schemata for “dentist,” “visiting the dentist” and “oral
hygiene” even before his or her first dental visit by post-
ing current pictures of the dentist, the waiting room,
and the pediatric operatory on the practice’s website, so
that parents can show their children who the dentist is
and what the dental office looks like. The website can
also suggest appropriate pictures about children’s dental
appointments and oral home care for parent and child
to look at together. These pictures can provide infor-
mation about what a dentist does and how to maintain
good oral health through behaviors at home. These prin-
ciples also apply for older children.
The photographs posted on the practice’s website can
help children notice that the dentist and other personnel
are smiling. “Smiling” is likely to be part of children’s
schemata of “good people” or “nice people.” Another
photograph might show the dentist using a large toy
toothbrush to “brush” the teeth of a plush alligator,
which can cue the parent to say: “Look, the dentist is
cleaning Mr. Alligator’s teeth! That helps him keep his
teeth nice and strong!” Since “nice” and “strong” are
positive qualities, this conveys that dentists are helpful
people, as well as that brushing is related to the health of
one’s teeth. Dentists can provide parents with descrip-
tions of what the dental philosophy of the practice is,
what will happen at a dental appointment to pass on to
the child, and additional information designed to help
ensure that the parent provides information about how
a dentist is helpful to children.
While infants use their vision to begin to build sche-
mata of concrete objects that they can see, such as dogs,
 14 T. Coolidge et al.
cats, trees, and flowers, they need input from caretakers
and other people to help build schemata for concepts
which may not be visible [4]. For example, a young child
2 who is taken to the dentist for the first time without the
kinds of preparation referred to above will probably be
able to see if the dentist is a member of the schema for
“man” or a member of the schema for “woman.” But it
will be much harder for the child to understand that this
person is a “dentist” unless the parent tells the child, or
the child watches a cartoon story explaining what a den-
tist is, what he or she does, and why he or she is impor-
tant for a child. Other invisible schemata include “strong
teeth” and “oral health.”
Young children also learn the scripts which govern
who is involved with a particular activity and how the
events are supposed to transpire [4]. For example, the
script for “day care” may include the child traveling to a
particular location with a parent, where he/she is greeted
by an adult who may help with removing a coat as the
parent leaves. The child is then free to enter a play area
where other children are. At a certain point, a meal or
snack may be served. At another point, the children are
expected to lie down and take a nap, or at least lie qui-
etly. Later, the parent will come back, the child will be
helped to put on his/her coat, and then parent and child
will return home.
Here, too, dentists can help by providing parents with
suggestions for how to describe the script for “going to
the dentist.” When children first visit the dental office,
they try to understand this new experience in light of
what they already know. When the new experiences do
not fit with their current schemata and scripts, the child
is more likely to respond with uncertainty, feelings of
being overwhelmed, or fear. If the clinician can pro-
vide detailed pictures or other visual examples on his/
her website of what will happen during an initial den-
tal visit, the parent and child can use this information
to help the child develop new schemata and a script for
“going to the dentist.” As a result, he or she will become
more relaxed and will behave more positively on the first
and future visits.
Eye Catcher
To help the child develop a script about what happens
at a dental appointment, the practice website could
include photographs of the door to the practice, what
one sees once that door is opened (e.g., the reception-
ist and waiting area, with toys, child art work on the
walls, perhaps a giant toothbrush), a child who is get-
ting parental help taking off a coat and hanging it up,
the dental operatory, the dentist talking with a child
in an operatory, a child being examined in a mother-­
supported position, and so on. The “script” ends with
photos of the dentist thanking the child for his/her
help, the child receiving a reward from a “treasure
box,” and the child and parent leaving the operatory
and returning to the waiting area, putting the coat
back on, and leaving the office. Once the child is at
the dental appointment, the dentist can help the child
elaborate the script by talking to him or her during
the appointment about what the dentist is doing and
why. This provides the child with more information
to add to his developing script about what happens
during a dental visit.
An additional bonus of developing a rich schema and
script about who dentists are, what they do, and why
they are important is that this can help protect a child
from developing dental fear and/or incorrect ideas about
dentists and dental visits. In 7 Chap. 4, it is pointed
out that children can become afraid of the dentist by
simply hearing another person say something such as:
“Dentists! I hate them! They hurt you!” However, if the
child has developed complex, positive schemata and
scripts for dentists and dental visits, he or she is much
less likely to be influenced by these negative statements
from others.
Revisiting the vignette of 15-month-old Sally, kick-
ing and crying are normal behaviors for a child of her
age – and perhaps up to a year older than her – so it
would be a mistake to conclude that she is an unruly
child (. Fig. 2.3). The initial kicking provides her
developing brain with information about the object
which she is sitting on. Closing her eyes, looking away
from the dentist’s face, and crying are signs of being
overwhelmed. The increased kicking is another sign of
..      Fig. 2.3 Some disobedience, or even aggression, is possible at the
transition from the sensorimotor to the preoperational stage
Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health
distress. There are a number of reasons why she might
be feeling this way. First, it is her first dental visit, so she
is working hard to figure out who this new person is and
what this new experience is all about. Second, she has
been put into a pediatric dental chair where she is sepa-
rated from her mother. Third, unless she has seen his/her
photograph ahead of time, she is now being approached
by a stranger. These combined are probably more than
she can tolerate. Examining Sally in a parent-supported
(as well as restrained) position (7 Fig. 5.15a, b) is much
less stressful, because in that position she can maintain
physical contact with her mother/father, which should
be soothing to her. This position also allows her parent
to lean in, so that Sally can be reassured by seeing his/
her familiar face, thus satisfying the central need that
young children have for physical parental touch and
reassurance during the sensorimotor and early preop-
erational stages.
Another cause for Sally’s distress is that the source
of control has shifted from herself to the stranger/den-
tist. Before the crying began, Sally was putting the toy
keys in her mouth and taking them back out again, a
typical behavior for children in this stage, who learn a
great deal about the world by putting things inside their
mouths. Notice that Sally was controlling when the keys
went inside and outside, and her tongue, inner cheeks,
and lips were exploring the keys as she moved them.
Contrast this with the dentist’s attempt to start an oral
exam by putting a mirror inside her mouth: suddenly,
someone else – a stranger – is controlling what gets put
inside her mouth, how it moves around, and when it is
removed.
Observations of children under 2 years of age receiv-
ing dental care indicated that, when the caretakers were
attentive to their children, the children were less dis-
tressed. The difficulty arises from the broad definition of
being “attentive.” While the physical contact of a mother-
supported exam may be important, it is not necessarily
sufficient. The lack of control and/or understanding of
being separate from the caregiver is distressing. Even if
the parent is physically present in the operatory, if he/she
is distracted – perhaps by being in conversation with the
dental assistant or checking his/her phone for texts – the
child is more likely to become distressed.
2.1.2 Preoperational Stage
Case Study
When 4-year-old Alex enters the operatory, he hops
up into the chair, slips, and bangs his chin on the
metal tray table. He sheds a few tears and is quickly
calmed by his mother. However, Alex remains appre-
hensive the entire visit even though he cooperates
15 2
with the clinician and the examination is successfully
completed. When Alex arrives home, his father asks
“How was your dental visit?” Despite learning that
he has healthy teeth and having had an otherwise
unremarkable clinical visit, Alex breaks into tears
and tells his father all about how he got hurt. Now,
here is the problem with memory: as time passes, Alex
may remember the fear he experienced at the dentist
office, but that memory has become detached from
the source of the fear. In other words, he is likely to
associate his fear with the dentist and the entire expe-
rience, rather than with the brief surprise and pain he
experienced when he hopped up into the chair.
In addition to Piaget’s stage theory, psychologists soon
found that children’s social environment also had a pro-
found influence on their cognitive development. Lev
Vygotsky, a contemporary of Piaget, believed that cul-
ture and, specifically, the social environment of a child
provide a tremendous contribution to cognitive develop-
ment. Of interest to the pediatric dentist is Vygotsky’s
belief that children have skills that allow them to learn
from others. Vygotsky identified what he called the
zone of proximal development (ZPD) as the difference
between skills the child has already acquired on his own
and what he would be capable of doing with some assis-
tance (or what is sometimes called “scaffolding”) from
older siblings or adults [5]. Dentists, too, can help chil-
dren learn new information by utilizing the concept of
the ZPD and move the child’s cognitive development
forward. For example, if a child opens his mouth only
slightly, the dentist can say: “Nice job, Tommy! Right
now I can see your front teeth. If you open your mouth
really wide, then I can see the rest of your teeth, too.”
Tommy is likely to open his mouth more widely, having
learned how this allows the dentist to see more of his
teeth.
As children progress to the preoperational stage
toward 2 years of age, they increasingly use symbols to
represent their world. During this time, language skills
are developing rapidly, and children are acquiring an
increasing number of mental images and schemata. What
this tells the clinician is that children can now engage in
games of make believe or pretend play. While a child
in this stage has not yet developed an understanding of
basic mental operations, two very important skills have
emerged: representing simple concepts (i.e., children can
tell whether two things are the same or different) and
he/she is beginning to understand the concepts of time.
Children can now think about the concept of yesterday
(the past) and soon (the future). These skills allow them
to begin to anticipate the consequences of their behav-
iors. Further, compared with infants, children in the pre-
operational stage are learning to control their impulses,
 16 T. Coolidge et al.

and thus they have more coping resources. Adults can Just as the parents help the child understand who
take advantage of the concept of the zone of proximal a dentist is and the upcoming dental visit by talking
development to help children develop coping resources. about what will happen, the dentist should talk to chil-
2 dren during the dental appointment itself, explaining
what he or she is doing and why he/she is doing it (“I
Case Study am counting your teeth to see how many you have”).
While it may be amusing to the child to experience other
Sammy walked slowly into the operatory and then
novel aspects of the dental office, such as feeling his/
stood hiding behind his mother. Sammy had been to
her body recline and return to a sitting position as the
the dentist once before, just after his first birthday,
back of a pediatric dental chair is lowered and raised,
but he had no memory of that event. Now he was
or fun to experience the water being squirted into his or
4 years old. His mother gently tried to coax him into
her mouth and then suctioned out by the “straw,” prob-
the chair, but he was very hesitant. She lifted him up
ably the most important behavior for the dentist is to
into the chair, and he immediately drew his knees to
talk to the child about what he/she is doing – and why –
his chest and put his head down.
before, during, and after any procedures or activities.
I introduce myself and tell Sammy that I want to
The descriptions and explanations serve two purposes.
take a look at his teeth to count them. Sammy doesn’t
First, they provide rationales for the child to help him/
look at me or respond. I go on to say that, to do this, I
her understand what is going on. Thus, they explain to
need him to lie flat in the chair and to open his mouth
the child what is happening, which is reassuring and can
for me. I suggest to him that perhaps he could pretend
help prevent the child’s imagination from incorrectly
he was a statue, and lie still. While Sammy is listening
assuming that something bad or dangerous is occurring
to me, he remains folded up in his little ball position.
in this new situation. Second, the information that is
Mom then says to Sammy: “Sammy, Melanie comes
conveyed helps the child develop the schemata related
to Dr. Dentist so he can keep her teeth healthy. She told
to dentists and oral health.
me that when she ‘lies still like a statue’ and opens her
In addition, clinicians need to remember that preop-
mouth really wide, it makes the Doctor’s job easier.”
erational children do not yet have the cognitive capaci-
I knew that Melanie was Sammy’s older sister,
ties of older children. For example, think about the
because she is my patient, too, but, since I had already
directions you may give to a child patient during an
asked Sammy to “lie still like a statue,” I had my
appointment. Do you ask the child to open wide? Then
doubts that his mother’s statement would work. I was
close. Then open wide, then close. Now, perhaps you
surprised and happy to watch Sammy uncurl himself,
want to check the bite after a new filling, so you ask the
put his hands at his side, and open his mouth! At
child to open his mouth and grind his teeth backward
the end of my exam, I complimented Sammy for his
and forward then side to side. Very young children will
excellent ability to lie still like a statue. Sammy said
not be able to inhibit the well-rehearsed sequence of
that lying still like a statue worked for Melanie, so he
opening and closing their mouths and switch to the new
trusted that it would work for him, too. His mother
grind backward and forward, side to side task.
went on to say: “Sammy really adores Melanie.” He
If tell-show-do (described in 7 Chap. 5) is used with
was unable to relate to pretend play as I had hoped,
preoperational children, the dentist should only refer to
but, because of the example that his older sister had
one step or action at a time. This is because children at
set, he developed a successful coping mechanism with
this stage cannot remember a series of things very well.
a gentle nudge from his mother, based on the concept
For example, if the dentist said “I need you to open your
of the zone of proximal development.
mouth very wide, and turn your head toward me, and
be very still,” the child may remember the initial action
that the dentist described (open mouth wide), or the last
At the same time, children in the preoperational stage action described (be very still), but not all three. (In Sect.
have difficulty viewing the world from someone else’s 2.2.1 of this chapter, we point out that, in general, mem-
perspective. This egocentrism means that children ory tends to be strongest for the initial experience, due
believe that other people perceive things in the same way to the primacy effect, and the last experience, due to the
as they do. From the child’s point of view, whatever he recency effect. The same is true for hearing a list or series
or she is seeing, hearing, or experiencing, the p
­ arent/sib- of words or descriptions. The issue with preoperational
ling/dentist must also be experiencing. In other words, children is that they are not able to remember all of the
the child cannot “put himself/herself in another’s shoes.” contents of the list or series that are in between the first
For example, in the previous scenario Sammy acted as if and last items as older children can.)
the dentist couldn’t see him or know that he was in the One of the best illustrations of how children in the
operatory, because he couldn’t see the dentist when he preoperational stage think differently from adoles-
was hiding behind his mother. cents and adults can be seen in the children’s failure
Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health
to understand the principle of conservation. The clas-
sic example is to show a young child two glasses of the
same size and shape, each filled to the same height with
water. The child can compare the two glasses and tell
you whether the amount of water in the glasses is the
same or different (in this case, she will tell you that it is
the same). Then, you can take a taller, thinner glass and
have the child watch you as you pour the water from
one of the first two glasses into this differently shaped –
taller and thinner – glass. Then, when you ask the child
whether the two glasses of water have the same amount
of water in them, or a different amount, she will confi-
dently tell you that they are different, and, in particular,
that the tall glass has more water in it. When you ask her
why, she will explain that the taller glass has more water
because the water level is higher!
This failure to understand that matter remains the
same despite the change in height (i.e., the failure to
understand conservation) extends to other changes in
appearance (e.g., two lines of ten pennies each are “the
same” as long as the two lines have the same length.
However, once the pennies are spread out in one of the
lines, then that line has “more” pennies in it.).
Why does the child fail to understand conservation?
Piaget said that children may only be able to focus on
one aspect of a situation at a time. Thus, in the example
of water, the child can only focus on the height of the
two glasses – without also being able to focus on the
width of the glasses, or the fact that the volume of water
must be the same even though it has been poured into a
taller glass, because the child saw the adult pouring the
water from the old container into the new one. On the
other hand, an older child is not fooled by the increased
height and will be able to tell you that the amount of
water is still the same. If you ask how he knows this, he
can say something such as: “You just poured the water
into a new glass. If you pour it back again, you will see
that it is the same amount as before.” The older child is
referring to the process of reversibility.
This means that dentists should not expect a child in
the preoperational stage to be able to think about men-
tally reversing actions. For example, the following state-
ment cannot be understood by preoperational children:
“If you had done a better job brushing, the tooth bugs
would not have become stuck to your teeth.”
On the other hand, the dentist can take advantage of
the fact that the preoperational child is likely to attribute
lifelike qualities to inanimate objects and natural events,
a process called “animism.” Thus, children of this age
respond well to statements such as: “Let’s let your tooth
rest on Mister Pillow” or “The super straw will suck up
all of the extra water.”
17 2
2.1.3 Concrete Operational Stage
Case Study
Six-year-old Carlos hops up in the operatory chair
with great energy and confidence. After a quick exam-
ination and a confirmation from the x-rays, I show
Carlos the weakness on the enamel on his lower molar.
When he asks, “How did that happen?” I explain about
the decay while also including behavioral steps he can
take to prevent the further breakdown of his tooth.
Carlos is now old enough to understand the concept
of reversibility such that he understands that, by skip-
ping teeth brushing before he went to bed this past
year, his enamel has weakened and the harmful bacte-
ria in his mouth have multiplied and are attacking his
tooth. Carlos can now perform basic mental opera-
tions, thus quickly calculating the effect his poor oral
care may have on the rest of his teeth. As Carlos is
now able to look at situations from a perspective out-
side of his own (i.e., is much less egocentric than the
preoperational child), he is able to understand what I
and his parents see. (For example, unlike 4-year-old
Sammy, Carlos knows that the dentist could see him,
or know that he was in the room, even if he tried to
hide behind his mother.)
I tell Carlos to imagine his teeth are like the bricks
on the side of my office building. Sometimes ivy and
moss start growing on the bricks and you might even
think they make it look nice. But, when we pull the
plants off of the brick, some of that hard brick goes
with the plants. The brick on the building still looks
good, but it is now weaker. When this happens over
a period of years, eventually the bricks are no lon-
ger hard and strong and in some cases crumble and
need to be removed. I explain to Carlos that this is
like his teeth and sugar. His teeth are like the bricks,
all polished and strong, and the pleasing to look at
ivy is like the raisins and lollipops he is so fond of. It
doesn’t happen overnight, but eventually, if the sugar
is allowed to stick to the teeth without being removed
every night, the enamel on his teeth, like the brick,
will weaken and crumble.
My story is met with a blank stare from Carlos,
who says that his teeth don’t have ivy and moss grow-
ing on them! Children at Carlos’ stage of cognitive
development have trouble with hypothetical and
abstract reasoning. Any directions that start with
“imagine” or “let’s pretend…” are doomed as children
at this stage understand concrete concepts and have
not yet developed the skill to think in the abstract.
 18 T. Coolidge et al.
2 before that happens.
..      Fig. 2.4 Elementary schoolchildren are at the concrete opera-
tional stage
By the time a young child is in elementary school, she
has entered the concrete operational stage (. Fig. 2.4).
She can understand some of the concepts that were dif-
ficult earlier, such as reversibility and conservation. The
ability to control impulses increases in this stage, allow-
ing the child to use an increasing number of strategies to
deal with difficult or unpleasant situations. The primary
limitation of this stage is that children cannot think
abstractly or with hypotheticals.
2.1.4 Formal Operational Thought
Case Study
Your hygienist put her head inside the operatory where
you are working on a patient, and asked: “May I see
you in your office when you have a moment, Doctor?”
A few minutes later, you excuse yourself and meet
with the hygienist. “It’s Kenny, Doctor. I’ve spoken
with him about his oral hygiene during the last two
visits, but he’s still not brushing his teeth very often.
And today I can smell cigarette smoke, which is new.”
Kenny is a 14-year-old who has been in your prac-
tice since he was in elementary school. He’s a bright
teen who is interested in marine biology, and hopes
to study this in college. You invite him to join you in
a private room. When you ask about his brushing, he
says “Yes, I know about brushing off the food bits,
but I don’t like to brush. I haven’t had a cavity in
years, so I figure that I’m not going to get anymore.”
He admits that he is smoking now, “like all the other
guys” in his circle of friends, but goes on to say that
he’ll never get lung cancer because he’ll quit way
Piaget believed that children will enter the final stage of
cognitive development – formal operational thought – at
around 11 or 12 years. While children in the concrete
operational stage can solve problems, they must physi-
cally manipulate objects in some way in order to do so.
By contrast, youth are increasingly able to solve prob-
lems by mental processes. Adolescents in this stage can
think about things and arrive at solutions without hav-
ing to actually manipulate objects. For example, if pre-
sented with the following information:
“Tom is taller than Bob, and Bob is taller than Joe,
and Joe is taller than Chris” and then asked: “Who is
taller, Chris or Tom?”, the adolescent in the formal
operational thought stage can answer: “Tom is,” because
he or she understands how to solve word problems using
his/her knowledge of logic. By contrast, a child in the
concrete operational stage will need to look at a drawing
showing the three people and their relative heights to
figure this out.
The use of logic signifies an increasing ability to use
abstract thought processes, such as using and under-
standing metaphors and analogies; ponder things that
don’t exist (“I wonder what the moon would be like if
there was water on it?”); think about abstract concepts,
such as “health,” “justice,” and “love”; think about the
outcomes of an action which hasn’t been taken yet; and
understand causation (. Fig. 2.5). Thus, an adolescent
can understand the scientific reasoning about why he/
she should use a toothbrush regularly, why consuming
acidic drinks or having a dry mouth can pose risks to
dental health, and the like. On the other hand, due to
what Piaget referred to as “adolescent egocentrism,”
even adolescents who can articulate the biological pro-
cesses related to caries development may act as if the
science doesn’t apply to them. Thus, some adolescents
do not practice oral self-care and/or do not attend a den-
tist regularly; these individuals are more likely to have
untreated dental needs [6–8].
The increased inhibitory abilities that were noted for
younger children continue in adolescence. For example,
in one cross-sectional study, adolescents younger than
16 years old stated that they preferred to take a smaller
reward immediately, rather than wait for a larger reward
in the future. On the other hand, the adolescents who
were 16 or older wanted to wait for the larger reward,
indicating a greater ability to inhibit the desire to have
the reward immediately. The older adolescents also
Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health
19 2

that the dentist knew about her hobbies and interests,

which included Irish dancing, and together they had
decided that she could distract herself by “practicing”
her Irish dancing steps during the treatment (as long
as she was able to curtail the arm movements, which
typically involved lifting her arms above her head).
The deliberate foot movements were a scaled-down
version of the kicks and other steps that were involved
in the dances.

Having a sense of control helps individuals cope with

stressful situations [18]. Since the amount of desired
control will vary from person to person and from cir-
cumstance to circumstance, it is important to consider
both the amount of desired control that an individual
has when faced with a stressful situation and the amount
of perceived control that the individual feels he/she actu-
ally has in that situation.
The Revised Iowa Dental Control Index (R-IDCI) is
..      Fig. 2.5 At formal operational stage, children and adolescents a nine-item scale which measures these two constructs
are capable of abstract thinking in the dental situation. Adult patients who experienced
less control in the dental setting than they preferred to
described themselves as being more likely to think about have rated themselves as having experienced higher lev-
the future, compared with the younger ones [9]. els of anxiety and pain during dental treatment, as well
Thinking about the future is associated with a num- as having higher levels of dental fear in general [19]. The
ber of health-promoting behaviors, such as engaging in nine-­item R-IDCI has also been used with youth aged
exercise and making healthy food choices [10]. Future 11–15 years in the United States, Australia, and Japan,
orientation is also related to obtaining regular health where it was compared with a measure of preferred con-
screenings. For example, adults who are more future-­ trol strategies for children in the dental setting (Child
oriented are more likely to have had a recent dental Dental Control Assessment, CDCA) [20] and measures
checkup [11]. By contrast, homeless youth who are less of dental fear [21]. The results indicate that the CDCA
future-oriented are more likely to go to a dentist when and the R-IDCI perform well with adolescents and
they have a problem, rather than for routine checkups, could provide the dentist with rich information about
and are more likely to neglect their oral home care [12]. patients’ preferences for various strategies that the den-
Compared with children, adolescents are more likely tist can use during a dental appointment, as well as the
to use cognitive, approach-oriented control strategies, patients’ potential for experiencing pain and anxiety
such as information seeking, positive self-talk, and cog- during dental treatment if they prefer to have greater
nitive distraction [13–17]. control than they actually feel that they have during
dental treatment.

Case Study
Eye Catcher
One of us (TC) observed a teen as she underwent a
Sample Revised Iowa Dental Control Index items:
restoration. The observer noticed that the teen was
Desired Control:
moving her feet in a deliberate way on the chair (while
55 To what degree would you like control over what
taking care not to jostle herself), and asked the teen
will happen to you in the dental chair?
about this once the treatment was completed. Sitting
upright, the patient explained that she had been anx-
Predicted Control:
ious about whether she would be able to handle the
55 Do you feel you have control of what will happen
discomfort of the injections and the length of time
to you in the dental chair?
that the treatment would take. She went on to say
 20 T. Coolidge et al.
Eye Catcher
55 Sample Child Dental Control Assessment Items:
2 55
55
I want the dentist to tell me what will happen.
I want the dentist to answer my questions.
55 I want the dentist to tell me how long things will
last.
2.2  sing Memory Principles to Help
U to tell your dad [i.e., the parent who was not in the
Prevent the Development of Fear
Returning to 4-year-old Alex, who banged his chin at
his dental appointment, let us focus on what dentists can
do to prevent children from developing dental fear. This
is particularly important given that we want children to
return for routine dental care on a regular basis, and it
is possible that children may also need to undergo some
appointments that involve restorations or other inva-
sive treatments. Unfortunately, the negative memory
from one appointment may impact a child’s behavior
on subsequent visits [22]. Given the pervasive negative
valence surrounding dental appointments in our culture
(how often has one heard “It was like pulling teeth” or
“Ugh, I’d rather have a root canal”), children may have
heightened anxiety and arrive at their first dental visit
prepared to experience something awful. Some research
focuses on restructuring memory of visits or procedures
so as to prevent negative memories growing with the
passage of time [23–25].
General memory principles help guide the restruc-
turing procedure followed in cognitive intervention [23].
These include:
Use the primacy effect concept identified by memory
researchers. We have already recommended that dental
offices offer stimuli (e.g., photos of the dentist and the
dental office on the practice website) and previsit activi-
ties (e.g., books for parents and children to look through)
to help prepare children for their initial visit. Dentists
also need to ensure that the initial visit – and the initial
aspects of that visit – is as positive as possible. These
initial experiences are likely to be strongly remembered,
as they are the primary experiences that the child has.
When children form their first impression of their visit,
they will use that information as a lens through which
they experience and interpret all subsequent informa-
tion, and have additional time to explore, think about,
and analyze this initial information. This results in a
strong encoding and thus a stronger recall.
Since 4-year-old Alex had a painful experience at
the onset of his dental appointment, it is not surpris-
ing that his memory of the visit – as he described it to
his father – focused on this initial experience. This dem-
onstrates the power of the primacy effect. However, if
the dentist (and/or parent) had found ways to use some
of the behaviors described below, Alex would have been
better able to put the initial experience in context.
Important behaviors for the dentist who wants to
prevent the development of dental fear:
55 Have the child repeat the information that you want
him/her to remember. You can ask the child “What
did you learn today?”, as well as “What are you going
operatory with the child during the visit] about your
trip to the dentist today?”
55 Have the child talk about what she learned and how
well she did today, because this helps to ensure that
she remembers these positive aspects.
55 If the child refers to “negative” behavior, reframe
this in a truthful way to put it in perspective, and
include a reference to some aspect of positive behav-
ior that you noticed. For example, if the child says “I
cried, it hurt,” you can reply: “Yes, it’s true that you
did cry when you got the shot, and I am sorry that it
hurt you. But you only cried for a minute or two, and
then you were able to lie very still and that helped me
finish the work quickly. Overall, you really did well
today!”
55 After walking the child back out to the waiting room,
be sure that she overhears you tell her parent what a
good job she did today.
55 Focus on simple, salient facts while suggesting
important ideas peripherally. Suppose the main
important idea that you want the child to under-
stand is: “Make sure you cover your teeth with
toothpaste every time you brush.” To make that
message salient, talk about how “the fluoride in
the toothpaste kills the bacteria that eat your tooth
enamel. When you cover your teeth with toothpaste,
you are protecting them.”
55 Children (and adults) find it easier to remember infor-
mation if it is associated with them. For example, the
dentist should talk to the child during the appoint-
ment about how well he is helping. The dentist can
say: “Thank you for lying nice and still.” “Thank you
for letting me know that you need a little break now.”
“You know how to open your mouth really wide!”
In addition to ensuring that the beginning of the dental
encounter is positive (primacy effect concept), accord-
ing to the recency effect concept the last experiences
at the dental office are also central to the child’s mem-
ory of the visit. In other words, the dentist needs to
ensure that these last experiences are positive. The end
of the appointment provides an excellent opportunity
Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health
to reinforce concepts first introduced, and any positive
behaviors exhibited. Remind children how they helped
the dentist take care of their teeth. The dentist can say:
“You really helped me today! You sat nice and still,
you opened your mouth really wide, which made my
job so much easier. You also followed my directions
really well. You know, you helped me so much today,
and that made my job so much easier.” Always praise
the child for something positive, even if the appointment
was difficult. For example, even the child who cries dur-
ing the entire examination can be told what a great job
he did opening his mouth very wide when the dentist
asked so that the dentist could see his teeth much more
easily.
To illustrate the power of the last experiences of
a dental visit, imagine the memory that this young
patient – observed at the end of an appointment which
included a restoration – will have of his dental visit:
The father heard his son crying in the operatory and
came to the doorway. When he saw his child in the den-
tal chair, extremely upset, he said: “Ahhh, now I know
what to do to punish you in the future. Next time you
misbehave I’m going to bring you back here!”
2.3  ailoring Oral Messages
T of food in the mouth, avoiding bacteria, which pro-
to the Individual Patient
Dentists (and other dental personnel) often find them-
selves wanting to give information or advice to their
patients and/or the parents of their patients. Sometimes
they feel frustrated when their advice doesn’t seem to be
heeded. We would like to offer some suggestions about
how to tailor the information in specific ways, which
have been found to be more effective in terms of result-
ing in actual behavior change.
Of note, individuals are motivated both by the prom-
ise of receiving rewards and the risk or threat of receiv-
ing punishment, although some individuals are more
motivated by one of these two possibilities [26]. An indi-
vidual’s relative preference for one of these two possi-
bilities can be assessed by the BIS/BAS Scale [26], where
BIS is short for the “behavioral inhibition system” (i.e.,
that which operates to reduce the risk of receiving pun-
ishment) and BAS is short for the “behavioral activa-
tion system” (i.e., that which operates to increase the
likelihood of receiving rewards). A 10-year longitudinal
study found that adolescents’ endorsement of the BIS
items increased with age [27], indicating that inhibition
tendencies increase with experience and maturation.
21 2
Eye Catcher
Sample BIS item: “I feel worried when I think I have
done poorly at something important.”
Sample BAS item: “When I want something I usu-
ally go all out to get it.”
Given the seeming paradox between understanding
the reasoning behind, say, suggestions to brush but at
the same time not brushing, dentists are likely to find
the results of one study team intriguing. In several
studies, Sherman, Updegraff, and Mann [28] experi-
mented with the wording of the messages they created
to learn whether they were successful in motivating
college students to change an oral behavior. First,
they created two messages about flossing. One was
gain-oriented (“Great Breath, Healthy Gums Only a
Floss Away”) and referred to the benefits of flossing,
while the other was loss-­oriented (“Floss Now and
Avoid Bad Breath and Gum Disease”) and referred
to the downsides of not flossing. Importantly, the
same information was included in both messages. For
example, the gain-oriented message included the state-
ment that “flossing your teeth daily removes particles
motes great breath,” while the loss-­oriented message
included the same information, but worded differ-
ently: “If you don’t floss your teeth daily, particles of
food remain in the mouth, collecting bacteria, which
causes bad breath.”
The team recruited college students and measured
their relative preferences for approaching (to receive
a reward) or avoiding (to avoid punishment) with the
BIS/BAS scale. The researchers postulated that the stu-
dents who were higher on BIS would respond more to a
message focused on losses, while the students who were
higher on BAS would respond more to a message focused
on gains. The students were then randomly assigned to
receive either the gain or the loss message. After they read
the message, they received individual packets of dental
floss. After a week, the students were asked how many
packets they still had. The results were that students who
had received the message which was congruent with their
motivational style flossed significantly more than the stu-
dents who had received the message which was incongru-
ent with their motivational style [28].
The take-away message is that the dentist who spe-
cifically tailors his/her description of the outcome of a
desired behavior (e.g., more frequent dental visits, such
 22 T. Coolidge et al.
as checkups; increase or decrease in oral self-care behav-
ior at home, etc.) to match the patient’s motivational
style (or the parent’s motivational style, in the case of
2 a child patient) is likely to be more effective, compared
with a dentist who tends to provide the same description
to all of his/her patients and parents. Dentists can create
gain- and loss-oriented descriptions of behaviors which
they would like to influence, such as reducing smoking,
increasing tooth brushing, and the like. Typically, these
messages contain the same information, but worded dif-
ferently to either focus on the costs or gains associated
with the behavior.
Eye Catcher
Sample part of a loss message for quitting smoking
for adolescents:
55 What are the costs of continuing to smoke?
–– Your appearance: By continuing to smoke,
you will have premature wrinkling and aging
of your face and lips. Your teeth will also be
more yellow, since cigarette smoke stains your
teeth….
Sample part of a gain message:
55 What are the benefits of quitting smoking?
–– Your appearance: By quitting smoking, you will
avoid premature wrinkling and aging of your
face and lips. Your teeth will also be whiter,
since cigarette smoke stains your teeth…
(Of course, other information – such as about risks/
gains to lungs, teeth, and sexual performance, the
amount of money that will be spent on cigarettes/
saved by stopping smoking, etc. – can be added to
these samples.)
Returning to the vignette about 14-year-old Kenny, it
appears that this adolescent is currently motivated by an
approach motivation (although the dentist could check
this by asking him to complete the BIS/BAS Scales), so
it would be best to frame messages that stress the ben-
efits of quitting smoking (i.e., quitting smoking means
that you could save X dollars per month; your clothes
and hair will smell fresh, since they won’t be exposed to
tobacco smoke; etc.) Similarly, it would be best to frame
messages about regular tooth brushing that stress the
benefits of this behavior (e.g., brushing regularly means
that your breath will be fresher, you’ll be more likely to
keep your teeth for a lifetime, etc.).
References
1. Bjorklund DF. Cognitive development: an overview. In: Zelazo
PD, editor. The Oxford handbook of Developmental Psychol-
ogy, Vol 1: body and mind. New York: Oxford University Press;
2013. p. 447–76.
2. Piaget J. The construction of reality in the child. New York:
Basic Books; 1954.
3. Meltzoff AN, Moore MK. Imitation of facial and manual ges-
tures by human neonates. Science. 1977;198:75–8.
4. Gelman SA. Concepts in development. In: Zelazo PD, editor. The
Oxford handbook of Developmental Psychology, Vol 1: body and
mind. New York: Oxford University Press; 2013. p. 542–63.
5. Vygotsky LS. Mind in society: the development of higher psy-
chological processes. Cambridge, MA: Harvard University
Press; 1978.
6. Coolidge T, Heima M, Johnson EK, Weinstein P. The dental
neglect scale in adolescence. BMC Oral Health. 2009;9:2.
7. Skaret E, Raadal M, Berg E, Kvale G. Dental anxiety and dental
avoidance among 12 to 18 year olds in Norway. Eur J Oral Sci.
1999;107:422–8.
8. Sarri G, Evans P, Stansffeld S, Marcenes W. A school-based
epidemiological study of dental neglect among adolescents in a
deprived area of the UK. Brit Dent J. 2012;213:E17. https://doi.
org/10.1038/sj.bdj.2012.1042.
9. Steinberg L, Graham S, O’Brien L, Woolard J, Cauffman E,
Banich M. Age differences in future orientation and delay dis-
counting. Child Dev. 2009;80:28–44.
10. Joireman J, Shaffer MJ, Balliet D, Strathman A. Promotion ori-
entation explains why future-oriented people exercise and eat
healthy: evidence from the two-factor consideration of future
Consequences-14 scale. Pers Soc Psychol B. 2012;38:1272–87.
11. Bradford WD. The association between individual time pref-
erences and health maintenance habits. Med Decis Mak.
2010;30:99–112.
12. Coolidge T, Pickrell J, Raykhman M, Trippel C, Riedy
CA. Smoking, dental attendance, and the CFC-14 in homeless
youth. Presented at the second international conference on time
perspective, July 29 – August 1, 2014; Warsaw, Poland.
13. Band EB, Weisz JR. How to feel better when it feels bad: Chil-
dren’s perspectives on coping with everyday stress. Dev Psychol.
1988;24:247–53.
14. LaMontagne LL, Hepworth JT, Johnson BD, Cohen F. Chil-
dren’s preoperative coping and its effects on postoperative anxi-
ety and return to normal activity. Nurs Res. 1996;45:141–7.
15. Hodgins MJ, Lander J. Children’s coping with venipuncture. J
Pain Symptom Manag. 1997;13:274–85.
16. Fields L, Prinz RJ. Coping and adjustment during childhood
and adolescence. Clin Psychol Rev. 1997;17:937–76.
17. Olson AL, Johanssen SG, Powers LE, Pope JB, Klein RB. Cog-
nitive coping strategies of children with chronic illness. Dev
Behav Pediatr. 1993;14:217–23.
18. Compas BE, Jaser SS, Dunn MJ, Rodriguez EM. Coping with
chronic illness in childhood and adolescence. Annu Rev Clin
Psycho. 2012;8:455–80.
19. Brunsman BA, Logan HL, Patil RR, Baron RS. The develop-
ment and validation of the revised Iowa dental control index
(IDCI). Pers Indiv Differ. 2003;34:1113–28.
20. Weinstein P, Milgrom P, Hoskuldsson O, Golletz D, Jeffcoat E,
Koday M. Situation-specific child control: a visit to the dentist.
Behav Res Ther. 1996;34:11–21.
Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health
21. Coolidge T, Heima M, Heaton LJ, Nakai Y, Höskuldsson Ó,
Smith TA, Weinstein P, Milgrom P. The child dental control
assessment (CDCA) in youth: reliability, validity and cross-cul-
tural differences. Eur J Paediatr Dent. 2005;6:35–43.
22. Quas JA, Bauer A, Boyce WT. Physiological reactivity, social
support, and memory in early childhood. Child Dev. 2004;75:
797–814.
23. Pickrell JE, Heima M, Weinstein P, Coolidge T, Coldwell SE,
Skaret E, Castillo J, Milgrom P. Using memory restructur-
ing strategy to enhance dental behaviour. I J Paediatr Dent.
2007;17:439–48.
24. Chen E, Zeltzer LK, Craske MG, Katz ER. Alteration of mem-
ory in the reduction of children’s distress during repeated aver-
sive medical procedures. J Consult Clin Psych. 1999;67:481–90.
23 2
25. Bruck M, Ceci SJ, Francouer E, Barr R. I hardly cried when I
got my shot! Influencing children’s reports about a visit to their
pediatrician. Child Dev. 1995;66:193–208.
26. Carver CS, White TL. Behavioral inhibition, behavioral acti-
vation, and affective responses to impending reward and pun-
ishment: the BIS/BAS scales. J Pers Soc Psychol. 1994;67:
319–33.
27. Almy B, Kuskowski M, Malone SM, Myers E, Luciana M. A
longitudinal analysis of adolescent decision-­making with the
Iowa gambling task. Dev Psychol. 2018;54:689–702.
28. Sherman DK, Updegraff JA, Mann T. (2008). Improving oral
health behavior: a social psychological approach. J Am Dent
Assoc. 2008;139:1382–7.
 25 3

Pediatric Body Growth

Panagiota Triantafyllou and Stephanie Roberts

Contents

3.1 Normal Growth – 26

3.1.1  rowth Phases – 26
G
3.1.2 Growth Evaluation – 26

3.2 Growth Disorders – 30

3.2.1 I ntrauterine Growth Retardation and Small for Gestational
Age Newborns – 30
3.2.2 Short Stature – 30
3.2.3 Tall Stature – 32

3.3 Puberty – 34
3.3.1 Disorders of Puberty – 34

References – 35

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_3
 26 P. Triantafyllou and S. Roberts
Growth and development in addition to onset and pro-
gression of puberty are important topics in the field
of pediatrics and that of pediatric dentistry. Growth is
the term which is referred to children’s linear growth,
whereas development is referred to cognitive and emo-
tional maturation and milestones’ achievement written
3 in 7 Chap. 2.
3.1 Normal Growth
Human growth is a complex and dynamic process which
starts at the time of ovum’s fertilization and continues
until the end of puberty with the fusion of the long
bones’ epiphyses. At any stage, normal growth is evidence
of good health. The process of growth is controlled by
many interacting factors such as endogenic (genotype),
exogenic (nutrition and environment), and internal regu-
latory systems (hormones and growth factors) [1–3]. The
role of the above factors depends on the stage of growth.
The rate of growth on the other hand is neither the same
nor symmetric for all the organs. There are four phases
of growth: the prenatal, the infantile, the childhood, and
pubertal [1–5].
Overview
Prenatal Conception to birth (newborn 0–28 days)
Infantile 1–23 months
Childhood 2–12 years
Puberty 12–16 years
3.1.1 Growth Phases
3.1.1.1 Prenatal Growth
The intrauterine development of the zygote into the
50-cm newborn is the first and most impressive period of
growth. It is divided into three trimesters. The comple-
tion of organogenesis in the first trimester is followed by
the rapid acceleration during the second trimester with
maximum velocity of 2.5 cm/week, whereas during the
third trimester it is mainly the weight which is acceler-
ated. Intrauterine growth depends on maternal nutri-
tional status, the size of uterus, the placenta, and the
influence of insulin growth factors (IGFs). Genetics and
growth hormone play a minor role during this period,
although skeletal dysplasias like achondroplasia or
severe growth factors’ deficiency do influence intrauter-
ine growth. In terms of hormones and in addition to the
insulin-like growth factors (IGFs), fetal insulin produc-
tion in response to maternal glycemia, placental lactogen,
and sex steroids is essential for fetal growth. Thyroid hor-
mones are very important for growth after birth but do
not seem to be essential during fetal period given that the
growth of newborns with athyreosis is unaffected. Male
fetus starts to produce testosterone at tenth fetal week.
Elevated testosterone levels perinatally drive to a higher
weight and less adipose tissue of male newborns [1–5].
3.1.1.2 Infantile Growth
Following birth, infants continue to grow rapidly. By
the end of first year of life, the infant has increased his
length 50% (approximately 25 cm) and has tripled his
weight. Growth during this period is influenced mainly
by nutritional factors and less by genetics, thyroid, and
growth hormone [1–4].
3.1.1.3 Growth in Childhood
In the second year of life, height velocity is 10–13 cm/
year, and in the third year it is 7.5–10 cm/year.
Thereafter, childhood growth is relatively constant and
from age 3 years to puberty, height velocity is 5–6 cm/
year. Weight gain is approximately 2–3 kg/year in both
genders. During this period growth is predominantly
regulated by growth hormone, IGFs, and thyroid hor-
mone. Nutrition is less important in this stage but a pos-
itive energy status is important to avoid falloff in linear
growth [1–5].
3.1.1.4 Pubertal Growth
Children generally enter puberty on average at age
10 years in girls and age 12 years in boys. Following
quiescence of the hypothalamic-pituitary-gonadal axis
after the mini-puberty of the fetal and neonatal period,
pubertal onset results from gradual increase in GnRH
pulsatility and secretion followed by increased pulsatile
release of LH, FSH, and sex steroids. Moreover, sex ste-
roids (mainly estradiol in girls and testosterone in boys)
stimulate growth directly and indirectly by augmenting
growth hormone production. The first clinical sign of
pubertal onset of girls is breast budding and in boys it
is testicular enlargement. Additionally, pubertal growth
spurt in girls begins at the onset of puberty, whereas in
boys it happens approximately 2 years later. The com-
bination of a longer period of prepubertal growth and
greater amplitude of pubertal growth results in greater
adult height in male [1–5].
3.1.2 Growth Evaluation
3.1.2.1 Weight and Height Measurement
Precise anthropometric measurements are the basis of an
accurate growth assessment. Infants are weighed with-
out any clothes and children with minimal clothing and
Pediatric Body Growth
without shoes. For children from birth to 2 years of age,
supine length should be measured, and it requires two
persons to obtain a reliable measurement. The one holds
child’s head and the other straightens the legs. Over the
age of 2 a stadiometer should be used to measure height
in standing position without shoes. Measurements
should be plotted on standardized growth charts [3, 5].
Standardized growth charts can be obtained from either
national surveys or the World Health Organization
website (. Figs. 3.1 and 3.2). For patients who have tri-
somy 21, Turner syndrome, Klinefelter syndrome, and
achondroplasia, specific growth charts are available that
should be used [3]. In every growth chart there are five
curves usually referred to third, 15th, 50th, 85th, and
97th percentile. For instance, when the height of a child
is plotted on the 15th percentile, it means that 15% of
children matched for age and gender are shorter and
85% taller than that child. To evaluate weight gain, it is
preferable to use BMI (body mass index) growth charts
according to which children are categorized as under-
weight, normal, overweight, or obese. In children less
than 2 years, weight-for-length is used instead of BMI.
Moreover, head circumference, arm span, upper seg-
ment/lower segment ratio, and sitting height are body
proportion measurements that can be considered for
growth evaluation if there is a clinical concern for short
or tall stature, falloff in growth velocity, or an underly-
ing syndrome.
3.1.2.2 Growth Velocity
Normal growth is assessed by growth velocity. It is
calculated by the difference of two measurements in a
time interval of 6–12 months. Shorter intervals such as
3 months may lead to inaccurate evaluation of growth.
There are specific charts for growth velocity (. Fig. 3.3).
Growth velocity follows seasonable variability given
that it is accelerating in spring and summer than fall and
winter [3, 6]. Assessment of growth velocity depends on
the stage of pubertal development and pubertal tempo
during puberty and depends on the timing of pubertal
growth spurt. Family history is an important part of the
history to assess the anticipated onset of puberty and
growth spurt.
3.1.2.3 Midparental Height or Target Height
The evaluation of a growth pattern should be based
on the genetic potential since adult height is in part
genetically determined. For instance, we do not worry
for a child growing at the tenth percentile if parents are
healthy and their height is also at the tenth percentile
and the child has a normal growth velocity for age. By
contrast, if the parents are very tall, even if this child’s
height is in normal range, it is short for the genetic
potential and needs further investigation. Therefore, the
27 3
child’s adult height potential can be estimated by cal-
culating midparental (MPH) or target, height. Having
measured parents’ heights, the target height is occur-
ring by calculating mean parental height and adding or
subtracting 6.5 cm for male or female child, respectively.
Two standard deviations for the calculated target height
is approximately ±10 cm [1].
3.1.2.4 Bone Age
Linear growth depends on skeletal maturation which
in normal children follows an orderly development.
Skeletal maturation depends on the appearance of
epiphyseal centers, the length of long bones, and the
fusion of the epiphyses that marks the cease of growth.
Estrogen fuses the growth plate in both girls and boys.
Bone age is a method of assessing skeletal maturation
by comparing left hand and wrist radiograph with
given age-­appropriate standard radiographs of healthy
children (. Fig. 3.4). There are two main methods for
the evaluation of bone age: a) the most widely used
Greulich and Pyle hand standards and b) the Tanner
and Whitehouse method mainly used in Great Britain
[1, 6–10]. Retarded bone age may be seen in hypothy-
roidism, growth hormone deficiency, Cushing’s syn-
drome, chronic malnutrition, and underlying chronic
disease. Advanced bone age results from hyperthyroid-
ism, precocious puberty, androgen excess, or obesity.
Furthermore, bone age, in addition to child’s height
at a specific moment, can be used for prediction of
final height, commonly performed using the Bayley-
Pinneau method [9, 10]. Height predictions must be
used in caution in children with abnormal growth pat-
terns and/or underlying pathology that may impact
growth.
3.1.2.5 Dental Age
The appearance of teeth in an orthopantomographic
(OPG) radiograph aids in estimating the dental age
of a child according to mineralization/maturation
stage of the dental hard tissues. Such information is
useful, inter alia, in anthropology and forensic medi-
cine/dentistry. Among several methods, the one most
commonly used is Demirjian’s, which is based on the
recording of all teeth – except for the third molars – of
the left side of the mandible from the OPG. It records
eight stages, beginning from the mineralization of
the tips of their cusps to full root apex formation, in
relation to chronological child age (. Fig. 3.5). The
method is considered relatively accurate (± 1 year) for
finding dental maturity of single children, although
there may be an overestimation in puberty [11]. Dental
age, despite being considered more reliable than erup-
tion age of the teeth, does not show a high correlation
with bone age [12].
 28 P. Triantafyllou and S. Roberts

a Height-for-age BOYS
5 to 19 years (percentiles)

190 97th 190

3 180
85th
180
50th

170 170
15th

3rd
160 160
Height (cm)

150 150

140 140

130 130

120 120

110 110

Months 100 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 100

Years 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age (completed months and years)
2007 WHO Reference

b Height-for-age GIRLS
5 to 19 years (percentiles)

180 180

97th

170 85th 170

50th
160 160

15th

150 3rd 150

Height (cm)

140 140

130 130

120 120

110 110

100 100

Months 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9
Years 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age (completed months and years)
2007 WHO Reference

..      Fig. 3.1 Height for age WHO curves from fifth to 19th year of age of children. Frequently used percentiles are marked at the right side.
a. Boys. b. Girls
Pediatric Body Growth
29 3

a Weight-for-age BOYS
5 to 10 years (percentiles)

45 45
97th

40 40

85th

35 35

50th
Weight (kg)

30 30

15th
25 25

3rd

20 20

15 15

Months 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9
Y e a rs 5 6 7 8 9 10
Age (completed months and years)
2007 WHO Reference

b Weight-for-age GIRLS
5 to 10 years (percentiles)

97th
45 45

40 40

85th

35 35
Weight (kg)

50th

30 30

15th

25 25
3rd

20 20

15 15

Months 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9
Y e a rs 5 6 7 8 9 10
Age (completed months and years)
2007 WHO Reference

..      Fig. 3.2 Weight for age WHO curves from fifth to tenth year of age of children. Frequently used percentiles are marked at the right side.
a. Boys. b. Girls
 30 P. Triantafyllou and S. Roberts

22
9 3.2 Growth Disorders
20 Boys 8
Girls 3.2.1 I ntrauterine Growth Retardation
18 7
and Small for Gestational Age
16
Centimetres per year

6 Newborns

Inches per year

3 14
Peak 5
12 The terms intrauterine growth retardation and small for
10 4 gestational age newborns many times are used identi-
8 3 cally. However, the first is the pathologic counterpart
6 to the second. The term intrauterine growth retardation
2 (IUGR) is referred to a newborn whose growth did not
4
1 achieve genetic potential, whereas the term small for ges-
2
tational age (SGA) is referred to a newborn with weight
0 0 and/or length below the third or tenth percentile for
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age
gestational age. Therefore, the SGA newborns have low
Rate of height increase birth weight and/or length due to genetic or constitu-
tional factors or intrauterine growth retardation results
..      Fig. 3.3 Height velocity curve for boys and girls (50th percentile) from maternal, placental, or fetal factors [3, 6, 13].

a b
Overview
55 Intrauterine growth retardation– newborn growth
did not achieve genetic potential
55 Small for gestational age – newborn’s weight and/or
length < third or tenth percentile for gestational
age.

The majority of IUGR newborns show catch-up growth

..      Fig. 3.4 a. Left-hand radiograph of a boy with bone age at
4 years. b. Left-hand radiograph of a girl with bone age at 8 years
and 10 months according to Greulich-Pyle method
in the next 2–3 years. However, 10–15% of them do not
exhibit catch-up growth and remain short throughout
life. The last 15 years of epidemiological studies have
shown that IUGR newborns have higher risk to develop
chronic diseases in adulthood such as metabolic syn-
drome, cardiovascular disease, obesity, and diabetes
mellitus type II [14]. The possible explanation for this
phenomenon is that their process of adaptation to a
limited supply of nutrients in utero drives to gene repro-
gramming that results in consequences in later life.

3.2.2 Short Stature

Short stature is defined as a height lower than the third

..      Fig. 3.5 Drawing of the eight stages of mineralization of a pre-
molar (upper row) and a permanent molar (bottom row), as these
teeth appear at the left side of the mandible in a panoramic radio-
graph, for the estimation of dental age using the Demirjian method
percentile or 2 SD under the mean height for age and
gender. Since stature is a characteristic that follows
a normal Gaussian distribution, that means that 2%
of population may be short and therefore not all the
children underneath the third percentile need further
investigation. Many of them have familial short stat-
ure, idiopathic short stature, or constitutional delay of
growth and puberty (. Figs. 3.6 and 3.7). It is impor-
tant to distinguish normal variants from pathological
short stature. Therefore, children with significant short
Pediatric Body Growth
31 3

Height-for-age BOYS
5 to 19 years (percentiles)

190 97th 190

85th
180 180
50th

170 170
15th
Mean
parental
3rd
160 160
Height (cm)

150 150

140 140

130 130

120 120

110 110

Months
100 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 100
Y ears 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age (completed months and years )
2007 WHO Reference

..      Fig. 3.6 Growth chart of a boy with familial short stature (below 3rd percentile)

Height-for-age BOYS
5 to 19 years (percentiles)

190 97th 190

85th
180 180
50th

170 170
15th Mean
parental
3rd height
160 160
Height (cm)

150 150

140 140

130 130

120 120

110 110

Months
100 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 100
Y ears 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age (completed months and years )
2007 WHO Reference

..      Fig. 3.7 Growth chart of a boy with constitutional delay of growth at puberty
 32 P. Triantafyllou and S. Roberts

stature, decreased growth velocity, or discordance from 3.2.3 Tall Stature

their genetic potential should be further investigated [3,
6, 14, 15]. Height that is more than 2 SD above the mean for age
Malnutrition, psychosocial deprivation, chronic dis- and gender is considered as tall. The majority of tall
eases, or chronic corticosteroid administration may cause children do not have underlying pathology and their tall
growth retardation. Intrauterine growth retardation may stature is either familial or constitutional [16, 17]. Tall
3 also lead to short stature in approximately 10–15% of stature is rarely a concern and a cause of referral, unless
cases. Endocrine disorders associated with growth retar- it is regarding very tall girls. Rarely, there is an under-
dation are growth hormone deficiency or resistance, lying cause like a syndrome or an endocrine disorder.
hypothyroidism, or Cushing’s syndrome. Growth hor- Syndromes that have tall stature as one of their present-
mone deficiency is the most common endocrine disorder ing features are Klinefelter’s (47, ΧΧΥ) and other chro-
that causes short stature. These children have decreased mosomal anomalies, and overgrowth syndromes such as
growth velocity and delayed bone age. Abnormal growth Sotos syndrome and Marfan syndrome (. Table. 3.2).
hormone action despite normal secretion is rare. Short Moreover, children with homocystinuria are character-
stature may be one of the main features of chromosomal ized by tall stature [3, 6, 16].
or genetic syndromes such as Turner syndrome, trisomy Endocrine disorders such as congenital adrenal
21 or Noonan syndrome, Russell-Silver syndrome, or hyperplasia, hyperthyroidism, and precocious puberty
Seckel syndrome, respectively (. Figs. 3.8 and 3.9). may result to linear growth acceleration. Nevertheless,
Additionally, skeletal dysplasias or disproportional parallel skeletal maturation results to early epiphyseal
growth may result on short stature (. Table 3.1), like closure and compromised final height. Extremely rarely
achondroplasia (. Fig. 3.10), spinal epiphyseal dyspla- tall stature is caused by excessive growth hormone secre-
sia, or SHOX deficiency [3, 6, 14, 15]. tion most commonly due to pituitary adenomas.

Height-for-age BOYS
5 to 19 years (percentiles)

190 97th 190

85th
180 180
50th Mean
parental
height
170 170
15th

3rd
160 160
Height (cm)

150 150

140 140

130 130

120 120

110 110

GH
Months
100 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 100
Y ears 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age (completed months and years )
2007 WHO Reference

..      Fig. 3.8 Growth chart of a boy with growth hormone deficiency before and after treatment with growth hormone (GH)
Pediatric Body Growth
33 3

..      Fig. 3.9 a Child with short stature for chronological age due to growth hormone deficiency. b The accompanying reduced bone growth
contributes to intense crowding of both dental arches. (Courtesy of Dr. I. Manoukakis)

..      Table 3.1 Differential diagnosis of short stature

Normal appearance Abnormal appearance

Normal HV Decreased HV Dysmorphic features Dysproportional short

stature
Malnutrition Normal or increased
weight
Familiar short stature Psychosocial Endocrine disorders Turner syndrome Achondroplasia
Constitutional delay of deprivation Noonan syndrome Hypochondroplasia
growth and puberty Malnutrition Down syndrome
Chronic disease Russell-silver syndrome
Seckel syndrome

HV height velocity
 34 P. Triantafyllou and S. Roberts

to play an important role. However, the regulation of

Overview
Obese or overweight children, especially those who
were overweight infants, may be tall for their age
throughout childhood. More commonly they have
accelerated bone age and they undergo early puberty
3 which may result in a shorter final height than expected.
3.3 Puberty
Puberty is the stage of growth and development when
a child becomes a young adult capable for reproduc-
tion. Adolescence, although it is a term widely used as
a synonymous to puberty, is referred to cognitive, psy-
chological, and social changes of this period. Puberty
is a complex biologic phenomenon, and a combination
of environmental, metabolic, and genetic factors seems
puberty initiation remains largely unknown.
During puberty the appearance of secondary sex-
ual characteristics with growth acceleration occurs as
a consequence of increased gonadotropin and sex ste-
roid secretion. Normal pubertal development occurs
between the ages of 8 and 13 years in girls and between
the ages of 9 and 14 years in boys. For clinical pur-
poses Tanner divided puberty in five stages. Tanner
stage I is prepubertal and stage V is the adult appear-
ance. Linear growth is completed 3–5 years from onset
[18–27].
In girls, the first evidence of puberty is breast enlarge-
ment which is called thelarche. Pubarche and axillary
hair follow but are due to concomitant adrenarche.
Menarche appears approximately 1.5–3 years later.
Although linear growth slows after menarche, an aver-
age of another 7 cm may be attained until growth will
be completed approximately at a bone age of 15 years.
In boys, the first sign of puberty is the enlargement of
the testes at a volume of ≥4 ml, followed by pubic hair
and penile growth. Peak height velocity occurs approxi-
mately 2 years later and growth is completed at about
the age of 17 years [18–27].

3.3.1 Disorders of Puberty

..      Fig. 3.10 Child with short stature for his chronological age due
to achondroplasia. (Courtesy of Dr. I. Manoukakis)
3.3.1.1 Precocious Puberty
When breast development (thelarche) occurs before
the age of 8 years in girls or testes enlargement occurs
before the age of 9 years in boys, puberty is considered
precocious. In some girls, puberty at the age of 6–7 years
may be normal. Paradoxically, these children are tall for
their age but they may end up short adults due to early
epiphyseal fusion.
Precocious puberty is more common in children with
a family history, in adopted children (increased risk),
and in children with certain mutations (i.e., MKRN3)
[28]. It is more common in girls and is usually idio-
pathic, whereas in boys there is usually an underlying

..      Table 3.2 Differential diagnosis of tall stature

Normal appearance Abnormal appearance

Normal HV Increased HV Dysmorphic features Dysproportional tall stature

In puberty No signs of puberty
Familial tall stature Precocious puberty Endocrine disorder ΧΥΥ syndrome Klinefelter syndrome
Obesity Sotos syndrome Marfan syndrome
Beckwith-Wiedemann syndrome Homocystinuria

HV height velocity
Pediatric Body Growth
defect. The earlier the age of onset, the more likely it is
to find an organic cause [18–21, 23, 25].
Precocious puberty is distinguished as central or
gonadotropin-dependent and peripheral or gonadotropin-­
independent. Central precocious puberty is caused by
activation of hypothalamic-pituitary-­gonadal axis, and it
is more common in girls. In the majority of cases it is idio-
pathic and rarely there is a central nervous system defect
(tumor, inflammation, trauma, radiotherapy, or hydro-
cephalous). In contrast, in peripheral precocious puberty
sex steroids’ production is autonomous mainly due to
hormone-producing tumors or McCune-Albright syn-
drome. Central precocious puberty is treated with GnRH
analogue in order to prevent early epiphyseal closure with
compromise in final height and to alleviate psychologi-
cal distress. In cases of peripheral precocious puberty, the
management is etiological (surgery in tumors, cortisone
replacement in congenital adrenal hyperplasia) [18–25].
3.3.1.2 Delayed Puberty
Delayed puberty is considered the absence of breast
enlargement by the age of 13 years in girls or the absence
of testes’ enlargement (≥4 ml) by the age of 14 years
in boys [23, 27, 29, 30]. Delayed puberty is more com-
mon in boys and more often it is constitutional with a
history of delayed puberty in a parent or an older sib-
ling. Children with constitutional delay of growth and
puberty are usually shorter for their age with delayed
bone age. However, bone age prediction is in line with
MPH; if predicted height is shorter, this is more worri-
some for underlying pathology. Their final height is usu-
ally normal as they have additional time for prepubertal
growth [30].
Constitutional delay of puberty has to be distin-
guished by underlying pathology such as permanent
central defect (hypothalamic/pituitary hormone defi-
ciency), primary gonadal failure, underlying chronic dis-
ease, or chromosomal disorders (Klinefelter syndrome
in boys or Turner syndrome in girls). [23–27, 29, 30]
References
1. Weintraub B. Growth Pediatric Rev. 2011;32:404–6.
2. Rosenbloom AL. Physiology of growth. Ann Nestle. 2007;65:97–
108.
3. Patel L, Clayton PE. Normal and disordered growth. In: Brook
C, Clayton P, Brown R, editors. Clinical pediatric endocrinology.
5th ed. Blackwell; 2005.
4. Juul A, Kreiborg S, Main KM. Growth and pubertal develop-
ment. Ch. 2. In: Koch G, Poulsen S, editors. Pediatric dentistry:
a clinical approach. 2nd ed. Wiley-­Blackwell; 2009.
5. Wales J. Growth and puberty. Ch 10. In: Lissauer T, Clayten
G, editors. Illustrated Textbook of Paediatrics. 2nd ed. Mosby;
2003.
6. Lifshitz F, Botero D. Worrisome growth. In: Lifshitz F, editor.
Pediatric endocrinology. 4th ed. New York; 2003. p. 1–46.
35 3
7. Greulich WW, Pyle SI. Radiographic atlas of skeletal develop-
ment of the hand and wrist. 2nd ed. Stanford, CA: Stanford
University Press; 1959.
8. Tanner JM, Whitehouse RH, Marshall WA, Healy MJR, Gold-
stein NH. Assessment of skeletal maturity and prediction of
adult height (TW2 method). 2nd ed. London: Academic Press;
1975.
9. Martin DD, Wit JM, Hochberg Z, Sävendahl L, Van Rijn
RR, Fricke O, et al. The use of bone age in clinical prac-
tice - part 1. Horm Res Paediatr. 2011;76:1–9. https://doi.
org/10.1159/000329372.
10. Martin DD, Wit JM, Hochberg Z, van Rijn RR, Fricke O, Werther
G, et al. The use of bone age in clinical practice - part 2. Horm
Res Paediatr. 2011;76:10–6. https://doi.org/10.1159/000329374.
11. Liversidge HM. The assessment and interpretation of Demir-
jian, Goldstein and Tanner's dental maturity. Ann Hum Biol.
2012;39:412–31.
12. Yan-Vergnes W, Vergnes JN, Dumoncel J, Baron P, Marchal-
Sixou C, Braga J. Asynchronous dentofacial development and
dental crowding: a cross-sectional study in a contemporary
sample of children in France. J Physiol Anthropol. 2013;32:22.
https://doi.org/10.1186/1880-­6805-­32-­22.
13. Claris O, Beltrand J, Levy-Marchal C. Consequences of intra-
uterine growth and early neonatal catch-up growth. Semin Peri-
natol. 2010;34:207–10.
14. Wit JM, Oostdijk W, Losekoot M, van Duyvenvoorde HA,
Ruivenkamp CA, Kant SG. Mechanisms in endocrinol-
ogy: novel genetic causes of short stature. Eur J Endocrinol.
2016;174:R145–73.
15. Argente J. Challenges in the Management of Short Stature.
Horm Res Paediatr. 2016;85:2–10.
16. Baron J, Sävendahl L, De Luca F, Dauber A, Phillip M, Wit JM,
Nilsson O. Short and tall stature: a new paradigm emerges. Nat
Rev Endocrinol. 2015;11:735–46.
17. Davies JH, Cheetham T. Investigation and management of tall
stature. Arch Dis Child. 2014;99:772–7.
18. Dattani MT, Hindmarsh PC. Normal and abnormal puberty. In:
Clinical pediatric endocrinology. Blackwell; 2005. p. 183–210.
19. Bordini B, Rosenfield RI. Normal pubertal development: part I:
the endocrine basis of puberty. Pediatr in Rev. 2011;32:223–9.
20. Bordini B, Rosenfield RI. Normal pubertal development: part
II: clinical aspects of puberty. Pediatr in Rev. 2011;32:281–92.
21. Bourguignon JP, Juul A. Normal puberty in a developmental
perspective. Endocr Dev. 2012;22:11–23.
22. Nussey S, Whitehead S. Chapter 6: gonad. In: endocrinology: an
integrated approach. Oxford: BIOS Scientific Publishers; 2001.
23. Lee PA. Puberty and its disorders. In: Lifshitz F, editor. Pediatric
endocrinology. 4th ed. New York; 2003. p. 211–38.
24. Abreu AP, Kaiser UB. Pubertal development and regulation.
Lancet Diabetes Endocrinol. 2016;4:254–64.
25. Latronico AC, Brito VN, Carel JC. Causes, diagnosis, and treat-
ment of central precocious puberty. Lancet Diabetes Endocri-
nol. 2016;4:265–74.
26. Abitbol L, Zborovski S, Palmert MR. Evaluation of delayed
puberty: what diagnostic tests should be performed in the seem-
ingly otherwise well adolescent? Arch Dis Child. 2016;101:
767–71.
27. Fenichel P. Delayed puberty. Endocr Dev. 2012;22:138–59.
28. Abreu AP, Dauber A, Macedo DB, Noel SD, Brito VN, Gill
JC, et al. Central precocious puberty caused by mutations in the
imprinted gene MKRN3. NEJM. 2013;368(26):2467–75.
29. Kaplowitz PB. Delayed puberty. Pediatr Rev. 2010;31:189–95.
30. Harrington J, Palmert MR. Clinical review: distinguishing con-
stitutional delay of growth and puberty from isolated hypo-
gonadotropic hypogonadism: critical appraisal of available
diagnostic tests. J Clin Endocrinol Metab. 2012;97:3056–67.
 37 4

Child Dental Fear,

Communication
and Cooperation
Trilby Coolidge and Nikolaos Kotsanos

Contents

4.1 Child Misbehavior – 39

4.2 Fear Definitions and Prevalence – 40

4.2.1  efinitions of Dental Fear, Anxiety, and Phobia – 40
D
4.2.2 Relationship between Child Misbehavior and Fear – 40

4.3 Etiologies of Dental Fear – 41

4.3.1  lassical Conditioning – 41
C
4.3.2 Social Learning Theory – 42
4.3.3 Cognitive – 43
4.3.4 Feelings of Helplessness and Loss of Control – 43
4.3.5 Genetic – 44
4.3.6 Family Stressors – 44
4.3.7 Temperament – 44
4.3.8 Parenting Style and Other Parenting Factors – 45
4.3.9 Parental Dental Fear – 46

4.4 Measuring Dental Fear – 46

4.4.1 S elf-Report Measures – 46
4.4.2 Behavior Rating Scale – 47

4.5  elationships between the Pain Threshold, Fear, and the

R
Experience of Pain – 47
4.5.1  roviding Children with Information about What Will Happen – 49
P
4.5.2 Dental Visits that Do Not Involve Invasive Procedures – 49
4.5.3 Impact of Treatment Aspects on the Child’s Sense
of Loss of Control – 49

4.6 Self-Management of Fear – 49

4.6.1 T he Importance of Age and Maturity – 49
4.6.2 Child Crying and Coping Behavior – 50
4.6.3 Therapeutic Management of Fear (Desensitization) – 50

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_4
4.7 Special Issues with Adolescents – 50
4.7.1  espond to Requests for Privacy – 51
R
4.7.2 Adolescents May Resist Going to the Dentist – 51

4.8 Communication in the Dental Environment – 52

4.8.1  onverbal Communication between the Dentist and the
N
Child Patient – 52
4.8.2 Verbal Communication between the Dentist and the
Child Patient – 53
4.8.3 Communication with Parents – 53
4.8.4 Communication with the Child – 54
4.8.5 Providing Written Information – 54
4.8.6 Empathy and Communication – 55

4.9 The Influence of the Dental Environment – 56

4.9.1  rovide Positive Stimuli before the Initial Visit – 56
P
4.9.2 Have Welcoming Reception, Staff and Waiting Areas – 56

References – 58
Child Dental Fear, Communication and Cooperation
39 4
4.1 Child Misbehavior a

A search in the old dental literature for descriptions of

children who did not readily cooperate with the dentist
revealed adjectives such as difficult, fidgeting, uncoop-
erative, disruptive, obstreperous, defiant, recalcitrant,
resistant, incorrigible, unmanageable, uncontrollable,
untreatable, etc. Since children usually do not make
their own dental appointments or come to the dentist
on their own, it is common today to refer to the dentist-­
child patient-parent triad, out of a recognition that par-
ents directly influence both the child and the dentist, as
well as indirectly influencing the child [1]. However, the
use of the pejorative terms listed above tends to shift
the blame of poor cooperation away from something
about the triad, or perhaps something about the dental
treatment itself, to some quality or qualities of the child
(. Fig. 4.1).
The dentist obviously has every good intention in b
approaching the child patient, just as he/she does with
adults. However, are good intentions and dental educa-
tion sufficient to ensure that a child will readily coop-
erate with the dentist? We argue that dentists who are
successful with children have a deeper knowledge about
what can cause a child to misbehave. Almost every child
can be trained to behave appropriately in the dental situ-
ation. Dentists learn diagnostic procedures to follow in
order to have the most accurate information about the
causes and solutions for dental problems patients have,
so that the best possible preventive care and treatment
can be offered to them. In a similar way, dentists who
work with children need to understand the common
..      Fig. 4.1 a A 3½-year-old child not willing to cooperate. b The
causes that may lead to behavioral problems, in order to
responsibility for the lack of cooperation is often ascribed to the child
prevent or manage such problems.
It is important to keep in mind that, by and large,
adults go to dentists of their own volition, while young
Overview children, especially, are taken to the dentist by their par-
Put in other terms, a dentist who works successfully ents or other adults. It is possible that the child would
with children: choose not to go to the dentist, if he or she was in a posi-
1. Has excellent (state-of-the-art) dental knowledge. tion to make the choice. Thus, the child who is brought to
2. Is able to provide dental treatment painlessly. the dentist may find himself/herself in a situation that is
3. Is able to acknowledge children’s feelings by under- not of his/her own preference, which may create negative
standing the causes of their reactions. feelings about being at the dentist. The child’s subjective
beliefs about what may happen at the dentist are closely
related to experiences of fear and anxiety, and appear to
Children and adolescents constitute a patient group with be stronger predictors of negative affect than the actual
differences across several parameters, such as age, abil- dental treatment is [2]. In addition, when young children
ity, personality, temperament, prior dental experiences, with dental fear and/or behavior management problems
dental health and hygiene, familial background, etc. are referred to a specialist, they are more likely to have
These parameters affect child behavior and reactions to manifest caries [3], which means that they are likely to have
the dental situation. This chapter focuses on analyzing to undergo invasive treatment, which in turn increases the
these factors to help the dentist understand and reduce risk of developing greater fear and/or of behaving poorly
the causes that may lead to child dental fear and/or poor at the dentist. Thus, such children need special attention
cooperation/misbehavior in the dental setting. in order to prevent these negative outcomes.
 40 T. Coolidge and N. Kotsanos
4.2 Fear Definitions and Prevalence
Definition
The Definition of Pain
The International Association for the Study of
Pain defines pain as follows:
4
»» An unpleasant sensory and emotional experi-
ence associated with actual or potential tissue
damage, or described in terms of such tissue
damage…. Pain is always subjective….Many
people report pain in the absence of tissue dam-
age or any pathophysiological cause; usually this
happens for psychological reasons. There is usu-
ally no way to distinguish their psychological
experience from that due to tissue damage if we
take the subjective report. If they regard their
experience as pain, and if they report it in the
same ways as pain caused by tissue damage, it
should be accepted as pain [4].
In accordance with this definition, we suggest that
pediatric dentists give credence to their patients’
reports of pain, even if the dentist believes that the
patient should not be feeling pain. Our experience is
that accepting the patient’s report goes a long way to
creating a relationship of trust between the patient
and the dentist.
4.2.1  efinitions of Dental Fear, Anxiety,
D the dental situation. Indeed, children with higher levels
and Phobia
Many people use the terms “fear” and “anxiety” inter-
changeably. We think that it is helpful to briefly describe
the differences between them. Fear refers to cognitive,
physiological, and behavioral responses to a perceived
threat. For example, a child who is afraid of the dentist
may respond to being at the dentist’s office with thoughts
such as: “It’s going to hurt!,” an increased heart rate, and
behaviors such as refusing to enter the waiting room, let
alone the operatory. Anxiety refers to the responses to a
threat which is more vague in nature (“Something bad
might happen!”) or may possibly occur in the future (“I
might have to go to the dentist again!”). If the anxiety-
provoking threat becomes imminent, the individual’s
response may be to become fearful. Thus, children who
have been anxious about going to the dentist may show
more fearful responses as the day and time of the dental
appointment nears.
In adults, phobia is a pattern of intense fear of a situ-
ation or object – recognized by the individual as being
extreme or irrational – which may lead to actively avoid-
ing the situation [5, 6]. Children may not be able to rec-
ognize their dental phobia as being irrational. Also, we
recommend that dentists not use active avoidance as a
criterion for determining if children are phobic about
dentistry, because younger children, especially, may not
be able to avoid going to dental appointments. It may
be more appropriate to call children phobic if they react
to an upcoming treatment with dread or need special
accommodations (such as a pediatric dentist who special-
izes in treating fearful children) to endure treatment [7].
For the remainder of this chapter, for simplicity’s
sake we will use the term “dental fear” to refer to dental
fear, dental anxiety, and dental phobia.
Researchers estimate that dental fear occurs in 5 to
20 percent of children and adolescents [8]; when studies
from a number of samples were compared, the research-
ers estimated that 9 percent of children and adoles-
cents had dental fear [7]. Dental fear is more common
in younger children [7, 9]. As 7 Chap. 2 describes, as
children mature they learn cognitive and other meth-
ods of coping, so that dental experiences become more
manageable and less frightening. In most samples, child
dental fear is higher in females [7].
4.2.2  elationship between Child
R
Misbehavior and Fear
As we have already implied in our definitions, some
dentally fearful children are more likely to misbehave in
of fear were more likely to be referred to a specialist in
behavior management [10]. A study found that paren-
tal rating of children’s level of dental fear was the best
predictor of whether or not a child misbehaved [11].
However, impulsivity (i.e., the lack of effortful control)
was found to be more important than dental fear in
predicting which children were referred to a specialist
because of misbehavior [12]. Other factors predicting
uncooperative behavior include younger age, a history
of toothache, parental assessment that the child will not
be cooperative, parental assessment that the child will
be anxious around strangers, and negative emotional-
ity [7, 13, 14]. Other risk factors for misbehavior include
psychiatric symptoms or diagnoses (such as autism and
Asperger’s syndrome) and learning problems [9].
We should caution that not all fearful children will
misbehave at the dental office, nor do all children who
misbehave have dental fear. A study of more than 3000
children found that about 25 percent of those with a
history of being uncooperative at the dentist had den-
tal fear, while about 60 percent of those who had dental
Child Dental Fear, Communication and Cooperation
41 4
fear also misbehaved [15]. We believe that dentists who Classical Conditioning
treat children are already alert to the possibility that the
child patient may misbehave and/or have dental fear,
because these make providing dental treatment more
Unconditioned Unconditioned
challenging. An additional reason for alertness is related Stimulus Response
to the potential ability of the dentist to make a positive
difference in the oral health of their patients, due to two
factors. First, children referred because of misbehavior Meat Salivation
and/or fear are more likely to have caries, compared
with their better-behaved peers [3]. Second, longitudinal
research indicates that having caries in childhood pre- Conditioned Conditioned
dicts having caries in adulthood [16]. Thus, the dentist Stimulus Response
who keeps concepts about dental fear and misbehavior
in mind as he or she works with pediatric patients may
Ring bell Salivation
be able to help patients minimize caries during their
childhood and thereby also reduce the risk of caries in
Without any conditioning, the dog automatically salivates
their adulthood.
when it sees the meat. If you ring a bell when you present the
meat, eventually the dog will salivate when it hears the bell.
The dog has been conditioned to respond to the bell.
4.3 Etiologies of Dental Fear
..      Fig. 4.2 Classical conditioning
4.3.1 Classical Conditioning

Many dental fears may be caused by classical condition-

ing. Recall Pavlov and his experiments with dogs. As you
probably know, dogs salivate when they see meat. This
is an automatic, or unconditioned, response. Pavlov dis-
covered that, if he sounded a bell when he presented the
meat, the dog would salivate in the future when it heard
the bell – even if the meat wasn’t presented. The dog had
been conditioned to respond to the bell with salivation
(. Fig. 4.2).
A child who experiences pain at the dentist may
develop a conditioned fear response to dentists, den-
tal operatories, the smells and sounds associated with
dentistry, or other stimuli that occurred when the pain
was experienced [8] (. Fig. 4.3). Through the process of
stimulus generalization, a child who has had a painful
experience outside of the dental office may also show
fear at the dentist. One typical example is a child who
had a painful vaccination given by a doctor wearing a
white coat. Such a child may respond with fear when
seeing a dentist wearing a white coat – or handling a ..      Fig. 4.3 Tooth extraction without proper pain control results in
syringe for local anesthesia. By the process of stimulus fear of the dentist
generalization, the child notices the similarities between
the dental and the previous situation and responds to create considerable barriers to optimal dental care. As
the dental situation with fear, based on the pain experi- Weinstein [18] pointed out in a model originally devel-
enced in the previous environment (. Fig. 4.4). oped for adults (i.e., for patients who have the ability to
Since obtaining dental treatment for dental prob- refuse to go to a dentist), dental fear caused by painful
lems is likely to happen at some point for a child, and treatment can lead to dental avoidance, which in turn
because continuing to obtain preventive dental ser- leads to greater risk of developing dental problems,
vices is desirable, a child’s conditioned dental fear may which creates a higher risk that the dental treatment will
 42 T. Coolidge and N. Kotsanos

Further, there is evidence that the child’s cognitions

about a dental experience can be changed. Pickrell et al.
[19] found that inviting a child to think about – and tell
his/her parents about – ways in which the child had done
well during an otherwise-stressful dental appointment
involving a dental injection resulted in decreased dental
fear, and more cooperative behavior, during a follow-up
appointment which also required a dental injection. In
4 addition, at the second appointment the children who
had discussed how they had done well after the first
appointment remembered the first appointment as being
less fearful than they had reported at the end of the
first appointment, while the children who had not had
the discussion about ways in which they had done well
remembered their fear level during the first appointment
..      Fig. 4.4 Acquisition of fear through stimulus generalization.
(Redrawn after Chadwick & Hosey [17])
as being slightly higher than they had rated it at the end
of the first appointment.

4.3.2 Social Learning Theory

Painful
Treatment
While many children (or their parents) can describe
having a painful dental experience which initiated the
child’s fear, other fearful children do not appear to have
Uncontrolled Self- had a history of having had painful dental experiences
Oral perceptions themselves. According to Social Learning Theory [20],
Pathology and Values we also learn from observing the behavior of others.
Thus, a child might hear another child on the playfield
say “Dentists are awful! I hate them because they hurt
me!” It is not uncommon for English-speaking adults
to say “I’d rather have a root canal than [undergo some
stressful experience],” which hearers understand as indi-
Avoidance of cating that root canal procedures at the dentist are very
Needed Fear painful. The natural conclusion is that many, most, or
Treatment perhaps even all dental procedures are painful. We also
learn from pictures and movies. Horror movies may
depict people brandishing dental drills as weapons,
Cycle of Fear which teaches viewers that dental instruments – and
possibly dentists themselves – are to be avoided as dan-
..      Fig. 4.5 Cycle of fear. (Based on Weinstein, 1990 [18])
gerous (. Fig. 4.6).
Since, according to this reasoning, children learn
be more painful when the patient finally does see a den- through observation, dental fear can be reduced by
tist, which continues to result in fear (. Fig. 4.5). exposing children to models who behave calmly dur-
Note that the cycle of fear includes self-perceptions ing a dental appointment. For example, dentally fearful
and values. Weinstein added this to his model because children who watched a video of a child calmly undergo-
not all people who experience pain related to dental ing a restoration under local anesthesia had significantly
treatment develop dental fear. The model suggests that lower anxiety when they subsequently underwent dental
cognitions regarding the nature of the situation, such treatment requiring anesthesia, compared with a con-
as placing a high value on dental treatment or seeing trol group who had viewed a video depicting the same
oneself to be a person with a high tolerance for pain, dentist and child, but which focused on hygiene instruc-
may protect the individual who experiences a painful tion, which was not the treatment that the children were
encounter from developing dental fear. about to undergo [21].
Child Dental Fear, Communication and Cooperation
43 4
4.3.4  eelings of Helplessness and Loss
F
of Control
The etiology of dental fear includes helplessness
and loss of control5 and also lack of trust (or fear of
betrayal) [25] as important factors in the child’s develop-
ment of dental fear. Adults with greater preferences for
being in control in the dental setting, but lowered per-
ceptions that they actually had control in that setting,
were at greater risk for having dental fear [26]. Children
8–10 years of age with greater dental fear stated that
they wanted to have more ways of controlling what hap-
pened to them at the dentist [27], while 11–15-year-olds
with greater dental fear also preferred to have more ways
of controlling their experiences at the dentist [28]. Thus,
lack of trust and loss of control constructs may be con-
sidered “cognitive” in the sense that they involve assess-
ments of the dental situation.

Tip

While children may not be able to have complete con-

trol during dental treatment, dentists can minimize
feelings of helplessness and loss of control by offering
their patients some control during the dental treatment.
For example, children can choose which tooth or teeth
they would like to have polished first or which type of
distraction they prefer. They can also be asked “Would
..      Fig. 4.6 Such pictures of dentists can cause dental fear in those
who observe them you like to take a little break now?” and taught to raise
the left hand and arm (i.e., the hand and arm farthest
from the dentist, to minimize hitting the dentist) to sig-
4.3.3 Cognitive nal “please stop” during treatment (. Fig. 4.7).

Armfield and colleagues have extensively explored the

extent to which certain cognitions about the dental situ-
ation may be related to the presence and/or severity of
fear. They propose that individuals who are more likely
to experience dental stimuli as uncontrollable, unpre-
dictable, dangerous, and/or disgusting are likely to feel
vulnerable in the face of such stimuli, which in turn
leads to an assessment that the situation is dangerous
[22]. In a sample of children, dental fear, subjective rat-
ings of poorer oral health, and ratings of higher cog-
nitive vulnerability were each significantly correlated
with the other two factors. When considered simultane-
ously, cognitive vulnerability was the stronger predictor
of dental fear [23]. Further research with this model
revealed that greater levels of cognitive vulnerability
were stronger predictors of children’s dental fear than
were having higher trait-like levels of negative affect, a
history of negative dental experiences, the number of ..      Fig. 4.7 Child requests that the treatment be temporarily stopped
dentally fearful relatives, age, or gender [24]. by raising the left hand and arm
 44 T. Coolidge and N. Kotsanos

4.3.5 Genetic or slowly), adaptiveness, shyness, activity level, and

self-­
control. Children with higher reactivity, lower
Some recent research indicates that there may be genetic adaptiveness, and lower self-control may have more
bases for dental fear. A study of adolescent twins found difficulty with new people and new situations and may
that the monozygotic siblings were more concordant pose greater behavioral challenges to dentists. Such
both in having dental fear and in their levels of dental children are more likely to cry, become afraid, and try
fear intensity, compared with the dizygotic siblings [29]. to avoid the situation (e.g., young children may try to
In adults, levels of dental fear are significantly more hide behind the parent) (. Fig. 4.8). Parents and other
4 similar for monozygotic twins compared with dizygotic adults can help children modulate these inborn ten-
twins [30]. Several recent studies have examined variants dencies, while increased abilities to cope with poten-
of the melanocorin-1 receptor gene (MC1R), common tial stressors help children behave more appropriately
in redheaded people. Adults with this variant have been as they age. When temperament is assessed by parental
found to have higher levels of dental fear and dental questionnaires, children who are shy, inhibited, and/or
avoidance, compared with those who do not have the are higher on negative emotionality are more likely to be
variant [31]. These variants, as well as other genetic sites, dentally fearful, while children who are higher on activ-
have also been identified with higher levels of fear of ity, impulsivity, and more rapid reactivity are less likely
pain [32, 33]. These data suggest that pediatric dentists to be cooperative [7, 11, 38].
should be particularly alert to the possibility that red-­ Dentists who are aware of the child’s tempera-
haired children – as well as other children with a family ment will be able to modify their behavior accordingly.
member with dental fear – may be more likely to have or For example, some children may need time to accept
develop dental fear themselves. the necessity of a tooth extraction, and therefore the
dentist would tell them about this at the appointment
where this has been decided (i.e., in advance of the
4.3.6 Family Stressors

Children of lower-income families are more likely to have

early childhood caries and/or caries [34–36]. Other fam-
ily stressors, such as divorce, having a parent in jail, and
exposure to neighborhood violence have also been pre-
dictive of caries; furthermore, greater numbers of stress-
ors are associated with increased risks for caries or other
dental problems [37]. Children of low-income families
are more likely to have higher levels of cariogenic bacte-
ria, higher levels of basal salivary cortisol secretion, and
caries, compared with children of higher-­income fami-
lies [34]. While some researchers had thought that such
findings were related to a relative lack of education in
the low-income parents, the findings of Boyce et al. [34]
are particularly striking because the parents generally
were fairly highly educated (57% had education beyond
the college level). The stress of growing up in a low-
income family possibly results in greater biological risks
for developing caries. Pediatric dentists should closely
monitor children of low-income families and families
experiencing other stressors, as well as counsel families
on sound oral health practices, to try to minimize the
development of caries in these at-risk children.

4.3.7 Temperament

Temperament refers to several behavioral dimensions

that are thought to be genetic and influence how the
child relates to his/her world. Examples include reac- ..      Fig. 4.8 This child will need more behavioral guidance from the
tivity (whether the child responds to a stimulus quickly dentist. (Redrawn from Chadwick & Hosey, 2003 [17])
Child Dental Fear, Communication and Cooperation
appointment for the extraction). On the other hand,
other children may experience heightened anxiety upon
hearing the news, in which case it would be preferable
to wait until the appointment for the extraction to let
the child know [39].
4.3.8  arenting Style and Other Parenting
P anxious during treatment, compared with children from
Factors
Baumrind [40] described three parenting styles, each
characterized by a combination of high vs. low tenden-
cies to dominate or control their children and high vs.
low displays of warmth directed toward their children.
Authoritarian parents exert high control over their chil-
dren and display low levels of warmth, authoritative
parents also exert high control but display higher lev-
els of warmth, while permissive parents exert little con-
trol and display high levels of warmth. A fourth style,
termed neglectful, was proposed characterized by low
control and low warmth [41] (. Fig. 4.9).
Among children whose behavior did not require
referral to a specialist, those who had authoritarian par-
ents had significantly higher dental fear scores [10]. In
a sample of young children, most (93%) of the children
whose parents were authoritative behaved cooperatively
during an initial dental visit. By contrast, only about
half of the children of permissive (58%) and authori-
tarian (45%) parents behaved cooperatively [42]. In one
sample, mothers who were authoritative were found to
have higher emotional intelligence than mothers who
were authoritarian or permissive. While parenting style
was not related to the children’s behavior in the dental
setting, higher levels of emotional intelligence in the
mother was predictive of greater cooperation in the
child [43].
Control
High Low
Low
Authoritarian Neglectful
Warmth
High
Authoritative Permissive
Parenting Styles
..      Fig. 4.9 Four parenting styles
45 4
One study found that children raised by permissive
families were more likely to need protective stabilization
and parental separation during treatment, compared
with children from authoritarian or authoritative fam-
ilies [44]. Another study by this team found that chil-
dren of permissive and authoritarian families displayed
more negative behavior and were rated as being more
authoritative families [1]. Of note is that these latter chil-
dren scored highest on a measure of “effortful control,”
which is related to the ability to control one’s behaviors.
Parenting style may also be related to the prevalence
of caries. Howenstein et al. [42] found that 80% of the
children of authoritative parents had no caries at their
initial dental visit, compared with only 3% of the chil-
dren of permissive parents and 9% of the children of
authoritarian parents.
Another study examined the roles that psychologi-
cally intrusive behaviors on the part of the parent (or
parents) may play in the development of dental fear [45].
This term refers to parental behaviors that are character-
ized by the child’s experiences of pressure to disavow his/
her own sensations and perceptions in favor of what the
parent asserts. Examples include parents who deny the
existence of the child’s pain, reject the child’s attempts to
express his or her own views when they differ from those
of the parent, shame or ridicule the child, or vacillate
between being over- and under-protective of the child.
These result in a child who is vulnerable to feeling a lack
of control in situations, because he/she hasn’t had the
developmentally appropriate experiences of successfully
managing unusual stimuli and experiences [ 45]. These
children are at greater risk for displaying negative behav-
iors [46]. Unfortunately, there is also evidence that the
child’s negative behaviors are likely to elicit additional
intrusive behaviors from the parent, which perpetuates
the child’s tendency to engage in negative behaviors
because he/she child has not been allowed to develop the
capacity to feel in control [47].
Parenting today may be harder than it was a gen-
eration or so ago [48]. Parents are less likely to provide
the high control of the authoritative and authoritar-
ian parenting styles, replaced by greater indulgence –
or even neglect – seen in the permissive and neglectful
parenting styles [49, 50]. More parents focus on verbal
­explanations or bribes to influence their children, and
fewer use physical discipline [49]. Parents place more
emphasis on reducing their child’s distress, which may
lead to decreased efforts to teach coping mechanisms
to children and/or increased requests for pharmaco-
logical interventions [50]. In two observational samples,
the majority (67–70%) of permissive parents intervened
during the appointment to have the dentist stop the
treatment of their child, compared with none of the
authoritarian or authoritative parents [1, 44].
 46 T. Coolidge and N. Kotsanos
Eye Catcher
One of the most powerful techniques for develop-
ing a strong dentist-parent alliance is drawn from
the principles of motivational interviewing, a set of
communication guidelines designed to help individu-
als change their behavior [51]. After the initial pleas-
antries with the parents who are bringing you a new
4 child patient for the first time, you can ask the parent
“What is your dental wish for Johnny?”
Our experience has been that most parents say
things such as “I hope he doesn’t ever have tooth-
ache,” “I’d like her teeth to be pretty,” “I want his
teeth to be nice and strong,” etc.
Notice that, for each of these goals, the same com-
bination of good oral care practices at home, coupled
with frequent checkups with you, will maximize the
odds that the goal will be reached. In other words,
you as the dentist have the same goal as the parent
does.
You can reinforce the parent’s goal: “OK, so your
wish is that Johnny never has a toothache. That’s a
great goal!” Then remind the parent of the goal later
on, when you discuss oral home care (“Not letting
Johnny fall asleep with a juice bottle is an important
way to prevent cavities and toothache”), coming back
to the dentist for regular checkups (“Regular check-
ups help me find any problems early on, another
important way to prevent toothaches”), and so on.
You can also write the goal down in the child’s chart,
so that you can refer to it at the beginning of subse-
quent visits. Now you have created a bond between
yourself and the parent: you are working together to
reach a common goal.
Motivational interviewing counselors often offer
their clients a “menu” of options, each of which is
designed to help them reach their goal. Similarly, you
can offer the parent a “menu” of options, all of which
are designed to meet the parent’s goal for the child.
You can say:
“Here’s a list of things that other parents have
done to help their children reach their goal of not
having toothache.” [Examples: “Don’t give her a bot-
tle with juice in it when it’s time for sleeping”; “After
he eats, wipe his teeth with a clean cloth”, “Don’t
put honey in her bottle of milk”.] “Which of these
do you think you could try?” This allows the parent
to answer something such as: “I think I can just give
him a bottle with water when I put him down for his
nap.” You can reinforce the parent’s choice (“That’s
a great option”) and then troubleshoot if necessary
(“I remember you told me that Grandma often gives
your child a bottle with juice when it’s time for a nap.
How could you make sure that this doesn’t happen?”).
This approach has been tested in several random-
ized clinical trials with children at higher risk for early
childhood caries. In one sample, at 12 and 24 months
after the discussion with the parents, the children
whose parents were in the motivational interviewing
group had significantly fewer caries, compared with
those who received more traditional oral health edu-
cation [52, 53].
4.3.9 Parental Dental Fear
Children whose parents are afraid of the dentist are at
higher risk of developing fear themselves, [54] and the
relationship between parental and child fear is generally
stronger for younger children [55]. Mothers who are den-
tally fearful are less likely to go to a dentist themselves at
least once a year, as well as less likely to have taken their
child to a dentist in the first 3 years of life [56]. Children
of fearful parents who avoided taking them to a dentist
were at increased risk of having caries and of displaying
misbehavior at a dental visit at age 5 [3]. It would be wise
for the pediatric dentist to routinely ask if a parent (or
other caretaker) is afraid of dentists or dental treatment,
as well as whether he/she goes to the dentist regularly.
4.4 Measuring Dental Fear
There are several ways of assessing children’s dental fear,
including self-report measures (questionnaires) that the
child completes, questionnaires about dental fear that
parents or others complete about, or on behalf of, the
child, and behavioral rating scales used by observers
to rate children’s behaviors, such as crying or resisting
treatment, that are assumed to indicate that the child is
afraid. For objective quantitative estimate some physi-
ological changes can be evaluated, like the heart rate,
breath rate, and palms sweating. The more recent mea-
surement of hormones cortisol and α-amylase in the
saliva for the estimation of dental stress has not shown
to be advantageous compared to changes in heart rate,
which remains an immediate and easier procedure [57].
4.4.1 Self-Report Measures
Perhaps the most commonly used self-report measure is
the Children’s Fear Schedule Survey – Dental Subscale
[58]. This measure consists of a list of 15 items or
descriptions of things that a child might encounter in
the dental setting, as well as a few items which refer to a
medical encounter. Each item is answered on a 5-point
Child Dental Fear, Communication and Cooperation
47 4

..      Table 4.1 Children’s Fear Survey Schedule – Dental Subscale [58]

Below are some things that you might be afraid of. Not afraid A little A fair Pretty much Very afraid
Circle the number that best represents how you feel at all afraid amount afraid

1. Dentists 1 2 3 4 5
2. Doctors 1 2 3 4 5
3. Injections (shots) 1 2 3 4 5
4. Having someone examine your mouth 1 2 3 4 5
5. Having to open your mouth 1 2 3 4 5
6. Having a stranger touch you 1 2 3 4 5
7. Having somebody look at you 1 2 3 4 5
8. The dentist drilling 1 2 3 4 5
9. The sight of the dentist drilling 1 2 3 4 5
10. The noise of the dentist drilling 1 2 3 4 5
11. Having somebody put instruments in your mouth 1 2 3 4 5
12. Choking 1 2 3 4 5
13. Having to go to the hospital 1 2 3 4 5
14. People in white uniforms 1 2 3 4 5
15. Having the nurse clean your teeth 1 2 3 4 5

scale, ranging from “Not afraid at all” to “Very afraid”
(. Table 4.1). The individual item scores are summed;
the total score may range from 15 to 75, with higher
scores indicating greater dental fear.
The CFSS-DS has been found to have good reliabil-
ity and validity [59, 60], although some authors have
pointed out that some of the items do not specifically
relate to pediatric dentistry (e.g., “Having to go to the
hospital”) and/or may not be highly related to pediat-
ric dentistry today (“People in white uniforms”) [61].
Initially created in English, the measure has now been
translated and validated in a number of additional
­languages.
Younger children may have an easier time complet-
ing the CFSS-DS if the items are read aloud to them
and if the numerical ratings are paired with something
such as the five images of the Facial Image Scale [61,
62]. Some authors have asked parents to fill out the
CFSS-­DS on behalf of their young children, but it is
not clear whether parents are accurate reporters about
their children’s fear [63, 64].
Another popular questionnaire for children is the
8-item Modified Child Dental Anxiety Scale [65]. One
version of this scale (Modified Child Dental Anxiety
Scale-faces (MCDASf)) [66] uses five facial images to
help children understand the task of selecting their rat-
ings of the eight items.
4.4.2 Behavior Rating Scale
The most commonly used behavior rating scale is the
Frankl scale [67]. Children are rated on a 4-point scale
according to their behavior in the dental office, ranging
from definitely negative (e.g., crying forcefully) to defi-
nitely positive (e.g., laughing). The ratings may be made
at different points during the dental encounter (e.g.,
entry into operatory, getting into the chair, accepting
the dental bib, etc., through to include behavior during
treatment and behavior at the end of the encounter), or
the dentist may simply notice what the child’s worst rat-
ing was during the encounter (. Table 4.2).
4.5  elationships between the Pain
R
Threshold, Fear, and the Experience
of Pain
The pain threshold is the level of stimulation above
which a patient becomes aware of pain. Pain tolerance
is usually higher than the pain threshold (except in very
young children) and represents the level of stimulation
which the patient can tolerate. Anxiety and physical ten-
sion – both of which are likely to be experienced by the
anxious person – cause the patient’s pain threshold to
be lower than it normally would be for that individual,
 48 T. Coolidge and N. Kotsanos

which increases the chances that stimuli will be experi-
enced as painful [5, 68]. Psychological methods of reduc-
ing fear and anxiety primarily raise the pain tolerance
level, rather than affecting the pain threshold [69]. In
addition, being able to handle discomfort in the dental
situation presupposes that one can control one’s anxiety.
Careful attention to children is required when there
is a possibility that they may experience pain, because
4 children differ in their awareness of, and reactions to,
pain. Children under the age of 3 or 4 may have a hard
time communicating when they experience painful
stimuli [70]. Older children, who typically have better
self-­discipline and know more ways to cope with what
might be stressful for their younger peers, may be able
to remain quiet and restrict their movements even in
circumstances when they feel some pain. However, it
is important for the dentist not to assume that a quiet,
immobile child does not feel discomfort. The dentist
may ask a child to use a graphic scale to rate any dis-
comfort or pain that he or she is feeling (. Fig. 4.10).
It is important that the dentist immediately notice
that the child is in pain and stop, provide more anesthe-
sia, or find a different way to provide treatment that is
pain-free, in order to prevent the classically conditioned
development of fear. In an adult with a long history
of safe, pain-free dental experiences, there is a smaller
chance that a negative dental experience will result in
fear. Since children have not had the chance to experi-
ence such a long history of pain-free dental encounters,
if a dentist lacks sensitivity or knowledge of proper
child guidance to deal with a child in pain, this may cre-
ate cooperation problems because the child has no other
effective ways of communicating that he or she is in pain
other than to rely on more primitive methods, such as
shouting, kicking, or thrashing about – which, in turn,
make dental treatment more difficult [72].

..      Table 4.2 Frankl rating scale [67]

Score Title Shorthand mark Description

1 Definitely negative
2 Negative
3 Positive
4 Definitely positive
− Refuses treatment, cries forcefully, fearfulness, or any other overt evidence of
extreme negativism
− Reluctance to accept treatment, uncooperative behavior, and some evidence of
negative attitude that is not pronounced
+ Acceptance of treatment, cautious behavior at times, willingness to comply
with the dentist, at times with reservation, but patient follows the dentist’s
directions cooperatively
++ Good rapport with the dentist, interest in the dental procedures, laughter and
enjoyment

..      Fig. 4.10 Wong-Baker face scale [71] for children 3 to 17 years old (above) and self-report Likert scale (below)
Child Dental Fear, Communication and Cooperation
4.5.1  roviding Children with Information
P 4.5.3
about What Will Happen
One way of reducing anxiety and addressing a ten-
dency to worry to the point of having catastrophic
ideas about what will happen is to provide children
with more information about what will happen during
their visit. This could be done in the form of a pam-
phlet or video that shows children undergoing exams,
radiographs, restorations, and the like. The dentist can
also allow children time to explore being in the chair in
various positions, touch some of the instruments, see
his/her own teeth in the mirror, and so on. The dentist
can also tell the children what the different steps in the
treatment are going to be, how long each will take, and
especially what the child is likely to feel during each
step [73].
4.5.2  ental Visits that Do Not Involve
D dentist, and its understanding tested, especially for the
Invasive Procedures
Researchers have found that children who have had sev-
eral dental checkup visits before having their first inva-
sive dental procedure were less fearful. In the terms of
classical conditioning, the dentist (conditioned stimu-
lus) has been presented to the children several times
in the absence of pain (unconditioned stimulus). This
makes it less likely that the first experience of the dentist
(conditioned stimulus) in an appointment that includes
pain (unconditioned stimulus) will result in fear of the
dentist (conditioned response). The initial pain-free
experiences help inoculate – or inhibit – the child from
developing fear. Therefore, one suggestion to avoid the
development of dental fear in children is to try to ensure
that the child’s initial dental visit does not include pain-
ful procedures [74, 75].
A second suggestion is to invite parents to bring
their child to the dentist for an initial “awareness visit”
to allow the children and their parents to meet the den-
tist [67]. A third suggestion is to ensure that children
have frequent exposures to dentists where possible; chil-
dren who only attend infrequently could have their vis-
its extended a bit to allow time for dentists to talk with
children and allow the children to look at and explore
dental instruments, in order to allow for exposure to
dentists and dental stimuli to decrease anxious feelings
that the children might have [2]. It is also noteworthy
that a higher number of filled teeth (which may be seen
as a proxy for having been to the dentist more often)
predict lower anxiety in children [74].
49 4
I mpact of Treatment Aspects
on the Child’s Sense of Loss of Control
Children may experience a sense of loss of control with
certain aspects of dental treatment, including when
dental tools that cause pain are in their mouths and the
children believe that they cannot end the painful stim-
uli themselves [76]. If the child believes that he/she is
going to feel pain that is greater than he/she can bear
(i.e., greater than his/her level of pain tolerance) without
having any way to control or end the pain, the result is
likely to be fear.
Speech is typically more difficult when the patient is
undergoing dental procedures, due to the dental dam,
instruments in the mouth, and the like. Being unable to
speak easily may also cause the child to feel a lack of
control. The signal we mentioned earlier (raising the left
arm to signal pain) can also be taught to the child to use
in case he or she wants to communicate something to the
case of local anesthesia administration.
4.6 Self-Management of Fear
Overview
People differ with regard to their pain threshold and tol-
erance levels, as well as in the ways in which they manage
the stress that may accompany dental experiences. Adults
have a variety of ways of coping with anxiety, including:
55 Distraction.
55 Prompting himself/herself to use deep breathing
and other forms of relaxation.
55 Turning to a supportive person for help [5].
Some dentists instinctively use similar approaches with
patients. For example, behaving with empathy toward a
patient’s anxieties increases the patient’s sense that the
dentist is a supportive partner in providing dental
treatment, resulting in increased trust and decreased
anxiety on the part of the patient [77, 78].
4.6.1 The Importance of Age and Maturity
Two additional factors are also important when dealing
with children. Their responses to the dental situation
will depend on the stage of their cognitive development
and linguistic abilities, both of which are related to age
 50 T. Coolidge and N. Kotsanos
and their level of emotional maturity. During a dental
visit, most children over the age of 3 are able to manage
any anxiety and, if they have proper guidance from the
dentist, behave cooperatively. However, some children
have not yet developed appropriate ways of coping and
therefore may respond to the strangeness or stressful-
ness of the dental appointment instinctively, such as
by crying or attempting to withdraw. Also, consistent
4 with the descriptions of parenting styles and/or intru-
siveness above, when parental discipline is lacking or
is overly strict, children’s coping abilities are usually
decreased [79].
4.6.2 Child Crying and Coping Behavior
Furthermore, the child’s reactions to pain will vary
depending on his/her background, including cultural
background [80]. Children frequently refer to their social
environment for clues about how to respond to stimuli.
For example, the child notices how others respond to
his/her crying and may modify his/her behavior accord-
ingly: Is crying accepted, or is the child supposed to
“toughen up” and withstand the uncomfortable stimu-
lus stoically? When is it appropriate to ask for help?
Here, the dentist’s first job is to determine the cause of
the crying. Even stubborn, hysterical crying has a cause:
this kind of crying reveals how anxious the child is in the
dental situation, which perhaps is a new one to the child
and certainly is a threatening one. The dentist needs to
respond with empathy as well as calmness, to help the
child feel safe and become able to cooperate. On the
other hand, crying that is the result of painful stimuli
reveals that there has not been enough local anesthesia.
Regardless of the cause, dentists who work with children
need to be able to respond to crying without losing their
self-control [81].
As we have seen, crying may be one response to the
stress of the dental situation. Adults and children alike
use some kind of strategy to deal with anxiety, which
can manifest anywhere on a continuum between com-
plete self-control (positive, cooperative behavior) to
complete rejection (negative, uncooperative behavior).
The dentist should evaluate a new pediatric patient’s
behavior carefully, to gain information about how well
this particular child is able to cope. Facial expressions,
crying, complaints, and body language all provide
diagnostic cues. A quick and practical way to estimate
and record a child’s behavior during the dental proce-
dure is through the use of the Frankl scale, described
earlier. It is useful to keep records of the child’s behav-
ior during dental visits so that the dentist can prepare
for the possible behavior of the child in subsequent
appointments.
4.6.3  herapeutic Management of Fear
T
(Desensitization)
The methodical introduction of children to dentistry is
accomplished through various techniques of behavioral
configuration through which the appearance of anxiety
and fear is prevented or reduced drastically (discussed
in 7 Chap. 5). However, when anxiety or fear is already
established, the dentist needs to use desensitization [82].
It is important that the patient remain calm while the
dentist gradually introduces stimuli which are related to
what the patient is afraid of. This is accomplished by
establishing with the patient what the least fearful stim-
uli are and presenting these first. As long as the patient
remains calm, the dentist can then gradually move on to
more fearful stimuli. This approach results in a break-
ing of the classically conditioned relationship between
the conditioned stimulus (e.g., dental stimuli) and the
conditioned response (e.g., fear), so that the child may
now experience the stimulus more calmly [5]. Some den-
tists may prefer to refer a child to a psychologist for the
desensitization. The advantages of the dentist himself/
herself carrying out the treatment are that the child
develops a trusting relationship with the person who will
then be carrying out the dental treatment, and the child
becomes familiar with the operatory and dental tools
that will be used in that treatment.
As described in 7 Chap. 5, this same technique of
gradual introduction of dental stimuli is used to prevent
children from developing dental fear. As a preventive
method, it becomes part of behavioral guidance.
4.7 Special Issues with Adolescents
As they mature, adolescents increasingly prefer to make
their own choices. While their parents are still the ones
who have the legal power to provide consent for dental
treatment, the dentist should ask the adolescent what
he or she would prefer to do and try, if possible, to be
guided by the adolescent’s preference.
Case Study
We had treated an adolescent for dental fear as a child
and encountered him again as an adolescent when he
was undergoing orthodontia. Although his mother
rolled her eyes as her son was describing this, we were
happy to see – literally – that the orthodontist had
accepted the adolescent’s requests for orange and
black wires as Halloween neared, and red and green
wires around Christmas.
Child Dental Fear, Communication and Cooperation
4.7.1 Respond to Requests for Privacy
Adolescents are also more likely to want to keep certain
things from their parents. For example, a dentist may
notice increased enamel erosion in an adolescent female,
and ask her about it. The patient might reveal that she is
pregnant or bulimic – and beg the dentist not to tell her
parents. Another adolescent might admit to using drugs,
and similarly say that he doesn’t want his parents to find
out. The dentist must delicately manage these kinds of
requests while still respecting the law, which typically
says that parents (or legal guardians) must give consent,
and which often is interpreted to mean that parents have
the right to know information about their child that is
relevant to medical treatment. There are exceptions to
these generalities. For example, in Washington state,
USA, minors may give consent for emergency treatment
if the parents are not available; in addition, minors may
receive birth control, mental health treatment, substance
abuse treatment, and other services without parental
consent. These exceptions will vary by laws applicable to
where the dentist’s practice is located.
4.7.2  dolescents May Resist Going
A make sure that you are making progress toward your
to the Dentist
As children become adolescents, they are increasingly
able to influence – or even decide – whether they will go
to a dentist for regular checkups. They may also be at
increased risk for caries as their parents are no longer
closely involved in monitoring diet or oral home care
[83]. Some adolescents who have a dentist that they can
go to will avoid going for dental care; these adolescents
are more likely to have caries, as well as more advanced
caries, compared with their peers who do go for check-
ups [83, 84].
Unlike the younger child who is usually brought to
the dentist by his/her parents, adolescents are increas-
ingly likely to make their own decisions about making
and keeping appointments for dental checkups as they
gain more autonomy. If they are fearful, they may well
be operating according to the cycle of fear, as described
earlier. An additional model of going or not going to a
dentist is useful to consider, reflecting the ambivalence
that some adolescents (and adults) may feel about den-
tal appointments if they are afraid. Dollard and Miller
[85] described the approach-avoidance conflict that
a person will encounter if some situation has both an
attractive (approach) and an undesirable (avoidance)
aspect to it. For fearful adolescents, dental care may
well have an attractive (approach) aspect (“I will get the
tooth fixed”; “I will get my teeth cleaned”), as well as an
undesirable (avoidance) aspect (“I will experience pain”;
51 4
“They will criticize me for not taking better care of my
teeth”). We have heard adolescents say things such as:
“I know I should go to the dentist – and I need to go to
the dentist – but I am too afraid to go.” This kind of
description reveals the ambivalence that fearful adoles-
cents may experience about going to the dentist.
The strength of the undesirable aspect – the avoid-
ance aspect – becomes stronger as the individual comes
closer to the ambivalent situation. For example, it
may be easy enough to contact a dentist to make an
appointment which will occur at some (distant) time
in the future. However, as the day of the appointment
draws closer, the ambivalent individual becomes more
fearful about what might happen at the appointment,
and, as this avoidance aspect becomes stronger than the
approach aspect, the individual is increasingly likely to
cancel the appointment (or not show up) [5].
To help counter the strength of the avoidance side,
the dentist can use the motivational interviewing tech-
nique described earlier. The dentist can ask something
such as “If I could perform a dental miracle for you,
what would it be?” and respond accordingly: “That is
a wonderful goal! I can help you with that goal. I will
make sure to check .............. every time you come, to
goal.” The purpose is not only to help the adolescent
believe that the dentist is “on his/her side” but also to
stress the positive reasons for coming to see the dentist.
This can help “tip the balance” so that the ambivalent
adolescent comes for his/her appointments.
In general, individuals vary with regard to whether
they are more likely to approach, or avoid, uncertain sit-
uations. Sherman and colleagues [86] found that college
students who read messages about flossing their teeth
which were framed to be consistent with their general
approach vs. avoidance motivational style were more
likely to floss, compared with those whose messages
were inconsistent with their motivational style.
Eye Catcher
Earlier, we described asking a parent what his/her
dental wish was for the child. You may recall that,
in our hypothetical responses, two parents requested
things they would like their children to have or to
attain (“I’d like her teeth to be pretty”; “I want his
teeth to be nice and strong”), while one requested
something he/she hoped would NOT have (“I hope he
doesn’t ever have toothache”). One could say that the
first two wishes were “approach” ones, while the third
one was an “avoidance” wish. Similarly, the dentist
treating an adolescent could ask him/her what his/her
dental wish, or dental miracle is – and listen to learn
 52 T. Coolidge and N. Kotsanos
if it is an approach wish or an avoidance wish. This
knowledge will help guide the dentist in his/her fram-
ing of information: “Brushing will help you achieve
your goal of keeping your teeth strong” would be
appropriate for a teen with an “approach” style (“I
wish that my teeth were stronger”), while “Brushing
will help you achieve your goal of avoiding cavities”
4 would be appropriate for a teen with an “avoidance”
style (“I wish that I didn’t get so many cavities.”).
4.8 Communication in the Dental
Environment
“Communicate” comes from a Latin word meaning to
participate. An old meaning of the word is to share.
Communication is the process by which two or more
people share information, ideas, messages, and the like
with each other. At times, the individuals have to ques-
tion one another and/or restate certain things to make
sure that everyone is understanding the information in
the same way. Once this is achieved, everyone involved
in the communication is “on the same page.”
Broadly speaking, communication includes two
aspects. One is verbal, including the content or meaning
of the words and phrases used by the speaker (or writer,
if the communication is written). When the communica-
tion is spoken, it also includes nonverbal aspects, such
as facial expressions, tone of voice, posture, emotion,
signals which alert the listener that the speaker is joking
or in some other way not speaking in a literal manner,
and the like. For effective communication to occur, the
nonverbal aspects must be in harmony with the verbal
aspect [87].
4.8.1  onverbal Communication between
N
the Dentist and the Child Patient
The importance of nonverbal communication is signif-
icant, even if it is not always immediately noticed. In
pediatric dentistry, nonverbal communication is likely
to play a larger part in dealing with young patients
than verbal communication does [87]. When speaking
to the child and the parent at the same time, attention
to the parent should not result in a reduction of the
continuous, two-way, nonverbal communication with
the child.
Tone of voice, facial expression, and posture can all
emphasize the verbal content of the dentist’s communi-
cation. A calm, soothing voice has a sedating result in
anxious children. The trust that the dentist inspires and
the comfort that he/she shows when inviting the child to
sit in the dental chair are conveyed by nonverbal mes-
sages. If the dentist does not express the congruent non-
verbal information, the resulting communication may
not be calming or comforting. Another way of express-
ing nonverbal communication is by calmly lowering the
dentist’s body so that his/her face is even with the face
of the child, as well as by displaying a facial expres-
sion that shows interest and confidence in the child
(. Fig. 4.11).
Visual contact is important in nonverbal commu-
nication. It conveys the friendly interest of one of the
communicating parties to the other. Thus, the dentist
can assume that a child who avoids visual contact is not
ready to cooperate. Physical contact can also be impor-
tant. A touch on the shoulder while speaking reassur-
ingly about forthcoming treatment resulted in more
cooperative behavior in children aged 7 to 10, compared
with children who only heard the reassuring verbaliza-
tion; however, touching did not affect the behavior of
younger children [88].
The dentist’s ability to understand children’s non-
verbal communications is crucial to guiding the child
to behave appropriately. An early study demonstrated
that increased experience and training during dental
..      Fig. 4.11 The dentist lowers his/her body so that his/her face is
even with that of the child
Child Dental Fear, Communication and Cooperation
53 4
school was related to greater accuracy in interpreting
these communications [89]. If the pediatric dentist is
unsure of how he or she is expressing these nonver-
bal aspects of communication, he/she may want to
have someone observe some of his/her interactions,
to provide feedback. Alternatively, he/she may decide
to record some interactions to be able to review them
afterward.

Overview
Nonverbal communication summarized:
Voice: A calm and reassuring tone inspires confi-
dence.
Expression: A smile is a powerful tool, especially in
the first dentist-patient interaction.
Eyes: Visual contact confirms that there is dentist-­
child communication.
Hand gestures: Avoid curt or sudden movements,
which can startle the child.
Body posture: A large height contrast between the
dentist and the child patient can be frightening for the
patient.
Place: A relaxing atmosphere in the dental office,
with child-friendly features and decorative aspects, can
help reduce fear. ..      Fig. 4.12 Dental terminology is often incomprehensible to
parents

4.8.2  erbal Communication between

V him/her is to ask him/her to tell you what you said, using
the Dentist and the Child Patient
Verbal communication is usually more success-
ful between adults because they share a common
­understanding of the words that are used. Children’s
cognitive capacities develop with age, so adults need
to modulate the words that they use to communicate
with them to make sure that these words are com-
mensurate with children’s developing comprehension.
Younger children do not understand expressions such
as “I’ll be done in a minute,” because they think more
literally than adults do. It is preferable to say some-
thing such as: “We are more than half-way through.”
Also, it is better to explain to children what the pedi-
atric dentist would like them to do, as well as the
reason for this. For example, the dentist could say:
“Please don’t move your feet, because this moves your
head, too.”
A simple way to check to make sure that another per-
son understands what you have tried to communicate to
his/her own words. This way, you can check to see if the
other person understood what you said – or is “read-
ing from the same page,” as we mentioned earlier. This
is particularly important when we want to make sure
that patients (or parents) understand dental terminol-
ogy, such as “plaque.” Dental professionals use dental
terminology among themselves, which is understand-
able given that they share a common knowledge base.
However, the pediatric dentist must make sure that the
parents and/or child understand what these terms mean.
The pediatric dentist will probably need to provide one
explanation to the parents and a simpler one to the child
(. Fig. 4.12).
4.8.3 Communication with Parents
Pediatric dentists need to communicate with parents as
well as children. Beyond gathering history and other
information from the parents that the child cannot
 54 T. Coolidge and N. Kotsanos
provide, and informing the parents of diagnostic find-
ings and potential dental treatments for these, we rec-
ommend that pediatric dentists pay particular attention
to whether the parents appear to be authoritative, per-
missive, or authoritarian and modulate their communi-
cations accordingly. This is because parents can impact
the dental situation through the way they structure
communications with their child and/or the dentist. For
4 example, children of permissive parents tend to respond
to the dentist’s communications to them during treat-
ment by replying to their parents rather than to the den-
tist, and the communication between the child and the
dentist becomes one-sided [1]. For this type of parent,
the dentist may need to clarify that he/she will be speak-
ing to the child during treatment and will expect the
child to reply to him/her – not to the parent. The dentist
may need to explain this and may want to practice this
with the child and the parent, reinforcing the child for
speaking to the dentist and reinforcing the parent for
not disrupting the child-dentist communication.
4.8.4 Communication with the Child
As was mentioned in 7 Chap. 2, verbal communica-
tion with children is limited by their stage of cognitive
development [90]. Up until about the age of 3 years,
children can only understand simple commands or
words about objects that they can see or manipulate
[87]. Between ages 3 and 5, most explanations are not
comprehensible. Instructions should be given in a way
that describes what the dentist would like the child to
do [91]. Children younger than about 10 have a hard
time understanding reversibility and therefore don’t
understand the concept of brushing their teeth to
reduce plaque levels [87].
Children do not understand verbal descriptions of
conditionals, or causal relationships, until about ages 11
to 13. If the dentist says to a child who has not reached
this ability “If you are good, I will give you a present,”
the child is likely to conclude that he or she is going to
get a present. Because “being good” is abstract, the child
also will not know what it is that the dentist is referring
to. Thus, the intended purpose of the dentist’s statement
is lost. For this reason, small gifts for good cooperation
should only be given as a reward at the end of the proce-
dure and not earlier (. Fig. 4.13).
It isn’t until the child reaches formal operational
thought, beginning around age 11, that the child is
capable of understanding conditionals and engaging in
..      Fig. 4.13 Rewarding good cooperation with a small gift
abstract thought. Now the child can think through prob-
lems and solutions, rather than use trial and error to try
to solve a problem. At this stage of development, the
child can understand concepts of oral disease causation
and progression and what he or she can do to prevent
this disease. However, a new feature often appears at this
time, called “the personal fable,” related to adolescent
egocentrism. This is a tendency to believe that one is
infallible. Thus, even though the adolescent can under-
stand the concepts of processes such as caries develop-
ment or addiction, he or she may still not brush his/
her teeth, or may take up smoking, out of the personal
fable: “That bad outcome [i.e., the caries or addiction]
won’t happen to me!“ [92] 7 Chap. 2 includes informa-
tion about tailoring oral health messages to adolescents,
to help encourage (or convince) them to develop good
oral care habits.
4.8.5 Providing Written Information
Two other points are also relevant [17]:
Some information can be given to the child before
the appointment, so that there is time for the child
to prepare mentally for what will happen during the
appointment. Usually, only a small amount of informa-
tion given at the dentist’s office is remembered by the
child, especially when there is anxiety about the dental
procedure.
Important information and directions (e.g., for home
oral care practices that will help minimize the develop-
ment of decay) should be given to the parents in writing,
as otherwise they may forget much of the information
after leaving the office.
Child Dental Fear, Communication and Cooperation
Dental Office Logo
Dear Parents,
Your child’s good oral health, like many other child
health needs, depends primarily on you. As indicated
by published studies, the fillings needed for restoring
your child’s decayed teeth will last only if you follow
the specific oral health program that you and I have dis-
cussed. It is a program designed to prevent dental
decay, which means that it will also help to ensure that
your child’s permanent teeth will be healthy when they
come in. You can think of the oral health program as a
prescription to follow for healthy teeth. (Note: The
dentist can substitute the parents’ dental wish for their
child, as described in the Eyecatcher about Motiva-
tional Interviewing, in place of the generic “for healthy
teeth.”) Please contact us if you have any questions
about the program.
55 Depending on your child’s age and manual dexter-
ity, you will brush your child’s teeth or carefully
supervise your child as he/she brushes his/her own
teeth. Pay particular attention to the back teeth,
and cleaning in between the teeth. Use a fluoridated
toothpaste.
4.8.6 Empathy and Communication
The dentist, who is the person who should be defining
the relationships in the dental office, should approach
the young patient through understanding, sensitiv-
ity, and caring and can maneuver by making compro-
mises in some less important aspect, such as inviting
the patient to decide whether the dentist should start
the examination or cleaning on the left or the right side
of the dentition. This approach conveys respect toward
the patient’s feelings and helps the patient maintain his/
her composure. Empathy is the ability of the dentist to
participate knowledgably and emotionally in the situa-
tion that the patient is experiencing, which has positive
effects on their mutual communication. The more that
the dentist can perceive the patient’s worries and desires
and understand what previous experiences the patient
has had with dentists, doctors, and other adults, the
more empathic the dentist will be able to be [93].
The attitude and behavior of the dentist can influence
the child’s anxiety and thereby his/her behavior. Dentists
who used reinforcement, asked how the child was feel-
ing, or provided specific instructions were more likely
to find that children cooperated, while dentists who
55 4
55 Give your child fluoride mouthwash to swish around
his/her teeth once or twice a day, at a different time
from brushing with the toothpaste.
55 Keep sugared or starchy snacking (such as potato
chips, candy, etc.) to a minimum. When these types of
materials are on the teeth, they hasten the process
that causes decay.
Other studies demonstrate the importance of bringing
your child back regularly for follow-ups with the dentist.
The dentist can monitor your child’s oral health and make
any recommendations for changes to your child’s oral
health program. Depending on your child, these follow-up
visits may be scheduled every 6 months or more frequently.
We will contact you when it is time to schedule the next
follow-up appointment. (Of course, if you see changes in
your child’s teeth, or have any questions, feel free to con-
tact us before the next follow-up appointment.) This is
proven to help the success of the preventive program.
We are more than happy to help you help your child
maintain good oral health!
Yours sincerely,
………………….
used coercion or delivered put-downs to the patients
were more likely to find that children did not cooper-
ate [91]. In a second study by this team, dentists were
more likely to respond to noncooperative children with
behaviors such as imposing rules, making commands,
ushering threats, and restraining them, rather than using
empathic responses, providing directions, giving rewards,
and the like [94]. The implications are that some dentists
may inadvertently reinforce noncooperative behavior.
Turning to the child’s perspective on dental treatment,
cooperative children rate their dentists as more helpful,
better communicators, more truthful, and less likely to
hurt them intentionally, compared with noncooperative
children [95].
Some examples of empathic communications to
the child, cognitions that the fearful or anxious child
is likely to have in response, and likely reasons for the
child’s improved behaviors are given in . Table 4.3.
Expressing desires or fear, or even anger, is normal, while
continuous whining or movement needs calm manage-
ment. When the dentist finds himself/herself in difficult
situations and/or feels pressured by a lack of time, he/
she becomes irritated and is more likely to deliver nega-
tive messages, such as “Stop moving/crying right now!”,
 56 T. Coolidge and N. Kotsanos

..      Table 4.3 Examples of empathic communications to the fearful child and their corresponding effects

Empathic communication to the child Possible thoughts of the Explanation of impact to child behavior
child in response

You seem unhappy or embarrassed. You seem to
mean that you didn’t want to come
I wish you did not need to be here. Surely you
want to go home right away
4 I wish we never needed to have to do some
things that you do not want
Sometimes even grown-ups do not want to go to
the dentist
You think we will do things that might hurt you?
We will simply count your teeth, take a couple
of pictures, and then you are free to leave
I am sorry for this noisy jerk you feel on your
tooth. Thank you for trying not to move so that
we can be done sooner
Maybe they understand
here how badly I feel.
Perhaps it is not so strange
that I feel this way
Hmm, I’ll be able to
manage. It won’t take long
before I can leave
I am doing all right
If the child is shy and/or resistant, he/she can learn
from our words. If he/she is crying, he/she can stop.
It’s not necessary to show his/her feelings by crying
because he/she senses that his/her feelings are
received and accepted by the dentist
The dentist shows he/she understands how the
child feels, while explaining what will happen next,
thus decreasing the child’s fear of the unknown
The dentist’s verbal descriptions of what the child
feels, the dentist’s positive reinforcement, and the
dentist’s explanation all reduce the child’s worry

to the child. These negative messages may temporarily
result in the cessation of uncooperative behavior, but
the effect is not long-lasting, the child’s sense of trust
in the dentist is reduced, and his/her fear is increased
[96]. It is better to convey information about how the
child’s behavior is interfering with the treatment, such
as calmly saying “Unfortunately, I can’t finish as quickly
as I would like to if you are moving/if you close your
mouth.” When dentists ask children if anything hurts,
provide specific positive reinforcement (“You are doing
a great job keeping your hands in your lap”), or pro-
vide direction, children are more likely to cooperate; on
the other hand, delivering put-downs (“Don’t act like a
baby”), setting rules, or trying to coerce the child results
in more uncooperative behaviors [91].
4.9  he Influence of the Dental
T
Environment
4.9.1  rovide Positive Stimuli before
P and Waiting Areas
the Initial Visit
A child’s first visit to a dental office will be characterized
by new stimuli, such as odors, sounds, and sights. The
multitude of unfamiliar stimuli and experiences may
overwhelm the child, who may respond with anxiety and
begin to cling closer to his/her parent. The American
Academy of Pediatric Dentistry [70] recommends that
child patients be exposed to “positive pre-visit imagery”
(p. 189), based on Fox and Newton [97], who found that
seeing photographs of children smiling as they sat in a
dental chair (and other photographs designed to convey
a positive feeling about dentistry) was associated with a
significant reduction in anxiety among children in the
waiting room, compared with seeing photographs of
neutral, non-dental stimuli. Dentists can help parents
simulate these findings by encouraging them to look at
the office website before the initial appointment, so that
they and their children can see photographs of the den-
tal office that show smiling children. Other photographs
could show the smiling receptionist, dentist, assistant,
and any other primary personnel that the child is going
to meet, the waiting room, the operatory with the den-
tal chair, and the like. This allows the parent and child
to spend some preparatory time at home talking about
what the child is likely to notice during the visit. In addi-
tion, as described previously, if possible an introductory
visit to the dental office – when no dental procedures are
carried out – can be helpful in ensuring that the initial
experiences with the dentist and the office are positive.
4.9.2  ave Welcoming Reception, Staff
H
The reception and waiting area creates a strong impres-
sion (and the initial impression for children who aren’t
able to view the office website photographs in advance),
in large part because it reflects the personality of the
dental office and therefore provides clues to the child
and parent about what kind of people they are likely
to encounter in the office and what is likely to happen
during the appointment itself (. Fig. 4.14). Pleasant
surroundings, attractive use of color, and gentle music
help create a positive mood and are attractive to the
child, thus reducing anxiety. Compliance with ADA
Child Dental Fear, Communication and Cooperation
a a
..      Fig. 4.14 Efforts toward creating positive impressions in a pedi-
atric dental clinic located in a larger university building. a: Signage to
direct parents and patients to the clinic. b: Entrance to the reception
and waiting area of the clinic
requirements for accessibility for children or par-
ents with mobility challenges conveys interest in, and
respect for, these families. On the other hand, a lengthy
waiting period can increase a child’s anxiety, as well as
create feelings of impatience on the part of the par-
ent. An effort to keep the appointments on time shows
that the dentist respects other people’s time. In case of
unforeseen delays, office personnel should apologize
to the parent and child and keep them informed of
how much longer the wait is likely to be. The dentist
might consider ensuring that new child patients and/or
younger patients be appointed for the first time slot of
the day and/or the first time slot after the lunch break
when possible, as a way of ensuring that these appoint-
ments start on time.
As a rule of thumb, children who are at the office
for the first time and who are sitting still without being
occupied by some activity may become worried about
57 4
..      Fig. 4.15 a Dental Playmobil toys allow children to explore their
dental visit. b Drawing makes waiting time more pleasant (subject to
restrictions imposed after the covid-19 pandemic)
what might happen to them in this new environment.
Therefore, it is important for the dentist to include areas
for playing and activities such as manipulating toys or
drawing. The waiting room should contain toys, books,
posters, and the like that are likely to appeal to chil-
dren of different ages and both genders. Containers of
attractive toys can be set out for children to explore, and
tables, chairs, paper, and crayons or colored pens can be
put out for drawing. Children’s drawings can be posted
on the wall in such a way that the artists – and other
children – can see them (. Fig. 4.15).
Dental receptionists often greet children and their
parents as they arrive at the dental office and make the
follow-up appointments as families leave. They may also
be the individuals with whom parents have their first
interaction with, as they call to seek the initial appoint-
ment for the child. Subsequently, parents and children
will also have interactions with the dentist, dental assis-
tants, and others during dental procedures. Therefore,
the dentist must ensure that all of the office staff are
skilled in communicating with pediatric patients and
their families.
 58 T. Coolidge and N. Kotsanos

References 21. Al-Namankany A, Petrie A, Ashley P. Video modelling and

reducing anxiety related to dental injections – a randomized
clinical trial. Br Dent J. 2014;216:675–9.
1. Aminabadi NA, Deljavan AS, Jamali Z, Azar FP, Oskouei
22. Armfield JM, Slade GD, Spencer AJ. Cognitive vulner-
SG. The influence of parenting style and child temperament on
ability and dental fear. BMC Oral Health. 2008; https://doi.
child-parent-dentist interactions. Ped Dent. 2015;37:342–7.
org/10.1186/1472-­6831-­8-­2.
2. Carrillo-Diaz M, Crego A, Armfield JM, Romero-Maroto
23. Carrillo-Díaz M, Crego A, Armfield JM, Romero M. Self-
M. Treatment experience, frequency of dental visits, and
assessed oral health, cognitive vulnerability and dental anxiety
children’s dental fear: a cognitive approach. Eur J Oral Sci.
in children: testing a mediational model. Comm Dent Oral Epi.
2012;120:75–81.
2012;40:8–16.
4 3. Wigen TI, Skaret E, Wang NJ. Dental avoidance behavior in par-
ent and child as risk indicators for caries in 5-year-old children.
24. Crego A. Carrillo-Díaz, Armfield JM, Romero M. applying
the cognitive vulnerability model to the analysis of cognitive
Int J Paed Dent. 2009;19:431–7.
and family influences on children’s dental fear. Eur J Oral Sci.
4. Anon. The need of a taxonomy. Pain. 1979;6:247–52.
2013;121:194–203.
5. Milgrom P, Weinstein P, Getz T. Treating fearful dental patients:
25. Chapman HR, Kirby-Turner NC. Dental fear in children – a
a patient management handbook. 2nd ed. Seattle, WA: Univer-
proposed model. Br Dent J. 1999;187:408–12.
sity of Washington Continuing Dental Education; 1995.
26. Logan HL, Baron RS, Keeley K, Law A, Stein S. Desired control
6. American Psychiatric Association. Diagnostic and statistical
and felt control as mediators of stress in a dental setting. Health
manual of mental disorders. 4th ed. Text Revision. Washington,
Psychol. 1991;10:352–9.
DC: American Psychiatric Association; 2000.
27. Weinstein P, Milgrom P, Hoskuldsson O, Golletz D, Jeffcoat E,
7. Klingberg G, Broberg AG. Dental fear/anxiety and dental
Koday M. Situation-specific child control: a visit to the dentist.
behaviour management problems in children and adolescents: a
Behav ResTher. 1996;34:11–21.
review of prevalence and concomitant psychological factors. Int
28. Coolidge T, Heima M, Heaton LJ, Nakai Y, Hőskuldsson Ó,
J Paed Dent. 2007;17:391–406.
Smith TA, Weinstein P, Milgrom P. The child dental control
8. Seligman LD, Hovey JD, Chacon K, Ollendick TH. Dental
assessment (CDCA) in youth: reliability, validity and cross-cul-
anxiety: an understudied problem in youth. Clin Psych Rev.
tural differences. Eur J Paed Dent. 2005;6:35–43.
2017;55:25–40.
29. Ray J, Wide Boman U, Bodin L, Berggren U, Lichentstein P,
9. Klingberg G. Dental anxiety and behavior management prob-
Broberg AG. Heritability of dental fear. J Dent Res. 2010;89:
lems in paediatric dentistry: a review of background factors and
297–301.
diagnostics. Eur Arch Paed Dent. 2008;9(Suppl 1):11–5.
30. Vassend O, Røysamb E, Nielsen CS. Dental anxiety in relation to
10. Krikken JB, van Wijk AJ, ten Cate JM, Veerkamp JSJ. Child
neuroticism and pain sensitivity. A twin study. J Anxiety Disord.
dental anxiety, parental rearing style and referral status of chil-
2011;25:302–8.
dren. Comm Dent Health. 2012;29:289–92.
31. Binkley CJ, Beacham A, Neace W, Gregg RG, Liem EB, Sessler
11. Gustafsson A, Broberg A, Bodin L, Berggren U, Arnrup K. Den-
DI. Genetic variations associated with red hair color and fear
tal behavior management problems: the role of child personal
of dental pain, anxiety regarding dental care and avoidance of
characteristics. Int J Paed Dent. 2010;20:242–53.
dental care. J Am Dent Assoc. 2009;140:896–905.
12. Arnrup K, Broberg AG, Berggren U, Bodin L. Temperamental
32. Randall CL, McNeil DW, Shaffer JR, Crout RJ, Weyant RJ,
reactivity and negative emotionality in uncooperative children
Maraziata ML. Fear of pain mediates the association between
referred to specialized paediatric dentistry compared to children
MC1R genotype and dental fear. J Dent Res. 2016;95:1132–7.
in ordinary dental care. Int J Paed Dent. 2007;17:419–29.
33. Randall CL, Wright CD, Chernus JM, McNeil DW, Feingold
13. Sharma A, Kumar D, Anand A, Mittal V, Singh A, Aggarwal
E, Crout RJ, Neiswanger K, Weyant RJ, Shaffer JR, Marazita
N. Factors predicting behavior management problems during
ML. A preliminary genome-wide association study of pain-
initial dental examination in children aged 2 to 8 years. Interna-
related fear: implications for orofacial pain. Pain Res Manag.
tional J Clin Pediatr Dent. 2017;10:5–9.
2017;7375468
14. Ramos-Jorge ML, Marques LS, Pavia SM, Serra-Negra JM,
34. Boyce WT, Den Besten PK, Stamperdahl J, Zhan L, Jiang Y,
Pordeus IA. Predictive factors for child behavior in the dental
Adler NE, Featherstone JD. 2010. Social inequalities in child-
environment. Eur Arch Paed Dent. 2006;7:253–7.
hood dental caries: the convergent roles of stress, bacteria and
15. Klingberg G, Berggren U, Carlsson SG, Norén JG. Child dental
disadvantage. Soc Sci Med. 2010;71:1644–52.
fear: cause-related factors and clinical effects. Eur J Oral Sci.
35. Kumar S, Tadakamadla J, Zinner-Gembeck MJ, Kroon J, Lalloo
1995;103:405–12.
R, Johnson NW. Parenting practices and children’s dental car-
16. Broadbent JM, Thomson WM, Poulton R. Trajectory patterns
ies experience: a structural equation modelling approach. 2017.
of dental caries experience in the permanent dentition to the
Comm Dent Oral Epi. 2017;45:552–8.
fourth decade of life. J Dent Res. 2008;87:69–72.
36. Tang C, Quinonez RB, Hallett K, Lee JY, Whitt JK. Examining
17. Chadwick BL, Hosey MT. Child taming: how to manage chil-
the association between parenting stress and the development of
dren in dental practice. London: Quintessence; 2003.
early childhood caries. Comm Dent Oral Epi. 2005;33:454–60.
18. Weinstein P. Breaking the worldwide cycle of pain, fear, and
37. Bright MA, Alford SM, Hinojosa MS, Knapp C, Fernandez-
avoidance: uncovering risk factors and promoting prevention for
Baca DE. Adverse childhood experiences and dental health in
children. Ann Behav Med. 1990;12:141–7.
children and adolescents. Comm Dent Oral Epi. 2015;43:193–9.
19. Pickrell JE, Heima M, Weinstein P, Coolidge T, Coldwell SE,
38. Klingberg G, Broberg AG. Temperament and child dental fear.
Skaret E, Castillo J, Milgrom P. Using memory restructur-
Ped Dent. 1998;20:237–43.
ing strategy to enhance dental behavior. Int J Paediatr Dent.
39. Hockenberry MJ, Wilson D. Wong’s essentials of pediatric nurs-
2007;17:439–48.
ing. 8th ed. Mosby/Elsevier: St. Louis MO; 2009.
20. Bandura A. Social learning theory. New York: Prentice-Hall;
40. Baumrind D. Current patterns of parental authority. Dev Psy-
1977.
chol Monogr. 1971;4:1–103.
Child Dental Fear, Communication and Cooperation
41. Lamborn SD, Mounts NS, Steinberg L, Dornbusch SM. Pat-
terns of competence and adjustment among adolescents from
authoritative, authoritarian, indulgent, and neglectful families.
Child Dev. 1991;62:1049–65.
42. Howenstein J, Kumar A, Casamasimo PS, McTigue D, Coury
D, Yin H. Correlating parenting styles with child behavior and
caries. Ped Dent. 2015;37:59–64.
43. Aminabadi NA, Pourkazemi M, Babapour K, Oskouei SG. The
impact of maternal emotional intelligence and parenting style
on child anxiety and behavior in the dental setting. Med Oral Cir
Bucal. 2012; https://doi.org/10.4317/medoral.17839.
44. Aminabadi NA, Farahani RMZ. Correlation of parenting style
and pediatric behavior guidance strategies in the dental setting:
preliminary findings. Acta Odont Scand. 2008;66:99–104.
45. Chapman HR, Kirby-Turner N. Psychological intrusion – an
overlooked aspect of dental fear. Front Psychol. 2018:1–19.
46. Olsen SF, Yang C, Hart CA, Robinson CC, Wu P, Nelson DA,
Nelson LJ, Jin S, Wo J. Maternal psychological control and pre-
school children’s behavioral outcomes in China, Russia, and the
United States. Iin Barber BK, ed. Intrusive Parenting: How Psy-
chological Control Affects Children and Adolescents. Washing-
ton DC: American Psychological Association, 2002; pp. 235–262.
47. Eisenberg N, Taylor ZE, Widaman KF, Spinrad TL. External-
izing symptoms, effortful control, and intrusive parenting: a test
of bidirectional longitudinal relations during early childhood.
Dev Psychopathol. 2015;27:953–68.
48. Long N. The changing nature of parenting in America. Ped
Dent. 2004;2:121–4.
49. Casamassimo PS, Wilson S, Gross L. Effects of changing
U.S. parenting styles on dental practice: perceptions of diplo-
mats of the American Board of Pediatric Dentistry. Ped Dent.
2002;24:18–22.
50. Law CS. The impact of changing parental styles on the advance-
ment of pediatric oral health. CDA J. 2007:192–7.
51. Miller WR, Rollnick S. Motivational i­nterviewing: preparing
people for change. 2nd ed. New York, NY: Guildford Press;
2002.
52. Weinstein P, Harrison R, Benton T. Motivating parents to pre-
vent caries in their young children: one-year findings. J Am Dent
Assoc. 2004;135:731–8.
53. Weinstein P, Harrison R, Benton T. Motivating mothers to pre-
vent caries: confirming the beneficial effect of counseling. J Am
Dent Assoc. 2006;137:789–93.
54. Coric A, Banozic A, Klaric M, Vukojevic K, Puljak L. Dental
fear and anxiety in older children: an association with parental
dental anxiety and effective pain coping strategies. J Pain Res.
2014;7:515–21.
55. Themessl-Huber M, Freeman R, Humphris G, MacGillivray S,
Terzi N. Empirical evidence of the relationship between paren-
tal and child dental fear: a structured review and meta-analysis.
International J Paed Dent. 2010;20:83–101.
56. Heima M, Heaton L, Gunzler D, Morris N. A mediation analy-
sis study: the influence of mothers’ dental anxiety on children’s
dental utilization among low-income African Americans. 2017.
Comm Dent Oral Epi. 2017;45:506–11.
57. Arhakis A, Menexes G, Coolidge T, Kalfas S. Heart rate, sali-
vary α-amylase activity, and cooperative behavior in previously
naïve children receiving dental local anesthesia. Pediatr Dent.
2012;34(7):e225–30.
58. Cuthbert MI, Melamed BG. A screening device: children at risk
for dental fears and management problems. ASDC J Dent Child.
1982;49:432–6.
59. Aartman IHA, van Everdingen T, Hoogstraten J, Schuurs
AHB. Self-report measurements of dental anxiety and fear in
children: a critical assessment. J Dent Child. 1998;64:252–8.
59 4
60. Porritt J, Buchanan H, Hall M, Gilchrist F, Marshman Z. Assess-
ing children’s dental anxiety: a systematic review of current mea-
sures. Comm Dent Oral Epi. 2012;41:130–42.
61. Buchanan H, Niven N. Validation of a facial image scale to
assess child dental anxiety. Int J Paed Dent. 2002;12:47–52.
62. Arapostathis KN, Coolidge T, Emmanouil D, Kotsanos
N. Reliability and validity of the Greek version of the Chil-
dren’s fear survey schedule-dental subscale. Int J Paed Dent.
2008;18:374–9.
63. Klein U, Manankil R, DeWitt P. Parents’ ability to assess dental
fear in their six- to 10-year-old children. Ped Dent. 2015;37:436–41.
64. Luoto A, Tolvanen M, Rantavuori K, Pohjola V, Lahti S. Can
parents and children evaluate each other’s dental fear? Eur J
Oral Sci. 2010;118:254–8.
65. Wong HM, Humphris GM, Lee GTR. Preliminary validation
and reliability of the modified child dental anxiety scale. Psychol
Rep. 1998;83:1179–86.
66. Howard KE, Freeman R. Reliability and validity of the faces
version of the modified child dental anxiety scale. Int J Paed
Dent. 2007;17:281–8.
67. Frankl SN, Shiere FR, Fogels HR. Should the parent remain
with the child in the operatory? J Dent Child. 1962;29:
150–63.
68. Rhudy JL, Meagher MW. Fear and anxiety: divergent effects on
human pain thresholds. Pain. 2000;84:65–75.
69. Baldwin WC, Weisenberg M. Effect of psychologic factors on
reactions to pain. In: Ripa LR, Barenie JA, editors. Manage-
ment of dental behavior in children. Littleton MA: PSG Pub-
lishing Company; 1979. p. 41–60.
70. American Academy of pediatric dentistry. Guideline on
behavior guidance for the pediatric dental patient. 2016;38:
185–98.
71. Wong DL, Baker CM. Pain in children: comparison of assess-
ment scales. Pediatr Nurs. 1988;14:9–17.
72. Versloot J, Craig KD. The communication of pain in paediatric
dentistry. Eur Arch Paediatr Dent. 2009;10:61–6.
73. Ripa LR. Attitudinal and environmental influences on children’s
behavior in the dental situation. In: Ripa LR, Barenie JA, edi-
tors. Management of dental behavior in children. Littleton MA
PSG; 1979. p. 27–40.
74. Nicolas E, Bessadet M, Collado V, Carrasco P, Rogerleroi V,
Hennequin M. Factors affecting dental fear in French children
aged 5-12 years. Int J Paed Dent. 2010;20:366–73.
75. Rantavuori K, Zerman N, Ferro R, Lahti S. Relationship
between children’s first dental visit and their dental anxiety in
the Veneto region of Italy. Acta Odont Scand. 2002:297–300.
76. Seligman MEP. Helplessness: on depression, development and
death. San Francisco CA: W.H. Freeman; 1975.
77. Sherman JJ, Cramer A. Measurement of changes in empathy
during dental school. J Dent Educ. 2005;69:338–45.
78. Tsiantou D, Lazaridou D, Coolidge T, Arapostathis KN, Kot-
sanos N. Psychometric properties of the Greek version of the
Toronto composite empathy scale in Greek dental students. Eur
J Dent Educ. 2013;17:208–17.
79. Zabin MA, Melamed BG. Relationship between parental dis-
cipline and children’s ability to cope with stress. J Beh Assess.
1980;2:17–38.
80. Folayan MO, Idenehn EE, Ojo OO. The modulating effect of
culture on the expression of dental anxiety in children: a litera-
ture review. Int J Paediatr Dent. 2004;14:241–5.
81. Zlotogorski Z, Zadik D, Evron D. The relationship between
learned resourcefulness and coping with crying in pediatric den-
tistry: a pilot study. Pediatr Dent. 1994;16:371–2.
82. Rachman SJ. Fear and courage. 2nd ed. New York: WH Free-
man; 1990.
 60 T. Coolidge and N. Kotsanos
83. Coolidge T, Heima M, Johnson EK, Weinstein P. The dental
neglect scale in adolescents. BMC Oral Health. 2009; https://doi.
org/10.1186/1472-­6831-­9-­2.
84. Skaret E, Raadal M, Berg E, Kvale G. Dental anxiety and dental
avoidance among 12 to 18 year olds in Norway. Eur J Oral Sci.
1999;107:422–8.
85. Dollard J, Miller N. Personality and psychotherapy. New York:
McGraw Hill; 1950.
86. Sherman DK, Mann T, Updegraff JA. Approach/avoidance
motivation: understanding the congruency effect. Motiv Emot.
4 2006;30:165–9.
87. Chambers DW. Communicating with the young dental patient. J
Am Dent Assoc. 1976;93:793–9.
88. Greenbaum PE, Lumley MA, Turner C, Melamed BG. Den-
tist’s reassuring touch: effects on children’s behavior. Ped Dent.
1993;15:20–4.
89. Brockhouse RT, Pinkham JR. Assessment of nonverbal commu-
nication in children. ASDC J Dent Child. 1980;47:42–5.
90. Piaget J. Judgement and reasoning in the child. Paterson, NJ:
Littlefield & Adams; 1964.
91. Weinstein P, Getz T, Ratener P, Domoto P. The effect of den-
tists’ behaviors on fear-related behaviors in children. J Am Dent
Assoc. 1982;104:32–8.
92. Elkind D. Egocentrism in adolescence. Child Dev. 1967;38:
1025–34.
93. Hojat M. Empathy in patient care: antecedents, development,
measurement, and outcomes. New York: Springer; 2007.
94. Weinstein P, Getz T, Ratener P, Domoto P. Dentists’ responses
to fear- and nonfear-related behaviors in children. J Am Dent
Assoc. 1982;104:38–40.
95. Welly A, Lang H, Welly D, Kropp P. Impact of dental atmo-
sphere and behaviour of the dentist on children’s cooperation.
Appl Psychophys Biof. 2012;37:195–204.
96. Venham LL, Gaulin-Kremer E. A child-­oriented philosophy of
dental management. Pediatr Dent. 1983;5:261–5.
97. Fox C, Newton JT. A controlled trial of the impact of exposure
to positive images of dentistry on anticipatory dental fear in
children. Com Dent Oral Epidemiol. 2006;34:455–9.
 61 5

Behavior Guidance
and Communicative
Management
Travis Nelson and Nikolaos Kotsanos

Contents

5.1 Definitions and Classification – 62

5.1.1 Classification of Behavior Guidance and Management Techniques – 62

5.2 Basic Behavior Guidance – 62

5.2.1 T ell-Show-Do – 63
5.2.2 Providing Control – 65
5.2.3 Ask-Tell-Ask – 65
5.2.4 Positive Reinforcement – 66
5.2.5 Distraction – 66
5.2.6 Modeling – 67
5.2.7 Voice Control – 68
5.2.8 Parental Presence – 68
5.2.9 Other Complementary Techniques – 69

5.3 Advanced Behavior Guidance – 71

5.3.1  rotective Stabilization – 71
P
5.3.2 Dealing with Demanding Behavior Problems – 74

5.4 Ethical and Legal Issues and Parental Consent – 76

References – 77

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_5
 62 T. Nelson and N. Kotsanos
5.1 Definitions and Classification
The cognitive approach to behavior guidance is based
on principles of social learning. Behavior is formed by
learning appropriate responses to specific stimuli. This
approach is referred to as a “stimulus-response” theory
[1]. At a dental visit the dentist methodically guides the
child’s reactions through continuous interaction with
patient and parent/caretaker [2]. Specific behavior guid-
ance techniques have been developed by combining
5 similar stimulus-response pairs. Combining these man-
agement techniques allows the clinician to provide the
best patient experience in the shortest possible time. The
aim of these interactions is to alleviate fear and anxi-
ety, while promoting an understanding of the processes
required to achieve and maintain oral health.
Overview
An evaluation of the child’s cooperative potential is
essential for treatment planning. Children can be clas-
sified into the following three groups according to their
ability to cooperate for dental treatment [1–3]:
1. Cooperative.
2. Potentially cooperative (e.g., shy, tense, fearful,
strong willed, emotionally immature, phobic, with
mild mental/motor impairment).
3. Unable to cooperate (e.g., younger than 2.5–3 years,
severely mentally impaired).
5.1.1  lassification of Behavior Guidance
C and quality of a sedation visit. Protective stabilization,
and Management Techniques
Most textbooks [1, 3, 4] and the American Academy
of Pediatric Dentistry (AAPD) guidelines have struc-
tured behavior guidance and management into indi-
vidual techniques, grouped and classified in a more or
less similar fashion. Broadly following the frequently
updated AAPD guidelines [2], these techniques can
be divided into basic and advanced approach strate-
gies.
5.1.1.1 Basic
55 Communicative techniques: tell-show-do, providing
control, positive reinforcement, distraction, ask-tell-­
ask, modeling (direct observation), voice control,
parental presence/absence, and possibly other ones
aimed at children and parents.
55 Pharmacological approaches: limited to the adminis-
tration of nitrous oxide minimal inhalation sedation.
5.1.1.2 Advanced
55 Protective stabilization.
55 Pharmacological approaches: procedural sedation
(enteral and parenteral) and general anesthesia
(GA).
The clinician’s verbal and nonverbal communication
skills, as described in 7 Chap. 4, are of outmost impor-
tance in the effective implementation of these tech-
niques. By mastering these techniques, practitioners can
successfully care for the majority of children using basic
non-pharmacologic approaches.
Contemporary care of children is contingent on
empathetic practice of dentistry. Organizations like
the AAPD recognize that fostering the emotional
development of the child is as important as mainte-
nance of their oral health. Guidelines published by the
AAPD reflect the profession’s value of caring for the
child as a whole [2]. Similarly, the European Academy
of Pediatric Dentistry (EAPD) provides a framework
for compassionate care of children in its official pub-
lications and editorials [5]. This approach is child-cen-
tered, taking into account the experience and opinions
of the patient and the family. It establishes a thera-
peutic relationship in which the patient’s needs are
respected in the context of the family’s feelings and
opinions [6–8].
In many countries, the clinician may combine purely
communicative techniques with pharmacological ones,
i.e., minimal inhalation sedation with nitrous oxide
or minimal to moderate procedural sedation [2, 5].
Incorporating non-pharmacologic behavior guidance
techniques generally improves the patient experience
sedation (except for nitrous oxide inhalation), and gen-
eral anesthesia are referred to as advanced behavior
management techniques by AAPD [2]. This means that
specific training is required to use these techniques [7].
Good training and experience are certainly required to
develop effective communicative behavior guidance too.
Individual techniques are described in this chapter, while
pharmacological techniques are described separately in
7 Chap. 8.
5.2 Basic Behavior Guidance
Children exhibit a wide range of physical, intellectual,
emotional, and social development and a diversity
of attitudes and temperament. It follows that dentists
use child appropriate behavior guidance techniques
while being tolerant and flexible in their implementa-
tion. While techniques should be evidence based and
Behavior Guidance and Communicative Management
63 5
societally accepted, it must always be remembered that
they must be integrated into an individualized behavior
guidance approach for each child. Consequently, behav-
ior guidance is as much an art as it is a science [2].

5.2.1 Tell-Show-Do

The dental office is a novel environment for young chil-

dren, and many present for the first visit with fear of the
unknown. “Tell-show-do” (TSD) helps alleviate anxiety
by deliberately teaching the child about specific aspects
of the dental experience. Gradually the young patient
becomes more comfortable in the new environment as
the unknown becomes known. TSD was first described
as a technique by Addelston over half a century ago, ..      Fig. 5.1 The tell-show-do technique: demonstrating how the
and it has been a mainstay of pediatric dental care ever dental explorer will be used to examine teeth by first “counting” the
since [8]. In the era of virtual based-on-screen games, it child’s fingernails
is sometimes being tested in modified ways with software
in smartphones [9], or as a standard anxiety-­reducing
technique paired with novel distraction technologies
based on TV or mobile apps [10, 11]. It is particularly
useful when employed alongside other basic techniques
such as providing control and positive reinforcement.

TSD Technique

The technique involves three steps:

1. Tell: describe instruments, materials, or proce-
dures with vocabulary adapted to the cognitive
ability of the child.
2. Show: demonstrate use of the item or technique
so the child may clearly see how it will be used
(. Fig. 5.1).
..      Fig. 5.2 The entire dental team should use the same terminology
3. Do: perform the procedure in the child’s mouth with patients. (Redesigned from Chadwick & Hosey [4])
exactly as demonstrated to the child.
During the second step (show) the child is shown
dental instruments and materials that have an unusual
In the first step of TSD (tell), it is important to use appearance, smell, or taste. This provides a multisensory
language that does not provoke anxiety and is easily experience that prepares the child for the dental proce-
understood by the child. This increases the patient’s dure. This is often enhanced by providing the child with
understanding and builds trust. For consistency it is a handheld mirror, allowing them to watch the procedure
important that all members of the dental team agree being performed during the third step (do) (. Fig. 5.3).
upon and use the same child-friendly terminology TSD is most effective when each step is very basic and is
(. Fig. 5.2). Consider the following examples of child-­ repeated until the child grasps the concept. This allows
friendly language: the patient to overcome fear before progressing to the
next step. It is important that the clinician remain con-
55 Hurt (→ bother). sistent throughout the process and avoid surprising the
55 Local anesthetic injection(→ sleepy juice). child by doing something that was not demonstrated
55 Explorer (→ tooth counter). (. Fig. 5.4).
55 Suction (→ vacuum cleaner). TSD is particularly useful with children who are in
55 Rubber dam (→ raincoat). Piaget’s preoperational stage of cognitive development,
55 Mouth prop (→ tooth chair). i.e., up to 6 to 7 years of age (see 7 Chap. 2). It is less
 64 T. Nelson and N. Kotsanos

effective in children under 3 years old (sensorimotor

5 desensitization protocols to overcome dental fear. This is
..      Fig. 5.3 A patient observing the dental procedure in a hand mirror
..      Fig. 5.4 Patient distressed by lip numbness from local anesthe-
sia. Explaining the “sleepy lip” sensation before administration may
prevent this reaction
stage) because they have not yet reached the cognitive
level required to understand and respond to complex
requests. While TSD may be effective for introducing a
wide variety of dental experiences to the child, accep-
tance varies depending on patient age, maturity, or den-
tal fear. A keen understanding of child development
and mastery of nonverbal communication aids the clini-
cian in interpreting the child’s reactions and facilitating
acceptance of dental procedures.
TSD is frequently implemented when employing
accomplished by gradually introducing new procedures
from least to more stressful (. Fig. 5.5). Children with
previous traumatic dental and medical experiences may
have more difficulty overcoming their fears, so progress
toward acceptance may be slower than with patients
who simply fear the unknown [2].
TSD is predicated on honesty. Its effectiveness is
undermined if the practitioner lies to the child or doesn’t
follow through with the procedure exactly as described.
Dentists can fall into this trap when parents have prom-
ised the child something that is not realistic, or by prom-
ising unrealistic things themselves. When a child asks
directly, “Will you give me a shot?”, he is indicating that
he has heard children receive injections at the ­dentist.
“No” is the wrong answer to this question. The dentist
can tactfully combine tell-show-do with other techniques,
such as distraction. For example, she could perhaps say
“in children we use sleepy jelly. Can you smell it? After
the jelly we use 5 drops of sleepy juice. We’ll count them.”
Local anesthesia is perhaps the only dental procedure not
introduced routinely by dentists in the tell-show-do man-
ner. This potentially prevents a negative reaction caused
by the child viewing the needle before the injection.
When appropriately modified, tell-show-do is very
useful with children who have mild to moderate dis-
abilities. For example, with hearing-impaired patients

6. Perform oral hygiene education and fluoride treatment

5. Complete the clinical and radiological examination

4. Count fingernails first with a dental explorer, then progress to teeth

3. Gently blow air on fingers, then on teeth

2. Have child sit on dental chair and begin with a toothbrush or dental mirror

1. Facilitate introductions and collect medical/dental history

..      Fig. 5.5 Example of a step-by-step approach to dental care

Behavior Guidance and Communicative Management
65 5
“show” may be emphasized more than “tell.” Speak
clearly, slowly, and in front of the patient. This allows
for lip-reading. It is also useful to have the parent func-
tion as an interpreter for patient requests. Avoid sud-
den noises and complex commands when working with
vision-impaired children. Allow the patient extra time
to touch and feel instruments. Children with severe
intellectual disability may have challenges responding
to basic behavioral techniques, but many can be suc-
cessfully treated in this manner if provided with addi-
tional time and a consistent treatment approach. Show
patients and families respect by avoiding language that
stigmatizes the patient, and always refer to the patient
using people-first language (e.g., child with Down syn-
drome, not Down syndrome child) [12].
..      Fig. 5.6 The patient holds a toy that emits a sound when a but-
ton is pressed. This allows them to pause the procedure and provides
a sense of control
5.2.2 Providing Control

Tell-show-do is quite effective for procedures that are

not painful; however, when the patient experiences dis-
comfort or pain (e.g., receiving local anesthesia), other
techniques may be necessary. Providing control is one
strategy that can be used effectively in these situations.
In this scenario the practitioner allows the child to have
some control over the procedure and discontinuation of
painful stimuli (. Fig. 5.6). Allowing the child to raise
their hand when a procedure becomes uncomfortable
gives the dentist the opportunity to address the cause of
pain and, at the same time, praise the child for reacting
as advised. This also allows the child to feel confident
that she will not be forced to tolerate a procedure that
is more difficult than she can handle. Providing control
is a basic behavior guidance strategy that can be com- ..      Fig. 5.7 “I don’t want you to use this when you fix my tooth”
bined with other communicative approaches, especially
positive reinforcement [2, 4]. 7 Chapter 4 describes the
One may provide the child with options: “what fla-
theoretical support for this approach.
vor jelly (topical anesthesia) would you like – cherry or
Some children attempt to postpone treatment using
banana?” These are examples of choices that engage the
delaying tactics. With these patients the dentist should
patient, yet do not materially alter the treatment. Offering
be flexible and accommodate patient concerns, while
choices shows the child that the dentist respects her feel-
reinforcing the importance of accomplishing the pro-
ings. It is better that children not be given more than two
cedure. Children sometimes also exert inappropriate
choices. This allows them to quickly and easily make a
levels of control, demanding accommodations that are
selection, and it eliminates the option of procedure refusal.
not possible (e.g., “I don’t want you to use this when
you fix my tooth.”) (. Fig. 5.7). This negative behav-
ior originates from fear of pain. To address the patient’s
5.2.3 Ask-Tell-Ask
concern, the dentist could use the following approach
together with providing control:
This technique is similar to tell-show-do, but the empha-
»» If you were a dentist, I would want you to tell me how sis is a bit different. The objective of tell-show-do is to
to fix your tooth. Today it is my job to take care of you. preemptively teach the patient about unfamiliar aspects
What’s important is you do not feel anything. Your job of the dental visit. Ask-tell-ask aims to address specific
will be to have this hand ready and raise it if anything anxieties that the patient has about dental treatment.
bothers you. The clinician first inquires about the patient’s specific
 66 T. Nelson and N. Kotsanos

concerns (“What are you worried about today?”). Then
he proceeds to tell the patient how the dental team will
address their concern (“We will use sleepy juice to make
sure it doesn’t hurt when we clean your tooth.”). Finally,
he asks if the patient understands the explanation and
if there are any additional concerns. The key feature of
this approach is alleviating anxiety by honing in on and
addressing specific patient concerns [2].
5.2.4 Positive Reinforcement
5 of a session recognizes good behavior and is an excel-
Children respond to feedback from their social envi-
ronment. They adopt or reject behaviors according
to the responses that they receive from others around
them. Providing the patient with positive reinforcement
increases the likelihood that a behavior will be repeated.
Similarly, enabling the patient to avoid discomfort and
unpleasant experiences (negative reinforcement) may
also promote desired behaviors. These behavioral con-
ditioning techniques, therefore, deliberately use rewards
to encourage desired behaviors. Rewards might include:
55 Verbal reinforcement, including positive tone of
voice or praise by the dentist or staff.
55 Nonverbal communication, such as facial expres-
sions, a pat on shoulder, or a high-five*.
55 Small prizes or gifts at the end of the visit.
*Touching the patient may be subject to Covid-19 pan-
demic restrictions or similar polices.
When a child encounters a painful stimulus and
appropriately raises his hand, he is reinforced in two
ways: (1) negative reinforcement as the painful stimulus
is removed and (2) positive reinforcement as the dentist
praises him for following instructions. In turn, praise
increases the patient’s self-esteem and feelings of accep-
tance. The amount of praise from the dental team and
parents should be proportional to the effort. It is often
advantageous to reserve the greatest praise for the end
of a dental visit.
Providing clear instructions and specific requests
improves child behavior. On the contrary, critical ques-
tions like “can’t you keep your mouth open wide?” are
not productive in managing child behavior [13]. Instead,
look for opportunities to reinforce positive behavior. We
can provide positive reinforcement throughout the visit
by praising the child for staying calm and still, keeping
their mouth open, and even for being a good listener.
Gentle words from the provider offer positive reinforce-
ment in themselves. The calm effect provides the child
with a sense of well-being and safety.
It is also most effective to put a positive spin on patient
education and oral health messages. Criticizing patients
and parents with statements like “you really shouldn’t eat
sweets so often” or “you need to do a better job brush-
ing your teeth” are not likely to generate positive results.
Instead, use messaging like “your teeth will stay healthy if
you drink juice during mealtimes instead of throughout
the day.” When providing brushing instruction, it is also
very helpful to praise the child’s brushing efforts while
actively demonstrating brushing techniques in a mirror.
In addition to verbal and nonverbal praise, the dentist
may present the child with a small gift. Simple prizes such
as colorful stickers and small toys are very well received
by children (7 Fig. 4.12). Providing the gift at the end
lent reinforcer [13]. On the other hand, promising a prize
before the child has demonstrated a desired behavior
may not have a positive effect, it’s more like bribery [14].
5.2.5 Distraction
Distraction redirects the child’s attention from an
uncomfortable sensation by occupying the mind with
more pleasant thoughts or activities. For example, chil-
dren awaiting treatment in the reception room can be
distracted by drawing and painting (. Fig. 5.8). During
dental treatment members of the dental team can
stimulate the imagination by telling stories, referenc-
ing patient hobbies (computer games, sports, or other
personal activities), and engaging the child through par-
ticipatory activities like holding a mirror. This can be a
good relationship building exercise, but there is little evi-
dence that focusing on non-dental issues is effective in
reducing dental fear [13]. On the other hand, TV, head-
phones with music, and other audiovisual technologies
are becoming very common in offices that care for chil-
dren [15, 16]. Virtual reality devices are a very immersive
..      Fig. 5.8 A child engaging in creative activity (drawing) in the
waiting room
Behavior Guidance and Communicative Management
form of distraction, and some findings suggest that
patients who use them may even experience lower levels
of procedural pain [17–19] (. Fig. 5.9).
Another technique that can be used with success
is providing the patient with breaks when they display
cooperative behavior (contingent distraction) [1]. It is
important to recognize that distraction does not work in
the absence of communication. In fact, very stimulating
forms of distraction such as television and video games
may interfere with communication and make treatment
more challenging.
Distraction can be passive or participatory. Asking
the patient to count the number of local anesthesia
drops that the dentist administers or participate in
breathing exercises is an example of participatory dis-
traction. A trick, such as shaking of the patient’s lip dur-
ing local anesthesia administration, is considered passive
a
b
..      Fig. 5.9 a. A girl is engaged in watching her favorite cartoon
on a ceiling monitor. b. Restorative dental work while watching and
listening to stories through audiovisual equipment
67 5
distraction. During the administration of local anesthe-
sia, most children are fairly anxious and their minds are
fully focused on the syringe. If the dentist informs the
patient that she will slowly count (e.g., five “drops”) and
does accordingly, the child is not only distracted, but is
given a time frame for the procedure (time structuring).
It is critical to recognize that distraction simply supports
a child’s cooperation and is not an alternative to insuf-
ficient local anesthesia. In fact, obtaining excellent local
anesthesia is perhaps the most critical step in facilitating
good patient behavior.
5.2.6 Modeling
Modeling focuses on shaping behavior using the prin-
ciples of learning theory and imitation. Studies have
shown that it can enhance cooperation [20, 21]. Modeling
is similar to the TSD technique, where an observing
child is “shown” a cooperative patient who models good
behavior (. Fig. 5.10). The interaction may be live or
filmed, at the convenience of the clinic. The observing
child is then expected to imitate the cooperative behav-
ior of the model. For that reason, the period of observa-
tion is generally several minutes long and is enhanced
by having the child view more than one cooperative
“model.” It is advantageous for the child-model to be
of a similar age, because children often respond very
well to others in their peer group [3]. It may also be con-
venient to have a sibling model good behavior. When
caring for siblings who have not experienced the dental
procedure, it is preferable to examine the one who looks
most calm and cooperative. This is not always the older
patient! When convenient, parents can also be recruited
to model behavior at the first dental visit. Parent model-
ing appears to significantly reduce the child’s stress dur-
ing the first examination [21].
..      Fig. 5.10 Modeling utilized for a fearful young patient
 68 T. Nelson and N. Kotsanos

5.2.7 Voice Control

Voice control focuses the patient’s attention on specific

instructions through alteration in volume, tone, and
speed of the dentist’s voice. Calm monotonous speech
may have a soothing effect, like soft music. Sudden firm
instructions like “stop crying and pay attention” restore
the child’s focus. On occasion a child may be redirected
when the clinician lowers herself to the child’s level and
quietly whispers instructions that the patient must focus
5 on to understand. This technique is generally most suc-
cessful with children who are only moderately uncooper-
ative and in those with reduced attention capacity. While
the name may imply that this is a verbal technique, it is
actually primarily a nonverbal method. This is because
the volume and tone of voice outweigh the verbal mes- ..      Fig. 5.11 Holding mother’s hand offers support to some children
sage. If used in the appropriate circumstances, voice
control can achieve short-term results, yet it should be
implemented with caution [22, 23]. In a modern liti- reflection of this contemporary approach, the AAPD
gious society, families must be forewarned if the dentist has incorporated parental presence/absence as a basic
chooses to use firm instructions. The firm approach is behavior guidance technique in published guidelines
not always well received by today’s parents [1]. and supports the dentist’s decision to include or sepa-
rate parents from the dental operatory [2].

5.2.8 Parental Presence 5.2.8.1 Parental Presence/Absence

Many dentists prefer for parents to remain outside the
dental operatory during treatment. This may be due to
historical practices and traditional “one to one” rela-
tionships common with adult patients. Parents can also
interfere with the child’s ability to concentrate on dental
procedures and may try inappropriately to be support-
ive with phrases like “don’t be afraid” or “did it hurt?”.
While they may be well-intentioned, those messages
increase distress in the patient and frequently make
treatment more challenging. Most pediatric practitio-
ners recognize that parents are most effective when they
function as silent supporters of their child.
Three or more decades ago pediatric dentists
allowed parents to be present during the child’s visit
much less frequently than they do today. Progressively,
dentists are more accepting of parental presence, even
during restorative sessions [24, 25]. Smaller family sizes,
changes in child-rearing practices, and parent emotional
needs have led many parents to expect greater involve-
ment in the dental visit. Parents who remain in the wait-
ing area may be concerned about their child’s ability
to cooperate and the dentist’s skills to manage them.
This is particularly true during the first appointment
(. Fig. 5.11). Over subsequent visits parents may have
less desire to be present as confidence in the child and
dentist increases [26]. Some dentists find that parental
presence allows a parent to understand the importance
of the child’s cooperation and at the same time appre-
ciate the clinician’s behavior management skills. As a
as a Behavior Shaping Technique
Children instinctively look to the parent for safety and
survival, a dependent relationship that is maintained
for at least the first decade of life (see 7 Chap. 2) [27].
Parent presence may therefore prove useful during new
experiences because separation anxiety is not added to
the novelty of the unknown environment. Very nervous
children may cling to the parent, as this imparts a feeling
of safety [28]. Many are used to their parent comforting
them when they are distressed, so they reflexively seek
parental protection and avoid the dental examination
and/or treatment (7 Fig. 4.8). While this may appear to
be a negative reaction, some have suggested that paren-
tal presence can be leveraged as a reward for coopera-
tion in initially noncooperative children [7, 29, 30].
In such cases we can reach out to the child before
he becomes completely uncommunicative with an empa-
thetic message like:
»» I know that you want to show your mother what a good
listener you can be today. She will stay right here with
us as long as you are able to listen to me. If you don’t
open wide, that shows us that you aren’t listening. That
means she will need to leave until you focus on what I
am asking. I would like to have her stay here with us.
Are you ready to show her how well you can open and
have your hand ready to raise if anything bothers you?
Before implementing this with the child, it is critical to
obtain consent from the parent. In practice, the tech-
nique works so well that it is actually quite rare for the
Behavior Guidance and Communicative Management
parent to leave the room [29]. Typically this approach
quickly facilitates cooperation in preschoolers and early
school-age children.
5.2.9 Other Complementary Techniques
Depending on the training and preferences of the practi-
tioner, other complementary strategies may be employed
in addition to these basic strategies.
zz Time structuring
Young children have a short attention span. Typically,
it is better to present procedures in “steps” rather than
minutes. The dentist gains the child’s confidence and
cooperation by explaining the basic steps involved in
the visit, i.e., local anesthesia, rubber dam placement,
caries removal, matrix band and wedge placement,
restoration placement, light curing, etc. in a way she
can easily understand. Structuring time in this way
allows her to understand when the session is nearing
an end [14].
zz Guided Imagery
Children will often begin a sentence with “I don’t like
...” or “I don’t want to ....” It is helpful to understand
that the child may raise concerns like this to assert his
feelings about the procedure. These types of statements
do not necessarily mean that the patient will not do what
is asked of him. Instead, these observations may be the
product of the child’s imagination. He may be wishing
for something that he understands may not actually
occur. It can be helpful to respond to these observations
with statements like, “It would be nice not having to....”
This demonstrates an appreciation for the child’s active
imagination and empathy for his feelings. In most cases,
children understand that what is asked of them needs
to be done. If we request cooperation calmly and con-
fidently, they often respond favorably [15]. The child’s
imagination is probably most active around the age of
4–5 years. We can leverage this in our interaction with
the patient. The clinician can guide the patient’s visit
with phrases like “Imagine that you are in space” or “...
pretend that you are Batman (or another character the
child likes) being brave for the dentist.” This type of
guided imagery is based on principles of hypnosis and
can be a powerful adjunctive technique [1].
zz Directed Breathing
Directed breathing is one of the most powerful ways
to reestablish a fearful patient’s focus. A crying child is
often too distracted by her distress to respond to direc-
tions. Instructing a fussy child to take deep, rhythmi-
cal breaths directs her attention on something concrete
69 5
and reduces crying. The act of breathing relaxes the
child and helps regulate the autonomic nervous system.
This technique is most effective when the dentist dem-
onstrates how the child should breathe by taking deep
breaths with her 4–5 times. Asking the child to relax her
muscles while breathing also helps relieve tension and
reduces anxiety [14].
zz Hypnosis
Combining distraction, relaxation, and monotone
speech can create a hypnotic state that reduces stress and
pain. Approximately one third of patients are receptive
to these techniques, but there are limited reports about
the effects of hypnosis in pediatric dentistry [4, 31, 32].
While there is some limited evidence to show effective-
ness, a systematic review suggested that there is not yet
enough support to broadly endorse the benefits of hyp-
nosis in the dental office [33].
zz Sound Analgesia
Soft melodic sounds or higher-volume rhythmic music
played through speakers or headphones is a form of
distraction known as sound analgesia. These techniques
have been used with fair results to improve child behav-
ior for short, potentially painful, procedures such as
local anesthesia [34]. While not well documented in the
dental literature, adult patients under laboratory pain
conditions experienced distraction and increased self-­
control while listening to music [35].
zz Humor
Laughter reduces the body’s stress reaction and con-
tributes to feelings of well-being. Humor is also regu-
larly used in the education sector as a useful tool for
maintaining student interest and causing relaxation.
Consequently, humor is employed often in medical and
dental settings. Members of the dental team can employ
this technique by telling age-appropriate jokes, invent-
ing rhymes, giving dental instruments funny names,
and making playful gestures [1]. As with all techniques,
authenticity is important and success is contingent on
the clinician’s temperament.
zz Memory Restructuring
Children frequently navigate difficult dental visits with-
out tears; however, that is not always the case. When the
patient has a negative experience, it can help to restruc-
ture her memory of the visit. Successful implementation
of this technique involves enhancing positive associa-
tions and minimizing negative aspects of the visit. After
treatment is complete, the dentist may engage in a car-
ing conversation with the child and parent. He should
verbally praise the child for some aspect of the visit that
she performed well. For example, the dentist might say,
 70 T. Nelson and N. Kotsanos
5 graphs), so she agreed to sit in the dental chair. After
..      Fig. 5.12 The use of a rubber dam and a mouth prop improves
the speed and quality of work
“I understand that today was hard for you. You did a
really good job of opening your mouth wide so that
we could finish quickly. I am so proud of you for being
brave today.” It is important to provide the child with
concrete examples of things that they did well. It is also
beneficial to praise the child in front of the parent and
ask that the parent praise them at home later that day in
the presence of other family members. Memory restruc-
turing has been demonstrated to be effective at reducing
dental fear and improving behavior at subsequent treat-
ment visits [2, 36].
zz The Use of Rubber Dam and Accessories
Instrumentation used in pediatric dentistry to provide
high-quality restorative outcomes (i.e., by maintain-
ing a clean, dry field) contributes indirectly to overall
treatment results by improving patient behavior. Many
children with dental behavior management problems
perform better after a rubber dam and a mouth prop
are placed (. Fig. 5.12). This creates a perception of a
barrier between the child and the technical procedures.
The mouth prop also allows the patient to relax with-
out having to focus on keeping his mouth open. Treating
patients in the supine position with a dental assistant
present reduces treatment time and improves safety
when the assistant holds the child’s hands during specific
aspects of the dental visit. Children with disabilities and
strong gag reflexes may require alternative positioning
for comfort and cooperation [37].
Two Examples of Behavior Guidance for Routine
Dental Treatment*
55 The Initial Examination
Anna, a healthy 3.5-year-old girl, presents to your
office. She is initially moderately fearful of many new
experiences, and she has some anxiety about the dental
visit. Your assistant told Anna that today you will only
count her teeth and take a few “pictures” (radio-
introducing yourself, you tell her about the dental mir-
ror. Next you lift it from the exam tray and show it to
her. You ask if she would like to touch it. Then you
present the explorer as a “tooth counter.” You explain
that it can be used to count teeth or fingernails. Then
you show how it can be used to count your own finger-
nails, pressing the explorer against the nails of your
gloved hand. When she has seen how the instrument is
used, you take Anna’s hand and begin to demonstrate
how you can count her fingernails too. Anna hesitates
and withdraws her hand. This indicates that she is not
yet ready to go from the “tell” into the “show” step. At
this point you move forward confidently, knowing that
it is generally more effective to proceed gently but per-
sistently. You count the first finger and she relaxes,
learning that the explorer doesn’t hurt and that she is
able to accept it. Counting her fingernails enhances her
confidence in what you have told her because what
happened was exactly what you promised. It was easy
and it didn’t hurt (. Fig. 5.1).
-And with this (air/water syringe) Anna, we blow a
little wind on the teeth…sending a light stream of air
onto her hand as you are holding it...this cleans and
dries them so that I can see really well. Now open big like
a lion so that I can count your teeth like we practiced.
Anna opens her mouth.
-Ah, thank you for opening so wide Anna (positive
reinforcement). What a nice healthy mouth! You begin
the dental examination, counting teeth and dictating
findings to your assistant.
55 Restorative Treatment
Alex is a healthy 5-year-old boy. He needs restoration
of his two left mandibular primary molars. You have
successfully administered a mandibular block, anes-
thetizing the inferior alveolar nerve (see 7 Chap. 7).
- You explain to him. Alex, now that your teeth are
sleeping on this side, I will cover them with this raincoat
(rubber dam). That way no more icky tastes will get on
your tongue, and no water or little bugs will stay in your
mouth. Do you want to feel it? See, it’s soft and made of
rubber!
Behavior Guidance and Communicative Management
He touches it.
- This little ring (rubber dam clamp) will hold it in
place like a button. If it bothers you at all, raise this hand
again. OK?
- This tooth chair (mouth prop) makes it easy to
keep your mouth open. Now open wide please. That’s
great, thank you!
The small size Molt mouth prop is inserted, not to
pry the teeth apart, but to help the mouth stay open
(. Fig. 5.13). Alex can watch this process in the mir-
ror, satisfying his curiosity and focusing his attention
on the procedure.
- Alex, anything that falls onto the raincoat will be
sucked up by this small vacuum cleaner (high-volume
suction). I will clean the little hole in your tooth with this
metal brush (diamond bur). Then I will fill it with little
putty and we will be all done.
You showed your patient the cylindrical diamond
bur and let him feel it on a finger nail (on a high-speed
hand piece but at very low speed). That will put him at
ease and reduce concerns about the unknown. You also
gave the patient control by allowing him to raise his
hand to pause the appointment if he experiences pain.
- Everything OK Alex?
He nods in agreement.
- Okay, let’s do it. Would you like to listen with head-
phones while watching this cartoon on the screen?
*Depending on the experience and the tempera-
ment of the pediatric dentist, steps may vary in content
and speed.
..      Fig. 5.13 Placing the mouth prop passively after asking the
patient to open his mouth
71 5
5.3 Advanced Behavior Guidance
Children may show a variety of negative behaviors
in the dental office, including a strong attachment to
their parents, avoiding eye contact, expressing strong
will, refusal to cooperate, and fight/flight reactions.
Fortunately, many children who display these behaviors
can be treated successfully using the right combination
of basic techniques. On the other hand, those strategies
are ineffective with some patients. Attempting to pro-
vide dental care for children who are unable to cooper-
ate with basic behavior guidance techniques can result in
poor outcomes and frustration for the child, parent, and
dentist (. Fig. 5.14). In these situations clinicians with
advanced training may consider use of protective sta-
bilization, procedural sedation, and general anesthesia
(GA) [2]. For the purposes of this chapter, we have lim-
ited our discussion to non-pharmacological techniques.
5.3.1 Protective Stabilization
Active Immobilization Operative dental care requires
good control of the field and the child’s movements. In
specific situations, safe treatment requires parents or
members of the dental team to actively hold the child’s
hands, limbs, or head for brief periods of time. This is
known as active immobilization. This is particularly com-
mon with young, precooperative children. Examples
include:
..      Fig. 5.14 Testing the dentist’s patience. (From Chambers
DW. Communicating with the young dental patient. JADA,
1976;93:793, with permission)
 72 T. Nelson and N. Kotsanos

55 Oral examination and single X-ray taking. a

55 Administration of local anesthetic.
55 Restoring a deeply carious molar tooth with glass
ionomer cement as an interim therapeutic restora-
tion (ITR).
55 Tooth extraction due to trauma or dentoalveolar
infection.

For more lengthy procedures, especially those involving

placement of multiple challenging restorations, a phar-
macological approach may be preferred to active immo-
5 bilization. However, one main benefit is that the latter
avoids the use of sedative medications, which may some-
times be contraindicated. When implemented, the dental
assistant usually aids in immobilizing the patient. This
could be an act as simple as holding the child’s hands
while the dentist administers an injection. Parents can b
also be used to help provide active immobilization. A
good example is when the parent holds a young child’s
hands while the dentist examines his mouth. Involving
parents is beneficial because the child may find their
touch comforting, while their consent is implied by their
participation. During future visits, the child should be
given the opportunity to have dental experiences that
reinforce autonomy and a positive perspective on dental
care [4].
Children under age 3 usually do not willingly sit in
the dental chair on their own. For that reason, a “knee
to knee” position works well when examining very
young children [38]. Another suitable position involves
having the parent sit at the base of the dental chair, with
the child’s legs draped over her lap (. Fig. 5.15). Both ..      Fig. 5.15 a. “Knee to knee” position for examination of children
positions allow the dentist to control the patient’s head, under the age of about 3 years. b. Alternative positioning of the
while the parent secures the feet and hands. They are young child in the dental chair with legs on mother’s lap and hands
essentially forms of active stabilization. Many children controlled by her
in this age group will cry and be unwilling to open their
mouths for an examination. To visualize the teeth and
avoid having the child bite down, the dentist may place
a finger on the posterior edentulous alveolar process as
a prop. It may also be necessary to assist older children
with disabilities in maintaining an open mouth pos-
ture during the exam. In such cases bite blocks/sticks
or finger cases made from rigid material may be used
(. Fig. 5.16).

Passive Immobilization Passive immobilization, or pro-

tective stabilization, is an AAPD-endorsed technique
that typically involves the use of a device that supports
the patient’s limbs and reduces bodily movement [2].
This enables the dental team to provide safe and effective ..      Fig. 5.16 Finger protection cases fabricated from rigid material
care for emergency procedures or for children with spe- may be used to maintain open mouth posture
Behavior Guidance and Communicative Management
73 5
cial needs who cannot cooperate willingly for dental a
examination. Most typically, passive immobilization
devices consist of padded boards with fabric fasteners
for securing hands and legs to the body. These devices
are manufactured in various sizes and are intended to
limit movement and prevent accidental injury from den-
tal instruments (. Fig. 5.17). Care should be taken to
avoid cutting off blood circulation or breathing by
applying the stabilization device too tightly. While not
suitable for lengthy procedures, stabilization may be well
received by some children with special needs (e.g., chil-
dren with spasticity). However, protective stabilization is
not to provide treatment in lieu of sedation or general
anesthesia if pharmacologic methods are indicated
(. Fig. 5.18).
It is important to explain the risks and benefits of b
protective stabilization to parents and to obtain con-
sent before use. Acceptance may vary depending upon
how the parent typically manages their child’s behavior
and how urgent the dental needs are [39]. In past sur-
veys protective stabilization was rather poorly accepted
by parents, usually being perceived as less accept-
able than general anesthesia [39, 40]. Acceptance of a
Papoose board (Olympic Medical Co, Seattle, Wash,
USA) was very high (90%) when the rationale for use
was thoughtfully presented by the dentist [41]. In the
USA, protective stabilization in pediatric offices is rela-
tively common, especially when combined with phar-
macological sedation [2]. In Europe, however, it is used
only by experienced clinicians under very specific cir-
cumstances [42]. c
Specialized mouth props are frequently used to assist
the child in maintaining an open mouth posture. The
Molt-type mouth prop consists of an anterior bite pad
attached to metal arms that may be opened through
a central hinge (. Fig. 5.19). This device works well
because it allows for a range of opening and the metal
arms sit outside the patient’s mouth, allowing the den-
tist/assistant to be able to prevent its dislodgement. It is
positioned in the posterior region opposite of the work-
ing side. It is very useful for children undergoing lengthy
operative appointments and in sedation/GA cases where
children are unable to open their mouths. It tends to
decrease muscle fatigue and is generally relatively well ..      Fig. 5.17 a, b. Papoose board® used to provide protective stabi-
received when it is introduced as a “tooth chair” or “bit- lization (Olympic Medical Co, Seattle, USA). c. Another example of
ing pad.” passive immobilization device (Specialized Care Co, Rainbow Wrap)
 74 T. Nelson and N. Kotsanos
a
5 –– Inhalation sedation with nitrous oxide.
b –– Guided breathing.
..      Fig. 5.18 a. Protective stabilization can be very well accepted by
some children with special needs. b. Patient with special needs cheer-
fully receiving care with protective stabilization
..      Fig. 5.19 Adult and child size Molt-type mouth props with sili-
cone tubes to prevent lip trauma while biting
Short Preference List of Behavior Guidance
Techniques
The management of the child’s behavior may include
the following techniques:
55 Always:
1. Approach with empathy and provide control.
2. Tell-show-do suited to child’s age.
3. Reinforce positive behavior.
55 Possibly:
–– Parental presence/absence.
–– Modeling.
–– Distraction.
–– Voice control.
–– Time structuring.
–– Guided imagery.
–– Protective stabilization.
5.3.2  ealing with Demanding Behavior
D
Problems
Medical conditions such as attention-deficit/hyperactiv-
ity disorder (ADHD) and autism spectrum disorders
affect child behavior. The specifics of these conditions
are discussed in 7 Chap. 22. In general, children with
special needs or intellectual disability often benefit from
a slow, structured approach to dental care. Some may
benefit from techniques such as desensitization therapy
[43]. Clinicians also encounter children who do not have
any known medical conditions that interfere with treat-
ment, yet still experience significant challenges in receiv-
ing dental care. Some specific examples are addressed
below.
5.3.2.1 Intense Fear of Dental Injection
Needle-phobia (7 Figs. 4.2) (. Fig. 5.20) is among the
most common fears in dentistry [14]. Patients with this
type of fear may benefit from techniques that involve
systematic desensitization. Such an approach would
involve rehearsing the injection procedure several times.
One might begin first with needle cap in place, then
proceed by placing the syringe in the mouth with the
needle exposed, and finally administer anesthetic. It is
imperative to provide the patient with control, allowing
him to pause the procedure immediately if he encoun-
ters pain. It is also beneficial to describe in detail what
the patient will feel before she experiences a sensation.
Expertise in administration of local anesthetic is criti-
cal. Administering anesthetic slowly with a light touch
Behavior Guidance and Communicative Management
..      Fig. 5.20 Drawing by a 6-year-old while awaiting treatment
..      Fig. 5.21 Demonstrating the brushing of lingual surfaces of
lower molars to a child’s parents. Its practice may reduce possible
gag reflex through progressive desensitization
minimizes discomfort and improves patient confidence.
When attempting desensitization, it should be noted
that ­overcoming dental fear in older patients may be
more difficult and time consuming than with younger
individuals [14].
5.3.2.2 Intense Gag Reflex
The gag reflex is seen in both adult and pediatric
patients. In children it is often discovered at the patient’s
first examination. The reflex is typically of a psycho-
logical origin, and severity ranges considerably among
patients. Possible contributing factors include pain, fear
of having foreign instruments in the mouth, and fear of
choking. Because the reflex may be based partially in
patient anxiety, nitrous oxide inhalation sedation may
have a relaxing effect that is particularly useful. Further
relaxation exercises, distraction, and systematic desensi-
tization may also help [37]. Adopting the latter, it can be
helpful to gradually introduce a stimulus, stopping short
of the patient gagging. This allows the patient to learn
that she can accept the triggering stimulus. Breathing
exercises may also be very helpful.
The gag reflex is often encountered when exposing
radiographs, taking maxillary impressions, placing a
rubber dam, providing fissure sealants, and on occasion
75 5
simply drying teeth with air [ 44]. When indicated for a
procedure, good local anesthesia significantly reduces
gagging and helps prevent nausea/vomiting. It is rec-
ommended that patients in whom the gag reflex is
anticipated arrive to the dental visit with an empty
stomach. This reduces nausea and limits vomiting. An
upright chair position is also recommended. If there is
no immediate need for restorative dentistry, instructing
the parent to assist the patient with brushing the molar
lingual surfaces for several weeks may help desensitize
sensitive areas (. Fig. 5.21). For children who need
immediate care but have a gag reflex that interferes
with treatment, referral to a pediatric dentist should be
considered.
An Example of Managing an Intense Gag Reflex
An 8-year-old boy presented to the dental office with
an intense gag reflex. The reaction was so strong that it
was not possible to properly examine his permanent
molars. He was also unable to receive diagnostic intra-
oral radiographs. He had urgent dental needs in the
upper left quadrant, so the dentist began treatment in
that area. Local anesthesia was administered and a
rubber dam clamp No. 13A was placed on the second
primary molar instead of the permanent one. The child
was seated upright, rather than supine in an effort to
reduce the reflex. This position made treatment more
challenging for the dentist, but it was completed suc-
cessfully. During the child’s appointment, the dental
team used behavior management techniques such as
positive reinforcement and distraction to reduce anxi-
ety and the gag reflex. Amazingly, at the next appoint-
ment the child had overcome his gag reflex to the point
where he was able to have intraoral radiographs. At
subsequent visits, the dentist was able to recline the
chair more and complete the treatment plan in a more
ergonomic position. At the recall visit in 6 months,
there was almost no evidence of a gag reflex.
5.3.2.3 Emotional` Immaturity and Language
Problems
Typically children aged 3–4 years are generally “coop-
erative” or “potentially cooperative” for dental care.
However, some children at this age present with unco-
operative behavior that is not manageable using a com-
municative approach. This is frequently because their
emotional immaturity prevents communication in stress-
ful situations (. Fig. 5.22). This is sometimes related
to child-rearing practices. For example, when parents
are uninvolved and assign parenting responsibilities to
other caretakers, the parent-child bond may be weak.
These children may not feel a sense of security from
 76 T. Nelson and N. Kotsanos
..      Fig. 5.22 A 4-year-old girl with mental impairment and urgent
restorative needs. She was scheduled for rehabilitation under general
anesthesia
the presence of their parent. Refugee children may have
encountered displacement, suffering, illness, and loss of
loved ones that makes it difficult for them to cope with
dental care [45, 46]. To compound the problem, many
refugee children do not speak the language of the den-
tal team. In such cases, the use of aversive voice control
or parental presence/absence is not usually appropriate.
Active immobilization may be used for emergencies, but
these children may need other advanced behavior guid-
ance techniques to accomplish extensive dental treat-
ment. If treatment needs are not urgent, the dentist may
pursue treatment options such as preventive approaches
[47] and deferred treatment with desensitization.
5.4  thical and Legal Issues and Parental
E their assent is paramount to successfully completing treat-
Consent
When a child’s behavior makes it impossible to provide
dental care in the traditional clinic setting, the clinician
must consider several factors [4]:
55 Can treatment be postponed or canceled? If so, what
are the potential consequences of doing so?
55 Is the child mature enough to assent to treatment, or
will the parent be the only party consenting for care?
55 Is advanced behavior guidance indicated, and if so
what are the potential consequences?
55 Has the parent been fully informed of their treat-
ment options?
55 Have cultural background, economics, and parent
preferences been considered?
For adult dental care, consent is implied when the patient
sits in the dental chair to receive treatment. With children,
..      Fig. 5.23 Societal norms have an impact in the well-established
triangle of parent-child-dental team interaction [1, 3]
consent is not granted in the same way. Consent for treat-
ment of minors must be provided by a legal guardian.
Informed consent entails providing parents with infor-
mation regarding benefits and risks of the proposed
treatment, as well as possible treatment alternatives. In
pediatrics, consent must take into account not only the
proposed treatment, but also the behavior management
plan. In situations where the parent provides legal autho-
rization to perform a procedure, the clinician should gen-
erally consider the child’s wishes. This may be challenging,
as preschool and school-age children may be reluctant to
accept treatment, in part because they don’t fully under-
stand how it will benefit them. Adolescents, on the other
hand, can generally understand treatment options and be
involved in the consent process like an adult patient [48].
When the child grants permission to perform a procedure,
it is known as assent. With older children and adolescents,
ment. Therefore, regardless of age, clinicians should aim
to involve children as willing participants in clinical care.
Contemporary parents expect to be very involved
in the informed consent process. Over time, social
changes affecting the parent-child relationships have
changed acceptance of some techniques and profes-
sional guidelines have been updated to reflect societal
changes [48] (. Fig. 5.23). In recent years we have also
seen a movement toward common guidelines between
the International, American, and European Pediatric
Dentistry associations.
Studies demonstrate that when provided with ade-
quate explanations, most parents accept communicative
techniques like tell-show-do and positive reinforcement.
Techniques that involve voice control and use of a “bite
rest” mouth prop are reasonably well accepted, but more
aversive techniques like “hand over mouth” and passive
stabilization receive low acceptance [39, 49]. While these
Behavior Guidance and Communicative Management
techniques are generally not seen as desirable by many par-
ents, those with uncooperative children are more willing to
agree to the use of more aversive techniques if the rationale
for use is well explained [40, 50]. Acceptance of sedation
and general anesthesia varies widely depending on culture
and the healthcare and legal system of each country. It is
always very important to provide detailed informed con-
sent before implementing pharmacological techniques [50].
Types of Consent Consent is an essential component of
healthcare delivery. Specifics of informed consent are gov-
erned by the laws of individual countries. Consent may be
implied – as when a parent observes the dental team per-
forming an examination – or it may be expressed in oral
or written form [50]. Written documentation offers the
dentist better legal protection than oral or implied con-
sent. Written consent provides evidence of the consent
process, which may decrease liability that stems from mis-
communication. In the case of oral consent, the presence
of a witness is recommended (e.g., the dental assistant),
and records should be kept in patient’s file. Written con-
sent should be procedure specific, as risks differ for restor-
ative procedures, extractions, protective stabilization, and
sedation or general anesthesia [50]. In all cases, the laws of
the country supersede any consent arranged between the
family and the dentist. In situations where a patient suf-
fers harm, responsibility is often ascribed to the dentist if
there is no evidence that informed consent was obtained
before a procedure [51]. The consent process is also an
important opportunity for the dentist to discuss the child’s
care and develop trust and rapport with families.
Clinician Temperament and Training Success in behavior
guidance relies on the experience, skill, and temperament
of the individual practitioner. Some clinicians are more
comfortable with advanced behavioral strategies such as
sedation and protective stabilization. Others may not have
had training in pharmacologic techniques and thus tend
to rely more on communicative behavior management.
Regardless of the clinician’s approach, it is critical that she
develop a strong working knowledge of the wide variety
of behavior guidance techniques. This allows her to imple-
ment strategies that are most likely to be successful in her
hands.
References
1. Wright G, Kupietzky A. In: Wright G, Kupietzky A, editors.
Non-pharmacologic approaches in behavior management. 2nd
ed. Behavior management in dentistry for children; 2014.
2. American Academy of Pediatric Dentistry. Behavior guidance
for the pediatric dental patient. The Reference Manual of Pedi-
atric Dentistry. Chicago, Ill: American Academy of Pediatric
Dentistry; 2020. p. 292–310.
77 5
3. Ripa L, Barenie J. Management of dental behavior in children.
Littleton, Mass.: PSG Publishing Co; 1979.
4. Chadwick B, Hosey M. Child taming: how to manage children in
dental practice. London: Quintessence; 2003.
5. Ten Berg M. Dental fear in children: clinical consequences. Sug-
gested behaviour management strategies in treating children
with dental fear. Eur Arch Paediatr Dent. 2008;9(Suppl 1):41–6.
6. Nelson T. The continuum of behavior guidance. Dent Clin N
Am. 2013;57(1):129–43.
7. Townsend JA. Behavior guidance of the pediatric dental patient.
Ch.23. In: Casamassimo PS, Fields Jr HW, Mc Tigue DJ, Nowak
AJ, editors. Pediatric dentistry. Infancy through adolescence. 5th
ed. Elsevier Saunders: St. Louis; 2013.
8. Addleston H. Child patient training: fortnightly review of the
chicago dental society; 1959. p. 7–9–27–9.
9. Raseena KT, Jeeva PP, Kumar A, Balachandran D, Anil A,
Ramesh R. A comparative study of tell-show-­do technique with
and without the aid of a virtual tool in the behavior manage-
ment of 6-9-year-old children: a nonrandomized, clinical trial.
J Indian Soc Pedod Prev Dent. 2020;38(4):393–9. https://doi.
org/10.4103/JISPPD.JISPPD_280_20.
10. Radhakrishna S, Srinivasan I, Setty JV, Murali Krishna DR,
Melwani A, Hegde KM. Comparison of three behavior modifi-
cation techniques for management of anxious children aged 4–8
years. J Dent Anesth Pain Med. 2019;19(1):29–36. https://doi.
org/10.17245/jdapm.2019.19.1.29.
11. Kharouba J, Peretz B, Blumer S. The effect of television distrac-
tion versus tell-show-do as behavioral management techniques
in children undergoing dental treatments. Quintessence Int.
2020;51(6):486–94. https://doi.org/10.3290/j.qi.a44366.
12. Communicating with and about people with disabilities: Centers
for Disease Control. https://www.cdc.gov/ncbddd/disability-
andhealth/materials/factsheets/fs-communicating-with-people.
html.
13. Weinstein P, Getz T, Ratener P, Domoto P. The effect of den-
tists' behaviors on fear-related behaviors in children. J Am Dent
Assoc. 1982;104(1):32–8.
14. Milgrom P, Weinstein P, Getz T. Treating fearful dental patients.
A patient management handbook. 2nd ed. Seattle: University
of Washington Continuing Dental Education; 1995. p. 167–70.
231–36, 313, 16
15. Ram D, Shapira J, Holan G, et al. Audiovisual video eyeglass
distraction during dental treatment in children. Quintessence
Int. 2010;41(8):673–9.
16. Prabhakar AR, Marwah N, Raju OS. A comparison between
audio and audiovisual distraction techniques in managing anx-
ious pediatric dental patients. J Indian Soc Pedod Prev Dent.
2007;25(4):177–82.
17. Asl Aminabadi N, Erfanparast L, Sohrabi A, Ghertasi Oskouei
S, Naghili A. The impact of virtual reality distraction on pain
and anxiety during dental treatment in 4-6 year-old children: a
randomized controlled clinical trial. J Dent Res Dent Clin Dent
Prospects. 2012;6(4):117–24.
18. Morris LD, Louw QA, Grimmer-Somers K. The effectiveness
of virtual reality on reducing pain and anxiety in burn injury
patients: a systematic review. Clin J Pain. 2009;25(9):815–26.
19. Khandelwal D, Kalra N, Tyagi R, Khatri A, Gupta K. Control of
anxiety in pediatric patients using "tell show do" method and audio-
visual distraction. J Contemp Dent Pract. 2018;19(9):1058–64.
20. Karekar P, Bijle MN, Walimbe H. Effect of three behavior
guidance techniques on anxiety indicators of children undergo-
ing diagnosis and preventive dental care. J Clin Pediatr Dent.
2019;43(3):167–72. https://doi.org/10.17796/1053-4625-43.3.4.
21. Farhat-McHayleh N, Harfouche A, Souaid P. Techniques for
managing behaviour in pediatric dentistry: comparative study of
 78 T. Nelson and N. Kotsanos
live modelling and tell-show-do based on children's heart rates
during treatment. J Can Dent Assoc. 2009;75(4):283.
22. Greenbaum PE, Turner C, Cook EW 3rd, Melamed BG. Den-
tists' voice control: effects on children's disruptive and affective
behavior. Health Psychol. 1990;9(5):546–58.
23. Wells MH, Dormois LD, Townsend JA. Behavior guidance: that
was then but this is now. Gen Dent. 2018;66(6):39–45.
24. Adair S, Waller J, Schafer T, Rockman R. A survey of mem-
bers of the american academy of pediatric dentistry on their
use of behavior management techniques. Pediat Dentist.
2004:159–66.
25. Ramos ME, Kao JY, Houpt M. Attitudes of pediatric dentists
toward parental presence during dental treatment of children. J
5 N J Dent Assoc. 2010;81(3):32–7.
26. Crossley ML, Joshi G. An investigation of paediatric dentists'
attitudes towards parental accompaniment and behavioural man-
agement techniques in the UK. Br Dent J. 2002;192(9):517–21.
27. Cassidy J, Shaver P, editors. Handbook of attachment theory,
research and clinical application. New York: Guilford Press; 1999.
28. Frankl S, Shiere F, Fogels H. Should the parent remain with the
child in the dental operatory? J Dent Children. 1962:150–63.
29. Kotsanos N, Coolidge T, Velonis D, Arapostathis KN. A form of
‘parental presence/absence’ (PPA) technique for the child patient
with dental behaviour management problems. Eur Arch Paediatr
Dent England. 2009:90–2.
30. McWhorter AG, Townsend JA. Behavior symposium work-
shop a report - current guidelines/revision. Pediatr Dent.
2014;36(2):152–3.
31. Oberoi J, Panda A, Garg I. Effect of hypnosis during Adminis-
tration of Local Anesthesia in six- to 16-year-­old children. Pedi-
atr Dent. 2016;38(2):112–5.
32. Peretz B, Bercovich R, Blumer S. Using elements of hypnosis
prior to or during pediatric dental treatment. Pediatr Dent.
2013;35(1):33–6.
33. Al-Harasi S, Ashley PF, Moles DR, Parekh S, Walters V. Hyp-
nosis for children undergoing dental treatment. Cochrane Data-
base Syst Rev. 2010;(8):Cd007154.
34. Aitken JC, Wilson S, Coury D, Moursi AM. The effect of music
distraction on pain, anxiety and behavior in pediatric dental
patients. Pediatr Dent. 2002;24(2):114–8.
35. Mitchell LA, MacDonald RA, Brodie EE. A comparison of the
effects of preferred music, arithmetic and humour on cold pres-
sor pain. Eur J Pain. 2006;10(4):343–51.
36. Pickrell JE, Heima M, Weinstein P, et al. Using memory restruc-
turing strategy to enhance dental behaviour. Int J Paediatr Dent.
2007;17(6):439–48.
37. Katsouda M, Tollili C, Coolidge T, Simos G, Kotsanos N,
Arapostathis KN. Gagging prevalence and its association with
dental fear in 4-12-year-old children in a dental setting. Int J
Paediatr Dent. 2018; https://doi.org/10.1111/ipd.12445.
38. Sacheti A, Ng MW, Ramos-Gomez F. Infant oral health is the
current standard of care. J Mass Dent Soc. 2012;61(3):22–7.
39. Boka V, Arapostathis K, Vretos N, Kotsanos N. Parental accep-
tance of behaviour-management techniques used in paediatric
dentistry and its relation to parental dental anxiety and experi-
ence. Eur Arch Paediatr Dent. 2014;15(5):333–9.
40. Eaton JJ, McTigue DJ, Fields HW Jr, Beck M. Attitudes of
contemporary parents toward behavior management techniques
used in. Pediatr Dent. 2005;27(2):107–13.
41. Frankel RI. The papoose board and mothers' attitudes following
its use. Pediatr Dent. 1991;13(5):284–8.
42. Roberts JF, Curzon ME, Koch G, Martens LC. Review: behav-
iour management techniques in paediatric dentistry. Eur Arch
Paediatr Dent. 2010;11(4):166–74.
43. Nelson T, Chim A, Sheller BL, Mc Kinney CM, Scott JM. Pre-
dicting successful dental examinations for children with autism
spectrum disorder in the context of a dental desensitization pro-
gram. J Am Dent Assoc. 2017;
44. Katsouda M, Coolidge T, Simos G, Kotsanos N, Arapostathis
KN. Factors associated with gagging during radiographic and
intraoral photographic examinations in 4-12-year-old children.
Eur Arch Paediatr Dent. 2020; https://doi.org/10.1007/s40368-
020-00535-9.
45. Gustafsson A, Arnrup K, Broberg AG, Bodin L, Berggren
U. Psychosocial concomitants to dental fear and behaviour man-
agement problems. Int J Paediatr Dent. 2007;17(6):449–59.
46. Salim NA, ElSa'aideh BB, Maayta WA, Hassona YM. Dental
services provided to Syrian refugee children in Jordan: a retro-
spective study. Spec Care Dentist. 2020;40(3):260–6. https://doi.
org/10.1111/scd.12460.
47. Raskin SE, Tranby EP, Ludwig S, Okunev I, Frantsve-Hawley
J, Boynes S. Survival of silver diamine fluoride among patients
treated in community dental clinics: a naturalistic study. BMC
Oral Health. 2021;21(1):35. https://doi.org/10.1186/s12903-­020-­
01379-­x.
48. Law CS, Karp JM. Behavior guidance symposium workshop B
report - training implications. Pediatr Dent. 2014;36(2):154–7.
49. Alammouri M. The attitude of parents toward behavior man-
agement techniques in pediatric dentistry. J Clin Pediatr Dent.
2006;30(4):310–3.
50. American Academy of Pediatric Dentistry. Informed consent.
The reference manual of pediatric dentistry. Chicago, Ill.: Amer-
ican Academy of Pediatric Dentistry; 2020, p. 470–355. Guide-
line on Informed Consent. Pediatr Dent 2015;37(5):95–7.
51. Sheller B. Challenges of managing child behavior in the 21st cen-
tury dental setting. Pediatr Dent. 2004;26(2):111–3.
 79 6

Examination, Diagnosis,
and Treatment Plan
Implementation
Stergios Arizos, Johan K. M. Aps, and Konstantinos N. Arapostathis

Contents

6.1 Examination and Diagnostic Process – 80

6.1.1  istory Taking – 80
H
6.1.2 Clinical Examination – 81
6.1.3 Radiographic Examination – 85

6.2 Implementing a Total Care Treatment Plan – 103

6.2.1  resentation of the Treatment Plan to Parents – 105
P
6.2.2 Factors Affecting the Progress of the Treatment Plan – 105
6.2.3 Referral to a Pediatric Dentist – 107

References – 109

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_6
 80 S. Arizos et al.
6.1 Examination and Diagnostic Process
The dental examination of the young patient is a com-
plex process, quite different from the equivalent in an
adult. It is not merely a simple oral checkup but a pro-
cess of collecting, analyzing, and evaluating data (medi-
cal, dental, social, personal, motor skills, cognitive and
learning skills, etc.). This process, while identifying any
dental problems (diagnosis), will reveal the child’s per-
sonality and family background in the scope of best
meeting the oral needs (treatment plan) of every young
patient.
6 close family and the broad social environment of the
Eye Catcher
The main element that differentiates the examination
of a child to that of an adult is that the child needs a
special approach by the examining dentist (behavior
guidance). Most often a child is not capable or unwill-
ing to provide accurate information about the back-
ground of a dental problem. Nor can he/she provide
information about the medical history. All the neces-
sary information will be provided by the child’s par-
ent or guardian who is obliged by law to accompany
the child to the dentist. Still this information is sub-
jective and needs to be treated critically by the clini-
cian because oftentimes it may be distorted by overly
anxious parents under emotional stress or others who
underreport their child’s complaints.
The actual symptoms will come to light during the
examination process, which need be properly structured
in stages orderly and clearly succeeding one another.
For example, discussing the child’s main complaint
with the parents/guardians at the same time with clini-
cal examination is incorrect. Even worse, history taking
while struggling to convince a child to sit in the dental
chair may lead to failure. Mistakes like these increase
the probability of a wrong diagnosis. The stages of the
diagnostic process are the following:
55 History taking.
55 Clinical examination.
55 Radiographic examination (if needed).
6.1.1 History Taking
History taking begins with the collection and record-
ing of personal data of the young patient and this has
some extra significance. Except that it is a practice’s legal
obligation to keep records with patients’ data, knowing
name, etc. aids in establishing a good way of commu-
nication with the young patient by demonstrating our
interest before he/she sits in the dental chair. An impor-
tant question is reason for the visit (e.g., routine checkup,
emergency because of trauma, pain, etc.). Thus, one can
avoid overlooking the prime reason of the visit, let’s say,
for example, an ectopic eruption of a tooth, and focus
instead on the need for pit and fissure sealants. A com-
plete medical and dental history of a patient includes
the familial and social history.
6.1.1.1 Family and Social History
Taking the family and the social history of the child is
a natural seamless procedure providing a picture of the
child. By means of an informal conversation about the
family (e.g., double or single parent, number of siblings,
place of residence (urban, rural), kind of school the child
attends, verbal communication skills and level, possible
extracurricular activities), important information is col-
lected. The parents’ – or guardians’ – education level,
often somehow drawn by their profession, may offer
insight into ease of communication about their child’s
oral health and oral home care. Their occupation and
the child’s social security number are useful for writing
prescriptions and for applying for financial coverage by
a social security or health insurance agent. Asking such
questions may often be perceived as indiscretion on the
part of the dentist; a relevant document may for that
reason be available in the waiting area.
6.1.1.2 Medical History
Taking a detailed medical history is paramount as some
pathological conditions may be predisposing factors for
oral health and thus affect the treatment plan or explain
manifest dental defects. Information relating to preg-
nancy and delivery, weight of the infant at birth, pre-
maturity and corresponding intubation, as well as days
spent in an incubator should all be recorded. Equally
important is the investigation of infection during the
neonatal period and infancy, while compliance to the
immunization program should also be confirmed.
Particular attention is needed in recording possible
syndromes and other congenital anomalies with a special
emphasis on congenital heart disease or heart surgery
that can be ground for developing bacterial endocardi-
tis. Parents often report the presence of a heart murmur
without being able to provide further details. In such
cases, further investigation of the condition by refer-
ring the child to a pediatrician or pediatric cardiologist
is necessary to determine the nature of the murmur and
whether antibiotic coverage for certain dental treat-
ments or a modified treatment plan is warranted.
Patients with diabetes (type I) or children with chronic
respiratory diseases (e.g., asthma) need s­ ometimes spe-
cial treatment, so it is important that the severity of these
Examination, Diagnosis, and Treatment Plan Implementation
conditions is further investigated. Chronic use of drugs
(e.g., corticosteroids) may often require modification of
drug level before dental treatment, always by consult-
ing the child’s attending physician. Highly detailed log-
ging is needed in patients with a history of neoplasia
or transplants. It therefore becomes obvious that taking
the medical history is a vital process for treatment plan-
ning and its overlooking may lead to situations that can
end up being life threatening. An example of a medical
history form is shown in . Fig. 6.1.
6.1.1.3 Dental History
The aim of dental history taking is, first, to investigate any
previous dental experience, in order to check the degree
of familiarity of the child with the dental environment.
Any previous dental treatment, along with administra-
tion of local anesthesia, the time elapsed since the child’s
last visit to the dentist, and whether this was pleasant or
unpleasant to the patient, should also be recorded. An
attempt is made to highlight any problems that existed in
the past, and detect any underlying fears toward dental
treatment, both on the side of the parent and the child.
This will aid in adopting a suitable approach strategy
that will effectively address all the possible previous neg-
ative experiences. Moreover, the history of any previous
facial or dental injuries also needs to be checked, along
with any treatment that was provided.
In case pain is the reason for the dental visit, a pain
history is next taken. This includes the assessment of
several characteristics such as the localization of pain
(soft tissue, tooth, maxillary, or mandibular), its nature
(acute, dull, spontaneous, or provoked), and its duration.
At this point caution is advisable, as children, especially
the ones below age 6 years, can rarely provide reliable
information about pain characteristics, unless the pain
is acute, recent, and so intense as to make them change
their habits. Pain details are a vital element for diagno-
sis. Parents can usually provide such details as well as
whether they have administered any analgesics (see also
7 Chap. 14 for emergencies). Finally, the dental his-
tory should include the child’s oral hygiene (frequency
of tooth brushing, use of fluoride toothpaste, any other
fluoride supplements) and dietary habits.
6.1.2 Clinical Examination
The clinical examination will additionally allow the cli-
nician to assess the degree of cooperation and the child’s
adaptation to the environment of the dental office.
Based on information derived from the patient’s medi-
cal and dental history, the clinician may request addi-
tional examinations, e.g., radiographic or microbiologic,
for the correct differential diagnosis. It is in other words
the next level of the diagnostic process, the one during
81 6
which the dentist comes in physical contact with the
young patient.
Essentially, the examination begins long before the
young patient seats in the dental chair, when the his-
tory forms are being filled in or, in cases of children
with intensely fearful disposition, just by observing their
behavior in the waiting room. So, relative to the child’s
age, the dentist can assess his/her physical growth and
gather information on maturity from the child’s mov-
ing, behaving, talking, and his/her facial expressions.
The observation of appearance and behavior may give
hints for possible disorders and syndromes that require
further investigation through the medical history.
The dentist can, besides assessing the oral cavity, have
a quick look at the child’s eyes, and at other exposed
parts of the body, such as hands and legs, for various
signs that may be related to the patient’s general health,
including possible signs of physical abuse. These include
bite marks, burns, abrasions, and bruises in different
stages of healing, which are located in parts of the body
that normally do not get traumatized. Irritation signs
and hyperplastic areas at the fingers may also provide
useful information about the existence of a bad habit,
such as digit sucking, while nails’ shape and color (curva-
ture, cyanosis) may advocate a congenital heart disease.
6.1.2.1 Extraoral Examination
As soon as the young patient takes his/her place in the
dental chair, the dentist proceeds to an assessment of
the facial structures, looking for anomalies that are typi-
cal for a syndrome (e.g., hypertelorism, forehead height,
etc.). The structure and the height of the lips as well
as the tone of both the labial and parietal muscles are
checked and assessed. Palpation of the neck and the
submandibular triangle follows, in checking for pres-
ence of enlarged or sensitive lymph nodes (. Figs. 6.2
and 6.3).
The examination of the temporomandibular joint
(TMJ) is also important. Palpation of the condyle head
area during mouth opening and closing is followed by
checking maximum mouth opening together with any
divergence of the mandible [1] (see also 7 Chap. 19).
6.1.2.2 Intraoral Examination
Intraoral examination aims to check the oral cavity for
any pathology and to familiarize the child with the den-
tal instruments. This is usually the moment at which the
first negative reactions of a young child may be expressed
(e.g., denying sitting in the dental chair, refusing to open
the mouth, asking not to be touched by some instru-
ment, etc.). Based on the information collected during
the medical and dental history taking, one should fol-
low appropriate behavior guidance in order to maintain
cooperation throughout the examination process and
the entire appointment.
 82 S. Arizos et al.

MEDICAL HISTORY

Name: ........................................................... Date of birth: .................................

Please answer the following questions about your child's medical history. Existing medical conditions and medications that can directly affect a dental treatment.
Your answers will help us to provide your child better care. If you do not understand a question, please ask your dentist.

Does your child have a history of: Does your child have a history of:

Congenital abnormalities……………………… Blackouts or seizures...................

H eart disease…………………………………. Epilepsy...................................

Heart murmur..................................................... Nocturnal enuresis.......................

Rheumatic fever..............................................

6 Anemia..........................................................

Bleeding disorders......................................

Is your child allergic to any of the following: Is your child:

Aspirin………………………………………… Vision impaired ……………………

Local anesthetics............................................... Hearing impaired.............................

Penicillin............................................................

Other antibiotics.................................................

Other drugs......................................................

Does your child have a history of: Has your child ever been:

Jaundice............................................................. Hospitalized.......................................

Hepatitis............................................................ Operated on under general anesthesia ..

Other liver disease............................................ Given a blood transfusion or derivatives in the last 10

years................................................
Renal disease....................................................

Diabetes............................................................

Other infections ………………………………

Has your child: Has your child recently taken any medication?

Asthma…………………………………………… If yes, please specify

Breathing difficulties ......................................... ..................................................................................

Bronchitis………………………………………… ..................................................................

Pneumonia…………………………………………

Has your child or another member of your family ever had problems after a general anesthesia?

If yes, please give details: ....................................................................................................................................

Has your child visited a pediatrician or another specialist during the last year? If so, please
specify......................................................................................................................

Is there anything else related to your child that you believe is important for a better approach and treatment by us? ................................
................................................................................................................................ better

Parent or guardian Name: .................................................................................................................................................

Parent or guardian Occupation:....................................................................................................................................
Signature: ..................................................................... Date:......................................................

..      Fig. 6.1 Example medical history form

Examination, Diagnosis, and Treatment Plan Implementation
..      Fig. 6.2 Palpation of the neck and the submandibular triangle,
in checking the presence of enlarged or sensitive lymph nodes
6.1.2.3 Soft Tissue Examination
Intraoral examination should start from the soft tissues
of the oral cavity and more specifically from the labial
and palatal mucosa, which should be checked for any
aberrations from the normal (e.g., redness, ulceration,
or vesicular lesions). As described in 7 Chap. 20, many
childhood diseases start with oral manifestations and
symptoms. The tonsils should be examined next for pos-
sible inflammation but mainly for their size and whether
this causes breathing difficulties, thus having long-term
effects on the shape of the maxilla and contributing
to occlusion problems. The palatal mucosa should be
examined followed by the lingual and the mucosa lining
the floor of the mouth. The latter is examined after ask-
ing the patient to touch with his/her tongue the palatal
surface of the maxillary incisors. This enables the den-
tist also to check the mobility of the tongue and the sub-
lingual frenum (tong-tie).
The examination is concluded with the inspection
of the buccal sulci and alveolar processes for any alter-
ation of shape and color. The examination in babies
and toddlers is usually being performed in a knee-to-
knee position (7 Fig. 5.15). In infants, the eruption
of the primary teeth is also checked for natal/neona-
tal teeth [2]. In older children, the alveolar processes
and the oral cavity in general are to be carefully exam-
ined for the presence of edema, sinus tracts (fistulae),
hyperplastic or short labial frenula, as well as gingival
recessions.
83 6
6.1.2.4 Examination of Periodontal Tissues
The examination of the periodontal tissues starts by
checking the degree of gingival inflammation and
the presence of calculus. Gingivitis is very common
throughout childhood. Gingival health and oral hygiene
are closely related and assessed by the gingival index
(GI) and plaque index (PI), respectively. The use of a
periodontal probe for examining specific teeth for gingi-
val attachment loss should start soon after the eruption
of first permanent molars [3], so that any periodontal
problems are detected early and appropriately treated
[4] (see also 7 Chap. 15). This examination is of even
greater value in medically compromised children under
immunosuppression or in children with syndromes asso-
ciated with periodontal disease (e.g., Down’s syndrome).
6.1.2.5 Examination of Hard Dental Tissues
The examination of the teeth is carried out with the aid
of a dental mirror under good lighting and after the
dental surfaces under examination are cleaned from
organic deposits and thoroughly dried (. Fig. 6.4). A
dental probe, if needed, should be used very carefully
without applying any pressure on dental enamel with
initial caries (sharp eyes, blunt probe principle) [5, 6, 7].
Implementation of other diagnostic techniques, such as
near-infrared light transillumination, to enhance clini-
cal diagnosis of caries and possibly replace dental radio-
graphs has proved useful, too [8]. Eruption timing and
sequence of the dentition is checked, especially in infants
with an incomplete primary dentition. Shape, morphol-
ogy, and location irregularities of teeth are recorded,
together with eroded or abraded dental surfaces, espe-
cially those with substantial enamel loss.
Eye Catcher
Enamel opacities are commonly observed in primary
and first permanent molars but also in any other
tooth. When yellow to brown in color, they are prone
to – and may already present at the examination
time – enamel breakdown which may lead to rapid
carious destruction; thus, their early identification
and timely treatment is a must. Special reference for
this condition (molar incisor hypomineralization) can
be found in 7 Chap. 17.
Dark pigmentation (black stain) in young ages is a find-
ing that worries parents and can be a cause for a dental
visit (. Fig. 6.5) because of aesthetic consequences [9].
The recording of dental carious lesions should be done
in detail and systematically, preferably with the aid of a
 84 S. Arizos et al.

Extraoral examination

Facial growth: ………………………………………………………………………………………

Profile: ………………………………………………………………………………………………

Soft tissues: …………………………………………………………………………………………

Lymph nodes: ………………………………………………………………………………………

TMJ: ………………………………………………………………………………………………..

6
Intraoral examination

Oral mucosa: ……………………………………………………………………………………….

Periodontal tissues: …………………………………………………………………………………

Oral hygiene : ……………………………………………………………………………………….

Occlusion type: ……………………………………………………………………………………..

Dental chart

..      Fig. 6.3 Part of an oral examination form. Its format may depend on the computer dental software

dental chart like the one shown in . Fig. 6.3. Present
teeth, lesions, and restorations are recorded per surface
(or part of a surface), as well as whether present res-
torations are acceptable. Special attention is necessary
in diagnosing and recording initial caries lesions, in
order to plan a preventive and/or conservative treatment
approach and monitor their evolution (. Fig. 6.6). All
these recordings are preferably made by an assistant
during examination of the teeth for time-saving reasons.
6.1.2.6 Examination of Dental Occlusion
The dental occlusion is a main component for the devel-
opment of functional orofacial structures as well as
aesthetics. Therefore, during dental examination, molar
relationship in the primary dentition, and first perma-
nent molar and canine relationship (by Angle classifica-
tion) in the mixed dentition, should be recorded. This,
combined with the presence of primate spaces and the
age of the patient, can provide key information about the
future development of the occlusion. Crossbites, anterior
or posterior, and possible early occlusal contacts should
always be recorded in order to consider preventing future
orthodontic needs [10, 11] (see 7 Chap. 11).
Additional important elements of a patient’s dental
record are also intraoral and extraoral photographs, as
well as impressions for the construction of plaster model
casts, if needed (or digital impressions as is increasingly
done nowadays). Taking intraoral photographs may be
useful to record and refer special conditions of hard
and soft oral tissues. They can be repeated as often as
Examination, Diagnosis, and Treatment Plan Implementation
..      Fig. 6.4 Examination of dental surfaces after they are dried with
the air syringe of the dental unit
..      Fig. 6.5 Dark stain on the primary teeth in a 20-month-old tod-
dler
required for monitoring a condition over time or for
informing patients and their parents for a specific prob-
lem and for the results of a dental intervention.
6.1.2.7 First Dental Examination and Recalls
Dental caries and its consequences are one of the most
frequent health problems of children at any age in most
societies (see 7 Chap. 12). The presence of caries in the
primary dentition is a strong predictor of its appear-
ance in the permanent dentition [12, 13]. Unfortunately,
the first visit of the child to the dentist often takes place
when a problem arises, e.g., pain of pulpal etiology, while
parents may be uninformed or negligent of proper child
oral hygiene. In such cases, young children are demanded
to be cooperative for particularly demanding dental
restorative needs. Therefore, to prevent oral diseases,
85 6
b
..      Fig. 6.6 a. Occlusal and cervical caries lesions in the primary
molars of a 7-year-old reviewed every 6 months. b After the applica-
tion of fluoride varnish at caries risk sites only
the recommendation of Pediatric Dentistry bodies for
the child’s first dental visit is to take place at eruption of
the first primary teeth or by age 12 months for educating
parents on everyday home preventive measures. Regular
dental follow-ups are also recommended, and, depend-
ing on caries risk, children need to be reviewed every few
months up to yearly [14]. In public health systems the
review intervals may exceed 1 year for some in shifting
resources in favor of children in highest caries risk [15].
6.1.3 Radiographic Examination
The use of diagnostic ionizing radiation (intraoral and
two- and three-dimensional extraoral radiographs) car-
 86 S. Arizos et al.
ries a potential stochastic biological risk (the so-called
stochastic effects of the linear non-threshold model)
[16–17]. Proper justification of the use of radiographs,
which means that the benefits outweigh the poten-
tial risks, should always be borne in mind. Children
are, after all, more susceptible to these potential risks
because their tissues have a higher mitotic activity and a
longer mitotic future (law of Bergonie and Tribondeau).
Especially the lens of the eye, the salivary glands, and
the thyroid gland deserve to be protected as much as
possible from the primary radiation beam if possible;
however, protective shielding should never cause nondi-
agnostic images [16, 18–20].
6 Guidelines on the use of radiographs in dentistry in
general are available from several professional dental
organizations (e.g. European Academy of Dental and
Maxillofacial Radiology, American Academy of Oral
and Maxillofacial Radiology, European Academy of
Paediatric Dentistry, American Academy of Pediatric
Dentistry, and the American Dental Association) [20–
22], and all have two messages in common, namely, that
the justification of exposing patients to diagnostic ion-
izing radiation should be beneficial to the patient, the
diagnosis (of caries, periodontal disease, periapical
pathology, or more bone spread pathology), and the
treatment planning and that radiographs should only
be taken after a thorough history taking and an intra-
oral exam. Moreover, the radiographic exam should
be based on a patient individual basis, meaning there
is no such thing as routine radiography (. Table 6.1).
It is justifiable to take radiographs to evaluate trauma,
healing, treatment, or development of the dentition and
the tooth bearing tissues, as long as the ALARA (as
low as reasonably achievable) principle is respected and
applied. In . Table 6.2 the decision criteria for dental
radiographic examination are summarized relative to
the information collected from the social, medical, and
dental history, as well as during the clinical examination.
It is obvious that taking good quality radiographs is
not always as easy in pediatric patients, as patients need
to be cooperative enough to comply with the technical
aspects of the radiographic procedure. As retakes imply
higher patient radiation doses, one has to assess which
radiographic techniques (e.g., occlusal versus periapi-
cal radiography) shall be used in each individual case
(. Fig. 6.7).
As for all steps in the treatment with children, one
has to explain at the individual child’s cognitive level
what is going to happen and how it will be achieved. In
order to make them understand better why they have
to put the image detector in their mouth or why they
have to stand still for a panoramic radiograph, it is use-
ful to show them a radiograph of another patient. This
will help them understand the process. Also explain
well what sounds the child will hear or just let the child
listen to the machine while it is doing a dummy run
(without the child or anyone else being irradiated)
(. Fig. 6.8).
6.1.3.1Examination with Intraoral
Radiographs
Imaging Techniques
The parallel technique is the preferred technique in
intraoral radiography as its principle generates geo-
metrically accurate images. The image detector should
be placed parallel to the teeth and the X-ray beam
should be aligned perpendicular to the image detec-
tor. The latter is best achieved with the use of proper
image detector holders which enable the primary beam
automatically to be directed perpendicular at the image
detector (e.g., Rinn® XCP or Rinn® Uni-Grip 360)
[23–26]. Alternatives to the parallel technique are the
bisecting angle technique and the occlusal and oblique
occlusal techniques. The latter two will be explained
in detail below. The bisecting angle technique requires
the primary X-ray beam to be directed perpendicularly
at the imaginary bisecting angle between the long axis
of the tooth and the long axis of the image detector.
. Figure 6.9 illustrates the technical difference between
the parallel technique and the bisecting angle technique
in the maxilla (. Fig. 6.9). This requires some practice
as elongation or foreshortening of the image is possible
if one uses the wrong angle and the primary X-ray beam
is not aimed perpendicular at the imaginary bisecting
line. In fact, occlusal and oblique occlusal radiographs
use the bisecting angle too. It is obvious that the bisect-
ing angle technique is only to be used when the paral-
lel technique is not possible, for whatever reason (e.g.,
severe gagging reflex or image detector is too large for
the child) [23]. . Fig. 6.10 shows examples of good and
bad images with both techniques. It is obvious that the
age of the patient and the cooperation play an impor-
tant part in the outcome of the image quality and hence
often the diagnostic yield.
Image Detectors
Image detectors can be analog film, photostimulable
phosphor storage plates (PSPP), or solid state sensors
(. Fig. 6.11). The latter are either charged coupled
devices (CCD) or complementary metal oxide semicon-
ductors (CMOS). These are, compared to the other two
image detectors, bulkier and therefore not always easily
tolerated by children. Both PSPP and solid state sensors
are digital image detectors. The PSPP resemble analog
film physically and are therefore often easier to use in
children. However, the PSPP are vulnerable to damaging
due to biting, bending, or sharp objects scratching the
surface (. Fig. 6.12), whereas the solid state sensors are
not. Artifacts on the PSPP will be reproduced every time
Examination, Diagnosis, and Treatment Plan Implementation
87 6

..      Table 6.1 Guidelines for prescribing dental radiographs

Guidelines for Prescribing Dental Radiographs

(based on and interpreted from Guidelines on prescribing dental radiographs for infants, children, adolescents, and persons with special
health care needs. Ad Hoc Committee on Pedodontic Radiology. American Academy of Pediatric Dentistry, reference manual, 2017/18)
(The selection of patients for dental radiograph examination. American Dental Association, US Food and Drug Administration.
7 www.­ada.­org)
Type of encounter Child with only a primary Child with a Adolescent with Adult, dentate or Adult,
dentition mixed dentition permanent partially edentulous completely
dentition edentulous

New patient1 being An “individualized” radio- An “individual- An “individualized” radiographic An

evaluated for dental graphic exam: ized” radio- exam: “individual-
disease and develop- Selected periapical or occlusal graphic exam: Posterior bitewings with a panoramic ized”
ment radiographs supplemented or Posterior radiograph or posterior bitewings radio-
not with posterior bitewings. bitewings with a with selected periapical radiographs. graphic
Bitewings are only indicated if panoramic Full-mouth periapical radiographs exam, based
proximal surfaces cannot be radiograph or are only indicated if the patient has on the
assessed without radiographic posterior clinical signs of generalized dental clinical
examination. Patients without bitewings with disease or a history of extensive signs and
clinical evidence of disease may selected dental treatment symptoms
be exempted from radiographic periapical
exposure at this time radiographs

Recall patient1 with no Posterior bitewing radiographs at 12- to 24-month Posterior Posterior bitewing Not
clinical caries and no intervals if proximal surfaces cannot be clinically bitewing radiographs at applicable
increased risk for assessed radiographs at 24- to 36-month
caries2 18- to 36-month intervals
intervals
Recall patient1 with Posterior bitewing radiographs at 6- to 12-month intervals if proximal Posterior bitewing Not
clinical caries or at surfaces cannot be clinically assessed radiographs at applicable
increased risk for 6- to 18-month
caries2 intervals
Recall patient1 with An “individualized” radiographic exam, which may consist of, but is not limited to, selected Not
periodontal disease periapical radiographs and bitewing radiographs, based on the clinician’s judgment applicable
Patient for monitoring Clinical and professional judgment will determine the need for Usually not indicated
of growth and radiographic examination and which type of radiographic examination
development of the is preferable
dentomaxillofacial
complex
Patient with other Clinical and professional judgment will determine the need for radiographic examination and which type of
circumstances including, radiographic examination is preferable
but not limited to,
proposed or existing
implants, pathology,
restorative or endodon-
tic needs, treated
periodontal disease, and
caries remineralization

1Clinical situations for which radiographs may be indicated include, but are not limited to, previous periodontal or endodontic treat-
ment, history of pain or trauma, familial history of dental anomalies, postoperative evaluation of healing (incl. Implant placement),
monitoring of remineralization, presence of dental implants, clinical evidence of periodontal disease, large or deep restorations, clini-
cally deep caries lesions, impacted and malpositioned teeth, presence of a sinus tract (fistula), clinically suspected sinus pathology,
growth abnormalities, known or suspected systemic disease with oro-dental implications, positive neurological findings in head and
neck, evidence of foreign objects in the dentomaxillofacial complex, pain, dysfunction or trauma to the temporomandibular joint,
facial asymmetry, abutment teeth for partial removable or fixed prosthesis, unexplained bleeding, dental sensitivity, swelling, morphol-
ogy, mobility, eruption, exfoliation and absence of teeth, and extensive dental erosion
2Factors increasing the risk for caries may include, but are not limited to, high level of caries experience or demineralizations, recurrent

caries, high titers of cariogenic bacteria, existing restoration(s) of poor quality, poor oral hygiene, inadequate exposure to fluoride,
prolonged breastfeeding or bottle-­feeding (especially nocturnal), frequent high sucrose content in diet, poor family dental health,
enamel defects, disability, hyposalivation, genetic abnormality affecting the teeth, many multisurface restorations, history of radio-
therapy and/or chemotherapy, eating disorder, substance abuse (alcohol, drugs), and irregular dental care
 88 S. Arizos et al.

..      Table 6.2 Criteria for dental radiographic examination in a

children [15]

Based on objective findings and Based on dental and

symptoms medical history

Caries History of pain

Pulp/periapical pathology Previous dental trauma
Traumatic injuries Postoperative
Eruption problems assessment
Developmental disorders Family history of
Internal discoloration of teeth dental anomalies
Orthodontic treatment planning Syndrome (e.g.,
Signs of edema ectodermal dysplasia)
Unexplained tooth mobility Systemic disease (e.g.,
6 Unexplained bleeding sickle cell anemia)
Deep periodontal pocket
Fistula formation
Unexplained dental sensitivity
Unusual alteration of space or tooth
movement
Lack of response to conventional
dental treatment
Unusual dental morphology
Assessment of developmental
disorders
Occlusal relationship changes

..      Fig. 6.7 Occlusal instead of periapical radiograph on a 3-year-­

old uncooperative child suffering from dental abscess due to dental
trauma

..      Fig. 6.8 a Presenting the radiographic plate to a young child with

the plate is exposed to X-rays. Therefore, handle them
with care and do never bend them. The PSPP require a
laser processor to acquire the image, while a solid state
sensor doesn’t. Many dentists will prefer the solid state
sensors because the image is acquired instantly; how-
ever, as mentioned before, one should remember they
are more bulky than the plates.
The solid state sensors come in a limited number of
sizes, whereas the PSPP come in the same sizes as analog
film (. Fig. 6.13). That makes the PSPP more suitable
learning difficulties, by using the “tell show do” technique in the
mouth of his favorite animal toy b. Acceptance of the radiographic
plate intraorally
for occlusal and oblique occlusal radiographs. When it
comes to diagnostic yield, both image detectors appear
to score equally [27–29].
Radiation doses associated with the fastest analog
film speed (E) are the same as for the digital image detec-
tors. In other words, a dentist using E-speed analog film
Examination, Diagnosis, and Treatment Plan Implementation
89 6
..      Fig. 6.9 Illustration of the
parallel technique (top) and the
bisecting angle technique
(bottom): the X-ray beam is
directed perpendicular at the
image detector, which is placed
parallel to the teeth, and the
X-ray beam is directed perpen-
dicular at the imaginary
bisecting angle (red line) between
the long axis of the tooth (green
line) and the long axis of the
image detector (yellow line)

does not cause higher radiation doses than a colleague
who uses digital image detectors, as the exposure times,
which are needed to acquire good quality diagnostic
images, are the same.
Image Detector Holders
Image detector holders provide good positioning of
the image detector inside the patient’s mouth and at the
same time enable accurate aiming of the X-ray source
to ensure the parallel technique is respected. One of the
most used image detector holders are Rinn® XCP and
Hawe Neos® (. Fig. 6.14). They also provide protec-
tion of the image detector and its stability inside the
patient’s mouth. The size and shape and model of the
image detector holders have to be paired with the type
of image detector and may even require a brand spe-
cific holder (e.g., Rinn XCP-Ora®). If paper tabs (e.g.,
Rinn ® bitewing loops) or foam tabs (e.g., Disposable
XCP® biteblock) are used to position the phosphor
storage plate or the solid state sensor in the patient’s
mouth, there is no extraoral aid to help one aim per-
pendicular at the image detector. It is obvious that
overlap between approximal surfaces is more common
if one does use these. When using the Snap-A-Ray®
Xtra Film and phosphor plate holder, or the Eezee-
Grip®, one has the same issues. For the solid state sen-
sors, the Snap-A-Ray ® DS exists, which is adapted to
hold the solid state sensor and which can be equipped
with a metal rod and a ring to aid extraoral X-ray beam
aiming (. Fig. 6.15).
 90 S. Arizos et al.

..      Fig. 6.10 At the top two

well-taken images, with good
geometry, and at the bottom,
two images with ill geometry and
hence less or no diagnostic yield

..      Fig. 6.11 Digital image detectors for intraoral radiography: example of a photostimulable phosphor storage plate (left) and example of
a solid state sensor (right)

Collimation and Protective Aprons or Shields
Collimation of the X-ray beam is important to
reduce the radiation dose and to reduce the scat-
tered radiation. When using a rectangular collimator
(. Fig. 6.16), one will reduce the patient’s radiation
dose with at least 50%. The use of a good image detec-
tor holder, which allows accurate X-ray beam align-
ment, is essential to obtain good quality radiographs.
It is not true that the use of a rectangular versus a
circular collimator causes more retakes [30–33]. In the
case of children, it is our duty to keep the radiation
dose as low as possible; hence, one should promote
and support the use of rectangular collimation in
pediatric dentistry.
Examination, Diagnosis, and Treatment Plan Implementation
..      Fig. 6.12 Three examples of images made with a damaged photostimulable phosphor storage plate and an image of a damaged plate
..      Fig. 6.13 PSPP come in the same sizes as analog film
A radiation-protective apron or thyroid gland shield
is meant to protect the tissues, which do not need to be
irradiated, from the primary radiation beam. Therefore,
they should be worn or held appropriately to protect
the thyroid gland. It is obvious that this needs to be
explained to the child in an age-appropriate fashion.
The use of a thyroid gland shield can be distracting for
the child and help in stressful situations where the child
has trouble gagging when the image detector is placed in
the mouth (. Fig. 6.17).
91 6
Bitewing Radiography
Bitewing radiographs provide a unilateral image of the
crowns and the cervical thirds of the posterior teeth in
both maxilla and mandible. They are in the first place
taken to assess the interproximal surfaces of the teeth,
which clinically are not visible if the contacts are closed.
That implies that if there are open contacts, bitewings
should not be taken for this reason. Bitewing radio-
graphs can also be used to assess interproximal bone
levels. If taken correctly, there should be no overlap
 92 S. Arizos et al.

..      Fig. 6.14 Examples of

image detector holders: at the
top the Rinn® XCP-DS®
holders for solid state sensors
and in the middle left the
Rinn® Flip-Ray® BW and on
the right the Rinn® Flip-Ray®
PA for photostimulable
phosphor plates and at the
bottom the Hawe Neos®
Kwik-Bite holder for analogue
film and photostimulable
phosphor plates

..      Fig. 6.15 Clockwise the

Snap-A-Ray® Film Holder, the
Eezee-­Grip® Digital Sensor
Holder, the Snap-A-Ray®, the
Snap-A-Ray® DS and the
Snap-A-Ray® Xtra Film, and
phosphor plate holder
Examination, Diagnosis, and Treatment Plan Implementation
..      Fig. 6.16 Rectangular collimators for intraoral radiography reduce the patient’s radiation dose by 50%
..      Fig. 6.17 Preparation for a radiographic checkup with proper
radiation protection
between the interproximal surfaces and the interdental
crest should also be well visible in the image. The com-
bination of clinical examination of air-dried clean teeth
and radiographs is the best way to diagnose interproxi-
mal and occlusal caries. In bitewing radiographs, besides
the crowns of the teeth, the interradicular space and the
lamina dura should also be included and assessed, as
this is where signs of pulpal inflammation expansion
can be found. In the primary dentition with closed inter-
proximal contacts, one will need only one bitewing per
side (usually size 0 of PSPP), which will enable one to
assess the distal surface of the primary canines to the
distal surface of the second primary molars.
In the mixed dentition one also needs only one bite-
wing radiograph per side (usually size 1 or 2 of PSPP).
These should include the distal surface of the canine to
the distal surface of the first permanent molar.
Once the second permanent molars have erupted,
two bitewing radiographs (usually size 2 of PSPP) may
be needed per side to include the distal surface of the
canine to the distal surface of the second permanent
molar. Later on, when also third molars have erupted,
two bitewing radiographs per side will be necessary to
cover all interproximal surfaces starting with the distal
surface of the permanent canine (. Fig. 6.18).
93 6
Modern panoramic machines can also take bitewing
radiographs. These extraoral bitewings require good
positioning in the panoramic machine. The advantage
of this is that patients do not have to hold the image
receptor in their mouth. These bitewing radiographs
show more than traditional bitewings, as can be seen in
(. Fig. 6.19). Literature has shown that the diagnostic
yield is very similar to intraoral bitewings [34–36]. If
crowding or ectopic eruption of teeth is present, over-
lapping contacts cannot or hardly be avoided, irrespec-
tive if the bitewings were intraoral or extraoral acquired
ones. The latter stresses even more the importance of a
good and thorough clinical examination.
It has been found that radiographic examination
aids in diagnosing up to eight times more proximal
caries lesions when compared to the clinical examina-
tion alone [37]. Clinical examination leads to the diag-
nosis of less than 50% of the existing proximal lesions,
while radiographic examination allows the diagnosis of
more than 90% of these lesions [38]. When it comes to
occlusal lesions, in an in vitro study of first permanent
and second primary molars, it was shown that radio-
graphic examination leads to higher rates of diagnosis
than just the clinical one [39]. This means that if clini-
cal ­examination is not combined with radiographs, an
important number of caries lesions remains undetected.
Since contemporary dentistry aims at the conservative
treatment of caries lesions, the role of radiographic
examination is particularly important in cases where ini-
tial proximal lesions or dentinal lesions situated below
clinically intact enamel can easily be diagnosed and
accordingly treated.
Each of the Academies of Paediatric Dentistry,
European (EAPD) [22] and American (AAPD) [20],
has issued their own protocol of radiological exami-
nation for the diagnosis of caries lesions in children
and adolescents. Both protocols recommend bitewing
radiographs, but they differ in the recommendations for
the radiological examination of new patients. Routine
radiological examination is not recommended for new
patients except for those who are at high caries risk and
only when proximal dental surfaces cannot be visually
 94 S. Arizos et al.

..      Fig. 6.18 Examples of

bitewing radiographs in the
primary dentition, the mixed
dentition, and the permanent
dentition

..      Fig. 6.19 Examples of extraoral bitewing radiographs taken with Planmeca® panoramic machines. (Courtesy of Mr. James Hughes,
Planmeca®, USA)
Examination, Diagnosis, and Treatment Plan Implementation
..      Table 6.3 Intervals of bitewing radiographic examination
reviews according to the protocol of the European Academy
of Paediatric Dentistry (EAPD) [22]
Age Caries risk
Low High
5-year-olds 36 months
8- or 9-year-olds 36 to 48 months
12- to 16-year-olds 24 months
Over 16 years old 36 months
inspected (AAPD), while all the above are proposed only
for the ages of 5, 8–9, 12–14, and 16 years old (EAPD).
This preference of the European Academy of Paediatric
Dentistry was based on findings of epidemiological
surveys that have demonstrated that, even in popula-
tions with low caries index, more than 1/3 of the chil-
dren in the abovementioned age groups had proximal
caries lesions that were missed during clinical examina-
tion [40–42]. Both Academies recommend similar time
95 6
intervals between radiographic examination reviews for
low caries risk patients (up to one proximal caries lesion
without any other indication of high caries risk) and
high caries risk patients (with proximal caries lesion in
enamel and/or in dentin). The corresponding protocol
of EAPD is shown in . Table 6.3.
12 months
12 months
Periapical Radiography
A periapical radiograph should provide a projection of
12 months
at least 2 mm beyond the tooth’s apex to show the tissues
12 months around the tooth (cancellous bone, lamina dura, and
periodontal ligament space). The best image will also be
made with the parallel technique with the use of proper
image detector holders which allow adequate alignment
of the X-ray beam with the image detector (. Fig. 6.14).
It is indicated for the diagnosis and assessment of any
pulpal or periapical pathology, dental anatomy, root
resorption, tooth exfoliation, dental trauma, eruption,
and periodontal problems and, in general, for the diag-
nosis of problems associated with a single tooth or a
small area of the oral cavity (. Fig. 6.20). Periapical
radiographs taken from two different horizontal or ver-

..      Fig. 6.20 Examples of periapical radiographs in children under different conditions

 96 S. Arizos et al.
tical angles can be used to identify the position of teeth
in three dimensions. This is called the parallax technique
or the buccal object rule. The first radiograph is taken
perpendicular at the tooth of interest. Then a second
radiograph is taken with the image detector in the same
position, but the X-ray source coming either more from
the mesial or more from the distal. If the object of inter-
est in the projection moved in the same direction as the
one the X-ray source was moved in, then the object is
located more lingual or palatal. The opposite holds for
objects located on the buccal. One can remember the
following mnemonic: “SLOB” which stands for “same
lingual opposite buccal.” An easy to remember trick is
6
a b
..      Fig. 6.21 Illustration of the parallax technique (SLOB rule, same
lingual opposite buccal). a To identify the exact location of the
impacted maxillary canine, two periapical radiographs are taken
from a different horizontal angle. The projection of the canine moved
in the same direction in which the X-ray machine was moved, which
implies the canine is positioned palatally. In this case the canine is. b
To identify the position of the supernumerary tooth that overlaps in
its projection with the left central maxillary incisor, one takes two
periapical radiographs from two different horizontal angles. The
to close one eye and hold your index and middle fin-
ger up in front of you so you can see only one finger.
Then move your head to the left or the right. The finger
that came in your field of view in which you turned your
head is the middle finger, which is further away than
your index finger. Your index finger will always move in
the opposite direction in your field of view. Solid state
sensors are an advantage when using the parallax tech-
nique as one can leave the image detector in the patient’s
mouth and only adjust the X-ray beam’s angle, which
is impossible with PSPP (. Fig. 6.21). The plate sizes
are the same with the ones used in bitewing radiographs
(. Figs. 6.22 and 6.23).
supernumerary tooth appears to be moving in the opposite direction
than in which the X-ray machine was moved; hence, the supernumer-
ary tooth is positioned labial to the central incisor. The dentifrice
tubes below explain the principle: the image in the middle shows only
one green labeled tube, but if one moves to the left or to the right
(change in horizontal angle), the red labeled tube is revealed. The red
labeled tube moved in the same direction as your head moved in. The
green labeled tube at the front moved in the opposite direction in
your field of view (SLOB or same lingual, opposite buccal)
Examination, Diagnosis, and Treatment Plan Implementation
a b
..      Fig. 6.22 a Periapical radiograph investigating the infra-­occluded second primary molar with a conventional size 0 plate. b Periapical
radiograph with a size 0 digital sensor. Periapical lesion of first primary molar and its surrounding tissues are well displayed
..      Fig. 6.23 a Periapical
radiograph with a size 2 plate,
depicting the two maxillary
central incisors after dental
trauma. b Periapical radiograph
with a size 1 plate, monitoring
previous intermediate pulp
capping on a maxillary first
permanent molar, but inad-
equately covering the apical area
Occlusal (Standard and Oblique) Radiography
The standard occlusal radiograph is ideal to image the
anterior mandibular or maxillary teeth. For the man-
dible, the image detector is placed on the occlusal plane
with the child sitting upright (occlusal plane is now par-
allel to the floor) and the X-ray beam aimed 45 degrees
upward through the tip of the chin (. Fig. 6.24). For
the maxilla, the image detector is also placed on the
occlusal plane with the child sitting upright, but the
X-ray beam aiming 65 degrees downward through the
bridge of the nose (. Fig. 6.25). These views provide a
periapical view of all four incisors and sometimes also
of the adjacent canines. In . Fig. 6.26 it is shown how
one can protect phosphor plates during occlusal radiog-
raphy. The use of two wooden tongue depressors taped
around the plate is simple and cheap. In young children,
a size 2 plate can be used with the long axis transverse in
the patient’s mouth. If two wooden tongue depressors
are taped around the plate, and the child is sitting on the
parent’s lap, the parent can hold the wooden spatulas to
stabilize the plate and the patient, and it provides also
the radiographer with information about the tilting of
the occlusal plane. The parent in this case should also
wear a protective apron. It is an easy technique in case
of dental trauma, a mesiodens, or suspected periapical
pathology when the above-described periapical radiog-
97 6
a
b
raphy fails or is impossible (. Figs. 6.24 and 6.25). In
orthodontia the standard upper occlusal radiograph is
often used to follow up with rapid maxillary expansion.
In cases where the aim is the diagnosis of pathologic
conditions located in the anterior region of the jaws, an
occlusal radiograph of the mandible or the maxilla can
be used, as an alternative or supplement to a periapical
one (. Fig. 6.27). It is clear that the use of solid state
sensors is a little more complicated in occlusal radi-
ography, but not impossible, especially in the primary
dentition.
Oblique occlusal radiographs can be used to image
primary molars, premolars, and permanent molars in
case a periapical radiograph is impossible for the child
to handle. For the mandible, the image detector, prefer-
ably a phosphor storage plate, is placed on the occlusal
plane with the child sitting upright so the occlusal plane
is parallel to the floor. The child is then asked to turn
the head in the opposite direction and the X-ray beam
is aimed at a 30 degree angle upward through the apices
of the teeth one wishes to visualize. The reason for the
head turning to the opposite side is because otherwise
the shoulders are in the way of the X-ray machine.
For the maxilla, the child is sitting upright and the
image detector is placed on the occlusal plane, which is
to be held parallel to the floor. The X-ray beam is then
 98 S. Arizos et al.
a
e f
..      Fig. 6.24 Standard occlusal radiograph of the maxilla and the
mandible. a Illustration of how the X-ray machine has to be posi-
tioned for both the upper standard occlusal (65 degree downward
angle) as well as the 45 degree mandibular occlusal radiograph. b is
an illustration of a standard upper occlusal radiograph of the entire
maxillary arch. c is an illustration of the technique used to image
only the anterior teeth. d shows that the technique can also be used
with smaller size 2 films as well. e is an illustration of the technique
to identify supernumerary and malformed teeth (solid state sensor
size 2 was used here), while in f it is used to check the tooth apices
b c
d
g
after dental trauma. h shows the application of this technique with a
size 2 solid state sensor used with the long axis transverse in the
patient’s mouth to diagnose the tooth apices in the case of an early
childhood caries. h is an illustration of a 45 degree angle, while i is an
true occlusal view of the mandible with the X-ray source placed per-
pendicular at the occlusal plane, which is a view used to investigate
the contours of the mandible and the floor of the mouth. j is an
illustration of a size 2 solid state sensor used with its widest dimen-
sions transverse in the mouth to investigate the eruption pattern of
the mandibular incisors
Examination, Diagnosis, and Treatment Plan Implementation
h i
..      Fig. 6.24 (continued)
a b
d e
..      Fig. 6.25 Examples of oblique occlusal radiographs taken on
patients with special needs. a is a view of the third quadrant, show-
ing osteitis around the roots of the severely decayed first primary
molar. b shows severe root resorption of the right lateral maxillary
incisor. c is a view of the first quadrant, showing the erupting right
aimed 60 to 65 degrees downward through the apices of
the teeth one wishes to visualize. . Figure 6.25 shows
examples of this technique, which can be used as an
alternative in case intraoral parallel technique is not fea-
sible in a patient. In young children (primary dentition),
only the size 2 radiographic plate is, in most situations,
99 6
j
c
lateral maxillary incisor. d is a view of the first quadrant, showing
the missing first primary molar and the developing first right premo-
lar. Also notice the bite and bending marks on this phosphor plate. e
is also of the first quadrant and shows the compromised eruption of
the second premolar
well tolerated. This radiograph replaces the periapical
ones of anterior teeth in young patients. In older chil-
dren, always according to the size of the mouth and
its opening, the size 4 radiographic plate (57x76 mm),
which is also available as a SPP plate, is usually used
(. Fig. 6.13). The use of a size 4 plate, if possible, is for-
 100 S. Arizos et al.
..      Fig. 6.26 Simple and economical trick to protect your photo-
stimulable phosphor plates from being bitten on or from being bent.
The use of tape and wooden tongue depressors can help prevent bite
6 marks and bending of the plates when used for occlusal and oblique
occlusal radiography
a b
c d
..      Fig. 6.27 Occlusal radiographs. a. Mandibular radiograph with
a size 4 plate, investigating delayed eruption of the permanent
canine. b. Maxillary radiograph for the examination of the anterior
region of the primary dentition, with a size 2 plate. c. Maxillary
giving if one has not exactly aligned the X-ray machine
and the image is elongated.
6.1.3.2 Examination with Extraoral
Radiographs
The most common technique used in extraoral radio-
graphic examination in children is a panoramic radio-
graph (orthopantomograph or dental panoramic
tomograph). The panoramic radiograph should be
collimated to the child’s size (use the machine in child
modus) in order not to over-radiate the patient. If the
patient was correctly positioned in the machine, the
panoramic radiograph provides a broad and complete
two-­dimensional overview of the maxillofacial complex.
However, one should always bear in mind that ghost
radiograph for the delayed eruption of left permanent incisor with a
size 2 plate. d. Maxillary radiograph investigating the ossification of
the median maxillary suture after rapid maxillary expansion (con-
ventional size 4 plate)
Examination, Diagnosis, and Treatment Plan Implementation
..      Fig. 6.28 Panoramic
radiograph of a child in the
mixed dentition. The image at
the top shows a well-collimated
panoramic radiograph of a
10-year-old patient. For the
image at the bottom, the adult
settings were used on a
4-year-old patient, and as such it
is not well collimated and shows
far too much of the orbits
images and distortions, inherent to the technique, are
always present (. Fig. 6.28). Especially in orthodontics
lateral and frontal cephalometric radiographs are com-
mon imaging modalities. Correct patient positioning is
also crucial to retain adequate diagnostic yield. Cone
beam computed tomography (CBCT) is an imaging
modality that provides three-dimensional images of the
hard tissues. CBCT comes in different field of view sizes,
but the field of view should always be as close as pos-
sible to the area of interest. The latter is important for
patient dose limitations. It needs to be emphasized that
patients must be able to understand the instructions and
must be able to stand or sit still long enough to obtain
high-quality images. Another extraoral radiographic
technique, the oblique lateral radiograph, requires large-­
sized PSPP in rigid cassettes and allows one to take
two-­dimensional images of the jaws if patients cannot
cope with intraoral radiography requirements or with
relatively long exposures required for panoramic radi-
ography. The latter technique will be described below.
Panoramic Radiography
Paramount in panoramic radiography is the position-
ing of the patient. Since there is no standardization in
panoramic radiography machines, the manufacturer’s
guidelines are to be followed accurately. Instructions dif-
fer between manufacturers. For children it is important
to use the child modus of the machine in order to reduce
101 6
the radiation dose but also to accommodate the focal
trough. There are panoramic machines that can scan
faster than the traditional 18 seconds (e.g., Morita®
Veraviewepocs). These fast scans cause a lesser patient
radiation dose (dose and time are linearly related). A
faster scan can also be an advantage if the patient can-
not stand still for 18 seconds.
A panoramic radiograph is a valuable tool for the
diagnosis of pathologic conditions or developmental
disorders in the primary, mixed, and permanent denti-
tion. For instance, several conditions such as impacted
teeth, ectopic eruption of teeth, mandibular fractures
(especially condylar), and cysts and tumors of the jaws
can easily be detected. However, panoramic radio-
graphs are not very helpful in the diagnosis of caries
lesions [43–45]. Guidelines issued by the EAPD and
the AAPD regarding the use of panoramic radiographs
in children and adolescents vary only in phrasing.
According to EAPD guidelines, panoramic radiographs
should be taken only when findings, during the clinical
or the intraoral radiographic examination, cannot be
explained when compared with normal oral anatomic
structures. They should not be used in asymptom-
atic children and adolescents [22]. On the other hand,
AAPD guidelines propose the use of panoramic radio-
graphs according to the specific needs of every patient
[20]. It all comes down to justification of the exposure
on a patient individual basis (. Fig. 6.29).
 102 S. Arizos et al.
b c
..      Fig. 6.29 a. Panoramic radiograph reveals two supernumeraries
obstructing eruption of central incisors. b, c. Two periapical radio-
graphs taken with a different angulation, where supernumeraries
Cephalometric Radiography
The use and interpretation of cephalometric radiograph
is described in 7 Chap. 9, as it deals mainly with the
development of orofacial structures and orthodontic
examination and assessment.
Cone Beam Computed Tomography (CBCT)
Medical CT (computed tomography) and CBCT are not
the same, although often both are called CT. Medical CT
uses a fan-shaped beam that is spiraled around the patient
several times with the patient in supine position, whereas
CBCT uses a cone-shaped beam that revolves around
an upright sitting or standing patient only once. Both
imaging modalities produce three-dimensional images.
Medical CT, however, is calibrated and uses so-­ called
Hounsfield units to identify tissue, air, and fluids in the
scans, which makes this imaging modality fit for hard and
soft tissue diagnosis, whereas CBCT can only be used for
teeth and bone diagnostic purposes. Unfortunately, CBCT
appear moving in the same direction with the X-ray machine; there-
fore, they lie behind (palatally) the unerupted central incisors
manufacturers have the liberty of choosing field of view,
exposure parameters, and resolution, and as such there is
no standard. For pediatric dentistry the applications for
CBCT are confined to dento-alveolar trauma, mesiodens,
developmental anomalies in the craniofacial complex, and
bony pathology, and therefore usually small field of view
scans are required only (. Figs. 6.30 and 6.31) [46, 47].
It is clear that for CBCT patients also need to be able to
understand what will happen and that they have to be able
to stay still long enough, because motion artifacts are det-
rimental for image quality and diagnostic yield [48–51].
Although guidelines are clear that CBCT should
not be used for caries detection, in 2014 Ertas et al.
published that for deep occlusal caries lesions CBCT
scored better than other radiographic techniques [52].
The exposure of the young and developing patient to
the radiation required for a CBCT, which is considerably
higher than in other conventional techniques, justifies its
use only in well-considered individual cases.
Examination, Diagnosis, and Treatment Plan Implementation
..      Fig. 6.30 Example of a small field of view (diameter 5 cm and
height 5.5 cm) cone beam CT image taken on a child for two super-
numerary teeth positioned palatal of the two central maxillary inci-
Oblique Lateral Radiography
The oblique lateral radiograph is a great alternative
in children and patients with special needs who can-
not cope with either panoramic or intraoral imaging.
The technique requires a cassette system (analog film
or phosphor storage plate in a rigid cassette), being
held against the cheek and nose of the patient, while
the X-ray beam is directed perpendicular at the cas-
sette from behind the mandibular body. The patient
needs to turn the head in the direction of the cassette
in order to create space between the cervical spine
and the contralateral body of the mandible. The so-
called radiographic keyhole is then created and allows
for an unobstructed view of the body of the man-
dible. . Figure 6.32 demonstrates the positioning of
the patient, the image receptor, and the tube head. It
also shows an example of such an image made in an
11-year-old boy with autistic spectrum disorder. This
technique is obviously an alternative and not a stan-
dard of care for every patient. Patients with special
needs and small children can benefit from this tech-
nique if a radiographic image is required.
103 6
sors. Clockwise the images represent the axial (caudal), the
parasagittal view (profile), the three-dimensional reconstruction of
the volume, and the coronal view (frontal)
6.2 I mplementing a Total Care
Treatment Plan
Following the completion of the examination process,
current needs and risk of future needs formulate a com-
prehensive treatment plan. This may consist of restorative
procedures possibly including tooth extraction(s) and
preventive or interceptive orthodontics or be confined to
purely preventive work. In any case, the treatment plan
should be governed by a total care philosophy, i.e.:
1. Be oriented to the etiological treatment of oral dis-
eases (dental caries, periodontal disease, etc.), in con-
junction with a preventive program that includes:
55 Home measures: proper oral hygiene, with relative
to risks of fluoride use, chlorhexidine, or other
chemical regimens, combined with dietary advice.
55 Professionally applied measures: dental prophy-
laxis, fissure sealants, fluoride application (e.g.,
varnish or silver diamine fluoride).
55 Collaborative professional with parent and child
tasks: reinforcing their active involvement and
compliance to the follow-up program.
 104 S. Arizos et al.

..      Fig. 6.31 Example of a cone beam CT image taken at the maxil- crown complicated fracture in a maxillary left permanent incisor
lary anterior teeth on a 10-year-old child for the diagnosis of a root-­

a b

..      Fig. 6.32 a, b. Oblique lateral radiography explained in pictures tic spectrum disorder, who appeared to have an ameloblastic fibroma
(X-ray beam parallel to the occlusal plane and oblique to the image coronally to the mandibular right first permanent molar, displacing
detector, which is held against the nose and cheek). c. An example of both molars and preventing their eruption
the resulting radiographic image of an 11-year-old boy with an autis-
Examination, Diagnosis, and Treatment Plan Implementation
105 6
2. Be in the best interest of the patient’s restorative
needs:
55 It should aim to restoring teeth with biocompat-
ible/bioactive materials.
55 Primary tooth restorations should be aimed to
last until normal tooth exfoliation.
3. Ensure proper growth and development of the occlu-
sion:
55 Monitoring and preventing occlusal discrepancies.
55 Coordinating with other specialties – e.g., ortho-
dontics, surgery, speech therapists, etc.
4. Appreciate parameters, such as:
55 The patient’s maturity or possible disabilities.
55 The family and social background for feedback
and compliance with treatment plan require-
ments. ..      Fig. 6.33 Radiographic findings are demonstrated to parents
avoiding dental terminology in an effort that they appreciate their
child’s dental needs
The treatment plan is recorded in the patient’s chart in
a coded way that saves time and facilitates future refer-
ence. The next step is to obtain approval (consent) from standable language, avoiding the excessive use of dental
the patient’s parents or guardians. terminology, and putting the emphasis on the long-term
benefits of child’s oral health and aesthetics rather than
the financial aspects of treatment. New future needs
6.2.1  resentation of the Treatment Plan
P may be connected with compliance to home care mea-
to Parents sures while own responsibilities for restorative mishaps
should be undertaken. The current situation should
A comprehensive treatment plan that includes priorities, not be dramatized by over-criticizing the parents for it.
alternatives, and consequences if no treatment is per- Explanations for the causes and positive attitudes for
formed should be presented to parents, based on exist- maintaining oral health lead to better informed and
ing guidelines. An honest approach helps establishing a active parents and children [53]. Motivational interview-
good relationship for parent and child. Demonstrating ing techniques described in 7 Chap. 4 are also useful in
the patient’s needs using visual educational facili- encouraging parents to actively support their children.
tates explanations to parents and increases acceptance
chances. Examples of such means are demonstrations
in-mouth, by intraoral camera, on a model of a child’s Eye Catcher
dentition, as well as by pointing any findings on intra-
There may be times that a thorough presentation is
oral, panoramic, or other radiographs (. Fig. 6.33).
not met with acceptance by parents. Not every parent
Parents are understandably not fully aware of the
is prepared or open to recognize the benefits of com-
extent of their children’s dental needs, which is why their
prehensive dental treatment. Some of them may (1)
detailed presentation may often surprise them. The den-
not appreciate the value of dental treatment, (2) not
tist’s sincere interest will help them to accept their role
comply with the preventive program, (3) miss their
and provide consent. A successful presentation should
appointments, or (4) fail their financial engagements.
provide accurate information about:
One may have to make some treatment plan compro-
mises in these cases, having always in mind the best
55 Their child’s oral health status including occlusion.
interest of the child.
55 The necessary restorative procedures.
55 The number of treatment visits required.
55 The individualized home care needed for successful
long-term results. 6.2.2  actors Affecting the Progress
F
55 The fees for services provided including procedures of the Treatment Plan
for insurance bodies.
Since the participation of parents is necessary for a treat-
Besides the content however, an effective presenta- ment plan to succeed, they should be properly informed
tion of a treatment plan requires communication skills. and prepared in order to play a supportive role and thus
This means inspiring confidence and showing pleasure avoid unwanted interferences in crucial points of the
for cooperation, while explaining it in a fully under- dentist-child communication. The preparation should
 106 S. Arizos et al.

be brief, not getting into unnecessary details and at the Ideally, oral hygiene is performed to the child and
same time encouraging the child to express questions demonstrated to the parent/guardian during the first visit.
directly to the dentist. For instance, if local anesthesia This except for the educational value has the benefit of
is about to be used in a following visit, questions by examining the child’s coping ability for future treatment
stressed parents should be answered beforehand, allow- and making a first positive contact (. Table 6.4). An
ing the dentist to focus on the child. Description of a exception would be an emergency treatment. The same
procedure that is about to begin to parents may stress a holds true for radiological examination. Its omission may
child waiting for the dentist to start working in his/her result in an incomplete diagnosis and, hence, incomplete
mouth. treatment plan (. Fig. 6.35), while accepting radio-
In order to ensure compliance with the preventive graphic examination is a good indicator of the child’s
program and acceptance of the applied behavior man- ability and readiness to cope with restorative treatment.
agement techniques, the dentist should establish a certain Another factor may be the existing dental health-­care
relationship with the child and the parent or guardian: system. In different countries, and even within the same
6 a so-called treatment alliance [53, 54], which is based on country, provision of dental health care for its young
mutual trust. The proportion of responsibility between
the child and the parent regarding the compliance with
the preventive program changes as the child grows. The ..      Table 6.4 The first two visits of a treatment plan that
responsibility for oral hygiene is often left entirely to the includes restorative treatment
child, even from a very young age (. Fig. 6.34), in a
frame of independency that pleases the parents, despite Prevention Acclimatization
that, as dental professionals see all the time, it is diffi-
First visit
cult for a 7-year-old to adequately brush his or her first
permanent molars. Moreover, it is important that oral Complete the clinical Show the patient the hand signal
examination and take that provides control to patient
hygiene education is given to the parent practicing it, radiographs. Discuss Gently dry teeth with the air
who may not necessarily be the one accompanying the treatment plan with syringe while using “tell show do”
child at the dental office. parents. Get informed Do tooth brushing in a friendly
consent praising manner
Disclose dental plaque Make sure that parents under-
and practice tooth stand their role during dental
brushing with both child treatment
and parent Show empathy: “Everything all
Educate parent on right?”, “do you like the taste?”
fluoride issues. Apply Inform the patient for the second
fluoride varnish visit
Provide dietary advice
Second visit
Assess plaque removal, Remind patient about the hand
and praise or reinforce signal
compliance Assess patient’s ability to
Assess compliance and cooperate and proceed accord-
reinforce on diet and the ingly, e.g., quadrant dentistry with
preventive program local anesthesia (use topical first
while introducing it)

..      Fig. 6.34 The responsibility of oral hygiene for a 3-year-old child ..      Fig. 6.35 Inadequate restorative treatment performed a year ago
belongs to the parents in the absence of radiographic examination
Examination, Diagnosis, and Treatment Plan Implementation
citizens may vary and not cover the entire spectrum of
needs. In many countries, there are national insurance
schemes providing very limited dental care for children,
and this severely affects implementing comprehensive
pediatric dental treatment. In other cases, children with
cooperation problems are referred from remote areas to
pediatric dentists, quite often with emergencies. Ideally,
the first visit ends with treatment planning after a thor-
ough examination and provision of a risk-based preven-
tive program, while quadrant restorative treatment is left
for the second or, if so decided, a later visit. Emergencies
however impose restorative treatment to start right away
in the first visit. Otherwise, considerations of time sav-
ing on behalf of the parent by cutting short the time
allowed for proper behavior guidance or by overload-
ing restorative work in the scope of reducing appoint-
ments may not be in the best interest of the young dental
patient.
In cases of full-mouth restorative needs, their schedul-
ing and execution per quadrant or sextant is preferable
for efficiency reasons on the dentist’s part, for reducing
the administrations of local anesthesia, and for mini-
mizing commuting for parents. A study showed that the
child’s stress before and after the administration of local
anesthesia by training pediatric dentists was reduced
only at the fourth restorative visit [55]. Regarding the
sequence of treatment, there has been advice to start or
to finish the treatment at a quadrant with mild restor-
ative requirements for easier acceptance or for improving
the child’s memories, respectively. The choice of jaw for
the first restorative session, due to the different type of
local anesthesia required (local infiltration versus inferior
dental nerve block), is in the discretion of the operator
depending on individual skills and experience or may be
left to the child’s preference for increasing acceptance.
Extractions of primary teeth, as well as minor surgical
operations, may be incorporated into quadrant works.
The content and speed of executing the treatment
plan and the productivity in pediatric dentistry in general
also depend on the way the provided services are orga-
nized. In industrialized countries, the dental team usually
consists of dental assistants, other dental auxiliary per-
sonnel with enhanced role (hygienists, dental therapists),
and office staff (. Fig. 6.36). Many routine dental tasks,
such as preventive work and follow-ups, are performed by
this personnel, while in other societies these are consid-
ered part of the (pediatric) dentist’s duties.
The use of behavior management techniques, such
as “tell show do,” offering partial control, positive rein-
forcement, etc., in combination with local anesthesia
and other auxiliary means, such as a rubber dam, is usu-
ally adequate for the completion of a treatment plan.
In cases of children with intense stress and fear, and/
or strong gag reflexes, however, minimal sedation with
nitrous oxide is often useful. For a better outcome, this
should be introduced to fearful children right from the
107 6
..      Fig. 6.36 A multiple-chair pediatric dental office with a theme
decoration and several work positions for auxiliary personnel
beginning of treatment. Avoiding any injection pain,
especially in stressed patients, makes the acceptance of
local anesthesia easier.
Eye Catcher
Many times, in cases of vulnerable children who are
unready to cooperate, flexibility in treatment plan-
ning is necessary. Instead of an ideal quadrant den-
tistry treatment, a more conservative approach, often
referred to as stabilization [53], combined with an
anti-caries agent like sodium diamine fluoride, is to be
preferred. The arrest of active caries lesions by use of
preventive measures and application of glass ionomer
cements in some cavities until their final restoration,
often referred to as “alternative” or “interim” restor-
ative treatment [56], is preferable in cases with low aes-
thetic demands (. Figs. 6.37 and 6.38). This strategy
is particularly useful in precooperative children below
the age of 3 or even in fearful potentially cooperative
ones at the beginning of their dental experience, if
there are no pain or inflammation emergencies. Thus,
children with similar clinical problems may follow dif-
ferent treatment plans based on their level of readiness
for acceptance of treatment. During the evaluation
process, acclimatization of the child continues with the
provision of preventive, nonoperative care. Unless par-
ents are able to comply with the preventive program,
perfect restorations alone in a child’s mouth, as further
explained in 7 Chap. 12, do not guarantee a long-term
therapeutic outcome.
6.2.3 Referral to a Pediatric Dentist
A study in American private practices had reported
that over 80% of the children attending a dental office
are cooperative patients [57]. For at least some of the
 108 S. Arizos et al.

a c d

6 b e f

..      Fig. 6.37 a. Severe neglect of a mouth of a 9.5-year-­old boy pre- are evident in the panoramic radiograph. c–f. Clinical condition of
senting with dental phobia and intense gag reflex during his first den- his molars
tal visit. Occlusal views were impossible to take. b. His dental needs

a b c

d e

..      Fig. 6.38 a. The mouth of the patient in . Fig. 6.37 in the next molars with deep lesions. d, e. Placement of GIC until compliance
day, after oral hygiene demonstration and its practice by him. b, c. with preventive program is established and acceptance of permanent
Partial caries removal with hand excavator from two first permanent treatment plan is improved
Examination, Diagnosis, and Treatment Plan Implementation
remaining 20%, a referral to a specialist pediatric dentist
would be preferable, in order to receive the comprehen-
sive care that they needed. Such patients may be:
55 Very young children below the age of 3, with severe
forms of early childhood caries, possibly requiring
treatment under general anesthesia.
55 Children with developmental dysplasias or syn-
dromes, such as clefts, ectodermal dysplasia, etc.
55 Children with serious medical problems, such as
heart or renal disease.
55 Children or adolescents with impairments (emo-
tional or physical) undermining the quality of the
proposed dental treatment.
55 Uncooperative children with severe anxiety or phobia.
The American Academy of Pediatric Dentistry
(AAPD) declares that it is unethical to ignore a dis-
ease because of age, behavior, or a disability [58]. Thus,
dentists have the moral obligation to refer the patients
whose needs are beyond their capabilities. The time of
referral is very important. The pediatric dental office
staff is trained and the environment designed appro-
priately for child patients with demanding treatment
needs. The identification of referral cases must be done
promptly, before the application of unsuitable behavior
management techniques or prior to the child’s expo-
sure to repeated unpleasant stimuli. When the latter is
allowed to occur, it creates fear, even phobia, conse-
quently making the addressed pediatric dentist’s task
considerably more difficult.
If a general practitioner refers a patient to an endo-
dontist, this is usually to provide treatment needed
for a specific tooth. After its completion, the patient
returns to the referring dentist. In the case of pediat-
ric dentistry, it is considerably different, as patients are
usually being referred for comprehensive dental care
and less often for a specific procedure prescribed by the
referring practitioner. This referral, in most cases, has
the same characteristics of a referral to an orthodon-
tist. Follow-up of the patient can either be performed
by the specialist or the general practitioner. The choice
may depend on the patient’s age, the parent’s desires,
or the referring dentist’s desires. The procedure is the
following:
55 If a dentist proposes that a child should preferably
be referred to a pediatric dentist, parental consent is
needed.
55 In case of an emergency, the referring practitioner
should notify the pediatric dentist accordingly, pre-
venting disruption of his or her schedule and con-
tributing to the best treatment for the patient.
55 Radiographs and other relevant information should
be forwarded to the pediatric dentist.
55 The pediatric dentist, in turn, should thank the refer-
ring practitioner, explaining the case management
and outcome.
109 6
If these simple rules are followed, a harmonious rela-
tionship is established between colleagues, and, most
importantly, high-quality dental care is provided to the
child patient.
References
1. Pérez RE. Temporomandibular disorders in children. In: Harfin
J, Satravaha S, Faltin Jr K, editors. Clinical cases in early orth-
odontic treatment. Cham: Springer; 2017.
2. Kana A, Markou I, Arhakis A, Kotsanos N. Natal and Neonatal
teeth: a systematic review of prevalence and management. Eur J
Paediatr Dent. 2013;14(1):27–32.
3. Clerehugh V, Tugnait A. Diagnosis and management of peri-
odontal diseases in children and adolescents. Periodontol 2000.
2001;26:146–68.
4. Califano JV. Research science and therapy committee American
Academy of periodontology. Periodontal diseases of children
and adolescents. J Periodontol. 2003;74(11):1696–704.
5. Baelum V. What is the appropriate caries diagnosis? Acta Odon-
tol Scand. 2010:65–79.
6. Brouwer F, Askar H, Paris S, Schwendicke F. Detecting second-
ary caries lesions: a systematic review and meta-analysis. J Dent
Res. 2016:143–51.
7. Lara-Capi C, Cagetti MG, Linstrom P, Lai G, Cocco F, Simark-
Mattsson, Campus G. Digital transillumination in caries detec-
tion versus radiographic and clinical methods: an in vivo study.
Dentaomaxillofacial Radiol. 2017: 20160417.
8. Kuenisch J, Soechtig F, Pitchika V, Laubender R, Neuhaus
KW, Lussi A, Hickel R. In vivo validation of near-infrared light
transillumination for interproximal dentin caries detection. Clin
Oral Invest. 2016:821–9.
9. Chen X, Zhan JY, Lu HX, et al. Factors associated with black
tooth stain in Chinese preschool children. Clin Oral Invest.
2014;18:2059. https://doi.org/10.1007/s00784-­013-­1184-­z.
10. Kanellis MJ. Orthodontic treatment in the primary dentition. In:
Bishara SE, editor. Textbook of orthodontics. Philadelphia: Pa,
Saunders; 2001. p. 248–56.
11. American Academy of Pediatric Dentistry. Guideline on man-
agement of the developing dentition and occlusion in pediatric
dentistry. Reference manual 17/18, Pediatric Dent. 39(6):334–47.
12. Li Y, Wang W. Predicting caries in permanent teeth from car-
ies in primary teeth: an eight-year cohort study. J Dent Res.
2002;81(8):561–6.
13. Helfenstein V, Steiner M, Marthaler TM. Caries prediction on
the basis of past caries including precavity lesions. Caries Res.
1991;25(5):372–6.
14. American Academy of Pediatric Dentistry. Periodicity of Exam-
ination, Preventive Dental Services, Anticipatory Guidance/
Counseling, and Oral Treatment for Infants, Children, and Ado-
lescents. Reference Manual 2018/19, 40 (No. 6); 194–204.
15. Tan EH, Batchelor P, Sheiham A. A reassessment of recall fre-
quency intervals for screening in low caries incidence popula-
tions. Int Dent J. 2006;56(5):277–82.
16. White SC, Mallaya SM. Update on the biological effects of ion-
izing radiation, relative dose factors and radiation hygiene. Aust
Dent J. 2012;57(1 Suppl):2–8.
17. Whaites E, Drage N. The biological effects and risks associated
with X-rays. In: Whaites E, Drage N, editors. Essentials of den-
tal radiography and radiology. 5th ed. Churchill Livingstone;
2013. p. 65–78.
18. Hoogeveen RC, Hazenoot B, Sanderink GCH, Berkhout WER.
The value of thyroid shielding in intraoral radiography. Dento-
maxillofacial Radiol. 2016:20150407.
19. Sansare KP, Khanna V. Karjodkar. Utility of thyroid collars
in cephalometric radiography. Dentomaxillofacial radiology.
2011:471–5.
 110 S. Arizos et al.
20. American Academy of Pediatric Dentistry. Prescribing den-
tal radiographs for infants, children, adolescents, and indi-
viduals with special health care needs. Reference Manual.
2017;39(6):205–7.
21. Horner K, Islam M, Flygare L, Tsiklakis K, Whaites E. Basic
principles for use of dental cone beam computed tomography:
consensus guidelines of the European academy of dental and
maxillofacial radiology. Dentomaxillofacial Radiol. 2009:187–95.
22. Kühnisch J, Anttonen V, Duggal MS, Loizides-Spyridonos M,
Rajasekharan S, et al. Best clinical practice guidance for pre-
scribing dental radiographs in children and adolescents: an
EAPD policy document. Eur Arch Paed Dent. 2020:21;375–86.
23. Whaites E, Drage N. Periapical radiography. In: Whaites E,
Drage N, editors. Essentials of dental radiography and radiol-
ogy. 5th ed. Churchill Livingstone. 2013. p. 85–118.
6 24. Whaites E, Drage N. Bitewing radiography. In: Whaites E, Drage
N, editors. Essentials of dental radiography and radiology. 5th
ed. Churchill Livingstone; 2013. p. 119–28.
25. White SC, Pharoah MJ. Projection geometry. In: White SC,
Pharoah MJ, editors. Oral Radiology – Principles and interpre-
tation. 7th ed. Elsevier; 2014. p. 84–90.
26. White SC, Pharoah MJ. Intraoral projections. In: White SC,
Pharoah MJ, editors. Oral Radiology – Principles and interpre-
tation. 7th ed. Elsevier; 2014. p. 91–130.
27. Gray BM, Mol A, Zandona A, Tyndall D. The effect of image
enhancements and dual observers on proximal caries detection.
Oral Surg Oral Med Oral Pathol Oral Radiol. 2017:e133–9.
28. Whaites E and Drage N. Image receptors. In: Essentials of dental
radiography and radiology. Whaites E and Drage N. Churchill
Livingstone, 5th ed. 2013. p.31–44.
29. Ludlow JB and Mol A. Digital imaging. In: Oral Radiology –
Principles and interpretation. White SC and Pharoah MJ. Else-
vier, 7th ed. 2014. p. 41–62.
30. Parrott LA, Ng SY. A comparison between bitewing radiographs
taken with rectangular and circular collimators in UK military
dental practices: a retrospective study. Dentomaxillofacial radi-
ology. 2011:102–9.
31. Zhang W, Abramovitch K, Thames W, Leon ILK, Colosi DC,
Goren AD. Comparison of the efficacy and technical accu-
racy of different rectangular collimators for intraoral radiog-
raphy. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2009;108:e22–8.
32. Goren AD, Bonvento MJ, Fernandez TJ, Abramovitch K,
Zhang W, Roe N, Seltzer J, Steinberg M, Colosi DC. Evalua-
tion of radiation exposure with Tru-Align intraoral rectangular
collimation system using OSL dosimeters. NY State Dental J.
2011:24–7.
33. Whaites E and Drage N. Dental X-ray generating equipment.
In: Whaites E, Drage N editors. Essentials of dental radiography
and radiology 5th ed. Churchill Livingstone; 2013. p. 25–30.
34. Terry GL, Noujeim M, Langlais RP, Moore WS, Prihoda TJ.
A clinical comparison of extraoral panoramic and intraoral
radiographic modalities for detecting proximal caries and visual-
izing open posterior interproximal contacts. Dentomaxillofacial
Radiol. 2016:20150159.
35. El-Ela WHA, Farid MM, Mostafa MSE-D. Intraoral ver-
sus extraoral bitewing radiography in detection of enamel
proximal caries: an ex vivo study. Dentomaxillofacial Radiol.
2016:20150326.
36. Gaalaas L, Tyndall D, Mol A, Everett ET, Bangdiwala A. Ex
vivo evaluation of new 2D and 3D dental radiographic
technology for detecting caries. Dentomaxillofac Radiol.
2016;45(3):20150281.
37. Stephen KW, Russell JI, Creanor SL, Burchell CK. Comparison
of fibre optic transillumination with clinical and radiographic
caries diagnosis. Community Dent Oral Epidemiol. 1987;15:90–4.
38. Pitts NB. The use of bite-wing radiographs in the management
of dental caries: scientific and practical considerations (review
article). Dentomaxillofac Radiol. 1996;25:5–16.
39. Ketley CE, Holt RD. Visual and radiographic diagnosis of
occlusal caries in first permanent molars and in second primary
molars. Br Dent J. 1993;174:364–70.
40. Raadal M, Amarante E, Espelid I. Prevalence, severity and dis-
tribution of caries in a group of 5-year-old Norwegian children.
Eur J Paed Dent. 2000:113–20.
41. Mejare I, Stenlund H, Julihn A, Larsson I, Permert L. Influence
of approximal caries in primary molars on caries rate for the
mesial surface of the first permanent molar in Swedish children
from 6 to 12 years of age. Caries Res. 2001;35(3):178–85.
42. De Vries HC, Ruiken HM, Konig KG, Van’t Hof MA. Radio-
graphic versus clinical diagnosis of approximal carious lesions.
Caries Res. 1990;24(5):364–70.
43. Ignelzi MA, Fields HW, Vann WF. Screening panoramic radio-
graphs in children: prevalence data and implications. Paed Dent.
1989;11(4):279–85.
44. Parks ET, Aps JK. Radiographic techniques. In: McDonald and
Avery’s Dentistry for the Child and Adolescent. 10th ed. Elsevier
St Louis Missouri, ISBN 978–0–323-28745-6; 2016. p. 17–38.
45. Hintze H and Espelid I. Radiographic examination and diagno-
sis. In: Koch G, Poulsen S, Espelid I, Haubek D, eritors. Pediat-
ric dentistry, a clinical approach. 3rd Ed. Wiley Blackwell; 2017.
p. 75–86.
46. Aps JKM. Cone beam computed tomography in paediatric den-
tistry: overview of recent literature. Eur Arch Paediatr Dent.
2013;14(3):131–40.
47. Van Acker JWG, Martens LC, Aps JKM. Cone-beam computed
tomography in paediatric dentistry, a retrospective observational
study. Clin Oral Invest. 2015; https://doi.org/10.1007/s00784-
015-1592-3.
48. Spin-Neto R, Matzen LH, Schropp L, Gotfredsen E, Wenzel
A. Factors affecting patient movement and re-­exposure in cone
beam computed tomography examination. Oral Surg Oral Med
Oral Pathol Oral Radiol. 2015;119:572–8.
49. Spin-Neto R, Matzen LH, Schropp L, Gotfredsen E, Wen-
zel A. Movement characteristics in young patients and the
impact on CBCT image quality. Dentomaxillofacial Radiol.
2016;20150426
50. Donaldson K, O’Connor S, Heath N. Dental cone beam CT
image quality possibly reduced by patient movement. Dentomax-
illofacial Radiol. 2012; https://doi.org/10.1259/dmfr/91866873.
51. Keris EY. Effect of patient anxiety on image motion artefacts in
CBCT BMC. Oral Health. 2017; https://doi.org/10.1186/s12903-
017-0367-4.
52. Ertas ET, Kucukyilmaz E, Ertas H, Savas S, Atici MY. A com-
parative study of different radiographic methods for detecting
occlusal caries lesions. Caries Res. 2014:566–74.
53. Chadwick BL, Hosey MT. Child Taming: How to manage chil-
dren in dental practice. Ch 4 and 6, pp. 29–36 and 47–56, Quin-
tessence, London; 2003.
54. Waggoner WF. Restorative dentistry for the primary dentition.
In: Casamasimo, Fields, McTigue, Nowak, editors. Pediatric
dentistry, infancy through adolescence. 5th ed.; 2013. p. 304–32.
55. Arhakis A, Menexes G, Coolidge T, Kalfas S. Heart rate, sali-
vary α-amylase activity, and cooperative behavior in previously
naïve children receiving dental local anesthesia. Pediatr Dent.
2012;34(7):e225–30.
56. American Academy of Pediatric Dentistry. Reference Manual.
Policy on interim therapeutic restorations (ITR). Reference
Manual. 2017-2018;39(6):57–8.
57. Baier K, Milgrom P, Russell S, Mancl L, Yoshida T. Children's
fear and behavior in private pediatric dentistry practices. Pediatr
Dent. 2004;26:316–21.
58. American Academy of Pediatric Dentistry. Policy on the ethi-
cal responsibilities in the oral health care management of
infants, children, adolescents and individuals with special health
care needs. Reference Manual. Pediatric Dent. 2017/18;39(6):
136–7.
 111 7

Local Anesthesia in Pediatric

Dentistry
Konstantinos N. Arapostathis and Jean-Louis Sixou

Contents

7.1 Equipment and Factors Relating to Local Anesthesia – 112

7.1.1 T opical Anesthetics – 112
7.1.2 Injectors and Needles – 112
7.1.3 Types of Local Anesthetics – Dosage – 113
7.1.4 Vasoconstrictors – 113
7.1.5 Rate or Speed of Injected Solution – 114
7.1.6 Temperature of Injected Solution – 114
7.1.7 Local Anesthesia Using Alternative Kinds of Injectors – 114

7.2 Main Local Anesthesia Techniques – 115

7.2.1 T opical Local Anesthesia – 115
7.2.2 Main Local Anesthesia Techniques with Infiltration
in Free Mucosa – 115
7.2.3 Main Palatal Anesthesia – 118
7.2.4 Injection within the Bone – 120
7.2.5 Other Anesthesia – 121

7.3  ehavior Guidance for the Administering

B
of Local Anesthesia – 122
7.3.1  reparing the Child – 122
P
7.3.2 Administration of Local Anesthesia – 123

7.4 Complications of Local Anesthesia – 125

7.4.1 L ocal Complications – 125
7.4.2 Systemic Complications – 126

References – 127

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_7
 112 K. N. Arapostathis and J.-L. Sixou

Prevention and controlling of pain during dental treat-
ment is one of the most important parameters in the
dentist’s attempt to provide for his/her patients a com-
plete and quality-based dental treatment. Especially
when the patients are children, successfully achieving a
high level of cooperation, building trust, preventing the
rise of dental phobia, and establishing a positive attitude
toward the dental act are definitively connected with the
minimization of discomfort and even complete absence
of pain while at the dentist [1–4]. Many studies have
arrived at the conclusion that the main causes of den-
tal phobia and avoidance of dental treatment are early
painful or otherwise negative dental experiences [3–7].
Painless dental treatment is achieved when the patient’s
fear and anxiety is controlled and is combined with the
7 effective administering of anesthesia.
7.1  quipment and Factors Relating
E tors used for controlled electronic administering on
to Local Anesthesia
Some of the equipment and factors that are directly
related to local anesthesia in pediatric dentistry are as
follows: the types of topical anesthetics, the injector, the
needles, the types of local anesthetics, the vasopressors,
the dosage based on the choice of anesthetic, the injec-
tion rate of the anesthetic, and the temperature of the
anesthetic solution.
7.1.1 Topical Anesthetics
Topical anesthetics are used to anesthetize the surface
of the mucous membrane at the point where the needle
will be inserted. They are usually available as gels (e.g.
benzocaine 20%), creams (e.g. lidocaine 5%), or sprays
(e.g. lidocaine 15%). In pediatric dentistry, gel is the sim-
plest to use, since its application on the desired part of
the mucous membrane can be controlled the easiest. In
addition, most products no longer have the bitter taste
related to the anesthetic itself, and some even come in
various fruit flavors. While toxic reactions from topical
anesthetics are rare, the use of large quantities should
be avoided due to the large concentration of anesthetic
in some of these products and its ease of infiltration [8,
9]. However, benzocaine-based topical analgesics are
slowly absorbed and are less likely to cause any over-­
dosage complications [10]. Topical anesthetics achieve
satisfactory anesthetization at a depth of approximately
2 mm when applied to a clean and dry area for an ade-
quate amount of time. Suggested times for topical anes-
thesia to become completely effective range between
30 seconds to 5 minutes, depending on the product and
the type of mucous membrane. These types of anesthet-
ics are not particularly effective, however, when deal-
ing with keratinized mucosa [9, 11, 12]. Cooling sprays,
although being efficient, should not be used, especially
in young children. Cold liquid can flow down the throat.
Furthermore, sudden arrival of the cold can frighten the
child.
7.1.2 Injectors and Needles
The carpule syringe is the most commonly used syringe
in adult and pediatric dentistry. It is made of metal or
plastic; mostly stainless steel can be sterilized and fea-
tures the ability to perform suction. Plastic devices seem
to be preferred by children [13]. When using it in child
patients, there are various innovative ways in which
syringes can be presented (. Fig. 7.1). There are also
other types of syringes which combine with their needle
counterparts, like the intraligamental syringe, the injec-
anesthesia including intraosseous anesthesia, and even
needleless jet injectors.
In relation to needles, there are various types, based
on the device used for administering the anesthetic.
Needles made for the carpule syringe are single-use, ster-
ilized, and individually wrapped in plastic packaging.
They are available in size 32–40, 22–25, and 10–13 mm
(extra long, short, and extra short, respectively, depend-
ing on the manufacturer) and 25, 27, and 30 G (Gauge,
which corresponds to 0.025, 0.020, and 0.015 mm in
lumen diameter). In pediatric dentistry, 30 and 27 G
needles are the most commonly used. However, it is rec-
ommended that the needle used for nerve block is not of
the smallest diameter (30 G), as using this type increases
the danger of the needle breaking [11, 14, 15]. In relation
to length, extra short 9–13 mm needles are suggested
for use in local infiltration anesthesia and transcortical
..      Fig. 7.1 Example of carpule syringe with suction ring and plastic
cover in the shape of a crocodile
Local Anesthesia in Pediatric Dentistry
..      Fig. 7.2 From top to bottom: 37 mm needle (extra long) with
25 G lumen. 22 mm (short) and 27 G needle, recommended for infe-
rior alveolar nerve block in child patients. 22 mm (short) and 30 G
lumen needle. 10 mm (extra short) and 30 G needle, recommended
for local infiltration anesthesia in child patients. The arrows on the
plastic piece of each needle indicate the bevel side of the tip
intraosseous anesthesia, while 22–25 mm needles are
suggested when performing inferior alveolar nerve block
in child patients [11, 15–17] (. Fig. 7.2). It has been
discovered that needle length does not correlate with
discomfort during insertion, while needle point condi-
tion does directly correlate with experienced pain. There
also seems to be conflicting evidence in relation to needle
diameter. As a result of these findings, the use of dif-
ferent needles for different types of insertion is advised,
especially in the case of palatal anesthesia [16, 18–20].
When injecting in attached mucosa (palatal mucosa,
attached gingiva), the flat part of the bevel at the tip of
the needle should be sought to come into parallel con-
tact with the periosteum for better and painless penetra-
tion in gingiva and injection of the anesthetic solution.
For this reason, needles have an indication for their
correct orientation. Some needles have a double bevel
to allow better penetration within bone in intraosseous
techniques (. Fig. 7.2).
7.1.3 Types of Local Anesthetics – Dosage
According to the European Academy of Paediatric
Dentistry guidelines, there is still a lack of information
for the use of local anesthetics in children aged under
4 years [10]. Three local anesthetics are considered most
appropriate in child patients. All three are amide type, are
safe, and are effective and rarely cause allergic reactions.
These are lidocaine, mepivacaine, and articaine [9, 10].
The solutions used in pediatric dentistry and their dura-
tion of action are presented in . Table 7.1. Lidocaine,
since its creation in 1943, remains one of the most widely
used local anesthetics [1] and is available in a 2% or 3%
solution with a vasoconstrictor of 1:80,000, 1:100,000,
113 7
..      Table 7.1 Commonly used local anesthetic solutions used
in pediatric dentistry and their duration length [3, 9]
Local anesthetic solutions Duration of anesthesia
Lidocaine 2% with epinephrine Pulpal: 60–90 minutes
1:100,000 Soft tissue: 3–4 hours
Articaine with epinephrine Pulpal: 45–75 minutes
1:200,000 Soft tissue: 3–4 hours
Mepivacaine 3% Pulpal: 20–30 minutes
Soft tissue: 2–3 hours
or 1:200,000. Mepivacaine possesses a slight vasodilat-
ing ability and in some ways, it can be argued, causes
minor scale vasoconstriction [9]. This ability renders it
the anesthetic of choice when use of a vasoconstrictor
is not suggested or contraindicated, such as when per-
forming minor, short-term dental work on very young
children. The duration of effective pulpal anesthesia is
short (20–30 min), but the quick relief from the unpleas-
ant numbing sensation of the neighboring soft tissue in
infiltration techniques in free mucosa is in fact an asset.
Articaine is available in a 4% solution with vasocon-
strictor 1:80,00, 1:100,000, 1:200,000, or 1:400,000. It
possesses increased intratissue infiltration but is contra-
indicated in patients with cardiac or respiratory condi-
tions and can even cause methemoglobinemia in high
doses. A high level of caution is required to avoid exceed-
ing the maximum permissible dosage of anesthetic solu-
tion in child patients [10, 21–23]. The exact dose of
anesthetic solution is frequently not calculated based on
the child’s weight, causing cases of overdose and toxic-
ity as a result. The unique physiology of the child’s body
(reduced ability for renal clearance and variations in
relation to metabolism, gastrointestinal flora, and serum
proteins) requires administering smaller doses of local
anesthetic to avoid dangerous toxic reactions from the
circulatory and central nervous system [3, 9, 10, 22, 23].
The maximum permissible dose for each anesthetic solu-
tion is presented in . Table 7.2.
7.1.4 Vasoconstrictors
Epinephrine (adrenaline) is the main vasoconstrictor
used today in dental local anesthesia. The addition of
a vasoconstrictor in anesthetic solutions slows the rate
of absorption by the tissues and thus reduces the chance
of occurrence of a toxic reaction while at the same time
increases the depth and duration of anesthesia. The safe
level of epinephrine in a solution is considered to be
1:200,000, 1:100,000, or 1:400,000. Dilution 1:400,000
associated with articaine has been shown to be accept-
 114 K. N. Arapostathis and J.-L. Sixou

..      Table 7.2 Maximum permissible dose of anesthetic solutions per each kg of body weight (1 cartridge = 1.8 ml) [3, 22]

Lidocaine 2% Mepivacaine 3% Articaine 4%

1 cartridge = 36 mg 1 cartridge = 54 mg 1 cartridge = 72 mg

Dosage 4.4 mg/kg 4.4 mg/kg 7 mg/kg

Weight Max. Dose Number of Max. Dose Number of Max. Dose Number of
cartridges cartridges cartridges
10 kg 44 mg 1.2 44 mg 0.8 70 mg 0.9
20 kg 88 mg 2.4 88 mg 1.6 140 mg 1.9
30 kg 132 mg 3.6 132 mg 2.4 210 mg 2.9
40 kg 176 mg 4.8 176 mg 3.2 280 mg 3.8
50 kg 220 mg 6.1 220 mg 4.0 350 mg 4.8

7 Maximum
Dose
300 mg 8.3 300 mg 5.5 500 mg 6.9

able and efficient for routine treatments in children [24,
25]. The addition of epinephrine lowers the pH of the
solution. It has been found that the lower pH of the
anesthetic solution increases discomfort during injec-
tion, and thus, epinephrine-free solutions are preferred,
when the length and type of dental treatment allow
it [26, 27]. Felypressin and norepinephrine are other
­vasoconstrictors available.
7.1.7  ocal Anesthesia Using Alternative
L
Kinds of Injectors
These are appliances that differ from traditional syringe
anesthesia or do not use needles. The most common of
these are: computer-controlled administering of anes-
thesia (C-CLAD), computer-controlled administering
of anesthesia and needle rotation, and needleless jet
injector anesthesia.

7.1.5 Rate or Speed of Injected Solution

It is recommended that injection of the anesthetic is
done at a slow pace. This way, the chances of anesthetic
toxicity are reduced and allow time for any unwanted
systemic action to occur before the entire solution is
injected. At the same time, lower pressure allows the
anesthetic to remain close to the injection point [19].
The ideal speed of injection is 1 ml/min, and for no rea-
son should it ever exceed 1.8 ml/min [9, 28]. While in
one study it appears that the rate of injecting the anes-
thetic did not reduce the effectiveness or cause coopera-
tion problems in children aged 5–6 [28], rapid injection
of anesthetic causes some degree of pain [29]. Use of
computer-­controlled injectors may be a way to help con-
trol the speed of injection and therefore lower the intra-
tissular pressure related to injection.
7.1.6 Temperature of Injected Solution
The temperature of the anesthetic does not seem to cor-
relate with pain experienced when it is above 15 °C. It
is suggested that anesthetic solutions be preserved at
ambient temperature, somewhere consequently not too
hot or cold [26, 29–31].
7.1.7.1 Computer-Controlled Administering
of Anesthetic Solution
These devices consist of an electronic unit, a footswitch
(The Wand-STA™, Sleeper One™, CCS™), or a hand-
switch (Dentapen™), needing a needle (specialized or
not) connected to the device (. Fig. 7.3). Pen-shaped
C-CLAD injectors (The Wand-STA™, Sleeper One™,
CCS™, Dentapen™) allow good support points.
Injection is controlled by the use of an electronic
device. It allows a drop-by-drop delivery during the first
seconds of injection which is very difficult to perform
using traditional syringes [32]. Another characteristic
is that injection is continuous and stable or increases
slowly after the first seconds: it therefore avoids pulses
of anesthetics that are associated to high intratissular
pressure around the needle and therefore to pain. Using
C-CLAD devices takes more time than regular anes-
thesia and comes at a higher cost, so much as to initial
purchase as to buying specific consumables for one of
them (The Wand-STA™). The different appearance of
the needle and syringe, when pen-shaped, appears to
reduce fear and pain in patients [13]. Although a sig-
nificant difference in pain levels was found in adults,
results are more ambiguous in children in usual infil-
tration techniques [33–35]. Recent literature reviews
Local Anesthesia in Pediatric Dentistry
..      Fig. 7.3 Various injectors for dental anesthesia. From left to
right: one with computer-controlled injection of anesthetics and
needle rotation (Quick Sleeper 5™), three injectors with computer-­
controlled injection of anesthetics (Sleeper One 5™, The Wand –
STA™, Dentapen™), and two manual injectors: one with balanced
weight distribution (Citoject™) and a usual metal syringe. Note that
The Wand-STA™ is linked to its system with a hose and Quick
Sleeper™ and Sleeper One™ with a wire
had different conclusions about C-CLAD in children:
positive [36, 37] or negative [38] opinion or lack of evi-
dence to conclude [39, 40]. The levels of dental phobia,
proper communication with the patient, and appropri-
ate presentation of the device are the most important
factors in influencing acceptance and cooperation with
the dentist. Two studies indicate that low-anxious chil-
dren receiving local anesthesia with the Wand™ dis-
play less pain-related behavior signs than low-anxious
children receiving local anesthesia with the traditional
syringe, while no differences are found in anxious chil-
dren whatever the kind of injector used (with or with-
out electronic assistance) [41, 42]. C-CLAD injectors
have shown promising results in lowering pain in chil-
dren during mandibular nerve blocks and intraliga-
mental injection [43, 44] and during palatal injections
(see further).
7.1.7.2  nesthesia without Use
A
of Needle – Jet Anesthetic Technique
With jet injection technique, the anesthetic is forwarded
through pressure to the tissues without using a needle.
The Injex™ device is a representative example of this
technique and used even in non-dental medical work
(. Fig. 7.4). A certain preparative process is required
before performing anesthesia unlike traditional meth-
ods, while the device and its consumables come at an
increased price. The device is applied vertically to the
115 7
mucosa of the alveolar process, slightly more cervi-
cally than where the apex of the tooth is calculated to
be. This technique yields successful anesthetic results in
regions where the device can be placed vertically to the
alveolar process (e.g., anterior teeth). However, there are
conflicting results as to the acceptance of the device by
child patients [6, 45]. It could prove to be very useful
in patients who have a fear of needles ­(aichmophobia/
belonephobia).
7.2 Main Local Anesthesia Techniques
7.2.1 Topical Local Anesthesia
Topical anesthesia is used to reduce pain from the inser-
tion of the needle in the mucosa. On a psychological
level, it introduces the patient to the idea of local anes-
thesia, as it is the first step in the process. Its applica-
tion consists of applying a small amount of gel or cream
onto a cotton swab and covering only the area where
the needle will be inserted. This area must remain clean
and dry before and during the entire process of apply-
ing the anesthetic (usually between 30 seconds to 5 min-
utes). One way of achieving this is for the patient to keep
his/her mouth open while the dentist holds the swab in
the right position and holds the oral cavity away from
the point of application, using a surgical suction tip to
remove saliva (. Fig. 7.5). The use of a suction tip also
reduces the chances of swallowing even small amounts
of the anesthetic, reducing the chance of a toxic reac-
tion, which is a possibility [46].
7.2.2  ain Local Anesthesia Techniques
M
with Infiltration in Free Mucosa
Eye Catcher
The techniques of administering local anesthesia to
children are essentially similar to those for adults. The
differences are basically related to their craniofacial
complex size and density. This has implications on
both the length and the gauge of needle selection.
There are two basic differences in the craniofacial com-
plex of children when compared to adults:
1. Anesthetic effectiveness is easier in child patients, as
the jawbones are less dense, allowing faster and bet-
ter diffusion of the anesthetic solution [1].
2. The smaller size of oral structures in children,
depending on their age, dictates a smaller depth of
needle penetration in mucosal tissues in traditional
infiltration techniques and allows access to the
 116 K. N. Arapostathis and J.-L. Sixou
a b
7 c
..      Fig. 7.4 a–c. Injex needleless jet injection syringe with necessary components to prepare administering local anesthesia. d. Position of
application
mandible from a modified position in the following
cases [9]:
(a) The inner mandibular foramen in children is
found at the height of the occlusal plane and not
7–8 mm above it, as it is with adults [47]
(. Fig. 7.6). As for its anteroposterior position
on the ramus, age does not seem to make any dif-
ference. The syringe is positioned above the pri-
mary molars, with direction from the opposite
half, at a 10-degree downward angle. Needle
penetration depth is about 15 mm and depends
on the mandible’s size [11, 29].
(b) In buccal nerve block anesthesia, injection takes
place upward and buccally from the last tooth on
the arch, using an amount less than 0.5 ml,
depending on age. This should always be done in
child patients for tooth extraction in case of infil-
tration technique. To place the dental dam clamp
without discomfort, an even smaller amount can
be injected at the depth of the gingivodental sul-
cus [29].
d
(c) The mental foramen in children is a little closer
to the first primary molar, and the injection point
for the anesthetic solution is chosen between the
two mandibular primary molars (. Figs. 7.7
and 7.8).
7.2.2.1 Local Infiltration Anesthesia
Local infiltration anesthesia has the same indications in
children as it does in adults. It is traditionally considered
as the anesthesia of choice for teeth, the periodontal tis-
sue, and palate in the maxilla and for the incisors and
surrounding periodontal tissue in the mandible. If this is
performed in an inflamed area, its action may be delayed
or suspended [3]. In the maxilla, local infiltration anes-
thesia on the target tooth is preferred over superior alve-
olar nerve block (. Figs. 7.9 and 7.10). An exception
can be made in cases of permanent molars whose apices
are covered by thick and/or fat zygomatic bone, or in the
case when the molar nerves are combined with branches
of palatine nerve [11]. Additional palatal anesthesia is
suggested as a supplementary procedure in pulpoto-
Local Anesthesia in Pediatric Dentistry
..      Fig. 7.5 Application of topical anesthetic. a. The area is dried.
b. Applying a small amount of anesthetic gel only in the area where
the needle is to be inserted
mies, endodontic treatment, or extractions or even when
placing the dental dam’s clamp (with the possibility of
alternative injection in the gingivodental sulcus). It is
frequently painful, due to the keratinized and uncom-
promising mucous membrane. To avoid pain from
needle insertion in the palate, in the cases where buccal
anesthesia has preceded, it is preferable for the needle to
be inserted vertically in the interdental papilla with buc-
cal direction and gradual injection of the anesthetic as
the needles arrive at the palatal surface. Injection stops
when ischemia (a whitish spot) is formed in the palatal
mucosa. Regular infiltration anesthesia of the palate can
follow [11] (. Fig. 7.11). An effective trick to alleviate
the sensation of pain in the palate is to apply pressure on
the mucosa with the posterior end of a dental tool near
the point of insertion during injection [29]. Another
possibility is to apply the flat part of the bevel of the
needle on the palatal surface. The needle is then inserted
117 7
..      Fig. 7.6 Top to bottom: movement of mandibular foramen in
primary dentition (children), mixed dentition, and permanent teeth
(adults)
at a 15–20° angle and slow injection performed at the
same time. An alternate solution to buccal infiltration
in this case is to use intraosseous techniques with needle
rotation (see below).
In anterior mandibular teeth, infiltration anesthe-
sia does not differ in children or adults [29]. Local
infiltration can be used to anesthetize the mandibu-
lar primary molars, due to lower bone density in child
patients. According to some researchers, this yields
good results when performing fillings and when pre-
paring for the installation of stainless steel dental
crowns [48, 49]. In cases of pulp treatment or extrac-
tion, inferior alveolar nerve block or intraosseous
anesthesia is preferred.
7.2.2.2 I nferior Alveolar Nerve Block
Anesthesia
The aim in inferior alveolar nerve (IAN) block is
the anesthetization of the mandibular teeth, except
for the incisors, while the buccal mucosa (anteriorly
to the mental foramen) and lingual mucosa are also
anesthetized. This way, quadrant dentistry can be
 118 K. N. Arapostathis and J.-L. Sixou

75

b
7 35

..      Fig. 7.7 Position of the mental foramen in children and adults

(with oblique needle direction)

performed easily while also avoiding multiple needle

insertions and guaranteeing adequate duration of the
anesthetic result. Penetration of the needle should
be done in the same direction as with adults, but
..      Fig. 7.8 a. Needle position. Insertion can be done at an even
at the height of the occlusal plane (. Figs. 7.6 and
more oblique angle. b. Injection of anesthetic between the two man-
7.12). Two available alternatives of IAN block have dibular primary molars
been proposed: the Gow-Gates technique (GG), per-
formed with the patient’s oral cavity wide open, and
the Vazirani-Akinosi technique (VA). This latter is a
closed-mouth block. Performed with both arches in
contact, it is indicated when there is limited mandibu-
lar opening and may become useful in some cases. At a
meta-analysis of studies in adults, VA showed similar
and GG higher success rates than the traditional IAN
block [50].

7.2.3 Main Palatal Anesthesia

There are five main palatal techniques that allow to anes-

thetize three to six teeth with a single injection, without
numbing of soft tissues (cheeks and upper lip): anterior
middle superior alveolar nerve block, naso-­ palatine
nerve, palatal approach anterior superior alveolar nerve
..      Fig. 7.9 Local infiltration anesthetic for maxillary primary molar
block, maxillary nerve block with palatal approach,
and greater palatine nerve block. The first three tech-
niques are more suitable for children and therefore are should precede. Slow injection of anesthetic solution is
further described below. With these, needle penetration always recommended to prevent pain from intratissue
may be more painful and therefore topical anesthesia overpressure.
Local Anesthesia in Pediatric Dentistry
7.2.3.1  nterior Middle Superior Alveolar
A is performed halfway between the midpalatine raphe
Nerve Block (AMSA)
The AMSA injection aims at anesthetizing maxillary
teeth and palatal tissues extending from the central inci-
sor to the buccal root of the first molar mesially. Most of
the time, teeth anesthetized range from the lateral inci-
sor to the second premolar or primary molar. Injection
..      Fig. 7.10 Buccal infiltration using the Sleeper One™ device
a b
..      Fig. 7.11 Palatal anesthesia with initial buccal approach.
a. Insertion of the needle horizontally, in the interdental papilla.
b. The anesthetic is injected gradually as the needle penetrates
119 7
and the crest of the free gingival margin at the premolar
level. After diffusion within the bone through nutrient
canals, the anesthetic solution is supposed to anesthe-
tize branches of anterior and middle superior alveolar
nerves and also areas covered by the greater palatine and
nasopalatine nerves. Computer-controlled injection has
been shown to induce less pain in children compared to
injection with traditional syringes [51, 52].
7.2.3.2 Nasopalatine Nerve Block
This anesthesia triggers the anterior portion of the
hard palate (soft and hard tissues) from canine to
canine. With this technique, teeth are more difficult to
anesthetize than bone and gingiva. This anesthesia is
therefore mainly interesting for treatment of superficial
or medium depth caries and for local surgery such as
removal of odontomas (. Fig. 7.13). It targets the inci-
sive foramen beneath the incisive papilla. As penetration
is generally performed parallel to the incisive papilla,
toward the palatal surface. c. New insertion of the needle with pala-
tal infiltration will follow
 120 K. N. Arapostathis and J.-L. Sixou
a one side may be better anesthetized than the other. Slow
7 b
..      Fig. 7.12 Inferior alveolar nerve block. a. Use of finger in con-
tact with the anterior lip of the mandible ramus as guidance. b. Pen-
etration of needle at the height of the occlusal plane
..      Fig. 7.13 Nasopalatine nerve block using the Quick Sleeper™
device for removing an anteriorly placed maxillary odontoma
injection is also recommended to reduce intratissular
pressure-­related pain.
7.2.3.3  alatal Anterior Superior Alveolar
P
Block (P-ASA)
This technique derives from the nasopalatine nerve
block. The injection site is similar. However, the needle
has to be inserted deeper, 6 to 10 mm, within the inci-
sive canal. Comparatively to the NP technique, P-ASA
allows better anesthesia of teeth and allows endodontic
treatments. Use of C-CLAD injectors for P-ASA has
been shown to be interesting in children [53, 54].
7.2.4 Injection within the Bone
Injecting within the bone can be performed in the inter-
dental septum (intraseptal anesthesia) or in the spongy
bone between two teeth (intraosseous anesthesia: IO).
7.2.4.1 Intraseptal Anesthesia
Injecting in the septum is difficult because of the high
density of the septal bone. Needle penetration and injec-
tion are hard to perform. Furthermore, diffusion of the
anesthetic solution occurs slowly through small canals
at the basis of the septum before reaching the spongy
bone [55]. Injecting in the four septae around a tooth
is necessary to get efficient anesthesia making intrasep-
tal anesthesia a complementary technique rather than a
first choice in children.
7.2.4.2 Intraosseous Anesthesia
Intraosseous (IO) injections make it possible to place
local anesthetic solutions directly into the cancellous
bone adjacent to the tooth to be anesthetized. The anes-
thetic solution injected diffuses on each side of the injec-
tion point using the intraosseous vasculature. It allows
anesthesia of two to six teeth according to the volume
injected. Surrounding soft tissues generally remain unaf-
fected. There are two ways to reach the interdental spongy
bone: through the cortical plate (transcortical anesthesia
[TC]) (. Fig. 7.14) or through the interdental septum
(osteocentral anesthesia [OC], also called transseptal
anesthesia) (. Fig. 7.15). Both ways can be used in ante-
rior and posterior teeth. However, OC is recommended
for posterior teeth because of easier access. The first step
is to anesthetize gingiva. The second step is to penetrate
the bone. The insertion point of the needle in TC is situ-
ated 1 to 3 mm below the mesial or distal septum adja-
cent to the tooth (teeth) to be anesthetized. In OC it is
situated at the top of the interdental septum, the needle
being inserted at a 40° angle. In young patients, mainly in
Local Anesthesia in Pediatric Dentistry
a b
..      Fig. 7.14 Transcortical anesthesia using a C-CLAD injector
(Sleeper One™). a. First step: Gingival anesthesia. The needle (9 mm
long, 30 G) is inserted with shallow angle with the flat part of the bevel
facing the gingival surface. The tip of the needle can be seen in subsur-
face situation as well as the whitening of gingiva due to the spreading
..      Fig. 7.15 Osteocentral anesthesia (also called transseptal anes-
thesia) using the Quick Sleeper™ injector. The first step is identical
to that of the transcortical technique. The needle (in this case a 27 G
13 mm long needle) is inserted at the top of the septum with a close-
to-40° angle. The angle depends on the width of the septal bone (dis-
tance between the buccal and palatal cortical plates). After
computer-controlled rotation of the needle, the computer-­controlled
injection of the anesthetic solution can be performed. Computer
control also allows low injection speed and therefore low intratissue
pressure and decreased risk of pain
primary dentition [25], penetration can be performed by
pushing the needle through the cortical plate or the inter-
dental septum. When children grow, septae and cortical
plates become harder. Rotating devices are necessary. One
of them is characterized by a computer control of needle
rotation and anesthetics injection (Quick Sleeper™) and
is more adapted to children than devices in which rota-
tion is based on drilling (Stabident™, X-Tip™). Slow
injection is recommended. Computer-controlled devices
with or without needle rotation are well adapted to IO
injections. Prospective studies performed with the Quick
Sleeper™ or Sleeper One™ devices have shown a 92%
121 7
c
of the anesthetic solution. b. Second step: The needle is in contact with
the cortical plate (90° angle). c. Third step: After passing through the
cortical plate (in this case without needle rotation), the anesthetic solu-
tion can be injected. Computer control allows low injection speed and
therefore low intratissue pressure and decreased risk of pain
to 97% success rate in children, including on MIH teeth,
with good acceptance from children, without postopera-
tive pain or papilla necrosis in the weeks following IO
injections [17, 25, 56, 57]. They suggest that IO injections
can be considered a good alternate or a supplement to
classic infiltration techniques in children and adolescents.
This was confirmed by a recent multicenter study com-
paring buccal infiltration and IO for treating first perma-
nent molars with deep carious lesions or moderate to high
severity (MIH) lesions in children and adolescents. Both
techniques showed similar efficacy but pain during the
insertion of the needle and injection was less with IO [58].
7.2.5 Other Anesthesia
7.2.5.1 Intraligamental Anesthesia
Intraligamental anesthesia (ILA) aims at injecting the
anesthetic solution directly within the periodontal liga-
ment. The solution injected finally reaches the cancel-
lous bone adjacent to the tooth. However, two thirds
of a cartridge are required to have diffusion at both the
crestal and periapical levels [59]. ILA is aggressive for the
periodontal apparatus and should be used additionally
in extraction of primary teeth and premolars, as addi-
tional anesthesia in oversensitive teeth (e.g., teeth with
amelogenesis imperfecta and molar incisor hypominer-
alization), in pulpotomies of primary teeth (excluding
the mandibular second molar) [60, 61], in diagnos-
tics when trying to find the cause of pain [20], and in
patients with hypertension and cardiac arrhythmia [11].
This type of anesthesia requires a special syringe or a
computer-controlled device (. Fig. 7.16).
Contraindications for intraligamental anesthesia are
children at high infectious risk because of the 96.6% rate
of bacteremia associated to ILA [62, 63], acute peri-
odontal inflammation, and teeth with partly developed
roots. When applied to primary teeth, concern has been
raised as to the formation of the succedaneous tooth
 122 K. N. Arapostathis and J.-L. Sixou
7 ..      Fig. 7.16 Intraligamental syringe
crown due to cytotoxic effects of the anesthetic solu-
tion, as reported in an animal study [61]. However, such
an effect was not confirmed in a long-term study using
computer-controlled injectors in children [64].
7.2.5.2 Intrapulpal Anesthesia
Intrapulpal anesthesia is an additional technique of
local anesthesia for controlling pain during pulp extirpa-
tion, in cases where regular techniques failed to produce
satisfactory levels of pulpal anesthesia. A prerequisite
of this technique is the exposure of the coronal pulp,
so that intrapulpal insertion of the needle and injec-
tion of the anesthetic is possible. It is contraindicated in
pulpotomies, as the vasopressor in the anesthetic solu-
tion obstructs correct diagnosis of pulpal condition.
This technique is painful in most of cases. It should be
considered a last chance technique. If used, root canal
therapy of the tooth should follow [9].
7.3  ehavior Guidance for the
B (pain, harm, pinch) should be avoided as well as neg-
Administering of Local Anesthesia
Quite frequently, the administering of local anesthe-
sia – meaning the process that aims to provide painless
dental treatment – causes fear, anxiety, and/or avoid-
ance of therapy. Fear of needles is one of the most
common sources of fear in patients. For this reason,
painless and effective administering of anesthesia is the
most important parameter concerning patients in pedi-
atric dentistry. The word “painless” has both physical
and psychological meanings. Painless administering is
possible from a technical standpoint, meaning correct
application of topical anesthesia, use of the appropri-
ate needle, slow injection of the anesthetic solution, and
limiting the amount of needle insertions [1]. This too
however depends on various other parameters, such as
correctly assessing the child patient’s maturity level and
his psychological preparation.
Local anesthesia should be administered in every
case of dental work which will involve pain, while there
are differing and dissenting opinions on the subject.
Some children fear the needle, while others the drill.
It is a logical consequence then that preparing a tooth
without local anesthesia in a child that fears the drill
will have a negative effect on the young patient’s anxi-
ety and fear levels, whereas careful application of local
anesthesia will help desensitize the tooth and calm the
patient. On the contrary, in a child who fears the needle,
one could suggest simple restorative treatments without
use of local anesthesia. If, however, the child feels pain
at a given point during this process, local anesthesia –
with appropriate insertion – should be used. As some
researchers have suggested, the choice can be given in
relatively mature child patients, so they can control, stop,
and ask themselves for local anesthesia if needed [65].
7.3.1 Preparing the Child
Correct and painless administration of anesthesia starts
with proper psychological preparation of the patient.
Initially, based on the young patient’s age and level of
understanding, the reason why anesthesia should be used
must be explained. An approach with empathy is always
important, more so in children who are fearful or have pre-
vious negative dental experiences. Before anesthesia takes
place, the process of what will happen and what the patient
will feel should be explained in a tell-­show-­do manner.
(a) Why is anesthesia being performed.
Using a vocabulary reflective of the child’s maturity,
it is explained that, e.g., “Just as you fall asleep and
can’t feel what’s going on around you, in the same
way your tooth will fall asleep, we will clean it, and
it will wake up white and strong.” Negative words
ative sentences such as “Do not be afraid,” “it will
not harm you” because patients focus on words like
“fear” and “pain” rather than the intended message.
(b) Desirable behavior on behalf of the child.
Before administering local anesthesia, it is necessary
to secure a good level of communication with the
patient (see 7 Chap. 4). At this stage, we remind
the child that as a “good helper.” he should have his
mouth open, not move his head, and, should he feel
pain, raise his hand (the one at the assistant’s side).
(c) Applying topical anesthetic.
Application of topical anesthetic takes place as dis-
cussed above (. Fig. 7.5). This contributes to the
patient feeling as slight pain as possible upon needle
insertion, but requires slow and steady injection of
the anesthetic as the needle bores deeper.
Local Anesthesia in Pediatric Dentistry
7.3.2 Administration of Local Anesthesia
Administering local anesthesia can be painless and
effective assuming three basic conditions are met.
(a) Working position for the clinician/patient/assistant.
The child patient should always be in the supine posi-
tion, so that the dentist has a good field of vision and
can hold the head (. Fig. 7.17). This is combined
with limiting the child’s view of the dental tools and
anesthetic devices [11]. The dentist places the child’s
head in a suitable position and the assistant hands
the prepared uncapped carpule syringe carefully so
that it’s out of his field of vision. Immediately after,
as injection of the anesthetic begins, the assistant
can remove through suction the remaining anes-
thetic which flows undesirably into the mouth, so
that the bitter taste does not cause vexation. At
the same time, he/she is ready to control instinctual
movement of the child due to pain (. Fig. 7.18).
..      Fig. 7.17 a, b. Administering of anesthesia. The patient is in the
supine position, so that the dentist has a good field of vision and can
hold the head
123 7
(b) Good preparation.
The syringe and its components can be assembled out-
side the child patient’s field of vision. Alternatively,
the dentist can ask for the child’s “help,” calling the
carpule, e.g., a pen or a spaceship, the needle a straw,
and the cartridge as a magical potion. As previously
described, plastic devices, especially pen-shaped, are
preferred by children [13]. The dentist may decide
to show the syringe and needle with or without its
cap, based on the experiences, temperament, and
maturity of the child. For instance, in a child with
negative experience, who insists on the idea that he’s
getting injected, the needle could be presented as a
metal straw, and a small portion be dripped onto,
e.g., the child’s nail, as a demonstration. Once the
patient sees through the mirror a drop fall onto his
tooth, to confirm that it does not hurt, the mirror
a
..      Fig. 7.18 a. The assistant hands over the syringe to the dentist
away from the child’s field of vision, having first removed the needle
cap. b. The assistant remains prepared to control the child’s instinc-
tual movement as the dentist administers inferior alveolar nerve
block anesthesia
 124 K. N. Arapostathis and J.-L. Sixou
a a
b
7 b
..      Fig. 7.19 a. Introducing local anesthesia through the tell-show-
­do method. b. Dripping a few drops by the child, combining tell-­
show-­do and distraction techniques (Courtesy of Dr. N Kotsanos)
is pulled away and the injection of the needle and
its solution is done painlessly. Others, after assess-
ing each individual case, may prefer to use the tell-­
show-­do method in administering local anesthesia
too (. Fig. 7.19).
(c) Needle insertion.
Partial injection, in infiltration techniques, is very
important following insertion at the point where
the topical anesthetic was applied so that the area
is anesthetized and that, in the case where the child
reacts or protests and the needle needs to be removed
from the mucosa, the next insertion is not painful.
To reduce the child’s discomfort when the needle is
inserted, pressure on the area can be applied. Other
tricks effective to distracting the child are rubbing
the palate externally or creating a minor jolt [10].
Following anesthesia, in most of infiltration
techniques, a scared young child may be surprised
and feel anxious, burst into tears, and considerably
..      Fig. 7.20 a, b. Informing the young patient how she will feel after
administering anesthesia
disrupt cooperation with the dentist. For this rea-
son, it must be explained to the patient – prior to or
right after anesthesia – that he/she might feel numb-
ness, swelling, or other abnormal sensations in the
cheek, adjusting the vocabulary to the child’s level
of understanding. The dentist must confirm that the
tooth will “wake up” and will be fine in due time,
based on if the anesthetic solution contained a vaso-
pressor. It is useful to show, using a mirror, that the
patient’s face has not changed (. Fig. 7.20).
In conclusion, for reasons of brevity, it is preferred
to emphasize the following, instead of getting into com-
plicated explanations about the injection:
55 Keeping the mouth opened well.
55 Focusing on the child’s ability to raise his hand.
55 Warning about the consequent, post-anesthetic sense
of numbness in infiltration techniques.
Local Anesthesia in Pediatric Dentistry
Eye Catcher
Palatal techniques, ILA, and IO injections are not
associated with soft tissue numbness (lips, cheeks,
tongue) and therefore with soft tissues self-biting.
However, each of them may lead to anxiety and pain
during needle penetration and injection of the anes-
thetic solution. Needle rotation in IO injections in
children above the age of 7 may be surprising for the
patients. Good preparation of the patient is therefore
required.
7.4 Complications of Local Anesthesia
Local anesthesia complications may happen locally, at
the point where the anesthetic was applied, or systemi-
cally [9, 10, 21–23, 66].
The amount and type of administered local anes-
thetic as well as potential unwanted reactions should be
noted in the patient’s file.
125 7
7.4.1.4 Cheek, Lip, or Tongue Injury
Biting, due to lack of understanding of the anes-
thetic phenomenon, is quite common in children and
patients with mental difficulties, especially in buccal
infiltration and inferior alveolar nerve block anesthesia
(. Fig. 7.21). This injury is accompanied by swelling
and pain. In open rupturing trauma, some topical anti-
septic like 2% chlorhexidine is required to avoid super-
infection [9]. As a preventative measure, children and
parents should be informed that biting, scratching, or
rubbing the anesthetized soft tissues should be avoided.
The application of a cotton bud between the tissues and
the dental arches to remind the patient is also suggested.
The risk of biting is decreased or absent in palatal tech-
niques (AMSA, P-ASA) and in intraosseous techniques.
7.4.1.5 Edema
An edema can be caused by needle trauma or a local
infection. It usually causes pain, malfunction, and even
appearance problems. Sometimes, if the problem is
acute enough, it may cause obstruction of the airways.
An edema caused by injury is a minor issue that recedes
within a few days without need for therapy [9].

7.4.1 Local Complications 7.4.1.6 Hematoma

A hematoma is created intraorally from extravasation of
7.4.1.1 Needle Breakage blood due to injury caused by the needle. It rarely causes
Needle breakage is a particularly rare occurrence, espe- any problems beyond a change in color of the mucosa.
cially since the appearance and establishment of single-­ Direct pressure applied to the hemorrhaging area helps
use needles in dental work. The main cause of this control the extent of the hematoma, which usually
complication is a sudden movement from the patient as recedes without intervention within 7–14 days. The use
the needle bores the muscular substrate or is in contact of analgesics to control pain is advised, as is the avoid-
with the periosteum. Thinner needles are more sensi- ance of hot foods and dressings for several hours [66].
tive as are those which have been previously bended by
7.4.1.7 Trismus
the dentist. As a preventative measure, changing needle
direction should be avoided once it is inside the tissues, Trismus, also called lockjaw, is a spasm of the masti-
while the hand holding the syringe should remain stable. cation muscles and a disorder of the trigeminal nerve,
Needle breakage may happen when rotating the needle which causes problems in the opening function of the
in intraosseous techniques. However, it breaks at the mouth. Muscle and vessel trauma, low-level infections,
basis of the plastic piece and the broken part is easily multiple needle insertions, and large doses of anesthetic
removed by the practitioner. are the most common causes that relate etiologically
with trismus. It is uncommon in pediatric dentistry.
7.4.1.2 Pain and Sense of Burning 7.4.1.8 Reaction to Vasoconstrictors
To avoid these, use of topical anesthesia and slow injec- Vasoconstrictors rarely cause serious complications.
tion of the anesthetic solution are essential. It should The most common local complication, found in the
be noted that the solution should be between room and maxilla and the region of the canines and primary
environmental temperature. molars/premolars, is the formation of a whitish area on
buccal skin. This corresponds to the point of injection
7.4.1.3 Paresthesia (. Fig. 7.22). Τhis is a vasomotor disorder, caused by
In rare instances, in infiltration techniques, prolonged vasoconstriction of small blood vessels in that area. The
anesthesia relating to burrowing of the nerve by the skin usually returns to its normal color during the ses-
needle (felt as an electric shock in the neural region) or sion. On rare occasions, this might manifest on the ipsi-
hemorrhaging around the nerve can occur [3]. This usu- lateral portion of the face, in which case the child and
ally recedes within 2 months. the parents should be put at ease.
 126 K. N. Arapostathis and J.-L. Sixou

a b

7
c d

..      Fig. 7.21 a. Lower lip injury due to biting, 2 days following infe- open rupture trauma from 2 weeks past. d. Abrasions caused by
rior alveolar nerve block. b. The extent of the same edema. c. Cre- scratching anesthetized area, 3 days after procedure
ation of gingival tissue in another child, following acute biting and

7.4.2 Systemic Complications Allergic reactions caused by topical anesthetics are

The systemic complications in local anesthesia are tox-
icity (overdosing) and allergic reactions [2, 8]. Toxicity
can be caused by exceeding the allowed dose or intravas-
cular injection of the anesthetic solution, which causes
suppression of cardiovascular and central nervous
system. Symptoms include tremors, shivering, spasms,
suppression of breathing, and even fainting. The safety
guidelines of administering anesthesia based on the
­ avoid intravascular injection.
child patient’s weight should always be followed.
classified as Type I reactions (anaphylactic reaction).
Amide-type topical anesthetics have been proven to be
the safest, and the number of reported allergic reactions
is very low. In the case of acutely allergic patients, the
testing of the caine family drugs by an allergist is sug-
gested. To avoid systemic complications, calculating
the maximum safe dose and not exceeding it is key, as
is slow injection and suction of the residual solution to
Local Anesthesia in Pediatric Dentistry
a
b Elsevier Mosby; 2013.
..      Fig. 7.22 a. Whitish region on the cheek due to vasomotor disor-
der following the administering of local anesthesia with buccal infil-
tration in the respective maxillary primary molars. b. A more
generalized case, 30 minutes after inferior alveolar nerve block.
Anesthetic solution used: 2% lidocaine with epinephrine 1:80,000
References
1. Wilson S, Ganzberg SI. Pain perception and control. In: Casa-
massino PS, Fields HW, McTigue DJ, Nowak AJ, editord. Pedi-
atric dentistry. Infancy through adolescence. 5th ed., Ch. 7. St
Louis: Elsevier Saunders; 2013.
2. Raadal M, Lundeberg S, Haukali G. Pain, pain control, and
sedation. In: Koch G, Poulsen S, editors. Pediatric dentistry. A
clinical approach. 2nd ed., Ch. 5. Munksgaard, Copenhagen;
2009.
3. American Academy of Pediatric Dentistry. Use of local anes-
thesia for pediatric dental patients. Reference Manual 2017/18;
39(6).
4. Klingberg G, Ridell K, Brogårdh-Roth S, Vall M, Berlin
H. Local analgesia in paediatric dentistry: a systematic review of
127 7
techniques and pharmacologic agents. Eur Arch Paediatr Dent.
2017;18(5):323–9.
5. Arapostathis KN, Coolidge T, Emmanuil D, Kotsanos N. Reli-
ability and validity of the Greek version of the Children’s
fear survey schedule – dental subscale. Int J Peadiatr Dent.
2008;18(5):374–9.
6. Saravia ME, Bush JP. The needleless syringe: efficacy of anes-
thesia and patient preference in children dental patients. J Clin
Pediatr Dent. 1991;15(2):109–12.
7. Munshi AK, Hegde A, Bashir N. Clinical evaluation of the
efficacy of anesthesia and patient preference using the needle-
less jet syringe in pediatric dental practice. J Clin Pediatr Dent.
2001;25(2):131–6.
8. McDonald RE, Avery DR, Dean JA, Jones JE: Local anesthe-
sia and pain control for the child and adolescent, In: Dean JA,
Avery DR, MacDonald RE, editors. Dentistry for the child and
adolescent. 9th ed., Ch. 13. Mosby: Elsevier; 2011.
9. Malamed SF. Handbook of local anesthesia. 6th ed. St Louis:
10. Kühnisch J, Daubländer M, Klingberg G, Dougall A, Spyrido-
nos Loizides M, Stratigaki E, Amar JL, Anttonen V, Duggal M,
Gizani S. Best clinical practice guidance for local analgesia in
paediatric dentistry: an EAPD policy document. Eur Arch Pae-
diatr Dent. 2017;18(5):313–21.
11. Fayle SA, Duggal ΜS. Local Analgesia. In: Duggal ΜS, et al.
editors. Restorative Techniques in Paediatric Dentistry. 2nd ed.,
Ch 2. Martin Dunitz, London; 2002.
12. Meechan JR, Robb ND, Seymour RA. Pain and anxiety control
for the conscious dental patient. New York: Oxford University
Press; 1998, Ch 6, pp. 87–100.
13. Kuşcu OO, Akyuz S. Children’s preferences concerning the phys-
ical appearance of dental injectors. J Dent Child. 2006;73(2):
116–21.
14. Davis MJ, Vogel LD. Local anesthetic safety in pediatric patients.
N Y State Dent J. 1996;62(2):32–5.
15. Kohli K, Ngan P, Crout R, Linscott CC. A survey of local and
topical anesthesia use by pediatric dentists in the United States.
Pediatr Dent. 2001;23(3):265–9.
16. Fuller NP, Menke RA, Meyers WJ. Perception of pain to three
different intraoral penetrations of needles. J Am Dent Assoc.
1979;99(5):822–4.
17. Sixou JL, Barbosa-Rogier ME. Efficacy of intraosseous injec-
tions of anesthetic in children and adolescents. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2008;106(2):173–8.
18. Carr MP, Horton JE. Clinical evaluation and comparison of 2
topical anesthetics for pain caused by needle sticks and scaling
and root planing. J Periodontol. 2001;72(4):479–84.
19. Flanagan T, Wahl MJ, Schmitt MM, Wahl JA. Size doesn’t
matter: needle gauge and injection pain. Gen Dent. 2007;55(3):
216–7.
20. Meechan JG. Pain control in local analgesia. Eur Arch Paediatr
Dent. 2009;10(2):71–6.
21. Virts BE. Local anesthesia toxicity review. Pediatr Dent.
1999;21(6):375.
22. Meechan J. How to avoid local anaesthetic toxicity. Br Dent J.
1998;184(7):334–5.
23. Harding AM. Pharmacologic considerations in pediatric den-
tistry. Dent Clin N Am. 1994;38(4):747.
24. Kämmerer PW, Krämer N, Esch J, Pfau H, Uhlemann U, Piehl-
meier L, Daubländer M. Epinephrine-­reduced articaine solution
(1:400,000) in paediatric dentistry: a multicentre non-interven-
tional clinical trial. Eur Arch Paediatr Dent. 2013;14(2):89–95.
25. Sixou JL, Marie-Cousin A. Intraosseous anaesthesia in children
with 4% articaine and epinephrine 1:400,000 using computer-
assisted systems. Eur Arch Paediatr Dent. 2015;16(6):477–81.
 128 K. N. Arapostathis and J.-L. Sixou
26. Oikarinen VJ, Ylipaavalniemi P, Evers H. Pain and tempera-
ture sensations related to local analgesia. Int J Oral Surg.
1975;4(4):151–6.
27. Meechan JG, Day PF. A comparison of intraoral injection dis-
comfort produced by plain and epinephrine-­containing lidocaine
local anesthetic solutions: a randomized, double-blind, split-
mouth, volunteer investigation. Anesth Prog. 2002;49(2):44–8.
28. Maragakis GM, Musselman RJ. The time used to adminis-
ter local anesthesia to 5 and 6 year olds. J Clin Pediatr Dent.
1996;20(4):321–3.
29. Wilson S. Local anesthesia and oral surgery in children. In:
Casamassino PS, Fields HW, McTigue DJ, Nowak AJ. Pediatric
dentistry. Infancy through adolescence. 5th ed., Ch. 28. St Louis:
Elsevier Saunders; 2013.
30. Rood JP. Some anatomical and physiological causes of failure to
achieve mandibular analgesia. Br J Oral Surg. 1977;15(1):75–82.
31. Ram D, Hermida LB, Peretz B. A comparison of warmed and
room-temperature anesthetic for local anesthesia in children.
7 Pediatr Dent. 2002;24(4):333–6.
32. Tzafalia M, Sixou JL. Administration of anesthetics using metal
syringes. An ex vivo study. Anesth Prog. 2011;58(2):61–5.
33. Rosenberg ES. A computer-controlled anesthetic delivery system
in a periodontal practice: patient satisfaction and acceptance. J
Esthet Restor Dent. 2002;14(1):39–46.
34. Sumer M, Misir F, Koyuturk AE. Comparison of the wand with
a conventional technique. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2006;101(6):e106–9.
35. Tahmassebi JF, Nikolaou M, Duggal MS. A comparison of pain
and anxiety associated with the administration of maxillary
local analgesia with wand and conventional technique. Eur Arch
Paediatr Dent. 2009;10(2):77–82.
36. Libonati A, Nardi R, Gallusi G, Angotti V, Caruso S, Coniglione
F, Marzo G, Mattei A, Tecco S, Paglia L. Pain and anxiety asso-
ciated with computer-controlled local Anaesthesia: systematic
review and meta-analysis of cross-over studies. Eur J Paediatr
Dent. 2018;19(4):324–32.
37. Pozos-Guillén A, Loredo-Cruz E, Esparza-­Villalpando V, Mar-
tínez-Rider R, Noyola-Frías M, Garrocho-­Rangel A. Pain and
anxiety levels using conventional versus computer-controlled
local anesthetic Systems in Pediatric Patients: a Meta-analysis. J
Clin Pediatr Dent. 2020;44(6):371–99.
38. Smolarek PC, Wambier LM, Rodrigues Chibinski AC. Does
computerized anesthesia reduce pain during local anesthesia in
pediatric patients for dental treatment? A systematic review and
meta-analysis. Int J Paediatr Dent. 2020;30(2):118–35.
39. Carugo N, Paglia L, Re D. Pain perception using a computer-
controlled anaesthetic delivery system in paediatric dentistry:
a review. Carugo N, Paglia L, Re D. Eur J Paediatr Dent.
2020;21(3):180–2.
40. Monteiro J, Tanday A, Ashley PF, Parekh S, Alamri H. Interven-
tions for increasing acceptance of local anaesthetic in children
and adolescents having dental treatment. Cochrane Database
System Rev. 2020;2:CD011024.
41. Versloot J, Veerkamp JS, Hoogstraten J. Pain behaviour and dis-
tress in children during two sequential dental visits: comparing
a computerised anaesthesia delivery system and a traditional
syringe. Br Dent J. 2008;205(1):E2.
42. Kuscu OO, Akyuz S. Is it the injection device or the anxiety
experienced that causes pain during dental local anaesthesia? Int
J Paediatr Dent. 2008;18(2):139–45.
43. Palm AM, Kirkegaard U, Poulsen S. The wand versus tradi-
tional injection for mandibular nerve block in children and
adolescents: perceived pain and time of onset. Pediatr Dent.
2004;26(6):481–4.
44. Baghlaf K, Alamoudi N, Elashiry E, Farsi N, El Derwi DA,
Abdullah AM. The pain-related behavior and pain perception
associated with computerized anesthesia in pulpotomies of man-
dibular primary molars: a randomized controlled trial. Quintes-
sence Int. 2015;46(9):799–806.
45. Arapostathis KN, Dabarakis NN, Coolidge T, et al. Compari-
son of acceptance, preference, and efficacy between jet injection
INJEX and local infiltration anesthesia in 6 to 11 year old dental
patients. Anesth Prog. 2010;57(1):3–12.
46. Bittmann S, Krüger C. Benzocaine-induced methaemoglobinae-
mia: a case study. Br J Nurs. 2011;20(3):168–70.
47. Benham NR. The cephalometric position of the mandibular
foramen with age. J Dent Child. 1976;43(4):233–7.
48. Wright GZ, Weinberger SJ, Martin R, Plotzke O. The effective-
ness of infiltration anesthesia in the mandibular primary molar
region. Pediatr Dent. 1991;13:278–83.
49. Oulis C.J, Vadiakas G, Vassilopoulou A. The effectiveness of
mandibular infiltration compared to mandibular block anaes-
thesia in children. Pediatr Dent. 1996;18(4):301–305.
50. Yu F, Xiao Y, Liu H, Wu F, Lou F, Chen D, Bai M, et al. Evalu-
ation of three block anesthesia methods for pain management
during mandibular third molar extraction: a meta-analysis. Sci
Rep. 2017:20;7:40987.
51. Jälevik B, Klingberg G. Pain sensation and injection techniques
in maxillary dento-alveolar surgery procedures in children--a
comparison between conventional and computerized injection
techniques (the wand). Swed Dent J. 2014;38(2):67.
52. Feda M, Al Amoudi N, Sharaf A, Hanno A, Farsi N, Masoud
I, Almushyt A. A comparative study of children's pain reac-
tions and perceptions to AMSA injection using CCLAD ver-
sus traditional injections. J Clin Pediatr Dent. 2010;34(3):
217–22.
53. Allen KD, Kotill D, Larzelere RE, Hutfless S, Beraghi S. Com-
parison of a computerized anaesthesia device with a tradi-
tional syringe in preschool children. Pediatr Dent. 2002;24:
315–20.
54. Ram D, Kassirer J. Assessment of a palatal approach-anterior
superior alveolar (P-ASA) nerve block with the wand® in paedi-
atric dental patients. Int J Paediatr Dent. 2006;16:348–51.
55. Woodmansey K. Intraseptal anesthesia: a review of a relevant
injection technique. Gen Dent. 2005;53(6):418–20.
56. Sixou JL, Marie-Cousin A, Huet A, Hingant B, Robert JC. Pain
assessment by children and adolescents during intraosseous
anaesthesia using a computerized system (QuickSleeper). Int J
Paediatr Dent. 2009;19:360–6.
57. Cabasse C, Marie-Cousin A, Huet A, Sixou JL. Computer-
assisted intraosseous anaesthesia for MIH teeth. A preliminary
study. Odont Stomatol Trop. 2015;38:5–9.
58. Smaïl-Faugeron V, Muller-Bolla M, Sixou JL, Courson F. Eval-
uation of intraosseous versus conventional infiltration anaes-
thesia in pediatric oral healthcare: combined split-mouth and
parallel-arm randomized controlled trial. Int J Paediatr Dent.
2019;29(5):573–84.
59. Garfunkel AA, Kaufman E, Marmary Y, Galili D. Intraliga-
mentary--intraosseous anesthesia. A radiographic demonstra-
tion. Int J Oral Surg. 1983;12(5):334–9.
Local Anesthesia in Pediatric Dentistry
60. Sharaf AA. Evaluation of mandibular infiltration versus
block anesthesia in pediatric dentistry. ASDC J Dent Child.
1997;64:276–81.
61. Brannstrom M, Lindskog S, Nordenvall KJ. Enamel hypoplasia
in permanent teeth induced by periodontal ligament anesthesia
of primary teeth. J Am Dent Assoc. 1984;109(5):735–6.
62. Roberts GJ, Simmons NB, Longhurst P, Hewitt PB. Bacterae-
mia following local anaesthetic injections in children. Br Dent J.
1998;185(6):295–8.
63. Sonbol H, Spratt D, Roberts GJ, Lucas VS. Prevalence, inten-
sity and identity of bacteraemia following conservative dental
129 7
procedures in children. Oral Microbiol Immunol. 2009;24(3):
177–82.
64. Ashkenazi et al. Effect of computerized delivery intraligamental
injection in primary molars on their corresponding permanent
tooth buds. Int J Paediatr Dent. 2010;20:270–5.
65. Gray M. Local analgesia in paedodontics. Br Dent J.
1994;177(10):366.
66. Ram D, Peretz B. Reactions of children to ­maxillary infiltration
and mandibular block injections. Pediatr Dent. 2001;23:343–6.
 131 8

Pharmacologic Behavior
Management (Sedation –
General Anesthesia)
Dimitrios Velonis, Dimitrios Emmanouil, and Keira P. Mason

Contents

8.1 Sedation – 132

8.1.1 I ndications – 134
8.1.2 Sedation Procedures – 135

8.2  inimal Sedation (Anxiolysis) and Moderate (Conscious)

M
Sedation – 137
8.2.1 I nhalation Sedation with Nitrous Oxide/Oxygen Mixture – 137
8.2.2 Moderate Sedation with Other Drugs – 143

8.3 General Anesthesia – 145

8.3.1  reoperative Evaluation and Admission to Hospital – 145
P
8.3.2 Induction of Anesthesia and Dental Treatment – 146

8.4 Safety Concerns About Sedation or General Anesthesia – 151

References – 151

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_8
 132 D. Velonis et al.

8.1 Sedation Sedation is defined as a state of central nervous sys-

In many parts of the world, parenting styles and child
protection laws have changed significantly over the last
30 or 40 years. These changes have affected parental
expectations of behavioral management of their child
at the dentist. The “helicopter parent,” a descriptive
term used for the parent who takes a “hovering” inter-
est in his/her child’s behavior, has affected the practice
of pediatric dentistry. In the past, parental presence
was neither allowed nor encouraged during dental
treatment. In some countries, it was common for the
dentist to apply restrictive behavioral management
techniques and this was preferred for reducing seda-
tion needs. Today, however, the majority of pediatric
dentists refrain from restrictive methods in favor of
pharmacologic behavioral management. Following this
8 increased use of sedation and general anesthesia (GA),
such training has become a critical component of the
curriculum of postgraduate pediatric dentistry training
programs [1].
tem (CNS) depression of consciousness. The specific
effects of sedatives on each individual are dependent
on the choice of medication(s), the dosage, the route
of delivery, and idiosyncratic responses to these med-
ications. The level of sedation follows a continuum
and ranges from minimal sedation for pain and anx-
iolysis to deep sedation. The American Society of
Anesthesiologists (ASA) and the American Acad-
emy of Pediatric Dentistry (AAPD) define the levels
of sedation as outlined by the ASA [2] (. Table 8.1,
. Fig. 8.1).
In minimal sedation patients respond to verbal com-
mands, while respiratory and circulatory functions are
unaffected and reflexes are mildly reduced.

Eye Catcher

With appropriate non-pharmacologic behavioral

management techniques, most children will cooper-
ate. There are some exceptions, like those with intense
anxiety, gag reflex, or certain phobias. Especially for
those who are unable to understand, follow instruc-
tions, or cooperate with behavioral techniques, mini- Minimal
mal or moderate sedation may be administered in Moderate
Deep
combination with non-pharmacologic techniques. GA
Sedation should be administered by trained person- Responds to stimuli
nel following the relevant guidelines, in appropriately Breathing/Airway
equipped treatment rooms. In some situations, deep
sedation or general anesthesia may be needed in a Cardiovascular
hospital setting. ..      Fig. 8.1 An arbitrary schematic representation of the continuum
of sedation to general anesthesia (GA)

..      Table 8.1 Level of CNS sedation [2] (older terms appear in parentheses)

Level of sedation
Minimal sedation Moderate sedation (conscious Deep sedation General anesthesia
(anxiolysis) sedation)

Patient Pt. responds to Pt. responds to verbal or light Pt. responds only after repeated No pt. response even to
response to verbal stimuli tactile stimuli (e.g., touch), eyes or painful stimuli, difficult to painful stimuli
stimuli usually closed arouse
Breathing – Not affected Adequate Potentially inadequate Usually inadequate
Airway No intervention needed Intervention may be needed Intervention needed
Cardiovascular Not affected Usually adequate Usually adequate Potentially inadequate
function
Pharmacologic Behavior Management (Sedation – General Anesthesia)
In moderate sedation, patients respond to verbal
commands. There is minimal risk of airway compromise,
and cardiovascular functions are usually unaffected.
In deep sedation there is partial or total loss of pro-
tective reflexes, and patients are not easily aroused but
will respond to persistent verbal or painful stimuli.
Spontaneous breathing may be compromised and open
airway support may be needed. Cardiovascular function
is usually stable; however, the risks during deep sedation
are similar to those of general anesthesia.
In general anesthesia protective reflexes are com-
pletely lost and patients require airway support.
Cardiovascular function is affected and physiologic
monitoring is needed.
The most important element of the new guidelines
is the introduction of the term “rescue.” Transition
from one stage of sedation to the next is always pos-
sible; therefore, all personnel must be appropriately
trained and certified to prevent and treat complications,
and decrease, or reverse the sedation if needed. Adverse
and unfortunate incidents have been reported in several
countries during dental sedation, even at doses which
were deemed within safe dosing limits [3, 4]. Several
associations, the American Academy of Pediatric
Dentistry included, have now updated guidelines. [2, 4]
Sedation Acceptance and Preferences in Different
Countries In the United States (USA), sedation has
been used for dental procedures for many years. 82% of
pediatric dentists, members of the American Academy of
Pediatric Dentistry, reported using sedation in more than
10% of their patients [5]. Nitrous oxide/oxygen inhala-
tion sedation is used widely by 3/4 of pediatric dentists
and more than half of general dentists [5, 6]. Similar to
findings in the USA, 75% of pediatric dentists worldwide
reported using nitrous oxide/oxygen inhalation sedation
alone or in combination with other drugs [7]. The same
sample of pediatric dentists estimated that 10–20% of
children could benefit from pharmacologic behavioral
management. In some dental schools, these sedation tech-
niques are a component of the undergraduate dental cur-
riculum [6].
In Europe there is a lack of uniformity in sedation
training and teaching. In Sweden, nitrous oxide/oxy-
gen sedation has been used since 1979. Appropriately
trained dentists administer the sedatives (most often
oral or rectal midazolam) and nitrous oxide/oxygen
inhalation sedation to patients classified as ASA I and
ASA II [8]. In the United Kingdom (UK), 28% of the
National Health Service (NHS) dentists reported using
sedation [9]. In Italy, sedation is administered by a
trained dentist or anesthesiologist, but comprehensive
training and certification requirements as well as legis-
133 8
lation have not been established [10]. Greece prohibits
the use of oral or nitrous oxide sedation by dentists in
a dental practice setting. The Association for Dental
Education in Europe (ΑDΕΕ) has issued sedation guide-
lines for dental graduates from European dental schools
[11]. According to these guidelines, every dental gradu-
ate should have a minimum background on pharma-
cologic behavioral management of both children and
adults. A recent resolution of the European Dentists
Council used an evidence-­based approach to propose
the training and use requirements for nitrous oxide in
dental practices. In order to comply with European
guidelines and for achieving conformity, it is upon the
dental schools and continued education providers to
provide such training and upon the legislators to pro-
vide the legal framework.
Preferences by dentists and acceptance by patients
and their parents also vary across the globe. For exam-
ple, in many dental offices in the USA and Canada, cer-
tified dentists or dentists-anesthesiologists administer
deep sedation for potentially difficult and painful proce-
dures, such as impacted third molar extractions.
In contrast, deep sedation is not used in dental offices
in the UK, as it is considered equivalent to general
anesthesia. Differences also exist for the preferred route
of administration (. Fig. 8.2). While rectal administra-
tion of midazolam is not the method of choice in the
UK and the USA, it is widely used in the Scandinavian
countries. The use of restraints during sedation is also
not uniformally accepted nor adopted worldwide. The
use of papoose board and wrap is still used during seda-
tion in the USA and is generally accepted by parents
and approved by the AAPD, but it is legally forbidden
in the UK and Scandinavian countries [8, 12].
..      Fig. 8.2 Oral administration of midazolam mixed with juice by
needleless syringe (courtesy of Dr. J. Veerkamp)
 134 D. Velonis et al.

Eye Catcher 8.1.1.1 Special Considerations

The ΑDΕΕ requires that every dental graduate
should have a minimum background on pharma-
cologic behavioral management of both children
and adults. In the USA, the American Dental
Association is changing the examination process for
dental graduates merging National Dental Board
Exams (NDBE) I and II into an integrated exam,
the INBDE (Integrated National Dental Board
Exam), effective 2020, in order to integrate content
from the biomedical, behavioral, and clinical sci-
ences [13].
8.1.1 Indications
8 The American Society of Anesthesiologists classifies
patients into six categories according to their physi-
cal status (. Table 8.2). Patients routinely selected for
treatment under sedation in the dental office are usu-
ally ASA I or ΙΙ. Patients classified as ASA III or ΙV are
often triaged to be managed and treated in a hospital
setting in cooperation with an anesthesiologist, as the
risk of complications and mortality increases the higher
the ASA category [2, 14].
Careful preoperative assessment and consulta-
tion with specialists may be necessary for a compre-
hensive evaluation and formulation of a sedation and
discharge plan. At any category, the addition of “E”
denotes emergency surgery. An emergency is defined
as existing when delay in treatment of the patient
would lead to a significant increase in the threat to life
or body part.
..      Table 8.2 American Society of Anesthesiologists (ASA)
classification [14]
ASA I A normal healthy patient
ASA II A patient with mild systemic disease without
substantive functional limitations (e.g., controlled
DM, HTN)
ASA III A patient with severe systemic disease with
substantive functional limitations (e.g., poorly
controlled DM, HTN)
ASA IV A patient with severe systemic disease that is a
constant threat to life
ASA V A moribund patient who is not expected to survive
without the operation
ASA VI A declared brain-dead patient whose organs are
being removed for donor purposes
in the Pediatric Patient
Children differ from adults in various aspects: ana-
tomical, physiological, emotional, social, and pharma-
cological. Understanding these differences is critical
in optimizing safe care during and following sedation.
Some of these anatomical and respiratory airway differ-
ences may include the following:
zz Anatomical
55 Large head size, short neck, large tongue, tonsils/
adenoids
55 Narrow nasal passages
55 Large epiglottis, short trachea
55 Cricoid cartilage is the narrowest part of a conically
shaped larynx (. Fig. 8.3)
55 Loose teeth
55 Anterior vocal cords
zz Respiratory
55 Low functional residual lung capacity (FRC)
55 High oxygen consumption (6 ml/kg/min instead of
3 ml/kg in adults)
55 Increased apnea incidents
55 Frequent upper respiratory infections
8.1.1.2  ssessment of Health Status
A
and Cooperation
The medical history of the child should be reported by
the parent or legal guardian. The following elements are
critical considerations in making a treatment plan:
55 Heart murmur or cardiac malformations.
55 Bleeding or hematologic disorders.
55 Respiratory disease, asthma, or recent respiratory
infection.
55 Gastroesophageal reflux disease (GERD).
55 Immune disorders.
55 Hepatic or renal dysfunction.
55 History of adverse reactions to sedation or general
anesthesia of the child or first-degree relative.
55 Previous surgical operations.
55 Allergies to foods and drugs.
55 Craniofacial abnormalities.
55 Obstructive sleep apnea, sleep disordered breathing,
and home physiologic monitors which may include
pulse oximeter.
55 Endocrine abnormalities.
55 Current and past medications, with special consider-
ation to:
–– Opioids or hypnotics.
–– Medications that may cross-react with sedatives
(e.g., macrolide antibiotics that prolong the action
of midazolam).
–– Bleomycin because nitrous oxide is contraindicated.
Pharmacologic Behavior Management (Sedation – General Anesthesia)
a b
..      Fig. 8.3 a. Fiberoptic photograph of the glottis and the entrance to the trachea in a child. b. Pediatric vs. adult airway. Cricoid cartilage
is the narrowest part of a funnel-shaped infant’s larynx (anterior side at right)
Decisions on selecting specific sedatives as well as route
of administration largely also depend on the child’s
behavior, ability to cooperate, and extent of treatment
required. A certain degree of cooperation is neces-
sary for successful completion of the dental procedure
under sedation. For example, a child that needs only an
extraction or a pulpotomy may be a good candidate for
midazolam. A child needing full quadrant restorative
treatment may benefit from a combination of oral seda-
tion with opioids, antihistamines, and/or nitrous oxide/
oxygen inhalation. A child with needle phobia or a sen-
sitive gag reflex may be treated under only nitrous oxide/
oxygen sedation. Still for nitrous oxide to be successful,
the child has to accept the mask and breathe through
the nose [8].
8.1.1.3  reparation of Child and Parent
P
for Sedation and Informed Consent
Before sedation is considered as an option, standard-
of-­care protocols should be followed, including a thor-
ough medical and dental history, comprehensive clinical
exam, and behavioral assessment or modification. The
proposed treatment plan(s) should be discussed with
the parent(s) and an informed consent obtained. The
informed consent should explain in easy-to-understand
terms, the procedure, the benefits and risks, as well as
alternatives to the proposed treatment plan [15].
Solid or liquid food in the stomach may pose a con-
siderable risk of aspiration in patients undergoing deep
sedation or general anesthesia secondary to suppres-
sion of protective reflexes. For moderate sedation, most
guidelines advocate that the patient have no solid food
6 hours prior, dairy products 4 hours prior, and water
or other clear liquids (apple juice) 2 hours prior to the
sedation. For minimal sedation with nitrous oxide/oxy-
135 8
gen inhalation sedation (NO/OS), fasting is not abso-
lutely necessary, but it is generally recommended that
the patient has not had a full meal 2 hours prior, albeit
the low incidence of vomiting (0.5%) appears irrespec-
tive of fasting time [16–18].
Whether minimal and moderate sedation or gen-
eral anesthesia is used, psychological preparation
of the child and family is of great importance. Non-­
pharmacologic behavioral management techniques
should be tailored to each situation. In some cases,
these techniques may be adequate and eliminate the
need for sedatives [12].
Postoperative instructions should be given both
verbally and in printed form. Fasting instructions, pos-
sible adverse reactions, and their management should be
detailed and emergency contacts clearly provided [15].
8.1.2 Sedation Procedures
8.1.2.1 General Prerequisites
For all sedation in the dental office, dentists and staff
should be certified and updated on all guidelines, poli-
cies, and procedures. At a minimum, basic life support
(BLS) training must be up to date. Sedation appoint-
ments are ideally scheduled during less busy hours in
the dental schedule. Checklists mostly include nil per
os (NPO) status, presence of escorting parent or legal
guardian, signed informed consent, documentation of
recent changes in physical status, contraindications to
treatment, and vital signs. The dentist should be accom-
panied by an assistant, as sedatives may produce delir-
ium or agitation. Chair-side presence of the parent or, in
some offices, observation through glass windows or via
camera should be made available [12].
 136 D. Velonis et al.

8.1.2.2 Monitoring and Resuscitation 8.1.2.3  ocumentation before and during

Equipment (General
Recommendations)
Recommendations for monitoring and resuscitation
equipment may vary slightly based on country guide-
lines or laws. A general list should include:
55 Automated external defibrillator (AED) and all nec-
essary equipment for BLS.
55 Central supply of oxygen, or two oxygen cylinders.
55 All necessary medications, materials, and devices for
respiratory and airway support (self-inflating bag,
laryngoscope, endotracheal tubes, laryngeal mask
airways, cardiovascular monitoring, capnograph,
electrocardiograph, blood pressure cuff).
55 Surgical suction, central or portable.
55 Pulse oximeter.
8 Monitoring of vital signs should be performed according
to targeted depth of sedation and should include clinical
observation, pulse oximetry, blood pressure monitoring,
capnography, and precordial or plain stethoscope [4, 19,
20] (. Table 8.3, . Fig. 8.4).
D
Sedation
Before sedation is administered, the patient’s medical
record must include [4, 20]:
55 Summary of dental history and treatment plan.
55 List of stimuli or conditions that trigger or exacer-
bate patient’s fear or anxiety.
55 Indications and rationale of sedation use.
55 Type of sedation route and dosages.
55 Signed informed consent from the parent/legal
guardian.
55 Medical history and history of previous use of seda-
tion or GA.
55 Confirmation of delivery of pre- and post-sedation
instructions.
During sedation, meticulous record keeping of the
sedation session is required both for scientific and legal
reasons. Detailed documentation on the outcomes or
adverse reactions is mandatory.
Immediately before administering sedation, the den-
tist or sedation provider must:

..      Table 8.3 Monitoring equipment and personnel requirements for sedation

Level of sedation
Minimal sedationa Moderate sedation Deep sedation

Monitoring − Clinical − Clinical observation − Clinical observation

observation − Precordial stethoscope − Precordial stethoscope
− Precordial − Pulse oximetry − Pulse oximetry
stethoscope − HR, BP, respiration − HR, BP, respiration
− Pulse oximetry − ECG recommended − ECG required
recommended − Capnography recommended − Capnography required
Personnel 2 persons 2 persons 3 persons
Observer trained Observer trained in PALS, may assist dental Independent observer trained in PALS
in PALS, may provider
assist dental
provider
Responsible Skilled to rescue a child with apnea, Skilled to rescue a child with apnea, laryngospasm,
practitioner laryngospasm, and/or airway obstruction and/or airway obstruction including the ability to
including the ability to open the airway, open the airway, suction secretions, provide CPAP,
suction secretions, provide CPAP, and and perform successful bag-valve-mask ventilation;
perform successful bag-valve-­mask recommended that at least one practitioner should
ventilation; recommended that at least one be skilled in obtaining vascular access in children
practitioner should be skilled in obtaining immediately available; trained in PALS
vascular access in children; trained in PALS

PALS Pediatric advanced life support

CPAP Continuous positive airway pressure
aFor minimal sedation generally not more than observation and intermittent assessment of sedation level is required, but because some

children will become moderately sedated, it is recommended that guidelines for moderate sedation will be readily applied
Pharmacologic Behavior Management (Sedation – General Anesthesia)
a b
c 8.2
d two levels of sedation can be achieved by the use of
..      Fig. 8.4 Monitoring equipment. a. Tabletop pulse oximeter. b.
Portable pulse oximeter. c. Capnograph. d. Precordial stethoscope
1. Perform a final check of the medical records and
answer any questions that may have risen in the
interim.
2. Perform a physical exam (blood pressure, heart rate,
chest and tracheal auscultation, extraoral exam,
weight and temperature recording).
137 8
Vital signs and physical exam findings are recorded on
the procedure monitoring record along with time, routes,
and dosage of sedatives. Vital signs and clinical assess-
ment are continuously monitored and ­ documented
every 5 minutes during this time period.
At the end of the dental treatment under sedation,
the following have to be on file:
55 Dental treatment performed.
55 Type of sedation used and patient response.
55 Documentation of adherence to fasting instructions
before sedation.
Oral and written instructions are provided at discharge
along with a 24-hour phone or pager number in case of
emergency [15].
 inimal Sedation (Anxiolysis)
M
and Moderate (Conscious) Sedation
Anxiolysis is defined as the reduction or elimination of
pain and anxiety in a conscious patient [2]. The main
purpose of conscious sedation in pediatric dentistry
(such as the combination of NO/OS and benzodiaz-
epines) is to bring the child into a state of relaxation,
making the behavioral modification techniques more
effective. Conscious sedation does not replace the effec-
tive communication between doctor and young patient,
nor can it create a sense of safety by itself. These first
inhalation sedation, oral sedation (most commonly
used methods in the dental practice), or their combina-
tion. Alternatively, it may be administered intramuscu-
larly, intravenously, intraperitoneally, or intranasally
(. Fig. 8.2). The drugs and techniques used should
have a wide margin of safety [11, 20].
8.2.1 I nhalation Sedation with Nitrous
Oxide/Oxygen Mixture
Nitrous oxide (N2O) is a nonirritating, colorless, odor-
less, tasteless gas, capable of producing anxiolysis and
mild-to-moderate analgesia and amnesia. It is the least
potent of all anesthetic gases used today. It is also an
effective analgesic and anxiolytic causing CNS depres-
sion with little effect on the respiratory system, known
also as “laughing gas” because it causes a feeling of
euphoria and relaxation [20, 21]. The AAPD, among
other organizations, recognizes NO/OS as a safe and
effective technique to reduce anxiety, produce analgesia,
 138 D. Velonis et al.
8 Nitrous oxide flowmeter
Oxygen flowmeter
Mixture percentage dial
Flow control knob
Oxygen flush
Air intake valve
Breathing tube connector
..      Fig. 8.5 Contemporary nitrous oxide/oxygen delivery system
and enhance effective communication between a patient
and health-care provider. Clinicians though should not
make the mistake of thinking that NO/OS, by itself, con-
trols behavior. It rather serves as an adjunct to behavior
management [17].
N2O was discovered in 1772 by the British J. Priestley
and was first used in dentistry in 1844 by H. Wells, an
American dentist, for tooth extractions. In 1868 it was first
used as a mixture with oxygen, and the delivery systems of
N2O/O2 that were developed in the decade 1955–1966 are
still used until today (. Fig. 8.5). N2O is one of the most
important discoveries of modern anesthesiology [22].
N2O has a rapid uptake, being absorbed quickly from
the pulmonary alveoli and held in a simple solution in the
serum. It is dissolved and transported in blood; it does not
combine with hemoglobin, and it does not undergo bio-
transformation. It is relatively insoluble, passing down a
gradient into other tissues and cells in the body, such as
the CNS. It is excreted quickly from the lungs. Elimination
of N2O occurs by means of expiration and its low solubil-
ity allows it to be removed rapidly [21]. At the molecular
level it has multiple mechanisms of action that charac-
terize its anesthetic, analgesic, and anxiolytic pharmaco-
logical properties. The anesthetic effect of N2O appears to
be caused by inhibition of NMDA glutamate receptors,
removing its excitatory influence on the nervous system.
Subanesthetic N2O concentrations produce only analgesic
and anxiolytic effects without loss of consciousness [23].
Analgesia and anxiolysis: N2O appears to manifest its
action on the GABA-A receptors. It causes elevation of
the pain threshold, in a dose-dependent manner, being
a weak analgesic, insufficient to ensure painless dental
treatment by itself. Its analgesic activity has long been
used in obstetrics for the relief of labor pain, in several
medical procedures, as well as in emergency departments
for reduction of fractures and wound suturing, even in
patients with cancer. It is important, however, to make
a clear distinction between the high anesthetic concen-
trations producing unconsciousness and the much lower
doses associated with analgesia and psychotropic effects,
i.e., anxiolysis and euphoria. The mechanisms involved
in the latter are not yet fully understood. However, there
is sufficient evidence to suggest that nitrous oxide’s anal-
gesic and anxiolytic actions are parallel to those of opi-
oids and benzodiazepines, respectively [24].
Anesthesia is the main use of N2O, which made it
widely known in medicine, as it was the first drug used
for induction of surgical anesthesia. Despite its low
potency, N2O is the most widely used general anesthetic.
If given alone, it would require hyperbaric conditions to
achieve general anesthesia; thus, it is used to reduce the
concentration of a second anesthetic gas, accelerating
the induction [25].
N2O inhalation sedation has several advantages: a rapid
onset of action (within 5 min) without the need for vascu-
lar access or painful administration. Recovery is also very
rapid (a child can be discharged within 15 min). The dosage
is easily adjusted to maintain a minimum sedation. It exerts
minimal effect on cardiovascular and respiratory function,
which, if observed, is more due to the relaxant activity
rather than a direct effect on the cardiovascular and respi-
ratory systems. It is the most common sedative procedure
among dentists and more so for pediatric dentists [5, 7].
Pharmacologic Behavior Management (Sedation – General Anesthesia)
139 8

Box
N2O sedation is the most commonly used sedation
procedure in dentistry:
1. Easy route of administration (no injection or
phlebotomy).
2. Rapid onset (5 minutes).
3. Easy dose titration.
4. Fast recovery (15 minutes).
5. Minimal effect on cardiovascular and respiratory
function.

8.2.1.1 Stages of Anesthesia

For general anesthesia, four stages are recognized in
Guedel’s classification [26]:
55 Stage 1: Induction (also referred to as analgesia).
55 Stage 2: Excitement stage.
55 Stage 3: Surgical anesthesia.
55 Stage 4: Overdose.

The stage 1 boundaries span from the induction of anes-

thesia to loss of consciousness. Patients still feel pain in
this stage.

Relative Analgesia and Planes of Analgesia

In 1968 Langa introduced a term to represent N2O
inhalation sedation, “relative analgesia” (RA) [27]. He
proposed that there are three planes of analgesia in the
first stage of general anesthesia. The planes vary from
moderate to total analgesia and are dependent on the
concentration of N2O in the mixture and the signs and
symptoms shown by patients. 25% N2O produces analge-
sia equivalent to 10 mg of morphine. 35% N2O provides
a maximum level of analgesia maintaining cooperation
and consciousness of the patient. 65% N2O can cause
the patient to enter stage 2 of anesthesia (excitement
stage). 80% N2O can produce hypoxia, hallucinations,
and respiratory, cardiovascular, liver, and kidney prob-
lems. 100% N2O causes anoxia [21]. The goal is that dur-
ing N2O inhalation sedation for dental procedures, the
patient always remains at the first stage of anesthesia.
In plane 1 (5–25% N2O) the patient appears normal,
relaxed, and awake; may feel slight tingling in toes, fin-
gers, tongue, or lips; and may giggle. Vital signs remain
normal. There are no definite clinical manifestations.
Plane 1 is usually of short duration.
In plane 2 or relative analgesia (20–55% N2O), the patient
may have a dreamy look, eyes appear “glassy” occasionally
with tears (. Fig. 8.6), reactions are slowed, and voice may
sound “throaty.” Patient will feel warm and drowsy, may
drift in and out of environment, and hear pleasant ringing
in ears. Partial amnesia may occur. Vital signs remain nor-
mal. Pain is reduced or eliminated but touch and pressure
are still perceived. Patient is less aware of the surroundings;
..      Fig. 8.6 Child under nitrous oxide sedation in stage 1, plane 2.
The eyes exhibit a dreamy look, with “glassy” appearance, main-
tained also during delivery of local anesthesia
sounds and smells are dulled. The term psychotropic anal-
gesic nitrous oxide (PAN) was introduced by Gillman and
Lichtigfeld to describe plane 2 of analgesia. This term clearly
distinguishes the concentrations of N2O used for anxioly-
sis/analgesia from the much higher doses used for anesthe-
sia wherein the patient is totally unconscious [28]. Plane 2
provides adequate N2O sedation and allows dentist-child
communication, although some clinicians prefer the dream
period, usually characterized by closed eyes and difficulty
with speech. . Figure 8.6 portrays a patient’s appearance
in plane 2. Plane 2 can be maintained for several hours, and
it is this that provides adequate suppression and simultane-
ously allows the dentist-child communication. Children in
plane 2 usually respond to questions by moving the head
rather than speaking. Facial features are relaxed and the
jaw usually sags open and remains open without the use
of mouth props. The eyes are usually closed but will open
in response to questions. The arms are heavy and will stay
where placed, and the hands are open. The legs often slide
off the side of the chair. All vital signs are stable. There is
no significant risk of losing protective reflexes and the child
is able to return to pre-procedure mobility. An ideal goal of
sedation is to reach this plane but not exceed it. This is the
desirable sedation level when performing N2O sedation.
 140 D. Velonis et al.

In plane 3 (55–70% N2O) patients assume an angry a

look with hard stare, pupils usually are centrally fixed
and dilated, and mouth tends to close frequently.
Patients are unaware of the surroundings and may hal-
lucinate. When patients are in plane 3, Roberts reported
that they may experience sensation of flying or falling
and uncontrolled spinning, or the chest may feel heavy
and the patient no longer cooperates [29].
For some patients, the feeling of “losing control”
may be troubling. Others may be claustrophobic and
unable to tolerate the nasal hood, finding it confining
and unpleasant. A patient’s experience after nitrous
oxide is believed to be similar to a posthypnotic state.
During N2O there is an enhancement of suggestibil-
ity and imaginative ability that may be utilized while b
managing the child’s behavior and improve the dental
experience. To that capacity N2O serves as a behavioral
management supplement. Careful selection of N2O/O2
8 sedation use will benefit many children in what seems as
a difficult start to dental treatment, so it is reported as
“preventive medication.” [30, 31]
Individual biovariability accounts for different reac-
tions to various concentrations of N2O. Some indi-
viduals experience several symptoms; others only a
few. Symptoms are intense for some and insignificant
for others. Sometime signs are obvious; at other times
they are subtle. Titration allows compensation for the
biovariability of any patient. Titrating N2O/O2 and care- ..      Fig. 8.7 a. Nasal hood for nitrous oxide delivery systems. b. Den-
ful observation of patient responses are key elements to tal restorative work under rubber dam isolation and delivery of N2O/
successful administration. O2 mixture through the nasal hood
Clinicians must know what signs and symptoms to
look for when administering and monitoring N2O seda-
tion. Keeping a constant vigil is imperative because mask by the child; hence, this treatment is not advised
pleasant sensations may quickly change and become for the resistant pediatric patient. It is a good prac-
unpleasant. Knowledge of the appropriate technique tice to give a mask to take home and practice breath-
and associated physical, physiologic, and psychological ing through the nose (. Fig. 8.7). At the outset, it is
changes minimizes negative patient experiences. important to check that the child does not have a cold
and can breathe through the nose. There are many child
8.2.1.2 Administration Technique management techniques to introduce the nasal mask
Before the first operative appointment, an introductory with explanations adjusted for the child’s level of com-
explanation must be given to the parent. It is important prehension. Some dentists prefer to have the child begin
to evaluate the child’s feelings of anxiety or fear during by breathing through the mouth. Others prefer to use
this visit and assure parents that the drug has no linger- scented nasal masks or a little dab of flavoring that can
ing after-effects and is routinely used safely. Additionally, be placed on the nasal mask beforehand to provide a
parents may be given a nitrous oxide parent information more pleasant smell. With the power of suggestion,
pamphlet and the opportunity to ask questions regard- many children will confirm that the funny gas smelled
ing the procedure. Informed consent for the procedure like chocolates or strawberries according to their choice.
and for the N2O sedation must be obtained and filed
in the patient’s chart. The patient’s record also should Titrating Gases for Sedation
include the indications for use of N2O sedation. A writ- First, it is important to check for a tight fit of the nasal
ten record detailing the concentration of nitrous oxide mask to ensure a closed circuit. Gas leakage contaminates
administered, monitored patient variables, the duration the clinician’s immediate environment (breathing zone)
of the procedure, posttreatment oxygenation procedure, and can irritate a child’s eyes (a check should be also
and any complications encountered or lack thereof made for any kinks in the gas lines that might obstruct
should be entered in the patient chart. the gas flow).
The most important factor for a successful nitrous Tidal volume is the amount of air moved in or out
oxide/oxygen procedure is the acceptance of the nasal of the lungs during quiet breathing. The goal is to match
Pharmacologic Behavior Management (Sedation – General Anesthesia)
the gas flow with the tidal volume. Total liters flow per
minute (L/min) is adjusted depending on the size and
age of the child. The reservoir bag should be approxi-
mately 2/3 full. Children aged 2–3 years (14 kg weight)
may be started with a flow under 3 L/min, increasing
the flow to 4 L/min at age 4 (20 kg), to 5 L/min at age 6
(28 kg), and almost 6 L/min above 10 years old (>40 kg)
[21]. Children need to be instructed to breathe properly.
Observing the movement of the reservoir bag is essential
to monitor breathing.
Once the volume of gas flow has been established
(about 2–3 minutes of oxygen), titration of gases for
sedation commences.
The use of the rubber dam also helps with proper
breathing. Once the dam is in place, mouth breathing is
difficult and nasal breathing is easier (. Fig. 8.7).
There are two methods to initially administer nitrous
oxide to children:
(a) Standard Titration Technique
The standard titration technique (also known as slow
titration technique or slow induction technique) is used
by many dentists for adults and older children. The tech-
nique begins slowly with 100% oxygen. After 2–3 min-
utes, gases are adjusted to approximately 20% N2O and
80% oxygen. Every 1–2 min, the gas ratio is altered. The
N2O level is increased about 10% and the oxygen flow
is lowered concomitantly. The total gas flow, which was
established at the outset, is maintained. Often, gas is
titrated near a 1:1 ratio for the injection and rubber dam
procedures and then decreased to about 30%. At the end
of the procedure, 100% oxygen should be delivered for
at least 3–5 minutes. This is specifically important while
treating children as they de-saturate rapidly [4]. As N2O
is 34 times more soluble than nitrogen in blood, diffu-
sion hypoxia may occur. The patient may be discharged
when returning to normal (pre-­sedation) levels of con-
sciousness and has regained normal speech and gait [32].
(b) Rapid Induction Technique
An alternative method for N2O administration is the
rapid induction technique [33]. Similar to the standard
titration technique, rapid induction begins with oxygen.
After 1–2 minutes, the gas is delivered at 50% N2O and
50% oxygen. It is maintained at this level for 5–10 min-
utes, and once injections have been given and a rubber
dam placed, the N2O level is decreased and the oxygen
is increased. This technique is most appropriate for
the very young child or the highly anxious patient as it
allows the clinician to deal with the behavior faster.
During nitrous oxide/oxygen analgesia/anxiolysis,
the concentration of N2O should not routinely exceed
50%. At concentrations greater than 50%, N2O may
cause deep sedation which in general has been found to
141 8
be associated with an increased risk of adverse events
[34]. For safety reasons, the dentist should always be
accompanied by assisting personnel. At least one staff
member must be present in the treatment room at all
times during the administration of nitrous oxide and the
patient should never be left unattended.
Generally, N2O should not be used as a substitute
for local anesthesia. N2O actually anesthetizes the soft
tissues, creates minimal discomfort from the injection,
and is highly recommended. However, to avoid any local
anesthesia discomfort, some clinicians take advantage
of the N2O analgesic properties and perform minor
procedures, like class I cavity restorations, without local
anesthesia [35].
8.2.1.3 Monitoring
Clinical observation of the patient’s responsiveness,
color, respiratory rate, and rhythm is adequate monitor-
ing for N2O/O2 sedation. Answering questions provides
an indication that the patient is breathing. No other
monitoring is required except in cases that an additional
pharmacologic agent is used [4].
8.2.1.4 Contraindications
N2O/O2 sedation cannot be used to control the behavior
of hysterical or defiant children with whom the dentist
cannot communicate. These children will not accept a
nasal mask or cooperate adequately in order to inhale
the nitrous oxide.
Common cold, upper respiratory infections (URI) or
bronchitis, allergies, hay fever, and any condition which
might lead to nasal blockage and prevent a child from
sufficiently inhaling N2O, are also contraindications.
Administering N2O to a child with a middle ear infec-
tion may cause a painful increase in middle ear pressure
and result in a ruptured eardrum. To patients with bowel
obstruction, it may lead to expansion of gas with readily
apparent adverse consequences. Other areas of trapped
gas may not be so clinically apparent; patients who have
undergone recent retinal surgery may have intraocular
gas that may expand during N2O administration, lead-
ing to intraocular hypertension and irreversible loss of
vision [36].
N2O can be safely administered to patients with
bronchial asthma and other forms of chronic obstruc-
tive pulmonary disease (COPD), because it is nonirritat-
ing to the bronchial and pulmonary tissues. Increased
stress can lead to an asthmatic attack; therefore, nitrous
sedation can be helpful. Exception is a small subset
of patients with severe pulmonary disease who utilize
hypoxic drive (lack of oxygen) to stimulate breathing,
rather than the normal mechanisms mediated by carbon
dioxide accumulation. These patients reflect a relative
contraindication to the use of N2O.
 142 D. Velonis et al.

N2O also can have a stronger effect on special

patients taking tranquilizers, analgesics, antidepres-
sants, and antipsychotic drugs or who have a depressed
level of consciousness. Other potential adverse events
such as myeloneuropathy associated with N2O adminis-
tration to a vitamin B12-deficient patient could result in
a serious complication [37]. Finally, use of N2O is con-
traindicated in children with methylenetetrahydrofolate
reductase (MTHFR) deficiency secondary to mutation
or polymorphism of the MTHFR gene (found to be
higher in children with autism) [17].

8.2.1.5 Adverse Effects

N2O/O2 under conditions stated in the guidelines (trained
personnel on carefully selected patients with appropri-
ate equipment and technique) is a very safe technique.
Review of nearly 36,000 administrations of 50% N2O
for non-dental procedures found that only 0.03% of
8 serious adverse events (somnolence, vomiting, bradycar-
dia, vertigo, headache, nightmares, sweating) may have
been caused by N2O [38]. Nausea and vomiting are the
most common adverse effects, occurring in 0.5–1.2% of
patients. Fasting is not required; it is advisable though
only a light meal to be consumed 2 hours prior to the
administration of N2O [18, 22].
..      Fig. 8.8 Scavenging system for evacuation of nitrous oxide from
the ambient air venting to the outside
8.2.1.6 Personnel Safety in Dental Surgery
Bone marrow suppression; liver, CNS, and testicular
dysfunction; decreased fertility and increased spontane- nitrous oxide exposure to staff [40]. The scavenging sys-
ous fetal loss; and peripheral neuropathy may possibly tem should vent outside. Additionally, it has been shown
occur with repeated and chronic exposure to nitrous that the double-mask system is more effective than the
oxide. The increased risk of spontaneous abortions and single-mask system in the removal of waste N2O [41].
malformations in humans is controversial, although ani-
mal studies show various risk potentials (feto-toxicity at
8.2.1.7  se of Nitrous Oxide/Oxygen
U
450–1000 ppm in rats). None of these adverse health
effects to personnel have been found when scavenging
Sedation in the COVID-19 Era
devices are used. Reduced fertility has been reported for Recently, an online early publication addressed new
those not using scavenging equipment and exposed to guidelines for the safe use of nitrous oxide inhalation
N2O more than 3 hours per week [39]. Still, it is advised sedation in the post-COVID era [42]. Briefly, although
that females should not administer nitrous oxide during the risk of producing significant aerosol with proper
the first trimester of pregnancy. use of nitrous oxide inhalation sedation in pediatric
In an effort to reduce occupational health hazards patients is low, proper technique and infection control
associated with N2O, the AAPD recommends expo- protocol were discussed, with the main difference being
sure to ambient N2O be minimized through the use of the instruction to the child to “breathe normally” as
effective scavenging systems and periodic evaluation opposed to “slow and deep breaths.” Emphasis was also
and maintenance of the delivery and scavenging sys- given in the selection criteria and the detailed infection
tems [17]. Scavenging (. Fig. 8.8) significantly reduces control protocol for the machinery and tubing used.
ambient N20 levels in the dentist’s breathing zone but
not to the level (25 ppm) recommended by the National Eye Catcher
Institute for Occupational Safety and Health (NIOSH).
Supplemental oral evacuation should be employed in N2O/O2 sedation used appropriately is a very safe
conjunction with the scavenging system during dental technique. There are no adverse effects of N2O to per-
procedures or when patient behaviors such as increased sonnel when scavenging devices are used.
talking or crying can result in increased environmental
Pharmacologic Behavior Management (Sedation – General Anesthesia)
8.2.2 Moderate Sedation with Other Drugs
Sedative drugs may be administered by oral, inhala-
tion, rectal, submucosal, intramuscular, or intravenous
routes. Oral sedation is regarded by many dentists to
be the simplest and most convenient sedation method
for managing the un-cooperative child patient. It is easy
to administer and there is no need for nasal hood or
injection.
8.2.2.1 Benzodiazepines
Benzodiazepines are the most widely used drugs for
minimal/moderate sedation. Most commonly used ben-
zodiazepines are midazolam and at a lesser degree diaz-
epam [15, 20]. They have sedative-hypnotic, anxiolytic,
amnesic, and anticonvulsant effects. Their mechanism
of action is inhibitory activation of the GABA receptor
complex, similar to N2O.
Diazepam (Valium), used to be a very common oral
sedation agent but due to its slow onset of action (1 hour)
and long period of elimination (50% in 24–48 hours),
has been substituted by midazolam [43].
Midazolam is today the most popular water-soluble
fast and short-acting benzodiazepine. Midazolam, like
..      Fig. 8.9 Midazolam in differ-
ent formulations and concentra-
a b
tions. a. Dormicum IV. b. Versed
oral syrup. c. Versed injectable.
d. Generic midazolam in
different concentrations. e.
Midazolam chemical form
d e
143 8
all benzodiazepines, exerts its clinical effect by bind-
ing to the GABA receptor complex which facilitates
the action of the inhibitory neurotransmitter gamma-­
aminobutyric acid [44]. It is most commonly adminis-
tered to children orally at a dose 0.3–1 mg/kg (usually
0.5 mg/kg) or rectally (0.3–0.4 mg/kg) with a maximum
dose of 10–12 mg. Intravenous and intramuscular dose
is usually 0.2 mg/kg. It is administered for minimal or
conscious sedation or for short-term diagnostic pro-
cedures. A suitable volume of the injectable form may
be mixed with sweetened juice to improve the flavor,
for oral administration at the corresponding dosage
(. Fig. 8.9). Midazolam is rapidly absorbed in the gas-
trointestinal tract and produces its peak effect in 30 min
with a short half-life of 1.5 h. This makes it a desirable
drug for short procedures [45]. The anterograde and ret-
rograde amnesia after midazolam is another advantage
of midazolam [46]. This has been questioned because
the amnesic effect mainly affects explicit memory, but
leaves implicit memory intact.
There are issues though with inter-individual varia-
tion of effects and its elimination that are highly dose-­
dependent as well as post-procedure agitation, which
occurs in 17% of pediatric patients pre-medicated with
c
Cl
N
 144 D. Velonis et al.
midazolam (0.3–0.5 mg/kg) [47]. Because of the possibility
of paradoxical reactions to midazolam, personnel must be
trained to reverse midazolam sedation by administration
of flumazenil, a benzodiazepine antagonist. The dosage is
0.01 mg/kg weight preferably intravenously, but can also
be administered intramuscularly or submucosally.
Clinical Case Presentation – Comprehensive Dental Treatment Under Sedation with a Combination of Oral
and Inhaled Drugs in a Pediatric ­Hospital-­Based Dental Clinic
A 4-year-9-month-old patient presented for emergency
treatment with lower right quadrant swelling and bloody
exudate from his tooth for 1 week. He had already been
placed on oral antibiotics by the pediatrician. Clinical
and radiographic exam revealed dentoalveolar abscess
associated with his mandibular first right primary molar
8 (. Fig. 8.10). As the patient had had a negative experi-
ence with dental treatment in the year prior and did not
cooperate for the treatment plan before, he was planned
for emergency extraction of this tooth on the same day
with oral midazolam (5 mg) and nitrous oxide sedation.
Informed consent for the procedure, passive restraint,
and the sedation were obtained. Preoperative assessment
and nil per os (NPO) status were confirmed and recorded.
His medical history was significant for failure-to-­thrive,
mild intermittent asthma (cold and exercise induced),
gastroesophageal regurgitation disease, and mild anemia
for which he was on medications. On his last complete
blood count (CBC), hemoglobin (Hg) was 11.3 g/dl. His
..      Fig. 8.10 Comprehensive dental treatment under sedation
with a combination of oral and inhaled drugs in a pediatric
hospital-based dental clinic. In the left, periapical radiographs
8.2.2.2 Other Drugs and Combination
Antihistamines such as hydroxyzine and promethazine
have a mild sedative effect along with antiemetic prop-
erties and are historically reported to have been used
either alone or in combination with other drugs and
N2O [20].
weight was 12 kg. He had no known drug or food aller-
gies and was hospitalized 1 year prior for 4 days for pneu-
monia and dehydration. He reportedly ate very little
food, which was limited to juice and pizza topping.
A comprehensive treatment plan was designed to
address his dental treatment needs. Completion of the
treatment plan can be viewed in . Fig. 8.10 and took
place in 11 appointments over a 7-month period. He
would only cooperate for radiographic exam under seda-
tion. Following the initial emergency tooth extraction
under sedation and passive restraint, restorative treat-
ment of teeth of upper left quadrant was done under
Valium, Vistaril, and nitrous oxide sedation, and all other
restorative sessions were completed with nitrous oxide
sedation alone. No sedation was needed for band fitting,
taking alginate impressions, and for cementation of the
space maintainers.
The prognosis for this child in general is good. His
oral hygiene improved dramatically. Arch space was man-
showing caries disease status and progress of dental treatment
over a 7-month period. In the right, intraoral photographs at
the recall visit after completion of the treatment plan
Pharmacologic Behavior Management (Sedation – General Anesthesia)
aged adequately. The prognosis was guarded for pulpoto-
mized mandibular first left primary molar that showed
root resorption and had to be monitored. He no longer
had complaints from his mouth and his eating habits had
also improved to include more food groups. Gradually
his behavior and cooperation improved. He was Frankl 4
at the last recall. He also did very well at that time for
intraoral photographs and radiographs without sedation.
He had gained almost 8 kg in 1.5 years.
Overall evaluation. This was a challenging case that
illustrates the differences in treating this child in several
visits with sedation in the office, as opposed to complet-
ing all dental treatment in one session under general
anesthesia. It took 7 months for the treatment plan to be
8.3 General Anesthesia
General anesthesia (GA) may be necessary for some
children’s restorative needs [43]. The parents must be
a part of the decision-making process, the benefits and
risks must be presented to them, and an informed con-
sent must be obtained [15]. The decision for GA can
never be based on providers’ or parents’ convenience.
The goals of an oral rehabilitation under GA are:
55 To bypass the stress and anticipated potential pain
associated with the dental treatment.
55 To provide safe and effective treatment, minimizing
the risk of adverse reactions or disruptive behavior.
55 To care for children with disabilities that interfere
with achieving a sufficient level of communication or
cooperation.
Indications for oral rehabilitation or dental treatment
under GA:
1. Children or adolescents unable to cooperate second-
ary to emotional, cognitive, psychological, or physi-
cal disability.
2. Children or adolescents for whom local anesthesia is
not an option either because of localized acute infec-
tion, allergies to local anesthetics, or anatomical con-
siderations.
3. Children or adolescents with extremely negative
behavior or phobias, resistant to non-­pharmacologic
behavioral management approaches.
4. Children or adolescents in need of extensive surgical
treatment.
Contraindications
1. Healthy and (potentially) cooperative children or
adolescents.
2. Children or adolescents with complicated medical
conditions (ASA III, IV).
145 8
completed, albeit with modifications, but in the end the
child’s behavior was successfully modified. Although
treatment in one visit under GA should be considered
and presented in such extensive cases, parental informed
consent is the decisive point. Treatment under GA may or
may not improve behavior [48–50]. This child was treated
between 2003 and 2004. At that time esthetic posterior
crowns were not as developed or widely used, and diaze-
pam (but also opioids and chloral hydrate) was used
more than nowadays. The authors present this case also
to point out that during the last 10–15 years procedural
sedation for dental treatment utilizes more often mid-
azolam and nitrous oxide sedation instead of diazepam
and opioids, and that polypharmacy is to be avoided.
3. Children with past history or at risk of adverse
events during sedation/anesthesia.
The majority of young pediatric dental cases that require
GA are children under the age of 3 with advanced dental
disease that require extensive, lengthy, sometimes pain-
ful treatment. The treatment plan must aim to treat all
present disease and restore structure and function, but
also avoid the need for retreatment. Therefore, primary
teeth that can be preserved with endodontic treatment
in the dental office setting should preferably be treated
with extraction and space maintenance in the operating
room. Preformed molar crowns (PMC) either metal or
esthetic ones are favored over amalgam or resin compos-
ite restorations in teeth with caries on multiple surfaces
[51]. The possibility of a second treatment under GA
may be considered in lengthy, complicated, extensive
cases when dental laboratory work is needed (i.e., pros-
thetics).
In the USA, deep sedation and GA can be performed
outside of the hospital setting, by an anesthesiologist
or dentist-anesthesiologist. This out-of-hospital option
provides benefits of reducing waiting time for appoint-
ments and cost of dental treatment up to 13 times [52].
8.3.1 Preoperative Evaluation
and Admission to Hospital
Once it has been decided that treatment for a pediatric
dental patient should be performed under GA, the den-
tist should evaluate the patient’s medical history, current
health status, and risk for life-threatening complications.
A pre-procedure anesthetic evaluation must be per-
formed and documented, prior to the scheduled date to
avoid unanticipated cancellations for unforeseen medi-
cal issues. Each hospital has its own set of protocols
 146 D. Velonis et al.

regarding whether the patient will be admitted as an

in-­patient or as an out-patient for same-day surgery.
These protocols also delineate when the patient should
be examined by a physician prior to the procedure, and
when laboratory studies are warranted.
In general, children classified as ΑSA I may present
to the hospital or ambulatory clinic 1 hour before the
procedure to complete the admission procedure and
preoperative evaluation [53]. Children classified as ASA
II or higher most often require a preanesthetic evalu-
ation before the day of the procedure. A preoperative
evaluation may include:
55 A complete blood count with differential.
55 A panel of coagulation tests.
..      Fig. 8.11 Setup of instruments in the OR, prepared before the
And where indicated by the medical history: procedure
55 A chest radiograph.
55 An electrocardiogram.
8
8.3.2 I nduction of Anesthesia and Dental
Treatment
8.3.2.1 Preparation of the Dental Team
for Operating Room Procedures
The operating room requires adherence to strict proto-
cols of sterility, efficiency, and conduct. Every operating
room used by the dental team should have stored instru-
ments, equipment, and materials in an adjacent room.
The instruments and equipment needed by the dental
team should be set up in the operating room before the
arrival of the patient (. Figs. 8.11 and 8.12). It is advis-
able to have a duplicate set of instruments and equip- ..      Fig. 8.12 Dental unit and portable x-ray unit, prepared before
ment as reserve. the procedure

8.3.2.2 Induction of General Anesthesia anxiolytic effects. An alternative approach is inhala-

The moment the parent separates from the child may be
emotionally challenging. Preparation of the child and
parent by the dental and medical team is very impor-
tant. A rule of thumb is that when children fall asleep
crying, they awake the same way [53]. Most anesthesi-
ologists prefer that the parent accompany the child into
the operating room until induction of anesthesia, reduc-
ing separation anxiety for both the parent and the child
[46, 53]. A study suggests that parental presence during
induction of GA is helpful only with a calm parent and
an anxious child, and not helpful when both parent and
child are both either calm or anxious [54].
Many anesthesiologists use pre-induction sedation
with midazolam or ketamine, administered 15–20 min-
utes prior to separation from parents for maximum
tion-induction with parental presence (. Figs. 8.13
and 8.14). A nasal or oral intubation is preferable for
dental treatment; a laryngeal mask is usually not com-
patible with the access needed for safe dental treatment
(. Fig. 8.15). The usual mixture of anesthetic gases is
comprised of N2O, Ο2, and sevoflurane. The dental team
during induction is on standby and ready to approach
with the dental equipment and proper adjustment of the
operating bed [54].
8.3.2.3 Dental Treatment
After the anesthesiologist secures the patient’s airway
and gives approval, the dentist(s) can proceed with tak-
ing dental radiographs if required (. Fig. 8.16). The
dentist and a sterile assistant prepare the patient for the
Pharmacologic Behavior Management (Sedation – General Anesthesia)
a a
b b
..      Fig. 8.13 a. Induction of general anesthesia with inhalation of
anesthetic gases. b. Child falling asleep
dental treatment, and the perioral area is cleansed with
a sterile 10 × 10cm gauze soaked in povidone iodine, fol-
lowed by one soaked in sterile water or saline solution.
The patient’s head is draped with folded sterile towels,
typically clamped together with towel clips (mosquitos)
or hemostatic forceps, leaving a triangular space around
the mouth. The throat pack is then placed tightly into
the pharyngeal space behind the soft palate and around
the tube. The time and presence of throat pack place-
ment are recorded. This throat pack prevents escape
of materials into the pharynx, or trachea, and should
be inspected continuously during the procedure and
kept as clean and dry as possible by the assistant with
the suction. With the throat pack in place, a thorough
intraoral and dental exam and procedure can be per-
formed. Intraoral examination findings are recorded,
and together with the radiographs (if taken), a final
treatment plan is formulated. The treatment plan is
147 8
..      Fig. 8.14 a. Administration of anesthetic gases to child in
. Fig. 8.11 and b. assisted ventilation with the bag valve. Child is
ready for starting an IV line and intubation
methodically executed, usually by quadrant. The mouth
is kept open with the use of a mouth prop (. Fig. 8.17).
Minor oral surgical procedures can also be per-
formed. Dental extractions preferably could be sup-
plemented with local anesthesia [51, 55]. The dentist
must inform the anesthesiologist about the time, type,
route, and quantity of local anesthetic to be used (pre-
emptive analgesia) and should regularly communicate
information on progress of the procedure and expected
time of completion. When all restorative and surgical
procedures have been completed, fluoride varnish is
applied to all teeth. The oral cavity and the pharynx
are thoroughly inspected for foreign bodies. The throat
pack is carefully removed and the time recorded.
Following extubation, the patient is then transferred
to the post-anesthesia care unit (PACU), where recovery
from the GA is monitored. The parents are reunited with
their child and are discharged after specific criteria are met.
 148 D. Velonis et al.

a a

b b

c ..      Fig. 8.16 a. Taking of intraoral radiographs in the OR. b. With

digital x-ray technology, the setup may consist of a digital sensor and
a laptop

Oral and written postoperative instructions are given

..      Fig. 8.15 a. Intubation with the use of a laryngoscope. b. Child
is now intubated and the nasotracheal tube connected to the anesthe-
sia machine. c. Intravenous administration of drugs (muscle relax-
ants, atropine, analgesics, antibiotics)
to the parents, which include possible prescription for
medications (analgesics, antibiotics), and a follow-
up appointment is scheduled in usually 2 weeks. The
amount of dental work and time spent in the operat-
ing room are often proportional to the feeling of post-
operative pain or discomfort. Patients that have had
more than ten teeth extracted are expected to experience
more postoperative pain. Because the pain is usually of
inflammatory origin, non-steroidal anti-inflammatory
drugs such as ibuprofen are preferred [56].
Pharmacologic Behavior Management (Sedation – General Anesthesia)
149 8

a b

c d

e f

..      Fig. 8.17 a. Placement of a throat pack. b. Comprehensive oral tube is notable. e, f. Advantages of working under GA, isolation of
exam. The mouth is kept open with the use of a mouth prop. c. two quadrants
Restorative treatment with rubber dam isolation. d. Nasotracheal
 150 D. Velonis et al.

Clinical Case Presentation – Oral Rehabilitation Under GA

A 20-month-old boy with severe ECC presented to a dental
clinic at a hospital-based medical center. The boy presented
with advanced dental disease, acute inflammation, and pain.
A partial oral examination revealed poor oral hygiene.
Because of the extensive restorative needs of the patient and
the lack of ability for cooperation in the dental clinic, it was
decided that the oral rehabilitation be performed under
GA. All stages of family preparation and preoperative exam-
ination were completed as described in previous paragraphs.
Dental treatment included extraction of all four maxillary
and the central mandibular primary incisors, pulpotomies
with PMC placement on the maxillary first molars, and com-
posite restorations on maxillary canines (. Fig. 8.18).
The dental prognosis is fair. Caries control with
parental education and participation was initiated,
dietary modifications, fluoride application at home and
the dental office, and behavioral management to promote
future cooperation without adjuvant medications.

a b

c d

e f

..      Fig. 8.18 Dental treatment in the OR of a 20-month-old
boy with severe early childhood caries (ECC). a. Starting an IV
line. b. Oral tracheal intubation. Nasal tracheal intubation was
not possible due to anatomic restrictions. c. Restorative treat-
ment without rubber dam isolation (second primary molars are
still unerupted) including PMC placement on maxillary first
primary molars. d. Short lingual frenum (ankyloglossia). e. Lin-
gual frenectomy. f. Immediate postoperative view after extrac-
tion of maxillary incisors and fluoride varnish application
Pharmacologic Behavior Management (Sedation – General Anesthesia)
8.4  afety Concerns About Sedation or
S References
General Anesthesia
During the past 15 to 20 years, a significant number of
adverse events and deaths have been reported in children
2–17 years old who received dental treatment under
sedation or general anesthesia. This has sparked a grow-
ing concern of the public about the safety of such pro-
cedures. Recent articles like the one that appeared in the
NY Times [57] highlight these issues and propose a set
of important questions that the parents should ask the
dentist prior to any treatment plan that includes seda-
tion or GA.
One study presented 95 cases that developed serious
complications following sedation for dental or other
medical treatment and reported that in 57% of the cases
there was permanent brain damage or death. In these
cases, the etiology was overdose of sedatives or anesthet-
ics and polypharmacy, i.e., use of multiple drugs with
or without nitrous oxide/oxygen at the same time [58].
Other causes were taking sedatives at home before treat-
ment, medications administered by staff without proper
training and experience, premature discharge, and the
choice of drugs with narrow therapeutic range (chloral
hydrate, phenobarbital, promethazine). An important
observation in this study was that adverse events were
noted even in cases where the right choice of drugs and
dosage has been made, at the fault of insufficient moni-
toring or emergency management.
Another study estimated that the risk of death fol-
lowing intravenous administration of sedative medica-
tions is 1 in 300.000 [59]. Regarding GA, death risk was
higher before 1980 (estimated at 1:5000), that is, before
the wide use of pulse oximetry and capnography. More
recently, death risk with GA was estimated by some
investigators at 1 in 100,000 cases for Europe, USA, and
Australia [60]. Parental acceptance for treatment under
GA seems to be also culture related (higher in the USA
[61], low in Jordan and Greece [62, 63]).
In conclusion, those that deliver dental treatment
under sedation or GA must have proper training and
certification and strictly adhere to all guidelines and
recommendations with respect to procedure selection,
drug selection, risk assessment, and choice of sedation
or anesthetic technique. Procedural sedation is a vital
part of the behavior management continuum. Every
day thousands of children are sedated safely all over
the world. Still in weighing the option to use procedural
sedation, we must strive to achieve a standard of “zero
tolerance” for adverse outcomes.
151 8
1. Casamassimo PS, Wilson S, Gross L. Effects of changing U.S.
parenting styles on dental practice. Pediatr Dent. 2001;24:18–22.
2. American Society of Anesthesiologists. Practice guidelines for
sedation and analgesia by non-­anesthesiologists. Anesthesiol-
ogy. 2002;96:1004–17.
3. Coté CJ, Notterman DA, Karl HW, Weinberg JA, McCloskey
C. Adverse sedation events in pediatrics: a critical incident anal-
ysis of contributing factors. Pediatrics. 2000;105:805–14.
4. Coté CJ, Wilson S. Guidelines for monitoring and Management
of Pediatric Patients before, during, and after sedation for diag-
nostic and therapeutic procedures: update 2016. Pediatr Dent.
2016;38:13–39.
5. Houpt M. Project USAP 2000--use of sedative agents by
pediatric dentists: a 15-year follow-up survey. Pediatr Dent.
2002;24:289–94.
6. Adair SM, Rockman RA, Schafer TE, Waller JL. Survey of
behavior management teaching in pediatric dentistry advanced
education programs. Pediatr Dent. 2002;26:151–8.
7. Wilson S, Alcaino EA. Survey on sedation in paediatric den-
tistry: a global perspective. Int J Paediatr Dent. 2011;21(5):
321–32.
8. Klingberg G. Pharmacological approach to the management of
dental anxiety in children--comments from a Scandinavian point
of view. Int J Paediatr Dent. 2002;12:357–8.
9. Morgan CL, Skelly AM. Conscious sedation services provided in
secondary care for restorative dentistry in the UK: a survey. Br
Dent J. 2005;198:631–5; discussion 625.
10. Zanette G, Robb N, Facco E, Zanette L, Manani G. Sedation in
dentistry: current sedation practice in Italy. Eur J Anaesthesiol.
2007;24:198–200.
11. Plasschaert AJM, Holbrook WP, Delap E, Martinez C, Walms-
ley AD. Association for Dental Education in Europe. Profile
and competences for the European dentist. Eur J Dent Educ.
2005;9:98–107.
12. Chadwick BL, Hosey MT. Child taming: how to manage chil-
dren in dental practice. Series: Quintessentials of dental practice,
Vol. 9. 2nd ed. United Kingdom: Quintessence Publishing; 2017.
13. Integrated National Board Dental Examination (INBDE).
https://www.­ada.­org/en/jcnde/inbde. Accessed 10 Jan 2019.
14. American Society of Anesthesiologists. Standards and Guide-
lines. ASA physical status (2014). https://www.­asahq.­org/
standards-­a nd-­g uidelines/asa-­p hysical-­s tatus-­c lassification-­
system. Accessed 9 Jan 2019.
15. American Academy of Pediatric Dentistry. Guideline for Moni-
toring and Management of Pediatric Patients During and After
Sedation for Diagnostic and Therapeutic Procedures. 2018–2019.
Pediatr Dent. Reference Manual. 2018;40:6.
16. Green SM, Krauss BS, Mason KP. Reevaluating fasting for pro-
cedural sedation. JAMA Pediatr. 2018;172:622.
17. American Academy of Pediatric Dentistry. Guideline on use
of nitrous oxide for pediatric dental patients. Pediatr Dent.
2016;39(6):273–7.
18. Kupietzky A, Tal E, Shapira J, Ram D. Fasting state and epi-
sodes of vomiting in children receiving nitrous oxide for dental
treatment. Pediatr Dent. 2008;30:414–9.
19. Hosey MT. UK National Clinical Guidelines in pediatric den-
tistry. Managing anxious children: the use of conscious sedation
in paediatric dentistry. Int J Paediatr Dent. 2002;12:359–72.
 152 D. Velonis et al.
20. Hallonsten A-L, Jensen B, Raadal M, Veerkamp J, Hosey MT,
Poulsen S. EAPD Guidelines on Sedation in Paediatric Den-
tistry. https://www.­eapd.­eu. 2005.
21. Emmanouil D, Kupietzky A. Nitrous oxide/oxygen inhala-
tion sedation in children. In: Wright GZ, Kupietzky A, editors.
Behavioral management in dentistry for children. Chichester,
UK: John Wiley & Sons; 2014. p. 145–58.
22. Wright AJ. History of anesthesia: early use of nitrous oxide. Bull
Anesth Hist. 1999;17:10–1.
23. Jevtović-Todorović V, Todorović SM, Mennerick S, Powell S,
Dikranian K, Benshoff N, Zorumski CF, Olney JW. Nitrous
oxide (laughing gas) is an NMDA antagonist, neuroprotectant
and neurotoxin. Nat Med. 1998;4:460–3.
24. Emmanouil DE, Quock RM. Advances in understanding the
actions of nitrous oxide. Anesth Prog. 2007;54:9–18.
25. Hornbein TF, Eger EI, Winter PM, Smith G, Wetstone D, Smith
KH. The minimum alveolar concentration of nitrous oxide in
man. Anesth Analg. 1982;61:553–6.
26. Guedel AE. Inhalation anesthesia—a fundamental guide. The
Macmillan Company; 1937.
27. Langa H. Relative analgesia in dental practice; inhalation anal-
8 gesia with nitrous oxide. Saunders. 1968;
28. Gillman MA, Lichtigfeld FJ. Pharmacology of psychotropic
analgesic nitrous oxide as a multipotent opioid agonist. Int J
Neurosci. 1994;76:5–12.
29. Roberts GJ. Inhalation sedation (relative analgesia) with oxy-
gen/nitrous oxide gas mixtures: 1. Principles Dent Update.
1990;17:139–42, 145–6.
30. Galeotti A, Garret Bernardin A, D’Antò V, Ferrazzano GF, Gentile
T, Viarani V, Cassabgi G, Cantile T. Inhalation conscious sedation
with nitrous oxide and oxygen as alternative to general anesthesia
in Precooperative, fearful, and disabled pediatric dental patients: a
large survey on 688 working sessions. Biomed Res Int. 2016:1–6.
31. Clark MS, Brunick AL. Handbook of nitrous oxide and oxygen
sedation. 3rd ed. St. Louis: Mosby; 2008.
32. Jastak JT, Orendurff D. Recovery from nitrous sedation. Anesth
Prog. 1975;22:113–6.
33. Simon JFJ, Vogelsberg GM. Behavior management in dentistry
for children. In: Wright GZ, editor. . Philadelphia: W.B. Saun-
ders Co.; 1975. p. 177–96.
34. Babl FE, Oakley E, Seaman C, Barnett P, Sharwood LN. High-con-
centration nitrous oxide for procedural sedation in children: adverse
events and depth of sedation. Pediatrics. 2008;121:e528–32.
35. Hammond NI, Full CA. Nitrous oxide analgesia and children’s
perception of pain. Pediatr Dent. 1984;6:238–42.
36. Lockwood AJ, Yang YF. Nitrous oxide inhalation anaesthesia in
the presence of intraocular gas can cause irreversible blindness.
Br Dent J. 2008;204:247–8.
37. Flippo TS, Holder WD. Neurologic degeneration associated
with nitrous oxide anesthesia in patients with vitamin B12 defi-
ciency. Arch Surg. 1993;128:1391–5.
38. Onody P, Gil P, Hennequin M. Safety of inhalation of a 50%
nitrous oxide/oxygen premix. Drug Saf. 2006;29:633–40.
39. Rowland AS, Baird DD, Weinberg CR, Shore DL, Shy CM,
Wilcox AJ. Reduced fertility among women employed as dental
assistants exposed to high levels of nitrous oxide. N Engl J Med.
1992;327:993–7.
40. Henry RJ, Primosch RE. Courts FJ the effects of various dental
procedures and patient behaviors upon nitrous oxide scavenger
effectiveness. Pediatr Dent. 1992;14(1):19–25.
41. Freilich MM, Alexander L, Sándor GKB, Judd P. Effectiveness
of 2 scavenger mask systems for reducing exposure to nitrous
oxide in a hospital-based pediatric dental clinic: a pilot study. J
Can Dent Assoc. 2007;73:615.
42. Gupta K, Emmanouli D, Sethi A. 2021. Use of nitrous oxide-
oxygen inhalation sedation in the COVID-19 era. Int J Paedi-
atr Dent. 2021. Letter to the editor. E-pub ahead of print DOI:
https://doi.org/10.1111/ipd.12745.
43. Creedon RL, Dock M. Pharmacological Management of patient
behavior. In: Mc Donald RE, Avery DR, editors. Dentistry for
the Child and Adolescent. 8th ed. St. Louis.: Mosby; 2004.
p. 297–324.
44. Blumer JL. Clinical pharmacology of midazolam in infants and
children. Clin Pharmacokinet. 1998;35:37–47.
45. Bhatnagar S, Das UM, Bhatnagar G. Comparison of oral mid-
azolam with oral tramadol, triclofos and zolpidem in the seda-
tion of pediatric dental patients: an in vivo study. J Indian Soc
Pedod Prev Dent. 2012;30:109–14.
46. Kain ZN, Hofstadter MB, Mayes LC, Krivutza DM, Alexander
G, Wang SM, Reznick JS. Midazolam: effects on amnesia and
anxiety in children. Anesthesiology. 2000;93:676–84.
47. Dahmani S, Brasher C, Stany I, Golmard J, Skhiri A, Bruneau B,
Nivoche Y, Constant I, Murat I. Premedication with clonidine is
superior to benzodiazepines. A meta analysis of published stud-
ies. Acta Anaesthesiol Scand. 2010;54:397–402.
48. Cantekin K, Yildirim MD, Cantekin I. Assessing change in
quality of life and dental anxiety in young children following
dental rehabilitation under general anesthesia. Pediatr Dent.
2014;36(1):12E–7E.
49. Fuhrer CT, Weddell JA, Sanders BJ, Jones JE, Dean JA, Tom-
lin A. Effect on behavior of dental treatment rendered under
conscious sedation and general anesthesia in pediatric patients.
Pediatr Dent. 2009;31(7):492–7.
50. Kupietzky A. Blumenstyk. A comparing the behavior of chil-
dren treated using general anesthesia with those treated using
conscious sedation. ASDC J Dent Child. 1998;65(2):122–7.
51. Gazal G, Bowman R, Worthington HV, Mackie IC. A double-
blind randomized controlled trial investigating the effectiveness
of topical bupivacaine in reducing distress in children follow-
ing extractions under general anaesthesia. Int J Paediatr Dent.
2004;14:425–31.
52. Rashewsky S, Parameswaran A, Sloane C, Ferguson F, Epstein
R. Time and cost analysis: pediatric dental rehabilitation with
general anesthesia in the office and the hospital settings. Anesth
Prog. 2012;59:147–53.
53. Zuckerberg AL. Perioperative approach to children. Pediatr Clin
N Am. 1994;41:15–29.
54. Kain ZN, Caldwell-Andrews AA, Maranets I, Nelson W, Mayes
LC. Predicting which child-parent pair will benefit from paren-
tal presence during induction of anesthesia: a decision-making
approach. Anesth Analg. 2006;102:81–4.
55. Anand P, Wilson R, Sheehy EC. Intraligamental analgesia for
post-operative pain control in children having dental extractions
under general anaesthesia. Eur J Paediatr Dent. 2005;6:10–5.
56. American Academy of Pediatric Dentistry (2012) Policy on
Pediatric Pain Management. Pediatr Dent Reference Manual.
2016;39(6):99–101.
57. Saint Louis C. 2017. Should Kids Be Sedated for Dental Work?
New York Times https://www.­nytimes.­com/2017/08/24/well/fam-
ily/should-­kids-­be-­sedated-­for-­dental-­work.­html. Accessed 10
Jan 2019.
58. Coté CJ, Karl HW, Notterman DA, Weinberg JA, McCloskey
C. Adverse sedation events in pediatrics: analysis of medications
used for sedation. Pediatrics. 2000;106:633–44.
Pharmacologic Behavior Management (Sedation – General Anesthesia)
59. Vaughan GG, Jarnigan TK, Montgomery MT. Morbidity and
mortality associated with the pharmacologic management of
pain and anxiety. Compendium. 1993;14:752, 754–6, 758.
60. Mellin-Olsen J, Staender S, Whitaker DK, Smith AF. The Hel-
sinki declaration on patient safety in Anaesthesiology. Eur J
Anaesthesiol. 2010;27:592–7.
61. Eaton JJ, McTigue DJ, Fields HW. Beck M attitudes of contem-
porary parents toward behavior management techniques used in
pediatric dentistry. Pediatr Dent. 2005;27(2):107–13.
153 8
62. Alammouri M. The attitude of parents toward behavior man-
agement techniques in pediatric dentistry. J Clin Pediatr Dent.
2006;30:310–3.
63. Boka V, Arapostathis K, Vretos N, Kotsanos N. Parental accep-
tance of behaviour-management techniques used in paediatric
dentistry and its relation to parental dental anxiety and experi-
ence. Eur Arch Paediatr Dent. 2014;15:333–9.
 155 9

Growth of the Craniofacial

Complex
Fernando Pugliese, Anastasios A. Zafeiriadis, and Mark G. Hans

Contents

9.1 Introduction – 156

9.1.1 The Changing Features of the Growing Face – 156

9.2 Prenatal Facial Growth and Development – 157

9.3 Concepts of the Growth Process – 160

9.4 Bone and Cartilage – 162

9.5 Growth of the Neurocranium – 164

9.5.1 T he Calvaria – 164
9.5.2 The Basicranium – 164

9.6 Growth of the Nasomaxillary Complex – 165

9.6.1 T he Maxillary Tuberosity and Arch Lengthening – 165
9.6.2 Palatal Remodeling and Alveolar Development – 166
9.6.3 Downward Maxillary Displacement – 167

9.7 Growth of the Mandible – 167

9.7.1 T he Ramus – 167
9.7.2 The Lingual Tuberosity – 168
9.7.3 The Mandibular Condyle – 168
9.7.4 Ramus Uprighting – 169

9.8 Cephalometrics – 170

9.9  ormal Variations in Facial Form and the Anatomic
N
Basis for Malocclusions – 172

References – 175

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_9
 156 F. Pugliese et al.
9.1 Introduction
9.1.1  he Changing Features
T
of the Growing Face
A baby’s face appears quite diminutive relative to the
much larger, more precocious cranium above and
behind it. Their respective proportions change signifi-
cantly, however (in early life). The growth of the brain
slows considerably after about the third or fourth years
of childhood, but the facial bones continue to enlarge
markedly for many years [1]. The eyes appear large in
the young child. As facial growth continues, the nasal
and jaw regions grow much faster and to a significantly
greater extent than the orbit and its soft tissues. As a
result, the eyes of the adult appear smaller in propor-
tion. The ears of the infant and child appear to be low;
in the adult however, although they in fact move down-
ward during continued growth, the face enlarges inferi-
orly even farther, so that the relative position of the ears
9 seems to rise. The young child’s forehead is upright and
bulbous. It continues to enlarge during the early years,
but the face expands much more, so that the proportion-
ate size of the forehead becomes reduced.
The childhood face appears quite broad. As develop-
ment continues, vertical facial growth overtakes expan-
sion in width to a marked extent, so that a relatively
narrower facial proportion characterizes the adult [2].
The nasal bridge is quite low in the child resulting in a
“pug nose.” It develops to a greater or lesser extent in
different facial types to become more prominent in most
adults. The eyes of the infant seem quite wide-set with
a broad-appearing nasal bridge separating them. This
is because the nasal bridge is so low, and also because
much of the width of the bridge has already been
attained in the infant.
The infant and young child have a nose that pro-
trudes very little with a short vertical dimension. The
shape and size of the infantile nose, however, give little
indication as to what will happen to it during subse-
quent growth. The lower part of the nose in the adult
is proportionately much wider and a great deal more
prominent. In the adult, the midface has become greatly
expanded, and the nasal floor has descended well below
the orbital floor. This change is quite marked because of
the enormous enlargement of the nasal chambers. Note
also the close proximity of the young child’s maxillary
arch and orbit, in contrast to their positions in the adult
(. Fig. 9.1).
While the cheekbone is prominent in early child-
hood, it is nonetheless quite diminutive and fragile com-
pared with that of the adult. The malar process and the
inferior part of the zygoma enlarge considerably during
childhood growth, even though the actual growth is in
..      Fig. 9.1 The entire adult face is deeper sagittally because of the
divergent directions of growth among all the various regional parts
that make it less “flat”. (From Enlow and Hans [3] with permission)
a backward direction. The protrusive modes of supra-
orbital and nasal growth cause the adult forehead and
nose to appear progressively more prominent relative to
the retrusively growing cheekbones and lateral orbital
rims. The entire adult face is deeper sagittally because of
the divergent directions of growth among all the various
regional parts, making it less “flat” (. Fig. 9.1).
As the whole face expands, the frontal, maxillary, and
ethmoidal sinuses enlarge significantly. The mandible of
the young child is still quite small in actual size, but also
proportionately, relative to the upper jaw and the face in
general, as it normally lags behind the maxilla in early
growth. However, it will usually grow twice as much as
the maxilla during puberty allowing it to “catch up” to
the maxilla in young adulthood. So it is sometimes dif-
ficult to predict during early childhood possible maloc-
clusions that might or might not become fully expressed
during later development. The chin is poorly formed in
the infant and gradually becomes more prominent year
by year, because of remodeling changes that take place.
The young child’s mandible appears to be pointed as it
is wide, short, and more “V”-shaped. In the adult, the
entire lower jaw becomes more anatomically diverse.
The development of the chin, together with massive
growth in the lateral areas of each ramus, expansion
of the masticatory musculature, and flaring of the
gonial regions, leads the whole lower face to take an
“U”-shaped configuration, resulting in a considerably
more full appearance. In the infant and young child, the
gonial region lies well inside (medial to) the cheekbone.
In the adult, the posterior-inferior corner of the man-
dible extends laterally out to the cheekbone or nearly so.
This gives the posterior part of the jaw a square appear-
ance (. Fig. 9.2).
The ramus of the adult mandible is much longer ver-
tically. It is also more upright at the junction between the
corpus and the ramus. Increases in vertical height of the
rami accommodate the vertical expansion of the nasal
Growth of the Craniofacial Complex
..      Fig. 9.2 Square appearance of the posterior part of the jaw.
(From Enlow and Hans [3] with permission)
region and the eruption of the upper and lower perma-
nent teeth. The premaxillary region normally protrudes
beyond the mandible in the infant and young child and
lies in line with, or forward of, the bony tip of the nose.
This gives a prominent appearance to the upper jaw and
lip. In subsequent facial development, however, the nose
becomes much more protrusive, and the tip of the nasal
bone comes to lie well ahead of the basal bone of the
premaxilla.
The anterior surface of the bony maxillary arch in
the infant has a vertically convex topography in contrast
to the concave contour of this region in the adult. The
adult maxillary alveolar bone is noticeably more pro-
trusive and proportionately more massive (in conjunc-
tion with the permanent dentition). The whole face,
vertically, is longer and more sloping as a result of the
changes outlined above. At birth, the overall length of
the cranium is approximately 60–65% complete, and it
increases rapidly. By 5 years old, it reaches about 90%
of its full size. In addition, much of the adult width
of the cranium is attained by the first or second year.
In the newborn, six fontanelles (“soft spots”) are pres-
ent between the bones of the skull roof. They become
covered at different times, but all have been reduced
to sutures by the 18th month. In the child, the slender
neck below a relatively large cranium, particularly in the
occipital region, gives a characteristic youthful appear-
ance to the whole head. This gradually disappears (to a
greater or lesser extent) until about puberty, when the
expansion of the neck muscles and other soft tissues
causes a proportionate decrease in the prominence of
the head relative to neck circumference, less noticeably
in females.
The external appearance of the baby’s face hides the
truly striking enormity of the dental battery developing
within it. When a crown tip first erupts, the parent natu-
rally believes that the process is just beginning and that
the tooth is only a tiny, but newsworthy, addition to the
pink mouth. They do not realize that the whole midface
157 9
is occupied by a vast magazine of unerupted teeth hid-
den to the eyes [4]. The thin covering and supporting
bone of the jaws is a much less commanding feature of
the young face.
>>Important
55 The growth of the brain slows considerably after
about the third or fourth years of childhood, but
the facial bones continue to enlarge markedly for
many years.
55 As development continues, vertical facial growth
overtakes expansion in width to a marked extent,
so that a relatively narrower facial proportion
characterizes the adult.
55 The mandible of the young child is still quite small
in absolute size, but also proportionately, rela-
tive to the upper jaw and the face in general, as it
normally lags behind the maxilla in early growth.
However, it will usually grow twice as much as the
maxilla during puberty allowing it to “catch up”
to the maxilla in young adulthood.
9.2  renatal Facial Growth
P
and Development
The “head” of a 4-week-old human embryo is mostly
just a brain covered by a thin sheet of ectoderm and
mesoderm. The location of the mouth is marked by a
tiny depression, the stomodeum. The eyes have already
begun to form by a thickening of the surface ectoderm
(the future lens), which meets an out-pouching from the
brain (the future retina). The eyes are still located at the
sides of the head, however (. Fig. 9.3). As the brain con-
tinues to grow and expand, the eyes rotate toward each
other and toward the midline of the future face. This
reduces the interorbital dimension, but only relatively,
as everything is actually increasing in size (. Fig. 9.4).
As the whole head expands, the thin membrane that
covers the stomodeum soon ruptures, and the pharynx
opens to the outside. The pharynx is the anterior-most
segment of the endodermally lined, embryonic gut. Its
lumen is bounded on the right and left sides by the pha-
ryngeal (or visceral) arches. Between the arches are the
pharyngeal clefts on the outside and the pouches on the
inside. Where each cleft meets its pouch, a mesoder-
mally reinforced contact between ectoderm and endo-
derm occurs. All these arches and some of the clefts and
pouches develop into specific adult structures in the face,
head, and neck. The tissues in each arch develop into
specific muscles, bones, and cartilages, and the arrange-
ment in the adult is carried forward from the pattern
that exists in the embryo. Each arch has a specific cranial
nerve which services the structures deriving from that
particular arch (. Fig. 9.5).
 158 F. Pugliese et al.

..      Fig. 9.3 Human face of about 4 weeks. 1, Stomodeal plate (buc-

9 copharyngeal membrane). 2, Mandibular arch (swelling or process).
3, Hyoid arch. 4, Frontal eminence (or prominence). 5, Optic vesicle.
6, Region where the maxillary process (or “swelling”) of the first arch
is just beginning to form. (Modified from Patten [5] with permission)

The first pharyngeal (or mandibular) arch gives rise

to the tissues that will eventually become the mandible
and its muscles. A bud develops from it to become the
“maxillary swelling,” and this is the primordium for
part of the maxillary arch that is soon to begin forming.
Meckel’s cartilage in the first arch serves as an anlage
for the malleus and incus. The mandible forms intra-
membranously lateral to it, while the cartilaginous con-
dyle later develops from a separate secondary cartilage ..      Fig. 9.4 Face at about 7 weeks. (From Enlow and Hans [3] with
(. Fig. 9.6). permission)
The second pharyngeal (or hyoid) arch’s cartilage
forms part of the hyoid apparatus and also the stapes.
Its mesenchyme develops into the stylohyoid muscle and
all the muscles of facial expression. These developing,
sheet-like muscles spread up and over the face like a
superficial sleeve. The third, fourth, and sixth pharyn-
geal arches (the fifth drops out) form the remainder of
the hyoid apparatus, the laryngeal cartilages, and the
muscles of the larynx. In addition, the parathyroids and
thymus develop from third and fourth arch tissue. The
main body of the tongue develops from the first arches
on the right and left, where they join in the floor of the
pharynx, by a fusion of the paired lingual swellings. The
root of the tongue develops from the third and fourth
arch tissue (. Fig. 9.7).
The first pharyngeal arch, at 5 weeks of age, develops
two sizable pairs of mandibular and maxillary swellings.
..      Fig. 9.5 Internal view of pharyngeal region. 1, Forebrain. 2, Sto-
Below the “forehead” is a pair of U-shaped swellings, modeum, 3, Cardiac prominence. 4, Maxillary process. 5, Mandibu-
the nasal primordia. In 2 more weeks a fast-moving lar process. 6, Pouch between second and third arches. (From Enlow
sequence of changes takes place, creating the face. On and Hans [3], modified from Langman [6], with permission)
Growth of the Craniofacial Complex
..      Fig. 9.6 Pharyngeal arch derivatives (I to VI). 1, Meckel’s carti-
lage. 2, Intramembranous bone developing around Meckel’s carti-
lage. 3, Superior part of body and lesser horn of hyoid. 4,
Sphenomandibular ligament. 5, Malleus. 6, Incus. 7, Stapes. 8,
­Styloid process. 9, Stylohyoid ligament. 10, Greater horn of hyoid
bone. 11, Inferior part of hyoid body. 12, Laryngeal cartilages. (From
Enlow and Hans [3] with permission)
..      Fig. 9.7 1, Body of tongue (lateral lingual swellings and tubercu-
lum impar). 2, Thyroid diverticulum. 3, Mandibular arch. 4, Pouch
between first and second arches. 5, Root of tongue (copula). 6, Ary-
tenoid swellings. 7, Trachea. 8, Esophagus. (From Enlow and Hans
[3] with permission)
159 9
..      Fig. 9.8 Face at about 5 weeks. 1, Frontal prominence. 2, Lateral
nasal swelling. 3, Eye. 4, Maxillary swelling. 5, Nasal pit. 6, Medial
nasal swelling. 7, Stomodeum. 8, Mandibular swelling. 9, Hyoman-
dibular cleft. 10, Hyoid arch. (From Enlow and Hans [3] with per-
mission)
each side, the maxillary swellings fuse with the medial
limbs of the nasal swellings forming the maxillary arch.
The middle portion is the “premaxillary” segment that
will later house the incisors and form the philtrum of
the upper lip. Above it, the medial limbs merge to create
the middle part of the nose; the lateral limbs become the
nasal wings. Bone is beginning to form in the maxillary
and mandibular arches, the eyes are continuing to be
displaced into more forward-orientated positions by the
enlarging brain, the ears lobes are forming, and there is
now a face. Within the face, a nasal septum has formed,
“shelves” from the right and left maxilla develop and
fuse at the midline to form a palate, and the oral and
paired nasal chambers thereby all become partitioned
from one another (. Fig. 9.8).
In shorter order, centers of ossification appear in
most of the other major bony parts of the face and cra-
nium, some intramembranously and some endochon-
drally. The bone tissue of each center spreads until the
definitive shape of each bone is attained. Then, the bone
begins to “remodel” as it grows. This remodeling process
first starts at around 14 weeks for most of the various
separate bones and their parts, and the same occurs gen-
erally for the fetal face and cranium. The principal dif-
ferences are in the anterior parts of the upper and lower
jaws and the zygoma. In the face of the child after 6 or
 160 F. Pugliese et al.
..      Fig. 9.9 Developing skull at about 9 weeks. 1, Occipital bone
(interparietal part). 2, Supraoccipital. 3, Dorsum sella (still cartilagi-
nous). 4, Squamous part of temporal. 5, Cartilage. 6, Styloid pro-
9 cess. 7, Occipital (basal part). 8, Frontal bone. 9, Crista galli (still
cartilaginous). 10, Nasal bone. 11, Malar. 12, Cartilage of nasal cap-
sule. 13, Maxilla. 14, Mandible (surrounding Meckel’s cartilage). 15,
Hyoid. 16, Thyroid cartilage. 17, Cricoid cartilage. Endochondral
sites of ossification are shown by dark stippling, and intramembra-
nous sites are shown in black. (From Enlow and Hans [3], modified
from Patten [5], with permission)
so years of age, these surfaces characteristically become
resorptive. Through fetal life and the early part of child-
hood, however, they remain depository, as the bony
maxillary and mandibular arches must expand sagit-
tally to accommodate the dentition [3]. Sometime before
about 5 or 6 years of age, however, the outer surfaces
of the forward part of both the maxilla and mandible
become resorptive. Subsequent lengthening of the bony
arch then proceeds only posteriorly. The characteristic
postnatal resorptive fields in the anterior parts of the
arches develop in conjunction with their continuing ver-
tical growth (. Fig. 9.9).
9.3 Concepts of the Growth Process
Bones grow by adding new bone tissue on one side
of a bony cortex toward the direction of progressive
growth and undergoing resorption on the other side.
This growth process is termed “drift.” The outside and
inside surfaces of a bone are completely blanketed by a
mosaic-­like pattern of “growth fields.” The outside sur-
face, however, is not all depository, as one might pre-
sume. About half of the periosteal surface of a whole
bone has a characteristic arrangement of resorptive
fields; a characteristic pattern of depository fields covers
the remainder. If a given periosteal area has a resorp-
tive type of field, the opposite (endosteal) surface of
that same area has a depository field and vice versa
..      Fig. 9.10 Note how the cortex on the right was formed by the
periosteum and the cortex on the left by the endosteum as both sides
shift in unison to the right. (From Enlow and Hans [3] with permis-
sion)
(. Fig. 9.10). The operation of growth fields covering
and lining the surface of a bone is actually carried out
by the membranes and other surrounding tissues rather
than by the hard part of the bone.
All the various resorptive or depository growth fields
throughout a bone do not have the same rate of growth
activity. Some fields grow much more rapidly, or to a
much greater extent, than others. Fields that have some
special significance or noteworthy role in the growth
process are often termed growth sites, such as the man-
dibular condyle (. Fig. 9.11). During remodeling, the
extent of bone deposition usually slightly exceeds that
of resorption so that the regional parts of a bone gradu-
ally enlarge as they remodel.
Remodeling is a basic part of the growth process
as the “drift” moves each regional part from one loca-
tion to another as the whole bone enlarges. This calls
for sequential remodeling changes in the shape and size
of each region. The ramus, for example, moves progres-
sively posteriorly by a combination of deposition and
resorption. The whole ramus is thus relocated posteri-
orly, and the posterior part of the lengthening corpus
becomes relocated into the area previously occupied
by the ramus. This progressive, sequential movement
of component parts as a bone enlarges is termed “area
relocation” (. Fig. 9.12).
The same deposition and resorption which produce
the overall growth enlargement of a whole bone carry
out relocation and remodeling at the same time. Growth
and remodeling are, in fact, inseparable parts of the same
Growth of the Craniofacial Complex
..      Fig. 9.11 Mandibular condyle as a growth site. (From Enlow and
Hans [3] with permission)
..      Fig. 9.12 Area relocation. (From Enlow and Hans [3] with per-
mission)
actual process. As a result, half of any given bone can
and must have a resorptive external surface as the bone
increases in overall size, as bones enlarge and change
shape via a complex combination of deposition of new
bone in some areas and resorption of bone in others.
In the maxilla, the palate relocates inferiorly by
periosteal resorption on the nasal side and periosteal
deposition on the oral side (. Fig. 9.13), while the
nasal chambers enlarge. About half of the palate is
thus resorptive and about half depository. The nasal
mucosa provides the periosteum on one side, and the
oral mucosa provides it on the other side.
As a bone enlarges by surface deposition in a given
direction, it is simultaneously physically displaced in
the opposite direction of other bones in direct contact
with it. This process is termed primary displacement
(or “translation”) (. Fig. 9.14). Essentially, the bone is
moved outward by the expansive force of all the growing
soft tissues surrounding it. As this takes place, new bone
is added immediately onto the contact surface, and the
two separate bones thereby remain in constant articular
junction. The nasomaxillary complex, for example, is in
161 9
..      Fig. 9.13 Palate inferiorly relocated. (From Enlow and Hans [3]
with permission)
contact with the cranium. The whole maxillary region is
displaced downward and forward away from the cranium
by the expansive growth of the soft tissues in the mid-
facial region. Displacement triggers new bone growth at
the various sutural contact surfaces between the naso-
maxillary composite and the cranial floor. Displacement
thus produces downward and forward growth by bone
deposition simultaneously taking place in an opposite
upward and backward direction (. Fig. 9.15).
A process of secondary displacement also occurs
during growth that involves the movement of a whole
bone caused by the separate enlargement of other
bones, which may be nearby or quite distant. For
example, increases in size of the bones that compose
the middle cranial fossa (in conjunction with growth of
the brain) result in a marked displacement movement
of the whole maxillary complex anteriorly and inferi-
orly, independently of the maxillary growth itself. The
effects of growth activities in relatively distant locations
are passed on, and all such changes must be taken into
account when analyzing the growth process and the
facial characteristics of any individual person.
>>Important
55 Bones grow by adding new bone tissue on one side
of a bony cortex toward the direction of progres-
sive growth and undergoing resorption on the
other side. This growth process is termed “drift.”
55 Remodeling is a basic part of the growth process
as the “drift” moves each regional part from one
location to another as the whole bone enlarges.
55 As a bone enlarges by surface deposition in a given
direction, it is simultaneously physically displaced
away in the opposite direction of other bones in
direct contact with it. The process is termed pri-
mary displacement (or “translation”).
55 A process of secondary displacement also occurs
during growth that involves the movement of a
whole bone caused by the separate enlargement
of other bones, which may be nearby or quite
distant.
 162 F. Pugliese et al.

..      Fig. 9.14 Displacement (or translation) process. (From Enlow and Hans [3] with permission)

9.4 Bone and Cartilage and it also grows interstitially by cell divisions of chon-
drocytes and by increases in the intercellular matrix.
Because of the unique nature of its intercellular matrix, Together with the noncalcified matrix, and the absence of
cartilage is a rigid and firm tissue, but it is not hard. vessels, these various features combine to allow the car-
Cartilage provides three basic functions. It gives flexible tilage to function and to grow in areas of direct pressure
support in appropriate anatomic places (the nasal tip, [7]. Because it can exist without a covering membrane, it
ear lobe, thoracic cage, tracheal rings); it is a pressure-­ is suited to articular surfaces, synchondroses, and epiph-
tolerant tissue located in specific skeletal areas where yseal plates; because it can expand interstitially, carti-
direct compression occurs (such as articular surfaces lage can thereby grow even without a membrane. As its
of joints); and it functions as a “growth cartilage” matrix is noncalcified, diffusion of substances can take
in conjunction with certain enlarging bones (e.g., a place through it and cell divisions are possible. Because
­synchondrosis, condylar cartilage, epiphyseal plate). there are no vessels to press closed, cartilage is pressure-
adapted and can grow where compression exists because
of its noncalcified, interstitial expansion features.
Eye Catcher Unlike cartilage, which is usually under compres-
sion, bone is tension-adapted [8]. Bone must have a
Cartilage is a nonvascular connective tissue that is
vascular, osteogenic covering soft tissue, and it can only
normally noncalcified. Vascularization and calcifica-
grow appositionally. Bone cannot grow directly in heavy
tion, however, are involved as steps in the replacement
pressure areas as its growth is dependent upon a sen-
of cartilage tissue by bone tissue in a normal embryo-
sitive, vascular membrane. Bone needs a membrane in
logic process called endochondral bone formation.
order to support its internal vascular system, which in
turn is essential because the matrix is calcified and will
not allow diffusion of oxygen and other substances to
Cartilage usually has a perichondrium, but it can exist and from cells. Once an osteocyte is encased in a calci-
without this covering membrane. Cartilage grows appo- fied matrix, it cannot grow by cell division, meaning that
sitionally by the activity of its chondrogenic membrane, a bone cannot grow interstitially.
Growth of the Craniofacial Complex
..      Fig. 9.15 Downward and forward maxillary displacement. (From Enlow and Hans [3] with permission)
In terms of embryologic origin, bones are formed
intramembranously (directly from mesenchymal stem
cells) in tension areas and endochondrally (formed first
in cartilage then converted to bone) in pressure areas.
“Growth cartilages” take part in the latter ossification
process. They provide for the linear growth of a bone
toward the direction of pressure. As interstitial carti-
lage expansion provides pressure-adapted growth on the
pressure side of the cartilage plate, an equal amount of
cartilage is removed and replaced by bone on the other
side. The remainder of the bone, including all its cortical
plates, grows by membranous ossification in conjunc-
tion with the periosteal and endosteal membranes.
The membranes associated with bone (periosteum,
sutures, periodontium) have their own internal growth
163 9
and remodeling process. The whole membrane, as a
sheet, undergoes extensive fibrous changes in order to
sustain constant connections with the bone by means of
collagenous fiber continuity from the membrane into the
matrix of the bone. As fibers in the membrane become
enclosed within the new bone deposits, the membrane-
produced fibers become incorporated as bone fibers.
This is accompanied by fibrous remodeling within the
membrane to provide continuity between membrane
and bone fibers. The membrane grows outward rather
than just backing off as bone is laid down by it. The
movements of muscle attachments along remodel-
ing surfaces of bones and the insertion of muscles on
resorptive bone surfaces are also carried out by this
membrane remodeling and relinkage process.
 164 F. Pugliese et al.
>>Important
55 Cartilage is a pressure-tolerant tissue located in
specific skeletal areas where direct compression
occurs (such as articular surfaces of joints); and
it functions as a “growth cartilage” in conjunction
with certain enlarging bones.
55 Unlike cartilage, which is usually under compres-
sion, bone is tension-adapted.
55 In terms of embryologic origin, bones are formed
intramembranously (directly from mesenchymal
stem cells) in tension areas and endochondrally
(formed first in cartilage then converted to bone)
in pressure areas.
9.5 Growth of the Neurocranium
9.5.1 The Calvaria
The bony lining surface of the whole cranial floor is
9 predominantly resorptive, in contrast to the endocranial
surface of the calvaria, which is predominantly deposi-
tory, as the meningeal surface of the skull roof is not
compartmentalized into a series of confined pockets.
The cranial floor, in contrast, has the endocranial fos-
sae and other depressions, such as the sella turcica and
the olfactory fossae. As the brain expands, the separate
bones of the calvaria are passively displaced corre-
spondingly in outward directions, through the soft tissue
stromata attached to them.
As the bones are displaced by the growing brain, they
become separated at their sutural articulations. The ten-
sion in the membranes causes deposition of new bone
on the sutural edges, thereby enlarging each bone in cir-
cumference. At the same time, the whole bone receives
a small amount of new deposition and resorption on
the flat surfaces of both ectocranial and endocranial
sides, respectively. This increases the overall thickness
and expands the medullary space between the inner and
outer tables. The arc of curvature of the whole bone
decreases, and the bone becomes flatter.
9.5.2 The Basicranium
The structure, dimensions, angles, and placement of the
various facial parts are affected by the size, shape, and
growth of the basicranium. The neural side of the cranial
floor requires an entirely different mode of development
compared to the calvaria because of its topographic
complexity and the tight curvatures of its fossae. The
endocranial surface of the basicranium is characteristi-
cally resorptive in most areas, because of the multiple
directions of enlargement and the complex magnitude of
remodeling required. Fossa enlargement is accomplished
by direct remodeling, involving deposition on the outside
with resorption from the inside, in conjunction with
sutural and growth at the cranial bases synchondroses.
The various endocranial compartments are separated
from one another by elevated bony partitions that are
depository in nature. As the fossae expand outward by
resorption, the partitions between them enlarge inward,
in proportion, by deposition. The midventral segment
of the cranial floor grows much more slowly than the
floor of the laterally located fossae. This accommodates
the slower development of the medulla, pons, hypo-
thalamus, optic chiasma, and so forth, in contrast to the
massive, rapid expansion of the hemispheres.
The basicranium also provides for the passage of
cranial nerves and the major cerebral blood vessels. The
process of remodeling growth provides for the chang-
ing stability of these nerve and vascular passageways,
as they do not become disproportionately separated
because of the massive expansion of the hemispheres of
the brain, as would happen if the basicranium enlarged
primarily at the sutures. The foramens undergo differ-
ential deposition and resorption, keeping pace with the
movement of the corresponding nerves or vessels they
house as the brain expands carrying them along.
The midline part of the basicranium is characterized
by the presence of synchondroses. Three synchondroses
are operative during the fetal and early postnatal peri-
ods: the intersphenoidal, the sphenoethmoidal, and the
spheno-occipital synchondrosis. The latter serves as the
principal “growth cartilage” of the basicranium dur-
ing adolescence and provides a pressure-adapted bone
growth mechanism. The spheno-occipital synchon-
drosis is retained throughout the adolescent growth
period as long as the brain and basicranium continue to
develop and expand. It ceases growth activity at about
12–15 years of age, and the sphenoid and occipital seg-
ments then begin to become fused in this midline area
through about 20 years of age [9]. Its presence provides
for the elongation of the midline portion of the cranial
floor by endochondral ossification.
Interstitial cartilaginous growth in the spheno-­
occipital synchondrosis with subsequent endochondral
bone formation causes primary displacement of the
bones involved. The sphenoid and the occipital bones
are actively separated by the primary displacement
process (. Fig. 9.16), and at the same time, new endo-
chondral (medullary fine-cancellous) bone is laid down
by the endosteum within each bone. Compact cortical
(intramembranous) bone is formed around this core
of endochondral bone tissue. The interior of the sphe-
noid bone eventually becomes hollowed to form the siz-
able sphenoidal sinus, which is formed secondarily and
enlarges progressively.
Disturbances in synchondrosal growth, such as
achondroplasia, result in significant shortening of the
cranial base, while growth of the calvaria and mandible
is largely unaffected [10]. Normal basicranial growth
Growth of the Craniofacial Complex
165 9
>>Important
55 As the brain expands, the separate bones of the
calvaria are correspondingly passively displaced
in outward directions, through the soft tissue stro-
mata attached to them.
55 Three synchondroses are operative during the
fetal and early postnatal periods: the intersphe-
noidal, the sphenoethmoidal, and the spheno-
occipital synchondrosis.
55 The spheno-occipital synchondrosis ceases growth
activity at about 12–15 years of age. Its presence
provides for the elongation of the midline portion
of the cranial floor by endochondral ossification.

9.6 Growth of the Nasomaxillary Complex

9.6.1  he Maxillary Tuberosity and Arch

T
..      Fig. 9.16 Primary displacement process that actively separates Lengthening
the sphenoid and the occipital bones. (From Enlow and Hans [3]
with permission) The horizontal lengthening of the bony maxillary arch
is produced by remodeling at the maxillary tuberosity
(. Fig. 9.17) [12]. This is a depository field in which
depends on genetically coded biologic processes occur- the backward-facing periosteal surface of the tuberos-
ring within the cartilage cells of the synchondrosis. ity receives continuing deposits of new bone as long as
However, although there is some intrinsic growth capac- growth in this part of the face proceeds. The arch also
ity in the basicranium, extrinsic control factors are also widens, and the lateral surface is, similarly, depository.
required. In contrast, the calvaria largely depend on the The endosteal side of the cortex within the interior of
growth of the brain and its surrounding endocranial the tuberosity (the maxillary sinus) is resorptive. The
and ectocranial matrix for growth control. cortex thus relocates progressively posteriorly and also,
As the middle and anterior cranial fossae become to a lesser extent, in a lateral direction with the maxillary
enlarged, the nasomaxillary complex is carried along sinus increasing in size as a result.
anteriorly with the floor of the anterior cranial fossa
from which it is suspended. At about 5 or 6 years of age,
frontal lobe growth and anterior cranial fossa expansion
are largely complete [11]. Therefore, any further develop-
mental protrusion of the forehead is a result of thickening
of the frontal bone and enlargement of the frontal sinus
within it. The temporal lobe and middle fossa, however,
continue to enlarge for several more years, and ongoing
expansion of each temporal lobe continues to displace
the frontal lobe forward, with this, in turn, causing ten-
sion in the osteogenic suture systems between these two
areas. The anterior fossae and the maxillary complex are
carried anteriorly by the frontal lobes, which are moved
forward because of temporal lobe enlargement behind
them. Each anterior cranial fossa enlarges in conjunc-
tion with the expansion of the frontal lobes. Wherever
sutures are present, they contribute to the increase in
the circumference of the bones involved. Thus, the sphe-
nofrontal, frontotemporal, sphenoethmoidal, fronto-
ethmoidal, and frontozygomatic sutures all participate
in a closely coordinated, traction-adapted bone growth
response to brain and other soft tissue enlargements.
The bones all become primarily displaced “away” from ..      Fig. 9.17 Maxillary tuberosity remodeling. (From Enlow and
each other as a consequence. Hans [3] with permission)
 166 F. Pugliese et al.

..      Fig. 9.18 Anterior and

inferior maxillary displacement
as it grows and lengthens
posteriorly and superiorly. (From
Moyers and Enlow [14] with
permission)

9 The maxillary tuberosity is a major “site” of maxillary

growth. It is growth in this area that creates space for the
eruption of the molar teeth. If one examines the “space”
available for the second or third molar in the mouth of
a 6-year-old, it is apparent that there is insufficient arch
length to accommodate this tooth. It is not possible to
determine if space will be available for this tooth to erupt
until after growth of the tuberosity is completed.
The whole maxilla undergoes a simultaneous process
of primary displacement in anterior and inferior direc-
tions as it grows and lengthens posteriorly and superi-
orly (. Fig. 9.18) [13].

Eye Catcher

Twenty-five years of age in males and 23 years in

females are probably the first point at which an accu-
rate assessment of “space” for third molar eruption
can be made. Until then these teeth should be consid-
ered unerupted and not impacted.

9.6.2  alatal Remodeling and Alveolar

P
Development
Even though the labial side of the whole anterior part
of the maxillary arch is resorptive, with deposition on
the palatal side, the palate and arch nonetheless increase
gradually in width (. Fig. 9.19), because of the V prin- ..      Fig. 9.19 Palatal remodeling. (From Enlow and Bang [13] with
ciple together with growth along the midpalatal suture. permission)
Growth of the Craniofacial Complex
..      Fig. 9.20 Ethmomaxillary complex downward displacement. (From Moyers and Enlow [14] with permission)
9.6.3 Downward Maxillary Displacement
The primary displacement of the whole ethmomaxil-
lary complex in an inferior direction (. Fig. 9.20) is
accompanied by simultaneous remodeling (resorption
and deposition) in all areas, inside and out, throughout
the entire nasomaxillary region. New bone is added at
the frontomaxillary, zygotemporal, zygosphenoidal,
zygomaxillary, ethmomaxillary, ethmofrontal, naso-
maxillary, nasofrontal, frontolacrimal, palatine, and
vomerine sutures resulting in displacement of the bones.
As the bones of the ethmomaxillary region are dis-
placed downward by the expanding soft tissues, sutural
bone growth takes place at the same time in response to
this, thus enlarging the bones as the soft tissues continue
to develop.
The downward movement of the teeth is accom-
plished by a vertical drift of each tooth in its own
alveolar socket as the socket itself also drifts inferi-
orly with it in lock-step by deposition and resorption.
Simultaneously, there is a passive carrying of the maxil-
lary dental arch as a whole, the palate and bony arch, all
167 9
associated soft tissues, and all of the alveolar sockets as
the entire maxilla is displaced downward as a unit [15].
>>Important
55 The maxillary tuberosity is a major “site” of max-
illary growth. It is growth in this area that creates
space for eruption of the molar teeth.
55 The whole maxilla undergoes a simultaneous
process of primary displacement in anterior and
inferior directions as it grows and lengthens pos-
teriorly and superiorly.
9.7 Growth of the Mandible
9.7.1 The Ramus
In terms of anatomy, the significance of the ramus of
the mandible is mostly that it provides an attachment
base for masticatory muscles, which, of course, com-
prises a basic function. However, the critical remodel-
ing and adjustments in ramus alignment, vertical length,
 168 F. Pugliese et al.

and anteroposterior breadth also provide an ever-­ 9.7.3 The Mandibular Condyle
changing fit with the growing maxilla and the limitless
structural variations of the face. Of course, it is not the This is an anatomic part of special interest because it
bony ramus itself that does this job, but its osteogenic, forms the articulation for the mandible and as such
chondrogenic, and fibrogenic connective tissues receiv- determines, at least in part, the relationship between the
ing local input control signals that produce its adjustive upper and lower teeth. Although the majority of the
shape and size through time. mandible is formed by intramembranous ossification,
The ramus is remodeled in a generally postero-­ the portion of the bony mandible that is derived from
superior manner while the mandible as a whole becomes condylar cartilage is endochondral in origin. During
displaced anteriorly and inferiorly, allowing posterior mandibular development, the condyle functions as a
lengthening of the corpus and dental arch. The posterior regional field of growth that provides an adaptation for
development of the mandibular bony arch simultane- its own localized growth circumstances, just as all the
ously proceeds by remodeling into the region previously other regional fields accommodate their own particular
occupied by the ramus. What was formerly ramus is con- localized growth conditions.
verted into what then becomes the mandibular corpus, The condylar growth mechanism itself is a clear-
which is thereby lengthened by this remodeling process. cut process. As seen in . Fig. 9.22, the endochondral
bone tissue (b) formed in association with the condylar
cartilage (a) is laid down only in the medullary por-
9.7.2 The Lingual Tuberosity
tion of the condyle. The enclosing bony cortices (c) are
produced by periosteal-endosteal osteogenic activity;
9 The lingual tuberosity is a major site of growth for the these vascular membranes are not subject to the com-
mandible just as the maxillary tuberosity is a major site pressive forces of articulation but, rather, are essen-
of growth for the upper bony arch. It is also the effective tially tension related because of muscle and connective
boundary between the two basic parts of the mandible: tissue attachments. The real functional significance of
the ramus and the corpus. the condylar cartilage thus involves an avascular and
The lingual tuberosity grows posteriorly by deposi- matrix-firm adaptation for regional pressure and mov-
tion on its posterior-facing surface. It protrudes notice- able articulation. This regional, endochondral bone-
ably in a lingual direction and it lies well toward the forming mechanism develops as a specific response to
midline from the ramus. The prominence of the tuberos- this particular local circumstance. The cartilage itself
ity is augmented by the presence of a large resorptive is not genetically programmed to grow and certainly
field just below it, which produces a sizable depression does not govern the course of growth in other areas of
called the lingual fossa. The combination of periosteal the mandible [16].
resorption in the fossa and deposition on the medial-­ The primary role of the condyle is to maintain the
facing surface of the tuberosity itself greatly accentuates articulation of the mandible with the neurocranium
the contours of both regions (. Fig. 9.21). through the glenoid fossa. The condyle is also capable
of adaptive and responsive growth and under normal
circumstances can withstand the compressive forces
of mandibular function. Thus, the condyle provides a

..      Fig. 9.22 Endochondral bone tissue b formed in association with

the condylar cartilage a is laid down only in the medullary portion of
..      Fig. 9.21 Mandibular lingual tuberosity growth by bone deposi- the condyle. The enclosing bony cortices c are produced by periosteal-­
tion on its posterior-facing surface. (From Enlow and Hans [3] with endosteal osteogenic activity. (From Enlow and Hans [3] with per-
permission) mission)
Growth of the Craniofacial Complex
pressure-­tolerant articular contact and has a multidi-
mensional growth capacity in response to ever-­changing,
developmental conditions. Depending on where in the
condylar cartilage mitotic divisions occur, that part of
the condyle (and ramus) thereby proliferates more verti-
cally or more posteriorly, as determined by input signals
that are related to both the demands of the dynamic and
static articulation of the teeth and the architectonic pat-
tern of “fitting” among the multitude of craniofacial
parts.
The rate and directions of condylar growth are
presumably subject to the influence of extracondylar
agents, including intrinsic and extrinsic biomechani-
cal forces and physiologic inductors, e.g., functional
movement of the mandible. One hypothesis is that
increased amounts of pressure on the cartilage serve to
inhibit the rate of cell division and proliferation, while
decreased amounts of pressure appear to stimulate and
accelerate growth. Moreover, the nature of the condy-
lar stimulus is more complex than simple forces acting
directly on the condyle; rather, nerve-muscle-connec-
tive tissue pathways are involved, and the changes
utilize a composite of such tissue responses and chain
feedbacks with the condyle as well as the other parts
of the mandible also participating. Sensory nerve
input from the periodontal membranes and from the
soft tissue matrix throughout the face picks up stimuli
that are passed on via motor nerves to muscles that, in
turn, alter the displacement and the positioning of the
mandible, which then affects the course of growth and
remodeling by the condyle and all other areas of the
growing mandible.
The condyle, of course, plays an important role
in mandibular growth [17]. It is directly involved as a
unique regional growth site; it provides indispensable
latitude for adaptive growth; it provides movable articu-
lation; it is pressure tolerant and provides a means for
bone growth (endochondral) in a situation in which
ordinary periosteal (intramembranous) growth would
not be possible. It is not just the condyle, however, that
participates as the key component; the whole ramus is
directly involved. The ramus bridges the pharyngeal
compartment and places the mandibular arch in an
occlusal position with the maxillary arch. The horizon-
tal breadth of the ramus determines the anteroposterior
position of the lower arch, and the height of the ramus
accommodates the vertical dimension and growth of
both the nasal and masticatory components of the mid-
face. The dimensions and morphology of the ramus are
directly involved in the attachments of the masticatory
muscles, and the ramus must accommodate their growth
and size. It is the growth and development of the whole
ramus, not merely the condyle, that accomplishes these
multiple and basic ends.
169 9
9.7.4 Ramus Uprighting
The ramus normally becomes more vertically aligned
during its development. As long as it is actively growing
in a posterior direction, this is accomplished by greater
amounts of bone addition on the inferior part of the pos-
terior border than on the superior part (. Fig. 9.23). A
correspondingly greater amount of matching resorption
on the anterior border takes place inferiorly rather than
superiorly. A “remodeling” rotation of ramus alignment
thus occurs. Condylar growth becomes directed in a
more vertical course along with the rest of the ramus.
Vertical lengthening of the ramus continues to take
place after horizontal ramus growth slows or ceases.
This is to match the continuing vertical growth of the
midface. To achieve this, condylar growth may become
more vertically directed, and a different pattern of ramus
remodeling can also become operative (. Fig. 9.24).
The direction of deposition and resorption reverses. A
forward growth direction can then occur in some indi-
viduals on the anterior border in the upper part of the
coronoid process. Resorption takes place on the upper
part of the posterior border. A posterior direction of
remodeling takes place in the lower part of the poste-
rior border. The result is a more upright alignment and a
longer vertical dimension of the ramus without a mate-
rial increase in breadth. This remodeling change, when it
occurs, appears to be more marked when the backward
relocation of the ramus, to provide for corpus lengthen-
ing, has decreased. There are probably other relation-
ships involved as well, including different facial and
headform types, although the biologic basis is presently
not fully understood.
The ramus undergoes a remodeling alteration in
which its angle becomes changed in order to retain
constant positional relationships between the upper
..      Fig. 9.23 The ramus normally becomes more vertically aligned
during its development, with greater amounts of bone additions on
the inferior part of the posterior border than on the superior part.
(From Enlow and Hans [3] with permission)
 170 F. Pugliese et al.
..      Fig. 9.24 Vertical lengthening of the ramus to match the contin-
ued vertical growth of the midface. (From Enlow and Hans [3] with
9 permission)
and lower arches. Otherwise, development among all
the diverse parts involved at different times, to differ-
ent degrees, and in different directions would result in
a marked misfit between the upper and lower jaws. The
composite of vertical growth changes of the mandibular
dentoalveolar arch, the ramus, and the middle cranial
fossae must match the composite of vertical nasomaxil-
lary growth changes to achieve a continuing facial bal-
ance. Any differential will lead to a displacement type of
mandibular rotation, either downward and backward or
forward and upward. Normal variations of facial type
and headform pattern are a common basis for such
mandibular rotations.
>>Important
55 The lingual tuberosity is a major site of growth
for the mandible just as the maxillary tuberosity
is a major site of growth for the upper bony arch.
55 Although the majority of the mandible is formed
by intramembranous ossification, the portion of
the bony mandible derived from condylar carti-
lage is endochondral in origin.
55 The horizontal breadth of the ramus determines
the anteroposterior position of the lower arch,
and the height of the ramus accommodates the
vertical dimension and growth of both the nasal
and masticatory components of the midface.
..      Fig. 9.25 Lateral cephalometric x-ray
9.8 Cephalometrics
Broadbent et al. [18] published a landmark paper describ-
ing the invention of a new kind of oriented radiograph
of the human skull. This radiograph was unique in one
important way. It was a standardized lateral and frontal
view of the human skull. The standards set forth in this
paper remain in use today. The evaluation of physiologi-
cal growth and its variants, together with its possible
diversions, similarly with the base of the skull and the
anatomical structures of the viscerocranium, depends
heavily upon the design and analysis of a cephalometric
x-ray [19]. The most commonly used type for the evalu-
ation of the sagittal and vertical relationships of the
anatomical structures of the craniofacial complex is the
lateral cephalometric x-ray (. Fig. 9.25). The frontal
x-ray, which evaluates the relationships on a lateral axis,
is rarely used.
Today, cephalometrics, the detailed analysis of
cephalograms, the standardized x-rays, is used in three
important ways by practitioners interested in facial
growth. First, it allows longitudinal study of facial
growth both in the absence and presence of orthodon-
tic treatment. Second, it provides a vocabulary of
terms to describe the morphology of the human face
Growth of the Craniofacial Complex
and jaws, and third, it provides five pieces of informa-
tion useful for orthodontic diagnosis and treatment
planning. These five elements that all orthodontists
derive from a combination of the clinical examination
and the lateral cephalometric radiograph are as fol-
lows:
1. The position of the maxilla relative to the cranial
base.
2. The position of the mandible relative to the cranial
base.
3. The position of the maxillary teeth relative to the
maxilla.
4. The position of the mandibular teeth relative to the
mandible.
5. The vertical proportions of the face.
..      Fig. 9.26 Digital tracing of a cephalometric x-ray prepared with Viewbox® cephalometric software (dHAL Software, Kifisia, Greece)
171 9
The practitioner needs to know if the anatomic features
of the patient are normal or abnormal with respect to
these parameters. The plan for treatment then follows.
For the analysis of a cephalometric x-ray, guiding points
are placed on drawings of anatomical elements that are
displayed in the cephalometric x-ray [19, 20]. This process
can be down by hand on special transparent paper or dig-
itally with the help of computer software (. Fig. 9.26).
In addition, with the help of cephalometric land-
marks, various other cephalometric variables are
defined. These variables can be:
1. Linear, when evaluating the distance between land-
marks or between landmarks and planes
2. Angular, when measuring the angles of cephalomet-
ric planes
3. Analogue, which evaluate the proportions of facial
parts
4. Mixed, which evaluate angles and distances
5. Circular, which measure arcs and circle sectors
 172 F. Pugliese et al.

!!Highlights 55 Facial angle, Lande angle.

The main points which can be located in a lateral 55 Growth angle.
cephalometric x-ray are as follows: 55 SNB angle.
55 N (nasion). 55 SNA angle.
55 S (sella turcica). 55 ANB angle.
55 Or (Orbitale) 55 Upper frontal facial height N-ANS.
55 Po (porion). 55 Lower frontal facial height ANS-Me.
55 ANS (anterior nasal spine).
55 PNS (posterior nasal spine). Dental measurements
55 Ar (articulare). 55 Angle of upper incisal axis with palatal plane.
55 Ba (basion). 55 Interincisal angle.
55 A (A point). 55 Angle of lower incisal axis with mandibular base
55 B (B point). plane.
55 Pg (pogonion).
55 Gn (gnathion). Soft tissue measurements
55 Me (menton). 55 Nasolabial angle.
55 Go (gonion). 55 Distance of upper lip from esthetic plane.
55 Prn (pronasale). 55 Distance of lower lip from esthetic plane.
55 Sns (subnasale soft).
55 Ls (labrale superius).
9 55 Li (labrale inferius).
9.9  ormal Variations in Facial Form
N
55 Pgs (pogonion soft).
and the Anatomic Basis
!!Highlights for Malocclusions
The main cephalometric planes used are:
55 Anterior skull base (S-N). There are two basic extremes in the shape of the head:
55 Frankfurt horizontal (FH or Po-O). dolichocephalic and brachycephalic. A third type, meso-
55 Palatal plane (ANS-PNS). cephalic, lies between the two extremes [27]. The oval-
55 Mandibular plane (Go-Gn or Go-Me). shaped dolichocephalic head form is horizontally long
55 Articulare-gnathion plane (Ar-Gn). and relatively narrow, in contrast to the more rounded
55 Facial plane (N-Pg). brachycephalic head form, which is horizontally shorter
55 Growth or Y-axis (S-Gn). and broader. Specific facial and occlusal types to these
55 Esthetical plane (E-Plane). head form shapes are as explained below.

Later follow the measurements of the dimensions and Definition

angles that describe the positions and relationships of
the skeletal elements, as well as the relationships of teeth
to their apical base. These measurements are then com-
pared to average reference values and standard deviations
defined by relevant x-ray studies for the demarcation of
what is “physiological” [21–26]. Based on the divergence
of values, parts of the face (skeletal, dental, and soft tis-
sue) are evaluated and the relationship between them is
defined, so the cause of the orthodontic problem can be
diagnosed (e.g., skeletal or dental anomaly) and the type
of face growth may be in turn evaluated.
!!Highlights
The main cephalometric measurements evaluated are:
Skeletal measurements
55 Angle of ramus of mandible.
55 Angle of mandible base.
55 Angle of maxillary plane – mandibular plane.
The cephalic index is the width of the head divided by its
length, multiplied by 100 and reported as a percentage:
55 Dolichocephalic, up to 75.
55 Mesocephalic, 75 to 80.
55 Brachycephalic is over 80.
Three general types of facial profile exist: orthognathic,
retrognathic, and prognathic [28]. The orthognathic
form is the everyday standard for a good profile. The
retrognathic face has a characteristic convex-­appearing
profile. The prognathic face is characterized by a con-
cave-appearing profile.
There are four general categories of occlusal pat-
terns: the “normal occlusion” and the Class I, the Class
II, and the Class III malocclusions. In the “normal” type
of occlusion, all the many underlying skeletal and dental
Growth of the Craniofacial Complex
factors combine to place the upper and lower teeth in
such a way that:
1. There is no undue amount of overjet.
2. All the teeth interdigitate perfectly, cusps fitting the
grooves of antagonist teeth.
3. There is no undue amount of overbite; the maxillary
front teeth do not overlap and cover the mandibular
front teeth by more than about one-third the crown
height of the lower incisors.
4. The maxillary canine is about one-half tooth width
distal to the mandibular canine.
5. The mesiobuccal cusp of the maxillary first molar
occludes with the mesiobuccal groove of the man-
dibular first molar (approx. One-half cusp behind).
The overall mandibular arch length is shorter than
maxillary arch length in the normal occlusion and
the more posterior positioning of the maxillary
molars accommodates the larger size of the upper
incisors. Normal differences also exist in root align-
ment, the incisor roots tip lingually, the canine roots
tip distally, and the molar and premolar roots are
essentially vertical.
The majority of the population, in fact, does not have
“normal” dentition. Most have a kind of malocclusion
which falls into one of the three general categories. This
system was first devised by Edward Angle and is thus
called the Angle Classification [29]. The Class I maloc-
clusion is the least severe type, and it mainly involves
dental variations from the ideal. The molar relation-
ship is normal, and disharmonies usually c­oncern the
crowding of anterior teeth. The profile is usually good,
although a few millimeters of retrognathia may nor-
mally be present. Overjet is not excessive. A variation of
the Class I occlusion involves “bimaxillary protrusion”:
proclination of both the upper and lower incisor regions.
This gives a noticeably “full” appearance to the mouth.
The Class II malocclusion is skeletally as well as den-
tally based. The various bones cause a positioning of the
teeth in such a way that a “Class II molar relationship”
exists. The maxillary first molar lies either directly over
or in front of the mandibular first molar, rather than
slightly behind, where it should be. In the most common
variety (Division 1) of the Class II type of malocclusion,
the maxillary incisors are protrusive with excessive over-
jet, and the profile is distinctly retrognathic. In another
variety (Division 2), however, overjet is not pronounced,
but a deep bite with palatally inclined incisors is pres-
ent, and sometimes the lateral maxillary incisors seem
to flare outward.
The Class III malocclusion is characterized by a
marked protrusion of the mandible, a prognathic profile,
and a molar relationship in which the lower first molar
173 9
lies mesially to the normal position. This is largely a
skeletally based type of occlusal variation.
There is a developmental and structural relationship
among these separate systems of classification (shape of
the whole skull, the facial profile, and occlusion) [21].
In individuals with a dolichocephalic head form,
the brain is horizontally long and relatively narrow.
This sets up a cranial base that is flatter, as the flexure
between the medial and anterior cranial floors is more
open. The whole nasomaxillary complex is thus placed
in a more protrusive position relative to the mandible
because of the horizontally longer cranial floor. It is
also lowered relative to the mandibular condyle, causing
a downward and backward rotation of the entire man-
dible. Finally, the occlusal plane becomes rotated into
a downward-­inclined alignment. These factors result in
a tendency toward mandibular retrusion and a Class II
molar relationship. The profile tends to be retrognathic
(. Figs. 9.27, 9.28). However, compensatory changes
may sometimes affect this.
Individuals with a brachycephalic head form have
a rounder and wider brain. This sets up a cranial base
that is more upright and has a more closed flexure,
which decreases the effective horizontal dimension of
the middle cranial fossa. The result is a relative retrusion
of the nasomaxilla and a more forward relative place-
ment of the entire mandible. This causes a greater ten-
dency toward a prognathic profile and a Class III molar
relationship. The occlusal plane as well as the ramus
of the mandible may be aligned upward, but various
..      Fig. 9.27 Dolichocephalic head form, causing a downward and
backward rotating of the mandible, resulting in a tendency toward
mandibular retrusion and a Class II molar relationship. (From
Enlow and Hans [3] with permission)
 174 F. Pugliese et al.

..      Fig. 9.28 Dolichocephalic

head form. (From Enlow and
Hans [3] with permission)

compensatory processes usually result in either a per-

9 pendicular or a downward-inclined occlusal plane and
..      Fig. 9.29 Brachycephalic head form, resulting in a relative retru-
sion of the nasomaxilla and more forward relative placement of the
entire mandible. This causes a greater tendency toward prognathic
profile and a Class III molar relationship. (From Enlow and Hans [3]
with permission)
slight backward rotation of the ramus (. Figs. 9.29 and
9.30). Other compensatory changes are also operative,
and these tend to counteract the built-in Class III ten-
dencies.
The basic nature of interrelationships among brain
form, facial profile, and occlusal type, as just described,
causes a predisposition toward characteristic facial
types and malocclusions among different types of pop-
ulations. These respective tendencies are built into the
basic plan of facial construction. However, most of us
also have intrinsic structural features; the built-in ten-
dencies are offset, to a greater or lesser extent; and we
thereby have at least reasonable facial proportions with
a Class I occlusion, even though the underlying tenden-
cies are still present. If these compensatory features do
not develop, however, or if they are insufficient, the
built-in tendencies then become expressed, and we have
a more or less severe malocclusion and a greater extent
of retrognathia or prognathia [30].
Growth of the Craniofacial Complex
175 9
..      Fig. 9.30 Brachycephalic
head form. (From Enlow and
Hans [3] with permission)

References 16. Mizoguchi I, Toriya N, Nakao Y. Growth of the mandible and

biological characteristics of the mandibular condylar cartilage.
Jap Dental Sci Rev. 2013;49:139–50.
1. Baer MJ, Harris JE. A commentary on the growth of the human
17. Meikle MC. The role of the condyle in the postnatal growth of
brain and skull. Am J Phys Anthrop. 1969;30:39–44.
the mandible. Am J Orthod. 1973;64:50–62.
2. Goldstein MS. Changes in dimension and form of the face and
18. Broadbent BH. A new x-ray technique and its application to
head with age. Am J Phys Anthrop. 1936;1:37–89.
orthodontia. Angle Orthod. 1931;1:45–66.
3. Enlow DH, Hans MG. Essentials of facial growth. 2nd ed. Ann
19. Bishara SE, Athanasiou AE. Cephalometric methods for assess-
Arbor: Needham Press; 2008.
ment of Dentofacial changes. In: Orthodontic Cephalometry.
4. Ntani G, Day PF, Baird J, Godfrey KM, Robinson SM, Cooper
St. Louis: Mosby-Wolfe; 1995. p. 105–24.
C, Inskip HM. Maternal and early life factors of tooth emer-
20. Riolo ML, Moyers RE, McNamara JA, Hunter WS. An atlas of
gence patterns and number of teeth at one and two years of age.
craniofacial growth: cephalometric standards from The Univer-
J Dev Orig Health Dis. 2015;6:299–307.
sity School Growth Study. Monograph 2, Craniofacial Growth
5. Patten BM. Human embryology. 3rd ed. New York, NY:
Series, Center for Human Growth and Development. Ann
McGraw-Hill; 1968.
Arbor: The University of Michigan; 1974. p. 379.
6. Langman J. Medical embryology. 2nd ed. Baltimore: Williams &
21. Downs WB. Variations in facial relations: their signifi-
Wilkins; 1969.
cance in treatment and prognosis. Am J Orthod. 1948;34:
7. Anderson CE. The structure and function of cartilage. J Bone
812–40.
Joint Surg. 1962;44:777–86.
22. Lande MJ. Growth behavior of the human bony facial profile as
8. Baumrind S. Reconsideration of the propriety of the “pressure-
revealed by serial cephalometric roentgenology. Angle Orthod.
tension” hypothesis. Am J Orthod. 1969;55:12–22.
1952;22:78–90.
9. Alhazmi A, Vargas E, Palomo JM, Hans M, Latimer B, Simpson
23. Steiner CC. Cephalometrics for you and me. Am J Orthod.
S. Timing and rate of spheno-occipital synchondrosis closure
1953;39:729–55.
and its relationship to puberty. PLoS One. 2017;12:e0183305.
24. Ballard CF. Morphology and treatment of class II division 2
10. Cendekiawan T, Wong RWK, Rabie ABM. Relationships
occlusions. Trans Euro Orthod Soc. 1956:44–55.
between cranial base synchondroses and craniofacial develop-
25. Ricketts RM. Esthetics, environment, and the law of orthodon-
ment: a review. The Open Anat J. 2010:67–75.
tics. Am J Orthod. 1968;54:272–89.
11. Nie X. Cranial base in craniofacial development: developmen-
26. Legan HL, Burstone CJ. Soft tissue cephalometric analysis for
tal features, influence on facial growth, anomaly, and molecular
orthognathic surgery. J Oral Surg. 1980;38:744–51.
basis. Acta Odontol Scand. 2005;63:127–35.
27. Margolis HI. A basic facial pattern and its application in clinical
12. Diamond M. Posterior growth of maxilla. Am J Orthod.
orthodontics. Am J Orthod. 1953;39:425–43.
1946;32:359–64.
28. Bergman RT. Cephalometric soft tissue facial analysis. Am J
13. Enlow DH, Bang S. Growth and remodeling of the human max-
Orthod Dentofac Orthop. 1999;116:373–89.
illa. Am J Orthod. 1965;51:446–64.
29. Angle EH. Treatment of malocclusion of the teeth, vol. 7. Phila-
14. Moyers RE, Enlow DH. Growth of the craniofacial skeleton. In:
delphia: White Dental Manufacturing Company; 1907.
Moyers RE, editor. Handbook of orthodontics. 4th ed. Chicago:
30. Enlow DH, Kuroda T, Lewis AB. Intrinsic craniofacial compen-
Yearbook Medical Publisher Inc.; 1988. p. 37–72.
sations. Angle Orthod. 1971;41:271–85.
15. Bjork A, Skieller V. Facial development and tooth eruption. Am
J Orthod. 1972;62:339–83.
 177 10

Tooth Eruption, Shedding,

Extraction and Related
Surgical Issues
Aristidis Arhakis, Ola B. Al-Batayneh, and Hubertus van Waes

Contents

10.1 The Physiology of Tooth Eruption – 178

10.1.1  hronology and Sequence of Tooth Eruption – 178
C
10.1.2 Mechanism of Tooth Eruption – 179

10.2 Symptoms of Tooth Eruption – 180

10.2.1 L ocal Treatment of Teething Symptoms – 181
10.2.2 Systemic Treatment of Teething Symptoms – 181

10.3 Disturbances in Tooth Eruption – 182

10.3.1  remature Tooth Eruption: Neonatal Teeth – 182
P
10.3.2 Delayed Tooth Eruption – 183
10.3.3 Other Disturbances in Tooth Eruption – 188

10.4 Shedding and Extraction – 196

10.4.1 S hedding of Primary Teeth – 196
10.4.2 Extraction and Surgical Techniques Related to Eruption – 196

10.5 Transplantation of Teeth – 200

10.5.1 E xtraction and Re-implantation of Permanent Teeth – 200
10.5.2 Transplantation of Teeth Anteriorly – 202
10.5.3 Intentional Re-implantation – 203

References – 205

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_10
 178 A. Arhakis et al.

10.1 The Physiology of Tooth Eruption ..      Table 10.1 Median age of eruption (Md) with one
standard deviation (S.D.) in months of primary teeth based
Eruption is the emergence of teeth from their devel- on a study carried out in n = 1988 Caucasian Arab children
opment position in the bone to the functional occlu- in Jordan [3]
sal position in the dental arch. This axial movement is Tooth Female
Male
divided into three phases: pre-eruptive phase, eruptive
Md S.D. Md S.D.
phase, and functional phase [1].
55 Pre-eruptive phase is observed before the beginning Maxilla
of root formation, during which the tooth germ Central incisor 10.5 0.7 10.6 0.6
moves within the tooth crypt.
Lateral incisor 12.9 0.6 13.1 0.6
55 The eruptive phase begins when the root starts to
form, while the tooth germ undergoes intraosseous Canine 20.6 0.6 19.8 0.7
and supraosseous movement until it enters the oral First molar 15.5 0.8 15.5 0.6
cavity and ends when tooth reaches occlusal plane.
Second molar 27.7 0.6 27.2 0.6
At this phase there are two substages: the first is the
intraosseous phase, followed by the extraosseous/ Mandible
preocclusal phase which starts after tooth penetra- Central incisor 8.3 0.9 8.1 0.7
tion through the alveolar process. At the end of this Lateral incisor 14.6 0.4 13.9 0.5
phase stabilization of periodontal tooth support
takes place, while root formation continues. Canine 20.9 0.6 19.8 0.8
First molar 16.1 0.8 15.8 0.6
The functional phase is the third and final phase, in which Second molar 27.7 0.5 27.2 0.6
10 the teeth move to maintain their positions of functional
occlusion and move toward the occlusal plane for some
time after reaching the initial occlusal contacts [1].

..      Table 10.2 Median age of eruption (M) with one

10.1.1  hronology and Sequence of Tooth
C standard deviation (S.D.) in years of permanent teeth based
on a study carried out in n = 2672 Caucasian Arab children
Eruption in Jordan [5]

Tooth Male Female

In primary teeth the sequence of eruption is the same
for both genders. The time of eruption is almost simi- M S.D. M S.D.
lar. On average, eruption begins at about the age of 8.2 Maxilla
± 0.8 months with the mandibular central incisors and Central incisor 7.25 0.89 7.11 0.78
ends approximately at the age of 2 years and 4 months
with the second primary molars (. Table 10.1). Thus, Lateral incisor 8.45 1.18 8.07 0.94
in most children the duration of primary tooth eruption Canine 11.56 1.51 11.09 1.43
lasts about 24 months [2]. First premolar 10.45 1.52 10.01 1.44
In permanent teeth, the eruption sequence is similar
to the primary teeth, except for the first molar, which is Second premolar 11.37 1.53 11.00 1.51
frequently the first tooth to erupt. Girls precede in erup- First molar 6.35 0.67 6.20 0.85
tion time and this difference between genders may reach Second molar 12.61 1.41 12.32 1.42
several months for the teeth that erupt last in the arches
[4]. Gross disturbances in the sequence of eruption are Mandible
less common in the permanent dentition, and, except Central incisor 6.48 0.67 6.32 0.81
for an interchange between mandibular canines and first Lateral incisor 7.51 0.89 7.34 0.85
premolars, it is to be taken with some consideration.
The eruption of the permanent dentition normally Canine 10.63 1.42 9.84 1.21
starts with the eruption of the mandibular incisors and First premolar 10.54 1.48 10.12 1.40
of either first maxillary or mandibular molars just after Second premolar 11.73 1.58 11.20 1.55
the age of 6 years and is completed with the eruption
of second molars at about age 12 (. Table 10.2). Thus, First molar 6.24 0.66 6.08 0.87
in most children, the total duration of eruption of per- Second molar 12.19 1.41 11.66 1.54
manent teeth (excluding third molars) lasts 6 years. The
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
eruption time in the permanent dentition shows more
pronounced variation compared to primary dentition,
normally ranging 6–18 months. The first to erupt per-
manent teeth have the minimum standard deviation of
their mean eruption time, whereas the later erupting
ones maxillary canines, premolars, and second perma-
nent molars have the maximal [4, 5].
Following the normal distribution of eruption times
both for primary and permanent teeth, one or two stan-
dard deviations are indicative of normality, as the range
is significant. For example, a clear medical and family
history for a 12-month-old boy with no erupted teeth,
who has a bulky alveolar ridge indicative of presence
of unerupted teeth, should be simply monitored clini-
cally. If there is a thin, potentially edentulous alveolar
ridge or the child is older, radiological examination and
then general medical examination are recommended
(. Fig. 10.1). Symmetrical teeth usually erupt almost
simultaneously, but other possible local factors should
a
b
c
..      Fig. 10.1 a By clinical evaluation, a 3-year-old girl is suspected
to have congenital absence of maxillary lateral incisors. b Radio-
graphic assessment reveals delayed development and eruption of lat-
eral incisors. c Their full eruption at the age of 4.5 years
179 10
be taken on account. Tooth eruption delay of several
months in respect to its timely erupted symmetrical one
in either jaw could be related to pathology and should
be checked radiographically (e.g., tooth impaction,
odontoma, etc.). For example, an 11-year-old child
­
that had the mandibular left first premolar erupted 6
months before the contralateral tooth should have a
radiographic examination if there is no mobility in the
predecessor primary molar.
10.1.2 Mechanism of Tooth Eruption
Tooth eruption has caused many historical discussions.
Various theories and opinions have been proposed
about the mechanism of tοοth eruption, such as the
theory of hydrostatic pressure in vessels and/or tissues
[6], a theory of the role of the periodontal ligament in
the eruption process [7], a theory of mobility/contrac-
tion of periodontal ligament fibroblasts [8], a theory
of root formation [6], and the bone remodeling theory
[9]. According to the prevailing opinion the dental fol-
licle has an important role in tooth eruption. Surgical
removal of the follicle has been shown to inhibit the
eruption process. Removing the coronal portion of den-
tal follicle causes disorder of bone resorption coronally
without affecting the bone deposition in the apical por-
tion, whereas the removal of the apical portion of the
follicle reduces bone formation apically but does not
inhibit the bone resorption process coronally [10]. If the
tooth germ is replaced with an artificial tooth in an oth-
erwise intact dental follicle, the artificial tooth still moves
toward the eruption position [9, 11]. These data suggest
that the dental follicle contributes to the eruption pro-
cess during the intraosseous phase, but does not explain
the continued extraosseous phase of eruption. After
the emergence of the crown of the tooth through the
alveolar bone, the enamel organ degenerates, becomes
thinner, and is known as reduced enamel epithelium
(. Fig. 10.2). The fusion of the reduced enamel epithe-
lium with the epithelium of the oral mucosa allows the
penetration of the erupting tooth without causing trau-
matic discontinuity of the oral mucosa [12].
The influence of innervation on tooth eruption
has been evaluated in experimental studies through an
epithelial-­mesenchymal interaction with the epithelial
rests of Malassez [13, 14]. Kjær proposed a new eruption
mechanism based on previous work, stating that the eti-
ology behind the eruption process is that an innervation-­
provoked pressure in the apical part of the tooth results
in an eruption that requires continuous adaptation from
the periodontal membrane and the active movement of
the crown follicle, destroying overlying bone tissue [15].
This attributes the process to the membrane covering
the apical part of the tooth root, the periodontal mem-
 180 A. Arhakis et al.
10 ..      Fig. 10.2 Total formation of the crown and emergence of the
tooth through the alveolar bone. A Beginning of root formation. B
The fusion of the reduced enamel epithelium with the epithelium of
the oral mucosa
brane, and the crown follicle as the three interrelated
structures, which are involved in the eruption process. It
is possible that a pressure apically changes the periodon-
tal membrane and at the same time triggers the crown
follicle to resorb the surrounding tissue. The hypothesis
suggested by Kjaer proposes that a tooth that will erupt
depends on the:
1. Space in the eruption path: created by the crown fol-
licle that destroys overlying bone tissue.
2. Lift or pressure from below: the root membrane
functions as a glandular membrane. The innervation
in the membrane causes, as in the glandular end cells,
an overpressure that displaces the root surface, peri-
odontal membrane, and pulp tissue, causing the
tooth to elevate in the eruption direction.
3. Adaptability in the periodontal membrane: this is
essential for eruption. This reorganization process
that occurs through cell necrosis—apoptosis—has
recently been proven and demonstrated in the inner-
most root-close layer of the periodontium in erupt-
ing teeth.
Early cytological studies of dog premolars showed that
there was an influx of mononuclear cells (monocytes)
into the coronal portion of the dental follicle postnatally,
with a simultaneous increase in the number of osteo-
clasts in the coronal part of the alveolar bony crypt [16].
Since the mononuclear cells have structural and enzy-
matic features of osteoclast precursors, it was proposed
that the dental follicle regulates bone resorption provid-
ing monocytes that are either converted to osteoclasts or
influence osteoclast function by the release of cytokines
and growth factors [17].
At a molecular level, there are signaling molecules
that potentially trigger and control the eruption of teeth
at a cellular level. Colony-stimulating factor-1 (CSFL1),
produced in the dental follicle, accelerates the eruption,
promoting influx of mononuclear cells and increasing
the number of osteoclasts that are observed in the early
stages of eruption [16, 18]. Interleukin L1a regulates
gene expression for the CSFL1 production in the dental
follicle cells. Epidermal growth factor (EGF) accelerates
tooth eruption, increasing interleukin L1a and inducing
bone absorption [19]. Besides the significant influence of
transforming growth factor b1 (TGF-b1) on active erup-
tion, a profound alkaline phosphatase activity is also
observed [20]. In patients with cleidocranial dysplasia,
a condition which is related with long delay or failure of
permanent teeth eruption, the mRNA levels of RANK,
osteoprotegerin (OPG), and CSF-1 were significantly
higher, compared to healthy individuals, indicating a
possible disturbance in the resorption and remodeling
of the bone [21].
10.2 Symptoms of Tooth Eruption
The eruption of primary teeth has been associated with
local or general symptoms. There are ¾ of infants or
toddlers who display these symptoms during the erup-
tion of anterior teeth and almost all during the erup-
tion of primary molars. At a local level, usually there
is inflammation of the gums that cover the tooth that is
about to erupt, increased salivation, and increased ten-
dency to bite. At a systemic level, usual manifestations
include general restlessness and crying and appetite loss
(or reduced feeling of hunger) [22–24]. A cross-sectional
survey conducted on 1500 parents attending Maternity
and Child Health Care Centers in Jordan showed that
almost 75% incorrectly attributed fever, diarrhea, and
sleep disturbances to teething. However, more than 50%
believed systemic symptoms are not related to the pro-
cess [24].
The dental follicle is a rich source of prostaglandins,
cytokines, and growth factors, substances that cause
local inflammation and pain. The symptoms are tem-
porary and are stated at any period before, during, and
after the emergence of the teeth in the mouth, having a
duration of about a week [22]. However, there are studies
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
181 10
that did not confirm the association of these ­symptoms
a
with the tooth eruption, concluding that these can be
attributed to coexisting reasons, not related with tooth
eruption [25]. An increase in body temperature up to
37.5 °C, with an absence of other clinical symptoms,
may be associated with teething. Nevertheless, higher
body temperature is not associated with tooth erup-
tion and the responsible reason should be detected by a
pediatrician [26]. Many parents report various teething
symptoms of their children, the most common of which
is oral pain.

Eye Catcher
b
Symptoms of primary tooth eruption should not be
approached as pathology. In most cases support, par-
ents’ reassurance, and their engaging in activities with
the child, like walks and toys, are the most effective
measures against the disturbances. In more severe sit-
uations, the choice of appropriate treatment, local or
systemic, is based on the existing symptoms.

10.2.1 Local Treatment of Teething

Symptoms
Especially during the teething period, due to the sensa-
tion of pain in the gums and mouth, infants and tod-
dlers have an increased tendency to put everything in
their mouth, to bite and rub their gums, trying to pro-
vide some relief from the pain. In pharmacies and shops
selling baby products, there is a wide variety of toys and
teething toys made of plastic, rubber, wood, and other
materials. Those which can be cooled before use operate
as analgesics through vasoconstriction (. Fig. 10.3).
Bread crust or biscuits containing no sugar or other
sweeteners can be used in the same way as teething toys.
However, products made from cereal flour should not
be used in infants less than 8 months old, in case some
of them are suffering from celiac disease (see 7 Chap.
17). The diagnosis is made after 8 months of life with
the emergence of intestinal symptoms caused by the
cereal gluten, which are intense if such foods are intro-
duced into the infant’s diet earlier. Raw, hard fresh-cut
fruits and vegetables are also effective and nutritious for
infants and healthy for their teeth.
There is a wide variety of pharmaceutical medica-
ments for local application on the gums, such as those
containing hyaluronic acid, licorice, clove, myrrh, and
arnica (. Fig. 10.3). They have mild action which
elapses quickly. Overdose should be avoided, especially
..      Fig. 10.3 a. Plastic ring containing water. Before use by the
infant, it can be refrigerated. b Advertisement of pharmaceutical
commercial product for relieving symptoms of teething
for ointments that contain lidocaine. In 2014 the FDA
issued a drug safety communication against the use of
lidocaine to treat teething pain. Notably, in 2011 a simi-
lar warning was issued against the use of benzocaine,
since it can cause severe methemoglobinemia. The use
of some analgesics such as salicylic acid (aspirin) can
provoke chemical burn or can have hemolytic effects in
infants with G6PD enzyme deficiency as they prevent
folic acid composition [23]; therefore, they should be
either avoided or used with caution.
10.2.2 Systemic Treatment of Teething
Symptoms
Systemic treatment is selected only if the local treat-
ment proves to be ineffective. It is administered with the
consent of the pediatrician when the disturbances of
teething (pain, insomnia, etc.) affect the quality of life
 182 A. Arhakis et al.

are rare cases of neonates (1: 2000–3500 births) born

..      Table 10.3 Dosage for usual analgesic/anti-inflammatory with one or more teeth present (natal, pre-birth) and
treatment
other cases where teeth erupt during the first month of
Acetaminophen/paracetamol
life (neonatal) [28]. These teeth regularly belong to the
normal primary dentition and only a very small percent-
Usual oral dosage: age may be supernumerary. In most of these cases, the
Children <12 years: 10–15 mg/kg/dose every 4–6 hours as prematurely erupting teeth are mandibular central inci-
needed (maximum 75 mg/kg/24 hours, but not to exceed 4.0 sors whose eruption is greatly accelerated for unknown
g/24 hours)
reasons. Because of the early eruption, these teeth do
Alternative dosing based on age of child not have sufficient root formation and often exhibit
Age Weight Dosage great mobility. Over 1/3 of natal teeth are lost within
the first year of life, while 2/3 of neonatal teeth generally
lbs kg mg3
shed prematurely [29].
0–3 months 6–11 2.7–5 40 Morphology, color, and structure of natal and neo-
4–11 months 12–17 5.1–7.7 80 natal teeth can often be different compared to primary
teeth that erupt normally. They can be conical, with
1–2 years 18–23 7.8–10.5 120
smaller dimensioned crown, incomplete structure, or
2–3 years 24–35 10.6–15.9 160 hypoplastic enamel, opaque or yellowish-brown col-
ored (. Fig. 10.4). Histologically, despite the normal
Ibuprofen
structure of the enamel prisms, early eruption appears
to inhibit the normal maturation of enamel resulting in
Usual oral dosage: a tendency for abrasion and staining, as pigments enter
10 Infants and children <50 kg: 4–10 mg/kg/dose every 6–8 hours
as needed (maximum single dose 400 mg; maximum dose 40
the porous enamel texture [30]. Natal and neonatal
teeth are found in healthy neonates, but have also been
mg/kg/24 hours)
observed in 50 different syndromes [28].
Alternative dosing based on age of child Two of the most common complications associated
Age Weight Dosage with (neo)natal incisors are injury of the mother’s nip-
ple and the Riga-Fede syndrome. During breastfeeding,
lbs kg mg3
the tongue of the infant embraces the mother’s areola,
6–11 months 6–11 2.7–5 40 passing out of the alveolar crest or even out of his lips.
4–11 months 12–17 5.1–7.7 80 The infants’ suckling incorrectly, possibly in order to
avoid the painful stimulus from the tooth to the lower
1–2 years 18–23 7.8–10.5 120
surface of the tongue, creates a condition that injures
2–3 years 24–35 10.6–15.9 160 the nipple and areola of mother’s breast and making
breastfeeding painful for the mother [26]. Riga-Fede
syndrome manifests as self-injury of the top or bottom
surface of the tongue of the infant. The lesion begins
of the child and parents. Before the administration of as a simple ulcer (see 7 Chap. 20, 7 Fig. 20.7) which
systemic therapy, i.e., analgesic/anti-inflammatory, the can develop into a bulky, fibrous mass with clinical
pediatrician should exclude other medical conditions, presentation of ulcerative granuloma. The problems
not related to teething [27] (. Table 10.3). in breastfeeding in both cases can lead to disturbances
in nutrition, reduced weight gain, and inhibition of
infant’s growth [31].
10.3 Disturbances in Tooth Eruption
Eye Catcher
10.3.1  remature Tooth Eruption: Neonatal
P
Teeth Natal and neonatal teeth should not be extracted
unless they are supernumerary (requires radiographi-
According to . Table 10.1, the mandibular primary cal confirmation) or if they create any problems for
central incisors may erupt early, e.g., at 5 months of age, the mother or the infant. In some cases, smoothening
and the eruption is considered normal. However, there of the incisal edge may prevent tongue ulceration [32].
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
183 10

a b

c d

..      Fig. 10.4 a Prenatal tooth in a newborn baby. b Eruption of a neonatal mandibular incisor. c, d Neonatal tooth that needed to be
extracted appears with immature and thin hard tissues

eruption (PFE). Typically more than one family mem-

Great mobility poses an additional risk of aspiration.
If extraction is indicated in a less than 10-day-old
newborn, due to the existing hypoprothrombinemia,
communication with the pediatrician is required in
order to check the adequacy of vitamin K and pre-
vent hemorrhagic disease of newborns [33].
10.3.2 Delayed Tooth Eruption
10.3.2.1 Generalized Delay in Tooth Eruption
Diseases of the endocrine glands, such as hypothyroid-
ism and hypoparathyroidism, and some chronic diseases
in which there is a delay in both physical and dental
development often cause delay in the emergence of the
primary and permanent dentition. Delayed eruption is
observed in at least 150 different syndromes [34].
One often overlooked but quite common cause for
failure of eruption is a so-called primary failure of
ber is affected. The reason behind it is a mutation on
the PTHR1 gene. Genetically verified diagnosis may
protect patients and orthodontists from long and futile
treatment, because orthodontic treatment alone does
not lead to success and can have a negative influence on
unaffected teeth and areas of the jaw [35, 36].
In cleidocranial dysplasia, there is typically a delay
in teeth eruption, which is more pronounced in the
permanent dentition, where it usually leads to their
­
impaction. The disorder is associated with the presence
of supernumerary teeth, defective osteoclastic activity,
and existence of bone formation defects (hypoplastic
clavicles, open skull sutures, short stature) (. Fig. 10.5).
For this reason, the eruption disorder also occurs in areas
with no supernumerary teeth [37]. People with tricho-­
dento-­osseous syndrome have normal height but also
exhibit disorders in bone remodeling (sclerotic lesions)
with reduced osteoclastic activity. Tooth eruption may
be delayed in the permanent dentition, often leading to
 184 A. Arhakis et al.
tooth impaction [38]. Hypoplastic enamel defects are
also observed (see 7 Chap. 17). In cases with pycnodys-
ostosis, individuals exhibit short stature and short limbs.
The skeleton, including the craniofacial complex, shows
osteopetrosis and brittleness. The increased density of
the jaw bones in combination with the intense crowding
causes inhibition of tooth eruption of the permanent
dentition and other anomalies [39]. Hypohidrotic ecto-
dermal dysplasia is mainly characterized by oligodontia;
however, cases of generalized delayed eruption have also
been reported [40].
Children with cleidocranial dysplasia, tricho-dento-­
osseous syndrome, and pycnodysostosis, who exhibit
great eruption delay, should be closely monitored from
an early age. The treatment is especially complicated
and is based on surgical extractions of supernumerary
teeth and exposing and assisting eruption of unerupted
teeth as part of a long-lasting orthodontic treatment.
Delayed eruption and impaction of permanent teeth
are observed in the absence of syndromes, sometimes
related with systemic diseases. Probably these conditions
are related to osteoblast/osteoclast malfunction mecha-
10 nisms that have not been clarified (. Figs. 10.6 and 10.7).
Terms used include ‘primary failure of eruption’, usually
referring to single teeth in the molar area, and ‘tooth erup-
tion delay’. The therapeutic approach may be simply mon-
itoring or, in some cases, similar to the above mentioned.
a
d e
..      Fig. 10.5 a Initial examination of cleidocranial dysplasia in a
13-year-old boy. b Confirmation of hypoplastic clavicles in chest
radiograph. c Open sagittal suture of the skull and lack of nasal
bone in anteroposterior cephalometric radiograph. d Occlusion class
III and a small maxilla and long delayed tooth eruption, which was
10.3.2.2 Localized Delay in Tooth Eruption
Very early loss of primary teeth due to severe carious
lesions or trauma of the anterior teeth is a common
cause of delayed eruption of the permanent successor.
Mainly in the case of trauma, this is likely to occur due
to the creation of more fibrous (scar) connective tissue
during healing. On the other hand, early eruption of the
permanent successor is usual, after severe inflammatory
alveolar osteolysis of microbial etiology (following a
septic pulp) of the primary predecessor (. Fig. 10.8).
In cases of profound delay, regardless of the cause, the
treatment plan may include surgical exposure and wait-
ing for either self or orthodontically assisted eruption
(. Fig. 10.9). Another relatively common cause of
delayed tooth eruption in healthy children is supernu-
merary teeth. Αdditionally, the presence of odontomas
is almost always related to inhibition of the eruption
of permanent teeth and orthodontic anomalies (see
7 Chap. 17).
Ankylosis of primary teeth, due to trauma in anterior
teeth or due to poorly understood reasons in posterior
teeth, may cause delayed eruption of the permanent suc-
cessor. Crown or root dilaceration and partial or com-
plete inhibition of root formation as consequences to
trauma or inflammation of primary teeth may delay or
inhibit the eruption of permanent incisors [41]. Differ-
ent types of cysts in the anterior or posterior region may
b
c
f
the chief complaint. e Greatly delayed dental age and supernumerary
maxillary incisors. f Surgical exposure and extraction of two super-
numerary and orthodontic tractions of permanent teeth in the den-
tal arch. (Courtesy of Dr. O. Kolokitha)
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
185 10

a b

..      Fig. 10.6 a Teeth of an 11-year-old boy with free medical history. b His panoramic radiograph shows characteristics of ‘tooth develop-
ment and eruption delay’ and ‘primary failure of eruption’ of the mandibular first molars

a b

c d

..      Fig. 10.7 a Delayed eruption of permanent teeth in an 8-year- child at age 11. Slight overeruption of the mandibular first perma-
old boy with a medical history of hydrocephalus. b Enlarged follicles nent molars 3 years after their surgical exposure. Late unassisted
of mandibular first permanent molars and possible minute folli- eruption of the opposing maxillary molars
cles of second molars in the panoramic radiograph. c, d The same

..      Fig. 10.8 a Premature

eruption of mandibular right
a b
first premolar at the age of 8
after intense inflammatory bone
resorption of microbial etiology
due to septic pulp necrosis of
primary predecessor. This is
probably the cause of the
hypomineralized defect of its
enamel. b Incomplete root
formation (approximately 1/3) of
the premolar
 186 A. Arhakis et al.
also inhibit normal eruption of the permanent teeth.
Most commonly dentigerous and midline cysts, which
appear radiographically as radiolucent lesions with a
well-defined cortex, are treated usually either with enu-
cleation or marsupialization [42] (. Fig. 10.10). Rarely
multiple dentigerous cysts with impacted teeth related to
syndromes are encountered (. Fig. 10.11).
The presence of a benign or malignant tumor could
cause a delay in the eruption of permanent teeth. The
adenomatoid odontogenic tumor is a benign, epithe-
lial, well-defined, single spaced tumor with a small
central radiopaque nucleus. It is mainly located in
a b
10
c
..      Fig. 10.9 a Delayed eruption of mandibular left first permanent
molar in an 8.5-year-old girl probably related to ‘primary failure of
eruption’ [36]. b Clinical appearance after the decision for orthodon-
tic traction. c Surgical exposure of mandibular left second premolar
and first permanent molar for the traction of the premolar in the
dental arch (traction of the molar will follow). d New panoramic
the anterior region of the maxilla. It may cause tooth
impaction and root dilacerations and is treated with
enucleation. When antineoplastic radiation is insti-
tuted in the craniofacial region for malignant tumors,
it may produce dental anomalies of permanent teeth
such as root formation arrest which may affect tooth
eruption [43]. Anterior teeth eruption delay may have
a psychological impact due to esthetics. A profound
delay in maxillary anterior teeth eruption may be
accelerated with surgical removal of the overlying con-
nective tissue, while even a simple incision may suffice
at times. Surgical treatment is however rarely necessary
radiograph shows the first permanent molar in traction process 3
years later. The eruption failure had resulted in sharp bends of the
root apices, when in close contact with the lower border of the man-
dible. e Successful outcome after laborious traction and the overall
4-year orthodontic treatment with extraction of two maxillary pre-
molars. (Courtesy of Dr. I. Manoukakis)
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
187 10

a b

c d

..      Fig. 10.10 a A midline cyst in the mandible of a 4.5-year-old sors at the age of 6 years. The hypoplastic labial area of the right
boy. b Ten months after enucleation of the cyst under general anes- permanent central incisor suggests early trauma (at the age of 1 year)
thesia. c, d Complete bone healing and eruption of the central inci- as a possible cause of the cyst, although there was no anamnesis

..      Fig. 10.11 Rare case of an 18-year-old girl with a phenotype of and a hypoplastic supernumerary in the left coronoid process (cour-
cleidocranial dysplasia and impaction of left maxillary canine, mul- tesy of Dr. S. Dalampiras)
tiple dentigerous cysts of premolars and molars even in the sinuses,
 188 A. Arhakis et al.
for functional reasons (. Fig. 10.12). Significant delay
may also occur in posterior teeth for unknown reasons
(. Fig. 10.7).
10.3.3 Other Disturbances in Tooth
Eruption
10.3.3.1 Ectopic Eruption of Permanent Teeth
Ectopic eruption of first permanent molars, unilateral
or bilateral, occurs with much greater frequency in the
maxilla than in the mandible (10:1). The main cause of
this disturbance is the disharmony of dental/osseous
growth in the area. The ectopic tooth has pronounced
proximal inclination with its proximo-occlusal ­crevice
entrapped at the disto-cervical constriction of the
crown of the second primary molar, having resulted in
its pathological root absorption distally. Diagnosis is
confirmed radiologically. In many cases the eruption
path is spontaneously corrected and the root resorp-
10 a b
..      Fig. 10.12 a Delayed eruption of maxillary right permanent cen-
tral incisor in an 8-year-old boy. b The radiograph does not reveal
any obstacle to its eruption. Maxillary right permanent central and
..      Fig. 10.13 Case of ectopic eruption of maxillary first molars in an 8-year-old boy which has self-corrected bilaterally. Distal cervical
resorptions of maxillary second primary molars occurred before self-correction
tion of the second primary molar may incidentally
be seen during routine radiographic examination
(. Fig. 10.13). An overall incidence of about 1% [44]
needs orthodontic intervention, possibly as presented
in 7 Chap. 11. Failure to provide any treatment may
cause extensive root resorption of the second primary
molar, its premature exfoliation with loss of space and
eruption with gross proximal inclination, and pala-
tal rotation of the maxillary first permanent molar
(. Fig. 10.14).
The maxillary permanent canines often find inad-
equate space as they usually erupt last (except perhaps
for the second molars), and this often leads to erup-
tion delays. Moreover, they may occasionally follow an
almost horizontal path of eruption becoming subject
to impaction (frequency 1.5–2%) [45]. This should be
suspected when the canines cannot be palpated labially
approximately 1.5 years before their normal eruption
time or when there is a gross asymmetry in their eruption
time (. Fig. 10.15). Impaction may be confirmed with
c
lateral incisors were left to self-erupt. c Eruption and good alignment
of all incisors 2 years later
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
189 10
..      Fig. 10.14 a Bite-wing
radiograph of a spacious a c
right-side primary dentition in a
4-year-old boy. b At age 6 years
an ectopic eruption of the
maxillary first permanent molar
is observed, along with severe
root resorption of the adjacent
second primary molar. c The
patient re-appeared 6 years later
with consequential palatal
eruption of the maxillary left
second premolar with significant b
drift of maxillary left first
premolar and first permanent
molar

a b

..      Fig.10.15 a Panoramic radiograph of a 14-year-old girl with alveolar bone in the canine region before their normal eruption time,
three impacted permanent canines, which require surgical exposure radiologic examination, and extraction of primary predecessors was
and orthodontic traction in the dental arch. b Early palpation of likely to have facilitated their proper eruption

a panoramic radiograph, and surgery with orthodontic
traction is undertaken as described in 7 Chap. 11.
Eruption of permanent anterior teeth can be diverted
as a result of crowding, local inflammation, or dental
trauma of the primary predecessor or due to the presence
of a mesiodens or odontoma. Ectopic eruption of the max-
illary permanent incisor usually occurs palatally and often
causes an anterior crossbite. Parents should be informed
during the routine recalls being observant of the eruption
position of maxillary incisors and seek early treatment in
case of palatal eruption. The treatment usually includes
extraction of the primary predecessor and crossbite cor-
rection if needed. Less often, maxillary central incisors
erupt labially at a higher position (. Fig. 10.16).
On the contrary, lingual eruption of mandibular
permanent incisors is much more frequent and is associ-
ated with resorption limited to the lingual root surface
of primary predecessors and their prolonged stay in the
dental arch. Since these are the first permanent teeth to
erupt, this condition alerts parents. The extraction of
 190 A. Arhakis et al.
a b
..      Fig. 10.16 a Ahead of time appearance of left permanent central
incisor in a labial ectopic location in a 7-year-old girl. b This, together
with the severe discoloration, inclination, and lack of apical root
a b
10
c correction of their position is risky both for reasons of
..      Fig. 10.17 a Eruption of permanent mandibular central incisor in
a lingual ectopic location in a 6-year-old boy. b Lateral (lingual) exter-
nal root resorption of the extracted primary predecessor incisor pre-
senting total lack of apical resorption. c Eruption of buccal cusps of
the maxillary premolars while primary predecessors are still present.
Extraction of the latter assists in quick alignment of the premolars
primary teeth is not necessary unless their retention cre-
ates functional problems (. Fig. 10.17). After shedding
or extraction, the tongue pressure soon improves align-
ment of the ectopic incisors. In cases of anterior crowd-
ing, extraction of adjacent primary anterior teeth is not
recommended because this simply postpones crowding
until the adjacent permanent teeth erupt.
resorption of the primary predecessor seen in the radiographic
image, suggests inflammation due to old lateral laxation trauma as
the cause for the anomalous eruption path of the permanent incisor
Ectopic eruption is often observed in other teeth,
including premolars, and, when there is no other ­pathology,
is related to the delayed shedding of primary molars and
often to their asymmetric root resorption. Interference
with mastication and inflammation often accompanied
by space loss are reasons to extract the primary molar.
Another kind of much more rare ectopic eruption is
the transposition of teeth, more often of the maxillary
canines with their adjacent teeth, very rarely being bilat-
eral (. Fig. 10.18). Since orthodontic movement and
preserving root integrity and periodontal health, leaving
the transposed teeth in their position and modifying their
shape, if necessary, is usually the treatment of choice.
10.3.3.2 Ankylosis of Primary Teeth
Ankylosis is the fusion of cementum with the alveo-
lar bone and may occur at any primary or permanent
tooth. It is far more common in primary molars with a
frequency of 7–14% [46]. It is considered as an eruption
disturbance that leads to gradually increasing infraoc-
clusion of the tooth. A dull (metallic) sound on tooth
percussion supports the diagnosis. When the successor
premolar is present, simple monitoring is required, as
in most cases the ankylosed primary molar shedding
follows its complete root resorption. This however
may occur with a delay of several months. When delay
is longer, some authors suggest extraction in order to
avoid drift of adjacent teeth and space loss [47, 48]
(. Fig. 10.19). Ankylosis may be visible in the—two-­
dimensional—radiograph by the absence of periodontal
space, depending on the extent and location of patho-
logical findings, i.e., mesial or distal part of the root
as opposed to buccal or lingual. Very often, ankylosis
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
191 10

a b

..      Fig. 10.18 a, b Bilateral transposition of permanent maxillary lateral incisors and canines in a 12-year old girl

a
b

c d

..      Fig. 10.19 a Radiographic image of bilateral ankylosis and sub- posite build-up of the right and extraction of the left second primary
mergence of mandibular second primary molars in a 13-year-old molar. d Further submergence of the primary molar build-­up is seen
boy. There is no permanent successor of his right one. b Clinical view 3 more years later
of occlusion at the right side. c Ideal occlusion 24 months after com-

is located in the furcation area in both primary and
permanent molars (. Fig. 10.20). With conventional
radiographs, the replacement resorption is often not vis-
ible; however, this can be seen on CBCT. In early anky-
losed primary molars, the crown is so infraoccluded that
it may become submerged into the gingiva or even the
alveolar bone (. Fig. 10.21). In this case, extraction is
the treatment of choice. This may be done under local
anesthesia depending on patient cooperation. Many of
these cases also require interceptive orthodontics (see
7 Chap. 11).
10.3.3.3 Eruption Cysts
Their appearance on the alveolar ridge is related to the
rupture of the dental follicle, shortly before primary or
permanent teeth eruption. They are exhibited as soft,
relatively translucent, single bluish swellings, contain-
ing serous fluid and blood with inflammatory elements
(. Fig. 10.22). They are more frequently seen in the
maxilla [49]. The diagnosis is clinical, while therapeu-
tic intervention usually is not necessary as the condition
is self-­resolved after tooth eruption. At times, biting
trauma by the opposing teeth causes discomfort to the
 192 A. Arhakis et al.

a b

10

..      Fig. 10.20 a Extracted ankylosed primary molar. b Radiograph of the molar tooth section shows replacement resorption in the furcation
area. This is a very common location for molar ankylosis in both primary and permanent dentition. (b: courtesy of Dr. H. Luder)

child. In this case, incision of the cyst after local anes-
thesia is an effective treatment, while in case of recur-
rence some authors suggest marsupialization or surgical
removal [50].
10.3.3.4 I nflammation Related to Eruption
of Teeth
The eruption of permanent teeth may infrequently be
accompanied with local soft tissue inflammation. This
inflammation is either purely periodontal as the pressure
of the erupting teeth causes local disturbances of the
periodontal ligament (. Fig. 10.23) or a consequence
of pulpal necrosis due to external resorption of a pri-
mary adjacent tooth (. Fig. 10.24). In the latter case,
extraction of the necrotic primary tooth may be indi-
cated. More common is pericoronitis of the last molar to
erupt (. Fig. 10.25). For the prevention of pericoronitis,
proper brushing is indicated during the eruption stage,
in order to reduce the possibility of infection in case
of biting trauma to the operculum. Treatment includes
washing with chlorhexidine solution 0.2%, which may
be more efficacious if administered under the operculum
with a syringe. In more extensive inflammation, systemic
antibiotic administration and analgesics are necessary.
In some cases the follicle of a slowly erupting per-
manent tooth can develop into a cyst. This occurs
quite often and is usually resolved spontaneously
if there is an opening toward the oral cavity. If the
tooth itself obturates the opening, a lateral cyst can
develop. This may need a surgical exposure/marsupi-
alization of the cyst, and a drain must be placed until
there is an epithelial connection between the gingiva
and the epithelium of the cyst. These cysts often look
like lateral periodontal defects. A scaling of the root
surface is contraindicated and would interfere with
complete healing (. Fig. 10.26) [51].
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
193 10

a b

c d

..      Fig. 10.21 a The mandibular right second primary molar is clinically absent in a 4-year-old boy. b Εxtensive ankylosis and absence of the
periodontal space is evident radiographically in the mesial root. c Occlusal clinical view 8 months later. d Radiographically, the follicle of the
second premolar may be seen located distally of the roots of the ankylosed primary molar. e Patient had moved and appeared again 4 years
later. f Severe inclination of the mandibular right first permanent molar is observed in the OPG, requiring orthodontic uprighting, following
the extraction of the submerged ankylosed second primary molar
 194 A. Arhakis et al.

..      Fig. 10.22 a Eruption cysts

a b
associated with: Α. maxillary
right permanent central incisor.
b Maxillary left first permanent
molar

..      Fig. 10.23 a Inflammation

a b
and fistula in a caries-free
8-year-old boy. b While
maxillary right permanent
lateral incisor is in eruption
process, bone resorption is
observed distal to its root.
Inflammation is attributed to
10 infection due to damage of the
periodontal ligament. Inflamma-
tion subsided by chlorhexidine
irrigation and was cured upon
lateral incisor eruption

a b c

..      Fig. 10.24 a Periodontal inflammation and fistula buccal to an radiograph shows external resorption of the lateral. c. Its extraction
erupting maxillary right permanent central incisor with vital pulp. reveals the extent of resorption with pulp necrosis, apparently from
The adjacent primary lateral incisor is sensitive to percussion. b The previous pressure during eruption of the permanent central incisor
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
195 10

a b

..      Fig. 10.25 a Inflammation accompanied by pain and buccal edema in a 6-year-old girl. b Pericoronitis of the erupting mandibular left
first permanent molar probably related to biting the operculum

..      Fig. 10.26 Buccal bifurcation cyst on a slowly erupting mandib- CBCT image, an opening lateral of its crown is visible. This orifice is
ular right first molar. Clinically the symptoms were like a pericoroni- needed to be opened surgically for cyst marsupialization
tis with a hard swelling buccal to the tooth on palpation. In the
 196 A. Arhakis et al.
10.4 Shedding and Extraction
10.4.1 Shedding of Primary Teeth
The shedding of primary teeth takes place after
complete resorption of their roots. Odontoclasts are
observed on the apical surface of their roots, and
their function is related to the pressure developed
by the dental sac of the erupting permanent tooth.
Odontoclastic activity continues after the full resorp-
tion of the supporting alveolar bone. If the perma-
nent successor is absent, the root of the primary tooth
is resorbed very slowly and it may take many years
or several decades (. Fig. 10.27). The etiology for
this intermediate condition is unknown. There are
various data on the differences between the “normal”
root resorption of primary teeth without successors
and the prevention of root resorption in permanent
teeth. For example, there are differences in the cells
of the periodontal ligament, which are degraded by
metalloproteinase activity that precedes the root sur-
face resorption. Similar cells of primary teeth produce
10 more collagenase compared to those of permanent
teeth and have a pronounced reaction to certain cyto-
kines such as L1a and TNF-A [52].
a wedge. Conical roots should be extracted using rota-
..      Fig. 10.27 a Over-retention of a mandibular second primary
molar. The resorption of most crown dentine indicates continued
extraosseous odontoclastic activity. b Panoramic radiograph of an
8-year-old girl. The maxillary second primary molars have normal
root resorption, while the mandibular ones that lack permanent suc-
cessors present no root resorption
10.4.1.1  remature Shedding of Primary
P
Teeth
Generalized premature shedding of primary teeth in
children is rare and may be a result of early aggressive
periodontitis with alveolar bone loss, usually when an
underlying systemic disease is present. In the Papillon-­
Lefevre syndrome the shedding of primary teeth usu-
ally occurs well before the eruption of permanent teeth,
which are also lost due to pathological periodontal
breakdown (. Fig. 10.28) [53]. Diseases of the blood
such as neutropenia and leukemia are also associated
with periodontal disease in children, probably because
of failure of the defense mechanism against periopatho-
genic bacteria [54]. Early loss of primary teeth is
the most common oral finding in hypophosphatasia
(. Fig. 10.29) [55]. In Chediak-Higashi syndrome there
is a severe immune deficiency with periodontal disease
of primary dentition. Early shedding of primary teeth is
also observed in Langerhans histiocytosis [56].
10.4.2 Extraction and Surgical Techniques
Related to Eruption
10.4.2.1 Extraction of Primary Teeth
When tooth extraction is planned, this should be after
careful clinical and radiographic considerations. The
principles of extraction include expansion of the bony
socket, use of a lever and fulcrum, and insertion of a
tional movement and a buccally directed movement for
removal from the socket. In multi-rooted teeth, a figure
eight movement to expand the socket should be started.
The final path of removal is toward the buccal aspect
as bone is thinner. In case of primary teeth with frag-
ile crowns or subgingival fractures after dental trauma,
..      Fig. 10.28 A 17-year-old girl with Papillon-Lefevre syndrome
and neglected oral hygiene. Loss of her last two maxillary permanent
teeth is imminent while the mandibular left third molar starts erupt-
ing
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
a b
..      Fig. 10.29 a 3½-year-old patient with early tooth loss. b Lost
teeth as collected by the mother. She reported that the teeth fell out
spontaneously with almost no bleeding. Root formation is not even
a b
d e
..      Fig. 10.30 Extraction of maxillary primary central incisors with
severe cervical carious lesions undermining the crown, septic pulp
necrosis, and fistulae. a Good subgingival grasping of the right cen-
tral incisor with appropriate forceps. b Easy extraction in a twisting/
use of an elevator to lever and luxate the tooth or root
fragment from its socket and a firm grip of the forceps
is needed. An elevator will help in loosening soft tissue
attachment from the tooth, luxation of teeth from the
surrounding bone before the application of dental for-
ceps, expansion of alveolar bone or socket, and removal
of broken, fractured, or retained roots or dental frag-
ments from their sockets. It is important to avoid exces-
sive forces, support the instrument to prevent injury to
adjacent structures, protect major structures, provide
adequate lighting, use a proper and stable fulcrum, and
197 10
finished. The patient was then referred to a hospital where hypophos-
phatasia was confirmed
c
f
pulling motion. c Inadequate cervical grasp of the central incisor
leads to its coronal fracture. d, e Twisting motion of the more sub-
gingivally grasped root. f The two extracted teeth
perform routine maintenance of instruments. Careful
debridement of socket should follow the use of eleva-
tors especially if bone has been fractured when used as
a fulcrum.
Anterior primary tooth extraction is a relatively easy
procedure, because of their single conical roots. The
tooth is firmly grasped, as subgingivally as possible, with
the appropriate forceps for primary teeth and extracted
by combined twisting/rotation and pulling motion
(. Fig. 10.30). Elevators are useful when tooth crown
destruction goes subgingivally. Movements of the crown
 198 A. Arhakis et al.
..      Fig. 10.31 Bisection of the tooth in buccal-lingual direction effected with a long cylindrical diamond-coated bur and completed with an
elevator that is inserted into the deep cut produced
toward buccal should be avoided during the extraction
10 in order not to force the apex of the primary tooth in
direction of the successor tooth and cause damage on
its developing crown. For the same reason, it is not indi-
cated to perform a curettage of the extraction alveolus.
Granulation tissue in this area is a reaction on the infec-
tion and will disappear spontaneously when the source
of infection is eliminated.
The extraction of second primary molars with no
significant root resorption, especially the mandibular
ones, can be very challenging and may result in loss of
child’s cooperation. This is because the mesio-­ distal
dimension of the roots is considerably larger than that
Managing Ankylosed Primary Molars
Sometimes early ankylosed primary molars do not follow
the eruption pattern of the adjacent teeth, and it is pos-
sible for their crown to be submerged into the gums or
even the alveolar bone. Conservative monitoring of
ankylosed primary molars is recommended. The clinician
should consider extraction if the permanent successor
has an altered path of eruption, if the ankylosed primary
molar is severely infraoccluded with the adjacent teeth
tipping to prevent the successor from erupting, or both.
The ankylosed molar often exfoliates spontaneously
within 6 months; however, when exfoliation is more
delayed, arch-length loss, occlusal disturbance, hooked
roots, or impaction of permanent successors may occur
of the crown. Therefore, after mandibular block anes-
thesia and additional buccal infiltration, bisection of
the tooth is often the preferred approach, based on
the radiographic image. A long diamond bur is placed
in a buccal-lingual direction, producing a deep groove,
where an elevator may be inserted to complete the bisec-
tion (. Fig. 10.31). Removal of the two parts is then
an easy and less stress bearing. Additionally, since the
ankylosis is often in the furcation area, the proposed
approach is very useful because the ankylosed area is
often removed by the bur. Extreme caution should be
taken to avoid injuries to the successor, which is a pos-
sibility if diligence is not practiced.
[57]. In this case, extraction, after adequate local anesthe-
sia, is the treatment of choice. The crown of the tooth is
captured with the appropriate forceps and, if needed,
with the simultaneous grip of alveolar bone cervically. In
most cases, where ankylosis is located in the furcation
area, it is useful to move the ankylosed tooth slowly in a
bucco-lingual direction until it is disengaged by causing
alveolar expansion. Less frequently, where the ankylosis
is at the root, root fractures are very likely and sometimes
the root will need to be extracted using a bur or by raising
a surgical flap. If elevators are used to luxate ankylosed
teeth, great caution must be taken not to luxate a recently
erupting neighboring tooth due to its short root and
therefore weak anchorage in the alveolar bone [58].
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
10.4.2.2  xtraction of Structures Impeding
E mond or steel bur in order to preserve the surrounding
Tooth Eruption
In cases where primary or permanent teeth do not erupt
into the oral cavity, it is necessary to radiographically
exclude or confirm the presence of obstacles such as
odontomas, supernumerary teeth, or other structures.
In the anterior region mesiodentes are quite common,
but supernumerary teeth can occur in most areas of
the dentition. If one or more obstacles are visible, it is
important to do a proper localization of these structures
by either a series of x-rays with different angulations or
a CBCT. The topographic relation to all other structures
must be evaluated carefully in order to plan the surgical
removal with the least collateral damage. Ideally, they
should be removed when permanent teeth adjacent to
the lesion exhibit about one half of their root develop-
ment to ensure no harm occurs to the normal perma-
nent teeth or interference with their eruption. Usually a
flap must be raised and the structures need to be exposed
by selective ostectomy with a round bur. In many cases
it proves to be useful to dissect the crown from the
root of an impacted tooth to be extracted with a dia-
a b
c d
..      Fig. 10.32 a Clinically missing maxillary right central incisor. b
The radiograph shows two mesiodentes, one of them horizontally. c
After a flap was raised, slight ostectomy with a round bur allowed
199 10
bone or teeth (. Fig. 10.32). Apparently, a multidisci-
plinary team including a pediatric dentist, orthodontist,
oral surgeon, and a periodontist in some cases can be
involved [59].
Odontomas present a severe obstacle for erupting
teeth and they should be removed completely. Surgical
removal (by enucleation) using a minimally invasive sur-
gical technique to remove the least amount of bone tis-
sue through a mucoperiosteal flap is indicated. In case
of odontomas, this may reveal a number of calcified
small structures looking like teeth (compound odon-
toma) or lesions of complex odontomas with or without
mineralized structures showing a tooth-like appearance.
Bone is removed using a low-speed dental hand-drill
and a tungsten carbide bur until the odontoma or crown
of mesiodens is exposed. In cases of compound odon-
tomas it is preferable to remove them together with the
intact follicle around them to make sure that all com-
ponents are removed and not a single little “tooth” is
left behind. Otherwise this could pose again a problem
for the eruption of other teeth (. Fig. 10.33). Adjacent
the first tooth to be removed with an elevator. d After further ostec-
tomy, the horizontal mesiodens was located and sectioned in two
parts prior to extraction
 200 A. Arhakis et al.

a b

c d

10

..      Fig. 10.33 a Clinically missing maxillary right primary canine. b fully rinsed and inspected. d Overview of the extracted hard-­tissue
Radiograph shows cloud-like radio-opaque structures. c After a flap bodies, some of them resembling tiny teeth, others more like com-
was raised and an ostectomy with a round bur, the follicle was plex odontomas
opened, the tooth-like structures were removed, and the alveola care-

teeth are seldom harmed by the excision since they are 10.5 Transplantation of Teeth
usually separated from the lesion by a septum of bone.
The patient can be treated under local anesthesia, 10.5.1 Extraction and Re-implantation
without any premedication depending on the patient’s of Permanent Teeth
behavior. The wound is carefully irrigated with physi-
ological solution and cleaned with a sterile dressing; the
After extraction or loss of a tooth, options that exist
flap repositioned and sutured with 3.0 absorbable suture
for the extraction space in a growing child may include
material [60].
replacement with a removable prosthesis, orthodontic
It has been suggested that specimens should be sent
space closure, use of the extraction space orthodonti-
for microscopic and histologic examination. Patient
cally to relieve crowding, or tooth replacement by auto-
care is specifically related to maintenance of proper
transplantation. Autotransplantation is related to the
oral hygiene including 0.2% digluconate chlorhexidine
transfer of a tooth from its alveolus to another site in the
prescription, ingestion of cold, soft meals, refrain-
same person. It is used for replacement of congenitally
ing from physical exercise/excessive physical activity
missing teeth or teeth lost due to trauma and dental dis-
during the next 48 hours, antibiotics, and pain man-
ease or those with poor prognosis after re-­implantation
agement, in addition to careful future clinical and
or revascularization procedures. The recipient site may
radiographical follow-up. Later orthodontic traction
be either an extraction site or a surgically prepared
might be needed in order to guide any impacted teeth
alveolus. A donor tooth chosen for autotransplantation
into their position, especially if they have completed
should be of limited value in the dentition, e.g., a third
root formation [59].
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
molar, a premolar in a crowded arch, or a supplemental
tooth. Some tilting of the distal tooth could still occur
due to the size discrepancy between donor and recipi-
ent teeth (e.g., permanent molar and premolar) [61].
Especially in cases with little space and therefore nec-
essary orthodontic treatment, this procedure may be a
very valid option to replace teeth and preserve esthetics
and alveolar bone.
If it is desired to achieve revascularization of a
transplanted tooth, the apex needs to have an opening
of at least 2 mm and the root length should be ¾ of the
expected length. If revascularization is successful, most
pulp chambers will show obliteration with time, which
is not a complication but a visible sign of vital tissue
inside the tooth (. Fig. 10.34). Teeth with an already
closed apex can also be transplanted, but because revas-
cularization is highly unlikely, a root canal treatment
is necessary. This can be done orthograde prior to the
transplantation or retrograde during the procedure [62].
Autotransplantation is performed under local anes-
thesia, and mucoperiosteal flaps are simultaneously
raised in the donor and recipient areas. The most impor-
tant factor for success is the extraction of the tooth to
be transplanted. The donor tooth should be carefully
and gently extracted using a forceps (avoiding exces-
sive pressure), keeping the radicular part intact and
a b
d e
..      Fig. 10.34 a Radiography of agenesis of mandibular second pre-
molar. Because maxillary premolar extractions were necessary for
the orthodontic treatment, it was decided to transplant one at the
201 10
untouched, and is transplanted to the recipient area
without extraoral storage. If partial healing of a previ-
ously extracted tooth socket had occurred, the recipi-
ent site can be prepared with a round bur. The created
alveolus should be larger than the tooth, which allows
the tooth to be placed without contact with the bone. If
the tooth is pressed against the bone, ankylosis is more
likely to occur. Once a transplanted tooth is put in place,
it needs to be fixed in position. To prevent ankylosis and
favor revascularization, it is necessary that the splint
allows a physiological mobility. Alternatively, the tooth
can also be kept in place with a suture, which can be
removed after 1 week. Another important factor is the
gingiva around a transplanted tooth: the tooth should
be positioned in a way that allows the gingiva to cover
the entire root surface. A tight gingival seal around
the tooth improves the prognosis. For this reason, it is
often advisable to put a tooth away from the occlusion,
if beforehand there was an anchylosed tooth that kept
the gingiva apically. Although a transplanted tooth can
generate bone growth, it is generally wise to implant it
in the bone and move it afterward orthodontically to its
desired position. The patient is prescribed chlorhexidine
rinse and amoxicillin for 1 week and then, clinically and
radiographically reviewed at 1 week, 1 month, 3 months,
and then every 6 months [63].
c
f
agenesis site. b Image immediately after transplantation. c–e Growth
of alveolar bone and root. f Increase in root length and pulp oblit-
eration are seen after 2 years
 202 A. Arhakis et al.
Eye Catcher
In cases of transplantations of premolars from the
maxilla into the mandible, it may be useful to implant
the tooth in a rotated position (. Figs. 10.34 and
10.35), because in this way the often narrow oro-­
buccal dimension of the alveolar ridge allows it better
to find enough room for the transplant, still preserv-
ing the buccal and lingual corticalis. Furthermore,
this approach also allows often a better gingival seal
after the extraction of a primary molar in that area.
Upon follow-up, radiographic examination of the auto-
transplanted tooth should reveal continued root growth,
no signs of root resorption, and intact lamina dura.
Also, there can be partial pulp obliteration in the trans-
planted tooth. The final crown-to-root ratio should be
less than 1. Clinically, the tooth should respond posi-
tively to ethyl chloride test and no periodontal lesions
present. Andreasen and others reported the long-term
prognosis of autotransplanted premolars after 13 years,
10 with 95% and 98% survival rates for teeth with incom-
plete and complete root formation, respectively [62].
There are several factors to ensure a successful auto-
transplantation; the donor tooth should preferably have
at least three quarters of the root formed, and it is nec-
essary to have an atraumatic technique to preserve an
intact periodontal ligament and Hertwig’s root sheath in
the donor tooth [64]. Pulp survival is also an important
a b
..      Fig. 10.35 a Clinical image immediately after transplantation of
maxillary second premolar to the mandibular left side. In the right
side, second premolar is also a transplant that has been implanted in
factor; an apical foramen diameter greater than 1 mm
decreases the risk of pulpal necrosis after transplan-
tation, and root resorption is more frequent in trans-
planted teeth with mature root development than in
teeth with immature roots [65]. On the other hand, teeth
in the early stages of root development show less post-
transplant root growth than those with more mature
roots but incompletely formed apices [66] as there is
a possibility of no additional root growth after trans-
plantation. Transplantation of a fully formed root will
require adequate endodontic therapy to ensure high sur-
vival rates [61].
10.5.2 Transplantation of Teeth Anteriorly
After traumatic loss of anterior teeth (avulsion or after
replacement resorption), their replacement poses diffi-
culties in adolescence. Implants are strictly contraindi-
cated because they behave as ankylosed teeth and don’t
follow or even impair the growth of the alveolar ridge.
Transplants can be a biological alternative. Usually pre-
molars are chosen; however, they only become available
in orthodontic cases with inadequate space indicating
extractions. Primary canines may be an alternative as
they can be extracted without long-term disadvantages.
If premolars are used to replace incisors, they need to
be re-formed by a composite buildup and sometimes the
palatal cusp needs to be reduced (. Fig. 10.36).
a rotated way to facilitate healing of a larger alveolus b After orth-
odontic rotation of the two second premolars, the clinical aspect is
unsuspicious. Tooth mobility is normal
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
a b
c d
..      Fig. 10.36 a Transplanted premolar in the place of an ankylosed
maxillary central incisor. Clinical view 2 weeks after transplantation.
For optimal gingival adaptation, the tooth had to be positioned in
the same location as the ankylosed tooth and then moved orthodon-
tically to its ideal position. b After reconstruction with composite.
10.5.3 Intentional Re-implantation
After severe trauma ankylosis of teeth is common. If
the resorbed area is small, the tooth can be mobilized
and immediately moved orthodontically to give the
cementum time and room to heal and re-establish a nor-
mal periodontium. If the ankylosed area is large, this
approach cannot be successful, because re-ankylosis
203 10
The palatal cusp was left in place and does not bother the patient. c
6 years after transplantation the composite reconstruction was dis-
colored and needs to be replaced. d Radiographically obliteration
was evident. There is no visible resorption, which corresponds with
the normal clinical mobility
occurs frequently. If occlusion and gingival situation
allow, the tooth can be extracted and inspected extra-
orally, ankylosed areas can be removed with a bur or
by cutting the apex, and then the tooth replanted and
splinted with a physiological mobility. A root canal
treatment with a retrograde post or filling the canal with
MTA is mandatory to prevent infection-related resorp-
tions (. Fig. 10.37).
 204 A. Arhakis et al.

a b

c d

10

..      Fig. 10.37 a Ankylosed maxillary right central incisor. Mobiliza- extract the tooth, resect the apical part, and put a retro-post prior to
tion and subsequent orthodontic forces did not result in healing of replantation in a more coronal position. c Clinical view 5 years after
the periodontal ligament and re-ankylosis was evident. b Radio- replantation. Mobility was normal. d Its radiographic image shows
graphically the replacement resorption was unclear. It was decided to no signs of resorption and normal periodontal space
Tooth Eruption, Shedding, Extraction and Related Surgical Issues
205 10
References 20. Oikawa T, Nomura Y, Arai C, et al. Mechanism of active erup-
tion of molars in adolescent rats. Eur J Orthod. 2011;33:221–7.
https://doi.org/10.1093/ejo/cjq053.
1. Marks SC Jr, Schroeder HE. Tooth eruption: theories and facts.
21. Dorotheou D, Gkantidis N, Karamolegkou M, Kalyvas D,
Anat Rec. 1996;245:374–93.
Kiliaridis S, Kitraki E. Tooth eruption: altered gene expression
2. Al-Batayneh OB, Shaweesh A. Clinical duration of eruption of
in the dental follicle of patients with cleidocranial dysplasia.
deciduous teeth in Jordanian children: a cross-sectional study.
Orthod Craniofac Res. 2013;16:20–7. https://doi.org/10.1111/
Arch Oral Biol. 2018;90:86–90. https://doi.org/10.1016/j.archo-
ocr.12000.
ralbio.2018.03.005.
22. Sood S, Sood M. Teething: myths and facts. J Clin Pediatr Dent.
3. Al-Batayneh OB, Shaweesh AI, Alsoreeky ES. Timing and
2010;35:9–13.
sequence of emergence of deciduous teeth in Jordanian children.
23. Dominguez-Rodriguez MV. Baby teething in early modern Eng-
Arch Oral Biol. 2015;60:126–33. https://doi.org/10.1016/j.archo-
land: theory and therapeutic practice. J Hist Dent. 2011;59:117–
ralbio.2014.08.014.
25.
4. Bruna Del Cojo M, Gallardo López NE, Mourelle Martínez
24. Owais AI, Zawaideh F, Al-Batayneh OB. Challenging par-
MR, De Nova García MJ. Time and sequence of eruption of
ents’ myths regarding their children’s teething. Int J Dent Hyg.
permanent teeth in Spanish children. Eur J Paediatr Dent.
2010;8:28–34. https://doi.org/10.1111/j.1601-­­5037.2009.00412.x.
2013;14:101–3.
25. Macknin ML, Piedmonte M, Jacobs J, Skibinski C. Symptoms
5. Shaweesh AI. Timing and sequence of emergence of permanent
associated with infant teething: a prospective study. Pediatrics.
teeth in the Jordanian population. Arch Oral Biol. 2012;57:122–
2000;105:747–52.
30. https://doi.org/10.1016/j.archoralbio.2011.08.014.
26. Ramos-Jorge J, Pordeus IA, Ramos-Jorge ML, Paiva SM. Pro-
6. Ten Cate A. Physiologic tooth movement eruption and shedding.
spective longitudinal study of signs and symptoms associated
In: Ten Cate A, editor. Oral histology. Development, structure
with primary tooth eruption. Pediatrics. 2011;128:471–6. https://
and function. St Louis: Mosby Co; 1997. p. 289–300.
doi.org/10.1542/peds.2010-­2697.
7. Berkovitz BK. The effect of root transection and partial root
27. Guidelines AAPD. Useful medications for oral conditions. Pedi-
resection on the unimpeded eruption rate of the rat incisor. Arch
atr Dent. 2017;39:492–8.
Oral Biol. 1971;16:1033–43.
28. Kana A, Markou L, Arhakis A, Kotsanos N. Natal and neonatal
8. Shore RC, Berkovitz BK, Moxham BJ. The effects of preventing
teeth: a systematic review of prevalence and management. Eur J
movement of the rat incisor on the structure of its periodontal
Paediatr Dent. 2013;14:27–32.
ligament. Arch Oral Biol. 1985;30:221–8.
29. Ruschel HC, Spiguel MH, Piccinini DD, Ferreira SH, Feldens
9. Marks SC Jr, Cahill DR. Experimental study in the dog of the
EG. Natal primary molar: clinical and histological aspects. J
non-active role of the tooth in the eruptive process. Arch Oral
Oral Sci. 2010;52:313–7.
Biol. 1984;29:311–22.
30. Cunha RF, Boer FA, Torriani DD, Frossard WT. Natal and neo-
10. Marks SC Jr, Cahill DR. Regional control by the dental follicle
natal teeth: review of the literature. Pediatr Dent. 2001;23:158–
of alterations in alveolar bone metabolism during tooth erup-
62.
tion. J Oral Pathol. 1987;16:164–9.
31. Costacurta M, Maturo P, Docimo R. Riga-­Fede disease and
11. Larson EK, Cahill DR, Gorski JP, Marks SC Jr. The effect of
neonatal teeth. Oral Implantol. 2012;5:26–30.
removing the true dental follicle on premolar eruption in the
32. Jariwala D, Graham RM, Lewis T. Riga-Fede disease. Br Dent J.
dog. Arch Oral Biol. 1994;39:271–5.
2008;204:171. https://doi.org/10.1038/bdj.2008.113.
12. Cahill DR, Marks SC Jr. Tooth eruption: evidence for the cen-
33. Kamboj M, Chougule R. Neonatal tooth-how dangerous can it
tral role of the dental follicle. J Oral Pathol. 1980;9:189–200.
be? J Clin Pediatr Dent. 2009;34:59–60.
13. Yang Z, Li Y, Ma X, Shen L, Zhao Z, Jin F. Role of the epithe-
34. Suri L, Gagari E, Vastardis H. Delayed tooth eruption: patho-
lial cell rests of Malassez in periodontal homeostasis and regen-
genesis, diagnosis, and treatment. A literature review. Am
eration – a review. Curr Stem Cell Res Ther. 2015;10:398–404.
J Orthod Dentofac Orthop. 2004;126:432–45. https://doi.
https://doi.org/10.2174/1574888x10666150312100957.
org/10.1016/S088954060400530X.
14. Fujiyama K, Yamashiro T, Fukunaga T, Balam TA,
35. Stellzig-Eisenhauer A, Decker E, Meyer-­Marcotty P, Rau C,
Zheng L, Takano-Yamamoto T. Denervation resulting in
Fiebig BS, Kress W, et al. Primary failure of eruption (PFE)-
dento-alveolar ankylosis associated with decreased Mal-
-clinical and molecular genetics analysis. J Orofac Orthop.
assez epithelium. J Dent Res. 2004;83:625–9. https://doi.
2010;71:6–16. https://doi.org/10.1007/s00056-­­010-­0908-­9.
org/10.1177/154405910408300808.
36. Aziz S, Hermann NV, Dunø M, Risom L, Daugaard-Jensen J,
15. Kjær I. Mechanism of human tooth eruption: review article
Kreiborg S. Primary failure of eruption of teeth in two siblings
including a new theory for future studies on the eruption
with a novel mutation in the PTH1R gene. Eur Arch Paediatr
process. Scientifica (Cairo). 2014;2014:341905. https://doi.
Dent. 2019;20:295–300. https://doi.org/10.1007/s40368-­018-­
org/10.1155/2014/341905.
00410-­8.
16. Wise GE, Marks SC Jr, Cahill DR. Ultrastructural features of
37. Shah A, Gill DS, Tredwin C, Naini FB. Diagnosis and manage-
the dental follicle associated with formation of the tooth erup-
ment of supernumerary teeth. Dent Update. 2008;35:510–2,
tion pathway in the dog. J Oral Pathol. 1985;14:15–26.
514–6, 519–20. https://doi.org/10.12968/denu.2008.35.8.510.
17. Marks SC Jr, Popoff SN. Bone cell biology: the regulation of
38. Jorgenson RJ, Warson RW. Dental abnormalities in the tricho-
development, structure and function in the skeleton. Am J Anat.
dento-osseous syndrome. Oral Surg Oral Med Oral Pathol.
1988;183:1–44. https://doi.org/10.1002/aja.1001830102.
1973;36:693–700.
18. Marks SC Jr, Cahill DR, Wise GE. The cytology of the dental
39. Alves Pereira D, Berini Aytés L, Gay EC. Pycnodysostosis.
follicle and adjacent alveolar bone during tooth eruption in the
A report of 3 clinical cases. Med Oral Patol Oral Cir Bucal.
dog. Am J Anat. 1983;168:277–89.
2008;13:E633–5.
19. Marks SC Jr, Gorski JP, Wise GE. The mechanisms and
40. Visinoni AF, Lisboa-Costa T, Pagnan NA, Chautard-Freire-
mediators of tooth eruption--models for developmental biolo-
Maia EA. Ectodermal dysplasias: clinical and molecular
gists. Int J Dev Biol. 1995;39:223–30. https://doi.org/10.1002/
review. Am J Med Genet A. 2009;149A:1980–2002. https://doi.
aja.1001680303.
org/10.1002/ajmg.a.32864.
 206 A. Arhakis et al.
41. Sennhenn-Kirchner S, Jacobs HG. Traumatic injuries to the pri-
mary dentition and effects on the permanent successors - a clini-
cal follow-up study. Dent Traumatol. 2006;22:237–41. https://
doi.org/10.1111/j.1600-­­9657.2006.00383.x.
42. Lazaridou D, Arhakis A, Lazaridou M, et al. Trauma, solitary
bone cyst and delayed eruption of permanent mandibular inci-
sors; an unusual case in a 7-year-old patient. Eur Arch Paediatr
Dent. 2011;12:275–7.
43. Kaste SC, Goodman P, Leisenring W, Stovall M, Hayashi RJ,
Yeazel M, et al. Impact of radiation and chemotherapy on risk of
dental abnormalities: a report from the Childhood Cancer Sur-
vivor Study. Cancer. 2009;115:5817–27. https://doi.org/10.1002/
cncr.24670.
44. Barberia-Leache E, Suarez-Clúa MC, Saavedra-­ Ontiveros
D. Ectopic eruption of the maxillary first permanent molar:
characteristics and occurrence in growing children. Angle
Orthod. 2005;75:610–5. https://doi.org/10.1043/0003-­­
3219(2005)75[610:EEOTMF]2.0.CO;2.
45. Ericson S, Kurol J. Radiographic examination of ectopically
erupting maxillary canines. Am J Orthod Dentofac Orthop.
1987;91:483–92.
46. Cardoso Silva C, Maroto Edo M, Soledad Alvaro Llorente M,
Barbería Leache E. Primary molar infraocclusion: frequency,
magnitude, root resorption and premolar agenesis in a Spanish
sample. Eur J Paediatr Dent. 2014;15:258–64.
47. Kurol J. Early treatment of tooth-eruption disturbances. Am J
Orthod Dentofac Orthop. 2002;121:588–91.
10 48. Kurol J, Magnusson BC. Infraocclusion of primary molars: a
histologic study. Scand J Dent Res. 1984;92:564–76.
49. Nagaveni NB, Umashankara KV, Radhika NB, Maj Satisha
TS. Eruption cyst: a literature review and four case reports.
Indian J Dent Res. 2011;22:148–51. https://doi.org/10.4103/0970-
­9290.79982.
50. Bodner L, Goldstein J, Sarnat H. Eruption cysts: a clinical
report of 24 new cases. J Clin Pediatr Dent. 2004;28:183–6.
51. Pelka M, van Waes H. Paradental cyst mimicking a periodontal
pocket: case report of a conservative treatment approach. Int J
Oral Maxillofac Surg. 2010;39:514–6. https://doi.org/10.1016/j.
ijom.2009.11.005.
52. Harokopakis-Hajishengallis E. Physiologic root resorption in
primary teeth: molecular and histological events. J Oral Sci.
2007;49:1–12.
53. Ullbro C, Crossner CG, Nederfors T, Alfadley A, Thestrup-
Pedersen K. Dermatologic and oral findings in a cohort of 47
patients with Papillon-Lefèvre syndrome. J Am Acad Dermatol.
2003;48:345–51. https://doi.org/10.1067/mjd.2003.197.
54. Oh TJ, Eber R, Wang HL. Periodontal diseases in the child and
adolescent. J Clin Periodontol. 2002;29:400–10.
55. Bloch-Zupan A, Vaysse F. Hypophosphatasia: oral cavity and
dental disorders. Arch Pediatr. 2017;24:5S80–4. https://doi.
org/10.1016/S0929-­693X(18)30020-­4.
56. Kumar A, Masamatti SS, Virdi MS. Periodontal diseases
in children and adolescents: a clinician's perspective part 2.
Dent Update. 2012;39:639–42, 645–6, 649–52. https://doi.
org/10.12968/denu.2012.39.9.639.
57. Tieu LD, Walker SL, Major MP, Flores-­Mir C. Management of
ankylosed primary molars with premolar successors: a system-
atic review. J Am Dent Assoc. 2013;144:602–11.
58. Raghoebar GM, Boering G, Stegenga B, Vissink A. Second-
ary retention in the primary dentition. ASDC J Dent Child.
1991;58:17–22.
59. de Oliveira BH, Campos V, Marçal S. Compound odontoma-
-diagnosis and treatment: three case reports. Pediatr Dent.
2001;23:151–7.
60. Pacifici A, Carbone D, Marini R, Pacifici L. Surgical man-
agement of compound odontoma associated with unerupted
tooth. Case Rep Dent. 2015;2015:902618. https://doi.
org/10.1155/2015/902618.
61. Mendes RA, Rocha G. Mandibular third molar autotransplan-
tation--literature review with clinical cases. J Can Dent Assoc.
2004;70:761–6.
62. Andreasen JO, Paulsen HU, Yu Z, Bayer T, Schwartz O. A long-
term study of 370 autotransplanted premolars. Part II. Tooth
survival and pulp healing subsequent to transplantation. Eur J
Orthod. 1990;12:14–24.
63. Cho SY, Lee CK. Autotransplantation of a supplemental pre-
molar: a case report. J Can Dent Assoc. 2007;73:425–9.
64. Thomas S, Turner SR, Sandy JR. Autotransplantation of
teeth: is there a role? Br J Orthod. 1998;25:275–82. https://doi.
org/10.1093/ortho/25.4.275.
65. Andreasen JO, Paulsen HU, Yu Z, Schwartz O. A long-term study
of 370 autotransplanted premolars. Part III. Periodontal healing
subsequent to transplantation. Eur J Orthod. 1990;12:25–37.
66. Andreasen JO, Paulsen HU, Yu Z, Bayer T. A long-term study
of 370 autotransplanted premolars. Part IV. Root development
subsequent to transplantation. Eur J Orthod. 1990;12:38–50.
 207 11

Orthodontic Knowledge
and Practice for the
Pediatric Dentist
Kitae Park, Anastasios A. Zafeiriadis, and Nikolaos Kotsanos

Contents

11.1  eneral Perspectives in Orthodontic Management of Children

G
and Adolescents – 208
11.1.1  rofile Evaluation – 208
P
11.1.2 Concluding Remarks on Profile Evaluation – 218

11.2  ge-Specific Perspectives in Orthodontic Management

A
of Children and Adolescents – 218
11.2.1 I ntervention in the Primary Dentition – 218
11.2.2 Intervention in the Mixed Dentition – 229
11.2.3 Harmful Oral Habits – 240

References – 244

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_11
 208 K. Park et al.
It is not an important consideration whether pediat-
ric dentists would perform orthodontic treatment on
their own or refer their patient to an orthodontist. This
should be a pediatric dentist’s own decision. With all
their patients, however, being growing children and ado-
lescents, they are dealing with problems related to dental
eruption and facial growth. Therefore, it is essential for
them to have good orthodontic knowledge that would
help make a strategic decision, even while performing
restorative treatment, e.g., deciding to save a badly cari-
ous primary molar by restoring it.
11.1  eneral Perspectives in Orthodontic
G treatment after skeletal growth is completed. Decisions
Management of Children
and Adolescents
In most cases, no sophisticated techniques are required
to solve simple orthodontic problems. It is more impor-
tant for pediatric dentists to have a broad understanding
of children’s orthodontic growth pattern, i.e., be able to
predict how children’s faces would grow up in the future,
rather than focusing on orthodontic techniques. Further,
to analyze orthodontic aspects, they should look to rec-
11 ognize the pediatric patients’ overall orthodontic profile
rather than focusing merely on their dental problems.
11.1.1 Profile Evaluation
How can we identify differences between orthopedic and
orthodontic problems? The differences are easily identi-
fied by examining the patient’s face (i.e., profile) rather
than looking into their mouth (. Fig. 11.1).
Orthodontic vs. Orthopedic Treatment
Orthopedic treatment is to correct skeletal dishar-
mony between the maxilla and mandible, while orth-
odontic treatment is to align the maxillary and/or
mandibular teeth by moving them. It is, therefore, rec-
ommended that orthopedic treatment be performed
at some point before skeletal growth is completed,
whereas there is no age limitation on provision of
orthodontic treatment. Thus, discerning orthodontic
from orthopedic problems would provide good crite-
ria to determine the appropriate age for each patient’s
treatment.
Generally, at age 4–5 years, after the primary dentition
is fully completed, children are to be distinguished based
on the convexity of their facial profile, that is to say they
can be divided into convex, straight, and concave profile
types, which would later be estimated as Class II, Class
I, and Class III malocclusion, respectively. By conduct-
ing oral examination with such estimation, pediatric
dentists can understand the big picture of characteristics
of each patient. Following the full eruption of the first
permanent molars, patients with convex or concave pro-
file are labeled as Class II or Class III malocclusion with
skeletal discrepancy of the maxilla and mandible. In this
case, suitable orthopedic treatment would be needed to
begin at some point before skeletal growth is completed.
Patients with straight profile, on the other hand, are con-
sidered that the relationship between the maxilla and
the mandible is within normal range. Age for possible
orthodontic treatment would consequently not be criti-
cal, and, in some cases, it might be of advantage to start
are therefore dependent on patient’s sagittal relation.
When a transverse discrepancy of the maxilla and man-
dible exists, treatment would have to begin while skeletal
growth is still in progress. This holds true even in the pres-
ence of a straight profile, because this discrepancy is still
considered a skeletal problem that requires orthopedic
treatment. A briefing for determining each malocclusion
treatment on the basis of the three different profiles is
given below.
11.1.1.1 Straight Profile
A patient with a straight profile is considered as hav-
ing no skeletal discrepancy between the maxilla and
the mandible (as long as there is no transverse discrep-
ancy), and accordingly no orthopedic treatment would
be required. Therefore, age for orthodontic procedure is
less critical. However, early treatment should be consid-
ered, if this straight profile patient has at least one of the
following findings:
1. Localized anterior crossbite causing traumatic
occlusion
Localized anterior crossbite can cause lateral or forward
functional deviation of the mandible and sometimes
lead to traumatic occlusion that would result in gingival
recession of the lower anterior teeth (. Fig. 11.2). Gin-
gival recession caused by traumatic occlusion should
be treated promptly upon detection, because it would
worsen at a rapid rate unless the ectopically driven tooth
is corrected. On the other hand, localized anterior cross-
bite, which does not cause mandibular functional devia-
tion or traumatic occlusion, is occasionally treated with
a comprehensive orthodontic treatment approach after
all the permanent teeth are fully erupted.
2. Localized severe rotation of the anterior teeth that
causes esthetic problem
Severe rotation of the anterior teeth can be caused by
arch length discrepancy or an impacted supernumer-
ary tooth. The resulting esthetic problem may have a
negative psychological impact on children, and there-
fore, treatment is recommended as early as possible
Orthodontic Knowledge and Practice for the Pediatric Dentist
Facial profile
First coming patient
..      Fig. 11.1 Understanding the big picture of orthodontic characteristics of each patient by profile evaluation
(. Fig. 11.3). In mild rotation cases of no psychological
patient concern, early treatment is not necessary, being
incorporated in the comprehensive orthodontic treat-
ment, when and if this is undertaken.
3. Distalization of the first permanent molar
Ectopic eruption of the first permanent molar can
cause premature exfoliation of the second primary
molar, which would in turn result in mesial drift of
the first permanent molar and shortage of space for
the second premolar normal eruption. Accordingly,
orthodontic treatment for distalization of the first
permanent molar if mesial drift has occurred would
be required prior to eruption of the second premolar
(. Fig. 11.4).
209 11
Orthopedic
Convex
treatment
Concave
Orthodontic
treatment
Straight
4. Eruption guidance of the permanent canine
Impaction of the maxillary permanent canines is a fre-
quently occurring clinical problem regardless of maloc-
clusion types. Numerous studies of Caucasian samples
report that maxillary canine impaction is found mostly
on the palatal side [1–4], while other studies show that in
East Asians impaction may occur more often on the labial
side [5–7]. The most common cause of labial impaction
is known as arch length discrepancy, while palatal impac-
tion has been related to trauma, aplasia of the adjacent
lateral incisor, peg lateralis, retained primary canine, or
even being of genetic origin although not clearly deter-
mined. The occurrence rate of eruption disturbance of the
maxillary permanent canine is known to be 1–3%, while
 210 K. Park et al.

a b

..      Fig. 11.2 Localized anterior crossbite can cause lateral or matic occlusion from anterior crossbite. b The traumatic occlusion
­forward functional deviation of the mandible and sometimes lead to was removed by correcting anterior crossbite
traumatic occlusion. a Gingival dehiscence has occurred by trau-

a b

11

..      Fig. 11.3 Because esthetic problem of severe rotation of the anterior teeth can psychologically have negative effect on the children, it is
recommended for them to have treatment as early as possible. a Before treatment. b After treatment

12% of canine impactions were accompanied by lateral
incisor root resorption [3, 4]. Therefore, it is important for
the pediatric dentist to suspect and diagnose impaction
of the maxillary permanent canine and perform an early
treatment to prevent it, in collaboration with the ortho-
dontist when necessary. That is, a radiographic examina-
tion should be implemented by age of 8 or 9 in the case
of absence of canine bulge. Panoramic radiographs show
that the canine and lateral incisor are overlapped until 6 or
7 years of age in most cases, and the canine tends to incline
distally after 8 years of age [8], having more vertical erup-
tion path after 9 years of age. Localization analysis using
panoramic radiographs showed that the distance between
the canine cusp tip and the occlusal plane was most useful
in predicting the possibility of canine impaction, and this
could be detected as early as 8 years of age [9].
For the treatment of eruption disturbance of the per-
manent canine, Ericson and Kurol suggests that primary
canine extraction improves the eruption path of the per-
manent canine, if the canine has enough eruption space
and is not accompanied with root resorption of the adja-
cent lateral incisor [4] (. Fig. 11.5). However, the effect
may vary from person to person, and accordingly bian-
nual clinical or radiographic examination would be rec-
ommended. There also has been preventive treatment for
canine impaction using maxillary expansion, which has
proven effective [10, 11]. Yet another approach has been
proposed to increase the effect by combining maxillary
expansion with wire appliances to additionally force the
root of the adjacent lateral incisor mesially [12].
5. Transverse discrepancy
If a child has transverse discrepancy between the maxilla
and the mandible, he/she is supposed to have a skeletal
discrepancy and need an orthodontic procedure (mainly
orthopedic treatment) although he/she has a straight
profile. It is recommended to begin the treatment as early
as possible, because the generalized posterior crossbite
causing mandible deviation may lead to permanent
facial asymmetry while growing up (. Fig. 11.6). Poste-
rior crossbite involving only one or two teeth not caus-
ing mandibular functional deviation would not need an
immediate treatment. Kanomi et al. conducted a CBCT
study on the effect of rapid maxillary expansion (RME)
Orthodontic Knowledge and Practice for the Pediatric Dentist
211 11

a b

c d

..      Fig. 11.4 a Mesial drift of ectopically erupted maxillary first molars using Nance button anchorage. c Nance holding arch was
permanent molars following the loss of the second primary molars. used for the retention. d Both the maxillary second premolars
b Fixed appliance has been used to distalize both the first permanent erupted well into the spaces created by orthodontic treatment

a b

..      Fig. 11.5 a Radiographic signs (eruption angulation path and tion path was improved. c Ectopic eruption of the permanent canine
downward eruption progress) were found on the upper left canine. b was fully corrected naturally
In 6 months after extraction of the upper left primary canine, erup-
 212 K. Park et al.

a b c

..      Fig. 11.6 a Left-side unilateral posterior crossbite causing man- expansion. c Mandibular functional deviation is corrected by maxil-
dibular functional deviation to the left side. b Upper removable lary expansion
expansion appliance with median screw was used to make maxillary

with children aged 6 to 15. They reported that either
bonded expander (McNamara-type RME) or banded
expander (Hyrax-type RME) was an effective treatment
option, but expansion efficiency decreased with age [13].
11.1.1.2 Convex Profile
A patient whose profile is convex is considered as Class II
malocclusion, which refers to sagittal maxilla-­mandible
discrepancy. That is to say, patients with convex profile
have either prognathic maxilla or retrognathic mandible,
or a combination of both. In the case of Class II maloc-
11 clusion, orthopedic treatment is required at some point
while skeletal growth is in progress.
treatment can be implemented even in the early mixed
dentition stage. Likewise, if the patient does not long
for treatment for her/his condition in spite of compara-
tively severe maxillary protrusion, one-phase treatment
can be undertaken in the late mixed dentition stage or at
growth peak (. Fig. 11.7). Proffit reported that “Early
treatment for most Class II children is no more effective,
and considerably less efficient, than later 1-stage treat-
ment during adolescence” but also described that “Class
II clinical trial results do not mean early Class II treat-
ment is never indicated” [17].
Conditions for Two-Phase Treatment

1. Very convex profile

Two-phase treatment means that orthopedic treat- 2. Increased overjet (more than 7 mm)
ment is to be performed in the early mixed dentition 3. Full-step Class II molar relationship
stage (phase 1 treatment) followed by orthodontic
treatment (phase 2 treatment) in the time of growth
peak or later. One-phase treatment means performing
the combination of orthopedic and orthodontic treat- In addition, gender also needs to be considered to deter-
ments simultaneously in the time of growth peak. mine when to start phase I orthopedic treatment for
Class II malocclusion. Girls tend to comply with the
treatment process using headgear or functional appli-
ance, if necessary, during pubertal growth peak because
Appropriate age and proper method of treatment for majority of them reach their pubertal growth peak dur-
Class II malocclusion have long been argued over two-­ ing elementary school years, while boys tend not to have
phase versus one-phase treatment. There has not been a good compliance with the process as they generally reach
single outcome showing a significant difference between at pubertal growth spurt in their middle school years
the two, although a variety of randomized clinical stud- when relatively more occupied with social relationships.
ies were carried out in the 1990s and early 2000s [14–16]. Moreover, if male patients undergo phase I orthopedic
Since then, it has been widely accepted that one-phase treatment in the early mixed dentition, it is difficult for
treatment is to be performed for Class II malocclusion the result to be maintained until phase 2 begins, because
around the time of growth peak, especially now that boys take longer to reach the pubertal growth peak
evidence-based treatment is being emphasized. and in turn a longer wait period is expected. Thus, if
However, a treatment method cannot be applied in the patient is a boy who has Class II malocclusion with
all cases uniformly and is to be changed or developed severe sagittal skeletal discrepancy, it would be another
based on the condition of each patient. To understand good option to begin phase I orthopedic treatment in
patients and determine their treatment method, in addi- the late elementary school years when boys are generally
tion, psychological parameters should be considered as in the late mixed dentition stage. . Figure 11.8 illus-
well as severity of malocclusion, as many studies have trates a patient who had a successful result of phase I
shown. Thus, if the patient is psychologically distressed orthopedic treatment performed at a relatively late age,
about severe maxillary protrusion, phase 1 orthopedic showed a favorable growth pattern, and kept the good
Orthodontic Knowledge and Practice for the Pediatric Dentist
..      Fig. 11.7 Flowchart for
Class II malocclusion in
children. It is desirable to
implement two-phase treatment
only when Class II malocclusion
is severe enough to correspond Selection criteria
with selection criteria. However,
if the patient is psychologically
distressed about severe maxillary
protrusion, phase 1 orthopedic
treatment can be considered even
in the early mixed dentition stage
Yes
Two
phases
orthopedic correction until his physical growth ended.
When orthopedic correction is successfully done, the
patient can be categorized as Class I malocclusion and
will be allowed to choose when to resume the follow-up
treatment any time he/she feels ready.
11.1.1.3 Concave Profile
A patient whose profile is concave is considered as Class
III malocclusion, which refers to sagittal discrepancy
between the maxilla and the mandible. That is to say,
patients with concave profile have either retrognathic
maxilla or prognathic mandible, or a combination of
both. In the case of Class III malocclusion, just as in
Class II, orthodontic procedure including orthopedic
treatment is required at some point while skeletal growth
is in progress.
While a localized anterior crossbite caused by a den-
tal problem can simply be treated using a removable
orthodontic appliance, Class III malocclusion of skel-
etal origin is generally treated with orthopedic treatment
methods using facemask or functional appliances, such
as a Frankel appliance. However, patients with concave
profile with midface deficiency are generally recom-
mended to use facemask that can improve the facial pro-
file by maxillary protraction (. Fig. 11.9). It has been
suggested that such functional appliances have dental
effect rather than orthopedic effect [18].
Facemask can be used for pediatric patients from the
primary dentition around 5 years of age until the late
mixed dentition, but mostly in the early mixed dentition
around 7–8 years of age. Patients are generally able to
obtain the desired result of maxillary protraction within
a year, leading to noticeable improvement of facial pro-
file. However, facemask cannot completely improve the
Class III traits. Thus, if potential Class III traits are
strongly predicted, the mandible would possibly grow
more than the maxilla, leading to anterior crossbite or
profile change into concave. Although there have been
213 11
Class II malocclusion
Full step class II molar
7 mm OJ
Severe convex profile
Yes No
One
Pt’s Desire phase
No
With pt’s Desire
One
phase
Two phase treatment can
be considered
a number of studies of growth pattern prediction after
facemask treatment, accurate predictions of patient’s
growth patterns are not likely to be possible [19–21]. In
the case of Class III malocclusion, therefore, it is impor-
tant to predict various possible outcomes, establish a
treatment plan for each outcome, and inform the out-
comes and plans to the patient and/or parents before the
treatment is started. In the same context, when growth
is about to end soon, the condition can be predicted in
three ways followed by each related treatment plan as
follows (. Fig. 11.10):
1. In case that good profile and occlusion are main-
tained as the result of favorable growth:
55 Final orthodontic treatment would be recom-
mended to improve esthetic or achieve functional
perfection, or no further treatment would have to
be performed depending on patient’s satisfaction.
2. In case that facial profile and occlusion are accept-
able because Class III growth pattern is not severe:
55 Compensation treatment would be recommended
when skeletal growth is completed, but facial pro-
file would not be improved because orthopedic
treatment is not included.
3. In case that Class III growth pattern is severe, clearly
showing a concave profile, and anterior crossbite
seems not to be able to be improved by orthodontic
treatment:
55 Orthognathic surgery would be applied only if
the patient and parents want to undergo the pro-
cedure.
Likewise, in the cases of Class III malocclusion treat-
ment, patient’s growth patterns tend to play a more
important part than the treatment itself, and success or
failure of the treatment tends to depend on the final
result. Regardless of the result, however, it would be
one of the predictions made prior to the treatment,
and accordingly every one of the results should not be
 214 K. Park et al.
11
..      Fig. 11.8 Later-state phase I treatment of Class II malocclusion.
a Severe overjet, convex profile, and Class II molar relationship in an
11-year, 1-month-old boy. b Pretreatment panoramic and cephalo-
metric radiographs showing late mixed dentition state and Class II
characteristics. c Posttreatment photographs showing improved
facial profile, overjet, and molar relationship. d Posttreatment pan-
oramic and cephalometric radiographs. Patient is in permanent den-
tition state and can be categorized as Class I malocclusion. e
Photographs in 4-year retention. Posttreatment results are well
maintained. f Cephalometric and panoramic radiographs in 4-year
retention. Phase I orthopedic correction is still well maintained
Orthodontic Knowledge and Practice for the Pediatric Dentist
215 11
c

..      Fig. 11.8 (continued)

 216 K. Park et al.

11

..      Fig. 11.8 (continued)

Orthodontic Knowledge and Practice for the Pediatric Dentist
217 11

Skeletal

Concave profile Improving profile

Orthopedic tx

Dental

Good profile Maintaining profile

Orthodontic tx

..      Fig. 11.9 Profile evaluation can be a good-decision process to
diagnose Class III malocclusion if it is skeletal origin or dental.
Localized anterior crossbite caused by dental problem can simply be
treated using removable orthodontic appliance, while Class III mal-
occlusion resulted from skeletal origin is generally treated with
orthopedic treatment methods using facemask or functional appli-
ances, such as Frankel appliance, etc. However, patients with concave
profile with midface deficiency are generally recommended to use
facemask that can improve the facial profile by maxillary protraction

Three conditions at
growth completion

Final
orthodontic
treatment

No or little relapse with fair profile

Orthopedic
treatment
Final
compensatory
orthodontic
treatment

Some class III relapse, but fair profile

Orthognatic
Surgery

class III relapse is pronounced in profile and occlusion

..      Fig. 11.10 Using facemask treatment, patients with Class III
malocclusion are generally able to obtain desired result of maxillary
protraction within a year, leading to noticeable improvement of
facial profile and occlusion. However, facemask cannot completely
improve the Class III traits. If potential Class III traits are strongly
predicted, the mandible would possibly grow more than the maxilla,
leading to anterior crossbite or profile change into concave. When
growth is about to end, the condition can be predicted in three ways
followed by each related treatment plan
 218 K. Park et al.
regarded as a failure. Although there have been vari-
ous prediction models of treatment result, each of them
does not provide an accurate growth pattern because
they are all based on retrospective studies [19–21].
Thus, it is critical to inform about various possible
results, and even a surgical option in the worst case, to
the patient and parents prior to Class III malocclusion
treatment.
One of the reasons why early orthopedic treatment
is implemented for Class III malocclusion, although
an optimal result is not always guaranteed, is that the
psychological aspect should be considered, same as in
Class II malocclusion cases. For example, if the patient
reaches middle or high school years without orthopedic
treatment for concave profile and anterior crossbite was
generally established at age 7–9, he/she will have more
chances to experience a psychological problem because
of his/her own appearance.
11.1.2  oncluding Remarks on Profile
C In the primary dentition, it is possible for abnormali-
Evaluation
Most parents want to know how their child would grow
up in terms of face and tooth appearance. Patients with
11 Class III malocclusion have the distinguishing cephalo-
metric features of this malocclusion type since being in
the primary dentition [22]. Pediatric dentists can make
a relatively simple prediction by observing the child’s
profile. This can be done easily and relatively accurately,
and the dentist can draw up a comprehensive layout
showing how the malocclusion would develop. Pediatric
dentists tend to primarily be interested in caries preven-
tion and treatment. However, they would not be able to
provide the best treatment or might even give unneces-
sary treatment, if they do not observe patient’s appear-
ance by just concentrating on intraoral examination.
For example, when a patient has canine impaction, a
dentist might only consider how to perform forced erup-
tion as the first thing. In this case as well, however, pro-
file evaluation should be the priority in order to make a
comprehensive treatment plan. . Figure 11.11 depicts
that a patient with lip protrusion can have totally differ-
ent treatment procedure. That is, a four first premolar
extraction approach can be chosen, but extracting the
impacted canine instead of the premolar would have
a much less copious and yet esthetically similar effect.
On the other hand, it would be desirable to save the
impacted canine of a patient with straight profile. In
the same context, the canine of the patient shown in
. Fig. 11.12 was saved through autotransplantation,
and such a treatment method was worth undergoing in
spite of some treatment failure possibilities. In conclu-
sion, using profile evaluation would play a key role to
establish an overall treatment plan that leads to the best
possible results for pediatric patients.
11.2 Age-Specific Perspectives
in Orthodontic Management
of Children and Adolescents
Preventive orthodontics can be useful in primary as well as
in mixed dentition. The dental clinician has to be aware of
what things to observe and look out for during all stages
of dental development and also be prepared to diagnose
and decide when the use of preventive orthodontics would
prove effective. This section addresses the most common
problems arising in the development of the occlusion
during primary and mixed dentition and their potential
effects on the permanent dentition, as well as the recom-
mended actions for their prevention and/or correction.
11.2.1 Intervention in the Primary
Dentition
ties to appear in the dental and skeletal relations of
the arches. However, no serious intervention is usually
needed at such an early age [23]. Having said that, there
have only been a relatively few clinical research papers
dealing with this age range, and their recommendations
are based on expert opinion rather than documenta-
tion. Where early orthodontic intervention is considered
pertinent, the possibility of comprehensive orthodontic
treatment in the permanent dentition should be taken
into account. If such a future need is foreseen, the cost/
benefit for intervening at such a young age should be
examined. The child’s ability to cooperate should also
be taken into account, as well as the possible burnout
effects of a lengthy course of treatment. During the
child’s dental examination, the type and extent of poten-
tial abnormalities should be observed and recorded.
These can be classified into the following categories.
11.2.1.1 Arch Space Anomalies
Crowded or widely spaced teeth are frequently observed
in the primary dentition. Except for the normal primate
spaces, widely spaced teeth and generalized spacing are
a normal characteristic of the primary dentition, pro-
gressively more so toward the late primary dentition as a
result of slow jaw growth in all directions (. Fig. 11.13).
Generalized spacing and primate spaces are useful for
the future arrangement of the significantly wider ante-
rior successor permanent teeth and consequently require
no intervention. In the case of crowding, intervention
is not necessary either, but this situation does require
frequent monitoring of the developing dentition as it is
likely that the crowding will be worse after the eruption
of the permanent teeth [24].
In the anterior region, the early loss of one or all inci-
sors does not necessarily lead to loss of space, especially
Orthodontic Knowledge and Practice for the Pediatric Dentist
..      Fig. 11.11 a In the panoramic radiograph, horizontal impaction
of the upper left canine is shown. In cephalometric radiograph,
flared upper and lower incisors causing lip protrusion are shown. b
Lateral facial photograph is showing lip protrusion, and therefore,
this patient can be a good candidate for four first premolar extrac-
219 11
tion orthodontic treatment. c, d In this patient, the upper left canine
was extracted instead of the first premolar for the spot of canine
impaction, which would have similar effect with one of extraction
orthodontic treatment. In the final result, good facial profile is
achieved by sacrificing the impacted canine
 220 K. Park et al.

11

..      Fig. 11.11 (continued)

Orthodontic Knowledge and Practice for the Pediatric Dentist
221 11

..      Fig. 11.12 a In the panoramic radiograph, similar horizontal arches with good facial profile. c, d In this patient, impacted canine
impaction of the upper left canine is shown. In cephalometric radio- was saved by autotransplantation, and in the final result, good facial
graph, good inclination of the upper and lower incisors is shown. b profile is maintained. For this patient, autotransplantation was
Facial and intraoral photographs are showing fairly well-aligned worth undergoing in spite of its probability of treatment failure
 222 K. Park et al.

11

..      Fig. 11.12 (continued)

Orthodontic Knowledge and Practice for the Pediatric Dentist
223 11

b ..      Fig. 11.14 One year after the loss of the primary central incisor.
Tilting of the lateral incisor has not affected total arch length with
canine relationship remaining stable

so far preferred, bearing a small portion of acrylic as a

maxillary cushion (. Fig. 11.17) [25, 26]; the possibility
of bilateral bonded wires should however not be over-
looked. It is certain that in the era of bonding, cemented
band appliances will gradually become less popular.
..      Fig. 11.13 a Normal primary dentition with primate space char- The problem of the second primary molar loss, prior
acteristics. b Early mixed dentition in a 6-year-old child with lower to the eruption of the first permanent molar, is more
anterior primary tooth crowding. Severe crowding is anticipated in difficult to solve. Cementing a “distal shoe” appliance
the permanent dentition
in the first primary molar, in the same appointment as
the extraction, has been advised traditionally. The distal
if the primary canines and molars remain in place, and end of the device enters the distal root alveolus of the
therefore, no space maintenance is needed. Tilting of extracted second primary molar, guiding the eruption
the adjacent teeth toward the lost tooth area may be of the first permanent molar (. Fig. 11.18). Following
observed, making the space look narrower, but this has adequate eruption of the first permanent molar, replace-
no effect on total arch length (. Fig. 11.14). If one or ment of the “distal shoe” with, e.g., a “band and loop”
more primary incisors are lost before canine occlusion, is required. The paradigm shift on caries control nowa-
which occurs at about the age of 2, no suggestions for days, as well as the level of technical difficulty of these
space maintenance have been proposed; the child’s inabil- early interventions, has made them less popular among
ity to cooperate constitutes a prohibitive factor anyway. pediatric dentists. Alternatively, space regaining may
In the case of the first primary molar loss, a space-­ be pursued after the first permanent molar completes
maintaining device should be applied, preferably of a eruption, following a mixed dentition space analysis.
fixed type, as this is likely to be much better tolerated by However, considering the difficulty of distalizing the
the young patient. In unilateral loss, the classic “band lower first permanent molar compared to the upper first
and loop” is preferred (. Fig. 11.15), although simpler permanent molar, using the distal shoe may still be an
appliances can be used, requiring less technical prepara- option in the lower arch.
tion. Such a device may be comprised of a suitably bent Fitting fixed appliances requires appropriate seating
stainless steel wire bonded to the etched enamel of the and removing instruments such as band-removing pliers.
adjacent teeth with composite resin (. Fig. 11.15d). The Band decementation or solder failure may occur in all
0.28′ (0.7 mm) diameter offers minimal elasticity, allowing fixed appliances, as well as detachment in those bonded
independent tooth movement for preventing its debond- with composite. Patients should be given instructions,
ing. This has shown success empirically, but no evidence and parents should be informed about the potential
exists as yet regarding its longevity. For bilateral loss in need for immediate repair.
the mandible, two independent “band and loop” appli-
ances may be cemented at the second primary molars. 11.2.1.2 Occlusal Anomalies
In the cases with at least two permanent lower incisors At the Vertical Plane
erupted, which already indicates a very early mixed den- Anterior open bite is commonly observed in the primary
tition, a lingual holding arch can be used (. Fig. 11.16). dentition, and most of the time, it is only dentoalveolar,
For bilateral loss in the maxilla, a Nance appliance was resulting from harmful oral habits, such as the use of the
 224 K. Park et al.
a b
c d
11
..      Fig. 11.15 a Band and loop on the cast. The wire is almost in
contact with the gums to minimize masticatory stress load and is
temporarily fixed to the lower second primary molar band with wax.
b The appliance is cemented to an upper second primary molar. c
Commercially available sets of bands for each quadrant of the pri-
..      Fig. 11.16 Lingual holding arch cemented on the second pri-
mary molars. It is shown here while the first premolars are erupting
and its removal is due
thumb or a pacifier as a comforter. Treatment in these
cases is focused on the discontinuation of the habit.
The open bite automatically regresses or fully corrects
itself, as the muscular balance between the tongue, the
mary and permanent molars are necessary for selecting the proper
band size. d Another type of unilateral space maintainer made chair
side by 0.7 mm wire bonded with resin composite to the primary
canine and second molar. It is shown here when its removal is due
because of eruption of the succeeding first premolar
lips, and the perioral muscular system is restored [25]
(. Fig. 11.19). Anterior open bite of skeletal nature is
difficult to treat and requires referral to an orthodontist
for monitoring and future intervention [24].
Increased overbite reaching or exceeding 100% is
also frequently observed in the primary dentition. It
requires no appliance therapy at this age, since in most
cases it corrects itself when the first permanent molars
come into occlusion.
At the Sagittal Plane
Anteroposterior discrepancies in the relationship of
the molars, as well as that of the anterior teeth, belong
to this category. In the anterior teeth, overjet may be
increased, but when negative, it is called a crossbite. The
relationship of the distal surface of the maxillary second
to that of the mandibular second primary molar guides
the future occlusal relationship of the first permanent
molars. In normal occlusion, the distal surfaces of the
maxillary second primary molars are nearly on the same
vertical line or about 1 mm distally to the occluding
mandibular ones (ideal relationship) (. Fig. 11.20).
Orthodontic Knowledge and Practice for the Pediatric Dentist
225 11

a b

..      Fig. 11.17 a Recent loss of the upper right primary lateral incisor and canine due to trauma. b A modified Nance appliance is cemented
to the second primary molars, with the addition of an artificial lateral for esthetical purposes

..      Fig. 11.18 a A mandibular

a c
second primary molar is about
to be extracted due to pathologi-
cal root resorptions at bifurca-
tion in a 4-year-old. b An X-ray
taken at the same session after
the attachment of a prefabri-
cated distal shoe appliance on
the restored first molar. c
Guiding of the first permanent
molar is in progress after
8 months. Following its full
eruption, another type space b
maintainer will be needed

Eye Catcher
Disorders at the anteroposterior/sagittal plane,
although they are more of a problem in the mixed den-
tition, may be observed in the primary dentition. Using
primary molar relationship information alone for pre-
dicting the relationship of jaws and dental arches in the
permanent dentition is not always safe, and the relation-
ship between the primary canines may be more helpful
in assessing disorders at the sagittal plane [25]. More
importantly, these occlusal examinations always should
be based on careful evaluation of facial profile, because
the big picture of the skeletal pattern of the patient can
be assumed accurately from facial evaluation.
Distal step occlusion of the second primary molars is fre-
quently observed, in combination with increased overjet
of the anterior teeth (. Fig. 11.21). This abnormality
usually has a skeletal basis but can also be related to
harmful oral habits. This is something that can be diag-
nosed based on clinical history and examination. Usu-
ally, these occlusal relationships of the primary molars
carry on to the permanent dentition, being indicators of
an Angle Class II malocclusion development. However,
orthodontic treatment is infrequently justified at such an
early age, as explained in 7 Sect. 11.1 of this chapter.
Less common in Caucasians and more so in East
Asians is the opposite disorder – called mesial step
occlusion – in combination with anterior crossbite, i.e.,
occlusion of the upper anterior teeth lingually to the
 226 K. Park et al.

a b

c d

..      Fig. 11.19 Disorders on the vertical plane. a, b Severe anterior open bite from thumb-sucking at 3 years of age. c Six months after habit
11 cessation. d Full self-correction 18 months later

..      Fig. 11.20 Normal occlusal relationships between the second
molars and canines in the primary dentition
respective lower teeth (. Fig. 11.22). The treatment
decision in these cases depends on their severity and
etiology, whether it is skeletal, dentoalveolar, or a func-
tional abnormality. Very frequently, however, this type
of occlusion is a precursor of an Angle Class III maloc-
clusion in the permanent dentition.
If the cause is a skeletal one, the child should be
treated at the appropriate time. Treatment in these cases
is usually long term. If the abnormality is combined
with a functional disorder, it should be corrected at this
age. Correction of multiple tooth anterior crossbite is
rarely successful through selective grinding, but there is
insufficient documentation to definitively indicate the
best treatment in these cases [27].
..      Fig. 11.21 The primary dentition with distal step occlusal rela-
tionship of the second primary molars and canines. There is a mod-
erate horizontal protrusion. This is a disorder in the sagittal
(anteroposterior) plane
A removable device is preferred, e.g., an anterior
bite plate with a jackscrew or spring attached to it, if
treatment by pushing the upper anterior teeth labially is
desired. A thin acrylic bite plate on the primary molars
frees the occlusion and eases correction of anterior
tooth occlusion (. Fig. 11.23). Using inclined planes
instead may not be effective to correct anterior cross-
bite in the primary dentition. Correction of an anterior
crossbite is maintained by the occlusion itself. However,
regular follow-ups are needed, since there is a tendency
for relapse in the permanent anterior teeth in a fair num-
ber of cases.
Orthodontic Knowledge and Practice for the Pediatric Dentist
At the Transverse Plane
Disorders of this category include posterior crossbite
(unilateral or bilateral), i.e., abnormalities in the bucco-
lingual relations of the posterior teeth, mainly related
to a narrower maxillary dental arch. These discrepan-
cies, if not treated at the appropriate time, may lead to a
multitude of complications in the permanent dentition,
such as severe dental wear, periodontal distraction, and
even skeletal problems like facial asymmetry. There is
insufficient documentation in the literature whether to
..      Fig. 11.22 The primary dentition with mesial step occlusal rela-
tionship between the second primary molars and canines and edge to
edge incisal relationship
227 11
treat posterior crossbite occlusion early, since in many
cases it is self-corrected with eruption of the permanent
molars and premolars. If further occlusal abnormali-
ties are foreseen, they may all be corrected later by a full
orthodontic treatment.
Correction of posterior crossbite is usually recom-
mended in cases where there is lateral shift of the man-
dible, and, at the maximum intercuspation of the two
arches, there is notable midline deviation. In the absence
of deviation with only dentoalveolar crossbite, treat-
ment is postponed until after the eruption of the first
permanent molars. The simple treatment possible is the
selective relief of tooth cusps interfering with normal
occlusion. This usually involves reverse inclined cusp
reduction of the upper and lower canines and leveling
the cusps of the primary molars in crossbite [28, 29]
(. Figs. 11.24 and 11.25).
In cases where the abnormality is judged as severe,
expanding the upper dental arch through some maxillary
appliance can be carried out. This can be removable, such
as a palatal bite plate with a midline jackscrew, or fixed,
such as a W-arch or a quad-helix. These fixed appliances
consist of bands that attach to the second primary molars
and palatal wire arches that are bent at various points for
activation, applying buccal pressure as far as the canines

a b

c d

..      Fig. 11.23 a Anterior crossbite. b Unsuccessful correction attempt with the use of an inclined plane. c Palatal bite plate with expansion
screw after 1 month’s use. d At the 6-month follow-up, a stable correction of the abnormality is observed
 228 K. Park et al.

(. Fig. 11.26). After crossbite correction, the appliance
should remain passively for a few months in the mouth
for securing the result and relapse prevention.
Apart from crossbite, there is also a much rarer occlu-
sal abnormality characterized by severe discrepancy jaw
sizes. There is a much wider maxilla or a very narrow
mandible, causing “telescopic” occlusion, bilaterally or
unilaterally (. Fig. 11.27). These cases have a skeletal
cause related to the basal bone of the jaws and require
monitoring for the appropriate orthodontic intervention.

b c

11

..      Fig. 11.24 a Posterior crossbite (right side) at the age of 6 years, with functional shift and midline deviation. b, c Before and after reduc-
ing the interfering cusps of involved the primary teeth

a b

..      Fig. 11.25 a Posterior crossbite at age 4 years with canine interference during lateral functional shift. Grinding of the maxillary and
mandibular right primary canines and molars was undertaken at this stage. b Occlusal relationship at age 10 with no further treatment
Orthodontic Knowledge and Practice for the Pediatric Dentist
a b
..      Fig. 11.26 a Functional posterior crossbite at 6 years of age as
the only occlusal abnormality. b One visit grinding of the left maxil-
lary and mandibular primary teeth (under local anesthesia) failed to
solve the problem in the following 6 months. c An 8-month applica-
a b
..      Fig. 11.27 Telescopic occlusion in the primary dentition. a Unilateral. b Bilateral. Tartar presence in the maxillary second primary
molars is probably related to impaired masticatory function
11.2.2 Intervention in the Mixed Dentition
All patients should be evaluated orthodontically at the
age of 6–7 years old, so that the need for treatment can
be evaluated and also scheduled in a proper timing, indi-
vidualized for each case.
11.2.2.1 Arch Space Anomalies
Space-related problems in the mixed dentition refer to
crowding or widely spaced teeth and are determined by
the mesiodistal dimension of the teeth in relation to the
available space in the dental arches.
229 11
tion of a quad-helix after the eruption of the maxillary first perma-
nent molars is shown here after reactivation of the anterior part. d
Overtreatment, better seen in the permanent molars, is necessary for
preventing relapse
Crowding
Crowding (primary) can occur from the early stages of
mixed dentition, caused by a disproportionate size rela-
tionship between the permanent teeth and the jawbones.
The appropriate mode and time of correction of the
crowding depends upon several factors, such as its mag-
nitude, smile esthetics, and other coexisting orthodon-
tic problems. Treatment options to relieve the crowding
may include the use of leeway space or the extraction of
permanent teeth. Orthodontic consultation should be
sought in such cases, as well as informing parents about
optimal treatment times.
 230 K. Park et al.

Apart from primary crowding, space loss due to
advanced dental caries or premature loss of a primary molar,
resulting to mesial drift of the first permanent molar, may
lead to secondary crowding (. Fig. 11.28). It is thus neces-
sary to maintain the primary teeth intact or restore them to
their normal size, also for occlusion purposes. Retention of
the second primary molars, in particular, aids in maintain-
ing stability of the entire dental arch length [30]. When a
a are already in occlusion, does not require space main-
b ally desirable [33]. In cases where the dental clinician
11
..      Fig. 11.28 a Space loss by mesial drift of a second molar in a
crowded primary dentition. b Space problem for the first premolars.
Severe early childhood caries has probably contributed to it
posterior primary tooth is lost, the need for a space main-
taining/regaining appliance should be examined. As most
of space loss – adjacent tooth drifting – occurs within the
first months after a premature primary molar extraction,
space maintenance should be considered without delay.
In many cases, maintaining space after premature
loss of the primary molars is important for preventing
crowding of the permanent teeth (. Fig. 11.29). There
is sufficient documentation that premature loss of the
first primary molar, when the first permanent molars
tenance [31, 32]. Apparent space loss may not reflect in
total arch space loss (. Fig. 11.30); it may be within
the limits of leeway space and therefore without clini-
cal importance. However, in the cases of incisor and/or
lip protrusion, or even at borderline space inadequacy,
maintaining space may be clinically important.
For the premature loss of the second primary molar,
there seems to be no documentation, but its loss is long
believed to cause appreciable decrease of the dental
arch length from the mesial drift of the first permanent
molar. The application of a space maintainer is gener-
cannot predict the need for future orthodontic treat-
ment, it is advisable to seek orthodontic consultation.
This is because, even if future orthodontic treatment
is deemed necessary, space maintenance may still be
desirable. In some cases, in which timely placing a space
maintener has been neglected, over-eruption of the
opposing second molar renders placing a space-main-
tainer obsolete since, at biting, that molar functionally
prevents mesial drift of its adjacent first permanent
molar (. Fig. 11.31). This possibility should not be a
reason for not including timely space maintenance in the
treatment plan.
Space maintenance can be achieved through the use
of fixed or removable dental appliances. The remov-
able Hawley appliance is a palatal acrylic plate retained

a b

..      Fig. 11.29 a Neglect in maintaining space after premature loss of the primary molars. b The panoramic radiograph shows the mesial drift
of all permanent molars and lack of space for the permanent maxillary canines and mandibular second premolar eruption
Orthodontic Knowledge and Practice for the Pediatric Dentist
by two Adams clasps, usually anchoring the appli-
ance on the first permanent molars, and a labial wire
arch, resting on the labial surface of the anterior teeth
(. Fig. 11.32). The mandibular lingual holding arch is
..      Fig. 11.30 Premature loss of the right mandibular first primary
molar has led to space loss. This seems mainly due to distal drift of
the right canine and incisors
a b
..      Fig. 11.31 a Neglect in maintaining space after early loss of both
the left mandibular primary molars. b Overeruption of the maxillary
second primary molar is preventing any further mesial drift of the
a b
..      Fig. 11.32 Removable Hawley appliance a For the maxilla. b For the mandible. The added screw has resulted in regaining the space lost
by premature extraction of the second primary molar
231 11
a fixed appliance made up of two bands cemented to
the first permanent molars and connected by an 0.036′
(0.9 mm) diameter wire arch that is passively applied to
the gingival third of the lingual surface of the permanent
incisors (. Fig. 11.33). For the maxilla, a transpalatal
arch or a Nance appliance can be used. Both consist of
bands cemented to the first permanent molars and are
connected together through a wire arch. The wire of the
transpalatal arch follows the dome of the hard palate,
while the Nance appliance rests at the anterior palatal
vault, by means of a small acrylic button for contact with
the palatal mucosa, thus being somewhat less “hygienic”
(see . Fig. 11.17 for the primary dentition). In the case
of bilateral loss in any jaw, a band and loop maintainer
may be used, as described above for the primary denti-
tion [33]. The composite bonded wire, suitably bent to
avoid occlusal loads, is again a viable alternative.
When space has already been lost, the application of
a fixed space regainer may be needed. The lip bumper is
one such device for the mandible. It consists of two buc-
cal tube bearing bands cemented to the first permanent
molars and a, wider than the dental arch, acrylic-­covered
mandibular permanent molar rendering the placing a space-­
maintainer obsolete
 232 K. Park et al.

wire arch that goes around the anterior area and in the
tubes. The lower lip muscle tone results in distalizing
(or rather uprighting) the molars. This process may be
accelerated by incorporating coil springs in the device.
For isolated unilateral space problems, a sectional fixed
appliance can be used, e.g., one that includes brack-
ets, tubes, partial archwire, and springs (. Fig. 11.34).
Removable devices, such as the Hawley appliance, may
also be used in combination with a jackscrew or finger
springs [34] (. Fig. 11.35).

a b

..      Fig. 11.33 a Loss of the second primary molars. Lingual holding arch wire rests passively on the gingival third of lower anterior teeth
lingual surface. b Transpalatal arch with loop for activation of the 0.36′ (0.9 mm) diameter wire

a b
11

..      Fig. 11.34 a Lower lip bumper for space regaining for the man- lis). b Space regaining for a second premolar with the use of spring
dibular left canine and first premolar (courtesy of Prof. N. Topouze- in a partial wire arch from the canine to first permanent molar

a b

..      Fig. 11.35 a Dual-purpose removable appliance for space maintenance (right side) and space regaining (left side, fitted with jackscrew).
b Activating the screw for space regaining
Orthodontic Knowledge and Practice for the Pediatric Dentist
11.2.2.2 Mixed Dentition Analysis
Eye Catcher
The goal of mixed dentition analysis is to predict the
width of the unerupted permanent teeth and calcu-
late whether these will fit in the available space, so
that an early diagnosis of potential problems in the
dental arches is allowed. Indications for preventive or
interceptive orthodontic treatment may thus be early
recognized and treatment decisions made, as well as
whether orthodontic consultation is necessary.
True width of primary molar
Apparent width of primary molar Apparent width of premolar
Other methods of analysis include those that use den-
tal ratio charts, since these are simple to use and do
not require X-rays. They are based on the analogy of
permanent mandibular incisor width to the canines
and premolars. Moyer’s mixed dentition analysis [36]
uses the sum of the four permanent mandibular incisor
width to predict the summed width of the maxillary or
mandibular permanent canine with the first and second
premolar in each side. Estimated values are presented
in . Table 11.1. Estimations are based on the width
of the mandibular rather than the maxillary incisors
because of the increased size variability of the upper
laterals. The width of expected permanent teeth was
calculated based on a sample of Caucasian children,
to which the method holds greater precision. Moyer’s
analysis tends to overestimate the size of permanent
teeth [35].
The Tanaka and Johnston analysis [37] also uses
the width of the mandibular incisors for calculating the
width of the canines and premolars. This method is pre-
sented in . Table 11.2. This method also has a tendency
to overestimate predicted tooth size but is particularly
easy to use, since it can be memorized and applied with-
out the use of charts [35]. Other methods, such as the
Staley and Kerber analysis, [38] use both radiographs for
width of the teeth and prediction charts. In conclusion,
..      Table 11.1 Predicted values of the sum of permanent canine and premolars width of one side with Moyer’s analysis (confidence
level 75%) [36]
Mandibular incisors 19.5 20 20.5 21 21.5 22
Canine Maxilla 20.6 20.9 21.2 21.3 21.8 22.0
plus
premolars Mandible 20.1 20.4 20.7 21.0 21.3 21.6
233 11
One method of mixed dentition analysis is to calcu-
late the width of the unerupted permanent teeth from
an undistorted X-ray image. For this reason, periapical
X-rays are preferred over panoramic ones, especially
when calculating canine tooth width [35]. This tech-
nique can be used for both jaws and all ethnic groups.
Precision of measurement depends on X-ray quality
including correct exposure angles. Correcting the X-ray
magnification is required, and this can be achieved by
comparing the width of a primary molar tooth in the
X-ray with its real width (clinical or on a plaster cast)
using the ratio [35]:
True width of premolar
=
mixed dentition analyses tend to be reliable, if they are
applied to the same ethnic groups from which the pre-
dicted values arose. They should be, however, avoided
if the radiographic examination reveals shape- and size-­
related abnormalities of the permanent teeth.
11.2.2.3 Dental Spacing
Spaces may be seen between any teeth, while in the
mixed dentition this phenomenon is usually found
between the two central incisors (diastema). The den-
tist does not need to close this until the lateral incisors
and canines have all erupted. In the majority of cases,
the horizontal forces exerted during the eruption of
these teeth close the diastema, and there is no need for
treatment. However, should the condition persist, the
possibility of an existing supernumerary (mesiodens)
or odontoma causing the abnormality should be inves-
tigated (. Fig. 11.36). In these cases, the mesiodens
is extracted, and then, the diastema may be closed
spontaneously without any treatment. If the diastema
remains after 6 months, orthodontic space closure may
be needed. This can be achieved through the use of a
removable Hawley appliance with springs pushing the
two central incisors mesially at the midline or by fixed
partial appliance, i.e., brackets on the incisors for pull-
ing them close with elastic forces (. Fig. 11.37).
22.5 23 23.5 24 24.5 25 25.5 26 26.5 27 27.5 28 28.5 29
22.3 22.6 22.9 23.1 23.4 23.7 24.0 24.2 24.5 24.8 25.0 25.3 25.6 25.9
21.9 22.2 22.5 22.8 23.1 23.4 23.7 24.0 24.3 24.6 24.8 25.1 25.4 25.7
 234 K. Park et al.

Furthermore, a diastema like this could persist if 11.2.2.4 Occlusal Anomalies

the upper lip frenum is bulky or its connective tissue
fibers attache too low between the two central incisors.
Diagnosis is made by pulling the upper lip, which causes
ischemia in an interdental papilla with a short frenum
and also with a radiograph, which may show an osse-
ous recession at the point of frenum fiber attachment.
In this case, closing the space should take place first and
frenum removal follow, so that the repair scarred gingi-
val tissue will help in maintaining the teeth in the correct
place [39].
..      Table 11.2 Prediction of the summed width of perma-
nent canine and premolars with Tanaka and Johnston
analysis [37]
Sum of mandibular + 11 mm = predicted width of maxillary
incisor width canine and premolars per side
2 + 10.5 mm = predicted width of mandib-
ular canine and premolars per side
At the Vertical Plane
Anterior open bite as a merely dentoalveolar anomaly
is very frequent in the mixed dentition. It occurs as a
reduced vertical growth of the anterior alveolar process
due to the persistence of a harmful oral habit. Skeletal
open bite is usually attributed to posterior downward
turn of the mandible during its growth. It may be found
only in the anterior region or be more severe in form and
extend all the way to the molar region. The more severe
forms of skeletal anterior open bite very frequently
require combined maxillofacial surgery with orthodon-
tic treatment (. Fig. 11.38).
The opposite anomaly seen on the vertical axis is
deep bite, characterized by increased vertical overlap
caused by either over-eruption of the anterior teeth or
decreased eruption of the posterior teeth (. Fig. 11.39).
Evaluation of occlusion should be performed, so that
potential interventions decided in the form of full orth-
odontic treatment [25]. Sometimes other consequences
may be present already, such as periodontal trauma.
In this anomaly too, its skeletal nature should be

11 a b

..      Fig. 11.36 a Midline diastema caused by the presence of an erupted mesiodens. b X-ray shows the presence of another unerupted
mesiodens

a b

..      Fig. 11.37 a A large midline diastema of the maxillary incisors. b Space closed with two brackets and elastic forces
Orthodontic Knowledge and Practice for the Pediatric Dentist
235 11

..      Fig. 11.38 A severe form of skeletal anterior open bite. Four years later without treatment, the open bite has increased

a b

..      Fig. 11.39 a A young patient’s mixed dentition with severe anterior deep bite (at proclined position). b This vertical plane anomaly con-
tributes to labial periodontal trauma of the mandibular central incisors

recognized, which is usually due to an anterior upward

turn of the mandible during its growth.

At the Sagittal Plane

These anomalies manifest with consequences in the pro-
traction of the anterior teeth (overjet). If the first per-
manent molar relationship is of an Angle Class II or
Class III malocclusion, it is most likely that this will have
respective consequences in the horizontal protraction
of the anterior teeth. Increased overjet in the maxillary
anterior region may be caused by forward relocation of
the anterior maxillary alveolar process and backward
relocation of the anterior mandibular alveolar process,
by increased labial inclination of the maxillary inci-
sors and increased lingual inclination of the mandibu-
lar incisors, and by maxillary prognathism, mandibular
retrognathism, or a combination of any of those fac-
..      Fig. 11.40 Class II occlusal relationship with severe overjet in
tors (. Fig. 11.40). Causes for the anterior dentoalve- the mixed dentition (Angle Class II). This is a disorder on the sagittal
olar divergence can be various harmful oral habits, but plane
 236 K. Park et al.
the cause of a generalized anomaly, especially when it
includes the basal base, is probably skeletal and should
be further investigated through lateral cephalometric
radiographs.
Eye Catcher
It has been suggested that early orthodontic treatment
in the mixed dentition of children with severe overjet
could reduce the risk of maxillary incisor fracture.
However, there was also a report that no significant
difference was shown in incisor fracture as a result
of dental trauma in children who had at least 7 mm
overjet corrected by early treatment, in comparison
to other children for whom treatment had been post-
poned until the permanent dentition [40]. The early
treatment with fixed appliances of a Class II maloc-
clusion in patients with severe overjet is not often
selected by the orthodontist, because orthodontic
treatment requires a longer treatment time this way,
possibly exhausting the child’s tolerance and coopera-
tion. If, however, other personal patient reasons exist,
e.g., risky athletic activities, low self-esteem because
of dental esthetics, etc., early intervention for overjet
11 correction may be justified.
The opposite commonly seen anomaly in the mixed
dentition at the sagittal plane is the anterior cross-
bite. This can be simply of dentoalveolar etiology
and may involve one or more anterior maxillary inci-
sors in lingual occlusion with the mandibular ones.
These cases are treated as described in the primary
dentition with a removable Hawley appliance with
springs (. Fig. 11.41). In the case of a single tooth,
a b
..      Fig. 11.41 a Neglected anterior crossbite of the maxillary left permanent central incisor. b Correction is attempted with a removable
Hawley appliance with Z-shaped spring and acrylic cover of the occlusal surfaces of the posterior teeth for occlusal relief
building an inclined plane with resin-modified glass
ionomer cement placed on the corresponding mandib-
ular incisors corrects the crossbite within 2–3 weeks. Its
removal is performed with great care to avoid incisal
enamel fractures. Mild cases of anterior crossbite in
early mixed dentition can potentially be solved by sim-
ply raising the bite for 2–3 weeks, thus allowing inci-
sor alignment by involuntary pressure of the tongue
(. Fig. 11.42).
When anterior crossbite is found in all the ante-
rior teeth, correct and timely diagnosis is required, to
determine if the problem is skeletal or merely func-
tional in nature. Skeletal-related anterior crossbite
(skeletal Angle Class III) is the disharmony of the jaw-
bones at the sagittal plane, while a narrow maxilla may
coexist, indicative of a width problem of the jaw basal
bones. In this anomaly, the anterior teeth may occlude
directly into crossbite without forward sliding of the
mandible (. Fig. 11.43). In the anterior crossbite of
functional cause, the anterior teeth are in a scissors
position, being forced to fall into crossbite for a stable
occlusion. In general, sagittal plane occlusal anoma-
lies require correct diagnosis and often full orthodon-
tic treatment; therefore, orthodontic consultation is
advisable.
At the Transversal Plane
Posterior crossbite in isolated teeth due to dentoalveolar
reasons is usually caused by diverging eruption of per-
manent teeth and is frequently observed in the mixed
dentition. Unilateral or bilateral posterior crossbite with
midline shift due to functional mandibular deviation
is also common in occurrence. In functional posterior
crossbite, there is always a lateral sliding element. The
most common cause is a disharmony in dental arch
width, with coexisting prominent cusps of the primary
Orthodontic Knowledge and Practice for the Pediatric Dentist
237 11

a b

..      Fig. 11.42 a Initial stages of a similar case with . Fig. 11.41. b right central incisor after 3 weeks by involuntary tongue pressure.
Bite raising with addition of composite resin on the occlusal surface Upon removing of the composite, occlusion alone will prevent
of the lower first primary molars. c Self-correction of the permanent relapse

..      Fig. 11.43 Severe crossbite with apparent skeletal characteristics of Angle Class III molar relationship

canines, causing a lateral shift of the mandible, which the skull. Orthodontic consultation is advisable in these
can be combined with functional anterior crossbite. cases.
Correction of crossbite in these cases is necessary and
can be achieved through the use of fixed or removable 11.2.2.5  ooth Number and Eruption-Related
T
appliances, as described earlier in the primary dentition, Anomalies
following the selective grinding of the primary teeth General information on tooth eruption disorders is pro-
involved [41]. Furthermore, skeletal-related crossbite can vided in 7 Chap. 10. This section will only discuss them
also occur related to size abnormalities in the maxilla in relation to the aligning of the dentition through orth-
or the mandible, reflecting asymmetries at the base of odontic means.
 238 K. Park et al.
a arch wire and spring in more severe ones (. Figs. 11.44
b izing the molars [43]. While suggested for ectopic erup-
c
11
d loss is bilateral or unilateral, if other occlusal problems
..      Fig. 11.44 a Severe caries in a 6-year-old. b Pseudo-ectopic erup-
tion of the maxillary first permanent molar hindered by the cervical
edge of the crown of the adjacent primary molar 6 months after
rehabilitation. c Inserting an elastic separator between the two teeth.
d X-ray taken 1 week later shows that eruption is unhindered
Ectopic Eruption of the First Permanent Molars
and Canines
Ectopic eruption of the first permanent molars usually
leads to substantial root resorption, resulting to early
loss of the adjacent second primary molars. This causes
a significant loss of space [42]. Prompt correction is
required, and this is usually done by pushing the perma-
nent molar crown back distally with various means, i.e.,
a wire loop in mild cases or a fixed appliance with partial
and 11.45). If the second primary molar is lost, space
regaining may be achieved through a removable appli-
ance (. Fig. 11.46).
Other common occlusal anomalies involving the
permanent canines are their ectopic eruption or impac-
tion, most usually occurring in the maxilla. Treatment
choices are discussed earlier in 7 Sect. 11.1 in this chap-
ter. Among those for preventing impaction is the use of
extraoral devices (headgear) to create space by distal-
tion, there is insufficient documentation that prompt
extraction of the primary canine prevents impaction of
the permanent one in the palate [44]. Canine impaction
is surgically corrected after raising a flap and bonding
a button to canine crown. This is connected to the wire
arch of a fixed orthodontic appliance via, e.g., a thin
metal chain, being pulled into its correct position in the
dental arch (. Fig. 11.47).
Congenitally Missing and Supernumerary Teeth
Maxillary lateral incisor agenesis creates esthetic prob-
lems by creating tooth spacing, drift of the adjacent
teeth, and midline deviations. In cooperation with the
orthodontist and possibly with the prosthodontist, it
has to be decided whether space should be maintained
for a prosthetic implant-based solution after growth is
complete or the space should be closed by moving the
canine proximally into the place of the lateral incisor.
These decisions depend upon whether lateral incisor
coexist, such as crowding of the anterior teeth in the
lower dental arch, maxillary anterior teeth width, and
possibly other factors. The facial type by its lateral view,
whether convex, concave, or straight, should always be
taken into account. In moving the canine to replace the
missing lateral, esthetic crown modification is usually
done with cusp grinding and composite resin buildup
[45] (. Figs. 11.48 and 11.49).
In the common occurrence of congenitally missing
mandibular second premolars, distal drift of the adja-
cent premolar and mesial drift of the first permanent
molar are observed. The need for space maintenance
is decided after considering several factors, such as the
number of congenitally missing teeth, the length of the
dental arch, the age, the skeletal background, and the
patient’s profile [46].
Mesiodens and other supernumerary teeth may
block eruption of the anterior teeth or drive them to
erupt ectopically, possibly with rotations and spac-
ing. Supernumerary permanent teeth most commonly
occur in the maxilla and, following their removal at the
appropriate time, frequently require orthodontic inter-
vention, which can either be local or part of a com-
prehensive treatment [47] (. Fig. 11.50). Generalized
Orthodontic Knowledge and Practice for the Pediatric Dentist
a b
..      Fig. 11.45 a Severe ectopic eruption of both maxillary first per-
manent molars. Orthodontic brackets bonded on their erupted part,
and spring bearing elastic wire is directly bonded on the three adja-
cent primary teeth for each side. b Corrected eruption in 8 weeks
a b
..      Fig. 11.46 a Ectopic eruption of a maxillary first permanent
molar with complete root resorption of the adjacent second primary
molar in a girl aged 7 years with a history of acute lymphoblastic
abnormalities with multiple supernumerary teeth, such
as cleidocranial dysplasia (CCD), may prove extremely
difficult and should be treated by a specialized ortho-
dontist in cooperation with a maxillofacial surgeon [48].
The Ankylosed Primary Molars
Ankylosed primary molars can lead to occlusal problems
as a result of their subsequent submergence. Extraction
and space maintenance is preferred in the case of succes-
sor premolar presence. In the case of premolar agenesis,
239 11
further assisted by newly inserted rubber rings. c Complete eruption
in 14 weeks. If the second primary molar root resorption later leads
to their premature loss, space maintenance may be needed
c
leukemia. b The primary molar was lost, leading to severe lack of
space. c Regaining is attempted using a Hawley appliance, fitted with
a jackscrew
orthodontic advice is useful for deciding the best suited
solution. Building the crown height of a primary molar
with severe infraocclusion prevents further diversion of
the adjacent teeth (7 Fig. 10.21). Monitoring should
continue, in view of the lack of alveolar bone growth
in height (as it physiologically occurs in the adjacent
teeth), a factor that will prove critical later in a potential
implant-related solution. Root resorption of the man-
dibular primary second molars without successors was
relatively slow, allowing them to remain in the dentition
 240 K. Park et al.

..      Fig. 11.47 a The maxillary

a b
impacted permanent canine. b
Canine uncovering by open
surgery technique, bonding of
button, and guiding into the
dental arch after extraction of
the over retained primary canine

a 11.2.3 Harmful Oral Habits

11
b such as anterior displacement of the maxillary incisors, lin-
..      Fig. 11.48 a Congenitally missing right maxillary lateral incisor
and microdontia of the left one with canine displacement. b Orth-
odontic alignment of the teeth with space left for future prosthetic
replacement of the right lateral. Palatal plate with an artificial right
lateral incisor for esthetics and space maintaining purposes is worn
for a 2–3-decade period, supporting the choice of their
preservation [49]. Ankylosis may also occur in various
permanent teeth because of periodontal damage as a
result of trauma, but etiology may remain obscure at
times (. Fig. 11.51).
11.2.3.1 Thumb-Sucking and Pacifier Overuse
Two common oral habits, which may prove harmful to the
dentition of preschool and school children, are sucking of
thumb or other fingers and the prolonged use of a pacifier.
In the infant, sucking objects is a natural reflex to what-
ever comes into contact with their lips. Thumb-sucking is
not considered detrimental to the dentition if discontin-
ued early, before the age of about 3, as consequences to
anterior dentoalveolar segment are usually self-corrected
upon habit cessation [50]. The prolonged thumb-sucking
or pacifier use may cause dentoalveolar abnormalities,
gual tilting of the mandibular incisors, or even posterior
crossbite due to palatal muscle hyperactivity, which exerts
pressure on the alveolar processes of the maxilla, thrusting
indirectly the tongue forward (. Fig. 11.52a). The severity
of these disorders is influenced by the frequency, intensity,
and duration of the habit, the position of the mandible, the
osteogenic capacity, and the child’s overall health. Thumb-
sucking is even more undesirable than prolonged use of a
pacifier, as the thumb is available to the child at any time
and cessation of the habit is thus more difficult to achieve.
The first step in the effort to cease the habit is to
inform parents about its harmful consequences and
persuade the young patient. Children do not appreciate
future own benefits but may merely obey instructions or
wish to please those who care for them. In many cases,
the use of a diary is effective, in which the parent records
how many times the habit was repeated, gradually aim-
ing toward its cessation. Progress should be accompa-
nied by rewarding and encouraging the child [50]. At
an early age, before the eruption of the maxillary per-
manent incisors, the use of a vestibular barrier is often
very helpful. It is inserted between the teeth and lips,
possibly reducing the need for the sucking habit and
Orthodontic Knowledge and Practice for the Pediatric Dentist
241 11

a b

..      Fig. 11.49 a Similar abnormality as in . Fig. 11.48. b, c In this ing the canine to a lateral incisor and buildup of the left lateral inci-
case, orthodontic movement of the right canine in the place of the sor with composite resin
missing lateral incisor was preferred to a prosthetic solution. Reshap-

a b

c d e

..      Fig. 11.50 a, b Eruption failure of the maxillary left central inci- with correct occlusion of the incisor. The high cervical gingival line
sor is due to a mesiodens in a 9-year-old girl. c, d Its surgical removal with reduced attached gingival requires gingivoplasty
followed by orthodontic traction of the permanent incisor. e Result
 242 K. Park et al.
mainly aiming to prevent tongue thrust during swallow-
ing (. Fig. 11.52). A fixed habit cessation appliance
bypasses the issue of compliance, but it is only advised
in cases where the child wants to stop the habit [51]. It
consists of two bands cemented to the molars and a wire
arch with grid that obstructs thumb entry into the mouth
(. Fig. 11.53). It must not interfere with occlusion and
..      Fig. 11.51 Severe infraocclusion of the second permanent molar
11 in an adult. Its ankylosis has occurred in childhood, possibly by
trauma to its periodontium during extraction of the adjacent first
permanent molar
a b
c d
..      Fig. 11.52 a Severe anomaly at the vertical plane (open bite) due to prolonged use of pacifier. b, c Commercial appliance and its use after
habit cessation for prevention of tongue thrust. d Very significant improvement in occlusion after 6 months
be painless, and its use should not expose the mouth to
potential injuries.
11.2.3.2  he Position of the Tongue at
T
Swallowing
Abnormal positioning of the tongue while swallow-
ing has in the past been referred to as infantile swal-
low, reverse swallow, or tongue thrust and has been
associated with the emergence of anterior open bite. It
is natural for infants to swallow with the mouth open,
that is without occluding, with the tongue positioned
between any teeth present and not coming into contact
with the palate. Upon completion of the primary den-
tition, infantile swallowing is replaced by adult swal-
lowing patterns, during which the tongue movement is
more complex. There are cases however where infantile
swallow persists and the tongue protrudes through the
anterior teeth, causing anterior open bite and/or other
dental abnormalities [52]. In the case of preexisting
open bite, the abnormal position of the tongue when
swallowing might be an adaptive movement, and the
problem that originally caused the open bite should be
addressed first.
Tongue thrusting may be quite prevalent in the mixed
dentition, up to 40% in some communities [53, 54]. In
many cases, tongue thrusting can be related to breath-
ing disorders, namely, tonsil hypertrophy and chronic
Orthodontic Knowledge and Practice for the Pediatric Dentist
243 11

a b

c d

..      Fig. 11.53 a Anterior open bite through persistent harmful sucking of thumb in the primary and mixed dentition. b Treatment by fixed
appliance for habit cessation. c, d Intermediate and final result before any further orthodontic intervention

mouth breathing. The participation of the tongue in
this functional imbalance of the oral musculature can
lead to the creation or increase of Angle Class II mal-
occlusion. The first treatment step for this disorder is
orofacial-­myofunctional therapy. Specifically, the young
patient should perform normal swallowing exercises at
regular periods of time throughout the day. An appli-
ance that obstructs tongue thrusting, similar to the type
used to stop thumb-sucking, could also be used.
11.2.3.3 Mouth Breathing
Mouth breathing and its relation to the emergence of
orthodontic abnormalities is a complex issue, because
it is hard to distinguish between exclusively mouth
breathers and nose breathers in the various studies. It is
believed that all people go through phases of nose and
mouth breathing during the day [55]. There is a weak
correlation between mouth breathing and the existence
of abnormalities that, together, constitute the so-called
“adenoid faces” (. Fig. 11.54). Characteristics include
an oblong face with an increased lower anterior height,
short or toneless lip, and maxillary/mandibular inci-
sor protraction. The existence of the aforementioned
abnormalities does not automatically justify surgi-
cal intervention in the adenoids or the nasal conchae,
since these characteristics can appear without the coex-
istence of mouth breathing [52]. In this case, the goal
of orthodontic treatment should be addressing patient’s
occlusal problems, while referral to an otolaryngologist
at the same time is considered pertinent so potential
problems can be diagnosed and the method and time of
action decided upon.
11.2.3.4 Nail-Biting
Nail-biting is a rare habit before ages 3–6 years. It has
been suggested that this habit is related to stress and
low self-esteem and that its frequency increases around
puberty. Chronic nail-biting does not cause disorders
in occlusion but is considered responsible for the wear-
ing of incisal edges and the appearance of small enamel
cracks, particularly in the maxillary incisors. Wire appli-
ances have been proposed to help onychophagic young
persons manage their chronic habit [56]. Some children
have the habit of biting pencils and other objects which,
if of a chronic nature, may have some effect on the posi-
tion of the involved teeth.
11.2.3.5 Lip Sucking
Sucking of the lip is easy to discern, since the lips and
some of the perioral skin of children who have this
habit are red and appear inflamed. Although this habit
does not have serious consequences for the teeth, it can
contribute to the maintaining of a preexisting occlusal
abnormality, especially if this habit takes place often, is
done intensely, and lasts long. Sucking of the lower lip
and its interference while swallowing may increase labial
 244 K. Park et al.
..      Fig. 11.54 a Characteristic
a b
“adenoid face” with chronic
mouth breathing. b Occlusal
anomaly of the dental arches. c
Tongue thrusting at swallowing
a b
11
..      Fig. 11.55 Occlusal anomaly with excessive overjet and overbite. Folding due to interference of the lower lip of the same patient while
the teeth are in occlusion at swallowing
inclination of the maxillary incisors as well as lingual
inclination of the mandibular incisors, thus contributing
to increased anterior overjet (. Fig. 11.55).
References
1. Al-Abdallah M, AlHadidi A, Hammad M, Dar-Odeh N. What
factors affect the severity of permanent tooth impaction? BMC
Oral Health. 2018;18(1):184. https://doi.org/10.1186/s12903-­
018-­0649-­5.
2. Brin I, Becker A, Shalhav M. Position of the maxillary perma-
nent canine in relation to anomalous or missing lateral incisors:
a population study. Eur J Orthod. 1986;8:12–6.
3. Ericson S, Kurol J. Radiographic examination of ectopically
erupting maxillary canines. Am J Orthod Dentofac Orthop.
1987;91:483–92.
4. Ngo CTT, Fishman LS, Rossouw PE, Wang H, Said O. Correla-
tion between panoramic radiography and cone-­beam computed
tomography in assessing maxillary impacted canines. Angle
Orthod. 2018 Jul;88(4):384–9. https://doi.org/10.2319/103117-
­739.1.
5. Jung YH, Liang H, Benson BW, Flint DJ, Cho BH. The assess-
ment of impacted maxillary canine position with panoramic
radiography and cone beam CT. Dentomaxillofac Radiol. 2012
Jul;41(5):356–60. https://doi.org/10.1259/dmfr/14055036.
6. Kim Y, Hyun HK, Jang KT. The position of maxillary canine
impactions and the influenced factors to adjacent root resorp-
tion in the Korean population. Eur J Orthod. 2012;34:302–6.
7. Liu DG, Zhang WL, Zhang ZY, Wu YT, Ma XC. Localization
of impacted maxillary canines and observation of adjacent inci-
sor resorption with cone-beam computed tomography. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2008;105:91–8.
8. Fernandez E, Bravo LA, Canteras M. Eruption of the perma-
nent upper canine: a radiologic study. Am J Orthod Dentofac
Orthop. 1998;113:414–20.
Orthodontic Knowledge and Practice for the Pediatric Dentist
9. Sajnani AK, King NM. Diagnosis and localization of impacted
maxillary canines: comparison of methods. J Investig Clin Dent.
2013;4:252–6.
10. Baccetti T, Sigler LM, McNamara JA Jr. An RCT on treatment
of palatally displaced canines with RME and/or a transpalatal
arch. Eur J Orthod. 2011;33:601–7.
11. McConnell TL, Hoffman DL, Forbes DP, Janzen EK, Wein-
traub NH. Maxillary canine impaction in patients with trans-
verse maxillary deficiency. ASDC J Dent Child. 1996;63:190–5.
12. Jang SY, Park K. Rapid palatal expansion for the treatment of
an ectopically erupting maxillary canine: case reports. J Korean
Acad Pediatr Dent. 2010;37:472–80.
13. Kanomi R, Deguchi T, Kakuno E, Takano-­Yamamoto T, Rob-
erts WE. CBCT of skeletal changes following rapid maxillary
expansion to increase arch-length with a development-dependent
bonded or banded appliance. Angle Orthod. 2013;83:851–7.
14. Tulloch JF, Proffit WR, Phillips C. Outcomes in a 2-phase ran-
domized clinical trial of early Class II treatment. Am J Orthod
Dentofac Orthop. 2004;125:657–67.
15. Dolce C, Schader RE, McGorray SP, Wheeler TT. Centrographic
analysis of 1-phase versus 2-phase treatment for Class II maloc-
clusion. Am J Orthod Dentofac Orthop. 2005;128:195–200.
16. O'Brien K, Wright J, Conboy F, Appelbe P, Davies L, Connolly
I, et al. Early treatment for Class II Division 1 malocclusion
with the Twin-block appliance: a multi-­center, randomized, con-
trolled trial. Am J Orthod Dentofac Orthop. 2009;135:573–9.
17. Proffit WR. The timing of early treatment: an overview. Am J
Orthod Dentofac Orthop. 2006;129:S47–9.
18. Baik HS, Jee SH, Lee KJ, Oh TK. Treatment effects of Frankel
functional regulator III in children with class III malocclusions.
Am J Orthod Dentofac Orthop. 2004;125:294–301.
19. Franchi L, Baccetti T, Tollaro I. Predictive variables for the out-
come of early functional treatment of Class III malocclusion.
Am J Orthod Dentofac Orthop. 1997;112:80–6.
20. Baccetti T, Franchi L, McNamara JA Jr. Cephalometric vari-
ables predicting the long-term success or failure of combined
rapid maxillary expansion and facial mask ­therapy. Am J Orthod
Dentofac Orthop. 2004;126:16–22.
21. Moon YM, Ahn SJ, Chang YI. Cephalometric predictors of
long-term stability in the early treatment of Class III malocclu-
sion. Angle Orthod. 2005;75:747–53.
22. Choi HJ, Kim JY, Yoo SE, Kwon JH, Park K. Cephalometric
characteristics of Korean children with Class III malocclusion
in the deciduous dentition. Angle Orthod. 2010;80:86–90.
23. Dean JMR, Avery D. Management of the developing occlusion.
In: Dentistry for the child and adolescent. 8th ed. St. Louis:
Mosby; 2004. p. 626–83.
24. Christensen JR, Fields HW. Orthodontic treatment in the pri-
mary dentition. In: Pinkham JR, Fields HW, McTigue DJ, edi-
tors. Pediatric dentistry. Infancy through adolescence. 3rd ed.
Philadelphia: Saunders; 1999. p. 440–61.
25. Kurol J, Rasmussen P. Occlusal development, preventive and
interceptive orthodontics. In: Koch G, Poulsen S, editors. Pedi-
atric dentistry. A clinical approach. Copenhagen: Blackwell-
Munksgaard; 2001. p. 322–48.
26. Tunc ES, Bayrak S, Tuloglu N, Egilmez T, Isci D. Evaluation
of survival of 3 different fixed space maintainers. Pediatr Dent.
2012;34:e97–102.
27. Borrie F, Bearn D. Early correction of anterior crossbites: a sys-
tematic review. J Orthod. 2011;38:175–84.
28. Lindner A. Longitudinal study on the effect of early interceptive
treatment in 4-year-old children with unilateral cross-bite. Scand
J Dent Res. 1989;97:432–8.
29. Thilander B, Wahlund S, Lennartsson B. The effect of early
interceptive treatment in children with posterior cross-bite. Eur
J Orthod. 1984;6:25–34.
245 11
30. Macena MC, Tornisiello Katz CR, Heimer MV, de Oliveira e
Silva JF, Costa LB. Space changes after premature loss of decid-
uous molars among Brazilian children. Am J Orthod Dentofac
Orthop. 2011;140:771–8.
31. Park K, Jung DW, Kim JY. Three-dimensional space changes
after premature loss of a maxillary primary first molar. Int J Pae-
diatr Dent. 2009;19:383–9.
32. Tunison W, Flores-Mir C, ElBadrawy H, Nassar U, El-Bialy
T. Dental arch space changes following premature loss of pri-
mary first molars: a systematic review. Pediatr Dent. 2008;30:
297–302.
33. Watt E, Ahmad A, Adamji R, Katsimpali A, Ashley P, Noar
J. Space maintainers in the primary and mixed dentition – a clin-
ical guide. Br Dent J. 2018;225(4):293–8. https://doi.org/10.1038/
sj.bdj.2018.650.
34. Kharbanda O, Dando J, Fricker J, Jayasekera T. Orthodontic
diagnosis and treatment in the mixed dentition. In: Cameron
AC, Widmer RP, editors. Handbook of pediatric dentistry. 2nd
ed. New York: Mosby; 2003. p. 287–321.
35. Proffit WR, Ackerman JL. Orthodontic diagnosis: the devel-
opment of a problem list. In: Proffit WR, Fields HW, editors.
Contemporary orthodontics. 3rd ed. St Louis: Mosby; 2000.
p. 147–95.
36. Moyers RE. Handbook of orthodontics. In: Moyers RE, editor.
Handbook of orthodontics. Chicago: Yearbook Medical Pub-
lishers; 1988. p. 369–79.
37. Tanaka MM, Johnston LE. The prediction of the size of
unerupted canines and premolars in a contemporary orthodon-
tic population. J Am Dent Assoc. 1974;88:798–801.
38. Staley RN, Kerber PE. A revision of the Hixon and Oldfather
mixed-dentition prediction method. Am J Orthod. 1980;78:
296–302.
39. Casamassimo PS, Christensen JR, Fields HW. Examination,
diagnosis and treatment planning. In: Pinkham JR, Fields HW,
McTigue DJ, editors. Pediatric dentistry infancy through adoles-
cence. 3rd ed. Philadelphia: Saunders; 1999. p. 446–74.
40. Koroluk LD, Tulloch JF, Phillips C. Incisor trauma and early
treatment for Class II Division 1 malocclusion. Am J Orthod
Dentofac Orthop. 2003;123:117–25; discussion 25–6.
41. Harrison JE, Ashby D. Orthodontic treatment for posterior
crossbites. Cochrane Database Syst Rev. 2001;(8):CD000979.
42. Yaseen SM, Naik S, Uloopi KS. Ectopic eruption – a review and
case report. Contemp Clin Dent. 2011;2:3–7.
43. Fleming PS. Need for further clarity on optimal approach to
ectopic canines. Evid Based Dent. 2012;13:81.
44. Parkin N, Benson PE, Shah A, Thind B, Marshman Z, Glenroy
G, et al. Extraction of primary (baby) teeth for unerupted pala-
tally displaced permanent canine teeth in children. Cochrane
Database Syst Rev. 2009;(2):CD004621.
45. Kokich VG. Managing orthodontic restorative treatment for
the adolescent patient. In: McNamara JA, Bruton WL, editors.
Orthodontics and dentofacialorthopedics. Ann Arbor: Need-
ham Press; 2001. p. 423–52.
46. Christensen JR, Fields HW. Treatment planning and manage-
ment of orthodontic problems. In: Pinkham JR, Fields Jr HW,
McTigue DJ, editors. Pediatric dentistry infancy through adoles-
cence. 3rd ed. Philadelphia: Saunders; 1999. p. 608–48.
47. Shah A, Gill DS, Tredwin C, Naini FB. Diagnosis and manage-
ment of supernumerary teeth. Dent Update. 2008;35:510–2,
514–6, 519–20.
48. Shen Z, Zou CC, Yang RW, Zhao ZY. Cleidocranial dyspla-
sia: report of 3 cases and literature review. Clin Pediatr (Phila).
2009;48:194–8.
49. Sletten DW, Smith BM, Southard KA, Casko JS, Southard
TE. Retained deciduous mandibular molars in adults: a radio-
 246 K. Park et al.
graphic study of long-term changes. Am J Orthod Dentofac
Orthop. 2003;124:625–30.
50. Huang B, Lejarraga C, Franco CS, Kang Y, Lee A, Abbott J,
Takahashi K, Bessho K, Pumtang-on P. Influence of non-orth-
odontic intervention on digit sucking and consequent anterior
open bite: a preliminary study. Int Dent J. 2015;65(5):235–41.
https://doi.org/10.1111/idj.12178.
51. Madiraju GS, Harika L. Effectiveness of appliance therapy in
reducing overjet and open bite associated with thumb sucking
habit. Minerva Stomatol. 2011;60(7–8):333–8.
52. Christensen JR, Fields HW, Adair SM. Oral habits. Ch. 26. In:
Casamassimo PS, Fields Jr HW, McTigue DJ, Nowak AJ, edi-
tors. Pediatric dentistry. Infancy through adolescence. 5th ed.
Philadelphia: Elsevier, St. Louis; 2013. p. 385–92.
11
53. Agrawal S, Koirala B, Dali M, Shrestha S, Bhagat T, Niraula
SR. Prevalence of oral habits of schoolchildren in the mixed den-
tition in Dharan, Nepal. J Dent Child (Chic). 2019;86(2):88–92.
54. Jalaly T, Ahrari F, Amini F. Effect of tongue thrust swallowing
on position of anterior teeth. J Dent Res Dent Clin Dent Pros-
pects. 2009;3(3):73–7. https://doi.org/10.5681/joddd.2009.019.
55. Warren DW, Hairfield WM, Dalston ET. Effect of age on nasal
cross-sectional area and respiratory mode in children. Laryngo-
scope. 1990;100:89–93.
56. Marouane O, Ghorbel M, Nahdi M, Necibi A, Douki N. New
approach to managing onychophagia. Case Rep Dent.
2016;2016:5475462. https://doi.org/10.1155/2016/5475462.
 247 12

Dental Caries Prevention

in Children and Adolescents
Nikolaos Kotsanos, Rosalyn Sulyanto, and Man Wai Ng

Contents

12.1 Dental Caries in Children and Adolescents – 248

12.1.1  athogenesis of Dental Caries – 248
P
12.1.2 Epidemiology and Treatment Needs – 252
12.1.3 Clinical Manifestation of Caries – 252
12.1.4 Caries Diagnosis and Record Keeping – 254
12.1.5 Caries Risk and Treatment Strategies – 259

12.2 Therapeutic Measures for Caries Control – 262

12.2.1 F luorides and Medicinal Means – 262
12.2.2 Dental Plaque Removal – 268
12.2.3 Pit and Fissure Sealants – 270
12.2.4 The Diet – 273
12.2.5 Patient Motivation and Recalls – 274

References – 277

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_12
 248 N. Kotsanos et al.
12.1  ental Caries in Children
D 12.1.1.1
and Adolescents
12.1.1 Pathogenesis of Dental Caries
Dental caries is the most common chronic disease of
childhood. After decades of research on the pathogene-
sis of caries, the “chemo-parasitic” theory, first proposed
by Miller at the end of the nineteenth century, prevailed
in the 1950s as the most acceptable one. Dental caries
is an infectious disease caused by oral microorganisms
[1]. In order for a tooth to become affected by caries,
adherence of mature dental plaque (intraoral biofilm)
to a tooth surface is required. Dental plaque harbors
a plethora of microorganisms (bacteria) on the tooth
surface (host). These microorganisms thrive on ferment-
able carbohydrates (substrate), producing organic acids
which in turn influence plaque in terms of its acidogenic
and acidophile synthesis. This is known as the “ecologi-
cal plaque hypothesis.” [2].
The composition and metabolic activity of microor-
ganisms in the biofilm, by the duration over which acids
remain on the tooth-plaque interface, affect the min-
eral balance of the hard tissues with their liquid envi-
ronment toward de- or remineralization. Contributing
factors include thickness/maturation of dental plaque,
frequency of exposure to fermentable carbohydrates
12 (pH drops), developmentally defective dental tissues,
reduced salivary flow and buffer capacity, and inad-
equate exposure to fluoride. Such factors may prolong
the effects of the acids responsible for tilting the balance
toward demineralization and create active disease condi-
tions. It is accepted that caries is a multifactorial disease,
in which many environmental, genetic, and behavioral
risk factors interact [3]. Arresting the caries process
(remineralization) can be achieved by controlling some
or most of the factors responsible for its activity.
Overview
The following factors are important determinants of
caries activity and progression:
55 Fermenting bacteria – mature (thick) dental plaque
55 Diet – frequent exposure to fermentable carbohy-
drates
55 Dental enamel – e.g., developmentally prone to
breakdown or hypoplastic
55 Chemotherapeutic agents – e.g., exposure to fluo-
ride
55 Host defense – e.g., saliva buffering capacity,
unspecified genetically mediated
55 Socioeconomic factors – affecting behavior, priori-
ties, means
The Physicochemical Process
Unlike in erosion or etching, carious dissolution of
enamel occurs in the subsurface, always under a thick
layer of biofilm (usually of several hundred microm-
eters). Organic acids (mainly lactic) are produced as
metabolic byproducts by the microorganisms. When
the pH in the biofilm-tooth interface has fallen below
a critical level of 5.2–5.7, dissolution of the ion compo-
nents of the apatite (Ca6[PO4]3[OH]2) undermines crys-
talline structure integrity. The resulting porous, partially
demineralized enamel loses its natural transparency and
appears chalky, i.e., as a “white spot” (. Fig. 12.1).
The enamel surface zone however is not critically
affected because de- and remineralization cycles pre-
serve it while chemical dissolution progresses into
deeper enamel. This is primarily owed to its continuous
repair by redeposition of dissolved mineral from deeper
enamel and/or from the biofilm reservoir when plaque
pH rises again above the critical level [4] (. Fig. 12.2).
Later, only after the carious lesion front has advanced
into the dentin, the relatively intact but insufficiently
supported surface zone collapses, resulting in a cavi-
tated lesion (. Fig. 12.3). Thus, during the early stage,
caries affecting the enamel is a physicochemical process
(demineralization), whereas cavitation is a late stage that
is caused by mechanical stresses.
Demineralization tends to follow anatomical path-
ways, enamel prisms, and dentinal tubules (. Figs. 12.3
and 12.4). If responsible caries risk factors have not
been addressed prior to cavitation, caries progression
toward the dentin includes proteolytic processes tak-
ing place in the presence of higher pH levels than those
required for demineralization. Effective biofilm removal
from inaccessible cavities is not possible through every-
day oral hygiene practices; therefore caries progression
becomes difficult to control. Exceptions may be shallow
cavitated lesions in accessible tooth surfaces (e.g., buc-
cal surfaces); these may be easily arrested by rigorous
plaque removal. Otherwise, restoring the tooth anatomy
with a biocompatible material allows again adequate
cleaning of all tooth surfaces.
12.1.1.2 Caries Microbiology
According to the “ecological plaque hypothesis,” plaque
is a structurally and functionally organized biofilm [2].
It is formed in an orderly way, and, in a healthy mouth,
it remains relatively stable (in a state of microbial
homeostasis) containing low amounts of potentially
pathogenic species of microorganisms. In an active dis-
ease state, a shift occurs whereby acid-producing and
acid-tolerant microorganisms become dominant in the
plaque. Many microorganisms, in particular Streptococci
and Lactobacilli, but also Diphtheroids, some fungi, and
Staphylococcus can produce enough acids to demineral-
ize hard dental tissues. Streptococcus mutans, which has
Dental Caries Prevention in Children and Adolescents
249 12
a

..      Fig. 12.1 a A proximal caries lesion in a mandibular first permanent molar seen after the extraction of the second primary molar. b Col-
lapsing of the superficial enamel zone allows retention of plaque in the small cavity

a b

..      Fig. 12.2 a Microradiograph of an enamel section with a small caries lesion with relatively intact surface zone. b Mapping of mineral loss
percentages in the various zones in the same lesion.

great acid-producing capacity, is considered the most

cariogenic of microorganisms and has been studied
more than any other bacterial species [5]. Streptococcus
sobrinus and Lactobacilli are also important pathogens
[6]. Streptococcus mutans and Lactobacilli are most
often the microbiological focus of clinical studies on
early childhood caries. However, the microbiota of car-
ies-associated biofilms is recognized to contain a wide
variety of bacteria [7].
In infants and preschool children, colonization of
dental plaque by Streptococcus mutans in newly erupted
primary teeth has been associated with the risk of caries
development. The earlier the colonization, the greater
the risk of severe-early childhood caries (S-ECC) [8].
Transmission of this microorganism frequently follows
a mother-to-child route (. Fig. 12.5) [9]. Effectively
controlling the mother’s levels of Streptococcus mutans
..      Fig. 12.3 Direction of progression of relatively small proximal
can delay its colonization to the child’s teeth.
carious lesions to the pulp in a permanent molar
 250 N. Kotsanos et al.
a b
..      Fig. 12.4 a Transmission electron microscope view of trans-
versely cut carious enamel which shows dissolution of crystals inside
the prisms. ×3,000. b Image of cut carious dentin by the same tech-
nique shows the demineralized collagen fibers and the presence of
bacteria in the enlarged dentinal tubules. ×5,000
12
..      Fig. 12.5 Usual way of oral microflora transmission from
mother to child
12.1.1.3 Other Caries Risk Factors
Saliva
The presence of normal salivary flow in and around the
biofilm is critical to maintaining good dental health.
Individuals who have significantly reduced salivary lev-
els are at high risk for developing dental caries. Many
qualitative and quantitative components of saliva have
been investigated regarding their effects on dental caries.
Factors such as buffer capacity, flow rate, fluoride level,
secretory levels of immunoglobulin IgA antibodies, per-
oxidase, hypothiocyanite ions, and adhesins are associ-
ated with an increased risk of dental caries [10]. In terms
of salivary flow, there is a difference between the rate
of unstimulated and stimulated flow. Stimulated saliva
is secreted after a chemical or mechanical stimulus, e.g.,
chewing gum. Less than 0.1 ml/min for unstimulated
and 0.5 ml/min for stimulated saliva are considered
reduced flow rates [11]. Examples of the consequences
of reduced salivary flow rate are the following:
1. During sleep, salivary flow is significantly reduced.
While milk is not considered cariogenic, frequent
intake by infants and toddlers from breast or the
nursing bottle during sleep, when salivary flow is
reduced, in the absence of effective toothbrushing
may lead to a rampant form of early childhood car-
ies, affecting the maxillary incisors and other teeth
sequentially as they erupt.
2. Severely reduced salivary flow rate after head and
neck radiation often results in rapid initiation and
progression of dental caries if appropriate preventive
measures are not implemented [12]
Socioeconomic Status
Children living in poverty have twice the rate of dental
caries compared to children living in more affluent fami-
lies. This disparity in caries rates continues through until
adulthood, although the differences dissipate in older age
groups [13]. There is also evidence that children of minor-
ity groups experience higher caries rates and unmet treat-
ment needs compared to national average [14]. Moreover,
in many areas of the world, minority children are more
likely to lack dental insurance coverage.
Tooth Morphology and Structure
The most common structural enamel defect is charac-
terized by defective mineralization of the first perma-
nent molars. This condition is currently termed molar
incisor hypomineralization (MIH) and it affects chil-
dren worldwide. Parts of the enamel being brittle due
to its porous structure, result in breakdown, being very
susceptible to rapid caries development (. Fig. 12.6).
It was estimated in one such study that the percent-
age of adolescents presenting with enamel breakdown
exceeded 7% [15]. These teeth require frequent moni-
toring for possible restorative treatment, and it should
be recognized that are often highly sensitive and diffi-
cult to fully anesthetize. The condition is also common
to primary molars, mainly the second ones, leading to
gross atypical cavitation in many cases of preschoolers.
Hypomineralized and hypoplastic areas such as deep
pits are often found in a variety of teeth, more often
molars, predisposing to caries as being impossible to
access during everyday oral hygiene practices.
Tooth Arrangement in the Dental Arch
Crowding of the dentition leads to greater plaque
retention and complicates the ability to maintain oral
hygiene, thereby increasing the risk of dental caries
and periodontal disease. However, there is inadequate
scientific evidence to support these empirical observa-
tions.
Dental Appliances and Restorations
Orthodontic and prosthetic appliances, both fixed
and removable, increase plaque retention and the risk
of dental caries. The most caries-prone tooth sites
are around the orthodontic brackets of anterior teeth
(. Fig. 12.7). Patients who are already high caries risk
prior to orthodontic treatment are in greatest risk dur-
ing treatment. They require intense supervision for
Dental Caries Prevention in Children and Adolescents
a b
..      Fig. 12.6 a First permanent molar with MIH showing break-
down of brittle enamel that is prone to caries formation. b The car-
ies-free dental arch of a 21-year-old who has a cariogenic diet and
b c
..      Fig. 12.7 a Primary caries lesions detected immediately after
removal of orthodontic brackets from the upper lateral incisors and
canines. b Unusual caries presentation at the incisal edges of the
lower incisors due to orthodontic retainers worn for two years with-
proper oral hygiene and monitoring of effective plaque
control, frequent home fluoride use, and professional
fluoride varnish applications [16]. Defective restora-
tions with interproximal overhangs increase plaque
retention thereby increasing the risk of caries, gingivitis,
and periodontal disease (. Fig. 12.8). Simply restor-
ing carious lesions does not lead to the reduction of
microbial load [17]. Consequently, whenever a patient
requires restoration(s), a rigorous risk-based preventive
plan should be adjunct to support the restorative treat-
ment plan.
251 12
average oral hygiene habits. He is likely the beneficiary of protective
hereditary salivary factors, good tooth anatomy, and lack of dental
arch crowding
out proper oral hygiene. c. Same patient as in b. Demineralized
enamel around the removed orthodontic brackets shows through the
transparent retainer in maxillary anterior teeth
Hereditary Factors
Hereditary (genetic) factors are often confused with
familial (environmental) factors that are responsible
for dental caries. This can lead to patients and parents
assuming fatalistic attitudes toward caries, especially in
the primary dentition. Genetics influences the arrange-
ment of teeth in the arch and in the expression of defense
mechanisms through the saliva as a vehicle [18], such as
secretory immunoprotein SIgA [19]. However, genetic
factors are not thought as important as environmental
factors in the prevention or control of caries.
 252 N. Kotsanos et al.
..      Fig. 12.8 Severely defective restorations on primary and perma-
nent molars. They were placed without the benefit of a radiographic
evaluation
12.1.2 Epidemiology and Treatment Needs
A number of researchers have found that children of
lower-income families are more likely to have early
childhood caries [20, 21]. For example, only 10% of 3-
to 6-year-olds enrolled in private kindergartens experi-
12 enced dental caries with an average dmfs index of 0.4,
compared to 23% and 1.3 respective caries values of
those enrolled in state-funded kindergartens [20]. Other
family stressors, such as divorce, having a parent in jail,
and exposure to neighborhood violence, have also been
predictive of caries; furthermore, greater numbers of
stressors are associated with increased risks for caries or
other dental problems [21]. Therefore, emphasizing the
impressive generalized decrease in caries rates of chil-
dren in the industrialized world, i.e., for 12-year-olds
between now and several decades ago, should not take
the focus away from the extent and severity of this per-
sistent disease of childhood in some societal strata or
in less privileged countries worldwide. Control of dental
caries in young children remains an intractable problem,
despite the great progress in scientific knowledge about
prevention. Families, especially those of low socioeco-
nomic status lack knowledge or motivation. Pediatric
dentists should closely monitor children of low-income
families and families experiencing other stressors, as
well as counsel families on sound oral health practices,
to try to minimize the development of caries in these
at-­risk children.
Although preventive measures in most countries, either
in home care or professionally applied, have contributed
to caries reduction in children, a significant number of
children in industrialized countries require restorative
dental treatment. For example in Germany before the
turn of the century, 40–50% of decayed primary teeth of
6- and 7- year-old children had untreated dental caries
[22]. In the United States, the national 2011–2012 survey
showed that 23% of 2- to 5-year-olds had caries, with
approximately 10% left unrestored. In 6- to 8-year-olds,
approximately 56% and 14% had caries in their primary
teeth and permanent teeth, respectively. Variations were
found in caries rates by race and ethnicity. Among 6- to
11-year-olds, 27% of Hispanic children had dental car-
ies in their permanent dentition as compared with 18%
of non-Hispanic white and Asian children. Unrestored
cavities in primary teeth for 2- to 8-year-olds were twice as
high for Hispanic and non-­Hispanic black children com-
pared with non-Hispanic white children [23].
12.1.3 Clinical Manifestation of Caries
In childhood and adolescence, dental caries almost
always initiates on enamel surfaces, as root surfaces are
not normally exposed in the oral cavity. The partially
demineralized primary enamel lesion appears opaque
white because the refractive index of the salivary con-
tent of its pores (water RI = 1.33) differs from that of
sound enamel (RI = 1.62). By drying the lesion with the
air syringe (air RI = 1.0), the contrast with surrounding
normal, translucent, enamel increases. Further, in case
of active carious lesions in areas of plaque retention and
reduced salivary flow, the white surface remains opaque
by the prevailing demineralization. If the plaque is not
frequently supplied with carbohydrates or the lesion
surface is kept plaque-free, it becomes glossy due to
prevailing remineralization. More often in occlusal pits
and fissures, influx of organic substances from saliva
and protein denaturation makes these initial lesions or,
sometimes the advanced too, appears stained very dark
(. Fig. 12.9).
Overview
Demineralized enamel surfaces (early carious lesions)
are commonly found in areas of plaque retention and
reduced salivary flow:
1. Pit, fissures, or other anatomical defects of enamel
2. Cervical smooth surface areas of teeth
3. Proximal surfaces, between gingival crest and the
contact areas
In the primary dentition, dental caries may initially show
a certain pattern, affecting primarily one of the surface
categories shown in the overview box, and later spread
Dental Caries Prevention in Children and Adolescents
a b
c d
..      Fig. 12.9 Early caries in clinical terms, a in pits and fissures of
primary molars, b at the cervical third of labial surfaces of mixed
dentition anterior teeth, c in the proximal surface of a second pri-
mary molar. d Demineralization is around and below the contact
to more categories. The diagnosis of early dentinal caries
affecting proximal surfaces of both the primary and per-
manent dentitions is possible from bitewing radiographs.
There are some predisposing factors which can critically
affect the clinical pattern of caries. Most common in the
permanent teeth are developmental defects such as MIH
and gross plaque retention around orthodontic brackets
(. Figs. 12.6 and 12.7). Hypomineralized second pri-
mary molars (HSPM) is another common factor in the
primary dentition, leading to atypical carious cavities
and atypical restorations (see 7 Chap. 17).
12.1.3.1 Severe Forms of Active Caries
Sometimes the de−/remineralization balance shifts
intensely toward demineralization resulting in the rapid
progression of caries. This rampant form of caries may
be equated with dental cleaning neglect and depending
on the patient’s age is an own responsibility or such of
the parent/guardian. Rapidly progressing caries may
appear at any age. S-ECC is a term used for the preschool
age, [24] it is quite widespread in lower socioeconomic
populations, and its treatment is discussed in the next
chapter. Rapidly progressing caries during adolescence
(. Fig. 12.10) is of particular concern. The diet of the
adolescents with often excessive soft drink consump-
tion, at a time when parental control weakens and peer
influence increases, may intensify the carious challenge
especially when they abstain from oral hygiene. Another
aggressive form of caries caused by severe salivary gland
253 12
e
area (ε), coinciding with the areas of plaque retention, e erythrosine-
dyed dental plaque on the pits and fissures of a first permanent
molar after brushing explains why these sites are prone to caries
malfunction may occur as a side effect of head and neck
radiotherapy. In all these forms of rapidly progressing
caries, caries activity is at its highest.
12.1.3.2 Arrested Caries
Small carious lesions are easy to arrest, primarily with
effective plaque removal. In some cases of advanced
chiefly occlusal cavitated lesions, more often in primary
molars, arrest may come as a natural phenomenon. The
enamel walls may break down resulting to an opened cav-
ity exposing the carious dentin to the oral environment
and thus presenting an opportunity to become arrested.
Demineralized dentin becomes ebony hard and very
dark in color by wear/remineralization (. Fig. 12.11).
The discoloration is owed to protein denaturation of the
partially demineralized dentin along with further degra-
dation of exogenous organic matter absorbed into the
porous dental tissues. Darkening of the enamel or the
dentin generally indicates a very slow mineral loss pro-
cedure or caries arrest.
Restoration of primary teeth with arrested carious
lesions may not be necessary except for the purpose
of improving aesthetics. Having said that, caution is
required as caries active proximal surfaces may coexist.
Small, arrested carious lesions are much more common
in the pits and fissures of molars and their dark color
aids diagnosis. These require close follow-up because
they might not be fully arrested and in such cases, restor-
ative treatment is necessary (. Fig. 12.9e).
 254 N. Kotsanos et al.

12.1.4 Caries Diagnosis and Record Keeping i.e., hard dental tissue distraction, pain, and presence of
­dentoalveolar inflammation.
It becomes apparent that dental caries is a chronic In the past decades, there has been increased inter-
disease, usually progressive in nature. Historically, est in etiologically treating dental diseases. In the twen-
treatment of dental caries has been synonymous with tieth century caries was being recorded using an index
surgical treatment (restorative treatment, prosthet- known as DMF (decayed, missing, filled, tooth or sur-
ics, dental materials, implants). This, by itself, did not faces). In the beginning of the current century, atten-
address the disease process but merely its symptoms, tion became focused on documenting and monitoring
of initial caries lesions of enamel. Introduced in 2005,
the “International Caries Detection and Assessment
a System” (ICDAS) [25] is an index that was developed
to include recording of early caries of enamel and
clinically visible dentin caries, by stage of progression.
Particular attention was paid to recording and manage-
ment of discolored enamel fissures, including treatment
options based on disease activity. The treatment and
follow-up of caries was therefore based on a system with
relatively standardized diagnostic criteria. Another sim-
ilarly detailed caries classification system is the “Nyvad”
visual-tactile classification system devised to enable the
detection of the activity and severity of caries lesions
with special focus on low caries populations [26]. On the
b other end, as most caries in developing countries remains
untreated, there is an index to evaluate the clinical con-
sequences in oral structures. This PUFA index records
severely decayed teeth with visible pulpal involvement
(P/p), ulceration caused by dislocated tooth fragments
12 (U/u), fistula (F/f), and abscess (A/a) [27].

>>Important
..      Fig. 12.10 a Severe early childhood caries. b Very high caries
activity in a young adolescent, manifesting also as initial caries
(demineralization) in the interproximal surfaces of mandibular per-
manent incisors
The International Caries Detection and Assessment
System (ICDAS) advantages:
55 Monitoring of the progression and arrest of cari-
ous lesions
55 Assessment of the effectiveness of treatment and
disease management approaches
55 May be used in both clinical and epidemiological
caries research

a b c

..      Fig. 12.11 a Arrested caries in primary incisors. b Arrested carious “open cavity” in a second primary molar (possibly predisposed by
primary molar hypomineralization) planned to be restored based on patient’s request. c After its restoration with composite
Dental Caries Prevention in Children and Adolescents
12.1.4.1  iagnostic Techniques, Tools,
D later in this chapter. Monitoring disease progression is
and Appliances
Three basic diagnostic means have traditionally been in
use in dentistry for the detection of early caries lesions.
1. Direct Visualization
In most cases, direct visual observation is the basic diag-
nostic technique. Adequate diagnosis is only possible
on tooth surfaces that are accessible, dried, and free
of plaque. Additional aids may be necessary to ensure
accurate diagnosis. Proximal surfaces of tooth surfaces
that are in contact cannot be visualized directly, unless
a suitable orthodontic elastic ring is inserted for a few
days pushing teeth apart for 1 mm or so.
2. Tactile Sensation
Mainly on occlusal surfaces, tactile sensation with an
explorer can contribute to diagnosis in deep pit and fis-
sures and assure the need for sealing them. However,
exerting pressure by a sharp explorer, a favorable prac-
tice of the past, imposes the risk of breaking undermined
demineralized enamel surface (ICDAS II grade 2 or 3)
and causing an iatrogenic microcavity (. Fig. 12.12).
Although a blunt probe has been suggested, [25] a sharp
explorer used with caution may at times be useful, just
as it is in plaque removal from deep pits and fissures
prior to their sealing.
3. Radiographic Examination
The radiographic examination of caries provides infor-
mation on the presence and depth of lesions of the proxi-
mal and occlusal surfaces (. Fig. 12.13). The sensitivity
of the radiographic technique should be considered for
a diagnosis that is as accurate as possible, as explained
..      Fig. 12.12 Creation of iatrogenic microcavity is possible if the
hypomineralized fissure of this newly erupted first maxillary perma-
nent molar is carelessly examined with a sharp explorer
255 12
usually coded, e.g. by categorizing radiolucent lesion
depth as confined to the
55 D1: enamel
55 D2: outer third of the dentin
55 D3: middle third of the dentin
55 D4: inner third of the dentin
12.1.4.2 Relationship of Clinical,
Radiographic, and Histological
Examinations
Nonoperative diagnostic methods do not allow for
accurate assessment of the depth of caries lesions and,
in general, the clinical examination is the least accurate.
The actual depth could be evaluated only by a histologi-
cal examination of the hard tissues. Their relationship is
shown in . Fig. 12.14. Newer methods and techniques
are continuously investigated for improved diagnostic
sensitivity. Thus far, new technologies have only acces-
sory role in clinical practice [28].
12.1.4.3 Detection of Early Caries
Not uncommonly, occlusal caries may have extended
well into dentin despite the presence of an apparently
intact overlying enamel surface. This condition of “hid-
den caries” poses a diagnostic difficulty. It is thought
that the widespread access to fluoride often promotes the
preservation of the surface enamel over subsurface cari-
ous lesions. In fact, the philosophy of arresting the pro-
gression of early carious lesions is based on the necessity
of preserving an intact surface over the partially demin-
eralized “body of the lesion” (. Fig. 12.15). The thick-
ness of the surface zone and even the depth of carious
lesion are probably positively influenced by the preserva-
tion of the original enamel surface (. Fig. 12.16). This
is known to contain more fluoride than the subsurface
enamel especially at young age [29], and, as fluoride is
released, it possibly favors the remineralization process.
To enable remineralization and caries arrest, it is
important that caries is detected as early as possible. To
date, several detection techniques have been introduced,
and respective appliances marketed by the dental indus-
try, for assessing the depth of small carious lesions on
occlusal and proximal surfaces. As technology continu-
ously evolves, new diagnostic equipment will probably
be released in the years to come. Comparative studies
over the past two decades have found advantages and
disadvantages for use of these alternative techniques in
caries detection. Despite their potential usefulness, none
of these have so far been able to replace the traditional
means as main diagnostic tools [28].
 256 N. Kotsanos et al.
a b
c d
..      Fig. 12.13 a, b Bitewing radiographs of a 5-year-old child with
caries on proximal surfaces of the primary molars. D1 lesion in the
mesial of lower right second molar, D2 in the distal of lower right
first molar and the mesial of upper left second molar, D3 in the distal
of upper right first molar, and D4 in the distal of upper and lower
left first and mesial of lower left second molars (with pulpal involve-
ment in the lower left molars). c, d Bitewings of the permanent denti-
12
12.1.4.4 Alternative Diagnostic Technologies
for Carious Lesions
Digital Image Fiber-Optic Trans-illumination
(DIFOTI)
Diagnosis of caries is possible with use of an intense
light beam transmitted through optical fibers to ante-
rior or posterior teeth at a buccolingual dimension. In
a few European countries, fiber-optic trans-illumination
has been used in place of bitewing radiography for more
than three decades. Several studies have concluded
that this technique shows the same efficacy compared
to the clinical examination. This technology has been
advanced with the introduction of a digital display. The
observed image is recorded by a charge-coupled device
(CCD) technology digital camera which is then sent to
a computer for analysis (. Fig. 12.17). DIFOTI has a
similar sensitivity to conventional radiographs, but lags
behind in assessing the depth of the lesion into dentin
[30, 31]. It is a relatively new technique which has not yet
undergone sufficient clinical research testing.
Fluorescence Techniques
Laser/Light Fluorescence
This technology was developed for the detection and
quantitative assessment of lesions on occlusal or
tion from the same patient at 15 years of age. Caries lesions D1 in the
distal of lower left second and right first premolars, D2 in the distal
of upper right first premolar and mesial of upper right first molar,
D3 in the distal of upper left second premolar, and D4 in the distal
of upper left first premolar. Some surfaces present with superimposi-
tions. In both sets, occlusal caries lesions are not detected radio-
graphically
accessible smooth surfaces. An optical fiber carries
light from a diode laser of 655 nm wavelength to the
dental surface under testing (. Fig. 12.18). The latter
absorbs the light; the organic and inorganic elements are
stimulated to produce infrared fluorescence. The sub-
stances emitting fluorescence are porphyrins (bacterial
metabolic products). The fluorescence is transferred to
another optical fiber back into the device resulting in a
numerical display from 0 to 99. Values above
​​ 20 indicate
the existence of decayed hard tissue.
Several in vitro and in vivo studies show sig-
nificant sensitivity in caries detection by the
DIAGNOdent (KaVo Dental Co) and VistaProof
(Durr Dental) systems. They demonstrate very good
reproducibility of measurements on the occlusal
surface. The measurements are influenced by several
factors including:
55 Enamel dehydration from persistent air drying
55 Presence of calculus, plaque, or discolorations
55 Presence of pit and fissure sealants [32]
Despite having sufficiently good caries detection sen-
sitivity, these devices are not able to give an indication
of the depth of the carious lesions in the dentin. For
proximal surfaces a needle-end optical fiber is available
for use [33].
Dental Caries Prevention in Children and Adolescents
a b
d e
..      Fig. 12.14 a Periapical radiograph (taken in vitro) of a premolar
which has been extracted for orthodontic reasons. On the left proxi-
mal surface, a radiolucency is observed on the outer half of enamel
and slightly in the underlined dentine (D2). On the other proximal
surface there are no findings. b The former exhibits a minor break-
down of the superficial enamel c The latter presents a white spot.
Quantitative Light-Induced Fluorescence (QLF)
The laser source is replaced by a single light source sys-
tem and appropriate filters with the light transferred
through a liquid-containing cable (. Fig. 12.19). Digital
CCD technology and software is used for recording and
analyzing the signals. Compared to visual examination,
QLF has been found to detect more and smaller early
carious lesions, prior to cavitation [34]. Several studies
have shown a good instrument sensitivity for displaying
loss or gain of minerals, which may be useful in assessing
preventive measures applied to enhance remineralization.
Its drawbacks include its inability to reach interproximal
lesions and its slow speed for image analysis. Therefore,
QLF cannot be recommended for routine use in the den-
tal office setting. At present, cost/benefit ratio data are
lacking for both DIFOTI and QLF technologies.
Digital Radiography
The effort to reduce the emitted Röntgen radiation
led to the adoption of the most sensitive conventional
radiographic F speed film which demonstrated high
257 12
c
Both could not be clinically detectable (in situ). d In longitudinally
splitting the tooth the extent of the two lesions is visible. The front
of the cavitated lesion is well into the dentin e The front of the white
spot is limited in the enamel. The observed cracks in the dentin are
due to dehydration
diagnostic reliability compared to previously available
D and E films [35]. Since the 1990s however, digital radi-
ography has become increasingly used in clinical dental
practice because the emitted radiation is much lower
while the image production is almost immediate. Digital
sensors replace the analog films, replacing the need for
chemical developing and fixer solutions. The typical dig-
ital imaging systems use CCD technology or the storage
phosphor plate (SPP).
CCD Technology
The CCD sensor has a ceramic base (. Fig. 12.20),
which is divided into multiple picture elements (pix-
els). Upon exposure to radiation, electric charges cor-
responding to energy-bearing photons hitting the sensor
are generated in each pixel. The analog signal, once
converted to digital, is shown on the computer screen in
various shades of gray [36]. In pediatric dentistry, there
are two significant disadvantages to the CCD technol-
ogy: the thickness the CCD sensors, their cord, and their
high cost.
 258 N. Kotsanos et al.

a b

c d

..      Fig. 12.15 a Low magnification of a scanning electron micro-
scope photomicrograph showing perikymata and enamel rod ends
seen on the enamel surface of a newly erupted premolar crown. b
Part of A is further magnified to show the evident discontinuity of
12 the surface at a perikyma (arrows) which may represent weak points
in caries attack. c Longitudinal section of sound enamel in the polar-
izing microscope showing the ending of six striae of Retzius at the
respective six perikymata on enamel surface. d Similarly cut enamel
section with artificially created small caries lesion imbibed in water
(R.I. =1.33). The 6-lobe pattern of subsurface demineralization is
probably related to entry points at the merging of six perikymata

b c

..      Fig. 12.16 a Microradiograph of enamel cut perpendicularly to
the long axis of the tooth with an artificial “carious” enamel lesion
imitating the natural caries lesion. In the right part (flattened) the
surface zone of enamel had beforehand been ground away. The
lesion surface zone in this part is much thinner and the depth of
demineralization much greater than in the left part with original
enamel. b Absence of adequately remineralized surface zone in an
artificial carious created in one half of a 3rd molar which has been
surgically extracted from an adolescent before full enamel matura-
tion was accomplished. c Prior exposure of the other half tooth to a
mineralizing solution (enriched with Ca++ and PO4---) before the
artificial caries formation favors development of a much smaller
lesion and well-remineralized enamel surface zone (b, c: sections in
water are observed in polarizing microscope)
Dental Caries Prevention in Children and Adolescents
a b
c 55 Reduction of radiation dose
..      Fig. 12.17 a Proximal enamel caries lesion of a premolar
detected by DIFOTI. b The same lesion is not detected by digital
radiograph [31]. c DIFOTI system with light-emitting handpiece and
image analysis devices
..      Fig. 12.18 DIAGNOdent device and handpiece (KaVo Dental,
Germany)
SPP Technology
These phosphor plates are similar in size and almost as
thin as the conventional radiographic films. They are
cordless and flexible (not quite as much as films) com-
pared to CCD sensors (. Fig. 12.21). These features
make their use more child-friendly and therefore pref-
erable in pediatric dentistry. They are somewhat more
sensitive than CCD, resulting to even less radiation dose
for the patient. Image formation is different in SPP tech-
nology. The SPP plate has no pixels but rather the ability
to reliably store an image for up to 10 minutes [37] in the
following way. Electrons activated by radiation photons
remain trapped for some time at higher energy layers.
259 12
The number of electrons is proportional to the intensity
of radiation. The plate is scanned in a reader machine
(. Fig. 12.22) and the electrons emit light at a particu-
lar wavelength as they return to initial resting position.
This signal is amplified producing the final image [36].
>>Important
Digital radiography has many advantages over the con-
ventional radiography film:
55 Direct image production
55 Avoidance of film and developer liquids
55 Reduction of time and cost
55 Ability to edit and enhance the image
55 Compatibility with keeping only electronic patient
records
55 Ease of duplication for copies to accompany referrals
Digital systems are priced at approximately $3–4000 for
CCD to $ 5–6000 for SPP with prices at a downward
trend. Image quality of digital systems is constantly
improving approaching that of conventional radio-
graphic film. The latter was rightly anticipated to be
fully replaced in the dental offices [38] and this has been
now a fact.
12.1.5 Caries Risk and Treatment Strategies
12.1.5.1 Caries Risk Assessment
Caries risk assessment is the cornerstone of a patient-­
centered approach to manage the caries disease process
and that is why it is important to establish a risk-based
frequency for professional recall visits. The American
Academy of Pediatric Dentistry (AAPD) has adopted a
caries risk assessment tool (CAT), and its last update was
more age specific for children up to age 12 years [39]. Other
similar tools like the Cariogram, CaMBRA, etc., are also
used for the same purpose. These tools assess the caries
risk of children at a specific time and should be periodi-
cally updated. An experienced clinician should analyze
the results, ideally after having examined the child.
Cariogram is an electronic tool conceived in Sweden
and presented as a pie graph (. Fig. 12.23). It requires
additional data to be entered, such as saliva and intra-
oral microflora, and includes the following ten factors
with different weight upon the final risk level:
1. Presence of caries lesions
2. Medical condition and medications
3. Salivary Lactobacilli and mutans Streptococci
counts
4. Diet content
5. Number of between meal snacks
6. Plaque amounts
7. Use of fluoride supplements
 260 N. Kotsanos et al.

a b

..      Fig. 12.19 a Image by QLF system of early caries on occlusal surface of molar. b QLF handpiece and laptop

a b

..      Fig. 12.20 a Front side of two different size CCD plates with ceramic base. b Backside
12
a b

..      Fig. 12.21 a SPP plates (at left) have similar size with the conven-
tional radiographic films No. 0 and 2 (at right). b Backside of SPP ..      Fig. 12.22 An SPP plate is inserted for scanning (Digora, Soredex,
plates KaVo Dental)

8. Saliva flow rate or permanent dentition. Their prognostic value greatly

9. Buffering capacity of saliva
10. The dentist’s clinical assessment
In general, most studies on caries risk prognostic tools
have been conducted in children, either in the primary
depends on the prevalence of caries in the population.
The presence of caries lesions in the primary dentition
is a strong predictor for the permanent dentition [39]
(see example of . Fig. 12.13). Oral breathing does not
appear to be a prognostic factor for dental caries [40].
Dental Caries Prevention in Children and Adolescents
..      Fig. 12.23 Screenshot of the Cariogram pie graph
Cariogram has been tested in several prospective studies.
It has been shown to have good sensitivity and specific-
ity for predicting caries in the permanent dentition, less
so for children in the primary dentition [41]. Designed
in the last part of the past century, i.e., before the era
developmental tooth anomalies like MIH and HSPM
have been closely associated with caries, it does not list
them in the risk factors.
>>Important
Risk factors for the prediction of future caries gener-
ally include
55 A higher dmfs or DMFS index than average for
the child’s age
55 The presence of demineralized enamel areas (pre-
cavitated caries lesions)
55 High levels of mutans Streptococci in saliva
55 Developmental defects of enamel
55 Low socioeconomic status
55 A diet that is high in sugar content
55 Presence of orthodontic or other dental appli-
ances
12.1.5.2 Presence of Extrinsic Black Stains
The presence of black stains on the tooth surfaces is
inversely associated with caries risk, both in the pri-
mary and the permanent teeth [42]. This however has
only been studied in children and there is not any lon-
gitudinal data. Its formation is significantly reduced
in the permanent dentition compared to the primary
dentition (. Fig. 12.24). Prevalence has reported to be
from 2.4 up to 16%. Its microflora consists mainly from
Actinomyces, differing to cariogenic plaque dominated
by Streptococci and Lactobacilli. This possibly explains
the lower caries prevalence of children with black stain.
261 12
Therefore, the presence of the black stain may be predic-
tive of low caries risk in childhood. The esthetic prob-
lem can be addressed by polishing the enamel with a
rotary ibrush and tooth polishing paste assisted by using
ultrasound tips in inaccessible to brush areas. Older chil-
dren may accept air-powder abrasive systems. Effective
toothbrushing may substantially prevent the formation
of black stain.
It should be mentioned that other types of extrin-
sic black stain may at times be observed on children’s
teeth, such as from an iron supplement (. Fig. 12.24d).
The clinical manifestation along with the patient’s
medical history aids in their diagnosis. Bacterial den-
tal plaque of characteristic orange color may appear
at times (. Fig. 12.25). Its composition has not been
investigated at present. Its removal is as easy as ordinary
dental plaque, unlike the black stain which requires pro-
fessional cleaning.
12.1.5.3 The Treatment Strategy of Caries
Primary prevention requires taking measures to promote
the nonoccurrence of a disease. Management strategies
of dental caries has the same basic purpose to control
the progression of the disease as early as possible, before
it leads to localized demineralization and subsequent
cavitation. Traditionally, for the dental profession and
the public alike, restoring carious cavities has been
synonymous with caries treatment, while measures for
maintaining a healthy dentition were considered pre-
vention. Thus, professional efforts to address caries as
an infectious disease have focused more on restorative
(surgical) and less on therapeutic (etiological) treatment.
The understanding of dental caries etiology and
of the role of therapeutic agents such as fluoride led
to interventions offered at the very early stages of
possible caries development, before the occurrence of
clinically detectable demineralization. Presently, treat-
ment interventions of dental caries include effective
communication (i.e., oral hygiene education by motiva-
tional interviewing and self-management) and clinical
measures aimed at preventing or controlling (healing)
of primary caries lesions. Although tooth repair with
restorative materials and endodontic and prosthetic
procedures (described in 7 Chapters 13 and 14) will
remain important to dentistry, these procedures merely
treat the symptoms of the disease and not the disease
itself [3].
 262 N. Kotsanos et al.

a b

c d

..      Fig. 12.24 Black stain a In a 20-month-old child b In a 13-year-­old adolescent. c Coexistence of black stain and caries in the primary
teeth of early mixed dentition. d Mild black stain as a result of long consumption of iron supplementation by a preschooler

dental caries are discussed. Its treatment must be offered

in conjunction with an individualized preventive program,
which considers local factors, such as developmental den-
12 tal defects, and general factors, including patient tempera-
ment, motivation, and manual dexterity skills.

..      Fig. 12.25 Orange plaque (biofilm) on first permanent and pri-
mary molars
12.2  herapeutic Measures for Caries
T effective engagement and motivation of the patient and
Control
The prevention of dental disease is perfectly interwoven
with the provision of comprehensive dental care to chil-
dren and is an essential part of the practice philosophy
of pediatric dentistry. Prevention concerns all oral dis-
eases, abnormalities of occlusion, and possible injuries.
Preventive measures for optimal occlusion and function of
the dental arches, periodontal diseases, and dental trauma
in children and adolescents are covered in their respective
chapters. In this chapter, only those measures related to
>>Important
Prevention and control of dental caries in children and
adolescents include four parallel strategies:
1. Enhancement of tooth resistance to caries with
fluorides and other remineralization agents
2. Effective mechanical removal of the biofilm
3. Pit and fissure sealants in caries susceptible tooth
sites
4. Controlling exposure to fermentable carbohydrates
Beyond the third strategy which remains the responsi-
bility of the dental clinician, all other strategies require
family with the clinician’s guidance toward behavioral
changes that would lead to caries control. These strate-
gies will now be explained in greater detail.
12.2.1 Fluorides and Medicinal Means
Fluoride
12.2.1.1
Mechanism of Action
By 1942, Dean et al. [43] observed the following findings
in conjunction with fluoride in drinking water:
Dental Caries Prevention in Children and Adolescents
55 Low caries indices associated with high fluoride con-
centrations
55 Increased “mottling” (fluorosis) of teeth associated
with higher concentrations of fluoride
55 A fluoride concentration of 1 part per million (ppm)
in drinking water provided the best result of maxi-
mum caries reduction without mottling
Based mainly on these findings, a fluoridation program
of drinking water was begun for the prevention of den-
tal caries at the community level in the United States.
This was followed by many epidemiological, laboratory,
and clinical studies to elucidate the mechanism of fluo-
ride action and the most effective ways for its implemen-
tation. It was long believed that its incorporation into
the enamel during its formation offered increased resis-
tance to dental caries but was later shown by artificial
caries formation in vitro that enamel fluoride content
was of lower importance [3]. At the same time, the claim
that the transformation of hydroxyl- to fluorapatite (by
replacement of OH− with F− ions) was responsible for
increased caries resistance became disproved, since only
a very small percentage of mineral volume underwent
such transformation.
The current understanding is that the presence
of fluoride at the tooth-plaque interface is impor-
tant (. Fig. 12.26). During de- and remineralization
activities, only a minimal amount of fluoride favors the
equilibrium to be tipped toward remineralization. In
addition, after a topical application of fluoride, CaF2
crystals are formed on tooth surfaces which are respon-
sible for the sustained pH-controlled release of fluoride.
It is therefore accepted that the anticaries effect of fluo-
ride is mainly topical [44]. Even when fluoride is avail-
able through a systemic route, such as from drinking
fluoridated water, its effects are mainly topical through
..      Fig. 12.26 Presence of fluoride of toothpaste in saliva and in
tooth-plaque interface
263 12
resecretion in saliva, which then enriches the dental
plaque.
Systemic Fluoride
Water Fluoridation
Water fluoridation is a systematic method of fluoride
delivery on a community level. Three hundred million
people around the world drink fluoridated water, with
1.0 ppm to be the optimal concentration of fluoride.
During the second half of the twentieth century, more
than 113 studies in 23 countries had already been pub-
lished showing an approximately 50% caries reduction
[45]. In the United States, the cost of fluoridation of
drinking water is 10 cents to 1.5 USD per person per
year, in inverse proportion to the size of the commu-
nity. Despite being an inexpensive and effective method
of caries prevention, there is some public opposition to
adding fluoride to drinking water. Most European coun-
tries have not adopted it, although its use is supported
by the European Academy of Paediatric Dentistry [46].
Milk Fluoridation
It has been used in some countries, mainly in indoor
childcare centers such as boarding schools and kinder-
gartens. In a randomized control clinical trial of 6-year-­
old children, those who consumed fluoridated milk from
the age of three years showed 76.4% lower DMFT and
31.3% lower dmft indices in comparison to the control
group [47]. Fluoride concentration in milk is usually
2.5–5.0 mg F/L. [48] Milk fluoridation has limited appli-
cations. Its use could be part of community health pro-
grams in target groups with high caries prevalence and
low compliance for toothbrushing [46].
Salt Fluoridation
Fluoridated salt is available in over 30 countries around
the world, e.g., Switzerland, Germany, France, and
Costa Rica. As a caries preventive measure, it is con-
sidered quite effective, but its effectiveness has not been
well documented. Moreover, its usefulness in children,
particularly those of young age, is very limited as chil-
dren generally follow a diet low in salt [48].
Fluoride Tablets and Drops
Fluoride tablets and drops may be prescribed by pedi-
atricians, family physicians, and dentists. Tablets of
0.25, 0.5, and 1 mg of fluoride are available. Each drop
contains 0.125 mg of fluoride. Although the fluoride
enters the blood circulation, its action is mainly local.
There is wide variation in the effectiveness of fluoride
supplementation in part because long-term compliance
is difficult to achieve [48, 49]. The European Academy
of Paediatric Dentistry recommends them only to chil-
dren of high caries risk on an individual basis [48]. The
 264 N. Kotsanos et al.

American Dental Association fluoride supplementation
schedule is based on the fluoride concentration of drink-
ing water and the age of the child [50].
Topical Fluorides
Home Use
Toothpaste
Over-the-counter fluoridated toothpaste is the most
effective vehicle of fluoride exposure. Fluoridated tooth-
paste may be the most important preventive measure
that is responsible for the dramatic reduction in caries
levels in developed countries since the 1970s. Its role in
preventing tooth decay has been documented by numer-
ous studies [51, 52] to be effective in reducing caries rates
by 21%–28% compared to non-fluoride toothpaste.
Fluoride is contained in toothpaste either in the form
of inorganic salts such as sodium fluoride (NaF), stan-
nous fluoride (SnF2), and monofluorophosphate fluo-
ride (MFP) or in the form of organic compounds such as
amine fluoride (NF4−) which theoretically offers greater
availability of free fluoride ions. Fluoride concentration
usually ranges from 1000 to 1450 ppm (. Fig.12.27).
Toothpastes with 5000 ppm F are specifically targeted
to special care patients, high caries risk adolescents, and
those with fixed orthodontic appliances, yet without
sound evidence for superior effectiveness [53].
In addition to fluoride and other possibly antimicro-
bial substances, toothpastes contain mainly two types
of active ingredients to enhance brushing effectiveness,
abrasives and surfactant factors to improve tooth and
plaque wetting. The main concern of fluoride toothpaste
use in young children is the risk of fluorosis – usually
mild in appearance – that is caused by chronic swallow-
ing [54]. Considering the child’s caries vs. fluorosis risk,
advice should be based on recommendations on the fluo-
ride concentration and amount of toothpaste according
to age (. Table 12.1). Because of the continued high car-
ies rates and the difficulty in predicting caries risk in tod-
dlers, the American Dental Association recommended
caregivers to start brushing children’s teeth at eruption
of the first tooth and with no more than a smear or a rice
grain size of fluoridated ­toothpaste twice a day [55, 56].

Fluoride Rinses
a Fluoride rinses usually contain NaF in different concen-
trations, ranging from 225 ppm (or less) to 800–900 ppm
fluoride. They are aimed at high-risk children, and the
high F rinses are recommended for less frequent use,
12 e.g., weekly. Because of the risk of swallowing, it would
not be recommended for preschoolers. Efficacy of fluo-
ride rinses in preventing caries is better documented for
permanent teeth [46].

Professional Application
Fluoride Gels and Varnishes
Fluoride gels contain 12,300 ppm fluoride either as
acidulated phosphate fluoride (APF) at pH 2.3 or as

b
..      Table 12.1 Recommended use of fluoride toothpastes in
children [46]

Age (ppm F) Frequency Amount (g) Size

(years) size

First 1000 Twice 0.125 Grain of

tooth–up daily rice
to 2 years
2–6 years 1000a Twice 0.25 Pea
daily
Over 1450 Twice 0.5–1.0 Up to
6 years daily full
length of
..      Fig. 12.27 a Middle: three toothpastes with 1450 or 1500 ppm brush
fluoride. Far left: arginine added toothpaste. Far right, 5.000 ppm
aFor children 2–6 years, 1000+ fluoride concentrations may be
fluoride toothpaste. b Toothpastes for children. Far left: 500 ppm
fluoride toothpaste (this concentration is not recommended any considered based on the individual caries risk
more). 2nd from the left: toothpaste containing ammonium fluoride.
3rd and the 4th: 1.000 ppm F toothpaste. Far right: 1.450 ppm fluo-
ride toothpaste
Dental Caries Prevention in Children and Adolescents
265 12
a b

..      Fig. 12.28 Disposable fluoride treatment trays: a. for primary dentition filled with APF foam. b. for mixed dentition with APF gel
(1.23%)

NaF at a neutral pH and are used placed in special trays

a
(. Fig. 12.28). The gel amount is about 2 ml per tray
(depending on the dentition), with the patient sitting
upright and with use of suction. Despite this precaution
it is not advised for preschoolers for the fear of inges-
tion. A 26–30% caries reduction has been reported [57].
Fluoride varnish is recommended 2–4 months
in high caries risk patients. The 2004 US Preventive
Services Task Force recommends that primary care cli-
nicians apply fluoride varnish to the primary teeth of all
infants and children starting at the age of primary tooth
eruption, with the goal to increase access to preventive
dental care to young children as early as possible [58].
Effectiveness may reach 50–70% when regularly applied
b
[59]. As the varnish contains 22,600 ppm fluoride, only a
small varnish quantity with proper teeth isolation is suf-
ficient for the entire dentition (. Fig. 12.29). It may be
used in high caries risk children of all ages, orthodontic
patients, and people with disabilities, applied as a thin
film only on surfaces at risk.

Silver Diamine Fluoride

Silver compounds, particularly silver nitrate, have been
used in dentistry since the 1840s [60] and have gained
renewed interest in recent years. Silver diamine fluoride
(SDF) was first used to treat caries in Japan in the 1960s
[61]. In 2014, 38% SDF was approved by the US Food
and Drug Administration (FDA) to treat dentin sensi-
tivity, and SDF has since gained increasing popularity
..      Fig. 12.29 a Quantity of fluoride varnish for the upper and lower
in the United States as an alternative to restorative treat- mixed dentition. b Placement as a thin film only on caries risk sur-
ment. Its major side effect of turning carious lesions faces with brush or probe
black has made it an attractive option primarily for
young patients or individuals with special health-care
needs who are not able to tolerate conventional restora- levels of evidence extracted from controlled clinical tri-
tions (. Fig. 12.30) [62]. als of SDF efficacy. Based on a meta-analysis of the
Limited evidence exists regarding SDF’s ability to extracted data, approximately 68% of cavitated car-
arrest and prevent caries. The AAPD recently pub- ies lesions were expected to be arrested two years after
lished guidance [63] on the use of SDF based on low SDF application with annual or biannual application.
 266 N. Kotsanos et al.
a b
..      Fig. 12.30 Caries of the maxillary left primary first molar a before SDF application and b after SDF application
Over a 30-month follow-up, SDF had 48% higher suc-
cess rate in caries lesion arrest compared to the controls.
The AAPD guidelines [63] endorsed the use of SDF for
the arrest of cavitated carious lesions in primary teeth as
12 part of a comprehensive caries management program.
Additionally, until more evidence becomes available,
close monitoring based on patient’s disease activity and
caries risk level is recommended.
Fluoride Toxicity
Many fluoride products are available for topical appli-
cation and some for systemic use. Some fluoride prod-
ucts are limited for professional application while some
are to be used by the patient at home. In countries with
available artificially fluoridated drinking water, children
may be exposed to various sources of fluoride, including
through the following routes:
i 1. Drinking water 1.0 mg F/day
2. Fluoride supplements 1.0 mg F/day (maximum)
3. Diet 0.5 mg F/day
4. Toothpaste 0.25 mg F/day (young children)
In such cases children may ingest more fluoride than
the optimal daily recommendation (1.0 mg F/day)
thus incurring the risk of mild dental fluorosis. Prior
to prescribing fluoride supplements, it is important to
establish the amount of fluoride available to a patient,
including through their drinking water, either bottled
or from public supply. Infants who consume formula
that is prepared with fluoridated water are at risk of
developing fluorosis in their permanent teeth, espe-
cially if such formula is consumed around the age of
2 years. Fluoride chewing gums containing 0.25 mg
fluoride per piece are available. In addition, some
foods, such as fish and tea, have considerable fluoride
concentration.
Acute Fluoride Toxicity
Acute toxicity may occur from ingestion of a large
amount of fluoride toothpaste, rinse, or any other
product that contains fluoride. The probably toxic dose
(PTD) – the minimum amount of fluoride swallowed
that would require intervention – is 5 mg F/Kg body
weight [64]. Symptoms and signs of acute fluoride poi-
soning in the order of appearance are nausea and vom-
iting and then for doses exceeding PTD are excessive
salivation, abdominal pain, diarrhea, and more serious
ones endangering life. Hospital treatment aims to stop
further absorption, remove fluoride from the body flu-
ids, and support the vital functions.
>>Important
For a 5-year-old child (average weight = 20 Kg),
the PTD is 100 mg fluoride. The various fluoride-­
containing products and the minimal quantity that
would result in a PTD if ingested are
55 100 ml of a 1000 ppm fluoride toothpaste
55 440 ml of a daily 225 ppm fluoride solution
55 110 ml of a weekly 900 ppm fluoride solution
Dental Caries Prevention in Children and Adolescents
55 8 ml of APF gel (12,300 ppm F)
55 4.4 ml fluoride varnish (22,600 ppm F)
Chronic Exposure to Fluoride: Dental Fluorosis
The main chronic adverse reaction of fluoride to the
dental tissues is dental fluorosis or mottling of the teeth.
Its clinical manifestation is pictured in 7 Chap. 17. The
ameloblast is sensitive to fluoride in both the secretory
and the maturation stages of enamel formation. For the
permanent maxillary central incisors, the period of maxi-
mum sensitivity of the ameloblasts to fluoride is between
15 and 24 months of age for boys and 21 to 30 months of
age for girls [65]. To avoid causing fluorosis, the total daily
fluoride intake should not exceed the limit of 0.1 mg F/
Kg body weight. In young children, the risk of fluorosis
increases when fluoride supplements are used together
with a 1000 or 1450 ppm F toothpaste. Most cases of flu-
orosis associated with fluoride toothpaste are mild [66].
12.2.1.2 Other Alleged Anticaries Agents
Casein
Casein phosphopeptide-amorphous calcium phosphate
(CPP-ACP) has been introduced over 10 years ago to
facilitate remineralization of incipient caries lesions.
Casein is a milk protein which has been previously inves-
tigated for its anticaries activity. This complex can main-
tain a supersaturated state in relationship to the enamel
and has been found to have a synergistic effect with the
fluoride in caries reduction [67]. Almost all clinical stud-
ies with CPP-ACP have investigated its remineralization
effectiveness of incipient caries lesions in the perma-
nent dentition of adolescents. A randomized clinical
trial in preschool children showed that CPP-ACP cream
(Recaldent, GC, . Fig. 12.31), applied with cotton
swab after brushing on school days for one year by the
school teacher, did not result in greater reduction in the
..      Fig. 12.31 Casein phosphopeptide-amorphous calcium phos-
phate (CPP-ACP, Recaldent, GC) in creamy form
267 12
mean caries rate compared with the sole use of fluori-
dated toothpaste [68].
Chlorhexidine
Chlorhexidine is an antimicrobial agent with a very
broad spectrum that is used extensively for the preven-
tion of periodontal disease. Its prolonged antimicro-
bial action lies in its adherence to the cell membrane of
bacteria, resulting in increased permeability and subse-
quent cell destruction. It is incorporated in toothpastes,
rinses, gels, and varnishes in concentrations of 0.02% for
daily use and 0.12% and 0.2% for therapeutic use. The
effectiveness of chlorhexidine has been documented in
several studies which demonstrate reductions of the gin-
gival and plaque indices in both adults and children of
about 30–40%. It has also been found that the applica-
tion of chlorhexidine varnish can reduce the levels of
Streptococcus mutans in the mouth, but this has not
been associated with a corresponding caries reduction
on either smooth surfaces or in pits and fissures [69, 70].
Prolonged use of chlorhexidine has adverse reac-
tions such as tooth discoloration and altering taste and,
therefore, its use is recommended for limited periods of
time. In children younger than 6 years of age, chlorhexi-
dine may be applied locally by an adult in the form of
a 0.2% chlorhexidine gel. Other antiseptic rinses, con-
taining alcohol, thymol, povidone iodine, and sodium
benzoate or other antiseptics are at times advertised for
plaque control. However, their effectiveness is inferior
compared to chlorhexidine solutions [71].
Xylitol
Xylitol is a sugar substitute, such as sorbitol, mannitol,
and aspartame. The goal of using sugar substitutes is to
replace the sugars with substances that are not metabo-
lizable by bacteria and therefore are not acid-producing.
Additionally, xylitol exhibits an antimicrobial action.
Mothers who chew a gum containing xylitol, sorbitol,
chlorhexidine, and fluoride, at least 2–3 times a day for a
year, had a significant reduction of Streptococcus mutans
transmission to their toddlers, and the children experi-
enced lower caries incidence when they were 4 years old
[72]. When they were examined for caries at age 10, no
long-term effect was present [73]. Xylitol has a pleasant,
refreshing taste and also comes in lozenges (. Fig. 12.32).
Probiotics
The rise in microbial strains that have become resistant
to antibiotics has recently led to a search for alternative
methods of preventing dental caries. Bacteriotherapy,
which aims to significantly displace pathogenic microor-
ganisms with harmless ones, has attracted the attention
of both researchers and food manufacturers resulting in
the introduction of the so-called probiotics. Some pro-
biotics contain species of Lactobacilli, Bifidobacteria,
 268 N. Kotsanos et al.
a dorsum, as well as other tissues in the oral cavity are
b
..      Fig.12.32 a Xylitol lozenges (Epic Dental, Murray, UT). b Pro-
biotic tablets (BioGaia, Stockholm, Sweden)
12
etc. and are mostly available in milk products, e.g.,
yogurts, and purportedly support the defense mecha-
nisms against diseases. These same groups of bacteria
also represent a significant part of the human intestinal
flora. Probiotics are also available in other forms, such
as tablets (. Fig. 12.32). The benefits of probiotics do
not currently seem to be sustainable in altering the oral
flora if their administration is not continuous. There are
some encouraging results regarding their antimicrobial
properties but effects on dental caries have not been
documented [74].
12.2.2 Dental Plaque Removal
Mechanical removal of dental plaque is an impor-
tant daily home-based preventive routine. This can
be accomplished with a toothbrush as well as some
additional important accessories, such as dental floss
and interdental brushes. Although the control of
plaque is discussed here with respect to caries and, in
7 Chap. 15 with respect to periodontal disease, it is
important also for another socially important condi-
tion, halitosis (bad breath or oral malodor). Volatile
sulfur compounds, metabolic products of the oral
microorganisms within the biofilm coating the tongue
mainly responsible [75].
Halitosis in children is usually a result of bacte-
rial colonization of the tongue dorsum. Effective oral
hygiene with thorough cleaning is the most simple and
basic way to tackle bad breath. Probiotic bacteria like
Lactobacillus salivarius WB21, green tea catechins, or
various antiseptic mouthwash are being tried in young
people with some success in reducing halitosis [76]. An
upper respiratory infection, presence of clefts, and oral
and nasal breathing odor could also be responsible for
halitosis.
12.2.2.1 Toothbrushing
Toothbrushing is a socially acceptable practice for
plaque removal for all age groups. Parents frequently
have questions regarding toothbrushing in terms of the
actual technique, frequency and duration, type of brush
(shape and size of head or handle, bristle hardness, elec-
tric versus manual), and toothpaste (amount and con-
centration of fluoride) to use.
Toothbrushes and Brushing Techniques
The method of toothbrushing needs to be simple, easy,
and effective when performed by children. The horizontal
scrub technique seems to most suitable for preschool chil-
dren [77]. This technique involves horizontal placement
of the brush at the gingival margin with small movements
back and forth. The lingual surfaces as well as the inter-
dental spaces of posterior teeth should be reached as these
are sites of greater caries risk and the primary molars are
among the last teeth to exfoliate (. Fig. 12.33). The par-
ticipation of parents is considered necessary for the most
posterior teeth until the age of 7–8 years, because relative
manual dexterity skills in most children are underdevel-
oped until then. Parental supervision of brushing for sev-
eral more years is recommended.
Toothbrush bristles should be made of nylon with
soft rounded edges to reach the interdental areas while
being gentle to the gingival tissues. Electric toothbrushes
are increasingly used nowadays having typically a round
head aiming to brush teeth one by one (. Fig. 12.34).
Contrary to manual toothbrushes, no hand movement
is necessary except for a slight turn of the toothbrush
head on each tooth surface so that the peripheral bris-
tles can access interdental spaces. Worn toothbrushes
lose their effectiveness and must be replaced when the
bristles appear bending. There is inadequate reliable
data to support effectiveness of either electric or manual
toothbrushes in children. Some studies show that some
electric ones may be superior for very young children or
offer advantages in children with disabilities [78, 79]. In
any case toothbrushing should be pleasantly accepted
for successful child’s oral hygiene.
Dental Caries Prevention in Children and Adolescents
269 12
Timing, Frequency, and Duration of Brushing
a
Since dental plaque begins to form on tooth surfaces with
the emergence of the first tooth in the oral cavity, tooth
cleaning should start as soon as the teeth erupt. At first,
the use of a piece of gauze is sufficient for plaque removal
from the first primary incisors. When many incisors are
erupted, and no later than the eruption of the first primary
molars, use of a toothbrush is a necessity (. Fig. 12.35).
Regarding the best time to brush the teeth, there con-
tinues to be no evidence as to whether brushing before
or immediately after breakfast, in the morning, or
before bedtime is best. Since salivary flow almost ceases
during sleep depriving teeth its protective role, it seems
logical to brush immediately before bedtime to minimize
plaque retention and to increase intraoral fluoride levels
b during sleep. Brushing should preferably be done twice
a day, for the added benefit of fluoride, but this depends
also on caries risk. As for brushing duration, two min-
utes may suffice for plaque removal [80]. Longer brush-
ing time is not easily achievable in children.

Eye Catcher

Good practice points on children brushing behavior

..      Fig.12.33 a Correct placement of the toothbrush onto the cervi-
cal and into proximal areas of the teeth. b Parental participation to
child’s toothbrushing. A finger of the opposite hand may improve
vision for correct toothbrush placement on posterior teeth
based on expert opinions and consensus are [46]
55 Each tooth surface is reached, and brushing
should exceed 1 min
55 Avoid rinsing with a lot of water
55 Use either a soft manual or power toothbrush

a b

..      Fig.12.34 a Hand toothbrushes, infant size (far right) to adolescent and adult size (left). b Recent technology electrical toothbrush
(Oral-B iO) working with microvibrations
 270 N. Kotsanos et al.
a a
b
..      Fig.12.35 a Eruption of the primary maxillary incisors signifies
12 the need of parental education on toothbrushing. b Demonstrating
the presence of plaque by erythrosine dye for the necessity of its
removal
12.2.2.2 Dental Floss and Interdental Brushes
Dental floss is a useful supplement allowing for inac-
cessible to toothbrush residual plaque removal from the
interproximal areas. This is especially the case in the pos-
terior teeth due to their much greater buccolingual width
than anterior teeth. The correct flossing technique is
demanding, making compliance difficult even by adults.
Special floss holders (. Fig. 12.36) make flossing easier
to accomplish, and its use in children could start after
contacts are established between the primary molars.
This is more important for caries risk children, provided
risk can be estimated. Educating high-risk early ado-
lescents in the correct use of dental floss seems a good
practice.
Interdental brushes are the alternative solution of
plaque removal from interdental areas (. Fig. 12.37).
Thin-sized such brushes are intended for daily use by
adolescents at risk for dental caries or periodontal dis-
ease. For added benefit, fluoride toothpaste or gel should
be added to the brush before applied to each interdental
space or combining interdental brushing with ordinary
brushing for practical purposes.
b
..      Fig. 12.36 a Various floss holders. The middle one has incorpo-
rated roll of floss for multiple uses. b. and c. Single use floss holders.
An incipient caries lesion is visible in the mesial of lateral incisor in b
12.2.3 Pit and Fissure Sealants
The depth and morphology of pits and fissures of occlu-
sal surfaces, especially in recently erupted teeth, do not
allow for effective plaque removal with the toothbrush
(. Fig. 12.38). With mature plaque behaving as a closed
ecosystem allowing for reduced saliva and fluoride
access, teeth with deep pits and fissures are particularly
vulnerable and often become carious within a short time
after their eruption [81]. Although the occlusal surfaces
represent only one-tenth of the total tooth surfaces in
the oral cavity, they may account for nearly 50% of the
cavitated lesions in children aged 6–12 years. A study
found that caries incidence on the occlusal surfaces of
permanent molars peak approximately two years after
they begin to erupt [82].
Dental Caries Prevention in Children and Adolescents
271 12

a a

..      Fig 12.38 a The pit and fissure system of a molar occlusal sur-
face by low magnification scanning electron microscopy. b Stagnant
..      Fig.12.37 a Different thin interdental brushes and suggested
plaque disclosed with erythrosine on a partially erupted first perma-
fluoride gel. b Demonstration of interdental brush use
nent molar

After Buonocore’s demonstration in 1955 that the

enamel surface can be etched with strong acids, reten- a b
tion of resinous materials sealing these vulnerable
areas became possible (. Fig. 12.39). Historically,
various polymeric materials have been used requiring
mixing two parts for chemical polymerization. Today,
one tube resin material is used as sealant, polymerized
under visible light of around 480 nm in mere 10 sec
with LED units operating at about 1000 mV or more
[83]. White or tooth-colored shades of sealant are most
popular. As with resin composite, incorporating fluo-
ride salts into sealant materials for fluoride release in
case of microleakage has been suggested, but clinical
testing found no superiority in caries prevention [84].

12.2.3.1 Sealant Placement Procedure

The clinical procedure for placement of a photopoly-
merizable resin sealant is as follows: ..      Fig.12.39 a Five years after having sealed a first permanent
1. Plaque deposits are carefully removed with a suitable molar, an incipient caries lesion can be seen in the fissures of the
brush at low speed, with a toothbrush, or by air partially erupted second permanent molar. b Sealing the occlusal fis-
sure system while its disto-palatal fissure is left to be sealed at the
abrasion. Their complete removal from deep pits and
next follow-up, after it is fully erupted
fissures in the first two options may be confirmed
with a sharp explorer (. Fig. 12.40).
 272 N. Kotsanos et al.

a a b

b c

c d

..      Fig.12.40 a A premolar was cleaned in situ with a cup-shaped

brush at low speed, prior to its extraction for orthodontic purposes.
b Use of erythrosine dye followed by rinsing with water reveals the
presence of significant quantity of residual plaque. c The application
of phosphoric acid 35% in vitro for 30 sec was ineffective in remov- e
ing this residual plaque that obviously prevented sufficient etching of
the respective area of enamel
12
2. Enamel etching with a 35% phosphoric acid for 30
secs followed by rigorous rinsing with water for
10 seconds.
3. A dry field is required with rubber dam or cotton roll
isolation.
4. Sealant is allowed to flow to all fissures avoiding
overfilling and bubble formation.
5. Photopolymerization for 20 seconds (time depends
on curing unit type).
6. Occlusion and adequate retention of sealant are ..      Fig. 12.41 Resin sealant placement in a recently erupted first
checked. permanent molar as part of a quadrant restorative treatment in a
child with high caries risk. a Immediately after completion of restor-
ative treatment. Amalgam was commonly used many years ago. b
Improper isolation leading to salivary contamination of
Application of phosphoric acid 35% gel. c Etching includes the buc-
the etched enamel results in reduced retention of the mate- cal pit that has incipient caries lesion. d Sealant is placed. e Final
rial. Although rubber dam isolation is desirable, the reten- clinical view of quadrant
tion of sealants placed on permanent molars with cotton
rolls was not significantly inferior [85]. However, if first penetration and retention. Sealants must be part of
permanent molar sealants are planned as part of quadrant a total preventive program that includes regular fol-
restorative dentistry in early mixed dentition, rubber dam low-ups. The cost/benefit ratio determines the neces-
isolation is preferred if it is possible to place the rubber sity of their use. Sealant placement has an associated
dam clamp on the permanent molar (. Fig. 12.41). cost – payment for the dental services, time loss for
parents/child – which is justified if caries can be pre-
12.2.3.2 Recommendations for Use vented and it can be documented. For this reason,
and Efficacy sealant placement is indicated for molars (or other
Sealants are placed in healthy pits and fissures of teeth) where the pits and fissures are at least at mod-
caries risk teeth or in those with incipient non-cav- erate caries risk [86]. Sealant placement in all chil-
itated caries confined to the enamel (ICDAS No. 3, dren may not be justified.
discolored groove, etc.). In the latter case, mechani- The timing for sealant placement in permanent molars
cal preparation (enameloplasty) may improve sealant with high caries risk is also important. It may take one
Dental Caries Prevention in Children and Adolescents
year from beginning of eruption to full occlusion. Partially
erupted teeth are more difficult to clean well, and there is
practically no self-cleaning while the tooth is out of occlu-
sion. Therefore, this period of partial eruption carries the
highest caries risk for the occlusal surfaces of molars [81]
(. Fig. 12.38b). A resin sealant may be placed as soon as
possible once the occlusal table is fully erupted. Until then,
a glass ionomer sealant may be placed if those tooth sur-
faces considered as high risk [87]. Alternatively, rigorous
brushing at home combined with topical fluoride applica-
tion on these surfaces every 3 months has been shown to be
effective in reducing caries development [88].
Satisfactory sealant retention rates 53% after ten and
35% and fifteen years have been reported [89]. Sealant
effectiveness for caries prevention varies between 83% in
the first year to 53% fifteen years after their initial place-
ment [90]. The retention rates of either conventional or
resin-modified glass ionomer sealants are substantially
lower than those of resin sealants [87, 91]. Yet, it seems
that the anticaries action of glass ionomer sealants is
extended for a period after their loss, possibly due to the
fluoride release from the small remnants of the material
in the fissures.
12.2.4 The Diet
The association of frequent intakes of a diet rich in car-
bohydrates and dental caries has been well documented
with landmark clinical studies performed in various age
groups several decades ago [92]. Sticky carbohydrates
such as biscuits, wafers, potato chips, etc. are cariogenic
and, when consumed at high frequency between meals,
contribute to a significant increase in caries rates. Liquid
carbohydrates, such as in soft drinks, sugar containing
juices, or other drinks, etc., are also highly cariogenic
but to a lesser extent, due to shorter oral clearance time
compared to the solid carbohydrates.
Sugar (sucrose) is the most implicated carbohydrate
in terms of acid production in the plaque. However,
glucose and fructose are also metabolized by microor-
ganisms which can lead to acid production. Nowadays,
in conjunction with the use of many different types of
sweeteners and syrups by the food industry, a simple
recommendation for reducing sugar intakes by children
is not enough. Consumption of foods such as bananas,
grapes, and other fruits, white bread, sugared cereals
(especially popular for children’s breakfast), pasta, pota-
toes, and even milk can all lead to acid production under
certain conditions and to a drop in plaque pH below the
critical value of 5.5 for dissolving hydroxyapatite.
Therefore, sugar concentration is not necessarily
considered to be the most important factor for caries
development. Other important factors that influence
the cariogenicity of a food item is its ability to adhere
to tooth surfaces (affecting oral clearance), the rate at
which it dissolves in saliva, its capacity to stimulate
273 12
the salivary glands for saliva production, and its own
ability to resist pH decrease (buffering capacity). The
most important factor is the total time that plaque pH
remains low, which is directly related to the frequency
of food intake [93]. The greater the number of meals
and snacks, the longer pH at plaque/enamel interface
remains low, thus favoring demineralization of the den-
tal tissues (. Fig. 12.42).
Sugars in the diet is an important component of car-
ies risk. Epidemiological studies such as the Vipeholm
study [92] however, although extremely valuable, were
conducted before the time of fluoride. A review of find-
ings shows that despite increases in sugar consumption,
communities that adopted frequent toothbrushing with
fluoride toothpaste experienced a significant decrease
in dental caries rates [94]. Therefore, proper preventive
measures of oral hygiene along with use of fluorides
may mitigate the effect of the diet on dental caries, and
the contemporary view is that dental caries is primarily
owed to tooth cleaning neglect.
Nevertheless, parents and their children should
be advised to adopt a balanced and healthy diet and
avoid snacks that favor the development of caries
(. Fig. 12.43). A useful tool for assessing a young
patient’s diet is to have the parent complete a three-day
diet form that records the time, type, and quantity of
food and drinks ingested. The dental professional would
be able to use that data to educate the family about the
various specific factors (high carbohydrate content, tex-
ture affecting oral clearance) that may be potentially
cariogenic and propose less harmful food and drink
replacements (. Fig. 12.44). Such forms are designed
to assist in providing customized dietary counseling,
and they have been met however with only partial suc-
cess and sometimes without success at all [95]. This is
one of the reasons they are not part of everyday prac-
tice of general practitioners, although other reasons
like perceived financial and time constraints play a role
[96]. Anyway, between meal snacks may need to be con-
trolled, with the number of meals plus snacks during the
day ideally being five (three main meals and two snacks).
It is important to emphasize avoiding harmful habits,
e.g., the use of bottle or at will breastfeeding during the
night or the use of a sweetened pacifier, which are sig-
nificant risk factors for S-ECC [97].
In addition to its association with dental caries,
frequent consumption of sugar containing drinks and
between meal snacks has also been linked with over-
weight and obesity [98]. Obesity has reached epidemic
proportions worldwide. In the United States, obe-
sity rates had quadrupled in children aged 6–11 and
almost doubled in adolescents aged 12–19 in a period
of 25 years [99], and a 2016 publication estimated the
percentage of obese children aged 2–19 years to be 17%
[100]. In some epidemiological studies of preschoolers,
a positive relationship between overweight and obese
children has been found with their caries index [101].
 274 N. Kotsanos et al.

a 8.0

7.0
Plaque pH

6.0

Critical pH*
8.0

8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Hours
breakfast coffee lunch sweet tea biscuit dinner coffee coffee
sweet sweet sweet
b 8.0

7.0
Plaque pH

6.0

Critical pH*
8.0

12 8
breakfast
9 10 11
coffee
12 13 14
lunch
15 16
tea
17 18 19
dinner
20 21 22 23
coffee
24 Hours

..      Fig. 12.42 Stephan curves with continuous recording of PH in contents leads to fewer pH drop episodes boosting remineralization
the plaque/enamel interface during a day. a Meals and multiple (Licensed under the Creative Commons Attribution-Share Alike 4.0
snacking prolong pH remaining below critical value and therefore International license, by Lolim95, Wikipedia commons)
increase caries risk. b Decreasing between meal snacking and sugar

Several other health risks associated with overweight
and obesity in childhood include type II diabetes, car-
diovascular diseases (hypertension, high cholesterol,
and dyslipidemia), psychological stress (depression and
low self-esteem), respiratory disease (obstructive sleep
apnea and asthma), and orthopedic (vlaisopodia and
slipped capital femoral epiphysis) and liver function
(steatohepatitis) [102].
12.2.5 Patient Motivation and Recalls
12.2.5.1 Patient Motivation
Dental caries is a chronic disease that is significantly
influenced by social and behavioral factors. When
patients have active caries, the disease process will
progress unless the risk factors that are responsible
for the disease are addressed. Effective control of the
disease requires patient self-management of the etio-
logical factors. An important role of the professional
dental care team is to not only help to educate the
patient and parents or family about disease etiology
but also to provide coaching and support to enable
the family to make lifestyle changes as improving
oral hygiene practices, dietary habits, and fluoride use
[103]. Traditional approaches involve the dental care
team telling the patient what to do. A close partnership
or collaboration between an informed and engaged
patient and family and a proactive dental care pro-
vider is necessary in order for the patient to make suc-
cessful sustainable changes to improve their caries risk
[104]. A significant challenge is to determine how to
help patients increase their motivation to make behav-
ior changes. This is particularly important at turbulent
times. In a relevant longitudinal study of adolescents
in Brazil, for example, the frequency of toothbrushing,
the use of dental services, and the self-perceived need
for dental treatment significantly decreased in com-
parison to immediately before the recent pandemic of
CoVid-19 [105].
Dental Caries Prevention in Children and Adolescents
275 12

..      Fig. 12.43 Pyramid of Harvard School of Public Health for cor- hsph.­h arvard.­e du/nutritionsource/healthy-­e ating-­p yramid/.
rect frequency per kind of diet intakes. It must be accompanied by Accessed on March 20, 2021
sufficient intake of liquid and daily physical exercise. 7 https://www.­

After learning about a patient’s specific caries risk

factors from a systematic caries risk assessment, a
member of the dental care team engages and coaches
the patient/parent or family with self-management goal
setting. . Figure 12.45 shows an example of a self-­
management goals handout. Knowing that change is
hard to make, usually no more than 1 or 2 goals are
selected to work on until the next visit. Goals may
include more frequent toothbrushing, dietary changes,
or using topical fluoride at home.
Motivational interviewing is a communication style
designed to affect change by increasing motivation and ..      Fig. 12.44 The logo (at left) of a Swiss inspired organization for
characterization of between meal snacks (at right) as dentally “safe”
(with permission)
 276 N. Kotsanos et al.

12

..      Fig. 12.45 Sample self-management goals handout ([108] with permission)

Dental Caries Prevention in Children and Adolescents
commitment to goals [106]. Motivation can be and often
is influenced by the health-care provider. What providers
do or say can make patients more or less likely to change
their behaviors. A key element of helping patients make
positive behavior changes is a strong partnership while at
the same time honoring their autonomy. Engagement and
trust can be created by focusing on desires, goals, hope,
and positive expectations and for the patient’s oral health.
Asking open-ended questions can help patients elicit
“change talk.” Motivational interviewing training is avail-
able, and practice is important to improve the skills needed
to help patients improve their motivation for change.
12.2.5.2 Recall Visit
Overview
During follow-up recall visits, patients should receive
as a part of their ongoing caries disease prevention and
management program:
55 Reevaluation of caries risk factors
–– Assessment of patient compliance to pro-
posed preventive measures and reactivation
as needed
–– Revisiting of self-management goals and
reaffirming those goals or establishing new
goals
55 Clinical examination to assess for new/recurrent
caries and the status of preventive or restorative
treatments, e.g., fissure sealants, restorations, pulp
treatments, arrest of early carious lesions, etc.
55 Evaluation of plaque control and effectiveness of
oral hygiene technique
–– Evaluation of dental occlusion, continu-
ously under change in children
55 Caries charting and monitoring
An effective treatment plan aimed at preventing dis-
ease recurrence should be supported by a functional
follow-­up system. The disease management program
should meet the individualized needs of each patient,
taking also into account their social and family char-
acteristics. This includes an accurate assessment of car-
ies risk and adherence to a follow-up schedule based
on it. The follow-­ups can be planned on an annual or
even less frequent interval for low caries risk patients,
every six months for medium caries risk patients and on
a quarterly basis or more frequently for high caries risk
patients [107]. Thus, for reasons of cost-effectiveness,
some children need not be reexamined every six months
or receive professional application of fluoride as long
they remain in the very low caries risk group. The con-
tent and intensity of preventive measures depend on the
caries risk group to which they belong at any time. If
277 12
there is active caries disease with rapidly evolving lesions
(cavities or “white spots”), the first step is to arrest them
or at least reduce their rate of progression. This requires
the education of the preventive program, coaching and
support to establish self-management goals, as well as
ultimately the long-term ability of the child or parent to
make sustainable changes to improve their caries risk.
This poses a challenging task to the clinician.
With advances in technology, traditional commu-
nication methods such as reminders by post have been
replaced by cell phone text messages, social network
messages, e-mails, etc. It is a good practice to remind
patients and/or parents of the benefits of compliance
with follow-ups. Most dental records software programs
automatically update and support the follow-up system.
In the absence of an automated electronic practice man-
agement system, the basic demographic and contact
information of each patient could be entered in a simple
electronic file corresponding to the appropriate follow-
­up month based on the caries risk of the patient. If the
patient responds, a new recall is set in the appropriate
month. Some incentives might enhance patient motiva-
tion or parent compliance with follow-up visits, e.g., a
low-cost policy for follow-ups, granting a new tooth-
brush for improved oral hygiene, praising the child, or
granting small gifts if there are no treatment needs.
References
1. Keyes PH. The infectious and transmissible nature of experi-
mental dental caries. Findings and implications Arch Oral Biol
1960;1:304–320.
2. Marsh PD. Dental plaque as a biofilm and a microbial com-
munity - implications for health and disease. BMC Oral Health.
2006;6(Suppl 1):S14.
3. Fejerskov O. Changing paradigms in concepts on dental caries:
consequences for oral health care. Caries Res. 2004;38(3):182–
91.
4. Chang NN, Jew JM, Fried D. Lesion dehydration rate changes
with the surface layer thickness during enamel remineralization.
Proc SPIE Int Soc Opt Eng. 2018;10473:104730D. https://doi.
org/10.1117/12.2296023.
5. Takahashi N, Nyvad B. Caries ecology revisited: microbial
dynamics and the caries process. Caries Res. 2008;42(6):409–18.
https://doi.org/10.1159/000159604.
6. Babaahmady KG, Challacombe SJ, Marsh PD, Newman
HN. Ecological study of Streptococcus mutans, Streptococcus
sobrinus and Lactobacillus spp. at sub-sites from approximal
dental plaque from children. Caries Res. 1998;32(1):51–8.
7. Li Y, Tanner A. Effect of antimicrobial interventions on the oral
microbiota associated with early childhood caries. Pediatr Dent.
2015;37(3):226–44.
8. Kohler B, Andreen I. Influence of caries-­preventive measures
in mothers on cariogenic bacteria and caries experience in their
children. Arch Oral Biol. 1994;39(10):907–11.
9. Berkowitz RJ, Jones P. Mouth-to-mouth transmission of the
bacterium Streptococcus mutans between mother and child.
Arch Oral Biol. 1985;30(4):377–9.
 278 N. Kotsanos et al.
10. Selwitz RH, Ismail AI, Pitts NB. Dental caries. Lancet.
2007;369(9555):51–9.
11. Zunt S. Evaluation of the dry mouth patient. Alpha Omegan.
2007;100(4):203–9.
12. Gupta N, Pal M, Rawat S, Grewal MS, Garg H, Chauhan D, et al.
Radiation-induced dental caries, prevention and treatment - a
systematic review. Natl J Maxillofac Surg. 2015;6(2):160–6.
13. Edelstein BL, Chinn CH. Update on disparities in oral health
and access to dental care for America's children. Acad Pediatr.
2009;9(6):415–9.
14. Sapourides DTV, Muronidis S, Kotsanos N. Caries experi-
ence among Greek Pomak children living in rural North-
Eastern Greece. A Cross-Sectional Study. Balkan J Stomatol.
2011;15(1):15–23.
15. Kosma I, Kevrekidou A, Boka V, Arapostathis K, Kotsanos
N. Molar incisor hypomineralisation (MIH): correlation
with dental caries and dental fear. Eur Arch Paediatr Dent.
2016;17(2):123–9. https://doi.org/10.1007/s40368-­016-­0221-­4.
16. Stecksen-Blicks C, Renfors G, Oscarson ND, Bergstrand F,
Twetman S. Caries-preventive effectiveness of a fluoride varnish:
a randomized controlled trial in adolescents with fixed orth-
odontic appliances. Caries Res. 2007;41(6):455–9.
17. Gregory RL, el-Rahman AM, Avery DR. Effect of restorative
treatment on mutans streptococci and IgA antibodies. Pediatr
Dent. 1998;20(4):273–7.
18. Wang X, Willing MC, Marazita ML, Wendell S, Warren JJ, Brof-
fitt B, et al. Genetic and environmental factors associated with
dental caries in children: the Iowa Fluoride Study. Caries Res.
2012;46(3):177–84.
19. Gregory RL, Gfell LE, Malmstrom HS. Differences in secretory
IgA and serum antibodies to Streptococcus mutans isolates from
caries-resistant and caries-susceptible subjects. Adv Exp Med
12 Biol. 1995;371B:1149–52.
20. Pikramenou V, Dimitraki D, Zoumpoulakis M, Verykouki E,
Kotsanos N. Association between dental caries and body mass
in preschool children. Eur Arch Paediatr Dent. 2016;17(3):
171–5.
21. Kumar S, Tadakamadla J, Zinner-Gembeck MJ, Kroon J, Lalloo
R, Johnson NW. Parenting practices and children’s dental car-
ies experience: a structural equation modelling approach. 2017.
Community Dent Oral Epidemiol. 2017;45(6):552–8.
22. Bolin AK. Children's dental health in Europe. An epidemiologi-
cal investigation of 5- and 12-year-old children from eight EU
countries. Swed Dent J Suppl. 1997;122:1–88.
23. Dye BA, Thornton-Evans G, Li X, Iafolla TJ. Dental caries and
sealant prevalence in children and adolescents in the United
States. NCHS. Data Brief. 2011-­2012;2015(191):1–8.
24. Policy on Early Childhood Caries (ECC): classifications, conse-
quences, and preventive strategies. Pediatr Dent. 2016;38(6):52–4.
25. Honkala E, Runnel R, Honkala S, Olak J, Vahlberg T, Saag
M, et al. Measuring dental caries in the mixed dentition by
ICDAS. Int J Dent. 2011;2011:150424.
26. Nyvad B, Baelum V. Nyvad criteria for caries lesion activity and
severity assessment: a validated approach for clinical manage-
ment and research. Caries Res. 2018;52(5):397–405. https://doi.
org/10.1159/000480522.
27. Monse B, Heinrich-Weltzien R, Benzian H, Holmgren C, van
Palenstein Helderman W. PUFA – an index of clinical conse-
quences of untreated dental caries. Community Dent Oral Epi-
demiol. 2010;38(1):77–82.
28. Chawla N, Messer LB, Adams GG, Manton DJ. An in vitro
comparison of detection methods for approximal carious lesions
in primary molars. Caries Res. 2012;46(2):161–9.
29. Kotsanos N, Darling AI. Influence of posteruptive age of
enamel on its susceptibility to artificial caries. Caries Res.
1991;25(4):241–50.
30. Bin-Shuwaish M, Yaman P, Dennison J, Neiva G. The correla-
tion of DIFOTI to clinical and radiographic images in class II
carious lesions. J Am Dent Assoc. 2008;139(10):1374–81.
31. Astvaldsdottir A, Ahlund K, Holbrook WP, de Verdier B,
Tranaeus S. Approximal caries detection by DIFOTI: in vitro
comparison of diagnostic accuracy/efficacy with film and digital
radiography. Int J Dent. 2012;2012:326401.
32. Seremidi K, Lagouvardos P, Kavvadia K. Comparative in vitro
validation of VistaProof and DIAGNOdent pen for occlusal
caries detection in permanent teeth. Oper Dent. 2012;37(3):
234–45.
33. Lussi A, Hack A, Hug I, Heckenberger H, Megert B, Stich
H. Detection of approximal caries with a new laser fluorescence
device. Caries Res. 2006;40(2):97–103.
34. Kuhnisch J, Ifland S, Tranaeus S, Hickel R, Stosser L, Heinrich-
Weltzien R. In vivo detection of non-­cavitated caries lesions on
occlusal surfaces by visual inspection and quantitative light-
induced fluorescence. Acta Odontol Scand. 2007;65(3):183–8.
35. Schulze RK, Nackat D, D'Hoedt B. In vitro carious lesion detec-
tion on D-, E-, and F-speed radiographic films. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2004;97(4):529–34.
36. Ludlow JBMA. In: PM WSC, editor. Oral radiology principles
and interpretation. 7th ed. St. Louis: Elsevier; 2014. p. 41–62.
37. Akdeniz BG, Grondahl HG, Kose T. Effect of delayed scanning
of storage phosphor plates. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2005;99(5):603–7.
38. Farman AG, Levato CM, Gane D, Scarfe WC. In practice: how
going digital will affect the dental office. J Am Dent Assoc.
2008;139(Suppl):14S–9S.
39. Guideline on Caries-risk Assessment and Management for Infants.
Children, and adolescents. Pediatr Dent. 2016;38(6):142–9.
40. Koga-Ito CY, Unterkircher CS, Watanabe H, Martins CA,
Vidotto V, Jorge AO. Caries risk tests and salivary levels of
immunoglobulins to Streptococcus mutans and Candida
albicans in mouthbreathing syndrome patients. Caries Res.
2003;37(1):38–43.
41. Tellez M, Gomez J, Pretty I, Ellwood R, Ismail AI. Evidence
on existing caries risk assessment systems: are they predictive
of future caries? Community Dent Oral Epidemiol. 2013;41(1):
67–78.
42. de Rezende VS, Fonseca-Silva T, Drumond CL, Ramos-Jorge
ML, Paiva SM, Vieira-Andrade RG. Do patients with extrinsic
black tooth stains have a lower dental caries experience? a sys-
tematic review and meta-analysis. Caries Res. 2019;53(6):617–27.
https://doi.org/10.1159/000500476.
43. Dean HTAF, Elvove E. Domestic water and dental caries. Public
Health Report (US). 1942;57:1155–79.
44. Buzalaf MA, Pessan JP, Honório HM, ten Cate JM. Mecha-
nisms of action of fluoride for caries control. Monogr Oral Sci.
2011;22:97–114. https://doi.org/10.1159/000325151.
45. Murray JJ. Efficacy of preventive agents for dental caries. Sys-
temic fluorides: water fluoridation. Caries Res. 1993;27(Suppl
1):2–8.
46. Toumba KJ, Twetman S, Splieth C, Parnell C, van Loveren C,
Lygidakis NΑ. Guidelines on the use of fluoride for caries pre-
vention in children: an updated EAPD policy document. Eur
Arch Paediatr Dent. 2019;20(6):507–16. https://doi.org/10.1007/
s40368-­019-­00464-­2.
47. Maslak EEAI, Kchmizova TG, Litovkina LS, Luneva N. The
effect of a milk fluoridation project in Volgograd. Caries Res.
2004;38(4):377.
48. Espelid I. Caries preventive effect of fluoride in milk, salt and
tablets: a literature review. Eur Arch Paediatr Dent. 2009;10(3):
149–56.
49. Poulsen S, Gadegaard E, Mortensen B. Cariostatic effect of daily
use of a fluoride-containing lozenge compared to fortnightly
Dental Caries Prevention in Children and Adolescents
rinses with 0.2% sodium fluoride. Caries Res. 1981;15(3):
236–42.
50. Rozier RG, Adair S, Graham F, Iafolla T, Kingman A, Kohn
W, et al. Evidence-based clinical recommendations on the pre-
scription of dietary fluoride supplements for caries prevention: a
report of the American Dental Association Council on Scientific
Affairs. J Am Dent Assoc. 2010;141(12):1480–9.
51. Marinho VC, Higgins JP, Sheiham A, Logan S. Fluoride tooth-
pastes for preventing dental caries in children and adolescents.
Cochrane Database Syst Rev. 2003;1:CD002278.
52. Twetman S. Caries prevention with fluoride toothpaste in chil-
dren: an update. Eur Arch Paediatr Dent. 2009;10(3):162–7.
53. Pretty IA. High fluoride concentration toothpastes for children
and adolescents. Caries Res. 2016;50(Suppl 1):9–14.
54. Mascarenhas AK, Burt BA. Fluorosis risk from early expo-
sure to fluoride toothpaste. Community Dent Oral Epidemiol.
1998;26(4):241–8.
55. American Dental Association Council on Scientific A. Fluo-
ride toothpaste use for young children. J Am Dent Assoc.
2014;145(2):190–1.
56. Guideline on Perinatal and Infant Oral Health Care. Pediatr
Dent. 2016;38(5):54–8.
57. Marinho VC, Higgins JP, Logan S, Sheiham A. Fluoride gels for
preventing dental caries in children and adolescents. Cochrane
Database Syst Rev. 2002;2:CD002280.
58. Moyer VA. US preventive services task force. Prevention of den-
tal caries in children from birth through age 5 years: US Preven-
tive Services Task Force recommendation statement. Pediatrics.
2014;133(6):1102–11.
59. Marinho VC, Higgins JP, Logan S, Sheiham A. Fluoride var-
nishes for preventing dental caries in children and adolescents.
Cochrane Database Syst Rev. 2002;3:CD002279.
60. Stebbins E. What value has Argenti Nitras as a therapeutic agent
in dentistry? Int Dent J. 1891;12(10):661–71.
61. Nishino M, Yoshida S, Sobue S, Kato J, Nishida M. Effect of
topically applied ammoniacal silver fluoride on dental caries in
children. J Osaka Univ Dent Sch. 1969;9:149–55.
62. Ng MW, Sulyanto RS. Chronic disease management of car-
ies in children and the role of silver diamine fluoride. CDA.
2018;46(1):23–34.
63. Crystal YO, Marghalani AA, Ureles SD, Wright JT, Sulyanto
R, Divaris K, et al. Use of silver diamine fluoride for den-
tal caries management in children and adolescents, including
those with special health care needs. Pediatr Dent. 2017;39(5):
135–45.
64. Whitford GM. Fluoride in dental products: safety consider-
ations. J Dent Res. 1987;66(5):1056–60.
65. Evans RW, Darvell BW. Refining the estimate of the critical
period for susceptibility to enamel fluorosis in human maxillary
central incisors. J Public Health Dent. 1995;55(4):238–49.
66. Tavener JA, Davies GM, Davies RM, Ellwood RP. The preva-
lence and severity of fluorosis in children who received tooth-
paste containing either 440 or 1,450 ppm F from the age of 12
months in deprived and less deprived communities. Caries Res.
2006;40(1):66–72.
67. Cochrane NJ, Saranathan S, Cai F, Cross KJ, Reynolds
EC. Enamel subsurface lesion remineralisation with casein phos-
phopeptide stabilised solutions of calcium, phosphate and fluo-
ride. Caries Res. 2008;42(2):88–97.
68. Sitthisettapong T, Phantumvanit P, Huebner C, Derouen
T. Effect of CPP-ACP paste on dental caries in primary teeth: a
randomized trial. J Dent Res. 2012;91(9):847–52.
69. Fennis-le YL, Verdonschot EH, Burgersdijk RC, Konig KG,
van’t Hof MA. Effect of 6-monthly applications of chlorhexi-
dine varnish on incidence of occlusal caries in permanent
molars: a 3-year study. J Dent. 1998;26(3):233–8.
279 12
70. Petersson LG, Magnusson K, Andersson H, Deierborg G, Twet-
man S. Effect of semi-annual applications of a chlorhexidine/
fluoride varnish mixture on approximal caries incidence in
schoolchildren. A three-year radiographic study. Eur J Oral Sci.
1998;106(2 Pt 1):623–7.
71. Maruniak J, Clark WB, Walker CB, Magnusson I, Marks RG,
Taylor M, et al. The effect of 3 mouthrinses on plaque and gin-
givitis development. J Clin Periodontol. 1992;19(1):19–23.
72. Thorild I, Lindau B, Twetman S. Caries in 4-year-old children
after maternal chewing of gums containing combinations of xyli-
tol, sorbitol, chlorhexidine and fluoride. Eur Arch Paediatr Dent.
2006;7(4):241–5.
73. Thorild I, Lindau B, Twetman S. Long-term effect of maternal
xylitol exposure on their children's caries prevalence. Eur Arch
Paediatr Dent. 2012;13(6):305–7.
74. Twetman S. Are we ready for caries prevention through bacterio-
therapy? Braz Oral Res. 2012;26(Suppl 1):64–70.
75. Bernardi S, Karygianni L, Filippi A, Anderson AC, Zürcher A,
Hellwig E, et al. Combining culture and culture-­independent
methods reveals new microbial composition of halitosis patients'
tongue biofilm. Microbiology. 2020;9(2):e958. https://doi.
org/10.1002/mbo3.958.
76. Higuchi T, Suzuki N, Nakaya S, Omagari S, Yoneda M, Hanioka
T, et al. Effects of Lactobacillus salivarius WB21 combined with
green tea catechins on dental caries, periodontitis, and oral mal-
odor. Arch Oral Biol. 2019;98:243–7. https://doi.org/10.1016/j.
archoralbio.2018.11.027.
77. Ceyhan D, Akdik C, Kirzioglu Z. An educational programme
designed for the evaluation of effectiveness of two tooth brush-
ing techniques in preschool children. Eur J Paediatr Dent.
2018;19(3):181–6. https://doi.org/10.23804/ejpd.2018.19.03.03.
78. Taschner M, Rumi K, Master AS, Wei J, Strate J, Pelka M. Com-
paring efficacy of plaque removal using professionally applied
manual and power toothbrushes in 4- to 7-year-old children.
Pediatr Dent. 2012;34(1):61–5.
79. Sharma A, Arora R, Kenchappa M, Bhayya DP, Singh D. Clini-
cal evaluation of the plaque-removing ability of four different
toothbrushes in visually impaired children. Oral Health Prev
Dent. 2012;10(3):219–24.
80. Creeth JE, Gallagher A, Sowinski J, Bowman J, Barrett K, Lowe
S, et al. The effect of brushing time and dentifrice on dental
plaque removal in vivo. J Dent Hyg. 2009;83(3):111–6.
81. Carvalho JC, Ekstrand KR, Thylstrup A. Dental plaque and
caries on occlusal surfaces of first permanent molars in relation
to stage of eruption. J Dent Res. 1989;68(5):773–9.
82. Harkane T, Larmas MA, Virtanen JI, Arjas E. Applying modern
survival analysis methods to longitudinal dental caries studies. J
Dent Res. 2002;81(2):144–8.
83. Wegehaupt F, Jorge F, Attin T, Tauböck T. Influence of short-
ened light-curing duration on the potential of resin-based
surface sealants to prevent Erosion. Oral Health Prev Dent.
2017;15(1):79–87. https://doi.org/10.3290/j.ohpd.a37717.
84. Lygidakis NA, Oulis KI. A comparison of Fluroshield
with Delton fissure sealant: four year results. Pediatr Dent.
1999;21(7):429–31.
85. Lygidakis NA, Oulis KI, Christodoulidis A. Evaluation of fis-
sure sealants retention following four different isolation and
surface preparation techniques: four years clinical trial. J Clin
Pediatr Dent. 1994;19(1):23–5.
86. Papageorgiou SN, Dimitraki D, Kotsanos N, Bekes K, van Waes
H. Performance of pit and fissure sealants according to tooth
characteristics: a systematic review and meta-analysis. J Dent.
2017;66:8–17.
87. Antonson SA, Antonson DE, Brener S, Crutchfield J, Larumbe
J, Michaud C, et al. Twenty-four month clinical evaluation of fis-
sure sealants on partially erupted permanent first molars: glass
 280 N. Kotsanos et al.
ionomer versus resin-based sealant. J Am Dent Assoc. 2012;143(2):
115–22.
88. Carvalho JC, Thylstrup A, Ekstrand KR. Results after 3 years of
non-operative occlusal caries treatment of erupting permanent first
molars. Community Dent Oral Epidemiol. 1992;20(4):187–92.
89. Romcke RG, Lewis DW, Maze BD, Vickerson RA. Retention
and maintenance of fissure sealants over 10 years. J Can Dent
Assoc. 1990;56(3):235–7.
90. Simonsen RJ. Retention and effectiveness of dental sealant after
15 years. J Am Dent Assoc. 1991;122(10):34–42.
91. Raadal M, Utkilen AB, Nilsen OL. Fissure sealing with a
light-cured resin-reinforced glass-ionomer cement (Vitre-
bond) compared with a resin sealant. Int J Paediatr Dent.
1996;6(4):235–9.
92. Gustafsson BE, Quensel CE, Lanke LS, Lundqvist C, Grahnen
H, Bonow BE, et al. The Vipeholm dental caries study; the effect
of different levels of carbohydrate intake on caries activity in
436 individuals observed for five years. Acta Odontol Scand.
1954;11(3–4):232–64.
93. Bowen WH. The Stephan curve revisited. Odontology.
2013;101(1):2–8. https://doi.org/10.1007/s10266-­012-­0092-­z.
94. van Loveren C, Duggal MS. The role of diet in caries prevention.
Int Dent J. 2001;51(6 Suppl 1):399–406.
95. Evans D. Some evidence that one-to-one dietary interventions
in the dental setting can change behaviour. Evid Based Dent.
2012;13(2):42.
96. Arheiam A, Brown SL, Burnside G, Higham SM, Albadri S,
Harris RV. The use of diet diaries in general dental practice in
England. Community Dent Health. 2016;33(4):267–73. https://
doi.org/10.1922/CDH_3928Arheiam07.
97. Feldens CA, Giugliani ER, Vigo A, Vitolo MR. Early feed-
ing practices and severe early childhood caries in four-year-old
12 children from southern Brazil: a birth cohort study. Caries Res.
2010;44(5):445–52.
98. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened bev-
erages and weight gain: a systematic review. Am J Clin Nutr.
2006;84(2):274–88.
99. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin
LR, Flegal KM. Prevalence of overweight and obesity among
US children, adolescents, and adults, 1999-­ 2002. JAMA.
2004;291(23):2847–50.
100. Ogden CL, Carroll MD, Lawman HG, Fryar CD, et al. Trends
in obesity prevalence among children and adolescents in the
United States, 1988-1994 through 2013-­2014. JAMA. 2016 Jun
7;315(21):2292–9. https://doi.org/10.1001/jama.2016.6361.
101. Pikramenou V, Dimitraki D, Zoumpoulakis M, Verykouki E,
Kotsanos N. Association between dental caries and body mass
in preschool children. Eur Arch Paediatr Dent. 2016;17(3):171–
5. https://doi.org/10.1007/s40368-­016-­0222-­3.
102. Krebs NF, Jacobson MS, American Academy of Pediatrics
Committee on N. Prevention of pediatric overweight and obe-
sity. Pediatrics. 2003;112(2):424–30.
103. Ng MW, Fida Z. Dental hygienist-led chronic disease manage-
ment system to control early childhood caries. J Evid Based
Dent Pract. 2016;16(Suppl):20–33. https://doi.org/10.1016/j.
jebdp.2016.01.015.
104. Edelstein BL, Ng MW. Chronic disease management strategies
of early childhood caries: support from the medical and dental
literature. Pediatr Dent. 2015;37(3):281–7.
105. Brondani B, Knorst JK, Tomazoni F, Dutra Cósta M, Vargas
AW, Noronha TG, Mendes FM, Ardenghi TM. Effect of the
COVID-19 pandemic on behavioral and psychosocial factors
related to oral health in adolescents: a cohort study. Int J Pae-
diatr Dent. 2021. https://doi.org/10.1111/ipd.12784.
106. Borrelli B, Tooley EM, Scott-Sheldon LA. Motivational inter-
viewing for parent-child health interventions: a systematic review
and meta-analysis. Pediatr Dent. 2015;37(3):254–65.
107. Patel S, Bay RC, Glick M. A systematic review of dental recall
intervals and incidence of dental caries. J Am Dent Assoc.
2010;141(5):527–39.
108. Ramos-Gomez FJ, Crystal YO, Ng MW, Crall JJ, Feather-
stone JD. Pediatric dental care: prevention and management
protocols based on caries risk assessment. J Calif Dent Assoc.
2010;38(10):746–61.
 281 13

Restoration of Carious Hard

Dental Tissues
Nikolaos Kotsanos and Ferranti Wong

Contents

13.1 Age up to 3 Years – 283

13.1.1 E arly Childhood Caries – 283
13.1.2 Atraumatic Restorative Treatment – 285

13.2 Age 3 to 6 Years – 286

13.2.1  rimary Molar Restorations – 286
P
13.2.2 Preformed Metal Crowns (PMC) – 287
13.2.3 Restoring Anterior Primary Teeth – 290

13.3 Age 6 to 12 Years – 291

13.3.1  it and Fissure Caries – 291
P
13.3.2 Proximal Surfaces of Permanent Teeth – 293
13.3.3 Excessively Carious Permanent Molars – 294

13.4 Age 12 to 18 Years – 294

13.4.1  roximal and Smooth Surface Caries – 294
P
13.4.2 Class II Cavities – 296

13.5 Isolating the Working Field by Rubber Dam – 297

13.5.1 E quipment – 299
13.5.2 Preparation and Placement – 300
13.5.3 Alternative Options for Isolation – 300

13.6 Restorative Materials in Pediatric Dentistry – 301

13.6.1  avity Matrices – 301
C
13.6.2 Cavity Lining/Base Materials – 301
13.6.3 Enamel and Dentin Adhesives – 302
13.6.4 Glass-Ionomer Cements – 303
13.6.5 Resin-Based Composites – 305
13.6.6 Dental Amalgam – 307

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_13
13.6.7  reformed Crowns – 307
P
13.6.8 Veneers and Prosthetic Appliances – 308

13.7 Restoration Failure and Contemporary Research – 309

13.7.1 F ailure and Repair of Restorations – 309
13.7.2 Improving the Dental Materials – 310

References – 311
Restoration of Carious Hard Dental Tissues
Restorative dental needs of children and adolescents
arise primarily as a consequence of dental caries.
Secondly, they arise from dental trauma, developmental
dental anomalies (more often molar incisor hypominer-
alization) including tooth aplasias, and, less frequently,
erosive dental wear. As explained in the introductory
7 Chap. 1, there are data for increasing number of
unmet needs with decreasing child age. Among other
reasons, this is apparently associated with the less-than-
optimal dental education in pediatric dentistry in most
societies in the past.
During transition from infancy to early childhood,
adolescence, and adulthood, restorative philosophy and
choice of techniques/materials need to suit the changing
conditions of the growing child, e.g., the type of den-
titions (primary or permanent) with their anatomical
differences and functional duration. Moreover, differ-
ent preventive principals and strategies may be suitable
according to the patient’s caries risk and age group in
order to achieve optimum results. All these factors affect
the treatment plan, and for this reason the caries man-
agement is presented in this chapter by age group.
13.1 Age up to 3 Years
This age group is characterized by the eruption of the
entire primary dentition and the process of establish-
ing functional occlusion. At the same time, although
the child cognitive development is rapid, it is still below
the level required to fully, and consistently, cooperate
with the dentist for restorative treatment. Therefore, it
is utmost important to identify these preschoolers with
high caries risk so that preventive advices and practices
can be given by educating them and, more crucially,
guiding parents to comply with their implementation.
13.1.1 Early Childhood Caries
Definition
The American Academy of Pediatric Dentistry
(AAPD) defines early childhood caries as “the pres-
ence of one or more decayed (non-cavitated or cavi-
tated lesions), missing (due to caries), or filled tooth
surfaces in any primary tooth in a child under the age
of six.” Furthermore, if this occurs before the age of
3 years, or if there are at least 4, 5, or 6 carious cavi-
ties at age 3, 4, or 5 years, respectively, the disease is
categorized as severe early childhood caries [1].
Early childhood caries (ECC) may affect any primary
teeth, more often molars. Severe early childhood caries
283 13
(S-ECC) may have any pattern of insult, affecting ante-
rior and/or posterior primary teeth. Poorly informed
parents are often surprised by how soon caries develops
in their child’s new teeth, before good oral hygiene, fluo-
ride, and other preventive measures are established.
One particular form of S-ECC, formerly referred
to as “baby bottle syndrome,” is characterized by car-
ies affecting mainly the maxillary primary incisors and
first molars. This pattern is attributed to the sequence
of eruption and therefore the exposure time of each
tooth to the cariogenic challenge [2]. The absence of
proper oral hygiene and fluorides together with unsuit-
able dietary habits are deemed to be the cause. However,
presence of severe developmental dental defects (e.g.,
primary molar hypomineralization or hypoplasia) are
known to promote this advancing form of caries [3,
4]. These dietary habits most often include allowing
the baby to go to sleep with a bottle containing milk
or other liquids with fermentable sugars, i.e., during the
period when salivary flow is minimal, thus depriving
teeth from its protective properties. This S-ECC form
may also occur as a result of prolonged breastfeeding
at will during the night, usually while the infant sleeps
with mother [5] (. Fig. 13.1). Breastfeeding is known
to promote physical and emotional health; its ad libitum
use (i.e., during sleep), however, after the first teeth erupt
is discouraged, as is bottle use when the child is able to
use a glass, i.e., after age 12 to 18 months [1].
Bottle-feeding-associated S-ECC first challenges the
labial surfaces of the maxillary incisors, which benefit
less by the protective effect of saliva. It subsequently
extends to adjacent surfaces such as palatal and inter-
proximal, as well as the occlusal and other surfaces of
the maxillary primary molars. The mandibular anterior
teeth remain without obvious damage until much later,
probably because of saliva protection and less contact
with the liquid intakes (. Fig. 13.2). If the deleterious
diet habit continues, other teeth such as canines and
..      Fig. 13.1 S-ESS in the form of nursing caries with advanced cer-
vical lesions in the maxillary incisors due to prolonged breast feeding
at will and absence of oral hygiene with fluoride
 284 N. Kotsanos and F. Wong
..      Fig. 13.2 Complete destruction of the maxillary primary inci-
sors (baby bottle tooth caries form of S-ECC) with fistula from right
central incisor and carious involvement of maxillary primary first
molars in a girl of 4 years. Mandibular anterior teeth are free of
clinical caries
second primary molars, even the interproximal surfaces
of the lower anterior teeth, may be involved.
13.1.1.1 Prevalence and Prevention
Colonization of cariogenic flora on the baby’s primary
teeth originates from individuals in close contact with
them, primarily mothers. Therefore, oral health and
hygiene of the mother could be a measure of ECC pre-
vention for the baby [6]. Bottle-feeding-related ECC
prevalence varies widely affecting the majority of chil-
13 dren in some isolated communities, and S-ECC is found
in much higher prevalence in families of low socioeco-
nomic background and/or remote rural areas [7]. For
their prevention, official pediatric bodies have set up the
first dental examination for babies before the their first
birthday, so that parents are adequately informed and
motivated on time [8] (see 7 Chap. 6).
13.1.1.2 Treatment and Restorations
With early diagnosis and implementation of therapeutic
measures, ECC lesions can be arrested and, with ongo-
ing eruption of teeth, remain inactive and require no
restoration, except for esthetic purposes (. Fig. 13.3).
The greatest difficulty in restoring heavily carious teeth
is insufficient cooperation of children under 3 years.
More specifically, addressing their restorative needs in
the dental office without sedation is hindered by:
55 The negative reaction of children fearing unknown
individuals in a stressful situation
55 The intense instinctive refusal of treatment even in
the least painful stimulus
55 The difficulty to maintain cooperation for a long
time during extensive restorations
In countries where in-office sedation is not possible with-
out an anesthesiologist present, dental rehabilitation is
..      Fig. 13.3 a Arrest of small labial cavities of maxillary primary
incisors and possibly of interproximal cavities in the midline. b
Despite late diagnosis of S-ECC (in the form of “baby bottle tooth
decay”), preventive practices are proven to be effective. Restorations
may follow for esthetics when the now 2-year-old patient becomes
cooperative
often necessary to be done in a hospital setting by a
trained pediatric dentist under general anesthesia admin-
istered by an anesthesiologist. This, however, significantly
raises the cost of treatment (see 7 Chap. 8). Therefore,
unless there are urgent needs due to pulpal inflammation
and pain, a biological (etiological) approach focusing to
the conversion of active caries lesions to inactive should
be preferred, at least until cooperation of the child may
allow definite restorations possible in the dental office.
This approach may include [8, 9]:
55 Effective oral hygiene with fluoride toothpaste
55 Discontinuing cariogenic diet habits
55 Frequent checkups at the dental office with fluoride
varnish application or perhaps other antimicrobial
agents (e.g., silver diamine fluoride)
If this therapeutic target is met, the certainly more
demanding dental restoration sessions can be post-
poned to age 3 years or older [9] (. Fig. 13.4). Effec-
tive counseling of the dental professionals by avoiding
judgmental remarks to the family is very important
because the success of nonsurgical caries management
depends on parental motivation, compliance, and coop-
eration. Indeed, keeping frequent, initially monthly or
bimonthly, appointments is critical due to the all too
often seen inadequate compliance.
Restoration of Carious Hard Dental Tissues
a a
b
..      Fig. 13.4 a S-ECC in a 4-year-old child with a poor restoration
on the maxillary right central. b Rehabilitation with light shade com-
posite restorations. Incipient caries lesions can be remineralized by
implementing oral hygiene/fluoride measures
..      Fig. 13.5 Arrest and color change to dark of small carious cavity
If this treatment is successful, lesion color usually
turns darker (. Fig. 13.5). This is a sign of arrested caries
from minerals and organic material influx and/or degra-
dation that stains the porous carious tissues. Deep carious
cavities need partial excavation with hand spoon excava-
tors, and/or rotary instruments at low speed, if tolerated
by the child. Local anesthesia may carefully be used only
if anticipated as acceptable to the child. Eventually a
semipermanent restoration is placed in the cavity, prefer-
ably with resin-modified glass-ionomer cement (RMGIC)
because of easy procedure and quick setting, good bond-
ing to dental tissues, and fluoride release.
285 13
b
..      Fig. 13.6 a, b Radiographic images of a child with very high-­
caries activity 18 months after receiving dental rehabilitation under
general anesthesia when 2 years old. c The noncompliance of par-
ents to caries preventive plan and follow-ups led to further multiple
new restorative needs
For very advanced carious cavities with pulp inflam-
mation and/or pain at this age, general anesthesia is the
preferred method to surpass the inability of the child to
cooperate. Adherence to the preventive strategy should
not be overlooked (. Fig. 13.6). Special efforts are
made to restore canines and second primary molars due
to their late exfoliation and, more importantly, for space
maintenance in accommodating the permanent teeth
in the future. Other pulpally involved anterior primary
teeth are preferably extracted, while there is also the
possibility of pulpotomy for primary molars. As to the
restoration materials for posterior teeth, amalgam, com-
posites (including compomers), RMGIC, or preformed
molar crowns (PMC) may be preferred depending on
cavity size and surfaces involved [10].
13.1.2 Atraumatic Restorative Treatment
Atraumatic restorative technique (ART) is a form of
less-than-optimal restorative treatment applied without
 286 N. Kotsanos and F. Wong

the need for rotary instruments in certain circumstances. a

Carious dentin and enamel are removed as best as pos-
sible with hand instruments, with special attention to
removing peripheral decay and unsupported enamel,
preserving pulp vitality and placing a glass-ionomer res-
toration. The purpose is to allow the deepest part of car-
ious dentin to remineralize by calcium and phosphate
ions, possibly of pulpal origin. This is accomplished by
depriving the microorganisms sealed in the deeper hard
and stained dentin from their nutrient substrate (carbo-
hydrates). The effectiveness of this approach in arresting b
caries lesions has been well-documented in clinical stud-
ies in class I cavities of permanent and primary teeth
[11] but has been found as inadequate for class II resto-
rations in primary molars [12].
ART is proposed mainly where technological infra-
structure is lacking. In countries or areas with contem-
porary services of pediatric dentistry, it could be used
as a temporary measure for children with inadequate
ability to cooperate with the view to later improved
cooperation. The term used is interim therapeutic res- ..      Fig. 13.7 a Disto-occlusal cavity in the mandibular primary right
torations (ITR), and these may be useful for children first molar of a 5-year-old after occlusal restoration in the same
tooth and sealant placement in the adjacent second molar before
under 3 years, or sometimes older, with S-ECC, as stated
18 months. b The radiographic examination reveals proximal caries
in implementing a flexible treatment plan in 7 Chap. 6. lesions of various depth on all four primary molars of this side

13.2 Age 3 to 6 Years

Caries in the proximal surfaces of primary molars is

13 very common in this age group. Its diagnosis before the
collapse of proximal enamel marginal ridge is mainly
based on the radiographic image. Due the buccolin-
gual width of the molars, unlike in anterior teeth, direct
visual assessment is difficult prior to cavitation and can
only be suspected by color change often seen occlusally.
In the occlusal, buccal, and lingual surfaces, where car-
ies is commonly found, visual assessment is relatively
easier. At age five, most restorative needs are in primary
molars (. Fig. 13.7). In low-caries populations, more
than 50% of proximal surface caries in primary molars
is limited to enamel radiographically [13]. This offers for
nonsurgical therapeutic interventions.
13.2.1 Primary Molar Restorations
In the past, the extensive use of amalgam in the primary
molars, just like in the permanent ones, required prepa-
rations with retentive cavity shape after caries removal.
The widespread use of adhesive materials nowadays
has reduced this need and has resulted to removing
less healthy tooth substance. Such materials include
resin composites and their acid modified hybrids (com-
pomers) as well as RMGIC [11].
..      Fig. 13.8 Tungsten carbide bur No. 330 (left) and various-shaped
small-sized diamond-coated burs for cutting enamel to prepare cavi-
ties in primary teeth
55 In class I cavities, preparation is limited to remov-
ing the carious dentin and the fragile unsupported
enamel around it. “Extension for prevention” into
other pits and fissures is not required as these could
be sealed, if needed. Access according to the pre-
dicted cavity size can be achieved with rotary cutting
burs, such as a tungsten carbide bur No. 330 or a
cylindrical diamond-coated bur (diamond for short),
in a high-speed handpiece (. Fig. 13.8). Regarding
the restorative material, any of the three abovemen-
tioned types of materials may be used. When, how-
ever, a significant part of the restoration is exposed
to heavy occlusal loads, a composite is preferred –
with prior GIC coating in deep cavities – to better
resist the abrasive forces (. Fig. 13.9).
Restoration of Carious Hard Dental Tissues
a b
c the matrix wear by the cylindrical diamond
..      Fig. 13.9 a Large class I cavities with partial enamel removal for
cavity access in the second primary molar. b Careful removal of cari-
ous dentin for avoiding exposure of any pulp horns (indirect pulp
treatment). c Composite restoration with incremental technique,
after cavity base lining with GIC
55 In class II cavities, opening through enamel, unless
the adjacent tooth is missing, is made by occlusal
access with a cylindrical diamond bur cutting in a
buccolingual direction, within the limits of the
intended size of the proximal box. This need not
reach so-called self-cleaning proximal areas, at least
for patients with daily oral hygiene, fluoride, and
regular recalls. The high injury rates of the neighbor-
ing enamel of the adjacent tooth necessitate its pro-
tection by:
1. Securing a sectional metal matrix in the interden-
tal space with a wooden wedge during box prepa-
ration (. Fig. 13.10)
2. Removal of unsupported enamel by hand chisels
to avoid such risk
The bulk of the softened dentin can easily be removed
with a spoon excavator. Peripheral dentin needs to be
thoroughly removed to allow adequate bonding and
prevent microleakage that may lead to secondary caries
development. This is succeeded by a round steel bur of the
proper size (usually No. 4 or 5) at low speed. Both these
traditional ways, and their combination works faster and
287 13
a b
..      Fig. 13.10 a Placing sectional metal matrix for disto-occlusal
cavity preparation of mandibular second primary molar to protect
the contacting mesial surface of the first permanent molar. b Note
more accurate than other newer techniques such using
polymer burs, Er:YAG laser, or the even slower chemo-
mechanical Carisolv® system [14]. Great caution should
be given to removing deep softened dentin because of the
risk of injuring the pulp horn, which also applies for the
class I deep cavities. Rounded internal cavity angles allow
better application of the restorative material, including
amalgam, to the cavity walls, and minimize stress con-
centration along the proximo-­occlusal pulpal walls. For
adhesive materials, the occlusal preparation should be
conservative in line with the principles of preventive resin
restorations (see later in this chapter).
Any of the three abovementioned resin composite,
compomer or RMGIC restorative materials may be
preferred as their failures have been similar or less than
amalgam in class II cavities [15]. In deep large cavities
involving greater buccolingual dimension proximally
(. Fig. 13.11), placement of a preformed metal crown
is preferred. RMGIC has also shown success, albeit
with considerable occlusal wear in large cavities [16]. An
open sandwich approach has also been used in primary
molars by covering the RMGIC material with a com-
posite layer (. Fig. 13.12), in order to take advantage
of each material properties [17]. However, its efficacy is
less well-documented than it is for permanent teeth [18].
13.2.2 Preformed Metal Crowns (PMC)
Although standard (small) class II cavities in primary
molars restored by pediatric dentists with RMGIC [19]
or composite [17] could last as long as PMCs, neither of
these materials has adequate evidence of good survival
for sizeable restorations. The good survival reported
on properly fitted PMCs is irrespective of size of cari-
ous destruction of the primary molars [19]. The main
drawback of the PMCs seems to be their esthetics, so
this disadvantage should be adequately explained to
the parents to accept their use. The esthetic problem is
overcome by choosing tooth-colored crowns, which are
 288 N. Kotsanos and F. Wong

..      Fig. 13.11 a Radio-

a b
graphic image of large
proximal-occlusal cavities in
the maxillary primary
molars. b Back-to-back wide
class II preparations with
sectional matrices and
wedge. Extended width of
the boxes is dictated by
carious dentin removal,
while retention is aided by
occlusal lock. c Inserting a
RMGIC material first in the
proximal box through the c d
appropriate tip. d The final
restorations

increasingly marketed as they are more appealing to

parents and children. These are several times the cost of
a PMC and require substantially more tooth prepara-
tion. Irrespective of the type of crowns, supply of a full
set of sizes (No. 2–7 for each type of primary or perma-
nent molars) is necessary for selecting the appropriate
type and size (. Fig. 13.13).
13 Despite of PMCs being anatomically preformed
(“contoured” and “crimped”), radiographic image of
their cervical outline is usually not as acceptable as the
clinical one (. Fig. 13.6). Radiographically, overhangs
in proximal tooth surfaces are often seen, contribut-
ing to some degree of periodontal inflammation, as it
was reported for permanent teeth [20]. This, however,
seems to be reversible, or at least asymptomatic, with
proper oral hygiene. The tooth preparation instruc-
tions, selection, and adjustment of the PMC must be ..      Fig. 13.12 Occlusal view of mandibular primary molars with
large proximal-occlusal RMGIC restorations at 24-month follow-up.
followed carefully [21]. The latter may impose some
The primary second molar was covered with a resin composite layer
difficulties in cases of primary molars with irregular (of whiter shade) using the open sandwich technique. The different
shape due to large proximal cavities, resulting in signifi- occlusal abrasion between the two materials is evident
cant loss of mesiodistal dimensions. In such cases, the
crown shape needs to be adjusted by appropriate con-
touring and crimping pliers (. Fig. 13.14), or even by 13.2.2.1 Fitting Procedure
flattening it mesiodistally with Howe utility pliers. These After anesthetizing the area sufficiently, the molar is
crown manipulations are only possible with plain non- occlusally reduced by a cylindrical diamond in high
veneered PMCs. At times, shortening a PMC may be speed for about 1.5 mm, maintaining the cuspal inclines
necessary to avoid extensive deep sitting subgingivally. of the crown. Gross decay can be removed by a hand
This may be achieved with metal-cutting scissors or a excavator. Proximal reduction, only as much as needed
heatless stone mounted on a low-speed handpiece, fol- for allowing crown insertion, is accomplished with a
lowed by smoothening with rubber wheel. When fitting thin tapered diamond (. Fig. 13.15). This is checked
is impossible, sometimes tricks like using opposite side with an explorer tip. Proximal preparation is done with
PMCs of the other jaw can be tried. appropriate care to avoid injury to the adjacent surfaces
Restoration of Carious Hard Dental Tissues
a a
b
..      Fig. 13.13 a Two 3 M ESPE (St. Paul, MN, USA) boxes with all
sizes of primary (left) and permanent molars (right). b Two Nu Smile
(Houston TX, USA) boxes with primary first molar crowns (left) and
upper anterior crowns (right) made entirely of zirconia
b or other endodontic treatment – discussed in 7 Chap.
a is cemented preferably with GIC. Gross excess can be
c d
..      Fig. 13.14 a Contouring and crimping PMC pliers. b Contouring
a PMC. c Crimping the cervical edge. d PMCs for first (left) and sec-
ond primary molars (right). The first and third PMC from left are not
festooned (older generation) always requiring adjustments by pliers
in contact. All line angles are rounded. The appropri-
ate size crown is selected by a trial-and-error procedure,
and in case the tooth size is between crown sizes, an
additional circumferential reduction eases seating the
smaller size. The slight elastic deformation of these
thin metal crowns allows for a snap fit with their pre-
contoured shape usually needing no other adjustment.
The tight cervical adaptation means mechanical reten-
tion of the crown and better respect to gingival health.
289 13
b
c
..      Fig. 13.15 Preparing a primary molar for PMC. a Occlusal
reduction. b Preparation of proximal surfaces for crown insertion. c
The green area shows final reduction
Seating the crown is usually easier in the lingual-
to-­
buccal direction for mandibular molars and in
the buccal-­ to-palatal direction for maxillary molars.
Carious dentin can be removed with a spoon excavator.
Deep cavities extending subgingivally may first be filled
with RMGIC. In case of pulp exposure, pulpotomy
14 – may precede crown placement. Finally, the PMC
wiped with a gauze before the cement is set and cement
residues removed from gingival sulcus by an explorer. If
the crown is going to be seated on the tooth the rubber
dam is clamped on, the dam is removed for cementa-
tion. In case of seating two PMCs in adjacent molars,
their trial must be simultaneous before cementing to
verify ­sufficient space in the mesiodistal dimension.
Regarding veneered or zirconia crowns, further reduc-
tion will probably be needed in all surfaces, and this
should be done following each manufacturer’s instruc-
tions (. Figs. 13.16 and 13.17).
Eye Catcher
The “Hall technique” is proposed for placing PMCs
in carious primary molars with neither tooth prepa-
ration nor caries removal [ 21, 22]. Its advocates sup-
port that the PMC can be pushed into place without
local anesthesia; the occlusion can easily be tolerated
by the child and adapted within several days. As this
technique is proposed as simple and easy to use, it
is gaining acceptability by both general practitioners
[23] and parents [24]. It has also been shown that the
longevity of PMCs placed by the Hall technique is as
good as that of conventional approaches with equal
success rates of 95% over an observational period of
77 months [25].
 290 N. Kotsanos and F. Wong
a b
e f
..      Fig. 13.16 a Restorative needs of a 4-year-old. b Following reha-
bilitation, a veneered PMC is requested by parents for maxillary
right first primary molar. c, d, e Crown preparation and radiographic
a III cavity can be prepared by either labial or lingual
13
b enamel bevel, followed by restoration with composite
..      Fig. 13.17 a Inability to fit the smallest size of zirconium crowns
due to space loss because of carious destraction of a first primary
molar. b Fitting the similar size PMC is feasible
13.2.3 Restoring Anterior Primary Teeth
Caries in the proximal contact surfaces of anterior
primary teeth suggests high-caries activity and the
need to implement an appropriate preventive program.
Common locations are the distal surface of the canines
and the mesial of upper incisors. In any case, a class
c d
g h
image. f After cementing the veneered PMC. Notice its esthetic dif-
ference with the mandibular PMC. g, h Occlusal view and radio-
graph at the 6-month follow-up
access, whichever results in less removal of healthy
tooth tissue. Carious dentin may be removed with a
round bur of appropriate size, in a low-speed hand-
piece. Any tooth-­colored restorative material may be
chosen. A lightly retentive cavity shape is given and,
if a composite is preferred, preparation differs only on
beveling the enamel. This is easier done with a small,
thin tapered diamond.
Reconstructing an incisal angle (class IV) fractured
due tο cariously undermined enamel requires a labial
using a sectional celluloid matrix or form. Following
the removal of deep carious dentin, the cervical cavity
aspect, being close to the pulp horn, could be lined with
GIC. Caries in the proximal surfaces of the lower pri-
mary incisors occurs less often and not always requires
restoration. Interproximal stripping with a thin tapered
diamond for creating self-cleaning conditions may be
sufficient treatment for these small cavities. When pri-
mary maxillary incisors are very heavily decayed, there
are at least two restorative options. One is by fitting a
veneered PMC (. Fig. 13.18) or, better, the newer
option of a full zirconia crown. Supply of the respective
sets of crowns is required for selecting the appropriate
size. After removing the decayed and additional tooth
tissue to enable fitting of the crown, this is cemented
with a GIC. In the absence of a set of those preformed
crowns, a second option is building the tooth up with
composite by using celluloid strip crowns [26]. When
there is no sufficient cervical enamel for retention of
the composite material, provided that the teeth have
Restoration of Carious Hard Dental Tissues
previously been endodontically treated, it is possible to
enhance retention either by fabricating a short stainless
steel wire post (. Fig. 13.19) or by a composite post
after an intracanal undercut is created in the root or its
filling material. Limiting such interventions in the cer-
vical third of the root avoids problems with the erup-
tion process of successors during root resorption and
a
b
..      Fig. 13.18 a Labial and palatal aspect of a veneered PMC for
upper incisors. b Similar crowns after cementation
a b
d e
..      Fig. 13.19 a Occlusal radiograph after endodontic treatment of maxillary right primary central incisor. b Custom-made wire post and
strip crown. c, d Securing the post with a fast-setting ZOE cement and, supragingivally, with composite. e After placing the composite filled
strip crown, excess composite flows cervically. f Final restoration after trimming excess material
291 13
shedding of primary incisors. However, the longevity of
these options is not as yet supported by clinical studies.
13.3 Age 6 to 12 Years
The first period of this age range, the early mixed den-
tition period, is marked by the eruption of permanent
first molars and incisors. These teeth require significant
preventive/therapeutic professional care, but frequently
restorative, too. Restorative dental care for primary
molars and possibly canines remains significant during
the whole mixed dentition period and is done as pre-
viously described in 7 Sect. 13.2. For this age span,
another minimally invasive approach has been put for-
ward as “nonoperative treatment” of active cavitated
approximal caries lesions in primary molars [27], in the
way it was again described for primary mandibular inci-
sors in 7 Sect. 13.2. This approach, however, is not truly
nonoperative as it requires partial caries removal by
high-speed cutting enamel to create open cavities and,
more ­importantly, it lacks adequate documentation.
13.3.1 Pit and Fissure Caries
The risk of the occlusal surfaces of first permanent
molars to develop caries is higher during eruption than
after they have reached occlusion [28]. Restoring cari-
ous lesions in these permanent tooth surfaces requires
investing significant dental resources in children under
age 12 and may start the restorative spiral into adult-
hood. Therefore, these surfaces constitute the main
c
f
 292 N. Kotsanos and F. Wong

..      Fig. 13.20 ICDAS codes and

criteria for treatment of fissures
with example photographs.
(From Bekes [34]. By permis-
sion)

ICDAS Code 0 ICDAS Code 1 ICDAS Code 2 ICDAS Code 3

(sound tooth surface) (first visual color (visual change in (localized enamel
change in enamel) enamel) breakdown)

Primary and secondary prevention Secondary Invasive

prevention treatment
Low caries risk:
Fissure sealing (in
Fluoridated toothpaste Fissure sealing individual cases)
Reduction of cariogenic food Restorative
therapy
Fluoride supplements

Topical fluoridation

High or medium caries risk:

Fissure sealing
13
target for preventive/therapeutic interventions in this
age, effected with the application of sealants that are
described in 7 Chap. 12. Small carious lesions in the
pits and fissures may be treated by minimal composite
restorations combined with sealing non-carious fissures.
It is common today for the benefit of communication,
to refer to sealants when the fissure system is healthy or
has minimal (non-cavitated) enamel demineralization,
while preventive resin restoration (PRR) implies that a
carious fissure requires limited dentin removal restored
by small amount of composite [29]. These preventive
restorations are also referred to as ultraconservative or
minimally invasive [30].
13.3.1.1 Preventive Resin Restoration (PRR)
Sealants not only prevent the onset of fissure caries but
may even lead to arrest of dentinal caries. Sealed radio-
graphically verified and active occlusal caries became
inactive and did not progress [31, 32]. The significance of
these findings is that good marginal seal stops substrate
penetration to underlying dentin caries bacteria turning
them inactive. Despite the scientific value of these stud-
ies, however, it remains good practice to remove infected
softened dentin before placing a restoration, because
the marginal integrity cannot be guaranteed in the long
run. Leaving affected (relatively hard) stained dentin in
deep cavities is considered a safe practice [33]. The buc-
cal surface of mandibular first molars and the palatal
surface of maxillary ones should be carefully followed
up as developmental deep pits are often exposed in these
surfaces by ongoing eruption. This requires placement
of a sealant or, if missed, a PRR or typical composite
restoration may be needed later (7 Fig. 12.41). The sec-
ond permanent molars may also be similarly vulnerable
during eruption at the late mixed to early permanent
dentition period. All fissure sealants should be periodi-
cally reexamined for defects and repaired with PRRs if
need be. Diagnostic criteria for selecting a sealant or a
PRR are schematically shown in . Fig. 13.20.
The PRR philosophy has been explained earlier in
the primary molars. Its placing procedure is as follows:
after plaque removal just as with sealant placement, a
minimum preparation of pits and fissures may be made
for improved access with a tapered or a small diameter
(0.5–0.8 mm) round diamond. The extent of demineral-
ized enamel and dentin dictates possible further cavity
Restoration of Carious Hard Dental Tissues
a b
c d
..      Fig. 13.21 a Aiming to restore a mildly carious first permanent
molar with PRR. b Caries removal leads to one of the cavities being
relatively large for PRR. c Etched enamel following a GIC base in
the deep cavity. d After adhesive and composite placement, the resto-
ration is completed with sealing non-carious fissures
opening (. Fig. 13.21). Removal of carious dentin is
carried out with a small (No. 1 to 4) round bur at low
speed. The aim is to combine:
55 Removal of carious dentin through conservative
enamel preparation and restoring with flowable com-
posite
55 Sealing non-carious fissures
Eye Catcher
For the removal of carious enamel and dentin, the
laser technology may alternatively be used. In recent
years, many studies have advocated its usefulness [35,
36]. There are several laser device types; those pre-
ferred for cutting hard tissues are primarily of the
erbium type, at two wavelengths, Er,Cr: YSGG at
2.780 nm and Er:YAG at 2.940 nm (. Fig. 13.22).
Their advantages include a painless procedure with
cavity preparation often not requiring the administra-
tion of local anesthesia, while the main disadvantage
still remains the relatively high cost of equipment.
Material of choice for replacing carious tissue
removal for the PRR is resin composite. Beveling and
etching the enamel, as well as etching the dentin for
5–8 seconds, precede coating with an adhesive. Com-
posite placement and sealing the non-carious fissures
follow. Long-term results for clinical behavior of such
restorations have shown high success rates of 93–95%
and absence of recurrent caries in 5–6 years [37, 38].
Restoring the typical, perhaps deep, class I cavity is
293 13
a b
..      Fig. 13.22 a hard tissue cutting laser device (Er, Cr: YSGG). b
Occlusal cavity preparation of a severely hypomineralized mandibu-
lar primary second molar without local anesthesia. (Courtesy of Dr.
K. Arapostathis)
performed in the same manner preferring incremental
placement of composite (. Fig. 13.23).
13.3.2  roximal Surfaces of Permanent
P
Teeth
13.3.2.1 Permanent First Molars
The first interproximal surface of a permanent tooth to
become carious is usually the mesial of the first molar. If
this surface is accessible (e.g., during preparing a disto-­
occlusal cavity in the adjacent second primary molar or
in the short time between its shedding and full eruption
of successor premolar), a conservative class V type res-
toration can be done with any of the materials suggested
above (. Fig. 13.24), as long as the cavity size does not
significantly weaken the mesio-occlusal marginal ridge.
Otherwise, a standard class II cavity is prepared for a
composite or an amalgam restoration, a procedure pre-
sented in restoration types for the next age group.
13.3.2.2 Permanent Incisors
Caries in the proximal surfaces of the permanent inci-
sors, much more frequently the maxillary incisors, occur
in high-risk children. Family awareness and motiva-
tion for the adoption of caries control practices should
be the main target, together with restorative approach
when cavitation is already established. Access to cav-
ity can be either palatal/lingual or labial, depending on
which results in the most conservative restoration. No
extension for self-retentive cavity shape is required apart
from beveling the enamel to increase micromechanical
retention of the composite, which is the preferred adhe-
sive material due to its mechanical properties and supe-
rior esthetics. In deep cavities, a GIC base may be used.
 294 N. Kotsanos and F. Wong
b c
..      Fig. 13.23 a Bite wing radiograph showing a deep cavity of man-
dibular left second permanent molar. b Preparation of various sizes
in the second premolar and the two molar cavities without removal
Other common needs for esthetic restorations of
permanent incisors in this age group are crown frac-
13 tures, due to trauma, and developmental anomalies of
the hard dental tissues. These are covered in the respec-
tive 7 Chaps. 16 and 17. In all cases, permanent restora-
tions are made with composite with the aid of a suitable
celluloid matrix, strip crown, or incisal angle mold as
described in the textbooks of restorative dentistry.
13.3.3  xcessively Carious Permanent
E risk, the dental clinician may be mostly involved with
Molars
Permanent first molars that are occasionally found to
have severely carious lesions at this young age are usu-
ally related to a condition termed “molar incisor hypo-
mineralization” (MIH), as described in 7 Chap. 17. The
developmental enamel defects, when severe, lead to early
breakdown of the brittle enamel, and this may have seri-
ous carious consequences if not timely cared for. Such
heavily destructed permanent molars may be restored
with composite or PMCs until the end of adolescence,
when these can be replaced with esthetic ceramic restora-
tions (. Figs. 13.25 and 13.26). Disinfecting the carious
cavities in general for 60 seconds with 2% chlorhexidine
d e
of the relatively hard dentine. c After a GIC base where appropriate.
d Etching the beveled enamel. e The finished composite ­restorations
or ozone has shown dramatic reduction in residual bac-
teria [39], and this may be especially useful in case of
partial caries removal before restorations are placed.
13.4 Age 12 to 18 Years
13.4.1 Proximal and Smooth Surface Caries
In this age group, depending on the adolescent’s caries
diagnostic, therapeutic, and/or restorative needs of the
proximal surfaces of the posterior teeth. The occlusal
surface of the second permanent molars also requires
due attention, with therapeutic strategies being no dif-
ferent than that for the first permanent molars described
earlier in this chapter. Before caries reaches the cavita-
tion level, informing and motivating the adolescents
on their caries risk, and on removing proximal plaque
with floss or small-sized interdental brushes, should be
the priority. Compliance of most teenagers, however,
to such instructions is usually suboptimal. The use of
fluoride toothpaste twice a day and fluoride varnish
treatment twice a year remain the realistic requirements
for the control of initial proximal lesions which can
Restoration of Carious Hard Dental Tissues
a b
..      Fig. 13.24 a While preparing the disto-occlusal surface of the
second primary molar, a small cavity is discovered in the mesial sur-
face of the permanent molar. b Following a conservative class V
be detected radiologically (see 7 Chap. 6). Even these,
however, along with restriction advise on carbohydrate
consumption frequency, are usually met only partially
so that the restorative approach often becomes inevi-
table in adolescents with high-caries activity.
Therefore, some knowledge on the speed of prog-
ress of proximal carious lesions may be useful. Data
from Sweden and the USA showed that in primary
teeth of mixed dentition, it required about a year for
initial lesions detected in bite-wing radiographs to
progress from outer to inner enamel half, while dou-
ble the time was necessary for similar progressions in
the first permanent molar, probably due to enamel
thickness reasons [40], For adolescents, this speed
was from 1.5 to 2 times slower, but in nearly half of
them, lesions had not progressed in 4 years. Newly
erupted teeth may be more caries susceptible, before
their enamel completes its posteruptive maturation, as
previously had shown by in vitro data [41]. Generally,
there were no consistent differences in the rate of pro-
gression between premolars versus molars or between
295 13
preparation, it was restored with composite before placing RMGIC
restorations to primary molars
high- and low-risk individuals [40]. In another study,
the distal surfaces of second premolars and the mesial
of the mandibular second molar presented faster
progression of dentinal radiolucencies than other
interproximal surfaces [42]. In this group of Swedish
adolescents, progression seemed slower with 75% of
enamel lesions surviving 4.8 years without reaching
the outer half of the dentin.
The choice between preventive/therapeutic and
restorative treatment of premolar and molar carious
lesions may present with dilemmas. In the presence of
a proximal radiolucency in the outer dentin, the impor-
tant factor for operative decision is the presence of, even
slight, cavitation (see also 7 Chap. 12). If this is not
possible to diagnose clinically, using a separating rubber
ring to achieve a temporary interdental space of 1 mm in
a few days could assist diagnosis. Restorative treatment
in questionable interproximal caries should therefore be
undertaken only if cavitation is diagnosed by visual or
tactile means or by monitoring radiographs, showing
progressing outer dentinal radiolucencies.
 296 N. Kotsanos and F. Wong
a b
c c
..      Fig.13.25 a Multiple surface breakdown of a maxillary first per-
manent molar in an 8-year-old due to molar incisor hypomineraliza-
tion. b The tooth has been restored with a PMC. c The precontoured
permanent molar PMCs do not usually need substantial adjustments
Eye Catcher
Iatrogenic damage of adjacent teeth during cav-
13 ity preparation is an important aspect. It has been
found that over 70% of proximal cavity preparations
caused – practically invisible – damage to the adja-
cent tooth surface, and this is considered to contrib-
ute to cariogenicity [43]. The resultant micro-niches
(7 Fig. 12.16), possibly on already demineralized
proximal enamel, probably favors further demineral-
ization. The way to avoid this has already been men-
tioned earlier in describing class II cavity preparation
in primary molars.
In labial/buccal surfaces, with the widespread use of
orthodontic brackets, halo-like “white spot” carious
enamel lesions are often found upon their removal
due to inadequate brushing and additional therapeutic
measures like regular fluoride varnish or casein supple-
ment applications [44]. In addition to restoring these
with composite, a relatively new technique of infiltrat-
ing the porous enamel structure with resin is proposed
for esthetic improvement. After removal of the less
porous surface layer with hydrochloric acid, subsurface
porous enamel is filled in two consecutive attempts with
thin resin, restoring its translucency (. Fig. 13.27).
a b
..      Fig. 13.26 a Preparation for esthetic cast ceramic restoration of
severely broken down/decayed permanent first molar in late adoles-
cence. b The ceramic inlay. c The finished restoration. (Courtesy of
Dr. P. Gerasimou)
The same technique is proposed for arresting incipi-
ent enamel caries in proximal surfaces, being suggested
as a cost-­effective long-term solution to its alternative
composite restoration [45, 46]. However, the lack of
radiopacity of this product (icon, DMG, Hamburg Ger-
many) presents some difficulty to monitor the proximal
caries lesion, while its cost per treatment is appreciable.
This technique as well as sealing proximal surfaces with
fissure sealant, following their separation by elastic
rings, has shown similar effectiveness in proximal caries
progression [47].
13.4.2 Class II Cavities
The classic class II cavity preparation with occlusal
extension is presently only preferred if the fissures of
posterior teeth are profoundly carious. Otherwise, the
old philosophy of “extension for prevention” is being
replaced by “sealing for prevention.” If amalgam is
selected, the long-established instructions of operative
dentistry for cavity preparation are followed rounding of
axio-pulpal angle for preventing material fracture at this
high-tension area. As composite is increasingly being
selected nowadays, no occlusal extension with only bev-
eling peripheral enamel for adequate micromechanical
Restoration of Carious Hard Dental Tissues
297 13

a b

..      Fig. 13.27 Maxillary incisors before a and after b resin infiltration of cervical enamel demineralized during orthodontic treatment.
(Courtesy Dr. A. Kavvadia)

retention is advisable. This cavity shape is often men- a

tioned as “box only” cavity preparation (. Fig. 13.28).
Long-term studies of this type of restorations show
adequate survival of 76% in 2.5–3 years [48] or 70% in
7 years [49].

Eye Catcher

For a successful “box only” type of restoration, due

attention should be paid to:
55 Ensure good peripheral enamel beveling and
incremental composite light polymerization b
55 Have appropriate differential etching of enamel
and dentin for ideal bonding
55 Aim for some retentive shape if caries undermines
areas subjected to occlusal load

Further preservation of sound dental tissue may be

achieved by not unnecessarily pushing proximal cav-
ity boundaries into self-cleaning areas (. Fig. 13.29),
unless patient has high-caries activity. Furthermore,
in large proximal surface cavities, preparation shape is
dictated by the extent of carious dentin removal, which
anyway reaches the self-cleaning region after the unsup-
ported enamel is chiseled away. In most cases, dentin
removed from deep cavities close to the pulp is replaced
by (RM)GIC (. Fig. 13.22). However, with improved
dentin bonding agents, the option of skipping this last
stage may be considered if polymerization shrinkage is
avoided by proper incremental placement of composite
to avoid microleakage.
For historical purposes, another cavity shape for
proximal surface caries is mentioned. “Tunnel restora-
tions” was proposed to gain access to the proximal lesion
by skillfully protecting the occlusal marginal ridge of the
posterior tooth. However, subjecting the marginal ridge
to occlusal loads was all too frequently met with fail-
ures, as shown by a study reporting significantly lower
..      Fig. 13.28 a “Box only” proximal cavity reparations in adjacent
maxillary primary molars. b Their compomer restorations just after
matrix removal
survival of such restorations (46%) than the “box only”
type (76%) in 2.5–3 years [48].
13.5 I solating the Working Field by
Rubber Dam
Keeping the operative field dry is a must in restorative
dentistry. The most effective method for isolating poste-
rior teeth is the use of rubber dam. Its introduction to
dentistry dates back to 1864 and has since been linked
with efficient quality quadrant dentistry. Its advantages
in pediatric dentistry include:
 298 N. Kotsanos and F. Wong

c
..      Fig. 13.30 Image of the past without the use of rubber dam

13

..      Fig. 13.29 a, b Following the opening of a 1 mm interdental

space after a 3-day separating ring insertion, preparation of ultra-
conservative cavities in adjacent premolars was possible maintaining
proximal crests. c The finished PMRC (compomer) restorations

55 Significantly aiding child cooperative behavior after
local anesthesia administration.
55 Improving visibility and access to the working field
by retracting and protecting adjacent soft tissues
(. Fig. 13.30).
55 Enabling quadrant dentistry.
55 Providing optimum moisture control with suction
use [50].
55 Contributing to an aseptic environment in endodon-
tic treatments [51] (. Fig. 13.31).
55 Contributing to patient safety by preventing inges-
tion/aspiration of foreign bodies, such as small
..      Fig. 13.31 The rubber dam greatly reduces contamination dur-
ing pulp treatments
instruments, debris from amalgam removal, irriga-
tion liquids, etc. [52]
55 Contributing to dental staff safety by significantly
reducing infected aerosols when coupled with high-­
volume suction to about 90–99% [53]. *
55 In minimal sedation sessions, it minimizes mouth emis-
sions of and exposure of dental personnel to nitrous
oxide with efficient mask and exhaust system [54].
Restoration of Carious Hard Dental Tissues
a c
..      Fig. 13.32 a Accessories for rubber dam use in children from top
anticlockwise: hole punch, clamp forceps, rubber dam elastic sheet
and metal frame, floss tied clamp, and scissors. b Commonly used
clamps in pediatric dentistry. Upper row for permanent molars: No.
On the other hand, the disadvantages of rubber dam
include:
55 Occasional difficulties in placing the clamp especially
to partially erupted teeth.
55 The possibility of it coming off if it is not tightly
secured.
55 The need for gingival anesthesia, in case local anes-
thesia is not necessary otherwise.
55 Difficulty in placement to patients with severe gag
reflex.
55 The difficulty of some child patients to swallow their
saliva.
55 Possible temporary injury to periodontal tissues.
55 Extended time required for the placement. This can
be minimized if the dam system is prepared by an
assistant and placed in one step.
* The importance of using rubber dam was especially
emphasized during the CoVid-19 pandemic.
In very young children, its first use needs additional
explanation time by tell-show-do and appropriate non-
technical vocabulary. Most of the above disadvantages
are in the dentist’s control and can be minimized with
experience.
13.5.1 Equipment
The accessories needed for placing a rubber dam to a
child’s mouth include [55] (. Fig. 13.32):
1. Clamps. A stable clamp needs to be touching the
tooth cervix at four points. The most commonly used
clamps in children are:
55 No. 14 and 14A for permanent molars and pos-
sibly 7A and W8A
299 13
8A, 14 (for fully erupted molars), 14A. Middle row second primary
molars: No. 27 W, 12A, 13A. Bottom row for permanent incisors:
No. 2. c Securing the rubber dam sheet for isolation of anterior teeth
with a floss loop and a piece of elastic cord (WedjetsR)
55 No. 12A and 13A for second primary molars and
possibly 27 W (mandible)
Wingless (W) clamps are available in addition
to those with wings. The latter, being more popu-
lar, are necessary for fitting the rubber dam if one
prefers the one-step technique (see below). It is
advisable to tie dental floss to the clamp bow and
secure it to the frame after clump placement in
case the clamp pops off the tooth. In isolating
anterior teeth, smaller-size clamps (e.g., No.2) can
be placed bilaterally or, alternatively, the dam
may be secured by tight loops of dental floss or
stabilized by elastic cords between teeth
(. Fig. 13.32c).
2. Rubber dam sheet. The latex or latex-­ free sheet is
available in a variety of colors, odors, and flavors to
please young patients. Darker colors increase contrast
with teeth. Medium thickness with dimensions 5 x 5
inches (12.5 x 12.5 mm) is most suitable for children.
3. The dam punch. Single- or multiple-size hole punches
are available. In everyday practice, small holes are
rarely used.
4. The dam frame. The frame keeps the elastic relatively
stretched after placement. It is available in metal or
plastic. The metal pins tend to secure the dam better
in the long run.
5. The clamp forceps. Available types have undercut
ends for securely transferring the clamp to the tooth.
Care is needed at removing forceps not to destabilize
the clamp.
6. Scissors. This is optional for cutting away the rubber
dam part if it covers the patient’s nose. It may also be
useful to poor nasal breathers for cutting a hole in
the working side of the sheet to allow for mouth
breathing.
 300 N. Kotsanos and F. Wong

13.5.2 Preparation and Placement a

Preparation Holes should be punched in a suitable posi-

tion in the elastic sheet so that, with the rubber dam in
place, the frame ends are in a safe distance from the eyes.
For restoring a disto-occlusal cavity, the clamp is prefera-
bly placed in the tooth posterior to it. The distance
between holes in the elastic may follow those marked on
the punch table, i.e., 3 mm, to avoid excess rubber at the
interdental cervical areas interfering with restoring the
cavities that extend subgingivally. An alternative way of
punching the elastic sheet is by merging the holes to a
length of 8–10 mm. After positioning the rubber dam, the
sheet opening is pulled and secured to the mesial surface
of the canine. This reduces the discomfort that may be felt
by the child during flossing the rubber dam past through b
tight contacts. Although not providing complete moisture
isolation as achieved by separate holes for individual
teeth, when aided by high suction, it is an easier and reli-
able method with widespread use for quadrant pediatric
dentistry.

Placement The rubber dam can be inserted by one- or

two-step moves. In the two-step placement, after attach-
ing the floss-tied clamp to the tooth, the elastic sheet is
brought into patient’s mouth, and the punched hole is
stretched with right and left index fingers over the clamp
bow first and then the clamp wings (. Fig. 13.33).
Once the floss has carefully been pulled through the
13 hole, the elastic sheet is stretched and hooked around
the frame, first at the bottom corner pins and then at the c
top ones. In the one step placement, the clamp is engaged
in the hole of the already hooked-to-frame elastic sheet
and the whole dam system transferred to the tooth by its
forceps (. Fig. 13.34). The clamp should be securely
anchored as cervically as possible to the tooth to pre-
vent coming off during the restoration procedure by
involuntary tongue pressure. In either case, the elastic
sheet is properly adjusted to teeth with minimal stretch
tension, and the floss is tied to the frame. The removal
of the rubber dam is easily done by its forceps in one
step.

13.5.3 Alternative Options for Isolation

For isolation of anterior teeth, alternatively, there
are plastic lip and cheek retractors of various types
(. Fig. 13.35). These are used mainly in bonding
orthodontic brackets and restoring carious or trau-
matized anterior teeth in cooperative children. For
isolating posterior teeth for sealant placement, or
in cases of partial eruption or extended subgingival
destruction of molars that makes clamp retention
impossible, moisture control can be achieved with
..      Fig. 13.33 Two-step placement of the rubber dam. a After secur-
ing the clamp and retrieving the floss through the hole, the two index
fingers stretch the rubber sheet at the hole area. b The rubber sheet is
stretched to pass the clamp bow first. c It is then stretched to pass
under the clamp wings and be ready for being hooked at the frame
cotton wool rolls. In the mandible, self-­retained cot-
ton roll holders are useful for simultaneous buccal
and lingual retraction.
Restoration of Carious Hard Dental Tissues
301 13
a b

..      Fig. 13.34 One step placement of the rubber dam a Forceps in clamp as it is engaged in the rubber dam. The elastic sheet is not exces-
sively stretched in the up-down direction. b Placing the rubber dam in the maxillary left second primary molar

a b c

..      Fig. 13.35 Examples of self-retained retractors. a OptiView™ (Kerr) b OptraGate (Ivoclar Vivadent). c Metal cotton roll holder for
mixed dentition mandibular posterior teeth

13.6  estorative Materials in Pediatric

R T-band, 2) custom-made pre-welded bands, 3) the
Dentistry
In selecting the right restorative material, the clinician
must bear in mind the anatomical and functional char-
acteristics and the differences between primary and
young or mature permanent teeth. For example, mas-
ticatory forces are significantly greater in adolescents
and the adult than in young children, exerting higher
occlusal load on restorations. Young permanent teeth
differ to more mature teeth in pulp chamber size and
have implications in their risk for pulp exposure. They
are also in a continuous eruption phase affecting the cer-
vical border of restorations.
Tofflemire band (API, Schweinfurt, Germany) (not
suitable for back-to-back restorations), 4) AutoMatrix,
Omni-Matrix, etc. (with special mounting handles).
In the case of tooth-colored materials for proximo-­
occlusal restorations, a custom piece of metal ribbon or
commercial preformed matrix piece can be placed and
fixed with a suitable wedge (. Fig. 13.11). In the case
of excessively large proximal cavities, special pressure
rings are available to improve contacts at the buccal and
lingual aspects of the cavity outline (. Fig. 13.37). In
anterior teeth, celluloid straight or angle matrices or
strip crowns could be used depending on cavity type and
size.

13.6.2 Cavity Lining/Base Materials

13.6.1 Cavity Matrices
Cavity matrices are used for proximo-occlusal restora-
tions with tight contact being secured with wedges of
suitable shape and size. In the case of amalgam restora-
tions, circular metal matrices are traditionally used to
withstand the increased condensation requirements [55]
(. Fig. 13.36). Such matrices may be 1) the adjustable
The glass-ionomer cement (GIC) is biocompatible and
is suitable material to replace the removed deep cari-
ous dentin, while other lining materials, such as zinc
oxide and eugenol (ZOE) cement, have been used in
the past. Its conventional or, perhaps better, its resin-
modified form (RMGIC) could be used in deep cavi-
ties [56]. There have been many reports, however, that
 302 N. Kotsanos and F. Wong
a covered by (RM)GIC. Alternatives to calcium hydrox-
b cal retention. They are polymeric materials containing
..      Fig. 13.36 a T-band for adjusting matrix diameter. b Appliance
(Rocky Mountain, USA) for welding custom-made ring matrices
after cutting appropriate lengths from a metal ribbon
13 a b
..      Fig. 13.37 a. Wedged Omni-Matrix™ (Ultradent, USA). b. Spe-
cial spring for improving contact of sectional metal matrices to prox-
imal cavity outline (shown here in the absence of a rubber dam)
neither a (RM)GIC base nor a calcium hydroxide lin-
ing is necessary under deep restorations [57–60]. It’s
common practice that minute quantity of quick setting
calcium hydroxide (Ca(OH)2) is used in the presence or
suspicion of accidental pulp exposure for its antibacte-
rial property and its ability to induce reparative dentin
formation. Because of its low compressive hardness
and increased solubility over time, it should always be
ide are MTA or Biodentine (Septodont, Saint-Maur-
des-­fosses Cedex, France), which are more often used in
permanent teeth (see 7 Chap. 14).
13.6.3 Enamel and Dentin Adhesives
The enamel and dentine adhesives bond composites
to these hard dental tissues of primary and perma-
nent teeth, thus allowing for more conservative cavity
preparations by reducing the need for macro-mechani-
methacrylate monomers (Bis-GMA) and/or other such
as urethane dimethacrylate (UDMA). Most monomers
have a hydrophobic group (methacrylate) for bonding to
composite and an acidic hydrophilic one (typically car-
boxylate or phosphate). After a brief dentin etching of
several seconds, the hydrophilic monomers of low vis-
cosity penetrate the superficially demineralized dentin.
Their entanglement with collagen fibers forms the so-­
called hybrid layer after polymerization (. Fig. 13.38).
For this exact purpose, excessive drying of etched dentin
should be avoided as it will lead to dehydration, shrink-
age, and collapse of the collagen fibers. This may cause
the formation of an inadequately thin hybrid layer [61].
a
..      Fig. 13.38 a Hybrid layer between bonding agent and dentin
(right) with projections within tubules. b Cut dentin after the detach-
ment of composite at scanning electron microscope. It is partly cov-
ered by bonding agent hybrid layer, while some dentinal tubules are
revealed
Restoration of Carious Hard Dental Tissues
Some bonding agents contain water aiming to rehydrate
collagen for improving bonding [62].
Bonding agents are under constant development to
improve their properties and inhibit long-term bond
deterioration, e.g., by adding cross-linkers to neutral-
ize the endogenous matrix metalloproteinases (MMPs),
which degrade the demineralized collagen dentin matrix
[63, 64]. They are going through successive generations
becoming more user-friendly, with application stages
reduced to two or even to one step.
The steps for bonding application are:
1. Apply the etchant – phosphoric acid 32–37%
(pH 0.1–0.4) – to enamel for 15–30 sec. It is also
applied to dentin for 5–8 sec to remove the smear
layer and demineralize the cut dentin surface (inter-
and peritubular) to open the lumen of dentinal
tubules and free collagen fiber ends. Achieving differ-
ent etching times for enamel and dentin presents
with some difficulty. For better control, it is recom-
mended that the acid is in colored gel form so that
can be selectively placed first in enamel.
2. After thorough rinsing of the etchant and careful
drying (full drying of enamel and gentle air-­drying
on dentin are again challenging), a primer is applied
to modify the dentin surface from hydrophilic to
hydrophobic, i.e., compatible with the adhesive agent
and the composite [57].
3. The bonding agent is spread on dentin and enamel
with excess liquid being blown away gently. After pho-
topolymerization, a portion of composite is applied
and polymerized for incrementally built restorations.
303 13
13.6.4 Glass-Ionomer Cements
Glass-ionomer cements (GIC) were introduced in den-
tistry in 1970. Although this name prevailed, the cor-
rect name in chemical terms is polyalkenoate cements.
The base is alumino-fluoro-silicate calcium (or stron-
tium) glass powder. Mixing with water-soluble polyalke-
noic acid produces an acid-base reaction. The reaction
releases fluoride ions at a high peak, which decreases sig-
nificantly after a few days [66]. The Ca and then Al ions
form bridges with carboxyl groups of the acid and the
cement changes from a gelatinous stage to solid within
several minutes (. Fig. 13.39). Other acidic compo-
nents are added, such as itaconic and polymaleic acids,
to improve the acid-base reaction, and tartaric acid is
added to accelerate the setting time [67].
At the initial reaction stage (2–5 min after mixing), the
acid is neutralized by Ca and Sr ions to form respective
salts. The formation of Al complexes at the end step stabi-
lizes the final structure (5–10 min after mixing). The setting
process continues to be very sensitive to water because this
may lead to leaching of Al ions and not allow the cement
a

In newer bonding agents, the second and third stages are b

combined into one stage (etch and rinse or total etch)
[62]. To use these products, a mild stream of air facili-
tates the evaporation of the solvent, which are ethanol
or acetone. For some formulations, continuous rubbing
of the adhesive agent for 15–20 secs is recommended.
Compliance with the manufacturer’s instructions for
each stage is very important to bonding success and
c
minimizes microleakage and postoperative sensitivity.
The so-called self-etch bonding agents are the seventh
generation, being one-step agents for quick and more
convenient bonding procedure (e.g., Prompt-L-­Pop, 3 M
ESPE). Etched reactants in these all-in-one products
remain dispersed in the adhesive [65]. Bonding strength
with enamel is reduced mainly due to the inferior etch-
ing, but some of these products achieve comparatively
good bonding to dentin [62, 65]. Eighth-generation uni- ..      Fig. 13.39 a Simplified drawing of the acid-base reaction between
versal adhesives differ to single-­bottle self-etch adhe- glass particles and polyacids of conventional GIC. The reacting
sives. Some contain reduced hydroxyethylmethacrylate outer sol-gel glass layer releases Ca, Al, and F ions. b Chains of Ca,
(HEMA; the most hydrophilic monomer) and water Al, and acidic polymers are formed as the GIC. The chains also react
with the dental surface (bottom part) to form a layer rich in Ca and
in their formulations. This allows for complete evapo-
PO4 ions. c In the set RMGIC (brown color), the faster light polym-
ration (with a 10-second air-­drying step) and therefore erization of the resin part protects the acid-base reaction from mois-
decreased risk of long-term bond degradation. ture. (By permission from: Mount [69])
 304 N. Kotsanos and F. Wong
to reach its full strength. Therefore, isolation and cement
protection for several hours are important. The main
advantage of hydrophilic GIC is its ability of molecular
bonding with hard dental tissues. Free carboxyl groups
either react with their Ca to form salts or they form chelat-
ing complexes (. Fig. 13.39). This is improved by wetting
the cut dentin with polyacrylic acid, which removes the
smear layer. After setting, water absorption causes hygro-
scopic expansion, which compensates the initial setting
contraction. Due to GIC bonding ability to dental tissues
and the slight moisture expansion of the material during
the first 24 hours, microleakage is minimized if the manu-
facturer’s instructions are followed.
In clinical studies of primary molar class II resto-
rations, the conventional, the high viscosity (increased
powder/liquid ratio), and the silver reinforced GICs did
not show optimal success rates [68–71]. The high vis-
cosity GIC, however, still finds application in the ART
technique that was presented earlier in this chapter.
Modifying GIC, by adding resin in the 1990s, greatly
improved its performance. By photopolymerizing the
resinous matrix, the resin-modified GIC restoration
(RMGIC) immediately obtains its outline form and is
ready for any possible trimming, like when checking
the occlusion. Its fracture resistance is also significantly
increased. Hence, RMGICs have largely replaced the
previous GIC forms as the preferred restorative materi-
als. The conventional GIC is now mainly used as luting
cement or for lining deep cavities. RMGIC restorations
13 in class II cavities of primary molars were shown to have
survival rates ranging from 76% to 97% in 2–4-year fol-
low-­up [ 72, 73] (. Fig.13.40). A disadvantage remains
its wear that may be notable in large restorations [16].
Nanofilled RMGIC (Ketac Nano, 3 M ESPE) has been
tested if it better preserves its outline form. It has shown
improved surface gloss but presented some enamel mar-
ginal deficiencies [74, 75] (. Fig. 13.41).
..      Fig. 13.40 3-year survival rates of class II restorations (from top
to bottom): three RMGICs, one PMRC (compomer), one conven-
tional GIC, and one amalgam. The conventional GIC is significantly
inferior to the others. (Courtesy of Dr. V. Qvist)
..      Fig. 13.41 Restorations of nanofilled RMGIC (Ketac Nano,
3 M ESPE) on three maxillary primary molars with no discernible
occlusal wear at 2-year follow-up. There is various marginal discolor-
ation, but this is seen to some extend with the resin sealant of the left
second primary molar
Besides the chemical adhesion to enamel and dentin,
other advantages of GICs include their significant fluo-
ride release and uptake ability and the similar thermal
coefficient with dentin together with a good biocom-
patibility. These latter properties make it an ideal den-
tin replacement material. For this reason, GIC is also
used in the so-called sandwich technique [17, 76]. The
RMGIC is used to replace dentin, while the composite is
used to replace enamel because it has better mechanical
and esthetic properties. By using an adhesive, chemical
bonding between the two materials is increased due to
their common resin constituents [77]. Despite the adhe-
sive properties of these materials, a minimally retentive
cavity shape is still advisable.
Eye Catcher
High fluoride release of (RM)GICs offering deminer-
alization protection over other groups of restorative
materials is well documented [78] (. Fig. 13.42). This
becomes clinically significant at restoration margins
[79] as defective restorations do not lead to secondary
caries (. Fig. 13.43). It has also been postulated that
this caries protection ability could extend to the con-
tacting proximal surfaces of adjacent teeth, but this
has not been confirmed [80]. In vitro research shows
that GIC could have low fluoride release for years,
and the material can be recharged and take up fluo-
ride when it is exposed to high fluoride environment
such as varnishes, toothpastes, or mouthwashes used
in preventive regimes [66]. As mentioned previously,
GIC is the material of choice as a luting cement for
PMC or orthodontic band cementation. It was also
tried for bonding brackets, but its bonding to enamel
was inferior to the standard composite bonding.
Restoration of Carious Hard Dental Tissues
..      Fig. 13.42 In vitro fluoride release graph shows superiority of a
RMGIC (Vitremer, 3 M ESPE) over other materials. Low-level
release continues and is shortly but significantly increased by
“recharging” the material with a fluoride rinse solution on the 51st
day
a b
..      Fig. 13.43 a, b Marginal fractures of unsupported enamel 2 and
2.5 years, respectively, after mandibular first primary molar restora-
tions. In both cases, there is no secondary caries of the exposed den-
tin, which is attributed to the fluoride release from the material.
Monitoring – instead of restoration replacement – is an option
13.6.5 Resin-Based Composites
There are many resin composite products in the dental
market. Features, such as esthetics and polishing abil-
ity, polymerization shrinkage, curing depth, and physi-
cal properties such as tensile strength and wear rate, are
mainly influenced by the quantity and size of filler par-
ticles included in the resin [10, 55]. Resin composites are
usually referred as:
55 Nanofilled, with a content of 50–60% amorphous
SiO2 particles of 20–75 nm in size
55 Microfilled having a particle size in the order of
0.1 μm or less
55 Minifilled with a particle size of about 0.1–1 μm
55 Macrofilled with a particle size of 10–100 μm
305 13
Furthermore, there are so-called hybrid and microhybrid
composites with a variety of particles of average size 1–3
and 0.2–0.7 μm, respectively, which were most commonly
used before the appearance of nanofilled ones.
The particles are usually irregular in shape and are
retained in the resin body with the aid of coupling agents.
Lately mono- or biphosphate methacrylate is preferably
used to give better spatial dispersion of particles due to its
electrically charged phosphate groups [81]. Large particle
size usually contributes to better mechanical strength of
the material. However, very small (nano) particles allow
higher filler content to increase strength and reduce
polymerization shrinkage by decreasing the resin content.
Also, the polishability and esthetics are improved. The
hybrid resins are produced to take advantages of these
combined properties. The high-content medium/low-
size particles have shown to have better wear resistance.
Though they achieve lower shrinkage (range 1–4.5%),
they should nevertheless still be placed by incremental
technique in large cavities. To decrease shrinkage and pre-
vent microleakage, polymerization can start with a lower
intensity curing light or aimed at the material through the
enamel wall [82]. Flowable composites have lower particle
content than hybrid ones. They are mainly used as liners
or as restoratives in minute cavities like the PRRs.
Before the era of dentin adhesives, evidence for
the survival of old composite restorations in primary
molars was poor compared to other materials [83].
Contemporary composites, however, have significantly
improved properties [10, 82]. When esthetics is impor-
tant, the composite is the material of choice for direct
restorations to all permanent and the anterior pri-
mary teeth. For primary teeth, special whiter shades
are available in the market (. Fig. 13.4). Due to its
micromechanical retention properties, the composite
allows dental tissue preservation with conservative cav-
ity preparations, while the resin content, unlike amal-
gam, allows for restoration repair. It, however, requires
more controlled placement conditions, particularly as
regards to isolation from moisture. Thus, rubber dam
use becomes more critical than with other materials. The
composite can also be combined with RMGIC as previ-
ously mentioned (. Figs. 13.12 and 13.44).
Today composites are photopolymerizable. This
curing method provides many advantages, particularly
regarding handling time, and prevents voids often pro-
duced with hand mixing. The appliance tip should be
placed as close to the material as possible, not touch-
ing the material at first. There are many types of curing
devices: halogen, LED (light emitting diode), plasma,
and laser. The most popular type is the LED [84, 85]
(. Fig. 13.45), which is run their fourth generation. They
are small, pen-like, cordless based on lithium batteries,
and polywave (exceeding the 400–500 nm range of blue
light) to cover wavelengths of all kinds of photoinitiators
 306 N. Kotsanos and F. Wong
a b
c d
e f
g
13
..      Fig. 13.44 Occlusal and proximal view of shed primary molars
with proximo-occlusal restorations for assessing occlusal wear of the
material. a, b Conventional GIC (ChemFil Molar, Dentsply) after
2 years in the mouth. c, d RMGIC (Vitremer, 3 M ESPE) after 4 years
in the mouth. e, f Combined RMGIC (Vitremer) with composite
(open sandwich) after 3 years in the mouth. The thin composite layer
has minimized occlusal wear. g Mesio-occlusal restoration with
nanofilled RMGIC (Ketac Nano, 3 M ESPE) after 52 months in the
mouth. Its limited occlusal wear is acceptable
b they performed well [90, 91].
a
..      Fig. 13.45 a, b Cordless contemporary photopolymerizing units
with rechargeable battery
in composites and bonding agents. Their light intensity,
ideally around 1000 mW/cm2 for fast curing, should be
checked periodically with appropriate radiometer and
include a “soft-start” mode of low light intensity for
reducing shrinkage stress [85]. Lately, a blue diode laser
(445 nm) has been tried for composite photopolymeriza-
tion with comparable efficacy to an LED unit [86].
Although it is thought that the presence of eugenol
prevents resin composite polymerization, quick setting
ZOE cements do not appear to decrease the compos-
ite bond strength with dentin [87]. Nevertheless, ZOE
should still be avoided in anterior teeth under composite
as it may cause staining compromising restoration color.
13.6.5.1 Polyacid-Modified Resin Composites
The polyacid-modified composites, more commonly
known as “compomers” (after combining composites
with glass ionomers), were introduced in 1990. They are
based on composite glycidyl methacrylate (bis-GMA),
dimethacrylate (bis-DMA), or other monomers bearing
carboxyl groups (acids), with additional fluoride con-
taining glass particles. They come in a paste form, like
conventional composites. After its photopolymeriza-
tion, the material absorbs moisture from saliva, and a
slow and mild acid-base-type reaction, similar to GIC
type, takes effect. This causes a slight material expan-
sion and fluoride release. However, in practice, the reac-
tion is likely limited to a depth of up to 100 μm only [88].
Initially, a non-etch technique with only self-­adhesive
methacrylate bonding agents was suggested as adequate
for retention. However, enamel etching, as with conven-
tional composites, was found to have better retention,
and it is now recommended as an essential step [89].
Fluoride release is appreciably less than that of GIC,
while restoration survival data exist for the compomers
that were first introduced in the dental market under the
trade names of Dyract (Dentsply, UK) and Compoglass
(Ivoclar Vivadent, Liechtenstein). Their mechanical
properties are better than RMGICs but slightly inferior
to conventional composites; therefore, they are recom-
mended for primary teeth and only for areas in perma-
nent teeth with reduced mechanical load. Clinical studies
with 2–3-year follow-up on primary molars showed that
13.6.5.2 Safety of Resin Biomaterials
Chemicals causing disturbances in endocrine gland
secretion, including bisphenol-A (BPA), are common
environmental pollutants with growing health concerns.
BPA is widely used in manufacturing plastics and may
be found in dental materials, either as an original com-
ponent or as a degradation/manufacturing by-product
of other components (e.g., bis-GMA) [92]. The most
significant potential exposure to BPA occurs immedi-
ately after placing resin sealants, bonding agents, and
Restoration of Carious Hard Dental Tissues
PRRs. There are a few studies showing possible BPA
associations with the immune system or the neuropsy-
chological development of children [93, 94]. Hence, it
is a potential health hazard warranting further investi-
gation. BPA-free composites have appeared in the den-
tal market as the AAPD recommends avoiding BPA
containing composites during pregnancy and proposes
measures for reducing potential exposure. These include
removal of the unpolymerized residual monomer from
the surface of sealants or composite restorations imme-
diately after placement by rubbing with rotary brush
and pumice powder, meticulous wiping with a cotton
roll, and copious rinsing with a water syringe [10]. The
use of rubber dam and high-volume suction also limit
possible exposure to BPA.
13.6.6 Dental Amalgam
Amalgam has been a highly successful restorative mate-
rial since its introduction to dentistry toward the end of
nineteenth century. Many of its advantages contributed
to this, namely, ease of handling, less demanding work-
ing conditions, its low cost, good physical properties,
and reduced microleakage at restoration margins [10].
The esthetic demands nowadays and the environmental
concern about its mercury content steadily decrease the
use of this metal alloy of silver, mercury, copper, and tin.
The good performance of amalgam restorations has
been documented by numerous studies. The 5-year sur-
vival of primary molar restorations was 91.5% for class
II and 96% for class I restorations when placed by an
experienced pediatric dentist [95]. Contemporary stud-
ies in primary molars, however, show no superiority over
other tooth-colored materials. Also, in sizeable cavities
or in multi-surface restorations, it is not as durable as
PMCs for primary molar teeth [96]. If it is preferred for
class II cavities, the width and depth of preparation at
cavity isthmus should be at least 1.2–1.5 mm. This fea-
ture adversely affects its use because it contravenes the
modern views of minimally invasive dentistry on pre-
serving healthy tooth structure (. Fig. 13.46). Great
care is also needed in checking the occlusion and avoid-
ing masticatory loads for several hours because of its
slow hardening process.
The continuous development of dependable tooth-­
colored materials inevitably led to declined use of den-
tal amalgam. Preference of Israeli parents for amalgam
was already low many years ago, mainly not only for
safety but also for esthetic reasons [97]. Long-lasting
posterior tooth restorations was at least as important as
esthetics for Scandinavian adolescents [98]. It appears
that, in addition to restoration longevity, esthetics and
ecology are important selection criteria, although com-
mercial reasons may also play an important role to the
307 13
a b
..      Fig. 13.46 a Class I amalgam restorations in maxillary primary
molars. b Class II amalgam restoration in mandibular first primary
molar. The second primary molar with incipient occlusal caries
received a sealant instead of a class I amalgam
shift toward tooth-colored materials. Today, many pedi-
atric dental practices rarely use amalgam, while in some
countries, its use has been banned for environmental
reasons.
13.6.7 Preformed Crowns
13.6.7.1 Primary Teeth
Preformed metal crowns (PMCs) offer full tooth cover-
age and came into use in 1950. It is an inexpensive choice
with the advantage of higher longevity than all other
restorative options for multi-surface carious primary
molars, e.g., those associated with hypomineralized sec-
ond primary molars (see 7 Chap. 17). As the fitting pro-
cedure is easily completed in one visit, it is the method of
choice for such cases [21, 99], and they are also favored
when restoring teeth of high-caries children under
general anesthesia in order to reduce later needs. The
basically stainless steel marketed PMCs (. Figs. 13.13
and 13.14) contain nickel and chromium (Fe 72%, Cr
18%, Ni 10%) [100]. Release of these elements was insig-
nificant after 1 week for causing any toxicity concerns,
while no serious allergies have been reported [100, 101].
For those who have esthetic demands, veneered PMCs
for anterior [102] and posterior primary teeth [103] are
available, but these are gradually replaced by the newer
full zirconium (Zr) crowns, made of zirconium oxide
[104]. The NuSmile (Houston, TX, USA) Zr crowns have
corresponding try-in crowns because contamination of
the Zr fitting surface can affect adhesion with luting
cement (. Fig. 13.47). The EZ-Pedo Crowns (Loomis,
CA, USA) have additional internal grooves (ZirLock®)
to increase their retention. Due to high strength of the
 308 N. Kotsanos and F. Wong

a b c

..      Fig. 13.47 Mandibular right primary first molar restored with a NuSmile zirconium crown. a preparation. b Try-in crown. c The cemented
zirconium crown

material, Zr crowns can withstand high occlusal forces, a

but they lack the flexibility of PMCs. This requires more
tooth preparation for seating the crowns. Nevertheless,
their popularity is high, due to acceptable effectiveness
and superior esthetics [104].

13.6.7.2 Permanent Teeth

For permanent molars, PMCs can be used as a mid-term
treatment option until late adolescence. They are suit-
able for restoring permanent molars with multi-surface
carious cavities and/or subgingival involvement, a con-
dition often found in patients with severe MIH. The b
PMCs for permanent teeth are contoured and crimped
13 cervically just as those for primary molars. They are
mainly used for full coverage of the first permanent
molars and rarely for the second molars (. Figs. 13.13
and 13.26). For more esthetic solutions, prefabricated
zirconia crowns were lately marketed as an option of
restoring severely broken down first permanent molars.
They need more extensive preparation in a similar way
to primary molars and data for long-term effectiveness.
c

13.6.8 Veneers and Prosthetic Appliances

In addition to the materials mentioned, indirect com-

posite veneers are sometimes used in children. For those
at the end of adolescence, cast materials such as porce-
lain veneers, full ceramic crowns, or other prostheses are
available (. Fig. 13.48). For a description of prepara-
tion and placement of these, the reader is directed to
relevant textbooks.
In the event of loss of anterior teeth from caries ..      Fig. 13.48 a Two cast ceramic veneers for the maxillary central
or dental trauma, transitional mobile or fixed prosthe- incisors. b The restored incisors. c Palatal view. (Courtesy of Dr.
P. Gerasimou)
sis may be fabricated mainly for esthetic and, less so,
for functional rehabilitation. By reaching adulthood, preferred solution is adding acrylic primary incisors in
a more permanent implant born prosthetic restora- a modified Nance appliance (see 7 Chap. 11). A small
tion can be provided. In the primary dentition, the amount of acrylic resin is bonded to the 0.36′ (0.9 mm)
Restoration of Carious Hard Dental Tissues
309 13
a a

b
b

..      Fig. 13.49 a Four acrylic primary incisors added in a modified
Nance appliance to replace the lost natural teeth. b Note the exten-
sion of wire and acrylic in the midline palate to provide space main-
tenance because of concomitant loss of both first primary molars
due to severe ECC
stainless steel wire to support the teeth (. Fig. 13.49).
For replacing the loss of a permanent incisor, a resin-
bonded bridge (“Maryland bridge”) may be used as a
semipermanent solution (. Fig. 13.50). In extensive
loss of anterior permanent teeth, a removable acrylic
denture can be provided until the end of adolescence
(. Fig. 13.51). Adjustments or fabrication of new
denture may be needed due to basal and alveolar
bone growth changes. It must be stressed that in the
latter case, a multidisciplinary approach with timely
consultation with orthodontist, implantologist, and
prosthetist regarding alveolar bone resorption, future
osseointegration requirements, and esthetics is war-
ranted.
13.7  estoration Failure and Contemporary
R (. Fig. 13.11).
Research
13.7.1 Failure and Repair of Restorations
New restorative materials and adhesive agents come
into the dental market all too frequently and documen-
tation usually lags behind, despite it being paramount
before any material is adopted by the clinicians. The low
..      Fig. 13.50 Resin-bonded bridge in late adolescence replaces an
earlier loss of the upper right central incisor due to trauma. a Labial
view. b Palatal aspect. (Courtesy of Dr. P. Gerasimou)
wear resistance of some materials in large restorations,
such as RMGIC, will result in time to altered outline
form occlusally in relation to the surrounding enamel
[16] (. Figs. 13.44 and 13.52). This may be repaired (if
desired) by adding some composite on the surface since
the resin part of RMGIC allows bonding between the
two materials. It is better to avoid this from the out-
set, either by a restoration made entirely of composite
or by an open sandwich restoration explained earlier
in this chapter. Another drawback is the difficulty for
establishing good contact points, especially in back-to-
back restorations, due to the weak packability of tooth-
colored materials. This may be overcome by carefully
over-­inserting the wedge to increase space between the
teeth during material condensation, so that good con-
tact can be reinstated after wedge removal. This is easier
achieved in children because of their less rigid alveolar
bone tissues and goes along with quadrant dentistry
The most common reason of restoration failure for
any material is secondary caries [105, 106]. Restorative
dentistry replaces failed restorations in 2 out of 3 cases
[107], and often these lead to pulp treatment. Another
reason of lesser importance is the esthetic concern
due to marginal discoloration of anterior teeth, which
is also indicative of secondary caries. While the com-
mon cause is leakage at restoration margins, profound
 310 N. Kotsanos and F. Wong

a a b

..      Fig. 13.52 a Significant occlusal wear of an extensive class II

RMGIC restoration (Vitremer, 3 M ESPE) in first primary molar
after 4 years. b Similar restoration in the first primary molar with a
nanofilled RMGIC (Ketac Nano, 3 M ESPE) shows no appreciable
occlusal wear after 3 years

problems due to inadequate local anesthesia or noni-

deal working conditions (e.g., without a rubber dam),
c which prevent adequate cavity visualization. Another
reason may be restoration fracture or loss, or even chip-
ping away of unsupported enamel in the proximal box
(. Fig. 13.43). Although restorations from resin-based
composite materials can be repaired, total replacement
of defective restorations by dentists is more common
than their repair [108].
The restoration failure reasons, except for those due
to dentist’s responsibility (knowledge, skill, choice of
13 material, and following manufacturer’s instructions),
may be attributed to the young patient and family (caries
activity, home use of caries preventive measures, dental
erosion, or occlusal wear). All these affect the survival
d of restorations but remain mostly under the dentist’s
control. For example, earlier studies showed superior-
ity of survival of amalgam restorations compared to
those with composite. More recent studies, however,
with the use of improved materials on one hand and the
increased dentists’ experience and familiarity with them
on the other, show that tooth-colored materials exhibit
on average comparable or, in some cases, higher survival
rates compared to amalgam [68] (. Fig. 13.40).

..      Fig. 13.51 a Tissue healing following the loss of two central and
one lateral permanent incisors of an 11-year-old girl with posterior 13.7.2 Improving the Dental Materials
cross bite. b Her panoramic radiograph. c Palatal acrylic plate with
an expansion screw and three acrylic replacement teeth. d Crossbite The present restoration failure rates because of sec-
correction and esthetic result in the 12-month follow-up. Close mon-
itoring until implant prosthesis at the end of adolescence is indicated
ondary caries suggest that there is still much room for
improvement in current restorative materials and, in
addition to improving adhesive and mechanical prop-
secondary caries is often related to lack of recognizing
erties, focus has been also in improving the biological
and removing all primary carious dentin from the cav-
profile of restorative materials [109]. Despite the proven
ity peripheral walls from the start. This frequent find-
protection exerted by the various fluoride vehicles used
ing in young patients may be related to cooperation
in caries prevention, the limited fluoride penetration in
Restoration of Carious Hard Dental Tissues
plaque restricts its protective effect in difficult to access
areas [110]. Consequently, the survival of restorations
could be significantly improved with materials having
bacteriocidal properties, better dental tissue adhesion,
and remineralizing properties. The relevant additives
should not adversely affect the mechanical properties of
those materials. There is extensive research on agents,
such as silver, zinc oxide, calcium fluoride, quaternary
ammonium, polyethylene amines, bioactive glass, and
nano(fluor)hydroxyapatite, to be incorporated into com-
posites – as well as to bonding agents – which are cur-
rently the most widely used esthetic dental restoratives.
This chapter concludes with a brief update of research
progress for novel restorative biomaterials with possible
future applications in pediatric dentistry.
Silver (Ag) compounds have a wide range of antimi-
crobial applications. Ag reacts with sulfhydrylic groups
of proteins preventing the unraveling and replication
of bacterial DNA, thus inhibiting their cell wall syn-
thesis and cell division [111]. Low Ag concentrations
(0.5–1.0%) in the form of nanofillers in a test CR exhib-
ited significant antibacterial action with mild, estheti-
cally acceptable for posterior teeth, effect on tooth
color [112]. Another biomaterial research approach
involves the use of bioactive glass. Its osseoinductive
and osteogenic properties guide progenitor stem cells
to produce bone tissue [113]. A test composite material
with low concentrations of Ag-bioactive glass particles
retained its combined antimicrobial and remineraliza-
tion properties without significantly compromising
mechanical performance in vitro [114]. Νanoparticles
of polymer quaternary ammonium salts incorporated
in dental materials can be copolymerized with the resin
and thus remain active longer in the composite [115]
(. Fig. 13.53). Bonding agents containing such salts
have shown to retain their antimicrobial properties after
artificial “aging” for 6 months in water [116]. The addi-
tion of chitosan, with or without calcium phosphate
particles, in composites induced their antimicrobial
activity while maintaining mechanical properties and
biocompatibility [117].
a b
..      Fig. 13.53 In vitro antibacterial activity of a composite contain-
ing methacryloyloxy-dodecylpyridinium bromide (MDPB) nanofill-
ers synthesized from quaternary ammonium. Compared to the
control a, the test composite b showed in the scanning electron
microscope (SEM) fewer colonies of mutans streptococci after a
24-hour incubation [115] (by permission)
311 13
Other approaches aim to increase to significant levels
the fluoride release ability of composites, just as it natu-
rally occurs with GIC. All these remain tested in vitro
so far. One similar attempt is to incorporate MgAl and
CaAl containing hydroxides in experimental compos-
ites to render them fluoride rechargeable [118]. Other
attempts include the development of a bioactive glass
composite adhesive for orthodontics that shows long
time release in acidic environment of ions F, Ca, and
PO4 ions with a potential to prevent formation and pro-
gression of early carious lesions around the brackets
[119]. Research continues and it is possible that future
tooth-colored restorative materials may also have caries
preventive properties, but these need to be tried clini-
cally to verify whether they increase restoration survival.
References
1. American Academy of Pediatric Dentistry. Policy on early
childhood caries (ECC): classifications, consequences, and pre-
ventive strategies. Reference manual 2018-19. Pediatr Dent.
2016;40(6):60–2.
2. Vadiakas G. Case definition, aetiology and risk assessment of
early childhood caries (ECC): a revisited review. Eur Arch Pae-
diatr Dent. 2008;9(3):114–25.
3. Owen ML, Ghanim A, Elsby D, Manton DJ. Hypomineralized
second primary molars: prevalence, defect characteristics and
relationship with dental caries in Melbourne preschool chil-
dren. Aust Dent J. 2018;63(1):72–80. https://doi.org/10.1111/
adj.12567.
4. Caufield PW, Li Y, Bromage TG. Hypoplasia-­associated severe
early childhood caries--a proposed definition. J Dent Res.
2012;91(6):544–50. https://doi.org/10.1177/0022034512444929.
5. Peres KG, Nascimento GG, Peres MA, Mittinty MN, Demarco
FF, Santos IS, et al. Impact of Prolonged Breastfeeding on Den-
tal Caries: A Population-Based Birth Cohort Study. Pediatrics.
2017;140(1):e20162943. https://doi.org/10.1542/peds.2016-­2943.
6. Adeniyi AA, Ogunbodede OE, Jeboda OS, Folayan OM. Do
maternal factors influence the dental health status of Nigerian
pre-school children? Int J Paediatr Dent. 2009;19:448–54.
7. Dogar F, Kruger E, Dyson K, Tennant M. Oral health of pre-
school children in rural and remote Western Australia. Rural
Remote Health. 2011;11(4):1869.
8. European Academy of Paediatric Dentistry. Guidelines on
prevention of early childhood caries: An EAPD Policy Docu-
ment. 2008. https://www.­eapd.­eu/uploads/1722F50D_file.­pdf.
Accessed 8 Jan 2019.
9. American Academy of Pediatric Dentistry. Policy on Early Child-
hood Caries (ECC): unique challenges and treatment options.
Reference manual 2018-19. Pediatr Dent. 2016;40(6):63–4.
10. American Academy of Pediatric Dentistry. Pediatric restorative
dentistry. Reference manual 2018–19. 40(6):330–342.
11. Frencken JE, Leal SC, Navarro MF. Twenty-­five-­year atraumatic
restorative treatment (ART) approach: a comprehensive over-
view. Clin Oral Investig. 2012;16(5):1337–46.
12. Kemoli AM, Opinya GN, van Amerongen WE, Mwalili
SM. Two-year survival rates of proximal atraumatic restorative
treatment restorations in relation to glass ionomer cements and
postrestoration meals consumed. Pediatr Dent. 2011;33(3):
246–51.
 312 N. Kotsanos and F. Wong
13. Amarante E, Raadal M, Espelid I. Impact of diagnostic cri-
teria on the prevalence of dental caries in Norwegian children
aged 5, 12 and 18 years. Community Dent Oral Epidemiol.
1998;26(2):87–94.
14. Celiberti P, Francescut P, Lussi A. Performance of four den-
tine excavation methods in deciduous teeth. Caries Res.
2006;40(2):117–23.
15. Hickel R, Kaaden C, Paschos E, et al. Longevity of occlusally-
stressed restorations in posterior primary teeth. Am J Dent.
2005;18(3):198–211.
16. Kotsanos N, Arizos S. Evaluation of a resin modified glass
ionomer serving both as indirect pulp therapy and as restor-
ative material for primary molars. Eur Arch Paediatr Dent.
2011;12(3):170–5.
17. Atieh M. Stainless steel crown versus modified open-
sandwich restorations for primary molars: a 2-year ran-
domized clinical trial. Int J Paediatr Dent. 2008;18(5):
325–32.
18. van Dijken JW, Kieri C, Carlén M. Longevity of extensive class
II open-sandwich restorations with a resin-­modified glass-iono-
mer cement. J Dent Res. 1999;78(7):1319–25.
19. Roberts JF, Attari N, Sherriff M. The survival of resin modified
glass ionomer and stainless steel crown restorations in primary
molars, placed in a specialist paediatric dental practice. Br Dent
J. 2005;198(7):427–31.
20. Koleventi A, Sakellari D, Arapostathis KN, Kotsanos N. Peri-
odontal impact of preformed metal crowns on permanent
molars of children and adolescents: a pilot study. Pediatr Dent.
2018;40(2):117–21.
21. Seale NS, Randall R. The use of stainless steel crowns:
a systematic literature review. Pediatr Dent. 2015;37(2):
145–60.
22. Innes NP, Evans DJ, Stirrups DR. Sealing caries in primary
molars: randomized control trial, 5-year results. J Dent Res.
2011;90(12):1405–10.
13 23. Innes NP, Marshman Z, Vendan RE. A group of general dental
practitioners' views of preformed metal crowns after participa-
tion in the hall technique clinical trial: a mixed-method evalua-
tion. Prim Dent Care. 2010;17(1):33–7.
24. Page LA, et al. Acceptability of the hall technique to parents and
children. N Z Dent J. 2014;110(1):12–7.
25. Banihani A, Duggal M, Toumba J, Deery C. Outcomes of the
conventional and biological treatment approaches for the man-
agement of caries in the primary dentition. Int J Paediatr Dent.
2018;28:12–22.
26. Kupietzky A. Bonded resin composite strip crowns for primary
incisors: clinical tips for a successful outcome. Pediatr Dent.
2002;24(2):145–8.
27. Hansen NV, Nyvad B. Non-operative control of cavitated
approximal caries lesions in primary molars: a prospective eval-
uation of cases. J Oral Rehabil. 2017;44(7):537–44. https://doi.
org/10.1111/joor.12508.
28. Carvalho JC, Ekstrand KR, Thylstrup A. Dental plaque and
caries on occlusal surfaces of first permanent molars in relation
to stage of eruption. J Dent Res. 1989;68(5):773–9.
29. Feigal RJ. Sealants and preventive restorations: review of effec-
tiveness and clinical changes for improvement. Pediatr Dent.
1998;20(2):85–92.
30. Freedman G, Goldstep F, Seif T. Ultraconservative resin restora-
tions. "watch and wait" is not acceptable treatment. Dent Today.
2000;19(1):66–8; 70-3.
31. Mertz-Fairhurst EJ, Curtis JW Jr, Ergle JW, et al. Ultraconserva-
tive and cariostatic sealed restorations: results at year 10. J Am
Dent Assoc. 1998;129(1):55–66.
32. Borges BC, de Souza BJ, Braz R, et al. Arrest of non-cavitated
dentinal occlusal caries by sealing pits and fissures: a 36-month,
randomised controlled clinical trial. Int Dent J. 2012;62(5):
251–5.
33. Schwendicke F, Frencken J, Innes N. Clinical recommendations
on carious tissue removal in Cavitated Lesions. Monogr Oral
Sci. 2018;27:162–6. https://doi.org/10.1159/000487843.
34. Bekes K (ed). Pit and fissure sealants. Springer, 2018
35. Kotlow L. Lasers and pediatric dental care. Gen Dent.
2008;56(7):618–27.
36. Olivi G, Genovese MD. Laser restorative dentistry in children
and adolescents. Eur Arch Paediatr Dent. 2011;12(2):68–78.
37. Welbury RR, Walls AWG, Murray JJ, McCabe JR. The manage-
ment of occlusal caries in permanent molars. A 5 years clinical
trial comparing minimal composite with an amalgam restora-
tion. Br Dent J. 1990;169:361–6.
38. Houpt M, Fuks A, Eidelman E. Composite/sealant restoration:
6 ½ year results. Pediatr Dent. 1988;10(4):304–6.
39. Durmus N, Tok YT, Kaya S, Akcay M. Effectiveness of the
ozone application in two-visit indirect pulp therapy of perma-
nent molars with deep carious lesion: a randomized clinical trial.
Clin Oral Investig. 2019. https://doi.org/10.1007/s00784-­019-­
02808-­0.
40. Shwartz M, Gröndahl HG, Pliskin JS, Boffa J. A longitudinal
analysis from bite-wing radiographs of the rate of progression of
approximal carious lesions through human dental enamel. Arch
Oral Biol. 1984;29(7):529–36.
41. Kotsanos N, Darling AI. Influence of posteruptive age of
enamel on its susceptibility to artificial caries. Caries Res.
1991;25(4):241–50.
42. Mejàre I, Källest LC, Stenlund H. Incidence and progression of
approximal caries from 11 to 22 years of age in Sweden: A pro-
spective radiographic study. Caries Res. 1999;33(2):93–100.
43. Qvist V, Johannessen L, Bruun M. Progression of approximal
caries in relation to iatrogenic preparation damage. J Dent Res.
1992;71(7):1370–3.
44. Lopatiene K, Borisovaite M, Lapenaite E. Prevention and treat-
ment of white spot lesions during and after treatment with
fixed orthodontic appliances: a systematic literature review.
J Oral Maxillofac Res. 2016;7(2):e1. https://doi.org/10.5037/
jomr.2016.7201.
45. Meyer-Lueckel H, Bitter K, Paris S. Randomized controlled
clinical trial on proximal caries infiltration: three-year follow-up.
Caries Res. 2012;6:544–8.
46. Schwendicke F, Meyer-Lueckel H, Stolpe M, et al. Costs and
effectiveness of treatment alternatives for proximal caries lesions.
PLoS One. 2014;9(1):e86992.
47. Martignon S, Ekstrand KR, Gomez J, Lara JS, Cortes A. Infil-
trating/sealing proximal caries lesions: a 3-year random-
ized clinical trial. J Dent Res. 2012;91(3):288–92. https://doi.
org/10.1177/0022034511435328.
48. Hörsted-Bindslev P, Heyde-Petersen B, Simonsen P, Baelum
V. Tunnel or saucer-shaped restorations: a survival analysis. Clin
Oral Investig. 2005;9(4):233–8.
49. Nordbø H, Leirskar J, von der Fehr FR. Saucer-­shaped cav-
ity preparations for posterior approximal resin composite
restorations: observations up to 10 years. Quintessence Int.
1998;29(1):5–11.
Restoration of Carious Hard Dental Tissues
50. Knight GT, Berry TG, Barghi N, Burns TR. Effects of two meth-
ods of moisture control on marginal microleakage between resin
composite and etched enamel: a clinical study. Int J Prostho-
dont. 1993;6:475–9.
51. Carrotte P. Endodontics: part 6. Rubber dam and access cavities.
Br Dent J. 2004;197:527–34.
52. Kremers L, Halbach S, Willruth H, et al. Effect of rubber dam
on mercury exposure during amalgam removal. Eur J Oral Sci.
1999;107:202–7.
53. Samaranayake LP, Reid J, Evans D. The efficacy of rubber dam
isolation in reducing atmospheric bacterial contamination.
ASDC J Dent Child. 1989;56:442–4.
54. Cohen EN, Brown BW Jr, Bruce DL, Cascorbi HF, Corbett TH,
Jones TW, Whitcher CE. A survey of anesthetic health hazards
among dentists. J Am Dent Assoc. 1975;90:1291–6.
55. Summit JB, Robbins W, Schwartz RS. Fundamentals of opera-
tive dentistry: a contemporary approach. 1st ed. Batavia: Illinois
Quintessence Publications Co Inc; 2001. p. 149.
56. Pontes DG, Guedes-Neto MV, Cabral MF, Cohen-Carneiro
F. Microleakage evaluation of class V restorations with conven-
tional and resin-modified glass ionomer cements. Oral Health
Dent Manag. 2014;13(3):642–6.
57. Banomyong D, Messer H. Two-year clinical study on postop-
erative pulpal complications arising from the absence of a glass-
ionomer lining in deep occlusal resin-­composite restorations. J
Investig Clin Dent. 2013;4(4):265–70. https://doi.org/10.1111/
j.2041-­1626.2012.00160.x.
58. da Rosa WLO, Lima VP, Moraes RR, Piva E, da Silva AF. Is a
calcium hydroxide liner necessary in the treatment of deep car-
ies lesions? A systematic review and meta-analysis. Int Endod J.
2018. https://doi.org/10.1111/iej.13034.
59. Corralo DJ, Maltz M. Clinical and ultrastructural effects of dif-
ferent liners/restorative materials on deep carious dentin: a ran-
domized clinical trial. Caries Res. 2013;47(3):243–50. https://doi.
org/10.1159/000345648.
60. Opal S, Garg S, Sharma D, Dhindsa A, Jatana I. In vivo effect
of calcium hydroxide and resin-modified glass ionomer cement
on carious dentin in young permanent molars: an ultrastructural
and macroscopic study. Pediatr Dent. 2017;39(1):1–8.
61. Takai T, Hosaka K, Kambara K, Thitthaweerat S, Matsui N,
Takahashi M, et al. Effect of air-drying dentin surfaces on
dentin bond strength of a solvent-free one-step adhesive. Dent
Mater J. 2012;31(4):558–63.
62. Pashley DH, Tay FR, Breschi L, Tjäderhane L, Carvalho
RM, Carrilho M, Tezvergil-Mutluay A. State of the art etch-
and-rinse adhesives. Dent Mater. 2011;27(1):1–16. https://doi.
org/10.1016/j.dental.2010.10.016.
63. Seseogullari-Dirihan R, Apollonio F, Mazzoni A, Tjaderhane L,
Pashley D, Breschi L, Tezvergil-Mutluay A. Use of crosslinkers
to inactivate dentin MMPs. Dent Mater. 2016;32(3):423–32.
https://doi.org/10.1016/j.dental.2015.12.012.
64. Sabatini C, Scheffel DL, Scheffel RH, Agee KA, Rouch K,
Takahashi M, et al. Inhibition of endogenous human dentin
MMPs by Gluma. Dent Mater. 2014;30(7):752–8. https://doi.
org/10.1016/j.dental.2014.04.006.
65. Agostini FG, Kaaden C, Powers JM. Bond strength of self-etch-
ing primers to enamel and dentin of primary teeth. Pediatr Dent.
2001;23(6):481–6.
66. Dionysopoulos P, Kotsanos N, Pataridou A. Fluoride release
and uptake by four new fluoride releasing restorative materials. J
Oral Rehabil. 2003;30(9):866–72.
313 13
67. Croll TP, Nicholson JW. Glass ionomer cements in pediatric
dentistry: review of the literature. Pediatr Dent. 2002;24(5):
423–9.
68. Qvist V, Laurberg L, Poulsen A, Teglers PT. Eight-year study
on conventional glass ionomer and amalgam restorations in pri-
mary teeth. Acta Odontol Scand. 2004;62(1):37–45.
69. Mount GJ. An atlas of glass- ionomer cements; A clinician’’s
guide. 3rd ed. London: Martin Dunitz; 2002.
70. Hübel S, Mejàre I. Conventional versus resin-­modified glass-
ionomer cement for class II restorations in primary molars. A
3-year clinical study. Int J Paediatr Dent. 2003;13(1):2–8.
71. Sidhu SK, Nicholson JW. A review of glass-­ionomer cements
for clinical dentistry. J Funct Biomater. 2016; 7(3): 16. Published
online 2016 Jun 28. https://doi.org/10.3390/jfb7030016.
72. Donly KJ, Segura A, Kanellis M, Erickson RL. Clinical per-
formance and caries inhibition of resin-­modified glass iono-
mer cement and amalgam restorations. J Am Dent Assoc.
1999;130(10):1459–66.
73. Chadwick BL, Evans DJ. Restoration of class II cavities in pri-
mary molar teeth with conventional and resin modified glass
ionomer cements: a systematic review of the literature. Eur Arch
Paediatr Dent. 2007;8(1):14–21.
74. Perdigão J, Dutra-Corrêa M, Saraceni SH, Ciaramicoli MT,
Kiyan VH. Randomized clinical trial of two resin-modified glass
ionomer materials: 1-year results. Oper Dent. 2012;37(6):591–
601. https://doi.org/10.2341/11-­415-­C.
75. Vance M, Lawson NC, Rupal M, Beck P, Burgess JO. Color and
gloss of Nano-filled resin-modified glass ionomers and resin
composites. J Esthet Restor Dent. 2015;27(5):293–9. https://doi.
org/10.1111/jerd.12118.
76. Andersson-Wenckert IE, van Dijken JW, Kieri C. Durabil-
ity of extensive class II open-sandwich restorations with a
resin-modified glass ionomer cement after 6 years. Am J Dent.
2004;17(1):43–50.
77. Fragkou S, Nikolaidis A, Tsiantou D, Achilias D, Kotsanos
N. Tensile bond characteristics between composite resin and
resin-modified glass-ionomer restoratives used in the open-sand-
wich technique. Eur Arch Paediatr Dent. 2013;14(4):239–45.
https://doi.org/10.1007/s40368-­013-­0055-­2.
78. Kotsanos N. An intraoral study of caries induced on enamel in
contact with fluoride-releasing restorative materials. Caries Res.
2001;35(3):200–4.
79. Raggio DP, Tedesco TK, Calvo AF, Braga MM. Do glass iono-
mer cements prevent caries lesions in margins of restorations
in primary teeth?: a systematic review and meta-analysis. J Am
Dent Assoc. 2016;147(3):177–85.
80. Tedesco TK, Bonifácio CC, Calvo AF, Gimenez T, Braga MM,
Raggio DP. Caries lesion prevention and arrestment in approxi-
mal surfaces in contact with glass ionomer cement restorations -
a systematic review and meta-analysis. Int J Paediatr Dent.
2016;26(3):161–72.
81. Breschi M, Fabiani D, Sandrolini L, Colonna M, Sisti L, Van-
nini M, et al. Electrical properties of resin monomers used in
restorative dentistry. Dent Mater. 2012;28(9):1024–31. https://
doi.org/10.1016/j.dental.2012.05.009.
82. Carvalho RM, Pereira JC, Yoshiyama M, Pashley DH. A review
of polymerization contraction: the influence of stress develop-
ment versus stress relief. Oper Dent. 1996;21(1):17–24.
83. Oldenburg TR, Vann WF Jr, Dilley DC. Comparison of com-
posite and amalgam in posterior teeth of children. Dent Mater.
1987;3(4):182–6.
 314 N. Kotsanos and F. Wong
84. Jandt KD, Mills RW. A brief history of LED photopolymeriza-
tion. Dent Mater. 2013;29(6):605–17. https://doi.org/10.1016/j.
dental.2013.02.003.
85. Soares LE, Liporoni PC, Martin AA. The effect of soft-start
polymerization by second generation LEDs on the degree of
conversion of resin composite. Oper Dent. 2007;32(2):160–5.
86. Drost T, Reimann S, Frentzen M, Meister J. Effectiveness of
photopolymerization in composite resins using a novel 445-nm
diode laser in comparison to LED and halogen bulb technol-
ogy. Lasers Med Sci. 2019;34(4):729–36. https://doi.org/10.1007/
s10103-­018-­2651-­1.
87. Ganss C, Jung M. Effect of eugenol-containing temporary
cements on bond strength of composite to dentin. Oper Dent.
1998;23(2):55–62.
88. Eliades G, Kakaboura A, Palaghias G. Acid-­ base reaction
and fluoride release profiles in visible light-cured polyacid-
modified composite restoratives (compomers). Dent Mater.
1998;14(1):57–63.
89. Krämer N, Frankenberger R. Compomers in restorative therapy
of children: a literature review. Int J Paediatr Dent. 2007;17(1):
2–9.
90. Marks LA, Faict N, Welbury RR. Literature review: restorations
of class II cavities in the primary dentition with compomers. Eur
Arch Paediatr Dent. 2010;11(3):109–14.
91. Papagiannoulis L, Kakaboura A, Pantaleon F, Kavvadia
K. Clinical evaluation of a polyacid-modified resin composite
(compomer) in class II restorations of primary teeth: a two-year
follow-up study. Pediatr Dent. 1999;21(4):231–4.
92. Fleisch AF, Sheffield PE, Chinn C, Edelstein BL, Landrigan
PJ. Bisphenol a and related compounds in dental materials.
Pediatrics. 2010;126(4):760–8. https://doi.org/10.1542/peds.2009-
­2693.
93. Maserejian NN, Trachtenberg FL, Hauser R, et al. Dental com-
posite restorations and neuropsychological development in chil-
dren: treatment level analysis from a randomized clinical trial.
13 Neurotoxicology. 2012;33(5):1291–7.
94. Maserejian NN, Shrader P, Brown OA, et al. Dental seal-
ants and composite restorations and longitudinal changes
in immune function markers in children. Int J Paediatr Dent.
2014;24(3):215–25.
95. Roberts JF, Sherriff M. The fate and survival of amalgam and
preformed crown molar restorations placed in a specialist paedi-
atric dental practice. Br Dent J. 1990;169(8):237–44.
96. Randall RC, Vrijhoef MA, Wilson NH. Efficacy of preformed
metal crowns vs amalgam restorations in primary molars: a sys-
tematic review. J Am Dent Assoc. 2000;131(3):337–43.
97. Peretz B, Ram D. Restorative material for children's teeth:
preferences of parents and children. ASDC J Dent Child.
2002;69(3):243–8, 233.
98. Espelid I, Cairns J, Askildsen JE, Qvist V, et al. Preferences
over dental restorative materials among young patients and
dental professionals. Eur J Oral Sci. 2006;114(1):15–21.
99. Seale NS. The use of stainless steel crowns. Pediatr Dent.
2002;24(5):501–5.
100. Keinan D, Mass E, Zilberman U. Absorption of nickel, chro-
mium, and iron by the root surface of primary molars cov-
ered with stainless steel crowns. Int J Dent. 2010;2010:326124.
https://doi.org/10.1155/2010/326124.
101. Ramazani N, Ahmadi R, Darijani M. Assessment of
nickel release from stainless steel crowns. J Dent (Tehran).
2014;11(3):328–34.
102. Oueis H, Atwan S, Pajtas B, Casamassimo P. Use of anterior
veneered stainless steel crowns by pediatric dentists. Pediatr
Dent. 2010;32(5):413–6.
103. Leith R, O’Connell AC. A clinical study evaluating success of
2 commercially available preveneered primary molar stainless
steel crowns. Pediatr Dent. 2011;33(4):300–6.
104. Donly KJ, Sasa I, Contreras CI, Mendez MJC. Prospective
randomized clinical trial of primary molar crowns: 24-month
results. Pediatr Dent. 2018;40(4):253–8.
105. Wendt LK, Koch G, Birkhed D. Replacements of restorations
in the primary and young permanent dentition. Swed Dent J.
1998;22(4):149–55.
106. Chrysanthakopoulos NA. Placement, replacement and longev-
ity of composite resin-based restorations in permanent teeth in
Greece. Int Dent J. 2012;62(3):161–6.
107. Maupomé G, Sheiham A. Criteria for restoration replacement
and restoration life-span estimates in an educational environ-
ment. J Oral Rehabil. 1998;25(12):896–901.
108. Gordan VV, Riley JL 3rd, Geraldeli S, et al. Repair or
replacement of defective restorations by dentists in the den-
tal practice-based research network. J Am Dent Assoc.
2012;143(6):593–601.
109. Balhaddad AA, Kansara AA, Hidan D, Weir MD, Xu
HHK. Melo MAS. Toward dental caries: Exploring nanopar-
ticle-based platforms and calcium phosphate compounds for
dental restorative materials. Bioact Mater. 2018;4(1):43–55.
https://doi.org/10.1016/j.bioactmat.2018.12.002. eCollection
2019 Mar. Review.
110. Watson PS, Pontefract HA, Devine DA, et al. Penetration of
fluoride into natural plaque biofilms. J Dent Res. 2005;84(5):
451–5.
111. Lansdown A. Silver in health care: antimicrobial effects and
safety in use. Curr Probl Dermatol. 2006;33:17–34.
112. Melo MA, Guedes SF, Xu HH, Rodrigues LK. Nanotechnol-
ogy-based restorative materials for dental caries management.
Trends Biotechnol. 2013;31(8):459–67.
113. Rezwan K, Chen QZ, Blaker JJ, Boccaccini AR. Biodegrad-
able and bioactive porous polymer/inorganic composite scaf-
folds for bone tissue engineering. Biomaterials. 2006;27:
3413–31.
114. Chatzistavrou X, Lefkelidou A, Papadopoulou L, Pavlidou E,
Paraskevopoulos KM, Fenno JC, et al. Bactericidal and bioac-
tive dental composites. Front Physiol. 2018;9:103. https://doi.
org/10.3389/fphys.2018.00103.
115. Imazato S, Chen JH, Ma S, et al. Antibacterial resin monomers
based on quaternary ammonium and their benefits in restor-
ative dentistry. Jpn Dent Sci Rev. 2012;48:115–25.
116. Zhang K, Cheng L, Wu EJ, et al. Effect of water-ageing on den-
tine bond strength and anti-biofilm activity of bonding agent
containing new monomer dimethylaminododecyl methacrylate.
J Dent. 2013;41(6):504–13.
117. Tanaka CB, Lopes DP, Kikuchi LNT, Moreira MS, Catalani
LH, Braga RR, Kruzic JJ, Gonçalves F. Development of novel
dental restorative composites with dibasic calcium phosphate
loaded chitosan fillers. Dent Mater. 2020;36(4):551–9. https://
doi.org/10.1016/j.dental.2020.02.004.
118. Hoxha A, Gillam DG, Agha A, Karpukhina N, Bushby AJ,
Patel MP. Novel fluoride rechargeable dental composites con-
taining MgAl and CaAl layered double hydroxide (LDH).
Dent Mater. 2020;36(8):973–86. https://doi.org/10.1016/j.den-
tal.2020.04.011.
119. Al-Eesa NA, Wong FSL, Johal A, Hill RG. Fluoride contain-
ing bioactive glass composite for orthodontic adhesives - ion
release properties. Dent Mater. 2017;33(11):1324–9. https://doi.
org/10.1016/j.dental.2017.08.185.
 315 14

Pulp Therapy in Pediatric

Dentistry
Aristidis Arhakis, Elisabetta Cotti, and Nikolaos Kotsanos

Contents

14.1  iagnosing Pulp Pathology of the Primary Tooth: Managing

D
the Emergencies – 316
14.1.1  iagnostic Procedure – 316
D
14.1.2 Management of Pulp-Related Emergency – 321

14.2 Treatment of Pulp Pathology in Primary Teeth – 323

14.2.1 I ndirect Pulp Capping of Primary Teeth – 323
14.2.2 Direct Pulp Capping of Primary Teeth – 325
14.2.3 Primary Molar Pulpotomy – 328
14.2.4 Pulpectomy/Root Canal Treatment of Primary Teeth – 331

14.3 Pulp Treatment of Young Carious Permanent Teeth – 334

14.3.1 I ndirect Pulp Capping – 335
14.3.2 Direct Pulp Capping – 336
14.3.3 Partial Pulpotomy and Cervical Pulpotomy – 337
14.3.4 Root Canal Treatment of Immature Carious Teeth – 337
14.3.5 Restoring the Color of Discolored Teeth – 341

References – 342

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_14
 316 A. Arhakis et al.

14.1  iagnosing Pulp Pathology

D a
of the Primary Tooth: Managing
the Emergencies
The need for pulp therapy during the practice of pedi-
atric dentistry emerges from the consequences of dental
caries, dental trauma, structural dental anomalies, and
b
undesirable iatrogenic trauma. The aim is to prevent or
treat pulp inflammation and bacterial penetration into
the pulp and the periapical tissues. When safeguarding
the vitality of the pulp is impossible, it is necessary to
perform endodontic (root canal) treatment, even in the
case of a permanent tooth with an immature root apex.
Otherwise, the bacterial infection may develop into an
acute dentoalveolar abscess or result to chronic inflam- ..      Fig. 14.1 a, b Relationship of the roots of second primary
mation of the periapical tissues. The aim of endodontic molars to the germ of the successor premolar at the age of 3.5 and 9
treatment of posterior primary teeth is to preserve them years, respectively (arrows)
until natural shedding, or at least until a stable occlusion
has been achieved [1]. In preserving the anterior teeth,
permanent and primary, esthetics is equally important
to function.
The anatomical differences of primary tooth 14.1.1 Diagnostic Procedure
roots compared to permanent teeth, their proximity to
the permanent successor tooth germs, their naturally 14.1.1.1 Medical History
occurring resorption, and, consequently, the limited time
these teeth remain in the dental arch, lead to modifica- When taking a medical history, diseases that may impose
tions of therapeutic principles, compared to permanent modifications to the treatment plan should be recorded.
teeth (. Fig. 14.1). Furthermore, pulp interventions of 55 Maintaining a tooth in a hemophilic patient is pre-
permanent teeth with immature root apices are deter- ferred for the added reason that its extraction would
mined by the decisive role the pulp plays in their matu- require prior caring for his/her coagulation issues,
ration. possibly by hospitalization.
55 The complex root canal anatomy of primary
14 Comparing clinical, radiographic, and histological
molars may explain some failures of endodontic
appearance of primary tooth pulp has led to some use-
ful observations. The onset of symptoms is preceded by treatment. Therefore, in patients with congenital or
hyperemia or even mild bacterial inflammation in the acquired imperfections of the cardiovascular sys-
pulp horns of a primary molar with an open cavity [2, 3] tem, extraction (under antimicrobial prophylaxis)
(. Fig. 14.2). When initial symptoms (provoked pain) is preferred [6].
are reported, the inflammation will have already spread 55 The same holds true for children with autoimmune
into at least part of the coronal pulp; yet this does not diseases, such as those with acute leukemia, due to a
necessarily imply the need for an invasive treatment. compromised immunological response. Again,
While pain is one of the commonest reasons why young extraction is preferred in conjunction with the appro-
patients seek dental treatment, many children present priate antimicrobial prophylaxis and in consultation
with cariously necrotic primary teeth without any pain with the child’s attending physician [6].
history [ 4, 5]. To ensure a sound diagnosis and a treat-
14.1.1.2 Dental History
ment, a careful medical and dental history should be
taken with as accurate as possible information on pain A child presenting at the dental surgery with toothache
characteristics; in addition, a detailed clinical and radio- poses a diagnostic challenge. This is the prioritization of
graphic examination is required. treatment goals:
Pulp Therapy in Pediatric Dentistry
a b
..      Fig. 14.2 a The very deep carious lesions in two mandibular
primary molars along with reported short duration provoked pain
suggest bacterial infiltration and inflammatory reaction, mainly at
55 Proper diagnosis, with an emphasis on recognizing
emergency cases
55 Alleviating any anxiety affecting the parents or the
child
55 Alleviating the child’s pain (avoiding extraction, if
possible)
The presence of pain may be associated with an inflam-
mation of pulpal, periapical, or periodontal etiology.
Pain history and characteristics determine whether
the case is an emergency. An accurate history taking
includes possible pain-evoking stimuli, its location,
intensity, duration, and frequency, as well as the factors
that alleviate or exacerbate it. Such questions are often
difficult to be answered, particularly by preschool age
children, and some information needs to be taken from
the parent, albeit with some reservations as to its accu-
racy [7]. Many children are prone to giving false answers
so as to avoid dental treatment they are afraid of, and
this is a typical phenomenon. For example, a fright-
ened child, after a sleepless night with toothache, when
finally faced with the dentist, may anticipate the likeli-
hood of a painful intervention; so they may report they
have no pain. On the other hand, some parents, possibly
somewhat negligent for not responding in good time,
may play down a child’s prior symptoms. Furthermore,
317 14
respective pulp horns. b Due to pulp proximity in the first molar,
the pulp was close to exposure after careful removal of the infected
dentin
as already mentioned, the fact that pain is not reported
does not exclude pulp inflammation in either primary
or permanent teeth. It remains possible that children
with pulpless primary teeth, even some with a fistula,
may not have a pain history, and their parents may con-
firm this. Children’s active lives and the low significance
attributed by many parents to primary teeth may result
in paying little attention to such matters. This often
results in the dentist having a rather difficult task when
trying to elicit an accurate pain history from the child
and their parents.
It is very important for arriving at correct diagno-
sis and treatment to make a distinction between two
types of dental pain. Evoked pain is generated by vari-
ous thermal, chemical, osmotic, or/and mechanical
stimuli and declines or disappears with the removal of
the stimulus. It should be noted that pain caused by
thermal stimuli to primary teeth is not as common as
in permanent dentition. A history of toothache caused
exclusively by evoked stimuli does not necessarily mean
nonreversible lesion to the pulp, whereas it is difficult
to accurately connect pain features with the extent of
pulpal inflammation [2]. The tooth usually presents a
carious cavity, in which food enters during mastica-
tion, and one or more of the stimuli mentioned above
causes pulpal pain. The absence of a contact point in
 318 A. Arhakis et al.
a bifurcation of molars, indicates advanced inflamma-
b c
..      Fig. 14.3 a A radiograph showing deep cavities of both man-
dibular primary molars. Carious dentin in the first molar seems to
be in contact with the pulp; this, and/or the loss of contact between
them, explains the evoked pain reported during mastication. b Their
restoration with RMGIC, with indirect pulp capping of the first pri-
mary molar. c Its asymptomatic survival until normal replacement
by the premolar after 3 years implies that the partial inflammation
of the pulp was reversible
14 cases of a proximo-occlusal cavity may also mean that
the pain is periodontal, arising from chronic wedging
of food and consequent localized periodontal inflam-
mation. The radiograph will indicate deep carious cavi-
ties, while there is often interdental alveolar bone loss
(. Fig. 14.3).
Spontaneous pain is not caused by a direct stimu-
lus; it occurs outside meal times, frequently in the
evening [7]. In primary teeth such pain has been corre-
lated with extensive inflammation throughout the pulp
tissue, both in the chamber and in the root canal(s),
where there may also be internal resorption. Therefore,
this is a nonreversible condition [8]. The child usually
avoids bringing any solid or liquid food into contact
with the teeth on the painful side. The responsible tooth
may present significant clinical symptoms, such as pain
on occlusion, or signs such as tenderness on pressure,
often in conjunction with mobility. Although there may
be no additional radiographic pathologic signs as yet,
the expansion of periodontal space, often visible in the
tion, i.e., generalized chronic pulpitis [8]. The evaluation
of clinical and radiographic data leads to considering a
decision for root canal treatment or extraction of the
tooth.
14.1.1.3 Clinical Examination
Extra- and intraoral examination with specific attention
to the following points will determine the urgency of a
case and if immediate treatment is required.
Cavity Size
Small cavities of primary molars present with radio-
graphic depth of caries reaching the inner dentin half
and would always show signs of partial inflamma-
tion in the corresponding pulp horns in a histological
examination [2] (. Fig. 14.2). This was found more fre-
quently in cases of class II rather than class I cavities [4].
Nevertheless, such inflammation seems to be reversible,
as inferred from clinical and radiographic-based suc-
cessful restorations. This may even be true in cases of
deep and extensive class II restorations (. Fig. 14.3) [9].
Edema
Intraoral edema (intraosseous and soft tissue infiltration
by inflammation products) is associated with pulp under-
going necrosis. The pulp infection exits to surrounding
tissues from the root apex in anterior (single root) teeth,
while in primary molars it usually exits from secondary
root canal branches in the furcation area. Inflammation
products diffuse through the alveolar bone usually with
buccal/labial direction and less frequently lingual/pala-
tal. However, as the existence of vital pulp is commonly
found in some root canals, local anesthesia is necessary
before starting root canal treatment [2]. If no treatment
is performed, the tissue pressure by edema will lead to
spontaneous drainage of inflammatory products (pus)
through a fistula, usually located next to the attached
gingiva (. Fig. 14.4).
Extraoral edema appears in the form of cellulitis
extending to the inter-muscle spaces of the face or
neck, often leading to intense local lymphadenitis. In
the mandible, this usually appears as a result of sep-
tic pulp necrosis in the first or second primary molar
or that in permanent molars of older children and
adolescents. In the maxilla, the inflammatory spread
of septic necrosis of the pulp of first primary molar
may extend to the child’s eye socket (. Fig. 14.5).
The drainage of the extraoral edema follows the route
of least resistance; pus drainage through the skin,
as sometimes encountered in permanent teeth, is an
exceptionally rare phenomenon for primary molars. If
Pulp Therapy in Pediatric Dentistry
319 14
..      Fig. 14.4 a The frequent
a b
finding of a fistula, relatively
closer to the (restored) maxillary
primary canine rather than the
responsible first primary molar,
raises a diagnostic issue. b The
radiograph reveals that the cause
is septic pulp necrosis of the
molar

a b

..      Fig. 14.5 a Spread of the edema with redness and a reduced Spread of osseous inflammation to the suborbital region due to sep-
capacity to open the mouth caused by dentoalveolar inflammation tic necrosis of the maxillary right first primary molar
of the mandibular right second primary molar in an 8-year-old. b

necessary, appropriate antimicrobial administration
(see below), either alone or with calcium hydroxide
root canal treatment, leads the edema to recession in a
matter of days [10].
Mobility
Pathologic mobility of primary teeth is accompanied
by radiographic findings. Mobility caused by edema is
related to non-vital pulp and can be treated with root
canal treatment. The outcome of the latter does not
depend on the extent of pathologic mobility [8].
Percussion
Pain caused by pressure on a tooth indicates that sup-
porting periodontal tissues are inflamed and radiogra-
phy may depict a periradical space increase if the tooth
has risen slightly in its alveolus. Upon occlusion, pain
is often felt in that case. Percussion testing may be very
painful, and make anxious children more frightened
of dentists. When deemed necessary, exercising mild
pressure on the tooth with a finger is sufficient.
Vitality Tests
The value of pulp vitality testing using electrical or ther-
mal stimuli, although high in permanent teeth, has dubi-
ous reliability in primary teeth. The subjective response
is often further influenced by the child’s anxiety or fear.
Furthermore, painful stimuli will negatively affect the
cooperation of a frightened child. Some new painless
techniques have been adapted for use in dental prac-
tice, such as measuring pulpal blood flow using Laser
Doppler Flowmetry [11]. Its use has extended to include
 320 A. Arhakis et al.
young permanent teeth in diagnosing the vitality (hemo-
dynamic function) of their pulp. Such techniques have
yet to gain ground in broader clinical applications.
14.1.1.4 Radiographic Examination
Absolute prerequisite for correct diagnosis and treat-
ment of pulp pathology is appropriate and recent
radiographic examination. Panoramic or other extra-
oral radiographs are unsuitable for diagnosing pulp or
the supporting bone pathology, as already described in
7 Chap. 6. Intraoral periapical or bite wings providing
images of the molar furcation area have significantly
higher diagnostic value concerning carious lesions, the
pulp and the periodontal condition. They provide infor-
mation on:
55 Proximity to the pulp in cases of deep carious lesions
55 Adequacy of restorative work
55 Success or failure of pulpotomy or pulpectomy out-
come [12]
The commonest radiographic findings related to pulp
pathology are as follows.
a graphic image of normal primary molar roots helps in
14
b
..      Fig. 14.6 a Root canal obliteration of maxillary right central
incisor probably caused by prior trauma. The periapical radiolu-
cent region indicates subsequent pulp necrosis. b Obliteration of the
mesial root of mandibular left second primary molar following pulp-
otomy (arrow)
Root Canal Obliteration
The intense production of tertiary dentin leading to a
drastic reduction of pulp tissue indicates pulp reaction
under chronic carious lesions or trauma. The resulting
pulp obliteration mainly involves anterior primary teeth
following injury and root canals of posterior primary
teeth following pulpotomy (. Fig. 14.6) [12, 13]. While
tooth monitoring becomes necessary, it does not imply
treatment failure.
Internal Root Resorption
Internal resorption may be visible radiographically when
it involves the mesial and/or distal aspects of root canals
while, if at initial stages it involves the lingual or buccal
sides, it may not be diagnosed. Therefore, when treating
a symptomatic pulp, preexisted resorption foci cannot be
excluded [14]. The presence of internal resorption follow-
ing pulp capping or pulpotomy is an indication of chronic
pulp inflammation, i.e., treatment failure. Although suc-
cessful root canal treatment cases have been presented
(. Fig. 14.7), in the absence of sufficient documentation
extraction remains the safest option.
External Root Resorption
This may be natural or pathologic. Knowledge of radio-
discerning pathologic resorption. It is normal for the
distal buccal roots of first primary molars to be rather
shorter than the distal buccal ones. Resorption of man-
dibular primary molar roots is affected by the position
of successor premolars. Pathologic bone resorption at
the bifurcation/trifurcation point of primary molars
may be accompanied by corresponding external root
resorption (. Fig. 14.8). In that case the correct treat-
ment is the extraction of the primary tooth [15].
Bone Radiolucency
Radiolucencies in primary molars resulting from pulp
infection almost always appear at the bifurcation area,
unlike permanent molars which mostly develop periapical
lesions. This has been attributed to the presence of many
accessory root canals in the bifurcation dentin of primary
molars [16] (. Fig. 14.9). Radiolucency starts by thicken-
ing of the periodontal space and resorption of lamina dura
meaning that inflammation has spread to the periodontal
tissues (. Fig. 14.10). When the radiolucency is small,
pulpectomy has high success rates, whereas empirical find-
ings point to extraction in cases of gross bone resorption [8].
Depth of Carious Lesion
Proximity to the pulp can be determined radiographi-
cally, unless buccal or lingual cavities are involved. If the
lesion is too close to the pulp, it is highly likely that the
pulp becomes exposed if all infected dentin is removed.
The history of pain helps assess the condition of the
pulp and allows options for indirect pulp capping or
pulpotomy [17], as presented below. A summary of the
Pulp Therapy in Pediatric Dentistry
321 14
..      Fig. 14.7 a Radiograph of
a b
an emergency pulpotomy per-
formed 4 weeks ago in a 4-year-
old girl (diagnostic radiographs
were then not possible due to
intense gag reflex). Internal
resorption in the distal root of
the mandibular second primary
molar and onset of furcation
bone resorption are seen; there
was probably a misdiagnosed
pulp condition. b Further prog-
ress of internal root resorption c d
after 2 weeks. c A root canal
treatment was undertaken and
completed at 8 weeks. d Success-
ful outcome of treatment at the
30 months follow-­up

pulp condition expected depending on diagnostic find-
ings is presented in . Table 14.1.
Diagnosis During Intervention
All too often the final diagnosis and treatment deci-
sion cannot be made before direct observation and
immediate assessment of the pulp tissue following its
exposure. Both the size of exposure and the nature of
the fluid excreted from the specific point are of diag-
nostic value [8]. Large exposed sites are not consid-
ered appropriate for direct pulp capping in primary
teeth [18]. Quick hemorrhage control signifies partial
inflammation and indicates a case for pulpotomy.
Intense hemorrhage (or suppurated blood flow) is his-
tologically related to inflammation extending into the
root canals of primary teeth. In this case, pulpectomy
is indicated, but not without prior radiographic
examination [8, 12].
Continuous hemorrhage from root canal entries
for more than a few minutes is a sign of hyperemic
inflammatory root pulp. If vasoconstrictors are
injected directly into the root canals (e.g., local anes-
thetic with epinephrine), this intervention in the
hemostatic capacity of the pulp deprives us of the
possibility of determining the extent of the inflamma-
tion.
14.1.2 Management of Pulp-Related
Emergency
When a child arrives as an emergency in a busy den-
tal surgery, it disrupts its smooth operation. A break
of, e.g., 30 minutes at some point between scheduled
appointments helps accommodate for possible emer-
gencies. If there is no emergency, this may be used to
deflate possible delays of prior sessions or for staff
relaxation and communication. This is particularly
useful for the first day of the working week, because
chances for an emergency add up at weekend holidays.
When there is an emergency case, the clinician is called
on to:
1. Minimize possible distress of small children often
unaccustomed with the dental environment
2. Perform necessary examinations for correct diagno-
sis and emergency treatment for patient relief
3. Book a new full clinical/radiographic examination
session for total care by enrolling the patient in the
regular dental practice schedule
Following the diagnosis, a treatment decision is reached
for either preserving or extracting the tooth, after the
informed consent of parents. If it is about a permanent
tooth, it is useful to have an orthodontic evaluation.
Emergency cases involving painful inflamed primary
teeth because of caries almost invariably concern molars.
On the relatively few occasions the emergency case
concerns carious anterior primary maxillary teeth, the
inflammation will have already spread to the periapical
tissues.
In cases of evoked pain to a primary molar, con-
servative treatment may be performed. Emergency
­treatment involves painless removal of some soft den-
tin with a spoon excavator, if possible, and temporarily
sealing cavity with GIC. If the clinician’s available time
and the child’s cooperation allow, radiographic exami-
nation and definite treatment by appropriate pulp ther-
apy may be preferred in this initial session; otherwise, a
new appointment may be arranged.
 322 A. Arhakis et al.

a b c

..      Fig. 14.8 a Major furcation bone resorption accompanied by period, but a wait-and-see approach was chosen. c After 3 years,
probable (missed) small external resorption of the adjacent distal a pathology-related deflection in the path of premolar eruption
root of mandibular second primary molar. b Root canal treatment together with lack of resorption of the primary molar roots are
did not lead to resolution of furcation pathology after a 5-month observed

..      Fig. 14.9 a Schematic rep-

resentation of the furcation a b
bone infection from accessory
root canals of a primary molar.
b Accessory and another much
smaller accessory root canals
at the bifurcation region of a
primary molar seen by scanning
electron microscopy [16] (by
permission)

14
..      Fig. 14.10 Radiographic examination of deep cavity of a first
mandibular primary molar reveals periodontal space thickening in
the furcation area along with internal root resorption (arrows)
If there is spontaneous pain in a primary molar, as is
often the case, definite treatment requires pulpectomy or
extraction, based on the radiographic image and other
factors described below. The dentist must be determined
to apply effective local anesthesia and be familiar with
this procedure in the case of an anxious or even fright-
ened child. Otherwise, it is better to refer the child to
a pediatric dentist, considering the consequences of a
failed, possibly painful, unscheduled session primarily on
the future cooperation of the child and secondarily on the
rest of the clinician’s daily schedule. Emergency interven-
tions may include means of pain control by anti-inflam-
matory/antimicrobial administering in cases of extensive
inflammation (. Fig. 14.5) or even drilling the tooth for
immediate drainage, antiseptic irrigation, and temporary
filling. There is no need to expose a localized abscess of
a primary tooth for pus drainage, because these usually
recede shortly if prior instructions are followed.
Pulp Therapy in Pediatric Dentistry
323 14

..      Table 14.1 Symptoms and signs in various pulp conditions of primary teeth

Diagnostic findings Partial chronic pulpitis Total chronic pulpitis Partial/total pulp necrosis

Mobility (pathologic) + +
Edema +
Tenderness on percussion/pressure + +/?
Vitality testing > >
Pain /? (evoked) + (spontaneous) +/
Intense hemorrhage on exposure +
Radiographic findings /+ +

14.1.2.1 Antimicrobial Medication

..      Table 14.2 Antimicrobial medication in suspension form
in Emergency Cases and usual dosage schemes for pediatric inflammations of dental
Acute orofacial infections are mostly of dental origin origin; in cases of serious infections the dosage can be doubled
and usually respond well to dental treatment. A funda-
mental principle of treating infections of dental origin Amoxicillin 40–50 mg/kg bw/24 hours, in 3
doses, for 7–10 days
is to control the endodontically established microbial
factor; this is achieved with extraction or root canal Amoxicillin with 40(32 + 8) mg/kg bw/24 hours, in 3
treatment of the tooth involved. If however these are clavulanic acid doses, for 7–10 days
left untreated, they may lead to a dangerous spread of Clindamycin 20–30 mg/kg bw/24 hours, in 3
the infection, e.g., to obstruction of airways [9]. In such doses, for 7–10 days
cases, the dentist may need to cooperate with the pedia- Clarithromycin 15 mg/kg bw/24 hours, in 3 doses,
trician and possibly hospitalize the child. Antimicrobial for 7–10 days
(antibiotic) medication should generally be adminis-
tered when the overall condition of the child is serious
or in cases of intense progressive cellulitis where there is to erythromycin [6, 14, 19]. Usual dosages are presented
a risk of the infection spreading to more vital organs. A in . Table 14.2.
conservative use of antibiotics is indicated for minimiz-
ing the risk of developing resistance to current antibi-
otic regimes [6, 14]. 14.2  reatment of Pulp Pathology
T
In many countries phenoxymethylpenicillin (penicil-
lin V) is still recommended, while if anaerobic infection
in Primary Teeth
is suspected, metronidazole may be used at a dose of 7.5
mg/kg of body weight every 8 hours for 5–6 days [14]. 14.2.1 I ndirect Pulp Capping of Primary
Semisynthetic penicillins are usually preferred, such as Teeth
amoxicillin and its more recent forms with the addition
of clavulanic acid. Another antimicrobial is clindamy- The aim of indirect pulp capping (IPC) is to main-
cin. Despite reservations in the past about side effects, tain pulp integrity. It has been proposed for teeth with
such as pseudomembranous colitis, clindamycin is used very deep carious lesions, in trying to avoid iatrogenic
due to its good absorption and antimicrobial spectrum, pulp exposure [20]. Prerequisite for IPC is the absence
which includes numerous anaerobic microbes. Dosage of clinical or radiographic signs of nonreversible pul-
is 15–40 mg/kg of body weight, divided into 3–4 equal pitis, and the only acceptable symptom may be short
doses. However, it may not be found in suspension and evoked pain that soon subsides without analgesics. In
being suitable for children weighing 35–40 kg or older, performing IPC, most bacteria-rich soft carious dentin
in adult dosages. is removed while the relatively hard, possibly discolored,
In cases of hypersensitivity to penicillin, in addi- dentin close to the pulp remains. This still contains some
tion to clindamycin, more recent forms of macrolides, bacteria, the number and activity of which is drastically
such as clarithromycin, are preferred, due to their bet- reduced when the cavity is restored with appropriate
ter pharmacodynamics and dosage schemes compared biocompatible material; its hermetic sealing deprives
 324 A. Arhakis et al.
Description of an Emergency Case
Dental History
A 4-year old boy with no medical history was referred
for consultation after a 9-day hospitalization with IV
antimicrobial and analgesic/anti-­inflammatory medica-
tion for a persistent submandibular edema (the patient’s
parents had sought emergency treatment at a local hospi-
tal’s pediatric department because of weekend holiday).
Prior intense pain was in remission, and his temperature
was 38 °C.
Dental Examination
The child was burned out and his cooperation low.
Extraorally
Chronic submandibular edema was still present
(. Fig. 14.11), while local submandibular lymph nodes
were found swollen and tender to palpation.
Intraorally
Clinically, the tongue presented a fungal infection.
Two clinically sound, class II back-to-back composite
resin restorations in the mandibular right first and second
primary molars were present. Inadequate oral hygiene
regionally, absence of intraoral edema but positive per-
cussion signs from the first primary molar, was evident.
14
c d
..      Fig. 14.11 a Persistent right submandibular edema after
9-day hospitalization of a 5-year-old. b The tongue presents
fungal infection secondary to long chemotherapeutic treatment.
c Radiograph reveals deep, back-to-back, restorations of man-
dibular right primary molars with residual carious dentin. A
The periapical radiograph indicated the mandibular
right first primary molar as the responsible tooth
(. Fig. 14.11).
Diagnosis
An extensive inflammation spread with no signs of
purulence, originating from the carious pulp of the man-
dibular right first primary molar, was diagnosed as the
cause. The tongue fungal infection had obviously been
caused by the continued administration of antimicrobials.
Treatment
Based on the radiographic image of its sound roots, it
was decided to immediately start root canal treatment of
the respective tooth, under inferior dental block anesthe-
sia and use of rubber dam.
Debriding and irrigating the canals with sodium
hypochlorite and filling root canals with calcium hydrox-
ide led to full edema resolution; after 10 days, root canal
filling with zinc and eugenol paste (ZOE) of the respec-
tive first primary molar and restoring both right first and
second primary molars were made possible under the
patient’s full cooperation. Oral hygiene was reinstituted,
and treatment success was confirmed in follow-ups
(. Fig. 14.11).
difuse furcation bony lesion suggests the first primary molar as
the responsible tooth (please disregard the dark thick artefact
line above its pulp chamber). d The annual follow-up radiograph
confirms the ­successful outcome of the root canal treatment
Pulp Therapy in Pediatric Dentistry
the bacteria of nutrients. The carious process is thus
interrupted and any carious dentin that remains hard-
ens (remineralizes) [7]. Following IPC, the pulp-dentin
complex is preserved by activating the reparative pulp
mechanism for secondary dentin apposition [21].
14.2.1.1 Technique
The tooth is anesthetized and isolated with rubber dam.
All carious dentin is removed except for that very close
to the pulp, which, if removed, might lead to pulp expo-
sure. This requires familiarization of the clinician with
the pulp chamber shape and dimensions of primary teeth
and with the radiographic image of deep primary molar
caries. The risk of exposure is much higher approaching
the primary tooth pulp horns, whether from the axial or
the supra-pulpal cavity wall (. Fig. 14.12). While it is
generally advised that following caries excavation only
hard and discolored dentin remains, in fast-progressing
active lesions no dentin with such characteristics is often
found. This increases the risk of unnecessary pulp expo-
sures. All these apply to anterior teeth as well. The prop-
erties of lining materials such as (RM)GIC allow for
minimal remnants of soft dentin surrounding the pulpal
horn [20]. These materials seem to possibly satisfy the
need for both an indirect capping material and a filling
material according to a clinical study [9], an approach
that also reduces chair time. The same principal governs
a For primary teeth in general, reentry to the cavity is not
b c
..      Fig. 14.12 a Radiographically the occlusal carious dentin in the
second primary molar is in contact with both pulp horns but not
with central supra-pulpal wall. b The preparation of this deep cavity
respects the pulp chamber shape. c Checking the finished restora-
tions for early contacts after rubber dam removal
325 14
the acceptance of sealing the soft infected dentin of pri-
mary molars under a PMC placed by the Hall technique.
Attention should be paid to fully removing carious
dentin located at the peripheral cavity walls and, partic-
ularly, the cervical one where most mistakes occur. The
restorative material must be seated on healthy dental
tissues (. Fig. 14.10). Otherwise, existing leakage risks
caries progression. The use of a round bur (usually Νο.
4 or 5) at very low rotation speed provides quite a good
sense of the hardness of deep dentin to be removed, in the
effort to avoid pulp exposure. On the contrary, the use of
a hand excavator, although very useful at initial removal
of gross carious dentin, when approaching the pulp is
more likely to result in its exposure. For the same reason,
the use of the dental probe to sense the dentin hardness
should be completely avoided, contrary to an old view
for checking if all carious dentin is removed. The ART
technique (discussed in 7 Chap. 13) for removing cari-
ous dentin using only hand instruments (usually without
local anesthesia) is another form of IPC [22].
14.2.1.2 Materials
If the pulp is healthy or with signs of reversible pulpitis,
it is sufficient to cover the pulpal cavity wall with conven-
tional GIC or RMGIC [23]. Other biocompatible mate-
rials may be used like a quick-setting calcium hydroxide
or ZOE. The latter was formerly used as temporary fill-
ing material in the so-called stepwise excavation [20].
recommended and IPC and restoration are better com-
pleted in one session. Although there is a view that lining
the deep cavity with calcium hydroxide is advantageous
due to the initially high pH, what seems to be impor-
tant is the tight seal from bacteria rather than the type of
material used to cover the pulpal wall of the cavity [21].
14.2.1.3 Effectiveness
IPC success rates of 83–96% have been reported for pri-
mary teeth that present no signs or symptoms of non-
reversible pulpitis [23]. IPC using preferably calcium
hydroxide and GIC is taught as the technique of choice
at 70% and 83% of American and British dental schools,
respectively [24]. IPC has the same indications as pulp-
otomy in primary molars with deep carious lesions with-
out pulp exposure [25] and may therefore be preferred
over pulpotomy, since their success is similar [26].
14.2.2 Direct Pulp Capping of Primary Teeth
Direct pulp capping (DPC) may be implemented when
the pulp tissue is exposed. The tooth must be asymp-
tomatic and, to avoid further contamination, one should
 326 A. Arhakis et al.
not risk a DPC without using a rubber dam. With extra
careful carious dentin removal, there may be cases that
exposure is borderline with no bleeding (. Fig. 14.13).
Following DPC, the pulp is expected to preserve its
vitality and “defend itself ” by reparative dentin deposi-
tion. This technique may be selected ideally for small
carious pulp exposure cases in permanent teeth with an
open apex. If we suspect that the inflammation extends
to a large part of the pulp chamber, treatment failure
and full-blown pulpitis are probable. In primary teeth,
DPC may be selected based on strict criteria indicat-
ing absence of pulp inflammation, i.e., in clinical terms,
absence of spontaneous or continuous pain of pulpal
origin and limited self-contained hemorrhage after min-
imal pulp exposure [17, 25]. The documentation of such
instructions is however low, based on a few old studies
and expert opinions; more recently, randomized con-
trolled clinical trials with contemporary pulp capping
materials support DPC as an option in carious primary
molars, with success rates comparable to pulpotomy [18,
27].
Instead of direct capping per se in cases of carious
primary teeth, some authors have adopted partial pulp-
otomy with calcium hydroxide or MTA (. Fig. 14.14).
In performing it, about 2 mm of pulp – the part con-
sidered to be inflamed – is removed using a high-speed
diamond bur. This variation has produced success rates
75% after 3 years [28]. Since it is a preferred option in
pulp exposures of traumatized permanent teeth, it is
described in 7 Chap. 16.
Technique
14 14.2.2.1
DPC procedure requires ideal conditions. Gross cari-
ous dentin removal at pulpal walls and cavity prepa-
ration must have been completed before exposure
occurs. Thus, the most dentin infected with bacteria
will have already been removed. If uncontrollable
hemorrhage is observed at minimal primary tooth
pulp exposure, extensive inflammation is present and
other pulp treatment options are chosen among those
presented below [20]. If there is little hemorrhage
leading soon to spontaneous hemostasis, possibly
aided with a short light dressing with a cotton pellet
dump in saline, DPC is possible. After gently drying
the pulpal wall, the minimally exposed primary tooth
pulp may be covered under no pressure with calcium
hydroxide (Ca[OH]2) or mineral trioxide aggregate
paste (ΜΤΑ), before placing a PMC or a well-sealed
restoration, which again does not require significant
condensation (. Fig. 14.15).
14.2.2.2 Materials
Biocompatible materials for DPC are the following.
Calcium Hydroxide
Pure calcium hydroxide (Ca[OH]2) has been, and still is,
the gold standard. Its water mixture provides good dis-
infection, because of high pΗ [12], and prevents micro-
bial growth; it has a superficial caustic effect to the pulp
tissue and is very soluble (it does not set). This is why
it is also employed in the form of quick-setting cement
with the addition of salicylate esters (commercial
brands, e.g., Dycal, Life, etc.); this increases mechani-
cal stability and easier handling (it sets very soon). As
a cement has much lower pH [9] which may explain the
lower success rates when compared with pure calcium
hydroxide in direct pulp capping. The pulp reacts form-
ing ideally a “bridge” of hard tissue, preserving pulp
vitality. The quality of this “bridge” has been studied
in permanent teeth and shown to be less solid than the
one formed with the use of ΜΤΑ [29], allegedly because
the latter bonds much better with dentin and remains
stable in the long-term, thus preventing microbial leak-
age. Nevertheless, calcium hydroxide is still the most
user-­friendly and affordable material [30].
Mineral Trioxide Aggregate (MTA)
The basic ingredients of ΜΤΑ is a mixture of dical-
cium and tricalcium silicate and tricalcium aluminate,
20% bismuth oxide added for radio-opaqueness and,
in smaller amounts, and iron and magnesium oxides. It
has found various dental applications as final root canal
sealer, in direct pulp capping and pulpotomy, root pen-
etration, and apical plugs [30, 31]. Less documentation
is available for the similar material Portland cement [32].
When the powder form is mixed with water, it becomes
colloidal and hardens within about three hours; its pH
is 12.5, similar to that of pure calcium hydroxide. The
main product of the reaction of these cements with
water is calcium hydroxide, which explains their similar
effect on the pulp. ΜΤΑ setting is accelerated in a humid
environment; this is why, after placing it at the exposure
site, dump cotton wool is temporized in the cavity, with
the final restoration placed the following day. This is
a disadvantage in clinical practice but some studies of
one visit for MTA application and restoration in pri-
mary teeth have shown good results [28]. ΜΤΑ strength
is at least equivalent to that of ΖΟΕ and other similar
cements. Disadvantages are its relatively high cost and
the necessity to be packaged in single doses because
atmospheric humidity degrades it, thus other packaging
forms have appeared (. Fig. 14.16).
Other Materials Under Investigation
Dentin bonding agents proposed for direct pulp cap-
ping do not promote the creation of secondary dentin,
and their bonding capacity to carious dentin is limited
leading to pulp inflammation [33]. TGF-β pathway
Pulp Therapy in Pediatric Dentistry
327 14

a b

c d

..      Fig. 14.13 a Extremely deep cavities in both mandibular primary
molars, radiographically in contact with the pulp cavity, and pos-
sible furcation involvement of the first one. There was history of only
provoked pain. b Occlusal aspect of oversize class II cavity prepara-
tions. c Wide borderline pulp exposure with no bleeding was evident
in both molars after extra careful carious dentin removal at pulpal
walls. Caries removal was complete at axial and cervical walls. d The
finished restorations with RMGIC after calcium hydroxide cover of
exposure site on both molars. e Follow-up radiograph at 30 months
shows pulp treatment success and healthy bone furcation

growth factor and bone morphogenetic proteins have 14.2.2.3 Effectiveness

been used in pulp capping cases in animal experiments
[34], but further investigation is necessary to explain
the mechanisms of their action and their potential for
clinical application. Other substances have also been
tested, such as an enamel matrix derivative, which has
performed successfully in a clinical primary teeth study
[35]; however, additional evidence is sought.
The relevant guidelines state that direct pulp capping
may only be selected in the absence of pulp inflamma-
tion [8, 25]. More recent findings regarding the use of
calcium hydroxide or MTA [18, 27, 36, 37] report high
success rates in carious primary molars, which approxi-
mate those of permanent teeth [38]. Until more random-
ized controlled trials (RCTs) are available on whether
 328 A. Arhakis et al.
a Pulpotomy is indicated following pulp exposure
b and internal or external pathologic root resorption
c Radiographic criteria for pulpotomy success are normal
..      Fig. 14.14 a Radiographic image of mandibular second primary
molar of a 6-year-old boy referring recent, short-duration, evoked
14 pain (its apical distal root resorption seems unrelated). b Partial
pulpotomy with MTA and placement of a PMC was preferred along
with restoring the first molar. c Progressive root canal obliteration is
observed under the MTA at 2-year recall
direct pulp capping is a reliable long-term option for
carious primary teeth as well, it should only be chosen
in the light of the precautions listed above [18, 30].
14.2.3 Primary Molar Pulpotomy
Pulpotomy is the excision and removal of the inflamed
crown pulp segment. The healthy radical segment
remains and is covered with some material so as to pro-
mote healing at the dissection point with the generation
of hard tissue, thus allowing the radical pulp to preserve
its vitality. In cases of anterior teeth, partial pulpotomy
or pulpectomy is preferred over pulpotomy because
there is no abrupt narrowing of the pulp chamber in its
transition to the radical pulp.
due to caries or injury in cases of asymptomatic teeth
with vital pulp or with pulpitis symptoms limited to the
crown pulp [8, 25]. The latter is confirmed when after
the excision of the crown pulp hemostasis is achieved
within a few minutes. Pulpotomy is contraindicated
for primary molars with extensive pulp inflammation,
something indicated by a history of spontaneous or
long-lasting pain, edema or abscess, tenderness on
percussion, pathologic mobility, furcation bone lesion,
[12]. Pulpotomy indications and contraindications are
not, in effect, different from those for indirect pulp
capping [8, 25], and this is why the former should be
selected over the latter only after pulp exposure has
occurred.
The evaluation of long-term pulpotomy success in
primary teeth is based on clinical and radiographic cri-
teria. Clinical success criteria are the absence of pain,
mobility, and inflammation including abscess or fistula.
periodontal space and no furcation or periapical radio-
lucency, as well as normal eruption path of the perma-
nent successor tooth.
14.2.3.1 Technique
After local anesthesia administration and rubber
dam placement, carious dentin is fully removed from
the cavity walls using a Νο. 4 or 5 round bur at a low
speed handpiece. Thus, additional bacterial contami-
nation when the pulp is exposed is prevented. If the
pulp is exposed, the supra-pulpal wall of the crown
chamber is removed using a cylindrical diamond bur
on a high-­speed handpiece with water spray. The bur
follows the outline of the crown chamber, as defined
by the pulp horns, starting from the exposure point
(. Fig. 14.17).
The pulp segment in the crown chamber may be
amputated using a new (sharp) sterilized excavator or a
new round No. 4–6 bur on a low speed handpiece. The
pulp is amputated at the root canals entries, a procedure
requiring familiarity with their topography. Ample rins-
ing of the pulp chamber with saline solution helps pre-
vent the entry of infected dentin debris into root canals.
The entire crown pulp must be carefully removed as any
inflamed remnants continue to bleed impeding diagnosis
and making it impossible to visually examine the root
canal entries. Root pulp hemorrhage is controlled by
placing a cotton wool plug impregnated with saline for
3 minutes (. Fig. 14.18). The tooth is considered suit-
able for pulpotomy only when hemorrhage stops after
that. Placing a cotton wool plug impregnated with 5%
sodium hypochlorite solution for 1 minute may help in
Pulp Therapy in Pediatric Dentistry
329 14
..      Fig. 14.15 a Radiograph
a b
of carious primary teeth. b
Pulp exposure of maxillary
second primary molar after
spontaneous hemostasis. c
The 2-year follow-up radio-
graph after DPC with ΜΤΑ
and IPC of maxillary and
mandibular second primary
molars, respectively, shows
the success of both pulp
treatments. d, e Clinical view
of the restorations
c d e

a b c

..      Fig. 14.16 a Individual packaging of white ΜΤΑ (ProRoot, Dentsply, and Angelus) in power sachets and distilled water. b White ΜΤΑ
(Medcem GmbH) with powder in capsules. c Allegedly less sensitive to moisture white ΜΤΑ (NuSmile)

the disinfection and hemostasis, although reservations
to that have been expressed [20, 25]. Root stumps are
particularly sensitive to new irritation, e.g., by new con-
tact with dry cotton fibers and bleeding may reappear. If
even minimal hemorrhage continues, the procedure may
be repeated once more. If it is still not controlled, this
indicates inflammation of the root pulp and pulpectomy
should follow [39].
Following hemostasis, the pulp stumps are covered
by the material of choice. The pulp chamber is then filled
under no pressure (before hardening starts) by fast set-
ting ZOE or by RMGIC. A PMC is carefully cemented
or another restoration placed providing complete cavity
sealing.
14.2.3.2 Materials and Effectiveness
of Pulpotomy
Various materials have been used for pulpotomy. The
ideal material should be bacteriostatic, nonirritating for
the pulp and surrounding tissues, promote pulp healing,
and not interfere with normal root resorption [12]. A
contemporary well-documented material is MTA, but
other medicaments and techniques are being or have
been used, as well.
Mineral Trioxide Aggregate
MTA as well as Portland cement are highly biocompat-
ible pulp capping materials not resorbed over time like
calcium hydroxide and present fewer toxic properties
 330 A. Arhakis et al.
a b
..      Fig. 14.17 a A cylindrical diamond bur has been used to cut
away supra-pulpal dentin of a mandibular second primary molar
with a large distal carious cavity. The supra-pulpal-dentin is ready
a b
d e
14
..      Fig. 14.18 a Series of pulpotomy actions following radiographic
examination, local anesthesia, and rubber dam isolation. a Hyper-
plastic pulpitis of mandibular left second primary molar. b Cavity
preparation with removal of supra-pulpal dentin with pear-shaped
diamond at high speed under water cooling. c Amputation of crown
than other materials [40–42]. Their mode of action was
explained earlier in DPC. A small quantity of 1–2 mm
thickness is placed at root canal entries. The absence of
internal root resorption, biocompatibility, and capac-
ity to induce “dentin bridge” creation has increased
MTA preference for pulpotomies. Some root canal
c
to be detached. b Cotton wool dumped in formocresol is pressed in
the pulp chamber after careful inflamed pulp remnants. c The pulpal
chamber with complete hemostasis
c
pulp and placement of cotton wool plug impregnated with saline
solution for 3 minutes. d Hemostasis is controlled. e Filling the pulp
chamber with quick-setting ZOE preparation following capping of
pulp stumps with MTA
obliteration is a frequent finding, but this does not seem
to be clinically significant (. Fig. 14.14). Success rates
are over 95% for 1- to 2.5-year follow-up period, [20,
43, 44], although lower rates have been reported when
placed by pediatric dentistry trainees (Dimitraki et al.
2019) [18].
Pulp Therapy in Pediatric Dentistry
Formocresol
Formocresol was the most popular primary tooth pulp-
otomy and reference material for more than 70 years.
In the new century, there has been renewed reflection
to the cytotoxicity and potential mutagenic action of
the formaldehyde (19%) it contains, which has caused
concern in the scientific community, leading to recom-
mendations for stopping its use [25]. Dilution of formo-
cresol with glycerine, at a ratio of 1:5, was found to be
as effective [43], and this has been employed more fre-
quently in recent decades to mitigate the undesirable
effects of formaldehyde. Formocresol is a potent anti-
septic that does not promote dentinogenesis but causes
fibrous degeneration and fixation, under the site of pulp
amputation. Despite animal studies eliciting its nega-
tive effects, formocresol has remained clinically accept-
able [45], and its use was until recently taught at dental
schools in the USA and Europe. Success rates have been
reported in the order of 80–90%, close to those for ΜΤΑ
[39, 46, 47].
Ferric Sulfate
When this coagulating agent comes into contact with
blood, a ferric ion and protein complex is formed in the
form of a membrane mechanically covering vessels and
inducing hemostasis. This complex covers the root canal
amputated pulp preventing clot formation (Srinivasan
et al. 2006) [46]. This 15-second impregnation with fer-
ric sulfate (. Fig. 14.17b) is followed by mild irrigation
of the crown chamber with water and light drying with
a moist cotton wool pellet. A ZOE cover of root canal
entries is succeeded by the permanent restoration. A wide
range of ferric sulfate success is reported (43–97%) which
is lower than those of MTA [17, 48]. Ferric sulfate has
no systemic toxic action. In the “post-formocresol era,”
it remains a popular medication in primary tooth pulp-
otomy [24, 49].
a b
..      Fig. 14.19 a External and internal resorption of mesial roots of
mandibular second primary molar and major furcation bone resorp-
tion in an 8-year-old boy call for its extraction. Some bone is visible
331 14
Other Techniques and Medications
A different approach is electrosurgery to cauterize the
pulp, leaving a clot at radical pulp stumps. A retrospec-
tive study reported high clinical and radiographic suc-
cess rates (96% and 84%, respectively) (Lin et al. 2014).
Additionally, various laser methods have been assessed
on animals and in dental praxis, such as Nd:YAG,
Er:YAG, carbon dioxide laser, laser diode, and argon
laser [50, 51]. Data so far do not support the general
adoption of laser and electric surgery techniques for pri-
mary molar pulpotomy.
14.2.4 Pulpectomy/Root Canal Treatment
of Primary Teeth
Pulpectomy means the full removal of pulpal tissue.
Following chemical and mild mechanical processing of
root canals, these are filled with a biocompatible mate-
rial to prevent any bacteria remaining within them. Root
canal treatment is indicated when there are signs and
symptoms of chronic pulpitis or necrotic pulp (pulpless
tooth) without radiographically apparent internal or
external pathologic root resorption. Local pus presence
is not a contraindication as it can be managed by end-
odontic drainage. Contraindications to root canal treat-
ment leave extraction as the alternative (. Fig. 14.19).
Extraction is preferred for primary teeth with extensive
crown destruction that cannot be restored even with a
PMC. When, in mixed dentition, the roots of a primary
molar have been resorbed, either naturally or pathologi-
cally, to the degree that there is no furcation bone up to
the permanent successor tooth crown, the primary molar
extraction is preferred and there is no need to maintain
space [3]. When space maintenance is an issue, preserv-
ing the primary tooth in the dentition is significant espe-
cially before the first permanent molars erupt [25].
on top of the successor’s crown, indicating the need for space main-
tenance. b, c Radiographic and clinical view with space maintainer in
place after 3.5 years, respectively
 332 A. Arhakis et al.
Anatomical Features of Primary Molar Roots
The shape and form of root canals in anterior teeth
are simple. In molars, however, many variations of
their basic anatomy exist, emphasizing the impor-
tance of the clinician being familiar with the mor-
phology of root canals to ensure successful root canal
treatment. Maxillary and mandibular primary molars
sometimes exhibit more than the usual three root
canals. In the mandible, a network of thin accessory
canals is usually found between buccal and lingual
aspect of the second molar distal root. In about one
quarter of second molars in both jaws, there is a very
wide root canal dividing before the apex (. Figs. 14.20
and 14.21) [ 52, 53]. Primary molar roots present con-
siderable curvature embracing the successor tooth
germ, so that care is needed to avoid perforating
them. The furcation lesions found almost exclusively
in primary molars with inflamed/necrotic pulps signi-
fies that mechanical debridement should focus in the
cervical half of the roots, thus reaching their apical
part with files being purposeless most of the time.
14.2.4.1 Technique
In the first session it is necessary to administer local
anesthesia to avoid any pain during pulpectomy and/
or debridement. It also makes the rubber dam more
..      Fig. 14.20 Root canal
variations of mandibular a a b
14 and maxillary b primary
molars [52] (by permission)
acceptable by the child. Removing the supra-pulpal
dentin is done as for pulpotomy, but the axial walls
may deviate more if necessary for easy access of root
canal filing and rinsing [54]. Every canal entry has to
be located and the canal tissue remnants removed by
appropriately sized Hedstroem or K files. The buccal
root canals of maxillary primary molars (particularly
the distal one) and the lingual root canals of man-
dibular primary molars are usually thinner, and pulp
extirpation or debridement usually starts with files Νο.
25–35 [54, 55]. The length of files preferred for primary
molar teeth is 21 mm since this, except for being suf-
ficiently long, facilitates working in the smaller open-
ing of a child’s mouth (. Fig. 14.22). If satisfactory
opening of the mouth is not possible, some authors rec-
ommend permanently bending a file (. Fig. 14.23). In
order to avoid files penetrating the apex, the working
length is set at 2–3 mm shorter than the actual one [54,
55].
Root canals are disinfected with 5% sodium hypo-
chlorite or chlorhexidine under continuous suction for
removing organic residues, while mildly filing slightly
short to apex [54]. In pulpitis not extending further
than the root canals, endodontic treatment may be com-
pleted in one session, while in pulpless (septic) teeth or
if inflammation extends to the alveolar bone, treatment
completion requires more than one session [17]. Two ses-
sions usually suffice, with root canals cleaned as above in
the first session, dried with paper points and filled with
Pulp Therapy in Pediatric Dentistry
333 14
a b c d

palatal

mesial

mesial
distal distal

..      Fig. 14.21 3-D models of second primary molars [52] (by per- resorption. c Mandibular molar with a single, wide root canal in the
mission). a Maxillary molar with auxiliary root canal in the apical distal root. d Mandibular molar with bifurcated root canal in the
half of mesiobuccal root. b Maxillary molar with early canal ter- middle and apical thirds of the distal root
mination in the palatal root, possibly the result of external root

b c

d e f

..      Fig. 14.22 a Periapical radiograph in this 5-year-old boy shows
moderate furcation bone resorption of mandibular right sec-
ond primary molar with deep occlusal cavity involving the pulp. b
After inferior alveolar nerve block anesthesia, the rubber dam was
placed. c Mild filing of mesiobuccal root (with 21 mm length, No.25
Hedstroem file) is done under rinsing with NaOCl. d Final restora-
tion of the cavity followed the filling of root canals with ZOE at
the next session. e Post-op radiograph. f The 3-year follow-up radio-
graph confirms the successful treatment outcome. Some resorption
of the inner wall of the mesial root is without clinical significance

calcium hydroxide with the help of a lentulo spiral or 14.2.4.2  oot Canal Filling Materials
R
high pressure syringe and temporized [56]. In the second and Effectiveness
session, 10–14 days later, rinsing is repeated and, if there The differences in growth/development, anatomy, and
is no exudate or other signs of inflammation, the root physiology between primary and permanent teeth
canals are dried by paper points and carefully filled with impose changes also in the criteria for root canal fill-
an appropriate paste (see types below). The pulp cham- ing materials. The ideal material for primary teeth
ber is then filled with a quick-setting ZOE preparation should.
[57, 58], a post-op radiograph taken, and final restora- 55 Be absorbable at a rate comparable to the rate of
tion or PMC placed. root resorption
 334 A. Arhakis et al.
..      Fig. 14.23 Hand instruments of 21 mm length for root canal
therapy. Top: Lentulo. Middle: Hedstroem Νο. 25 file. Bottom:
Bended Νο. 30 file for mesial roots, in cases of inadequate mouth
opening
55 Be harmless to periapical tissues and the germ of the
permanent successor tooth
55 Be absorbed quickly if pushed through the apex
55 Be antiseptic
55 Be easy to handle
55 Bond to the canal walls
55 Show no contraction
55 Be easy to remove if such a need arises
55 Be radio-opaque
55 Not cause tooth discoloration
Gutta-percha points are excluded, unless there is aplasia
14 of permanent successor, and, consequently, preserving
the primary tooth in the arch is important, even if it is
heavily carious. The materials that most closely fulfill
most of the abovementioned criteria and used today are
ZOE and iodoform paste.
The use of ZOE is taught in 2/3 of undergraduate
programs in the USA [49] and recommended by most
pediatric dentistry and endodontology bodies. A moder-
ate foreign body reaction in cases of overfilling and dif-
ferent absorption rates than those of the root remain its
disadvantages [59]. However, its residues may remain in
the alveolar bone for a long time without any significant
clinical impact.
The difficulty in adequate pulp removal/debride-
ment of root canals in primary molars, particularly
when working without a rubber dam, the uncertainty
regarding the impact of handling files or medication
on developing permanent successor, and the frequent
cooperation problems encountered when working with
child patients under stress discourage many dentists
from preferring this technique. Nevertheless, reported
success rates of root canal treatment are quite high (78–
93%) [10]. The fact that, in the case of primary teeth,
less strict radiographic success criteria may be applied in
comparison with permanent teeth does not decrease the
value of such results. Iodoform paste has shown clinical
and radiographic success rates of 84% [60]. In a study
of 30 primary incisors and 51 primary molars with 78%
successful root canal treatment rates using ΖΟΕ, some
undesirable sequelae were observed in permanent suc-
cessor teeth, such as premolar deviation from eruption
path at a frequency of 21%, palatal eruption of maxil-
lary incisors in crossbite at 20%, as well as prolonged
retention of primary teeth at 36% [61].
14.3  ulp Treatment of Young Carious
P
Permanent Teeth
Procedures to manage the anterior teeth with pulpal
involvement following trauma in children and adoles-
cents are presented in 7 Chap. 16. Indeed, trauma is by
far the main reason for pulpal damage of these teeth in
youth. For the biological background of these proce-
dures and root canal treatment of teeth with mature
roots and closed apices, readers are referred to appro-
priate endodontology books and relevant publications.
In this chapter we report specifically diagnostic proce-
dures and treatment options and protocols for treating
young permanent teeth presenting pulp pathology com-
bined with deep carious cavities. Most of such teeth are
molars, the first ones in particular.
The root canal treatment of permanent immature
teeth (open apices) aims at allowing root development
and restoring function. If the prognosis is poor, preserv-
ing these teeth along with their supporting bone until
adulthood allow for a permanent solution (prosthetic/
implant). These decisions should be made in the best
interests of the young patient and may include orthodon-
tic consultation. For example, extraction rather than end-
odontic treatment of a badly broken down tooth at an
appropriate time followed by orthodontic space closure
may be preferred as a best solution in the long run [62].
Eye Catcher
The pulp tissue of young permanent teeth, particu-
larly those with an open apex, responds more posi-
tively to microbial inflammation and trauma, due to
the better hemodynamics of its vascular network, and
to the broader communication with the densely vas-
cularized periapical tissues [63]. On traumatic or iat-
rogenic exposure, pulpal tissue is healthy and can be
entirely preserved, if properly treated. When the pulp
is exposed in the presence of carious dentin, it always
presents some degree of infection and inflammation
that is already chronic (. Fig. 14.24) or in the process
of partial or total necrosis.
Pulp Therapy in Pediatric Dentistry
335 14
..      Fig. 14.24 a Hemorrhagic
pulp exposed while preparing a b
occlusal cavity in a young per-
manent molar with spontaneous
pain history indicates nonrevers-
ible pulpitis. b. Septic carious
dentin with pulp abscess (hema-
toxylin/eosin stain, By permis-
sion [64])

Concerning the diagnosis of probable pathology of a

young permanent teeth based on clinical signs and
symptoms as well as radiographic findings, readers are
referred to . Table 14.1 which presents a summary
regarding primary teeth, the only exception being that
permanent pulp response to sensitivity testing is more
reliable.

14.3.1 Indirect Pulp Capping

b
IPC in the case of young permanent teeth follows the
procedures described for the corresponding pulp treat-
ment of primary teeth. If preferred, capping should
embrace the clinical and radiographic criteria to con-
firm the absence of nonreversible pulp inflammation
(. Fig. 14.25). An alternative is represented by the
“stepwise excavation” procedure [25] which, when per-
manent teeth are involved, is often preferably com-
pleted in two sessions, with an interval between the two
that may extend to several months. These teeth usu- ..      Fig. 14.25 a Cotton wool pellet impregnated in ethyl chloride
ally present symptoms of evoked pain. In the first ses- spray for cold pulp testing. b Electrometric testing for pulp vitality is
sion, after all carious dentin has been removed except done without gloves for contactivity purposes
for that in direct proximity to the pulp, quick-setting
calcium hydroxide preparation is inserted and covered
with a GIC filling for the period mentioned. This treat- (reparative) dentin is deposited on the respective pulpal
ment aims at alleviating the symptoms and drastically wall. The advantage of this technique is that the practitio-
reducing the risk of pulp exposure upon reentering the ner is given the opportunity to evaluate the success of the
cavity [65, 66], because during the time interval tertiary treatment and modify the therapeutic scheme accordingly.
 336 A. Arhakis et al.

Another approach is to complete tooth restoration
in one session by stepwise excavation, just as is done for
primary teeth (. Fig. 14.26). This does not offer the
possibility to confirm the reversibility of pulp inflam-
mation securing a safer prognosis. In choosing the best
option, all the relevant factors for the individual patient
must be considered on a case-by-case basis, because
long-term prognosis in the relevant literature does not
favor either of the two options [67].
14.3.2 Direct Pulp Capping
Evidence on the suitability of carious permanent teeth
for DPC, as well as the relevant clinical procedure,
do not differ from that presented for primary teeth.
Traditionally, the material of choice has been calcium
hydroxide, while the more recent so-called Bioactive
Endodontic Cements have shown excellent results [68].
One such is a calcium silicate cement (Biodentine™,
Septodont, France), which appears to promote equally
dense reparative dentin as that produced by ΜΤΑ [69]
(. Fig. 14.27). In the past, adhesive dentin agents were
experimentally used in contact with the exposed pulp,
but they did not meet with success. This supports the
view that besides hermetically sealing the cavity from
bacteria, the capping material should promote repara-
tive dentin formation.
When a small carious exposure of healthy or, more
likely, reversibly inflamed pulp occurs, and after pos-
sible hemorrhage is controlled, the capping material of
choice is placed over the exposure without pressure. If
it is a quick-setting calcium hydroxide, it is then coated
with a GIC followed by a sound restoration to fully pre-
vent microleakage. If the choice is MTA, it should be
covered with a dump cotton pellet before the tooth is
temporarily filled. It takes a few hours for the MTA to
set, so cotton is removed and final restoration placed at

a b

14 ..      Fig. 14.26 a Deep occlusal carious lesion of mandibular first permanent molar. b Indirect pulp capping with quick-setting calcium
hydroxide, GIC lining and final composite restoration in one session appears to be successful at the 6-month review

..      Fig. 14.27 a Deep carious lesion of mandibular

a b
first permanent molar in a 17-year-old girl with a
history of provoked pain. b Non-­hemorrhagic pulp
exposure during partial caries excavation. c The cav-
ity is filled with Biodentine™ cement for 6 months,
before composite resin replaced the outer part of the
cement for a permanent restoration. d Biodentine™
capsule and water dose

c d
Pulp Therapy in Pediatric Dentistry
a b
..      Fig. 14.28 a Deep carious lesion of a mandibular first perma-
nent molar without a history of spontaneous pain. Despite the effort
toward indirect pulp capping, exposure occurred, and the pulp was
a later time. If the material is Biodentine™ cement, it
can be left as a temporary filling material for up to 6
months or be coated after its 12-minute setting time with
the permanent restoration (. Fig. 14.28) [70]. Direct
capping is considered successful if the pulp survives
and the radiograph confirms the deposition of repara-
tive dentin at the exposure site. Furthermore, in teeth
with an open apex, success is confirmed when the root
continues developing and apex formation is completed
(apexogenesis).
The effectiveness of DPC in young permanent teeth
with deep carious cavities has been better documented
than in primary teeth; consequently the technique is
included in the relevant guidelines [71]. If only teeth
with vital pulp with no more than reversible pulpitis
are selected, and a sound procedure is followed, studies
show that DPC of permanent teeth shows success rate
of 73% for over 3 years follow-up [72] or even 80% for
6 years follow-up [73]. In a specialist endodontic private
practice, success rates at 9 years follow-up of 98% for
young teeth with mature apex have been reported, which
rose to 100% in the 15 teeth with immature apices [38].
Eye Catcher
Various bioactive molecules are being investigated,
including growth factors and molecules of extracel-
lular enamel or dentin matrix. These are considered
capable of activating the endogenous stem or ances-
tor cells, enhancing the local regenerative potential.
Animal studies have shown that the use of bioactive
molecules in pulp capping produced a thicker layer of
homogenous reparative dentin, while research contin-
ues in the quest whether carious dentin is capable of
repair [74]. For example, collagen infiltrated with
hydroxyapatite and silicon nanoparticles provided
scaffolding for increased crystal formation toward
carious dentin remineralization, if environmental
conditions were favorable [75].
337 14
directly capped with Biodentine™ cement. b This radiograph was
taken 4 months later, before placing a permanent restoration. The
tooth was asymptomatic
14.3.3  artial Pulpotomy and Cervical
P
Pulpotomy
In partial pulpotomy only the superficially inflamed
pulp next to exposure site is removed, and the healthy
pulp is covered with any biological material listed above
for DPC. It is considered the treatment of choice for
permanent incisors with crown fractures that expose the
pulp; for a description of the procedure see 7 Chap. 16.
In a carious exposure of a permanent molar, this tech-
nique is considered to be more successful than DPC and
especially indicated for teeth with undeveloped apices
[76]. Partial pulpotomy is acceptable as a permanent
pulp treatment (. Fig. 14.29).
Wide acceptance of DPC and partial pulpotomy in
young permanent teeth affected by caries has restricted
the choice of cervical (deep) pulpotomy exclusively to
cases when hemorrhage can only be controlled at the
level of pulp stumps at the entries to root canals. Even
then, it is meaningful to choose this procedure only in
immature teeth so that apices may be completed, while
in mature teeth full pulpectomy and root canal treat-
ment should be preferred [77]. Once again, the capping
materials of choice for deep pulpotomy are MTA or
calcium hydroxide (. Fig. 14.30). A theoretical disad-
vantage of the technique, in case of failure, may be the
difficulty to access root canals for further treatment due
to possible formation of a hard tissue bridge under the
capping material.
14.3.4  oot Canal Treatment of Immature
R
Carious Teeth
The detailed procedures of endodontic procedures of
mature teeth can be found in textbooks of endodon-
tology. In this part of a pediatric dentistry book, the
emphasis is given to the treatment of irreversible pulpal
inflammation or pulp necrosis, with or without apical
 338 A. Arhakis et al.
a ces. Recent advances in regenerative endodontics have
b c
..      Fig. 14.29 a Deep carious cavity with pulp involvement in a
mandibular first permanent molar of a 14-year-old girl. b Partial
pulpotomy of inflamed part of the pulp, dressing with MTA and
temporary restoration. c At the 6-month review, the restored by
PMC tooth is asymptomatic
14
a c
d e
..      Fig. 14.30 a An emergency case of immature carious first per-
manent molar with extensive crown pulp inflammation. b Hemosta-
sis and placement of MTA at root pulp stamps following cervical
periodontitis, in immature carious teeth with open api-
offered more biological possibilities for immature teeth
[78]. The majority of young carious permanent teeth
that usually require root canal treatment are first molars
with pulpitis, most usually in patients with severe forms
of Molar Incisor Hypomineralization. These patients
often present as emergencies with history of recent spon-
taneous pain, often complaining of a sleepless night.
Following the taking of periapical radiograph and diag-
nosis, effective local anesthesia to allow cooperation of
the young patient, and rubber dam placement, access to
the pulp chamber and root canals is achieved.
14.3.4.1 Apexification
Under copious irrigation with 1.5% sodium hypochlo-
rite, delicate instrumentation is carried out using hand
files to remove the inflamed/necrotic content. Sodium
hypochlorite in teeth with immature apices may be alter-
nated with irrigation by sterile saline solution. A file
working length is set 1–2 mm before the radiographic
apex, since the open apex often has uneven shape. At
this point either traditional apexification or “MTA
plug” techniques may be selected [79].
For the traditional apexification technique, after dry-
ing with absorbent paper cones or intracanal aspirating
tips, the canals are carefully filled with calcium hydrox-
ide (powder or paste), using a lentulo spiral or a syringe
and endodontic pluggers, until the material meets the
apical tissues. Calcium hydroxide can help dissolve small
amounts of residual necrotic pulp tissues while exerting
pulpotomy. c Radiographic image with temporary filling. d Contin-
ued apexogenesis is seen at the 6-month review. A preformed metal
crown had been placed. e Clinical occlusal view
Pulp Therapy in Pediatric Dentistry
antisepsis [80]. The access cavity of the tooth is sealed
with a temporary restoration which should be at least
3 mm thick. The goal of the apexification treatment is to
promote healing of the periapical tissues and the forma-
tion of an apical hard tissue barrier which will act as a
stop for a future endodontic obturation. The apical bar-
rier is achieved within a period which ranges from 6 to
18 months (average 12 months), during which the canal
may need calcium hydroxide refilling two or three times
because of gradual resorption at its apical portion [81].
The need, however, to change calcium hydroxide during
the apexification is debated. After the clinical procedure
is completed, the patient will be followed at 1 week, 1
month (for symptoms), and then every six months with
a clinical and radiographic evaluation. The formation
of the apical barrier is confirmed radiographically. The
roots are permanently filled with gutta-percha (best if
thermoplasticized) and root canal sealer (. Fig. 14.31).
If the “MTA apexification” procedure is selected,
after the canal has been instrumented and disinfected,
a preformed barrier of MTA blocks the open apex for
a minimum length of three millimetres [25]. The MTA
barrier can be introduced in the canal with different
carriers and compacted using endodontic pluggers. If
the tooth is very immature (i.e., stage 1–2), then the
entire canal may be filled with MTA. Following posi-
tioning of the apical barrier, the access cavity is sealed
with a wet cotton pellet and a temporary cement. In the
next appointment the tooth is reaccessed, the MTA is
checked for its proper setting, the remaining root is filled
with gutta-percha and sealer, and the tooth is restored
with adhesive techniques. According to some authors,
the treatment can be also completed in one appoint-
ment, without waiting for the MTA to set. The patient is
checked for symptoms after one week and followed-up
clinically and radiographically to monitor the mineral-
ized barrier. The advantage of using a preformed apical
a b
..      Fig. 14.31 a Radiograph of a heavily carious and abscessed
mandibular first permanent molar with large diffused periapical
radiolucency at immature distal root. b Obturation of the canals
with gutta-percha following the temporary calcium hydroxide fill
339 14
plug consists in completing the endodontic treatment
of an immature tooth soon, by sealing the open apex
and still promoting the hard tissue barrier formation in
the next 6 to 18 months as in the traditional technique
(. Fig. 14.32). The MTA’s very hard consistency, how-
ever, does not forgive mistakes.
This procedure can be followed both in traumatized
teeth and in teeth with carious pulp necrosis. If the
tooth is necrotic, local anesthesia may not be necessary,
except for a minimal amount to numb the gingiva for
clamp placing. MTA apexification may be performed
using also alternative bioactive cements [79]. Successful
apical barrier formation, following the placement of an
MTA apical plug in 22 pulpless immature permanent
incisors, was as high as 95% [82]. For posterior carious
permanent teeth with open apices, there have been only
case reports [83, 84].
14.3.4.2 Revascularization
In the context of a “regenerative” endodontic approach,
revascularization of the pulp space of anterior trauma-
tized immature necrotic teeth has been attempted in an
effort to avoid later root fractures because of thin canal
walls [78]. The rationale of this technique is to activate
the stem cells of the apical papilla. According to the sug-
gested protocols, the tooth should be lightly rinsed in the
coronal to middle third of the root. A delicate instru-
mentation to this level may be also attempted. The disin-
fected space is then filled with a triple antimicrobial paste
(ciprofloxacin, metronidazole, and minocycline), and
the tooth is temporized (. Fig. 14.33). In the absence
of symptoms, three weeks later, the tooth is reopened,
using an anesthetic solution without vasoconstrictor,
the canal is rinsed, and bleeding is induced by pushing
an endodontic file passed the working length [85]. When
a coagulum is formed, the coronal portion of the root is
sealed with MTA or other bioactive endodontic cement,
c
and ongoing healing of the periapical tissues. c Three-year follow-up
radiograph of the tooth with preformed metal crown showing com-
plete healing, resorption of the extruded material, and intact lamina
dura [84] (By permission)
 340 A. Arhakis et al.
..      Fig. 14.32 Radiograph of a carious mandibular
left second premolar presenting apical lesion around its
immature root apex. b K file is in the root canal without
local anesthesia. c The restored tooth with MTA plug at
a distance from open apex. d After one year, apical clo-
sure and the excellent periapical healing are seen
a b
14
..      Fig. 14.33 a Periapical radiograph showing the mandibular per-
manent right first molar of a 7-year-old boy, affected by deep caries
and showing signs of apical periodontitis at the apex of the distal
root. The tooth did not respond to sensitivity test. Tooth revascu-
larization treatment was attempted using triple antibiotic paste. b
and the tooth is hermetically restored. By this procedure
the stem cells from the papilla should be able to migrate
and use the coagulum as a scaffold, and growth factors
are released from the dentinal walls. The migration of
stem cells should recreate the pulp tissue. So far, the
clinical cases studied have shown success in achieving
a b
c d
c
6-months recall: the tooth is asymptomatic and the bone lesion is
healing. c 18 months recall: the tooth is still asymptomatic, periapi-
cal tissues look healthy, the root canal walls appear thickened, and
the apical opening narrowed, but the root has not increased its length
thicker dentinal walls and consequently more fracture-­
resistant roots [86, 87]. Histopathology reports have
shown that the endodontically grown tissue was mostly
of periodontal origin being cementum bone-like and
fibrous connective tissue [78, 88]. The revascularization
mechanism, the type of tissue coming in contact with
Pulp Therapy in Pediatric Dentistry
a b
d e
..      Fig. 14.34 a Partial pulpotomy with white MTA in an 8-year-old
girl, of the immature maxillary right central incisor having suffered
a complicated crown fracture. b The 3-month radiographic follow-
­up shows the reattachment of the fragment with composite resin. c
Successful outcome after 5 years, with some canal obliteration. d, e
pulpal walls, and the long-term clinical consequences
are therefore still under investigation.
Finally, several experimental animal studies and
recent limited trials in humans indicate that stem cell
treatment may play a significant role in the future of
dentistry. The first applications will most probably con-
cern the pulp and periodontal tissues, after the possible
epigenetic stability of populations emerging from stem
cell cultures has been investigated. What have also to be
determined are the protocols to test regenerated dental
tissues before they are clinically used to ensure desirabil-
ity of shape, size, and color [89].
14.3.5  estoring the Color of Discolored
R and unobstructed lingual approach to the pulp cavity is
Teeth
Since gray MTA has been considered responsible for the
discoloration due to its ferric oxide content, white MTA
has been developed and marketed, particularly for use
with anterior teeth. Despite the use of white MTA, how-
ever, in 5 of the 22 anterior teeth receiving root canal
treatment in a clinical study of children of an average age
of 10 years, some crown discoloration was observed [82].
It has indeed been observed after the use of white MTA
341 14
c
f
The patient however complained of localized crown discoloration at
the fracture line, which becomes more evident as enamel and den-
tin are progressively removed. f The discoloration was related to the
MTA. Most of it was removed and cavity restored with opaque and
enamel-colored composite resin
even in conservative pulp treatments of permanent inci-
sors (. Fig. 14.34). Discoloration related to endodontic
treatment has always been an aesthetic problem, aris-
ing in pulpless teeth before or after treatment. Before
treatment, it is caused by the degeneration of necrotic
pulp tissues due to patient neglect for seeking treatment.
After endodontic treatment, it stems from inadequate
treatment procedures allowing leakage, for example,
an unsuitable access shape to pulp chamber allowing
for degenerating pulp remnants to remain unnoticed.
Restoring normal color by internal bleaching may be
achieved following the procedure described below.
After radiographic examination of the tooth and
placement of the rubber dam, the filling is removed
achieved. The pulp contents are removed up to a few
millimeters beyond the clinical cervix; using a round
bur at a low speed, discolored dentin is removed in so
far that tooth strength is not compromised. A thin layer
of cement, e.g., white GIC, is cervically placed so as to
prevent microleakage of the bleaching agent into the
root or the periodontium through the dentinal tubules.
The dentin is etched internally and then cleaned of fatty
ingredients with an acetone impregnated cotton wool
pellet.
 342 A. Arhakis et al.
a b
..      Fig. 14.35 a-d Gradual color restoration in four sessions of a discolored maxillary right central permanent incisor that had received root
canal treatment. (Courtesy of Dr. P. Beltes)
The cavity is filled up to the dentin borders with a
dense paste produced by mixing sodium perborate pow-
der with 3% hydrogen peroxide. The enamel walls are
cleaned and a temporary restoration, e.g., RMGIC,
offers a hermetic seal [90]. If necessary, the process is
repeated. In the last session, the cavity and tooth are
thoroughly rinsed with water, due to a risk of chemical
damage to the gingiva and of external cervical resorp-
tion of the root by the bleaching agents. Then cavity is
wiped with cotton wetted with chloroform and restored
with a white shade of composite (further enhancing the
bleaching effect) after etching and bonding. If every
stage is performed with care, the outcome is good and
stable, particularly in light yellow and gray discoloration
cases, as compared to those of dark yellow and black
(. Fig. 14.35) [91].
References
1. Laing E, Ashley P, Naini FB, Gill DS. Space maintenance. Int
14 J Paediatr Dent. 2009;19:155–62. https://doi.org/10.1111/j.1365-­
263X.2008.00951.x.
2. Duggal MS, Nooh A, High A. Response of the primary pulp to
inflammation: a review of the Leeds studies and challenges for
the future. Eur J Paediatr Dent. 2002;3:111–4.
3. Kassa D, Day P, High A, Duggal M. Histological compari-
son of pulpal inflammation in primary teeth with occlusal or
proximal caries. Int J Paediatr Dent. 2009;19:26–33. https://doi.
org/10.1111/j.1365-­263X.2008.00962.x.
4. Finucane D. Rationale for restoration of carious primary teeth:
a review. Eur Arch Paediatr Dent. 2012;13:281–92.
5. Tickle M, Milsom KM, Humphris GM, Blinkhorn AS. Parental
attitudes to the care of the carious primary dentition. Br Dent J.
2003;195:451–5. https://doi.org/10.1038/sj.bdj.4810600.
6. American Academy of Pediatric Dentistry. Antibiotic pro-
phylaxis for dental patients at risk for infection. Pediatr Dent.
2017;39:374–9.
7. Santamaria RM, Innes NP, Machiulskiene V, Evans DJ, Splieth
CH. Caries management strategies for primary molars: 1-yr
randomized control trial results. J Dent Res. 2014;93:1062–9.
https://doi.org/10.1177/0022034514550717.
8. Rodd HD, Waterhouse PJ, Fuks AB, Fayle SA, Moffat MA. Brit-
ish Society of Paediatric Dentistry. Pulp therapy for primary
molars. Int J Paediatr Dent. 2006;16(Suppl 1):15–23. https://doi.
org/10.1111/j.1365-­263X.2006.00774.x.
c d
9. Kotsanos N, Arizos S. Evaluation of a resin modified glass
ionomer serving both as indirect pulp therapy and as restor-
ative material for primary molars. Eur Arch Paediatr Dent.
2011;12:170–5.
10. Ballesio I, Campanella V, Gallusi G, Marzo G. Chemical and
pharmacological shaping of necrotic primary teeth. Eur J Paedi-
atr Dent. 2002;3:133–40.
11. Roeykens H, De Moor R. The use of laser Doppler flowmetry in
paediatric dentistry. Eur Arch Paediatr Dent. 2011;12:85–9.
12. Fuks AB. Vital pulp therapy with new materials for primary
teeth: new directions and treatment perspectives. Pediatr Dent.
2008;30:211–9.
13. Sonmez D, Sari S, Cetinbaş T. A comparison of four pulpotomy
techniques in primary molars: a long-term follow-up. J Endod.
2008;34:950–5. https://doi.org/10.1016/j.joen.2008.05.009.
14. Alaluusua S, Veerkamp J, Declerck D. Policy document for the
use of antibiotics in paediatric dentistry. 2002. https://www.­
eapd.­eu/uploads/20A87CB2_file.­pdf. Accessed at 22 Jan 2019.
15. Peretz B, Nisan S, Herteanu L, Blumer S. Root resorption pat-
terns of primary mandibular molars and location of the pre-
molar successors: a radiographic evaluation. Pediatr Dent.
2013;35:426–9.
16. Lugliè PF, Grabesu V, Spano G, Lumbau A. Accessory foramina
in the furcation area of primary molars. A SEM investigation.
Eur J Paediatr Dent. 2012;13:329–32.
17. Smaïl-Faugeron V, Glenny AM, Courson F, Durieux P, Muller-
Bolla M, FronChabouis H. Pulp treatment for extensive decay in
primary teeth. Cochrane Database Syst Rev. 2018;5:CD003220.
https://doi.org/10.1002/14651858.CD003220.pub3.
18. Dimitraki D, Papageorgiou SN, Kotsanos N. Direct pulp capping
versus pulpotomy with MTA for carious primary molars: a ran-
domised clinical trial. Eur Arch Paediatr Dent. 2019;20(5):431–
40. https://doi.org/10.1007/s40368-­019-­00419-­7.
19. Segura-Egea JJ, Gould K, Şen BH, Jonasson P, Cotti E, Maz-
zoni A, et al. European Society of Endodontology position
statement: the use of antibiotics in endodontics: a review. Int
Endod J. 2018;51:20–5. https://doi.org/10.1111/iej.12781.
20. Dhar V, Marghalani AA, Crystal YO, Kumar A, Ritwik P,
Tulunoglu O, et al. Use of vital pulp therapies in primary
teeth with deep caries lesions. Pediatr Dent. 2017;39(5):
146–59.
21. Coll JA, Seale NS, Vargas K, Marghalani AA, Al Shamali S,
Graham L. Primary tooth vital pulp therapy: a systematic review
and Meta-analysis. Pediatr Dent. 2017;39(1):16–123.
22. Massara ML, Alves JB, Brandao PR. Atraumatic restorative
treatment: clinical, ultrastructural and chemical analysis. Caries
Res. 2002;36:430–6. https://doi.org/10.1159/000066534.
23. Boutsiouki C, Frankenberger R, Krämer N. Relative effective-
ness of direct and indirect pulp capping in the primary denti-
tion. Eur Arch Paediatr Dent. 2018;19:297–309. https://doi.
org/10.1007/s40368-­018-­0360-­x.
Pulp Therapy in Pediatric Dentistry
24. Ni Chaollai A, Monteiro J, Duggal MS. The teaching of man-
agement of the pulp in primary molars in Europe: a preliminary
investigation in Ireland and the UK. Eur Arch Paediatr Dent.
2009;10:98–103.
25. American Academy of Pediatric Dentistry. Guideline on pulp
therapy for primary and immature permanent teeth. Pediatr
Dent. 2016;38:280–8.
26. Coll JA. Indirect pulp capping and primary teeth: is the primary
tooth pulpotomy out of date? Pediatr Dent. 2008;30:230–6.
27. Tuna D, Olmez A. Clinical long-term evaluation of MTA as
a direct pulp capping material in primary teeth. Int Endod J.
2008;41:273–8.
28. Trairatvorakul C, Koothiratrakarn A. Calcium hydroxide partial
pulpotomy is an alternative to formocresol pulpotomy based on
a 3-year randomized trial. Int J Paediatr Dent. 2012;22:382–9.
https://doi.org/10.1111/j.1365-­263X.2011.01211.x.
29. Leye Benoist F, Gaye Ndiaye F, Kane AW, Benoist HM, Farge
P. Evaluation of mineral trioxide aggregate (MTA) versus cal-
cium hydroxide cement (Dycal®) in the formation of a dentin
bridge: a randomised controlled trial. Int Dent J. 2012;62:33–9.
https://doi.org/10.1111/j.1875-­595X.2011.00084.x.
30. Schwendicke F, Brouwer F, Schwendicke A, Paris S. Differ-
ent materials for direct pulp capping: systematic review and
meta-analysis and trial sequential analysis. Clin Oral Investig.
2016;20:1121–32. https://doi.org/10.1007/s00784-­­016-­1802-­7.
31. Srinivasan V, Patchett CL, Waterhouse PJ. Is there life after Buckley’s
Formocresol? Part I - a narrative review of alternative interventions and
materials. Int J Paediatr Dent. 2006;16:117–27.
32. Steffen R, van Waes H. Understanding mineral trioxide aggre-
gate/Portland-cement: a review of literature and background
factors. Eur Arch Paediatr Dent. 2009;10:93–7.
33. Costa CA, Hebling J, Hanks CT. Current status of pulp cap-
ping with dentin adhesive systems: a review. Dent Mater.
2000;16:188–97.
34. Tziafas D, Alvanou A, Komnenou A, Gasic J, Komnenou
A. Effects of recombinant basic fibroblast growth factor, insu-
lin-like growth factor-II and transforming growth factor-beta
1 on dog dental pulp cells in vivo. Arch Oral Biol. 1998;43:
431–44.
35. Al-Hezaimi K, Javed F, Al-Fouzan K, Tay F. Efficacy of the
enamel matrix derivative in direct pulp capping procedures: a
systematic review. Aust Endod J. 2013;39:171–5. https://doi.
org/10.1111/j.1747-­4477.2012.00357.x.
36. Garrocho-Rangel A, Flores H, Silva-Herzog D, Hernandez-
Sierra F, Mandeville P, Pozos-Guillen AJ. Efficacy of EMD
versus calcium hydroxide in direct pulp capping of primary
molars: a randomized controlled clinical trial. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2009;107:733–8. https://
doi.org/10.1016/j.tripleo.2008.12.017.
37. Kotsanos N, Arapostathis KN, Arhakis A, Menexes G. Direct
pulp capping of carious primary molars. A specialty practice
based study. J Clin Pediatr Dent. 2014;38:307–12.
38. Bogen G, Kim JS, Bakland LK. Direct pulp capping with min-
eral trioxide aggregate: an observational study. J Am Dent
Assoc. 2008;139:305–15.
39. Lin PY, Chen HS, Wang YH, Tu YK. Primary molar pulpot-
omy: a systematic review and network meta-­analysis. J Dent.
2014;42:1060–77. https://doi.org/10.1016/j.jdent.2014.02.001.
40. Witherspoon DE, Small JC, Harris GZ. Mineral trioxide aggre-
gate pulpotomies: a case series outcomes assessment. J Am Dent
Assoc. 2006;137:610–8.
343 14
41. Barbosa AV, Sampaio GC, Gomes FA, de Oliveira DP, de
Albuquerque DS, Sobral AP. Short-term analysis of human
dental pulps after direct capping with Portland cement. Open
Dent J. 2009;3:31–5. https://doi.org/10.2174/18742106009030
10031.
42. Stringhini Junior E, Vitcel ME, Oliveira LB. Evidence of pulp-
otomy in primary teeth comparing MTA, calcium hydroxide,
ferric sulphate, and electrosurgery with formocresol. Eur Arch
Paediatr Dent. 2015;16:303–12. https://doi.org/10.1007/s40368-­
015-­0174-­z.
43. Moretti AB, Sakai VT, Oliveira TM, Fornetti AP, Santos CF,
Machado MA, et al. The effectiveness of mineral trioxide
aggregate, calcium hydroxide and formocresol for pulpotomies
in primary teeth. Int Endod J. 2008;41:547–55. https://doi.
org/10.1111/j.1365-­2591.2008.01377.x.
44. Ng FK, Messer LB. Mineral trioxide aggregate as a pulpotomy
medicament: an evidence-based assessment. Eur Arch Paediatr
Dent. 2008;9:58–73.
45. Milnes AR. Persuasive evidence that formocresol use in pediatric
dentistry is safe. J Can Dent Assoc. 2006;72:247–8.
46. Sakai VT, Moretti AB, Oliveira TM, Fornetti AP, Santos CF,
Machado MA, et al. Pulpotomy of human primary molars with
MTA and Portland cement: a randomised controlled trial. Br
Dent J. 2009;207:E5. https://doi.org/10.1038/sj.bdj.2009.665.
47. Holan G, Eidelman E, Fuks AB. Long-term evaluation of pulp-
otomy in primary molars using mineral trioxide aggregate or
formocresol. Pediatr Dent. 2005;27:129–36.
48. Fuks AB, Papagiannoulis L. Pulpotomy in primary teeth: review
of the literature according to standardized criteria. Eur Arch
Paediatr Dent. 2006;7:64–71.
49. Dunston B, Coll JA. A survey of primary tooth pulp therapy
as taught in US dental schools and practiced by diplomates
of the American Board of Pediatric Dentistry. Pediatr Dent.
2008;30:42–8.
50. Odabaj ME, Bodur H, Baris E, Demir C. Clinical, radiographic,
and histopathologic evaluation of Nd:YAG laser pulpotomy on
human primary teeth. J Endod. 2007;33:415–21.
51. Saltzman B, Sigal M, Clokie C, Rukavina J, Titley K, Kulkarni
GV. Assessment of a novel alternative to conventional formo-
cresol-zinc oxide eugenol pulpotomy for the treatment of
pulp- ally involved human primary teeth: diode laser-mineral
trioxide aggregate pulpotomy. Int J Paediatr Dent. 2005;15:
437–47.
52. Fumes AC, Sousa-Neto MD, Leoni GB, Versiani MA, da Silva
LA, da Silva RA, et al. Root canal morphology of primary
molars: a micro-computed tomography study. Eur Arch Paedi-
atr Dent. 2014;15:317–26. https://doi.org/10.1007/s40368-­014-­
0117-­0.
53. Ozcan G, Sekerci AE, Cantekin K, Aydinbelge M, Dogan
S. Evaluation of root canal morphology of human primary
molars by using CBCT and comprehensive review of the litera-
ture. Acta Odontol Scand. 2016;74:250–8. https://doi.org/10.310
9/00016357.2015.1104721.
54. Pozos-Guillen A, Garcia-Flores A, Esparza-­Villalpando V, Gar-
rocho-Rangel A. Intracanal irrigants for pulpectomy in primary
teeth: a systematic review and meta-­analysis. Int J Paediatr Dent.
2016;26:412–25. https://doi.org/10.1111/ipd.12228.
55. Pramila R, Muthu MS, Deepa G, Farzan JM, Rodrigues
SJ. Pulpectomies in primary mandibular molars: a compari-
son of outcomes using three root filling materials. Int Endod J.
2016;49:413–21. https://doi.org/10.1111/iej.12478.
 344 A. Arhakis et al.
56. Barcelos R, Santos MP, Primo LG, Luiz RR, Maia LC. ZOE
paste pulpectomies outcome in primary teeth: a systematic
review. J Clin Pediatr Dent. 2011;35:241–8.
57. Chandrasekhar S, Prasad MG, Radhakrishna AN, Saujanya K,
Raviteja NVK, Deepthi B, Ramakrishna J. A comparative In
vivo efficacy of three spiral techniques versus incremental tech-
nique in obturating primary teeth. J Indian Soc Pedod Prev Dent.
2018;36:71–5. https://doi.org/10.4103/JISPPD.JISPPD_365_16.
58. Walia T, Ghanbari AH, Mathew S, Ziadlou AH. An in vitro
comparison of three delivery techniques for obturation of root
canals in primary molars. Eur Arch Paediatr Dent. 2017;18:17–
23. https://doi.org/10.1007/s40368-­016-­­0258-­­4.
59. Chen X, Liu X, Zhong J. Clinical and radiographic evaluation
of pulpectomy in primary teeth: a 18-months clinical random-
ized controlled trial. Head Face Med. 2017;13:12. https://doi.
org/10.1186/s13005-­017-­0145-­1.
60. Holan G, Fuks AB. A comparison of pulpectomies using ZOE
and KRI paste in primary molars: a retrospective study. Pediatr
Dent. 1993;15(6):403–7.
61. Coll JA, Sadrian R. Predicting pulpectomy s­ uccess and its rela-
tionship to exfoliation and succedaneous dentition. Pediatr
Dent. 1996;18(1):57–63.
62. Conde MCM, Chisini LA, Sarkis-Onofre R, Schuch HS, Nör
JE, Demarco FF. A scoping review of root canal revasculariza-
tion: relevant aspects for clinical success and tissue formation.
Int Endod J. 2017;50:860–74. https://doi.org/10.1111/iej.12711.
63. Hargreaves KM, Giesler T, Henry M, Wang Y. Regenera-
tion potential of the young permanent tooth: what does the
future hold? J Endod. 2008;34:S51–6. https://doi.org/10.1016/j.
joen.2008.02.032.
64. Slootweg PJ. Dental pathology, Ch. 8. In: Disorders of the den-
tal pulp. 2nd ed. Springer-Verlag; 2013.
65. Ricketts DN, Kidd EA, Innes N, Clarkson J. Complete or
ultraconservative removal of decayed tissue in unfilled teeth.
Cochrane Database Syst Rev. 2006;3:CD003808. https://doi.
org/10.1002/14651858.CD003808.pub2.
66. Hayashi M, Fujitani M, Yamaki C, Momoi Y. Ways of enhanc-
ing pulp preservation by stepwise excavation-­ a systematic
14 review. J Dent. 2011;39:95–107. https://doi.org/10.1016/j.
jdent.2010.10.012.
67. Thompson V, Craig RG, Curro FA, Green WS, Ship JA. Treat-
ment of deep carious lesions by complete excavation or par-
tial removal: a critical review. J Am Dent Assoc. 2008;139:
705–12.
68. Parinyaprom N, Nirunsittirat A, Chuveera P, Na Lampang S,
Srisuwan T, Sastraruji T, et al. Outcomes of direct pulp capping
by using either ProRoot mineral trioxide aggregate or biodentine
in permanent teeth with carious pulp exposure in 6- to 18-year-old
patients: a randomized controlled trial. J Endod. 2018;44:341–8.
https://doi.org/10.1016/j.joen.2017.10.012. Epub 2017 Dec 21
69. Tran XV, Gorin C, Willig C, Baroukh B, Pellat B, Decup F,
et al. Effect of a calcium-silicate-based restorative cement
on pulp repair. J Dent Res. 2012;91:1166–71. https://doi.
org/10.1177/0022034512460833.
70. Rajasekharan S, Martens LC, Cauwels RGEC, Anthonappa RP,
Verbeeck RMH. Biodentine™ material characteristics and clini-
cal applications: a 3 year literature review and update. Eur Arch
Paediatr Dent. 2018;19:1–22. https://doi.org/10.1007/s40368-­
018-­0328-­x.
71. Santos PSD, Pedrotti D, Braga MM, Rocha RO, Lenzi
TL. Materials used for indirect pulp treatment in primary
teeth: a mixed treatment comparisons meta-analysis. Braz Oral
Res. 2017;31:e101. https://doi.org/10.1590/1807-­­3107/2017.
vol31.0101.
72. Aguilar P, Linsuwanont P. Vital pulp therapy in vital permanent
teeth with cariously exposed pulp: a systematic review. J Endod.
2011;37:581–7. https://doi.org/10.1016/j.joen.2010.12.004.
73. Dammaschke T, Leidinger J, Schafer E. Long-­term evaluation
of direct pulp capping--treatment outcomes over an average
period of 6.1 years. Clin Oral Investig. 2010;14:559–67. https://
doi.org/10.1007/s00784-­009-­0326-­9.
74. Chatzistavrou X, Papagerakis S, Ma PX, Papagerakis P. Innova-
tive approaches to regenerate enamel and dentin. Int J Dent.
2012;2012:856470. https://doi.org/10.1155/2012/856470.
75. Besinis A, van Noort R, Martin N. Remineralization potential
of fully demineralized dentin infiltrated with silica and hydroxy-
apatite nanoparticles. Dent Mater. 2014;30:249–62. https://doi.
org/10.1016/j.dental.2013.11.014.
76. Mejare I, Cvek M. Partial pulpotomy in young permanent
teeth with deep carious lesions. Endod Dent Traumatol. 1993;9:
238–42.
77. Bjørndal L, Reit C, Bruun G, Markvart M, Kjaeldgaard M,
Näsman P, et al. Treatment of deep caries lesions in adults:
randomized clinical trials comparing stepwise vs. direct com-
plete excavation, and direct pulp capping vs. partial pulpotomy.
Eur J Oral Sci. 2010;118:290–7. https://doi.org/10.1111/j.1600-­-
0722.2010.00731.x.
78. Simon SR, Tomson PL, Berdal A. Regenerative endodontics:
regeneration or repair? J Endod. 2014;40:S70–5. https://doi.
org/10.1016/j.joen.2014.01.024.
79. Harlamb SC. Management of incompletely developed teeth
requiring root canal treatment. Aust Dent J. 2016;61(Suppl
1):95–106. https://doi.org/10.1111/adj.12401.
80. Hasselgren G, Olsson B, Cvek M. Effects of calcium hydroxide
and sodium hypochlorite on the dissolution of necrotic porcine
muscle tissue. J Endod. 1988;14:125–7. https://doi.org/10.1016/
S0099-­2399(88)80212-­7.
81. Deepti A, Shifa S, Muthu MS, RathnaPrabhu V. Apical closure
of immature molar roots: a rare case report. Int J Clin Pediatr
Dent. 2008;1:54–7.
82. Moore A, Howley MF, O'Connell AC. Treatment of open apex
teeth using two types of white mineral trioxide aggregate after ini-
tial dressing with calcium hydroxide in children. Dent Traumatol.
2011;27:166–73. https://doi.org/10.1111/j.1600-­9657.2011.00984.x.
83. Woelber JP, Bruder M, Tennert C, Wrbas KT. Assessment of
endodontic treatment of c-shaped root canals. Swiss Dent J.
2014;124:11–5.
84. Musale PK, Kothare S. Non-surgical endodontic manage-
ment of immature permanent mandibular first molar: a 3 year
follow-up. Eur Arch Paediatr Dent. 2018;19:373–7. https://doi.
org/10.1007/s40368-­018-­0350-­z.
85. Cotti E, Mereu M, Lusso D. Regenerative treatment of an
immature, traumatized tooth with apical periodontitis: report
of a case. J Endod. 2008;34:611–6. https://doi.org/10.1016/j.
joen.2008.02.029.
86. Cehreli ZC, Isbitiren B, Sara S, Erbas G. Regenerative
endodontic treatment (revascularization) of immature
necrotic molars medicated with calcium hydroxide: a case
Pulp Therapy in Pediatric Dentistry
series. J Endod. 2011;37:1327–30. https://doi.org/10.1016/j.
joen.2011.05.033.
87. Tzanetakis GN, Giannakoulas DG, Papanakou S, Gizani S,
Lygidakis N. Regenerative endodontic therapy of immature per-
manent molars with pulp necrosis: a cases series and a literature
review. Eur Arch Paediatr Dent. 2021;22(3):515–25. https://doi.
org/10.1007/s40368-020-00550-w.
88. Shimizu E, Ricucci D, Albert J, Alobaid AS, Gibbs JL, Huang
GT, Lin LM. Clinical, radiographic, and histological observa-
tion of a human immature permanent tooth with chronic apical
abscess after revitalization treatment. J Endod. 2013;39:1078–
83. https://doi.org/10.1016/j.joen.2013.04.032.
345 14
89. Mitsiadis TA, Papagerakis P. Regenerated teeth: the future
of tooth replacement? Regen Med. 2011;6:135–9. https://doi.
org/10.2217/rme.14.78.
90. Marin PD, Heithersay GS, Bridges TE. A quantitative compari-
son of traditional and non-peroxide bleaching agents. Endod
Dent Traumatol. 1998;14:64–8.
91. Abbott P, Heah SY. Internal bleaching of teeth: an analysis of
255 teeth. Aust Dent J. 2009;54:326–33. https://doi.org/10.1111/
j.1834-­7819.2009.01158.x.
 347 15

Periodontal Diseases
in Children and Adolescents
Aikaterini-Elisavet Doufexi and Frank Nichols

Contents

15.1 Diseases Restricted to Gingiva – 348

15.1.1  ingivitis – 348
G
15.1.2 Localized Juvenile Spongiotic Hyperplasia – 350
15.1.3 Gingival Hyperplasia – 351

15.2 Periodontitis – 352

15.2.1  hronic Periodontitis in Children and Adolescents – 353
C
15.2.2 Periodontitis Associated with Systemic Disease – 356
15.2.3 Diabetes Mellitus and Periodontal Disease – 357
15.2.4 Acute Ulcerative Gingivitis/Periodontitis – 357

15.3 Mucogingival Deformities – 358

15.3.1  ingival Recession – 358
G
15.3.2 Frenum Pull – 358

References – 360

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_15
 348 A.-E. Doufexi and F. Nichols
Children and adolescents commonly present with peri-
odontal diseases. The dental clinician should be aware
of and be able to diagnose and timely treat such diseases
for the following reasons: [1]
1. The prevalence of periodontal disease in children
and adolescents is high.
2. Superficial or localized periodontal lesions in chil-
dren may lead to more severe and generalized peri-
odontal diseases in adulthood.
3. There is strong evidence for an association between
general-systemic diseases and periodontal diseases.
4. Families at high risk for periodontal disease (e.g.,
due to predisposing genetic factors) can be identified
early and placed into individualized prevention pro-
grams and more vigilant treatment.
5. The prevention and treatment of most forms of peri-
odontal disease is straightforward and effective.
Eye Catcher
The most common periodontal disease in children
and adolescents is gingivitis. Common in youth are
also mucogingival problems, gingival hyperplasias,
and necrotizing ulcerative gingivitis/periodontitis.
Periodontal attachment loss occurs infrequently in
children, but when it does, it is usually aggressive.
Severe periodontal attachment loss in children and
adolescents should raise concern for an underlying
systemic disease of genetic predisposition.
15.1 Diseases Restricted to Gingiva
15.1.1 Gingivitis
15
15.1.1.1 Definition, Epidemiology,
and Clinical Findings
Chronic gingivitis is a reversible disease of periodontal
tissues with signs and symptoms of gingival inflamma-
tion without attachment loss. Under the general title
“gingivitis,” we could describe three different forms:
(a) Acute or chronic gingivitis of exclusively microbial
etiology.
(b) Gingivitis in which the inflammatory reaction is modi-
fied by hormones, specifically gonadotrophins (elevated
estrogen and/or progesterone levels in puberty, during
pregnancy, and when taking oral contraceptives).
(c) Gingivitis secondary to drug-induced gingival
hyperplasia.
The primary etiologic factor associated with these forms
of gingivitis is dental plaque on tooth surfaces of chil-
dren. Other factors may be important predisposing
factors that complicate the development of the inflam-
matory process, i.e., by differentiating host response.
Gingivitis presents with the same clinical findings in chil-
dren and adults: gingival redness, edema of free gingi-
vae, bleeding on probing, and often loss of stippling [2].
The gingival margin becomes rounded due to edema and
bleeds upon any mechanical challenge (. Fig. 15.1). If
gingivitis is left untreated, the gingival tissue can become
more fibrous and the interdental papillae may appear
hyperplastic, thereby increasing the depth of the gingi-
val crevice [2]. This leads to pocket development without
loss of attachment (“pseudo-pocket”).
Epidemiological data indicate that in children aged
4–9 years, gingivitis occurs at rates of 40–60%. Its
prevalence increases with age [3]. Approximately 82%
of teenagers suffer from gingivitis in the USA, while
in various other countries teenagers show a similar or
higher prevalence [4, 5]. Experimental gingivitis studies
after discontinuation of oral hygiene showed that longer
time was required for its appearance in children than in
adults [6–9]. The bleeding index (GI, gingival index) in
various age groups (children, adolescents, adults), with
similar plaque index scores, was also found to increase
with age [7]. The different inflammatory responses in
various age groups could be partially attributed to dif-
ferent levels of hormones, particularly in females.
The inflammatory response of the gingiva to plaque
accumulation is typically more severe around erupting
permanent teeth and is frequently termed “eruption
gingivitis.” [10] The main reason is simply related to
the substantially greater bacterial load due to ineffec-
tive oral hygiene in the tooth eruption sites. Access to
and cleaning of the tooth eruption area with the brush
requires more time and effort. Another reason might
be that degenerative changes in the attached epithelium
undergoing remodeling at the eruption site may lead to
a diminished immune response with an altered ability to
mount a suitable inflammatory response [10].
15.1.1.2 Microbiological and Histological
Findings
Although the signs and symptoms of gingivitis in chil-
dren are less pronounced than in adults, the microbiota
is generally similar and is characterized by elevated
levels of subgingival Prevotella sp., Actinomyces sp.,
­
Capnocytophaga sp., Leptotrichia sp., and Selenomonas
sp. [11–13]. Histologically, gingivitis in children is char-
acterized by ulceration of the epithelium of the gingival
sulcus and infiltration of the underlying connective tissue
by inflammatory cells [2]. Dominant cells in the region
of gingival inflammation are T lymphocytes in contrast
to adult gingivitis where B lymphocytes predominate.
The total number of leukocytes in the sulcus is generally
reduced in children compared to adult gingivitis [2, 14,
15]. Moreover, elevated estrogen and progesterone levels
in adolescents may contribute to increased vascularity
and a more pronounced inflammatory response of gin-
gival tissue to bacterial plaque [2, 11, 16].
Periodontal Diseases in Children and Adolescents
349 15
a b

c d

..      Fig. 15.1 a. A seven-year-old boy with chronic generalized gingi- bleeding upon plaque removal are educational to the child. d. Clini-
vitis manifested by edema of free gingivae. b. Heavy plaque deposits cal appearance 6 weeks after the treatment of gingivitis (oral hygiene
due to the absence of oral hygiene are evident to the naked eye. c. instructions, removal of deposits). Tooth crowns appear longer, due
Plaque disclosure with fuchsine dye and demonstrating spontaneous in part to the resolution of edema

15.1.1.3 Etiology and Treatment

The causal relationship of dental plaque with gingivi-
tis has been demonstrated with experimental gingivitis
studies in both adults and children [6, 7, 12]. However,
several predisposing factors, local and systemic, regulate
the onset of disease [8]. Such local factors for gingivitis
in children and adolescents are those favoring plaque
accumulation and retention, including:
1. Carious cavities.
2. Overhanging restorations.
3. Hypoplastic cervical tooth areas.
4. Orthodontic anomalies, particularly with severe
tooth crowding (. Fig. 15.2).
5. Fixed orthodontic appliances (. Fig. 15.3). ..      Fig. 15.2 A girl 14 years of age scheduled for orthodontic treat-
ment. Ineffective oral hygiene and tooth crowding contributed to
On the other hand, factors that affect host defense localized gingivitis (edema of free gingivae). Arrows indicate the
localized gingival recession, consistent with ectopic (labial) tooth
responses may include: positioning

55 Mouth breathing which leads to dry mouth, causing

Gingivitis in children and adolescents is fully reversible
local vasoconstriction and thus reducing microbial
with effective daily plaque removal and possibly addi-
defense responses. Clinical signs of mouth breathing
tional oral hygiene measures. It is imperative for the
are the glossy dry surface of the gingiva and mucosa,
clinician to demonstrate oral hygiene practice to ado-
enlarged interdental papillae and free gingival margin,
lescents – and/or to parents of younger children – and
and bleeding on probing [8]. These findings are usually
evaluate their performance frequently. If calculus is pres-
most pronounced in the maxillary anterior region.
ent, scaling with hand or ultrasonic instruments is neces-
55 Increased levels of estrogen and progesterone in ado-
sary. Reevaluation every 6 months is necessary, especially
lescence may contribute to increased vascularity of
in children with orthodontic abnormalities or children
gingival tissue, and this may be associated with
wearing fixed orthodontic appliances, and if oral hygiene
increased bleeding index scores and inflammation [2,
is poor, this ought to be more frequent [8]. Care of local
8] (. Figs. 15.3, 15.4).
and systemic predisposing factors is also very important
55 Various systemic diseases that will be discussed as a
[2, 8]. For example, mouth breathing should be identified
separate entity.
 350 A.-E. Doufexi and F. Nichols

a a

b
b

..      Fig. 15.3 a. Clinical appearance of hyperplastic form of gin-

givitis, modified by hormonal changes of puberty in a 14-year-old
female under orthodontic treatment. Edematous gingivae are indica-
tive of inflammation. b. After removal of orthodontic brackets, good
oral hygiene, and periodontal treatment, periodontal health is fully
restored. The result could (and should) have been achieved with
equal success during the orthodontic treatment

and cared for by the dental clinician and orthodontist

and possibly by the otorinolaryngologist [8].
15
Eye Catcher
An important goal for adolescents is to increase
their motivation and make them a partner in their
oral hygiene effectiveness self-assessment of the
techniques, as parental supervision ceases or is not
welcome. Success in addressing this challenge will
support their self-esteem and awareness to care for
their own health and aesthetics and will help them
minimize bad breath and gingival bleeding.
15.1.2  ocalized Juvenile Spongiotic
L and papillated lesion affecting one tooth, but cases with
Hyperplasia
Localized juvenile spongiotic gingival hyperplasia (LJSGH)
is a poorly understood distinctive inflammatory hyperpla-
sia occurring in children and juveniles but may infrequently
occur in adults. It was reported, for example, that, out of
27 cases with a median age of 13 years, three were patients
..      Fig. 15.4 a. Clinical image of severe gingivitis in a 15-year-old
male presenting with heavy calculus and bacterial accumulation
and orange stain. b. Initial treatment with ultrasonic scaling was
followed by oral hygiene instructions. c. At follow-up, a degree of
gingival inflammation persists. The fear of bleeding at brushing com-
bined with pubertal hormonal effects in some adolescents calls for
additional topical chemotherapeutic support, e.g., periodic use of
chlorhexidine
over 60 years of age [17]. The most commonly affected site
is the anterior maxillary gingiva, without any explanation
offered for this so far. LJSGH presents as a solitary, red,
multiple affected teeth have been reported [18]. There is
an abrupt transition from LJSGH to normal mucosa.
Typical microscopic findings include elevated areas of
variably acanthotic, spongiotic nonkeratinized epithelium
(. Fig. 15.5). There are no sex hormone (estrogen or pro-
gesterone) receptors as investigated immunohistochemi-
cally. No etiologic relationship has been established.
Periodontal Diseases in Children and Adolescents
351 15

a b

..      Fig. 15.5 a. Clinical image of localized juvenile spongiotic gin- Histological picture of LJSGH. The epithelium demonstrates hyper-
gival hyperplasia (LJSGH) in a 10-year-old boy extending full width plasia, spongiosis, and exocytosis. A dense mixed inflammatory cell
in the attached gingiva of the right central and only in the free infiltrate is seen in the underlying connective tissue. (Courtesy of Dr.
gingiva of the left central incisor (courtesy of Dr. R. Steffens). b. N. Nikitakis)

LJSGH does not respond to conventional oral a

hygiene measures unlike and plaque-related and/or
puberty-related gingivitis. Anecdotal evidence of spon-
taneous remission has been mentioned. Excision or
cryotherapy has been met with some success and may be
tried in a symptomatic or cosmetically unsightly lesion.
However, as there is no long-term follow-up documenta-
tion, in the cases of asymptomatic lesions, observation
would be justified [18].
Plasma cell gingivitis (PCG), being again a rare, also
benign inflammatory condition of unclear etiology pos-
sibly involving allergic reaction to food additives such as
cinnamon, seems to not be so frequent in children. When
encountered, standard, professional oral hygiene proce- b
dures and nonsurgical periodontal therapy, including
antimicrobials, have been reported to produce marked
improvement [19].

15.1.3 Gingival Hyperplasia

15.1.3.1 Drug-Related Gingival Hyperplasia
The main cause of gingival hyperplasia is systemic medi-
cations. Severely hyperplastic gingivae produce aesthetic
problems but may also impair mastication, tooth erup-
tion and position, and speech, as well as act as predis- ..      Fig. 15.6 a. Clinical features of hyperplastic gingivitis in a
posing factors for periodontal destruction. Four drugs, 10-year-old child under phenytoin. Gingival enlargement is evident
phenytoin, nifedipine (and other calcium channel block- with coexisting acute and chronic inflammation. b. Plaque deposits
are the absolute prerequisite for the inflammatory process and sec-
ers), cyclosporine, and amphetamine, have been identi-
ondary hyperplasia to occur
fied as the most common cause of gingival hyperplasia
in children and adolescents [8, 20]. In more than 50%
of drug-related cases, hyperplasia is caused by the administration to children and has increased incidence
chronic administration of phenytoin (. Fig. 15.6), a and intensity compared to adults. Gingival hyperplasia
drug used to treat epilepsy. Gingival hyperplasia occurs is mainly localized in the anterior region [20]. The com-
2–3 weeks after the initiation of systemic medication bined administration of nifedipine and cyclosporine in
 352 A.-E. Doufexi and F. Nichols
children under organ transplantation and therapy of
autoimmune diseases increases the frequency and sever-
ity of gingival hyperplasias [20].
Another group of drugs associated with gingival
hyperplasia are amphetamines administered to children
with attention deficit hyperactivity disorder (ADHD).
These children may represent up to 5–10% of the school
population in the USA and nowadays constitute the
largest percentage of children referred for treatment of
gingival hyperplasia [8]. Interestingly, most studies show
a positive correlation between the frequency and sever-
ity of hyperplasia and plaque index and bleeding index,
despite there being no clear causal relationship between
poor oral hygiene and gingival hyperplasia [20].
The most effective treatment of drug-induced gingi-
val hyperplasia is to replace the drug causing the hyper-
plasia [21]. This, however, is solely in the responsibility
of the attending physician, and in most cases medica-
tion substitution is not possible. Therefore, treatment of
drug-induced gingival hyperplasia is mainly preventive
and includes:
55 Emphasis on oral hygiene instruction.
55 Frequent (every 3 months) professional removal of
hard and soft bacterial deposits.
55 Use of antimicrobial solutions.
Initial treatment includes oral hygiene instructions,
maintenance therapy with root planing, and, in some
cases, surgical removal of hyperplastic gingivae (gingi-
vectomy) [22]. It should be noted that, in 40% of these
patients, recurrence of hyperplasia after gingivectomy
appears 18 months after surgical treatment, which is
frequently associated with gingival inflammation due to
15 poor compliance [21, 22]. Surgical interventions should
necessarily be followed by frequent and meticulous
maintenance therapy.
15.1.3.2  ongenital Fibrous Gingival
C 15.2
Hyperplasia
Other causes of gingival hyperplasia in children and
adolescents are congenital fibrous hyperplasia, neu-
rofibromatosis type I, and leukemia [20]. Hereditary
gingival fibromatosis (HGF) is an inherited autosomal
dominant syndromic disease (. Fig. 15.7). The syn-
drome may be associated with epilepsy, mental retar-
dation, and hypertrichosis, but in most cases gingival
hyperplasia is the only clinical manifestation. It presents
with equal frequency in boys and girls, and usually its
onset coincides with eruption of the permanent denti-
tion [20]. Histologically, it differs from the drug-related
gingival hyperplasia mainly in that the gingival connec-
tive tissue shows a high percentage of collagen fibers
..      Fig. 15.7 Hereditary gingival fibromatosis in a 30-month-old
boy with primary molars covered with fibrous gingivae. (Courtesy
of Dr. R. Steffens)
and absence of inflammatory cells. Although the fibrous
gingival hyperplasia does not directly cause alveolar
bone loss, it creates gingival anatomical conditions that
predispose for plaque accumulation with bone loss as a
possible consequence. The most common complications
are tooth migration, resulting in tooth spacing and over-­
retention of primary teeth. Indicated treatment is gingi-
vectomy for the improvement of aesthetics, speech, and
masticatory function [20] (. Fig. 15.8).
Neurofibromatosis type I, also termed von
Recklinghausen’s disease, is an inherited disease with
varying expression, depending on the type of mutation
that causes it (see 7 Chap. 21). Intraorally, gingival
hyperplasia may present with tooth impaction, orth-
odontic anomalies, high plaque and caries indices, and
periodontal attachment loss.
Periodontitis
The previous classification of periodontal diseases in
1999 [23] describes three forms of periodontitis, i.e.,
chronic periodontitis, aggressive periodontitis, and
periodontitis as a manifestation of systemic disease.
The first category, chronic periodontitis, occurs exclu-
sively in adults by this classification. The most cur-
rent classification in 2018 [24] excludes the category
of aggressive periodontitis and classifies periodontal
disease to stages and grades. Stages are supposed to
describe the disease state, whereas grades are supposed
to describe the rate of disease progression and the sys-
temic and environmental factors that can affect disease
progression.
Periodontal Diseases in Children and Adolescents
a e
c
h i
..      Fig. 15.8 a–d. Clinical appearance of congenital fibrous gin-
gival hyperplasia in a 10-year-old girl. The patient presents with
“pseudo-­pockets” and swollen gingivae composed of fibrous tissue,
especially in the upper and lower anterior regions. Exceptions are the
Eye Catcher
Children and adolescents can experience one of the
following forms of periodontitis based on the most
recent classification of periodontal diseases in 2018:
1. Chronic periodontitis.
2. Periodontal disease as a manifestation of systemic
disease.
Aggressive periodontitis can occur in children and ado-
lescents and can be generalized or localized. Chronic
periodontitis in young individuals is caused by specific
bacteria and dysfunction of the immune system.
15.2.1 Chronic Periodontitis in Children
and Adolescents
Chronic periodontitis occurs not only in adults but
also in children and adolescents. Briefly, the clinical
signs include rapid attachment loss and severe gingival
inflammation and may show a familial aggregation [11,
23] (. Fig. 15.9). Secondary features include defects
in phagocytosis and excessive activity of macrophages/
353 15
f g
j
interdental papillae between the maxillary central and lateral inci-
sors, which have clinical signs of chronic inflammation, i.e., smooth,
red, and spongy texture. e–j. The radiographic images show normal
bone levels in the hyperplastic anterior region
monocytes. Polymorphonuclear leukocytes may have
reduced capacity for chemotaxis and phagocytosis,
reduced bactericidal capacity, and reduced capacity to
produce leukotrienes [11, 25–27]. Chronic periodonti-
tis in children and adolescents progresses more rapidly
than the chronic periodontitis in adults and can be local-
ized or generalized in distribution [11, 28].
Localized aggressive periodontitis – as defined by
the previous classification in 1999 – is characterized
by attachment loss around at least two permanent first
molars or incisors and up to two other teeth in the
absence of systemic disease [11, 29] (. Fig. 15.10).
Retrospective studies in patients with localized aggres-
sive periodontitis show that attachment loss in the
primary teeth can precede that in the teeth of the
permanent ­ dentition [30]. In contrast, generalized
aggressive periodontitis is determined by recording
attachment loss in three or more teeth other than
molars or incisors [11]. Some clinicians and periodon-
tal researchers believe that localized aggressive peri-
odontitis is not a precursor disease to other forms of
periodontitis, while others maintain that it can evolve
into generalized aggressive periodontitis [11, 31, 32]
(. Figs. 15.11 and 15.12). The incidence of aggressive
 354 A.-E. Doufexi and F. Nichols
a1 a2
b1 b2
c1 c2
..      Fig. 15.9 Three African-American sisters present with character-
istics of aggressive periodontitis, such as severe periodontal lesions,
loss of teeth due to periodontal disease at a young age, periodon-
tal destruction in incisors and molars, and genetic predisposition.
a1–3. The oldest girl of the family (19 years old) has already lost a
central incisor and a first lower molar due to periodontal disease.
The lower molar has been replaced with a fixed partial denture. Dur-
ing periodontal surgery advanced intraosseous periodontal lesions
were detected in the mandibular molar region of the contralateral
side. b1–3. The middle sister (17 years old) has already shown buc-
cal displacement of the upper central incisors. Radiographs showed
15
a b
..      Fig. 15.10 a. Significant attachment loss on the buccal surface
of the mandibular right first permanent molar of a 7-year-old girl
detected with the periodontal probe, while there are minimal clinical
signs of inflammation (edema and bleeding on probing). b. Radio-
graphic examination of the area reveals some bone loss of the newly
erupted first molar, compatible with a probably self resolving buccal
bifurcation cyst. This does not comprise localized aggressive peri-
odontitis. (Courtesy of Dr. N. Kotsanos)
a3
b3
c3
c4
significant periodontal destruction around the maxillary central
incisors, which can account for their significant buccal displacement.
Radiographic evidence indicates also the advanced periodontal
lesions around the first maxillary molars. c1–4. The youngest girl
of the family shows significant loss of the attachment between the
upper central incisors with the characteristic loss of papilla. By con-
trast, there is no loss of periodontal attachment in the lower incisors.
According to the dental history, both parents lost their teeth due to
periodontal disease. Overall, the pediatric dentist should collaborate
with a periodontist in the diagnosis, prevention, and treatment of
aggressive periodontitis in children
periodontitis – generalized or localized – ranges
between 0.1 and 3.8% depending on the report and has
a higher frequency in African-Americans (2.5%) than
in Caucasians.
15.2.1.1 Clinical, Microbiological,
and Immunological Findings
Based on many clinical reports and impressions, the
prevailing clinical view holds that localized chronic peri-
odontitis in children and adolescents is characterized by
a relatively low accumulation of supragingival plaque
and calculus, but others report similar accumulation of
supragingival plaque as with other forms of periodontitis
[11, 29, 33–35]. Bacteria that have been associated caus-
ally with the disease are usually anaerobic gram-­negative
rods [36, 37]. Many periopathogenic bacteria isolated
from diseased sites are common with those of adult
patients with chronic periodontitis, but show greater
prevalence in patients of younger age. Some of these
Periodontal Diseases in Children and Adolescents
a b
d e
..      Fig. 15.11 a. 9-year-old boy with localized aggressive periodon-
titis. A. Acute hyperplastic inflammatory lesion is seen in the gin-
giva of the maxillary and mandibular molars. b, c. The radiographic
examination reveals significant alveolar bone loss in the central max-
illary and the lateral mandibular incisors. d. Eighteen months later,
are Porphyromonas gingivalis (P.g.), Peptostreptococcus
micros, Campylobacter rectus, and Tannerella forsythia.
The Aggregatibacter (formerly Actinobacillus) acti-
nomycetemcomitans (A.a.) is also a periopathogenic
bacterium and is frequently recovered as a substantial
percentage of the flora at localized periodontitis sites.
Among the five different serotypes of A.a. isolated, sero-
type b has been associated with aggressive and chronic
periodontitis and serotype c with periodontal health.
However, a single subgingival organism has not been
implicated as the causative organism for localized peri-
odontitis [4, 11, 12, 38–40]
Both localized and generalized periodontitis in chil-
dren and adolescents are characterized by dysfunction of
the immune system. Patients show polymorphonuclear
leukocyte dysfunction and impaired immunoglobin pro-
duction (immunoglobins come from B lymphocytes).
For both localized and generalized periodontitis, poly-
morphonuclear leukocytes typically show impaired
chemotaxis (although this is not universal) and reduced
GP-110 expression, which is a glycoprotein found on the
neutrophil cell surface and acts as a receptor of chemo-
tactic factors. The IgG immunoglobulins are classified
into four isotype classes (IgG1–4). After infection with
355 15
c
radiographic examination reveals significant bone loss on the molars
as well. e. Five years after baseline examination, the periodontitis
has progressed significantly with the maxillary right second premo-
lar having a hopeless prognosis. (Courtesy of Drs. N. Kotsanos and
A. Gofa)
A.a., the IgG2 antibody produced against A.a. is spe-
cific for the high molecular weight lipopolysaccharide
(HMWLPS) generated by A.a. [11]. Production of IgG2
antibodies against A.a. appears to be protective against
aggressive periodontitis [11, 41, 42] since patients with
higher concentrations of IgG2 show less attachment
loss compared to patients with lower titers of IgG2.
The immune response in young patients with chronic
periodontitis is determined by other factors as well. For
example, the levels of IgG2 in serum are influenced by
genetic and environmental factors. Specifically, high
levels of serum IgG2 have been detected in Blacks with
aggressive periodontitis, while low levels of IgG2 are
typically observed in subjects with a smoking history
[11]
15.2.1.2 Treatment
As mentioned before, aggressive periodontitis is prob-
ably caused by either a specialized subgingival flora or a
dysfunctional immune reaction to the subgingival flora.
Thus, the treatment of aggressive periodontitis aims to
reduce the microbial load and to strengthen host defense
mechanisms [11].
 356 A.-E. Doufexi and F. Nichols
..      Fig. 15.12 a. Routine radiographic examination for
a b
detection of caries revealed localized aggressive peri-
odontitis in the primary molars in an 8-year-old girl with
no systemic disease. The patient was scheduled for oral
hygiene instructions and root scaling and planing. b.
Three years later no attachment loss was detected for the
permanent teeth, as the patient was prompt in following
her recall appointments after phase I periodontal therapy
c d
Eye Catcher
The antimicrobial therapeutic approach for chronic
periodontitis in children and adolescents is similar to
the classical periodontal disease management proto-
col, i.e., the combination of the following:
(a) Conventional debridement treatment with root
scaling and planing.
(b) Surgical treatment.
(c) Local or general administration of antibiotics
(antimicrobials) [11].
The treatment of chronic periodontitis requires eradi-
cation of the biofilm by root scaling and planing and
typically includes surgical intervention and the admin-
istration of antibiotics (. Fig. 15.13). Indeed studies
15 indicate that levels of A.a. were significantly reduced
only after periodontal surgery, while the conservative
treatment with the administration of antibiotics does
not significantly reduce the levels of A.a. [3, 11, 42, 43].
Since in most cases of periodontitis other periopatho-
genic bacteria are detected besides A.a., administra-
tion of systemic antibiotics is often recommended [11].
Young people usually have an excellent healing capacity,
and, therefore, the combination of surgery and systemic
administration of antibiotics can be successful in pro-
moting substantial osseous fill in infrabony lesions or
furcation involvement associated with aggressive peri-
odontitis.
In localized periodontitis, tetracyclines are the sys-
temic antibiotics most frequently used. Specifically, the
administration of doxycycline (100 mg once a day for
13 days) in combination with surgical debridement-root
scaling and planing has been found to significantly reduce
the levels of A.a. [44–47]. Metronidazole in combination
with amoxicillin with or without clavulanic acid has also
been used with successful results, especially in the cases
of resistant to tetracyclines A.a. Administration of met-
ronidazole (250 mg) in combination with amoxicillin
(375 mg 3 times daily for 7 days) may be more effective
in eradicating (or substantially reducing) the A.a. and
P.g. in most patients with rapid progression of periodon-
titis [2, 11, 48]. The same antibiotic regimen can be used
in the cases of generalized periodontitis. Use of alter-
native antibiotics may be required in patients who do
not respond to conventional antibiotic therapy. In this
case, laboratory techniques, such as bacterial culture,
polymerase chain reaction (PCR) detection of genetic
products, ELISA, or DNA probes, can be used to detect
periopathogenic bacteria or that resist conventional
antibiotic treatment [11].
15.2.2 Periodontitis Associated
with Systemic Disease
Periodontal disease associated with systemic disease may
be a manifestation of these diseases. Examples include:
1. Papillon-Lefèvre syndrome (7 Fig. 10.29)
2. Hypophosphatasia
3. Neutropenia
4. Chediak-Higashi syndrome
5. Histiocytosis X
6. Acrodynia
7. HIV infection
8. Leukocyte adhesion deficiency
9. Leukemias
Leukemia is the most common cancer in children, and
the characteristic clinical appearance of the gingiva may
help in the early diagnosis of this disease. The clinical
signs of leukemia are gingival inflammation and hyper-
plasia due to invasion of the connective tissue and the
Periodontal Diseases in Children and Adolescents
a
b
c d
..      Fig. 15.13 a. A 5-year-old boy with no systemic diseases who
was diagnosed with aggressive periodontitis shows significant clini-
cal signs of acute gingival inflammation (edema and loss of stippling
appearance). b. Radiographic examination reveals significant attach-
ment loss in deciduous molars. The patient was treated with root
underlying bone by transformed leukocytes. Children
with leukemia might have fever, bleeding disorders, and
malaise. Gingivitis signs and symptoms in children with
leukemia will be recurrent, if the systemic disease is not
treated. Periodontal disease associated with systemic dis-
eases in children and adolescents typically shows severe
symptoms, including severe inflammation, ulceration,
rapid bone loss, tooth mobility, and tooth loss. For fur-
ther reading on the relationship between systemic dis-
eases and periodontal disease, the reader is directed to
Williams and Paquette [49], while other diseases, such as
neutropenia, histiocytosis X, HIV infection, and leuke-
mia, are further described in 7 Chaps. 20 and 21.
15.2.3  iabetes Mellitus and Periodontal
D are associated not only through common biological
Disease
It should be noted that, according to the classification of
periodontal disease in 1999, diabetes is not included in the
category of periodontitis as a manifestation of systemic
disease. Nevertheless, diabetes, particularly type I diabe-
tes, is an important predisposing condition for all forms
of periodontitis [50, 51]. Several researchers have studied
the relationship between juvenile diabetes and aggressive
periodontitis. Children with type I diabetes, especially with
uncontrolled diabetes, have a higher bleeding index over
healthy subjects [52, 53]. The prevalence of aggressive peri-
odontitis in children with type I diabetes has been found to
be 10% [54]. Attachment loss in diabetic children is usually
localized to molars and incisors, but it can also be general-
ized. A.a. and Capnocytophaga sp. have been isolated from
357 15
e
scaling and planing and systemic antibiotics. c–e. Eighteen months
after treatment completion, the patient presents with periodontal
health. The patient complied with frequent recall appointments.
Orthodontic treatment will be initiated in the future for the posterior
crossbite. (Courtesy of Drs. N. Kotsanos and D. Apatzidou)
subgingival plaque of diabetic children with periodontitis
[55]. Therefore, children with type I diabetes are at higher
risk of developing destructive periodontal disease.
A significant correlation is also reported between
body fat index and the presence of periodontitis in
children and adolescents [56]. The authors conclude
that a healthy diet and physical activity may be factors
that inhibit the onset and progression of periodontitis.
The mechanism linking obesity with periodontitis may
involve elevated levels of cytokines including IL-8 and
TNF-α in crevicular fluid of obese patients that might
contribute to periodontal destruction. However, there
are some common predisposing factors for obesity and
periodontitis, such as unhealthy diet and low socioeco-
nomic status. Therefore, it appears that the two diseases
mechanisms but also through common risk factors.
15.2.4  cute Ulcerative Gingivitis/
A
Periodontitis
The frequency of acute periodontal disease and par-
ticularly acute necrotizing periodontal diseases in chil-
dren and adolescents is very low – less than 1% – in
Europe and the USA, [8, 11] while they occur more fre-
quently in children and adolescents of developing coun-
tries in Africa, Asia, and South America (2–5%) [11].
Necrotizing ulcerative gingivitis usually occurs in young
children with systemic disease, while in adolescence it is
associated with high levels of physical or mental stress.
The two most common diagnostic criteria for necrotizing
 358 A.-E. Doufexi and F. Nichols
a 15.3
b years, recession is typically detected on the buccal sur-
..      Fig. 15.14 A 17-year-old girl presented with clinical signs of
acute ulcerative gingivitis (pain, halitosis, necrosis of the dental
papilla, pseudomembranes). a. Characteristic ulcerative lesions in
dental papillae. The patient was a heavy smoker, and she reported
that she was under significant stress and malnourished. b. Formation
of pseudomembranes in a dental papillae area
ulcerative gingivitis are necrosis of the interdental papil-
lae and the acute pain (. Fig. 15.14). Bacteria associ-
ated with acute ulcerative gingivitis include spirochetes,
especially Borrelia vincentii and Prevotella intermedia.
Eye Catcher
Predisposing factors for acute necrotizing ulcerative
periodontal diseases are viral infections including
infection with HIV, systemic diseases, poor nutrition,
smoking, inadequate sleep, and mental and physical
stress. Necrotizing ulcerative periodontitis is charac-
terized by formation of pseudomembranes, necrosis
of interdental papillae, and acute pain. It is exceed-
15 ingly rare in children and is usually associated with
severe immunodeficiency associated with AIDS or
ARC (AIDS-related complex).
If necrotizing ulcerative gingivitis is left untreated, it
may progress to periodontitis. Treatment of necrotiz-
ing ulcerative gingivitis involves removing plaque and
calculus, oral hygiene instructions, administration of
metronidazole or penicillin if there are other systemic
symptoms, and frequent recall appointments. If the
patient is a smoker, he/she should be informed about
the role of nicotine to gingival tissue responses and
referred for smoking cessation therapy. Scaling using
ultrasound has proven to be very efficient and leads to
rapid relief of symptoms. It is also recommended to
use a soft toothbrush, at least in the initial phase of
therapy, because of severe pain with each contact of
the gingiva, and mouthwashes with 1.5% hydrogen per-
oxide or 0.2% chlorhexidine can cause significant burn-
ing sensation.
Mucogingival Deformities
15.3.1 Gingival Recession
Localized recession occurs in 10–15% of children and
adolescents. Recession usually occurs on labial surfaces
of the lower incisors in children, whereas during teenage
faces of the canines, premolars, and molars. Causes and
predisposing factors for gingival recessions in children
and adolescents are [8]:
1. Poor oral hygiene, especially if the patient is under-
going orthodontic treatment.
2. Traumatic toothbrushing.
3. Malpositioned teeth.
4. Thin gingival biotype.
5. Piercing of tongue and lips.
6. Frenum pull.
7. Traumatic habits (. Fig. 15.15).
It is important to identify the exact causes (traumatic
toothbrushing or inflammation) and predisposing fac-
tors (gingival biotype, teeth alignment) before treating
gingival recession. For example, the buccal alveolar
bone position on the facial aspect of a tooth may be a
predisposing factor for recession. Before any surgical
treatment of recession on a facially tipped tooth, the
tooth position must be corrected by orthodontic treat-
ment. After the completion of realigning, the existence
and severity of recession is reassessed, and usually no
further surgical treatment of the recession is needed.
Piercing of the tongue and lips is one of the mod-
ern causes of gingival trauma that may cause recession
[8]. The continuous pressure on the gingiva created by
tongue jewelry can also cause severe attachment loss in
addition. Studies show that about 1/3 of patients with
tongue jewelry have at least one area of lingual recession
and 80% of patients with lip jewelry have one or more
areas of recession [57, 58]. Informing patients about
the consequences of piercing can prevent future reces-
sion due to piercing (. Fig. 15.16). Recognition of the
factors responsible for the genesis of recession can also
help to prevent failure of mucogingival surgery.
15.3.2 Frenum Pull
Another common finding in children is frenum pull
between the maxillary central incisors accompanied by
diastema (. Fig. 15.17). In most cases there is no reason
for immediate treatment until eruption of permanent
incisors and canines, when usually the diastema closes
spontaneously. If the patient elects to have orthodontic
treatment, surgical incision or excision of the frenum is
Periodontal Diseases in Children and Adolescents
a b
..      Fig. 15.15 a, b. A 4-year-old boy presented for dental caries
treatment. Clinical examination revealed extensive gingival reces-
sion in the area of the maxillary lateral incisors. The child confessed
a b
..      Fig. 15.16 a. Lip jewelry can cause chronic trauma intraorally
to corresponding periodontal tissues. b. The adolescent girl agreed
to change to flat surface buttoning to prevent this from happening
postponed until the end of orthodontic treatment and
only if it impedes the movement of the two central inci-
sors. On the other hand, there are reports that frenum
excision before orthodontic treatment may provide bet-
ter access for frenum removal due to the presence of
the diastema. Moreover, some studies indicate that the
diastema might disappear only by frenum excision with
no orthodontic treatment, suggesting that early surgical
intervention may be more cost-effective as well as less
time-consuming [59, 60].
The excision of the frenum can be accomplished in
various ways, i.e., surgical removal can be as simple as
a frenotomy or may include apical displacement of the
frenum and a free gingival graft. A free gingival graft
in the frenectomy area might cause aesthetic concerns
due to different thickness and color between the graft
and the adjacent gingiva. Moreover, a frenectomy can
be accompanied with a lateral sliding flap by which pri-
mary closure can be achieved over the site where the fre-
num was previously located [60, 61].
The ankyloglossia (tongue-tie) is a malformation
characterized by high attachment of a short lingual
frenum, occurring at a frequency of about 1.5–4.5%.
The short lingual frenum limits the tongue movement
anteriorly and superiorly in the mouth, limiting its
359 15
scratching his gingiva with his nails. Treatment will include gingival
recession as well as management of underlying stress. (Courtesy of
Dr. Arhakis)
mobility and causing difficulties with physiological
functions.
Various frenum classifications have been proposed in
the literature. One of them is the following [7]:
(a) Light (a very thin frenum of mucosa).
(b) Moderate (the frenum and the genioglossus muscles
showing fibrous consistency).
(c) Complete (the tongue is attached to the floor of the
mouth).
Ankyloglossia may result in difficulty with speech, but
this is usually not serious. However, surgical excision
of a short lingual frenum in a few cases contributed to
the restoration of the speech of young patients who had
severe difficulties in speech. Because the evaluation of
the results from each speech therapist is subjective, con-
troversy exists in speech therapy studies as to whether the
surgical correction of ankyloglossia improved speech.
Whether there is real benefit after surgical excision of
the lingual frenum could be assessed by randomized
controlled clinical trials comparing speech difficulties
before and after frenectomy [62].
Frenectomy of the lingual frenum is indicated if the
child cannot touch the labial surface of the lower inci-
sors with his/her tongue. If decided in infancy, it can be
done under general anesthesia (7 Fig. 8.18). In coop-
erative children it may be performed under local anes-
thesia with cautious placement of a few sutures due to
the vascularity of the floor of the mouth. It has recently
been reported that frenectomy can be done by the use of
diode, Nd:YAG, or CO2 laser, a method associated with
less postoperative pain and discomfort and also better
healing compared to traditional surgical techniques.
The laser excision technique is simple and efficient, read-
ily achieves the required frenum release with minimal
bleeding, and can be accomplished without anesthesia
even in infants with severe ankyloglossia.
 360 A.-E. Doufexi and F. Nichols

a b

c d

..      Fig. 15.17 a, b. Frenum pulls on the upper lip in the primary and d. Medium ankyloglossia in a 7-year-old girl. The patient did not
permanent dentitions, respectively. Frenum excision is better post- undergo surgical treatment, since her speech was not impaired.
poned until after orthodontic treatment. c. The high frenum attach- (Courtesy of Dr. N. Kotsanos)
ment can impair plaque control and promote gingival inflammation.

References 13. Murakami S, Mealey BL, Mariotti A, Chapple ILC. Dental

plaque-induced gingival conditions. J Periodontol.
2018;89(Suppl 1):S17–27.
1. Pari A, Ilango P, Subbareddy V, Katamreddy V, Parthasarthy
14. Ramseier CA, Anerud A, Dulac M, Lulic M, Cullinan MP,
H. Gingival diseases in childhood - a review. J Clin Diagn Res.
Seymour GJ, Faddy MJ, Bürgin W, Schätzle M, Lang
2014;8:ZE01–4.
NP. Natural history of periodontitis: disease progression and
2. Oh TJ, Eber R, WangHL. Periodontal diseases in the child and
tooth loss over 40 years. J Clin Periodontol. 2017;44:1182–91.
adolescent. J Clin Periodontol. 29:400–10.
15. Seymour GJ, Crouch MS, Powell RN. The phenotypic charac-
3. Burt B. Position paper: epidemiology of periodontal diseases. J
terization of lymphoid cell subpopulations in gingivitis in chil-
Periodontol. 2005;76:1406–19.
dren. J Periodontal Res. 1981;16:582–92.
4. Albandar JM. Epidemiology and risk factors of periodontal
16. Nakagawa S, Fujii H, Machida Y, Okuda K. A longitudinal
15 5.
diseases. Dent Clin N Am. 2005;49:517–32, v-vi.
Albandar JM, Tinoco EM. Global ­epidemiology of periodon-
study from prepuberty to puberty of gingivitis. Correlation
between the occurrence of Prevotella intermedia and sex hor-
tal diseases in children and young persons. Periodontol 2000.
mones. J Clin Periodontol. 1994;21:658–65.
2002;29:153–76.
17. Wang MZ, Jordan RC. Localized juvenile spongiotic gingival
6. Loe H, Theilade E, Jensen SB. Experimental gingivitis in man.
hyperplasia: a report of 27 cases. J Cutan Pathol.
J Periodontol. 1965;36:177–87.
2019;46(11):839–43. https://doi.org/10.1111/cup.13549.
7. Matsson L, Goldberg P. Gingival inflammatory reaction in
18. Siamantas I, Kalogirou EM, Tosios KI, Fourmousis I,
children at different ages. J Clin Periodontol. 1985;12(2):98–
Sklavounou A. Spongiotic gingival hyperplasia synchronously
103.
involving multiple sites: case report and review of the literature.
8. Studen-Pavlovich D, Ranalli DN. Periodontal and soft tissue
Head Neck Pathol. 2018;12(4):517–21.
prevention strategies for the adolescent dental patient. Dent
19. Arduino PG, D'Aiuto F, Cavallito C, Carcieri P, Carbone M,
Clin N Am. 2006;50:51–67.
Conrotto D, et al. Professional oral hygiene as a therapeutic
9. Bimstein E, Lustmann J, Soskolne WA. A clinical and histo-
option for pediatric patients with plasma cell gingivitis: pre-
metric study of gingivitis associated with the human deciduous
liminary results of a prospective case series. J Periodontol.
dentition. J Periodontol. 1985;56:293–6.
2011;82(12):1670–5. https://doi.org/10.1902/jop.2011.100663.
10. Trombelli L, Farina R. A review of factors influencing the inci-
20. Doufexi A, Mina M, Ioannidou E. Gingival overgrowth in chil-
dence and severity of plaque-induced gingivitis. Minerva
dren: epidemiology, pathogenesis, and complications. A litera-
Stomatol. 2013;62:207–34. Review.
ture review. J Periodontol. 2005;76:3–10.
11. Califano JV. Position paper: periodontal diseases of children
21. Dongari-Bagtzoglou A. Drug-associated gingival enlargement.
and adolescents. J Periodontol. 2003;74:1696–704.
J Periodontol. 2004;75:1424–31.
12. Moore WE, Holdeman LV, Smibert RM, Cato EP, Burmeister
22. Ilgenli T, Atilla G, Baylas H. Effectiveness of periodontal ther-
JA, Palcanis KG, Ranney RR. Bacteriology of experimental
apy in patients with drug-induced gingival overgrowth. Long-
gingivitis in children. Infect Immun. 1984;46:1–6.
term results. J Periodontol. 1999;70:967–72.
Periodontal Diseases in Children and Adolescents
23. Armitage GC. Development of a classification system for peri-
odontal diseases and conditions. Ann Periodontol. 1999;4:1–6.
24. Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine
DH, et al. Periodontitis: consensus report of workgroup 2 of
the 2017 world workshop on the classification of periodontal
and Peri-implant diseases and conditions. J Periodontol.
2018;89(Suppl 1):S173–82.
25. Cogen RB, Roseman JM, Al-Joburi W, Louv WC, Acton RT,
Barger BO, et al. Host factors in juvenile periodontitis. J Dent
Res. 1986;65:394–9.
26. Van Dyke TE, Hoop GA. Neutrophil function and oral disease.
Crit Rev Oral Biol Med. 1990;1:117–33.
27. Van Dyke TE, Zinney W, Winkel K, Taufiq A, Offenbacher S,
Arnold RR. Neutrophil function in localized juvenile peri-
odontitis. Phagocytosis, superoxide production and specific
granule release. J Periodontol. 1986;57:703–8.
28. Waerhaug J. Subgingival plaque and loss of attachment in peri-
odontosis as evaluated on extracted teeth. J Periodontol.
1977;48:125–30.
29. Catunda RQ, Levin L, Kornerup I, Gibson MP. Diagnosis of
aggressive periodontitis: a dilemma? Quintessence Int.
2018:49173–80.
30. Sjödin B, Matsson L, Unell L, Egelberg J. Marginal bone loss
in the primary dentition of patients with juvenile periodontitis.
J Clin Periodontol. 1993;20:32–6.
31. Brown LJ, Albandar JM, Brunelle JA, LöeH. Early-onset peri-
odontitis: progression of attachment loss during 6 years. J
Periodontol. 1996;67:968–75.
32. Gunsolley JC, Califano JV, Koertge TE, Burmeister JA,
Cooper LC, Schenkein HA. Longitudinal assessment of early
onset periodontitis. J Periodontol. 1995;66:321–8.
33. Albandar JM, Brown LJ, Brunelle JA, Löe H. Gingival state
and dental calculus in early-onset periodontitis. J Periodontol.
1996;67:953–9.
34. Araujo M. Localized juvenile periodontitis or localized aggres-
sive periodontitis. J Mas Soc Summer. 2002;51:14–8.
35. Butler JH. A familial pattern of juvenile periodontitis (peri-
odontosis). J Periodontol. 1969;40:115–8.
36. Newman MG, Socransky SS. Predominant cultivable microbi-
ota in periodontosis. J PeriodontalRes. 1977;12:120–8.
37. Slots J. Subgingival microflora and periodontal disease. J Clin
Periodontol. 1979;6:351–82.
38. Asikainen S, Lai CH, Alaluusua S, Slots J. Distribution of
Actinobacillus actinomycetemcomitans serotypes in periodon-
tal health and disease. Oral Microbiol Immunol. 1991;6:
115–8.
39. Han NM, Xiao XR, Zhang LS, Ri XQ, Zhang JZ, Tong YH,
et al. Bacteriological study of juvenile periodontitis in China. J
Periodontal Res. 1991;26:409–14.
40. Moore WE, Moore LV. The bacteria of periodontal diseases.
Periodontol. 2000. 1994;5:66–77.
41. Califano JV, Gunsolley JC, Nakashima K, Schenkein HA,
Wilson ME, Tew JG. Influence of anti-­Actinobacillus actino-
mycetemcomitans Y4 (serotype b) lipopolysaccharide on sever-
ity of generalized early-onset periodontitis. Infect Immun.
1996;64:3908–10.
42. Califano JV, Pace BE, Gunsolley JC, Schenkein HA, Lally ET,
Tew JG. Antibody reactive with Actinobacillus actinomycetem-
comitans leukotoxin in early-onset periodontitis patients. Oral
Microbiol Immunol. 1997;12:20–6.
43. Albandar JM. Aggressive periodontitis: case definition and
diagnostic criteria. Periodontol 2000. 2014;65:13–26. Review.
44. Aitken S, Birek P, Kulkarni GV, Lee WL, McCulloch CA. Serial
doxycycline and metronidazole in prevention of recurrent peri-
361 15
odontitis in high-risk patients. J Periodontol. 1992;63:
87–92.
45. Miller KA, Branco-de-Almeida LS, Wolf S, Hovencamp N,
Treloar T, Harrison P, Aukhil I, Gong Y, ­Shaddox LM Long-
term clinical response to treatment and maintenance of local-
ized aggressive periodontitis: a cohort study. J Clin Periodontol.
2017;44:158–68.
46. van Winkelhoff AJ, de Graaff J. Microbiology in the manage-
ment of destructive periodontal disease. J ClinPeriodontol.
1991;18:406–10.
47. Saxén L, Asikainen S, Kanervo A, Kari K, Jousimies-Somer
H. The long-term efficacy of systemic doxycycline medication
in the treatment of localized juvenile periodontitis. Arch Oral
Biol. 1990;35(Suppl):227S–9S.
48. van Winkelhoff AJ, Tijhof CJ, de Graaff J. Microbiological
and clinical results of metronidazole plus amoxicillin therapy
in Actinobacillus actinomycetemcomitans-­ associated peri-
odontitis. J Periodontol. 1992;63:52–7.
49. Williams RC, Paquette W. Periodontal disease as a risk for sys-
temic disease, Ch. 21. In: Lindhe J, Lang NP, Karring T, edi-
tors. Clinical periodontology and implant dentistry. 5th ed.
Wiley-Blackwell; 2008.
50. Díaz Rosas CY, Cárdenas Vargas E, Castañeda-­Delgado JE,
Aguilera-Galaviz LA, Aceves Medina MC. Dental, periodontal
and salivary conditions in diabetic children associated with
metabolic control variables and nutritional plan adherence. Eur
J Paediatr Dent. 2018;19:119–26.
51. Lalla E, Cheng B, Lal S, Kaplan S, Softness B, Greenberg E,
Goland RS. Lamster IB:119-126. Diabetes mellitus promotes
periodontal destruction in children. J Clin Periodontol.
2007;34:294–8.
52. Sadeghi R, Taleghani F, Mohammadi S, Zohri Z. The effect of
diabetes mellitus type I on periodontal and dental status. J Clin
Diagn Res. 2017;11(7):ZC14–7.
53. Sbordone L, Ramaglia L, Barone A, Ciaglia RN, Iacono
VJ. Periodontal status and subgingival microbiota of insulin-
dependent juvenile diabetics: a 3-year longitudinal study. J
Periodontol. 1998;69(2):120–8.
54. Al-Zahrani MS, Bissada NF, Borawskit EA. Obesity and peri-
odontal disease in young, middle-aged and older adults. J
Periodontol. 2003;74:610–5.
55. Kieser JA, Thomson WM, Koopu P, Quick AN. Oral piercing
and oral trauma in a New Zealand sample. Dent Traumatol.
2005;21:254–7.
56. Campbell A, Moore A, Williams E, Stephens J, Tatakis
DN. Tongue piercing: impact of time and barbell length on lin-
gual gingival recession and tooth chipping. J Periodontol.
2002;73:289–97.
57. Kamble A, Shah P, Velani PR, Jadhav G. Laser-­assisted multi-
disciplinary approach for closure and prevention of relapse of
midline diastema. Indian J Dent Res. 2017;28:461–4.
58. Koora K, Muthu MS, Rathna PV. Spontaneous closure of mid-
line diastema following frenectomy. J Indian Soc Pedod Prev
Dent. 2007;25:23–6.
59. Suter VG, Heinzmann AE, Grossen J, Sculean A, Bornstein
MM. Does the maxillary midline diastema close after frenec-
tomy? Quintessence Int. 2014;45(1):57–66.
60. Horton CE, Crawford HH, Adamson JE, Ashbell TS. Tongue-
tie. Cleft Palate J. 1969;6:8–23.
61. Suter GA, Bornstein M. Ankyloglossia: facts and myths in
diagnosis and treatment. J Periodontol. 2009;80:1204–19.
62. American Academy of Pediatric Dentistry. Policy on the use of
lasers for pediatric dental patients. Reference Manual.
2017/18;39(6):93–5.
 363 16

Dentoalveolar Trauma
of Children and Adolescents
Cecilia Bourguignon, Aristidis Arhakis, Asgeir Sigurdsson,
and Nikolaos Kotsanos

Contents

16.1 Introduction to Dentoalveolar Trauma – 364

16.1.1  lassification – 364
C
16.1.2 Epidemiology – 364
16.1.3 Etiology of Dental Trauma – 366
16.1.4 Examination: Diagnosis – 367

16.2 Dental Trauma to Primary Teeth – 370

16.2.1 F ractures of Primary T – 370
16.2.2 Luxation Injuries to Primary Teeth – 372
16.2.3 Follow-Up and Complications of Trauma to Primary Teeth – 376
16.2.4 Consequences of Primary Tooth Trauma to Their Permanent
Successors – 377

16.3 Dental Trauma to Permanent Teeth – 380

16.3.1 F ractures of Permanent Teeth – 380
16.3.2 Luxation Injuries to Permanent Teeth – 389
16.3.3 Post-traumatic Complications of Permanent Teeth – 396
16.3.4 Follow-Ups of Injured Permanent Teeth – 401
16.3.5 Endodontic Evaluation and Management of Injured Permanent
Teeth – 401

16.4 Prognosis of Injured Teeth – 405

16.5 Orthodontic Management of the Traumatized Dentition – 406

16.6 Prevention of Dentoalveolar Trauma – 407

16.6.1 Mouth-guards – 407

References – 409

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_16
 364 C. Bourguignon et al.
16.1 Introduction to Dentoalveolar Trauma
Injuries to the lower face occur in about one third of
the general population and most of them are managed
by dental practitioners. Dental and oral injuries occur
frequently in children and may have medical, functional,
and psychological consequences. The term dentoalveo-
lar, or dental as a short expression, refers to injuries to
the teeth themselves, to their supporting periodontal lig-
ament and bone, to soft tissues covering the oral cavity
or being in contact with the teeth, or to a combination
thereof. Such injuries may cause pain, inflammation,
and discomfort of different intensities. They are often
combined with injuries in other parts of the face or body.
Dental traumas in children usually cause extreme anxi-
ety both to themselves and to their parents. Treatment
may thus be a challenge for the dentist. If optimal prog-
nosis is to be ensured, good knowledge, careful plan-
ning, efficiency, and a calm attitude are “must to have”
skills for the dental practitioner.
16.1.1 Classification
The present classification is based on a system adopted
by the World Health Organization (WHO) in 1992 in its
Application of international classification of diseases to
dentistry and stomatology. Later, JO and FM Andreasen
suggested some adjustments in the classification, which
include the groups below [1].
Injuries to the hard dental tissues and the pulp:
55 Incomplete enamel fracture. Fracture without
enamel loss (enamel infraction)
55 Complete enamel fracture. Loss confined to the
enamel
55 Crown fracture (enamel/dentin), no pulp exposure;
also known as uncomplicated crown fracture
16 55 Crown fracture (enamel/dentin), pulp exposed; also
known as complicated crown fracture
55 Crown/Root fracture with or without pulp exposure
55 Root fracture; no enamel involvement
Injuries to the periodontal tissues:
55 Concussion. Periodontal trauma without tooth loos-
ening
55 Subluxation. Loosening without tooth displacement
55 Extrusive luxation. Partial excursion of the tooth
while still in its socket
55 Lateral luxation. Non-axial (horizontal) tooth dis-
placement
55 Intrusion. The tooth is impacted into the alveolar
bone
55 Avulsion. Complete excursion of the tooth out of its
socket
a b
..      Fig.16.1 a Extraoral wound 24 hours after its suturing. The soft
tissue laceration was due to impact on hard floor surface, which also
led to palatal displacement of the right maxillary primary incisors. b
Intraoral lacerated mucosal marks from the traumatized teeth
In addition to the above groups, there are “injuries to
the supporting bone” and “injuries to gingiva or oral
mucosa included” [1]. Dentoalveolar trauma is often
accompanied by soft tissue injuries. Unless there is
bleeding that interferes with dental treatment, soft tissue
injuries should be dealt with only after the tooth/pulp is
securely treated. If there is an open soft-tissue injury, it
needs disinfection and suturing so that proper healing
may be achieved (. Fig. 16.1). Radiographic examina-
tion of the soft tissues may be necessary, as described
later, regarding tooth fractures. If there is notable swell-
ing, the edema will start subsiding the third day after
trauma (. Fig. 16.2). Tooth displacement (luxation)
is often accompanied by alveolar bone fracture, which
is discussed in the subchapter on this topic. There may
also be maxillary or mandibular trauma, most often
occurring at the mandibular condyles. Oral injuries
are common among teenagers, usually after a fight
(. Fig. 16.3), but may also be a component of more
serious non-oral injuries, for example, those occurring
at motor accidents. Whether mandibular/maxillary frac-
tures should be treated simply by splinting or if surgical
correction is necessary lies beyond the scope of a pediat-
ric dentistry textbook, and readers are referred to other
sources, e.g., maxillofacial surgery literature.
Eye Catcher
Traditional classifications usually separate endodon-
tic from periodontal injuries. This is not in principle
justified, since injuries usually affect both tissues con-
comitantly. Additionally, there are mutual relations
between these tissues from a healing and prognosis
perspective.
16.1.2 Epidemiology
Oral traumas where patients seek help at dental practices
and hospitals are frequent and represent 5% of all body
trauma cases. Their incidence is probably even higher,
Dentoalveolar Trauma of Children and Adolescents
a b
..      Fig. 16.2 a Upper lip edema a few hours after a 2-year-old tod-
dler had fallen. b Intraoral view of the dentoalveolar trauma
a
b [3–5]. Of particular interest is the finding that 87% of
..      Fig. 16.3 a Chin blow in a 17-year-old boy following a fight. The
TMJ is painful and the occlusion hindered by lateral displacement of
the mandible. b Coronoid process and condyle fractures (arrows) in
the patient’s right ramus as seen in the panoramic radiograph
because in mild dental trauma cases patients often do
not seek treatment or are not officially registered, since
they do not represent issues of concern to them [2].
16.1.2.1 Primary Teeth
At least 30% of children have suffered some type of
trauma to their primary teeth [2]. Such injuries occur
most frequently between the ages of 2 and 5 years
and about 80–85% of them are caused by falls [3, 4]
365 16
Number of Accidents
25
22
21 21
20 19
17
15
10
5
5
2
1
0
up to 1 up to 2 up to 3 up to 4 up to 5 up to 6 up to 7 up to 8
..      Fig. 16.4 Age distribution of 106 successive patient arrivals with
200 traumatized primary teeth at University of Gottingen Dental
Clinic, Germany [3]
(. Fig. 16.4). The teeth most frequently involved in
trauma are central maxillary primary incisors at a rate
of 68–75%, since they are more exposed than any other
teeth on the dental arch. The next most frequent group is
that of lateral maxillary primary incisors and maxillary
canines [2, 4]. Posterior tooth trauma is rather rare, and
it is typically caused by jaw fracture; it usually involves
longitudinal crown-root fractures (. Fig. 16.5). More
rarely, such trauma may be accompanied by mandibular
condyle fracture.
Although the reported range of findings is wide,
varying from 1:1 to 3:1, boys generally appear to be
more susceptible than girls to primary tooth trauma
children arriving at a dental practice because of trauma
have already suffered prior trauma to one or two teeth
[6]. Thus, a recent dental trauma radiograph may show
atypical root resorption, indicating an older trauma for
which no treatment had been sought (. Fig. 16.6).
16.1.2.2 Permanent Teeth
A study from Denmark reported a 22% dentoalveolar
trauma incidence for permanent teeth [2]. There is a
huge variation in trauma prevalence, explained by dif-
ferences in trauma investigation methodology, age
group choice, geographical regions, and various socio-
economic factors. Still, among youngsters with ante-
rior permanent teeth, boys have been reported to be
about twice as likely to suffer dental trauma than girls;
however, this gap is likely to be diminishing now [7, 8].
The highest incidence is encountered among individu-
als of up to 10 years, while during adolescence, there
is a marked reduction in numbers, almost leveling off
in adult life [4] (. Fig. 16.7). The distribution of per-
manent teeth most frequently involved in trauma is
similar to that of primary teeth, and it is presented in
. Table 16.1. The most frequent condition is isolated
dental trauma, but there are cases of multiple dental
traumas as well [4, 7].
 366 C. Bourguignon et al.

a b c d

..      Fig. 16.5 a Crown-root fracture with pulp exposure of a man- and placement of a stainless-steel crown after removal of the frac-
dibular primary first molar after blow to the chin. b Radiographic tured fragment rather than tooth extraction. Regular monitoring of
image of the crown-root fracture. c, d Treatment involved pulpotomy the tooth is necessary

16.1.3 Etiology of Dental Trauma

Dental trauma etiology is associated with accidents and

impacts related to biological, socioeconomic, psycho-
logical, and behavioral factors [4].

16.1.3.1 Primary Teeth

..      Fig. 16.6 The parents were not aware of any trauma episode; the
occlusal radiograph, however, shows changes consistent with prior
trauma to primary central incisors: an apical radiolucency is visible
on the right one; there is pathological root resorption of both and
pulp canal obliteration of the left one
The main cause for dentoalveolar trauma in primary
dentition is the unstable gait of young children, which
results in frequent falls at home or at school. Falls are
frequent causes for the avulsion of primary teeth among
children aged 9 months to 4 years. Other common causes
are collision and falls while playing at school or cycling
accidents [4, 10]. The abused child syndrome is another,
less frequent, etiological factor that might escape the
attention of dental practitioners. Incidents that seek
delayed medical help are suspicious for child battering
or abuse (. Fig. 16.8) [10].

a b
Dental trauma distribution
60 90
Permanent teeth
16 50
80
Primary teeth
70
NUMBER OF PATIENTS

40 60
Males Females
50
30
40
20 30

20
10
10

0 0
0-4 5-9 10-14 15-19 20-24 25-29 30-34 35-39 >40 Assault Bike Fall MVA Other Play Sport Work
AGE GROUPS (YEARS) CAUSE OF INJURY

..      Fig. 16.7 A sample of 323 Australian individuals who sought do not become apparent prior to school age. b Causes of traumatized
treatment for dental trauma [4]. a Distribution of patients according primary and permanent teeth (MVA motor vehicle accident)
to age and gender. Prevalence differences between males and females
Dentoalveolar Trauma of Children and Adolescents
367 16
interference or impact on fixed surfaces of reduced
..      Table 16.1 Distribution of frequency of permanent
hardness mainly causes luxation injuries. The outcome
incisors dental trauma
is, of course, dependent on the force of the impact. The
Lam, Abbott Roberts and most common predisposing factor is increased over-
et al. 2008 [4] Longhurst 1996 [9] jet with protrusion of maxillary incisors. It has been
reported that an increase from 0–3 mm to 3–6 mm
Upper central incisors 63% 73% leads to twice as many trauma rates, while if protru-
Upper lateral incisors 18% 18% sion exceeds 6 mm, incidence triples [14] (. Fig. 16.9).
Lower central incisors 10% 6%
Insufficient lip coverage seems to play a role as well. The
Swedish Council on Technology Assessment in Health
Lower lateral incisors 5% 3% Care (SBU) presented a systematic overview in 2005 of
the literature and concluded (evidence 3) that there is
an increased risk of a traumatic dental injuries (TDI)
Eye Catcher to the upper front teeth if the patient has a pronounced
overjet with protrusion in combination with inadequate
Biological factors that affect the type of primary lip coverage [15]. Hyperactive children, as well as those
tooth trauma are the structure of the supporting alve- with frequent epileptic seizures or motor disabilities, are
olar bone, which is of reduced hardness among young also more susceptible to dental trauma, depending on
children and therefore sustains higher deformity, and the severity of their disability and on whether they are
root length, which is shorter when compared to per- on medication or not [16, 17].
manent anterior teeth. Due to these factors, tooth dis-
placement is more frequent (85%) than tooth fracture
(15%) in primary teeth [6]. 16.1.4 Examination: Diagnosis
16.1.4.1 Medical History
A medical history is taken to find out about possible
16.1.3.2 Permanent Teeth allergies, coagulation disorders, cognitive disorders,
Almost half of permanent tooth trauma cases in the or other information that might affect the treatment
7–18-year-old age group occur at school. Of the rest, plan. Part of this history taking should be assessment
10% are caused by road accidents, if bicycles are also of any possible central nervous system (CNS) injuries,
included [2]. Sport injuries are frequent, particularly in like brain concussion or intracranial hemorrhage. This
contact sports, such as football, basketball, handball, is because every dental trauma is by definition a head
and boxing [11]. However, many of those “sport” inju- injury, and it has been shown in a systematic review of
ries actually do not occur during an organized event but over 12,750 mild head injuries that the mean prevalence
rather in backyard play where prevention is much harder of intracranial hemorrhage was over 8% [18]. The most
to achieve [12]. Naturally, rates may vary among societ- common signs of a CNS injury are loss of consciousness
ies with different lifestyles. or post-traumatic amnesia; however, delayed reactions
Crown fractures are caused by direct impact of like loss of/or diminished consciousness, situational
teeth against hard objects or surfaces [13]. Soft tissue confusions, headache getting worse, nausea/vomiting,

..      Fig. 16.8 a Case of an abused child for whom

a b
delayed medical help was sought. b The panoramic
radiograph indicates alveolar fracture in the ante-
rior maxilla with extrusion of three incisors (cour-
tesy of Dr. C. Stavrianos)
 368 C. Bourguignon et al.
a b
c chest radiograph.
..      Fig. 16.9 a Face of an 8-year-old with increased risk of dental
trauma due to overjet of maxillary central incisors >10 mm. b, c
A 7-year-old girl with epilepsy. There is a 15 mm maxillary perma-
nent central incisor overjet with deep bite. Previous trauma caused
an enamel-dentin fracture. A sinus tract is now evident labially to the
right central incisor
and or behavioral changes/unexplained irritation can
be also signs [19]. Therefore, it is essential to do at least
some rudimentary CNS evaluation prior to any further
treatment is rendered. If there are any signs of brain
injury, the patient needs to be referred immediately to
appropriate emergency services.
16.1.4.2 Dental Trauma History
Whether at the initial phone call or once the patient has
arrived at the dental office, the dentist needs to know what
happened. For collecting reliable and comparable data, it
is recommended that a standardized dental trauma sheet
should be filled out [20]. The most important questions
that should be answered first are the following:
55 When did the injury happen? The time intervening
16 between the injury and the beginning of treatment
is decisive for selecting the therapeutic protocol and
for prognosis.
55 Where did the injury happen? This information is
important in order to find out how far the patient is
from the dental office and also for social or/and legal
purposes. If the injury happened in contaminated
soil, anti-tetanus protection should be checked.
55 How did the injury happen? The nature of the impact
can lead to suspicions about the type of injuries to
be expected. For example, a blow to the chin often
results in condyle fracture or crown/root fracture in
molars or premolars.
55 Was there loss of consciousness or other signs/symp-
toms? If the patient fainted, vomited, had amnesia,
suffered headaches, or presented hemorrhage or
loss of cerebrospinal fluid from the nose or the ears,
he needs to be referred to a hospital immediately.
Dizziness, which may occur quite a few hours after
the accident, or photophobia and difficulty in visual
focusing are also indicators of possible craniocere-
bral injury.
55 Have the teeth been counted? Is any missing? If there
is suspicion that a tooth may have been aspired into
the respiratory tract, the patient is referred for a
55 Is there any difficulty in closing mouth or a maloc-
clusion? If yes, there might be tooth displacement,
alveolar process or jaw fracture, displacement, or/
and fracture of a TMJ component.
55 Did any tooth become mobile? If yes, a luxation
injury is suspected.
16.1.4.3 Extraoral Examination
The patient is checked for the presence of abrasions,
edemas, bruising, hematomas (particularly in the con-
junctivas), and hemorrhagic foci. Facial bones should be
palpated to locate any abnormalities that might lead to
fracture diagnosis. If the edema or pain does not allow
direct palpation, appropriate radiographs should be
taken. The patient is to be asked to open and close his/
her mouth so as to identify whether there is limitation or
deviation in the mandibular movement and to diagnose
condyle fractures (e.g., temporomandibular disorders,
see 7 Chap. 19, 7 Fig. 19.4).
16.1.4.4 Intraoral Examination
The patient is carefully examined for:
55 Edema or hemorrhaging in the gums or the mucosa
55 Malocclusion
55 Missing, displaced, loosened, or fractured teeth or
teeth with enamel cracks. The following are also
examined:
1. Mobility: at the horizontal and vertical levels,
considering the normal mobility of primary teeth
ready to fall out and of permanent teeth recently
erupted.
2. Percussion: sensitivity or pain means injury to the
periodontal ligament, while a sound similar to
that of an impacted metal object indicates the
tooth has intruded into the bone,
3. Crown discoloration: it is likely to happen a few
days after the accident, or it might have pre-
existed due to prior injury to the same tooth.
4. Reaction to sensitivity testing: the first few days,
measurements may be unreliable but should be
done because the information is useful for com-
parison purposes at later sessions or to other
noninjured teeth.
Every injury to the lower face needs to be assessed for
possible traumas caused to dental tissues and for any
coexisting periodontal tissue trauma [21].
Dentoalveolar Trauma of Children and Adolescents
369 16
16.1.4.5 Radiographic Examination
It is imperative that radiographs should be taken, depend-
ing on the tooth and the type of trauma, so that clear con-
clusions may be drawn concerning the presence or absence
of a root fracture, the potential displacement of the injured
tooth, the periapical and periodontal condition, the stage
of root development, and, in the case of a primary tooth,
its relation to its permanent successor [22]. Since maxil-
lary central incisors are most frequently affected teeth, the
IADT (International Association of Dental Traumatology)
recommends that three periapical radiographs be taken
with different horizontal angulations, plus an occlusal
radiograph [21]. Radiographic examination is imperative
in certain reviewing checks, based on the protocols rec-
ommended, because, in the long run, this is a fundamen-
tal criterion of a successful or unsuccessful outcome. For
example, halting of normal pulp space width reduction in
young teeth or discovery of a periradicular radiolucency
or of a pathologic external root resorption on primary or
permanent teeth confirms pulp tissue necrosis and infec-
tion. This is explained by the diffusion of necrotic/septic
material from the root canal through the apex and dentinal
tubules. In these situations, endodontic treatment needs to ..      Fig. 16.10 Positioning a young child on the parent’s lap, while
be started as soon as possible. the parent is holding between fingers a No. 2 biting plate, for taking
a radiograph of the anterior primary teeth
Radiographic examination of primary teeth in very
young children who cannot cooperate is performed
with them sitting on the parent’s lap while the parent is
a
holding a No. 2 biting conventional or phosphor plate
(. Fig. 16.10). In cases of crown fractures and wounds
of adjacent soft tissues, such as lips or tongue, the latter b
need to be examined radiographically to check for possi-
ble shard laceration. The radiographic exposure time has
to be reduced accordingly [23] (. Fig. 16.11).
Although cone beam examinations should be avoided
in young patients in order to minimize radiation exposure,
they may be helpful visualization aids for better diagnosis.
They should be prescribed occasionally, only when needed ..      Fig. 16.11 a Previous day’s chin blow of a 7-year-old boy and
to improve treatment decision-­making (see 7 Chap. 6). associated crown fracture of maxillary permanent left central inci-
sor. Lip laceration is suspicious for possible lip entry of the fragment.
>>The IADT (International Association of Dental b Radiograph of lower lip confirms the presence of crown fragment
Traumatology) Guidelines
Since 2001, the International Association of Dental recommendations for patients and dentists. The IADT
Traumatology (IADT) has through its Board of Guidelines are endorsed by the American Association
Directors developed a series of guidelines for treatment of Endodontists (AAE) and by both the American and
of all types of traumatic injuries affecting primary and European Academies of Pediatric Dentistry (AAPD,
permanent teeth. The IADT has additionally revised EAPD). Based on the IADT’s Guidelines, a recent
and updated these guidelines in 2007, 2012, and 2020 interactive website called Dental Trauma Guide, at
[21, 23, 24]. The 2012 IADT Trauma Guidelines can 7 http://www.­dentaltraumaguide.­org, was created
be loaded using this link: 7 www.­iadt-­dentaltrauma.­ as a joint venture between IADT and Copenhagen
org or the smartphone application “ToothSOS.” The University Hospital under the supervision of Dr. Jens
IADT is in the continuous process of revising and Andreasen, eminent author and researcher for dental
updating its guidelines to provide the best treatment trauma [25].
 370 C. Bourguignon et al.
a to avoid lip and tongue injury. When a fracture is more
b c
..      Fig. 16.12 a Hypoplasia of maxillary right central primary inci-
sor and absence of the lateral incisor in a 2-year-old born at 26th
week. b Radiograph shows the lateral with severe dysplasia (odon-
toma). c This photograph of another boy explains why a metal laryn-
goscope for achieving intubation may be incriminated for causing
such trauma to forming incisors, had this been necessary in the pre-
maturely born infant
16.2 Dental Trauma to Primary Teeth
Before describing trauma to erupted teeth, one needs to
refer first to the fact that children who had to undergo
orotracheal intubation for various reasons (premature
delivery, corrective surgical treatment, etc.) are more
likely to present dental abnormalities. Such abnor-
malities are considered to be resulting from trauma to
the alveolar process caused by the metal laryngoscope
during intubation at a time when the development/cal-
cification of anterior maxillary primary teeth is taking
place (. Fig. 16.12). There is evidence of analogous
trauma cases in the permanent dentition, and this is a
16 risk that pediatric anesthesiologists should be aware
of [26].
16.2.1 Fractures of Primary T
16.2.1.1  namel Infraction, Enamel-Dentine
E A crown-root fracture varies depending on the fracture
Crown Fracture Without Pulp
Exposure
This usually occurs in the mesial incisal angle or the
incisal edge of central maxillary incisors. Radiographic
examination with a periapical radiograph should follow
the clinical examination.
zz Treatment
In limited fractures, which do not significantly affect
esthetics, it is preferable to grind sharp enamel borders
extensive involving the dentin, restoration with com-
posite resin may be performed in children capable of
cooperating. Otherwise, because dentinal tubules are
exposed, it is imperative that these should be covered
with glass ionomer cement, a process demanding far less
cooperation [23].
zz Follow-up
No follow-up is necessary in the case of infractions. In
an enamel-dentin fracture without pulp exposure, clini-
cal recall should be performed at 6–8 weeks after the
injury [23] (See also . Table 16.2).
16.2.1.2 Crown Fracture with Pulp Exposure
Such cases represent 5% of traumas in primary denti-
tion, and most times, there is hemorrhage or the edge
of the pulp horn revealed appears as a red spot [6, 23,
27]. Following clinical examination, it is imperative that
an anterior occlusal radiograph be taken so as to assess
the integrity, the developmental stage, or the extent of
physiologic root resorption.
zz Treatment
Treatment recommended for pulp exposure includes
pulpotomy, either partial or complete, and root canal
treatment, provided the patient is capable of cooperat-
ing. When the two techniques were used for primary
incisors with caries, success rates showed no signifi-
cant difference [28]. The fractured crown is then recon-
structed using composite resin (. Fig. 16.13). If there
is no hemorrhage from a recent trauma (within a few
hours), the pulp may be covered immediately. In cases
of patients incapable of cooperating, extraction might
be necessary [23, 29].
zz Follow-up
The first clinical recall is performed after a week
has passed. Clinical and radiographic recall is per-
formed at 6–8 weeks and a year later [23] (See also
. Table 16.2).
16.2.1.3 Crown-Root Fracture
line position, and there is usually pulp exposure. This
fracture type usually appears to 2–4% of primary denti-
tion teeth [6]. The fracture might be vertical in the case
of incisors; otherwise, the coronal component is the one
that presents the highest mobility and small to medium
displacement [6, 23]. The radiolucent line of the fracture
is sometimes discernible in periapical radiographs.
zz Treatment
If pulp exposure cannot be clinically or radiographi-
cally excluded, the two components have to be
Dentoalveolar Trauma of Children and Adolescents
371 16

..      Table 16.2 IADT recommended clinical and radiographic follow-up scheme on dental trauma of primary teeth [23]

Type 1st w 4w 8w 6m 1y Annuallya

Enamel fracture
Enamel-dentine fracture c+rb
Crown fracture with pulp exposure c+rb c+rb c+r
Crown-root fracture c+rb c+rb c+r
Root fracture:
Without crown part displacement c+rb c+rb c+rb c+rb
Extraction of crown part c+rb c+rb
Concussion – Subluxationb c+rb c+rb c+rb
Lateral luxation c+rs+rb s+rb c+rs+rb c+rs+rb c+rs+rb c+rb
Intrusive luxation c+rb c+rb c+rb c+rb
Extrusive luxation c+rb c+rb c+rb c+rb
Avulsion c+rb c+rb
Alveolar bone fracture c+rb c+r+s c+rb c+r c+rb

c clinical examination, r radiographic examination, s splint removal, rs review if repositioned and splinted
aAnnually until exfoliation
bRadiographs are only indicated where clinical findings are suggestive of pathosis

a b c

..      Fig. 16.13 a Clinical and radiographic image of crown fractures both central incisors with composite resin. c Twelve months after
to both maxillary primary central incisors in a 3-year-old child. the initial injury no pathologic findings are observed (courtesy Dr.
The left central presents with extensive pulp exposure. b Images G. Vadiakas)
after pulpotomy of the left central incisor and crown buildup of

separated. If the pulp is not exposed, remove the mov-
able part of the tooth and, if feasible, reconstruct the
remaining part. If the pulp is exposed and restoration
of the radicular part is being considered, after the
crown has been removed root canal treatment ensues.
In cases when patients are not very cooperative or when
the fracture line ends intraosseous, which is a rather
frequent finding, the treatment of choice is extraction
[29, 30] (. Fig. 16.14).
zz Follow-up
Clinical recalls are performed after a week has
passed and then 6–8 weeks later. Clinical and radio-
graphic recall is performed at 1 year. Consequently,
 372 C. Bourguignon et al.

a a

b
b

..      Fig. 16.14 a Complicated crown-root fracture of maxillary pri- c

mary right central incisor. b The apparent vertical fracture line in the
occlusal radiograph is a reason for extraction

clinical recall during annual check-up sessions suffices

until the permanent successor erupts [23] (see also
. Table 16.2).

16.2.1.4 Root Fracture d

Root fractures appear at a 24% rate in primary denti-
tion, mainly involving central incisors [6]. The tooth
becomes mobile and sensitive to percussion, while the
crown part may have been displaced.

zz Treatment
If the coronal fragment is not displaced and is immo-
bile, no treatment is necessary [23]. If it is slightly mobile
and if the child is cooperative, splinting with wire and
composite resin may be recommended. Parents need to
16 be informed that after the splint is removed, the tooth
may become mobile and may fall out after some time,
especially if a new trauma occurs. In cases when the
crown part has been displaced and prevents occlusion,
or when a root fracture is accompanied by alveolar bone
trauma, the treatment of choice is to extract the coro-
nal fragment and leave in situ the apical fragment. To
prevent trauma to the permanent successor germ, the
apical fragment is allowed to be normally resorbed [23,
29] (. Fig. 16.15).
zz Follow-up
If the coronal fragment has been splinted, the case
should be reviewed in a week. The splint should be left
in place for 4 weeks. Clinical recalls are performed after
6–8 weeks and 1 year has passed after the injury. Regular
annual clinical recall suffices until the permanent tooth
erupts (see also . Table 16.2).
..      Fig. 16.15 a Radiographic imaging of horizontal root fracture
of a maxillary primary right central incisor. b The ensuing edema
results in extrusion of the coronal fragment from the socket. c Root
canal treatment of the coronal fragment up to the fracture line;
incisal crown reduction was done to avoid traumatic occlusion.
d At 12 months follow-up, the apical fragment has been normally
resorbed, while there is also root canal obliteration of the left central
incisor. Follow-up is necessary
16.2.2 Luxation Injuries to Primary Teeth
16.2.2.1 Concussion
This is encountered in about 11% of primary dentition
trauma [6]. There is no clinical movement, mobility of
the tooth, or significant hemorrhage from the gingival
sulcus, because there is no significant periodontal liga-
ment rupturing. However, there is pain on percussion.
Radiographically, the periodontium presents no patho-
logic post-traumatic finding [23]. Due to mild symptoms,
such cases are often missed by parents who only visit the
dentist if signs/symptoms, like discoloration, appear [31].
Dentoalveolar Trauma of Children and Adolescents
zz Treatment, Follow-up
The tooth should remain under observation, with clini-
cal recall at 1 and 6–8 weeks after the injury [23].
16.2.2.2 Subluxation (Loosening)
This is quite a frequent phenomenon and concerns
about 1/3 of dental trauma to primary dentition [6]. The
tooth injured has not been displaced but has become
mobile due to partial periodontal ligament rupture. This
mobility might be mild to medium, horizontal, or verti-
cal in direction. The gingival sulcus often presents lim-
ited hemorrhage. In the radiograph, periodontal tissues
appear normal [23].
zz Treatment
If the patient is cooperative, when mobility exceeds 2 mm
(at the incisal edge), splinting is applied for 2 weeks; if
oral hygiene is good, tooth mobility will tend to return
to normal.
zz Follow-up
Clinical recall at 1 and 6–8 weeks after the injury [23]
(see also . Table 16.2).
16.2.2.3 Lateral Luxation
Lateral luxation or displacement is the type of trauma
when the crown is displaced horizontally, more fre-
quently in a palatal direction, and interferes with occlu-
sion. Lateral luxation is frequently accompanied by
alveolar bone injury [23, 32]. Initial radiographic exami-
nation comprises of an anterior occlusal and an extra-
oral lateral radiograph. The former is used to detect any
periapical space enlargement, while the latter sometimes
allows the clinician to determine the proximity to the
permanent tooth germ or the labial alveolar bone plate
displacement (. Fig. 16.16) [23].
zz Treatment
A study that followed 545 displaced primary incisors
indicated that only 5–22% of them did not return to
their original position with time [5]. Gently digit repo-
sitioning of the tooth, followed with a 4 weeks flexible
a b
..      Fig. 16.16 a Lateral laxation of maxillary primary left central
incisor seen the next day of the accident. b Palatal displacement is
emphatically shown in the occlusal radiograph. c Because of trau-
matic occlusion, tooth repositioning under local anesthesia was
373 16
splinting, is an option [23]. However, repositioning a
laterally displaced primary tooth carries a higher risk
of pulp necrosis [32]. Furthermore, due to their age
and fear following the injury, young patients are often
noncooperative. To avoid another possible injury to
permanent successors, it is preferable not to attempt
to reposition a laterally displaced primary tooth. It
is recommended that it should be left to return natu-
rally to its position with the help of tongue pressure
[31]. In cases of minor occlusal interference, selective
grinding is recommended. Extraction is considered
when the crown has been significantly displaced labi-
ally causing significant occlusal interference and in
neglected cases of such trauma when there is often
perforation in the vestibular alveolar bone plate
(. Fig. 16.17) [23].
zz Follow-up
Clinical recalls takes place at 1 week, 6–8 weeks,
6 months, and after 1 year. Regular annual clinical recall
suffices until the permanent tooth erupts [23] (see also
. Table 16.2).
16.2.2.4 Intrusive Luxation
Intrusive luxation is insertion of the tooth deep into the
alveolar bone, which suffers fracture of various severity
levels. Compared to other types of trauma intrusion is one
of the most common, particularly in the early primary
tooth dentition, with the primary tooth displacement
causing sometimes serious complications to the perma-
nent successor tooth [23]. The tooth is immobile and, on
percussion, produces a dull metallic sound, characteris-
tic of ankylosis (i.e., direct contact to supporting bone).
Complete intrusion of the tooth into the socket may be
wrongly perceived by parents as tooth loss (. Fig. 16.18).
Differential diagnosis is based on radiographic data.
The most common apex displacement is in a labial
direction. Palatal displacement toward the permanent
tooth germ occurs only if the child has an object in the
posterior teeth when she/he falls. The direction in which
tooth displacement occurred is revealed through palpa-
tion and radiographic examination. Lateral extraoral
c d
successfully attempted in this cooperative 3-year-old and tooth
splinted rigidly. d At the 6-month recall, the tooth was free of signs
and symptoms
 374 C. Bourguignon et al.
radiograph shows both the apex displacement new posi-
tion and the very likely fracture of the vestibular pala-
tal bone plate, as well as its relationship with the labial
surface of the permanent successor (as in . Fig. 16.16).
a
b . Table 16.2).
..      Fig. 16.17 a Neglected trauma of primary maxillary central inci-
sors. Severe crown discoloration of both teeth and inflammatory fen-
estration of alveolar bone plate and mucosa related to the right one.
b Occlusal radiograph shows apical radiolucencies indicative of pulp
necrosis and infection
16
a b
..      Fig. 16.18 a Multiple intrusion of three maxillary incisors and
avulsion of the fourth one in a 26-month-old. b The parents per-
ceived two incisors as lost. c Extraoral radiograph of another intru-
sive incident shows both central incisor apices in labial displacement
zz Treatment
In a study with 172 intruded primary incisors, the apex
had been intruded in labial direction in 80% of the cases;
only 2 presented ankylotic signs and all remaining ones
erupted, while 2/3 survived without complications at the
3 years recall after the injury [33]. Therefore, the tooth
is left to erupt irrespective of the direction of displace-
ment [23] and wait for spontaneous healing of the alveo-
lar bone. Tooth descent is completed in 4–8 weeks, but
its final position may be lagging behind its initial one
(. Fig. 16.19). If there is suspicion that the apex has
been displaced into the germ of the permanent succes-
sor, which may possibly be seen radiographically, or if
the tooth does not erupt, extraction is chosen [33].
zz Follow-up
Clinical recalls take place at 1 week, 6–8 weeks,
6 months, and after 1 year. Regular annual clinical recall
suffices until the permanent tooth erupts [23] (see also
16.2.2.5 Extrusive Luxation
In cases of extrusive luxation, the tooth has been
extruded but remains attached in the socket and is some-
what mobile, while it also interferes with occlusion. The
incidence of extrusive luxation is low (3.8%) as compared
to other displacement dental trauma [6]. Radiographic
assessment presupposes a periapical radiograph using a
No 0 plate or an equivalent digital sensor.
zz Treatment
If the tooth is not interfering with the occlusion, it
should be left to spontaneously reposition itself. If
after having fractured the alveolar plate. The nasal spine is visible
more superiorly. The trace drawing indicates the previous tooth and
bone plate positions (stippled lines) in relation to intruded positions
(continuous lines)
Dentoalveolar Trauma of Children and Adolescents
a b
..      Fig. 16.19 a Intrusion of maxillary primary left central incisor
(after 24 hours) in a 16-month-old boy. b Spontaneous re-eruption
with 45° rotation in 8 weeks. c Radiograph of the tooth with reten-
tion (splinting with the right central incisor) at 4-year follow-up,
extrusion is more than 3 mm and the tooth excessively
mobile, extraction might be the treatment of choice [23].
zz Follow-up
Clinical recalls take place at 1 week, 6–8 weeks, and after
1 year. Regular annual clinical recall suffices until the
permanent tooth erupts [23] (see also . Table 16.2).
16.2.2.6 Avulsion
Avulsion means the tooth is completely out of its socket
and its prevalence represents 5–18% of displacement
trauma. About 90% of avulsed teeth are primary max-
illary incisors [6]. Radiography confirms that the tooth
was not intruded. It is good to search for the avulsed
tooth, because there is also a risk that the tooth went
accidentally into the respiratory tract. Symptoms in such
cases are coughing, tachypnea, and high temperature
[23].
zz Treatment
If there is complete avulsion of a primary tooth, its
replantation is not recommended (. Fig. 16.20), con-
trary to a permanent tooth, due to either the direct risk
of causing mechanical injury to the underlying perma-
nent tooth germ or to indirect risk resulting from pos-
sible inflammation. Replantation might be possible only
under ideal conditions of immediate repositioning when
the infant is cooperative. Besides, complications may
arise such as the following: pulp necrosis and infection
requiring either endodontic treatment or extraction and
ankylosis of the replanted primary tooth and pathologic
root resorption. There have been some reports of pri-
mary avulsed teeth that were replanted, most of which,
however, were ultimately removed 2–24 months later due
to subsequent complications [34]. Although there are
no functional impairments, i.e., related to mastication
or articulation, this premature loss of anterior primary
teeth is often of esthetic concern to parents. If they so
wish, a suitable fixed restoration may be constructed
(7 Fig. 13.49).
375 16
c d
after orthodontic alignment was undertaken when age 3 years at
parents’ request. Pulp obliteration indicates pulp remained vital. d
Clinical view at age 6 years
a b
..      Fig. 16.20 a Dentition after avulsed maxillary primary left cen-
tral incisor. b Parents brought the avulsed primary tooth only to be
informed that its replantation is not recommended
zz Follow-up
It is necessary to perform clinical review at 6–8 weeks.
Further follow-up at 6 years of age is indicated to
monitor eruption of the permanent tooth [23] (see also
. Table 16.2).
16.2.2.7 Alveolar Bone Fracture
This usually accompanies displacement of one or sev-
eral teeth, which move together on inspection because
they are attached to the fractured bone segment. A peri-
apical radiograph provides information about the extent
of the fracture and its relation to other primary and the
permanent successor teeth (. Fig. 16.21).
zz Treatment
Treatment comprises of repositioning the fractured bone
segment and displaced teeth, if possible, and their splint-
ing for 4 weeks [23]. If there is contusive trauma to the
gingiva or the mucosa, this is sutured. Good oral hygiene
performed by the parents improves healing.
zz Follow-up
The first clinical recall is performed 1 week after the
injury. Clinical and radiographic examination should
then be done at 4 weeks and then 1 year. Regular annual
clinical recall suffices until the permanent tooth erupts
[23] (see also . Table 16.2).
 376 C. Bourguignon et al.

a dentinal tubules and are degraded, affecting the color

of the tooth. In mild trauma cases, such discoloration
may reverse, whereas, in more serious cases leading to
pulp necrosis, it persists and often is the only early post-­
traumatic finding. Such endogenous discoloration may
be distinguished into three categories:
55 A pink shade appears a few days following the
tooth trauma, usually after mild concussion or
subluxation trauma types; this is mainly due to
intrapulpal hemorrhage (extravasation of eryth-
rocytes). Such discoloration may subside in a few
weeks, indicating some recovery of the pulpal tis-
b
sue, or grow darker.
55 A yellowish shade may be associated diminished
pulp by root canal obliteration (see below). This
color change is evident several months after
trauma.
55 A dark shade, usually blue-gray or brown-gray, most
likely indicates pulp necrosis (. Fig. 16.22). Such
discoloration is often observed and usually appears
gradually within a period of 2 months after the
injury [29]. The involved tooth may remain until it
..      Fig. 16.21 a Neglected trauma in the maxillary primary right
central incisor to right canine region 2 weeks after the injury. Soft
sheds naturally, without any other pathologic find-
tissue healing is delayed due to alveolar process fracture. b The radio- ings. Dark discoloration on its own is not an indica-
graph reveals part of the fracture line (arrows) tion for root canal treatment or extraction, unless
there are radiographic signs of periapical pathosis,
16.2.3  ollow-Up and Complications of
F
Trauma to Primary Teeth a

Follow-ups are extremely important to prevent or detect

complications early. They should be carried out for all
types of trauma as in . Table 16.2.
Besides complications to their permanent successors,
traumatic injuries of primary teeth may cause any of the
following complications to these own teeth:

16 16.2.3.1 Pulpitis
Pulpitis is the initial reaction of the pulp in cases of
direct tooth injury such as in fractures or in cases of
b
luxation injuries. Pulpitis may be fully reversed or lead
to pulp degeneration and necrosis without any pain or
symptoms. Teeth with reversible pulpitis may be sen-
sitive to concussion. However, pulpitis may be due to
bacterial contamination, whether the fracture exposes
the pulp or not, whereupon septic pulp necrosis ensues
with signs of periapical inflammation. In such cases root
canal treatment becomes necessary, or, if there is no
patient cooperation, the tooth has to be extracted [29].

16.2.3.2 Discoloration of the Traumatized
Tooth
Discoloration appears in almost half of primary tooth
trauma cases [5]. It is common for the pulp capillaries
to bleed following trauma. Blood elements enter the
..      Fig. 16.22 a The dark brown-gray shade of symptomless max-
illary primary right central incisor indicates pulp necrosis. b The
radiograph shows small apical radiolucency and a larger one at
asymptomatic left central incisor, which has a slightly wider root
canal than its right counterpart. Follow-ups are necessary to deter-
mine if treatment becomes necessary
Dentoalveolar Trauma of Children and Adolescents
a
b cooperation. Or they may be of the ankylosis type when
..      Fig. 16.23 a Yellowish shade and partial re-eruption of a maxil-
lary primary right central incisor, after having suffered intrusion in
the past. b The occlusal radiograph shows marked pulp canal oblit-
eration
and/or symptoms and signs of periapical inflamma-
tion, such as pain, appearance of an abscess, or fis-
tula. Parents are informed accordingly; besides
attending the usual dental recalls, they also need to
regularly raise the upper lip of their child and check
for these signs [23].
16.2.3.3 Pulp Canal Obliteration
It is usually discovered clinically by the yellowish color of
the crown of such teeth. The pulp chamber and root canals
become significantly stenotic by mineralized dentin like
tissue formed at fast rate (. Fig. 16.23). This phenome-
non is quite frequent and appears in 52% of intruded teeth
[33]. Pulpal necrosis has been observed in only 10% of
primary teeth with pulp space obliteration within 3 years
[35]. Therefore, prognosis should be considered favorable,
and these teeth do not need root canal treatment if there is
no periapical lesion shown in the radiograph and no clini-
cal signs of pulp necrosis and infection.
16.2.3.4 Pulp Necrosis
Pulp necrosis is a frequent, yet unpredictable, conse-
quence of primary tooth trauma, with an incidence rate
of 25% [5]. Diagnosis is based on signs and symptoms
such as pain, swelling, fistula, tooth mobility, gray crown
377 16
discoloration, as well as radiographic findings, such as
periapical lesion and pathologic root resorption.
16.2.3.5 Root Resorption
Post-traumatic root resorptions may vary greatly.
Within a few months, the largest part of the root may be
resorbed. External root resorptions occur when trauma
damaged the cementum and the periodontal ligament,
such as in severe luxation injuries. They may be of the
inflammatory type, in case of pulp infection. The ques-
tion then arises whether to do root canal treatment or
extract the primary tooth, depending also on patient
the alveolar bone comes into direct contact with the
tooth root. During the normal exfoliation process, the
root may be resorbed leading to the disappearance of
the ankylotic area. If the eruption of the permanent
successor is delayed or ectopic, the ankylosed primary
tooth has to be extracted [29]. These resorptions should
not be confused with physiologic primary tooth resorp-
tion.
16.2.4 Consequences of Primary Tooth
Trauma to Their Permanent
Successors
Eye Catcher
Permanent teeth may suffer consequences from
­traumatic injuries to predecessor primary teeth only
if they are at an early developmental or mineraliza-
tion stage. That’s why knowledge relevant to tooth
formation timing and sequence is important (please
see 7 Chap. 17). Since the most frequently trauma-
tized primary teeth are the maxillary incisors, the per-
manent teeth mostly suffering such consequences are
their homologous successor teeth. Regarding enamel
defects, these are more frequently found in the labial
surface because this surface is close to the apex of pri-
mary incisors.
Traumatic injuries to primary teeth may affect the
underlying permanent successors by any of the follow-
ing mechanisms:
55 Direct physical damage (. Fig. 16.24)
55 Aseptic inflammation ensuing soon after trauma
55 Septic inflammation following pulp infection of the
primary tooth
55 Combination of the above
The most common sequalae are:
 378 C. Bourguignon et al.

..      Fig. 16.24 a Maxillary

primary left central incisor of a b
a 6.5-year-­old boy a week after
intrusion injury on a steel object.
b A difficult to interpret finding
at the periapical radiograph led
to a decision for CBCT, which
revealed an incisal fracture of
the permanent successor inflicted
by the primary tooth root. c At
1-year follow-up, the successor
tooth has not erupted presenting
a hard palatal swelling related to
the incisal fragments. d The peri-
c d
apical radiograph reveals its root
anomaly probably as an intrusive
domino effect. e The fractured
permanent incisor erupted 8
months later

16.2.4.1  hite or Yellow-Brown Spots

W a
on the Enamel
These hypomineralized porous enamel spots have the
appearance of demarcated opacities of various size on
the enamel (. Fig. 16.25). Their frequency of appear-
16 ance is as much as 23% of primary tooth trauma cases
and do not seem to correlate with any specific trauma
type [36, 37].
zz Treatment
Because porous enamel of such spots usually occupies
the full thickness of the enamel, grinding and compos-
ite resin restoration are preferred, similar to the restora-
tion of hypomineralized incisors in an MIH case (see
7 Chap. 17). Using the opaque tint of composite resin
may allow a more conservative removal of the enamel.
The microabrasion technique is not indicated. The more
recent technique of resin infiltration, using the Icon®
kit, for instance, may be effective.
16.2.4.2 Enamel Hypoplasia
This comprises 12% of trauma-related developmen-
tal defects. Such lesions occur when the permanent
successor germ is still developing, i.e., before it is ade-
quately mineralized. The type of trauma to the primary
b
..      Fig. 16.25 a Well-demarcated white enamel opacities; differen-
tial diagnosis is necessary between trauma to predecessor primary
teeth and molar incisor hypomineralization (MIH). b Severe mid-­
crown enamel hypoplasia of a maxillary left permanent central
incisor probably related to trauma/inflammation of the predecessor
primary tooth
dentition that most often leads to appearance of such
lesions is intrusive and extrusive laxations [37]. The
hypoplastic enamel region may be small or extensive
and may include areas of hypomineralization as well
(. Fig. 16.25). Radiographically, hypoplasias may
often be diagnosed prior to tooth eruption.
zz Treatment
Such lesions should be treated by removal of discolored
enamel and/or dentin and restoration with composite
resin.
Dentoalveolar Trauma of Children and Adolescents
16.2.4.3 Crown Dilaceration
Such dysplastic defects are due to primary tooth impact
onto the germ of the permanent successor tooth, result-
ing to a bend at the developing cervical part, which is
softer in relation to the already mineralized crown [36,
37]. In a report of anterior permanent teeth with dysplas-
tic defects related to primary tooth trauma, dilaceration
was found in 25% of the cases [37]. Crown angulation
varies depending on the developmental phase and the
germ location at the time of injury, as well as on the
direction of the trauma-causing force. The crown of
dilacerated maxillary incisors is usually rotated anteri-
orly and nasally (7 Fig. 17.20). Almost half of these
teeth remain impacted. About 3% of trauma cases to
primary dentition lead to such abnormalities [36]. It is
inferred that the accidents occur earlier than age 5 years,
i.e., when more than half or all the permanent crown has
developed. Most commonly correlated trauma cases are
extrusive and intrusive laxations of predecessor primary
teeth [37].
zz Treatment
As soon as dilaceration is discovered, it is followed up
using lateral extraoral radiographic examination and
probably other auxiliary radiographs, like CBCT. If the
tooth does not erupt, a decision about extraction and
orthodontic correction of the diastema or orthodonti-
cally guiding the tooth to occlusion must be made. If
the latter solution is chosen, attention is necessary in
the case of intense tooth dilaceration, because crown
a b
d e
..      Fig. 16.26 a Radiographic image of dysplastic unerupted four
maxillary permanent incisors in an 8-year-old boy with a history
of severe trauma at age 9 months. A “wait and see” approach was
adopted. b He returned 1 year later with left-side labial edema. c,
d The partially erupted left lateral already had septic pulp, prob-
ably due to pulp communication with the oral environment due to
379 16
rotation during the descent may lead to vestibular root
appearance [38]. The decision depends on the crown
integrity and the severity of dilaceration. If the tooth
erupts on its own, its position in the dentition is assessed
along with the possibility of correcting the crown shape
using composite resin.
16.2.4.4 Other Rare Developmental Disorders
Rare dysplasias of successor permanent teeth are
reported as follows [36, 37]:
55 Odontoma-type dysplasia (. Fig. 16.26)
55 Root duplication
55 Lateral root bending (. Fig. 16.27)
55 Partial or complete interruption of root develop-
ment continuity
55 Permanent tooth germ necrosis
Types of trauma most often correlated with these spe-
cific abnormalities are intrusive and extrusive laxations
of primary teeth [37].
zz Treatment
In some cases, such as lateral root bending, dysplastic
permanent teeth do erupt. If possible, orthodontic trac-
tion is applied to the dentition if certain teeth erupted,
to temporarily conserve alveolar osseous mass until
more permanent treatment is possible. In the remaining
cases, however, extraction and correction of the space is
recommended to allow future prosthetic restoration [36,
37].
c
f
dysplasia. e, f Patient aged now 12 years is under orthodontic treat-
ment, while the right central with dysplastic crown has been tempo-
rarily built up, the left central and right lateral have been extracted
as untreatable, and the left lateral was endodontically treated. Final
esthetic/prosthetic rehabilitation will follow orthodontic treatment
as a multidisciplinary approach case
 380 C. Bourguignon et al.
a b
c d
..      Fig. 16.27 a Labial ectopic and delayed eruption of maxillary
permanent left central incisor in an 8-year-old boy with a serious
oral trauma history at age 2 years. b Its radiograph reveals lateral
root bending, a sort of mild dilaceration. c, d The annual review, fol-
lowing the extraction of predecessor primary incisor, shows further
descent and almost complete apex development
16.2.4.5 Consequences to Permanent Tooth
Eruption
Following trauma to anterior primary teeth, there are
often disorders observed in the time or path of per-
manent successor tooth eruption (see 7 Chap. 10).
Delayed permanent tooth eruption was noted in 1/3 of
primary tooth trauma cases [39]. It is reported that this
may last up to 1 year and adversely influence occlusion
in the mixed dentition. A permanent tooth may often be
at crossbite along with delayed presence of the primary
tooth in the dentition (7 Fig. 11.42), while there have
been cases of ectopic labial eruption observed (7 Fig.
16 10.17). On the contrary, it is rather rare for a perma-
nent tooth to erupt prematurely following the loss of its
primary predecessor due to trauma, because there is no
bone destruction present, as is the case when the tooth is
extracted due to severe carious periapical inflammation.
16.3 Dental Trauma to Permanent Teeth
16.3.1 Fractures of Permanent Teeth
16.3.1.1 Enamel Infraction
Incomplete enamel fracture (infraction) is frequent (10–
12.5%) in permanent teeth, but often missed [2, 7]. It is
caused by direct impact onto a hard object or surface
and may appear along with other fracture types to the
same or adjacent teeth. There is no loss of tooth mass.
a
b
..      Fig. 16.28 Incomplete enamel fractures (infractions). a Clinical
view b By LED illuminating the maxillary permanent central inci-
sors at an appropriate angle, the infractions become visible on both
incisors of right side
zz Diagnosis
Cracks follow various directions and stop close to the
dentin-enamel junction [40]. Diagnosis is facilitated by
the light scattering observed, due to the crack, when a
light beam falls almost perpendicularly to the longitu-
dinal tooth axis (. Fig. 16.28). Radiographic examina-
tion is recommended [41]. Response to pulpal sensitivity
tests is normal. In case of severe infractions, etching and
sealing with bonding resin should be considered; other-
wise, no treatment is required.
zz Follow-up
Clinical and radiographic recalls are not necessary in
the cases of sole infractions [21] (see also . Table 16.3).
Pulpal necrosis rate is 3.5% and most probably caused
by tooth concussion or loosening, which occurred at
the same time as the enamel infraction but escaped
attention. When an associated luxation injury is sus-
pected, the cracked tooth should be followed more
closely (see further down in this chapter in the 7 Sect.
16.3.4).
16.3.1.2 Complete Enamel Fracture
In this type of crown fracture, there is a partial enamel
loss due to impacting on a hard object. The range of
incidence rates in permanent teeth (26–76%) depends on
the extent to which treatment is sought for such small
injuries [2, 42].
zz Diagnosis
After the appropriate trauma form has been completed,
an investigation should ensue as to whether additional
trauma of a different kind occurred, such as root fracture.
Root developmental stage affects tooth prognosis [41].
Dentoalveolar Trauma of Children and Adolescents
381 16

..      Table 16.3 Follow-up table for fractured permanent teeth, according to IADT Guidelines 2020 [21]

4w 6–8 w 3m 4m 6m 1y 5y

Enamel infraction
Complete enamel c+r c+r
fracture
Enamel-dentine fracture c+r c+r
without pulp exposure
Enamel-dentine fracture c+r c+r c+r c+r
with pulp exposure
Crown-root fractures c+r c+r c+r c+r c+r c+r
Root fracture c+r+s c+r c+r+s* c+r c+r c+r

This follow-up regimen is recommended when there is no luxation injury associated to the fracture at the time of trauma. If a con-
comitant luxation injury occurred, the luxation follow-up regimen prevails (please look . Table 16.4)
c+r: clinical and radiographic examination
s: splint removal (for mid-root and apical third fractures)
s*: splint removal (for cervical third fractures)

zz Treatment a
Treatment, depending on fragment size and patient’s
esthetic requirements, may comprise grinding to
improve incisal edge appearance or crown reconstruc-
tion using tooth fragment if available or composite resin
(. Fig. 16.29).

zz Follow-up
Clinical and radiographic recalls as well as vitality tests b
should be performed at 6–8 weeks and 1 year after the
injury [41, 21] (see also . Table 16.3). Pulpal necrosis
rate is a mere 1.7% [43]. However, if an associated luxa-
tion injury occurred or is suspected, the tooth should be
monitored more closely (see further later in this chap-
ter on the topic “Follow-ups for Luxation Injuries of
Permanent Teeth”)
..      Fig. 16.29 Enamel fracture at the incisal edge of maxillary per-
16.3.1.3 Enamel-Dentine Fracture Without manent right central incisor and its reconstitution with composite
Pulp Exposure (Uncomplicated resin
Crown Fracture)
This is the highest fracture incidence (40%) to perma- in pulp infection risk has the thickness of dentin remain-
nent teeth [2]. The tooth needs to be restored the soonest ing after the injury.
possible, not only for comfort or esthetic purposes but
also to prevent pulpal microbial infection due to expo- zz Diagnosis
sure of a high number of dentinal tubules to the oral Radiographic examination is imperative to exclude the
environment in addition to avoiding issues such as devi- possibility of root fracture or tooth displacement [21].
ation of adjacent teeth or overeruption of antagonists.
It has been calculated that 1 mm2 of dentin contains zz Treatment
about 20,000–45,000 dentinal tubules, which provide Restoring young permanent incisors with a ceramic
direct communication between the pulp and the oral crown should be avoided. Reconstruction of the frac-
cavity and allow bacteria as well as chemical and ther- tured incisor crown with composite buildup is the treat-
mal stimuli to be transmitted [44, 45]. A significant role ment of choice. Rubber dam should always be used.
 382 C. Bourguignon et al.
Isolating with a double lip retractor is not sufficient,
since breathing vapors contaminate the etched surfaces
and compromise adhesion. Local anesthesia is not
always necessary, since even if a thin dentin wall remains,
it may be covered with a base such as glass ionomer
cement (GIC) and blowing or rinsing the tooth causes
no pain any more [21]. According to some authors, bev-
eling broken enamel reinforces retention and improves
esthetic result. Following rubber dam placement, dentin
coverage if needed, etching, and the application of an
adhesive, the composite resin (CR) should be applied
using a celluloid partial or full strip crown, depending
on whether the fracture is angular or almost horizontal,
respectively (. Figs. 16.30 and 16.31).
A more elaborate composite resin buildup may be
made by taking a silicone impression and pouring a
plaster model which is sent to a lab technician who will
reconstruct the tooth and fabricate a “silicone key” or a
mouth-guard. The clinician will then use one of those as
a palatal matrix to gradually add layers of enamel and
dentin composite in different shades and forms trying
to mimic a natural tooth. Finishing and polishing are
essential steps to obtain a good tooth-composite inter-
face and an esthetically pleasing restoration [21].
If the broken fragment is found intact, it is an
interesting esthetic option to consider bonding it back
a b
16
..      Fig. 16.30 a Clinical view of enamel-dentine oblique crown fractures on three maxillary permanent incisors of a 9-year-old child. b, c
Clinical and radiographic view after the crown buildup was made using composite resin. (Courtesy Dr. G. Vadiakas)
a b c d
..      Fig. 16.31 a Enamel-dentine crown fracture without pulp expo-
sure on mandibular permanent right lateral incisor after covering the
dentin with GIC and enamel beveling. b Appropriate size strip crown
filled with composite. c Placement of strip crown on the fractured
[46–48]. The technique involved is described as follows.
The crown fragment should be kept moist or be rehy-
drated in water for at least 15 minutes before it is bonded
[49]. This improves bonding quality and strength. A
length of adhesive wax may be added to the incisal edge
of the broken fragment so as to facilitate manipulations.
It has been suggested that the enamel on both fractured
surfaces be beveled prior to reattachment, but this may
prevent optimal coaptation of the two fragments. The
enamel of both fragments is then etched and the adhe-
sive applied. By placing and light curing a minimal
quantity of composite resin between the two edges, the
broken piece is accurately repositioned. Any gaps left
are filled and the fracture line is reinforced with more
composite resin. In the last three decades, this restora-
tion type has been in use (. Fig. 16.32); some authors
have reported on technique details. For example, bev-
eling of the fracture line did not seem to increase the
strength of the restoration [46]; however, it aids in mask-
ing the fracture line. Adding composite resin on the frac-
ture line did not increase bond strength when compared
to using solely the adhesive on its own [48]. No sound
clinical data regarding time endurance as compared to
solely composite resin reconstruction techniques have
been reported. Rubber dam isolation should always be
used in restorative procedures, even if there is no pulp
c
tooth followed etching and bonding. All was done under rubber dam
isolation, which is now removed for finishing the restoration. d One-
year recall
Dentoalveolar Trauma of Children and Adolescents
383 16

a b c d

..      Fig. 16.32 Reattachment of a fractured crown fragment in a fragment using a non-radiopaque composite available at early 1990s.
9-year-old girl. a Oblique enamel-dentine crown fracture on maxil- d Recall of the adult patient 14 years later with no other interven-
lary permanent left central incisor. b, c Reattachment of the tooth tion. A slight shade change of the composite can be detected

a
exposure, to avoid saliva and breathing humidity con-
tamination (. Fig. 16.33).

zz Follow-up
Clinical examinations including vitality testing and
periapical radiographs need to be repeated at 6–8 weeks
and 1 year following the injury. Pulpal necrosis has been
shown to occur in 9% of such traumas [50], but this rate
also depends on how soon after trauma the pulp was b
protected. If trauma to periodontal tissues happened
as well, pulpal necrosis likelihood rises to 28% [51–
53]. The presence of a periapical radiolucency or root
development interruption of young permanent incisors
means that the pulp became necrotic and infected. This
makes root canal treatment imperative [21] (see also
. Table 16.3).

16.3.1.4  namel-Dentine Fracture with Pulp

E ..      Fig. 16.33 a, b Rubber dam isolation improves adhesion of com-
Exposure (Complicated Crown
Fracture)
These crown fractures are also called “complicated frac-
tures.” The pulp is exposed to the oral environment and
bacterial contamination starts immediately. That’s why
treatment should be provided the soonest possible.
zz Diagnosis
Crown fracture with pulp exposure does not automati-
cally cause pain, but sensitivity to hot and cold stimuli,
as well as low intensity pain during mastication [21]. The
scale of pulp exposure and the time interval between
injury and treatment are parameters with a direct effect
on the inflammatory reaction extending into the pulp.
At the initial examination, pulp sensibility tests are
unreliable and pulp vitality can be perceived visually.
Radiographic examination is imperative, similar to the
previous types of trauma, so as to exclude the possibility
of root fracture and to confirm apex status [21].
zz Treatment
The aim of pulpal treatment is to maintain pulp vital-
ity to allow immature teeth to complete their root
posite buildups. There are several ways to apply the rubber dam:
placing the clamps away, as shown here, is one of them. Alterna-
tively, dental floss can be knotted on each tooth. WedjetsR can also
be used interdentally. Direct clamping of an immature incisor is not
recommended due to the high risk of fracture of these fragile teeth
development. Root canal treatment should thus be
avoided. Treatment depends on root formation stage
and degree of pulpal inflammation. Such treatment
options include the following: (1) direct pulp capping,
(2) partial pulpotomy, (3) cervical pulpotomy, or (4)
root canal treatment. The first three treatment types
are described below, while for root canal treatment,
the reader is invited to look in this chapter in section
“Endodontic Management of Injured Teeth.” All these
treatment options should always be carried out under
rubber dam isolation.
Direct pulp capping The success rate of this procedure is
lower than Cvek’s partial pulpotomy; therefore, direct
pulp capping is not frequently recommended [54, 55].
Ideal clinical prerequisite conditions for direct pulp cover
are to observe a vital pulp where the pulp exposure is lim-
ited (up to about 1 mm) and for the intervention to take
 384 C. Bourguignon et al.
place soon after the trauma (up to several hours). Besides,
the pulp should be free of inflammation owed to another
cause, e.g., deep caries. Technique steps are:
55 Local anesthesia without vasoconstrictor.
55 Tooth isolation with rubber dam.
55 Cleaning of tooth surfaces and disinfection of
tooth and rubber dam with iodine, chlorhexidine, or
sodium hypochlorite.
55 Rinsing and disinfection of the pulpal exposure with
saline solution, chlorhexidine, or sodium hypochlorite.
Blood clot presence reduces the likelihood of heal-
ing, either by preventing direct contact of therapeutic
agents with pulp tissue or because the space left after
its decomposition is inviting bacterial presence [56].
55 Once hemostasis is obtained, calcium hydroxide (CH)
powder mixed with saline or anesthetic solution to the
consistency of a paste is applied; this remains the gold
standard for pulp coverage. Alternatively, ΜΤΑ® has
been used in the recent past years and has been shown
to favor dentin bridge formation and pulp vitality
maintenance as well. However, MTA, whether gray or
white, has been shown to create tooth discoloration,
and its use is not recommended anymore for pulp
capping [21, 57], especially in anterior teeth. Bioden-
tine®, a new bioceramic cement, seems to be a prom-
ising material for pulp capping, but more studies are
a b
16
d e
..      Fig. 16.34 a The maxillary permanent left central incisor of an
8-year-old boy presents a horizontal crown fracture with pulp expo-
sure. The right one presents an oblique crown fracture without pulp
exposure. b The radiographic examination shows that the incisors
have open apices. c View of the pulp exposure. Following placement
needed before its widespread use can be safely recom-
mended.
55 When Ca(OH)2 is used as the pulp dressing material,
it should be covered hermetically. Glass ionomer
cements seem to provide an adequate marginal seal
before the tooth is restored with composite resin [58].
Partial pulpotomy In cases of more extensive pulp expo-
sure and delayed arrival at the surgery (up to 2 days fol-
lowing the injury), partial pulpotomy is preferred (Cvek
technique) in order to remove the inflamed portion of the
pulp first [54]. The aim is to obtain a dentin bridge forma-
tion below the cover material. The technique is recom-
mended for either mature or immature teeth. After
anesthesia and rubber dam isolation, the technique steps
are the same as described above for direct pulp capping;
however, an additional step is required, the partial ampu-
tation of the pulp before the placement of the capping
material [21] (. Fig. 16.34).
The amputation is done as follows:
55 A small reservoir of approximately 2 mm deep is
created by amputation of the exposed pulp with a
high-­speed sterile bur under copious water spray. A
diamond causes less damage than a low-speed bur or
an excavator (. Fig. 16.35a) [59, 60].
c
of the rubber dam, the exposed pulp is excised to about 2 mm deep,
Ca(OH)2 paste is applied on the remaining pulp, and GIC covers the
paste and the exposed dentin of both teeth. d The final crown build-
ups with composite resin. e Post-op radiographic image. (Courtesy
Dr. G. Vadiakas)
Dentoalveolar Trauma of Children and Adolescents
a 3–4 days. This is sometimes indicated for teeth that have
b ture line may lie under the gingiva. In these cases, the cer-
..      Fig. 16.35 Cvek’s partial pulpotomy. a A small reservoir, almost
a box of approximately 2 mm, is created by amputation of the
exposed pulp with a high-speed sterile bur under copious water spray.
A diamond causes less pulp damage than a low-speed bur or an exca-
vator. b After obtaining hemostasis, the pulp is covered with a thick
calcium hydroxide paste (mixture of calcium hydroxide powder with
saline or anesthetic solution). A hermetic seal covering the calcium
hydroxide should then be placed before fragment bonding or com-
posite buildup. Please note rubber dam isolation during treatment
55 Pulp bleeding can be arrested by placing a cotton
pellet soaked in saline on the pulp stump with light
pressure for a few minutes or by rinsing gently the
pulp wound with sodium hypochlorite [61]. Allowing
time for hemorrhage control is important. However,
if hemostasis is not achieved, this likely means that
the inflammation extends beyond the prepared zone
and that it is necessary to amputate the pulp further,
more cervically.
55 In Cvek’s pulpotomy technique, the pulp is then cov-
ered with a thick calcium hydroxide paste (mixture
of calcium hydroxide powder with saline or anes-
thetic solution) (. Fig. 16.35b) [54, 60].
Cervical pulpotomy As in the case of pulp exposures due
to caries (see 7 Chap. 14), cervical pulpotomies are usu-
ally performed on immature permanent teeth when the
objective is to attempt to maintain root pulp vitality. This
is preferred in cases when the inflammation is quite
advanced due to major pulp exposure and when a long-
time interval since trauma has elapsed, maybe exceeding
385 16
also suffered other injuries as well [54]. The technique is
the same as partial pulpotomy; however, pulp amputation
is done at the cervical level of the tooth.
Restoration After any of the three pulp treatments
described above, crown restoration is performed as
already discussed, with composite resin reconstruction,
possibly with the “silicon key” technique, or with reat-
tachment of the broken crown fragment. Quite often
though, tooth eruption is in process, and part of the frac-
vical area may be restored by using resin modified glass
ionomer cement (RMGIC) or, even better, the total
reconstruction can be made by using exclusively RMGIC,
which can be considered as temporary until the tooth has
sufficiently erupted.
zz Follow-up
In all three treatment modalities described above to
tackle exposed vital pulps, clinical and radiographic
examinations, in combination with sensibility testing, are
important and should be repeated on follow-up visits at
6–8 weeks, 3 months, 6 months, and 1 year following the
injury [21] (see also . Table 16.3). Clinically, it should
be confirmed that there is no pain or apical inflammation
and that the crown color is normal. Radiographs should
confirm continuing root development (. Figs. 16.36
and 16.37). If a periapical radiolucency appears, root
canal treatment should be performed.
a b
..      Fig. 16.36 Partial pulpotomy and fragment reattachment. a
Radiographic image of crown fracture with pulp exposure of maxil-
lary permanent left central incisor in a 7-year-old child. The root
is at an early developmental stage. Treatment comprised of partial
pulpotomy and reattachment of the broken piece. b Treatment objec-
tives were achieved: completion of root development and absence of
pathologic findings at 3-year follow-up. However, some pulp space
obliteration is evident coronally. Follow-ups should be continued.
(Courtesy Dr. G. Vadiakas)
 386 C. Bourguignon et al.
a b
..      Fig. 16.37 Cervical pulpotomy. a Radiographic preoperative
view of horizontally crown fractured maxillary permanent central
incisors in an 8-year-old boy, who presented with a week’s delay.
The left one has pulp exposure with minimal vitality signs and the
right one responds normally. Both teeth are immature. b A cervical
pulpotomy was performed on the left incisor, and both teeth were
restored with composite. This is at the 12-month recall
zz Prognosis
In complicated crown fractures, the pulp survival rates
for pulp capping range from 63% to 88%. Success rates of
partial pulpotomy range from 94% to 100% [62]. When,
however, dental trauma with pulp exposure is accompa-
nied by periodontal tissue trauma (luxation injury), pulp
necrosis likelihood increases up to 14% [51, 62].
16.3.1.5 Crown-Root Fracture
Crown-root fractures to permanent anterior teeth are
not so common. They have been reported to appear in
0.5–5.5% of all dental trauma cases to permanent teeth
[2]. Treatment depends on the depth of the fracture line
within the bone socket and the ensuing difficulty of iso-
lation and restoration. The more apically the fracture
16 line ends, the worse the prognosis [63, 64].
zz Diagnosis
Diagnosis is achieved through clinical and radiographic
examination to exclude the possibility of additional root
fracture or displacement. CBCT can be considered for
better visualization of the fractured path, its extent, and
its relationship to the marginal bone [21]. The typical
crown-root fracture is oblique in a labial-palatal direc-
tion (. Fig. 16.38); it starts a few mm supragingivally
on the labial surface and ends 2–5 mm subgingivally in
the palatal aspect. In this case, radiographic diagnosis
presents some difficulties. If the crown component is
retained in place by periodontal fibers, it may present
a wide range of mobility levels, depending on how far
subgingivally its palatal border lies. There is usually a
pulp exposure. More rarely, the fracture line may be
almost parallel to the longitudinal tooth axis.
zz Treatment
Prior to attempting any treatment, a decision must be
made on whether the remaining tooth structure will be
mechanically strong enough to support a future restora-
tion. If not so, it is wise to consider the possibility of
submerging the root, rather than attempting to extrude
it to create restorable margins. Options for treating this
type of fracture are discussed below:
Eye Catcher
Treatment options for crown-root fractures depend
on the subgingival extension of the fracture line, on
whether the fracture is located in an esthetically sen-
sitive region and on the stage of root development.
Due to the endodontic, periodontal, and prosthetic
issues involved, tooth overeruption using orthodon-
tic forces or surgical extrusion is often carried out in
order to expose the fracture line to the gingival level
so that proper treatment and restoration may be per-
formed under humidity and hemorrhage control. In
immature teeth of children and teenagers, the advan-
tages/disadvantages of orthodontic traction or surgi-
cal extrusion should be put into balance, especially in
patients at risk for new trauma episodes. They are not
necessarily good options for immature teeth.
Removal of the crown part and restoration This is the
most conservative way to treat a fracture, and it may be
preferred if part of the fracture line lies only slightly sub-
gingivally [63, 64]. The crown part may be restored by
reattaching the broken fragment, by composite resin
buildup or through a prosthetic crown. However, isolation
problems usually prevent ideal ­bonding at the subgingival
border [21].
Gingivectomy (and osteotomy, if necessary) This may be
indicated in cases where the subgingival fracture line lies
in a region of no esthetic concern, e.g., in the palatal sur-
face [21, 63]. However, there is risk of failure due to the
development of persistent periodontal inflammation pal-
atally.
Orthodontic extrusion of the tooth with or without gingivo-
plasty (. Fig. 16.39) This approach is more time-­
consuming when compared to the surgical approach,
since it usually takes 5 weeks to obtain 2–3 mm extrusion,
as well as at least another 8–10 weeks of splinting to retain
the tooth in its new position [65, 66]. The depth of the
fracture line is important because the crown/root ratio fol-
lowing extrusion should be at least 1:1 after crown recon-
struction. Since there is concomitant displacement of the
bone and periodontal tissues along with the tooth move-
Dentoalveolar Trauma of Children and Adolescents
a b
..      Fig. 16.38 Crown-Root fracture. Surgical extrusion of the
tooth. a Radiographic view of the crown-root fracture of a maxil-
lary permanent right central incisor in an 11-year-old boy. A previ-
ous dentist had started the endodontic treatment and had placed a
radiopaque paste inside the canal. b Clinical view of the tooth after
removal of the temporary filling. The fracture line extends subgingi-
vally well below the crestal bone level. c Clinical view after surgical
a b
..      Fig. 16.39 Crown-root fracture of 11-year-old boy is candidate
for orthodontic traction. a Clinical image of maxillary permanent
right central incisor after emergency treatment. b A mobile mesio-­
palatal fragment is apparent (arrow). c The periapical radiograph
ment, lateral fiberotomy has to be performed every
7–10 days during the orthodontic traction period.
Alternatively, bone and gum remodeling may be per-
formed in a single procedure at the end of orthodontic
traction.
Surgical extrusion of the tooth This is an intentional par-
tial avulsion so that the root is repositioned to a more
coronal position to allow fracture margins to lie at the
level of the gingiva (. Fig. 16.38). Following splinting in
the new position, the tooth should receive root canal
treatment. Prognosis is good, but there is 5% possibility
for the root to resorb within 3 years [67] or, according to
other authors, 12% in 4 years [68, 69].
Extraction Finally, there is the option of extracting the
tooth if none of the solutions above is suitable. Prosthetic
treatment at a later stage may, however, be quite complex,
because alveolar bone resorption increases with time [21].
This is why the solution of allowing the tooth root to
remain, through the excision and removal of only the cor-
onal fragment followed by suturing of the gingiva, has
387 16
c d
repositioning of the tooth in a more coronal position in order to cre-
ate restorable margins. Root canal treatment was finalized, and the
crown was buildup with composite. d Radiographic view at 9-year
follow-up. The tooth is still functioning and asymptomatic and no
pathologic signs are present. Due to coronal repositioning, its tooth
apex is located more coronally compared to the left central incisor
c d
fails to document the course of this fracture line. d One angle of the
cone beam tomographic scans reveals the fracture line to end mesi-
ally at crestal bone level (arrow)
been proposed [70] (please see the “Replacement
Resorption (Ankylosis)” section later in this chapter).
Retaining the root contributes toward maintaining alveo-
lar crest volume so that it may be removed as late as pos-
sible after puberty, only if necessary and when the timing
of implant placement is deemed appropriate [71]. A mid-
term prosthetic appliance will have to be made for the
patient. Allowing the root to remain submerged and
placement of a Maryland bonded bridge is also a very
good option for these patients.
zz Follow-up
Clinical and radiographic examinations, in conjunc-
tion with vitality testing, are important and should be
repeated at 1 week, 6–8 weeks, 3 months, 6 months,
and then yearly for at least 5 years [21] (see also
. Table 16.3).
16.3.1.6 Root Fracture
Root fracture is a combination of pulp, dentin,
cementum, and periodontal membrane trauma; it
appears relatively rarely at a rate of 0.5–7.5%. Teeth
 388 C. Bourguignon et al.
most often involved are maxillary central incisors, at
a rate of 75%. In young patients, whose permanent
incisors are immature and at various eruption stages,
root fracture is a rather rare event [72]. Socket elas-
ticity probably makes such teeth more susceptible
to displacement and avulsion rather than root frac-
ture. Root fractures may be horizontal (transverse),
oblique, or vertical (longitudinal). The latter often
appears in mature teeth with an intraradicular post
and prognosis is bad. Horizontal and oblique frac-
tures are more frequent and are distinguished into
simple and multiple ones. Simple ones have a better
prognosis. They are distinguished into apical third,
middle third, and cervical third fractures of the root.
Prognosis is worse in cervical to middle third frac-
tures due to less periodontal support during their
potential healing process.
zz Diagnosis
Horizontal and oblique root fractures may be dif-
ficult to diagnose clinically. Indeed, sometimes
they may be erroneously diagnosed as tooth loos-
ening (subluxation) or lateral displacement (lateral
luxation) since clinical characteristics are the same.
Furthermore, they may be missed, due to the pres-
ence of a more visible dental trauma, such as a crown
fracture. Involved teeth might be sensitive to percus-
sion and palpation, and the coronal fragment may be
slightly displaced lingually, labially, and/or incisally
(. Fig. 16.40) [65].
a b
16
..      Fig. 16.40 a Periapical radiographic view of maxillary perma-
nent right central incisor presenting a horizontal middle third root
fracture. b The cone beam coronal view shows the same. c However,
the cone beam sagittal view reveals that the fracture line is oblique
and more complex: from the labial, it starts horizontally but then
It is also likely that the radiograph does not reveal
a root fracture immediately after the injury, but at a
later point in time. This is most probably due to either
­hemorrhage or granulomatous tissue formation at the
fracture line, which gradually displaces the coronal
fragment incisally [73]. Additionally, depending on the
direction of the radiograph beam, some root fractures
may be undetectable. That’s why, according to IADT,
radiographic assessment comprises taking three periapi-
cal radiographs from different angles, plus an occlusal
radiograph [21].
Cone beam computerized tomography (CBCT)
examination is also extremely helpful to diagnose the
true extent of root fractures. The real trajectory of frac-
ture lines is usually undetectable in a single periapical
radiograph (. Fig. 16.40).
zz Treatment
The basic principle for treating root fractures in perma-
nent teeth is to reposition the luxated and mobile coronal
fragment and immobilize it with a splint (. Fig. 16.41).
Repositioning is performed under local anesthesia and
confirmed through radiographic examination. Splinting
is performed, for instance, with a passive twist flex wire
and composite resin on the labial surface of affected and
adjacent teeth. The splint should be semiflexible and
passive, without applying forces on the teeth. Splinting
should remain for about 4 weeks but may stay up to
4 months if the fracture is located at the cervical third
of the root [21].
c
takes a vertical direction downward to the alveolar bone crest pala-
tally. There is a chance that the fracture may heal. Before the advent
of cone beam examination, many oblique root fractures were misdi-
agnosed as “horizontal” and healed
Dentoalveolar Trauma of Children and Adolescents
Eye Catcher
Four types of reactions have been described following
a root fracture [73, 74]:
1. Hard tissue healing. The fracture heals through the
formation of a dentinoid or cementoid callus unit-
ing the fragments. It is the “ideal” kind of healing.
2. Healing with interposition of connective tissue.
3. Healing with interposition of connective tissue
and bone between the fragments.
4. Interposition of granulation tissue between the
fragments. This failure to heal is related to pulpal
necrosis and infection of the coronal fragment.
Clinically, the tooth is sensitive to horizontal or ver-
tical percussion, while an abscess is likely to appear
at the fracture level. Radiographically, the fracture
line widens, there is lamina dura loss, and there are
alveolar bone radiolucencies at the fracture level.
zz Follow-up
Regardless of fracture type, clinical and radiographic
examinations should be performed at 4 and 6–8 weeks
as well as at 4, 6, and 12 months and yearly for
5 years, in accordance to the IADT Guidelines [21].
a b
d e
..      Fig. 16.41 a Root fracture in the middle third with extrusive
and lateral luxation of maxillary permanent left central incisor in
a 12-year-old boy (closed apex). b, c The tooth was repositioned,
and a semiflexible wire passive splint was bonded with composite.
Incisal edge was ground by 1 mm to avoid occlusal interference. d
389 16
The protocol for clinical and radiographic recalls of
fractured permanent teeth is summarized further in
. Table 16.3.
zz Prognosis
Immature teeth are more likely to heal and maintain
pulp vitality as compared to mature teeth [75, 76]. Pulp
necrosis appears in 20–44% of root fractures [77, 78].
Necrosis usually concerns the coronal fragment only
(. Fig. 16.41), while the apical component remains
vital in almost all cases [75, 79]. As with every fracture
type, a negative response to sensibility testing does not
necessarily indicate pulp necrosis. The degree of disloca-
tion of the coronal fragment is one of the most impor-
tant factors influencing prognosis, and reapproximating
the two halves is key to pulpal healing [77].
16.3.2 Luxation Injuries to Permanent Teeth
16.3.2.1 Concussion
When a permanent tooth suffers concussion, there is
minimal trauma to periodontal tissues and pulp. The
impact is usually along the tooth axis and there is no
displacement or mobility of the tooth.
c
f
Five weeks later root canal treatment of the coronal fragment was
initiated due to pain symptoms. e At the 3-year follow-up, the tooth
remains asymptomatic with normal mobility but with crown 1 mm
shorter. f Healing has occurred by bone tissue between the frag-
ments. Note the canal obliteration of the apical fragment
 390 C. Bourguignon et al.

zz Diagnosis when there is no tooth mobility or interference with

The tooth is asymptomatic, although in some cases mild
pain may appear during mastication and it may be sen-
sitive to percussion. There is no laceration of periodon-
tal fibers or hemorrhage from the gingival sulcus. Pulp
vitality testing usually leads to positive results, since
pulp vascularity is hardly affected. The clinical and
radiographic image of the tooth is normal.
zz Treatment
Treatment comprises monitoring of pulp vitality.
Proper oral hygiene and a soft diet for 2 weeks are rec-
ommended [21].
zz Follow-ups
Clinical and radiographic recall is performed at 4 and
6–8 weeks and 1 year following the injury [21]. Prognosis
is very good. After 11-year follow-up, 4% necrosis
of mature teeth and 0% of immature teeth have been
reported [80].
16.3.2.2 Subluxation (Loosening)
zz Diagnosis
During clinical examination, there might be hemor-
rhage from the gingival sulcus. There is some tenderness
to percussion. On palpation there is small, usually hori-
zontal tooth mobility due to partial laceration of peri-
odontal fibers. Due to periodontal edema, there may
be premature contact with antagonists, which may lead
to traumatic occlusion [21] (see also . Table 16.4). No
response to initial pulp sensibility testing may indicate
pulp injury. Radiographic image is usually normal [10].
zz Treatment
Treatment other than monitoring is usually not needed
but, depending on symptoms and the extent of mobil-
16 ity, passive and flexible splinting may offer relief to the
patient in some cases. The splint may soon be removed
occlusion, and in any case, it should not be kept for
more than 2 weeks for the risk of promoting external
root resorption [21].
zz Follow-ups, prognosis
Clinical and radiographic recall is at 4 and 6–8 weeks,
6 months, and 1 year following the injury [21] (see also
. Table 16.4). Prognosis depends on the extent of peri-
odontal tissue trauma and on stage of root development.
Pulp necrosis in 0–2% immature teeth and 3.5–15%
mature teeth after 7–11 years has been reported [81].
16.3.2.3 Lateral Luxation
It is most frequent in the 8–12-year age group [82, 83].
zz Diagnosis
The tooth is displaced in a new position, and there is
bleeding from the gingival sulcus. It may either be quite
mobile or be immobile. If the coronal part has been
displaced in a palatal direction, it often interferes with
occlusion. The tooth apex is frequently displaced labi-
ally, locked out of its socket, with the buccal plate of its
alveolar bone frequently fractured and displaced labially
with it. This can be well visualized in cone beam exam-
ination, but palpation of the buccal plate is also very
informative. This occurs more frequently to maxillary
incisors with fully developed apices; the tooth sound is
metallic on percussion, similar to ankylosed teeth.
The responses to pulp sensibility testing may be
negative initially, but in cases of open apex without
apical displacement, they may become positive after
about 3 weeks [21]. Radiographic examination com-
prises of 4 radiographs (periapical, occlusal, and
two eccentric exposures in opposite direction to each
other) to check for potential root fracture, possible
periapical alveolar space creation, and stage of root
development [22].

..      Table 16.4 Follow-up table for luxation injuries of permanent teeth, according to IADT Guidelines 2020 [21]

2w 4w 8w 12w 6m 1y Annuallya

Concussion c+r c+r

Subluxation c+r+s c+r c+r c+r
Lateral luxation c+r c+r+s c+r c+r c+r c+r c+r
Intrusive luxation c+r c+r+s c+r c+r c+r c+r c+r
Extrusive luxation c+r+s c+r c+r c+r c+r c+r c+r

aFor at least 5 years

c+r: clinical and radiographic examination
s: splint removal
Dentoalveolar Trauma of Children and Adolescents
a b
..      Fig. 16.42 a, b Lateral luxation of right lateral with subluxation
of right central incisor in a 10-year-old girl. c Emergency manage-
ment consisted of repositioning the lateral, removing the very mobile
zz Treatment
Laterally luxated maxillary incisors may be reposi-
tioned ideally during the first 12 hours after the injury,
under local anesthesia, − buccal and/or palatal – or
after infraorbital nerve block [84]. To disengage a
locked apex, it is pressed from the buccal, using a fin-
ger with simultaneous mild pull of the tooth crown
incisally, which also achieves concurrent reduction
of any alveolar bone fracture that may be present
(. Fig. 16.42). Tooth splinting should be semiflex-
ible and performed with a passive wire retained on the
labial tooth surfaces using small amounts of composite
resin for dental/gingival hygiene. The purpose of splint-
ing is to maintain the tooth in position, while allowing
physiologic mobility. This has been shown to improve
periodontal healing and be helpful in the prevention of
ankylosis. The splint is usually kept for 4 weeks [21],
since lateral luxation is usually associated with alveo-
lar bone fracture. No investigation using a periodontal
probe is allowed during this time. If it is certain that
no associated bone fractured occurred, the splint time
may be reduced to 2 weeks. The integrity of the alveo-
lar bone plate is checked radiographically and, in case
of marginal bone breakdown, splinting is extended for
another 3–4 weeks [21]. If the trauma is not recent, it is
preferable to reposition the tooth through orthodontic
forces after initial periodontal healing [85]. The patient
should be rescheduled to come at 2 weeks post-trauma
to check good initial healing, perform endodontic
evaluation, and possible removal of the splint. If the
injured tooth is mature and the apex was severely dis-
placed, the chances of pulp survival are low and end-
odontic treatment should likely be performed soon in
order to prevent pulp infection and inflammatory root
resorption. Pulp space healing, most often by sponta-
neous revascularization, may be expected in 70% of
immature teeth with this type of injury [86].
zz Follow-up, prognosis
Initial clinical and radiographic recall is performed at 2,
4, and 6–8 weeks after the injury. Later recalls should be
391 16
c
primary canine, and carefully etching available teeth on either side
for splinting with flexible orthodontic wire and composite resin
performed at 6 months, 1 year, and every year for 5 years
[21] (see also . Table 16.4). There are quite a few dif-
ferent reports of laterally luxated teeth surviving. One
study reports that immature teeth present low rates of
pulp necrosis (9%), while mature teeth present high rates
(77%) [80].
16.3.2.4 Intrusive Luxation
Intrusive luxation occurs due to axial force applied to
the tooth’s incisal edge. This is considered to be the most
serious trauma type, since it is associated with extensive
lesions of the pulp, periodontal cells, and cementum
and often with alveolar bone plate fracture [87]. It is a
traumatic lesion of particularly bad prognosis, particu-
larly if the patient did not comply with proper treatment
(. Fig. 16.43).
zz Diagnosis
Intrusion is often a component of serious trauma
involving several teeth and bone fracture. Clinically, the
crown of the injured tooth appears shorter than that of
adjacent teeth. Diagnosis is easier during puberty. On
the contrary, among 7–8-year-old children, the intruded
tooth looks like an erupting one, and differential diag-
nosis can benefit from mild percussion, which produces
a metallic sound [82]. Since this is displacement trauma,
radiographic examination should include four radio-
graphs, as in the case of lateral luxation. The absence of
periodontal tissue at the apical region or along the entire
radical length is a typical finding [21].
zz Treatment
There are no satisfactorily documented recommenda-
tions as yet concerning the treatment of a permanent
tooth that has suffered intrusion. Treatment depends
on the degree of root development and degree of intru-
sion.
zz Immature teeth
Teeth with open apices have the potential to re-erupt
spontaneously to their original position. This may
 392 C. Bourguignon et al.
a b
c d
..      Fig. 16.43 Consequences of a neglected intrusion case. a Serious
trauma to an 8-year-old girl at the playground swing, with intrusion
of all 4 maxillary permanent incisors and severe lateral luxation of
many primary teeth. b Same patient 8 weeks later. Partial re-­eruption
of the incisors (more limited for the right central one, which is also
rotated). c Patient reappearance 20 months after the initial injury.
a b
d e
16
..      Fig. 16.44 a Intrusion and non-complicated crown fracture of
a maxillary permanent left central incisor in an 8-year-old. b Pala-
tal view. c Radiographic view (open apex). d Six months monitor-
ing after pulp protection with glass ionomer cement. Spontaneous
happen within 3 months [88, 89]. Given that about
2/3 of such teeth become necrotic during this waiting
period, the teeth need to be monitored so that necrosis
may be diagnosed in good time [86, 90]. If within a few
weeks there is no sign of re-eruption, the tooth is repo-
sitioned using orthodontic means [21] (. Fig. 16.44).
The right central incisor did not re-erupt and produces an ankylotic
sound on percussion, while the left lateral incisor presents a fistula.
d Root development continued in the right lateral and left central
incisors, but not in the other two incisors. Prognosis for right central
incisor is bad, especially that its presence is impeding anterior alveo-
lar bone growth. Family compliance is needed to improve prognosis
c
re-­eruption occurred, but only partially. e Outcome 12 months later,
after repositioning the left central incisor by orthodontic means and
stabilization splinting over a 3-month period
If the intrusion is severe, more than 7 mm, the IADT
Guidelines recommend to reposition the tooth either
surgically or orthodontically. It has also been proposed
that a mild attempt to disengage the tooth using a tooth
extraction forceps should be made immediately after the
injury [21].
Dentoalveolar Trauma of Children and Adolescents
zz Mature teeth
If the tooth is intruded less than 3 mm, it is worth trying
to wait for spontaneous re-eruption. If after 2–4 weeks
there is no sign that re eruption is on its way, surgical
or orthodontic repositioning is indicated. If the mature
tooth is intruded more than 7 mm, surgical reposition-
ing is recommended by the IADT Guidelines [21]. The
figures below show orthodontic (. Fig. 16.45) and sur-
gical (. Fig. 16.46) repositioning of intruded mature
teeth, the former being considered a more acceptable
solution from a biological point of view. Surgical repo-
sitioning is performed using bone forceps and digital
compression to the socket. After repositioning, splint-
ing is required for 4–8 weeks [21]. Because the rates of
necrosis are high among such teeth [82], it is necessary
for root canal treatment to start earlier than 3 weeks
after the injury, at about 10 days, with temporary intra-
canal Ca(OH)2 filling initially for a few months and
gutta-percha final filling later on. Soft food is recom-
mended for 10–14 days as well as good oral hygiene
including local application of chlorhexidine (0.1%)
twice a day for a week [21].
zz Follow-up, prognosis
Clinical and radiographic examination, regardless of
the degree of root development, similarly to lateral
luxation, should be performed at 2, 4, and 6–8 weeks, 6
a b
..      Fig. 16.45 Orthodontic repositioning of intruded teeth. a Severe
intrusion of both maxillary central incisors, concomitant with exten-
sive crown fracture in a 14-year-old adolescent from a bike accident.
b Starting orthodontic repositioning with traction of central incisors.
393 16
and 12 months, and every year for 5 years [21] (see also
. Table 16.4). Healing is complex due to the high likeli-
hood of pulp necrosis and external tooth resorptions,
both replacement and inflammatory. After follow-up
of many years, it was confirmed that the pulp became
necrotic in 2/3 of intruded permanent teeth with open
apex and in 98–100% of those with a closed apex [89].
16.3.2.5 Extrusive Luxation
Extrusive luxation is caused by a lateral force impact
that leads to serious injury of the periodontal ligament.
The tooth may still be kept in position by some peri-
odontal fibers.
zz Diagnosis
Clinically the tooth appears to have “gone down,” with
a longer clinical crown, and there is bleeding from the
soft tissues around the tooth. The tooth is very mobile.
There is usually no response to pulp sensitivity testing.
Radiographic examination reveals increased width of
the periodontal space [21].
zz Treatment
Repositioning might have been performed immediately
at the site of the accident. If performed in the dental
office, following local anesthesia, the tooth is pushed
back into the socket with mild digital pressure. In case
c
c Completion of root canal treatment. d Crown buildups with com-
posite resin and alignment of incisors using fixed orthodontic appli-
ances. Clinical and radiographic follow-ups will continue. (Courtesy
of Dr. G Vadiakas)
 394 C. Bourguignon et al.
a b
d e
..      Fig. 16.46 Surgical repositioning of intruded teeth. a, b Severe
intrusion of maxillary permanent right central incisor, moderate
intrusion of left central incisor, fracture to their crowns, and con-
comitant fracture of the alveolar bone plate in a 10-year-old girl.
Teeth are quite mature. c Immediate surgical repositioning of central
incisors with forceps. Caution should be taken not to damage the
of recent trauma, the blood clot will spread out from the
apical region of the socket. In extrusions neglected for
several days, the blood clot has become organized. Some
authors recommend orthodontic intrusion of those
teeth if they are mature. If, however, the tooth is severely
interfering with occlusion, it may be extracted and repo-
sitioned in its normal position following clot curettage
(. Fig. 16.47). Flexible splinting, with a passive wire
16 and composite resin, ensues for 2 weeks to allow time
for periodontal ligament healing. The patient is given
the same instructions as those given for intrusion injury.
Continuous monitoring of the tooth is necessary
so that any root resorption may be noticed. In cases
of immature teeth, pulp space revascularization is con-
firmed if root development continues. In mature and
immature teeth, continuous negative reaction to pulp
sensibility testing, presence of apical radiolucency,
swelling, or fistula indicates pulpal necrosis, whereupon
root canal treatment is indicated.
zz Follow-up, prognosis
Following clinical and radiographic examination
2 weeks after the injury, the splint is removed. Recall fol-
lows the protocol applied for luxation injuries [21] (see
also . Table 16.4). Tooth preservation rates are high fol-
lowing extrusion injuries, while pulpal survival depends
c
f
root cementum with the forceps. d Splinting with orthodontic wire
and composite resin and suturing of interdental gingival papillae. e
Esthetic restorations with composite resin following root canal treat-
ment of the two central incisors. Soft tissues healed well. f 4-year
follow-up radiographic image without signs of root resorption or
other pathologic findings. (Courtesy of Dr. G Vadiakas)
on the stage of root development. In immature teeth,
pulpal necrosis rates are 9%, while in mature teeth, rates
reported are 55–98% [80, 91].
The protocol for clinical and radiographic recalls in
cases of luxated permanent teeth is summarized in this
chapter, in the 7 Sect. 16.3.4, in . Table 16.4.
16.3.2.6 Avulsion
This type of trauma appears more frequently among
young individuals, when the apex has not yet fully devel-
oped and the alveolar bone is more resilient. The aim
of emergency treatment is to replant the avulsed tooth
as soon as possible, ideally within minutes, at the site of
the accident. Parents, sport coaches, and the population
in general should be instructed to do so [24]. If debris
are present on the root surface, they should be gently
removed by rinsing the tooth in water, milk, or saline
prior to replantation. No wiping or scraping should be
done, since they damage the cementum and periodontal
ligament cells covering the root surface. The combina-
tion of the three parameters presented below determines
the treatment of choice as well as the prognosis.
55 Root development stage: Spontaneous pulp space
revascularization is considered unlikely in the case
of a replanted mature tooth (closed apex). In a
tooth with open apex, the likelihood of pulp space
Dentoalveolar Trauma of Children and Adolescents
a b
d e
..      Fig. 16.47 Extrusive luxation with delayed repositioning. a A
17-year-old girl presents 6 days after extrusive luxation of maxil-
lary permanent right central incisor, with crown fracture of this and
the left lateral incisor. There is significant occlusion interference. b
Radiograph shows that the teeth are mature (closed apex). The apical
socket space probably contains an organized clot. c, d The extruded
incisor is extracted and, after the blood clot is curetted away, is
revascularization and, consequently, of the root
continuing development is higher, particularly if
the root surface is treated with tetracyclines, such
as doxycycline or minocycline, prior to replantation
[92, 93].
55 Time the tooth remained out of the socket: The lon-
ger the tooth remains outside its socket, the higher
the likelihood of periodontal cell necrosis due to
desiccation. Consequently, the sooner replantation
takes place, the more favorable the results [94–98].
If the extra-alveolar dry time is less than about
15 minutes, periodontal tissues may well heal. If
the tooth remains outside its socket for more than
an hour, even in humid environment, healing is
impaired and any therapeutic intervention aims at
limiting the phenomenon of replacement resorp-
tion [95].
55 Tooth preservation medium: A preservation medium
may decelerate the destruction of periodontal cells
caused by dehydration.
–– An extra-alveolar dry environment (air) soon
causes necrosis of periodontal fibers resulting in
root resorption [95].
395 16
c
f
immediately replanted and splinted for 2 weeks. e Signs of pulp canal
obliteration on both teeth at the 8 months recall. f Reconstruction of
the crowns with composite resin at this stage, although this should
have been carried out earlier in order to cover the exposed dentin.
Follow-up continues in case of root canal treatment need and signs
of root resorption
–– Hank’s Balanced Salt Solution (HBSS) is an iso-
tonic solution with a neutral pH, which contains
ingredients necessary for cellular metabolism and
is suitable for cell culture [99].
–– Viaspan solution is used in medicine for preserv-
ing organs to be transplanted; therefore, it is ideal
for preserving teeth [100]. However, neither of
these two solutions are readily available.
–– Dentosafe® and Save-A-Tooth® are kits that con-
tain a medium for the preservation of avulsed teeth.
They are a cell culture medium that contains min-
eral salts, amino acids, vitamins, and glucose [101].
–– Milk is a good medium for PDL preservation and
is readily available. It has the appropriate osmotic
properties, neutral pH, and nutrients and no toxic
ingredients. Low-fat milk seems to be most suit-
able as compared to full fat and low temperature
possibly improves cell survival [101, 102].
–– Other media. Saliva is less suitable than milk,
because it is more hypotonic, but it is always read-
ily available. Saline solution is preferable to water,
which is the most hypotonic and causes quicker
cell lysis [103].
 396 C. Bourguignon et al.
Emergency Treatment of an Avulsed Tooth
Mature Teeth (Closed Apex)
The tooth has already been replanted The proper posi-
tion of the replanted tooth is verified clinically and radio-
graphically. The area is thoroughly rinsed and any gingival
lacerations are sutured. The tooth is cleaned and splinted
with a passive and flexible splint for 2 weeks. Even though
antimicrobial medication is sometimes prescribed (e.g.,
tetracyclines, for patients older than 8 years) to prevent
socket infection and inflammatory root resorption, there
is no strong evidence as of today to support systemic anti-
biotic use [24]. If the tooth has contacted soil, the child
should be referred to the pediatrician, unless anti-tetanus
coverage is documented.
Soft food is recommended for 10–14 days, brush-
ing with a soft toothbrush and local application of
chlorhexidine 0.1% 2 times a day for a week [24]. After
7–10 days, root canal treatment should start; Ca(OH)2
should be applied in the canal for at least 3–4 weeks
before the final gutta-percha filling. However, in cases of
teeth with signs of inflammatory resorption, Ca(OH)2
should be applied for at least 3 months [104]. This
approach reached success rates of 97% after an 8-month
period [105].
The tooth remained outside its socket up to 60 minutes in a
favorable medium (like milk, Hank’s, Viaspan, Dentosafe®
solution) The tooth is grasped by the crown while the
root and socket are rinsed with saline solution. The tooth
is repositioned into its socket with mild digital pressure;
its position is checked clinically and radiographically, and
then the tooth is splinted with a passive and flexible
splint. The same procedures as in the previous case are
followed [24].
Time outside the socket exceeds 60 minutes dry The likeli-
hood of successful periodontal healing is minimal and,
16 therefore, efforts are made to delay the onset of ankylosis
and root replacement resorption as long as possible [106].
The root is rinsed, and any soil residues or nonviable soft
tissue attached to the root surface is removed gently using
gauze; the socket is rinsed with saline solution [24]. It has
been suggested that the tooth is bathed in a 2% stannous
fluoride solution so as to delay resorption [107]. The
tooth is repositioned and the same procedures as in previ-
ous cases are followed. Root canal treatment may take
place extraorally before the replantation or 7–10 days
later [24].
Immature Teeth (Open Apex)
The tooth has already been replanted The procedure fol-
lowed is the same as for teeth with closed apex. Because
there is a possibility that the pulp space may become
revascularized, root canal treatment is not performed
until later, only if pulp necrosis gets confirmed
(. Fig. 16.48). An apexification procedure is then needed
(please look further down in this chapter).
The tooth remained outside the socket up to 60 minutes in a
favorable medium The process followed is the same as
for closed apices, with the administration of antimicrobial
preparations and root canal treatment performed as soon
as pulp necrosis is confirmed (. Fig. 16.49) [104].
Time outside the socket exceeds 60 minutes dry Prognosis is
poor, but replantation should still be done, not only for
mid-term esthetic, functional, and psychological pur-
poses but also for preserving the outline of the alveolar
bone, the ultimate aim being to facilitate bonded bridge
or implant placement later and improve soft tissue
esthetics. The final outcome is ankylosis and root resorp-
tion with possible tooth loss, although there have been
reports of cases, albeit exceptional, with a favorable out-
come.
zz Follow-up
Clinical and radiographic examinations are performed
4 weeks later, at 3 months, 6 months, and 1 year, with con-
tinuous annual follow-ups [24] (see also . Table 16.5).
16.3.3  ost-traumatic Complications of
P
Permanent Teeth
A range of complications may appear following trau-
matic injuries to permanent teeth. The most common
are pulp canal obliteration, pulp necrosis, and different
types of root resorption.
16.3.3.1 Pulp Canal Obliteration
Root canal obliteration, as in the case of primary teeth,
leads gradually to pulp chamber and root canal steno-
sis. It can be interpreted as a tentative healing and as
a defense mechanism. There are several ways by which
pulp space obliteration can occur. It is not fully under-
stood how cells are activated to drastically accelerate
intracanal calcified tissue production. The clinical result
of this phenomenon is reduction or complete loss of
tooth sensitivity and a shade change of the crown.
Eye Catcher
Obliterated teeth tend to become discolored, usually
toward yellow but sometimes toward brown-gray. If
endodontic treatment was necessary, intracoronal
bleaching may be performed on those teeth after root
canal filling and placement of a hermetic seal on top
of it (see 7 Chap. 14 and 7 Fig. 14.35). Otherwise,
external bleaching may be attempted (see 7 Chap. 17).
Dentoalveolar Trauma of Children and Adolescents
397 16

a b

c d e

..      Fig. 16.48 a Avulsion of 5 maxillary teeth in 6.5-year-old girl:
both permanent central incisors and 3 primary, left canine, and
both lateral incisors. Central incisors remained dry for 10 minutes
and then placed in milk for another 1 hour 40 minutes. Following
replantation, sutures to the attached gingiva (secured with a spot
of composite) held teeth in place for 1 week in the absence of adja-
cent teeth to splint with. b Radiograph immediately after replanta-
tion. c Radiographs at 14 months show that revascularization and
obliteration of the pulp space is occurring in the avulsed right central
incisor. d The teeth are asymptomatic with no sign of ankylosis. e
The 30-month radiograph shows complete obliteration of the right
central incisor’s pulp space. Meanwhile paucity of root development
and apical radiolucency of the left central incisor had dictated ini-
tiation of endodontic treatment. An apexification procedure using
Ca(OH)2 was selected

a b c d

e f g h

..      Fig. 16.49 a Avulsion of the maxillary permanent right central
incisor (dry for 10 minutes, in milk for another 40 minutes) and
partial extrusion of right lateral incisor with alveolar fracture and
lacerations to labial gingiva in an 8-year-old boy. b Avulsed incisor
rinsed with saline. c, d Replantation of avulsed central incisor and
repositioning of extruded lateral incisor, sutured gingiva and splint-
ing using passive orthodontic wire and composite resin. Exposed
dentin was protected with GIC and hygiene instructions given. e,
f Following the restoration of the crown fracture, after 12 weeks,
an apical radiolucency is observed on the right central incisor. g
After Ca(OH)2 filling followed by Portland cement apical plug (not
radiopaque), the remaining canal was filled with gutta-­percha. The
6-month radiograph shows apical healing while the extruded lateral
incisor shows root canal obliteration. h At 2 years, infraocclusion is
the result of ankylosis of the avulsed tooth
 398 C. Bourguignon et al.
..      Table 16.5 Follow-up table for avulsion injuries of permanent teeth, according to IADT Guidelines 2020 [21]
2w 4w
Avulsion c+r +s c+r
aFor at least 5 years
c+r: clinical and radiographic examination
s: splint removal
Despite radiographically appearing full root canal oblit-
eration, a minimal canal space might exist, depending
on how the obliteration evolved. Pulp space oblitera-
tions are most often observed in cases of immature teeth
(with open apices), which suffered extrusion traumas or
lateral luxation and intrusion, thus raising suspicions
that the disorder may be related to pulp space revascular-
ization mechanisms [108]. Only in 8–13% of such cases
was pulp necrosis observed, and periapical inflamma-
tion appeared 5–20 years after the injury, which brings
the 20-year pulp survival estimation to 84% [105, 109,
110]. Endodontic treatment is usually feasible even in
such necrotic cases, albeit with some difficulty, because
the root canal remains accessible and prognosis is good
[111]. However, the calcified tissue may form from a
coronal to apical direction without leaving a canal space
as we usually know it. Or the pulp space might get colo-
nized by an osteoid or cementoid type of calcified tis-
sue (. Fig. 16.48) originating from the periradicular
tissues, in which cases there is no presence of a “canal”
structure. That’s why, before intervening endodontically
on those teeth, a careful preoperative investigation must
be made by comparing previous periapical radiographs
to understand how the obliteration developed. Addi-
tionally, a preoperative cone beam tomographic exami-
16 nation (CBCT) is recommended (. Fig. 16.50). The use
of the operative microscope is helpful to find and treat
infected obliterated canals. Referral to a trained endo-
dontist is advised.
16.3.3.2 Pulp Necrosis
Pulp necrosis is the most common post-traumatic
complication. It often occurs in cases of displacement
(luxation) injuries, where pulp neurovascular supply
has usually been severed [51]. It occurs less often in
teeth with open apices, because small displacements of
those teeth do not necessarily lead to apical blood ves-
sel rupture; even if rupture does occur, a young pulp
has a higher potential for healing. Pulp necrosis usu-
ally appears in the first 3 months after the injury; how-
ever, in some cases, it might take up to 2 years for it to
be confirmed. Diagnosis is based on symptom assess-
ment; clinical examination, including palpation, percus-
sion, sensibility testing, and evaluation of tooth color
3m 6m 1y Annuallya
c+r c+r c+r c+r
changes; and radiographic findings such as presence of
radiolucencies and signs or root and/or bone resorption.
Laser Doppler flowmetry and oximetry are promising
technologies that have been shown to allow reading of
pulp status or pulp space revascularization status in a
matter of few weeks [112–114].
Change of tooth color Even relatively mild trauma such
as concussion and subluxation may lead to blood supply
rupture or disruption at the apical foramen. Intrapulpal
hemorrhage can cause the crown to become slightly pink.
If the blood supply recovers, which means that the pulp
preserves its vitality, normal tooth color is self-restored. If
the tooth crown gradually turns gray – several weeks or
even months after the injury – then suspicion of necrosis
is raised, since this discoloration likely indicates necrotic
pulp tissue decomposition [115].
Pulp sensibility testing Most permanent teeth that have
suffered loosening (subluxation) or displacement (luxa-
tion) do not initially respond to cold or electrometric
vitality testing; yet, several regain their sensitivity later,
within 2–3 months. However, there have been cases, when
it was up to 2 years before teeth regained their normal
reaction. Besides, young patients and immature teeth
seem to respond in an unreliable fashion to pulp sensitiv-
ity testing [116]. Therefore, a negative response to cold or
to electric sensibility test per se is not sufficient, and root
canal treatment should be postponed until at least one
more clinical or radiographic indication of pulp necrosis
arises. Last but not least, sometimes the nerve fibers seem
to be the last ones to die, possibly giving false-positive
responses to testing [117]. For all these reasons, pulp sen-
sitivity interpretation can be seen as a “challenging art.”
Radiographic signs of pulp necrosis Radiographic tech-
nique should be reproducible, so that, as time passes,
images may be compared to each other. Radiographs to
help diagnose pulp necrosis should only be taken at a
point in time when pathologic findings are expected to be
present. This may be 3 weeks after the injury, although it
often takes quite a few months before an apical radiolu-
cency becomes visible in the radiograph [24]. In teeth with
open apices, necrosis of Hertwig’s epithelial root sheath
Dentoalveolar Trauma of Children and Adolescents
a b
..      Fig. 16.50 Pulp canal obliteration. Maxillary permanent right
central incisor of a 28-year-old female had suffered a severe luxa-
tion injury while she was a child. a Periapical radiograph showing
means that apex development is inhibited. Signs of root
resorption and root development interruption of imma-
ture teeth are also indicators of possible pulp necrosis.
16.3.3.3 Root Resorption
A tooth displacement (luxation) trauma often results in
some form of root resorption [118].
Partial surface resorption In such cases, small cavities
appear on the root surface, covered by periodontal mem-
brane; these can be confirmed with 3D radiographic tech-
niques (cone beam computer tomography, CBCT) [119].
This form of resorption is transient and self-limiting and
appears frequently after mild luxation injuries. No treat-
ment is required if the pulp is vital.
Replacement resorption (ankylosis) This is a serious
complication, mainly associated with intrusion or delayed
replantation of an avulsed tooth. It is related to severe and
extensive destruction of the cementum and periodontal
ligament, resulting in fusion (ankylosis) of the alveolar
bone with dentin. Clastic cells then resorb the root, which
is gradually replaced by bone. A characteristic metal
sound is produced on percussion, and the tooth is deprived
of physiological mobility. Radiographically, areas of peri-
odontal ligament space have disappeared. Within a few
years, full resorption may be seen with complete root
replacement by bone (. Fig. 16.51). In young patients,
the affected tooth tends to become infraoccluded as both
growth of the alveolar process and eruption of adjacent
teeth continue. Decoronation has been suggested as a
temporary measure to maintain alveolar ridge dimen-
sions [120, 121] (. Fig. 16.52). If replacement root
resorption evolves slowly, buccal, lingual, and vertical
bone dimensions will be better preserved for longer, and
this facilitates implant placement later. Implants should
be placed as late as possible since alveolar bone growth
has been shown in patients aged 35–45 years old, indicat-
399 16
c
absence of a visible canal. b, c Cone beam examination (CBCT)
shows no trace of a visible canal. The tooth is asymptomatic with no
signs of pathology. No treatment other than follow-ups is necessary
a b
..      Fig. 16.51 Replacement resorption. Maxillary permanent right
central incisor was avulsed and replanted when patient was 9 years
old. a 6-month post-injury. There is an ankylotic sound to the per-
cussion test and radiographically there are signs of replacement
resorption (arrow). b At 18 months replacement resorption is clearly
visible: the periodontal ligament space has almost completely disap-
peared all around the right central incisor root; the bone is in direct
contact with the root dentin; the root is getting gradually replaced by
bone. In this case, the pulp seems to have remained vital
ing it is continuous throughout life [122–125]. Ankylosis
clearly complicates full mouth orthodontic planning as
well as future prosthetic or implant treatments.
Inflammatory root resorption As in replacement root
resorption, this type of resorption is related to severe and
extensive damage to the cementum and periodontal liga-
ment, the root protective layers. But it’s also related to
associated pulp necrosis and infection. Bacterial by-­
products and endotoxins from the infected pulp travel
through the dentinal tubules toward the root surface. In
areas deprived of cemental and precemental layers, they
act as stimuli for the body’s defense mechanisms. An
intense odontoclastic activity results on the root surface,
 400 C. Bourguignon et al.
a b c f
d e
..      Fig. 16.52 Replacement resorption and decoronation. Maxillary
permanent right central incisor was avulsed, replanted, and splinted.
The extra-alveolar time was 3 hours dry. a Radiographic view imme-
diately after replantation and splinting. b–d Ankylosis evolution at
4 weeks, 15 months, and 30 months. e The avulsed incisor became
severely infrapositioned due to ankylosis. f Clinical view of the
which is responsible for the resorption. In children aged
6–10 years, this type of resorption tends to be extremely
aggressive, causing sometimes tooth loss in a matter of a
few weeks. This happens, because at this age, dentinal
tubules are wide and the distance from the pulp canal to
the root surface is small [126, 127].
Radiographically, inflammatory root resorptions
may appear initially as if the periodontal ligament
space is wider and irregular on both the alveolar bone
16 and on the root side. Subsequently, distinctive radio-
lucent lesions will form on the root surface and in the
adjacent bone. The first signs of inflammatory root
resorption (most commonly located in the cervical
1/3rd of the root) can be apparent radiographically as
early as 2 weeks after the injury, especially in young
teeth [128].
If diagnosed early, inflammatory root resorption can
be successfully treated. The key to successful treatment
is to completely disinfect the root canal space. Calcium
hydroxide intracanal medication has been shown to be
beneficial to treat inflammatory root resorption, and its
use is recommended [21, 24, 105] (. Fig. 16.53). Once
the canal space is disinfected, radiolucencies around the
root should disappear, and the periodontal ligament
width may return to normalcy and follow the new con-
tours of the root surface. Final filling of the canal with
gutta-percha and sealer ensues.
g h
decoronation surgery. g Radiographic view immediately after dec-
oronation. h Radiographic view 13 months post-­decoronation. Note
the bone formation coronally to the resorbing root. The presence of
the decoronated root helps to delay bone volume loss and maintain
alveolar ridge dimensions
Cervical root resorption These resorptions are usually
late complications of dental trauma, so they will not be
fully discussed in the scope of this chapter. In short words,
cervical resorptions tend to appear below the epithelial
attachment of the tooth and are inflammatory in nature.
It has been assumed that the presence of sulcular bacteria
is responsible for the maintenance of the lesion once it has
formed [129]. They occur equally in vital and in non-vital
teeth.
Radiographic evaluation will reveal a radiolucent
area in the cervical area of the tooth adjacent to the
crestal bone (. Fig. 16.54). The lesion seems to have
the tendency to develop confined in dentin, in an apical/
incisal direction along the pre-cementum and the pre-
dentin, but without perforating those protective layers
and without penetrating into the pulp canal space or
into the PDL space [130–133]. Their management can
be complex, particularly if diagnosed late, where either
the involved tooth ends up with a periodontal pocket or
needs to be extracted.
Internal resorption This is a rare post-traumatic com-
plication likely caused by chronic pulp inflammation. It
appears without any clinical symptoms and is usually
diagnosed radiographically years after the injury. If the
tooth involved is treated early, before the resorption
extends and causes root perforation, root canal treat-
Dentoalveolar Trauma of Children and Adolescents
401 16

a b c d e

..      Fig. 16.53 Inflammatory root resorption. Accident of an
11-year-­ old female caused avulsion of maxillary permanent left
central incisor, which was replanted several hours after the injury. a
Diagnostic radiograph 1 year after the injury. There is a radiolucent
zone in the bone all around the root. Radiolucent “holes” on the root
and on the adjacent bone are also visible. Diagnosis of inflammatory
resorption is made. b Endodontic treatment with calcium hydroxide
is started and the canal space “disappears.” c After 5 months, the
radiolucent zones around the root have subsided; there is calcified
tissue apposition on the root resorption lacunas; normal periodon-
tal ligament width is reestablished. These signs are positive as they
indicate that healing is in progress and that the resorption process
has likely stopped. d The root canal is filled and the access cavity
is restored. e 2 year follow-up. The tooth is fine but still has to be
frequently monitored, especially that orthodontic treatment was
deemed necessary

ment may be successful to stop the resorption

(. Fig. 16.55).

16.3.4  ollow-Ups of Injured Permanent

F
Teeth
All traumatized teeth should be carefully reevaluated
periodically after an injury, irrespective of its apparent
severity. . Tables 16.3, 16.4, and 16.5 show the IADT’s
recommendations for a recall schedule after each type
of injury [21, 24].

16.3.5 Endodontic Evaluation

and Management of Injured
Permanent Teeth
16.3.5.1  ulp Status Evaluation and Diagnosis
P present. Resorption of the cervical type is visible disto-cervically. In
Following Trauma
It is important to remember that a tooth can sustain
multiple injuries at the same time. This does impact the
outcome. For example, a luxation injury can occur in
combination with an uncomplicated crown fracture [52,
53, 134, 135]. After emergency treatment, a close follow-
­up is essential to ensure that that the pulp has survived.
If guidelines are followed, more favorable outcomes can
be expected when compared to cases treated without
..      Fig. 16.54 Cervical resorption. Radiograph of tooth # 11,
6 years after trauma of a 15-year-old male. Root development
stopped; an apical radiolucency indicative of pulp space infection is
this case, endodontic treatment should be carried out first, prior to
managing the resorption per se
compliance to the guidelines [136]. At every evalua-
tion, a radiograph needs to be taken as well as all clini-
cal signs and symptoms associated with pulp necrosis
explored. The pulp might remain unresponsive to sen-
sibility testing for several months; however, if no other
signs are evident, it is advisable to do no treatment but
rather schedule recalls, especially if the patient’s tooth is
 402 C. Bourguignon et al.
a b
..      Fig. 16.55 Internal resorption. a The coronal part of the canal is
obliterated. The arrow points at mid-root where the internal resorp-
tion is located. b After endodontic treatment and root filling. End-
odontic treatment was necessary to stop the internal resorption process
immature. Additional signs to look for are color changes
of the crown, the width of the periodontal ligament,
periapical lesions, and other signs of infection, like fis-
tula, tissue swelling, and/or pain [80, 110, 137, 138]. If
in doubt about the pulp status diagnosis, a timely refer-
ral to a specialist is strongly recommended, because root
resorption associated with necrotic and infected pulp
space can cause quite a rapid and irreversible loss of
root structure in a matter of weeks.
16.3.5.2  eeping the Pulp Alive and Favoring
K appointment, if so indicated [21, 24].
Spontaneous Pulp Space
Revascularization
As mentioned previously in this chapter, one of the main
16 goals of post-traumatic management is the maintenance
of pulp space vitality. For instance: if proper emergency
treatment is provided to crown-fractured teeth, whether
with or without pulp exposure, the pulp has high chances
of remaining vital; because of the larger vascular supply
and larger apical opening in immature teeth, pulpal sur-
vival or spontaneous pulp space revascularization is a pos-
sibility subsequent to severe luxation injuries [118, 139].
It is a desirable mode of healing. However, while waiting
for this revascularization, the tooth has to be monitored
against the risk of pulp necrosis, infection, and root resorp-
tion, which can severely compromise the tooth.
16.3.5.3 Endodontic Treatment of Necrotic
Teeth
Signs and symptoms of pulp necrosis and infection are
as follows: pain, swelling or discomfort, fistula, exces-
sive mobility, sensitivity to palpation and percussion,
periapical radiolucency, color changes, persistent unre-
sponsiveness to sensitivity testing, or nondevelopment
of the root. Once the pulp has been diagnosed with
certainty as necrotic, endodontic treatment should be
instituted as soon as possible. The endodontic approach
will be dictated by the stage of root development, type
of injury, and time elapsed since the traumatic episode.
Treatment often involves an apexification procedure (see
further down in this chapter). All types of endodontic
treatment should always be carried out with rubber dam
isolation. It is not advisable to clamp the traumatized
tooth but rather rely on clamping adjacent teeth or on
using widgets or dental floss.
1. Endodontic Treatment of Necrotic Mature (closed
apex) Teeth
In decreasing order, the most severe injuries to
the PDL and pulp are intrusion and avulsion, lateral
luxation, extrusion, subluxation, and concussion.
When there is little or no chance of pulp survival
in mature teeth, endodontic therapy should be ini-
tiated between 7 and 10 days post-trauma in order
to prevent the necrotic pulp from becoming infected
[21, 24]. Endodontic treatment should not be started
at the emergency visit for two reasons. Firstly, addi-
tional manipulation of the tooth soon after the
injury could further traumatize the periodontal liga-
ment [24, 140, 141]. Secondly, too early application
of calcium hydroxide can have a detrimental effect
on periodontal ligament healing [140–142].
Since a luxated or avulsed tooth may still be
mobile 7–10 days after trauma, it is advised to start
the endodontic treatment while the tooth is still
splinted. The splint can be removed at the end of the
Currently, the most widely accepted intracanal
medicament is calcium hydroxide [Ca(OH)2] paste,
either in premixed form or by mixing powder with
sterile water or anesthetic solution [143–147]. It has
been shown that if Ca(OH)2 is placed for 2 weeks
into the root canal of a traumatized tooth prior to
it becoming infected (i.e., within about a fortnight),
the treatment outcome is favorable [104, 148]. If end-
odontic treatment is started later and an established
infection exists prior to the placement of Ca(OH)2, it
is recommended that the Ca(OH)2 remains in place
for several months prior to the final root canal obtu-
ration. This is to reduce the risk of inflammatory
root resorption [104].
2. Endodontic treatment of necrotic immature (open
apex) teeth
As the pulp of immature teeth is needed for root
development, it is of good clinical practice to moni-
tor its status and consider the pulp as vital until there
is clear evidence showing the contrary (at least two
signs and symptoms indicating pulp necrosis and
Dentoalveolar Trauma of Children and Adolescents
infection). Only when a pulp is definitely diagnosed
as necrotic should endodontic treatment be initiated.
Several approaches exist: classical apexification, api-
cal plug apexification or the so-called Regendo, or
pulp space “revascularization” procedures.
a. Classical apexification
The classical apexification is a procedure where
the root canal of an open apex tooth is cleaned
and filled repeatedly with calcium hydroxide
[Ca(OH)2] dressings to stimulate the formation of
a natural hard tissue barrier at the apical portion
of the root. After this biological calcified barrier
has formed, it is possible to obturate the canal
system without or with decreased risk of over
extending the root filling material [149, 150].
It is a prerequisite to disinfect the canal space
to create a suitable environment for stimulating
apical barrier formation. Disinfection is achieved
by thorough, but gentle, irrigation with sodium
hypochlorite and by placing a relatively thin
mixture (less than tooth paste thick) of calcium
hydroxide powder mixed with anesthetic solution
or saline solution. It is not recommended to use
barium sulfate in the mixture because it prevents
assessment of the calcium hydroxide placement
in the canal space. The mixture is spun into the
canal space. After 3 weeks, the patient is recalled,
and the thin mixture irrigated out. At this time, a
thick, almost dry, mixture of calcium hydroxide
and sterile solution is packed to the full length of
the tooth using pluggers or inverted gutta-­percha
cones to seat it to the full length of the root. Once
a radiograph indicates that the intracanal mix-
ture is as dense as dentine all the way to the apex
(. Fig. 16.56), a temporary restoration such as
IRM® should be placed in the access cavity.
The patient should then be recalled every
3 months and the density of the mixture evalu-
ated radiographically. Currently, it is not recom-
mended to replace the mixture if it appears to be
intact at these recall appointments [24]. The time
required to achieve the apical barrier formation
varies between 6 and 24 months with an average
of 1 year +/− 7 months [151]. Once the presence
of the barrier has been confirmed both radio-
graphically and clinically, the final root canal
obturation can be done (. Fig. 16.57).
b. Apical plug apexification
In the last 20 years, the use of mineral trioxide
aggregate (MTA™, Dentsply, Tulsa, OK, USA)
as an artificial apical plug has gained popularity
in order to allow root canal obturation sooner
than with the classical approach [152]. However,
it is important to note that MTA™ has minimal
bactericidal effect on several bacterial species
403 16
[153, 154]. Additionally, but only after its wide-
spread use during many years, it was observed
that MTA™ causes tooth discoloration. New bio-
ceramic materials such as Biodentine® or Total
Fill® have been suggested recently to replace
MTA. As of today, there is neither enough data
yet regarding outcome when these materials are
used nor regarding the possibility that they may
cause late discolorations.
Given that bacteria are the single most impor-
tant factor to maintain inflammatory root resorp-
tion, it is strongly advised to follow a two- to
three-step apexification procedure when the canal
space is likely infected. The protocol is to disin-
fect and medicate the canal for 7–14 days with a
thin calcium hydroxide paste. Secondly, an arti-
ficial apical barrier is created by compacting the
chosen apical plug material into the apical area
(. Fig. 16.58). When MTA was used as the plug
material, a wet cotton pellet needed to be placed
in the canal for at least about 4 hours, so that the
MTA could set. An extra treatment session was
thus required.
CollaCote™ or calcium sulfate can be placed
apically beforehand to help preventing extrusion
of the material in the apical area. The rest of the
canal is then obturated. It is delicate to place the
apical plug material correctly at the apex. An
operating microscope is needed, as magnification
and good lighting are essential.
c. Pulp space revascularization of necrotic infected
teeth (Revitalization or ‘Regenerative’ endodon-
tics)
a b
Ca(OH)2 packing Ca(OH)2 washout
..      Fig. 16.56 Calcium hydroxide placement and washout. Necrotic
maxillary permanent right central incisor is very immature, and cal-
cium hydroxide apexification is carried out. a Radiograph immedi-
ately after a dense packing of (barium sulfate free) pure Ca(OH)2
mixed with anesthetic solution or saline is placed in the whole canal
length until the apex. Note that the canal “disappears” and takes
the radiopacity of dentin. b After 3 months, some Ca(OH)2 washed
out, and the wide diameter of the canal becomes visible again. If the
apical barrier has not formed yet, a new dense Ca(OH)2 is placed
again in the canal for 3 months. The final root canal obturation is
performed when the natural apical calcified barrier has formed
 404 C. Bourguignon et al.
a b c d
9m
..      Fig. 16.57 Calcium hydroxide apexification. a Pre-op radiograph
of very immature maxillary permanent right central incisor with a
wide-open apex and very thin root walls. Endodontic treatment had
been started by another dentist. The canal is gently but thoroughly
cleaned, irrigated, disinfected, and packed with Ca(OH)2. b, c After
..      Fig. 16.58 Artificial apical plug apexification with MTA. The
material is placed apically, a wet cotton pellet is placed next to it,
16 and the remaining root canal is obturated in a later treatment session
Until recently, it was thought that there was
no possibility to promote regrowth of vital tissue
into infected root canal spaces of teeth with open
apexes [155–157]. Now it has been realized that
under certain conditions, it is possible not only
to heal periapical lesions associated with necrotic
and immature teeth but also more interestingly
to stimulate tissue growth inside the canal space
of these teeth [158, 159]. This is accomplished by
reducing the bacterial load, first by thorough irri-
gation and then by intracanal placement of either
a dual or triple mix of antibiotics (metronida-
zole, ciprofloxacin, and possibly minocycline) or
alternatively a Ca(OH)2 dressing for a few weeks
[160–163]. Minocycline is not used anymore in
the antibiotic mixtures because it causes tooth
e
9m obtur 4 years
9 months of Ca(OH)2 protocol, an apical barrier has formed and is
clearly visible. d Trial with a gutta-percha cone to check the apical
stop. Full canal obturation is then performed. e At 4-year follow-­up.
The tooth is asymptomatic and stable
discolorations. The key to success is to be able
to disinfect the canal space and then to create a
scaffolding for the ingrowing tissue [164]. Several
teams worldwide are working on developing syn-
thetic scaffolds to be placed within the canals.
Presently, the scaffolding is created by allowing
a blood clot to form at the second appointment,
after the disinfecting paste has been washed out
by irrigation. An endodontic instrument is then
placed through the apex into the periapical tis-
sues to induce bleeding within the root canal.
Once a clot has started to organize itself, a double
seal is placed in the access cavity, down close to
the cervical area. Using a bioceramic material is
recommended to cap the blood clot, and then a
traditional restoration is placed on top [162]. The
success rate of this procedure, where the root
end continues to grow and/or mature, is reported
between 27% and 55% and the survival rate of the
teeth much higher [165–167]. If the tooth does not
respond to treatment, then the traditional apexifi-
cation procedure is still an option. It is important
to remember that the response to this revascular-
ization procedure can take months if not years to
materialize [167]. Also, the vital tissue obtained
so far, at least in animals, is rarely an authentic
pulp tissue [92, 168]. That’s why the present pro-
cedures should rather be called “revitalization”
than “regenerative” procedures (. Fig. 16.59).
Post-endodontic considerations for immature
traumatized teeth
Non-vital immature teeth have thin roots with
weak dentine walls and are especially at risk of
root fracture at the neck of the tooth [105, 150,
169]. The cervical area of the tooth may be rein-
forced using etched and bonded composite resin,
allowing space, if indicated, for a post [170, 171].
If little coronal tooth structure remains, a fiber
Dentoalveolar Trauma of Children and Adolescents
a b
..      Fig. 16.59 “Revitalization” of necrotic and infected immature
tooth. a Pre-op radiograph. The incisor is very immature. b Aspect
after the main treatment steps irrigation, disinfection of the canal
with a dual antibiotic paste for 3 weeks, creation of bleeding to fill
post may be bonded into the root canal. Metallic
posts should be avoided. Compared to metal posts,
fiber posts have the advantage of some flexibility.
If they fail, they are more likely to become de-
cemented rather than cause a root fracture [172].
3. Endodontic treatment in the presence of inflammatory
root resorption
As seen earlier in this chapter, calcium hydrox-
ide as an intracanal medication has proven to be an
effective method to halt the progression of external
inflammatory root resorption (. Fig. 16.53) espe-
cially if detected early [104, 173]. Ca(OH)2 paste
should be used in a thick, almost dry consistency. It
should be renewed at 3 weeks and every 3 months
because it may wash out. Treatment should be con-
tinued until all signs of inflammatory root resorption
have healed and until a normal periodontal ligament
width has reestablished. This can take anywhere
from 6 to 24 months. The access of the tooth should
be temporized with an appropriate restorative mate-
rial such as IRM™ as it is of upmost importance to
keep bacteria away of the canal space.
16.4 Prognosis of Injured Teeth
Injured mature and immature teeth treated in an appro-
priate and timely fashion have a good chance of sur-
vival, up to 20 years or more and even if the injury was
405 16
c
the canal space, and placement of a hermetic access cavity restora-
tion. c At 4-year follow-up. Some “revitalization” of the pulp canal
space has occurred, with calcified tissue formation in some areas
severe (i.e., in cases of avulsions and intrusions). Several
older studies show this [94, 118, 174], and the current
knowledge about factors affecting the survival of these
teeth has considerably improved in recent years [85, 88].
In particular, teeth treated in compliance with today’s
IADT’s Guidelines seem to have an even better chance
of survival than those treated years ago [136, 175]. If
proper emergency management is provided, as well
as later treatment as deemed necessary on follow-ups
(such as timely endodontic treatment), the prognosis of
injured teeth turns out to be very good.
In the case of avulsed teeth, for instance, the most
important factor affecting prognosis, apart from extra-
oral dry time and timely endodontic treatment, has
been reported to be the stage of root development. A
better survival rate was observed for mature teeth [98].
Certainly, as seen earlier in this chapter, endodontic
treatment of immature teeth is quite challenging when
compared to mature teeth, but the main reason why
their survival rate is reduced is their thin and fragile den-
tinal walls. Immature teeth tend to fracture easily even
to minor impacts occurring repeatedly in everyday life,
especially if they developed areas of resorption located
cervically [105]. That’s why attempts should be made to
prevent those resorptions. Some years ago, the long-­term
use of calcium hydroxide has been blamed as a causative
factor for immature teeth fractures. The study design of
these in in vitro studies was far from ideal though [169].
It’s worth noting that calcium hydroxide apexification
 406 C. Bourguignon et al.
has been successfully used (97%) for decades in the treat-
ment of injured teeth [105, 176].
In situations where the prognosis of an injured tooth
is deemed dark due to developing ankylosis in a grow-
ing child, or due to high risk of tooth fracture (related
to fragile dentinal walls or loss of tooth structure due
to the presence of resorption areas), it’s advisable to
check if the patient will need premolar extraction for
orthodontic reasons. In the affirmative, one should
consider the possibility of extracting the problematic
traumatized incisor, rather than the healthy premolar.
Autotransplantation of a premolar to replace the incisor
might be a possibility. Proper overall treatment planning
and coordination between different dental specialties is
then needed (. Fig. 16.60) [177].
16.5 Orthodontic Management
of the Traumatized Dentition
The particular orthodontic management of intruded
teeth, crown-root fractured, and ankylosed teeth is pre-
sented in this chapter within the specific injury types.
Orthodontic treatment is so common nowadays, that it
often involves movement of anterior teeth with a history
of trauma. Before any treatment is initiated, the ortho-
dontist needs to inquire with the patient and his parents
if any dental injury occurred, both recently and in the
past. Additionally, full mouth periapical radiographs
should be taken, not only a panoramic radiograph, in
order to make a thorough preoperative evaluation. The
orthodontist also needs to take into consideration the
impact of orthodontic treatment on long-term progno-
sis of such traumatized teeth [178]. Orthodontic treat-
ment should always be interpreted as an added trauma
to the teeth. Therefore, orthodontic forces should be
light and short-acting and aimed at limited goals when
16 moving previously injured teeth.
Depending on the severity of trauma, it’s wise to wait
before initiating orthodontic treatment. In the case of
a b
..      Fig. 16.60 Autotransplantation of a premolar. a These avulsed
and replanted maxillary central incisors were undergoing severe
replacement root resorption at follow-ups. It was decided to use the
patient’s premolars to substitute them. b Clinical view 2 weeks after
autotransplantation of the immature second maxillary premolars
and their splinting in the position of the extracted compromised
mild luxation injuries, such as concussion and sublux-
ation, a 3-month observation time should be sufficient.
In moderate to severe injuries, such as extrusion, intru-
sion, lateral luxation, and replantation of avulsed teeth,
a minimum of 6 months to 1 year is advised. In root-frac-
tured teeth, the recommended observation time is 1 year.
In crown-fractured teeth, when the dentist is certain that
no associated luxation injury occurred at the time of
trauma, a 3-month observation time is still advised [179].
Eye Catcher
Traumatized teeth presenting root resorption before
orthodontic treatment are at high risk of further
resorption as a result of intense orthodontic force
application [180]. Thus, no orthodontic treatment
should be initiated on teeth presenting apical or lat-
eral radiolucencies or signs of root resorption. The
related pathologies should be treated first, usually
with endodontic treatment. Only when healing is
observed, orthodontic forces may begin to be applied
but under careful and frequent clinical and radio-
graphic monitoring every 3 months. Parents should
be informed about possible contingencies happening
during or after treatment of injured teeth, as compli-
cations may occur. Sometimes a treatment paucity or
even total orthodontic treatment interruption is nec-
essary for those teeth.
From a preventive perspective, increased overjet with
protrusion of maxillary incisors is a common pre-
disposing factor for dental injuries in the permanent
dentition. It has been reported that an increase from
0–3 mm to 3–6 mm leads to twice as many trauma rates,
while if protrusion exceeds 6 mm, incidence triples [14]
(. Fig. 16.9). Insufficient lip coverage seems to play a
role as well. Preventive consultation with an orthodon-
tist is thus advisable for these patients.
c d e
incisors. c Radiographic view of the premolars 2 weeks after the
operation and after the splint had been removed. d One-year fol-
low-­up radiographic examination showing sound progress in apical
development. e Reshaping of the premolars into incisor crowns by
palatal grinding and composite reconstruction after the end of orth-
odontic treatment. (Courtesy of Dr. Μ. Duggal)
Dentoalveolar Trauma of Children and Adolescents
16.6 Prevention of Dentoalveolar Trauma
Accidents, including road accidents, are a major threat
against the physical integrity and life of children. They
are the top death cause during the first year of life and a
major cause for hospital care and disability in industri-
ally developed countries.
Facial and dental trauma is due to various causes,
many of which cannot be easily prevented. They hap-
pen more often during children’s leisure time and dur-
ing play [11, 13]. In preschool years, and particularly in
early infancy, when balance in movement and percep-
tion of danger are limited, there should be no obstacles
on the ground, no stairs, furniture, or other hard objects
with sharp angles in areas within which children move.
Furthermore, athletic activities among children and ado-
lescents have significantly expanded in recent years, par-
ticularly related to body contact sports. Injuries occurring
during high speed and impact force sports, such as on ice
or snow, result in more facial or skull trauma, which may
be life-threatening, and require protective equipment, such
as a helmet. Lower speed and impact force sports (e.g.,
basketball) result in dental trauma. Injuries in sports are
more frequent than those due to fights or road accidents
[181]. The need for educating children, parents, teachers,
coaches, and owners of recreational venues in prevention
and first-aid management of injuries is self-evident.
In the permanent dentition, patients having pro-
clined incisors with increased overjet and insufficient lip
coverage tend to suffer more dental injuries. A preven-
tive consultation with an orthodontist is thus advisable
for these patients.
..      Table 16.6 Advantages and disadvantages of the three basic types of mouth-guards based on Bourguignon and Sigurdsson [184]
Advantages
Type I +Very low cost
+Immediate placement
Type II +Relatively low cost
+Better protection than Type I
+Possibility of Refit
+ Immediate placement
Type III + Good fit and stay in place
+ Sound retention
+They cover the entire dentition
+Less discomfort for breathing/speech
+More acceptable to athletes
+Choice of thickness
407 16
16.6.1 Mouth-guards
A dentist does not only provide treatment but can also
assist in preventing trauma consequences by fabricating a
mouth-guard. This is a sturdy functional device that pro-
tects against dental, periodontal, and supporting alveolar
bone trauma. Depending on the sport and the level of
involvement in it (professional, amateur), the appropriate
type of mouth-guard should be used. A study investigat-
ing amateur athletes among newly recruited soldiers in the
army, who were issued with free-­of-­charge type II mouth-
guards, showed that, although very few of them wore the
device, users suffered milder dental trauma [182].
A mouth-guard has to meet numerous requirements:
It should be resilient, comfortable, odorless, affordable,
retentive, and properly fitting; its borders should be
smooth and even, it should have the necessary thick-
ness at critical regions, it should not prevent speech or
breathing, it should not be cumbersome, and it should be
easy to fabricate [183]. No type of mouth-guard fulfils all
these requirements, and every type has its own pros and
cons. In general, disadvantages have to do with difficul-
ties caused to speech or breathing, with the effect on an
athlete’s appearance, with the difficulty of their adapt-
ability to various individuals, their volume, and their
cost. The use of commercial mouth-guards prevents
intense voluntary exhaling but has no negative conse-
quences on pulmonary ventilation during the athlete’s
training.
There are three types of mouth-guards. Their advan-
tages and disadvantages are presented in . Table 16.6
[184].
Disadvantages
−Limited size numbers (small, medium, and large)
−reduced fit
−Lack of retention
−Continuous occlusion/bite necessary
−Obstruct athlete’s speech/breathing
−No absolute fit
(better than type I)
−Lack of retention,
−Continuous occlusion/bite necessary
−They are more cumbersome
−They loosen easily with use
−High cost
−Increased fabrication time
 408 C. Bourguignon et al.
55 Type I: Various, commercially available, prefabri-
cated mouth-guards which cannot be adjusted to a
specific individual, one or two sizes that are intended
to fit most. Some have a “spring” fit and do cover
both arches others require the athlete to clench to
keep the mouth-guard in place. (. Fig. 16.61).
55 Type II: These are fabricated from a thermoplastic
material. They are heat adapted to the teeth, albeit
not ideal, by the athlete and can provide satisfactory
protection. The right size of mouth-guard is selected
and rendered relatively pliable, following the manu-
facturer’s instructions (by submerging it into very
16
..      Fig. 16.61 Type I – Prefabricated mouth-guards. (With permis-
sion [184])
a b
..      Fig. 16.62 Type II – Heat-adapted mouth-guards. (With permission [184])
hot water). The mouth-guard is then transferred to
the mouth, where it is adjusted and fitted while cool-
ing (. Fig. 16.62).
55 Type III: One layer or multilayer custom-made
mouth-guards, fabricated by a dentist. They allow
any type of adaptation during their fabrication, tak-
ing into consideration regions of chronic trauma,
dental-mandibular problems and the type of sport.
An athlete can enjoy free flow of air during strenu-
ous exercise, while teeth and mandible are protected.
This type is ideal for athletes undergoing orthodon-
tic treatment with fixed devices on both jaws
(. Fig. 16.63).
One of the most common materials for mouth-guard
fabrication nowadays is ethylene-vinyl acetate (EVA).
Mouth-guards can be fabricated using different devices
and in various colors; this may also be useful, for exam-
ple, in water polo sports, where, if lost, the mouth-­guards
..      Fig. 16.63 Type III – Custom-made mouth-guards require an
impression. (With permission [184])
c d
Dentoalveolar Trauma of Children and Adolescents
are easily visible at the bottom of the pool. Sound and
hygienic maintenance is ensured by keeping the guards
in a special case, by avoiding very hot water when clean-
ing them and by placing them, every so often, in an anti-
septic solution. Furthermore, such guards should not be
exposed to the sun or high temperatures to avoid warp-
ing [185].
References
1. Andreasen JO, Andreasen FM. Essentials of traumatic injuries
to the teeth: a step-by-step treatment guide. 3rd ed. Copenhagen:
Munksgaard; 2008.
2. Andreasen JO, Ravn JJ. Epidemiology of traumatic dental inju-
ries to primary and permanent teeth in a Danish population
sample. Int J Oral Surg. 1972;1:235–9.
3. Sennhenn-Kirchner S, Jacobs HG. Traumatic injuries to the pri-
mary dentition and effects on the permanent successors - a clini-
cal follow-up study. Dent Traumatol. 2006;22:237–41.
4. Lam R, Abbott P, Lloyd C, Kruger E, Tennant M. Dental trauma
in an Australian rural centre. Dent Traumatol. 2008;24:663–70.
5. Borum MK, Andreasen JO. Sequelae of trauma to primary
maxillary incisors. I. Complications in the primary dentition.
Endod Dent Traumatol. 1998;14:31–44.
6. Cardoso M, de Carvalho Rocha MJ. Traumatized primary teeth
in children assisted at the Federal University of Santa Catarina,
Brazil. Dent Traumatol. 2002;18:129–33.
7. Glendor U. Epidemiology of traumatic dental injuries – a 12
year review of the literature. Dent Traumatol. 2008;24:603–11.
8. Oldin A, Lundgren J, Nilsson M, Noren JG, Robertson A. Trau-
matic dental injuries among children aged 0-17 years in the BITA
study - a longitudinal Swedish multicenter study. Dent Trauma-
tol. 2015;31:9–17.
9. Roberts G, Longhurst P. Oral and dental trauma in children and
adolescents. Oxford University Press; 1996. p. 25–35, 67–80.
10. Schatz JP, Joho JP. A retrospective study of dento-alveolar inju-
ries. Endod Dent Traumatol. 1994;10:11–4.
11. Stockwell AJ. Incidence of dental trauma in the Western Austra-
lian School Dental Service. Community Dent Oral Epidemiol.
1988;16:294–8.
12. Glendor U, Koucheki B, Halling A. Risk evaluation and type
of treatment of multiple dental trauma episodes to permanent
teeth. Endod Dent Traumatol. 2000;16:205–10.
13. Rauschenberger CR, Hovland EJ. Clinical management of
crown fractures. Dent Clin N Am. 1995;39:25–51.
14. Jarvinen S. Incisal overjet and traumatic injuries to upper per-
manent incisors. A retrospective study. Acta Odontol Scand.
1978;36:359–62.
15. Holm AK, Axelsson S, Bondemark L, Brattström V, Hansen K,
Marké LÅ. Bettavvikelser och tandreglering i ett hälsoperspe-
ktiv. En systematisk litteraturöversikt. SBU Statens beredning
för medicinsk utvärdering (The Swedish Council on Technology
Assessment in Health Care). Stockholm: SBU; 2005.
16. Gawlak D, Luniewska J, Stojak W, Hovhannisyan A, Strozynska
A, Manka-Malara K, et al. The prevalence of orodental trauma
during epileptic seizures in terms of dental treatment - Survey
study. Neurol Neurochir Pol. 2017;51:361–5.
17. Karolyhazy K, Kivovics P, Hermann P, Fejerdy P, Aranyi
Z. Five-year follow-up of oral health and seizure condition of
patients with epilepsy: a prospective observational study. Com-
munity Dent Health. 2010;27:233–7.
18. Hofman PA, Nelemans P, Kemerink GJ, Wilmink JT. Value of
radiological diagnosis of skull fracture in the management of
409 16
mild head injury: meta-analysis. J Neurol Neurosurg Psychiatry.
2000;68:416–22.
19. McCrory P, Meeuwisse WH, Aubry M, Cantu RC, Dvorak J,
Echemendia RJ, et al. Consensus statement on concussion in
sport: the 4th International Conference on Concussion in Sport,
Zurich November 2012. J Athl Train. 2013;48:554–75.
20. American Academy on Pediatric Dentistry Council on Clinical
Affairs Committee on the A. Guideline on management of acute
dental trauma. Pediatr Dent. 2008–2009;30:175–83.
21. Bourguignon C, Cohenca N, Lauridsen E, Flores MT, O'Connell
AC, Day P, et al. International Association of Dental Traumatol-
ogy guidelines for the management of traumatic dental injuries:
1. Fractures and luxations. Dent Traumatol. 2020;36:314–30.
22. Kullman L, Al SM. Guidelines for dental radiography imme-
diately after a dento-alveolar trauma, a systematic literature
review. Dent Traumatol. 2012;28:193–9.
23. Day P, Flores MT, O'Connell A, Abbott PV, Tsilingaridis G,
Fouad AF, et al. Ιnternational Association of Dental Trau-
matology guidelines for the management of traumatic dental
injuries: 3. Injuries in the Primary Dentition. Dent Traumatol.
2020;36:343–59.
24. Fouad AF, Abbott PV, Tsilingaridis G, Cohenca N, Lauridsen
E, Bourguignon C, et al. International Association of Dental
Traumatology guidelines for the management of traumatic den-
tal injuries: 2. Avulsion of permanent teeth. Dent Traumatol.
2020;36:331–42.
25. Andreasen JO, Lauridsen E, Gerds TA, Ahrensburg SS. Dental
Trauma Guide: a source of evidence-based treatment guidelines
for dental trauma. Dent Traumatol. 2012;28:142–7.
26. Mourao J, Neto J, Luis C, Moreno C, Barbosa J, Carvalho J,
et al. Dental injury after conventional direct laryngoscopy: a
prospective observational study. Anaesthesia. 2013;68:1059–65.
27. Cardoso M, de Carvalho Rocha MJ. Association of crown dis-
coloration and pulp status in traumatized primary teeth. Dent
Traumatol. 2010;26:413–6.
28. Howley B, Seale NS, McWhorter AG, Kerins C, Boozer KB,
Lindsey D. Pulpotomy versus pulpectomy for carious vital
primary incisors: randomized controlled trial. Pediatr Dent.
2012;34:112–9.
29. McTigue DJ. Overview of trauma management for primary and
young permanent teeth. Dent Clin N Am. 2013;57:39–57.
30. Malmgren B, Andreasen JO, Flores MT, Robertson A, DiAnge-
lis AJ, Andersson L, et al. Guidelines for the management of
traumatic dental injuries: 3. Injuries in the primary dentition.
Pediatr Dent. 2017;39:420–8.
31. Garcia-Godoy F, Garcia-Godoy FM. Reasons for seeking treat-
ment after traumatic dental injuries. Endod Dent Traumatol.
1989;5:180–1.
32. Soporowski NJ, Allred EN, Needleman HL. Luxation injuries of
primary anterior teeth--prognosis and related correlates. Pediatr
Dent. 1994;16:96–101.
33. Holan G, Ram D. Sequelae and prognosis of intruded primary
incisors: a retrospective study. Pediatr Dent. 1999;21:242–7.
34. Zamon EL, Kenny DJ. Replantation of avulsed primary inci-
sors: a risk benefit assessment. J Can Dent Assoc. 2001;67:386.
35. Jacobsen I, Sangnes G. Traumatized primary anterior teeth.
Prognosis related to calcific reactions in the pulp cavity. Acta
Odontol Scand. 1978;36:199–204.
36. Andreasen JO, Ravn JJ. The effect of traumatic injuries to pri-
mary teeth on their permanent successors. II. A clinical and
radiographic follow-up study of 213 teeth. Scand J Dent Res.
1971;79:284–94.
37. Andreasen JO, Sundstrom B, Ravn JJ. The effect of traumatic
injuries to primary teeth on their permanent successors. I. A
clinical and histologic study of 117 injured permanent teeth.
Scand J Dent Res. 1971;79:219–83.
 410 C. Bourguignon et al.
38. Topouzelis N, Tsaousoglou P, Pisoka V, Zouloumis L. Dilacera-
tion of maxillary central incisor: a literature review. Dent Trau-
matol. 2010;26:427–33.
39. Brin I, Fuks A, Ben-Bassat Y, Zilberman Y. Trauma to the pri-
mary incisors and its effect on the permanent successors. Pediatr
Dent. 1984;6:78–82.
40. Ravn JJ. Follow-up study of permanent incisors with enamel
cracks as a result of an acute trauma. Scand J Dent Res.
1981;89:117–23.
41. DiAngelis AJ, Andreasen JO, Ebeleseder KA, Kenny DJ, Trope
M, Sigurdsson A, et al. Guidelines for the management of trau-
matic dental injuries: 1. Fractures and luxations of permanent
teeth. Pediatr Dent. 2016;38:358–68.
42. Petti S, Glendor U, Andersson L. World traumatic dental injury
prevalence and incidence, a meta-­analysis - One billion living
people have had traumatic dental injuries. Dent Traumatol.
2018;34(2):71.
43. Robertson A. A retrospective evaluation of patients with
uncomplicated crown fractures and luxation injuries. Endod
Dent Traumatol. 1998;14:245–56.
44. Garberoglio R, Brannstrom M. Scanning electron microscopic
investigation of human dentinal tubules. Arch Oral Biol.
1976;21:355–62.
45. Tziafas D, Kolokuris I. Effect of pulpal inflammation on bacte-
rial penetration of acid-etched and non-­etched dentin. Endod
Dent Traumatol. 1987;3:75–9.
46. Dean JA, Avery DR, Swartz ML. Attachment of anterior tooth
fragments. Pediatr Dent. 1986;8:139–43.
47. Worthington RB, Murchison DF, Vandewalle KS. Incisal edge
reattachment: the effect of preparation utilization and design.
Quintessence Int. 1999;30:637–43.
48. Arapostathis K, Arhakis A, Kalfas S. A modified technique on
the reattachment of permanent tooth fragments following dental
trauma. Case report. J Clin Pediatr Dent. 2005;30:29–34.
49. Poubel DLN, Almeida JCF, Dias Ribeiro AP, Maia GB, Mar-
tinez JMG, Garcia FCP. Effect of dehydration and rehydration
intervals on fracture resistance of reattached tooth fragments
using a multimode adhesive. Dent Traumatol. 2017;33:451–7.
50. Zadik D, Chosack A, Eidelman E. The prognosis of traumatized
permanent anterior teeth with fracture of the enamel and dentin.
Oral Surg Oral Med Oral Pathol. 1979;47:173–5.
51. Robertson A, Andreasen FM, Andreasen JO, Noren JG. Long-
term prognosis of crown-fractured permanent incisors. The
effect of stage of root development and associated luxation
16 injury. Int J Paediatr Dent. 2000;10:191–9.
52. Lauridsen E, Hermann NV, Gerds TA, Ahrensburg SS, Kreiborg
S, Andreasen JO. Combination injuries 1. The risk of pulp necro-
sis in permanent teeth with concussion injuries and concomitant
crown fractures. Dent Traumatol. 2012;28:364–70.
53. Lauridsen E, Hermann NV, Gerds TA, Ahrensburg SS, Kreiborg
S, Andreasen JO. Combination injuries 2. The risk of pulp
necrosis in permanent teeth with subluxation injuries and con-
comitant crown fractures. Dent Traumatol. 2012;28:371–8.
54. Cvek M. A clinical report on partial pulpotomy and capping
with calcium hydroxide in permanent incisors with complicated
crown fracture. J Endod. 1978;4:232–7.
55. Heide S, Kerekes K. Delayed direct pulp capping in permanent
incisors of monkeys. Int Endod J. 1987;20:65–74.
56. Hafez AA, Cox CF, Tarim B, Otsuki M, Akimoto N. An in vivo eval-
uation of hemorrhage control using sodium hypochlorite and direct
capping with a one- or two-­component adhesive system in exposed
nonhuman primate pulps. Quintessence Int. 2002;33:261–72.
57. Belobrov I, Weis MV, Parashos P. Conservative treatment of a
cervical horizontal root fracture and a complicated crown frac-
ture: a case report. Aust Dent J. 2008;53:260–4.
58. Gruythuysen RJ, Weerheijm KL. Calcium hydroxide pulpotomy
with a light-cured cavity-sealing material after two years. ASDC
J Dent Child. 1997;64:251–3.
59. Heide S, Mjor IA. Pulp reactions to experimental exposures in
young permanent monkey teeth. Int Endod J. 1983;16:11–9.
60. Cvek M, Lundberg M. Histological appearance of pulps after
exposure by a crown fracture, partial pulpotomy, and clinical
diagnosis of healing. J Endod. 1983;9:8–11.
61. Suzuki P, de Souza V, Holland R, Murata SS, Gomes-Filho JE,
Dezan Junior E, et al. Tissue reaction of the EndoREZ in root
canal fillings short of or beyond an apical foramenlike commu-
nication. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2010;109:e94–9.
62. El-Meligy OA, Avery DR. Comparison of mineral triox-
ide aggregate and calcium hydroxide as pulpotomy agents in
young permanent teeth (apexogenesis). Pediatr Dent. 2006;28:
399–404.
63. Zhen M, Wang C, Hu WJ, Zhang H, Li LS, Wei YP, et al. Peri-
odontal evaluation of crown-root fractured teeth following mod-
ified crown lengthening surgery. Br Dent J. 2017;222:21–5.
64. Ranka M, Shah J, Youngson C. Root fracture and its manage-
ment. Dent Update. 2012;39:530–2.
65. Feiglin B. Clinical management of transverse root fractures.
Dent Clin N Am. 1995;39:53–78.
66. Faria LP, Almeida MM, Amaral MF, Pellizzer EP, Okamoto R,
Mendonca MR. Orthodontic extrusion as treatment option for
crown-root fracture: literature review with systematic criteria. J
Contemp Dent Pract. 2015;16:758–62.
67. Caliskan MK, Turkun M, Gomel M. Surgical extrusion of
crown-root-fractured teeth: a clinical review. Int Endod J.
1999;32:146–51.
68. Tegsjo U, Valerius-Olsson H, Frykholm A, Olgart K. Clinical
evaluation of intra-alveolar transplantation of teeth with cervi-
cal root fractures. Swed Dent J. 1987;11:235–50.
69. Elkhadem A, Mickan S, Richards D. Adverse events of surgi-
cal extrusion in treatment for crown-root and cervical root frac-
tures: a systematic review of case series/reports. Dent Traumatol.
2014;30:1–14.
70. Salama M, Ishikawa T, Salama H, Funato A, Garber D. Advan-
tages of the root submergence technique for pontic site develop-
ment in esthetic implant therapy. Int J Periodontics Restorative
Dent. 2007;27:521–7.
71. Malmgren B, Tsilingaridis G, Malmgren O. Long-term follow
up of 103 ankylosed permanent incisors surgically treated with
decoronation – a retrospective cohort study. Dent Traumatol.
2015;31:184–9.
72. Maki K, Nishioka T, Seo R, Kimura M. Management of a root
fracture in an immature permanent tooth. J Clin Pediatr Dent.
2005;30:127–30.
73. Andreasen FM, Andreasen JO. Resorption and mineralization
processes following root fracture of permanent incisors. Endod
Dent Traumatol. 1988;4:202–14.
74. Hovland EJ. Horizontal root fractures. Treatment and repair.
Dent Clin North Am. 1992;36:509–25.
75. Andreasen JO, Andreasen FM, Mejare I, Cvek M. Healing of
400 intra-alveolar root fractures. 1. Effect of pre-injury and
injury factors such as sex, age, stage of root development, frac-
ture type, location of fracture and severity of dislocation. Dent
Traumatol. 2004;20:192–202.
76. Feely L, Mackie IC, Macfarlane T. An investigation of root-
fractured permanent incisor teeth in children. Dent Traumatol.
2003;19:52–4.
77. Zachrisson BU, Jacobsen I. Long-term prognosis of 66 per-
manent anterior teeth with root fracture. Scand J Dent Res.
1975;83:345–54.
Dentoalveolar Trauma of Children and Adolescents
78. Jacobsen I, Zachrisson BU. Repair characteristics of root
fractures in permanent anterior teeth. Scand J Dent Res.
1975;83:355–64.
79. Andreasen JO, Andreasen FM, Mejare I, Cvek M. Healing of
400 intra-alveolar root fractures. 2. Effect of treatment factors
such as treatment delay, repositioning, splinting type and period
and antibiotics. Dent Traumatol. 2004;20:203–11.
80. Andreasen FM. Pulpal healing after luxation injuries and root
fracture in the permanent dentition. Endod Dent Traumatol.
1989;5:111–31.
81. Crona-Larsson G, Bjarnason S, Noren JG. Effect of luxa-
tion injuries on permanent teeth. Endod Dent Traumatol.
1991;7:199–206.
82. Lauridsen E, Hermann NV, Gerds TA, Kreiborg S, Andreasen
JO. Pattern of traumatic dental injuries in the permanent denti-
tion among children, adolescents, and adults. Dent Traumatol.
2012;28(5):358–63.
83. Nikoui M, Kenny DJ, Barrett EJ. Clinical outcomes for per-
manent incisor luxations in a pediatric population. III. Lateral
luxations. Dent Traumatol. 2003;19:280–5.
84. Andreasen FM. Pulpal healing following acute dental trauma:
clinical and radiographic review. Pract Proced Aesthet Dent.
2001;13:315–22; quiz 24.
85. Andreasen JO, Andreasen FM, Skeie A, Hjorting-­Hansen E,
Schwartz O. Effect of treatment delay upon pulp and periodon-
tal healing of traumatic dental injuries - a review article. Dent
Traumatol. 2002;18:116–28.
86. Andreasen FM, Pedersen BV. Prognosis of luxated permanent
teeth – the development of pulp necrosis. Endod Dent Trauma-
tol. 1985;1:207–20.
87. Andreasen JO, Bakland LK, Matras RC, Andreasen FM. Trau-
matic intrusion of permanent teeth. Part 1. An epidemiologi-
cal study of 216 intruded permanent teeth. Dent Traumatol.
2006;22:83–9.
88. Andreasen JO, Bakland LK, Andreasen FM. Traumatic intru-
sion of permanent teeth. Part 3. A clinical study of the effect
of treatment variables such as treatment delay, method of repo-
sitioning, type of splint, length of splinting and antibiotics on
140 teeth. Dent Traumatol. 2006;22:99–111.
89. Andreasen JO, Bakland LK, Andreasen FM. Traumatic intru-
sion of permanent teeth. Part 2. A clinical study of the effect
of preinjury and injury factors, such as sex, age, stage of root
development, tooth location, and extent of injury including
number of intruded teeth on 140 intruded permanent teeth.
Dent Traumatol. 2006;22:90–8.
90. Medeiros RB, Mucha JN. Immediate vs late orthodontic
extrusion of traumatically intruded teeth. Dent Traumatol.
2009;25:380–5.
91. Dumsha T, Hovland EJ. Pulpal prognosis following extru-
sive luxation injuries in permanent teeth with closed apexes. J
Endod. 1982;8:410–2.
92. Ritter AL, Ritter AV, Murrah V, Sigurdsson A, Trope M. Pulp
revascularization of replanted immature dog teeth after treat-
ment with minocycline and doxycycline assessed by laser Dop-
pler flowmetry, radiography, and histology. Dent Traumatol.
2004;20:75–84.
93. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M, Fatti
P. Effect of topical application of doxycycline on pulp revas-
cularization and periodontal healing in reimplanted monkey
incisors. Endod Dent Traumatol. 1990;6:170–6.
94. Andreasen JO, Hjorting-Hansen E. Replantation of teeth.
I. Radiographic and clinical study of 110 human teeth replanted
after accidental loss. Acta Odontol Scand. 1966;24:263–86.
95. Andreasen JO, Borum MK, Jacobsen HL, Andreasen
FM. Replantation of 400 avulsed permanent incisors. 4.
411 16
Factors related to periodontal ligament healing. Endod Dent
Traumatol. 1995;11:76–89.
96. Andreasen JO, Borum MK, Andreasen FM. Replantation
of 400 avulsed permanent incisors. 3. Factors related to root
growth. Endod Dent Traumatol. 1995;11:69–75.
97. Andreasen JO, Borum MK, Jacobsen HL, Andreasen
FM. Replantation of 400 avulsed permanent incisors. 2.
Factors related to pulpal healing. Endod Dent Traumatol.
1995;11:59–68.
98. Andreasen JO, Borum MK, Jacobsen HL, Andreasen
FM. Replantation of 400 avulsed permanent incisors. 1.
Diagnosis of healing complications. Endod Dent Traumatol.
1995;11:51–8.
99. Hiltz J, Trope M. Vitality of human lip fibroblasts in milk,
Hanks balanced salt solution and Viaspan storage media.
Endod Dent Traumatol. 1991;7:69–72.
100. Trope M, Friedman S. Periodontal healing of replanted dog
teeth stored in Viaspan, milk and Hank’s Balanced Salt Solu-
tion. Endod Dent Traumatol. 1992;8:183.
101. Sigalas E, Regan JD, Kramer PR, Witherspoon DE, Opper-
man LA. Survival of human periodontal ligament cells in
media proposed for transport of avulsed teeth. Dent Trauma-
tol. 2004;20:21–8.
102. Blomlof L, Lindskog S, Hedstrom KG, Hammarstrom L. Vital-
ity of periodontal ligament cells after storage of monkey teeth
in milk or saliva. Scand J Dent Res. 1980;88:441–5.
103. Blomlof L, Lindskog S, Hammarstrom L. Periodontal healing
of exarticulated monkey teeth stored in milk or saliva. Scand J
Dent Res. 1981;89:251–9.
104. Trope M, Moshonov J, Nissan R, Buxt P, Yesilsoy C. Short vs.
long-term calcium hydroxide treatment of established inflam-
matory root resorption in replanted dog teeth. Endod Dent
Traumatol. 1995;11:124–8.
105. Cvek M. Prognosis of luxated non-vital maxillary incisors
treated with calcium hydroxide and filled with gutta-percha.
A retrospective clinical study. Endod Dent Traumatol. 1992;8:
45–55.
106. Soder PO, Otteskog P, Andreasen JO, Modeer T. Effect of dry-
ing on viability of periodontal membrane. Scand J Dent Res.
1977;85:164–8.
107. Selvig KA, Bjorvatn K, Claffey N. Effect of stannous fluoride
and tetracycline on repair after delayed replantation of root-
planed teeth in dogs. Acta Odontol Scand. 1990;48:107–12.
108. Jacobsen I, Andreasen JO. Traumatic injuries: examination,
diagnosis, and immediate care. In: Koch G, Poulsen S, editors.
Pediatric dentistry. A clinical approach. 2nd ed. Wiley-Black-
well; 2009.
109. Robertson A, Andreasen FM, Bergenholtz G, Andreasen JO,
Noren JG. Incidence of pulp necrosis subsequent to pulp canal
obliteration from trauma of permanent incisors. J Endod.
1996;22:557–60.
110. Andreasen FM, Zhijie Y, Thomsen BL, Andersen PK. Occur-
rence of pulp canal obliteration after luxation injuries in the
permanent dentition. Endod Dent Traumatol. 1987;3:103–15.
111. Robertson A. Pulp survival and hard tissue formation subse-
quent to dental trauma. A clinical and histological study of
uncomplicated crown fractures and luxation injuries. Swed
Dent J Suppl. 1997;125:1–65.
112. Yanpiset K, Vongsavan N, Sigurdsson A, Trope M. Efficacy
of laser Doppler flowmetry for the diagnosis of revascular-
ization of reimplanted immature dog teeth. Dent Traumatol.
2001;17:63–70.
113. Caldeira CL, Barletta FB, Ilha MC, Abrao CV, Gavini G. Pulse
oximetry: a useful test for evaluating pulp vitality in trauma-
tized teeth. Dent Traumatol. 2016;32:385–9.
 412 C. Bourguignon et al.
114. Gopikrishna V, Tinagupta K, Kandaswamy D. Compari-
son of electrical, thermal, and pulse oximetry methods for
assessing pulp vitality in recently traumatized teeth. J Endod.
2007;33:531–5.
115. Andreasen FM. Transient apical breakdown and its relation to
color and sensibility changes after luxation injuries to teeth.
Endod Dent Traumatol. 1986;2:9–19.
116. Fuss Z, Trowbridge H, Bender IB, Rickoff B, Sorin S. Assess-
ment of reliability of electrical and thermal pulp testing agents.
J Endod. 1986;12:301–5.
117. Pileggi R, Dumsha TC, Myslinksi NR. The reliability of elec-
tric pulp test after concussion injury. Endod Dent Traumatol.
1996;12:16–9.
118. Andreasen JO. Luxation of permanent teeth due to trauma. A
clinical and radiogrpahic follow-up study of 189 injured teeth.
Scand J Dent Res. 1970;78:273–86.
119. Cohenca N, Silberman A. Contemporary imaging for the diag-
nosis and treatment of traumatic dental injuries: a review. Dent
Traumatol. 2017;33:321–8.
120. Malmgren B, Cvek M, Lundberg M, Frykholm A. Surgical
treatment of ankylosed and infrapositioned reimplanted inci-
sors in adolescents. Scand J Dent Res. 1984;92:391–9.
121. Malmgren B, Malmgren O. Rate of infraposition of reim-
planted ankylosed incisors related to age and growth in chil-
dren and adolescents. Dent Traumatol. 2002;18:28–36.
122. Thilander B, Odman J, Jemt T. Single implants in the upper
incisor region and their relationship to the adjacent teeth.
An 8-year follow-up study. Clin Oral Implants Res. 1999;10:
346–55.
123. Thilander B. Dentoalveolar development in subjects with nor-
mal occlusion. A longitudinal study between the ages of 5 and
31 years. Eur J Orthod. 2009;31:109–20.
124. Bernard JP, Schatz JP, Christou P, Belser U, Kiliaridis S. Long-
term vertical changes of the anterior maxillary teeth adjacent
to single implants in young and mature adults. A retrospective
study. J Clin Periodontol. 2004;31:1024–8.
125. Oesterle LJ, Cronin RJ Jr. Adult growth, aging, and the sin-
gle-tooth implant. Int J Oral Maxillofac Implants. 2000;15:
252–60.
126. Andreasen JO, Reinholdt J, Riis I, Dybdahl R, Soder PO,
Otteskog P. Periodontal and pulpal healing of monkey incisors
preserved in tissue culture before replantation. Int J Oral Surg.
1978;7:104–12.
127. Andreasen JO. Relationship between surface and inflammatory
16 resorption and changes in the pulp after replantation of perma-
nent incisors in monkeys. J Endod. 1981;7:294–301.
128. Stalhane I, Hedegard B. Traumatized permanent teeth in chil-
dren aged 7-15 years. Sven Tandlak Tidskr. 1975;68:157–69.
129. Trope M. Cervical root resorption. J Am Dent Assoc. 1997;128
Suppl:56S–9S.
130. Heithersay GS. Invasive cervical resorption following trauma.
Aust Endod J. 1999;25:79–85.
131. Heithersay GS. Invasive cervical resorption: an analysis of
potential predisposing factors. Quintessence Int. 1999;30:
83–95.
132. Heithersay GS. Treatment of invasive cervical resorption: an
analysis of results using topical application of trichloracetic
acid, curettage, and restoration. Quintessence Int. 1999;30:
96–110.
133. Heithersay GS. Clinical, radiologic, and histopathologic
features of invasive cervical resorption. Quintessence Int.
1999;30:27–37.
134. Wang C, Qin M, Guan Y. Analysis of pulp prognosis in 603
permanent teeth with uncomplicated crown fracture with or
without luxation. Dent Traumatol. 2014;30:333–7.
135. Lauridsen E, Hermann NV, Gerds TA, Ahrensburg SS,
Kreiborg S, Andreasen JO. Combination injuries 3. The risk of
pulp necrosis in permanent teeth with extrusion or lateral luxa-
tion and concomitant crown fractures without pulp exposure.
Dent Traumatol. 2012;28:379–85.
136. Bucher K, Neumann C, Thiering E, Hickel R, Kuhnisch
J. Complications and survival rates of teeth after dental trauma
over a 5-year period. Clin Oral Investig. 2013;17:1311–8.
137. Hermann NV, Lauridsen E, Ahrensburg SS, Gerds TA,
Andreasen JO. Periodontal healing complications following
extrusive and lateral luxation in the permanent dentition: a
longitudinal cohort study. Dent Traumatol. 2012;28:394–402.
138. Hermann NV, Lauridsen E, Ahrensburg SS, Gerds TA,
Andreasen JO. Periodontal healing complications following
concussion and subluxation injuries in the permanent dentition:
a longitudinal cohort study. Dent Traumatol. 2012;28:386–93.
139. Cvek M, Cleaton-Jones P, Austin J, Lownie J, Kling M, Fatti
P. Pulp revascularization in reimplanted immature monkey
incisors – predictability and the effect of antibiotic systemic
prophylaxis. Endod Dent Traumatol. 1990;6:157–69.
140. Lengheden A, Blomlof L, Lindskog S. Effect of immediate cal-
cium hydroxide treatment and permanent root-­filling on peri-
odontal healing in contaminated replanted teeth. Scand J Dent
Res. 1991;99:139–46.
141. Lengheden A, Blomlof L, Lindskog S. Effect of delayed cal-
cium hydroxide treatment on periodontal healing in contami-
nated replanted teeth. Scand J Dent Res. 1991;99:147–53.
142. Blomlof L, Lengheden A, Lindskog S. Endodontic infection
and calcium hydroxide-treatment. Effects on periodontal heal-
ing in mature and immature replanted monkey teeth. J Clin
Periodontol. 1992;19:652–8.
143. Bystrom A, Claesson R, Sundqvist G. The antibacterial effect
of camphorated paramonochlorophenol, camphorated phenol
and calcium hydroxide in the treatment of infected root canals.
Endod Dent Traumatol. 1985;1:170–5.
144. Cvek M. Clinical procedures promoting apical closure and
arrest of external root resorption in non-vital permanent inci-
sors. Trans Int Conf Endod. 1973;5:30–41.
145. Cvek M. Treatment of non-vital permanent incisors with cal-
cium hydroxide. II. Effect on external root resorption in luxated
teeth compared with effect of root filling with guttapucha. A
follow-up. Odontol Revy. 1973;24:343–54.
146. Haapasalo HK, Siren EK, Waltimo TM, Orstavik D, Haapas-
alo MP. Inactivation of local root canal medicaments by den-
tine: an in vitro study. Int Endod J. 2000;33:126–31.
147. Sjogren U, Figdor D, Spangberg L, Sundqvist G. The antimi-
crobial effect of calcium hydroxide as a short-­term intracanal
dressing. Int Endod J. 1991;24:119–25.
148. Trope M, Yesilsoy C, Koren L, Moshonov J, Friedman S. Effect
of different endodontic treatment protocols on periodontal
repair and root resorption of replanted dog teeth. J Endod.
1992;18:492–6.
149. Steiner JC, Dow PR, Cathey GM. Inducing root end closure of
nonvital permanent teeth. J Dent Child. 1968;35:47–54.
150. Kerekes K, Heide S, Jacobsen I. Follow-up examination of end-
odontic treatment in traumatized juvenile incisors. J Endod.
1980;6:744–8.
151. Kleier DJ, Barr ES. A study of endodontically apexified teeth.
Endod Dent Traumatol. 1991;7:112–7.
152. Steinig TH, Regan JD, Gutmann JL. The use and predictable
placement of Mineral Trioxide Aggregate in one-visit apexifica-
tion cases. Aust Endod J. 2003;29:34–42.
153. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Anti-
bacterial effects of some root end filling materials. J Endod.
1995;21:403–6.
Dentoalveolar Trauma of Children and Adolescents
154. Estrela C, Bammann LL, Estrela CR, Silva RS, Pecora
JD. Antimicrobial and chemical study of MTA, Portland
cement, calcium hydroxide paste, Sealapex and Dycal. Braz
Dent J. 2000;11:3–9.
155. Ostby BN. The role of the blood clot in endodontic therapy.
An experimental histologic study. Acta Odontol Scand.
1961;19:324–53.
156. Öhman A. Healing and sensitivity to pain in young replanted
human teeth. An expermimental, clinical and histological
study. Odontol Tidskr. 1965;73:168–227.
157. Myers WC, Fountain SB. Dental pulp regeneration aided by
blood and blood substitutes after experimentally induced peri-
apical infection. Oral Surg Oral Med Oral Pathol. 1974;37:
441–50.
158. Iwaya SI, Ikawa M, Kubota M. Revascularization of an imma-
ture permanent tooth with apical periodontitis and sinus tract.
Dent Traumatol. 2001;17:185–7.
159. Banchs F, Trope M. Revascularization of immature perma-
nent teeth with apical periodontitis: new treatment protocol? J
Endod. 2004;30:196–200.
160. Hoshino E, Kurihara-Ando N, Sato I, Uematsu H, Sato M,
Kota K, et al. In-vitro antibacterial susceptibility of bacteria
taken from infected root dentine to a mixture of ciprofloxacin,
metronidazole and minocycline. Int Endod J. 1996;29:125–30.
161. Sato I, Ando-Kurihara N, Kota K, Iwaku M, Hoshino E. Ster-
ilization of infected root-canal dentine by topical application
of a mixture of ciprofloxacin, metronidazole and minocycline
in situ. Int Endod J. 1996;29:118–24.
162. Trope M. Treatment of the immature tooth with a non-vital pulp
and apical periodontitis. Dent Clin N Am. 2010;54:313–24.
163. Nagata JY, Soares AJ, Souza-Filho FJ, Zaia AA, Ferraz CC,
Almeida JF, et al. Microbial evaluation of traumatized teeth
treated with triple antibiotic paste or calcium hydroxide with
2% chlorhexidine gel in pulp revascularization. J Endod.
2014;40:778–83.
164. Thibodeau B, Teixeira F, Yamauchi M, Caplan DJ, Trope
M. Pulp revascularization of immature dog teeth with apical
periodontitis. J Endod. 2007;33:680–9.
165. Nagata JY, Gomes BP, Rocha Lima TF, Murakami LS, de
Faria DE, Campos GR, et al. Traumatized immature teeth
treated with 2 protocols of pulp revascularization. J Endod.
2014;40:606–12.
166. Khademi AA, Dianat O, Mahjour F, Razavi SM, Younessian
F. Outcomes of revascularization treatment in immature dog's
teeth. Dent Traumatol. 2014;30:374–9.
167. Jeeruphan T, Jantarat J, Yanpiset K, Suwannapan L, Khew-
sawai P, Hargreaves KM. Mahidol study 1: comparison of
radiographic and survival outcomes of immature teeth treated
with either regenerative endodontic or apexification methods: a
retrospective study. J Endod. 2012;38:1330–6.
168. Wang X, Thibodeau B, Trope M, Lin LM, Huang GT. Histo-
logic characterization of regenerated tissues in canal space after
the revitalization/revascularization procedure of immature dog
teeth with apical periodontitis. J Endod. 2010;36:56–63.
413 16
169. Andreasen JO, Farik B, Munksgaard EC. Long-­term calcium
hydroxide as a root canal dressing may increase risk of root
fracture. Dent Traumatol. 2002;18:134–7.
170. Rabie G, Trope M, Garcia C, Tronstad L. Strengthening and
restoration of immature teeth with an acid-etch resin tech-
nique. Endod Dent Traumatol. 1985;1:246–56.
171. Trope M, Maltz DO, Tronstad L. Resistance to fracture of
restored endodontically treated teeth. Endod Dent Traumatol.
1985;1:108–11.
172. Mannocci F, Machmouridou E, Watson TF, Sauro S, Sher-
riff M, Pilecki P, et al. Microtensile bond strength of resin-
post interfaces created with interpenetrating polymer network
posts or cross-linked posts. Med Oral Patol Oral Cir Bucal.
2008;13:E745–52.
173. Cvek M, Sundstrom B. Treatment of non-vital permanent
incisors with calcium hydroxide. V. Histologic appearance of
roentgenographically demonstrable apical closure of immature
roots. Odontol Revy. 1974;25:379–91.
174. Andreasen JO, Hjorting-Hansen E. Replantation of teeth.
II. Histological study of 22 replanted anterior teeth in humans.
Acta Odontol Scand. 1966;24:287–306.
175. Werder P, von Arx T, Chappuis V. Treatment outcome of 42
replanted permanent incisors with a median follow-up of 2.8
years. Schweiz Monatsschr Zahnmed. 2011;121:312–20.
176. Kahler B, Swain MV, Moule A. Fracture-­toughening mecha-
nisms responsible for differences in work to fracture of hydrated
and dehydrated dentine. J Biomech. 2003;36:229–37.
177. Waldon K, Barber SK, Spencer RJ, Duggal MS. Indications for
the use of auto-transplantation of teeth in the child and adoles-
cent. Eur Arch Paediatr Dent. 2012;13:210–6.
178. Kindelan SA, Day PF, Kindelan JD, Spencer JR, Duggal
MS. Dental trauma: an overview of its influence on the man-
agement of orthodontic treatment. Part 1. J Orthod. 2008;35:
68–78.
179. Malmgren O, Goldson L, Hill C, Orwin A, Petrini L, Lundberg
M. Root resorption after orthodontic treatment of traumatized
teeth. Am J Orthod. 1982;82:487–91.
180. Levander E, Malmgren O. Evaluation of the risk of root
resorption during orthodontic treatment: a study of upper inci-
sors. Eur J Orthod. 1988;10:30–8.
181. Tuli T, Hachl O, Hohlrieder M, Grubwieser G, Gassner R. Den-
tofacial trauma in sport accidents. Gen Dent. 2002;50:274–9.
182. Zadik Y, Levin L. Does a free-of-charge distribution of boil-
and-bite mouthguards to young adult amateur sportsmen
affect oral and facial trauma? Dent Traumatol. 2009;25:69–72.
183. Newsome PR, Tran DC, Cooke MS. The role of the mouth-
guard in the prevention of sports-related dental injuries: a
review. Int J Paediatr Dent. 2001;11:396–404.
184. Bourguignon C, Sigurdsson A. Preventive strategies for trau-
matic dental injuries. Dent Clin N Am. 2009;53:729–49, vii.
https://doi.org/10.1016/j.cden.2009.06.002. PMID: 19958909.
185. Park JB, Shaull KL, Overton B, Donly KJ. Improving mouth
guards. J Prosthet Dent. 1994;72:373–80.
 415 17

Developmental Defects
of the Teeth and Their Hard
Tissues
Nikolaos Kotsanos, Petros Papagerakis, Haim Sarnat,
and Agnès Bloch-­Zupan

Contents

17.1 Disturbances in Tooth Number, Size, and Morphology – 416

17.1.1  Short Introduction to Dental Development – 416
A
17.1.2 Causes of Disturbances and Correlations with Overall Health – 420
17.1.3 Clinical Expression of Disturbances and their Treatment – 421

17.2 Malformations of Dental Tissue Structure – 430

17.2.1 T he Structure of Enamel, Dentin, and Cementum – 430
17.2.2 Clinical and Histological Appearance, Etiology, and Diagnosis – 432

17.3 Developmental Discoloration of Dental Tissues – 454

17.4 Conclusion – 456

References – 459

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_17
 416 N. Kotsanos et al.
17.1  isturbances in Tooth Number, Size,
D about the completion of primary tooth formation or its
and Morphology
17.1.1  Short Introduction to Dental
A utero and of the third molars at about the age of 5 years,
Development
Primary teeth develop from oral ectoderm-derived cells,
which differentiate into ameloblasts that form enamel,
and cranial neural crest-derived mesenchyme cells,
which differentiate into odontoblasts and cementoblasts
forming dentin and cementum, respectively. These two
cell types (epithelial and mesenchyme) interact to con-
trol the entire process of tooth initiation, morphogen-
esis, and cytodifferentiation [1].
Oral ectoderm-derived epithelial cells first form the
dental laminae. Tooth formation begins with the thick-
ening of the dental lamina and its ingrowth into the
underlying cranial neural crest-derived mesenchyme at
the sixth to eighth week in utero for the entire primary
dentition. This folding of the epithelium along with a
condensation of the adjacent ectomesenchymal cells
leads to the formation of tooth germs or buds. Organized
clusters of these cells are called the dental placodes. A
very important transient structure named the enamel
knot is derived from the dental placodes. The enamel
knot functions as a signaling center of epithelial/mes-
enchymal interactions, which are responsible for tooth
morphogenesis. In fact, the enamel knot’s signaling cen-
ters will determine the individualized crown shape for
each tooth. This is done by controlling the appropri-
ate size and number of cusps by complex mechanisms
involving the differential expression of numerous genes
including MSX for incisors, BARX-1 for molars, etc.,
and then going through the morphological cap and bell
stages [2, 3] (. Figs. 17.1 and 17.2).
Once morphogenesis is completed, the dental crown
cytodifferentiation stage starts, during which neural
crest-derived ectomesenchymal cells facing the enamel
17 organ differentiate into odontoblasts and subsequently
epithelial cells from the inner dental epithelium differ-
entiate into ameloblasts. Both odontoblasts and ame-
loblasts produce extracellular organic matrix (dentin
and enamel, respectively) in the space between them,
as they move apart from each other. Almost simultane-
ously, mineralization of these two tissues with calcium
phosphate (hydroxyapatite) starts at the cusps and then
proceeds cervically [1]. The permanent teeth develop
by further proliferative activity lingual to each primary
tooth bud (anterior teeth and premolars) and backward
extension (molars) of the dental lamina. Their budding
(anlage) starts during the bell stage of primary tooth
development, and their formation will begin later, at
eruption. This means that formation of the first perma-
nent tooth (first molar) begins at about the 20th week in
but traces of mineralized tips of cusps cannot be seen
radiographically before birth for the first and before
year 8 for the third permanent molar [1].
Like the formation of other organs of the fetus, the
histodifferentiation of ameloblasts, odontoblasts, and
cementoblasts and the deposition of their matrix are
regulated by complex mechanisms [1, 4]. Interaction
between epithelial and mesenchymal cells, also between
extracellular matrix and cells, and between different
types of epithelial and mesenchymal cells is continu-
ous and tightly regulated. The gene regulation of cell
differentiation has been examined in animal studies
using molecular biology. Advances in molecular genet-
ics have allowed the identification of hundreds of genes
that are related to dental developmental disorders. The
regulating (signaling) molecules (growth factors) are
peptides which are secreted and bind to specific recep-
tors in adjacent cells. These molecules belong to specific
families, like bone morphogenetic protein (BMP), fibro-
blast growth factor (FGF), hedgehog signaling routes,
and Wnt families [2, 3, 5]. Their role has been studied in
transgenic mice and shown that the inhibition of tran-
scription activity inhibited odontogenesis [3].
In addition to growth factor signaling initially char-
acterized in mice models, the last few years, direct DNA
sequencing of patients with genetic traits has discovered
an increasing number of genes involved in tooth number,
tooth form, and dental structural anomalies (. Tables
17.1, . 17.2, and . 17.3).
These genes include almost any type of proteins such
as transcription factors, extracellular proteins, adhesion
molecules, and even proteins with still unknown func-
tions. Most of these newly discovered genes with key
roles in tooth development play also key roles in differ-
ent organs, but some are only expressed in dental tissues
and have only tooth-specific phenotype such as amelo-
genin mutations causing amelogenesis imperfecta (AI).
However, even amelogenin, the so-called “exclusive”
enamel protein, might be present in other tissues and
organs like the brain [28].
During the morphogenesis of the teeth includ-
ing their root formation, the dental papilla constantly
interacts directly and indirectly with the surrounding
periodontal and bone tissues. During the eruption of
the tooth, the surrounding cementum and bone tissues
undergo continuous remodeling, with resorption in
front of the erupting bud and apposition behind it, thus
allowing for tooth eruption (see 7 Chap. 10).
Developmental Defects of the Teeth and Their Hard Tissues
417 17
..      Fig. 17.1 Dental develop-
ment from tooth bud stage
through to enamel mineraliza-
tion at cusp tips. (From Bekes K.
(Ed) Pit and Fissure Sealants.
2018, Springer. By permission)

Placode Bud Cap Early bell

Signaling centers Mesenchymal centers

Wnt
Shh BMP
BMP FGF
FGF Activin
Edar

..      Fig. 17.2 Epithelial-mesenchymal tissue interactions and epithe-
lial signaling centers regulating tooth morphogenesis. Epithelial sig-
naling centers express signals of four signal families and Edar, the
receptor of ectodysplasin (Eda). The early signaling center in the
placode regulates epithelial budding, while the primary enamel knot
regulates the shift from the bud to cap stage and then to the bell
stage. The secondary enamel knots regulate tooth cusp formation in
molar teeth. Reciprocal signals (in green square) are expressed in
mesenchyme. Arrows indicate signaling across the two tissues and
within the epithelium [3]. (By permission)
 418 N. Kotsanos et al.

..      Table 17.1 Non-syndromic oligodontia: selected gene mutations responsible for non-syndromic variations in number and shape
of teeth

Gene Mutation Molecule type Phenotype

MSX1 [6] M61K and R196P (missense) Transcription factor (binds Hypodontia (AD or AR)
S105X, Q187X, and S202X (nonsense) DNA through its homeodo- Oligodontia (AD)
main) Possible cleft palate
PAX9 [7] K114X (nonsense) Transcription factor (binds Oligodontia (AD)
L21P, R26W, R28P, G51S, and K91E (missense) DNA through its paired Molar Hypodontia (AD)
G73fsX316, R59fsX177, and V265fsX316 domain) Peg-shaped laterals (AD)
(frameshift)
AXIN2 [8] Arg656Stop, 1994–1995insG (LOF) Wnt signaling regulator Incisor agenesis (unknown)
Associated with
Colorectal carcinoma

AD autosomal dominant, AR autosomal recessive

..      Table 17.2 Syndromic oligodontia (most common syndromes)

Syndrome Phenotype Gene Protein OMIM

product

Axenfeld-Rieger syndrome [9] Oligodontia PITX2/PAX6 Transcription 180,500

Eye and umbilical defects factor
Hypohidrotic ectodermal dysplasia Oligodontia EDA Signal 305,100
Small peg-shaped teeth EDAR receptor 129,490
Hypoplastic teeth and glands EDARΑDD Signal 224,900
mediator
Transcription
factor
EEC syndrome Ectodermal dysplasia TP63 Transcription 129,900
Ectrodactyly factor 604,273
Cleft palate
CLPED syndrome Ectodermal dysplasia PVRL1 Cell adhesion 225,060
Cleft lip/palate molecule
(nectin-1)
Cleidocranial dysplasia Supernumerary teeth RUNX2 Transcription 119,600
Impaired eruption factor
17 Deficient bone formation
Tricho-dento-osseous syndrome (TDO) Taurodontism DLX3 Transcription 129,510
Enamel hypoplasia factor
Hair and bone defects
Autosomal dominant lacrimo-auriculo-dento-­ Microdontia FGF10 Growth 602,115
digital (LADD) syndrome (149730) [10] and Oligodontia FGFR2 factor and
autosomal dominant aplasia of lacrimal and Irritable eyes (176943) receptors
salivary glands (ALSG; 180,920) Dryness of the mouth FGFR3
Anomalies mainly affecting (134934)
lacrimal glands and ducts, salivary
glands and ducts, ears, teeth, and
distal limb segments
Down syndrome [11] Mental impairment Trisomy 21 190,685
Stunted growth
Macroglossia
Oligodontia (mainly in the lower
incisors)
Developmental Defects of the Teeth and Their Hard Tissues
419 17

..      Table 17.2 (continued)

Syndrome Phenotype Gene Protein OMIM

product

ADULT syndrome [12] Ectrodactyly TP63 Tumor 103,285

Syndactyly protein
Excessive freckling
Broad nasal bridge
Midfacial hypoplasia
Lacrimal duct anomalies
Limb mammary syndrome (LMS) [13] Severe limbs anomalies, TP63 Tumor 603,543
Mammary hypoplasia/aplasia protein
Cleft palate and bifid uvula
Ehlers-Danlos (type VII, dermatosparaxis) Severe skin and mucosal fragility ADAMTS2 Proteinase 225,410
syndrome [14]
Incontinentia pigmenti [15] Skin hyperpigmentation IKKα (NEMO) Transcription 308,300
Peg-shaped teeth factor
Delayed eruption and impaction activator
Witkop syndrome [16] Nail dysgenesis MSX1 Transcription 189,500
factor
Apert syndrome [17] Syndactyly FGFR2 Growth 101,200
Exophthalmia factor
Hypoplastic midface receptor
Class III malocclusion
Blepharocheilodontic syndrome [18] Eyelid anomalies CDH1 Adhesion 119,580
Bilateral cleft lip and palate CTNND1 molecules
Microdontia with peg-shaped
teeth
Charcot-Marie-tooth disease type 2 [19] Muscle weakness NEFL Neuro-­ 607,684
Sensory loss filaments
Grinding of the teeth
Ellis-van Creveld syndrome [20] Short limb dwarfism EVC1 Transmem- 225,500
Postaxial polydactyly EVC2 brane
Partial cleft lip proteins
Peg-shaped laterals
Conical and microdontic teeth
Enamel hypoplasia
Frontometaphyseal dysplasia [21] Hearing loss FLNA Filamin A 305,620
Cleft palate (actin-­
Joint contracture binding
protein)
Hay-Wells syndrome [22] Ankyloblepharon TP63 Tumor 106,260
Ectodermal dysplasia protein
Cleft palate and/or cleft lip
Johanson-blizzard syndrome [23] Small nose that appears “beak UBR1 Ubiquitin 243,800
shaped” protein ligase
Microdontia
Kartagener’s syndrome [24] Sinusitis DNAI1 Dynein 244,400
Bronchiectasis DNAHC11 protein
Male infertility DNAH5 complex
Enamel hypoplasia
Missing lateral incisors
Williams syndrome [25] Cardiovascular abnormalities Deletion in the 189,500
Mental retardation long arm of
Malocclusion chromosome 7
Taurodontism
Pulp stones
 420 N. Kotsanos et al.

..      Table 17.3 Syndromic hyperdontia (most common syndromes)

Condition Mutation Molecule Phenotype

type

Cleidocranial dysplasia RUNX2 Transcrip- Bone dysplasia

(CCD) tion factor Defective development of the cranial bones and by the
Complete or partial absence of the collar bones
Supernumerary teeth
Apert [17] FGFR2 Receptor Premature fusion of certain skull bones (craniosynostosis)
Syndactyly
Supernumerary teeth
Sturge-weber [26] GNAQ (G G protein Sturge-weber syndrome has three major features: a red or pink
protein subunit birthmark called a port-wine birthmark, a brain abnormality called a
alpha q) leptomeningeal angioma, and increased pressure in the eye (glaucoma)
Supernumerary teeth
Crouzon FGFR2 Receptor Premature fusion of certain skull bones (craniosynostosis)
Hearing loss
Supernumerary teeth
Cleft lip Multifactorial N/A Cleft lip
Supernumerary teeth
Gardner syndrome APC Wnt Multiple colorectal polyps and various types of tumors, both benign
(adenomatous polyposis signaling (noncancerous) and malignant (cancerous)
of the colon) [27] regulator Supernumerary teeth

17.1.2 Causes of Disturbances

and Correlations with Overall Health
Tooth number, size, and shape are determined during the
initiation and morphogenesis stages of odontogenesis.
These disturbances of the teeth are associated and interre-
lated. Coexistence of missing (aplasia, agenesis) and small
or even conical teeth is often reported in the same patient
and his relatives and was termed “continuous variation”
by Brook [29, 30]. It seems that an anomaly at an early
stage of odontogenesis can lead to complete inhibition or
restriction of the formation of the tooth. Such phenom-
17 ena are often observed in the third molars, second premo- ●
lars, and upper lateral permanent incisors and are termed
..      Fig. 17.3 Example drawing of transmission pattern in autoso-
“terminal reduction.” The epithelial buds of these teeth are
mal dominant inheritance of a boy. □, male patient; ○, female
formed last within their group of teeth (incisors, premolars, patient; ■, affected
molars). This indicates that the aplasia is related to a quan-
titative deficit of the dental placode [31, 32]. The terms used
for congenitally missing teeth are hypodontia (1–5 miss- sion links of such anomalies need to be recorded at the
ing teeth), oligodontia (>5 missing teeth), and anodontia initial consultation, and a pedigree should be designed as
(complete agenesis), whereas additional teeth are described the example shown here (. Fig. 17.3).
by the term supernumerary teeth or hyperdontia. The majority of gene mutations that have been iden-
Many of the disturbances in tooth development are tified as causes of variations in the number and shape
attributed to local or systemic environmental causes, while of teeth are related to genes responsible for the tran-
there are some whose etiology remains unclear. Genetically scription of macromolecules of odontogenesis that act
regulated disturbances are caused by gene mutations, and at very early stages summarized here for non-syndromic
thanks to advances in genetic research, many of these oligodontia (. Table 17.1) and syndromic oligodontia
have already been identified [33]. The hereditary transmis- (. Table 17.2).
Developmental Defects of the Teeth and Their Hard Tissues
421 17
The main genes associated with tooth agenesis,
regardless of the presence or not of a general syndrome,
include the MSX1, PAX9, IRF6, AXIN2, WNT10A,
EDA, EDAR, and EDARADD genes [3, 33].
As an example, the autosomal dominant trait of
hypodontia is caused by gene mutation in MSX1 and
PAX9, which are mediators in the interaction of epi-
thelial/mesenchymal cells. Agenesis of the second pre-
molars and third molars is almost always associated
with mutations in MSX1. On the other hand, the eti-
ology of hypohidrotic ectodermal dysplasia, which is
characterized by severe oligodontia, small peg-shaped
anterior teeth, and severe reduction of the hair, nails, ..      Fig. 17.4 Cleidocranial dysplasia. Supernumerary teeth, delayed
sweat glands, and other epithelial appendages, is associ- eruption, and retention of the primary teeth
ated with the loss of function of ectodysplasin (EDA),
the signaling molecule that together with the EDAR and (Gardner syndrome) [37]. However mutations in AXIN2
EDARADD belongs to the family of tumor necrosis fac- and APC genes are rare.
tors (TNF). However, these same genes (EDA, EDAR, On the other hand, genetic mutations are also found
EDARADD) are responsible for non-syndromic hypo−/ in patients presenting supernumerary teeth as phenotypic
oligodontia and may not be associated with additional traits (. Table 17.3). Among the most common syndromic
ectodermal symptoms. conditions presenting numerous supernumerary teeth is
WNT10A gene, another mediator of the Wnt cleidocranial dysplasia (cleidocranial dysostosis) which is
­pathway, has also been suggested as a major cause of inherited as an autosomal dominant trait on chromosome
tooth agenesis. More than half of the patients present- 6 p21 (. Fig. 17.4). Dysfunction in molecule RUNX2 sig-
ing with non-syndromic oligodontia in a specialized nificantly affects osteoblasts and bone remodeling and the
center had bi- or monoallelic WNT10A mutations [34], epithelial/mesenchymal cell interactions during early odon-
which means that the mutations in this gene are the togenesis [2]. Typically manifested by underdeveloped or
most common cause of these types of oligodontia [35]. missing clavicles, in severe cases the shoulders can be brought
Furthermore, WNT10A mutations have been identified together in the midline. Other signs are delayed closure of
in a large proportion of patients with oligodontia and the fontanelle, prominent forehead, hypertelorism, multiple
mild phenotypes of ectodermal dysplasia. Significant teeth, delayed eruption, and retention of the primary teeth.
differences are found among the ectodermal dysplasia
phenotypes caused by the EDA and WNT10A genes.
Those indicate that there are at least two different routes 17.1.3  linical Expression of Disturbances
C
of occurrence [36].
and their Treatment
In other cases of non-syndromic oligodontia, there
may also be other genetic mutations, such as in AXIN2,
an inhibitor of the Wnt signaling pathway [5]. Research Eye Catcher
has linked genetic background of dental agenesis of this
The management of dental anomalies and associated
pathway with some forms of cancer. The normal route
rare diseases requires interactions with specialized
of Wnt catenin shows such a relation. For example, a
dedicated centers with long term expertise. In Europe,
strong relationship has been found between the gene
per definition, rare diseases affect less than 1 in 2,000
AXIN2, tooth agenesis, and the development of colon
persons. Among 7,000 rare mostly genetic diseases,
cancer, suggesting that tooth agenesis may in some cases
900 have orodental manifestations. These diseases
be a sensitive cancer indicator [8]. This is particularly
affect 25 million people in Europe. Expert centers
true for cases of oligodontia without ectodermal dys-
have been identified and certified by national health
plasia, where the dentist should inform the physician,
authorities and plans focused on rare diseases [33]. As
in order to suggest to the patient a genetic mutation test
examples, one could mention TAKO – Resource cen-
of AXIN2 to exclude the possibility of predisposition
ter for oral health in rare medical condition in Norway
to cancer. It has also been reported that mutations in
and the Rare disease reference center for rare oral and
the APC gene, another “tumor suppressor gene” of the
dental diseases O-Rares in Strasbourg France (see
Wnt pathway, involved in tooth number variations, may
7 https://www.­orpha.­net/ for a list of centers).
be associated with polyps in the colon and osteomas
 422 N. Kotsanos et al.
17.1.3.1  ariations in Tooth Number:
V most common ones, in order of frequency, are Down
Epidemiology and Clinical
Phenotypes
In the primary dentition, the incidence of hypodon-
tia is 0.6% and of supernumerary teeth is 0.3% or
less. Both hypodontia and hyperdontia appear more
frequently in the maxillary lateral incisor region [38],
while oligodontia and anodontia occur very rarely in
the primary dentition – mainly in cases of ectodermal
dysplasia (. Fig. 17.5). Hypodontia in the primary
dentition usually leads to missing corresponding per-
manent teeth [39].
In the permanent dentition, hypodontia is much more
frequent, ranging from 2.6% to 11.3%, depending on
ethnicity and sample characteristics. Terminal reduction
is manifested and includes the third molar, second pre-
molar, as well as the maxillary lateral incisor and man-
dibular incisors at a prevalence of 4% [40]. In a young
Korean population with hypodontia in the high end of
prevalence spectrum, mandibular incisors were missing
about equally as frequent (34%) as the second premolars
[41]. Hypodontia involves usually one to two teeth, is
often symmetrical, and is rather more frequently found
in girls than in boys [40]. Non-syndromic oligodontia is
more rare, while anodontia occurs very rarely in cases
of ectodermal dysplasia. Hypodontia and microdontia
of the maxillary lateral incisors are related, and they are
inherited as an autosomal dominant trait, but knowl-
edge about the exact pathogenetic mechanism is limited
[41] (. Fig. 17.6). There are more than 100 syndromes
that include missing teeth. Information about these can
be found in digital databases such as OMIM (Online
Mendelian Inheritance in Man) and ORPHANET. The
a b
17
c d
..      Fig. 17.5 a Congenitally missing primary mandibular canines
resulting in diastemas. b The radiograph confirms their agenesis. c, d
Agenesis of the right and a large (fused?) left maxillary primary inci-
syndrome, cleft lip and palate, and ectodermal dyspla-
sia. Other less frequent are Rieger syndrome and incon-
tinentia pigmenti (. Fig. 17.6).
The prevalence of supernumerary permanent teeth
not related to syndromes is about 1.5%. They are more
frequently found in boys in the pre-maxilla, mostly near
the midline and called mesiodens (see 7 Chap. 10) [42,
43]. They are sometimes multiple hypoplastic supernu-
meraries found in the form of compound odontomas
(see later in this chapter). The presence of one or more
forth molars is relatively rare (. Fig. 17.7). In children
with cleft lip and palate, supernumerary as well as miss-
ing teeth at the cleft area are common. However, in cleft
lip and palate, missing teeth may not concern solely
teeth in the cleft area but also more distant teeth point-
ing toward a role of the responsible gene both in palate
and tooth development [ 44].
zz Treating Children with Missing Teeth
In the primary dentition, there is often no need for treat-
ment, unless aesthetics or function (mastication) is sig-
nificantly affected, as in cases of syndromic oligodontia.
The problem then might also be social, and, for opti-
mized integration of the child in society, prosthesis in
the primary dentition would be considered from 3 years
onward. Depending on the severity of the deficit, vari-
ous types of partial dentures can be constructed once
child cooperation can be achieved. In the permanent
dentition, the treatment plan should have a long-term
vision. Orthodontic assessment and treatment should
come before any prosthetic solution, particularly in the
anterior area. The most common problem is the agenesis
e
sor. e Anodontia of a 5.5-year-old boy with ectodermal dysplasia. (e:
courtesy Dr. E. Kotsiomiti)
Developmental Defects of the Teeth and Their Hard Tissues
423 17

a b

c d

e f

..      Fig. 17.6 Agenesis of permanent teeth. a, b Hypodontia in a of 11 permanent teeth (8 premolars, maxillary canines, and right lateral).
10-year-old boy and his father. Both have aplasia of a permanent lower Microdontia of her left lateral incisor. e, f Syndromic oligodontia in a girl
incisor. c, d Non-syndromic oligodontia of a 10-year-old girl. Agenesis with incontinentia pigmenti. Clinical and radiographic appearance

of upper lateral incisors. One solution could be aligning

the canine into the space of the lateral and then modify-
ing the shape of the canine to mimic a lateral incisor [45]
(. Fig. 17.8).
However, if the orthodontic assessment requires
maintaining the space of the lateral incisors (see
7 Chap. 11), an intermediate prosthetic solution can
be offered by bonding an artificial lateral incisor in a
removable appliance or directly onto the adjacent teeth
(7 Fig. 13.50). An implant solution may follow growth
..      Fig. 17.7 Panoramic radiograph of a 22-year-old with four super-
numerary molars (fourth permanent molars). The patient complained
of pressure during eruption of the third molars. (Courtesy Dr. V. Boka)
 424 N. Kotsanos et al.
..      Fig. 17.8 Shape correction by composite built-up of maxillary
canines after orthodontic space closure. It was intended to mimic
missing lateral incisors
completion in young adulthood. Because of limited evi-
dence, these clinical options are currently based on case
reports [46]. Severe oligodontia and conical anterior
teeth are often part of different expressions of ectoder-
mal dysplasia and contribute to a reduced height of the
alveolar process. The appliance chosen for reinstatement
of aesthetics and function will require adaptation to the
growing oral structures. A multi-disciplinary approach
including pediatric dentists, orthodontists, prosthodon-
tists, periodontists, and others is of advantage.
zz Treating Children with Supernumerary Teeth
In the primary dentition, there is usually no need for
intervention, unless the treatment plan requires an
extraction of the superfluous tooth/teeth. The timing
17 of the extraction is of great importance, especially when
it comes to extraction of a supernumerary permanent
tooth. It depends mainly whether or not it is performed
around the eruption time of the permanent tooth.
Waiting for the supernumerary tooth to erupt can reduce
the degree of difficulty of the extraction (. Fig. 17.9).
Impacted supernumerary teeth that are not expected
to erupt, such as inverted mesiodens, require exact
localization with various radiographic means, such as
CBCT. Usually, a surgical flap is prepared under local
anesthesia to carefully access and extract the tooth
(. Fig. 17.10). In cases where surgical exposure of the
tooth requires bone removal, care should be given to the
..      Fig. 17.9 a The presence of two supernumerary primary maxil-
lary lateral incisors. Extraction is only indicated for the one erupted
in the palate. b Supernumerary primary maxillary incisor (mesiodens)
aligned in the dental arch
periodontal tissues of adjacent teeth, because any minor
damage might result in ankylosis (see also 7 Chap. 10).
17.1.3.2  ariations in Size, Shape,
V
and Morphology of Teeth
Eye Catcher
Tooth type, size, and morphology are genetically
determined, but genetic factors may control mineral-
ization, too, as seen, for example, in certain types of
amelogenesis imperfecta. Environmental factors how-
ever may play their role in the morphology and shape
of the teeth and beyond those importantly disturb
their mineralization. Environmental factors can cause
injuries to the developing tooth bud through direct
trauma; deregulation of biological mechanisms by
high fever, inflammation, drugs, and chemicals; radio-
therapy of adjacent tissues; effect of cytotoxic agents;
and other serious insults.
zz Variations in Size
Abnormal tooth size may be local or generalized.
Microdontia is a relatively common finding. It may
Developmental Defects of the Teeth and Their Hard Tissues
a b
d e
..      Fig. 17.10 a Over-retention of the primary right central incisor
in a 7.5-year-old girl is being investigated radiographically. b The
presence of a mesiodens in a labio-palatal direction inhibits the suc-
cessor’s eruption. c Eight months following surgical removal of the
mesiodens, the impacted central incisor descent is slow, possibly
..      Fig. 17.11 Generalized mild microdontia of a 12-year-old girl,
particularly prominent in the premolar area producing diastemata
affect a group of the teeth (. Fig. 17.11), but more usu-
ally individual teeth, mainly the maxillary lateral incisor
(incidence 0.3% for primary and 1% for permanent ones)
[8]. In this case the crown is narrower and often conical.
Generalized microdontia is found in some syndromes,
e.g., Down syndrome, pituitary short stature, and ecto-
dermal dysplasia. Generalized macrodontia is found
rarely associated with syndromes, e.g., KGB, otodental,
or Ekman-Westborg-Julin (. Fig. 17.12). As an indi-
vidual finding, if ever present, it may resemble a double
tooth (gemination or fusion), which is a common dental
anomaly.
425 17
c
impeded by the already erupted lateral. This indicates its traction
along with space regaining. d This is now possible with a partial wire
arch. e A patient at a 3-year recall. No further orthodontic treatment
was necessary
Teeth with microrrizia (short roots) occur rarely,
e.g., in some cases of osteopetrosis or as a consequence
of radiation or chemotherapy during root formation
(. Fig. 17.13), and such cases need differential diag-
nosis from dentin dysplasia type I (rootless) or molar
incisor malformation (MIM) described later in the
chapter. Another type is known as short root anom-
aly (SRA), characterized by short roots, more so in
the incisors. Other teeth may exhibit the abnormal-
ity, and, rarely, there are generalized cases. The root/
crown ratio may be 1:1 or lower with crown anatomy
and periodontal tissues appearing normal. SRA was
quite common (1.3%) in a young Finnish population
[47]. There is a poorly understood genetic background.
Patients with SRA did not exhibit a significant change
of root length after orthodontic treatment when com-
pared to controls [48].
zz Variations in Shape/Morphology
Apart from the third molars, the permanent tooth that
presents diversities in shape with greater frequency is the
maxillary lateral incisor. Another variation that occurs
in both dentitions, usually in the palatal surface of
maxillary central incisors, is the talon cusp. This could
appear as an isolated trait or be part of a syndrome, like
the Rubinstein-Taybi, in which it represents a hallmark
diagnostic trait. Depending on its size, a talon cusp may
 426 N. Kotsanos et al.

..      Fig. 17.12 a Generalized

macrodontia in a 10.5-year-old a b
boy with Ekman-Westborg-Julin
syndrome. b Complete absence
of space for the erupting canines.
He needs orthodontic consulta-
tion for premolar extraction

a b

..      Fig. 17.13 a Stunted root formation (at age 15). At age 8.5 years, molars are unaffected, while maxillary laterals have near-­terminal
the patient was diagnosed with leukemia and received chemotherapy. root resorption
b A 12-year-old girl with generalized short root anomaly. The first

interfere with occlusion (. Fig. 17.14). The Carabelli’s

cusp located on the palatal surface of the upper first per- a b
manent molars is very common causing little problems.
Other extra cusps should be suspicious for dysplasia
(. Fig. 17.15).
Dens invaginatus is the result of the inner enamel
epithelium submerging in the underlying mesenchyme.
The folding of enamel within dentin has usually a tubu-
c d
lar form which may be limited to the crown or might
reach the root and create conditions for bacterial inva-
sion and pulpal infection. It affects more often lateral
incisors; possible suspicion from altered size, the pres-
17 ence of prominent palatal cingulum, or other surface
defects is checked by tactile and radiographic examina-
tions for diagnosis (. Fig. 17.16). Taurodontism may
occur in both dentitions as a rare dental anomaly, it is
however more commonly found in some syndromes. The
underlying mechanism is related to late invagination of
..      Fig. 17.14 a, b Talon cusps on the palatal surface of primary
Hertwig’s epithelial root sheath, which is responsible for maxillary central incisors. During tooth eruption talon cusps may
root formation. Radiographic examination shows long require periodic grinding. b Their radiograph shows particularly
pulp chambers with their floor in a more apical position wide root canals. c Big talon cusps in the palatal surface of the per-
so that the short roots’ appearance resembles a bull’s manent maxillary central incisors in a 10-year-old boy interfere with
occlusion. d The radiograph confirms normal roots
head (. Fig. 17.17).
The descriptive term “double teeth” includes the
fusion of two or more tooth germs and the gemina- i­ncidence of double teeth is more common in the ante-
tion of a normal with a supernumerary tooth or the rior area of the primary dentition in Caucasians (0.7
incomplete division of a tooth bud (. Fig. 17.18). The to 1.6%), and there is a high probability (20–75%) of
Developmental Defects of the Teeth and Their Hard Tissues
a b
..      Fig. 17.15 a One year after sealing this seemingly intact second
permanent molar, the patient complains of pain at biting. b The
radiograph shows apical periodontitis. c In drilling for endodontic
a c
..      Fig. 17.16 a Invagination of mandibular lateral incisor with pulp necrosis and a fistula in a 10-year-old boy. b Lingual aspect. c The
radiograph shows an anomalous wide root with enamel submergence
a
b c
..      Fig. 17.17 a Taurodontism of primary mandibular molars in a
6-year-old with one successfully pulpotomized. Elongated pulp cham-
bers in expense of root length and very late formation of successor
premolars. b, c Taurodontism of the first permanent molars and max-
illary primary molars in a 9-year-old with amelogenesis imperfecta
427 17
c
treatment, a large void in the dentin (arrow) is thought as infection
channel prior to sealing. The anomalous mesio-buccal cusp should
have raised suspicion
a missing permanent successor [49]. The crown may be
twinned or simply very wide and thus be wrongly per-
ceived as isolated macrodontia (. Fig. 17.19). The pulp
chamber is usually one large, but in case of fusion, there
may be two separate chambers. Differentiation between
gemination and fusion and diagnosis of macrodontia
and Talon cusp are carried out also by radiographic
examination and comparison to the contralateral tooth.
Dilaceration is a sharp angulation in the cervix,
root, or crown of a permanent tooth. It is most com-
monly caused by trauma to the corresponding primary
tooth, while the permanent one is about completing
crown formation. Odontomas refer to the creation of
a dental hamartoma or tumor of unknown etiology.
It may be extra dental formation(s) or a traumatized
developing tooth germ. It occurs mainly in the perma-
nent dentition; their size varies from few millimeters to
1 or 2 centimeters and usually inhibits the eruption of
one or more teeth. It appears in the form of compound
odontoma composed of multiple smaller supernumer-
 428 N. Kotsanos et al.

a b c

..      Fig. 17.18 a Fusion of maxillary lateral with a supernumerary tion with composite inhibits further caries in the fusion line and
tooth in a 3-year-old boy, with advanced caries in the fusion line. b improves aesthetics in the primary dentition
Radiograph showing the fused root ending in two apices. c Restora-

17
c d

..      Fig. 17.19 a Abnormally wide left permanent maxillary central gual aspect reveals fusion with the respective supernumerary teeth.
incisor of this 7-year-old appears as a macrodont. Its incisal edge has The course of cervical line and the exogenous pigmentation in the
one more mamalon than usual. b The root does not reveal signs of teeth “mid-line” support this diagnosis; a radiograph can verify it
fusion. c Wide mandibular central incisors in a 5-year-old boy. d Lin-
Developmental Defects of the Teeth and Their Hard Tissues
429 17
..      Fig. 17.20 a, b Compound
odontoma located palatally to a b c
maxillary central incisor of a
7-year-old girl, merely affecting
its eruption path. c The eight
surgically extracted supernu-
merary microdonts. d Complex
odontoma in an 8-year-old girl
prevents eruption of mandibu-
lar left first permanent molar.
Its eruption occurred spontane-
ously after extraction of the d
odontoma with local anesthesia

ary teeth or in the form of complex odontoma, which

is characterized by irregularly mixed hard dental tissues
or a combination of both called composite odontoma
(. Fig. 17.20).
Many other very rare forms of dental anomalies
a
have been described that it is not intended to present
here, and their etiology may be unknown. Just an exam-
ple is an exophytic hard dental tissue growth observed in
otherwise well-formed mandibular incisors [50].

zz Restoration of Dental Anomalies in Size, Shape, and

Morphology
In many cases, teeth with size and shape variations may
be modified by cutting and/or building with composite
resin to restore or improve their shape. Peg-shaped lateral
incisors are a typical example (. Fig. 17.21) just as was
described earlier for altering the shape of maxillary per-
manent canines to mimic lateral incisors (. Fig. 17.8). b
In the case of talon cusp, which usually contains a pulp
horn, grinding is done gradually, e.g., every 3 months,
to allow the formation of reparative dentin and avoid
pulp infection and necrosis. Drilling deep invagination
should be carefully planned to avoid pulp exposure. The
success of a possible endodontic treatment depends on
the complexity of the invagination and the access to the
root canal. Some cases are particularly difficult and end
up in extraction. Early sealing of suspicious palatal pits
of incisors may prevent carious complications.
In case of asymptomatic double primary teeth, there
is no need for any intervention apart from covering the ..      Fig. 17.21 a Hypoplastic “peg-shaped” lateral incisors of a
dysplastic fissures for caries prevention. If there are 15-year-old girl. b Reshaping with composite resin restoration in a
symptoms, extraction is preferred. In case of permanent strip crown with no tooth preparation to meet her aesthetic demand
 430 N. Kotsanos et al.
double tooth, if the shape of the pulp chamber permits
it, endodontic treatment is indicated, provided that an
aesthetic restoration, either conservative or prosthetic,
can follow. The sharp angulation in dilaceration often
results in impaction of the tooth. If possible, the tooth is
surgically exposed and guided into the correct position
in the dentition [51] (. Fig. 17.22). Surgical removal of
odontomas is usually carried out under local anesthe-
sia. In young children, nitrous oxide inhalation or some
other kind of sedation will aid child cooperation.
17.2 Malformations of Dental Tissue
Structure
17.2.1  he Structure of Enamel, Dentin,
T selectively enhance the attachment and proliferation of
and Cementum
Enamel, dentin, and cementum are three of the body’s
mineralized tissues. Enamel is of epithelial origin and
covers the crown of each tooth. In contrast, dentin
and cementum are of mesenchymal origin. Dentin
forms the bulk of the tooth and extends within both
the crown and root. It is of yellowish tint, in contrast
to the much whiter and harder enamel. Cementum is
deposited only in the root area. Each tooth is anchored
onto its socket (alveolar bone) by the periodontal liga-
ment (PDL) that connects cementum to the alveolar
bone through s­ pecialized made-of-collagen fibers [52].
Eye Catcher
Enamel, dentin, and cementum contain about 96%,
70%, and 50% (by weight) inorganic minerals, respec-
tively, mostly calcium and phosphate salts, such as
hydroxyapatite and others, as in other calcified tissues
in the body [53]. Their organic matrices are different.
The ameloblasts that are derived from ectoderm pro-
17 duce mainly amelogenin, enamelin, ameloblastin,
kallikrein, and other proteins. The odontoblasts, orig-
inating from mesenchyme (ectomesenchyme neural
crest), produce mainly collagen type 1 and some non-­
collagenous materials such as mucopolysaccharides.
The apposition of the matrix occurs between the
ameloblasts and odontoblasts as they keep retreating
from the dentino-enamel junction. The ameloblasts
end up at the surface of the rod-structured enamel
they had produced. The odontoblasts having left
behind the dentinal tubules (that contain their den-
tinal processes) remain at the periphery of the pulp
and continue to function throughout the life of the
tooth pulp, producing secondary and tertiary dentin
depending on the stimuli [1] (. Fig. 17.23).
At the formation of the organic substrate, mineralization
plays an essential role with simultaneous incorporation of
inorganic minerals at about 30%. Then, a period of matu-
ration follows. This is a period of slower (lasting several
months to a few years) completion of mineralization by
removal of the remaining matrix proteins by proteases and
replacement by minerals. The process advances from the
cusps to the cervical margin of the tooth and right down
the root. Cementum and periodontal ligament are essen-
tial for root formation and tooth eruption. Cementum
is an avascular mineralized tissue that covers the entire
root surface. It is the interface between the dentin and
the periodontal ligament and contributes to periodontal
tissue repair and regeneration after damage. The organic
extracellular matrix of cementum contains proteins that
cell populations residing within the PDL space [1].
All dental mineralized tissues are formed in a circa-
dian rhythm, which in light microscope sections are seen
as curved incremental lines, called after Retzius in enamel
and von Ebner in dentin. In the enamel of primary teeth
and sometimes also in the bucco-mesial cusp of the first
permanent molar, an accentuated incremental line can be
seen that corresponds to the time of birth which leaves a
record of the change from intra- to extra-­uterine life – the
neonatal line [54] (. Fig. 17.24). Its importance is that it
helps estimate the timing of events in the child’s life. In
forensics, it allows to decide if a child was born alive.
Formation of enamel and dentin is circadian, char-
acterized by daily repeated activity that controls cell
morphology, gene expression, secretion, and degrada-
tion/removal of the proteins. All secretory, mineraliza-
tion, and maturation stages are of vital importance for
the final product and are regulated by relevant genes. As
a result of differences in the circadian rhythm profile, the
thickness and hardness of the enamel can vary greatly;
this will affect the susceptibility of the tooth to caries,
abrasion, and breakdown [53, 55]. Malformations in the
structure of both hard tissues may occur due to disor-
ders during tissue differentiation, formation, mineral-
ization, and maturation stages. They are associated with
many causative factors, environmental and/or genetic. A
mild disturbance may be seen in light microscopy as an
accentuated line or if more severe as a hypoplastic defect
or opacity. These insults may be chronologically associ-
ated with possible causative events and assist diagnosis.
17.2.1.1 Mineralization Chronology
of the Teeth
Despite its variation, chronology of odontogenesis is
always described as the mean average of observations
and shown in . Fig. 17.25. The mineralization of the
crown of the primary tooth starts from the cusps in the
first half of the fourth month in utero until the middle
Developmental Defects of the Teeth and Their Hard Tissues
c d
..      Fig. 17.22 a Maxillary central incisor dilaceration in a periapical
radiograph. b The CBCT gives a three-dimensional spatial relation-
ship of the dilacerated incisor. c, d Traction through orthodontic
of the fifth month in utero (second molars). The crowns
are completed during the first year of life, during the
first months for the incisors and the last months for the
canines and second molars. The formation of roots is
completed at the age of 1.5–3 years (. Table 17.4). The
mineralization of the first permanent molars and inci-
sors (excluding the upper lateral) begins roughly at birth,
431 17
treatment made aligning possible [51]. (By permission from Am J
Orthod Dentofacial Orthop)
while canines and the upper lateral incisors start to min-
eralize at the start and the end of the first year, respec-
tively. Premolars and second molars mineralize between
the age of 2 and 4 years (delays for the second premolars
are frequent), and third molars between the age of 8 and
13 years (. Table 17.5). The completion of mineraliza-
tion of the crown takes about 5–7 years, while the roots
 432 N. Kotsanos et al.

require about equal time, with the pace of mineraliza-
tion and ultimately its duration being greater in the teeth
formed later (like the second molars and premolars).
Girls are usually about 6 months ahead of boys in
completing mineralization of the teeth. The figure show-
a b
ing the stages of the mineralization of the teeth in the
panoramic radiograph is useful in calculating dental age.
17.2.2 Clinical and Histological
Appearance, Etiology, and Diagnosis
A detailed clinical examination and history-taking help
diagnose the type of dental defect and deliver appropri-
ate treatment, possibly by multi-disciplinary approach
with other health professionals if a systemic disorder is
suspected (. Table 17.6).

17.2.2.1  evelopmental Dental Defects

1 μm
..      Fig. 17.23 The start of enamel formation in a mouse tooth in the
transmission electron microscope. a Ameloblast is located on the
upper left side. Collagen fibers (CF) with characteristic vertical
stripes. b Right below, enamel rods are in connection with collagen
of predentin and the cellular membrane of the ameloblast, where
mineralization is about to start [53]. (By permission)
D
with Environmental Origin
Developmental defects of enamel can be manifested as
reduced matrix formation, causing reduced quantity of
enamel (hypoplasia), or as loss of its translucency (seen
as opacity) and hardness. Both can be caused by systemic
or local causes. The size and location of the defects will
depend on the severity, duration, and time of the insult,
i.e., the stage of enamel development at that time. If an

a b

17

..      Fig. 17.24 a Photomicrograph of hard longitudinal tooth section showing the neonatal line (NNL) [54]. (By permission). b Drawing of
human primary incisor showing the neonatal line (P pulp, D dentin, E enamel)
Developmental Defects of the Teeth and Their Hard Tissues
433 17
..      Fig. 17.25 The chronology
14
of the formation/mineralization
of all teeth (except for the third 12
permanent molars) appears on 10
the left (in months) for primary 32 8
teeth and on the right (in years) 24 6
for permanent teeth (0 is birth
16 4
time). The curved lines on the

Permanent teeth (years)

Primary teeth (months)
root relate to the root length at 8 2
eruption. Tooth length is propor- 0 0
tional to duration of its
formation. Primary teeth are
light blue in color. Tooth parts at 0 0
the bottom signify the formation 8 2
stage at birth time
16 4
24 6
32 8
10
12
14

..      Table 17.4 The chronology of mineralization and eruption of the primary teeth

Start of mineralization Crown completion Tooth eruption Root completion

(intrauterine week) (age in months) (age in months) (age in years)
Tooth Maxilla Mandible Maxilla Mandible Maxilla Mandible Maxilla Mandible

Central incisor 14th 14th 11/2 21/2 10 8 11/2 11/2

Lateral incisor 16th 16th 21/2 3 11 13 2 11/2
Canine 17th 17th 9 9 19 20 31/4 31/4
First primary 15th 15th 6 51/2 16 16 21/2 21/4
molar
Second primary 19th 18th 11 10 29 27 3 3
molar

..      Table 17.5 The chronology of mineralization and eruption of the permanent teeth

Start of mineralization Completion of the crown Eruption Completion of the root

(age in years) (age in years) (age in years)
Tooth Maxilla Mandible Maxilla Mandible Maxilla Mandible Maxilla Mandible

Central incisor 3rd month 3rd month 4½ 3½ 7½ 6½ 10½ 9½

Lateral incisor 3rd month 3rd month 5½ 4 8½ 7½ 11 10
Canine 4th month 4th month 6 5½ 11½ 10½ 13½ 12½
First premolar 20 months 22 months 7 6¼ 10½ 10½ 13½ 13½
Second premolar 27 months 28 months 7½ 7½ 11 11½ 14½ 15
First permanent 32nd week in 32nd week in 4½ 3½ 6½ 6 10½ 10½
molar utero utero
Second 27 months 27 months 7½ 7½ 12½ 12 15½ 16
permanent molar
Third permanent 8 years 9 years 14 14 20 20 22 22
molar
 434 N. Kotsanos et al.

..      Table 17.6 Hereditary dental hard tissues defects (most common)

Condition Phenotype Gene Protein product OMIM

Enamel
Amelogenesis Hypoplasia, hypomaturation dose AMELX (X-linked) Amelogenin, enamel 301,200
imperfecta type IA dependent matrix protein
[56]
Amelogenesis Hypoplasia ENAM (AD) Enamelin matrix 104,500
imperfecta type IB Dose dependent protein
Severe hypoplastic pitted enamel with
grooves
Amelogenesis Hypomineralized pigmented enamel KLK4 (AR) Maturation stage 204,700
imperfecta type enamel proteinase
IIA1
Amelogenesis Hypomineralized pigmented enamel MMP20 (AR) Enamel proteinase 612,529
imperfecta type (secretory stage)
IIA2
Amelogenesis Hypomaturation, grossly opaque enamel WDR72 (AR) Membrane 613,211
imperfecta type leading to discoloration and breakdown trafficking protein
IIA3 (endocytosis)
Amelogenesis Hypomaturation AI C4ORF26 (AR) May encode an 614,832
imperfecta type extracellular matrix
IIA4 acidic phosphopro-
tein
Amelogenesis Hypomaturation AI SLC24A4 (AR) Na/K exchanger 301,201
imperfecta type
IIA5
Amelogenesis Localized or generalized hypomineral- FAM83H (AD) Not characterized 130,900
imperfecta type III ized enamel
Dose dependent
Amelogenesis Hypoplastic AI with taurodontism DLX3 (AD) Transcription factor 104,510
imperfecta type IV;
AI4
Amelogenesis Generalized hypoplastic and failure of FAM20A (AR) Not characterized 614,253
imperfecta and tooth eruption, gingival hypertrophy
gingival fibromato-
sis syndrome
Dentin

17 Shields type Osteogenesis imperfecta COL1A1 (AD) or COL1A2 Collagen 125,490

I-DGI-I [57] Brown to blue discoloration and attrition Mutations can reduce the
in both the deciduous and permanent amount of collagen (less
dentitions severe) or produce defective
Pulpal obliteration collagen (more severe
The degree of expressivity is variable phenotype)
Shields type Opalescent dentin DSPP (AD) Dentin sialophos- 125,420
I-DGI-II [58] Pulpal obliteration phoprotein
Bulbous crowns
Discoloration in both dentitions
Developmental Defects of the Teeth and Their Hard Tissues
435 17

..      Table 17.6 (continued)

Shields type Multiple pulp exposures in the deciduous DSPP (AD) Dentin sialophos- 125,500
I-DGI-III teeth phoprotein
(Brandywine Bell-shaped permanent teeth
isolate) [ 59] Early abscess
Shell teeth
Dentin dysplasia Permanent and deciduous teeth crowns SMOC2 (AD) – 125,400
type I (DD-I) [ 60] have normal shape and color in most
cases
Diminished root development with
unusual mobility and early exfoliation
Periapical radiolucencies in non-carious
teeth
Dentin dysplasia Dentin dysplasia II is distinguished from DSPP (AD) Dentin sialophos- 125,420
type II (DD-II) [61] DGI-II because the permanent teeth are phoprotein
normal in color but show “thistle-tube
pulp chambers” and pulp stones on
radiographs
Cementum
hypoplasia
Tricho-dento-­ Taurodontism DLX3 (AD) Transcription factor
osseous (TDO) Enamel hypoplasia
syndrome [62] Kinky, curly hair at birth
Increased thickness and density of the
cranial bones
Amelogenesis Hypomaturation-hypoplastic AI type DLX3 (AD) Transcription factor 104,510
imperfecta (type IV; Taurodontism
AI4) [63]
Cleidocranial Supernumerary teeth RUNX2 Transcription factor 119,600
dysplasia [64] Impaired eruption
Deficient bone and cementum
Formation
Epidermolysis Enamel hypoplasia PLEC1 Intermediate 226,650
bullosa (several) Cementum dysplasia COL17A1; LAMA3; filament-binding 226,670
Taurodontism LAMB3; LAMC2; Components of 226,700
ITGB4 hemidesmosomes 226,730
Hypophosphatasia Increased urine phosphoethanolamine ALPL Membrane enzyme 241,510
[65] bowing of long bone that converts
Bony fractures pyrophosphate to
Cementum hypoplasia or aplasia phosphate
Premature exfoliation of primary teeth
(around age 3–4 years old)
Cementum
hyperplasia
Gnathodiaphyseal Various amounts of cementum-like ANOCTAMIN 5;(ANO5) 166,260
dysplasia calcified mass are found in x-rays
Cemento-osseous It is a benign condition of the jaws that Unknown
dysplasia may arise from the fibroblasts of the
periodontal ligaments it is most common
in African-American females
 436 N. Kotsanos et al.
insult occurs at the initial formation phase of the organic
substrate of the enamel, it can cause hypoplasia, i.e., quan-
titative deficit of enamel. The enamel can be thinner or
of relatively normal thickness but with pits or grooves.
If it affects mineralization, either initial or late stage, the
result would be hypomineralization or hypomaturation,
respectively, i.e., qualitative defect of enamel with loss of
its translucency. In hypomineralization there is usually a
more severe deficiency in minerals than in hypomaturation
resulting in softer less protective enamel.
The opacities may be diffuse or well demarcated.
Literally speaking, these terms are clinical as they are
observed visually, while the terms hypomineraliza-
tion and hypomaturation are histological ones despite
they are often being used interchangeably. The DDE
(Developmental Defects of Enamel) Index was pro-
posed by the International Dental Federation (FDI) to
distinguish and epidemiologically record these develop-
mental defects of enamel, namely, 1) hypoplasia, 2) dif-
fuse opacities, and 3) demarcated opacities. There are
however other means or indices for classifying some
defect entities like amelogenesis imperfecta or molar
incisor hypomineralization (see later in the chapter).
Histological examination with a polarizing micro-
scope shows that the appearance of hypomineralized
enamel under the microscope is not very different than
enamel demineralized by the carious process, i.e., it is
porous and opaque. Thus, other clinical characteristics
like the topography are important for differential diag-
nosis. Hypomineralization opacities may be white or
yellowish to brown. Discoloration may increase in time,
due to degradation of the organic components and/or
the influx of pigments from the oral environment. After
tooth eruption, severely hypomineralized enamel may
be broken down by mastication forces (post-eruptive
breakdown). This is an acquired finding and may not
be mistaken as hypoplasia. The distinction is based on
the rounded defect boundaries in the case of hypopla-
sia. Opaque enamel adjacent to a hypoplastic defect is
17 not uncommon and indicates more lasting disturbance,
­initiated at the formation stage of enamel.
The medical history is important for diagnosis of
developmental disturbances, i.e., maternal health dur-
ing pregnancy, perinatal period events, and child health
in the infantile period. Any disturbance, like high fever,
sickness, or use of certain drugs, can be a contributing
factor to the defect, if it disturbs ameloblast function
and mineralization, so the child’s medical history should
also be accurately recorded. Type of birth, full term or
premature birth, whether intubation was necessary,
complications during childbirth, breastfeeding, fluoride
supplementation, and past serious illnesses or high fever
are important notes of history-taking. Radiographic
findings, other relevant findings in the hair or nails, and
searching for similar defects in first-degree relatives may
be very useful for diagnosis [66].
A single-affected tooth usually signifies a local cause,
a group of symmetric teeth affected a systemic envi-
ronmental (chronological) one, and when whole denti-
tions are affected (primary and permanent) signifies a
genetic cause. Systemic defects of environmental origin
often involve the enamel as the ameloblasts are consid-
ered sensitive to low oxygen pressure and to high body
temperature. At birth, for example, the normal but sud-
den change in diet and oxygenation is being recorded in
enamel – and dentin – of primary teeth with the neo-
natal line. Difficult or premature birth/low birth weight
of the infant might cause accentuation of that line [67].
Clinically apparent developmental dental defects
caused by environmental reasons may occur throughout
the course of tooth formation, before, during, and after
birth. After the age of 7, mineralization and maturation
of all crowns are expected to be complete, apart from the
third molars (. Fig. 17.25). When the causes are systemic,
there would usually be relatively symmetrical defects in all
teeth developing during the time of the insult. When the
causes are local, they involve a single region or a single
tooth. If the cause, either systemic or local, acts for a given
period, it may affect only a part of the crown of the tooth.
Knowing the time of the formation of all teeth, a clinician
can figure out the time and inquire for the specific cause.
zz Molar Incisor Hypomineralization (MIH)
Molar incisor hypomineralization (MIH) affects the
enamel of one or more first permanent molars and usu-
ally the incisors, too. MIH is the most common qualita-
tive, developmental disorder of the enamel. The crown
of the first permanent molar erupts with irregular, well-­
demarcated, opaque discolored areas (hypomineralized
enamel). At the time of eruption, the tooth surface is
believed to be intact. With time, depending on the sever-
ity of hypomineralization, progressive discoloration
and/or post-eruptive breakdown (PEB) of enamel may
occur [68, 69] (. Fig. 17.26). The consequent increased
plaque accumulation often causes severe caries, leading
to rapid crown destruction.
In the past high caries era, molars with severe MIH
became heavily carious very quickly, often resulting in
extraction. Diagnosis was difficult and escaped attention
(. Fig. 17.27), but, as the prevalence of dental caries in
children and adolescents became significantly reduced,
MIH came to be easily recognized. Epidemiology finds
prevalence varying greatly throughout the countries
between 3.5 and 40% with a mean world average of
14.2%, as suggested by a meta-analysis [70]. The high-
est has reported in countries of Northern Europe and
Brazil, but this is constantly updated as new reports
are increasingly published (. Fig. 17.28). Most cases
Developmental Defects of the Teeth and Their Hard Tissues
are mild, and more severe forms of MIH with enamel
breakdown accounted for 13% in 8-year-olds and signif-
icantly more, i.e., 35%, in 14-year-olds of all MIH cases
in one of those studies [69].
a b
c
..      Fig. 17.26 Severity examples in MIH. a Demarcated opacity of
white and brown color in a newly erupted molar (mild MIH but with
the potential to become severe with time). b Severe MIH at newly
erupted molar with breakdown becoming carious. c Demarcated
white opacity (mild form) in a central incisor. MIH severity of the
child is determined by the worst affected tooth
..      Fig. 17.27 Three mandibular molars of this 8-year-old with severe MIH have become heavily carious. The same is true for one of the
hypomineralized second primary molars (HSPM)
437 17
The typical appearance of MIH involves mainly
the first permanent molars and, in at least half of the
cases, the permanent incisors. These 12 teeth are fre-
quently mentioned as the index teeth for MIH. The
lesions in incisors cause mostly aesthetic concerns
and present breakdown infrequently. Those in the
molars can cause significant destruction, pain, and
functional problems. Microscopically the pulp shows
signs of hyperemia and mild inflammation, probably
due to the invasion of bacteria and bacterial prod-
ucts through the porous enamel and via the dentinal
tubules [71]. These histological findings in the pulp
might explain the intense sensitivity of the affected
teeth to thermal and osmotic stimuli, which tend
to drive children to avoid brushing, reinforcing the
vicious caries cycle, and are responsible for the dif-
ficulties in reaching adequate anesthesia levels during
restoration.
Eye Catcher
The appearance of MIH-type lesions in primary
molars – in the second one in particular, hence the
acronym HSPM, hypomineralized second primary
molar – is quite common, about half the MIH
­prevalence. Its severe form has been recognized as the
cause for the large, atypical, carious cavities of these
teeth (. Fig. 17.29). The relationship between the
occurrence of HSPM and MIH suggests a shared
cause and indicates that clinically the first can be used
as a predictor for the latter [72]. Usually less severe
MIH-type defects may be found in any other perma-
nent teeth with prevalence per tooth compared to that
in incisors (. Fig. 17.30). While severe defects are
rare, opacities often appear less well demarcated in
premolars and second permanent molars [73].
 438 N. Kotsanos et al.
..      Fig. 17.28 Histogram based on MIH prevalence reports in the literature until 2013. In some countries a second or third study (in red and
green, respectively) had been conducted with the majority of studies being in European countries (left half of the horizontal axis) until that time
a b
..      Fig. 17.29 a, b Hypomineralized primary molars and caries.
Radiolucent dentinal lesions on both mandibular right molars are
due to caries, but the clinical view suggests lesions are developed on
a HSPM background. c Brown opacity (still mild MIH) in a maxil-
17
Histologically, the lesions usually involve the entire
thickness of the enamel (. Fig. 17.31). Therefore,
unless very mild, they cannot be removed by superficial
(micro-)abrasion. The hardness of the porous enamel is
significantly reduced, with rods appearing thinner and
with empty spaces between them in scanning electron
microscope [74]. Despite the systemic nature of the
disease, the lesions are not characterized by symmetry
as they affect from one to four molars with defects of
various sizes and in different tooth locations [68]. Con-
sidering the period of formation/mineralization of the
enamel, causative factors of typical MIH should act
mainly during the perinatal period or in the first year
of life (. Fig. 17.32). The etiology is primarily environ-
mental, and a proposed mechanism incriminates serum
c d
lary second permanent molar. d Mandibular second permanent
molar with severe MIH-type lesion with breakdown-driven carious
cavity while at an eruption process
albumin entrapment, which blocks normal enamel pro-
tein removal for uneventful replacement by mineral [75],
but this is still open to further research. Causative fac-
tors have not been fully clarified. Among those impli-
cated are premature birth and low birth weight, birth
complications and cesarean section, mother illness at
late pregnancy, early childhood diseases especially in the
respiratory system in combination with high fever epi-
sodes, administration of amoxicillin, varicella, exposure
to bisphenol A during pregnancy, and late introduc-
tion of gruel [76]. A genetic component involving gene
expression during dental enamel formation or affect-
ing the immune response cannot be ruled out, while no
explanation has yet been offered for the asymmetrical
clinical presentation of MIH.
Developmental Defects of the Teeth and Their Hard Tissues
439 17
..      Fig. 17.30 Per tooth 140
prevalence and severity of White opacity yellow/brown opacity
MIH-­type opacities in all 120 poster uptive breakdown atypical restoration
permanent teeth of 14-year-old atypical extraction
adolescents. [73] (By permission) 100

80

60

40

20

0
17 16 15 14 13 12 11 21 22 23 24 25 26 27

47 46 45 44 43 42 41 31 32 33 34 35 36 37
0

20

40

60

80

100

120

140

a b

..      Fig. 17.31 a Longitudinally split surface of MIH molar. Areas of enamel hypomineralization are more opaque and extend in its full
depth being absent in the cervical area. b Similar appearance of HSPM mainly in its occlusal enamel. [74] (By permission)

zz Restoration of Teeth with MIH
Older studies reporting MIH restorative outcomes
reported that children with MIH had a tenfold chance
of restorative needs in their first permanent molars and
three times more chance of repeated treatment in the
same teeth [77]. A treatment plan should respect the
severity level; mild MIH may be treated by remineraliza-
tion or sealants, and severe MIH requires restorations
or crowns [77, 78]. Thus, in mild cases, monitoring and
preventive programs are sufficient, including placing
sealants in occlusal fissures, despite the reduced reten-
tion expected in molars with MIH [79]. The applica-
tion of 5% NaOCl rinse to remove part of the organic
content of hypomineralized enamel before etching does
not appear to increase the tag length of resin sealant
[80], while the use of adhesive agents before the sealant
application seems to increase its retention [79]. In cases
where breakdown of severely hypomineralized enamel
is observed or anticipated, the extent of its removal at
cavity preparation poses a dilemma. A good clinical
 440 N. Kotsanos et al.

..      Fig. 17.32 Typical severe MIH in an 8-year-old boy. The mother tion started prenatally – are more resistant to breakdown than the
had prolonged labor with full-term birth complications. It is remark- rest of the enamel. Incisors have a mild form, so far
able that cusp tips of the first permanent molars – where mineraliza-

guide is to remove as much affected enamel as possi-

a b
ble by means of a round steel bur in a low-speed hand
piece only. Another conservative approach in hypo-
mineralized fissure areas may be to extensively cover
them with resin composite and thus prevent breakdown
(. Fig. 17.33). Enamel opacity color bears relation to
severity, with yellow/brown having more chance for
breakdown than white opacities [81]. In selecting restor-
ative material, resin composite bonding with sound
adjacent enamel seems advantageous [82] and thus is
preferred to amalgam, which is associated with further ..      Fig. 17.33 a Minimal preparation with low-speed hand piece in
17 marginal fractures when its margins are not placed in the slightly broken down central fissures of recently erupted maxillary
entirely sound enamel [77]. second permanent molar. b Successful survival of the overlaid com-
As a medium-term solution to prevent rapid decay posite restoration on occlusal and palatal surfaces in the 5-year recall
following the early breakdown of enamel until the full
eruption of molars with severe MIH, or in fearful, appre- a b
hensive children, restoration with resin-modified glass
ionomer cement (RMGIC) is proposed (. Fig. 17.34).
Placing PMC in the first molars with severe multi-surface
defects is a relatively easy and inexpensive option until
adulthood and may then be followed by ceramic crowns
or onlays. In very severe cases, extracting at an appro-
priate age (ideally 8–11 years with mandibular molars
on the earlier range side) drives the second molars drift
mesially and close the space spontaneously or with min-
imal orthodontic correction [83] (. Fig. 17.35). For the ..      Fig. 17.34 a Newly erupted maxillary second permanent molar
with severe MIH (breakdown and caries). b Cavity protection with
affected incisors, the use of a small amount of opaque RMGIC and postponement of definitive restoration
Developmental Defects of the Teeth and Their Hard Tissues
a b
..      Fig. 17.35 a, b An 11-year-old boy with severe MIH in the man-
dibular first molars, one with endodontic needs and normal relation
of incisors. The recent formation of bifurcation of mandibular sec-
ond permanent molars together with the existing developing third
and appropriate shade of resin composite produces usu-
ally good aesthetic results (. Fig. 17.36), while micro-
abrasion with infiltration techniques may be options
for very mild cases (. Fig. 17.37). Rarely if ever caries
becomes an issue to anterior teeth with MIH.
zz Molar Incisor Malformation
It was not until 2014 that severe root hypoplasia of
the first permanent molars, coexistent in at least half
of the reported cases with similar findings in primary
second molars, crown hypoplasia of permanent inci-
sors, and less often hypoplastic defects to other teeth,
was reported [84, 85]. The term currently used is molar
incisor malformation (MIM). The molar crowns
seem normal clinically, while radiographically the
pulp chambers appear very flattened. Their roots are
anomalous in shape, thin or short, or are nearly absent
(. Fig. 17.38).
While no prevalence data are yet available, it does
not seem to be a rare dental anomaly [86]. Systemic
illnesses in the first year of life, more often involving
neural structures, are present in the majority of MIM
cases, and these possibly pose an insult to developing
dental tissues. MIM pathogenesis is currently being
searched more intensely. The anomaly seems to begin
at about the formation of cervical enamel and dentin,
severely affecting the integrity of the pulp chamber and
canals and the Hertwig’s root sheath. The first perma-
nent molars present usually with signs and/or symp-
toms of non-­cariogenic pulp inflammation or necrosis.
These teeth often become mobile and lost early; if not,
their malformed roots rarely can be successfully treated
endodontically. No treatment other than their extrac-
tion seems appropriate, as MIM is typically seen early
in panoramic radiographs when molar space closure is
still possible.
zz Enamel Fluorosis
Fluoride (F) has led to significant reduction in den-
tal caries incidence in the previous decades world-
441 17
c
permanent molars justifies a decision to extract the affected first
molars. c Complete eruption of mandibular permanent teeth in
18 months. Persisting spaces may be managed with orthodontic
treatment
a b
c d
..      Fig. 17.36 a Maxillary lateral incisors of an 11-year-old girl, one
with mild and one with severe MIH. b Restoration of the left one:
partial removal of hypomineralized enamel in depth, but complete
peripherally, with bevel in healthy enamel. c The final restoration
with composite after placing a thin layer of opaque. d Case of severe
MIH in a 25-year-old man. PMCs were placed in three first perma-
nent molars 18 years ago. The effect of time is evident in the opaci-
ties and breakdown of lateral incisors, which had received no
restoration
wide. When long-term accumulation of higher than
the accepted doses of F occurs, it can cause incom-
plete enamel mineralization (hypomaturation), result-
ing clinically in diffuse opacities, which can be mild
to very severe. The most porous areas, after tooth
eruption, become strongly discolored, hence the old
name mottled teeth (. Fig. 17.39). In mild to moder-
ate cases, superficial enamel is worn away in time by
occlusal forces. This may be mimicked in the dental
clinic for aesthetic purposes. The fluorosis severity is
classified into five to nine categories according to vari-
ous existing indices (Dean, TSIF, TFI, etc.) [87]. The
pathogenic mechanism of fluorosis also involves other
factors such as matrix metalloproteinases (MMPs)
mentioned also in the mechanism of amelogenesis
imperfecta.
Severe fluorosis occurs after chronic ingestion
of water containing much higher than the desired
 442 N. Kotsanos et al.

a b

..      Fig. 17.37 a Maxillary incisors with demarcated white opacities. b The centrals were treated with microabrasion (scrubbing the affected
areas with slurry of 18% hydrochloric acid and pumice) and additional resin infiltration in the right one

(0.7–1 ppm) fluoride ion concentration. This occurs

a naturally in certain areas of the world, for example,
Tanzania, China, etc. Aesthetic restoration of these
teeth is achieved by direct or indirect restorations and
veneers or with porcelain or zirconia crowns. Mild to
moderate forms of fluorosis may be found endemically
in almost every country [87].
Mild forms of fluorosis can also occur, from drink-
ing natural or even artificially fluoridated water, use of
fluoridated water in baby formulas, or by prolonged
ingestion of fluoride toothpaste around the age of
2 years (see “Toxicity of Fluoride” in 7 Chap. 12).
b The clinical picture is in the form of diffuse horizon-
tal areas, which is the most common, and needs dif-
ferentiation from other similar lesions, such as those
of hypomaturation-­type amelogenesis imperfecta (see
below). Histologically, in fluorosis, the porous lesion of
enamel, in contrast to those observed in MIH, involves
only the outer part, of a few hundred microns of the
enamel. Therefore, with dental wear that occurs with
age, or with micro-abrasion technique [88] applicable
at the dental office, the white or discolored undesirable
look of some of the lesions can be improved dramati-
17 c cally (. Fig. 17.40).

17.2.2.2  namel Dysplasias Related

..      Fig. 17.38 a Panoramic radiograph of a 9-year-old girl with
MIM involving all first permanent and second primary molars. b Her
clinical presentation is as yet relatively normal. c A 13-year-old boy
with MIM. All first molars have dysplastic roots with apical radiolu-
cencies, while the second molars seem unaffected. In view of all third
molar presence, he should have been treated as a 4X6 extraction case
at a younger age
E
to Diseases or Drugs
Metabolic disturbances, drugs, and many other insults
during tooth formation, if beyond the biologic thresh-
old of the cell or the individual, can harm the sensitive
ameloblasts and cause cessation of matrix formation
(hypoplasia) or disturbed mineralization that will leave
a mark on the surface of the tooth, as a developmen-
tal defect. The timing, duration, and intensity of the
insult will determine the position, extent, and severity
of the defect.
Clinically, partial or total lack of enamel can be
observed in a tooth or expressed as pitting, striations,
Developmental Defects of the Teeth and Their Hard Tissues
443 17
a b

..      Fig. 17.39 a Mild enamel fluorosis of an adolescent (TFI = 1–2). about 2 ppm fluoride during her preschool years. Points of break-
Even in the recommended concentration of artificially fluoridated down are seen in the superficial enamel (TFI = 5), while the discolor-
water, 10% of the children may present mild fluorosis. b Moderate ation is acquired, attributed to pigment penetration (TFI,
fluorosis (TFI = 4–5) in a young woman after drinking water with Thylstrup-Fejerskov index of fluorosis)

and fissures, single or multiple, with smooth edges. a

In systemic conditions, the lesions will be symmetri-
cal or as generalized hypoplasia [89]. Some medical
conditions can cause developmental dental defects,
and the medical history of the child is important for
linking with the etiology of the defect (. Fig. 17.41).
Premature birth, serious chronic viral and bacterial
infections, high fever, and conditions with a possible
effect on calcium metabolism may be responsible, as
well [68, 76]. b
Some conditions that may have that effect are listed
below:

55 Toxic effect of drugs, chemical elements, or sub-

stances (fluoride, tetracycline, dioxins).
55 Severe malnutrition, neonatal hypocalcaemia, rick-
ets from hypovitaminosis D, and jaundice.
55 Thyroid and parathyroid disorders and hyper-­
hemoglobinemia. c
55 Mother’s diabetes, metabolic disorders of the infant
(e.g., liver, kidney, or celiac disease), and others.

zz Localized Defects from Environmental Causes

Traumatic intrusion of a primary incisor might destroy
the ameloblasts of the bell stage tooth anlage and cause
a hypoplastic defect in the crown of the permanent
successor. A chronic abscessed primary molar might
cause bone infection and injure the developing premo-
d
lar tooth germ. The type and size of the damage in the
permanent tooth depends on the stage of development
of the tooth bud, as well as the intensity and duration
of the insult [76].
Other reasons of localized hypoplasia or defect are
radiotherapy: in the formation phase of some teeth, it
may cause hypoplasia, microdontia, complete inhibi-
tion of the formation of some teeth, or stunting the
growth of their roots. Hypoplasia of primary inci-
sors is observed in some premature infants may be ..      Fig. 17.40 a Mild enamel fluorosis in a 10-year-old boy raised in
due to trauma from the metal laryngoscope intuba- Hong Kong with artificially fluoridated water (then 0.7 ppm). The
possible cause was the additional ingestion of fluoride toothpaste
tion attempt (. Fig. 16.12). It has been suggested that during preschool age. b Appearance after micro-abrasion with Prema
such enamel defects of the primary dentition may be (Premier Dental Products) of right and with abrasion with composite
serious predisposing factors for severe ECC [89]. polishing diamond bur of left incisors. The aesthetic result is similar.
c Moderate enamel fluorosis in maxillary incisors of an 8-year-old. d
Important aesthetic improvement after micro-­abrasion with Prema
 444 N. Kotsanos et al.

a b

c d

17

..      Fig. 17.41 a Severe enamel hypomineralization of a toddler aged
16 months with a history of premature birth at 25 weeks of preg-
nancy. b Chronological enamel hypoplasia of a 10-year-old with a
history of hypoparathyroidism diagnosed soon after birth. c Chron-
ological enamel hypoplasia of an 11-year-old girl with no recorded
history. It is proposed that the insult occurred during the first year of
life, and it did not affect the upper lateral incisors (intact left maxil-
lary canine is primary). d Chronological enamel hypoplasia of an
8-year-old girl with a history of meningococcal septicemia in the age
of 10 months. e The unilateral full-depth enamel hypoplasia of a
newly erupted second permanent molar could be attributed to the
young patient’s medical history of severe respiratory infection at age
3 years
Developmental Defects of the Teeth and Their Hard Tissues
445 17
17.2.2.3  ental Defects with Genetic
D
..      Table 17.7 Classification of amelogenesis imperfecta
Background based on phenotype and the mode of inheritance, according
zz Amelogenesis Imperfecta (AI) to Witkop [93]
Amelogenesis imperfecta, the only known inherited
malformation of the enamel, occurs with variable Type 1. Hypoplastic Enamel inheritance
frequency of approximately 1:4000–14,000, but an 1Α Hypoplastic, generalized pitted Autosomal
extremely high (1:700) prevalence in a closed commu- dominant
nity of Sweden has been reported [90–92]. According 1Β Hypoplastic, localized pitted Autosomal
to a current definition, AI is a group of heterogeneous dominant
genetic conditions or rare diseases that affect the struc-
1C Hypoplastic, localized pitted Autosomal
ture and appearance of enamel of all or almost all recessive
teeth, inherited with different modes of transmission
1D Hypoplastic, diffuse smooth Autosomal
(autosomal dominant (AD), autosomal recessive (AR),
dominant
X-linked). AI may rarely be associated with other mor-
phological or biochemical lesions [93]. The autosomal 1E Hypoplastic, diffuse smooth X-linked dominant
mode of transmission involves about 95% of cases, and 1F Hypoplastic, diffuse tough Autosomal
the sex linked 5%. dominant
AI manifests through a variety of phenotypes, and 1G enamel agenesis Autosomal
this has led to many attempts to build a classification recessive
[91–98], some of which add also mode of inheritance and
Type 2. Hypomaturation
eventually histological background. Additionally, the
development of genetic research has contributed to the 2Α diffuse pigmented Autosomal
recessive
designation of specific genes to different types of AI [96]
and thus arose classifications with molecular basis [97]. 2Β diffuse X-linked recessive
Most genetic defects are associated with the malfunc- 2C snowcapped teeth X-linked
tions of enamel proteins participating in the composition
2D snowcapped teeth Autosomal
of the enamel matrix or in enamel maturation consisting
dominant (?)
in the replacement of the protein content by mineral to
reach the optimal 96–98% mineralization. For example, Type 3. Hypocalcified
lack of a guanine (nitrogen base) in exon 9 of ENAM 3Α diffuse Autosomal
causes premature termination of translation and synthe- dominant
sis of an enamelin protein with 276 amino acids instead 3Β diffuse Autosomal
of 1142 [99]. Among the genes that cause AI, FAM83H recessive
(AD) causes more and the most severe malformations
Type 4. Hypomaturation-hypoplastic with taurodontism
(hypomineralized, yellowish brown) throughout the
crown. However, the action mechanisms remain unclear. 4Α Hypomatured-hypoplastic with Autosomal
taurodontism dominant
In . Table 17.7, a classification of 14 groups and AI sub-
sets is presented, by Witkop [93] which is based on the 4Β Hypoplastic-hypomatured with Autosomal
phenotype and the mode of transmission. taurodontism dominant
The hypoplastic type is characterized by reduction of
the whole thickness of the enamel of all teeth in primary
and permanent dentition. It may have pitted appear-
ance (type 1A) or rarely vertical grooved enamel defects. probably multifactorial, and it is thought to be mainly
Especially in 1D and 1E types, characterized by a very a result of genetic effects. The future discovery of genes
thin layer of enamel, teeth appear smaller and have no involved both in formation of the craniofacial complex,
contact points (. Fig. 17.42). Although the prevalence and amelogenesis may elucidate the relevant molecular
of anterior open bite in the general population is 3.7%, mechanisms [102].
in patients with AI, it varies from 24% to 60%, indicat- The types hypomatured and hypocalcified (old term
ing a strong correlation between them [100, 101]. It is for synonymous hypomineralized) are characterized by
 446 N. Kotsanos et al.
a b
d e
..      Fig. 17.42 Hypoplastic type of amelogenesis imperfecta. a Pit-
ted (subtype 1A by Witkop [93]) in a 12-year-old girl. Tooth cusps
present with milder hypoplasia. b Rare hypoplastic type with vertical
striations that give wrinkled appearance in an 8-year-old girl (first
described in Darling’s classification [94]. c The mandibular first
molar of cases in B significantly lacks enamel requiring composite
normal thickness of undermineralized enamel, which
is porous and thus is relatively brittle with reduced
resistance to masticatory forces (. Fig. 17.43). It is a
qualitative and not a quantitative dental defect. The
hypocalcified type presents with lower concentration of
mineral salts, is subject to enamel wear, and coexists in a
high percentage with anterior open bite and accumula-
tion of plaque and calculus. In the hypomaturation type,
open bite is also present but with lesser prevalence, with
increased unaesthetic effect, due to oral pigment accu-
mulation in the porous enamel and possibly increased
tooth sensitivity.
The hypomatured-hypoplastic with taurodontism
[103] is less common and may coexist in certain syn-
17 dromes. Its relationship with the tricho-dento-osse-
ous syndrome (TDO syndrome: curly hair, AI, bone
thickening particularly in the skull bones) is typical
(. Fig. 17.44). However, taurodontism can coexist with
hypoplastic and incomplete enamel maturation in the
absence of the syndrome. Note that taurodontism is of
ectodermal origin, as Hertwig’s sheath, which stimulates
the formation of the root, is a product of the enamel
organ. In this type, the enamel has a yellow/brown stain-
ing and is pitted (hypoplastic) especially on labial sur-
faces.
c
f
restoration. d Hypoplastic subtype 1D by Witkop [93]. e, f More
severe form of same subtype as in d, allowing for bonding of direct
composite veneers in maxillary incisors. The super thin enamel can
be observed in the radiograph leading to dental arch with spaces.
PMCs were placed on permanent molars for maintaining vertical
dimension
zz Dental Rehabilitation of AI
The main problem and chief complaint of children
and adolescents with any type of AI are the aesthetic
appearance of the teeth and possibly pain as the teeth
might be very sensitive. The form and color of the teeth
become a very significant element in reducing the qual-
ity of life of people with AI, young as well as adult.
AI has marked an impact on the psychosocial health
of the affected people. Furthermore, there are other
issues, such as orthodontic abnormalities, mainly open
bite. Up to 60% of individuals have open bite in hypo-
calcified AI, as well as more dental caries, sensitivity
to thermal stimuli, and difficulties in mastication. The
multiplicity of treatment needs is best met by interdis-
ciplinary approach [101]. Due to the nature of enamel,
when restorations are needed, adhesive materials are
preferred to amalgam. In more severe cases, PMCs may
be placed in the first permanent and second primary
molars, while, if preferred, aesthetic zirconia crowns
are now available demanding more preparation efforts
[112]. In the primary dentition however, the severity of
AI is generally milder.
Placing PMCs on molars helps primarily prevent
attrition and maintain the vertical dimension of the face.
Restorative options in the anterior area depend on the
Developmental Defects of the Teeth and Their Hard Tissues
447 17

a c

b d

..      Fig. 17.43 a, b Hypomineralized type of AI in a 12-year-old girl. ents intense post-eruptive brown discoloration and some break-
All teeth present enamel worn/broken down to various degrees. c down. d Mild phenotype hypomaturation-type AI with little enamel
Young adult with severe hypomaturation type of AI. Enamel pres- breakdown

a b c

..      Fig. 17.44 a A 14-year-old Caucasian boy with TDO syndrome with severe tooth wear that soon led to pulpal complications and
and characteristic curly light blond hair. b Wide pulp chambers and cervical root fracture which led to crown loss of left central incisor
taurodontism are seen in permanent molars. c Hypoplastic enamel are evident in the maxilla
 448 N. Kotsanos et al.
Box Gene Investigation and Correlation of AI with Other Diseases or Syndromes
Enamel formation depends on Ca2 + transport through the
ameloblasts, namely, Ca2 + entry from the blood vessels
and its exit from the opposite side of the ameloblast to
form a hydroxyapatite. The recent identification of muta-
tions in genes involved in the homeostasis of calcium ions
such as STIM1 (encoding a protein that activates the
transmembrane entry of Ca2 + to prevent depletion of its
stocks into the endoplasmic reticulum) and SLC24A4 (Na
+, K +, Ca2 + transporter), mutations which cause hypo-
maturation type AI, offered new insights into the molecu-
lar management of Ca2+ in ameloblasts [104]. Depletion of
Ca2 + changes the structure of the protein STIM1, which is
a calcium sensor located in endoplasmic reticulum [105].
STIM1 is then translocated close to the cell membrane
where it is linked and activates Orai1, a cell membrane cal-
cium channel. Once the STIM/Orai system is activated,
they mediate the transport of Ca2 + from outside to inside
the cell in many cell types, including T cells, muscle cells,
and ameloblasts [106].
Mutations in Orai1 and STIM1 cause immunodefi-
ciency 9 and 10, respectively, and predispose to congeni-
tal myopathy, ectodermal dysplasia, as well as enamel
malformations [104].
The progressive fragmentation of proteins (degrada-
tion) which are secreted in pre-enamel and will be
removed to make room for the prismatic hydroxyapatite
crystals to increase in width and thickness during miner-
alization is caused by proteolytic enzymes. The most
important of these is a metalloproteinase, the enamelysin
MMP20. Mutations of MMP20 inhibit the smooth pro-
cess of protein degradation and growth of crystals and
cause hypomaturation type of AI, which is transmitted as
an autosomal recessive disease [107]. The hypomatured
enamel detaches relatively easily from dentin, while the
yellowish discoloration is evident since tooth eruption
and increases with time as pigments from the mouth enter
porous enamel.
17 The hypoplastic type of AI is mainly associated with
mutations in amelogenin AMEL and enamelin ENAM
genes, and, previously, it did not seem to have obvious
association with syndromes. Mutations in FAM20A gene
have been identified as causative agents of a syndromic
type of hypoplastic AI with almost absent enamel. The
enamel-renal syndrome (ERS) (combination of AI and
nephrocalcinosis) and the AI-fibrous gingival hyperplasia
are both associated with mutations in FAM20A gene and
are allelic rare diseases [108] (. Fig. 17.45).
FAM20A is a glycoprotein, a kinase phosphorylating
extracellular matrix proteins involved in mineralization.
Therefore, the hypoplastic type of AI, which is related
..      Fig. 17.45 Hypoplastic-type AI and nephrocalcinosis. Com-
plete lack of enamel associated with severe renal calcifications,
associated with mutation in FAM20A gene
causally with mutation in FAM20A, is, at least partially, a
result of an abnormal calcification process of phospho-
proteins secreted into the enamel, probably by phosphor-
ylation failure. Mutations of FAM20A are associated
with erratic calcification traces in the gums, periodontal
tissue, dental pulp, lungs, and kidneys. Clinical findings
in patients presenting with FAM20A mutations include
fibrous gingival hyperplasia, aggressive periodontitis,
thin alveolar bone, secondary hyperparathyroidism, and
nephrocalcinosis/nephrolithiasis. Nephrocalcinosis may
be asymptomatic up to young adulthood. The first signs
may be recurrent infections of the urinary system, pyelo-
nephritis, renal colic, and excretion of kidney stones [109,
110]. The timely referral of juveniles with hypoplastic AI
for kidney ultrasound may confirm early AI-renal syn-
drome, while a neglected nephrocalcinosis or nephroli-
thiasis would lead to significant morbidity. Therefore,
cases of AI-fibrous gingival hyperplasia should be
screened for FAM20A mutations and evaluated carefully
for renal findings.
FAM20C, a gene of the same family as FAM20A,
presents interest, as its mutations are discovered in
patients with Raine syndrome, a rare, autosomal reces-
sive, fatal osseosclerotic bone dysplasia that has similar
clinical findings as the ones observed in patients with
FAM20A mutations, like fibrous gingival hyperplasia and
ectopic calcification [111]. These are some examples of
genetic research, and it is expected that many more genes,
with unknown roles in amelogenesis, will be recognized in
the future as causative of AI.
Developmental Defects of the Teeth and Their Hard Tissues
449 17

a b c

..      Fig. 17.46 a Direct minimal composite veneers in some inci- and . Fig. 17.43b, maxillary anterior teeth (after canine further
sors of hypoplastic AI of . Fig. 17.42b confirm clinically, after eruption) and premolars have received composite veneers on the
3 years, the possibility of etching and adhesion to enamel. In both vestibular ­surfaces, as a medium-term aesthetic solution. Regular
hypoplastic (b) and hypocalcified (c) AI types of . Fig. 17.42e observation is mandatory for possible composite detachments

type and severity of AI. In most case of hypoplastic and

a
in some mild phenotypes of hypomineralized and hypo-
maturation type of AI, the enamel can be etched satis-
factorily [113], so as to allow direct aesthetic composite
veneers in the anterior teeth (. Fig. 17.46). These may
require frequent repairs. Strip crowns have been used
successfully for many years for restorations with com-
posite of the crown of decayed anterior primary teeth.
This clinical procedure requires only minimal prepa-
ration of the tooth. The long-term outcome of such b
direct restorations in permanent hypoplastic teeth after
10 years of follow-up was satisfactory in a retrospective
study of 21 teeth; [114] however, more firm evidence is
required [115]. Veneers and ceramic crowns as perma-
nent restorations should be delayed until cervical mar-
gin becomes more permanent (. Fig. 17.47). The use of
intraoral scanner and CAD-CAM technics may facilitate
the use of veneers during teenage years. Enamel bonding
issues complicate the, often necessary, orthodontic treat-
ment, while the frequency of interventions and the long ..      Fig. 17.47 a An 18-year-old young woman with mild phenotype
monitoring may have a burnout effect and discourage the of hypomaturation-type AI had direct composite veneers in anterior
patient, so a positive approach by the dentist is necessary. teeth for years and desires aesthetic improvement. b After the cemen-
tation of ceramic veneers. (Courtesy Dr. P. Gerasimou)

zz Dentinogenesis Imperfecta (DGI)

Dentinogenesis imperfecta is a hereditary dentin dyspla-
sia divided in three types [116], Shields types I, II, and
III, based on clinical, radiographic, and histologic find-
ings. Except for a few cases of DGI type I, the hereditary
malformations of dentin are transferred as dominant
traits. The most frequent types are I and II with an over-
all prevalence of approximately 1:6000–8000. Type III
has been described only in an isolated community of
Brandywine Maryland, USA. DGI-Shields I is the den-
tal expression of a generalized disorder of connective
tissue, osteogenesis imperfecta (OGI). In 90% of OGI
cases, mutations are found in genes encoding collagen
type 1 (COL1A1 and COL1A2). Frequent findings in
OGI are increased frequency of hypodontia, class III
malocclusion, and posterior cross bite. In 50% of OGI
patients, the teeth will show DGI characteristics clini-
cally, but they will all present dentin defects if analyz-
ing the structure or ultrastructure of dentin under a
microscope. In dentinogenesis imperfecta Shields II,
the causative genetic defect is located in the long arm
of chromosome 4 (4q21). DGI types II and III are basi-
cally dental conditions with no bone involvement.
The genetic defect of almost all other heritable
dentin dysplasias than DI involves dentin sialoph-
osphoprotein (DSPP) encoding gene, which means
that DGI types II and III are allelic conditions [115].
Furthermore, a study of patients with DGI and DSPP
mutations concluded that they exhibited also enamel
abnormalities, different from those of the dentin, indi-
cating that DSPP may also participate in early stages
of amelogenesis [117]. Histologically the abnormal den-
tin has few tubules with atypical direction (swirls) and
many branches, with inclusions of cells and small blood
vessels (. Fig. 17.48).
 450 N. Kotsanos et al.

..      Fig. 17.48 a DGI: Pulp

obliteration, histological a b
section. Mantle dentin on the
outside is normal, while the rest
is globular, irregularly formed
dentin. The enamel was lost in
the preparation. b DGI-1
pathological dentin with large
interglobular spaces, inclusion
of cells and small blood vessels

..      Fig. 17.49 a DGI of a 5-year-old a b

child in occlusion. Early eruption of
mandibular permanent central
incisors. b The occlusal view of
mandible shows that the second
primary molars still preserve almost
completely their enamel. c DGI of his
38-year-old father. d The occlusal view
of his mandible shows fractures, most
severe in the posterior teeth c d

zz Dental Rehabilitation in DGI dimension. Therefore, PMCs should be placed early on

Over time the abnormal dentin accumulates to the point
of pulp obliteration. Dentin mineralization is defec-
tive, with reduced hardness; dentin does not support the
enamel, which detaches and exposes the softer dentin that
will wear off quickly (. Fig. 17.49). In the permanent
dentition, the production of abnormal secondary/ter-
17 tiary dentin continues to fill the pulp chamber and canal,
so that they appear radiographically fine as a thread
(. Fig. 17.50). The support of the enamel is better, but it
varies due to defects in the enamel-dentin junction [117].
The permanent teeth are much more resistant to occlusal
forces than the primary teeth, but they have a character-
istic brown-gray opalescent color. Radiographically the
teeth show short roots, bulbous crowns that constrict at
the cervix, and pulpal obliteration [117].
The main problems are the invasion of exposed den-
tinal tubules by bacteria-provoking pulp necrosis and
subsequent untreatable periapical infections due to the
disappearance of pulpal spaces related to anarchic den-
tin production; the aesthetics, mainly of the permanent
dentition; and the abrasion of the primary and per-
manent teeth, often resulting in reduced vertical facial
primary molars and if possible aesthetic crowns with
white facing on the maxillary primary incisors for psy-
chological reasons. Therefore, early diagnosis and treat-
ment are important. The first permanent molars usually
show some wear, although to a much lesser degree than
that of primary molars, yet regular monitoring is rec-
ommended from eruption. In cases of little abrasion, a
layer of composite can be directly mounted on, although
placing PMC may be preferred. When adolescence is
over, ceramic crowns solve both problems, aesthetic and
functional. The exclamation of the patient with DGI
in . Fig. 17.50 after he received full mouth ceramic
crowns was: “I can finally smile.”
zz Dentin Dysplasia (DD)
It was first described in 1920 as “rootless teeth.” [118]
DD type I presents with extremely short roots and small,
almost obliterated coronal pulps, with often apical lesions
appearing in the absence of caries (. Fig. 17.51). The
teeth become mobile and are lost early, the treatment being
only prosthetic rehabilitation of the oral cavity. There have
been cases of DD I with autosomal dominant (SMOC2
Developmental Defects of the Teeth and Their Hard Tissues
gene) transmission [119] associated with major microdon-
tia, oligodontia, and tooth shape abnormalities. The prev-
alence is rare (1:100,000). DD type II may resemble DGI
type II radiographically and clinically in the permanent
teeth but with milder discoloration/opalescence. Subtypes
of the two main types have even been proposed. It is sug-
gested that type II is caused by mutations in DSPP, the
largest member of SIBLING family of glycoproteins, or it
is associated with a DGI type II allele gene [120].
17.2.2.4  ental Defects Unclassified
D There have been unerupted teeth, molars in partic-
as to Etiology
zz Regional Odontodysplasia
Regional odontodysplasia (ROD) is an uncommon
dental anomaly with unclarified etiology. Recently, a
suggestion of common genetic background with genes
involved in tooth agenesis, namely, a codon mutation of
the PAX9, has been put forward [121]. This disorder is
characterized by severe malformation of all dental tis-
sues of some teeth in a certain region, seemingly having
affected the specific part of the dental lamina. It affects
primary and permanent teeth in that side of the jaw,
more often the maxilla, rarely crossing the midline and
even more rarely affecting both jaws. The affected teeth
have radiographically a “ghost tooth” appearance. Their
a b
c lesions mentioned in 7 Chap. 20, the enamel may have
..      Fig. 17.50 a, b The radiographs of a 20-year-old man with DGI
show pulp chamber and root canal obliteration in all teeth. c Their
clinical side view with brown opalescent color
a b
..      Fig. 17.51 a Panoramic radiograph of adolescent with Dentin Dysplasia type I. Arrows show clinically caries-free molars with periapical
radiolucencies. b, c Rootless teeth erupt and are shed soon
451 17
eruption is usually delayed, or they do not erupt at all.
Following eruption, local infections of the alveolar bone
are frequently observed [122]. In favorable cases full
coverage could prevent pulp inflammation. Otherwise,
the management consists of surgical extraction of the
dysplastic teeth and the placement of prosthesis, par-
tial dentures in childhood, and implants/fixed following
adolescence (. Fig. 17.52).
zz Intra-Coronal Dentin Radiolucencies
ular, seen in routine radiographic examinations to
have coronal dentin radiolucencies often reaching or
involving the overlying enamel (. Fig. 17.53). They
may be of non-­progressive or progressive nature, and,
in the latter case, following eruption, these teeth may
become cavitated and therefore not be recognized
as such. The term used is pre-eruptive intra-coronal
radiolucency/resorption (PEIR), suggesting that they
are a result of resorption of as yet unexplained cause.
In that sense they may not belong in developmental
dental defects but are presented here until their etiol-
ogy is clarified. Their presence has been associated
with unfavorable tooth position or eruption path.
Their prevalence is reported as about 3%, but this
varies greatly in studies [123].
17.2.2.5  ystemic Diseases and Syndromes
S
with Dental Defects
Celiac disease is a condition of the small intestine caused
by immunological sensitivity to gluten gliadin protein of
wheat products. The prevalence is 3–8:1000, and there
is a familial tendency, meaning a genetic component
which so far has not been elucidated. Except for oral
chronologic hypoplasia or hypomineralization defects,
but usually only on the incisal third of the incisors, as
the intolerance is diagnosed in infancy and its effects
controlled by strict avoidance of all wheat sources [124–
126] (. Fig. 17.54).
Rickets is caused by prolonged deficiency in vita-
min D that is essential for calcium absorption and
c
 452 N. Kotsanos et al.
a b
c d
..      Fig. 17.52 a Regional odontodysplasia (ROD) in all half of
maxillary primary dentition. The affected teeth have erupted. b The
permanent teeth have similar “ghost tooth” appearance radiographi-
cally. c After affected primary teeth extraction under general anes-
thesia, a partial denture was placed. d A rare case of ROD crossing
the midline
a
¯ reach the enamel. Moderate cusp wear of the teeth
¯
¯
b permanent molars and in premolars is also recom-
17
..      Fig. 17.53 a Panoramic radiograph of a 13-year-­old girl at reten-
tion after orthodontic treatment. The radiolucencies of suprapulpal
dentin observed in both unerupted second mandibular molars with
unfavorable eruption paths (arrows) were not vissible at the radiograph
taken pre-­orthodontically. b Large dentin radiolucency in an erupting
mandibular first permanent molar in a 6-year-old girl with free medi-
cal history. Her mother had idiopathic very short stature. The tooth
will be restored as soon as it erupts to prevent pulp complications
thus mineralization of bones and teeth [127]. Vitamin
D is absorbed from food but needs sun exposure to
the skin for its activation. Rickets affects children
and adolescents. It is called osteomalacia in adults,
..      Fig. 17.54 Zones of hypoplastic enamel as severe chronologic
dental defects in the anterior teeth of a 9-year-old child with celiac
disease history
and, in the skeleton, it may cause kyphosis. The teeth
appear with symmetrical enamel hypoplastic-hypo-
mineralized defects, consistent with the period of
hypocalcemia.
Familial hypophosphatemia is a rare hereditary rick-
ets resistant to vitamin D, usually X-linked (PHEX),
affecting more severely boys. The low levels of phos-
phorus in the blood may be caused by dysfunction
caused by renal over-reabsorption or perhaps by intes-
tinal mal-­absorption or altered vitamin D metabolism
in the kidneys. Dental findings are defective dentin
formation with extensions of pulp horns that often
leads to microbial penetration and pulp inflamma-
tion, necrosis, and abscesses. Treatment is endodontic
or full coverage of the molars with crowns to prevent
pulp exposure, PMC in children, or ceramic later, but
preventive sealing of all the fissures in primary and
mended [128]. Additional findings are class III occlu-
sion, shorter cranial base, and mandibular ramus [129]
(. Fig. 17.55).
Hypophosphatasia is a metabolic disorder with low
alkaline phosphatase activity and bone rickets findings,
particularly in the legs. It is inherited as an autosomal
dominant or recessive trait. It can be fatal in infancy,
although many cases diagnosed prenatally have a good
prognosis [130]. In milder types, delayed eruption and
premature tooth loss, before 3 years of age, are observed,
particularly in the anterior primary teeth (. Fig. 17.56).
This is attributed to decreased and dysplastic cementum,
while dentin is rather normal [131]. Similar dental find-
ings have been recorded in young adults and may lead to
loss of the teeth.
Epidermolysis bullosa is a group of rare heteroge-
neously inherited diseases of mucosal and epidermal
bonding to the connective tissue, which are gener-
Developmental Defects of the Teeth and Their Hard Tissues
ally characterized by blister formation in response to
mechanical trauma. In one of the three types in which
it mainly manifests, generalized enamel hypoplasia is a
common finding. Dental treatment is difficult with spe-
..      Fig. 17.55 A 9-year-old boy with hypophosphatemia and class
III occlusion. Hypoplastic enamel is evident in all anterior teeth,
permanent and primary, mostly noticeable in their incisal parts
..      Fig. 17.56 This 3.5-year-old boy with hypophosphatasia had
three mandibular incisors shed already
a b
..      Fig. 17.57 A 10-year-old boy with APECED. a Enamel hypoplasia is evident in an erupting second premolar. b Drug-resistant tongue
candidiasis
453 17
cial precautions, as light pressure or tension on the lips
or cheeks, for example, causes blisters. It is interesting
to notice that genes involve in epidermolysis bullosa
(AR) have also been reported as causative in hypoplas-
tic AI when transmitted as an autosomal dominant dis-
ease [132].
Ehlers-Danlos syndrome is a group of connective tis-
sue disorders; at least eight types are related to the syn-
thesis of collagen, mainly transmitted as an autosomal
dominant trait. The physical findings are loose joints
(including TMJ) and super elastic skin, while dental
findings include hypoplastic enamel, abnormal dentin
and tooth roots with pulp stones, and also early loss of
the teeth [133].
APECED (autoimmune polyendocrinopathy-candi-
diasis-ectodermal dystrophy, OMIM #240300) is a rare
autosomal recessive autoimmune disease. It is due to a
mutation in a single gene named AIRE in chromosome
region 21q22.3. Among other ectodermal disorders,
enamel defects in both primary and permanent denti-
tions appear to be common (. Fig. 17.57). Inherited
developmental dental disorders are observed in many
rare diseases or syndromes, for example, in tuberous scle-
rosis with pitted hypoplastic enamel [134], osteopetrosis
with pitted hypoplastic enamel and oligodontia [135]
(. Fig. 17.58), and others.
The restoration of the anterior teeth with hypopla-
sia or hypomineralization defects has been discussed
in 7 Chap. 13 and earlier in this chapter in the resto-
ration of the teeth with MIH. Special attention is paid
to removing discolored enamel and/or using an opaque
composite color for camouflage toward a more aesthetic
result. At the appropriate age, some cases will require
porcelain veneers and other prosthetic solutions for bet-
ter and more permanent aesthetics.
 454 N. Kotsanos et al.
a b
..      Fig. 17.58 a, b Clinical view and panoramic radiograph of a
7-year-old girl with osteopetrosis and neglected mouth. c One of two
mandibular first permanent molars removed because of infection
a b
..      Fig. 17.59 a Green discoloration of primary teeth of a 4-year-
old girl (with manifest caries), which was operated for liver trans-
plantation in the seventh month. The discoloration is due to
17.3 Developmental Discoloration
of Dental Tissues
Developmental discolorations are endogenous, and
their clinical appearance is often modified after expo-
sure to the oral environment and to daylight. They are
mainly caused by:
55 Blood degradation products (e.g., congenital por-
phyria, atresia of the bile duct) [136] (. Fig. 17.59)
17 55 Incorporation of drugs or dyes during mineraliza-
tion (e.g., tetracycline)
55 Hypoplasia/hypomineralization (e.g., some types of
AI and DI)
In these instances, the final tooth color is a combined
result of internal and external discoloration. With soci-
etal norms demanding white smiles, children and espe-
cially adolescents are often concerned not only with
discolored teeth but with the natural overall tooth color,
all too often asking for “tooth whitening.”
c
(under antibiotic coverage until prolonged bone healing) shows
anomalous root with cementosis
bilirubinemia. In the anterior teeth, it is evident only cervically
because most of their crown had been formed and mineralized
already. b The second primary molars suggest coexistence of HSPM
zz Tetracycline-Induced Discoloration
Chronic intake of tetracycline, its hydrochloric salt in
particular, causes brown-grey discoloration. This drug
was prescribed in the past for the management of typhoid
and cystic fibrosis, in young patients. Many children had
subsequently yellow/brown or gray teeth, depending on
the formulation that was administered [137]. That was
because tetracycline has a strong tendency for binding to
tissues in the mineralization phase, like dentin and bone.
While staining of bones is lost in a few years due to its
remodeling, it remains permanently in the dentin. When
the teeth are exposed to light, the integrated tetracy-
cline becomes darker and thus unsightly (. Fig. 17.60).
When sections of the dentin are exposed to ultraviolet
light, fluorescent characteristic lines are present cor-
responding to the dentin growth lines (mineralization
fronts) during the days of intake (. Fig. 17.61). This
allows dating the time of drug intake, as well as animal
research on bone and tooth development. Histologically
it seems that tetracycline does not color the enamel as
much, but its transparency allows the discolored den-
Developmental Defects of the Teeth and Their Hard Tissues
455 17

a a b

..      Fig. 17.61 a Longitudinal section of premolar tooth under fluo-

rescence microscope of an adolescent who received tetracycline for
4 days during the mineralization phase of this tooth’s crown. They are
obvious in the dentin (along von Ebner lines) and less so in enamel
(along Retzius incremental lines). b Similar section of the first man-
dibular premolar suggesting multiple intakes of tetracycline for cystic
fibrosis treatment in the 1970s [137]

of normal color is very variable, but the final preferences

should be left to the patient. As a health scientist, the
..      Fig. 17.60 a The yellow zones in a young adult’s cervical area of dentist should not enforce his opinions regarding this
maxillary incisors correspond to tetracycline intake at the age of subjective matter, and after taking into account possible
2–3 years of age. b Aesthetic improvement with direct composite
veneers
different perceptions between parents and children, he
should give satisfactory solutions within the framework
of professional ethics. Tooth bleaching has become very
tin to shine through. Several decades ago, since the side
popular. Techniques are based on the application of a
effect of tetracycline became known, their administra-
composition of hydrogen peroxide (H2O2), while add-
tion to children younger than 8 years and pregnant
ing energy in the form of heat, light or laser radiation
women has been replaced by other antimicrobial drugs,
shortens the application time (. Fig. 17.62). Although
and the phenomenon is nowadays rare.
successful use of the process has been reported even
A few cases are still seen in young people. As in other
in children, the technique is recommended only after
intrinsic discoloration cases, the aesthetic correction is
puberty and always taking precautions to avoid chemi-
made with veneers of opaque composite resin in chil-
cal trauma to the gums and pulp irritation [139, 140].
dren or with ceramic materials after the clinical cervical
Some tooth sensitivity may at times appear after bleach-
tooth margin has been finalized.
ing. Young people may also benefit from using “whit-
ening” dentifrices. Discolorations due to developmental
zz External Bleaching of Discolored Teeth
defects of dental tissues do not respond to bleaching, so
The importance that many adolescents attribute to the
other techniques are preferred, mainly by covering the
appearance of teeth varies, and aesthetic views differ
discolored teeth, e.g., direct or indirect aesthetic veneers.
between dentists, parents, and children [138]. The sense
 456 N. Kotsanos et al.

b c

..      Fig. 17.62 Bleaching methods with trays. a, b At home (with carbamide peroxide 16% in transparent tray). c At the dental office (with
hydrogen peroxide 35%) with the assistance of a ZOOM lamp. (Curtesy Dr. K. Giannakopoulos)

17.4 Conclusion
Dental anomalies have extremely complex causes and
phenotypes making often clinical decisions very diffi-
cult for general, pediatric, and other dental specialists.
It is imperative for dentists to acquire a good knowledge
of the causes and differential diagnosis for each den-
tal anomaly to precisely diagnose and be able to offer
the optimal treatment to each patient. The attached
table aims to contribute toward a successful differen-
tial diagnosis and provide useful clues for treatment
(. Table 17.8).

17
Developmental Defects of the Teeth and Their Hard Tissues
457 17

..      Table 17.8 Differential diagnosis and clinical decision guidance for dental anomalies

Abnormal tooth number

Hypo−/oligodontia
DDX Genotype/phenotype Notes

Selected 1. MSX1: No significant difference between the number of teeth missing The dentist is expected to order
non-syndromic on the left and right; the absence of maxillary first premolars is the most genetic tests: [142]
familial tooth distinguishing feature of an MSX1 mutation [141] 1. Defects are often first discovered
agenesis 2. PAX9: No significant difference between the number of teeth missing by the dentist
on the left and right; the absence of the second molars is the most 2. Can be associated with cancer
distinguishing feature of PAX9 mutations 3. The list of candidate genes is
3. AXIN2: Incisor agenesis and colorectal cancer or precancerous lesions short: WNT10, LRP6…
of variable types
Syndromic 1. Ectodermal dysplasia (EDA, EDAR, EDARΑDD): Abnormalities of two Because dental treatment is complex;
oligodontia or ectodermal structures such as the hair, teeth, nails, sweat glands, a multi-disciplinary approach is best
(most likely salivary glands, cranial-facial structure, and digits. Frontal bossing, longer Children may need dentures as early
candidates) or more pronounced chins, and broader noses are very common [143] as 2 years of age
2. Achondroplasia (FGFR3): Disproportionate short stature, shortening of Multiple denture replacements are
the proximal limbs, short fingers and toes with trident hands, and often needed as the child grows, and
intelligence are generally normal [144] dental implants may be an option in
3. Incontinentia pigmenti (IKBKG): Development of harder skin growths late adolescence or adulthood, once
with grey or brown patches. Hair loss (alopecia), dental abnormalities, the jaw is fully grown
eye abnormalities that can lead to vision loss, and lined or pitted finger- Orthodontic treatment may also be
nails and toenails. Mainly affects males (X-linked) necessary
4. Orofaciodigital syndrome-I (OFD1): Malformations of the face, oral
cavity, and digits with polycystic kidney disease and variable involve-
ment of the central nervous system. X-linked (males) [145]
5. Robin sequence (SOX9): A sequential chain of signs that start with
micrognathia, followed by retraction of the tongue (glossoptosis) and
upper airway obstruction. U-shaped cleft palate is very common [146]
6. Rieger syndrome (PITX2, FOXC1): Mild craniofacial abnormalities,
and various abnormalities of the eye, especially glaucoma [147]
Supernumerary teeth/hyperdontia
Non-syndromic Mostly single or double supernumeraries, results in crowding, delayed Rare in relation to syndromic
supernumerary eruption, diastema, rotations, cystic lesions, and resorption of the
teeth adjacent teeth
Syndromic 1. Cleidocranial dysplasia (RUNX2): Clavicles are poorly developed or There are several treatment strategies
hyperdontia absent so the shoulders are brought close together, supernumerary to treat CCD
(most likely teeth, enamel-dentin hypoplasia, delayed teeth eruption, bone Dental practitioners’ awareness for
candidates) hypoplasia clinical/radiological characteristics of
2. Gardner’s syndrome (APC): Adenomatous polyps of the gastrointesti- Gardner’s syndrome; early detection
nal tract which usually undergoes malignant change by the fourth of associated polyps could be
decade. Mandibular lesion consisting of clumped toothlets [147–150] lifesaving
Enamel defects
AI variants Type I (AMELX/ENAM): Hypoplastic, thin enamel. Enamel on the Subjects with AI regardless of the
cervical 1/3 of the crowns is usually most severely affected, and horizontal variant showed accelerated dental
groves of severely hypoplastic enamel could be evident age [151]
Type II (MMP20/KLK4/WDR72/C4orf26/ SLC24A4): Hypomaturation, There is a sixfold increase in
softer enamel with normal thickness. The enamel has a milky to shiny tendency of AI patients to show
agar-brown color in newly erupted teeth but may become more deeply impaction of the permanent teeth
stained in contact with exogenous agents; it tends to chip away and associated anomalies such as
Type III (FAM83H): Hypocalcified. The enamel has a cheesy consistency follicular cysts
and can be scraped from the dentin with a dental explorer. Newly erupted Forty-two percent of AI patients
teeth are covered with a dull, opaque white honey-colored or yellow-­ presented with skeletal and/or dental
orange-­brown enamel open bite compared to 12% in
Type IV (DLX3): Hypomature hypoplastic enamel with taurodontism. unaffected family members
Enamel has a variation in appearance, with mixed features from type 1
and type 2 AI. All type 4 AI have taurodontism in common
Dental fluorosis Mottled teeth: Early stage or mild (opaque, white spots, narrow white
lines following the perikymata) and late stage or severe (enamel appears
yellowish and pitted with white-brown lesions that look like cavities) [152]
(continued)
 458 N. Kotsanos et al.

..      Table 17.8 (continued)

Abnormal tooth number

Hypo−/oligodontia
DDX Genotype/phenotype Notes
Molar incisor Enamel opacities of the affected permanent molars and usually incisors Multifactorial disease (perinatal
hypomineraliza- (index teeth). They appear yellow, brown, cream, or white [153]. Other illness, fevers, other unknown
tion teeth may be involved factors)
Syndromic 1. Pseudohypoparathyroidism (GNAS): Short fourth and fifth metacarpals Alopecia is seen only in some vitamin
enamel and rounded facies, tetany, enamel hypoplasia, interglobular dentin, D-resistant rickets
hypoplasia (most delayed eruption [154]
likely candidates) 2. Epidermolysis bullosa (PLEC1, COL17A1, LAMA3, LAMB3,
LAMC2, and ITGB4, among others): Easy blistering of the skin and
mucous membranes, enamel hypoplasia, cementum dysplasia, taur-
odontism
3. Vitamin D-dependent rickets type I and II (CYP27B1, VDR): Pitted
type enamel hypoplasia [155] short stature, yellowish-to-brownish enamel
4. Vitamin D-resistant rickets (PHEX, CLCN5, DMP1, FGF23): Excessive
pulp horn, interglobular dentin, “spontaneous” abscesses, bowed or
knock-kneed legs, and a deformed chest and skull, with prominent frontal
and parietal bones causing a distinctive “square headed,” taurodontism,
poorly defined lamina dura, and hypoplastic alveolar ridge [156]
Dentin defects
DD-I (dentin Unknown gene: Rare autosomal dominant condition with clinically
dysplasia type I) normal crowns and diminished root development. After an initial layer of
normal dentin forms, there are repeated cycles of odontoblast death
followed by new odontoblast recruitment leading to “cascading waterfall”
histological appearance and pulp obliteration [157]
DGI-I/OGI COL1A1 and COL1A2 mutation: Associated with osteogenesis imper- Bisphosphonates – The nitrogen-­
(dentinogenesis fecta, primary teeth are more severely affected compared to the perma- containing in particular – Are being
imperfecta type nent dentition, commonly involving lower incisors and canines administrated to OGI patients to
I/osteogenesis increase bone mass and reduce the
imperfecta) incidence of fracture. Autosomal
dominant or recessive inheritance
DGI-II, DGI-III DSPP mutations: DGI-II, DGI-III, and DD-II are likely to be the same
and DD-II disease.
No effect on bone. The effect of DSPP mutations on the protein may
determine the severity of the clinical phenotypes: (1) DD-II, partial pulp
obliteration and mild discoloration; (2) DGI II, complete pulpal
obliteration and discoloration in both dentitions; and (3) DGI III, pulpal
exposure and early abscess
Regional Non-hereditary: Ghost teeth appear more radiolucent than normal. These There is no predilection for race, but
17 odontodysplasia teeth are very brittle, and many of these teeth do not erupt [122] females are more likely to get
regional odontodysplasia
Syndromic 1. Ehlers-Danlos syndrome (ADAMTS2, PLOD1, TNXB…): Loose joints,
dentin hypopla- stretchy skin and abnormal scar formation
sia (most likely 2. Vitamin D-resistant rickets (mentioned in the enamel section)
candidates) 3. Pseudohypoparathyroidism (mentioned in the enamel section)
4. Epidermolysis bullosa (mentioned in the enamel section)
Cementum defects
Cementum hypo- 1. Hypophosphatasia (ALPL): Acellular and cellular cementum defect, Lab tests for hypophosphatasia:
plasia (most excessive mobility of teeth, and premature exfoliation of teeth, usually Fasting serum ALP is lower 24 hr.
likely candidates) missing the front teeth. Also present abnormal enamel (less severe in urine PEA elevated
primary dentition), pulp chamber bigger Serum PLP will be elevated
2. Epidermolysis bullosa (mentioned in the enamel section)
3. Cleidocranial dysplasia (mentioned in the hyperdontia section)
Cementum 1. Gnathodiaphyseal dysplasia (ANO5): Reduced bone mineral density
hyperplasia (most (osteopenia, various amounts of cementum like calcified mass [158]
likely candidates) 2. Cemento-osseous dysplasia (unknown): Benign, arise from the
fibroblasts of the periodontal ligaments, periapical the lesion occurs in
the mandibular incisors [159]
Developmental Defects of the Teeth and Their Hard Tissues
459 17
References 18. Ababneh FK, Al-Swaid A, Elhag A, Youssef T, Alsaif S. Bleph-
aro-cheilo-dontic (BCD) syndrome: expanding the phenotype,
case report and review of literature. Am J Med Genet A.
1. Nanci A. Chapter 5: Development of the tooth and its sup-
2014;164(6):1525–9. https://doi.org/10.1002/ajmg.a.36465.
porting tissues. In: Ten Cate’s oral histology. St Louis: Mosby;
19. Gemignani F, Marbini A. Disease course of Charcot-
2008. p. 79–107.
Marie-tooth disease type 2 and comorbidity. Arch Neu-
2. Jussila M, Thesleff I. Signaling networks regulating tooth
rol. 2004;61(9):1470. https://doi.org/10.1001/archneur.61.9.
organogenesis and regeneration, and the specification of den-
1470-­a.
tal mesenchymal and epithelial cell lineages. Cold Spring Harb
20. Kalaskar R, Kalaskar AR. Oral manifestations of Ellis-van
Perspect Biol. 2012;4(4):a008425. https://doi.org/10.1101/csh-
Creveld syndrome. Contemp Clin Dent. 2012;3(Suppl 1):S55–
perspect.a008425.
9. https://doi.org/10.4103/0976-­237X.95106.
3. Balic A, Thesleff I. Tissue interactions regulating tooth devel-
21. Giuliano F, Collignon P, Paquis-Flucklinger V, Bardot J, Philip
opment and renewal. Curr Top Dev Biol. 2015;115:157–86.
N. A new three-generational family with frontometaphyseal dys-
https://doi.org/10.1016/bs.ctdb.2015.07.006.
plasia, male-to-female transmission, and a previously reported
4. Simmer JP, Papagerakis P, Smith CE, Fisher DC, Roun-
FLNA mutation. Am J Med Genet A. 2005;132A(2):222.
trey AN, Zheng L, et al. Regulation of dental enamel shape
https://doi.org/10.1002/ajmg.a.30396.
and hardness. J Dent Res. 2010;89(10):1024–38. https://doi.
22. Tadini G, Santagada F, Brena M, Pezzani L, Nannini P. Ecto-
org/10.1177/0022034510375829.
dermal dysplasias: the p63 tail. G Ital Dermatol Venereol.
5. Fraser GJ, Bloomquist RF, Streelman JT. Common develop-
2013;148(1):53–8.
mental pathways link tooth shape to regeneration. Dev Biol.
23. Santhosh BP, Jethmalani P. Johanson-Blizzard syndrome:
2013;377(2):399–414. https://doi.org/10.1016/j.ydbio.2013.02.007.
dental findings and management. J Contemp Dent Pract.
6. Chhabra N, Goswami M, Chhabra A. Genetic basis of dental
2013;14(3):544–7.
agenesis–molecular genetics patterning clinical dentistry. Med
24. Merrett SJ, Durning P. Kartagener's syndrome: unusual dental
Oral Patol Oral Cir Bucal. 2014;19(2):e112–9.
morphology. Int J Paediatr Dent. 2005;15(3):220–3. https://doi.
7. Stockton DW, Das P, Goldenberg M, D'Souza RN, Patel
org/10.1111/j.1365-­263X.2005.00629.x.
PI. Mutation of PAX9 is associated with oligodontia. Nature
25. Wong D, Ramachandra SS, Singh AK. Dental management
Genet. 2000;24(1):18–9.
of patient with Williams Syndrome-A case report. Contemp
8. Lammi L, Arte S, Somer M, Jarvinen H, Lahermo P, Thesleff
Clin Dent. 2015;6(3):418–20. https://doi.org/10.4103/0976-­
I, et al. Mutations in AXIN2 cause familial tooth agen-
237X.161908.
esis and predispose to colorectal cancer. Am J Hum Genet.
26. Akers AL, Ball KL, Clancy M, Comi AM, Faughnan ME,
2004;74(5):1043–50. https://doi.org/10.1086/386293.
Gopal-Srivastava R, et al. Brain vascular malformation con-
9. Meyer-Marcotty P, Weisschuh N, Dressler P, Hartmann J,
sortium: overview, progress and future directions. J Rare Dis-
Stellzig-Eisenhauer A. Morphology of the sella turcica in
ord. 2013;1(1):5.
Axenfeld–Rieger syndrome with PITX2 mutation. J Oral
27. Yu F, Cai W, Jiang B, Xu L, Liu S, Zhao S. A novel mutation
Pathol Med. 2008;37(8):504–10. https://doi.org/10.1111/j.1600-­-
of adenomatous polyposis coli (APC) gene results in the forma-
0714.2008.00650.x.
tion of supernumerary teeth. J Cell Mol Med. 2018;22(1):152–
10. Rohmann E, Brunner HG, Kayserili H, Uyguner O, Nürnberg
62. https://doi.org/10.1111/jcmm.13303.
G, Lew ED, et al. Mutations in different components of FGF
28. Deutsch D, Haze-Filderman A, Blumenfeld A, Dafni L, Leiser
signaling in LADD syndrome. Nat Genet. 2006;38(4):414–7.
Y, Shay B, et al. Amelogenin, a major structural protein in min-
https://doi.org/10.1038/ng1757.
eralizing enamel, is also expressed in soft tissues: brain and cells
11. Anuthama K, Prasad H, Ramani P, Premkumar P, Natesan A,
of the hematopoietic system. Eur J Oral Sci. 2006;114(Suppl
Sherlin HJ. Genetic alterations in syndromes with oral manifes-
1):183–9. https://doi.org/10.1111/j.1600-­0722.2006.00301.x.
tations. Dent Res J (Isfahan). 2013;10(6):713–22.
29. Brook AH. A unifying aetiological explanation for anomalies
12. Berk DR, Armstrong NL, Shinawi M, Whelan AJ. ADULT
of human tooth number and size. Arch Oral Biol. 1984;29(5):
syndrome due to an R243W mutation in TP63. Int J Derma-
373–8.
tol. 2012;51(6):693–6. https://doi.org/10.1111/j.1365-­4632.
30. Brook AH, Jernvall J, Smith RN, Hughes TE, Townsend
2011.05375.x.
GC. The dentition: the outcome of morphogenesis leading
13. van Bokhoven H, Jung M, Smits AP, van Beersum S, Rüschen-
to variations of tooth number, size and shape. Aust Dent J.
dorf F, van Steensel M, et al. Limb mammary syndrome: a
2014;59(Suppl 1):131–42. https://doi.org/10.1111/adj.12160.
new genetic disorder with mammary hypoplasia, ectrodac-
31. Schalk-van der Weide Y, Bosman F. Tooth size in relatives
tyly, and other hand/foot anomalies maps to human chromo-
of individuals with oligodontia. Arch Oral Biol. 1996;41(5):
some 3q27. Am J Hum Genet. 1999;64(2):538–46. https://doi.
469–72.
org/10.1086/302246.
32. Bishop K, Addy L, Knox J. Modern restorative management of
14. Pauker PS, Stoler MJ. Clinical manifestations and diagnosis
patients with congenitally missing teeth: 1. Introduction, ter-
of Ehlers-Danlos syndromes. Up to date. Waltham: Wolters
minology and epidemiology. Dent Update. 2006;33(9):531–4. ,
Kluwer-Health; 2016.
537. https://doi.org/10.12968/denu.2006.33.9.531.
15. Wu HP, Wang YL, Chang HH, Huang GF, Guo MK. Dental
33. Bloch-Zupan A, Sedano H, Scully C. Dento/oro/craniofacial
anomalies in two patients with incontinentia pigmenti. J For-
anomalies and genetics. Boston: Elsevier; 2012. https://doi.
mos Med Assoc. 2005;104(6):427–30.
org/10.1016/C2011-­0-­06093-­3.
16. Jumlongras D, Bei M, Stimson JM, Wang WF, DePalma SR,
34. Arte S, Parmanen S, Pirinen S, Alaluusua S, Nieminen P. Can-
Seidman CE, et al. A nonsense mutation in MSX1 causes Wit-
didate gene analysis of tooth agenesis identifies novel mutations
kop syndrome. Am J Hum Genet. 2001;69(1):67–74. https://
in six genes and suggests significant role for WNT and EDA
doi.org/10.1086/321271.
signaling and allele combinations. PLoS One. 2013;8(8):e73705.
17. Dalben Gda S, das Neves LT, Gomide MR. Oral findings in
https://doi.org/10.1371/journal.pone.0073705.
patients with Apert syndrome. J Appl Oral Sci. 2006;14(6):
35. Yu P, Yang W, Han D, Wang X, Guo S, Li J, et al. Mutations
465–9.
in WNT10B are identified in individuals with oligodontia. Am
 460 N. Kotsanos et al.
J Hum Genet. 2016;99(1):195–201. https://doi.org/10.1016/j.
ajhg.2016.05.012.
36. Arzoo PS, Klar J, Bergendal B, Norderyd J, Dahl N. WNT10A
mutations account for ¼ of population-­based isolated oligo-
dontia and show phenotypic correlations. Am J Med Genet A.
2014;164A(2):353–9. https://doi.org/10.1002/ajmg.a.36243.
37. Oku T, Takayama T, Sato Y, Takada K, Hayashi T, Takahashi
M, et al. A case of Gardner syndrome with a mutation at codon
1556 of APC: a suggested case of genotype-­phenotype cor-
relation in dental abnormality. Eur J Gastroenterol Hepatol.
2004;16(1):101–5.
38. Kramer PF, Feldens CA, Ferreira SH, Spiguel MH, Feldens
EG. Dental anomalies and associated factors in 2- to 5-year-
old Brazilian children. Int J Paediatr Dent. 2008;18(6):434–40.
https://doi.org/10.1111/j.1365-­263X.2008.00918.x.
39. Whittington BR, Durward CS. Survey of anomalies in primary
teeth and their correlation with the permanent dentition. N Z
Dent J. 1996;92(407):4–8.
40. Rølling S, Poulsen S. Agenesis of permanent teeth in 8138
Danish schoolchildren: prevalence and intra-­oral distribution
according to gender. Int J Paediatr Dent. 2009;19(3):172–5.
https://doi.org/10.1111/j.1365-­263X.2008.00958.x.
41. Kim YH. Investigation of hypodontia as clinically related
dental anomaly: prevalence and characteristics. ISRN Dent.
2011;2011:246135. https://doi.org/10.5402/2011/246135.
42. Mahabob MN, Anbuselvan GJ, Kumar BS, Raja S, Kothari
S. Prevalence rate of supernumerary teeth among non-syn-
dromic South Indian population: an analysis. J Pharm Bioallied
Sci. 2012;4(Suppl 2):S373–5. https://doi.org/10.4103/0975-
­7406.100279.
43. Delli K, Livas C, Bornstein MM. Lateral incisor agenesis,
canine impaction and characteristics of supernumerary teeth in
a South European male population. Eur J Dent. 2013;7(3):278–
83. https://doi.org/10.4103/1305-­7456.115410.
44. Nicholls W. Dental anomalies in children with cleft lip and pal-
ate in Western Australia. Eur J Dent. 2016;10(2):254–8. https://
doi.org/10.4103/1305-­7456.178317.
45. Kavadia S, Papadiochou S, Papadiochos I, Zafiriadis
L. Agenesis of maxillary lateral incisors: a global overview
of the clinical problem. Orthodontics (Chic). 2011;12(4):
296–317.
46. Andrade DC, Loureiro CA, Araújo VE, Riera R, Atallah
AN. Treatment for agenesis of maxillary lateral incisors: a
systematic review. Orthod Craniofac Res. 2013;16(3):129–36.
https://doi.org/10.1111/ocr.12015.
47. Apajalahti S, Hölttä P, Turtola L, Pirinen S. Prevalence of
short-root anomaly in healthy young adults. Acta Odontol
17 Scand. 2002;60(1):56–9.
48. Cutrera A, Allareddy V, Azami N, Nanda R, Uribe F. Is Short
Root Anomaly (SRA) a risk factor for increased external api-
cal root resorption in orthodontic patients? A retrospective
case control study using cone beam computerized tomog-
raphy. Orthod Craniofac Res. 2019;22(1):32–7. https://doi.
org/10.1111/ocr.12254.
49. Yuen SW, Chan JC, Wei SH. Double primary teeth and their
relationship with the permanent successors: a radiographic
study of 376 cases. Pediatr Dent. 1987;9(1):42–8.
50. Kotsanos N, Velonis D. Management of bulbous exophytic
malformations of permanent mandibular incisors. Pediatr
Dent. 2012;34(7):500–2.
51. Chang NY, Park JH, Kim SC, Kang KH, Cho JH, Cho JW,
et al. Forced eruption of impacted maxillary central inci-
sors with severely dilacerated roots. Am J Orthod Dento-
fac Orthop. 2016;150(4):692–702. https://doi.org/10.1016/j.
ajodo.2016.04.018.
52. Papagerakis P, Mitsiadis T. Development and structure of teeth
and periodontal teeth. In: Primer on the metabolic bone dis-
eases and disorders of mineral metabolism, John P. Bilezikian
(Editor-in-Chief), pp.901–910, 9th Edn, Wiley-Blackwell. 2018.
53. Simmer JP, Richardson AS, Hu YY, Smith CE, Ching-Chun
HJ. A post-classical theory of enamel biomineralization and
why we need one. Int J Oral Sci. 2012;4(3):129–34. https://doi.
org/10.1038/ijos.2012.59.
54. Kurek M, Żądzińska E, Sitek A, Borowska-­Strugińska B, Ros-
set I, Lorkiewicz W. Neonatal line width in deciduous incisors
from neolithic, mediaeval and modern skeletal samples from
north-central Poland. Ann Anat. 2016;203:12–8. https://doi.
org/10.1016/j.aanat.2015.02.006.
55. Zheng L, Ehardt L, McAlpin B, About I, Kim D, Papag-
erakis S, et al. The tick tock of odontogenesis. Exp Cell Res.
2014;325(2):83–9. https://doi.org/10.1016/j.yexcr.2014.02.007.
56. Wright JT, Carrion IA, Morris C. The molecular basis of hered-
itary enamel defects in humans. J Dent Res. 2015;94(1):52–61.
https://doi.org/10.1177/0022034514556708.
57. Shields ED, Bixler D, el-Kafrawy AM. A proposed classifica-
tion for heritable human dentine defects with a description of a
new entity. Arch Oral Biol. 1973;18(4):543–53.
58. Zhang J, Wang J, Ma Y, Du W, Zhao S, Zhang Z, et al. A novel
splicing mutation alters DSPP transcription and leads to den-
tinogenesis imperfecta type II. PLoS One. 2011;6(11):e27982.
https://doi.org/10.1371/journal.pone.0027982.
59. Dong J, Gu T, Jeffords L, MacDougall M. Dentin phospho-
protein compound mutation in dentin sialophosphoprotein
causes dentinogenesis imperfecta type III. Am J Med Genet A.
2005;132(3):305–9. https://doi.org/10.1002/ajmg.a.30460.
60. Toomarian L, Mashhadiabbas F, Mirkarimi M, Mehrdad
L. Dentin dysplasia type I: a case report and review of the liter-
ature. J Med Case Rep. 2010;4:1. https://doi.org/10.1186/1752-­
1947-­4-­1.
61. Lee SK, Hu JC, Lee KE, Simmer JP, Kim JW. A dentin sialoph-
osphoprotein mutation that partially disrupts a splice acceptor
site causes type II dentin dysplasia. J Endod. 2008;34(12):1470–
3. https://doi.org/10.1016/j.joen.2008.08.027.
62. Price JA, Wright JT, Walker SJ, Crawford PJ, Aldred MJ, Hart
TC. Tricho-dento-osseous syndrome and amelogenesis imper-
fecta with taurodontism are genetically distinct conditions.
Clin Genet. 1999;56(1):35–40.
63. Dong J, Amor D, Aldred MJ, Gu T, Escamilla M, MacDou-
gall M. DLX3 mutation associated with autosomal dominant
amelogenesis imperfecta with taurodontism. Am J Med Genet
A. 2005;133(2):138–41. https://doi.org/10.1002/ajmg.a.30521.
64. Bufalino A, Paranaíba LM, Gouvêa AF, Gueiros LA, Martelli-
Júnior H, Junior JJ, et al. Cleidocranial dysplasia: oral features
and genetic analysis of 11 patients. Oral Dis. 2012;18(2):184–
90. https://doi.org/10.1111/j.1601-­0825.2011.01862.x.
65. Hu JC, Plaetke R, Mornet E, Zhang C, Sun X, Thomas HF,
et al. Characterization of a family with dominant hypophos-
phatasia. Eur J Oral Sci. 2000;108(3):189–94.
66. Hennekam RCM, Krantz ID, Allanson JE. Gorlin's syndromes
of the head and neck. Oxford University Press. 5th ed. 2010.
67. Eli I, Sarnat H, Talmi E. Effect of the birth process on
the neonatal line in primary tooth enamel. Pediatr Dent.
1989;11(3):220–3.
68. Weerheijm KL, Duggal M, Mejàre I, Papagiannoulis L, Koch
G, Martens LC, et al. Judgement criteria for molar incisor
hypomineralisation (MIH) in epidemiologic studies: a sum-
mary of the European meeting on MIH held in Athens, 2003.
EurJ Paediatr Dent. 2003;4(3):110–3.
69. Kevrekidou Α, Kosma Ι, Arapostathis Κ, Kotsanos Ν. Molar
incisor hypomineralisation of eight- and 14-year-old children:
Developmental Defects of the Teeth and Their Hard Tissues
prevalence, severity, and defect characteristics. Pediatr Dent.
2015;37(5):455–61.
70. Dave M, Taylor G. Global prevalence of molar incisor hypo-
mineralisation. Evid Based Dent. 2018;19(3):78–9. https://doi.
org/10.1038/sj.ebd.6401324.
71. Fagrell TG, Lingström P, Olsson S, Steiniger F, Norén JG. Bac-
terial invasion of dentinal tubules beneath apparently intact
but hypomineralized enamel in molar teeth with molar incisor
hypomineralization. Int J Paediatr Dent. 2008;18(5):333–40.
https://doi.org/10.1111/j.1365-­263X.2007.00908.x.
72. Elfrink ME, ten Cate JM, Jaddoe VW, Hofman A, Moll HA,
Veerkamp JS. Decidious molar hypomineralization and molar
incisor hypomineralization. J Dent Res. 2012;91(6):551–5.
https://doi.org/10.1177/0022034512440450.
73. Kevrekidou A, Kosma I, Kotsanos I, Arapostathis KN, Kot-
sanos N. Enamel opacities in all other than molar incisor hypo-
mineralisation index teeth of adolescents. Int J Paediatr Dent.
2020; https://doi.org/10.1111/ipd.12735.
74. Alifakioti E, Arhakis A, Oikonomidis S, Kotsanos N. Struc-
tural and chemical enamel characteristics of hypomineralised
second primary molars. Eur Arch Paediatr Dent. 2020; https://
doi.org/10.1007/s40368-­020-­00557-­3.
75. Perez VA, Mangum JE, Hubbard MJ. Pathogenesis of molar
hypomineralisation: aged albumin demarcates chalky regions
of hypomineralised enamel. Front Physiol. 2020;11:579015.
https://doi.org/10.3389/fphys.2020.579015.
76. Fatturi AL, Wambier LM, Chibinski AC, Assunção LRDS,
Brancher JA, Reis A, et al. A systematic review and meta-­
analysis of systemic exposure associated with molar incisor
hypomineralization. Community Dent Oral Epidemiol. 2019;
https://doi.org/10.1111/cdoe.12467.
77. Kotsanos N, Kaklamanos EG, Arapostathis K. Treatment
management of first permanent molars in children with molar-
incisor hypomineralisation. Eur J Paediatr Dent. 2005;6(4):
179–84.
78. Linner T, Khazaei Y, Bücher K, Pfisterer J, Hickel R, Küh-
nisch J. Comparison of four different treatment strategies in
teeth with molar-incisor hypomineralization-­ related enamel
breakdown-A retrospective cohort study. Int J Paediatr Dent.
2020;30(5):597–606. https://doi.org/10.1111/ipd.12636.
79. Lygidakis NA, Dimou G, Stamataki E. Retention of fissure
sealants using two different methods of application in teeth
with hypomineralised molars (MIH): a 4 year clinical study.
Eur Arch Paediatr Dent. 2009;10(4):223–6.
80. Gandhi S, Crawford P, Shellis P. The use of a 'bleach-etch-seal'
deproteinization technique on MIH affected enamel. Int J Pae-
diatr Dent. 2012;22(6):427–34. https://doi.org/10.1111/j.1365-­
263X.2011.01212.x.
81. Farah R, Drummond B, Swain M, Williams S. Linking the
clinical presentation of molar-incisor hypomineralization to its
mineral density. Int J Paediatr Dent. 2010;20(5):353–60. https://
doi.org/10.1111/j.1365-­263X.2010.01061.x.
82. Lygidakis NA, Chaliasou A, Siounas G. Evaluation of com-
posite restorations in hypomineralised permanent molars: a
four-year clinical study. Eur J Paediatr Dent. 2003;4(3):143–8.
83. Jälevik B, Möller M. Evaluation of spontaneous space clo-
sure and development of permanent dentition after extrac-
tion of hypomineralized permanent first molars. Int J
Paediatr Dent. 2007;17(5):328–35. https://doi.org/10.1111/
j.1365-­263X.2007.00849.x.
84. Lee HS, Kim SH, Kim SO, Lee JH, Choi HJ, Jung HS, et al.
A new type of dental anomaly: molar-incisor malforma-
tion (MIM). Oral Surg Oral Med Oral Pathol Oral Radiol.
2014;118(1):101–9. https://doi.org/10.1016/j.oooo.2014.03.014.
461 17
 85. Witt CV, Hirt T, Rutz G, Luder HU. Root malformation
associated with a cervical mineralized diaphragm - a distinct
form of tooth abnormality? Oral Surg Oral Med Oral Pathol
Oral Radiol. 2014;117(4):e311–9. https://doi.org/10.1016/j.
oooo.2013.06.030.
  86. Wright JT, Curran A, Kim KJ, Yang YM, Nam SH, Shin TJ,
et al. Molar root-incisor malformation: considerations of
diverse developmental and etiologic factors. Oral Surg Oral
Med Oral Pathol Oral Radiol. 2016;121(2):164–72. https://
doi.org/10.1016/j.oooo.2015.08.024.
  87. Cleaton-Jones P, Hargreaves JA. Comparison of three fluo-
rosis indices in a Namibian community with twice opti-
mum fluoride in the drinking water. J Dent Assoc S Afr.
1990;45(5):173–5.
  88. Croll TP. Enamel microabrasion: observations after 10 years.
J Am Dent Assoc. 1997;128(Suppl):45S–50S.
 89. Caufield PW, Li Y, Bromage TG. Hypoplasia-­ associated
severe early childhood caries--a proposed definition. J
Dent Res. 2012;91(6):544–50. https://doi.org/10.1177/
0022034512444929.
  90. Sundell S. Hereditary amelogenesis imperfecta. An epidemio-
logical, genetic and clinical study in a Swedish child popula-
tion. Swed Dent J Suppl. 1986;31:1–38.
  91. Bäckman B, Holm AK. Amelogenesis imperfecta: prevalence
and incidence in a northern Swedish county. Community Dent
Oral Epidemiol. 1986;14(1):43–7.
 92. Crawford PJ, Aldred M, Bloch-Zupan A. Amelogenesis
imperfecta. Orphanet J Rare Dis. 2007;2:17. https://doi.
org/10.1186/1750-­1172-­2-­17.
 93. Witkop CJ Jr. Amelogenesis imperfecta, dentinogenesis
imperfecta and dentin dysplasia revisited: problems in clas-
sification. J Oral Pathol. 1988;17(9–10):547–53.
  94. Darling AI. Some observations on amelogenesis imperfecta
and calcification of the dental enamel. Proc R Soc Med.
1956;49(10):759–65.
 95. Stephanopoulos G, Garefalaki ME, Lyroudia K. Genes
and related proteins involved in amelogenesis imperfecta.
J Dent Res. 2005;84(12):1117–26. https://doi.org/10.1177/
154405910508401206.
  96. Aldred MJ, Savarirayan R, Crawford PJ. Amelogenesis imper-
fecta: a classification and catalogue for the 21st century. Oral
Dis. 2003;9(1):19–23.
  97. Wright JT, Torain M, Long K, Seow K, Crawford P, Aldred
MJ, et al. Amelogenesis imperfecta: genotype-­phenotype stud-
ies in 71 families. Cells Tissues Organs. 2011;194(2–4):279–83.
https://doi.org/10.1159/000324339.
  98. Rowley R, Hill FJ, Winter GB. An investigation of the asso-
ciation between anterior open-bite and amelogenesis imper-
fecta. Am J Orthod. 1982;81(3):229–35.
 99. Mårdh CK, Bäckman B, Holmgren G, Hu JC, Simmer JP,
Forsman-Semb K. A nonsense mutation in the enamelin gene
causes local hypoplastic autosomal dominant amelogenesis
imperfecta (AIH2). Hum Mol Genet. 2002;11(9):1069–74.
https://doi.org/10.1093/hmg/11.9.1069.
100. Ravassipour DB, Powell CM, Phillips CL, Hart PS, Hart TC,
Boyd C, et al. Variation in dental and skeletal open bite maloc-
clusion in humans with amelogenesis imperfecta. Arch Oral
Biol. 2005;50(7):611–23. https://doi.org/10.1016/j.archoral-
bio.2004.12.003.
101. Ramos AL, Pascotto RC, Iwaki Filho L, Hayacibara RM,
Boselli G. Interdisciplinary treatment for a patient with open-
bite malocclusion and amelogenesis imperfecta. Am J Orthod
Dentofac Orthop. 2011;139(4 Suppl):S145–53. https://doi.
org/10.1016/j.ajodo.2009.05.031.
 462 N. Kotsanos et al.
102. Wright JT, Deaton TG, Hall KI, Yamauchi M. The mineral
and protein content of enamel in amelogenesis imperfecta.
Connect Tissue Res. 1995;32(1–4):247–52.
103. Seow WK. Taurodontism of the mandibular first perma-
nent molar distinguishes between the tricho-dento-­ osseous
(TDO) syndrome and amelogenesis imperfecta. Clin Genet.
1993;43(5):240–6.
104. Wang S, Choi M, Richardson AS, Reid BM, Seymen F,
Yildirim M, et al. STIM1 and SLC24A4 are critical for enamel
maturation. J Dent Res. 2014;93(7 Suppl):94S–100S. https://
doi.org/10.1177/0022034514527971.
105. Zhu J, Feng Q, Stathopulos PB. The STIM-­Orai pathway:
STIM-Orai structures: isolated and in complex. Adv Exp
Med Biol. 2017;993:15–38. https://doi.org/10.1007/978-­3-­319-­
57732-­6_2.
106. Zheng L, Zinn V, Lefkelidou A, Taqi N, Chatzistavrou X,
Balam T, et al. Orai1 expression pattern in tooth and craniofa-
cial ectodermal tissues and potential functions during amelo-
blast differentiation. Dev Dyn. 2015;244(10):1249–58. https://
doi.org/10.1002/dvdy.24307.
107. Papagerakis P, Lin HK, Lee KY, Hu Y, Simmer JP, Bartlett
JD, et al. Premature stop codon in MMP20 causing amelo-
genesis imperfecta. J Dent Res. 2008;87(1):56–9. https://doi.
org/10.1177/154405910808700109.
108. Kantaputra PN, Kaewgahya M, Khemaleelakul U, Dejkham-
ron P, Sutthimethakorn S, Thongboonkerd V, et al. Enamel-
renal-gingival syndrome and FAM20A mutations. Am J
Med Genet A. 2014;164A(1):1–9. https://doi.org/10.1002/
ajmg.a.36187.
109. Tagliabracci VS, Engel JL, Wen J, Wiley SE, Worby CA, Kinch
LN, et al. Secreted kinase phosphorylates extracellular proteins
that regulate biomineralization. Science. 2012;336(6085):1150–
3. https://doi.org/10.1126/science.1217817.
110. Ashkenazi M, Rafe Z, Sarnat H, Levin L. Nephrocalcinosis
associated with continuous enamel hypoplasia and severe
alveolar bone loss: a case report and l­iterature review. Pediatr
Dent. 2014;36(3):250–3.
111. Ababneh FK, AlSwaid A, Youssef T, Al Azzawi M,
Crosby A, AlBalwi MA. Hereditary deletion of the entire
FAM20C gene in a patient with Raine syndrome. Am J Med
Genet A. 2013;161A(12):3155–60. https://doi.org/10.1002/
ajmg.a.36160.
112. Cohn C. Zirconia prefabricated crowns for pediatric patients
with primary dentition: technique and cementation for
esthetic outcomes. Compend Contin Educ Dent. 2016;37(8):
554–8.
113. Seow WK, Amaratunge A. The effects of acid-­etching on
17 enamel from different clinical variants of amelogenesis imper-
fecta: an SEM study. Pediatr Dent. 1998;20(1):37–42.
114. Alonso V, Caserio M. A clinical study of direct compos-
ite full-coverage crowns: long-term results. Oper Dent.
2012;37(4):432–41. https://doi.org/10.2341/11-­229-­S.
115. Dashash M, Yeung CA, Jamous I, Blinkhorn A. Inter-
ventions for the restorative care of amelogenesis imper-
fecta in children and adolescents. Cochrane Database Syst
Rev. 2013;6:CD007157. https://doi.org/10.1002/14651858.
CD007157.pub2.
116. Barron MJ, McDonnell ST, Mackie I, Dixon MJ. Heredi-
tary dentine disorders: dentinogenesis imperfecta and den-
tine dysplasia. Orphanet J Rare Dis. 2008;3:31. https://doi.
org/10.1186/1750-­1172-­3-­31.
117. Lee SK, Lee KE, Hwang YH, Kida M, Tsutsumi T, Ariga T,
et al. Identification of the DSPP mutation in a new kindred and
phenotype-genotype correlation. Oral Dis. 2011;17(3):314–9.
https://doi.org/10.1111/j.1601-­0825.2010.01760.x.
118. Cherkaoui Jaouad I, El Alloussi M, Laarabi FZ, Bouhouche
A, Ameziane R, Sefiani A. Inhabitual autosomal recessive
form of dentin dysplasia type I in a large consanguineous
Moroccan family. Eur J Med Genet. 2013;56(8):442–4. https://
doi.org/10.1016/j.ejmg.2013.05.003.
119. Bloch-Zupan A, Jamet X, Etard C, Laugel V, Muller J, Geof-
froy V, et al. Homozygosity mapping and candidate prioritiza-
tion identify mutations, missed by whole-­exome sequencing,
in SMOC2, causing major dental developmental defects. Am
J Hum Genet. 2011;89(6):773–81. https://doi.org/10.1016/j.
ajhg.2011.11.002.
120. McKnight DA, Simmer JP, Hart PS, Hart TC, Fisher
LW. Overlapping DSPP mutations cause dentin dysplasia and
dentinogenesis imperfecta. J Dent Res. 2008;87(12):1108–11.
https://doi.org/10.1177/154405910808701217.
121. Koskinen S, Keski-Filppula R, Alapulli H, Nieminen P, Ant-
tonen V. Familial oligodontia and regional odontodysplasia
associated with a PAX9 initiation codon mutation. Clin Oral
Investig. 2019; https://doi.org/10.1007/s00784-­019-­02849-­5.
122. Alotaibi O, Alotaibi G, Alfawaz N. Regional odonto-
dysplasia: an analysis of 161 cases from 1953 to 2017.
Saudi Dent J. 2019;31(3):306–10. https://doi.org/10.1016/j.
sdentj.2019.04.012.
123. Al-Batayneh OB, Al Tawashi EK. Pre-eruptive intra-coronal
resorption of dentine: a review of aetiology, diagnosis, and
management. Eur Arch Paediatr Dent. 2020;21(1):1–11.
https://doi.org/10.1007/s40368-­019-­00470-­4.
124. Giuca MR, Cei G, Gigli F, Gandini P. Oral signs in the diag-
nosis of celiac disease: review of the literature. Minerva Sto-
matol. 2010;59(1–2):33–43.
125. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB,
Drago S, et al. Prevalence of celiac disease in at-risk and
not-at-risk groups in the United States. Arch Intern Med.
2003;163(3):286–92.
126. Raether D, Klingberg G, Magnusson L, Norén JG. Histology
of primary incisor enamel in children with early onset celiac
disease. Pediatr Dent. 1988;10(4):301–3.
127. Papagerakis P, Hotton D, Lezot F, Brookes S, Bonass W, Rob-
inson C, et al. Evidence for regulation of amelogenin gene
expression by 1,25-dihydroxyvitamin D(3) in vivo. J Cell Bio-
chem. 1999;76(2):194–205.
128. Linglart A, Biosse-Duplan M, Briot K, Chaussain C, Esterle
L, Guillaume-Czitrom S, et al. Therapeutic management of
hypophosphatemic rickets from infancy to adulthood. Endocr
Connect. 2014;3(1):R13–30. https://doi.org/10.1530/EC-­
13-­0103.
129. Al-Jundi SH, Dabous IM, Al-Jamal GA. Craniofacial
morphology in patients with hypophosphataemic vita-
min-D-resistant rickets: a cephalometric study. J Oral
Rehabil. 2009;36(7):483–90. https://doi.org/10.1111/j.1365-­-
2842.2009.01963.x.
130. Wenkert D, McAlister WH, Coburn SP, Zerega JA, Ryan
LM, Ericson KL, et al. Hypophosphatasia: nonlethal disease
despite skeletal presentation in utero (17 new cases and litera-
ture review). J Bone Miner Res. 2011;26(10):2389–98. https://
doi.org/10.1002/jbmr.454.
131. van den Bos T, Handoko G, Niehof A, Ryan LM, Coburn
SP, Whyte MP, et al. Cementum and dentin in hypophos-
phatasia. J Dent Res. 2005;84(11):1021–5. https://doi.
org/10.1177/154405910508401110.
132. Prasad MK, Geoffroy V, Vicaire S, Jost B, Dumas M, Le
Gras S, et al. A targeted next-generation sequencing assay for
the molecular diagnosis of genetic disorders with orodental
involvement. J Med Genet. 2016;53(2):98–110. https://doi.
org/10.1136/jmedgenet-­2015-­103302.
Developmental Defects of the Teeth and Their Hard Tissues
133. Malfait F, Francomano C, Byers P, Belmont J, Berglund B,
Black J, et al. The 2017 international classification of the
Ehlers-Danlos syndromes. Am J Med Genet C Semin Med
Genet. 2017;175(1):8–26. https://doi.org/10.1002/ajmg.c.
31552.
134. Lygidakis NA, Lindenbaum RH. Pitted enamel hypoplasia
in tuberous sclerosis patients and first-degree relatives. Clin
Genet. 1987;32(4):216–21.
135. Athanasiadou E, Vlachou C, Theocharidou A, Tilaveridis I,
Vargiami E, Antoniadis K, et al. When a pedodontic examina-
tion leads to the diagnosis of osteopetrosis: a case report. Spec
Care Dentist. 2020;40(1):113–20. https://doi.org/10.1111/
scd.12427.
136. Battineni S, Clarke P. Green teeth are a late complication of
prolonged conjugated hyperbilirubinemia in extremely low
birth weight infants. Pediatr Dent. 2012;34(4):103–6.
137. Kotsanos N. Prevalence of tetracycline deposits in premo-
lar teeth extracted for orthodontic purposes. Br Dent J.
1982;152(3):91–2.
138. Shulman JD, Maupome G, Clark DC, Levy SM. Perceptions
of desirable tooth color among parents, dentists and children.
J Am Dent Assoc. 2004;135(5):595–604.
139. Lee SS, Zhang W, Lee DH, Li Y. Tooth whitening in chil-
dren and adolescents: a literature review. Pediatr Dent.
2005;27(5):362–8.
140. Kugel G, Gerlach RW, Aboushala A, Ferreira S, Magnuson
B. Long-term use of 6.5% hydrogen peroxide bleaching strips
on tetracycline stain: a clinical study. Compend Contin Educ
Dent. 2011;32(8):50–6.
141. Mu YD, Xu Z, Contreras CI, McDaniel JS, Donly KJ, Chen
S. Mutational analysis of AXIN2, MSX1, and PAX9 in two
Mexican oligodontia families. Genet Mol Res. 2013;12(4):4446–
58. https://doi.org/10.4238/2013.October.10.10.
142. Rey T, Tarabeux J, Gerard B, Delbarre M, Le Béchec A, Stoet-
zel C, et al. Protocol GenoDENT: implementation of a new
ngs panel for molecular diagnosis of genetic disorders with
orodental involvement. Methods Mol Biol. 1922;2019:407–52.
https://doi.org/10.1007/978-­1-­4939-­9012-­2_36.
143. Pinheiro M, Freire-Maia N. Ectodermal dysplasias: a clini-
cal classification and a causal review. Am J Med Genet.
1994;53(2):153–62. https://doi.org/10.1002/ajmg.1320530207.
144. Horton WA, Hall JG, Hecht JT. Achondroplasia. Lan-
cet. 2007;370(9582):162–72. https://doi.org/10.1016/S0140-­
6736(07)61090-­3.
145. Gurrieri F, Franco B, Toriello H, Neri G. Oral–facial–digi-
tal syndromes: review and diagnostic guidelines. Am J Med
Genet A. 2007;143(24):3314–23. https://doi.org/10.1002/
ajmg.a.32032.
463 17
146. Selvi R, Mukunda PA. Role of SOX9 in the etiology of Pierre-
Robin syndrome. Iran J Basic Med Sci. 2013;16(5):700–4.
147. Alhashimi N, Abed Al Jawad FH, Al Sheeb M, Al Emadi B,
Al-Abdulla J, Al Yafei H. The prevalence and distribution of
nonsyndromic hyperdontia in a group of Qatari orthodontic
and pediatric patients. Eur J Dent. 2016;10(3):392–6. https://
doi.org/10.4103/1305-­7456.184162.
148. Singh K, Singh A, Kumar P, Gupta N. Prosthodontic man-
agement of a patient with Gardner's syndrome: a clinical case
report. Dent Res J (Isfahan). 2014;11(2):276–80.
149. Aletaha M, Fateh-Moghadam H. Gardner syndrome. J Oph-
thalmic Vis Res. 2012;7(3):257–60.
150. Öner AY, Pocan S. Gardner's syndrome: a case report. Br Dent
J. 2006;200(12):666–7. https://doi.org/10.1038/sj.bdj.4813719.
151. Seow WK. Dental development in amelogenesis imperfecta: a
controlled study. Pediatr Dent. 1995;17(1):26–30.
152. Ritter AV. Talking with patients dental fluorosis. J Esthet
Restor Dent. 2005;17(5):326–7. https://doi.org/10.1111/j.1708-
­8240.2005.tb00139.x.
153. Weerheijm KL, Jälevik B, Alaluusua S. Molar–incisor hypo-
mineralisation. Caries Res. 2001;35(5):390–1. https://doi.
org/10.1159/000047479.
154. de Nanclares GP, Fernández-Rebollo E, Santin I, García-
Cuartero B, Gaztambide S, Menéndez E, et al. Epigenetic
defects of GNAS in patients with pseudohypoparathyroid-
ism and mild features of Albright’s hereditary osteodystro-
phy. J Clin Endocrinol Metab. 2007;92(6):2370–3. https://doi.
org/10.1210/jc.2006-­2287.
155. Kitanaka S, Kato S. Vitamin D-dependent rickets Type I
and Type II. The genetics of osteoporosis and metabolic
bone disease. Humana Press. 2000;95–110. https://doi.
org/10.1007/978-­1-­59259-­033-­9_6.
156. Inoue Y, Segawa H, Kaneko I, Yamanaka S, Kusano K,
Kawakami E, et al. Role of the vitamin D receptor in FGF23
action on phosphate metabolism. Biochem J. 2005;390(1):325–
31. https://doi.org/10.1042/BJ20041799.
157. Ye X, Li K, Liu L, Yu F, Xiong F, Fan Y, et al. Dentin dyspla-
sia type I—novel findings in deciduous and permanent teeth.
BMC Oral Health. 2015;15:163. https://doi.org/10.1186/
s12903-­015-­0149-­9.
158. Rolvien T, Koehne T, Kornak U, Lehmann W, Amling M,
Schinke T, et al. A novel ANO5 mutation causing gnathodi-
aphyseal dysplasia with high bone turnover osteosclerosis. J
Bone Miner Res. 2017;32(2):277–84. https://doi.org/10.1002/
jbmr.2980.
159. Alsufyani NA, Lam EW. Osseous (cemento-­osseous) dyspla-
sia of the jaws: clinical and radiographic analysis. J Can Dent
Assoc. 2011;77:b70.
 465 18

Tooth Wear in Children

and Adolescents
Nikolaos Kotsanos and Dowen Birkhed

Contents

18.1 Various Types of Tooth Wear – 466

18.1.1  ttrition and Abrasion – 466
A
18.1.2 Erosive Tooth Wear – 466

18.2 Tooth Wear and Bruxism in Children – 467

18.3 Dental Erosion – 467

18.3.1  revalence and Severity – 467
P
18.3.2 Aetiology of Dental Erosion – 469
18.3.3 Examination and Diagnosis – 470
18.3.4 Prevention of Erosion – 471
18.3.5 Restoration of Erosive Lesions – 471

References – 472

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_18
 466 N. Kotsanos and D. Birkhed

There are different types of tooth wear, but in children

and adolescents, dental erosion is the most common
type. Since it relates to teeth lifetime and oral function,
erosive tooth wear is usually lower in the primary than
in the permanent dentition. The dentin of primary teeth
can however be more rapidly exposed mainly due to
thinner enamel than in corresponding permanent teeth
[1]. Significant wear of young permanent teeth results in
restorative needs and must therefore be diagnosed as
early as possible and treated promptly.
Dental erosion has increased during the last decades
in many countries, and most studies relate this to an
increased consumption of soft drinks and to changes of
lifestyle [2, 3]. Erosive tooth wear is a cumulative multi-
factorial process starting from the eruption of the teeth.
To some extent, it may be considered as a normal condi-
tion rather than an oral disease since the acid is of no
pathological origin [4, 5]. ..      Fig. 18.1 The facets of lateral incisors in this primary dentition
denote that attrition is involved in the tooth wear mechanism

18.1 Various Types of Tooth Wear

a
18.1.1 Attrition and Abrasion

Both attrition and abrasion are related to mechanical

wear, and acids are not involved as is in the case for den-
tal erosion. Attrition is caused by tooth-to-tooth con-
tact and is in most cases considered physiological. When b
it comes to “bruxism” (excessive teeth grinding), which
is a more severe form of attrition, it often takes place
during the night, which produces distinctive sound and
is perceived by the patient’s environment.
Abrasion is another form of mechanical wear
induced by the interaction between teeth and foreign
objects or substances. Both these two types of tooth
wear (attrition and abrasion) are not always easily dis- ..      Fig. 18.2 a Uniform occlusal tooth wear of a 6-year-old girl.
Notice the beginning of lobular incisal edge flattening of the newly
tinguishable. Pronounced occlusal wear has been found erupted mandibular left central incisor. b Similarities in her mother’s
in skulls of past centuries and is attributable to chewing dentition. There was no history connecting either of them with false
unrefined foods that act as a foreign substance. In brux- dietary behaviours
ism, hard dental tissue micro-particles breaking off may
act as an abrasive substance for the teeth [6]. Clinically, Abrasion usually appears in adolescence as saucer-­
18 occlusal wear creates flat surfaces (facets) that fit each shaped cervical wear due to over brushing with incorrect
other in antagonist teeth (. Fig. 18.1). Similarly, attri- horizontal movements, even worse when a hard bristle
tion shortly leads to the flattening of the lobular cutting brush is used. Prevention is important because cervical
edge of newly erupted anterior teeth (. Fig. 18.2). abrasion can be more intense with increasing age and is
Abrasion due to foreign objects may become appar- often acquiring a wedge-shaped form combined with
ent after intensive tooth brushing with toothpaste. gingival recession (. Fig. 18.3).
Abrasion appears to be influenced by the frequency,
duration and force of brushing [7] but is insignificant
when brushing is carried out without toothpaste. 18.1.2 Erosive Tooth Wear
Abrasion can be avoided by using toothpaste with low
abrasivity and brushing with a gentle hand [8, 9]. On the Dental erosion is defined as the loss of tooth structure
other hand, toothpastes with whitening and stain by acid dissolution without the involvement of bacteria.
removal properties often have high abrasivity [10]. It can be caused either by outer factors (drinks and
Tooth Wear in Children and Adolescents
467 18
a understandably, does not correlate with age [17]. The
most frequently affected tooth surfaces of attrition both
in children and adults are the occlusal surfaces of molars
and the incisal edges of anterior teeth by being the prime
surfaces subject to the function of mastication
(. Figs. 18.4 and 18.5).

b
Eye Catcher

The extent of synergy between attrition and erosive

action cannot be easily estimated. Studies of sculls
from past centuries reveal that the dentition was phys-
iologically worn due to unrefined diets requiring
much heavier mastication [18]. On the other hand, in
..      Fig. 18.3 a Saucer-shaped erosive tooth wear of an 18-year-old modern populations, the ideal occlusion is repre-
male with overuse of lemons and juices. His gingival recession points sented by a dentition without wear, with a small
to tooth brushing as a contributory factor. b Generalized erosive (3–4 mm) overjet and vertical incisal coverage.
tooth wear modified by wedge-shaped abrasive wear in the posterior
teeth due to his damaging brushing technique. (Courtesy Dr. C. Pax-
imada)
Observation of contemporary attrition patterns sug-
other acidic food products) or by inner factors (regurgi- gests that mandibular movement in sleep bruxism may
tation and vomiting). It may appear on virtually plaque-­ be associated with current tooth attrition [19]. The prev-
free tooth surfaces. Following dissolution of the outer alence of both self-reported and partner-reported sleep
layer of enamel and/or dentin, the resulting surface is bruxism in young adults was found to be significantly
more susceptible to mechanical wear of tooth brushing more common in the attrition group compared to the
or mastication forces. Therefore, it is often a combina- controls [20]. The prevalence of bruxism in children is
tion of dental erosion and abrasion. The primary tooth high, about 37% for preschool and 50% for first-grade
enamel appears to be more prone to erosion than the primary school children in the USA, according to paren-
permanent one in frequent consumption of acidic drinks tal records [20, 21]. In 4- to 9-year-old children with
[11]. The salivary flow rate, buffering capacity and cerebral palsy, 70% of them exhibited bruxism [22]. In
mucoprotein content affect the sensitivity-susceptibility 6-year-old children, bruxism resulted in greater wear of
of individuals to dental erosion [12]. primary canines [23]. Significantly more attrition is
Another type of tooth wear pathology, called abfrac- observed in young men than in women [24].
tion, makes the enamel vulnerable to masticatory shear Significant attrition is often observed in dental
stress in the cervical area and is apparent in older age anomalies characterized by reduced tooth hardness,
[13]. All previously described types of wear can act either developmental (e.g. molar incisor hypomineral-
simultaneously, but the morphology of defects may sub- ization, MIH) or inherited ones (e.g. dentinogenesis and
stantially vary depending on the predominant aetiologi- amelogenesis imperfecta, . Fig. 18.6). Measures to pre-
cal factor [14]. The combination of these processes can vent severely worn teeth in such children include restora-
cause synergistic results (. Fig. 18.3), as the softer tion of occlusal surfaces of primary or permanent teeth
enamel and dentin after an erosive acid attack are more with composite or preformed metal crowns.
prone to abrasion by an immediate brushing action [15].
Such effects are more obvious in some enthusiastic
brushers in adolescence. 18.3 Dental Erosion

18.3.1 Prevalence and Severity

18.2 Tooth Wear and Bruxism in Children
Physiological tooth wear (attrition) increases with age,
and in modern societies, it is estimated that the accept-
able wear rate of the posterior teeth is approximately
15–20 μm/year [16]. The severity of any type of patho-
logical wear depends on parafunctional habits and,
Dental erosion seems to be the worst contemporary type
of dental wear, and the dental community shows an
increasing concern in the current century. Erosion began
being recorded in Britain since 1993, and the prevalence
had shown to increase within a few years [25]. There are
more erosion prevalence studies in children and adoles-
 468 N. Kotsanos and D. Birkhed

..      Fig. 18.4 a Tooth wear of a

a
5-year-old. b The occlusal and
incisal wear is thought as owed
to reported night bruxism,
which, in combination to
existing primary molar
hypomineralization, led also to
breakdown visible on the
bucco-occlusal crest of first
molar. c Occlusal wear of an
Essix splint used at night verifies
the action of attrition forces

b c

mean prevalence in deciduous teeth between 30% and

18
..      Fig. 18.5 Severe occlusal wear extensively exposing the dentin in
a 5.5-year-old with night bruxism. The greater wear in the anterior
region is attributed to edge-to-edge type of occlusion. (Courtesy Dr.
S. Papapetrou)
cents than in adults, which is mainly due to the ease of
finding the respective study samples. A recent review of
the global prevalence of erosive tooth wear shows a
50% and in permanent teeth between 20% and 45% [26].
The wide variation in prevalence has been attrib-
uted except for dietetic habits to the multiplicity of
indices measuring tooth erosion. Some studies indicate
a positive association between dental erosion and car-
ies in teenagers [27, 28], while other reports find no
such association.
Concerning the primary teeth, erosion was found in
5.7% of preschool Chinese children, in 31% in Saudi
Arabia and in 47% of 5-year-old Irish children [29–31].
A recent meta-analysis of all the studies published in the
literature over the past three decades on the prevalence
of dental erosion in preschool children showed that
tooth wear into the dentin of deciduous teeth in children
increases linearly with age [32]. A German study
reported that the prevalence and risk factors of erosive
tooth wear in 3- to 6-year-old kindergarten children
increased from 2004–2005 to 2014–2015 [33].
In adolescence, prevalence data shows great variabil-
ity, ranging from 37% to 100% in various European
countries and the USA, and a variety of tooth numbers
with erosive lesions [34, 35]. A Greek study, using a
Tooth Wear in Children and Adolescents
..      Fig. 18.6 Mandibular first molars of a 9-year-old odontogenesis
imperfecta patient with worn out/disintegrated enamel casps expos-
ing the defective dentin
newer index (BEWE, Basic Erosive Wear Examination,
which does not evaluate wear depth but measures ero-
sive tooth wear semi-quantitatively by its extent on
tooth surfaces), recorded erosion in 65% of primary
teeth of 8-year-olds and in 37% of permanent teeth of
14-year-olds [36].
18.3.2 Aetiology of Dental Erosion
The aetiological factors for dental erosion can be divided
into those of extrinsic and intrinsic origin.
18.3.2.1 Extrinsic Factors
1. Diet: The parameter of diet has been the most exten-
sively studied factor regarding dental erosion. There
are several reviews on the influence of diet on tooth
erosion prevalence in children and adolescents [37–
39]. Overconsumption of acidic drinks (soft drinks
and fruit juices), citrus fruits and lemon or vinegar is
the most common aetiological factor (. Fig. 18.7).
Despite the wide variation among populations – in
1995 one in ten US students consumed at least four
soft drinks daily [40] and in 2001 in Britain at least
three soft drinks daily [41] – children generally con-
sume more soft drinks and juices than adults. In Brit-
ain, 2/5 of fruit drinks are consumed by children up
to 9 years old [42]. The soft drink consumption has
been tripled in the USA in the last 20 years of the
past century [43]. The acidity of some popular drinks
aimed at young people ranges from pH = 2.6 (Coca-
Cola, Sprite) and 3.0 (ice tea) to 3.4 (Red Bull) [44].
Except for the acidity, the erosive potential of a bev-
erage depends on its inorganic content, its resistance
to pH neutralization (buffer capacity) and possibly
other chemical properties. At the same acidity levels,
citric acid causes more erosion in vitro than phos-
phoric acid [44], while the addition of calcium (and a
469 18
a
..      Fig. 18.7 a Erosive tooth wear in a 15-year-old admitting overus-
ing lemon in his diet. Maxillary central incisors present glossy sur-
face with obvious enamel thickness reduction. b Incisal view of
thinness
small amount of phosphate and fluoride) in juices
may reduce their erosive potential [45].
2. Medicines: Several studies have discussed the use of
various medicines and their role for causing dental
erosions in primary and permanent teeth [46–48].
One factor to take into consideration is the length of
the treatment and the intake frequency of the drug.
Thus, a causal relationship has been found for the
frequent use of acetylsalicylic acid (aspirin) that is
used in the treatment of juvenile rheumatoid arthri-
tis as well as for ascorbic acid (vitamin C) [49, 50].
Both positive [51] and negative relationships [52]
with erosion have been reported with asthma inhala-
tion drugs.
3. Behaviour factors: There are some factors related to
diet and particularly to drinking habits that can affect
the erosion risk, such as swishing or retaining the soft
drink, lemon or citrus fruits in the mouth before
swallowing [53]. Other patient-­ related factors are
intake frequency, lifestyle and oral hygiene [54]. It is
not clear how socioeconomic status affects the preva-
lence of dental erosion. Most studies show a positive
association with low socioeconomic status, but there
are also some studies showing the opposite. A Chi-
nese study in particular found that preschool children
of higher socioeconomic status (higher parent educa-
tional level) drank more fruit juices daily [29]. When
comparing factors potentially related to the occur-
rence of dental erosion in high- and low-erosion
groups of young Saudi men, it was found that drink-
ing habits was a significant factor [55]. Moreover, the
contact time between the tooth and the acid may be a
more important risk factor for dental erosions com-
 470 N. Kotsanos and D. Birkhed

pared to frequency of dietary acid intake or fre-

quency of tooth brushing [56]. Logistic regression of
392 Swedish adolescents showed predictive variables
for high consumption of carbonated soft drinks, and
thereby for dental erosion, to be unhealthy dietary
habits, less physical activity, high BMI and long time
spent in front of TV/computer [57].

18.3.2.2 Intrinsic Factors

kGastroesophageal Reflux Disease (GERD) and
Vomiting
The hydrochloric acid (HCl) of the stomach reaches the ..      Fig. 18.8 An 18-year-old young man with GERD and severe ero-
sion of the maxillary teeth (perimylolysis). Please observe that the
mouth through vomiting or regurgitation and causes palatal cusps of the premolars, especially the one on left side, are
dental erosion especially in the palatal surfaces of upper eroded and that the amalgam fillings, which are not affected of the
anterior teeth, called perimylolysis (. Fig. 18.8). Lack stomach acid, are shiny and “stand out” on the palatal surfaces of
of treatment of this condition results in the destruction the first molars and on the one of the premolars. The patient also has
of posterior teeth mainly their palatal cusps and occlu- approximal caries in the anterior teeth, which is more noticeable
because of the erosion of the palatal surfaces
sal surfaces. These acid-demineralized occlusal surfaces
are less resistant to occlusal wear, and the result is a
combination of chemical erosion and attrition.
Erosion from chronic vomiting is uncommon in chil- a
dren. The vomiting may be spontaneous or induced and
related with pathological conditions, e.g. irritable intes-
tine syndrome, nausea or migraine and epilepsy [58].
Long-lasting emetic episodes starting from preschool
age and continuing during child’s growth show a reduced
frequency in adulthood suggesting a self-limiting condi-
tion. Vomiting is most common in the first 3 months of
pregnancy. Vomiting is also sometimes self-induced by
young women or even adolescents suffering from buli-
mia or anorexia nervosa [59, 60]. b
New-born babies often show GERD, but after the
age of 1 year with the eruption of the first primary teeth,
the frequency of this condition is reduced to 8% [61].
Moreover, a study in 2- to 16-year-old children with
GERD showed no significantly increased dental erosion
and concluded that perhaps the reflux of gastric acids in
children is constrained in the esophagus [61]. Dentists
however should keep in mind that children do not usu-
ally report this reflux because they consider it as normal.
..      Fig. 18.9 a Erosive tooth wear of an 18-year-old female with
“sour taste preference” with pronounced incisal edge translucency of
18 maxillary central incisors. b Erosion is complicated with incisal
18.3.3 Examination and Diagnosis enamel breakdown of a 25-year-old male who likes to bite lemons

The clinical examination includes inquiring for dietary
habits, tooth brushing method, other habits, presence of
GERD and estimation of salivary secretion rate and
buffer capacity. Diagnosis is based on visual examina-
tion because all types of dental wear occur in clinically
accessible surfaces. A relatively early finding of erosive
tooth wear is the glossy appearance due to loss of sur-
face structure (perikymata) of the enamel. A frequent
later finding is an increased incisal edge transparency of
the crown of anterior teeth (. Fig. 18.9). The most fre-
quently affected sites are the occlusal surfaces of pri-
mary molars and palatal or labial surfaces of upper
anterior teeth [34, 35]. This is associated with the pre-
dominant erosive factor, e.g. GERD or frequent con-
sumption of acidic products. In advanced stages, dentin
exposure can be observed (. Fig. 18.10). Depending on
the prime aetiological and contributing factors, this may
be in the palatal surface of anterior teeth or the occlusal
surfaces of posterior teeth, starting with cupping in the
cusp tips (. Fig. 18.6). Generally, the early stages of
erosion are difficult to diagnose, especially before sig-
nificant depth of enamel has been lost and dentin expo-
Tooth Wear in Children and Adolescents
a proved wrong, revealing the difficulties in identifying
b
c ral to a gastroenterologist if necessary. Chewing ant-
..      Fig. 18.10 a Severe erosive tooth wear of the central incisors in a
20-year-old male with a history of 1.5lt daily consumption of cola
drink. Note the minimal wear with stain deposited on the misaligned
laterals’ labial surfaces. b Generalized wear of the palatal surfaces
with exposed dentin in the lateral incisor. c Wear (and approximal
caries) in his posterior maxillary teeth. (Courtesy Dr. C. Paximada)
sure and/or hypersensitivity is apparent, unless there is
experience and specific interest in dental wear.
Different index systems for grading dental wear
severity in the clinical situation have been described. The
most widely used tooth wear index is the one by Smith
and Knight [62] using four grades – from 0 (no signs of
dental wear) to 4 (pulp exposure or tertiary dentin). The
number of such indices reported in the literature is
extremely large amounting to dozens. The preferred
index should be relatively simple so as to be used in epi-
demiological studies with large population samples,
while it should be sensitive enough to accurately depict
wear depth and extent on all tooth surfaces. Some indi-
ces like the “Basic Erosive Wear Examination” (BEWE)
record only the most severely (regarding the surface
area) affected tooth surface in each sextant of the denti-
tion [63, 64]. Regarding the depth of erosive lesions, the
comparison of clinical to histological assessments has
shown that 1/3 of recordings of dentin exposure were
471 18
true depth or lesions [65].
18.3.4 Prevention of Erosion
In the permanent teeth, dental erosion may develop
early in life and may commonly be progressive [66].
Dentists should therefore be aware of this fact and per-
form regular screenings for erosion and recording of
associated lifestyle factors [66]. Concerning the diffi-
culty in early recognition of erosion, proper training of
dental practitioners can help its diagnosis and preven-
tion. Measures include [67–69]:
55 Detailed recording of diet for 4 continuous days
(with 1–2 holidays), including the exact time, quan-
tity and type of consumption, the time of brushing,
evaluation of the erosive potential of acidic foods/
drinks and instructions to decrease them
55 Evaluation of GERD or vomiting reflexes and refer-
acid tablets [70] or mouth washing with soda solution
to neutralize acids
55 Brushing teeth with a soft tooth brush and low
abrasivity toothpaste at a time that does not coin-
cide with the presence of acidic pH in the saliva, e.g.
at least 20 min after taking acidic food or drinks
[71–73]
55 Personalized fluoride treatment (includes fluoride
varnish or gel, brushing with high fluoride concen-
tration toothpaste or stannous fluoride) [74] or pos-
sibly other enhancing agents
55 Instructions for inspection and possible improve-
ment of saliva parameters, e.g. by chewing gum [54]
18.3.5 Restoration of Erosive Lesions
Eye Catcher
Just as with dental caries, restoring teeth with erosive
lesions is not a causative treatment. It may however
be useful for arresting their progression, for relieving
possible hypersensitivity and for functional and aes-
thetic reasons. Restorative treatment does not replace
preventive (causative) treatment, for the added reason
that many restorative materials are affected by enamel
erosion acids.
Composites are considered as the first choice of restor-
ative treatment. Small to moderate occlusal lesions can
be filled after using dentin bonding adhesives. In cervi-
cal lesions, glass ionomers are said to be inappropriate
 472 N. Kotsanos and D. Birkhed
a b
c d
..      Fig. 18.11 a Erosive tooth wear of a young female needing resto-
ration. b Initial reduction of labial tooth surfaces using a special bur
with depth guide. c Near-final preparations for porcelain veneers. d
because they are susceptible to erosion too [75, 76],
although resin-modified glass ionomers are likely be
more durable and suitable. In severely worn anterior
teeth except for composite resin restorations with cellu-
loid matrix (strip crown), porcelain veneers can be used
at the end of adolescence (. Fig. 18.11). There is no
data available about their longevity, other to limited evi-
dence in teeth with caries or crown fractures.
There have been many publications lately on the
management of tooth wear with crowns and indirect
restorations [77–81]. The conclusions from these litera-
18 ture reviews are that there is no strong evidence to sug-
gest that any material is better than another. Direct or
indirect materials may be feasible options to restore
severely worn teeth. However, most of these reviews are
focusing on rehabilitation of severely worn teeth in
adults and very few on younger individuals.
References
1. Kreulen CM, Van't Spijker A, Rodriguez JM, Bronkhorst EM,
Creugers NH, Bartlett DW. Systematic review of the prevalence
of tooth wear in children and adolescents. Caries Res.
2010;44:151–9.
Final restorations of the six maxillary anterior teeth. (Courtesy Dr.
P. Gerasimou)
 2. Carvalho TS, Lussi A, Jaeggi T, Gambon DL. Erosive tooth
wear in children. Monogr Oral Sci. 2014;25:262–78.
 3. Johansson AK, Omar R, Carlsson GE, Johansson A. Dental
erosion and its growing importance in clinical practice: from
past to present. Int J Dent. 2012;2012:632907.
  4. Ganss C. Is erosive tooth wear an oral disease? Monogr Oral Sci.
2014;25:16–21.
  5. Ganss C, Lussi A. Diagnosis of erosive tooth wear. Monogr Oral
Sci. 2014;25:22–31.
  6. Xhonga FA. Bruxism and its effect on the teeth. J Oral Rehabil.
1977;4:65–7.
  7. Dyer D, Addy M, Newcombe RG. Studies in vitro of abrasion by
different manual toothbrush heads and a standard toothpaste. J
Clin Periodontol. 2000;27:99–103.
  8. Addy M, Hunter ML. Can tooth brushing damage your health?
Effects on oral and dental tissues. Int Dent J. 2003;53(Suppl
3):177–86.
  9. Philpotts CJ, Weader E, Joiner A. The measurement in vitro of
enamel and dentine wear by toothpastes of different abrasivity.
Int Dent J. 2005;55:183–7.
10. Schemehorn BR, Moore MH, Putt MS. Abrasion, polishing,
and stain removal characteristics of various commercial denti-
frices in vitro. J Clin Dent. 2011;22:11–8.
11. Hunter ML, West NX, Hughes JA, Newcombe RG, Addy
M. Erosion of deciduous and permanent dental hard tissue in
the oral environment. J Dent. 2000;28:257–63.
12. Amaechi BT, Higham SM. Eroded enamel lesion remineraliza-
tion by saliva as a possible factor in the site-­specificity of human
dental erosion. Arch Oral Biol. 2001;46:697–703.
Tooth Wear in Children and Adolescents
13. Grippo JO. Abfractions: a new classification of hard tissue
lesions of teeth. J Esthet Dent. 1991;3:14–9.
14. Lussi A, Hellwig E. Risk assessment and preventive measures.
Monogr Oral Sci. 2006;20:190–9.
15. Attin T, Siegel S, Buchalla W, Lennon AM, Hannig C, Becker
K. Brushing abrasion of softened and remineralised dentin: an
in situ study. Caries Res. 2004;38:62–6.
16. Lambrechts P, Braem M, Vuylsteke-Wauters M, Vanherle
G. Quantitative in vivo wear of human enamel. J Dent Res.
1989;68:1752–4.
17. Bartlett D, Dugmore C. Pathological or physiological erosion--is
there a relationship to age? Clin Oral Investig. 2008;12(Suppl
1):S27–31.
18. Kaifu Y. Changes in the pattern of tooth wear from prehis-
toric to recent periods in Japan. Am J Phys Anthropol.
1999;109:485–99.
19. Okura K, Shigemoto S, Suzuki Y, Noguchi N, Omoto K, Abe S,
Matsuka Y. Mandibular movement during sleep bruxism
assoc ated with current tooth attrition. J Prosthodont Res.
2017;61:87–95.
20. Jonsgar C, Hordvik PA, Berge ME, Johansson AK, Svensson P,
Johansson A. Sleep bruxism in individuals with and without
attrition-type tooth wear: an exploratory matched case-control
electromyographic study. J Dent. 2015;43:1504–10.
21. Insana SP, Gozal D, McNeil DW, Montgomery-­ Downs
HE. Community based study of sleep bruxism during early
childhood. Sleep Med. 2013;14:183–8.
22. Peres AC, Ribeiro MO, Juliano Y, César MF, Santos RC. Occur-
rence of bruxism in a sample of Brazilian children with cerebral
palsy. Spec Care Dentist. 2007;27:73–6.
23. Rios D, Magalhães AC, Honório HM, Buzalaf MA, Lauris JR,
Machado MA. The prevalence of deciduous tooth wear in six-
year-old children and its relationship with potential explanatory
factors. Oral Health Prev Dent. 2007;5:167–71.
24. Seligman DA, Pullinger AG, Solberg WK. The prevalence of den-
tal attrition and its association with factors of age, gender, occlu-
sion and TMJ symptomatology. J Dent Res. 1988;67:1323–33.
25. Nunn JH, Gordon PH, Morris AJ, Pine CM, Walker A. Dental
erosion - changing prevalence? A review of British National chil-
drens' surveys. Int J Paediatr Dent. 2003;13:98–105.
26. Schlueter N, Luka B. Erosive tooth wear - a review on global
prevalence and on its prevalence in risk groups. Br Dent J.
2018;224:364–70.
27. Isaksson H, Birkhed D, Wendt LK, Alm A, Nilsson M, Koch
G. Prevalence of dental erosion and association with lifestyle
factors in Swedish 20-year olds. Acta Odontol Scand.
2014;72:448–57.
28. Mulic A, Tveit AB, Skaare AB. Prevalence and severity of dental
erosive wear among a group of Norwegian 18-year-olds. Acta
Odontol Scand. 2013;71:475–81.
29. Luo Y, Zeng XJ, Du MQ, Bedi R. The prevalence of dental ero-
sion in preschool children in China. J Dent. 2005;33:115–21.
30. Al-Malik MI, Holt RD, Bedi R. Erosion, caries and rampant
caries in preschool children in Jeddah, Saudi Arabia. Commu-
nity Dent Oral Epidemiol. 2002;30:16–23.
31. Harding MA, Whelton H, O’Mullane DM, Cronin M. Dental
erosion in 5-year-old Irish school children and associated fac-
tors: a pilot study. Community Dent Health. 2003;20:165–70.
32. Corica A, Caprioglio A. Meta-analysis of the prevalence of
tooth wear in primary dentition. Eur J Paediatr Dent.
2014;15:385–8.
33. Tschammler C, Müller-Pflanz C, Attin T, Müller J, Wiegand
A. Prevalence and risk factors of erosive tooth wear in 3-6 year
old German kindergarten children – a comparison between
2004/05 and 2014/15. J Dent. 2016;52:45–9.
473 18
34. Jaeggi T, Lussi A. Prevalence, incidence and distribution of ero-
sion. Monogr Oral Sci. 2006;20:44–65.
35. Provatenou E, Kaklamanos E, Kevrekidou A, Kosma I, Kot-
sanos N. Erosive tooth wear and related risk factors in 8- and
14-year-old Greek children. Caries Res. 2016;50:
349–62.
36. Margaritis V, Mamai-Homata E, Koletsi-­Kounari H, Polychro-
nopoulou A. Evaluation of three different scoring systems for
dental erosion: a comparative study in adolescents. J Dent.
2011;39:88–93.
37. Salas MM, Nascimento GG, Vargas-Ferreira F, Tarquinio SB,
Huysmans MC, Demarco FF. Diet influenced tooth erosion
prevalence in children and adolescents: results of a meta-analy-
sis and meta-regression. J Dent. 2015;4:865–75.
38. O'Toole S, Mullan F. The role of the diet in tooth wear. Br Dent
J. 2018;224:379–83.
39. Lussi A, Jaeggi T, Zero D. The role of diet in the aetiology of
dental erosion. Caries Res. 2004;38(Suppl 1):34–44.
40. American Academy of Pediatrics, Committee on School Health.
Soft drinks in school. Pediatrics. 2004;113:152–3.
41. Al-Dlaigan YH, Shaw L, Smith A. Dental erosion in a group of
British 14-year-old school children. Part II: influence of dietary
intake. Br Dent J. 2001;190:258–61.
42. Rugg-Gunn AJ, Lennon MA, Brown JG. Sugar consumption in
the United Kingdom. Br Dent J. 1986;161:359–64.
43. Cavadini C, Siega-Riz AM, Popkin BM. US adolescent
food intake trends from 1965 to 1996. Arch Dis Child.
2000;83:18–24.
44. Lussi A, Jaeggi T. Chemical factors. Monogr Oral Sci.
2006;20:77–87. West NX, Hughes JA, Addy M. The effect of pH
on the erosion of dentine and enamel by dietary acids in vitro. J
Oral Rehabil. 2001;28:860–4.
45. Barbour ME, Parker DM, Allen GC, Jandt KD. Human enamel
erosion in constant composition citric acid solutions as a func-
tion of degree of saturation with respect to hydroxyapatite. J
Oral Rehabil. 2005;32:16–21.
46. Lussi A, Carvalho TS. Analyses of the Erosive Effect of dietary
substances and medications on deciduous teeth. PLoS One.
2015;10:e0143957.
47. Hellwig E, Lussi A. Oral hygiene products, medications and
drugs - hidden aetiological factors for dental erosion. Monogr
Oral Sci. 2014;25:155–62.
48. Scatena C, Galafassi D, Gomes-Silva JM, Borsatto MC, Serra
MC. In vitro erosive effect of pediatric medicines on deciduous
tooth enamel. Braz Dent J. 2014;25:22–7.
49. Sullivan RE, Kramer WS. Iatrogenic erosion of teeth. J Dent
Child. 1983;50:192–6.
50. Asher C, Read MJ. Early enamel erosion in children associated
with the excessive consumption of citric acid. Br Dent J.
1987;162(10):384–7.
51. Al-Dlaigan YH, Shaw L, Smith AJ. Is there a relationship
between asthma and dental erosion? A case control study. Int J
Paediatr Dent. 2002;12:189–200.
52. Dugmore CR, Rock WP. Asthma and tooth erosion. Is there an
association? Int J Paediatr Dent. 2003;13:417–24.
53. Johansson AK, Lingström P, Imfeld T, Birkhed D. Influence of
drinking method on tooth-surface pH in relation to dental ero-
sion. Eur J Oral Sci. 2004;112:484–9.
54. Buzalaf MAR, Magalhães AC, Rios D. Prevention of erosive
tooth wear: targeting nutritional and patient-­related risks fac-
tors. Br Dent J. 2018;224:371–8.
55. Johansson AK, Lingström P, Birkhed D. Comparison of factors
potentiall related to the occurrence of dental erosion in high-
and low-erosion groups. Eur J Oral Sci. 2002;110:
204–11.
 474 N. Kotsanos and D. Birkhed
56. O'Toole S, Bartlett D. The relationship between dentine hyper-
sensitivity dietary acid intake and erosive tooth wear. J Dent.
2017;67:84–7.
57. Hasselkvist A, Johansson A, Johansson AK. Association
between soft drink consumption, oral health and some lifestyle
factors in Swedish adolescents. Acta Odontol Scand.
2014;72:1039–46.
58. O'Sullivan E, Milosevic A. UK National Clinical Guidelines in
Paediatric Dentistry: diagnosis, prevention and management of
dental erosion. Int J Paediatr Dent. 2008;18(Suppl 1):29–38.
59. Bartlett D. Intrinsic causes of erosion. Monogr Oral Sci.
2006;20:119–39.
60. Osatakul S, Sriplung H, Puetpaiboon A, Junjana CO, Cham-
nongpakdi S. Prevalence and natural course of gastroesophageal
reflux symptoms: a 1-year cohort study in Thai infants. J Pediatr
Gastroenterol Nutr. 2002;34:63–7.
61. O'Sullivan EA, Curzon ME, Roberts GJ, Milla PJ, Stringer
MD. Gastroesophageal reflux in children and its relationship to
erosion of primary and permanent teeth. Eur J Oral Sci.
1998;106:765–9.
62. Smith BG, Knight JK. An index for measuring the wear of teeth.
Br Dent J. 1984;156:435–8.
63. Mulic A, Tveit AB, Wang NJ, et al. Reliability of two clini-
cal scoring systems for dental erosive wear. Caries Res.
2010;44:294–9.
64. Bartlett D, Ganss C, Lussi A. Basic Erosive Wear Examination
(BEWE): a new scoring system for scientific and clinical needs.
Clin Oral Investig. 2008;(Suppl 1):S65–8.
65. Ganss C, Klimek J, Lussi A. Accuracy and consistency of the
visual diagnosis of exposed dentine on worn occlusal/incisal sur-
faces. Caries Res. 2006;40:208–12.
66. Hasselkvist A, Johansson A, Johansson AK. A 4 year prospec-
tive longitudinal study of progression of dental erosion associ-
ated to lifestyle in 13-14 year-old Swedish adolescents. J Dent.
2016;47:55–62.
67. Amaechi BT, Higham SM. Dental erosion: possible approaches
to prevention and control. J Dent. 2005;33:243–52.
68. Carvalho JC, Scaramucci T, Aimée NR, Mestrinho HD, Hara
AT. Early diagnosis and daily practice management of erosive
tooth wear lesions. Br Dent J. 2018;224:311–8.
18
69. Carvalho TS, Colon P, Ganss C, Huysmans MC, Lussi A, Schlu-
eter N, et al. Consensus Report of the European Federation of
Conservative Dentistry: erosive tooth wear, diagnosis and man-
agement. Swiss Dent J. 2016;126:342–6.
70. Lindquist B, Lingström P, Fändriks L, Birkhed D. Influence of
five neutralizing products on intra-oral pH after rinsing with
simulated gastric acid. Eur J Oral Sci. 2011;119:301–4.
71. Ganss C, Schlueter N, Friedrich D, Klimek J. Efficacy of waiting
periods and topical fluoride treatment on toothbrush abrasion
of eroded enamel in situ. Caries Res. 2007;41:146–51.
72. O’Toole S, Bernabé E, Moazzez R, Bartlett D. Timing of dietary
acid intake and erosive tooth wear: a case-­control study. J Dent.
2017;56:99–104.
73. Lussi A, Lussi J, Carvalho TS, Cvikl B. Toothbrushing after an
erosive attack:will waiting avoid tooth wear? Eur J Oral Sci.
2014;122:353–9.
74. Huysmans MC, Young A, Ganss C. The role of fluoride in ero-
sion therapy. Monogr Oral Sci. 2014;25:230–43.
75. Jaeggi T, Grüninger A, Lussi A. Restorative therapy of erosion.
Monogr Oral Sci. 2006;20:200–14.
76. Johansson A, Johansson AK, Omar R, Carlsson GE. Rehabili-
tation of the worn dentition. J Oral Rehabil. 2008;35:548–66.
77. Milosevic A. Clinical guidance and an evidence-­based approach
for restoration of worn dentition by direct composite resin. Br
Dent J. 2018;224:301–10.
78. Loomans BAC, Kreulen CM, Huijs-Visser HECE, Sterenborg
BAMM, Bronkhorst EM, Huysmans MCDNJM, Opdam
NJM. Clinical performance of full rehabilitations with direct
composite in severe tooth wear patients: 3.5 years results. J Dent.
2018;70:97–103.
79. Mesko ME, Sarkis-Onofre R, Cenci MS, Opdam NJ, Loomans
B, Pereira-Cenci T. Rehabilitation of severely worn teeth: a sys-
tematic review. J Dent. 2016;48:9–15.
80. Mehta SB, Banerji S. The restorative management of tooth wear
involving the aesthetic zone. Br Dent J. 2018;224:333–41.
81. Varma S, Preiskel A, Bartlett D. The management of tooth
wear with crowns and indirect restorations. Br Dent J.
2018;224:343–7.
 475 19

Temporomandibular Disorders
in Children and Adolescents
Linda Van den Berghe and Louis Simoen

Contents

19.1  he Orofacial System: Principles of Occlusion

T
and Function – 476
19.1.1  entric Positions of the Lower Jaw and
C
Temporomandibular Joint – 476
19.1.2 Rest Position – 477
19.1.3 Eccentric Positions – 477
19.1.4 Eccentric Mandibular Movements – 477
19.1.5 Vertical Dimension in Occlusion – 477

19.2 Disorders of the Orofacial System – 478

19.2.1 E pidemiology – 478
19.2.2 Etiology – 478
19.2.3 Anamnestic Records – 480
19.2.4 Clinical Examination – 480
19.2.5 Imaging – 480
19.2.6 Diagnosis – 480
19.2.7 Treatment Strategies – 482

19.3 Summary – 482

References – 482

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_19
 476 L. Van den Berghe and L. Simoen
The content of this chapter is not intended to represent
the extensive knowledge of the normal and pathological
function of the temporomandibular system. The basic
aim is to help the dentist understand the basic principles
of normal functioning of the masticatory system [1, 2]
and the extent, symptomatology, and etiology of tem-
poromandibular disorders in children and adolescents,
in order to enable general practitioners to contribute to
treatment.
19.1  he Orofacial System: Principles
T strongest joint of the whole human body. Both units
of Occlusion and Function
The orofacial system (OFS) is the biological system of
an individual where physiological functions of mastica-
tion, swallowing, speech, and breathing are performed.
It consists of a number of elements and tissues that act
together and form functional units. The components of
the OFS are:
(a) The temporomandibular joints (TMJs).
(b) The maxilla or upper jaw and mandibula or lower
jaw.
(c) The teeth and periodontium.
(d) The attached muscles of mastication.
Functions of the OFS are neuromuscular driven, involv-
ing both the central and peripheral nervous system and
muscles. What we accept as normal or efficient function-
ing of the OFS is not only determined by the mandibu-
lar movements but also by the proprioceptive control of
the spatial positions of the lower jaw.
Eye Catcher
In the literature and in practice, the topic dental
occlusion and its role in function or dysfunction of
the masticatory system is often the subject of discus-
sions and controversy. The variety of theories offer-
ing different specific guidelines for clinical approach
is confusing and, moreover, often only based on per-
sonal clinical expertise or foundations and not always
relying on actual scientific evidence [1, 2].
19
Maxillomandibular relationships exist as the positions or
movements of the mandible with or without contacts of
the occlusal surfaces of the teeth present in the oral cav-
ity of each individual. The mandibular position with
tooth contacts should be differentiated in a static posi-
tion or occlusion and an eccentric or dynamic position
or articulation. Without dental contacts the mandibular
movements are generated with distinction between the
eccentric or border movements, on the one hand, and the
functional movements, on the other hand. The rest posi-
tion of the lower jaw is a variable position without tooth
contacts, depending on the momentarily orofacial mus-
cular tension status.
These relationships should also be considered in the
temporomandibular joint. The TMJ is often the subject
of diagnostic failure of certain signs or symptoms in the
masticatory system, due to incomplete or even absent
“medical” knowledge concerning its anatomy and physi-
ological functioning. It is a specific type of joint: it is a
twin joint and contains an articular disc; it is about the
(condyles) move simultaneously according to their ana-
tomic features and in harmony with the occlusal or den-
tal configuration and enable functional luxation,
generally throughout lifetime.
19.1.1  entric Positions of the Lower Jaw
C
and Temporomandibular Joint
19.1.1.1 Maximum Intercuspation
The maxillomandibular position also known as maxi-
mal occlusion represents the relation of both jaws with
existing maximal contacts of opposing occlusal surfaces.
The proprioceptive sense develops during infancy.
Clinical reproducibility of this relation in the TMJs is
doubtful and, therefore, it is never recommended to be
used as a reference for dental reconstruction purposes.
19.1.1.2 Centric Relation/Centric Occlusion
Centric relation (CR) is known as the maxillomandibu-
lar relation in the TMJ where the hinge movement or
rotation of the mandible takes place, around the so-­
called hinge axis, virtually connecting the center of both
condyles. This determination is important as it is repro-
ducible and therefore an important parameter in restor-
ative dentistry, for instance, in youngsters with
oligodontia or amelogenesis imperfecta or even in eden-
tulous patients. The articular condyles effortlessly hold
the rearmost, upmost, and midmost (RUM) position or
centric relation in the TMJs. This position is individu-
ally determined and varies according to the personal
anatomy of the condyles and the morphology of the gle-
noid fossa.
The corresponding interocclusal contact between
upper and lower jaws can be registered between antagonis-
tic premolars and molars, not in the anterior region
(canines and incisors), and is called centric occlusion (CO).
According to the epidemiologic research, in a major-
ity of individuals, there is indeed a difference between
centric and maximal occlusions, the so-called long
­centric occlusion. Centric and maximal occlusion can be
similar, always showing maximal intercuspation of all
Temporomandibular Disorders in Children and Adolescents
present teeth with the condyles in the reproducible RUM
position, which is called the point centric occlusion [1, 2].
19.1.2 Rest Position
Is a postural position of the mandible depending highly
on the neuromuscular activation or state of the mastica-
tory system. The mandible is suspended with an interoc-
clusal distance, the freeway space, which is supposed to
be maintained after dental reconstruction, but which is
also able to adapt to minimal and slow changes in the
equilibrium between elevator and depressor masticatory
muscles. It cannot be considered as strictly reproducible
and is mostly calculated by clinicians as an interdental
space between 1 and 4 mm. It can be adversely affected
by certain emotional conditions (anxiety, depression)
and loss of teeth related to parafunctional habits or
bruxism as these conditions can influence the neuromus-
cular balance in the masticatory system.
19.1.3 Eccentric Positions
Eccentric Occlusal Positions of the Mandible (Also
Known as Articulation).
These positions are static, with certain tooth con-
tacts, depending on the occlusal or articulating type of
the individual dentition. The ideal features in the adult
dentition are:
1. Lateral excursion to the working side featuring only
canines, called the canine guidance.
2. Lateral excursion to the working side with involve-
ment of canines, premolars, and/or molars, called a
group contact.
3. After lateral excursion, at the non-­working or bal-
ancing side, tooth contacts disappear and is called
the unilateral clearance.
4. Maximal protrusion is reached with frontal or incisal
guidance, involving incisors and/or canines with
bilateral disocclusion or clearance between premo-
lars and molars.
During lifetime teeth can show continuous differentia-
tion due to functional or natural loss of tooth substance,
possibly enhancing or changing the eccentric positions
of the lower jaw.
19.1.4 Eccentric Mandibular Movements
All mandibular movements can be traced and projected
in the three spatial planes: the sagittal, the frontal or
coronal, and the horizontal plane. When borderline,
477 19
these movements are reproducible, and within these lim-
its, functional movements are developed. The latter are
highly variable, depending on the neuromuscular status
of the system.
When recorded at the anterior teeth, a characteristic
three-dimensional diagram is generated known as the
Posselt envelope of motion:
1. In the horizontal plane, we distinguish maximal pro-
trusion, maximal retrusion to centric relation, and
maximal lateral excursions.
2. In the frontal or coronal plane, we distinguish maxi-
mal opening and closing in maximal intercuspation
and maximal lateral excursions.
3. In the sagittal plane, we distinguish maximal protru-
sion, maximal retrusion to centric relation, and max-
imal opening and closing.
When recorded at the TMJ:
1. In the horizontal projection, we distinguish the ante-
rior-posterior translation and the lateral eccentric
movements, at the working side, with the rotating
condyle making the so-called Bennet movement or
Bennet shift*, and at the non-working (balancing)
side, with the translating condyle following the path-
way of the Bennet angle.
2. In the frontal projection, we distinguish the opening
movement and the lateral eccentric movements, with
the Bennet shift* at the working side and the path-
way of the Bennet angle at the non-working side.
3. In the lateral projection, we distinguish the opening
movement with the condyle moving according to the
condylar rotation around the hinge axis and followed
by an anterior-inferior translation, following the
pathway of the condylar plane, making an average
angle of 30–35° with a reference horizontal line or
plane.
*The Bennet movement or shift of the working condyle
is a bodily displacement and may be absent or very dis-
crete.
For extensive documentation of all these principles,
see Dos Santos Jr. (2007) [2].
19.1.5 Vertical Dimension in Occlusion
The vertical dimension is the morphologic facial height
which can be measured with the teeth in maximum
intercuspation. Theoretically it only changes three times
throughout the human life evoked by enhanced bone
growth. The first stage appears together with the erup-
tion of the deciduous molars, the second stage between
the ages of 6 and 8 years triggered by the start of the
eruption of the permanent molars, and the third stage
 478 L. Van den Berghe and L. Simoen

between the ages of 12 and 16 years during the last and a lack of clinical reports on striking comorbidities
growth phase. in adults as well as in children and adolescents, e.g.,
During the function of the masticatory system (e.g., sleep or sleep breathing disorders. Nevertheless in gen-
chewing, swallowing, speech), the feature of the mobile eral, the signs and symptoms in children and adolescents
lower jaw or mandible and fixed upper jaw or maxilla, are light and variable over time in the vast majority and
the organization of the dental arches and the dental can be characterized as mild or moderate [4–9].
anatomy (shape) determine the individual ability of the Exceptionally, in some cases with rare diseases, such as
natural mandibular movements. In other words, har- juvenile idiopathic arthritis (JIA), it can progressively
mony should exist between shape and function. Careful lead to severe functional limitations and pain [10].
evaluation and registration of the individual determi- Although at an early age (5–7 years) signs and symp-
nants are mandatory in clinical practice, however with- toms of temporomandibular disorders are not usually
out overestimation as well as oversimplification of the found, some disorders can be detected in one third of
basic principles of occlusion. In biologic or anatomic children with primary teeth [4]. The existence of com-
absence of harmony or even installed disharmony (after plaints (headaches, clicking TMJ), with some of them
restorative treatment), adaptation mechanisms derive in already known by the parents, is confirmed in 36% of
the majority of the human beings; in other words, dis- children aged 7–14 years old, while 64% of those chil-
harmony not necessarily causes traumatic events, such dren apparently show also symptoms (mainly pain on
as temporomandibular pain or dysfunction. palpation of the masticatory muscles) [11, 12].
In long-term studies, signs and symptoms show great
variation in their appearance with the progress of time.
19.2 Disorders of the Orofacial System Some findings, such as clicking, seem to come and go in
an unpredictable way. Indeed, in a 10-year monitoring
Temporomandibular disorders (TMD, the term adopted of children of 7, 11, and 15 years old, no significant pro-
in 1983 by the ADA) contain a number of problems portion of unchanged signs or symptoms of TMD
involving the masticatory muscles, the TMJ, and associ- could be registered [13], while 20 years after the comple-
ated structures. This term is synonymous with the term tion of the monitoring of the same individuals, not any
craniomandibular disorders (CMD) of the OFS. The recrudescence could be found within this remarkably
American Academy of Pediatric Dentistry (AAPD) long period of time [14].
accepts in its guidelines that TMD can also be observed
in adolescents, children, or infants [3]. The role of the
general dentist is regularly underestimated as it comes to 19.2.2 Etiology
observation, detection, differential diagnosis, and treat-
ment strategies. In the majority of patients, temporomandibular disor-
ders are of multifactorial origin. A long time ago, the
dental profession associated occlusal relationships with
19.2.1 Epidemiology temporomandibular pain and dysfunction. Unfortunately,
no or little scientific evidence can be found any longer for
The prevalence of TMD signs in adults is estimated the majority of these associations as in the past only
between 30 and 50% in general population samples. assumptions were made regarding the relationship
They are the most common cause of pain of the non-­ between what is known, the principles of occlusion, and
odontogenic origin in the orofacial system in about 5 to what was not known, the pathophysiology of pain.
12% of the patients seeking treatment. An important Mechanistic concepts can no longer be accepted as expla-
distinction should be made between signs and symp- nation or as therapy models for pain-related disorders.
toms, on the one hand, and patients’ complaints, on the A possible etiologic factor, which can contribute to
19 other hand. the occurrence of temporomandibular disorders in chil-
The occurrence of temporomandibular disorders in dren, is trauma. Lateral or bilateral intra-articular or
children is much more difficult to map and tends to be epicondyle fractures are often the result of trauma to
lower than in adults, with an increasing trend in the sec- the chin, after falling, which is a very common finding in
ond and third decade of life. The variation in reports is childhood [15] and can eventually lead to ankylosis of
mostly due to study design concerning, among others, the maxilla [16]. In isolated cases of condylar fractures
study populations (general population or patient sam- in children, conservative treatment, using functional
ples), examination methods, and discrepancies between orthodontic appliances as activator, may result in com-
definitions and variables. Important confounders are the plete recovery of the fracture and lead to the natural
study methods and/or results from adult populations function of the TMJ and the OFS [17].
Temporomandibular Disorders in Children and Adolescents
Oral parafunctional behaviors such as lip, cheek bit-
ing, thumb sucking, and abnormal posturing of the jaw
have no functional purpose, are common in all age
groups, and occasionally can have some negative effects
on the masticatory system. Nail biting and excessive
chewing gum use on the contrary can cause more impor-
tant overloading of the masticatory muscles and the
TMJ, compared to the negative effects of bruxism.
19.2.2.1 Bruxism
In adults, bruxism is classified as either sleep bruxism,
mainly characterized by tooth grinding, or awake brux-
ism, often characterized as tooth clenching. Both forms
can be found in children and adolescents, with a global
prevalence of 8–38% [18–21].
The etiology of bruxism cannot be explained by
mechanistic concepts but is multifactorial. Its origin has
to be searched in the central nervous system. Genetic
but also peripheral environmental factors should be
considered as the most evident influences nowadays.
Tooth clenching while awake can lead to masticatory
muscle fatigue and numbness (with difficulties to open the
mouth widely or chewing hard food), clicking of the TMJ,
and sometimes an uncomfortable occlusion. In other
words, awake bruxism is a potentially higher etiologic risk
factor for the emergence of myogenous or arthrogenous
symptoms of TMD in childhood and adolescence [20].
Sleep bruxism will mostly do no harm in children
concerning the teeth and the masticatory system, regard-
less the, sometimes, loud sounds produced and reported
by the parents. They should always be informed about
possible non-dental comorbidities. In fact, in the litera-
ture, sleep bruxism can be found to be associated with
headache and sleep breathing disorders (snoring and
obstructive sleep apnea), possibly resulting in growth
disturbances of the maxilla and mandible [21], sleep dis-
turbances, and behavioral disorders (e.g., hyperactivity,
attention-deficit/hyperactivity disorder ADHD, fatigue,
and attention deficit at school), but evidence is still
insufficient to establish a cause-effect relationship [21].
The same lack of evidence exists about permanent dam-
age to the dentition resulting from sleep bruxism during
childhood. Tooth wear of primary teeth has a low pre-
dictive value for wear of the permanent dentition [22].
19.2.2.2 Does Malocclusion Cause TMD?
Occlusal interferences, open bite, cross bite, and missing
posterior teeth cannot be considered as etiologic risk fac-
tors for TMD [23]. Unilateral posterior cross bite
(UPCB) is shown to be weakly associated with clicking
of the TMJ and masticatory muscle pain [23, 24] but can
on the other hand strongly be associated with facial
asymmetry, disturbance of the masticatory cycle, reduced
bite force, and masticatory muscle hypertrophy. Therefore
479 19
correction of UPCB is recommended in children to
reduce the physiologic adaptation demands [23, 24].
19.2.2.3 Does TMD Cause Malocclusion?
Structural and developmental changes and acquired and
inflammatory disorders of the TMJ cause skeletal and
dental changes and frequently lead to marked facial
asymmetry. This is known for unilateral condylar hyper-
plasia and osteochondroma of the condyle, together with
condylar asymmetry and open bite, but without the emer-
gence of functional disturbances and TMD. Idiopathic
condylar resorption causes frontal open bite but in a
majority of cases without functional limitations or risk
of development of TMD [23].
On the contrary, idiopathic juvenile rheumatoid
arthritis (IJRA) is known to involve the TMJs (50–78%)
and to cause arthralgia, progressive limitation of jaw
movements, destructive changes during mandibular
growth, progressive class II, frontal open bite, and
arthritic condylar changes (flattening and erosions) [23].
Recognition before the start of orthodontic therapy is
mandatory (clinical and magnetic resonance imaging
(MRI)) and should be confirmed with laboratory tests
as it is an inflammatory disorder.
19.2.2.4 TMD and Orthodontics
If the patient shows signs or symptoms of TMD before
the start of orthodontic therapy, a tailor-made treat-
ment plan is mandatory and should consider the demand
and preferences of the patient (even in adolescents, cer-
tainly in young adults) together with extensive informa-
tion search. Timing and balance between function and
esthetics are important issues.
The relationship of the occurrence of symptoms of
TMD with occlusal factors and orthodontic treatment
in childhood has been the subject of controversy for a
long time. Systematic reviews and meta-analyses espe-
cially from the last decade are reassuring concerning the
risk for developing TMD during and after orthodontic
treatment [23–28].
Orthodontic therapy performed during adolescence
generally does not increase or decrease the chances of
developing TMD later in life. Signs and symptoms of
TMD occur also in healthy individuals and can increase
with age, particularly during adolescence; thus, TMD
originating during orthodontic treatment is mostly not
related to that treatment [24]. Occlusal interferences are
temporarily created, but in a majority of the patients,
this will cause transient discomfort with a temporarily
risk for increased muscle pain or clicking in the
TMJ. Only in cases with a history of low adaptive capac-
ity (bruxism, parafunctions) or occlusal hypervigilance,
mandibular loading should be decreased, and conserva-
tive TMD management should be considered first.
 480 L. Van den Berghe and L. Simoen
The extraction of the teeth as part of an orthodontic
treatment plan does not increase the risk of developing
TMD (e.g., extraction of premolars and the risk for con-
dylar posterior displacement) [24–28]. There is no ele-
vated risk for TMD associated with any particular type
of orthodontic mechanics, although a stable occlusion is
a reasonable treatment goal. Not achieving a specific
gnathologic ideal occlusion does not result in TMD
signs or symptoms [24]. No method of prevention for
TMD has been demonstrated yet.
Before, during, and after orthodontic therapy, always
screen for TMD and for oral behaviors, and instruct the
patient to avoid parafunctions. The psychological pro-
file of the patient including his capacity of amplification
of sensations (e.g., occlusal changes) has to be evaluated
in advance and has to result in a customized treatment
plan.
19.2.3 Anamnestic Records
Any dentist who works with children should include in
the dental examination the TMJs and orofacial struc-
tures, being capable of evaluating related complaints,
symptoms, or findings. The anamnestic record should
include a dental as well as a medical part, and the patient
should be asked about possible complaints such as head-
ache, ear pain, or more extensive facial pain, clicking in
the TMJs (. Fig. 19.1) [7]. Previous dental trauma and
all the conditions causing, especially, chronic orofacial
pain, with information on the origin, location, quality,
intensity, and duration of pain, should be recorded.
It is not always obvious to obtain the right answers
to some questions; parents should be involved and
informed extensively. The nature of the questions should
certainly avoid confusion, as the same limitations can be
experienced in adults as well. Adapted visual analogue
scales like the Universal Pain Assessment Tool (UPAT)
can be useful tools for TMD pain history-taking in
youngsters (. Fig. 4.10) [29].
Questions for TMD history taking:
• Do you feel pain in the face or jaw or the mandible?
19 • Do you often suffer from headache?
• Do you feel tired or pain when you chew?
• Do you feel pain when you open your mouth too much?
• Do you hear sounds from the TMJ and are they
associated with pain?
• Do you clench or grind your teeth? (also ask the parent)
• Do you bite your nails or chew gum frequently?
• What is the sleep position you prefer?
..      Fig. 19.1 Proforma for the dental record and the findings of pos-
sible TMJ disorders [7]
19.2.4 Clinical Examination
According to the Axis I examination protocol of the
Diagnostic Criteria for Temporomandibular Disorder
(DC-TMD) [30], the extraoral examination should
include simultaneous bilateral palpation of the TMJ
and the most palpable masticatory muscles, namely, the
temporal and the masseter muscles (. Fig. 19.2).
During examination so-called functional pain on (maxi-
mal) opening of the mouth (. Fig. 19.3) and lateral
movements of the mandible, or possible irregular jaw
deviations or TMJ sounds have to be recorded. Except
for dental (e.g., tooth wear, caries) and periodontal (e.g.,
gingivitis, early-onset periodontitis) inspection, the
intraoral examination for the presence of muscle pain
on palpation is optional and not considered as manda-
tory any longer. The examination for the determination
of the pain must be done very carefully, because the
child can express any pressure on palpation as a pain
experience. Children must be able to open their mouth
maximally between 35 and 40 mm like adults. The lat-
eral excursions of the mandible in children reach
approximately 8–12 mm (each side), but the measure-
ment is not reliable in very young children, due to the
possible problem for them to follow instructions.
19.2.5 Imaging
The panoramic radiograph is the recommended primary
imaging tool to document the history and examination
protocol in case of TMD in children as well as in adults.
The obtained dental, periodontal, and TMJ information is
in most cases sufficient to identify or confirm the presence
or absence of structural pathology and rarely will affect
the primary diagnosis and choice of baseline conservative
therapy. Only in cases where there is injury, long-lasting
pain, significant limitation of mobility, abnormal change
of the occlusion, a progressive pathologic joint condition
with facial asymmetry, numbness in the region of the man-
dible, a general joint disease (IRA), etc., further imaging
of the TMJs is desired [31]. In these cases magnetic reso-
nance imaging (MRI) and cone-beam computed tomogra-
phy (CBCT) are the tools of choice nowadays.
19.2.6 Diagnosis
According to the worldwide scientifically approved diag-
nostic criteria of temporomandibular disorders (DC-­
TMD) [30], two major TMD entities should be
distinguished: the pain-related and the non-pain-related
disorders (defined as the temporomandibular dysfunc-
tions). The pain-related disorders, regularly coexisting
Temporomandibular Disorders in Children and Adolescents
..      Fig. 19.2 a Palpation of
the temporal muscle. b
Palpation of the masseter
muscle
..      Fig. 19.3 Maximal opening with location for palpation of the
TMJ
in individuals, can be of muscular (myogenous) origin
called myalgia, myofascial pain, myofascial pain with
referral, or TMD-related headache, depending on the
source(s) of pain situated in the masticatory muscles, or
can be of arthrogenous origin, called arthralgia situated
in the TMJ. Myogenous as well as arthrogenous pain is
mainly the result of overloading of the masticatory sys-
tem on the muscular and/or temporomandibular articu-
481 19
lation level. In isolated cases, it is the result of
inflammatory processes including myositis or arthritis
as in (juvenile) rheumatoid arthritis with involvement of
the TMJ. The non-pain-related disorders or dysfunc-
tions of the masticatory system originate from intra-­
articular dysfunction and the TMJ disc dislocations
with or without reduction, also called the internal
derangements, or originate from TMJ hypermobility
implications, defined as luxation or subluxation of the
disc-condyle complex. The most typical characteristic
of these dysfunctions is the TMJ clicking noise often
experienced as disturbing or even threatening and may
lead to certain levels of debilitation of mandibular
movements [32]. Temporomandibular joint arthrosis
due to degenerative processes and in most cases charac-
terized by crepitation of the TMJ cannot be considered
as a pain-related disorder, in its strict sense of existence.
As already mentioned, the role of occlusal factors in
the etiology of temporomandibular disorders in chil-
dren is controversial. As mentioned before in this chap-
ter (see 7 Sect. 19.2.2), the presence of a unilateral
posterior cross bite (UPCB) is about the only parameter
who should be taken into consideration and treated in
youngsters as a risk factor on the long term, when rely-
ing on scientific evidence [23].
Differential diagnosis of TMD with some diseases
such as dental pain, sinusitis, otitis, mastoiditis, Eagle’s
syndrome, etc., is mandatory, and it is at least the task of
the dentist to coordinate multidisciplinary investiga-
tions in case of the presence of such suspected non-­
dental pathologies or comorbidities.
 482 L. Van den Berghe and L. Simoen
19.2.7 Treatment Strategies
Children presenting with orofacial pain or dysfunctions
show, in a majority, important and sometimes unpre-
dictable fluctuations of their complaints and/or symp-
toms in time, individually as well as in general. Different
issues should be taken into consideration: the transient
and benign character of most of the signs and their ori-
gin, in the first place, and, in a minority but not less
important, the coexistence of TMD with non-dental
comorbidities such as sleep breathing disorders and
headache (see 7 Sect. 19.2.2). Prophylactic early inter-
ventions such as extensive occlusal adjustment and orth-
odontic treatment, with exception of laterally forced
cross bites (see 7 Sect. 19.2.2), to prevent TMD in chil-
dren, are no longer supported scientifically. Simple con-
servative and reversible measures are strongly
recommended as the latter have proven already for
decades, effectiveness on the long term, in adults as well
as in children.
After history-taking and clinical examination, com-
prehensive explanation and information should be pro-
vided to the child but also to the parents or present
accompanying person. Reassurance about the innocent
character of the condition and the favorable prognosis
of simple treatment is mandatory and possible in most
cases. Treatment has to start with education about avoid-
ing unnecessary loading of the masticatory system, such
as nail biting, tongue thrusting, and excessive use of
chewing gum, if present as oral parafunctional activities.
Different small, take-home programs can be pre-
sented depending on the individual needs (in the pres-
ence of, e.g., clicking, fear for mobilization of the jaw in
case of painful muscle splinting) can improve proprio-
ceptive neuromuscular facilitation and offer sufficient
pain management. Therapeutic exercises (e.g., careful
stretching, mobilization of the lower jaw, opening, and
lateral excursions with resistance) are an important part
of physical as well as cognitive behavioral therapy and
merit a place in the treatment of TMD in children and
adolescents, depending on the understanding and com-
pliance of the child.
>>Night Guards
19 The use of night guards is controversial and should be
considered with care in the deciduous and mixed denti-
tion as they can have negative effects on physiologic
growth and development patterns. Hard acrylic splints
as used in adults for main protective reasons should
be avoided even in the presence of sleep bruxism. In
fact, it should be stressed that in children sleep bruxism
tends to decrease at the age of 9 or 10 years and most
of the children will not continue to grind their teeth
during adolescence or adulthood [19, 20].
Only if the existence of a non-dental comorbidity is sus-
pected with potentially severe consequences such as
chronic fatigue, attention deficit, sleep apnea or hypop-
nea, and headache, the patient should be referred for
specialized differential diagnosis. In these cases disturb-
ing sleep bruxism in combination with snoring is often
present, and it is recommended to refer to the ear-nose-­
throat (ENT) doctor or pneumologist, to exclude aller-
gies or tonsillary obstruction of the upper airway. Other
comorbid risks factors such as the use of psychoactive
drugs, underlying stress-related factors, and neurologic
diseases should be recognized by the dentist and are
important reasons for referral.
19.3 Summary
Temporomandibular disorders in children and adoles-
cents are common and can mostly be characterized as
mild and transient. Extensive history-taking in the pres-
ence of the parents or accompanying persons is manda-
tory, in order to try to exclude non-dental comorbidities
as soon as possible (e.g., snoring, apnea, headache, ENT
pathologies, rheumatoid arthritis). The latter should get
priority for multidisciplinary differential diagnosis.
Bruxism, occlusal discrepancies, and orthodontic ther-
apy are no longer considered as primary or perpetuating
etiologic factors for TMD. Careful functional examina-
tion should include recording of mandibular move-
ments, extraoral palpation of the TMJ and informative
masticatory muscles, and evaluation of the joint noises.
Therapy has to start with extensive counseling adapted
to the child’s age and maturity and should always be
conservative and reversible like cognitive education and
therapeutic exercises. The use of hard acrylic night
guards should be avoided in the majority of youngsters
with deciduous or mixed dentition. Similar as in adults,
orthodontic therapy and orthognathic surgery are not
the primary treatment options of choice for pain or dys-
function of the temporomandibular system in children
or adolescents neither.
References
1. Ramfjord SP, Ash MM. Anatomy and physiology of mastica-
tory muscles and temporomandibular joints. In: Occlusion. In:
W.B. Saunders; 1995. p. 4–23.
2. Dos Santos JJ. Maxillomandibular relations and movements. In:
Occlusion. Principles and Treatment. Quintessence books; 2007.
p. 1–37.
3. American Academy of Pediatric Dentistry. Guidelines on
acquired temporomandibular disorders in infants, children and
adolescents. Reference Manual 2012–2013. Pediatr Dent.
2012;34(6):258–3.
Temporomandibular Disorders in Children and Adolescents
4. Bonjardim LR, Baviao MB, Carmagnani FG, et al. Signs and
symptoms of temporomandibular joint dysfunction in children
with primary dentition. J Clin Pediatr Dent. 2003;28(1):53–8.
5. Magnusson T, Carlsson GE, Egermark I. Changes in subjective
symptoms of craniomandibular disorders in children and ado-
lescents during a 10 year period. J Orofac Pain. 1993;7(1):76–2.
6. Magnusson T, Carlsson GE, Egermark I. Changes in clinical
signs of craniomandibular disorders from the age of 15 to 25
year. J Orofac Pain. 1994;8(2):207–5.
7. Magnusson T, Helkimo M. Temporomandibular disorders. In:
Koch G, Poulsen S, Espelid I, Haubek D, editors. Pediatric den-
tistry. a clinical approach. Wiley Blackwell; 2017. p. 309–15.
8. Nilsson IM. Reliability, validity, incidence and impact of tem-
poromandibular pain disorders in adolescents. Swed Dent J
Suppl. 2007;183:7–6.
9. Toscano P, Defabianis P. Clinical evaluation of temporoman-
dibular disorders in children and adolescents: a review of the
literature. Eur J Paediatr Dent. 2009;10(4):188–2.
10. Juvenile CR, Arthritis I. Overview and involvement of the tem-
poromandibular joints, prevalence, systemic therapy. Oral Max-
illofacial Surg Clinics. 2015;27(1):1–10.
11. Alamondi N, Farsi N, Salako N, Feteih R. Temporomandibular
disorders among school children. J Clin Pediatr Dent.
1998;22:323–9.
12. Bertoli FM, Antoniuk SA, Bruck I, Xavier GR, Rodrigues DC,
Losso EM. Evaluation of the signs and symptoms of temporo-
mandibular disorders in children with headaches. Arq Neurop-
siquiatr. 2007;65(2A):251–5.
13. Motegi E, Miyazaki H. Oqura I, et al. an orthodontic study of
temporomandibular joint disorders. Part 1: epidemiological
research in Japanese 6-18 year olds. Angl Orthodontist.
1992;62(4):249–6.
14. Verdonck A, Takada K, Kitai N, et al. The prevalence of cardi-
nal TMJ dysfunction symptoms and its relationship to occlusal
factors in Japanese female adolescents. J Oral Rehabil.
1994;21(6):687.
15. Kaban LB, Mulliken JB, Murray JE. Facial fractures in children:
an analysis of 122 fractures in 109 patients. Plast Reconstr Surg.
1977;59:15–20.
16. Kaban L. Acquired abnormalities of the temporomandibular
Joint. In: Kaban L, Troulis M, editors. Pediatric Oral and Max-
ilofacial Surgery. Philadelphia PA Saunders; 2004. p.340–376.
17. Chatzistavrou EK, Basdra EK. Conservative treatment of iso-
lated condylar fractures in growing patients. World J Orthod.
2007;8(3):241–8.
18. Barbosa Tde S, Miyakoda LS, Pocztaruk Rde L, et al. Temporo-
mandibular disorders and bruxism in childhood and adoles-
cence: review of the literature. Int J Pediatr Otorhinolaryngol.
2008;72(3):299–4.
483 19
19. Manfredini D, Restrepo C, Diaz-Serrano K, Winocur E, Lob-
bezoo F. Prevalence of sleep bruxism in children: a systematic
review of the literature. J of Oral Rehab. 2013;40:631–2.
20. Saulue P, Carra MC. Bruxism in children and adolescents. In:
Laluque JF, Brocard D, d’Incau E, editors. Understanding Brux-
ism. Current Knowledge and Practice. Quintessence Publishing;
2017. p.63–71.
21. Carra MC, Bruni O, Huynh N. Topical review: sleep bruxism,
headaches and sleep-disordered breathing in children and ado-
lescents. J Orofac Pain. 2012;26:267–6.
22. Nyström M, Könönen M, Alaluusua S, Evälahti M, Vartiovaara
J. Development of horizontal tooth wear in maxillary anterior
teeth from five to 18 years of age. J Dent Res. 1990;69:1765–70.
23. Michelotti A, Iodice G. The role of orthodontics in temporo-
mandibular disorders. J Oral Rehab. 2010;37(6):411–7.
24. Sonnesen L, Bakke B, Solow B. Temporomandibular disorders
in relation to craniofacial dimensions, head posture and bite
force in children selected for orthodondic treatment. Eur J
Orthod. 2001;23(2):179–92.
25. Mc Namara JA Jr, Seligman DA, Okeson JP. Occlusion orth-
odontic treatment and temporomandibular disorders. A review.
J Orofac Pain. 1995;9(1):73–90.
26. Vanderas AP, Papagiannoulis L. Multifactorial analysis of the
etiology of craniomandibular dysfunction in children. Int J Pae-
diatr Dent. 2002;12(5):336.
27. Dibbets JM, van der Weele LT. Long-term effects of orthodontic
treatment, including extraction, on signs and symptoms attrib-
uted to CMD. Eur J Orthod. 1992;14(1):16–20.
28. Kim MR, Graber TM, Viana MA. Orthodontics and temporo-
mandibular disorders: a meta-analysis. Am J Orthod Dentofac
Orthop. 2002;121:438–6.
29. Dugashvili G, Van den Berghe L, Menabde G, Janelidze M,
Marks L. Use of the universal pain assessment tool for evaluat-
ing pain associated with TMD in youngsters with an intellectual
disability. Med Oral Patol Oral Cir Bucal. 2017;22(1):88–4.
30. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic criteria
for temporomandibular disorders (DC/TMD) for clinical and
research applications: recommendations of the international
RDC/TMD consortium network and orofacial pain special
interest group. J Orof Pain Headache. 2014;28(1):6–27.
31. American Academy of Pediatric Dentistry. Treatment of tem-
poromandibular disorders in children: summary statements and
recommendations. J Am Dent Assoc. 1990;120:265–9.
32. Visscher CM, Ohrbach R, van Wijk AJ, Wilkosz M, Naeije
M. The Tampa scale for kinesiophobia for temporomadibular
disorders (TSK-TMD). Pain. 2010;150:492–500.
 485 20

Oral Lesions in Children

and Adolescents
Stephen Porter and Alexandros Kolokotronis

Contents

20.1 Common Oral Mucosal and Bony Abnormalities – 487

20.1.1 E rythema Migrans (Geographic Tongue) – 487
20.1.2 Palatal Torus (Torus Palatinus) – 488
20.1.3 Mandibular Torus (Torus Mandibularis) – 488
20.1.4 Cysts – 488

20.2 Reactive Overgrowths – 488

20.2.1  yogenic Granuloma – 488
P
20.2.2 Fibroepithelial Polyp – 489
20.2.3 Peripheral Ossifying Fibroma – 489
20.2.4 Peripheral Giant Cell Lesion – 489
20.2.5 Congenital Granular Cell Tumor (Congenital Epulis
of the Neonates) – 490
20.2.6 Other Swellings – 490

20.3 Vascular Malformations (Hamartomas) – 490

20.3.1  emangioma – 490
H
20.3.2 Lymphangioma – 491

20.4 Oral Ulceration – 491

20.4.1 T raumatic Oral Ulceration – 491
20.4.2 Aphthous Ulceration and Related Disease – 492
20.4.3 Oral Ulceration Secondary to Systemic Disease of Childhood – 494

20.5 Infectious Diseases in Childhood – 495

20.5.1  iral Infections – 495
V
20.5.2 Bacterial Infections – 500
20.5.3 Fungal Infections – 502

20.6 Mucocutaneous Disease – 503

20.6.1 E rythema Multiforme – 503
20.6.2 Allergic Reactions – 504
20.6.3 Other Mucocutaneous Disease – 504

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_20
20.7 Hematological Disease – 505
20.7.1  ematological Malignancies – 505
H
20.7.2 Disorders of Blood Cells – 506
20.7.3 Bleeding Disorders – 508

20.8 Salivary Gland Disease – 510

20.8.1  ucocele – 510
M
20.8.2 Ranula – 510
20.8.3 Sialolithiasis – 510
20.8.4 Acute Suppurative Sialadenitis (Suppurative Parotitis,
Bacterial Sialadenitis, Bacterial Parotitis) – 511
20.8.5 Recurrent Parotitis of Childhood (Juvenile Recurrent Parotitis) – 511
20.8.6 Xerostomia (Oral Dryness) – 511
20.8.7 Drooling – 512

References – 512
Oral Lesions in Children and Adolescents
487 20
While the majority of child patients attending an oral
health care service will have plaque-related oral disease
such as caries and gingivitis, and more rarely congeni-
tally driven disease of the teeth and/or jaws, a spectrum
of disease can occasionally affect the mouths of chil-
dren. In particular, a wide variety of disorders can affect
the oral mucosa and more rarely the salivary glands.
Such disease may reflect many different pathological
mechanisms, and while most usually arise in adults,
some such as the autoinflammatory disorder periodic
fever, aphthous ulceration, pharyngitis, and adenitis
(PFAPA) and recurrent parotitis of childhood seem to ..      Fig. 20.1 a, b Erythema migrans of the tongue – often termed
geographic tongue
be almost unique to pre-pubertal individuals. Similarly,
very occasionally children manifest disease expected of
adulthood (e.g., lichen planus or Sjogren’s syndrome).
Regardless of these trends, it is essential that clinicians
managing the oral health of children have an awareness
of the more common disorders and when to refer the
patient to an appropriate specialist.
Some of the disorders relevant to oral medicine that
arise in children:
1. May be the first manifestation of significant systemic
disease (e.g., ulceration or purpura of acute leuke-
mias)
2. Can be the most troublesome manifestation of a sys-
temic disease (e.g., oral ulceration of Crohn’s dis- ..      Fig. 20.2 Erythema migrans of the buccal mucosa
ease)
3. Can lessen the quality of life of the affected patients change in site and appearance without an identifiable
(e.g., oral ulceration of any cause) precipitant. Sometimes there is accompanying fissuring
4. May compromise the general health of child (e.g., of the tongue, and rarely areas of erythema can arise on
failure to thrive due to loss of appetite caused by oral other oral mucosal surfaces (. Fig. 20.2).
ulcers) The areas of redness may sometimes, but not always,
5. May reflect systemic disease that requires dental care be painful, discomfort being brought on by a wide vari-
to be particularly essential and/or modified ety of agents that may include chocolate, cheese, and
tomatoes. Similarly, the signs of erythema migrans can
The present chapter reviews the various disorders of the be precipitated or modified by different foods.
oral mucosa and salivary glands that may commonly
arise in children. Detailed discussion of the many other
Eye Catcher
diseases that may arise in childhood can be found else-
where. The precise cause of erythema migrans is unknown
although it may occasionally arise in patients with a
history of atopic disease, cutaneous psoriasis, and
20.1  ommon Oral Mucosal and Bony
C possibly inflammatory bowel disease. There have been
Abnormalities reports of erythema migrans arising in patients with
SARS-2-Cov (COVID 19), but it is unlikely that this is
20.1.1  rythema Migrans (Geographic
E a specific oral feature of this infection. The disease is
Tongue) a manifestation of mild localized acute inflammation.

Erythema migrans is a common disorder, perhaps occur-
ring in up to 3% of individuals and may often arise in
childhood. It affects both genders and occurs in children
of all ethnic groups [1, 2]. It manifests as discrete areas
of erythema surrounded by a creamy white border on
the dorsum of the tongue (. Fig. 20.1). The areas may
Diagnosis can be based solely upon the clinical features,
and there is no requirement for any additional investiga-
tions. The treatment of erythema migrans remains unsat-
isfactory and principally comprises avoidance of
identified precipitants and local application of anesthetic
agents such as benzydamine hydrochloride. There is no
 488 S. Porter and A. Kolokotronis
evidence of the long-term behavior of this disorder, but it
is not potentially malignant and does not affect growth.
20.1.2 Palatal Torus (Torus Palatinus)
Palatal tori are common and arise in all genders and all
ethnic groups [3]. They become more manifest as a child
grows. They present as symmetrically enlarged, painless,
bony enlargements of the vault of the hard palate. Tori do
not warrant any treatment in childhood and do not seem
to interfere in the use of removable orthodontic appliances.
20.1.3 Mandibular Torus (Torus
Mandibularis)
Mandibular tori are less common than those of the pal-
ate and arise independent of the latter [4]. They tend to
manifest as a child grows and present as painless bony
enlargements on the lingual aspect of the mandible in
the area of the permanent premolars. Mandibular tori
have no systemic significance and do not warrant treat-
ment in childhood.
20.1.4 Cysts
In total, 65–85% of newborn may present with small intra-
oral cysts and/or nodules. The term Epstein’s pearls refers to
small cysts which are located on the junction of hard and
soft palate, exclusively, in the middle line. They have a hemi-
spherical shape and white color, and when their size extends
over 3 mm, they may be visible at birth or a few days after.
Similarly appearing swellings termed Bohn’s nodules are a
single or multiple small cysts which are located on buccal or
lingual aspects of the alveolar mucosae, more often the
mandibular surface [5] (. Fig. 20.3).
20
..      Fig. 20.3 Bohn’s nodule on the buccal side of alveolar process of
the maxilla in a 3-month newborn
a
b
..      Fig. 20.4 a Cyst of the incisive papilla in a 3½-year-old boy. b A
relevant radiolucent lesion is distinguishable in the anterior occlusal
maxillary radiograph
Both types of cysts contain keratin, and it is easy for
the clinician to reach a diagnosis based on clinical signs
with no further investigation. New cysts may continue
to emerge for up to 2 months after birth, all of which
are, eventually, self-limited and disappear spontane-
ously within a few days or up to 3 months after birth.
Older children (with deciduous teeth and more often
permanent teeth) can develop eruption cysts which are
described in 7 Chap. 10 as eruption disorders [6]. There
are a number of cyst types that may occur in childhood
(e.g., cyst of the incisive papilla (. Fig. 20.4) or other
odontogenic cysts), details of which are available in
appropriate maxillofacial surgery textbooks.
20.2 Reactive Overgrowths
20.2.1 Pyogenic Granuloma
Pyogenic granulomas are inflammatory lesions that usu-
ally manifest on the gingivae, particularly interdentally.
They are not notably common in the first decade of life
[7, 8]. They represent an overabundant local inflamma-
tory reaction to plaque retention. They are thus typically
associated with overhanging restorations, broken-down
carious teeth, or other local plaque-­retaining factors.
They manifest as sessile (i.e., broad-­based: red, purple, or
occasionally yellow/brown) swellings that bleed easily
with gentle pressure. They are usually painless with
patients only reporting the presence of a swelling, local
bleeding, or slight dysgeusia (. Fig. 20.5).
Oral Lesions in Children and Adolescents
..      Fig. 20.5 Pyogenic granuloma before and after its excision.
(Courtesy Dr. H. van Waes)
Pyogenic granulomas may sometimes resolve sponta-
neously but usually require excision together with correc-
tion of the underlying cause. They can arise in females in
the second trimester of pregnancy and then enlarge as the
pregnancy progresses. Following the birth of the child,
these lesions often spontaneously regress, and, if not,
then excision with removal of any plaque-retaining fac-
tors is warranted. Breast feeding does not prolong the
presence of pyogenic granulomas. Such lesions can very
rarely arise on the oral mucosae in response to physical
trauma. The risk of such post-traumatic pyogenic lesions
is possibly increased in patients receiving cyclosporin
therapy and/or those with graft-versus-host disease
(GvHD).
20.2.2 Fibroepithelial Polyp
These are common swellings that arise at sites of trauma.
They are most likely on the buccal, labial, or lingual sur-
faces and are actually uncommon in children [9]. They
manifest as sessile rubber-like swellings with either a
normal overlying mucosa or less commonly a homoge-
neous white surface that reflects repeated local trauma
(e.g., biting) (. Fig. 20.6). These lesions have no malig-
nant potential but should be excised as they may hinder
speech and/or eating and if repeatedly bitten may bleed
or occasionally enlarge. Occasionally a long-standing
489 20
..      Fig. 20.6 Fibroepithelial polyp located at the mucosa of the
lower lip
..      Fig. 20.7 Clinical image of a peripheral giant cell granuloma
pyogenic granuloma may evolve into a fibroepithelial
polyp (and are sometimes termed a fibrous epulis).
20.2.3 Peripheral Ossifying Fibroma
These are uncommon, exclusively arising on the gingi-
vae, and have the clinical appearance of a fibroepithelial
polyp but are found radiologically and/or histopatho-
logically to have evidence of mild ossification [10]. They
have no associations with systemic disease, are not
potentially malignant, and warrant excision. They are
unlikely to re-occur.
20.2.4 Peripheral Giant Cell Lesion
This tends to present as a sessile swelling of the gingi-
vae and tends to arise in the first decade of life and
particularly the mixed dentition period [11]. The
lesions are single, sessile swellings that have a red, blue,
or purple color (. Fig. 20.7). They are reminiscent of
pyogenic granulomas, can be initiated by plaque-
retaining factors, and can only be truly distinguished
 490 S. Porter and A. Kolokotronis
by the differing histopathology – giant cell lesions con-
tain multi-­nucleated giant cells, while pyogenic granu-
lomas have no giant cells but have a polymorphonuclear
leukocyte-­dominating acute inflammatory picture.
There is no erosion/destruction of the underlying bone.
Treatment and indeed diagnosis require excision and
subsequent histopathological examination of the
lesions. Recurrence is possible when surgical excision is
not radical.
Peripheral giant cell granuloma is exclusively seen on
gingivae (formerly giant cell epulis). Central giant cell
granuloma is a bony lesion found especially in long
bones and rarely in the mandible.
20.2.5  ongenital Granular Cell Tumor
C
(Congenital Epulis of the Neonates)
This, although not a reactive lesion, is a gingival over-
growth. It is a rare soft tissue anomaly that presents as a
swelling or nodule of the alveolar ridge (typically the
upper) [12]. The overlying mucosa is generally of nor-
mal appearance (. Fig. 20.8). It is present at birth and
tends to resolve spontaneously over several months.
These swellings have the potential to interfere in feeding
(although rarely do). Surgical excision can be under-
taken but is rarely warranted.
20.2.6 Other Swellings
There is a wide spectrum of other causes of soft tissue
swellings of the soft tissues of the mouth. These
include benign or (very rarely) primary malignancies
of the oral tissues, metastatic deposits (e.g., leukemic
deposits (see later)), mucoceles, fibromas associated
with tuberous sclerosis, hemangiomas of Sturge-Weber
syndrome, neurofibromas in Neurofibromatosis or
multiple endocrine neoplasia type 2B (MEN2B), and
others [13].
a b
20
..      Fig. 20.8 a, b Congenital granular cell tumors or congenital epulis of neonates
Eye Catcher
The list of causes of soft tissue swellings is perhaps
endless; hence perhaps the key factors to consider
about any swelling are as follows:
1. Is the lesion enlarging quickly and/or destructive?
2. Does the swelling have a likely (i.e., easily identifi-
able) cause?
3. Are there any unusual features in the medical history?
4. Is the swelling interfering in normal oral function?
If the answers to any of these are worrisome, it is
advisable that the patient is investigated in a multidis-
ciplinary manner with appropriate specialists.
20.3 Vascular Malformations (Hamartomas)
20.3.1 Hemangioma
Hemangiomas represent abnormal collections of nor-
mal non-arterial blood vessels [14]. They may be an iso-
lated feature or part of a congenitally driven disorder
such as Sturge-Weber syndrome. Hemangiomas mani-
fest as solitary red, blue, or purple sessile swellings that
typically blanche with gentle pressure (. Fig. 20.9).
They usually arise on the tongue or buccal mucosae
although if part of Sturge-Weber syndrome are exten-
sive and follow the distribution of one or more divisions
of usually one trigeminal nerve.
Eye Catcher
Hemangiomas that manifest at birth often regress
over the early years of life although some have a ham-
artous behavior – enlarging as the child grows. Most
hemangiomas do not interfere in oral function, rarely
if ever they bleed and hence rarely warrant complex
investigation (e.g., radiology or histopathology) or
treatment (e.g., removal or embolization).
Oral Lesions in Children and Adolescents
a b
..      Fig. 20.9 a Clinical image of a small hemangioma. b Picture of a
large hemangioma of the lower lip in a 7-year-old girl. There were
also hemangiomas at the right half of the tongue and the pharynx. c
20.3.2 Lymphangioma
Lymphangiomas are much more uncommon than hema-
giomas [15]. They typically manifest on the tongue as
minute brown, red, and/or purple swellings peppered
across the dorsum of the tongue. Rarely large lymphan-
giomas can arise, usually on mobile surfaces of the mouth,
and have a golden appearance that upon closer examina-
tion comprises small “bubble”-like swellings that have a
blood-colored center – akin to frog spawn (. Fig. 20.10).
Lymphangiomas are painless and do not usually
interfere in oral function, although they may occasion-
ally ooze a greasy fluid if bitten. Small lymphangiomas
do not warrant investigation or treatment although the
large ones may warrant investigation (e.g., lymphangiog-
raphy/ultrasound scanning and/or histopathology) and
occasionally treatment (e.g., excision or embolization).
20.4 Oral Ulceration
20.4.1 Traumatic Oral Ulceration
Oral and sometimes gingival ulceration due to trauma is
common in childhood, particularly as young children
often put items in their mouths for a wide variety of rea-
sons, may fall while having an object in their mouths, or
inadvertently drink chemicals, drugs, or detergents.
The ulceration caused by trauma clearly depends
upon the causative agent and what the child was doing at
the time of the traumatic injury [16]. The site and extent
of ulceration clearly depend on the cause of the injury.
The ulceration may be superficial or deep but in general
is localized. The trauma of injuries to the palate can be
particularly severe if a child has fallen while biting in an
object – there can be severe tearing of the palatal mucosa
down to the level of the mucoperiosteum. The ulceration
of trauma caused by the ingestion of chemicals is usually
superficial but can involve several surfaces of the mouth
[17]. If the child has spat the material out, the ulceration
491 20
c
The same case when the patient was aged 12 years. The expansion of
the lower lip hemangioma is notable
..      Fig. 20.10 Lymphangioma of the dorsal surface of the tongue
may only affect the anterior aspects of the mouth,
although if swallowed there will be ulceration and edema
of the posterior aspects of the mouth and pharynx.
Depending upon the cause and the time since injury,
trauma to the oral mucosae and gingivae may actually
have a spectrum of features that include erosions, ulcer-
ations, swellings, petechiae, bruising bullae, and/or areas
of hyperkeratosis (. Fig. 20.11).
The diagnosis of most instances of traumatic ulcer-
ation is based upon the history of known injury and the
clinical features. However, if there is a suspicion that the
ulceration has been deliberately self-inflicted, there is a
need to consider if the child is distressed and thus reflects
their social circumstances.
Eye Catcher
The management of most traumatic ulceration usu-
ally comprises:
1. Ensuring that the cause is identified and further
avoided
2. Placing an adherent paste (such as carboxymeth-
ylcellulose) over the area of ulceration
3. Use of an antimicrobial mouthwash to avoid any
infection
4. Local application of an analgesic agent (e.g., ben-
zydamine hydrochloride or lidocaine)
 492 S. Porter and A. Kolokotronis

The areas usually heal with little scarring; however, if
there is extensive ulceration, as may occur with chemical
injuries, scarring is possible and can lead to restricted
mouth opening. The risk of subsequent restricted open-
ing may be lessened with the use of splints (either cus-
tom made or simple wood sticks) and more rarely
surgical removal of scars (. Fig. 20.12).
20.4.1.1  iga-Fede Disease and Riga-Fede
R clinical picture affects the buccal mucosa (. Fig. 20.14),
Granuloma
Riga-Fede disease and Riga-Fede granuloma are associ-
ated with the presence of neonatal teeth which can trau-
matize the oral mucosa of the newborns [18]. The former
is characterized by a small area of ulceration on the ven-
tral and/or dorsal surface of the anterior tongue. The
ulcer may be covered by a whitish pseudomembrane
without cervical lymphadenopathy (. Fig. 20.13). In
instances where there is an epithelial hyperplasia, the
term Riga-Fede granuloma is sometimes used as a
descriptor. The treatment of these disorders is discussed
in 7 Chap. 10.
20.4.1.2 Chronic Mucosal Biting
Chronic oral mucosal biting is not uncommon in children
and young adults who experience a stressful period, feel
unsafe, or have psychological problems. The resulting
the bilateral sides of tongue, or labial mucosa. The
affected surfaces are rarely ulcerated but instead have
areas of ragged white patches that represent hyperkerato-
sis. The lateral borders of the tongue may have homoge-
nous white patches, while there may be more obvious,
and white, occlusal lines of the buccal mucosae.
The areas of white patch are localized to the areas
that can be reached by the teeth and may be unilateral or
bilateral. The disorder is painless and usually only
detected during a clinical examination.

a Eye Catcher

Treatment of chronic oral mucosal biting is rarely

required although there is a need to consider as to
why the patient has developed this habit and occa-
sionally consider the use of a soft occlusal splint to
lessen any damage to the mucosal surfaces.

20.4.2  phthous Ulceration and Related

b Disease
..      Fig. 20.11 a Traumatic ulcers on dorsal surface of a young
patient’s tongue. b Clinical image of a chemical burn
A
Recurrent aphthous stomatitis (RAS) is a common dis-
order characterized by recurrent episodes of superficial
oral mucosal ulceration in otherwise well individuals.
The ulcers are usually ovoid and have a yellow to brown
center and surrounding erythematous halo [19].
Three types of clinical presentation may arise of
which minor RAS (MiRAS) accounts for at least 80% of
all presentations. Minor RAS is characterized by crops
of about five ulcers of less than 1 cm in diameter that
arise every few weeks on the non-keratinized surfaces of

a b c

20

..      Fig. 20.12 a Electric burn on the lips due to biting an electrical cable. b Construction of a mobile device with flaps to aid ulcer healing
without complications on the corner of the mouth. c Clinical view after healing
Oral Lesions in Children and Adolescents
493 20

..      Fig. 20.13 Clinical image of an infant with Riga-Fede disease

due to injury by neonatal teeth
b

..      Fig. 20.15 a, b Clinical image of minor recurrent stomatitis in

the buccal vestibule

..      Fig. 20.14 Chronic biting buccal mucosa in a teenage girl

a
the oral mucosa (. Figs. 20.15 and 20.16). The ulcers
heal spontaneously over about 10–14 days and do not
cause scarring.
Major RAS (MaRAS) comprises larger but fewer
ulcers than those of MiRAS, have an irregular outline,
and arise on any mucosal surface. MaRAS heals sponta-
neously over several weeks and can cause some scarring
(e.g., of the soft palate). A very rare type of RAS is b
termed (erroneously) herpetiform RAS (He RAS). This
has no connection to herpetic infection and is character-
ized by 10s to 100s of 1 mm size on any oral mucosal
surface. The small ulcers supposedly coalesce into larger
irregular outlined ulcers – but there are a few good
descriptions of this.

Eye Catcher
Recurrent aphthous stomatitis usually arises in the
second decade of life, but about 10% of the affected
individuals develop disease younger than this. The
cause of RAS is unknown and certainly does not
reflect psychological distress, allergic reactions or
foodstuffs, or viral or other infections.
There remains no effective means of stopping the emer-
gence of the ulceration of RAS; hence the goal of treat-
ment is to lessen the duration (and hence associated pain)
of each episode [20, 21]. The present evidence suggests
..      Fig. 20.16 a Two minor aphthous ulcers on the lateral aspect of
the tongue. b Clinical image of a major aphthous ulcer at a similar
location
that there is no specific means of lessening the duration of
ulcers, but typical strategies center upon topical cortico-
steroids such as fluticasone (given as a spray or mouth-
wash), betamethasone mouthwash, or prednisolone
mouthwash. Painful symptoms may be lessened with ben-
zydamine hydrochloride dabbed on areas of ulceration or
used as a spray or, less appropriately, for children, as a
mouthwash. Occlusive pastes such as carboxymethylcel-
lulose-based agents can also be useful, but it is often dif-
 494 S. Porter and A. Kolokotronis
ficult for a child patient or their parent/guardian to
achieve this. Systemic immunosuppressive therapies are
only warranted when RAS is notably severe interfering in
feeding, sleep, or lessening quality of life. Such immuno-
suppressive therapies are out with the practice of pediat-
ric dentistry.
Ulcers similar to MaRAS can arise in patients with
anemia (e.g., secondary to gluten-sensitive enteropathy
(coeliac disease (see below) or ileocecal Crohn’s disease)
or neutropenias (e.g., in leukemias), but the affected
individuals may have other oral or extra-oral features of
these disorders (see below). Two disorders in which
RAS-like ulceration is suggested to be particularly com-
mon are Behcet’s disease and FPAPA syndrome.
Behcet’s disease, also called “Adamandiades-Behcet,”
is an uncommon disorder that arises in adults and rarely
in children. It is sometimes considered to be an autoin-
flammatory disorder (i.e., inflammation that arises
spontaneously) clinically characterized by episodes of
RAS-like ulceration that arises at least three times
yearly, superficial genital ulceration that occurs at least
once per year, ocular disease (posterior uveitis), skin
rashes (various – including vesicular-type eruptions and
erythema nodosum) as well as painful joints ­(arthralgia),
and a spectrum of other possible manifestations.
Behcet’s disease tends to arise in individu-
als with genetic origins associated with the Eastern
Mediterranean (e.g., Turkey), across lower Asia and
up to Japan (i.e., the old “Silk Routes”), suggesting
perhaps an immunogenetic etiology [22]. With respect
to pediatric dentistry, oral ulcers are akin to those of
RAS although it is suggested that these may more com-
monly affect the hard palate and be MaRAS than with
typical RAS disease. The management of BS is out with
the specialty of pediatric dentistry but typically includes
systemic immunosuppression strategies, including the
use of biological disease-modifying drugs.
20.4.2.1 Systemic Autoinflammatory
Disorders
Periodic fever, aphthous ulceration, pharyngitis, and
adenitis (PFAPA, previously termed Marshall’s syn-
drome) is a rare systemic autoinflammatory disorder
(SAID) characterized clinically by periodic episodes of
fever, sore throat, cervical lymphadenopathy, and super-
ficial oral ulceration [23] (. Fig. 20.17). The accompa-
20 nying fever thus sets it apart clinically from RAS. It
represents a periodic release of IL-1β that then drives
inflammation. The exact trigger for the episodes is not
known although as the disease may abate following ton-
sillectomy there is a suggestion that it is bacterially
driven. Present management is centered upon tonsillec-
tomy and use of anti-IL1 monoclonal therapies.
..      Fig. 20.17 Multiple aphthous-like ulcers during the onset of a
febrile episode in a patient with PFAPA
20.4.3  ral Ulceration Secondary
O
to Systemic Disease of Childhood
20.4.3.1 Gastrointestinal Disease
A number of gastrointestinal disorders can give rise to
oral ulceration and other manifestations in the mouth.
20.4.3.2 Crohn’s Disease
Crohn’s disease is a chronic bowel inflammatory dis-
ease, which may involve orofacial region in about 20%
of cases. The etiology remains unknown. Frequently,
the first manifestation occurs at the age of 14–15 years.
Any part of gastrointestinal tract, i.e., from the mouth
to the anus, may be affected. It, usually, occurs with
mild abdominal pain, diarrhea, and slight weight loss
[24].
When there are intraoral clinical signs during clinical
examination, these may be the first or the only manifes-
tations of the disease. These clinical signs vary. There
may be diffuse or nodular swelling of oral and/or peri-
oral tissue, giving the picture of granulomatous disease
(e.g., granulomatous cheilitis) (. Fig. 20.18), ulcerative
lesions which may resemble aphthous ulcerations, or
large deep ulcers surrounded by mucosal tags which can
be present on the buccal mucosae or the buccal vesti-
bules. In addition, there may be swelling of the buccal
and/or labial mucosa that is soft and termed “cobble-
stoning.” In some patients, there may be erythema
migrans of the tongue (geographic tongue). A lower
motor neuron palsy of the facial nerve is possible but
extremely rare in children. In some individuals there
may be pyostomatitis vegetans which is characterized by
the development of multiple, diffuse small abscesses
[24–27] (. Fig. 20.19). The management of the oral
aspects of Crohn’s disease is out with the clinical prac-
tice of pediatric dentistry although as with all child
patients affected individuals should be provided with
appropriate advice to minimize the risk of plaque-­
related oral disease.
Oral Lesions in Children and Adolescents
a 20.5
b Mumps.”
..      Fig. 20.18 a Clinical image of labial swelling and angular cheili-
tis in a patient with Crohn’s disease. b Colonoscopy reveals ulcerative
lesions within the intestinal mucosa
..      Fig. 20.19 Pyostomatitis vegetans
20.4.3.3 Gluten-Sensitive Enteropathy
(Coeliac Disease)
Gluten-sensitive enteropathy (GSE) is an immunologi-
cally mediated disorder in which there is notable inflam-
mation of the small bowel induced by wheat proteins
such as gluten. It may arise in childhood and manifest
with abdominal pain, altered bowel habit, failure to
thrive, and many other features depending upon its
severity. Oral ulceration similar in appearance to that of
RAS is not uncommon and indeed may be the first clin-
ically detectable sign of GSE. The ulceration arises as a
consequence of hematinic deficiencies (e.g., folate and
iron) secondary to the loss of small bowel function [13,
28–30]. Additionally, the affected children may also have
enamel defects (see also 7 Chap. 17).
495 20
Infectious Diseases in Childhood
A number of infections can give rise to oral ulceration
in childhood. The ulcers are typically superficial, but,
unlike RAS, the affected patients are systemically unwell
and the episodes of ulceration are not recurrent [31, 32].
Infections that give rise to white patches are considered
in 7 Sect. 20.5.3, although consideration is also given
in this chapter to “Human Papilloma Virus and
20.5.1 Viral Infections
Viral infections caused by herpes simplex type 1 or
Coxsackie viruses are by far the most common infec-
tious causes of oral ulceration in childhood.
20.5.1.1 Herpes Simplex
Herpetic infection can manifest as a primary (herpetic
gingivostomatitis) or, rarely in childhood, secondary
infection (herpes labialis). Primary herpetic gingivosto-
matitis arises about 7–10 days following initial exposure
to herpes simplex (typically via oral secretions). The
infection is typically caused by HSV-1, although HSV-2
can be causative (this not necessarily being related to
oro-genital contact). Infection usually occurs in pre-
school years, although it can also occur in the teenage
years and early 20s. In recent years there has been a shift
away from the early age occurrence toward the later
one – possibly reflecting improved hygiene within nurs-
eries or schools.
Primary infection commences with fever lasting
2–5 days, pharyngeal pain, and cervical lymphadenopa-
thy with the later evolution to short-lasting vesicles that
break down to form painful oral ulceration. The ulcers
can arise on any oral mucosal surface, are superficial,
and coalesce into large irregular areas of ulceration. The
gingivae become erythematous, swollen, and ulcerated
(and can be mistaken as acute necrotizing ulcerative gin-
givitis (ANUG). The affected patients have notable mal-
aise, drooling, and anorexia. The ulceration and
understandable poor plaque control may give rise to
oral malodor. The clinical picture can thus be alarming
to patients and their parents/guardians [33]
(. Figs. 20.20 and 20.21).
The clinical features are particularly distinct, the
only differential diagnosis realistically being ery-
thema multiforme (see below). There is a little need
for any confirmatory investigations such as viral
DNA identification or establishing a rise in anti-HSV
antibody levels between the acute and convalescent
phases.
 496 S. Porter and A. Kolokotronis
The clinical features usually resolve over about
1 week, and treatment is generally directed toward
reducing the pain and pyrexia with non-steroidal anti-­
inflammatory drugs (e.g., paracetamol or ibuprofen)
and ensuring adequate fluid intake. Antiviral therapy is
rarely warranted unless (1) the clinical picture seems to
be notably severe at an early stage and/or (2) the child is
known to be immunocompromised. The antiviral of
choice is aciclovir (e.g., 15 mg/kg of body weight, 5 times
a day for 5–7 days – although higher doses may be con-
sidered for immunocompromised patients). The pro-
drugs valaciclovir and famciclovir are sometimes used
for immunocompromised children, and cidofovir is a
possible option when aciclovir resistance (which is rare)
is likely.
Most children do not have later episodes of herpetic
gingivostomatitis, this being most likely in some child
patients with immunodeficiency states. Herpetic infec-
tion will have episodes of the secondary infection – her-
pes labialis.
Herpes labialis (sometimes termed “cold sores”) is
common and actually can arise in individuals who have
no recollection of having had the illness of primary her-
pes simplex infection. Herpes labialis is rare in the first
decade of life but becomes more likely after this age. It is
a b
..      Fig. 20.20 a, b Clinical image of primary herpetic gingivostoma-
titis in a 16-month-old infant. Vesicles are observed on the perioral
cutaneous region surrounded by a red halo, while mucosal inflamma-
tion and confluent vesicles may be seen intraorally
a b
20
..      Fig. 20.21 a Typical clinical picture of primary herpetic gingivo-
stomatitis. There are multiple vesicles surrounded by red halo. There
also is coexisting, disease-specific, gingivitis together with a crusting
clinically characterized by episodes of infection, usually
at the same site of the vermillion border of the lip that
comprises a sequence of paresthesia, erythema, vesicu-
lation, pustule formation, ulceration, and eventual heal-
ing. The cycle of clinical features occurs over about
5 days, and affected individuals do not have any other
clinical features directly caused by the HSV infection.
Episodes of herpes labialis usually have a precipitant
that presumably causes a mild reduction in immunosur-
veillance and resultant viral replication within the tri-
geminal ganglion. Commonly reported precipitants
include upper or lower respiratory tract infections,
exposure to sunlight, pregnancy, and psychological dis-
tress. Many patients however report that they felt “run
down” just prior to the onset of herpes labialis.
The diagnosis of herpes labialis is based upon the
clinical history and features. There is usually no justifi-
cation for confirmatory investigations. Therapy that
only reduces the symptoms and signs by 1–2 days can be
topical aciclovir (5% cream) or topical penciclovir (1%
cream). Each agent needs to be applied before the onset
of vesiculation; otherwise clinical benefit is unlikely –
although it is suggested that penciclovir can still be of
some benefit when applied late (as opposed to aciclovir).
Eye Catcher
Children with herpes labialis do shed the virus from
lesions, and presumably oral fluids, thus should not
be in close contact with individuals who are not
known to be immune to herpes simplex or elderly or
immunocompromised persons.
20.5.1.2 Herpes Zoster (Varicella Zoster)
Herpes zoster gives rise to a primary infection termed
chickenpox and a secondary disorder called shingles.
The virus is transmitted via the droplet route. ­Chickenpox
occurs in early childhood and arises in waves of infec-
c
of the right labial angle of the young patient. b, c Cases of the same
disease localized in the tongue and the palate, respectively
Oral Lesions in Children and Adolescents
497 20
tion in groups of children that typically arise in the win- a
ter months of a country. The affected children experience
gradual onset of pyrexia, headache, and malaise fol-
lowed by the emergence of a red vesiculopapular rash
that gives rise to small pustules that ulcerate and heal.
Complications such as meningitis and encephalitis are
possible but rare. The complete clinical picture lasts
about 7–10 days. Oral ulceration – usually just a small
number of superficial ulcers – can occur alongside the
cutaneous rash and should be managed symptomati-
cally (. Fig. 20.22) [32, 34].
Shingles, the secondary infection of herpes zoster, is b
rare in childhood although it is more likely in children
with certain primary or secondary immunodeficiencies.
Shingles typically arises from the dorsal root nuclei of
the thorax and abdomen and thus does not give rise to
oral lesions. Oral ulceration can occur if there is reacti-
vation of the virus in the trigeminal ganglion and mani-
fests as superficial small ulcers that follow the distribution
of one branch or division of the nerve (. Fig. 20.23). A
rare feature of shingles is pain in a tooth that precedes
the onset of the ulceration.
..      Fig. 20.23 a Typical clinical picture of herpes zoster infection of
The management of shingles in childhood is similar
the third branch of the trigeminal nerve in a 4-year-old patient. b
to that of primary herpetic gingivostomatitis although The unilateral distribution of rash and mucosal lesions are distinc-
higher dosages of acyclovir are warranted. In view of tive characteristics of the disease
the possibility that the shingles is a reflection of an
underlying immune defect, it is important that the
affected children are managed both by pediatric dentists fever lasting 1–2 weeks, lymphadenopathy (predomi-
and pediatricians. nantly cervical) and sometimes abdominal pain due to
hepatosplenomegaly, and a pink macular skin rash. In
20.5.1.3 Infectious Mononucleosis the oropharyngeal region, the uvula, the fauces, and
Infectious mononucleosis (IN) is a type of glandular the tonsils are swollen, red, and painful. Sometimes
fever caused by Epstein-Barr virus (EBV). The majority there are multiple petechiae on the hard and soft pal-
of cases occur in the second and third decade and reflect ates and small numbers of superficial oral ulcers
salivary transmission, for example, via kissing. The (. Fig. 20.24).
infection has a long incubation period of 4–7 weeks [32]. The numbers of leukocytes in peripheral blood are,
Clinically IN commences with general symptoms typically, moderately increased (10.000–15.000/mm3),
onset. The first symptoms are malaise, headache, high but in some cases, they are intensely increased. There are
also atypical lymphocytes. It is essential for the disease
to be distinguished from acute leukemias since they
share some similar clinical and laboratory features. The
detection of antibodies to EBV (heterophile antibodies)
is a specific laboratory examination called mono-test
and previously the Paul Bunnell test.
The normal course of the disease is self-limiting.
Complications or recurrence is rare and only likely in
those with immunodeficiency or immunosuppression.
Because there are no specific therapeutic agents against
the particular virus, the treatment of the patient is symp-
..      Fig. 20.22 Clinical image of mild varicella infection. On the
tomatic – for example, with analgesics and/or antipyret-
perioral cutaneous region, there are a small number of erosive lesions
(rash), while on the vermillion border of the lips, there are small ero- ics. Systemic corticosteroids have occasionally been used
sions resulting from vesicular rupture (arrows) when there is severe pharyngeal edema.
 498 S. Porter and A. Kolokotronis

b
..      Fig. 20.24 Petechiae and bruising on the border of soft and hard
palate in a teenager with infectious mononucleosis

20.5.1.4 Hand Foot and Mouth Disease

This is caused by various types of Coxsackie virus. It
tends to arise in school children in the first decade of
life. The virus is transmitted from person to person by
direct contact, and the incubation period of the disease
ranges from 3 to 9 days. The disease begins with a fever,
..      Fig. 20.25 Hand-foot-and-mouth disease. a The vesicular ery-
chills, rhinorrhea, and malaise. Almost simultaneously,
thematous patches in the oral cavity are evident. b The vesicular rash
there is a vesicular enanthema of the oral mucosa, on the fingers of the young patient
which is usually located at the front of the oral cavity.
The vesicles rapidly rupture to give rise to small ero-
sions covered by whitish pseudomembranes and sur-
rounded by red halo, which resemble minor aphthous
ulcerations. The subjective symptoms are mild although
there may be lymphadenopathy. In a very short time, a
small number of vesicles may be observed on the skin
of the upper and lower limbs (mainly the pulps of the
fingers) and rarely on the buttocks or knees
(. Fig. 20.25). There is no specific therapy for this dis-
order, lesions resolve within 7–10 days, and therapy
should be directed toward lessening pain and any ..      Fig. 20.26 Herpangina affecting the soft palate
pyrexia [31, 32].

20.5.1.5 Herpangina 20.5.1.6 Measles

Herpangina is caused by Coxsackie A viruses – in con-
trast to its name which suggests herpesvirus participa-
tion. Transmission of the virus occurs by direct
contact, and the incubation time is 4–7 days [3].
Herpangina, normally, begins with high fever that
lasts for 1–4 days, sore throat, difficulty in swallowing,
rhinorrhea, weakness, muscle pain, and possibly vom-
iting and/or diarrhea. Almost simultaneously, there
are a small number of vesicles which are typically
20 found on the soft palate, uvula, faucal arches, and
pharynx. Very quickly the blisters rupture, leaving
erosions covered by whitish ­pseudomembranes, sur-
rounded by red halo which are, clinically, similar to
aphthous ulcerations (. Fig. 20.26). The normal
course of the disease is self-limiting over about
8–12 days, and any treatment should be directed
toward lessening symptoms [31, 32].
Measles is caused by the homonymous virus. It affects
mainly children of school age. It is transmitted by
droplets, and the incubation period ranges from 10 to
12 days. The disease usually occurs in epidemics, which
occur every 2–4 years. The clinical manifestations
begin with general symptoms (fever, headache, mal-
aise) rapidly followed by rhinorrhea and laryngotra-
cheobronchitis manifesting as a cough. Almost
simultaneously, asymptomatic intraoral lesions
develop which are located mostly on buccal mucosa.
They are consisted by small whitish confluent spots
(Koplik spots, similar to chips of chalk), which are
based on an erythematous base and disappear after
2–3 days. Moreover, local lymphadenopathy coexists.
A few hours later, a maculopapular rash takes place.
Typically, the disease manifests firstly behind the ears
and extends to the neck, cheeks, chest, upper limbs,
Oral Lesions in Children and Adolescents
and then the body and lower limbs. After the fever
which, usually, lasts 6–9 days, the rash starts to dimin-
ish and after a week resolves [32].
Concerning the defense against measles, there is a
preventive vaccination, which protects young people
around 90%. Usually the measles vaccine is applied
along with that for mumps and rubella (MMR vaccine),
in two doses.
20.5.1.7 Mumps
In view of the wide availability of effective vaccination,
mumps should now be considered a disorder of the
past – nevertheless not all children receive this vaccine;
hence, a small number of children and adults may still
manifest this disease. Mumps is an acute generalized
paramyxovirus infection of children and young adults.
Mumps typically affects the major salivary glands,
although involvement of other structures can occur
including the pancreas, testes, ovaries, brain, breast,
liver, joints, and heart.
Mumps is transmitted via the droplet route and has
an incubation time of approximately 14–18 days.
Patients present with initial pyrexia, chills, and facial
pain. The parotids are typically bilaterally enlarged,
although this may initially be unilateral. There is often
swelling of the submandibular glands together with
lymphadenopathy, giving rise to profound facial and
neck swelling (. Fig. 20.27). Rarely sublingual swelling
may be so profound as to cause elevation of the tongue
and dysphagia and dysarthria. The salivary swelling
tends to diminish after approximately 4–5 days and may
precede more complicated aspects of the illness.
Affected patients may be unwell for about 1 week,
but complications can include orchitis (infection of the
testes – usually in post-pubertal years), mild pancreati-
tis, and viral meningitis or encephalitis. Cardiac, hepatic,
and joint infection can occur, and they are rare and do
not generally cause notable complications. However
long-term neurological damage, including deafness, is
rarely possible [35].
a b
..      Fig. 20.27 Mumps. a Bilateral swelling of the major salivary
glands. b Unilateral swelling of the right parotid gland
499 20
There is no specific treatment for mumps, analgesia
and appropriate fluid intake being the mainstays of
therapy. It has been suggested that corticosteroids may
be effective for severe parotitis, but generally these are
not required unless the patients have other systemic
symptoms such as orchitis. Mumps can generally be pre-
vented with appropriate vaccination (mumps/measles/
rubella (MMR)) [36].
20.5.1.8 Human Papilloma Virus Infections
Human papilloma virus (HPV) is a DNA virus that
comprises about 200 different genotypes that infect
epithelial cells. They may be classified as cancer-caus-
ing (i.e., oncogenic types) and non-cancer-causing
(i.e., non-­oncogenic types). The virus is transmitted
by close contact. Oral infection with HPV in children
is almost always is with non-oncogenic types. The
exact route of acquisition of HPV in children is rarely
identifiable although presumably some children bite
warts of their fingers and hence transfer the virus to
the mouth. There is no good evidence that pediatric
oral HPV infection is a consequence of abuse of any
kind [13].
20.5.1.9  ommon Warts (Verruca Vulgaris,
C
Squamous Papilloma)
This is the most presentation of HPV infection of the
mouth. These manifest as slow-growing, solitary raised
white nodules that have a cauliflower-like appearance
(. Fig. 20.28). They can arise on any oral mucosal or
gingival surface and are painless. They have no malig-
nant potential and should be removed by scalpel exci-
sion (which allows histopathological confirmation of
the diagnosis) or less commonly by laser ablation or
thermocoagulation. In general these lesions do not
recur. Occasional children with immunodeficiencies
such as HIV disease may have multiple or recurrent oral
..      Fig. 20.28 Wart of the vermillion border of the upper lip in a
17-year-old patient (arrow)
 500 S. Porter and A. Kolokotronis
..      Fig. 20.29 Multifocal epithelial hyperplasia (or Heck’s disease)
warts that will lessen if the underlying immune dysfunc-
tion can be corrected.
20.5.1.10  ultifocal Epithelial Hyperplasia
M Confirmation of the diagnosis of OHL requires histo-
(MEH, Heck’s Disease)
This is a very rare disorder that usually arises in early
childhood and manifests as multiple flat or nodular/
popular warts affecting any oral mucosal or gingival
surface (. Fig. 20.29). There are often so many warts
that can become large, such that speech and/or eating
can become difficult as patients incidentally bite the
lesions. The exact route of acquisition of the infection is
unknown although suggested routes have been via the
vaginal tract during child delivery or via utensils [37].
The disorder is said to be most common in individu-
als of Inuit (i.e., American-Indian) genetic origin and
hence likely in children living in Greenland and Central
America (although it can arise in children without such
ethnicity/residency). The disorder tends to spontane-
ously resolve in the late second decade, but before this
therapy is difficult as the only reliable means of treating
the warts is by scalpel or laser excision or thermocoagu-
lation. Topical imiquimod or interferon alpha have been
used by there are no good data to suggest that they are
reliably effective.
20.5.1.11 Human Immunodeficiency Virus
(HIV)
Pediatric HIV disease still arises across the globe
although the number of children becoming infected is
falling. Children typically have become infected either in
utero or less commonly during birth or very rarely as a
consequence of breastfeeding. The fall in new pediatric
infection reflects the availability of anti-retroviral ther-
20 apy (ART) although, unfortunately, not all children with
HIV are identified and hence are not receiving ART.
In the past, when ART was not notably effective,
children with HIV infection could develop a wide range
of infections as well as Kaposi’s sarcoma (KS) and non-­
Hodgkin’s lymphoma (NHL) reflecting the progressive
loss of cell-mediated immunity [38, 39]. The present dis-
cussion focuses upon the most common oral manifesta-
tions of pediatric HIV disease – although oral ulceration
is not itself a common feature of HIV infection of child-
hood. The most likely features of undiagnosed or poorly
controlled HIV infection are:
kPseudomembranous candidiasis (thrush)
See 7 Sect. 20.5.3.
kOral hairy leukoplakia
This manifests as painless adherent white patches of the
tongue and/or floor of the mouth. It is caused by
Epstein-Barr virus (EBV) and is not potentially malig-
nant. The extent of the OHL usually reflects the degree
of the patient’s immune dysfunction – indeed if ART is
effective, any pre-existing OHL may melt away only
returning if ART (now rarely) becomes ineffective.
pathological examination of lesional tissue together
with the identification of EBV proteins or DNA within
the tissue. There is no specific therapy for OHL, and
indeed as the lesion is painless and not potentially malig-
nant, there should never be a need to consider any ther-
apy such as acyclovir [40].
kKaposi’s sarcoma
This only arises in HIV disease when there is severe
immunosuppression. This is a tumor of blood vessels
caused by human herpes virus-8 (HHV-8). It manifests
as a red, blue, or purple macule, papule, or nodule typi-
cally on the hard/soft palate of one side of the mouth
although another common site is the upper gingivae. It
is locally destructive and hence can cause ulceration and
possibly bony destruction. The management of Kaposi’s
sarcoma of the mouth is usually undertaken by oncol-
ogy teams but may include local radiotherapy or sys-
temic chemotherapy as well as treatment of any
undiagnosed or poorly controlled HIV disease [31, 32].
kOther features
As noted above, a plethora of other oral disorders
can arise in children with HIV disease. These may
include ANUG, severe HSV, and occasionally VZV
infection, systemic mycoses, unusual bacterial infec-
tions (e.g., Borrelia henselae), as well as large oral or
pharyngeal ulcers of unknown cause. All unusual fea-
tures of HIV disease should be managed by appropri-
ate specialists.
20.5.2 Bacterial Infections
20.5.2.1 Impetigo
Impetigo is a cutaneous disease. It does not affect the
oral mucosa but gives rise to golden-colored vesicles or
small blisters of the perioral or perinasal skin – although
Oral Lesions in Children and Adolescents
a
b
..      Fig. 20.30 a, b Bullous impetigo of the perioral area skin affect-
ing a male and a female teenager. In such cases differential diagnosis
from herpetic infections is important
in extreme cases, it can affect several other sites of the
face. It tends to arise in young infants and early-year
school children without any pre-existing skin disease,
although it may complicate disease such as eczema or
arise the following simple injuries such as cuts and
grazes. Children with diabetes mellitus may be at
increased risk of impetigo. It is usually caused by
Streptococcus pyogenes and/or Staphylococcus aureus.
There are two types of impetigo: bullous impetigo
(usually caused by Staphylococcus), which affects neo-
nates, infants, and toddlers, and the non-bullous impe-
tigo, which affects more often school-age children
(. Fig. 20.30). The prognosis is generally good, and the
treatment includes administration of antimicrobial
drugs usually topically or/and systemically [41]. ­Effective
topical antimicrobials include mupirocin and fusidic
acid 2%. These agents are commercially available as
ointments and should be applied to the lesions two to
four times daily for 7–10 days.
20.5.2.2 Scarlet Fever
The cause of scarlet fever is the Streptococcus pyogenes
erythrogenic toxin. The infection is transmitted through
inhalation of droplets, and the mean incubation time is
2–4 days [1]. The clinical expression of the disease
includes initially pharyngotonsillitis, painful bilateral
regional lymphadenitis, and general symptoms (fever
lasting usually 5–6 days, severe headache, weakness,
etc.). The typical micro-macular rash appears soon in
the great folds of the body (axillae and inguinal region)
501 20
and spreads to the rest of the body. It is characteristic
that the rash is absent from the perioral and paranasal
region (Filatoff sign).
In the oral cavity-intensive inflammatory, mucosal
erythema and white tongue coating can be present from
the initial stages of the disease. The tip and the lateral
borders of the tongue are intensively erythematous.
During the third to fifth day of the disease, the white
coating of the tongue is gone, and the tongue is inten-
sively erythematous with swollen fungiform papillae and
is called raspberry tongue. The disease results in perma-
nent immunity to erythrogenic toxin but not to strepto-
cocci. Penicillins are typically effective.
20.5.2.3 Tuberculosis
Tuberculosis (TB) is caused by Mycobacterium tubercu-
losis usually acquired via the droplet route from some-
one with open pulmonary TB. It can be acquired via
other routes, but this is most unusual. TB remains a sig-
nificant health problem in countries with poor econo-
mies where there is social poverty, malnutrition, and
lack of health care resources. However, in view of migra-
tion and travel, children and adults living in high-­
resource countries can present to clinics with clinically
detectable TB. In addition, undetected HIV disease
increases the risk of TB [42].
In childhood and adolescence, the disease appears
more often as chronic submandibular or cervical lymph-
adenopathy which is called scrofula (. Fig. 20.31). Oral
ulceration – usually single ulcers – or labial enlargement
can be features of TB but are remarkably rare. Although
highly unlikely in children, TB can cause destruction of
..      Fig. 20.31 Tuberculosis-associated cervical lymphadenitis
(scrofula) in a young patient. The fistula opening and the erythema
of the overlying skin are obvious
 502 S. Porter and A. Kolokotronis

the adrenal cortex and the later development of hyper-
pigmentation of the buccal mucosae (“Addisonian pig-
mentation”). The diagnosis of TB is out with the clinical
practice of pediatric dentistry but typically requires
identification of the causative organism via molecular
analyses – culture is now considered to be a second line
for the identification of TB. The management of TB is
typically undertaken by infectious disease specialists.
Protection from TB is achieved with BCG vaccination –
hence why all healthcare providers must receive this
prior to commencing clinical work.
Eye Catcher
White patches of the mouth can be subgrouped into
adherent (i.e., do not easily wipe off) and non-­
adherent. Except for thrush, non-adherent white
patches may usually be just food debris. They may
also be found as necrotic tissue in oral mucositis sec-
ondary to local radiotherapy or systemic chemother-
apy [13]. Adherent white lesions may be seen in
congenital rare disorders, such as dyskeratosis con-
genita and pachyonychia congenita.

20.5.2.4  cute Necrotizing Ulcerative

A
Gingivitis 20.5.3.1 Pseudomembranous Candidiasis
The diagnosis and general therapy are outlined in (Thrush)
7 Chap. 15. Very rarely acute necrotizing ulcerative This manifests as gelatinous white to yellow, curd-like
gingivitis can extend to the periodontal tissues (necro- white patches that are easily wiped off to leave areas of
tizing periodontitis) and/or the oral mucosa (necrotiz- erythematous erosion. It tends to present on the soft
ing stomatitis), and in such instances, the treatment is palate, fauces, or posterior buccal mucosae but can
the same as above although systemic antibiotics are occur anywhere in the mouth (even on the gingivae)
essential. (. Fig. 20.32) [45].
The presence of thrush always reflects a local and/or
systemic cause that requires acknowledgment or identi-
Eye Catcher fication. Common causes are the present or recent use of
broad-spectrum antibiotics (e.g., amoxicillin or tetracy-
Children with severe malnutrition are at risk of acute
clines) or corticosteroids (particularly inhaled or admin-
necrotizing ulcerative gingivitis necrosis spreading to
istered systemically). Long-standing oral dryness may
the underlying muscle and indeed facial skin in which
cause thrush, but this would be rare in children. Of
case the disorder is termed NOMA. This disorder
importance however, thrush can be an early feature of
tends to arise in geographic areas with extreme pov-
immunodeficiency (e.g., due to HIV disease, leukemia,
erty (e.g., some African countries). Then malnutrition
or undiagnosed/poorly controlled diabetes mellitus).
is the consequence of a poor economy brought on by
Hence, it is essential that the cause of thrush is always
political unrest and sometimes warfare. NOMA can
identified.
have a devastating impact upon the facial growth of
Thrush is caused by the superficial mycotic infection
children and may result in lifelong facial disfigure-
candida. Candida albicans is the usual infecting species
ment that requires many, often complex, surgical pro-
although many other candida types may also give rise to
cedures to overcome [43, 44].
this clinical disorder.
The management of thrush principally rests upon
20.5.2.5 Other Bacterial Infections the identification and management (where possible) of
any underlying cause. In some instances the thrush will
A wide range of other bacterial infections of the mouth,
resolve spontaneously, for example, following comple-
most giving rise to oral ulceration, can arise in children,
but these almost always arise in severely immunocom-
promised states such as undiagnosed late HIV disease,
primary immunodeficiency, or hematological malig-
nancy [31].
20
20.5.3 Fungal Infections

The most common oral fungal infection in childhood is

oral candidiasis, especially the acute pseudomembra-
nous candidiasis (thrush), appearing in the form of
­non-­adherent white patches. ..      Fig. 20.32 Pseudomembranous candidiasis
Oral Lesions in Children and Adolescents
tion of courses of antibiotics or systemic corticoste-
roids, while with some patients, it is impossible to remove
any underlying cause – for example, corticosteroid
inhaler use for asthma. In such instances there may be
no need to provide therapy as thrush is usually not
symptomatic and is not known to have any malignant
potential. Where therapy is required, topical agents such
as nystatin suspension may be useful, and when disease
is severe, does not resolve with nystatin, and/or is symp-
tomatic, there may be a need for systemic fluconazole
therapy. Topical anti-fungal gels such as those with
miconazole or clotrimazole may be alternative thera-
pies, but they are unlikely to be easy to apply. There is
rarely any requirement to confirm the diagnosis of
thrush by microbiological means (e.g., culture): (1) can-
dida is a common commensal of healthy persons and (2)
the candida load (or count) does not predict disease
severity or likely response to therapy. Long-term use of
anti-fungals can increase the risk of the emergence of
anti-fungal resistance, but this is only a concern in
patients who are severely immunocompromised.
Candida can give rise to a number of clinical presen-
tations other than thrush and they include the following:
kDenture-associated stomatitis
In children, a red appearance beneath the acrylic plate
of a prosthetic or a removable orthodontic appliance.
This is painless, and therapy is directed to improving
appliance hygiene and occasionally placing miconazole
gel on the fitting surface of the appliance.
kChronic erythematous candidiasis
A red patch in the center of the dorsum of tongue. This
is painless and may arise in children using corticosteroid
inhalers for long periods. A similar patch may occasion-
ally also arise on the hard palate (sometimes termed
chronic erythematous candidiasis). This rarely warrants
any therapy (i.e., anti-fungals) as it is painless, is not
potentially malignant, and in any case is unlikely to
resolve if the patient continues to have corticosteroids.
kAngular cheilitis
Red patches at the corners of the mouth. This is rare in
children and if present may be associated with severe
anemia or immunodeficiency (e.g., HIV disease). The
lesions can be painful and are infected with Candida
and/or Sstaphylococcus aureus. Treatment should be
principally directed toward resolving the underlying
cause, although nystatin suspension plus local applica-
tion of miconazole gel may hasten healing.
kChronic hyperplastic candidiasis
This manifests as adherent white or speckled (i.e., red
and white) patches of the oral mucosa. It is very rare in
503 20
children, can only be diagnosed by histopathological
examination of lesional tissue, and if present may be a
sign of known or unknown long-standing immunodefi-
ciency (e.g., worsening HIV disease, congenital defects
of cell immunity, or chronic mucocutaneous candidia-
sis) (see below). Topical or systemic anti-fungal agents
may lessen or resolve such disease, but there is little good
data on effective therapy, and in any case, there should
be a focus upon identifying and where possible resolving
any underlying cause.
kChronic mucocutaneous candidiasis (CMC)
This is a group of rare disorders that reflect a number
of defects of cell-mediated immunity [46]. They are col-
lectively characterized by recurrent candida infection of
mucosal surfaces and/or skin. Oral disease can manifest
in childhood and presents as recurrent episodes of any
of the above clinical presentations of candida infection
of the mouth. The most significant CMC type is auto-
immune polyendocrinopathy-candidiasis-ectodermal
dystrophy (APECED) characterized by autoimmune
destruction of the endocrine tissue (e.g., parathyroid,
adrenal cortex, pancreas, ovaries, testes) such that the
affected children may have enamel hypoplasia or hypo-
calcemia of the developing teeth and Addisonian pig-
mentation [46, 47]. CMC is sometimes accompanied by
an iron deficiency; hence, children may have oral ulcer-
ation angular cheilitis and/or glossitis (i.e., a smooth
tongue). The management of CMC is out with the
practice of pediatric dentistry although clearly enamel
anomalies in APECED may warrant treatment.
Except for candidiasis, there are some systemic
mycotic infections such as mucormycosis, aspergillosis,
histoplasmosis, and blastomycosis, which may cause
ulceration in immunocompromised children.
20.6 Mucocutaneous Disease
Immune-mediated mucocutaneous disease that may
affect the mouths of children is extremely rare.
Pemphigus types have been reported in children (ero-
sions/ulcers), but perhaps the most common, although
rare, of these disorders to arise in children would be ery-
thema multiforme.
20.6.1 Erythema Multiforme
Erythema multiforme (EM) very rarely arises in children.
This is an unusual hypersensitivity disorder that may
arise in response to medication and occasionally infec-
tion (e.g., HSV or Mycoplasma pneumoniae. The more
different drugs that an individual is receiving, the greater
 504 S. Porter and A. Kolokotronis
a Eye Catcher
b ble – it is too late)
..      Fig. 20.33 a Clinical image in Stevens-Johnson syndrome. b In
Steven-Johnson syndrome, ulcerative lesions often arise on the ver-
milion borders of the lips
the likelihood of EM. This disorder comprises four clini-
cal presentations: erythema multiforme minor, EM,
major, Steven’s Johnson syndrome (SJS) (. Fig. 20.33),
and toxic epidermal necrolysis syndrome (TENS). The
minor type comprises ulceration of a mucosal surface or
less than 10% of the skin, while the other types involve
more extensive mucocutaneous ulceration with TENS
giving rise to more than 30% of the skin being affected
[48, 49].
Mucosal and/or cutaneous disease may sometimes,
but not always, be accompanied by target lesions (con-
centric rings of white and red) that may affect any cuta-
neous surface but particularly the palmar and plantar
surfaces. A detailed discussion of EM is out with the
scope of this chapter, but if EM is suspected, it is essen-
tial that patients are rapidly referred to appropriate spe-
cialists.
20.6.2 Allergic Reactions
Allergic reactions, i.e., hypersensitivity responses in
response to oral healthcare procedures, are very rare.
20 The most common allergic reaction that is likely to arise
is a type 1 reaction (i.e., immediate hypersensitive) to
penicillin. This is clearly most likely when a patient with
known allergy to penicillin is mistakenly prescribed this
drug. The clinical presentation of penicillin allergy var-
ies from mild urticaria (i.e., skin rash) to angioedema
(swelling of the lips, tongue, pharynx, and larynx) and
anaphylaxis (urticaria, asthma, angioedema, anoxia,
and possible death).
Allergic reaction is a most severe adverse effect; hence,
there is always a need to review the medical history of
child patients before prescribing penicillin or indeed
any systemic medication. The management of possi-
ble angioedema and anaphylaxis varies across the
globe, but the major principles (regardless of the pre-
cipitant) are as follows:
1. Removal of the potential cause (usually impossi-
2. Call for professional support
3. High flow oxygen
4. Repeated intramuscular adrenaline (every 5 min-
utes) until professional support arrives
Hypersensitivity reactions to a wide range of other
agents used in pediatric dentistry are possible and
include natural elastic gum (latex, e.g., gloves, rubber
dam) (. Fig. 20.34) and, in rare cases, after contact
with materials which do not contain latex (e.g., various
metals, such as nickel which is used in orthodontic mate-
rials [50, 51]) (. Fig. 20.35). The reactions to these
agents vary in severity and timing; some may be rapid
(within a few minutes, e.g., angioedema in response to
an impression material) or slow (within 48–72 hours,
e.g., perioral rash with some instruments) [50–53].
Reactions to local anesthetics are almost unheard of
although some patients or their parents report that they
are “allergic” when in fact upon closer discussion they
are found to have possibly fainted or just “felt unwell”
or “tired.” If a genuine allergy to components of local
anesthetic solutions is suspected, then it is important
that the patient is referred to a suitable specialist for
detailed evaluation.
20.6.3 Other Mucocutaneous Disease
Unlike adults, children are not liable to develop autoim-
mune disease such as immunobullous disease nor oral
lichen planus, although clearly these can occasionally
arise in children or young adults. A detailed discussion
of these is out with the scope of this book. However, it
must be borne in mind that oral lichen planus-like dis-
ease can arise in children with graft-versus-host disease.
Graft-versus-host disease (GvHD) arises in children
who receive a bone marrow allograft (e.g., in the man-
agement of leukemia) in which, as the term suggests, the
graft exerts a cytotoxic response upon the host. The oral
consequences of GvHD include early oral superficial
ulceration and later the emergence of white patches, ero-
sions, and ulcers on the mucosae and/or gingivae that
mimic those of oral lichen planus. Other features include
Oral Lesions in Children and Adolescents
a loss of salivary gland function (hence xerostomia), mul-
b childhood that may give rise to oral manifestations and/
c solid (e.g., lymphomas and tumors of Langerhans
..      Fig. 20.34 Three images demonstrating the progress of a proba-
ble allergic reaction to rubber dam latex. a Edematous reaction of
the left buccal area 2 hours after the dental treatment. b Exanthema
after 3 days. c The same region 15 days later
a b
..      Fig. 20.35 a Unusual allergic reaction (type IV-delayed hyper-
sensitivity), which arose during orthodontic treatment of a young
female. Diagnostic evaluation by an allergist revealed hypersensitiv-
ity to nickel (degree ++++). b Complete clinical signs of remission
after the removal of the brackets. The orthodontic treatment was
completed by using nickel-free brackets. (Courtesy by Dr. O. Kolok-
itha)
505 20
tiple mucoceles, and pyogenic granulomas (that may be
driven by cyclosporin). This immunosuppressant may
also cause gingival enlargement [54].
20.7 Hematological Disease
There are a vast array of hematological disorders of
or have the impact upon the acute care of pediatric den-
tistry. The present discussion is not intended to be defin-
itive but to provide an overview of relevant aspects of
hematological disease.
Hematological disease reflects either altered cellular
number or function of cells derived from bone marrow
(i.e., reticulocytes, white blood cells, and platelets) or
the proteins of the coagulation pathways. Hematological
disease also includes non-solid (e.g., leukemias) and
cells).
20.7.1 Hematological Malignancies
20.7.1.1 Lymphomas
Lymphomas are hematological solid tumors. They
broadly split into Hodgkin’s disease (HD) and non-­
Hodgkin’s lymphoma (NHL). Hodgkin’s disease usually
arises from nodal lymphoid tissue and spreads locally
from one group of nodes to another (and can include
the liver and spleen); a characteristic histopathological
feature of HD is the presence of Reed-Sternberg cells. In
contrast NHL usually commences in extra-nodal sites
(e.g., tonsils, Peyer’s patches, brain, viscera), spreads
erratically, and is histopathologically dominated by
abnormal lymphocytes (usually). The cause of most
lymphomas is unknown although some NHL may be
caused by EBV or Helicobacter pylori. Lymphomas are
in general uncommon in children although some NHL
are more common in children than adults.
20.7.1.2 Hodgkin’s Disease
Hodgkin’s disease arises in young individuals (15–
30 years old). Initially there is painless swelling of one or
few lymph nodes belonging to one group – and of note
the cervical group is often the first to be affected. Patients
can develop “B” symptoms of weight loss, pyrexia, and
lethargy. Involvement of the mouth is very rare [55]
although if disease affects the bone marrow patients will
be liable to opportunistic infection (e.g., acute pseudo-
membranous candidiasis) or have features of thrombo-
cytopenia. Gingival swelling due to HD has been
reported, and there are occasional reports of bone
involvement (manifesting as radiolucencies). Hodgkin’s
 506 S. Porter and A. Kolokotronis
disease is managed by hematological oncology teams
and usually has a good prognosis.
20.7.1.3 Non-Hodgkin’s Lymphoma
This is a notably broad group of malignancies. Children
are rarely affected although Burkitt’s lymphoma tends to
arise in children and usually affects the jaw bones manifest-
ing as large bony swellings, gingival enlargement, tooth
mobility, and possible pathological fracture. Non-
Hodgkin’s lymphoma can arise in the mouths of children
with severe HIV disease and may manifest as large areas of
necrotic ulceration of the gingivae and/or oral mucosae. As
with HD, such disease is managed by hematology oncolo-
gists, but unlike HD, it has a variable prognosis [56–58].
20.7.1.4 Langerhans Cell Histiocytosis
This comprises a group of rare tumors of myeloid den-
dritic cells. Although uncommon it can give rise to nota-
ble oral features and by virtue of its systemic effects has
the possibility of complicating the care of children
requiring pediatric dentistry [59, 60]. It comprises three
clinical presentations: eosinophilic granuloma, Hand-­
Schüller-­Christian syndrome, and Letterer-Siwe disease.
The terminology is sometimes variable such that the
non-localized form of eosinophilic granuloma is termed
histiocytosis X. These disorders tend to arise in children
and young adults.
Eosinophilic Granuloma
This is usually a localized disease that arises in late child-
hood. The skull and often the jaws, especially the man-
dible, are common sites of involvement. Jaw disease can
cause mobility of the teeth in the affected area, and
pathological fracture (of the mandible) can rarely occur.
Radiology can reveal radiolucent areas that are observed,
and the teeth may have the appearance of floating on the
top of the radiolucency. Usually, the overlying oral
mucosa may be ulcerated. The jaws can be affected
in localized multisystem disease (that can involve the
lungs, liver, spleen, bone marrow, or CNS) [61].
Hand-Schüller-Christian Disease
This is a variant of disease that includes the clinical tri-
adof:
20 (a) Osteolytic lesions (in 100% of the affected individuals)
(b) Diabetes insipidus (reflecting destruction of the pos-
terior pituitary gland (50%)
(c) Exophthalmos (10%)
However, these features do not arise simultaneously, and
there may be lymphadenopathy, cutaneous rashes, and
hepatosplenomegaly. The jaws can be affected in the
same way as eosinophilic granuloma [62].
Letterer-Siwe Disease
This is rare but the most severe type of Langerhans
cell histiocytosis and tends to arise in young children
(e.g., 2 years of age). Affected children develop a seb-
orrheic rash, ear discharge, and features of severe
multisystemic disease including anemia, thrombocy-
topenia, neutropenia, lymphadenopathy, and/or hepa-
tosplenomegaly is the most severe type of Langerhans
cell disease. The oral manifestations can be those of
eosinophilic granuloma, but in addition there may be
features of anemia (e.g., superficial ulceration), neu-
tropenia (e.g., candida infections), and thrombocyto-
penia (e.g., petechiae and ecchymoses) [63].
20.7.1.5 Leukemia
Leukemias are hematological non-solid tumors in which
there are clones of neoplastic, immature, or mature lym-
phocytes or granulocytes. They are principally divided
into four main types:
• Acute myelogenous leukemia (AML)
• Acute lymphoblastic leukemia (ALL)
• Chronic myelogenous leukemia (CML)
• Chronic lymphocytic leukemia (CLL)
Apart from these four major types, there are also vari-
ous (and many) subtypes. Children and young adults
tend to have a greater risk of acute than of chronic leu-
kemias. Acute lymphoblastic leukemia is the most com-
mon type in childhood. Further details of the
implications of leukemia for pediatric dentistry are pro-
vided in 7 Chap. 21; however, in general, the oral mani-
festations encompass those of loss of bone marrow
function, complications (both short- and long-term) of
therapy, leukemic deposits (as with acute lymphoblastic
leukemia), and gingival deposits of acute myeloid leuke-
mia that manifests as gingiva enlargement [64].
20.7.2 Disorders of Blood Cells
The majority of red cell defects in children center around
anemia (i.e., a reduction in hemoglobin and red cells).
20.7.2.1 Anemia
Anemia in adults tends to reflect a deficiency of one or
more of the hematinics (iron, vitamin B12, and folate
(folic acid)), and certainly, for example, children with
undiagnosed gluten-sensitive enteropathy are at risk of
this. Young adults with bulimia nervosa and/or anorexia
nervosa may be at risk of anemia due to a lack of intake
of folic acid or iron. Anemias cause oral ulceration, a red
smooth dorsum of the tongue (“atrophic glossitis”), and
angular cheilitis. Vitamin B12 deficiency (e.g., in Crohn’s
disease) may also cause a soreness of the tongue. Anemias
must be managed by appropriate specialists [65].
Oral Lesions in Children and Adolescents
The dominating anemias of childhood and in par-
ticular certain parts of the globe are the hemolytic ane-
mias due to hemoglobinopathies – thalassemia and
sickle cell disease.
20.7.2.2 Thalassemia
Thalassemias are a group of hemolytic inherited (fol-
lowing the autosomal recessive pattern) diseases which
are caused by hemoglobin composition disorders and
particularly by reduced production of α (α-thalassemia)
or β (β-thalassemia) hemoglobin A (HbA) peptide
chains. In the Mediterranean there are in general three
following forms of β-thalassemia; other thalassemias
are much less common and indeed can be life-­
threatening.
kβ-Thalassemia major
55 This manifests in the first few months of life and is
characterized by severe hemolytic anemia, delayed
body development, recurrent infections, and spleno-
megaly. Affected individuals have features of ane-
mia. With time bony enlargement can arise as a
consequence of extra-medullary bone marrow
expansion, and this particularly affects the long
bones and skull. Radiologically there may be expan-
sion of the diploic space with trabeculae having a
“hair on end” appearance [66–69] (. Fig. 20.36).
Enlargement of the mandible and more commonly
the maxilla can give rise to a liontine (“lion-like”)
appearance. The oral features of thalassemia are
now rare in children in view of the advances in treat-
ment – indeed bone marrow transplantation is now
sometimes undertaken.
..      Fig. 20.36 Lateral skull radiograph of a child with thalassemia
major. The “hair-on-end” skull is depicted
507 20
kβ-Thalassemia intermedia
This may be caused by double heterozygosity (combina-
tion of α- and β-thalassemia). It is rare and presents
almost the same clinical picture of with thalassemia
major – but is milder.
kβ-Thalassemia minor
55 This rarely gives rise to severe anemia or the features
of major disease.
20.7.2.3 Sickle Cell Disease
The sickle cell diseases reflect a defect in the structure of
the globin chain – i.e., there are a normal number of
chains (unlike thalassemias), but the structure and func-
tion are defective. When there is a reduction in blood oxy-
genation, the reticulocytes become sickle in shape, do not
pass along small blood vessels with ease, and may cause
obstruction of vessels. Sickle cell disease has some nota-
ble racial (hence geographical) variation being most likely
in individuals of a Black Africa decent. Affected individ-
uals are prone to hemolytic anemia and intermittent
vaso-occlusal disease. The abnormal red blood cells
become sequestered in the spleen, and with severe disease,
there is a loss of splenic function and risk of pneumococ-
cal infection. The vaso-occlusal disease varies in presenta-
tion between patients but in its most severe form can
cause acute pain crisis that may be precipitated by infec-
tion, extreme temperature, hypoxia, dehydration, psycho-
logical or physical stress, or even menstruation [70, 71].
A detailed discussion of sickle cell disease is out with
the scope of this chapter but key issues relevant to pedi-
atric dentistry include effective preventative care to
avoid a risk of periapical infection precipitating a pain-
ful crisis, the need for general anesthesia, avoidance of
the use of agents likely to suppress respiratory function,
avoidance of non-steroidal anti-inflammatory drugs in
patients with possible or known renal disease, and
awareness that patients with severe sickle cell anemia
can develop pain in single non-carious teeth that is a
manifestation of a pulpal infarct.
20.7.2.4 Neutropenia
Neutropenia reflects a reduction in the number of poly-
morphonuclear neutrophils. In children this can reflect
congenital disease such as chronic neutropenia and cyclic
neutropenia or be a consequence of bone marrow failure
(e.g., with leukemias and lymphomas) or due to a reduc-
tion in bone marrow function due to drug therapy (e.g.,
cytotoxics or immunosuppressives). Rarely autoimmune
disease may cause an autoimmune neutropenia [72, 73].
In general, neutropenias increase the risk of recur-
rent infections of the respiratory and urinary tracts
and skin, and children may have recurrent episodes
 508 S. Porter and A. Kolokotronis
of pyrexia of unknown cause. Depending upon the
cause and hence severity of the neutropenia, the oral
cavity can be greatly affected. Common features are
deep ulceration of the mucosae or gingivae (these are
sometimes said to lack an inflammatory halo), pro-
found gingivitis, and cervical lymphadenopathy. Oral
pseudomembranous candidiasis can also arise. In
long-­standing profound anemia, there is a risk of
aggressive periodontitis with resultant tooth mobility
and even early loss of the primary dentition. In cyclic
neutropenia the neutrophil count tends to spontane-
ously reduce about every 3–4 weeks such that patients
develop all of the above features in a cyclical manner.
Eye Catcher
There are a wide range of rare disorders in which neu-
trophil function (e.g., adherence, chemotaxis, phago-
cytosis, or killing) can be defective. In general, these
disorders increase the risk of aggressive periodontitis
although some may also cause orofacial
granulomatosis-­type disease.
20.7.3 Bleeding Disorders
Cessation of bleeding rests upon vasoconstriction, the
formation of the primary platelet plug, and the subse-
quent establishment of a clot. Defects of any of these
elements have the potential to increase the risk of
post-­injury bleeding and in severe disease cause spon-
taneous bleeding. The present discussion focuses upon
the more common or well recognized of this group of
disorders.
20.7.3.1 Hereditary Hemorrhagic
Telangiectasia (HHT,
Osler-Weber-Rendu Syndrome)
This is an uncommon autosomal dominant disorder of
blood vessel formation characterized by mucocutaneous
telangiectasias and arteriovenous malformations in var-
ious internal organs (e.g., lungs, liver, and brain). The
telangiectasias have a high likelihood to occur in the
nose, mouth, and gastrointestinal tract; they bleed easily
causing, for example, repeated and/or severe epistaxis
20 and unknown gastrointestinal bleeding leading to ane-
mia [74, 75].
Affected children and adults may have multiple small
1–3-mm-diameter telangiectasias on the face, periorally,
on the lips, and on any oral mucosal of gingival surface.
Patients may also have oral signs of anemia. Other fea-
tures may include the risk of brain abscess, hemorrhagic
stroke, hepatic failure, and risk of high-output cardiac
failure.
Aside from its oral manifestations, the implications
of HHT for pediatric dentistry center upon the need
for effective preventative dental care to avoid the need
for general anesthesia, careful nasal intubation (if
essential) to avoid epistaxis, and cessation of spontane-
ous bleeding of oral telangiectasias with chemical cau-
terization and post-surgical (e.g., post-extraction)
bleeding with chemical cauterization and/or tranexamic
acid [76].
20.7.3.2 Thrombocytopenia
Thrombocytopenia – reduced platelet count – is uncom-
mon in childhood although when present it has many
causes that range from autoimmune disease such as idio-
pathic thrombocytopenic purpura (ITP) and systemic
lupus erythematosus (SLE), viral infection (when there is
usually a short-term fall in platelet count), congenital
disease (e.g., Wiskott-Aldrich syndrome and Fanconi
anemia), malignancy (e.g., leukemias or other tumors of
the bone marrow), or loss of bone marrow function due
to radiotherapy, chemotherapy, or immunosuppressives.
As detailed previously the oral features of thrombo-
cytopenia comprise a variable number of petechiae and/
or ecchymoses. The petechiae (small red-to-purple flat
dots that when larger are termed purpura) can arise on
any oral mucosal and/or gingival surface, while the
ecchymoses (large bruises) are more likely at sites of
trauma such as the palate and buccal mucosae. When
there is a severe reduction in platelet numbers (e.g.,
below 20,000/mm3), there may be spontaneous gingival
bleeding. Cleary children with severe thrombocytopenia
will have cutaneous purpura and bruising and be liable
to epistaxis and gastrointestinal tract bleeding. Bleeding
within viscera is uncommon.
The management of thrombocytopenia clearly
depends upon the severity of the platelet deficiency and
the underlying cause. Aside from its oral features, the
implications of thrombocytopenia center upon avoiding
bleeding with infiltrations (in general the platelet count
should be above 20,000/mm3) or regional blocks (the
count should be above 50,000/mm3), ensuring effective
post-surgical hemostasis and avoidance of drugs likely
to increase bleeding (e.g., NSAIDs), and considering
any interaction between dentistry and the underlying
disease or its treatment (e.g., possible corticosteroid
cover for children receiving long-term corticosteroids).
Finally, there should be a focus upon the prevention of
childhood dental disease – hence avoiding the need for
any invasive dental treatment [77].
Oral Lesions in Children and Adolescents
There are a number of disorders in which platelet
numbers are normal but their function abnormal
(thrombasthenias). In general patients with such disease
should be managed with the similar considerations as
for thrombocytopenia.
20.7.3.3 Coagulopathies
There is a wide spectrum of defects of the clotting mech-
anism. These may be of congenital defects of the clotting
factors (e.g., the hemophilias) or secondary to hepatic or
gastrointestinal disease (e.g., vitamin K deficiency sec-
ondary to gluten-sensitive enteropathy) or the use (all be
it rarely in children) of anti-coagulants – especially cou-
marin agents such as warfarin. The present discussion
will center upon more well recognized congenital clot-
ting factor deficiency disorders.
Hemophilia A
Hemophilia A is an X-linked (i.e., the affected gene lies
on the chromosome X) recessive inherited disease that
gives rise to a reduction or absence of Factor VIII. As
an X-linked recessive disorder, females may be carriers
or very rarely affected, while males are at risk of having
the disease.
Hemophilia A accounts for 85% of all instances of
hemophilia and has an incidence of about 1:5000 live
births. Depending upon the level of the Factor VIII defi-
ciency, there are three forms: severe (when levels are
<1% of normal), moderate (2–5% of normal), and mild
(6–40%). Carriers can also have reduced levels of Factor
VIII but not to the same degree as those with the dis-
ease. Severe disease accounts for about 50% of the
affected individuals and can give rise to spontaneous
bleeding, particularly joints and deep structures.
Moderate disease may cause spontaneous bleeding,
while mild does not – although as with all types of dis-
ease there is a risk of prolonged bleeding after trauma.
Without treatment hemophilia may cause anemia, hem-
arthroses (that may limit mobility), and a risk of infec-
tion. Life-threatening bleeding is possible with severe
disease.
The general management of hemophilia depends
upon the severity of the clotting defect but in general
centers upon the use of factor replacements (now recom-
binant and not derived from blood donations), agents to
stimulate release of endogenous stores of clotting fac-
tors (e.g., desmopressin, desamino-8-D-argininine vaso-
pressin (DDAVP), the use of antifibrinolytic agents such
as tranexamic acid to stabilize clot retention, and avoid-
ance of trauma. Patients who develop inhibitors (i.e.,
antibodies to Factor VIII) may be given activated pro-
thrombin complex concentrate (FEIBA). In the past the
use of human-derived factor concentrates led to patients
with hemophilia A (or indeed any type) acquiring HIV
resulting in most instances in early death from
509 20
AIDS. Similarly, HCV transmission occurred in some
instances. It is now highly unlikely that any child or
young adult who has received factor concentrates in
recent years will be infected with HCV and certainly not
HIV [77–80].
Eye Catcher
The implications of hemophilia A to pediatric den-
tistry principally center upon preventative care to
ensure avoidance of invasive dental procedures (or
the need for local anesthesia) and avoidance of post-­
surgical bleeding. This latter must include:
1. Early liaison with the patient’s hematology team
to determine the need for, and provision of, factor
concentrates or DDAVP and the appropriateness
of any planned local anesthesia
2. As atraumatic as possible dental treatment
3. Assurance of prolonged post-surgical hemostasis
with placement of hemostatic agents in extraction
sockets, effective closure of wounds with resorb-
able sutures, and the use of tranexamic acid
mouthwash
Non-steroidal anti-inflammatory drugs such as ibu-
profen should be avoided for pain relief in view of
their potential to induce gastric erosion or reduce
platelet function.
Hemophilia B (“Christmas Disease”)
This is another X-linked recessive coagulopathy in which
there is a deficiency of Factor IX. Although less com-
mon than hemophilia A, its clinical presentation, man-
agement, and dental implications mirror those of
hemophilia A.
von Willebrand’s Disease
von Willebrand’s disease (vWD) is the most common of
all congenital bleeding disorders. It is an autosomal
dominant disorder that reflects a deficiency of the
amount or function of von Willebrand factor (vWF)
that stabilizes Factor VIII and also allows platelets to
adhere to blood vessel endothelium. There are three
types of vWD (I, mild; II, moderate; and III, severe)
with patients with the mild type generally only requiring
DDAVP, while those with moderate and severe require
concentrates of Factor VIII and vWF. In general, the
implications of vWD are similar to those of hemophilia
A, although patients who are affected occasionally have
only been identified following episodes of prolonged
post-extraction bleeding. In addition, in view the com-
bined platelet/clotting factor defects, patients may have
oral petechiae or spontaneous gingival bleeding [81].
 510 S. Porter and A. Kolokotronis
20.8 Salivary Gland Disease
Salivary gland disease in childhood is rare but, as with
adults, most commonly comprises loss of function and/
or swelling of one or more glands.
20.8.1 Mucocele
Mucoceles are swellings of minor salivary glands that
typically present as a single painless sessile translucent
blue swelling, typically of the lower lip (although can
occasionally arise within the mouth) (. Fig. 20.37).
Patients often inadvertently or deliberately bite the
lesions (in the hope that they will burst and resolve) and
report having a salty and/or oily discharge. Multiple
mucoceles have been observed in some children with
GvHD and can occur in otherwise well children [82].
Mucoceles are probably caused by trauma, but
patients rarely recall any likely causative event.
Mucoceles reflect one of two histopathological pictures:
a tear within the wall of duct causing salivary to extrava-
sate into the adjacent connective tissue (“mucous extrav-
asation cysts”) or a much less commonly ductal
obstruction by a small sialolith or scar (“mucous reten-
tion cysts”) or has a tear in which saliva is passing into
the connective tissues.
Regardless of the cause, mucoceles should be
removed. Surgical (i.e., scalpel) excision has the advan-
tage that the lesional tissue can be histopathologically
examined but has the disadvantage of sometimes being
difficult – for example, when the mucocele bursts during
removal – and has a small risk of post-surgical paresthe-
sia or anesthesia. Cryotherapy is simple and rapid to
undertake, but post-treatment pain and swelling can be
significant and distressing for the patient; there is no
sample for histopathological examination. Any muco-
cele of the upper lip warrants histopathological exami-
nation, while the vast majority of these will be
extravasation or retention lesions – just once in a while,
they will be a reflection of salivary gland malignancy.
20.8.2 Ranula
A ranula represents a mucocele of a sublingual and/or
20 submandibular gland. These are usually a developmen-
tal anomaly and manifest as a translucent/blue swelling
of the floor of the mouth (. Fig. 20.38). The swellings
are painless, of variable size – although they can be sev-
eral centimeters in diameter – but rarely interfere in
speech, swallowing, or breathing. They are classified as
superficial (when they lie above mylohyoid), deep (i.e.,
lie beneath mylohyoid), and perhaps plunging (lying
..      Fig. 20.37 Mucocele located at the ventral surface of the tongue,
the second most frequent location following the lower lip mucosa
..      Fig. 20.38 Ranula of the tongue and floor of the mouth
above and below the mylohyoid). Ranulas usually have
no associations with systemic disease although they
have been observed in patients with HIV salivary gland
disease or on ART [35, 83–85].
For the investigation and treatment of ranulas,
patients should be referred to oral surgery. The investi-
gation of possible ranulas requires ultrasound scanning,
and where there remains any doubt (which is unlikely),
magnetic resonance imaging may be considered. Small
ranulas may not warrant removal although if consid-
ered large or are interfering in oral function excision is
indicated.
20.8.3 Sialolithiasis
Sialolithiasis is inflammation within a salivary gland as
a consequence of ductal obstruction by sialoliths (sali-
vary calculi). This disorder is uncommon in children but
when present is likely to manifest as painful swelling in
the submandibular region. The pain is precipitated by
gustation hence when an individual thinks of food or
eats. The pain is often burning or stretching in nature
and typically arises just before or during eating or drink-
ing. The swelling is diffuse, and the gland may be tender
to touch. Rarely the gland can become infected giving
rise to a purulent discharge from the submandibular
duct or sublingual fold, dysgeusia and oral malodor, as
well as submandibular lymphadenopathy. Pyrexia and
malaise are very rare [35, 86, 87].
The precise cause of sialolith formation remains
unknown although occasionally a correlation with
Oral Lesions in Children and Adolescents
..      Fig. 20.39 Occlusal radiograph of the mandible in which a sialo-
lith (marked with the arrow) is depicted as circular, homogeneous,
and radiopaque entity located at the left half of the floor of the
mouth
nephrocalcinosis has been suggested (but not hyper-
parathyroid disease). It has also been observed in a small
number of children with HIV salivary gland disease.
The management of possible sialolithiasis tends to fall
under the specialties of oral medicine or oral surgery but
is centered upon identification of the site and size of sial-
oliths (e.g., via plain radiography (. Fig. 20.39), ultra-
sound scanning, and/or sialoendoscopy) and removal of
calculi directly (e.g., those within the submandibular
duct) via sialoendoscopic retrieval (with or without litho-
tripsy), or, rarely, removal of a chronically inflamed
gland. Sialolithiasis is rarely recurrent [35, 88, 89].
20.8.4  cute Suppurative Sialadenitis
A The precise etiology of recurrent parotitis remains
(Suppurative Parotitis, Bacterial
Sialadenitis, Bacterial Parotitis)
Acute suppurative sialadenitis is an uncommon disorder
characterized by painful swelling – usually of the parotid
glands (suppurative parotitis), purulent discharge from
the duct of the affected gland, associated dysgeusia, and
cervical lymphadenopathy. When the disease is severe,
there may be accompanying pyrexia, malaise, and a risk
of abscess formation and parapharyngeal space infec-
tion – including Ludwig’s angina.
Acute suppurative sialadenitis can affect children and
adults. Prematurity may be a risk factor for disease in
childhood, and sialadenitis can occur in newborns. Acute
suppurative sialadenitis may also be a feature of Sjogren’s
syndrome. Aseptic sialadenitis has been observed in pre-
term children receiving long-term orogastric tube feed-
ing. Immunodeficiency and concurrent illness may
predispose to childhood suppurative parotitis [35, 90].
The causative infection is usually mixed, and hence
microbiological investigation of pus or saliva is rarely of
notable diagnostic benefit. Management is principally
directed toward resolving the infection and later identi-
511 20
fying and where possible treating any underlying risk
factor. Typical therapeutic regimes are effective hydra-
tion and systemic antimicrobials. Typically employed
antibiotics are anti-staphylococcal penicillins (e.g., flu-
cloxacillin, amoxicillin, or co-amoxiclav), cephalospo-
rins, or clindamycin, although the precise choice of
antibiotic will often depend upon any likely causative
organism that is identified (although as noted above in
most instances there is a little need for detailed microbio-
logical evaluation of pus or saliva). Complications of
acute suppurative sialadenitis in childhood are rare [91].
20.8.5  ecurrent Parotitis of Childhood
R
(Juvenile Recurrent Parotitis)
Recurrent parotitis of childhood is characterized by
recurrent parotid inflammation. It can arise at any age,
but the usual age of onset is 3–6 years. Childhood-onset
disease is usually more common in males, while adult-­
onset disease normally arises in females. The disease gives
rise to pain and swelling in one parotid gland that may
last up to 14 days. Fever and overlying erythema are com-
mon, and occasionally white muco-pus can be expressed
from the parotid duct. The number of attacks varies from
1 to 5 per year, but some patients may have up to 20 epi-
sodes of swelling per year. The frequency of recurrence
tends to peak between 5 and 7 years of age, and up to 90%
of patients have resolution of disease by puberty.
Sialography and ultrasonic scans reveal sialectasis.
unclear, but certainly almost all affected patients are
otherwise well.
Analgesia is the mainstay of therapy. Antibiotics do
not shorten attacks. Intraductal saline with or without
dilatation of Stenson’s duct and intraductal antibiotics
(or methyl violet to induce sclerosis) have been proposed
as have included sialoendoscopy and ductal dilatation
with a sialoballoon. Suggested invasive procedures
include ligation of Stenson’s duct, transection of chorda
tympani, or transection of Jacobsen nerve in the middle
ear. Radical methods such as total or sub-total paroti-
dectomy have also been proposed, but as the disease
tends to resolve, spontaneously there seems a little place
for such invasive measures [35, 92, 93].
20.8.6 Xerostomia (Oral Dryness)
Reduced salivary gland function with resultant oral dry-
ness is rare in children and young adults. A loss of sali-
vary output can greatly impact upon oral function and
hence lessen quality of life. Affected individuals may
have dysarthria, dysphagia (especially with dry foods),
 512 S. Porter and A. Kolokotronis
dysgeusia, an increased risk of caries (e.g., of the cervi-
cal areas or at the margins of restorations), plaque-­
related gingivitis, oral candidiasis, and acute suppurative
sialadenitis) [94].
Despite its reported rarity, it is likely that some chil-
dren will have long-standing oral dryness. The most
likely cause will be long-term use of medication that
have an anti-muscarinic action (e.g., benzodiazepines,
tricyclic (or other) antidepressants, opiates, antihista-
mines). Other possible causes in childhood would
include radiotherapy-induced salivary gland destruction
(some children will have had radiotherapy for unusual
head and neck malignancies), salivary gland agenesis
(that may be an isolated anomaly or arise as part of
ectodermal dysplasia), HCV sialadenitis, HIV salivary
gland disease, or autoimmune disease (e.g., Sjogren’s
syndrome). A detailed discussion of these disorders is
out with the scope of this chapter; however the key prin-
ciples of the management of long-standing oral dryness
relevant to pediatric dentistry are as follows:
1. Prevent plaque-related oral disease.
2. Identify and manage oral complications relevant to
pediatric dentistry.
3. Arrange referral of patients to appropriate special-
ists (e.g., oral medicine) for the management of other
complications.
20.8.7 Drooling
Drooling is the unintentional loss of saliva from the
mouth. It may arise as a consequence of impaired neu-
romuscular function, though less frequently it can be
due to an increased production of saliva (idiopathic or
drug-induced). In children, the most common cause of
drooling is cerebral palsy [35, 95, 96].
Eye Catcher
Drooling is common in normally developed babies
but considered abnormal after age 4 years. It is associ-
ated with a wide spectrum of clinical and functional
complications such as impaired speech and eating,
perioral skin breakdown, as well as wetting and stain-
ing of clothing. Aspiration-related and pulmonary
complications are possible.
20
Drooling is known to be difficult to treat. Management
can be conservative or more invasive. Conservative treat-
ments include changes in diet or habits, oral-motor exer-
cises, intra-oral devices such as palatal training devices,
and medical treatments such as botulinum toxin injec-
tions. More invasive treatments include surgical reposi-
tion of the ducts of the submandibular glands such that
they open into the pharynx.
Pharmacological therapy for drooling encompasses
the use of anticholinergic agents, such as glycopyrrolate,
benztropine, and scopolamine to decrease saliva secre-
tion through the parasympathetic autonomic nervous
system. Botulinum toxin decreases the severity of drool-
ing with statistical significance in children. The duration
of effect can vary from 6 weeks to 6 months. However,
there remains the need of establishing the ideal dose and
form of application. Botulin toxin treatment may how-
ever cause increased saliva thickness, dysphagia, dry
mouth, and risk of pneumonia. Resection of the major
glands is possible, but there is a risk of xerostomia, visi-
ble scar, and facial nerve weakness [96, 97].
References
1. González-Álvarez L, García-Pola MJ, Garcia-­Martin JM. Geo-
graphic tongue: predisposing factors, diagnosis and treatment. A
systematic review. Rev Clin Esp. 2018;218(9):481–8.
2. Jainkittivong A, Langlais RP. Geographic tongue: clinical char-
acteristics of 188 cases. J Contemp Dent Pract. 2005;6:123–35.
3. Kumar Singh A, Sulugodu Ramachandra S, Arora S, Dicksit
DD, Kalyan CG, Singh P. Prevalence of oral tori and exostosis in
Malaysian population – a cross-sectional study. J Oral Biol Cra-
niofac Res. 2017;7(3):158–60.
4. Chaubal TV, Bapat R, Poonja K. Torus Mandibularis. Am J
Med. 2017 Oct;130(10):e451.
5. Fromm A. Epstein’s pearls, Bohn’s nodules and inclusion-cysts
of the oral cavity. J Dent Child. 1967;34:275–87.
6. de Oliveira AJ, Silveira ML, Duarte DA, Diniz MB. Eruption
cyst in the neonate. Int J Clin Pediatr Dent. 2018;11(1):58–60.
7. Maymone MBC, Greer RO, Burdine LK, Dao-­Cheng A, Ven-
katesh S, Sahitya PC, et al. Benign oral mucosal lesions: clinical
and pathological findings part I – benign oral mucosal lesions. J
Am Acad Dermatol. 2018. pii: S0190-­9622(18)32887-1.
8. Cheney-Peters D, Lund TC. Oral pyogenic granuloma after bone
marrow transplant in the pediatric/adolescent population: report
of 5 cases. J Pediatr Hematol Oncol. 2016;38(7):570–3.
9. Monteiro LS, Albuquerque R, Paiva A, de la Peña-Moral J,
Amaral JB, Lopes CA. A comparative analysis of oral and max-
illofacial pathology over a 16-year period, in the north of Portu-
gal. Int Dent J. 2017;67(1):38–45.
10. Nadimpalli H, Kadakampally D. Recurrent peripheral ossifying
fibroma: case report. Dent Med Probl. 2018;55(1):83–6.
11. Chrcanovic BR, Gomes CC, Gomez RS. Peripheral giant cell
granuloma: an updated analysis of 2824 cases reported in the
literature. J Oral Pathol Med. 2018;47(5):454–9.
12. Gardner P, Rozzelle A. Congenital granular cell tumor: case
report and review. Case Rep Pediatr. 2018;2018:4389158.
13. Porter SR, Mercadante V, Fedele S. Oral manifestations of sys-
temic disease. Br Dent J. 2017;223(9):683–91. https://doi.
org/10.1038/sj.bdj.2017.884.
14. Tucci FM, De Vincentiis GC, Sitzia E, Giuzio L, Trozzi M, Bot-
tero S. Head and neck vascular anomalies in children. Int J Pedi-
atr Otorhinolaryngol. 2009;73(Suppl 1):S71–6.
15. Bhayya H, Pavani D, Avinash Tejasvi ML, Geetha P. Oral
lymphangioma: a rare case report. Contemp Clin Dent.
2015;6(4):584–7.
Oral Lesions in Children and Adolescents
16. Scully C, Porter S. Orofacial disease: update for the dental clini-
cal team: 2. Ulcers, erosions and other causes of sore mouth.
Part II. Dent Update. 1999;26(1):31–9.
17. Gilvetti C, Porter SR, Fedele S. Traumatic chemical oral ulcer-
ation: a case report and review of the literature. Br Dent J.
2010;208(7):297–300.
18. Kanumuri PK. Riga Fede Disease. J Neonatal Surg. 2017;6(1):20.
19. Scully C, Porter S. Oral mucosal disease: recurrent aphthous sto-
matitis. Br J Oral Maxillofac Surg. 2008;46(3):198–206.
20. Porter SR, Al-Johani K, Fedele S, Moles DR. Randomised con-
trolled trial of the efficacy of HybenX in the symptomatic treat-
ment of recurrent aphthous stomatitis. Oral Dis.
2009;15(2):155–61. https://doi.
org/10.1111/j.1601-­0825.2008.01503.x.
21. Brocklehurst P, Tickle M, Glenny AM, Lewis MA, Pemberton
MN, Taylor J, Walsh T, Riley P, Yates JM. Systemic interven-
tions for recurrent aphthous stomatitis (mouth ulcers). Cochrane
Database Syst Rev. 2012;9:CD005411.
22. Scully C, Hodgson T, Lachmann H. Auto-­inflammatory syn-
dromes and oral health. Oral Dis. 2008;14(8):690–9.
23. Colbert RA, Sun HW, Wood GM, Barham BK, Jones A, Aksen-
tijevich I, et al. Periodic fever, aphthous stomatitis, pharyngitis,
and adenitis (PFAPA) is a disorder of innate immunity and Th1
activation responsive to IL-1 blockade. Proc Natl Acad Sci U S
A. 2011;108(17):7148–5.
24. Michailidou Ε, Arvanitidou S, Lombardi T, Kolokotronis A,
Antoniades D, Samson J. Crohn’s disease diagnosed by oral
lesions: report on five patients. Quintess Int. 2009;40:581–5.
25. Sainsbury CP, Dodge JA, Walker DM, Aldred MJ. Orofacial
granulomatosis in childhood. Br Dent J. 1987;163(5):154–7.
26. Stein SL, Mancini AJ. Melkersson-Rosenthal syndrome in child-
hood: successful management with combination steroid
and minocycline therapy. J Am Acad Dermatol. 1999;41(5 Pt
1):746–8.
27. Al Johani KA, Moles DR, Hodgson TA, Porter SR, Fedele
S. Orofacial granulomatosis: clinical features and long-term out-
come of therapy. J Am Acad Dermatol. 2010;62(4):611–20.
28. Wierink CD, Van Diermen DE, Aartman IHA, Heymans
HSA. Dental enamel defects in children with coeliac disease. Int
J Paediatr Dent. 2007;17(3):163–8.
29. Bossù M, Bartoli A, Orsini G, Luppino E, Polimeni A. Enamel
hypoplasia in coeliac children: a potential clinical marker of
early diagnosis. Eur J Paediatr Dent. 2007;8(1):31–7.
30. Costacurta M, Maturo P, Bartolino M, Docimo R. Oral mani-
festations of coeliac disease.: a clinical-statistic study. Oral
Implantol (Rome). 2010;3(1):12–9.
31. Porter SR. Viral infection of the oral cavity. In: Wilson M, edi-
tor. Food constituents and oral health: current status and future
prospects. Cambridge: Woodhead Publishing; 2009. p. 19–50.
32. Porter S, Leão JC, Gueiros LA. Oral and Maxillofacial Viral
Infections. In: Farah C, Balasubramaniam R, McCullough MJ
(eds). Contemporary Oral Medicine. Springer; 2019. pp. 983–1007
33. Sälberg M. Oral viral infections of children. Periontol.
2000;49:87–95.
34. Kolokotronis A, Louloudiadis K, Fotiou G, Matiais A. Oral
manifestations of infections due to varicella zoster virus in oth-
erwise healthy children. J Clin Pediatr Dent. 2001;25:107–12.
35. Porter SR, Mercadante V, Fedele S. Non-­neoplastic salivary
gland disease. In: Watkinson JC, Clarke RW, editors. Scott-
Brown’s otorhinolaryngology: head & neck surgery. 8th ed. CRC
Press; 2017. Part 3. p. 345–456.
36. Livingston KA, Rosen JB, Zucker JR, Zimmerman CM. Mumps
vaccine effectiveness and risk factors for disease in house-
holds during an outbreak in New York City. Vaccine.
2014;32(3):369–74.
513 20
37. Said AK, Leao JC, Fedele S, Porter SR. Focal epithelial hyper-
plasia - an update. J Oral Pathol Med. 2013;42(6):435–42.
38. Araújo JF, Oliveira AEF, Carvalho HLCC, Roma FRVO, Lopes
FF. Most common oral manifestations in pediatric patients HIV
positive and the effect of highly active antiretroviral therapy.
Cien Saude Cole. 2018;23(1):115–22.
39. Baghirath PV, Krishna AB, Gannepalli A, Ali MM. Oral
manifestations of HIV in children receiving anti-­
­ retroviral
therapy in Hyderabad, India. Eur Arch Paediatr Dent.
2013;14(6):389–95.
40. Greenspan JS, Greenspan D, Webster-Cyriaque J. Hairy leuko-
plakia; lessons learned: 30-plus years. Oral Dis. 2016;22(Suppl
1):120–7.
41. Kolokotronis A, Doumas S, Lambroudi M, Lysitsa S, Epivatia-
nos A, Antoniades D. Facial and perioral primary impetigo: a
clinical study. J Clin Pediatr Dent. 2005;29:341–6.
42. Ilyas SE, Chen FF, Hodgson TA, Speight PM, Lacey CJ, Porter
SR. Labial tuberculosis: a unique cause of lip swelling compli-
cating HIV infection. HIV Med. 2002;3(4):283–6.
43. Folayan MO. The epidemiology, etiology, and pathophysiology
of acute necrotizing ulcerative gingivitis associated with malnu-
trition. J Contemp Dent Pract. 2004;5(3):28–41.
44. Enwonwu CO, Falkler WA, Idigbe EO. Oro-­ facial gangrene
(noma/cancrum oris): pathogenetic mechanisms. Crit Rev Oral
Biol Med. 2000;11(2):159–71.
45. Millsop JW, Fazel N. Oral candidiasis. Clin Dermatol.
2016;34(4):487–94.
46. Carey B, Lambourne J, Porter S, Hodgson T. Chronic mucocuta-
neous candidiasis due to gain-of-function mutation in STAT1.
Oral Dis. 2019;25(3):684–92. https://doi.org/10.1111/odi.12881.
47. Capalbo D, Improda N, Esposito A, De Martino L, Barbieri F,
Betterle C, et al. Autoimmune polyendocrinopathy-­candidiasis-
ectodermal dystrophy from the pediatric perspective. J Endocri-
nol Investig. 2013;36(10):903–12.
48. Bott L, Santos C, Thumerelle C, et al. Severe Stevens-Johnson
syndrome in 4 children. Arch Pediatr. 2007;14(12):1435–8.
49. Al-Johani KA, Fedele S, Porter SR. Erythema multiforme and
related disorders. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2007;103(5):642–54.
50. Kolokitha OE, Chatzistavrou E. A severe reaction to ni-contain-
ing orthodontic appliances. Angle Orthod. 2009;79(1):186–92.
51. Sifakakis I, Eliades T. Adverse reactions to orthodontic materi-
als. Aust Dent J. 2017;62(Suppl 1):20–8.
52. Nainar SM. Dental management of children with latex allergy.
Int J Paediatr Dent. 2001;11(5):322–6.
53. Syed M, Chopra R, Sachdev V. Allergic reactions to dental mate-
rials – a systematic review. J Clin Diagn Res. 2015;9(10):
ZE04–9.
54. Condò R, Maturo P, Perugia C, Docimo R. Oral lesions in pae-
diatric patients with graft-versus-host disease. Eur J Paediatr
Dent. 2011;12(1):50–4.
55. Kämmerer PW, Schiegnitz E, Hansen T, Draenert GF, Kuffner
HD, Klein MO. Multiple primary enoral soft tissue manifesta-
tions of a Hodgkin lymphoma--case report and literature review.
Oral Maxillofac Surg. 2013;17(1):53–7. https://doi.org/10.1007/
s10006-­012-­0321-­1.
56. Bowzyk Al-Naeeb A, Ajithkumar T, Behan S, Hodson DJ. Non-
Hodgkin lymphoma. BMJ. 2018;362:k3204.
57. Kemp S, Gallagher G, Kabani S, Noonan V, O'Hara C. Oral
non-Hodgkin's lymphoma: review of the literature and World
Health Organization classification with reference to 40 cases.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2008;105(2):194–201.
58. de Arruda JAA, Silva LVO, Kato CNAO, Schuch LF, Batista
AC, Costa NL, et al. A multicenter study of malignant oral and
 514 S. Porter and A. Kolokotronis
maxillofacial lesions in children and adolescents. Oral Oncol.
2017;75:39–45.
59. Allen CE, Merad M, McClain KL. Langerhans-­cell histiocyto-
sis. N Engl J Med. 2018;379(9):856–68.
60. Monsereenusorn C, Rodriguez-Galindo C. Clinical characteris-
tics and treatment of langerhans cell histiocytosis. Hematol
Oncol Clin North Am. 2015;29(5):853–73.
61. Kannan K, Alwithanani N, Salama M, Kumar M, Uthappa R,
Ahamed M. Eosinophilic granuloma in jaw bone: a pare pediat-
ric case report. Ethiop J Health Sci. 2016;26(5):487–90.
62. Lalitha CH, Manjula M, Srikant K, Goyal S, Tanveer S. Hand
schuller christian disease: a rare case report with oral manifesta-
tion. J Clin Diagn Res. 2015;9(1):ZD28–30. https://doi.
org/10.7860/JCDR/2015/10985.5481.
63. Madrigal-Martínez-Pereda C, Guerrero-­Rodríguez V, Guisado-
Moya B, Meniz-García C. Langerhans cell histiocytosis: litera-
ture review and descriptive analysis of oral manifestations. Med
Oral Patol Oral Cir Bucal. 2009;14(5):E222–8.
64. Javed F, Utreja A, Bello Correa FO, Al-Askar M, Hudieb M,
Qayyum F, et al. Oral health status in children with acute lym-
phoblastic leukemia. Crit Rev Oncol Hematol. 2012;83(3):303–
9. https://doi.org/10.1016/j.critrevonc.2011.11.003.
65. McCord C, Johnson L. Oral manifestations of hematologic
disease. Atlas Oral Maxillofac Surg Clin North Am.
­ 85.
2017;25(2):149–62.
66. Tyler PA, Madani G, Chaudhuri R, Wilson LF, Dick EA. The
radiological appearances of thalassaemia. Clin Radiol.
2006;61:40–52.
67. Hazza’a AM, Al-Jamal G. Radiographic features of the jaws and
teeth in thalassemia major. Dentomaxillofac Radiol.
2006;35:283–8.
68. Duggal MS, Bedi R, Kinsey SE, Williams SA. The dental man-
agement of children with sickle cell disease and beta-thalassae-
mia: a review. Int J Paediatr Dent. 1996;6(4):227–34.
69. Helmi N, Bashir M, Shireen A, Ahmed IM. Thalassemia review:
features, dental considerations and management. Electron Phy-
sician. 2017;9(3):4003–8.
70. da Fonseca M, Oueis HS, Casamassimo PS. Sickle cell anemia: a
review for the pediatric dentist. Pediatr Dent. 2007;29(2):159–69.
71. Alrayyes S, Compton AA, Kawar N. Oral health considerations
for pediatric patients with sickle cell disease. Dis Mon.
2018;64(6):302–5.
72. Tirali RE, Yalçınkaya Erdemci Z, Çehreli SB. Oral findings and
clinical implications of patients with congenital neutropenia: a
literature review. Turk J Pediatr. 2013;55(3):241–5.
73. Porter SR, Luker J, Scully C, Oakhill A. Oral features of a family
with benign familial neutropenia. J Am Acad Dermatol.
1994;30(5 Pt 2):877–80.
74. Hopp RN, de Siqueira DC, Sena-Filho M, Jorge J. Oral vascular
malformation in a patient with hereditary hemorrhagic telangi-
ectasia: a case report. Spec Care Dentist. 2013;33(3):150–3.
75. Kühnel T, Wirsching K, Wohlgemuth W, Chavan A, Evert K,
Vielsmeier V. Hereditary hemorrhagic telangiectasia. Otolaryn-
gol Clin N Am. 2018;51(1):237–54.
76. Scully C. Scully’s medical problems in dentistry. Edinburgh:
20 77.
Elsevier; 2014. p. 212–75.
Malmquist JP. Complications in oral and maxillofacial surgery:
management of hemostasis and bleeding disorders in surgical
procedures. Oral Maxillofac Surg Clin North Am.
2011;23(3):387–94.
78. Rasaratnam L, Chowdary P, Pollard D, Subel B, Harrington C,
Darbar UR. Risk-based management of dental procedures in
patients with inherited bleeding disorders: development of a
dental bleeding risk assessment and treatment tool (DeBRATT).
Haemophilia. 2017;23(2):247–54.
79. Abed H, Ainousa A. Dental management of patients with inher-
ited bleeding disorders: a multidisciplinary approach. Gen Dent.
2017;65(6):56–60.
80. Smith JA. Hemophilia: what the Oral and maxillofacial surgeon
needs to know. Oral Maxillofac Surg Clin North Am.
2016;28(4):481–9.
81. van Galen KP, Engelen E, Mauser-Bunschoten EP, van Es RJ,
Schutgens RE. Antifibrinolytic therapy for preventing oral
bleeding in patients with haemophilia or Von Willebrand disease
undergoing minor oral surgery or dental extractions. Cochrane
Database Syst Rev. 2015;12:CD011385.
82. Porter SR, Scully C, Kainth B, Ward-Booth P. Multiple salivary
mucoceles in a young boy. Int J Paediatr Dent. 1998;8(2):149–51.
83. Zhao YF, Jia Y, Chen XM, Zhang WF. Clinical review of 580
ranulas. Oral Surg Oral Med Oral Pathol Oral Radiol Endodon-
tol. 2004;98(3):281–7.
84. Sigismund PE, Bozzato A, Schumann M, Koch M, Iro H, Zenk
J. Management of Ranula: 9 years’ clinical experience in
pediatric and adult patients. J Oral Maxillofac Surg.
­
2013;71(3):538–44.
Garofalo S, Mussa A, Mostert M, Suteu L, Vinardi S, Gamba S,
et al. Successful medical treatment for ranula in children. Oral
Surg Oral Med Oral Pathol Oral Radiol. 2014;117(4):e289–e97.
86. Lustmann J, Regev E, Melamed Y. Sialolithiasis: a survey on 245
patients and a review of the literature. Int J Oral Maxillofac
Surg. 1990;19(3):135–8.
87. Nahlieli O, Eliav E, Hasson O, Zagury A, Baruchin AM. Pediat-
ric sialolithiasis. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2000;90:709–12.
88. Eun YG, Chung DH, Kwon KH. Advantages of intraoral
removal over submandibular gland resection for proximal sub-
mandibular stones. Laryngoscope. 2010;120(11):2189–92.
89. Beahm DD, Peleaz L, Nuss DW, Schaitkin B, Sedlmayr JC,
Rivera-Serrano CM, et al. Surgical approaches to the subman-
dibular gland: a review of literature. Int J Surg. 2009;7(6):503–9.
90. Brook I. The bacteriology of salivary gland infections. Oral
Maxillofac Surg Clin North Am. 2009;21(3):269–74.
91. Fattahi TT, Lyu PE, Van Sickels JE. Management of acute sup-
purative parotitis. J Oral Maxillofac Surg. 2002;60(4):446–8.
92. Capaccio P, Sigismund PE, Luca N, Marchisio P, Pignataro
L. Modern management of juvenile recurrent parotitis. J Laryn-
gol Otol. 2012;126(12):1254–60.
93. Katz P, Hartl DM, Guerre A. Treatment of juvenile recurrent
parotitis. Otolaryngol Clin N Am. 2009;42(6):1087–91.
94. Wolff A, Fox PC, Porter S, Konttinen YT. Established and novel
approaches for the management of hyposalivation and xerosto-
mia. Curr Pharm Des. 2012;18(34):5515–21.
95. Meningaud JP, Pitak-Arnnop P, Chikhani L, Bertrand
JC. Drooling of saliva: a review of the etiology and management
options. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2006;101(1):48–57.
96. Scully C, Limeres J, Gleeson M, Tomás I, Diz P. Drooling. J Oral
97.
Pathol Med. 2009;38(4):321–7.
Reddihough D, Erasmus CE, Johnson H, McKellar GMW,
Jongerius PH. Botulinum toxin assessment, intervention and
aftercare for paediatric and adult drooling: international consen-
sus statement. Eur J Neurol. 2010;17(SUPPL. 2):109–21. https://
doi.org/10.1111/j.1468-­1331.2010.03131.x.
 515 21

The Young Dental Patient

with Systemic Disease
Aristidis Arhakis and Nikolaos Kotsanos

Contents

21.1 Neoplasms – 516

21.1.1  ental Findings and Treatment – 517
D
21.1.2 Dental Care Protocol – 518

21.2 Cardiovascular Diseases and Chemoprophylaxis – 518

21.2.1  icrobial Endocarditis and Dental Care – 519
M
21.2.2 Prevention Protocol for Dental Patients – 520

21.3 Diabetes Mellitus – 521

21.3.1 Dental Findings and Treatment – 521

21.4 Asthma – 521

21.4.1 Dental Findings and Treatment – 522

21.5 Chronic Renal Failure – 522

21.5.1 Dental Findings and Treatment – 523

21.6 Gastroesophageal Reflux Disease – 523

21.6.1 Dental Findings and Treatment – 523

21.7 Juvenile Idiopathic Arthritis – 524

21.7.1 Dental Findings and Treatment – 524

References – 524

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_21
 516 A. Arhakis and N. Kotsanos
The prevalence of the diseases in childhood has been
studied in some populations, with comparisons being dif-
ficult due to differences in defining systemic diseases or to
ages included in these estimations. In 2006 in the USA,
after clinical examination of approximately 5000 children
2–14 years old, it was found that the prevalence of obesity
and chronic health conditions (including asthma, diabe-
tes, mobility, and learning problems) was 26.6%, about
double than just 12 years ago, with the increase being
more notable in African Americans [1]. In another study
of children 0–15 years old in Southern Sweden, 8.4% suf-
fered from a chronic disease. With the exception of regu-
lar recalls and necessary health care, the disease had a
minor influence on the quality of life of 70% of them,
while 8% needed continuous assistance or had reduced
survival [2]. The mortality was however higher in socially
deprived areas with additional aggravating factors of
poor nutrition, lack of breast-feeding, and smoking.
Improvements on medicinal treatment and nursing
have contributed to a significant increase of survival of
patients with life-threatening chronic diseases. For exam-
ple, the survival of patients with leukemia and malignant
neoplasms of the brain (comprising the majority of the
child/adolescent cancer) reaches 50% until the age of 30.
The cystic fibrosis life expectancy has now exceeded
40 years, twice than what was just some decades ago.
More than 85% of children with serious systemic diseases
in industrialized countries live beyond the age of 20.
Most of the time, these children are being followed up in
clinics without hospitalization needs. Their care is often
based on medical protocols, and dentists must be alert of
the potential effects of systemic diseases on the children’s
oral health and their treatment needs. In most instances,
they ought to seek cooperation with the medical team [3].
This chapter aims to addressing the most prevalent medi-
cal conditions in childhood and how oral care should be
adapted to comply with their medical needs.
Eye Catcher
The prevention, control, and treatment of oral dis-
ease in children and adolescents with systemic disease
must include:
1. Initially, after diagnosis of the systemic disease,
referring the child for dental assessment
2. Contacting the attending physician for possible inter-
actions with general health or administered drugs
3. Evaluation of the effect of systemic disease, socio-
21 economic status, available care, and local possibly
aggravating factors like saliva and function of
oral structures on caries, periodontal, and other
oral risks
4. Oral hygiene implementation and the overcoming
of possible difficulties, use of pharmaceutical
adjuncts like chlorhexidine, sealant placement,
and diet instructions (considering the systemic
disease)
5. Regular recalls for motivation on oral care and its
evaluation, reassessment of saliva flow rate, car-
ies, and periodontal disease
21.1 Neoplasms
Less than 1% of total cancer cases appear in childhood.
It is estimated that 1 in 285 children will be diagnosed
with cancer before age 20 years. The most frequent
malignancies in childhood affect blood, followed by
tumors of the brain, lymphomas, neuroblastomas (most
common in infants), Wilms tumors (nephroblastoma),
osteosarcomas (including Ewing’s), and sarcomas of
soft tissues (rhabdomyosarcomas). Factors that are
most likely involved in child carcinogenicity are radia-
tion (ionizing and non-ionizing) and infections (in the
child, mother, and environment). Acute lymphoblastic
leukemia is the most frequent malignancy (30%), mani-
festing mostly at ages of 2–5 years. The survival rate has
dramatically improved and is now 85% in the industrial-
ized world, with prognosis being poorer in infants and
young adults [4, 5].
Treatment of acute lymphoblastic leukemia nor-
mally takes 2–2.5 years, consisting of three phases:
induction (or remission induction), consolidation
(intensification), and maintenance. The first aims at the
elimination of leukemic blast cells from blood and bone
marrow, restoring normal hematopoiesis in 96–99% of
children. The second phase takes somewhat less in
strengthening the first one, while the third phase lasts for
at least 2 years maintaining the result. The medicines
usually used are glucocorticoids (prednisone, dexameth-
asone), methotrexate, vincristine, mercaptopurine, and
asparaginase. Most of them were developed before 1970.
However, dosages and timetable combinations in che-
motherapy have been optimized resulting in the current
high survival rate. Transplantation of progenitor cells
(bone marrow) is another option.
Osteosarcomas are surgically treated. Ewing’s sarco-
mas are treated with combination of surgical therapy,
radiotherapy, and chemotherapy for a period of
1–2 years. Basal cell carcinomas are treated either surgi-
cally or with radiotherapy. Relatively little progress has
been made in the treatment of tumors of the brain and
neuroblastomas. Neurosurgery remains the main sup-
portive treatment, accompanied by radiotherapy.
The Young Dental Patient with Systemic Disease
21.1.1 Dental Findings and Treatment
In the most acute lymphoblastic leukemia cases, clinical
signs in the mouth are painful ulcerations in the mucous
membranes and automatic or evoked gum bleeding. The
white blood cells in the peripheral blood are increased
(often >100,000/ml), although in a few cases, they may
be within normal limits or decreased (under- or non-­ Mucositis, ulcerations, and infections Mucositis of the
leukemic forms).
Eye Catcher
Both radiotherapy and chemotherapy cause serious
oral complications in children at a greater frequency
than in adults [6]. The chemotherapeutic drugs and
radiotherapy target cells with high mitotic activity,
which is high also in normal cells of children in com-
parison to adults. The levels of leukocytes are affected
and fall 5–7 days after each cycle of chemotherapy,
lasting for 14–21 days. A few days after the leukocyte
number recovery, the next cycle of chemotherapy
could follow.
Chemotherapeutics affect drastically the renewal
of the cells of the oral epithelium and may cause
problems such as ulcers (71%), lip lacerations (38%),
dry mouth (11%), mucositis (9%), lymphadenopathy
(7%), candidiasis (4%), and other infections (4%) [7].
In some cases, disturbances appear in the craniofacial
development or the formation of the teeth.
Dry mouth Dry mouth, caused by radiotherapy due to
dramatic decrease of saliva production from the salivary
glands, increases the likelihood of infections in the mouth
and affects speech, chewing, and swallowing. Dry mouth
is accompanied by a feeling of burning tongue and thirst.
For children these symptoms are usually temporary, either
..      Fig. 21.1 a, b Commercial a b
preparations as saliva substitutes
to reduce the dry mouth
sensation. c Chewing gum with
xylitol
517 21
due to less radiation dose or due to greater regenerative
capacity of their salivary glands. The use of substitutes
for saliva, soda or 50% glycerol solution in water with
added drops of lemon juice, reduce the feeling of dry
mouth [8]. Sugar-free chewing gums with xylitol contrib-
ute to activation of salivary glands (. Fig. 21.1).
mouth and throat appears in 50–80% of children under-
going cancer therapy (. Fig. 21.2). Symptoms are felt by
the first week of radiotherapy or chemotherapy and
retract after the end. Mouth rinsing four to five times a
day with a 3% H2O2 or soda solution relieves mild muco-
sitis symptoms. In more severe forms, anti-inflammatory
and anesthetic preparations are used. There is also encour-
aging evidence supporting that low-­level laser irradiation
therapy reduces significantly the duration of the mucositis
caused by chemotherapy [9].
Oral infections from fungi, viruses, and bacteria are
the result of immunosuppression, dry mouth, and/or
mucous membrane lesions. The most common infection
is candidiasis (thrush), for which the antifungal drugs
nystatin, miconazole, etc., are administered. For the
healing of ulcers, topical application of iodine solution
or cetylpyridinium chloride three to four times daily
gives satisfactory results. Younger patients undergoing
antineoplastic treatment are more prone to infections
associated with the herpes virus. The infection can be
localized (cold sores) or display severe herpetic gingivo-
stomatitis (see 7 Chap. 20). The severity of the infection
depends on the size of immunosuppression.
Dysgeusia and eating disorders Dysgeusia (foul taste)
can be a lasting symptom in young patients undergoing
chemotherapy or radiotherapy and affects especially the
taste of bitter and acidic, while that of salt and sweet is
not seriously affected. It can be treated by the administra-
tion of zinc sulfate during meals. These changes are due to
c
 518 A. Arhakis and N. Kotsanos
a 21.1.2
b the antineoplastic therapy, dental infections should at
..      Fig. 21.2 a An improved stage of mucositis following chemother-
apy of a patient with leukemia at ages 4 and 6 years. b His panoramic
radiograph at age 14 years shows several teeth with short roots
swelling of the taste buds, becoming normal 6–12 months
after therapy [10]. Eating disorders are associated with the
disease itself, while anorexia may be related to complica-
tions of antineoplastic therapy such as mucositis, dry
mouth, and loss of taste or nausea.
Abnormalities of teeth and jaws Children being at the
growth period are subject to developmental abnormali-
ties. These may be related to dental and/or skeletal devel-
opment, like maxillary or mandibular hypoplasia or
dental root growth (short roots, early root completion)
(. Fig. 21.2), oligodontia, enamel hypoplasia, and dis-
turbance of tooth eruption time, all dependent on the
radiotherapy or chemotherapy time and duration [10].
Neurotoxicity Neurotoxicity is a side effect resulting
from certain types of chemotherapy drugs such as alka-
loids and vincristine. The resulting facial pain is continu-
ous and dull but may be reported by the young patient as
toothache. Usually the symptoms subside a week after the
end of chemotherapy [11].
Rampant caries Particularly, in those patients undergo-
ing head and neck radiation therapy, there is the risk of
a rampant form of dental caries within months after
21 therapy, as a result of a combination of dry mouth and
negligence of undertaking preventive measures, i.e., very
good oral hygiene and use of fluoride (. Fig. 21.3).
Extractions and minor surgical interventions can be
done under prophylactic antibiotic chemotherapy with-
out fear of necrosis or infection, if they are least trau-
matic [6, 11].
Dental Care Protocol
Before starting antineoplastic therapy, it is very important
for minimizing oral complications to begin with prophy-
laxis and care of the existing dental needs. This includes
adopting the right dietary habits and brushing with a soft
toothbrush and fluoridated toothpaste. Complementary
use of fluorides (described in 7 Chap. 12) may be required
for children at high caries risk, with dry mouth, and those
undergoing head and neck radiation [6]. When there is no
time for complete dental rehabilitation before the start of
least be removed, e.g., by extractions and periodontal
therapy, because they can lead to systemic infections when
the patient will become immunocompromised [12]. In pri-
mary teeth, extraction is a safer treatment option to end-
odontic treatment, while in permanent dentition, the latter
is acceptable if it could be completed and allow at least a
week for assessing a successful outcome [7]. Tooth extrac-
tions, after platelet and blood neutrophil counts, can be
performed at least 10 days beforehand, to allow time for
wound healing. Fixed orthodontic appliances are removed
if patient do not apply adequate oral hygiene or if there is
a severe mucositis.
During antineoplastic therapy toothbrushing is regu-
larly performed despite the reduction of platelets [6], if
necessary with extra soft toothbrush respecting the sensi-
tive soft tissues. Dental treatment is done only in emer-
gency situations, in cooperation with attending physician
[7, 12]. After the end of antineoplastic therapy, any unfin-
ished dental treatment could be completed and a recall
program followed, as in healthy children. In those suffer-
ing from severe mucositis, the remaining mucosal lesion is
taken care of and examined histologically if needed.
Compliance in preventive program is often poor because
of both children and parents’ fatigue, after a long demand-
ing process of therapy. Burnout by cancer treatment is
usually greater by adolescents than children [13].
21.2 Cardiovascular Diseases
and Chemoprophylaxis
Heart diseases in infants and children are among the
most frequent chronic diseases of childhood and are
divided into congenital and acquired forms. Congenital
heart diseases, owed to malformation of the heart and/
or large vessels, have a prevalence of five to eight cases
per 1000 live births. The time of occurrence and the
severity vary. Almost half of them are diagnosed in the
first year of life, while others may remain undetected for
years. Cardiomyopathies and some types of arrhythmias
usually coexist with other congenital anomalies of the
heart or occur as a complication of the surgical correc-
The Young Dental Patient with Systemic Disease
a b
c d
e f
..      Fig. 21.3 a, b Dental treatment needs of a 4-year-old boy with
acute lymphoblastic leukemia. All needs were met before chemother-
apy. c New caries in primary molars and burnout neglect of oral
hygiene following a 3-year miss of recalls. d Extensive hypomineral-
tion. Acquired heart diseases are rare in infancy. These
include endocarditis, myocarditis, Kawasaki disease,
pericarditis, and acquired arrhythmia. Some of these
can be fatal or lead to disabilities.
21.2.1 Microbial Endocarditis
and Dental Care
Endocardial microbial infection is characterized by for-
mation of shoots, mainly in heart valves, and has a high
mortality rate if not treated promptly (. Fig. 21.4).
Chemoprophylaxis recommendations along with the
views on morbidity causes for bacterial endocarditis
have undergone many changes over time. Theoretical
risk prevalence is very low (1:150,000 for adults at high
risk who received chemoprophylaxis and three times
higher for those who did not) [14].
519 21
ization of permanent incisors, visible after new supervised oral
hygiene. e Juice-drinking abuse and bruxism have contributed to
additional erosive wear. f The 18-month recall shows arrest of caries
lesions as a result of the reinstituted preventive program
A small number of incidents have been directly
correlated with previous dental treatment [15]. Micro-
organisms – especially virulent streptococci – cause
endocarditis typically associated with the normal flora
of the mouth. Colonization occurs at irregularities of
cardiovascular endothelium due to anatomical defects,
disease, or foreign body. The real cause is considered
to be consecutive bacteremia episodes and not isolated
incidents, e.g., tooth extraction or the placement of rub-
ber dam and matrix with wedge [16]. Thus, the most
important bacterial endocarditis prevention measure
in high-risk individuals is daily oral hygiene, since the
extent of bacteremia (the number of bacteria entering
the blood flow) is related to the severity and extent of
the already existing gingivitis [17]. Preventing bacterial
endocarditis is not only by chemoprevention, but is sup-
ported by the treatment of any infection that could lead
to bacteremia [14].
 520 A. Arhakis and N. Kotsanos
..      Fig. 21.4 A schematic
representation of a longitudinal
heart section with possible sites
of bacterial endocarditis vegeta-
tions
21.2.2  revention Protocol for Dental
P >>Important
Patients
The protocol adopted by the European Academy of
Paediatric Dentistry for the prevention of bacterial
endocarditis in children with an increased risk is as fol-
lows: amoxicillin, 50 mg/kg body weight (maximum
dose of 2 gr) as a single dose per os 1 hour before dental
surgery. In case of allergy to penicillin, clindamycin is
selected, 20 mg/kg body weight (maximum dose of
600 mg). In case of intramuscular or intravenous admin-
istration, the above is proposed to be done, half an hour
before the dental treatment: ampicillin 50 mg/kg body
weight (maximum dose of 2 gr). In case of allergy to
penicillin, clindamycin is administered, 15 mg/kg body
weight (maximum dose of 600 mg) [15].
>>Important
Patients proposed to take chemoprophylaxis are classified into
two groups
High risk. Patients with a history of bacterial endocarditis,
congenital cyanotic heart diseases (e.g., transposition of the
great vessels, tetralogy of Fallot), and iatrogenic arteriovenous
communications in systemic or pulmonary circulation. Patients
with cardiac implants who develop cardiac valvular diseases.
21 Congenital heart defects, which are fully treated, surgically or
using a catheter, requiring antibiotic coverage in the first
6 months after surgery.
Medium risk. Patients with congenital heart defects, acquired
valve dysfunction, hypertrophic cardiomyopathy, mitral valve
prolapse with valvular regurgitation, and/or thickening of the
leaflets.
Dental treatments for which chemoprophylaxis is proposed
• Tooth extraction or any other surgical procedure
• Periodontal treatment, root scaling, and pocket depth
measurement
• Implant placement or avulsed tooth re-implantation
• Chemo-mechanical root canal preparation, if exceeding
root apex
• Subgingival placement of antimicrobial fibers or films
• Orthodontic band placement
• Intraligamentary local anesthesia
• Scaling and tooth or peri-implant prophylaxis
Studies have shown that, in children who had recently
received chemotherapy (antibiotics), colonization of
strains resistant to the antibiotic administered was
more frequent [18]. The British Society for Antimicro-
bial Chemotherapy proposes revision of the current
protocol, by administering preventive chemoprophy-
laxis only in high-risk patients for endocarditis as well
as in those with high mortality risk when ill. Generally,
there is a worldwide debate and frequent revisions on
chemoprophylaxis necessity for various patient catego-
ries. For patients who require multiple appointments
for dental treatment, an interval of at least 14 days
between sessions is proposed, in order to reduce the
risk of developing resistant strains of the administered
antimicrobial for chemoprophylaxis. Furthermore,
mouthwash with chlorhexidine 0.2% solution for
1 minute prior to dental treatment, if possible, is pro-
posed.
The Young Dental Patient with Systemic Disease
521 21
21.3 Diabetes Mellitus Eye Catcher

Diabetes is characterized by elevated blood sugar levels
due to reduced production of insulin by the beta cells of
the islets of Langerhans in the pancreas. Diabetes is
divided in type I (insulin-dependent or teenage) and type
II (non-insulin-dependent or adult) form. The incidence
of diabetes is low in infants, increases in school age chil-
dren, and reaches the rate of 1:500 among children at the
age of 17, in Europe. Diagnosis is made by medical his-
tory, clinical presentation, and laboratory urine and
blood tests. Originally, a child suffering from this disease
has symptoms such as polyuria, polydipsia, drowsiness,
anorexia, weight loss, and constipation. Regarding the
treatment, monitoring blood sugar is needed as well as
suitable diet and daily insulin administration. Three
meals and two to three sugar-free between-meal snacks,
low fat and rich in fiber, are required [19, 20].
21.4
Diabetes’ implications on a young patient could be:
1. Hypoglycemic coma: Chills and cold skin, fast
pulse, stress, confusion, convulsions, and coma. If
the patient retains his/her senses, sugar or honey
through the mouth must be given. The patient
recovers usually within 5–10 minutes. If they lost
their senses, 1 mg of glycogen intramuscularly or
10–20 ml 20–50% dextrose is intravenously
injected [19].
2. Hyperglycemic coma: (Due to lack of insulin) dry
mouth and skin, fast and weak pulse, low blood
pressure, and tendency to vomit. Immediate intra-
venous administration of fluids (bicarbonate salt
8.4%) and direct communication with the physi-
cian or hospital for insulin are required [19].
Asthma

21.3.1 Dental Findings and Treatment Asthma is a chronic inflammatory condition of the air-
ways, characterized by recurrent episodes of wheezing,
Flow rate of saliva in diabetic children is reduced due to breathlessness, retrosternal (back of chest) dull pain,
the dehydration associated with polyuria, but caries and coughing, particularly at night and early morning
index is not affected, probably due to low frequency of [23]. More severe bronchial obstruction leads to diffi-
carbohydrate intake. Only in uncontrolled diabetes and culty in breathing and tachycardia [24]. Asthma is a het-
erogeneous disease, especially in early childhood, and is
uncontrolled diet a child can be considered as high car-
caused both by endogenous and environmental factors.
ies risk [19]. More correlation has been established
The most common of the latter is exposure to allergens,
between diabetes and periodontal disease, especially in
infections, and airway exposure to nonspecific stimuli
adults. The longer the diabetes history, the more serious such as cigarette smoke. Activity at low temperatures
are the periodontal problems, particularly in non-­ causes symptoms in 80% of children with asthma. The
insulin-­dependent diabetes and uncontrolled one [21]. emotional state and stress may also trigger an asthma
When blood glucose is elevated, increased amounts of attack [25].
glucose are found in the saliva and gingival fluid.
The best time for dental treatment is during morning
Eye Catcher
hours, when blood sugar is stable. Before treatment the
dentist is necessary to consult the pediatrician for the Asthma affects 5–10% of children. Depending on the
patient’s dosage, and frequency of insulin administra- frequency and intensity of symptoms and the need for
tion, diet, blood glucose level, and any other problem medication, it is classified into four categories: mild,
may coexist. Low resistance of diabetic children to moderate, severe, and very severe. Three quarters
infections has to be always in mind. Orofacial infections belong to the mild category with little daily episodes
must be treated immediately as they can trigger the or short-term crises [26]. The majority (60%) of chil-
appearance of ketosis. Conducting ordinary dental dren with asthma show no symptoms until the age of
treatment and minor surgical procedures under local 6 years.
anesthesia does not require special precautions. In more
extensive surgical procedures, special attention has to be Medicinal treatment of chronic asthma in children
given to avoid hypoglycemia, in order to prevent a pos- includes two main groups of drugs, bronchodilators,
sible delay in healing because of impaired phagocytosis. and anti-inflammatory. Mild asthma is usually treated
Adrenaline contained in local anesthetics does not by inhaling beta-2 agonists alone, usually every
increase the blood glucose levels [22]. 4–6 hours. In patients with moderate asthma, anti-­
 522 A. Arhakis and N. Kotsanos
a b
c d
..      Fig. 21.5 a Fixed-dose inhalation apparatus for asthma. b In
very young children, it is used with chamber and mask covering both
the mouth and nose. c, d MIH-type mild and severe molar hypomin-
eralization of MIH appearance, respectively, in a young boy with
asthma. (Courtesy Dr. G. Vadiakas)
inflammatory drugs are sometimes given proactively,
but not for treating an acute episode [27, 28]. Inhaled
steroids administered per os two times a day provide
good control. In acute severe asthma, the usual treat-
ment is a short-acting beta-2 antagonist [27, 28]. The lat-
ter is applied by a nebulizer or fixed-dose device in a
hospital (. Fig. 21.5). Systemic administration of cor-
ticosteroids is also proposed [28].
21.4.1 Dental Findings and Treatment
Although there is no general agreement, caries indices
seem to increase with the severity of asthma and while the
patient is under medication [29]. The presence of ferment-
able carbohydrates, such as lactose, to ensure a more toler-
able taste of the inhaled medications may be responsible. It
is reported that up to 80% of inhaled medication stays in
the mucosa remaining in the oral cavity. In children with
asthma, increased dental erosion was observed. This was
ascribed to more frequent carbonated and/or low pH fluid
intake – according to preference styles of adolescents – due
21 to dry mouth sensation caused by commonly observed
oral breathing [30]. Some reduction in the flow rate of
saliva is expected from the activity of beta-2 blockers, and
more plaque and gingivitis have been found [31]. Increased
calculus is observed, possibly related to high calcium and
phosphate levels in the saliva secreted by the submandibu-
lar salivary and parotid glands [29, 30].
The respiratory function of the patient may improve
if the dental chair is placed in a less inclined position. It
is appropriate to use a rubber dam and high-volume
suction for minimizing aerosols. Dental visits should be
as short as possible to prevent the child feeling fatigue.
Aspirin and other non-steroidal anti-inflammatory
medications are to be avoided [27]. Erythromycin
should not be administered in patients receiving the-
ophylline, because the former interferes in the metabo-
lism of the latter, thereby increasing blood theophylline
to possibly toxic levels. Inhalation sedation with N2O/
O2 for dental treatment can be helpful, as it does not
irritate the lung epithelium and may prevent asthmatic
attacks [32]. In the event of an asthmatic attack, dental
treatment is discontinued; the patient is placed in a
comfortable position, sitting or standing, and an inhaled
beta-2 blockers is administered directly. If there is no
improvement, the patient is given corticosteroids and
epinephrine subcutaneously at a dose of 0.01 mg/kg of
a 1:1000 (maximum dose 0.3 mg), while medical assis-
tance is sought [33].
21.5 Chronic Renal Failure
Chronic renal failure is progressive bilateral destruction
of nephron function, which results in the kidneys being
unable to maintain the internal environment balance for
which they are responsible [34]. Before the age of 5, the
disease is caused by genetic abnormalities in the kidneys,
such as hypoplasia, and in the urinary tract, manifested
by vesicoureteral reflux. At age 5–15 years, the disease is
usually caused by lesions of the glomeruli (e.g., glomer-
ulonephritis) or hereditary kidney diseases (cystic fibro-
sis, nephrotic syndrome). The degree of dysfunction of
the kidneys determines the symptoms the child exhibits.
Initially it complains of malaise, headache, vomiting,
anorexia, polyuria, and polydipsia. Later there is a pro-
gressive disorder of electrolytes and dehydration after
metabolic acidosis, increased pressure, heart failure, and
uremia. Younger patients suffering from the disease
have some physical growth retardation and muscular
weakness, while their skin color is pale with a brown hue
[34]. It is ranked the fourth most serious illness in the
USA, with attack frequency of urinary tract infection at
1% for boys and 3% in girls before the age of 10 years.
Diagnosis is made by medical history, clinical examina-
tion, and laboratory tests. Depending on the severity of
the disease and the stage of development, the treatment
is divided into three categories: conservative treatment,
dialysis, and kidney transplantation [35].
The Young Dental Patient with Systemic Disease
21.5.1 Dental Findings and Treatment
The oral manifestations of the disease depend on the
age at which the disease occurs, the duration, severity,
and the cause. Changes are observed in both the soft
and the hard tissues. One of the most important findings
in the soft tissue is pale mucosa from anemia which is
due to decreased secretion of erythropoietin by the kid-
ney [36]. Intraoral hematomas and ecchymosis and mild
coagulation problems are due to the sensitivity of the
walls of the capillaries and the reduced energy of the
plasma II agent.
Dental Findings at Chronic Renal Failure
The teeth and bones of the jaws are affected when
kidney failure occurs during tooth formation/min-
eralization (chronologic enamel hypoplasia/hypo-
mineralization) or in critical periods of bone
growth, possibly leading to orthodontic anomalies
[37]. The uremia affects the bone remodeling caus-
ing disappearance of lamina dura and creating bone
lesions which histologically resemble giant cell
tumors, as in hyperparathyroidism [36]. Despite the
disappearance of the lamina dura, if there are no
other bone lesions, mobility of the teeth is not usu-
ally observed. Discolored teeth have been reported
from deposition of blood pigments due to uremia or
by prolonged use of tetracyclines [38]. Reduced den-
tal caries and increased deposition of calculus are
also reported [39].
Dental treatment varies depending on the child’s medi-
cal condition and its treatment phase. Routine dental
treatment should be avoided when the serum urea nitro-
gen is >60 mg/dl and the rate of creatinine is >1.5 mg/dl.
Arterial blood pressure and hemorrhagic tendency of
the patient should be monitored. Aspirin should be
avoided, and the responsible physician contacted before
administering any medication, because of the limited
ability of the kidneys to metabolize and excrete it.
Antibiotics are not considered necessary, unless there is
active inflammation. If herpetic gingivostomatitis
occurs in very young children, total liquid intake is mon-
itored to ensure electrolyte balance [40].
A child who is receiving hemodialysis needs some
extra precautions. Before any dental restoration is
undertaken in patients with surgically inserted artificial
anastomosis, chemoprophylaxis is necessary. The hand
or foot on which the anastomosis is mounted should
not be used to administer drugs and be free to move for
preventing blood clotting. Many of these children are
taking anticoagulants (coumarin) to prevent blood
523 21
clots. Their administration should be stopped 48 hours,
in order for normal hemostasis to be achieved if hem-
orrhagic dental procedures are anticipated [41]. The
number of transfusions these children undergo because
of blood loss classifies them at high risk for hepatitis.
The dentist should therefore take the necessary precau-
tions.
For a patient who has had a kidney transplant, fur-
ther precautions are needed, because of taking cortico-
steroids and immunosuppressants to prevent foreign
body expulsion. One of the side effects of these drugs
is that they cover the symptoms of inflammation so
that infections become a frequent cause of death in
these patients. Therefore, it is vital to communicate
with the attending physician for antibiotic coverage
before any dental procedure, for minimizing inflamma-
tion chances [37].
21.6 Gastroesophageal Reflux Disease
Gastroesophageal reflux disease (GERD) is the entrance
of gastric or intestinal contents into the esophagus with
or without vomiting [42, 43]. About 7–8% of infants and
toddlers manifest daily episodes of GERD of short
duration (<3 minutes), especially after meals and at bed-
time, with no or minimal symptoms [44]. A low degree
of reflux with no other symptoms is observed in normal
neonates, especially preterm, and up to 7–week-old
infants due to immaturity of the lower esophageal
sphincter [45]. In cases of very intense reflux, blood tests
and urine tests should be carried out to rule out other
causes such as gastroenteritis or pylorostenosis [46]. In
children and adults, drugs are administered to increase
the base pressure of the lower esophageal sphincter
(metoclopramide, domperidone) and antacids to neu-
tralize stomach acid [47]. Surgical treatment for children
is reported in cases of failure of medical treatment, per-
sistent vomiting, stenosis, recurrent pneumonia, and
life-threatening complications, such as respiratory arrest
[48].
21.6.1 Dental Findings and Treatment
Dental findings relate to erosion of the teeth by stomach
hydrochloric acid regurgitation, and, together with their
prevention and treatment, they are described in the rel-
evant 7 Chap. 18. However, findings in children with
GERD are not as frequent as one would expect, as only
a limited percentage (14–17%) of them exhibit erosive
tooth wear [49, 50]. This is possibly because other fac-
tors are involved in the association between GERD and
dental erosion.
 524 A. Arhakis and N. Kotsanos
a b c event of general anesthesia, patients may have problems
..      Fig. 21.6 a, b Face image and postero-anterior cephalometric
radiograph of a 12-year-old girl with juvenile idiopathic arthritis
(JIA) showing the asymmetric development of the mandible. c Seri-
ous degenerative changes of the condyle and temporal trench (arrow)
of an 11-year-old boy with JIA. (Courtesy Dr. S. Sidiropoulou)
21.7 Juvenile Idiopathic Arthritis
Juvenile idiopathic arthritis (JIA, formerly juvenile
rheumatoid arthritis, or Still’s disease) is a chronic
inflammatory arthritis that occurs before the age of
16 years. The prevalence is about 1–2:10,000, but there
are differences in the geographical distribution.
Pathogenesis is linked to autoimmune and genetic fac-
tors, while there may be hormonal and infectious in
addition to other environmental factors. Patients with
JIA exhibit fever, skin rash, and lymphedema. JIA
types are defined by the number of joints affected.
The joint has a raised temperature and is usually swol-
len, sensitive to touch, and painful to move, charac-
terizing a chronic, non-­purulent inflammation [51].
Prescribing non-­ steroidal anti-inflammatory drugs
such as acetylsalicylic acid (aspirin) is the treatment
of choice, offered by pediatric rheumatologists. In
case these prove inefficient, sulfasalazine or drugs
with immunosuppressive action such as steroids and
azathioprine are used. Prolonged use of corticoste-
roids may result in growth retardation; thus, they can
be injected intra-articularly. The patient should do
daily exercise, e.g., swimming, and use splints for sup-
port to prevent joint deformities [52].
21.7.1 Dental Findings and Treatment
In 20% of patients with multi-joint type JIA, the tem-
poromandibular joint (TMJ) is also affected.
Radiographically, a flattening of the mandible head is
observed, while in 10% of cases, there is contralateral
surface hardening of the mandible which significantly
affects the growth morphology of the child’s face with
JIA (. Fig. 21.6). These changes affect the growth of the
21 craniofacial system and the functioning of the mandible,
limiting its movement. The mandible of children with
JIA is smaller and retrognathic, and early o ­ rthodontic
treatment can help the condyle discharge at exacerbated
disease episodes [53]. Oral hygiene is particularly impor-
tant as children prefer medication in syrup form. In the
due to restricted chest movements [54].
References
  1. Van Cleave J, Gortmaker SL, Perrin JM. Dynamics of obesity
and chronic health conditions among children and youth.
JAMA. 2010;303:623–30. https://doi.org/10.1001/jama.2010.104.
 2. Westbom L, Kornfält R. Chronic illness among children in a
total population. An epidemiological study in a Swedish primary
health care district. Scand J Soc Med. 1987;15:87–97.
  3. Compas BE, Jaser SS, Dunn MJ, Rodriguez EM. Coping with
chronic illness in childhood and adolescence. Annu Rev Clin
Psychol. 2012;8:455–80. https://doi.org/10.1146/annurev-­
clinpsy-­032511-­143108.
  4. Ward E, DeSantis C, Robbins A, Kohler B, Jemal A. Childhood
and adolescent cancer statistics, 2014. CA Cancer J Clin.
2014;64:83–103. https://doi.org/10.3322/caac.21219.
  5. Pui CH, Mullighan CG, Evans WE, Relling MV. Pediatric acute
lymphoblastic leukemia: where are we going and how do we get
there? Blood. 2012;120:1165–74. https://doi.org/10.1182/blood-­
2012-­05-­378943.
  6. Levi LE, Lalla RV. Dental treatment planning for the patient
with oral cancer. Dent Clin N Am. 2018;62:121–30. https://doi.
org/10.1016/j.cden.2017.08.009.
 7. Barbería E, Hernandez C, Miralles V, Maroto M. Paediatric
patients receiving oncology therapy: review of the literature and
oral management guidelines. Eur J Paediatr Dent. 2008;9:188–
94.
  8. Ray-Chaudhuri A, Shah K, Porter RJ. The oral management of
patients who have received radiotherapy to the head and neck
region. Br Dent J. 2013;214:387–93. https://doi.org/10.1038/sj.
bdj.2013.380.
 9. Migliorati C, Hewson I, Lalla RV, Antunes HS, Estilo CL,
Hodgson B, et al. Systematic review of laser and other light ther-
apy for the management of oral mucositis in cancer patients.
Support Care Cancer. 2013;21:333–41. https://doi.org/10.1007/
s00520-­012-­1605-­6.
10. Epstein JB, Barasch A. Oral and dental health in head and neck
Cancer patients. Cancer Treat Res. 2018;174:43–57. https://doi.
org/10.1007/978-­3-­319-­65421-­8_4.
11. Hong CH, Napeñas JJ, Hodgson BD, Stokman MA, Mathers-
Stauffer V, Elting LS, et al. A systematic review of dental disease
in patients undergoing cancer therapy. Support Care Cancer.
2010;18:1007–21. https://doi.org/10.1007/s00520-­010-­0873-­2.
12. AAPD. Guideline on dental management of pediatric patients
receiving chemotherapy, hematopoietic cell transplantation,
and/or radiation. Pediatr Dent. 2016;38:334–42.
13. Hockenberry-Eaton M, Hinds PS. Fatigue in children and ado-
lescents with cancer: evolution of a program of study. Semin
Oncol Nurs. 2000;16:261–72. discussion 272-8
14. Duval X, Alla F, Hoen B, Danielou F, Larrieu S, Delahaye F,
et al. Estimated risk of endocarditis in adults with predisposing
cardiac conditions undergoing dental procedures with or with-
out antibiotic prophylaxis. Clin Infect Dis. 2006;42:e102–7.
https://doi.org/10.1086/504385.
15. Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM,
Levison M, et al. Prevention of infective endocarditis: guidelines
from the American Heart Association: a guideline from the
American Heart Association Rheumatic Fever, Endocarditis
and Kawasaki Disease Committee, Council on Cardiovascular
Disease in the Young, and the Council on Clinical Cardiology,
Council on Cardiovascular Surgery and Anesthesia, and the
The Young Dental Patient with Systemic Disease
Quality of Care and Outcomes Research Interdisciplinary Work-
ing Group. J Am Dent Assoc. 2007;138:739–45, 747–60. https://
doi.org/10.1161/CIRCULATIONAHA.106.183095.
16. Roberts GJ, Jaffray EC, Spratt DA, Petrie A, Greville C, Wilson
M, et al. Duration, prevalence and intensity of bacteraemia after
dental extractions in children. Heart. 2006;92:1274–7. https://
doi.org/10.1136/hrt.2004.046581.
17. Forner L, Larsen T, Kilian M, Holmstrup P. Incidence of bacte-
remia after chewing, tooth brushing and scaling in individuals
with periodontal inflammation. J Clin Periodontol. 2006;33:401–
7. https://doi.org/10.1111/j.1600-­051X.2006.00924.x.
18. Prendergast BD. The changing face of infective endocarditis.
Heart. 2006;92:879–85. https://doi.org/10.1136/hrt.2005.067256.
19. Lamster IB, Lalla E, Borgnakke WS, Taylor GW. The relation-
ship between oral health and diabetes mellitus. J Am Dent
Assoc. 2008;139:19S–24S.
20. Pinhas-Hamiel O, Zeitler P. The global spread of type 2 diabetes
mellitus in children and adolescents. J Pediatr. 2005;146:693–
700. https://doi.org/10.1016/j.jpeds.2004.12.042.
21. Chapple IL, Genco R. Diabetes and periodontal diseases: con-
sensus report of the Joint EFP/AAP Workshop on Periodontitis
and Systemic Diseases. J Periodontol. 2013;84:S106–12. https://
doi.org/10.1902/jop.2013.1340011.
22. Siudikiene J, Machiulskiene V, Nyvad B, Tenovuo J, Nedzel-
skiene I. Dental caries and salivary status in children with type 1
diabetes mellitus, related to the metabolic control of the disease.
Eur J Oral Sci. 2006;114:8–14. https://doi.
org/10.1111/j.1600-­0722.2006.00277.x.
23. Widmer RP. Oral health of children with respiratory diseases.
Paediatr Respir Rev. 2010;11:226–32. https://doi.org/10.1016/j.
prrv.2010.07.006.
24. Maupomé G, Shulman JD, Medina-Solis CE, Ladeinde O. Is
there a relationship between asthma and dental caries? A critical
review of the literature. J Am Dent Assoc. 2010;141:
1061–74.
25. Bateman ED, Hurd SS, Barnes PJ, Bousquet J, Drazen JM,
FitzGerald JM, et al. Global strategy for asthma management
and prevention: GINA executive summary. Eur Respir J.
2008;31:143–78. https://doi.org/10.1183/09031936.00138707.
26. Thomas M, Kay S, Pike J, Williams A, Rosenzweig JR, Hillyer
EV, et al. The Asthma Control Test (ACT) as a predictor of
GINA guideline-defined asthma control: analysis of a multina-
tional cross-sectional survey. Prim Care Respir J. 2009;18:41–9.
https://doi.org/10.4104/pcrj.2009.00010.
27. Zhu JF, Hidalgo HA, Holmgreen WC, Redding SW, Hu J, Henry
RJ. Dental management of children with asthma. Pediatr Dent.
1996;18:363–70.
28. Boothe DM. Drugs affecting the respiratory system. Vet Clin
North Am Exot Anim Pract. 2000;3:371–94.
29. Thomas MS, Parolia A, Kundabala M, Vikram M. Asthma and
oral health: a review. Aust Dent J. 2010;55:128–33. https://doi.
org/10.1111/j.1834-­7819.2010.01226.x.
30. Paganini M, Dezan CC, Bichaco TR, de Andrade FB, Neto AC,
Fernandes KB. Dental caries status and salivary properties of asth-
matic children and adolescents. Int J Paediatr Dent. 2011;21:185–
91. https://doi.org/10.1111/j.1365-­263X.2010.01109.x.
31. Mehta A, Sequeira PS, Sahoo RC, Kaur G. Is bronchial asthma
a risk factor for gingival diseases? A control study. N Y State
Dent J. 2009;75:44–6.
32. Malamed SF. Sedation: a guide to patient management. Mosby:
St Louis; 1985. p. 529–30.
33. Widmer RP. Oral health of children with respiratory diseases.
Paediatr Respir Rev. 2010;11:226–32. https://doi.org/10.1016/j.
prrv.2010.07.006.
34. Vogt BA, Avner ED. Chronic Renal Disease. In: Kliegman RM,
Behrman RE, Jenson HB, Stanton BF, editors. Nelson Textbook
525 21
of Pediatrics. 18th ed. Philadelphia: Saunders; 2007.
p. 2210–4.
35. Van De Voorde RG, Warady BA. Management of chronic renal
disease. In: Avner ED, Harmon WE, Niauder P, Yoshikawa N, edi-
tors. Pediatric nephrology. Heidelberg: Springer; 2009.
p. 1661–92.
36. Proctor R, Kumar N, Stein A, Moles D, Porter S. Oral and den-
tal aspects of chronic renal failure. J Dent Res. 2005;84:199–208.
https://doi.org/10.1177/154405910508400301.
37. Olczak-Kowalczyk D, Gozdowski D, Pawłowska J, Grenda
R. The status of dental and jaw bones in children and adoles-
cents after kidney and liver transplantation. Ann Transplant.
2012;17:72–81.
38. Summers SA, Tilakaratne WM, Fortune F, Ashman N. Renal
disease and the mouth. Am J Med. 2007;120:568–73. https://doi.
org/10.1016/j.amjmed.2006.12.007.
39. Andrade MR, Antunes LA, Soares RM, Leão AT, Maia LC,
Primo LG. Lower dental caries prevalence associated to chronic
kidney disease: a systematic review. Pediatr Nephrol.
2014;29:771–8. https://doi.org/10.1007/s00467-­013-­
2437-­4.
40. Saif I, Adkins A, Kewley V, Woywodt A, Brookes V. Routine and
emergency management guidelines for the dental patient with renal
disease and kidney transplant. Part 1. Dent Update. 2011;38:179–
82, 185–6. https://doi.org/10.12968/denu.2011.38.3.179.
41. Saif I, Adkins A, Kewley V, Woywodt A, Brookes V. Routine and
emergency management guidelines for the dental patient with renal
disease and kidney transplant. Part 2. Dent Update. 2011;38:245–8,
250–1. https://doi.org/10.12968/denu.2011.38.4.245.
42. Michail S. Gastroesophageal reflux. Pediatr Rev. 2007;
28:101–10.
43. Guimarães EV, Marguet C, Camargos PA. Treatment of gastro-
esophageal reflux disease. J Pediatr. 2006;82:S133–45. https://
doi.org/10.2223/JPED.1555.
44. Nelson SP, Chen EH, Syniar GM, Christoffel KK. Prevalence of
symptoms of gastroesophageal reflux during childhood: a pedi-
atric practice-based survey. Pediatric Practice Research Group.
Arch Pediatr Adolesc Med. 2000;154:150–4.
45. Poets CF. Gastroesophageal reflux: a critical review of its role in
preterm infants. Pediatrics. 2004;113:e128–32.
46. Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R. Global
Consensus Group The Montreal definition and classification of
gastroesophageal reflux disease: a global evidence-based consen-
sus. Am J Gastroenterol. 2006;101:1900–20. https://doi.
org/10.1111/j.1572-­0241.2006.00630.x.
47. Ray SW, Secrest J, Ch'ien AP, Corey RS. Managing gastroesoph-
ageal reflux disease. Nurse Pract. 2002;27:36–53.
48. Sunku B, Marino RV, Sockolow R. A primary care approach to
pediatric gastroesophageal reflux. J Am Osteopath Assoc.
2000;100:S11–5.
49. Linnett V, Seow WK, Connor F, Shepherd R. Oral health of
children with gastro-esophageal reflux disease: a controlled
study. Aust Dent J. 2002;47:156–62.
50. Ersin NK, Onçağ O, Tümgör G, Aydoğdu S, Hilmioğlu S. Oral
and dental manifestations of gastroesophageal reflux disease in
children: a preliminary study. Pediatr Dent. 2006;28:279–84.
51. Weiss JE, Ilowite NT. Juvenile idiopathic arthritis. Pediatr Clin N
Am. 2005;52(2):413–42. https://doi.org/10.1016/j.pcl.2005.01.007.
52. Kahn P. Juvenile idiopathic arthritis - an update on pharmaco-
therapy. Bull NYU Hosp Jt Dis. 2011;69:264–76.
53. Sidiropoulou-Chatzigianni S, Papadopoulos MA, Kolokithas
G. Mandibular condyle lesions in children with juvenile idio-
pathic arthritis. Cleft Palate Craniofac J. 2008;45:57–62. https://
doi.org/10.1597/07-­014.1.
54. Beena JP. Juvenile idiopathic arthritis: review of the literature
and case report. J Dent Child (Chic). 2013;80:25–30.
 527 22

Disabilities, Neuropsychiatric
Disorders, and Syndromes
in Childhood and Adolescence
Nikolaos Kotsanos, Luc A. M. Marks, Konstantinos N. Arapostathis,
and Kazumi Kubota

Contents

22.1 Introductory Comments – 528

22.1.1  ccess and Design of the Dental Practice – 528
A
22.1.2 Prevalence and Preventive Care – 529
22.1.3 Difficulties for the Dental Treatment of Special Needs Patients – 529

22.2 Patients with Disabilities – 530

22.2.1  erebral Palsy and Physical Disability – 530
C
22.2.2 Cognitive Developmental Disabilities – 532
22.2.3 Sensory Disabilities – 533

22.3 Patients with Neuropsychiatric/Psychological Disorders – 534

22.3.1  utism Spectrum Disorders (ASD) – 534
A
22.3.2 Attention Deficit Disorders – 535
22.3.3 Epilepsy – 537
22.3.4 Disorders of Nutrition and Weight – 537

22.4 Diseases and Syndromes with Genetic Background – 539

22.4.1  own Syndrome – 540
D
22.4.2 Ectodermal Dysplasia – 541
22.4.3 Cystic Fibrosis – 542
22.4.4 Muscular Dystrophy – 543
22.4.5 Familial Mediterranean Fever – 544
22.4.6 Clefts – 544
22.4.7 Osteogenesis Imperfecta – 545
22.4.8 Other Syndromes and Craniofacial Anomalies – 546

References – 550

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_22
 528 N. Kotsanos et al.

22.1 Introductory Comments
This chapter is about children and young persons with
physical, sensory, intellectual, mental, medical, psycho-
logical, emotional, cognitive, or behavioral conditions
which require the use of specialized services. These con-
ditions may arise from genetic/mutation; developmental,
acquired, traumatic, and environmental causes; or any
combination. Terms such as “disabled,” “special needs”
and “mental retardation” produce different feelings to
people and bring up different images, depending on the
education, the culture, the acquired experiences, and the
society in which they live. The awareness of societies
providing access to people who are disadvantaged to the
social network has shifted the emphasis to the skills that
these people may develop, rather than their weaknesses.
Thus, the degree of functional adaptation of persons with
disability in contemporary society is determined not only
by their physical impairment but also by the supportive
adaptation of the environment and the public services.
Eye Catcher
The International Classification of Functioning, Dis-
ability and Health (ICF) of the World Health Organi-
zation (7 http://www.­who.­int/classifications), which
is an international standard for the description and
measurement of health and disability, emphasizes the
social aspects of disability and does not face it only as
“medical” or “biological” malfunction.
The International Classification of Diseases
(ICD-11 update, 7 https://www.­who.­int/classifica-
tions/icd/revision/en/) operates as a standard diagnos-
tic tool with multiple purposes, e.g., epidemiological
data, clinical treatment of diseases, etc.
new knowledge for the oral health and quality of life of
these people. Special care dentistry is concerned with “The
improvement of oral health of individuals and groups in
society who have a physical, sensory, intellectual, mental,
medical, emotional or social impairment or disability or,
more often, a combination of a number of these factors”
[2]. Dental clinicians in order to be able to meet the specific
needs of people with disabilities require adequate educa-
tion and training and a friendly accessible practice. Educa-
tion must start at the undergraduate curriculum of dental
school for providing the skills with not just theoretical but
also clinical training [1].
22.1.1  ccess and Design of the Dental
A
Practice
Access to a dental clinic should be suitably designed so
that people with disabilities do not face significant b
­ arriers
that make them feel disadvantaged [3] (. Fig. 22.1). The
following provisions should be obeyed:
55 Parking area, properly labeled
55 Access corridor with a gradient up to 1:10
55 Automatic doors and elevator spacious for wheelchairs
55 Flat-level waiting area, no carpets, and spacious
public areas, e.g., toilet
55 Easy to transfer the patient working room with pro-
visions for efficient four-handed dentistry (attention
to high suction and other dental equipment noises
for some patients)
a

The oral health of people with disabilities is often infe-

rior (depending on the disability) than in the general
population. This is not so for biological reasons, but
because usually preventive oral care of them depends
b
on education and motivation of caregivers, while restor-
ative care depends on suitable adaptation of dental care
units as well as on insurance and social welfare coverage.
Socioeconomic factors are also important, as disability
is more frequent in families with a low income. Further
influencing factors could be lower education and the
limited interest of dental practitioners [1].
However, as science progresses and societies become
more sensitive worldwide, the burden is gradually overcome,
22 and the dental needs of people with disability or chronic
disease are better met. The International Association for
Disability and Oral Health (iADH) and the corresponding
..      Fig. 22.1 a Parking space marked for a person with kinetic dis-
national societies are interested and active, disseminating abilities. b Rump access to a dental office situated above ground level
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
529 22
22.1.2 Prevalence and Preventive Care

Estimates of the prevalence of patients with special

needs depend on what levels of disability are accounted
for. A number of 100 million is reported for children
with moderate to severe disability in general with preva-
lence of 6–10% in various countries [4]. Increased fre-
quency for several types of disability and disorders is
reported for boys, poorest population groups, as well as
those with lower education [5, 6]. Single-parent families
are at a greater risk to have one or more children with
disabilities than the general population.
The improvement of medical care and access to it has
contributed to increased survival and quality of life for
those people. With regard to their oral status, patients
with special needs have generally greater rehabilitation ..      Fig. 22.2 A visit to institutionalized patients for planning to
needs than the general population. For some disabilities meet their needs
and disorders, there is a greater frequency of occlusal
anomalies and dental trauma [7, 8]. Their diet consists higher levels of stress on the dental treatment. Behavior
in some cases of soft food due to their reduced chewing management could include communication techniques,
capacity, while food may stay longer in the mouth due protective immobilization, or, in case of failure of coop-
to hypotonic muscular activity. More caries, periodontal eration, recourse to general anesthesia, particularly for
disease, large calculus deposits, and lack of treatment rehabilitation needs that require immobilization of the
are observed especially in patients living in institutions patient. As a guide, from 564 patients who went to a unit
[4, 9] (. Fig. 22.2). Education for dental hygiene must dealing with people with special needs in Brazil, about
be given both to patients as well as parents and other half were treated adequately with local anesthesia, while
people who are responsible for their care. from those sent to the operating room for general anes-
thesia, 32% had intellectual impairment, 18.5% cerebral
palsy, 10.2% Down syndrome, 16.3% other rare syn-
22.1.3 Difficulties for the Dental Treatment dromes, and 9.2% autism [10].
of Special Needs Patients
Treating these patients on the dental chair may pres- Classification Regarding the Ability of Self-Care
ent with difficulties. They often show a limited period
55 Independent. These can carry out themselves their
of concentration, and this is why working time should
daily needs with minimum supervision by persons
be short, while others suffer from muscular spastic-
of their environment.
ity making dental treatment more difficult. Depending
55 Partially dependent. These can carry out them-
on the needs and the possibility of cooperation, one
selves their daily needs after training by specially
may choose between intraoral and panoramic X-rays,
trained persons. This requires patience and perse-
although any radiographic examination is often diffi-
verance from both the instructor and the recipi-
cult. Ease of access to radiological examination should
ent.
be taken into consideration. Some clinicians prefer to
55 Fully dependent. These are people whose daily
perform dental treatment with the patient remaining on
activities are carried out by other people.
their special chair, and there is specially designed equip-
ment for that purpose. Others prefer to move the patient
from the wheelchair to the dental chair if possible main-
taining that this allows better working conditions and This chapter is structured in three sections for children
patient control (. Fig. 22.3). and young persons with disabilities, disorders, or syn-
The communicating difficulties make necessary the dromes/inherited diseases, each:
involvement of parents, which is anyway useful for tak- 55 Defining and briefly describing each condition
ing the medical history and providing informed consent. 55 Reporting the expected oral/dental findings and sug-
Anecdotally, patients with special needs usually have gesting the best possible approach and treatment
 530 N. Kotsanos et al.
a
b following terms are used:
..      Fig. 22.3 a Special wheelchair reclining base for dental work
without moving the patient. b Moving the patient in the dental chair
with caregiver’s assistance
22.2 Patients with Disabilities
22.2.1  erebral Palsy and Physical
C way into society (. Fig. 22.4). Unfortunately, there is
Disability
This is a condition relating to non-progressive dam-
age to the central nervous system (CNS = brain, spinal
cord, and cerebellum). The term cerebral palsy describes
a group of movement disorders of posture and move-
ment of the body that occur early in life and are not
amenable to cure. Some improvement may be possible
through kinesiology exercises and/or surgery. The effect
of the causative factors may be imposed while in utero,
in the perinatal period or at age 0–3 years, causing, e.g.,
decrease in oxygenation of the developing brain if occur-
ring during the perinatal period. In the majority of cases,
CNS damage occurs during intra-uterine life from viral
and bacterial infections [11]. Other frequent causes are
head injuries. Prevalence is about 2:1000, but in prema-
ture infants (of 20–27 weeks’ gestation), this figure may
22 be tenfold. Pre- or perinatal etiology diseases, like most
cerebral palsy cases, have shown a downward trend.
There are various forms of cerebral palsy: spastic
(65%), athetoid (20%), ataxic (5%), dyskinetic (5%), and
atonic (5%), although some cases may be mixed. In the
first type, muscle rigidity and stiffness are predominant,
while in the second, slow jerky movements while in the
ataxic loss of balance is manifested. In approximately
50% of cases, there is coexisting mental disability and
possibly impairment of hearing, vision, or touch, while
epilepsy is also frequent [12].
Eye Catcher
Depending on the limbs affected by cerebral palsy, the
55 Quadriplegia: affecting all four limbs
55 Diplegia: affecting one upper plus one lower limb
on the same side
55 Paraplegia: affecting both lower limbs
Cerebral palsy is a serious medical and social problem.
Unfortunately, only 25–30% of patients become socially
and professionally self-sufficient. In their particularly
difficult medical rehabilitation effort, several specialties
(pediatricians, neonatologists, pediatric neurologist,
geneticists, physiatrists, neurosurgeons, orthopedic
surgeons) and many paramedical professions (physio-
therapists, occupational therapists, physical educators,
speech therapists, psychologists, etc.) may be involved.
This includes the pediatric dentist who recognizes the
right of the patient to be integrated in the best possible
no medicinal cure. For those who also suffer from epi-
lepsy, antiepileptic drugs and perhaps muscle relaxants
are used for reducing seizures.
22.2.1.1 Dental Findings and Treatment
Big overjet with intense Angle class II molar relationship
and other malocclusions are commonly found in young
people with cerebral palsy (. Fig. 22.5). Drooling is
also a frequent finding (. Fig. 22.6), associated with a
reduced ability to maintain an upright head position and
keep the lips sealed. Increased tooth wear due to ero-
sion by GERD or to attrition by severe tooth grinding is
also very common [13]. Periodontal disease is also more
common because of plaque removal difficulties, mouth
breathing, and chronic administration of drugs with side
effects to gingivae. Inadequate caregiver’s involvement
to deliver preventive care and, in many cases, unfavor-
able dietary habits contribute to increased dental caries.
There are speech problems, while frequent tooth inju-
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
531 22
a b c

d e

..      Fig. 22.4 a An 18-year-old quadriplegic girl with intellectual treatment. d End result with having condensed laterals to replace the
impairment. b Her dental occlusion for which she (and mother) lost central incisors. Lingual retainer was maintained for 2 years. e
wished aesthetic improvement. c The dysplastic/carious ectopic max- Appearance after 12 years for scheduled regular periodontal treat-
illary central incisors were extracted, followed by fixed appliance ment. The patient has been very happy with her smile

a b c

..      Fig. 22.5 a Quadriplegic adolescent with extreme overjet and traumatic occlusion. b, c Fitting a removable Hawley appliance to reduce
overjet, while the bite plane for the lower incisors aims at raising the bite for preventing occlusal trauma

ries occur due to unstable movement and balance. There
may also be a dysfunction of the temporomandibular
joint, which is likely due to neuromuscular mechanism
imbalance. As this is frequently underestimated, evalua-
tion tools may be used for this purpose [14].
The difficulty of dealing with cerebral palsy persons
in the dental surgery puts emphasis on oral hygiene edu-
cation of the patients themselves and/or their caregivers.
This requires training and evaluation. Toothbrush han-
dles may need modification to facilitate those with lim-
ited manual dexterity (. Fig. 22.7), and the increasingly
used electric toothbrushes seem beneficial [15]. An infor-
mation session is recommended to ensure compliance
of parents and caregivers in avoiding frequent intake
of carbohydrates (cookies, etc.) as well as using patient
acceptable routes for topical fluoride use. Because swal-
lowing is very often not fully controlled, large amounts
of fluoride toothpaste should be avoided. In treating
gingivitis or periodontitis, chlorhexidine rinses or gels
can periodically be used.
In the dental surgery, control of involuntary jaw
movements is assisted by molts (. Fig. 22.7) or other
supportive devices. Pads, towels, and other means may
be suitable for comfort, avoiding placing the patient in
a perfect horizontal position if this impairs swallow-
ing. Warning of sudden movements and noises, e.g.,
high-­volume suction, helps reduce adverse reflexive
movements. Intraoral stimuli are applied slowly and
gradually to evaluate reactions – including the gag
reflex – and the use of rubber dam is necessary for
working in posterior teeth. Sealants fall well into caries
preventive strategies, while few steps and high-strength
 532 N. Kotsanos et al.
a b
..      Fig. 22.6 a An adolescent with cerebral palsy wearing bib
because of drooling. b Severe bilateral fibrous hyperplasia in the oro-
pharyngeal region significantly reduces the airway. It is possibly
related to administered antiepileptic medication
a Chronic self-mutilation of the lower lip and tongue of a teenager with
b
..      Fig. 22.7 a Improving the grip of toothbrush handle for persons
with impaired holding ability. b Molt-type metal mouth prop and
self-made acrylic block for maintaining mouth open
restorative materials are preferred to withstand
the patient’s masticatory forces, often applied with
increased intensity and ­frequency due to neuromuscu-
lar disorders and habits. Regular follow-up depends on
the patient’s risk.
Some children have a self-injurious behavior con-
tinuously biting their oral soft tissues or hands, just
as observed in Lesch-Nyhan syndrome. In these cases,
devices of various types can be employed to prevent self-­
harm [16, 17] (. Fig. 22.8).
22.2.2 Cognitive Developmental
Disabilities
22 Intellectual and developmental impairments – instead
of the outdated stigmatizing term “mental retarda-
tion” – characterizes a person of significantly lower
a b
..      Fig. 22.8 a Scarred arm with hair growth associated with sucking
and biting stimuli of a 14-year-old girl with intellectual impairment. b
Lesch-Nyhan syndrome. c Fitting of palatal plate to raise bite and
thus prevent lip trauma by anterior teeth
mental development than average [7, 9]. Categorization
of this reduced cognition ability is based on the intellec-
tual quotient (IQ). The disability manifests itself early in
childhood. There may be various syndromes, hereditary
causalities, or injuries and diseases affecting the person
either perinatally or in childhood. They can coexist with
other disorders of various systems such as cardiological,
sensory, behavioral, or psychiatric disorders, concentra-
tion deficit, restlessness, hyperactivity, epilepsy, etc [18].
It is manifested in a wide range of ways. In very mild
cases, the child may need a little support such as “reme-
dial teaching” but be able to attend a regular school,
while in severe cases, he/she may need continuous sup-
port by a caregiver.
22.2.2.1 Dental Findings and Treatment
Oral diseases are not different for children with mental
and developmental disabilities. Many of them, however,
because they are lacking in skills or motivation, need
help with their oral hygiene. The electric toothbrush may
increase their ability to brush effectively [15]. Additional
data are listed below in the most typical case of this cat-
egory of patients, namely, Down syndrome. Treatment
challenges of these patients are higher than their coun-
terparts without disabilities. Responsibility falls in the
family, adequate training of dentists, and state welfare
for preventive and therapeutic dental care (. Fig. 22.9).
In terms of dental care, these patients need short
sessions after first becoming familiar with the environ-
ment and the staff, which ideally should be the same in
successive sessions. Assistance by parents/caretakers to
increase communication with patient can be beneficial.
Communication techniques such as tell-show-do can
be adapted to suit the individual case, and photos can
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
a to understand their environment. Assimilating the neces-
b describe own characteristics. This improves communica-
c
..      Fig. 22.9 a Intraoral view of a 35-year-old female with mental
retardation and phobia. b A panoramic radiograph was possible and
shows extensive treatment needs. The mandibular left second molar
is indicated for extraction. c One week after dental rehabilitation
under general anesthesia, immediately after cementation of bridge-
work under sedation
be used as educational tools. Reward (i.e., high-five
handling) or feedback after each session can be seen as
important, while the transition from simple to difficult
procedures must be done carefully.
22.2.3 Sensory Disabilities
22.2.3.1 Visual Impairment (Blindness)
The prevalence of blind children depends apparently on
country socioeconomics, with reported ratios of around
0.1/1000 in the richest and 1.1/1000 in the poorest [19].
Factors that can cause visual disturbances may act in the
fetal period (microphthalmia, optic atrophy and eye devel-
opment abnormalities, and viral or bacterial infections
such as syphilis, tuberculous meningitis, measles, rubella)
or after birth (trauma, hypertension, premature birth, leu-
kemia, diabetes, glaucoma). Children with congenital or
acquired complete loss of vision must rely on other senses
533 22
sary information is done with the help of parents.
22.2.3.2 Dental Findings and Treatment
There seems to be no difference in the prevalence of car-
ies and periodontal infection in children with partial or
complete loss of vision, although some studies show an
increased incidence [20]. Regarding the correct approach
for blind children, it is a good idea for the dentist to first
tion, especially if done with humor. The patient is given
eyeglasses, both for protection in the case of photophobia
and for a sense of security. The tell-show-­do technique
is applied mainly through touch, though other senses
are also involved such as tasting or smelling materials,
while reference to sight is avoided. The same applies for
the demonstration of oral hygiene, holding the patient’s
hand as we move the toothbrush around the dentition.
Sudden noises are avoided, and priority is given to
maintaining a calm atmosphere. If the child shows diffi-
culty in speaking, other ways, such as the Braille system
or, more often, his/her escort, can mediate for commu-
nication. The visually impaired child may show more
apprehension than that with total blindness because
of vaguely seeing instrument shapes and needing more
explanations. Sometimes cooperation difficulties are
with parents who may feel guilt and show overprotec-
tion or denial. Therefore, it is important to achieve good
communication with parents and clarify everyone’s roles.
22.2.3.3 Hearing Problems (Deafness)
One in 600 newborns may exhibit some degree of deaf-
ness. Hearing loss may begin before birth (viral infec-
tions; ototoxic drugs such as streptomycin, neomycin,
and aspirin; syphilis; hereditary factors as in some syn-
dromes) or perinatally (injury, anoxia, erythroblastosis).
Viral infections, ototoxic drugs, and injuries can also
cause deafness after birth. Early diagnosis and correc-
tion of hearing loss are important for the normal devel-
opment of communication [21].
Eye Catcher
If deafness occurs before the development of speech,
the latter cannot develope. Depending on what vol-
ume is recognized by a person, deafness can be char-
acterized as mild (20–40 db), moderate (41–70 db),
severe (71–90 db), and profound (> 90 db). At times
various ways have been developed to communicate
with the deaf, such as written messages, sign lan-
guage, “lip reading” telecommunication devices, and
cochlear implants.
 534 N. Kotsanos et al.
22.2.3.4 Dental Findings and Treatment
Those with hearing disabilities have more dental needs
than other children. Possible reasons may be related
to socioeconomic status, non-regular attendance and
underestimation of dental needs, and practical difficul-
ties during dental sessions owed to communication prob-
lems and poor cooperation. Some samples of school-age
children and adolescents up to adulthood who attend
special schools show increased periodontal disease lev-
els, while institutionalized hearing-impaired and blind
children have shown increased caries and calculus [9, 21].
Before the initial visit, the parent must be informed
about the process and be the one who will introduce the
child to dental surroundings. An illustrated brochure
or a children’s book that describes the first dental visit
may be useful for that. The escorting adult can help with
communication. Explanations prior to the treatment
help child cooperation. During history-taking, speech
ability and degree of hearing disability are assessed.
Verbal communication is done at a slow pace with short
sentences. It is done without the use of masks to allow
“lip reading,” despite that even the best lip readers
understand only 30–40% of the verbal message [7].
22.3 Patients with Neuropsychiatric/
Psychological Disorders
22.3.1 Autism Spectrum Disorders (ASD)
At one end of the spectrum is the typical form of autism,
while at the other end is the high-functionality Asperger
syndrome. The pervasive developmental disorder (PDD)
falls within the spectrum, although it is a broader term that
also includes other disorders. Autism in its typical form is
a disorder of cognitive and emotional development that
causes problems in learning, communication, and rela-
tionships with others. The prevalence of total spectrum in
the USA is just over 1% and four to five times more com-
mon in boys than in girls [22]. The observed increase in
prevalence in recent decades may be due to better recogni-
tion and coexists with other diseases or syndromes.
Eye Catcher
The diagnosis of autism is made after a detailed medi-
cal, psychological, and neurological examination of
the patient and must satisfy the following four crite-
ria:
1. Serious disturbance of reciprocal social relations
22 2. Severe disruption of communication development
that usually includes the verbal one
3. The behavior, interests, and imagination are lim-
ited and repetitive (stereotypical behavior
4. Early identification (up to age 3–5 years)
The exact etiology of ASD is unknown. Although it is
believed that they are mostly genetic in origin, environ-
mental factors may modulate the phenotypic expres-
sion. People with autism have a limited ability to learn.
Disorders of behavior include self-harm, aggression,
anger, desire for eating paradoxical items, and other
psychiatric symptoms. About 1/4 show seizures start-
ing either in early childhood or in adolescence and get
chronic antiepileptic treatment. The disease progression
cannot be foreseen. Therapeutic intervention includes
psychosocial and possibly pharmacological approach.
Recently there have been some positive results with the
introduction of ketogenic diet, which many children
have been able to follow [23]. This diet is administered
for many years in drug-resistant epilepsy, comprising
of high-fat, adequate amount of protein for growth but
insufficient carbohydrate levels for metabolic needs, forc-
ing the body to use fat instead of glucose for its energy
needs. Special training techniques, such as “treatment
and education of children with autism” (TEACCH) and
speech therapy, may also be useful.
Although there are many similarities between
Asperger syndrome and classic autism, people with
Asperger have far fewer problems with verbal communi-
cation and usually have average or superior intelligence,
i.e., no autism-associated learning disabilities. Usually
they have some obsessions and experience stress in unex-
pected changes in their program. There are several ther-
apeutic procedures that can improve their quality of life
such as interaction, behavior therapy, and even changes
in diet. With appropriate support, people with Asperger
syndrome are able to live an independent life and not
usually present particular challenges in the dental invi-
ronment [24].
22.3.1.1 Dental Findings and Treatment
There are few reports on oral status of young people
with autism, and it seems that plaque and gingivitis
are increased, apparently due to difficulties in effective
brushing of those who care for them. It is not certain
that caries is increased; dental care needs however are
unmet to a greater degree, possibly because of diffi-
culties in seeking treatment or achieving cooperation.
Visual education may help, e.g., for toothbrushing, by
placing structured color images and/or symbols (e.g.,
Picture Exchange Communication System (PECS) or
ΜΑΚΑΤΟΝ), in the bathroom for the various stages of
brushing. Similar images can help introduce the den-
tal environment and dental treatment, providing visual
guidance (. Fig. 22.10). Other reports suggest the use of
modern technology, e.g., tablet-type devices to create sim-
ple stories with appropriate guidance messages of young
patients and improve dental examination acceptance [25].
In the dental surgery, more than one visit may be
required to familiarize children with autism to the envi-
ronment. This is done better if contact is with the same
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
..      Fig. 22.10 A series of images of dental experience that can be used for visual education of children with autism
dental staff who also learns the patient behavioral ste-
reotypes and elements that may cause agitation. The
communication deficit and diminished ability to follow
instructions make cooperation difficult, and usually
referral to a pediatric dentist is necessary. Basic behav-
ior guidance techniques with parental presence may be
used, with “tell-show-do” along with short instructions
to focus attention. The use of firm-structured procedures
benefits compliance and cooperation (. Fig. 22.11).
The dentist should aim for eye contact and direct com-
munication. Sessions should be short avoiding any pain
stimuli. Because of intense and unpredictable reactions
to facial or mouth touch, a calm sensory adaption pro-
cess helps many children. Favorite music or other parent-­
provided routine occupation may also help. Having said all
that, many children with autism are not able to cooperate
and need treatment under general anesthesia.
22.3.2 Attention Deficit Disorders
Attention-deficit/hyperactivity disorder (ADHD), the
most common childhood neurobehavioral disorder, is
a functional brain disorder. Although the parent may
often report a lively child as hyperactive, the term should
be used only for children who have:
55 Uncontrollable behavior or activities
55 Excessive impulsiveness
55 Concentration deficit
55 Constant fidgeting
Typical ADHD behaviors are exhibited when asking the
child to follow rules, such as to stay quiet in the dental
office waiting room. The etiology of the disorder is not
fully understood but has genetic background [26]. The
neurobiological dysfunction relates to the anterior lobe
of the brain and probably involves an imbalance in the
535 22
neurotransmitters dopamine and norepinephrine. Onset
of hyperactivity may be related to or be independent of
family factors, e.g., special demands by teacher or the
parents and the relationship they have with the child,
such as lack of love, rejection, overprotective behavior,
continuous strict discipline problems, etc. Autism, the
obsession, and the continuously high levels of stress can
cause similar disorders, overlap, and present comorbid-
ity with autism spectrum [27].
ADHD prevalence from 3 up to 10% in children has
been reported. A review of studies among children and
adolescents in China found an overall prevalence of
6.3% [28]. Boys are affected more often than girls. The
diagnosis is usually made at the start of primary school.
Comorbidity is almost the rule for ADHD in childhood.
Oppositional defiant disorder that includes frequent
and persistent anger and irritability is frequent with
ADHD. Treatment includes family and teacher counsel-
ing. Methylphenidate (Ritalin) and amphetamine deriva-
tives are used to improve the behavior and concentration
with good results for most patients [29, 30]. From the
neurological perspective ADHD has a good progno-
sis, but the risk for psychiatric disorders in adulthood
remains.
22.3.2.1 Dental Findings and Treatment
The importance of oral hygiene should be particularly
stressed as these children have a delayed development
of motor skills, and thus there is a greater need for
brushing with the help of parents. Many of those chil-
dren are sensitive to sounds, light, odors, and bad taste.
Cooperation for dental treatment is usually reduced, as
if they were younger in age. In communicative manage-
ment, the dental clinician should focus on the child, keep
continuous eye contact, and use short sentences with
clarity and firmness [31] (. Fig. 22.12). Continuous
positive reinforcement increases confidence of the child,
 536 N. Kotsanos et al.

..      Fig. 22.11 a A poten- a d

tially cooperative 20-year-old
patient in the autism
spectrum. He was treated in
the pediatric dentistry
postgraduate clinic with
mere communicative
behavior guidance. b, c
Radiograph of right oral
quadrant before and after
the restorations. d, e At the
18-month follow-up, the
patient complies to the b
preventive program with
parental help

..      Fig. 22.12 a, b A
a b
4.5-year-old patient with
ADHD complains about
provoked pain from lower
right quadrant. c, d Pursuing
visual contact and maintain-
ing a calm and firm
approach made diagnostic
radiographs and dental
treatment completion
possible by merely commu-
nicative behavior guidance

c d

22
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
as already presented in 7 Chap. 5. Sedation may help,
but its use requires caution as bizarre behaviors have
been reported. In severe cases of ADHD, general anes-
thesia is recommended.
22.3.3 Epilepsy
The term epilepsy is used to describe a complex of
symptoms comprising of recurrent seizures (fits) with
a sudden, abnormal discharge of brain neurons accom-
panied by loss or impairment of consciousness, usually
succeeded by convulsions. The prevalence of epilepsy
in the general pediatric population is about 0.5%, but
it accompanies many other diseases, e.g., it coexists in
20–25% of autism cases [32] and in 4.5% of ADHD
[30]. Diagnosis is clinical, based on patient’s history,
and concluded with the electroencephalogram, which
further defines the extent and the part of the brain
that is involved. When discharge occurs in the motor
cortex, it induces seizures, while when the parietal or
occipital cortex is involved, the patient exhibits visual,
auditory, or olfactory hallucinations. The most com-
mon type is the primary or idiopathic with no obvi-
ous reason for release. There is a secondary type as a
result of head injury; illness, e.g., meningitis; or anoxia
during birth. The course of childhood epilepsy can-
not be predicted. In children with multiple disabilities,
epilepsy episodes may last longer. Depending on the
type and severity, appropriate medications should be
administered.
Generalized epilepsy seizures extend from the out-
set to both brain hemispheres, they may be accompa-
nied by convulsions, and the patient usually exhibits
immediate loss of consciousness. In partial epilepsy,
discharges occur in one focal region of the cerebral
cortex and affect a specific part of the body; they may
subsequently become generalized and spread to both
hemispheres of the brain. There are other more recent
efforts by the International League Against Epilepsy
(ILAE) regarding classification and understanding
(generalized seizures, focal seizures, and unclassified
seizures) [33].
Another distinction concerns the tonic-clonic epilepsy
(grand mal) and absence seizure (petit mal). The first usu-
ally begins abruptly but may be preceded by a brief warn-
ing about the coming seizure. Eye pupils become dilated,
eyes rotate upwards and sideways, and the person may
experience momentary malfunction of respiratory move-
ments and cyanosis. Tonic convulsions last 10–30 seconds,
followed by a phase of clonic seizures lasting several min-
utes. The muscles contract violently, and outflow of saliva
is observed, as well as perspiration and often involuntary
537 22
discharges of the bowel and bladder. Muscle contrac-
tion subsides gradually until it stops. Usually the child
remains unconscious after the seizure, sinking into a deep
sleep of at least 1 hour. The second absence occurs almost
exclusively in children. It is characterized by less intense
convulsions, momentary loss of consciousness, an expres-
sionless face, and discontinuity of voluntary movements
with rhythmic tremor of the whole body. Fits are short
(about 10 seconds) and the child recovers quickly.
22.3.3.1 Dental Findings and Treatment
Of particular interest from the dental perspective
is the chronic administration of phenytoin because
a side effect is gingival hyperplasia, more severely
affecting the anterior segment. In extreme situations
it significantly covers the teeth creating aesthetic con-
cerns. Meticulous plaque removal, along with frequent
scaling if needed, decreases the effect, but still surgi-
cal resection of hyperplastic gingiva may be needed.
Permanent regression of hyperplasia 6 months after
drug discontinuation is seen. Among other relevant
drugs, carbamazepine and sodium valproate have
similar side effects, though to a lesser degree (see also
7 Chap. 15).
There is a much greatly possibility for anterior tooth
fracture in people experiencing seizures [34]. Immediate
treatment for dental trauma should not be overlooked
and provided in a calm manner because intense anxiety
may be a precipitating factor for seizures.
Eye Catcher
In the event of an epileptic episode occurring in the
dental surgery, the child should be protected from
falling. If the patient is on the floor, a pillow is placed
under his/her head. We do not try to stop the seizure
but only to ensure free airway especially in cases of
increased salivation or vomiting. We should not,
however, try to open the patient’s mouth when tightly
closed [35]. Records on the type and frequency of sei-
zures and the administered drugs are kept.
22.3.4 Disorders of Nutrition and Weight
These include obesity and psychogenic disorders of
nutrition. Anorexia nervosa, bulimia nervosa, and binge
eating disorder are classified in the category F50 of
ICD-10 (WHO 2004). Psychogenic disorders seem to
be an increasing problem, are most commonly found in
(post-)adolescent girls, and are in fact symptoms caused
by underlying psychological and emotional instabili-
ties. The focus on food distracts from handling painful
 538 N. Kotsanos et al.

emotions when their management by normal reasoning that it should be mandatory for young adolescents. A
is not possible. Eating disorders occur in girls about 10 review of the literature refers to the prognosis as having
times more often than in boys. good outcome 43%, improvement 36%, chronic course
20%, and mortality 5% [41].
22.3.4.1 Anorexia Nervosa
Predisposing factors in this disorder may be personal, 22.3.4.2 Bulimia
familial, or socio-cultural. The main symptom of In bulimia (nervosa) there are recurrent episodes of
anorexia nervosa is the dependence on body shape and overeating and an excessive preoccupation of weight
irresistible tendency of losing weight [36, 37]. Anorexic control. Patients may have normal weight that is
young girls look at first sight as decisive people with achieved by purging/vomiting and ways similar to
confidence, but actually they set unachievable goals.
They are never happy and vision themselves as failed
a
(. Fig. 22.13). Weight loss is achieved by many tech-
niques such as avoiding fatty foods, vomiting after meal,
strenuous exercise, and medication use, for example,
diuretics, appetite suppressants, etc. [38]. If the onset of
anorexia happens pre-pubertal, the sequence of events b
of puberty is delayed or inhibited in the absence of the
required body fat.
The prevalence is about 1:10,000 young women, but
in the peak age group 19–24 years, it may be more than
1:1000 with an average age of onset at 17 years [39]. The
body mass index (BMI = weight kg/height m2) for 16
years old and above is 20, while for 14–15 years must be
at least 18.5–19.5 [40] (. Fig. 22.14). Therapeutically,
anorexic patients with average weight less than 20% ..      Fig. 22.13 a Anorexic young women view themselves as being
below normal should first be treated as outpatients. overweight. b Weight loss is pursued by voluminous vomiting after
Family therapy is more useful, and many experts believe lunch

a b

22
..      Fig. 22.14 Curves of body mass index (BMI) for boys a and girls for 18-year-olds) signify obesity. Underwight degrees, from mild to
b. BMI values lying between yellow lines is normal, above yellow line severe, lie under the yellow line (18.5 for 18-year-olds)
(marked 25 for 18-year-olds) signify overwight and above red line (30
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
539 22
anorexia nervosa. This is a newer disease described in a
1979 [37]. Diagnostic criteria for bulimia nervosa by
ICD-10 are continuously being occupied and irresistibly
desiring food in large quantities consumed in short peri-
ods. Another term used is binge eating which somewhat
differs from overeating meaning that one may eat alone,
rapidly, and without control producing feelings of dis-
gust, regret, or guilt. An overeating episode contains
almost exclusively carbohydrates and fats, for example,
pastries, chocolates, biscuits, bread, honey, butter, and
cheese. In the psychiatric comorbidity, elevated rates of b
depression (46%), anxiety disorders (43%), and psycho-
tropic drug abuse (49%) have been reported.
Cognitive behavioral therapy is the primary treatment
for bulimia. Besides establishing normal diet program, it
includes eliminating the coexisting psychiatric symptoms
with psychotherapy and antidepressants for preventing
relapse, since the course of the disease is characterized
by remissions and exacerbations. Prognosis 6 years after
the end of treatment was good for the 60% of patients, ..      Fig. 22.15 Children’s obesity is related to modern lifestyle
30% of patients had intermediate, and 10% had a poor
outcome by mortality of 1.1% and 3.7% anorexia [42]. to be elevated in obese adolescents [45, 46]. The advice
against the increased consumption of carbohydrates to
Dental Findings and Treatment obese adolescents should not be limited to dental effects
The most common oral finding is the erosion of the only, but to general health, like the prevention of cardio-
teeth and particularly the palatal surfaces of maxillary vascular disease.
incisors [43]. It is associated with induced vomiting, but
no linear correlation has been found. These patients
should avoid frequent drinks with abrasive potential, 22.4  iseases and Syndromes with Genetic
D
such as acidic beverages or fresh fruits containing citric
acid (see also 7 Chap. 18). Immediately water washing
Background
their mouth or even taking antacids in the presence of
Alterations in the genetic material occur in many differ-
frequent vomiting may be of some help.
ent ways. Changes in the DNA sequence (mutations) are
22.3.4.3 Obesity responsible for the appearance of different traits in the
organism (phenotype). Gene mutations involve a small
Obesity is the increase of BMI due to a significant
number of bases, while the term chromosomal muta-
increase in body fat. In industrialized societies this
tions is used when a larger part of the chromosome is
occurs in 10–15% of children. In a sample of preschool
involved. The mutations contribute to genetic diversity
children, 7.2% were overweight and 2.7% obese [44].
in the population and are responsible for many heredi-
Severe obesity (BMI > 30) occurs in approximately 10%
tary diseases, as well as many cancer types. Mutations
of adults. When obesity continues into adulthood, it
can occur in any genital or body cell of an organism.
leads to high cholesterol and predisposes to cardiovas-
Only mutations in genital cells, however, can be passed
cular diseases, diabetes, and hypertension. The factors
from one generation to the next.
contributing to childhood obesity may be associated
with modern lifestyles, psychological family char-
acteristics, socioeconomic status, and cultural views Eye Catcher
(. Fig. 22.15). Overweight children do not usually seek
to exercise and, in addition to consultation and proper Some chronic diseases and most craniofacial abnor-
diet, should be directed to physical exercise and sports. malities, especially those related with syndromes,
show inheritance from parents to children through
Dental Findings and Treatment genes. The genes are located in a particular order
It has been found in the laboratory that cells of adipose and in pairs, one from the father and one from the
tissue secrete pro-inflammatory cytokines. Associations mother, at the 22 pairs of autosomal chromosomes
between overweight and obese children with dental car- and the 23rd pair of sex chromosomes. Their position
ies are found since preschool age, but not without con- is described on the short (p) or long (q) arm, after the
tradictions. Other findings suggest gingivitis or caries respective chromosome number (e.g., 21q11.1).
 540 N. Kotsanos et al.
Most genes regulate cells to produce enzymes or other
proteins, and these in turn control the phenotype. Gen-
erally, phenotype is transferred through autosomal or
X-linked type of inheritance. Sometimes a mutation
occurring at a gene transcription can cause a genetic
disease. Some diseases are inherited with the predomi-
nant type, while others with the recessive type. With the
predominant type, a mutant gene from one parent is
enough to transfer a disease to the offspring. In con-
trast, with the recessive type of inheritance, the mutant
gene needs to exist in both parents. In a hereditary dis-
ease transmitted by the recessive type, the probability of
both parents being carriers is very small but increasing
in cases of consanguineous marriages between close rel-
atives, such as in areas with characteristics of geographi-
cal/racial isolation.
22.4.1 Down Syndrome
Down syndrome is the most common chromosomal
abnormality. It is estimated that 65–80% of Down syn-
drome conceptions result in miscarriage [47]. About 95%
of cases have an extra chromosome 21 (trisomy 21) due to
non-segregation of chromosomes 21 in the first or the sec-
ond meiotic division at the father or mother genome. The
rest of the 5% may exhibit other chromosomal anomalies
such as chromosome migration, trisomy of only part of
chromosome 21 (often 21q21–21q22.3), or mosaicism. In
mosaicism, individuals have two cell lines, trisomic and
normal, and usually the pathologic phenotype is not fully
expressed [48]. Although Down syndrome may occur in
births from mothers of all ages, the risk increases with
increasing age of the mother (. Fig. 22.16). The inci-
dence is 0.9/1000 births at maternal age less than 33
..      Fig. 22.16 Predicted risk of births with Down
syndrome by maternal age
22
years, 2.8/1000 when the age is 35–38 and 38/1000 when
the mother is over 44 years old [47, 48].
22.4.1.1 Clinical Features
Children with Down syndrome are characterized by
growth retardation of both motor and cognitive func-
tions. They show reduced skeletal growth with an aver-
age height of 151 cm for men and 141 cm for women.
Mental retardation is usually moderate, with the
­intelligence quotient (IQ) ranging between 30 and 50
with a mean of 36.5. Characteristics of the syndrome
are slanted eyes, spots on the iris, strabismus, myopia,
nystagmus, flat and small nasal bridge, dysplastic ears
with low grip, short and wide neck with thick folds of
the skin in the neck, wide hand with characteristic con-
tinuous (simian) line on the palms, brachydactyly (short
fingers), clinodactyly, genital malformations, congenital
heart disease, and muscular hypotonia.
Congenital heart disease rate in children with Down
syndrome is high (40–60%). Most frequent heart con-
ditions are common atrioventricular canal (39%), arte-
rial septal defects (29–42%), ventricular septal defects
(14–43%), open ductus arteriosus (17%), and tetralogy
of Fallot (6%) [49, 50]. Other pathological conditions
associated with the syndrome are mainly hematological
and neoplastic disorders (leukemia), impaired immune
response, and hypothyroidism [51, 52]. In older patients,
pathological changes are found in the brain, similar to
atrophic changes in Alzheimer’s disease. Seizures of
grand mal or petit mal type are reported in 1–10%.
22.4.1.2 Dental Findings and Treatment
Individuals with Down syndrome show the following
oral characteristics: fissured tongue (61%), macroglossia
or protruding tongue (42%), narrow palate (67%), angu-
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
lar cheilitis, protruding lower lip, and occlusal and skele-
tal disorders such as reduced medium growth of the face
[51, 52]. Angle class III malocclusion is observed due
to mandibular protrusion associated with muscle hypo-
tonia, evident since infancy (pseudo-­prognathism) [52].
Despite normal salivary flow rate, these individuals may
exhibit drooling. To exercise the hypotonic tongue and
prevent protrusion and drooling, it has been proposed
to use the Castillo-Morales palatal plate (. Fig. 22.17).
It is based on involuntary pushing reflex of the tongue
against a palatal foreign body, and it has been used since
age 6 months and in cases of cerebral paralysis [52].
The most common dental anomalies are related to the
number (hypodontia) and the morphology of the teeth
(microdontia, taurodontism). Late eruption with pro-
longed primary tooth shedding and more variable dental
age are observed [53]. Regarding caries there are conflicting
541 22
reports with most of them suggesting reduced susceptibil-
ity [47, 48, 54]. The major oral health problem is periodon-
tal disease, partly owed to poor oral hygiene because of
reduced dexterity of these patients [55–58]. Compared to
the healthy population, periodontal disease is character-
ized with earlier onset and increased severity. This is related
to immune system dysfunctions such as impairment of T
cells, inadequate phagocytotic capacity, and elevated levels
of prostaglandin E2 in the gingival sulcus fluid. Although
children with trisomy 21 have an increased inflammatory
reaction against periopathogenic bacteria compared to
healthy children, periodontal disease progression can be
prevented by regular preventive care [55–58].
Dental treatment of patients with Down syndrome
varies depending on intellectual impairment and exist-
ing medical pathologies. Regarding the former, problems
relate to behavior management, mainly due to commu-
nication difficulties to allay fear and reverse negativity.
Most patients however may be treated at the dental
office by specialists (. Figs. 22.18 and 22.19) [57, 58].
After taking a detailed medical history, it may be neces-
sary to communicate with the treating cardiologist for
the patient’s ability to respond to the dental treatment
plan and possible prophylaxis.

22.4.2 Ectodermal Dysplasia

Ectodermal dysplasia is a general term used to describe

the clinical manifestations of an inherited condition
caused by maturation abnormalities of ectoderm dur-
..      Fig. 22.17 Castillo-Morales appliance is a palatal plate with a
raised area at palate dome as a stimulus for tongue activation ing embryogenesis. More than 100 types of ectodermal

b d

c e

..      Fig. 22.18 a The face of a cooperative 8-year-old girl with Down syndrome. b, c Occlusal view with severe caries. d, e Her mouth after
restorative work and sealants placed in all first permanent molars
 542 N. Kotsanos et al.
a b
..      Fig. 22.19 a OPG of a cooperative 13-year-old with Down syn-
drome showing agenesis of maxillary lateral incisors and one man-
dibular central incisor. His parents requested orthodontic correction
dysplasia have been recorded. Its overall prevalence in
the USA is 1:1300. The hypo-hidrotic type is responsible
for about 80% of cases and is transmitted by X-linked
recessive trait (Xq13.1 gene) or rarely by autosomal
recessive or dominant trait. Several organs of ectoder-
mal origin such as teeth, glands, hair, and nails have
severe developmental defects. Oligodontia and hypopla-
sia in the form of conical anterior teeth are standard
features and contribute to a reduced height of alveolar
process. Reduced height of the lower face and promi-
nent lips, nasal obstruction due to nasal crusting, and
skin dryness are among additional features. The hair is
usually sparse blond, and the eyebrows and eyelashes
are absent. The salivary and lacrimal secretion is usually
reduced. The severely impaired function of sweat glands
leads to failure of body temperature self-regulation
resulting in these children suffering at hot temperatures.
They mostly show normal intelligence and average life
expectancy.
22.4.2.1 Dental Findings and Treatment
To address oligodontia, a removable prosthetic appli-
ance can be helpful in function and aesthetics provid-
ing psychological support (. Fig. 22.20). Children as
young as 3 years old can get used to these appliances
successfully, but reconstruction is necessary with growth
and dentition changes [59]. If permanent teeth erupt in
suitable places, having their shape built up with com-
posite and wearing partial dentures are an acceptable
interim solution [59]. There are sporadic reports on cases
of mini-dental implants since the beginning of puberty
[60], but implants are mainly placed for long-term suc-
cess in the third decade of life [61]. The intervention of
22
c
of a protrusive mandible. b The patient at advanced treatment stage.
c A happily smiling patient after having finished treatment. (Cour-
tesy of Dr. Manoukakis)
an orthodontist is often needed in this multidisciplinary
approach. Such a team may include pediatric dentist,
orthodontist, prosthodontic, psychologist, and later
oral surgeon.
22.4.3 Cystic Fibrosis
Cystic fibrosis is a genetic disorder that affects mostly the
lungs and pancreas. It previously caused death at a young
age, but currently life expectancy is close to 50 years. It is
inherited as an autosomal recessive trait, with a frequency
of approximately 1 in 2000 births [62], and is more com-
mon in people of North European ancestry. It is caused
by the presence of mutations in both copies of the gene
for the cystic fibrosis transmembrane conductance regu-
lator (CFTR). This is a channel protein that controls the
flow of H2O and Cl− ions in and out of cells. The main
feature of the disease is the production of much thicker
secretions that obstruct pores and channels particularly
in the pancreas and lungs, resulting in pancreatic insuf-
ficiency at an early age. The sputum laid in the inner sur-
face of lung airways traps bacteria in the small airways
which cause inflammation. The symptoms include per-
sistent cough, wheezing, breathlessness, and recurrent
serious chest infections, e.g., pneumonia. Chronic respi-
ratory disease progressively destroys the lungs, leading
the patient to respiratory failure, which led to 94% of
mortality [63]. Glands including intestinal, gall bladder,
the intrahepatic bile, and submaxillary can be clogged by
mucus. The heterozygous may ­experience minor distur-
bances in transport epithelium, but have no clinical mani-
festation [63, 64].
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
..      Fig. 22.20 a 5-year-old boy a b
with hypohidrotic ectodermal
dysplasia. b, c Oligodontia and
conical mandibular canines. d
Partial denture for maxillary
missing teeth. e At age 8 years
he is happy with his mid-term
solution of maxillary denture
and a mandibular fixed
bridgework, preferred for d e
stability
Eye Catcher
Treatment of cystic fibrosis depends on the stage of
the disease and the involved organ. The removal
of mucus from the lungs and respiratory tract is an
important part of daily treatment and is achieved with
chest physiotherapy including possible pat on the back
and chest. Antimicrobial and mucolytic drugs are also
administered. Furthermore, approximately 90% of
individuals with cystic fibrosis take pancreatic enzymes
and vitamins that help absorb nutrients of food [64].
Success of gene therapy in other monogenic diseases
has created interest in cystic fibrosis gene therapy [65].
22.4.3.1 Dental Findings and Treatment
Despite earlier reports of lower caries prevalence in chil-
dren and adolescents with cystic fibrosis, a systematic
review of the literature did not show difference than the
general population [66]. Patients with cystic fibrosis after
recurrent respiratory infections may experience blockage
of the nasal cavity and sinus. During dental treatment,
actions that may aggravate the symptoms of the disease
must be avoided. Intense air streams, such as during
nitrous oxide and oxygen inhalation sedation, may dry
secretions in the airway, causing further obstruction and
respiratory tract infections. General anesthesia is also con-
traindicated when respiratory function is limited. Local
anesthesia is perfectly acceptable. To reduce the potential
for inhalation of aerosols, rubber dam should be used [67].
543 22
c
22.4.4 Muscular Dystrophy
Muscular dystrophy is a disease which affects muscle
fibers causing necrosis and replacement with adipose
and connective tissue. It is an inherited disease and
is caused by a mutation that modifies the metabolism
of the muscular tissue. It manifests progressively by
affecting new muscles. There are at least eight types
of muscular dystrophies that are distinguished by the
muscles that are affected first, the age at which they
occur, and their evolution. There is no treatment to
stop the disease [68], but the attention is given to car-
diovascular problems. The Duchenne muscular dystro-
phy is the most common myopathy and occurs in boys
of 3–5 years of age. It is a serious recessive X-linked
form of muscular dystrophy which eventually leads to
loss of gait and death. With a prevalence of 1:3500
boys, muscular dystrophy is the most common type
[68], and these children need a wheelchair when about
12 years old and have a life expectancy of 20 years [69].
In Becker muscular dystrophy, symptoms appear later,
at about 12 years of age, and life expectancy is higher.
22.4.4.1 Dental Findings and Treatment
Cardiomyopathies and respiratory diseases are contra-
indications for general anesthesia. Muscular dystrophy
can also coexist with malignant hyperthermia. When the
facial muscles are affected, the face remains expression-
less and lips unable to get whistling position. There may
be occlusion disorders, but no increased caries suscepti-
bility is reported (. Fig. 22.21) [70].
 544 N. Kotsanos et al.
..      Fig. 22.21 Muscular dystrophy of a 13-year-old boy with age-­
appropriate dentition, tooth crowding, and caries attributed to inad-
equate oral hygiene practice by parents
22.4.5 Familial Mediterranean Fever
The familial Mediterranean fever is an autosomal
recessive disorder characterized by recurrent epi-
sodes of independent high fever and acute inflam-
mation and pain, particularly in abdominal region.
It is manifested before the age of 20, and there are
about 30 mutations responsible for it. It is observed
in populations living around the Mediterranean Sea,
Armenians, Israeli (especially Sephardic), Arabs,
and Turks, and its manifestation is favored by mar-
riages between relatives [71]. The amyloidosis that is
observed is distinguished in systematic, localized, and
familial. Therapeutically, daily use of colchicines is
recommended to prevent fever episodes and develop-
ment of amyloidosis [72].
22.4.5.1 Dental Findings and Treatment
The dental clinician should differentiate the familial
Mediterranean fever from periodic fever [73], the aph-
thous stomatitis, pharyngitis and adenitis (PFAPA)
syndrome and Behcet’s disease, which exhibit oral mani-
festations. Periodontitis is a very frequent finding in
patients with familial Mediterranean fever who exhibit
amyloidosis and needs regular treatment [74].
22.4.6 Clefts
From about 5000 inherited conditions, 700 involve cra-
niofacial abnormalities, which constitute a large and
heterogeneous group. Clefts are by far the most com-
mon craniofacial abnormalities, and 2/3 of them involve
the head and the neck [75]. They are the result of failure
of facial tissues to join properly during organogenesis
in utero. The clefts of the maxilla are among the most
frequent malformations occurring in humans and may
be separate entities or coexist with other malformations
(e.g., eyes, ears, etc.) or be part of clinical semiology of
22 syndromes (e.g., Pierre Robin). About 70% are individ-
ual clefts. The cleft may involve the lip, the palate (hard
and soft), or a combination of them including the alveo-
lar process. It may be unilateral or bilateral and com-
plete or incomplete (. Fig. 22.22). The prevalence is
about 1/700–800 live births, and the order of frequency
is broadly combined clefts (45%), cleft palate (30%), and
cleft lip (25%).
The etiology appears to be multifactorial and genetic
(mutations in genes such as SKI/MTHFR and IRF6), as
well as environmental factors (alcohol consumption and
treatment with corticosteroids during the first months
of pregnancy, folic acid deficiency, etc.) have been impli-
cated [76].
22.4.6.1 Dental Findings and Treatment
Children with clefts, especially those with alveolar
process and palate cleft, face multiple and complex
problems that require immediate and long-term man-
agement. Difficulties may arise with feeding, speech,
hearing, oral diseases, cognitive deficits, and emo-
tional and social issues. Inflammation of the mid-
dle ear through the oropharynx is frequent, due to
improper development of the muscles involved in the
functioning of the Eustachian tube. Other problems
involve orthodontic anomalies, missing teeth, and
delayed or even ectopic eruption of the teeth and are
best addressed by an interdisciplinary team approach.
Caries prevalence is often referred to be increased
(even three times higher) in children with clefts, but the
sample of those children in these studies includes chil-
dren with syndromes that may have low dexterity or
inadequate preventive care [77, 78]. Other studies did
not find differences [79]. The teeth of the maxilla are the
most affected by caries and especially near the cleft. The
gingival index and bleeding from the sulcus in children
and young people with clefts are also significantly higher
than in control groups [80]. Discomfort and fatigue with
problems in the oral cavity may contribute to neglect of
oral hygiene. Early prevention and treatment of caries
and gingivitis is important, and the participation of a
­pediatric – or special care dentist – is essential in the cleft
palate team.
Correction treatment extends from birth until
the completion of management at full development,
i.e., early adulthood. Surgical and orthodontic needs
should be timely met; surgical protocols can vary as
to the therapeutic intervention time but will generally
start by following the “rule of 10”: 10 weeks of age,
weighing 10 kg, and hemoglobin 10 g/dl. The lip is cor-
rected first and then, before speech starts, the palate.
Surgical correction has often undesirable appearance
with narrow palate with irregular dome (. Fig. 22.23).
Orthodontic treatment aims to enlarge the palate and
align the teeth. The ectopic eruption of first permanent
molars is frequent (approximately 10%) due to crowded
upper arch [81].
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
545 22
a b

..      Fig. 22.22 a Surgically corrected cleft lip with asymmetry at lip and left nasal flap. b Partial cleft palate (at left), unilateral (at middle),
and bilateral lip-palate cleft (at right)

22.4.7 Osteogenesis Imperfecta a

Osteogenesis imperfecta (OI) is clinically, biochemically,

and genetically a rare heterogeneous group of disorders
in the collagen of connective tissue with a prevalence of
1:20,000 to 50,000. The disease is characterized by frag-
ile bones suffering frequent fractures, by short stature
and blue color of the sclera of the eyes (. Fig. 22.24).
In 90% of cases, mutations in the genes COL1A1 and
COL1A2 are responsible [82]. Two of the four types in
which OI has long been classified usually coexist with
b
dentinogenesis imperfecta. Patients in these OI types
present significant dental needs explained in 7 Chap.
17. Later an extension of the classification was pro-
posed to include four additional OI types.

Overview
The main typical characteristics of osteogenesis imper-
fecta types that include dentinogenesis imperfecta:
55 Short stature, retarded growth
55 Bone fractures, non-induced*
55 Skin hyperelasticity ..      Fig. 22.23 a Surgically corrected palatal cleft in a 9-year-old
55 Hearing loss with neglected oral hygiene, before the start of orthodontic treat-
55 Blue sclera ment. b End result of orthodontic treatment and prosthetic rehabili-
55 Opalescent teeth tation for missing maxillary lateral incisors. Unsatisfactory palatal
55 Dental pulp obliteration healing with fistula is evident. (Courtesy of Dr. l. Ioannidou)

*In case there are cooperation problems, the dental cli-
nician must bear in mind that protective stabilization is
better avoided due to the high risk of bone fractures.
22.4.7.1 Bisphosphonates
An issue pediatric dentists must be aware of is the sug-
gested administration of bisphosphonates (BP) for the
treatment of OI. By suppressing bone metabolism, they
block osteoclastic activity, increasing bone resistance
to fractures [83]. In adults receiving BPs intravenously,
a high incidence of osteonecrosis of the jaw has been
reported [84]. No occurrence of osteonecrosis for OI
pediatric patients treated with BPs has been reported;
this however does not preclude cases emerging in the
future because the osteonecrosis risk is related to the
cumulative dose and duration of therapy [85]. Treatment
with BPs does not need to be interrupted when primary
teeth close to shedding are extracted, possibly because
there is little supporting bone [86]. Oral flora may also
play a key role in pathogenesis of jaw osteonecrosis;
therefore, good oral hygiene is important for its preven-
tion. The elimination of dental disease and oral infec-
tion is important prior to intravenous BP therapy, and
this stresses the need for multidisciplinary approach [87].
Given the action of BPs on inhibition of bone resorp-
tion, the potential for these agents to delay tooth eruption
 546 N. Kotsanos et al.
was experimentally shown in animals. As OI itself has
been found to lead to advanced dental development [87],
BP treatment had a delaying effect, resulting in no differ-
ent rate of dental development than healthy children [88].
22.4.7.2 Malocclusion
Malocclusion is very frequent finding in OI patients,
mainly as mandibular protrusion [86]. Orthodontic
treatment of OI patients is difficult, as orthodontic sur-
gery may be needed in many cases and slower remodeling
rate may delay tooth movement. Also tooth movement
has to be interrupted, and orthodontic surgery is notre-
commended if BP therapy is instituted. There have been
some successful case reports. For example, in growing
patients affected by OI and treated with BPs, it was pos-
sible to apply rapid maxillary expansion with no compli-
cations at 1-year follow-up [89].
22.4.8  ther Syndromes and Craniofacial
O some functions well. The syndrome is characterized
Anomalies
The syndromes that are accompanied by dental abnor-
malities have been reported briefly in 7 Chap. 17. This
is a very brief presentation of rather rare syndromes
with dental interest, either due to special characteristics
of the lower face or due to peculiarities in their dental
..      Fig. 22.24 Blue sclera of the eye of a patient with osteogenesis
imperfecta. (Courtesy of Dr. H. Sarnat)
a b c d
22
..      Fig. 22.25 a An 8-year-old girl with Crouzon syndrome and
exophthalmos. b Note the craniosynostosis. c Small maxilla with low
triangular palatal dome, near-normal mandible, and skeletal open
treatment. Suspicion during pregnancy can often be
confirmed by amniocentesis and chromosome analy-
sis (karyotype). Diagnosis is usually made easily and
quickly by applying molecular techniques after recent
advances in genetics. Documentation is constantly
updated at the OMIM database.
Tourette syndrome is a neurodevelopmental disorder
characterized by the presence of multiple motor and
vocal tics. Tics are sudden, rapid, repetitive, arrhythmic,
stereotypical contractions of motor or vocal muscles.
The vast majority of cases are inherited, but no gene
responsible is yet identified. It occurs in 4–6:1000 births
and is three to four times more common in boys. A sys-
tematic review did not find any reports for unexpected
adverse effects or drug interactions in relation to seda-
tion or GA for dental treatment [90].
The fragile X chromosome syndrome occurs
1:4000–5000 births of males. In girls it is less fre-
quent because in 70% of them the other X chromo-
by autistic-like behaviors, while learning impairment
and behavioral problems may coexist. For these rea-
sons difficulties arise in dental treatment [91].
The Crouzon and Apert syndromes (. Figs. 22.25
and 22.26) may be rare (1:25,000 and 1:100,000 births,
respectively) but are the most common involving cra-
niosynostosis, i.e., premature seam synostosis of the
infant’s head. There is micrognathia with crowded teeth
and posterior position of the maxillary requiring den-
tal and orthodontic evaluation very early. In Apert syn-
drome, the mandible appears normal [92]. The incidence
of mental impairment can be up to 20% for Crouzon
and 30% for Apert syndrome.
Treacher Collins syndrome is a rare disorder
(1:50,000 births), and it is caused by autosomal domi-
nant inheritance (40%) or a new mutation (60%) of gene
TCOF1 in chromosome 5q32. The zygomatic bones are
hypoplastic or missing. The ear flaps exhibit dysplasia
that often includes the acoustic meatus (hearing disor-
ders). In severe cases the airway gets blocked. Eating
problems and sleep apnea are often observed; how-
bite. d Her panoramic radiograph shows ectopic eruption of maxil-
lary permanent molars related to the small maxilla
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
a a
..      Fig. 22.26 a A 7-year-old boy with Apert syndrome. b Small
maxilla, near-normal mandible, and skeletal open bite, just as with
Crouzon syndrome. c Very low triangular palatal dome with fissure
at midline
ever, intelligence is usually not affected. The mandible
is hypoplastic contributing to the deformity of the face
(. Fig. 22.27). The surgical restoration process is pro-
longed including bone grafts, usually taken from the
skull, while soft tissue deformities are restored using
flaps, muscle transfers, and skin grafts [93].
Turner syndrome affects only girls with a prevalence
of 1:2500, although 98% of embryos with this syn-
drome are aborted. One of the two sex X chromosomes
is missing (whole or part of it) or exhibits anomalies.
The clinical signs vary. More than half patients present
symptoms such as deceleration of bone development
(short stature), underdeveloped ovaries, lymph edema
(swelling) of the hands and feet, shape disorders of
nails and ears, short and broad neck with low hairline
margin of the head, predisposition to obesity, frequent
ear infections, etc. The maxilla is generally narrow with
elevated triangular palate and crowded teeth, while the
547 22
..      Fig. 22.27 a Deformity of the face of a 3-year-old boy with
Treacher Collins syndrome. Frontal projection with hypertelorism,
middle face bone asymmetry including the eye sockets and hypoplas-
tic zygomatic bones, hypoplastic mandible, and severe dysplasia of
ear flaps with impaired hearing. b Intraorally, there are basal bone
asymmetries with cross-bite and anterior open bite, agenesis of three
primary lateral incisors, and delay in the eruption of a lower cuspid
mandible tends to be broad, and often micrognathic
(. Fig. 22.28) 20–40% prevalence of cardiovascular
diseases is reported, most with valvular heart disease.
The average height of the affected women is 143 cm.
Growth hormone therapy is initiated when the child’s
height starts to drop under the fifth percentile position
(see 7 Chap. 3), which usually occurs from the age of
2. Even though intelligence is within normal levels,
young girls are hyperactive, anxious, and immature
and fall behind in learning and social interaction [98].
Noonan syndrome appears similar to Turner syn-
drome but affects both genders with a prevalence of
1:1000–2500 births. IQ ranges between 48 and 130,
with an average of 86 and 25% exhibit intellectual
impairment. Children with Noonan syndrome must be
checked for heart function. Diagnosis is based on clini-
cal appearance (. Fig. 22.29) [99].
Neurofibromatosis type I (NF1 or von
Recklinghausen’s disease) is inherited by autosomal
dominance. Its prevalence is 1:4000–5000 births, and
the defective gene is in chromosome 17 (17q11.2).
Suspicion of the disease is linked to the presence of
 548 N. Kotsanos et al.

Box
Most oral health epidemiological studies in children with maxillofacial disorders have been conducted on children
with clefts, while research is scarce on other disorders. An obvious reason for this is their rarity. Thus, a review of 19
patients with syndromes of skull synostoses (ten with Apert’s, five with Crouzon’s, two with Pfeiffer’s, and two with
Saethre-Chotzen’s) showed high plaque index and need for extensive dental restorations [94]. Another study on 57
children with skull synostoses (17 of them non-syndromic), which were part of an oral care program from an interdis-
ciplinary clinic, found the exact opposite results, highlighting the success of preventive care in these patiens [95].
Higher oral disease levels were observed in two other reviews on 15 children with Treacher Collins syndrome and on
31 with Ehlers-Danlos syndrome, the latter exhibiting worse periodontal health and increased TMJ disorders with
regressive dislocations [96, 97].

a a

b
b

..      Fig. 22.28 a The face of a 10-year-old girl with Turner syndrome

and mild intellectual impairment. Short neck and short nose with
wide nasal flaps. b Posterior cross-bite and mild Angle class III mal-
c
occlusion, due to narrow maxilla. The mandible is normal

light brown (café au lait) spots on the skin, either neu-

rofibromas or freckles in the armpit or bubonic region.
Children with NF1 may exhibit skeletal anomalies,
sight disorders, and learning disabilities with attention
deficit. A dental study of 50 children with NF1 showed
a high prevalence of class III malocclusion and prob-
lems with mandible and TMJ [100]. Neurofibromas are
observed intraorally in 4–7% of cases with most usual
locations on the tongue, cheeks, the floor of the mouth, ..      Fig. 22.29 a Young adult patient with Noonan syndrome, char-
22 and the palate. Malignant transformation is observed acteristic curly hair, and intellectual impairment. b Her panoramic
radiograph. c Restorative work and fixed prosthetic rehabilitation
in 3–5% of cases [101]. Neurofibromatosis type II is
was performed under general anesthesia and included the extrac-
quite rarer and characterized by vestibular neurofibro- tions of mandibular laterals and left first premolar. One maxillary
mas and meningiomas. These confer instability, hear- central incisor was missing already
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
549 22
a b c d

..      Fig. 22.30 a A young adult patient with neurofibromatosis type achieved by tactile spelling in patient’s palm. d All restorative and
II. b Multiple caries and erosion due to high soft drink consumption. fixed prosthetic work was performed with local anesthesia (multidis-
c Due to advanced blindness and deafness, communication was ciplinary treatment at Pediatric Dentistry and Prosthodontics
Departments)

ing, and/or sight loss, which become more severe in

adulthood [101] (. Fig. 22.30).
Prader-Willi syndrome is the most frequent obesity
cause of genetic etiology. It occurs with a prevalence of
1:10,000–25,000 and is caused by non-expression of genes
of the 15q11–q13 area of chromosome 15 of father’s ori-
gin. The syndrome’s main characteristics are neonatal
lethargy, hypotonia, eating problems, retarded growth
during neonatal period, variable degrees of intellectual
impairment, hyperphagia (of hypothalamic origin), and
..      Fig. 22.31 Congested teeth in the mouth of a 7-year-old boy
obesity and often underdeveloped jaws (. Fig. 22.31). with Prader-Willi syndrome. There are gross demarcated enamel
Twenty-five percent of obese adults suffer from diabetes opacities in the mandibular incisors and heavy plaque deposits on
mellitus type II with an average starting age of 20 years. many teeth
Moreover, elongated face with slim upper lip and broad
nose is observed [102].
Finally, there are many other syndromes and max- syndrome (. Fig. 22.32), the Lesch-Nyhan syndrome
illofacial anomalies that one can see in a specialized (. Fig. 22.8), etc. Others like Carpenter syndrome and
center or find in the OMIM base [103]. Some with Canavan disease (most prevalent in Ashkenazi Jews)
possible dental interest are the 22q11 deletion syn- may be either extremely rare or have medical relevance
drome (former DiGeorge’s), the tricho-dento-osseous only, and their description here is not considered nec-
syndrome (7 Fig. 17.43), the incontinentia pigmenti essary.
 550 N. Kotsanos et al.

a b c

..      Fig. 22.32 a Incontinentia pigmenti in a 6-year-old girl with small freckles appearing at the lower face. b Severe oligodontia. c Hypoplas-
tic anterior primary teeth at age 4 years

References tual disability. Med Oral Patol Oral Cir Bucal.

2017;22(1):e88–94.
15. Doğan MC, Alaçam A, Aşici N, Odabaş M, Seydaoğlu G. Clin-
1. Baumeister SE, Davidson PL, Carreon DC, Nakazono TT,
ical evaluation of the plaque-removing ability of three different
Gutierrez JJ, Andersen RM. What influences dental students to
toothbrushes in a mentally disabled group. Acta Odontol
serve special care patients? Spec Care Dentist. 2007;27(1):15–
Scand. 2004;62(6):350–4.
22.
16. Fardi Κ, Topouzelis N, Kotsanos Ν. Lesch-Nyhan syndrome. A
2. Joint Advisory Committee for Special Care Dentistry. A case
preventive approach to self-mutilation. Int J Pediatr Dent.
for need: proposal for a speciality in special care dentistry.
2003;13:51–6.
BSDH, 2003. http://www.­bsdh.­org.­uk/misc/ACase4Need.­pdf.
17. Cauwels RG, Martens LC. Self-mutilation behaviour in Lesch-­
3. Dougall A, Fiske J. Access to special care dentistry, part 1.
Nyhan syndrome. J Oral Pathol Med. 2005;34(9):573–5.
Access. Br Dent J. 2008;204(11):605–16. https://doi.org/10.1038/
18. Vedi K, Bernard S. The mental health needs of children and
sj.bdj.2008.457.
adolescents with learning disabilities. Curr Opin Psychiatry.
4. Jones L, Bellis MA, Wood S, Hughes K, McCoy E, Eckley L,
2012;25(5):353–8.
Bates G, Mikton C, Shakespeare T, Officer A. Prevalence and
19. Gilbert CE, Anderton L, Dandona L, Foster A. Prevalence of
risk of violence against children with disabilities: a systematic
visual impairment in children: a review of available data. Oph-
review and meta-analysis of observational studies. Lancet.
thalmic Epidemiol. 1999;6(1):73–82.
2012;380(9845):899–907.
20. Shetty V, Hegde AM, Bhandary S, Rai K. Oral health status of
5. Altarac M, Saroha E. Lifetime prevalence of learning disability
the visually impaired children--a south Indian study. J Clin
among US children. Pediatrics. 2007;119(Suppl 1):S77–83.
Pediatr Dent. 2010;34(3):213–6.
6. Norwood KW Jr, Slayton RL, Council on Children With Disabili-
21. Jain M, Bharadwaj SP, Kaira LS, Bharadwaj SP, Chopra D,
ties; Section on Oral Health. Oral health care for children with
Prabu D, Kulkarni S. Oral health status and treatment need
developmental disabilities. Pediatrics. 2013;131(3):614–9. https://
among institutionalised hearing-impaired and blind children
doi.org/10.1542/peds.2012-­3650. Epub 2013 Feb 25.Review.
and young adults in Udaipur, India. A comparative study. Oral
7. Crall JJ. Improving oral health for individuals with special
Health Dent Manag. 2013;12(1):41–9.
health care needs. Pediatr Dent. 2007;29:98–104.
22. Autism and Developmental Disabilities Monitoring Network
8. Mc Donald RE, Weddell JA, Sanders JB, Jones JE. Dental
Surveillance Year 2008 Principal Investigators; Centers for Dis-
problems of children with disabilities, Ch. 23. Ιn: Ralph E
ease Control and Prevention. Prevalence of autism spectrum
McDonald; David R Avery; Jeffrey A Dean, Dentistry for the
disorders--autism and developmental disabilities monitoring
child and adolescent. 8th ed, 2004, 524. St. Louis, Mosby.
network, 14 sites, United States, 2008. MMWR Surveill Summ.
9. Simon EN, Matee MI, Scheutz F. Oral health status of handi-
2012;61(3):1–19.
capped primary school pupils in Dar es Salaam, Tanzania. East
23. Evangeliou A, Vlachonikolis I, Mihailidou H, Spilioti M, Skar-
Afr Med J. 2008;85(3):113–7.
palezou A, et al. Application of a ketogenic diet in children
10. Limeres Posse J, Vázquez García E, Medina Henríquez J,
with autistic behavior: pilot study. J Child Neurol.
Tomás Carmona I, Fernández Feijoo J, Diz DP. Pre-­assessment
2003;18(2):113–8.
of severely handicapped patients suitable of dental treatment
24. Woodbury-Smith MR, Volkmar FR. Asperger syndrome. Eur
under general anesthesia. Med Oral. 2003;8(5):353–60.
Child Adolesc Psychiatry. 2009;18(1):2–11.
11. McIntyre S, Taitz D, Keogh J, Goldsmith S, Badawi N, Blair
25. Lefer G, Rouches A, Bourdon P, Lopez CS. Training children
E. A systematic review of risk factors for cerebral palsy in chil-
with autism spectrum disorder to undergo oral assessment
dren born at term in developed countries. Dev Med Child Neu-
using a digital iPad® application. Eur Arch Paediatr Dent.
rol. 2013;55(6):499–508.
2019;20(2):113–21. https://doi.org/10.1007/s40368-­018-­­0398-­­9.
12. Gladstone M. A review of the incidence and prevalence, types
26. Thapar A, Cooper M, Eyre O, Langley K. What have we learnt
and aetiology of childhood cerebral palsy in resource-poor set-
about the causes of ADHD? J Child Psychol Psychiatry.
tings. Ann Trop Paediatr. 2010;30(3):181–96.
2013;54(1):3–16.
13. Peres AC, Ribeiro MO, Juliano Y, César MF, Santos RC. Occur-
27. Taurines R, Schwenck C, Westerwald E, Sachse M, Siniatchkin
22 rence of bruxism in a sample of Brazilian children with cere-
bral palsy. Spec Care Dentist. 2007;27(2):73–6.
M, Freitag C. ADHD and autism: differential diagnosis or
overlapping traits? A selective review. Atten Defic Hyperact
14. Dugashvili G, Van den Berghe L, Menabde G, Janelidze M,
Disord. 2012;4(3):115–39.
Marks L. Use of the universal pain assessment tool for evaluat-
28. Wang T, Liu K, Li Z, Xu Y, Liu Y, Shi W, Chen L. Prevalence
ing pain associated with TMD in youngsters with an intellec-
of attention deficit/hyperactivity disorder among children and
Disabilities, Neuropsychiatric Disorders, and Syndromes in Childhood and Adolescence
adolescents in China: a systematic review and meta-analysis.
BMC Psychiatry. 2017;17(1):32. https://doi.org/10.1186/
s12888-­016-­1187-­9.
29. Warikoo N, Faraone SV. Background, clinical features and
treatment of attention deficit hyperactivity disorder in children.
Expert Opin Pharmacother. 2013;14(14):1885–906.
30. Socanski D, Aurlien D, Herigstad A, Thomsen PH, Larsen
TK. Epilepsy in a large cohort of children diagnosed with
attention deficit/hyperactivity disorders (ADHD). Seizure.
2013;22(8):651–5.
31. Blomqvist M, Holmberg K, Fernell E, Ek U, Dahllöf G. Oral
health, dental anxiety, and behavior management problems in
children with attention deficit hyperactivity disorder. Eur J
Oral Sci. 2006;114(5):385–90.
32. Canitano R. Epilepsy in autism spectrum disorders. Eur Child
Adolesc Psychiatry. 2007;16(1):61–6.
33. Korff CM, Scheffer IE. Epilepsy classification: a cycle of evolu-
tion and revolution. Curr Opin Neurol. 2013;26(2):163–7.
34. Percival T, Aylett SE, Pool F, Bloch-Zupan A, Roberts GJ,
Lucas VS. Oral health of children with intractable epilepsy
attending the UK National Centre for Young People with Epi-
lepsy. Eur Arch Paediatr Dent. 2009;10(1):19–24.
35. Haller JS. Epilepsy in the dental office: concern, care and man-
agement. N Y State Dent J. 2008;74(3):46–7.
36. Bruch H. Anorexia Nervosa: therapy and theory. Am J Psy-
chiatry. 1982;139(12):1531–8.
37. Russell G. Bulimia nervosa: an ominous variant of anorexia
nervosa. Psychol Med. 1979;9:429–48.
38. Beumont PJV. The clinical presentation of Anorexia nervosa
and Bulimia nervosa. In: Brownell KD, Fairburn GC, editors.
Eating disorders and obesity; 1995. p. 151–8.
39. Lucas AR, Beard CM, O’Fallon WM, Burland LT. 50-year trends
in the incidence of anorexia nervosa in Rochester Minneapolis: a
population-based study. Am J Psychiatry. 1991;148:917–22.
40. Touyz WS, Beumont PJV. Behavioral treatment to promote
weight gain in AN. In: Garner D, Garfinkel P, editors. Hand-
book of eating disorders. The Guilford Press; 1997. p. 361–71.
41. Steinhausen P. The course and outcome of anorexia nervosa.
In: Brownell K, Fairburn C, editors. Eating disorders and obe-
sity. The Guilford Press; 1995. p. 234–7.
42. Fichter MM, Quadflieg N. Six-year course of bulimia nervosa.
Int J Eat Disord. 1997;22(4):361–84.
43. Milosevic A, Brodie D, Slade P. Dental erosion, oral hygiene
and nutrition in eating disorders. Int J Eat Dis. 1997;21:195–9.
44. Trikaliotis A, Boka V, Kotsanos N, Karagiannis V, Hassapidou
M. Short communication: Dmfs and BMI in preschool Greek
children. An epidemiological study. Eur Arch Paediatr Dent.
2011;12(3):176–8.
45. Fadel HT, Pliaki A, Gronowitz E, Mårild S, Ramberg P, Dahlèn
G, Yucel-Lindberg T, Heijl L, Birkhed D. Clinical and biologi-
cal indicators of dental caries and periodontal disease in ado-
lescents with or without obesity. Clin Oral Investig.
2014;18(2):359–68.
46. Irigoyen-Camacho ME, Sanchez-Perez L, Molina-Frechero N,
Velazquez-Alva C, Zepeda-Zepeda M, Borges-Yanez A. The
relationship between body mass index and body fat percentage
and periodontal status in Mexican adolescents. Acta Odontol
Scand. 2014;72(1):48–57.
47. Gorlin RJ, Cohen MM, RCM H. Syndromes of the head and
neck. 4th ed. Oxford University Press; 2001. p. 35–42.
48. Desai SS, Fayetteville NY. Down syndrome. A review of the
literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
1997;84:279–85.
49. Tobias ES, Connor JM, Ferguson-Smith MA. Essential medi-
cal genetics. 6th ed , Ch. 18. Willey-Blackwell; 2011. p. 241–53.
551 22
50. Abanto J, Ciamponi AL, Francischini E, Murakami C, de
Rezende NP, Gallottini M. Medical problems and oral care of
patients with Down syndrome: a literature review. Spec Care
Dentist. 2011;31(6):197–203.
51. Sharath Α, Muthu MS, Sivakumar N. (Α) Oral findings of
Down syndrome in Chennai city, India. Indian J Dent Res.
2008;19(3):230–5.
52. Limbrock GJ, Hoyer H, Scheying H. Regulation therapy by
Castillo-Morales in children with Down syndrome: primary
and secondary orofacial pathology. ASDC J Dent Child.
1990;57(6):437–41.
53. Moraes MEL, Bastos MS, Santos LR, Castilho JC, Moraes
LC, Medici FE. Dental age in patients with Down syndrome.
Braz Oral Res. 2007;21(3):259–64.
54. Sharath Α, Muthu MS, Sivakumar N. (Β) Dental caries preva-
lence and treatment needs of Down syndrome children in
Chennai, India. Indian J Dent Res. 2008;19(3):224–9.
55. Morinushi T, Lopatin DE, Nakao R, Kinjyo SA. Comparison
of gingival health of children with down syndrome to healthy
children residing in an institution. Spec Care Dentist.
2006;26(1):13–9.
56. Deps TD, Angelo GL, Martins CC, Paiva SM, Pordeus IA,
Borges-Oliveira AC. Association between dental caries and
down syndrome: a systematic review and meta-analysis. PLoS
One. 2015;10(6):e0127484. https://doi.org/10.1371/journal.
pone.0127484.
57. Oredugba FA. Oral health condition and treatment needs of a
group of Nigerian individuals with Down syndrome. Down
Syndr Res Pract. 2007;12(1):72–7.
58. Descamps I, Marks LA. Oral health in children with Down
syndrome: parents’ views on dental care in Flanders (Belgium).
Eur J Paediatr Dent. 2015;16(2):143–8.
59. Kotsiomiti E, Kassa D, Kapari D. Oligodontia and associated
characteristics: assessment in view of prosthodontic rehabilita-
tion. Eur J Prosthodont Restor Dent. 2007;15(2):55–60.
60. Sfeir E, Nassif N, Moukarzel C. Use of mini dental implants in
ectodermal dysplasia children: follow-up of three cases. Eur J
Paediatr Dent. 2014;15(2 Suppl):207–12.
61. Chrcanovic BR. Dental implants in patients with ectodermal
dysplasia: a systematic review. J Craniomaxillofac Surg.
2018;46(8):1211–7. https://doi.org/10.1016/j.jcms.2018.05.038.
62. Strausbaugh SD, Davis PB. Cystic fibrosis: a review of epidemi-
ology and pathobiology. Clin Chest Med. 2007;28(2):279–88.
63. Boucher RC. New concepts of the pathogenesis of cystic fibro-
sis lung disease. Eur Respir J. 2004;23(1):146–58.
64. Mogayzel PJ Jr, Naureckas ET, Robinson KA, et al. Pulmo-
nary Clinical Practice Guidelines Committee. Cystic fibrosis
pulmonary guidelines. Chronic medications for maintenance of
lung health. Am J Respir Crit Care Med. 2013;187(7):680–9.
65. Chi DL. Dental caries prevalence in children and adolescents
with cystic fibrosis: a qualitative systematicreview and recom-
mendations for future research. Int J Paediatr Dent.
2013;23(5):376–86. https://doi.org/10.1111/ipd.12042. Epub
2013 Jun 12
66. Chi DL. Dental caries prevalence in children and adolescents
with cystic fibrosis: a qualitative systematic review and recom-
mendations for future research. Int J Paediatr Dent.
2013;23(5):376–86.
67. da Fonseca MA. Dental and oral care for chronically ill chil-
dren and adolescents. Gen Dent. 2010;58(3):204–9.
68. Klingler W, Jurkat-Rott K, Lehmann-Horn F, Schleip R. The
role of fibrosis in Duchenne muscular dystrophy. Acta Myol.
2012;31(3):184–95.
69. Flanigan KM. The muscular dystrophies. Semin Neurol.
2012;32(3):255–63.
 552 N. Kotsanos et al.
70. Engvall M. On oral health in children and adults with myo-
tonic dystrophy. Swed Dent J Suppl. 2010;203:1–51.
71. Touitou I. The spectrum of Familial Mediterranean Fever
(FMF) mutations. Eur J Hum Genet. 2001;9:473–83.
72. Khoury S, Dusek J, Anderson G, Vigneswaran N. Systemic
amyloidosis manifesting as localized, severe periodontitis. J
Am Dent Assoc. 2004;135(5):617–23.
73. Wurster VM, Carlucci JG, Edwards KM. Periodic fever syn-
dromes. Pediatr Ann. 2011;40(1):48–54.
74. Cengiz MI, Bagci H, Cengiz S, et al. Periodontal disease in
patients with familial Mediterranean fever: from inflamma-
tion to amyloidosis. J Periodontal Res. 2009;44(3):354–61.
75. Wells M. Oral health status of children with craniofacial
anomalies. Pediatr Dent. 2013;35(3):E79–86.
76. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and
maxillofacial pathology. 3rd ed. St. Louis: Saunders; 2009.
77. Bokhout B, Hofman FX, van Limbeek J, et al. Incidence of
dental caries in the primary dentition in children with a cleft
lip and/or palate. Caries Res. 1997;31(1):8–12.
78. Ahluwalia M, Brailsford SR, Tarelli E, et al. Dental caries,
oral hygiene, and oral clearance in children with craniofacial
disorders. J Dent Res. 2004;83(2):175–9.
79. Lucas VS, Gupta R, Ololade O, et al. Dental health indices and
caries associated microflora in children with unilateral cleft lip
and palate. Cleft Palate Craniofac J. 2000;37(5):447–52.
80. Perdikogianni H, Papaioannou W, Nakou M, et al.
Periodontal and microbiological parameters in children and
adolescents with cleft lip and /or palate. Int J Paediatr Dent.
2009;19(6):455–67.
81. Bjerklin K, Kurol J, Paulin G. Ectopic eruption of the maxil-
lary first permanent molars in children with cleft lip and/or
palate. Eur J Orthod. 1993;15(6):535–40.
82. van Dijk FS, Cobben JM, Kariminejad A, Maugeri A, Nikkels
PG, van Rijn RR, et al. Osteogenesis imperfecta: a review with
clinical examples. Mol Syndromol. 2011;2:1–20. https://doi.
org/10.1159/000332228.
83. Ierardo G, Bossù M, D'Angeli G, Celli M, Sfasciotti
G. Bisphosphonates therapy in children with osteogenesis
imperfecta: clinical experience in oral surgery. Oral Implantol.
2017;10:311–6. https://doi.org/10.11138/orl/2017.10.3.311.
84. Chahine C, Cheung MS, Heda TW, Schwartz S, Glorieux
FH, Rauch F. Tooth extraction socket healing in pediatric
patients treated with intravenous pamidronate. J Pediatr.
2008;153:719–20. https://doi.org/10.1016/j.jpeds.2008.05.003.
85. Maines E, Moniti E, Doro F, Morandi G, Paolo C, Antoniazzi
F. Children and adolescent treated with neridronate for osteo-
genesis imperfecta show no evidence of any osteonecro-
sis of jaw. J Bone Miner Metab. 2012;30:432–8. https://doi.
org/10.1007/s00774-­011-­0331-­3.
86. Okawa R, Kubota T, Kitaoka T, Kokomotoa Κ, Ozono Κ,
Nakano K. Oral manifestations of Japanese patients with
osteogenesis imperfecta. Pediatr Dent J. 2017;27:73–8. https://
doi.org/10.1016/j.pdj.2017.02.001.
87. Bhatt RN, Hibbert SA, Munns CF. The use of bisphospho-
nates in children: review of the literature and guidelines for
dental management. Aust Dent J. 2014;59:9–19. https://doi.
org/10.1111/adj.12140.
22
88. Vuorimies I, Arponen H, Valta H, Tiesalo O, Ekholm M,
Ranta H, et al. Timing of dental development in osteogen-
esis imperfecta patients with and without bisphosphonate
treatment. Bone. 2017;94:29–33. https://doi.org/10.1016/j.
bone.2016.10.004.
89. Ierardo G, Calcagnile F, Luzzi V, Ladniak B, Bossu M, Celli
M, et al. Osteogenesis imperfecta and rapid maxillary expan-
sion: report of 3 patients. Am J Orthod Dentofac Orthop.
2015;148:130–7. https://doi.org/10.1016/j.ajodo.2015.01.029.
90. Hansen JK, Jacobsen PE, Simonsen JL, Hovgaard O, Haubek
D. Tourette syndrome and procedures related to dental treat-
ment: a systematic review. Spec Care Dentist. 2015;35(3):99–
104. https://doi.org/10.1111/scd.12098.
91. Amaral COFD, Straioto FG, Napimoga MH, Martinez
EF. Caries experience and salivary aspects in individuals with
fragile X syndrome. Braz Oral Res. 2017;31:e79. https://doi.
org/10.1590/1807-­3107BOR-­2017.vol31.0079.
92. Krarup S, Darvann TA, Larsen P, et al. Three-dimensional
analysis of mandibular growth and tooth eruption. J Anat.
2005;207(5):669–82.
93. Asten P, Skogedal N, Nordgarden H, Axelsson S, Akre
H, Sjögreen L. Orofacial functions and oral health associ-
ated with Treacher Collins syndrome. Acta Odontol Scand.
2013;71(3–4):616–25. https://doi.org/10.3109/00016357.2012.
700065.
94. Dalben GS, Costa B, Gomide MR. Oral health status of chil-
dren with syndromic craniosynostosis. Oral Health Prev Dent.
2006;4(3):173–9.
95. Mustafa D, Lucas VS, Junod P, et al. The dental health and
cariesrelated microflora in children with craniosynostosis.
Cleft Palate Craniofac J. 2001;38(6):629–35.
96. da Silva DG, Teixeira das Neves L, Ribeiro Gomide M. Oral
health status of children with Τreacher Collins syndrome.
Spec Care Dentist. 2006;26(2):71–5.
97. De Coster PJ, Martens LC, De Paepe A. Oral health in preva-
lent types of Ehlers-Danlos syndromes. J Oral Pathol Med.
2005;34(5):298–307.
98. Faggella A, Guadagni MG, Cocchi S, Tagariello T, Piana
G. Dental features in patients with Turner syndrome. Eur J
Paediatr Dent. 2006;7(4):165–8.
99. Mallineni SK, Yung Yiu CK, King NM. Oral manifestations
of Noonan syndrome: review of the literature and a report of
four cases. Romanian J Morphol Embryol. 2014;55(4):1503–9.
Review
100. Bardellini E, Amadori F, Flocchini P, et al. Oral findings in 50
children with neurofibromatosis type 1. A case control study.
Eur J Paediatr Dent. 2011;12(4):256–60.
101. Javed F, Ramalingam S, Ahmed HB, Gupta B, Sundar C,
Qadri T, et al. Oral manifestations in patients with neurofi-
bromatosis type-1: a comprehensive literature review. Crit Rev
Oncol Hematol. 2014;91(2):123–9. https://doi.org/10.1016/j.
critrevonc.2014.02.007. Epub 2014 Mar 12. Review
102. Bailleul-Forestier I, Verhaeghe V, Fryns JP, Vinckier F,
Declerck D, Vogels A. The oro-dental phenotype in Prader-­
Willi syndrome: a survey of 15 patients. Int J Paediatr Dent.
2008;18(1):40–7.
103. https://www.­omim.­org. Online Mendelian inheritance in man.
 553 23

Child-Centred Dentistry:
Engaging and Protecting
Children
Zoe Marshman and Helen Rodd

Contents

23.1 Introduction – 554

23.2 Oral Health-Related Quality of Life – 554

23.2.1 Measures Used – 554

23.3 Decision-Making and Consent – 555

23.3.1 I nvolving Children in Clinical Decisions – 555
23.3.2 Principles of Consent – 556

23.4 Safeguarding – 556

23.5 Service Evaluation – 557

23.5.1 PROMs and PREMs – 557

23.6 Oral Health Research and Ethics – 558

23.6.1 T he Rationale for Child Engagement – 558
23.6.2 Methodological Considerations – 558
23.6.3 Ethical Issues – 559

23.7 Conclusion – 560

References – 560

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6_23
 554 Z. Marshman and H. Rodd

23.1 Introduction
a suffix to indicate the age range for which the instru-
All children have a right to high-quality dental care and ment has been validated (e.g. CPQ8–10 is intended for
to be involved in decisions about their own oral health. children aged 8 to 10 years) and the number of items
This fundamental principle is embedded in many global included in the questionnaire (e.g. CPQ-16SF indi-
policies, such as the United Nations Convention on the cates that it is a 16-item ‘short form’ version of the
Rights of the Child [1] and the Council of Europe full CPQ). Each measure has inherent strengths and
Guidelines on Child-Friendly Health Care [2]. These limitations which have been critiqued in a previous
publications seek to promote the welfare and wellbeing review [3].
of children as a whole. Regrettably, there are still many
countries and cultures around the world where children’s
positions remain tokenistic or violated (see 7 https:// The past two decades have seen a steady increase in the
www.­humanium.­org/en/child-­rights for the current sit- development of validated questionnaires for measuring
uation). children’s OHRQoL. In essence, these seek to quantify
The goal of child-centred dentistry is not simply to the degree to which a child’s oral status affects their lives
ensure that children’s mouths are disease- and symptom-­ in relation to a variety of psychosocial and functional
free. Rather, emphasis is placed on listening to and valu- domains (. Fig. 23.1). The most commonly used
ing young patients’ opinions in order to better meet their response format requires the participant to state how
perceived oral health needs. This chapter will highlight often their mouth/lips/teeth have affected them over a
concepts which are inherent to child-centred practice, given time period (e.g. 3 months). In contrast, a few
principally oral health-related quality of life, decision-­OHRQoL instruments ask the respondent about the
making and consent, safeguarding, service evaluation, severity, rather than frequency, of any impacts. The
research and ethics. majority of current measures are not condition specific,
meaning that they can be applied to all children, irre-
spective of their oral status. However, some investiga-
23.2 Oral Health-Related Quality of Life tors have argued the case for more ‘sensitive’ measures
which are designed to measure the impact (and evaluate
The notion of health-related and, more specifically, oral the subsequent treatment effect) of a specific condition,
health-related quality of life (OHRQoL) is now well such as caries, malocclusion or developmental enamel
integrated within modern clinical practice. The premise defects. The recently developed caries-specific measure
underlying OHRQoL is that an individual’s oro-facial (CARIES-QC) is one such example, and this has been
condition may impact more widely than on function and validated for use with 5- to 16-year-old children who
symptoms alone, having potential effects on social and have caries experience [4]. To illustrate these fundamen-
emotional aspects. Thus, dental disease/disorders, as tal differences, . Fig. 23.2 provides examples of both a
well as associated dental interventions, can be evaluated generic OHRQoL measure which has a frequency
in terms of how they impact on OHRQoL. The tradi- response format (CPQ11–14) and a condition-specific
tional biomedical (surgical) approach to treating dental measure which has a severity response format
disease has been largely superceded by a more biopsy- (CARIES-QC).
chosocial approach, where treatment outcomes can be It should also be noted some child OHRQoL mea-
measured in terms of positive or negative change to self-­ sures have been designed for completion by adults/car-
reported wellbeing. ers/clinicians, as a proxy, rather than by children
themselves, such as the parental perceptions of child
OHRQoL questionnaire (P-CPQ) [5]. These question-
23.2.1 Measures Used naires require the parent/carer to indicate how much
they think their child’s oral health condition is having an
impact on the given areas. This approach is clearly
Eye Catcher appropriate for very young children or those with severe
learning disabilities, but it is recognised that
To date, the most well-known and widely translated ­child-­reported and parental/proxy-reported impacts do
instruments for measuring children’s OHRQoL not necessarily concur [6–8]. Indeed, there is evidence to
include the Child Perceptions Questionnaire (CPQ), suggest that parents tend to under-report the severity of
the Child Oral Impact on Daily Performances impacts associated with their own child’s oral condition.
(C-OIDP) and the Child Oral Health Impact Profile The child OHRQoL literature is a rapidly emerging
23 (COHIP). The questionnaire notation often includes field. The main body of work, to date, has used OHRQoL
measures to describe the oral health of a target popula-
Child-Centred Dentistry: Engaging and Protecting Children
555 23

Items
Theoretical domains

• Interactions
• Friendships
Social well-being
• Being teased
• School performance

• Pain (acute/chronic)
Oral symptoms
• Discomfort

OHRQoL
• Self esteem
Psychological well-being • Self concept
• Embarrassment/shyness

• Eating/drinking
• Speaking
Function
• Sleeping
• Sports, music etc

..      Fig. 23.1 Theoretical domains and examples of different items that may be included within oral health-related quality of life (OHRQoL)
questionnaires

tion in relation to caries experience, malocclusion, trau-

Example A. Extract from CPQ11-14 matic dental injury, facial differences or dental anomalies
[6–10]. A number of studies have used OHRQoL instru-
In the past 3 months, how often have you felt shy or embarrassed
ments as patient-reported outcome measures to demon-
because of your teeth, lips, jaws or mouth?
strate the benefits of various clinical interventions
 Never
[11–13]. However, this is where further work is needed as

these measures may lack the sensitivity to detect


Once or twice treatment-­related change for specific conditions.


Sometimes
 Often

23.3 Decision-Making and Consent


Every day or almost every day
23.3.1 I nvolving Children in Clinical
Example B. Extract from CARIES-QC Decisions

How much do your teeth annoy you?
 Not at all
A bit
A lot
..      Fig. 23.2 Examples of different response formats used in child
oral health-related quality of life measures: a response according to
the frequency of an impact as used in the generic Child Perceptions
Questionnaire (CPQ) and b response according to the severity of an
impact in the caries-specific Child Experiences of Caries Question-
naire (CARIES-QC)
Clinicians have a responsibility to ensure that they
actively involve young patients, along with their parents/
carers, in managing their oral health. This aspiration
presents acknowledged challenges, especially when
looking after very young children or those with learning
disabilities. It should also be recognised that children
may differ greatly as to how much or little they actually
wish to be involved in decision-making, taking an active
or passive role [14]. Nonetheless, the overarching prin-
ciple remains: children have the right to be involved in
treatment decisions that relate to them [2]. To achieve
this aim, children should be presented with information
in a format and language that they can understand,
 556 Z. Marshman and H. Rodd
whilst being sensitive to the values and views of their
carers. The UK Patient Information Forum provides
invaluable advice for how to develop high-quality and
developmentally appropriate information for young ser-
vice users [15].
The value of shared decision-making is well recog-
nised within paediatric healthcare as a whole, and a
number of interventions have been used to facilitate this
process [16]. In recent years there has been a growth in
the popularity and availability of patient decision aids
(PDAs) to support healthcare encounters. These inter-
ventions seek to help patients in healthcare decisions,
thereby reducing decisional conflict and increasing
patient satisfaction and knowledge. Although these have
mostly been directed towards parents, some PDAs have
been specifically designed for adolescent dental patients,
in the context of choices relating to orthodontic treat-
ment [17] and sedation/general anaesthesia [18]. Rapid
advances in social media and information technology
may also offer child-appropriate and engaging means of
providing information about dental conditions and
treatment options.
23.3.2 Principles of Consent
Integral to decision-making is the formal consent/
assent process. The legalities of the consent process
vary across the world, but the parent/guardian is usu-
ally required to sign a written consent form prior to
treatment. Where possible, the assent of the child is to
be encouraged. The legal age at which the child can pro-
vide written consent again varies across the world but is
usually over the age of 16–18 years. There has been
much debate as to whether a child, younger than the
required legal age, can in fact agree to treatment them-
selves. The principle of ‘Gillick’ or ‘Fraser’ competence
supports the right of children in the United Kingdom
to agree to treatment themselves, providing they are
perceived to fully understand the treatment options and
implications [19]. The clinician has the overarching
responsibility of ensuring that they always act in the
child’s best interests.
The issue of physically restraining a child for neces-
sary dental treatment remains controversial [20]. In
some countries it is an accepted practice to use physical
restraint, also referred to as protective stabilisation, with
or without additional pharmacological regimens.
However, in other countries, this is not part of routine
care, with some bodies viewing it as an ‘assault’ or
infringement of the child’s rights.
23
Eye Catcher
The child’s best interests are central, and in the case
of a very young pre-cooperative child who requires an
urgent examination, it would seem appropriate to
seek the parent’s approval to hold the child, in a safe
and controlled manner. However, restraining an older
child against their will, thereby posing physical dan-
ger to the child and staff, would not be a good prac-
tice. This serves only to reinforce the child’s dental
anxiety and mistrust with the potential for long-term
negative impacts.
23.4 Safeguarding
It is abhorrent that we live in a world where children are
exposed to emotional, physical or sexual abuse as well as
neglect. It remains imperative therefore that the whole
dental team is vigilant and competent in the identifica-
tion and expedient management of all types of abuse. It
is widely cited that non-accidental injuries involve the
head and neck regions in 50% of all injuries; thus, pre-
sentation in the dental setting may be more common
than other healthcare services [21]. Children under the
age of 2 years are reportedly at greatest risk of safe-
guarding concerns. Some important signs and risk fac-
tors of a child’s vulnerability may include those shown
below [22, 23].
>>Important
Patient/parent interactions
–– Delayed presentation of injury
–– History of any injury inconsistent with clinical
findings
–– Withdrawn child
–– Lack of parental empathy
–– Inappropriate comments
Physical signs
–– Failure to thrive (low body mass index)
–– Dirty and smelly
–– Inappropriately dressed
–– Untreated head lice or other infections (e.g. impe-
tigo)
–– Multiple bruises, of different vintage
–– Unusual injuries, bites, burns, pinch marks
Family risk factors
–– History of drug/alcohol dependency
–– History of domestic violence
–– Parent subject to abuse as a child
Child-Centred Dentistry: Engaging and Protecting Children
–– Low socioeconomic status
–– Chaotic and lifestyle stressors, multiple children
from different fathers
–– Unemployment, financial stress
–– Frequent past attendances at emergency depart-
ments
–– Child not attending school
This is an area that clinicians find particularly difficult,
with many reported barriers to addressing potential
abuse, including lack of training, concern about how
their questioning may be received by the family and
worry that they may make things worse for the child.
Support and resources should be available to support
clinicians in this challenging area. Furthermore, manda-
tory training in safeguarding should be undertaken by
all dental health professionals. It is also important that
the dental team receive regular updates on wider issues
such as female genital mutilation and child trafficking,
as intelligence about these practices continues to grow.
Physical abuse may be more readily identifiable than
neglect per se, which may therefore remain unchal-
lenged. The question has to be asked as to whether
severe dental caries, which is ubiquitous in some popula-
tions, in itself constitutes neglect and thus warrants
social care referral and intervention. The general con-
sensus is that dental neglect is a ‘persistent failure to
meet a child’s basic oral health needs, likely to result in
the serious impairment of a child’s oral or general health
or development’ [24]. It may also be a manifestation of
general neglect. The scenario of a parent failing to bring
their child for a scheduled general anaesthetic appoint-
ment for necessary dental extractions, following a previ-
ous presentation of pain and/or infection, has to be
viewed seriously and neglectful of the child’s basic oral
healthcare needs.
The wider issue of failed dental/medical attendances
is also debated within the safeguarding arena. The term
‘was not brought’ has been proposed by some as a more
appropriate terminology than other descriptors, such as
‘did not attend’ or ‘failed to attend’ [25]. Conceptually,
children are mostly reliant on an adult to bring them to
their dental appointments, and therefore they them-
selves should not be labelled as ‘non-attenders’. Every
clinician should adhere to an agreed local/national pro-
tocol for following up on children who were not brought
to their scheduled dental appointments. This will ensure
that children who are known to be ‘at risk’ are not over-
557 23
looked and a clear pathway is identified for subsequent
information sharing, multiagency support and social
care referral where necessary.
23.5 Service Evaluation
There are currently around 2.2 billion children in the
world, representing a large sector of health service users.
Thus one can readily see the argument for greater child
representation, as key stakeholders, in consultations about
quality assurance and planning of healthcare ­services. An
example of this commitment to involve children comes
from a 2016 survey of the quality of care received by
British children during their hospital admission (see
7 http://www.­cqc.­org.­uk/sites/default/files/20171128_
cyp16_statisticalrelease.­pdf). Questionnaires were com-
pleted by almost 35,000 children aged 8–15 years and
provided important feedback about good practice and
where things could be further improved.
23.5.1 PROMs and PREMs
Many healthcare sectors routinely employ patient-­
reported outcome measures (PROMs) and patient-­
reported experience measures (PREMs) as part of
ongoing overall service evaluations [26]. Whereas PROMs
tend to measure the impact of a clinical intervention in
improving a patient’s perceptions of their own health,
PREMs capture a patient’s objective experience of spe-
cific aspects of healthcare (e.g. were they seen on time,
were the staff friendly). Within children’s oral health, the
use of PROMs and PREMs is still emerging as high-
lighted by a systematic review on child-reported out-
comes for cleft lip and palate care [27]. The management
of traumatic dental injuries is another key area where the
need for standardised patient-reported outcome mea-
sures has been recognised [28]. Child OHRQoL question-
naires, as described previously, are probably the most
frequently used PROM within clinical research, including
clinical trials, with the aim of measuring the effectiveness
of an intervention from the child’s perspective [29].
Picker (7 www.­picker.­org) is an international char-
ity, established in 2000, that provides expertise for devel-
oping effective tools to capture patients’ experiences,
thereby improving the quality of health and social care.
 558 Z. Marshman and H. Rodd
Tip
The ‘Children’s Friends and Family Test’ is one of the
freely available resources that can be used to measure
children’s experiences of healthcare (access at 7 http://
www.­p icker.­o rg/wp-­c ontent/uploads/2015/04/
BIG_6260-­P 2778_CYP-­F FT-­Q uestion-­Form_CW_
TD-­_No-­Online_050215_FINAL_A4.­pdf).
It was developed following wide consultation with chil-
dren themselves, who were able to comment on the
wording, response format and overall design. This is
considered an exemplary child PREM, which can be
completed as a hard copy or online via a smartphone
app or website.
23.6 Oral Health Research and Ethics
23.6.1 The Rationale for Child Engagement
Children can be enthusiastic and reliable research par-
ticipants, offering unique insights to investigators. A key
driver to greater child engagement has come from the
social sciences where research practice has shifted from
being ‘on’ children to ‘with’ children and acknowledges
them as experts in their own lives [30]. It is paramount
that young people are given the opportunity to contrib-
ute to clinical research in order to improve future health-
care services and to promote greater understanding of
childhood conditions.
With appropriate approaches, children of all ages
and abilities can be involved throughout the research
process. Even prior to study commencement, children
can be consulted to prioritise the research topic and sug-
gest questions to be posed, thereby ensuring that the
research is actually relevant to them. They can also pro-
vide invaluable advice on the study design and recruit-
ment and retention of participants [31, 32]. Interestingly,
there has been a fundamental shift in the priorities of
many funding bodies, who now stipulate that there must
be evidence of significant patient and public involve-
ment within a proposed research programme. As well as
recruiting children to oral health research, it is impor-
tant that the findings of such research are conveyed in
such a way that children can readily access and under-
stand them.
Over the last decade, the contribution of children to
oral health research has become much more transpar-
ent. Previously, however, there was a paucity of dental
research that actively involved children, as highlighted
in a 2006 systematic review [33]. This enquiry was
23
repeated in 2014 and evaluated all child-related dental
studies, published between 2006 and 2014, with the aim
of determining to what degree children had been actively
involved [34]. Children’s participation was classified
according to the following four categories:
1. Children fully engaged, contributing to the research
process or having their own words used.
2. Children as research subjects, completing measurers
designed by adults.
3. Children’s input sought via a proxy, parent or clini-
cian.
4. Children seen simply as objects with no engagement
at all.
The key finding was that, although only 20% of the con-
temporary literature involved children fully as active
participants, this was a considerable improvement on
the 7% engagement identified by the previous review. It
is encouraging, therefore, to see how child dental
research has continued to move towards greater partici-
pation in recent years. There are still missed opportuni-
ties, however, particularly within more ‘traditional’
research areas, such as clinical trials.
23.6.2 Methodological Considerations
Broadly speaking, children can be engaged in oral health
research through quantitative or qualitative approaches
or a combination of the two [35, 36]. Quantitative meth-
ods essentially seek to measure or define something.
They rely on the use of questionnaires or scales, poten-
tially providing a vast amount of numerical data, usu-
ally from large cohorts, which are conducive to statistical
analyses and interpretation. With today’s modern tech-
nologies and social media explosion, the burden of
administration and analysis can be greatly reduced by
using online surveys. Caution does have to be exercised,
however, when using non-validated questionnaires for
research purposes, as these could undermine the reliabil-
ity of the data. However, the stages involved in develop-
ing and validating a child-centred questionnaire are
complex and time-consuming. Another caveat relates to
the ‘adaptation’ of adult questionnaires for use with
children, as the meaning of words and response formats
may be entirely inappropriate. Furthermore, items of
importance to young people may have been omitted
altogether.
Qualitative enquiries, on the other hand, do not seek
to measure things, but rather to describe things through
people’s own accounts. As such, they can gain more
meaningful insights into behaviours, opinions and moti-
vations. A wide variety of approaches can be employed
Child-Centred Dentistry: Engaging and Protecting Children
..      Fig. 23.3 Two young sisters engaged in a participatory activity relating to genetic research about amelogenesis imperfecta, drawing their
‘family trees’
including interviews, focus groups, film-making, video
or written diaries. These techniques can also be sup-
ported by participatory activities such as drawing,
model-making or role play (. Fig. 23.3). Qualitative
methods offer some advantages to quantitative
approaches in that they facilitate participation of
younger children or those with specific learning or lan-
guage disabilities. They also allow a deeper insight into
a topic as children are generally given the opportunity to
say what they like, without being too restricted by the
researcher’s agenda. Conversely, this approach may pro-
vide data that are irrelevant or difficult to analyse and
interpret. Assuring the quality of qualitative research
remains equally as important as for quantitative
research.
23.6.3 Ethical Issues
Alongside considerations for meaningful research par-
ticipation comes the requirement for ethical research
conduct. In addition to the general principles that gov-
ern ethical research practice as whole, there are some
special considerations that relate to children’s participa-
tion. A valuable resource for those undertaking research
with children is the comprehensive 2015 report produced
by the Nuffield Council of Bioethics, entitled ‘Children
and clinical research: ethical issues.’ Over 500 children,
parents, clinicians and researchers were consulted to
make proposals as to how children and young people
559 23
can be ethically be involved in research as well as identi-
fying roles and responsibilities of all involved.
Tip
The accompanying website provides excellent films, ani-
mations and other resources for involving children in
health research (accessed at 7 http://nuffieldbioethics.­
org/project/children-­research).
It is imperative that children are protected from any
emotional or physical harm as a result of their research
participation. Clearly the research must be well justified,
in terms of addressing an important question and the
need to be conducted with children specifically. Any
risks and burdens of participation must also be as low as
possible. Children (as well as their parents/carers) should
be provided with information about the proposed study
in a clear and easy-to-understand format, so they can
make up their own mind, with no time pressure as to
whether or not they would like to participate. The asso-
ciated assent or consent forms should also be easy to
comprehend. It is important that there is not seen to be
a power imbalance between the researcher and the child.
So, for example, the person doing an interview should be
independent and not someone who is actually providing
the child’s treatment, as children may not feel comfort-
able saying what they really think. Finally, although
confidentiality is key to research governance, children
 560 Z. Marshman and H. Rodd
should be made aware that if they disclose something
that concerns the research team from a child protection
point of view, the researcher may have to share this
information.
23.7 Conclusion
Paediatric dentistry, by the very nature of the specialty,
has always striven to be patient-centred. However, con-
tinued transformation within social, educational and
health policy has driven more robust and evidence-based
approaches to the way in which children are engaged
within dentistry.
References
1. The United Nations International Convention on the Rights of
the Child. https://downloads.unicef.org.uk/wpcontent/
uploads/2010/05/UNCRC_united_nations_convention_on_the_
rights_of_the_child.pdf. Accessed 11.2.21.
2. Lenton S, Ehrich J. Approach to child-friendly health care--the
Council of Europe. J Pediatr. 2015;167:216–8.
3. Yang C, Crystal YO, Ruff RR, Veitz-Keenan A, McGowan RC,
Niederman R. Quality appraisal of child Oral health-related
quality of life measures: a scoping review. JDR Clin Trans Res.
2020;5(2):109–17.
4. Gilchrist F, Rodd HD, Deery C, Marshman Z. Development and
evaluation of CARIES-QC: a caries-specific measure of quality
of life for children. BMC Oral Health. 2018;18:202. Published
online: https://doi.org/10.1186/s12903-018-0662-8.
5. Jokovic A, Locker D, Stephens M, Kenny D, et al. Measuring
parental perceptions of child oral health-­related quality of life. J
Public Health Dent. 2003;63:67–72.
6. Li YJ, Gao YH, Zhang Y. The impact of oral health status on
the oral health-related quality of life (OHRQoL) of 12-year-olds
from children's and parents' perspectives. Community Dent
Health. 2014;31:240–4.
7. Dantas-Neta NB, Moura LF, Cruz PF, Moura MS, et al. Impact
of molar-incisor hypomineralization on oral health-related qual-
ity of life in schoolchildren. Braz Oral Res. 2016;30:e117.
8. Reissmann DR, John MT, Sagheri D, Sierwald I. Diagnostic
accuracy of parents' ratings of their child's oral health-related
quality of life. Qual Life Res. 2017;26:881–91.
9. Eckstein DA, Wu RL, Akinbiyi T, Silver L, Taub PJ. Measuring
quality of life in cleft lip and palate patients: currently available
patient-reported outcomes measures. Plast Reconstr Surg.
2011;128:518e-26e.
10. Zaror C, Martínez-Zapata MJ, Abarca J, Díaz J, et al. Impact of
traumatic dental injuries on quality of life in preschoolers and
schoolchildren: a systematic review and meta-­analysis. Commu-
nity Dent Oral Epidemiol. 2018;46(1):88–101.
11. Knapp R, Gilchrist F, Rodd HD, Marshman Z. Change in chil-
dren's oral health-related quality of life following dental treat-
ment under general anaesthesia for the management of dental
caries: a systematic review. Int J Paediatr Dent. 2017;27:302–12.
12. Hasmun N, Lawson J, Vettore MV, et al. Change in Oral health-
related quality of life following minimally invasive aesthetic
treatment for children with molar incisor Hypomineralisation: a
23 prospective study. Dent J (Basel). 2018;6(4):61. https://doi.
org/10.3390/dj6040061.
13. Aimée NR, Damé-Teixeira N, Alves LS, et al. Responsiveness of
Oral health-related quality of life questionnaires to dental caries
interventions: systematic review and Meta-analysis. Caries Res.
2019;53(6):585–98.
14. Hall M, Gibson B, James A, Rodd HD. Children's experiences of
participation in the cleft lip and palate care pathway. Int J Paedi-
atr Dent. 2012;22:442–50.
15. Patient Information Forum. Guide to Producing Health Information
for Children and Young People. 2014. https://www.pifonline.org.uk/
wp-content/uploads/2014/11/PiF-Guide-Producing-Health-Informa-
tion-Children-and-Young-People-2014.pdf. Accessed 11.2.21.
16. Wyatt KD, List B, Brinkman WB, Prutsky Lopez G, et al. Shared
decision making in pediatrics: a systematic review and Meta-
analysis. Acad Pediatr. 2015;15:573–83.
17. Marshman Z, Eddaiki A, Bekker HL, Benson PE. Development
and evaluation of a patient decision aid for young people and
parents considering fixed orthodontic appliances. J Orthod.
2016;43:276–87.
18. Hulin J, Baker SR, Marshman Z, Albadri S, Rodd HD. Develop-
ment of a decision aid for children faced with the decision to
undergo dental treatment with sedation or general anaesthesia.
Int J Paediatr Dent. 2017;273:44–55.
19. Nunn J, Foster M, Master S, Greening S. British Society of Pae-
diatric Dentistry: a policy document on consent and the use of
physical intervention in the dental care of children. Int J Paedi-
atr Dent 2008;Suppl 1:39–46.
20. Peretz B, Gluck GM. The use of restraint in the treatment of
paediatric dental patients: old and new insights. Int J Paediatr
Dent. 2002;12:392–7.
21. Welbury RR, Murphy JM. The dental practitioner's role in pro-
tecting children from abuse. 2. The orofacial signs of abuse. Br
Dent J. 1998;24(184):61–5.
22. American Academy of Pediatrics Committee on Child Abuse
and Neglect; American Academy of Pediatric Dentistry; Ameri-
can Academy of Pediatric Dentistry Council on Clinical Affairs.
Guideline on oral and dental aspects of child abuse and neglect.
Pediatr Dent. 2008-2009;30(7 Suppl):86–9.
23. Harris C, Welbury R. Top tips for child protection for the
GDP. Dent Update. 2013;40:438–40.
24. Bhatia SK, Maguire SA, Chadwick BL, Hunter ML, et al. Char-
acteristics of child dental neglect: a systematic review. J Dent.
2014;42:229–39.
25. Powell C, Appleton JV. Children and young people's missed
health care appointments: reconceptualising 'Did not Attend' to
'Was not Brought' – a review of the evidence for practice. J Res
Nursing. 2012;17:181–92.
26. Weldring T, Smith SMS. Patient-reported outcomes (PROs) and
patient-reported outcome measures (PROMs). Health Serv
Insights. 2013;6:61–8.
27. Ranganathan K, Vercler CJ, Warschausky SA, MacEachern MP,
et al. Comparative effectiveness studies examining patient-
reported outcomes among children with cleft lip and/or palate: a
systematic review. Plast Reconstr Surg. 2015;135:198–211.
28. Sharif MO, Tejani-Sharif A, Kenny K, Day PF. A systematic
review of outcome measures used in clinical trials of treatment
interventions following traumatic dental injuries. Dent Trauma-
tol. 2015;31:422–8.
29. Gilchrist F, Marshman Z. Patient-reported outcomes (PROs) in
clinical trials in paediatric dentistry. Int J Paediatr Dent.
2020;31(Suppl 1):31–7.
30. Clark A, Flewitt R, Hammersley M, Robb M (eds). Understand-
ing Research with Children and Young People (published in
association with The Open University). 2013. Sage publications
ltd, London (ISBN: 9781446274934).
Child-Centred Dentistry: Engaging and Protecting Children
31. Marshman Z, Innes N, Deery C, Hall M, et al. The management
of dental caries in primary teeth - involving service providers
and users in the design of a trial. Trials. 2012;22;13:143.
32. Weintraub JA, Breland CE. Challenges, benefits, and factors to
enhance recruitment and inclusion of children in pediatric den-
tal research. Int J Paediatr Dent. 2015;25:310–6.
33. Marshman Z, Gibson BJ, Owens J, Rodd HD, et al. Seen but not
heard: a systematic review of the place of the child in 21st-cen-
tury dental research. Int J Paediatr Dent. 2007;17:320–7.
561 23
34. Marshman Z, Gupta E, Baker SR, Robinson PG, et al. Seen and
heard: towards child participation in dental research. Int J Pae-
diatr Dent. 2015;25:375–82.
35. Marshman Z, Hall MJ. Oral health research with children. Int J
Paediatr Dent. 2008;18:235–42.
36. Gilchrist F, Rodd HD, Deery C, Marshman Z. Involving chil-
dren in research, audit and service evaluation. Br Dent J.
2013;214:577–82.
 563

Supplementary
Information
Index – 565

© Springer Nature Switzerland AG 2022

N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry,
https://doi.org/10.1007/978-3-030-78003-6
 565 A–B

Index

A Apexification technique 338–339

Aphthous ulceration 492–494
Abfraction 467 Apical plug apexification 403
Abrasion 466 Arch length discrepancy 209
Actinomyces sp. 348 Arch space anomalies 218–223, 229–233
Active immobilization 71, 72 Artificial apical plug apexification 404
Acute fluoride toxicity 266–267 Aspirin 522
Acute hyperplastic inflammatory 355 Association for Dental Education in Europe (ΑDΕΕ) 133, 134
Acute lymphoblastic leukemia 516 Asthma 521, 522
Acute necrotizing ulcerative gingivitis (ANUG) 495, 502 Atraumatic restorative technique (ART) 285
Acute orofacial infections 323 Attention deficit hyperactivity disorder (ADHD) 352,
Acute suppurative sialadenitis 511 535–537
Acute ulcerative gingivitis 357–358 Attrition 466
Adamandiades-Behcet 494 Autism spectrum disorders (ASD) 534–536
Aesthetic restorative materials 3 Autoimmune polyendocrinopathy-candidiasis-ectodermal
Allergic reactions 504, 505 dystrophy (APECED) 453, 503
Alveolar bone fracture 375 Autotransplantation of premolar 406
Amelogenesis imperfecta (AI) Avulsion 375
–– definition 445
–– dental rehabilitation 446, 449
–– gene investigation and correlation 448
–– hypomatured-hypoplastic with taurodontism 446, 447
B
–– hypoplastic type 445, 446 Bacterial infections
–– masticatory forces 446, 447 –– acute necrotizing ulcerative gingivitis 502
–– mechanisms 445 –– impetigo 500, 501
American Academy of Pediatric Dentistry (AAPD) guidelines 3, –– scarlet fever 501
62, 259 –– tuberculosis 501, 502
Analgesia 138, 511 Bacteriotherapy 267
Anamnestic records 480 Basic erosive wear examination (BEWE) 471
Anemia 506 Basic life support (BLS) training 135
Anesthesia 138–140 Behavior guidance
Angle Class II malocclusion 225, 235, 243 –– ask-tell-ask aims 65
Angle Class III malocclusion 226, 235 –– classification 62
Angle Class III molar relationship 237 –– definition 62
Angular cheilitis 503 –– demanding behavior problems
Ankyloglossia 359 –– emotional immaturity and language problems 75, 76
Ankylosed primary molars 239 –– gag reflex 75
Ankylosis 190–193 –– intense fear of dental injection 74, 75
Anorexia nervosa 538 –– directed breathing 69
Anterior cross bite 227 –– distraction 66, 67
Anterior middle superior alveolar nerve block (AMSA) injection 119 –– ethical, legal issues and parental consent 76, 77
Anterior open bite 234, 243 –– guided imagery 69
Anteroposterior discrepancies 224 –– humor 69
Anxiolysis –– hypnosis 69
–– antihistamines 144 –– memory restructuring 69
–– benzodiazepines 143, 144 –– modeling 67
–– definition 137 –– outcomes 71
–– evaluation 145 –– parental presence 68, 69
–– nitrous oxide/oxygen mixture –– positive reinforcement 66
–– adverse effects 142 –– protective stabilization
–– breathing practice 140 –– active immobilization 71, 72
–– contraindications 141, 142 –– passive immobilization 72–74
–– in COVID-19 era 142 –– providing control 65
–– informed consent 140 –– routine dental treatment
–– inhalation sedation 137–140 –– initial examination 70
–– monitoring 141 –– restorative treatment 70, 71
–– personnel safety 142 –– rubber dam and accessories 70
–– rapid induction technique 141 –– sound analgesia 69
–– rubber dam 141 –– ‘Tell-show-do’ technique 63–65
–– standard titration technique 141 –– time structuring 69
–– patient history 144, 145 –– voice control 68
566 Index

Behavior management –– endodontic treatment 4

–– classification 62 –– evidence-based dental care 3
–– and guidance 2 –– fluoride use 4
–– techniques 107 –– future trends 6
Behavior observation 81 –– interventions 5
Behaviour factors 469, 470 –– oral health care demands 5
Behcet’s disease 494 –– orthodontic treatment 5
Benzodiazepines 143, 144 –– preschool children report 4, 5
Bioactive Endodontic Cements (BECS) 336 –– prevalence and severity 4
Biodentine® 384 –– smile aesthetics 5
BiodentinTM cement 337 –– special care needs children 5
Bisphenol-A (BPA) 306 Child Oral Health Impact Profile (COHIP) 554
Bisphosphonates (BP) 545, 546 Child Perceptions Questionnaire (CPQ) 554
Bite wing radiograph 294 Child-centred dentistry
Bleeding disorders –– consent 556
–– coagulopathies 509 –– decision-making 555, 556
–– HHT 508 –– ethical issues 559, 560
–– thrombocytopenia 508, 509 –– oral health research 558, 559
Blood cells –– oral health-related quality of life 554, 555
–– anemia 506, 507 –– principle 554
–– neutropenia 507, 508 –– safeguarding 556, 557
–– sickle cell diseases 507 –– service evaluation 557
–– thalassemias 507 Childhood caries
Bottle-feeding associated S-ECC 283 –– age up to 3 years
Bulimia 538, 539 –– ART 285
–– ECC 283–285
–– S-ECC 283
C –– age 3 to 6 years
–– PMF 287–289
Calcium hydroxide 326 –– primary molar restorations 286–287
Calcium hydroxide apexification 404 –– restoring anterior primary teeth 290–291
Canavan disease 549 –– age 6 to 12 years
Candida albicans 502 –– molar incisor hypomineralization 294
Capnocytophaga sp. 348 –– pit and fissure caries 291–293
Cardiovascular diseases –– proximal surfaces of permanent teeth 293–294
–– microbial endocarditis and dental care 519 –– age 12 to 18 years
–– prevalence 518 –– alternative options for isolation 300–301
–– prevention protocol 520 –– cavity lining/base materials 301–302
Cariogram pie graph 261 –– cavity matrices 301
Carpenter syndrome 549 –– class II cavities 296–297
Casein phosphopeptide 267 –– dental amalgam 307
Casein phosphopeptide-amorphous calcium phosphate (CPP-­ –– dental materials 310–311
ACP) 267 –– enamel and dentine adhesives 302, 303
Castillo-morales palatal plate 541 –– equipment 299–300
Cavity lining/base materials 301–302 –– failure and repair of restorations 309–310
Cavity matrices 301 –– glass ionomer cements 303, 304
Celiac disease 451 –– permanent molars 308
Central nervous system (CNS) injuries 367 –– preformed metal crowns 307
Centric relation (CR) 476, 477 –– preparation and placement 300
Cephalometric radiograph 102 –– proximal and smooth surface caries 294–296
Cephalometrics 170–172 –– resin based composites 305–307
Cerebral palsy 530–532 –– veneers and prosthetic appliances 308–309
Cervical pulpotomy 337, 385, 386 Children’s Fear Schedule Survey–Dental Subscale (CFSS-DS) 47
Cervical resorption 401 Children’s participation 558
Cervical root resorption 400 Children's rights 6, 7
Charge-coupled device (CCD) technology 256 Chin blow 365
Chemoprophylaxis Chlorhexidine 267
–– microbial endocarditis and dental care 519 Chronic erythematous candidiasis 503
–– prevalence 518 Chronic generalized gingivitis 349
–– prevention protocol 520 Chronic gingivitis 348
Child engagement 558 Chronic hyperplastic candidiasis 503
Child oral health Chronic mucocutaneous candidiasis (CMC) 503
–– airborne Covid-19 6 Chronic mucosal biting 492, 493
–– appointment delays 6 Chronic periodontitis 353–356
–– dental auxiliary personnel 5 Chronic renal failure 522, 523
–– dental caries 4 Chronic respiratory disease 80, 542
Index
567 B–D
Class I amalgam restorations 307 –– tooth brushing 268, 269
Class II cavities 296–297 –– diagnosis and record keeping
Class II malocclusion 212–214, 218 –– detection of early caries 255
Class II RMGIC restoration 310 –– DIFOTI 256
Class III malocclusion 213 –– digital radiography 257–259
Classical apexification 403 –– direct visualization 255
Clefts 544, 545 –– laser/light fluorescence 256
Cleidocranial dysplasia (CCD) 183–185, 239 –– non-operative diagnostic methods 255
Coagulopathies 509 –– QLF 257
Coeliac disease 495 –– radiographic examination 255
Cognitive development –– tactile sensation 255
–– children’s thought process 12 –– diet 273–274
–– concrete operational stage 12, 17, 18 –– epidemiology and treatment 252
–– formal operational thought 12, 18, 19 –– fluoride gels 264
–– preoperational stage 12, 15–17 –– fluoride rinses 264
–– preventing dental fear 20, 21 –– fluoride tablets and drops 263
–– sensorimotor stage 12–15 –– fluoride toxicity 266–267
–– short-and long-term goals 12 –– fluoride varnish 265
–– tailoring oral messages 21, 22 –– mechanism of action 262–263
Colony-stimulating factor-1 (CSFL1) 180 –– milk fluoridation 263
Communication –– pathogenesis of
–– aspects 52 –– caries microbiology 248–250
–– with children 54 –– dental appliances and restorations 250–251
–– empathy and 55, 56 –– fermentable carbohydrates 248
–– nonverbal communication 52, 53 –– hereditary (genetic) factors 251
–– with parents 53, 54 –– physico-chemical process 248
–– verbal communication 53 –– salivary flow 250
–– written information 54 –– socio-economic status 250
Complicated crown fracture 383–386 –– thickness/maturation of dental plaque 248
Computer controlled administering of anesthesia (C-CLAD) 114, –– tooth morphology and structure 250
115 –– patient motivation 274–277
Concussion 372–373 –– presence of black stains 261
Cone beam computed tomography (CBCT) 102–104, 388 –– prevention and control of 262
Cone beam tomographic examination (CBCT) 398 –– probiotics 267–268
Congenital granular cell tumor 490 –– recall visit 277
Congenital heart disease 81, 540 –– silver diamine fluoride 265
Consent 556 –– toothpaste 264
Contemporary attrition 467 –– treatment strategy of 261
Cotton wool pellet 335 –– water fluoridation 263
COVID-19 6, 142 –– xylitol 267
Coxsackie virus 498 Dental education 2
Craniofacial anomalies 546–548 Dental erosion
Craniomandibular disorders (CMD) 478 –– abfraction 467
Crohn’s disease 494, 495 –– clinical examination and diagnosis 470, 471
Crouzon and Apert syndromes 546, 547 –– definition 466
Crowding 229 –– extrinsic factors 469, 470
Crown angulation 379 –– intrinsic factors 470
Crown dilaceration 379 –– prevalence and severity 467–469
Crown-root fracture 366, 370, 386, 387 –– prevention 471
Cvek’s partial pulpotomy 385 –– restoration 471, 472
Cystic fibrosis 542, 543 Dental fear
Cystic fibrosis transmembrane conductance regulator (CFTR) 542 –– behavior rating scale 47, 48
–– child misbehavior 39–41
–– classical conditioning 41, 42
–– cognitive vulnerability 43
D –– communication
Decision-making 555, 556 –– aspects 52
Dental amalgam 307 –– with children 54
Dental anxiety 40 –– empathy and 55, 56
Dental caries 85 –– nonverbal communication 52, 53
–– caries risk assessment 259–261 –– with parents 53, 54
–– chlorhexidine 267 –– verbal communication 53
–– clinical manifestation 252–253 –– written information 54
–– CPP-ACP 267 –– definition 40
–– dental plaque removal –– dental environment 56, 57
–– depth and morphology of pits and fissures 270–273 –– family stressors 44
568 Index
Dental fear (cont.)
–– genetic bases 44
–– helplessness and loss of control 43
–– issues with adolescents 50–52
–– pain threshold and experience of pain
–– attention to children 48
–– dental check-up visits 49
–– graphic scale 48
–– information providing 49
–– pain tolerance 47
–– sense of loss of control 49
–– parental dental fear 46
–– parenting styles 45, 46
–– physiological changes 46
–– self-management
–– age and maturity 50
–– child crying and coping behavior 50
–– therapeutic management 50
–– self-report measures 46, 47
–– social learning theory 42, 43
–– temperament 44, 45
–– uncooperative child behavior 39
Dental floss 270
Dental fluorosis 267
Dental health 3
Dental history 81
Dental knowledge 7, 8
Dental radiographic examination
–– criteria for 87, 88
–– extra oral radiographs
–– CBCT 102–104
–– cephalometric radiograph 102
–– ghost images and distortions 100–101
–– oblique lateral radiograph 103, 104
–– panoramic radiography 101, 102
–– guidelines 86
–– intraoral radiographs
–– bitewing radiographs 91, 93–95
–– collimation 90, 93
–– image detector holders 89, 92
–– image detectors 86, 88–91
–– imaging techniques 86, 89, 90
–– periapical radiograph 95–97
–– protective apron/thyroid gland shield 91
–– standard occlusal radiograph 97–100
–– patient radiation doses 86, 88
–– potential risks 86
Dental spacing 233–234
Dentin dysplasia (DD) 451
Dentinogenesis imperfecta (DGI) 449–451, 545
Dentist-child communication 139
Dentoalveolar trauma
–– classification 364
–– definition of 364
–– dental trauma history 368
–– epidemiology 364–366
–– etiology of 366–367
–– extraoral examination 368
–– IADT guidelines 369
–– intraoral examination 368
–– medical history 367
–– orthodontic management 406
–– permanent teeth (See Permanent teeth)
–– prevention of 407–409
–– primary teeth
–– follow-up and complications of 376–377
–– fractures of 370–372
–– luxation injuries 372–375
–– traumatic injuries 377–380
–– prognosis of injured teeth 405–406
–– radiographic examination 369
Dentosafe® 395
Denture-associated stomatitis 503
Developmental dental defects
–– developmental discolorations 454–456
–– differential diagnosis and treatment 456–458
–– tissue structure malformations
–– enamel, dentin and cementum 430, 432, 433
–– environmental developmental defects (See Environmental
developmental defects)
–– tooth number, size and morphology disturbances
–– causes and correlations 418–421
–– dental development 416–420
–– epidemiology and clinical phenotypes 422, 423
–– expert centers 421
–– supernumerary teeth 424, 425
–– syndromic oligodontia 422, 424
–– variations 424–431
Diabetes mellitus 357
–– definition 521
–– dental findings and treatment 521
DIAGNOdent (KaVo Dental Co) 256
Diet 273–274, 469
Digital image fiber-optic trans-illumination (DIFOTI) 256
Digital radiography 257–259
Direct pulp capping (DPC) 325–327, 336–337, 383
Disabilities
–– access and design 528
–– cerebral palsy and physical disability 530–532
–– classification 529
–– cognitive development 532, 533
–– dental treatment 529, 530
–– prevalence and preventive care 529
–– sensory
–– hearing problems (deafness) 533, 534
–– visual impairment blindness 533
Distal step occlusion 225
Disto-occlusal cavity 286, 287
Double teeth 426
Down syndrome 532
–– clinical features 540
–– dental findings and treatment 540–542
–– incidence 540
Drooling 512
Dry mouth 517
Duchenne muscular dystrophy 543
Dysgeusia 517
E
Early childhood caries (ECC) 283–285
Eating disorders 517
Ecological plaque hypothesis 248
Ectodermal dysplasia 541, 542
Ectopic eruption 209, 238
Ehlers-Danlos syndrome 453, 548
Enamel and dentine adhesives 302, 303
Enamel fracture 381
Enamel hypoplasia 378
Enamel-dentine crown fracture 370, 382
Endocardial microbial infection 519
Environmental developmental defects
–– amelogenesis imperfecta
–– definition 445
Index
569 D–G
–– dental rehabilitation 446, 449 –– contraindications 145
–– gene investigation and correlation 448 –– dental treatment 146–149
–– hypomatured-hypoplastic with taurodontism 446, 447 –– indications 145
–– hypoplastic type 445, 446 –– induction 146–148
–– masticatory forces 446, 447 –– operating room procedure 146
–– mechanisms 445 –– oral rehabilitation goals 145
–– dentin dysplasia 451 –– patient history 150
–– dentinogenesis imperfecta 449–451 –– pre-operative evaluation 145, 146
–– enamel dysplasia 442–444 –– safety 151
–– enamel fluorosis 441–443 –– stages 139, 140
–– histological examination 436 Genetic diseases
–– hypomineralization and hypomaturation 436 –– clefts 544, 545
–– intra-coronal dentin radiolucencies 451, 452 –– cystic fibrosis 542, 543
–– medical history 436 –– down syndrome 540–542
–– MIH 436–442 –– ectodermal dysplasia 541, 542
–– mineralization and maturation 436 –– familial mediterranean fever 544
–– molar incisor malformation 441, 442 –– muscular dystrophy 543, 544
–– ROD 451, 452 –– osteogenesis imperfecta 545, 546
–– systemic diseases and syndromes 451–454 –– syndromes and craniofacial anomalies 546–550
–– systemic/local causes 432, 434–435 Gingival health 3
Eosinophilic granuloma 506 Gingival hyperplasia 351, 352
Epidermolysis bullosa 453 Gingival index (GI) 83
Epilepsy 537 Gingival recession 358
Epstein Barr virus (EBV) 497 Gingivitis 348–350
Er:YAG laser 287 Glass ionomer cements (GIC) 303, 304
Erythema migrans 487, 488 Gluten-sensitive enteropathy (GSE) 495
Erythema multiforme (EM) 503, 504 Graft-versus-host disease (GvHD) 504, 505
Eudomembranous candidiasis 502 Growth
European Academy of Pediatric Dentistry (EAPD) 62 –– area relocation 160, 161
Ewing’s sarcomas 516 –– bone age 27, 30
Extraoral examination 81, 83, 84 –– bone and cartilage 162, 163
Extra oral wound 364 –– cephalometrics 170–172
Extrusive luxation 374, 393–395 –– childhood growth 26
–– dental age 27, 30
–– growing face features 156, 157
–– growth fields 160
F –– infantile growth 26
Facemask 213 –– IUGR 30
Facemask treatment 217 –– malocclusions 172–175
Familial hypophosphatemia 452 –– mandible
Familial mediterranean fever 544 –– lingual tuberosity 168
Family and social history 80 –– mandibular condyle 168, 169
Ferric sulphate 331 –– ramus 167, 168
Fibroepithelial polyp 489 –– ramus uprighting 169, 170
Fluoride 471 –– mandibular condyle 160, 161
Fluoride gels 264 –– MPH/target height 27
Fluoride rinses 264 –– nasomaxillary complex
Fluoride tablets and drops 263 –– arch lengthening 165
Fluoride toxicity 266–267 –– maxillary tuberosity 165, 166
Fluoride varnish 265 –– palatal remodeling and alveolar development 166
Formocresol 331 –– primary displacement 167
Fragile X chromosome syndrome 546 –– neurocranium
Frankel applian 213 –– basicranium 164, 165
Frankl rating scale 47, 48 –– calvaria 164
Frenum pull 358–359 –– palate inferiorly relocation 161
Functional posterior crossbite 229 –– prenatal facial growth and development
Fungal infections 502, 503 –– characteristic postnatal resorptive fields 160
Furcation bone infection 322 –– cranial nerve 157, 158
–– eyes location 157, 158
–– hyoid arch 158, 159
–– interorbital dimension 157, 158
G –– mandibular arch 158, 159
Gastroesophageal reflux disease (GERD) 470, 523 –– oral and paired nasal chambers 159
Gastrointestinal disease 494 –– prenatal growth 26
Gene mutations 539 –– primary displacement 161–163, 165
General anesthesia (GA) 285 –– process 26
–– admission to hospital 145, 146 –– pubertal growth 26
570 Index

Growth (cont.) Incontinentia pigmenti syndrome 549, 550

–– puberty Indirect pulp capping (IPC) 323, 325, 335–336
–– delayed puberty 35 Inequalities 4, 5
–– development 34 Infectious mononucleosis (IN) 497, 498
–– environmental, metabolic and genetic factors 34 Inferior alveolar nerve (IAN) block 117, 118, 120
–– precocious puberty 34, 35 Inflammatory root resorption 401
–– rate of growth 26 Informed consent 7
–– secondary displacement 161 Intellectual quotient (IQ) 532
–– SGA 30 Intelligence quotient (IQ) 540
–– short stature 30–34 Interdental brushes 270
–– tall stature 32, 34 Interim therapeutic restorations (ITR) 286
–– velocity 27, 30 Internal resorption 400, 402
–– weight and height measurement 26–29 International association for disability and oral health (iADH) 528
Growth hormone deficiency 32 International Association of Dental Traumatology (IADT) 369
International caries detection and assessment system (ICDAS) 254
International classification functionality, disability and health
H (ICF) 528
Hall technique 289 Intraligamental anesthesia (ILA) 121, 122
Hamartomas 490, 491 Intraoral examination
Hand-foot-and-mouth disease 498 –– dental occlusion 84, 85
Hand-Schüller-Christian disease 506 –– hard dental tissues 83–85
Hank’s Balanced Salt Solution (HBSS) 395 –– pathology 81
Hearing problems (deafness) 533, 534 –– periodontal tissues 83
Heck’s disease 500 –– soft tissue 83
Hemangiomas 490, 491 Intraosseous anesthesia 120, 121
Hematological disease Intrapulpal anesthesia 122
–– anemia 506 Intraseptal anesthesia 120
–– bleeding disorders Intrauterine growth retardation (IUGR) 30
–– coagulopathies 509 Intrusion of maxillary primary left central incisor 375
–– HHT 508 Intrusive luxation 373, 391, 393
–– thrombocytopenia 508, 509
–– Hodgkin’s disease 505
–– langerhans cell histiocytosis 506 J
–– leukemias 506 Jet injection technique 115, 116
–– lymphomas 505 Juvenile idiopathic arthritis (JIA) 524
–– neutropenia 507, 508
–– NHL 506
–– sickle cell diseases 507 K
–– thalassemias 507
Hemophilia A 509 Kaposi’s sarcoma 500
Hemophilia B 509
Hemorrhagic pulp 335
Hereditary gingival fibromatosis (HGF) 352
L
Hereditary hemorrhagic telangiectasia (HHT) 508 Labial ectopic and delayed eruption 380
Herpangina 498 Langerhans cell histiocytosis 506
Herpes labialis 496 Laser/light fluorescence 256
Herpes simplex 495, 496 Lateral luxation 373
High molecular weight lipopolysaccharide (HMWLPS) 355 Lateral root bending 379
Hodgkin’s disease (HD) 505 Left-side unilateral posterior crossbite 212
Human herpes virus-8 (HHV-8) 500 Leptotrichia sp. 348
Human Immunodeficiency virus (HIV) 500 Lesch-Nyhan syndrome 549
Human papilloma virus (HPV) 499 Letterer-Siwe disease 506
Hydrochloric acid (HCl) 470 Leukemias 356, 506
Hydroxyethylmethacrylate (HEMA) 303 Lingual holding arch 224
Hyperglycemic coma 521 Lip jewelry 359
Hypersensitivity reactions 504 Lip sucking 243–244
Hypoglycemic coma 521 Local anesthesia
Hypohydrotic ectodermal dysplasia 184 –– behavior guidance
Hypomineralized second primary molars (HSPM) 253 –– administration 123–125
Hypophosphatasia 452 –– fear of needles 122
Hypoplasia 370 –– patient preparation 122
Hyrax-type RME 212 –– C-CLAD 114, 115
–– craniofacial complex of children 115–118
–– dosage 113, 114
I –– IAN block 117, 118, 120
Idiopathic juvenile rheumatoid arthritis (IJRA) 479 –– ILA 121, 122
Impetigo 500, 501 –– injected solution
Index
571 G–O
–– rate/speed 114 Molar incisor malformation (MIM) 441, 442
–– temperature 114 Monofluorophosphate fluoride (MFP) 264
–– injection within bone Mouth breathing 243
–– intraseptal anesthesia 120 Mouth-guards 407–409
–– IO anesthesia 120, 121 Moyers' analysis 233
–– injectors and needles 112, 113 Moyers' mixed dentition analysis 233
–– intrapulpal anesthesia 122 Mucoceles 510
–– jet injection technique 115, 116 Mucocutaneous disease 503
–– local complications –– allergic reactions 504, 505
–– cheek, lip/tongue injury 125, 126 –– erythema multiforme 503, 504
–– edema 125 –– GvHD 504, 505
–– hematoma 125 Mucositis 517
–– needle breakage 125 Multifactorial disease 248
–– pain and sense of burning 125 Multifocal epithelial hyperplasia (MEH) 500
–– paraesthesia 125 Mumps 499
–– trismus 125 Muscular dystrophy 543, 544
–– vasoconstrictors 125, 127
–– local infiltration anesthesia 116–119
–– palatal techniques N
–– AMSA injection 119 Nail biting 243
–– nasopalatine nerve block 119, 120 Nance button anchorage 211
–– P-ASA 120 Necrotic immature (open apex) teeth 402
–– systemic complications 126 Necrotic mature (closed apex) teeth 402
–– topical anesthesia 115, 117 Needle-phobia 74, 75
–– topical anesthetics 112 Neoplasms
–– vasoconstrictor 113 –– acute lymphoblastic leukemia 516
Local infiltration anesthesia 116–119 –– clinical finding and treatment 517–519
Localized aggressive periodontitis 353 –– dental care protocol 518
Localized anterior crossbite 208, 210, 217 –– osteosarcomas 516
Localized gingivitis 349 Neurofibromatosis type I (NF1) 352, 547, 549
Localized juvenile spongiotic gingival hyperplasia (LJSGH) 350, Neuropsychiatric/psychological disorders
351 –– ADHD 535–537
Localized periodontitis 356 –– ASD 534–536
Luxation injuries 372–375 –– epilepsy 537
Lymphangiomas 491 –– nutrition and weight 537–539
Lymphomas 505 Neurotoxicity 518
Neutropenia 507, 508
M Nitrous oxide (N2O)
–– adverse effects 142
Malocclusion 479, 546 –– breathing practice 140
Mandibular anterior teeth 284 –– contraindications 141, 142
Mandibular primary molars 317 –– in COVID-19 era 142
Mandibular torus 488 –– informed consent 140
Marginal fractures 305 –– inhalation sedation 137–140
Masticatory system 478 –– monitoring 141
Maxillary impacted permanent canine 240 –– personnel safety 142
Maxillary incisors 297 –– rapid induction technique 141
Maxillary lateral incisor agenesis 238 –– rubber dam 141
Maxillary primary canine 319 –– standard titration technique 141
Maxillary primary left central incisor 373 Non-complicated crown fracture 392
Maxillary primary right central incisor 291, 372 Non-Hodgkin’s lymphoma (NHL) 500, 506
Maxillofacial disorders 548 Noonan syndrome 547, 548
McNamara-type RME 212 NuSmile 307
Measles 498, 499 NuSmile zirconium crown 308
Medical history 80–82 Nutrition 537–539
Medicines, dental erosion 469 Nyvad’ visual-tactile classification system 254
Medium ankyloglossia 360
Melanocorin-1 receptor gene (MC1R) 44
Mesio-buccal root 333
Mesiodens 238
O
Methacryloyl-oxy-dodeca-pyridinium bromide (MDPB) 311 Obesity 539
Microflora transmission 250 Odontoma-type dysplasia 379
Midparental height (MPH) 27 Omni-matrix ™ 302
Milk fluoridation 263 One-phase treatment 212
Mineral trioxide aggregate paste (ΜΤΑ) 326, 329–330 OptiView™ (Kerr) 301
Mixed dentition analysis 233 Oral dryness 511, 512
Molar-incisor hypomineralization (MIH) 296, 378, 436–442 Oral hairy leukoplakia (OHL) 500
572 Index

Oral health-related quality of life (OHRQoL) 554, 555 Orofacial system (OFS)
Oral hygiene 106 –– anamnestic records 480
Oral hygiene instructions 350 –– centric relation/centric occlusion 476, 477
Oral lesions –– clinical examination 480, 481
–– bacterial infections –– components 476
–– acute necrotizing ulcerative gingivitis 502 –– diagnosis 480, 481
–– impetigo 500, 501 –– eccentric mandibular movements 477
–– scarlet fever 501 –– eccentric positions 477
–– tuberculosis 501, 502 –– epidemiology 478
–– fungal infections 502, 503 –– etiology 478–480
–– hematological disease –– functions 476
–– anemia 506 –– imaging 480
–– bleeding disorders 508, 509 –– maxillomandibular relationships 476
–– Hodgkin’s disease 505 –– maximum intercuspation 476
–– langerhans cell histiocytosis 506 –– rest position 477
–– leukemias 506 –– treatment strategies 482
–– lymphomas 505 –– vertical dimension 477, 478
–– neutropenia 507, 508 Orofacial-myofunctional therapy 243
–– NHL 506 Orthodontic brackets 239, 251
–– sickle cell diseases 507 Orthodontic management
–– thalassemias 507 –– harmful oral habits
–– lymphangiomas 491 –– lip sucking 243–244
–– mucocutaneous disease 503 –– mouth breathing 243
–– allergic reactions 504, 505 –– nail biting 243
–– erythema multiforme 503, 504 –– pacifier overuse 240–242
–– GvHD 504, 505 –– position of tongue at swallowing 242–243
–– oral mucosal and boney abnormalities –– thumb sucking 240–242
–– cysts 488 –– intervention in mixed dentition
–– erythema migrans 487, 488 –– arch space anomalies 229–233
–– mandibular torus 488 –– dental spacing 233–234
–– palatal torus 488 –– Moyers' mixed dentition analysis 233
–– reactive overgrowths –– occlusal anomalies 234–237
–– congenital granular cell tumor 490 –– partial archwire and springs 232
–– fibroepithelial polyp 489 –– Staley and Kerber analysis 233
–– peripheral giant cell lesion 489, 490 –– Tanaka and Johnston analysis 233
–– peripheral ossifying fibroma 489 –– tooth number and eruption related anomalies 237–240
–– pyogenic granulomas 488, 489 –– intervention in primary dentition
–– swellings 490 –– arch space anomalies 218–223
–– salivary gland disease –– occlusal anomalies 223–229
–– acute suppurative sialadenitis 511 –– profile evaluation
–– drooling 512 –– convex profile 212–218
–– mucoceles 510 –– orthodontic vs. orthopedic treatment 208
–– ranula 510 –– straight profile 208–210
–– recurrent parotitis 511 Orthodontic treatment 2
–– sialolithiasis 510, 511 Orthodontics 479, 480
–– xerostomia 511, 512 Orthopantomographic (OPG) radiograph 27, 30
–– ulceration (See Oral ulceration) Osler-Weber-Rendu syndrome 508
–– vascular malformations 490, 491 Osteogenesis imperfecta (OI)
–– viral infections –– bisphosphonates 545, 546
–– hand foot and mouth disease 498 –– classification 545
–– herpangina 498 –– malocclusion 546
–– herpes simplex 495, 496 –– prevalence 545, 546
–– herpes zoster 496, 497 Osteopetrosis 453
–– HIV 500 Osteosarcomas 516
–– HPV 499 Over-the-counter fluoridated toothpaste 264
–– infectious mononucleosis 497, 498
–– measles 498, 499
–– MEH 500 P
–– mumps 499 Palatal anterior superior alveolar block (P-ASA) 120
–– warts 499 Palatal torus 488
Oral ulceration Panoramic radiography 101, 102
–– aphthous ulceration 492–494 Partial pulpotomy 337, 338, 341, 384, 385
–– Crohn’s disease 494, 495 Passive immobilization 72–74
–– gastrointestinal disease 494 Patient-reported experience measures (PREMs) 557
–– GSE 495 Patient-reported outcome measures (PROMs) 557
–– traumatic oral ulceration 491–493 Perikymata 258
Orange plaque (biofilm) 262 Perimylolysis 470
Index
573 O–R
Periodontal diseases Preventive resin restoration (PRR) 292–293
–– frenum pull 358–359 Prevotella sp. 348
–– gingival hyperplasia 351, 352 Primary failure of eruption (PFE) 183
–– gingival recession 358 Primary molar hypomineralization 254
–– gingivitis 348–350 Primary molar pulpotomy 328–331
–– LISGH 350, 351 Primary molar restorations 286–287
–– periodontitis Probably toxic dose (PTD) 266
–– acute ulcerative gingivitis 357–358 Pseudomembraneous candidiasis 500
–– chronic periodontitis 353–356 Psychotropic analgesic nitrous oxide (PAN) 139
–– diabetes mellitus and 357 Puberty
–– localized aggressive periodontitis 353 –– delayed puberty 35
–– with systemic disease 356 –– development 34
Peripheral giant cell lesion 489, 490 –– environmental, metabolic and genetic factors 34
Peripheral ossifying fibroma 489 –– precocious puberty 34, 35
Permanent teeth Public health systems 85
–– endodontic evaluation and management of 401–405 Pulp canal obliteration 399
–– follow-ups of 390, 398, 401 Pulp necrosis 398
–– fractures of Pulp sensibility testing 398
–– complete enamel fracture 380–381 Pulp therapy
–– complicated crown fracture 383–386 –– cariously necrotic primary teeth 316
–– crown-root fractures 386, 387 –– diagnostic procedure
–– enamel infraction 380 –– clinical examination 318–320
–– root fracture 387–389 –– dental surgery 316–318
–– uncomplicated crown fracture 381–383 –– medical history 316
–– luxation injuries to –– radiographic examination 320–321
–– avulsion 394–396 –– symptoms and signs in 323
–– concussion 389–390 –– management of emergency 321–324
–– extrusive luxation 393, 394 –– treatment of
–– intrusive luxation 391, 393 –– direct pulp capping 325–327
–– lateral luxation 390–391 –– indirect pulp capping 323, 325
–– subluxation (loosening) 390 –– primary molar pulpotomy 328–331
–– post-traumatic complications of 396–401 –– pulpectomy/root canal treatment 331–334
Pervasive developmental disorder (PDD) 534 –– young carious permanent teeth
Pharmacologic behavioral management –– cervical pulpotomy 337
–– general anesthesia (See General anesthesia (GA)) –– direct pulp capping 336–337
–– sedation –– immature carious teeth immature carious teeth 337–341
–– acceptance and preferences 133, 134 –– indirect pulp capping 335–336
–– anatomical airway 134, 135 –– partial pulpotomy 337
–– anxiolysis (See Anxiolysis) –– restoring color of discolored teeth 341–342
–– BLS training 135 Pulpitis 376
–– child and parent preparation 135 Pyogenic granulomas 488, 489
–– deep sedation 133
–– definition 132
–– documentation 136, 137 Q
–– general anesthesia 133 22q11 deletion syndrome 549
–– guidelines 132 Qualitative methods 559
–– health status and cooperation assessment 134, 135 Quantitative light-induced fluorescence (QLF) 257
–– informed consent 135 Quantitative methods 558
–– minimal sedation 132
–– moderate sedation 133
–– monitoring and resuscitation equipment 136, 137
–– parental expectations 132
R
–– physical status 134 Rampant caries 518
–– pre-operative assessment and consultation 134 Ranula 510
–– respiratory airway 134 Rapid induction technique 141
–– safety 151 Rearmost, upmost, and midmost (RUM) 476
Phenoxymethylpenicillin 323 Recurrent aphthous stomatitis (RAS) 492
Physical disability 530–532 Recurrent parotitis 511
Plaque index (PI) 83 Regenerative’ endodontic approach 339, 403
Plasma cell gingivitis (PCG) 351 Regional odontodysplasia (ROD) 451, 452
Polyacid modified composites 306 Relative analgesia (RA) 139, 140
Posterior cross bite 228 Replacement resorption (ankylosis) 387, 399
Postgraduate education 8 Resin based composites 305–307
Post-traumatic root resorptions 377 Resin-modified glass ionomer cement (RMGIC) 304, 440
Prader-Willi syndrome 549 Revised Iowa Dental Control Index (R-IDCI) 19
Predominant type 540 Rickets 452
Preformed metal crowns (PMCs) 145, 287–289, 307 Riga-Fede disease 492, 493
574 Index

Riga-Fede granuloma 492, 493 Standard titration technique 141

Root canal obliteration 320, 396 Stannous fluoride (SnF2) 264
Root canals 332 Stephan curves 274
Root duplication 379 Steven’s Johnson syndrome (SJS) 504
Root fractures 372, 387–389 Streptococcus mutans 248, 249
Rubber dam isolation 383 Subluxation (loosening) 373
Supernumerary teeth 238
Systemic auto-inflammatory disorder (SAID) 494
S
Safeguarding 556, 557
Sagittal maxilla-mandible discrepancy 212
T
Salivary gland disease Tall stature 32, 34
–– acute suppurative sialadenitis 511 Target height 27
–– drooling 512 Telescopic occlusion 229
–– mucoceles 510 Tell-show-do technique 533
–– ranula 510 Temperament 44, 45
–– recurrent parotitis 511 Temporomandibular disorders (TMD), see Orofacial system (OFS)
–– sialolithiasis 510, 511 Temporomandibular joint (TMJ) 81
–– xerostomia 511, 512 Thalassemias 507
Save-Tooth® 395 Thrombocytopenia 508, 509
Scarlet fever 501 Tongue thrusting 242
Second primary molar 325 Tooth brushing 268, 269
Sedation Tooth brushing method 470
–– acceptance and preferences 133, 134 Tooth decay (DMFT) 4
–– anatomical airway 134, 135 Tooth eruption
–– BLS training 135 –– ankylosis 190–193
–– child and parent preparation 135 –– delayed eruption
–– deep sedation 133 –– generalized delay 183, 184
–– definition 132 –– localized delay 184–188
–– documentation 136, 137 –– ectopic eruption 188–191
–– general anesthesia 133 –– eruption cysts 191, 194
–– guidelines 132 –– eruption mechanism 179, 180
–– health status and cooperation assessment 134, 135 –– eruption sequence 178, 179
–– informed consent 135 –– eruptive phase 178
–– minimal sedation 132 –– functional phase 178
–– moderate sedation 133 –– inflammation 192, 194, 195
–– monitoring and resuscitation equipment 136, 137 –– neonatal teeth 182, 183
–– parental expectations 132 –– pre-eruptive phase 178
–– physical status 134 –– primary teeth
–– pre-operative assessment and consultation 134 –– extraction 196–200
–– respiratory airway 134 –– shedding 196, 197
Selenomonas sp. 348 –– teething symptoms
Sensory disabilities –– cross-sectional survey 180
–– hearing problems (deafness) 533, 534 –– dental follicle 180
–– visual impairment blindness 533 –– local treatment 181
Service evaluation 557 –– systemic treatment 181, 182
Severe early childhood caries (S-ECC) 283 –– transplantation
Severe infra-occlusion 242 –– extraction and re-implantation 200–202
Severe periodontal lesions 354 –– intentional re-implantation 203, 204
Shingles 497 –– teeth anterior 202, 203
Short stature 30–34 Tooth revascularization treatment 340
Sialolithiasis 510, 511 Tooth wear
Sickle cell diseases 507 –– attrition and abrasion 466, 467
Silver diamine fluoride (SDF) 265 –– bruxism 467–469
Skeletal discrepancy 210 –– erosion
Skeletal open bite 234 –– abfraction 467
Sleep bruxism 467, 479 –– clinical examination and diagnosis 470, 471
Small for gestational age (SGA) 30 –– definition 466
Social learning theory 42, 43 –– extrinsic factors 469, 470
Sodium fluoride (NaF) 264 –– intrinsic factors 470
Soft tissue swellings 490 –– prevalence and severity 467–469
Sound analgesia 69 –– prevention 471
Space regaining 232 –– restoration 471, 472
Space-maintainer obsolete 231 Topical anesthesia 115, 117
Special care dentistry 528 Topical anesthetics 112
Squamous papilloma 499 Total care treatment plan 103
Index
575 R–Z
–– factors 105–108 –– herpangina 498
–– presentation to parents 105 –– herpes simplex 495, 496
–– specialist pediatric dentist, referral to 109 –– herpes zoster 496, 497
Tourette syndrome 546 –– HIV 500
Toxic epidermal necrolysis syndrome (TENS) 504 –– HPV 499
Transmission electron microscope 250 –– infectious mononucleosis 497, 498
Transpalatal arch 231 –– measles 498, 499
Transverse discrepancy 208, 210 –– MEH 500
Traumatic dental injuries (TDI) 367 –– mumps 499
Traumatic oral ulceration –– warts 499
–– causes 491 VistaProof (Durr Dental) systems 256
–– chronic mucosal biting 492, 493 Visual impairment blindness 533
–– diagnosis 491 Vomiting 470
–– Riga-Fede disease and granuloma 492, 493 von Recklinghausen disease 352, 547, 549
Treacher Collins syndrome 546, 547 von Willebrand’s disease (vWD) 509
Tricho-dento-osseous syndrome 549
Tuberculosis (TB) 501, 502
Tuberous sclerosis 453 W
Tunnel restorations 297
Warts 499
Turner syndrome 547
Water fluoridation 263
Two-phase treatment 212
Weight loss 538
White or yellow-brown spots 378
White ΜΤΑ 329
U
Unilateral posterior crossbite (UPCB) 479
Upper left canine 219 X
Upper lip edema 365
US dental schools 2 Xerostomia 511, 512
X-linked recessive trait (Xq13.1 gene) 542
Xylitol 267
V
Varicella zoster 496, 497
Verruca vulgaris 499
Z
Viral infections Zone of proximal development (ZPD) 15
–– hand foot and mouth disease 498 Z-shaped spring 236