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The document is a description of the book 'Pediatric Endodontics: Current Concepts in Pulp Therapy for Primary and Young Permanent Teeth' edited by Anna B. Fuks and Benjamin Peretz, which focuses on advancements in pediatric dentistry, particularly in pulp therapy. It emphasizes a shift towards conservative treatment approaches for pulp injuries in children, highlighting the importance of understanding the biological aspects of the pulp and the implications for treatment. The book aims to provide comprehensive knowledge for dental professionals to improve care for pediatric patients.

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100% found this document useful (1 vote)
34 views84 pages

Pediatric Endodontics Current Concepts in Pulp Therapy For Primary and Young Permanent Teeth 1st Edition Anna B. Fuks Instant Download

The document is a description of the book 'Pediatric Endodontics: Current Concepts in Pulp Therapy for Primary and Young Permanent Teeth' edited by Anna B. Fuks and Benjamin Peretz, which focuses on advancements in pediatric dentistry, particularly in pulp therapy. It emphasizes a shift towards conservative treatment approaches for pulp injuries in children, highlighting the importance of understanding the biological aspects of the pulp and the implications for treatment. The book aims to provide comprehensive knowledge for dental professionals to improve care for pediatric patients.

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Bradley
Pediatric
Endodontics
Current Concepts in
Pulp Therapy for Primary and
Young Permanent Teeth

Anna B. Fuks
Benjamin Peretz
Editors

123
Pediatric Endodontics
Anna B. Fuks • Benjamin Peretz
Editors

Pediatric Endodontics
Current Concepts in Pulp Therapy
for Primary and Young Permanent Teeth
Editors
Anna B. Fuks Benjamin Peretz
Department of Pediatric Dentistry Department of Pediatric Dentistry
The Hebrew University Hadassah The Maurice and Gabriela Goldschleger
School of Dental Medicine School of Dental Medicine
Jerusalem Tel Aviv University
Israel Tel Aviv
Israel

ISBN 978-3-319-27551-2 ISBN 978-3-319-27553-6 (eBook)


DOI 10.1007/978-3-319-27553-6

Library of Congress Control Number: 2016933125

Springer Cham Heidelberg New York Dordrecht London

© Springer International Publishing Switzerland 2016


This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recita-
tion, broadcasting, reproduction on microfilms or in any other physical way, and transmission or infor-
mation storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar
methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publica-
tion does not imply, even in the absence of a specific statement, that such names are exempt from the
relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, express or implied, with respect to the material contained herein or for any errors
or omissions that may have been made.

Printed on acid-free paper

Springer International Publishing AG Switzerland is part of Springer Science+Business Media


(www.springer.com)
This book is dedicated to
Moises Fuks, my beloved husband and
long-term companion and friend
and to
Tamar, Neta and Alona Peretz, my beloved
and precious family
Anna B. Fuks and Benjamin Peretz
Preface

The initial idea for writing this book came because we felt that there has been an explo-
sion of scientific knowledge on the understanding of the pulp tissue in the last two
decades, which, in turn, affect the proper treatment for various pulp pathological condi-
tions. This immense advancement has included the primary pulp also, and pediatric
dentistry today, with regard to pulp treatment, can provide a better, more problem-ori-
ented therapy and treatment to the affected primary pulp. Therefore, when we were
approached by the Springer representative to write this book, we gladly agreed.
We felt that there was a need for students, undergraduate and postgraduate alike, as
well as for the professional community to be familiarized with the current “state of the
art” on pediatric endodontics. We made all efforts to cover the various aspects of the
dentin-pulp complex in pediatric dentistry: from the understanding of biological con-
cepts of the healthy pulp, through the pulp reactions to the deleterious effects of car-
ies, to the various treatment modalities for each type of pulp injury, to the adverse
reactions to various pulp dressing materials, and to the postoperative prognosis.
The better understanding of these topics led us to conclude that a conservative
approach in the treatment of reversibly inflamed pulp needs to be emphasized. Thus,
considerable attention has been given to the conservative approach to pulp treatment
in primary and young permanent teeth. Our message stresses the paradigm shift
toward conservative treatment modalities, relying on an accurate diagnosis based on
signs and symptoms to assess the appropriateness of the technique for a specific case.
Notwithstanding, the traditional modes of treatment are also covered.
Understanding the new concepts regarding pulp treatment will guide practicing
pediatric dentists and general dentists to select the proper mode of treatment.
A special emphasis has also been given to the future of pulp treatment, in light of
the innovative knowledge on stem cells. At present, there is a consensus that the
future of medicine and dentistry, particularly of pulp treatment, lies in the thorough
research on stem cells.
We hope that this text will be useful to all students and dentists who treat chil-
dren, to provide a better care for their teeth.

Jerusalem, Israel Anna B. Fuks


Tel Aviv, Israel Benjamin Peretz

vii
Contents

1 Pediatric Endodontics: Past and Present Perspectives


and Future Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Anna B. Fuks and Benjamin Peretz
2 The Primary Pulp: Developmental and Biomedical
Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
Anna B. Fuks, Josimeri Hebling, and Carlos Alberto de Souza Costa
3 Clinical Pulpal Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
Marcio Guelmann
4 Indirect Pulp Treatment, Direct Pulp Capping,
and Stepwise Caries Excavation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
James A. Coll
5 Pulpotomy Techniques: Cervical (Traditional) and Partial . . . . . . . . . 51
Kaaren G. Vargas, Anna B. Fuks, and Benjamin Peretz
6 Pulpectomy and Root Canal Treatment (RCT)
in Primary Teeth: Techniques and Materials . . . . . . . . . . . . . . . . . . . . . 71
Moti Moskovitz and Nili Tickotsky
7 Restoration of Pulp-Treated Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
Kevin J. Donly and Jungyi Alexis Liu
8 Pulp Therapy for the Young Permanent Dentition . . . . . . . . . . . . . . . 117
Eyal Nuni
9 The Future: Stem Cells and Biological Approaches
for Pulp Regeneration. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
Jacques E. Nör and Carolina Cucco

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163

ix
Pediatric Endodontics: Past and Present
Perspectives and Future Directions 1
Anna B. Fuks and Benjamin Peretz

Contents
1.1 Pediatric Endodontics ........................................................................................................ 2
1.2 Historical Perspective ........................................................................................................ 3
1.3 The Scope of the Book....................................................................................................... 3
1.4 The Aim of the Book ......................................................................................................... 4
References ................................................................................................................................... 5

Dentistry for children is one of the most needed of all specialties in dentistry. Yet,
unawareness of newer concepts of present-day pediatric dentistry practice and the
ultimate goals to be achieved still exist. The value of teaching pediatric dentistry can-
not be overestimated as inadequate or unsatisfactory dental treatment during child-
hood may damage permanently the entire masticatory apparatus, leaving the individual
with many of the dental problems so common in today’s adult population [1].
The utmost goals of modern pediatric dentistry are to bring children into the
permanent dentition after natural exfoliation of their healthy and/or properly treated
primary teeth and instill a positive attitude toward keeping habits of optimal dental
and oral health.

A.B. Fuks, DDS (*)


Department of Pediatric Dentistry, The Hebrew University
Hadassah School of Dental Medicine, Jerusalem, 12272, Israel
e-mail: [email protected]
B. Peretz, DMD
Department of Pediatric Dentistry, The Maurice and Gabriela
Goldschleger School of Dental Medicine, Tel Aviv, Israel
e-mail: [email protected]

© Springer International Publishing Switzerland 2016 1


A.B. Fuks, B. Peretz (eds.), Pediatric Endodontics: Current Concepts in Pulp
Therapy for Primary and Young Permanent Teeth,
DOI 10.1007/978-3-319-27553-6_1
2 A.B. Fuks and B. Peretz

1.1 Pediatric Endodontics

Pediatric dentistry is a unique specialty that deals with the total and comprehensive
oral health care of children. As such, it involves all aspects of oral care ranging from
prevention to restorative treatments. Historically, pediatric dentistry has evolved
from an extraction-oriented practice at the beginning, where primary teeth with
inflamed pulps were mostly extracted, and no focus has been put on preserving the
pulp, to a specialty based on emphasizing prevention of oral and dental diseases.
A more conservative approach has been developed during the last decades
regarding dental caries and specific modes of treatment such as minimal invasive
dentistry and an increase use of prevention materials (mainly containing fluoride).
This approach has been attributed to both developed diagnostic criteria and tools
and to the new dental products and materials in the market. This approach goes
further with regard to pulp therapy. It has long been established that the human
dental pulp has a remarkable potential for self-healing when encountering a severe
insult, especially in young patients, mainly due to the high degree of cellularity and
vascularity. Incomplete caries removal, stepwise excavation, and indirect pulp treat-
ment have been proposed to treat reversibly inflamed pulps. In addition, several
techniques for managing irreversibly inflamed or necrotic pulps have been intro-
duced in pediatric dentistry practice. Exposure of the pulp may occasionally be due
to caries but may also occur by accident during cavity preparation or by fracture of
the crown of the permanent maxillary incisors in particular.
Despite the extensive progress that has been achieved in prevention of dental
caries worldwide, and the variety of treatment modalities to treat inflamed and/or
infected pulp, a remarkable number of complications of untreated or poorly treated
primary teeth and/or young immature permanent teeth are still encountered. This
demands exact diagnosis, thorough knowledge of pulpal conditions and therapies,
and also the value of the individual tooth for the occlusal development. Hence, pedi-
atric endodontics has its own characteristics and includes the pulpal treatment of
primary and young immature permanent teeth. It must always be seen in the total
context of the dentition and the patient.
A review of the anatomy of primary teeth readily explains the frequent need for
pulp therapy in these teeth. Specifically, Finn [1] and Ash [2] described twelve basic
differences between primary and permanent teeth that can be summarized as fol-
lows: the enamel is thinner on primary teeth than on permanent teeth, and the thick-
ness of the dentin between the pulp chambers and the enamel in primary teeth is less
than in permanent teeth. The pulp, therefore, is correspondingly closer to the outer
surface, and dental caries can progress and penetrate into the dentin more rapidly,
leaving the tooth more susceptible to infection. Thus, pulp exposures caused by car-
ies occur more frequently in primary teeth. If infection spreads to the alveolar bone,
the developing permanent tooth may also be affected.
Pulp treatment of young permanent teeth must take into consideration the life
expectancy of the young patient and provide the best conditions for the roots to
develop and mature.
The practitioner should be familiar with the different treatment approaches to be
able to select the most appropriate modality for each specific clinical situation.
1 Pediatric Endodontics: Past and Present Perspectives and Future Directions 3

1.2 Historical Perspective

The first method of capping exposed pulps was described by Phillip Pfaff, a dentist
at the court of the Prussian King Friedrich II in Berlin in 1756 who used gold
foils [3]. Several agents for direct pulp capping have been recommended ever since.
The assumption that the pulp tissue must be irritated by cauterization in order to
heal prevailed until the end of the nineteenth century, and most materials were used
empirically. At the beginning of the twentieth century, it became obvious that micro-
organisms were the reason for pulp inflammation, and more attention was drawn to
disinfecting agents that, although effective, were very cytotoxic. The lack of proper
tools for achieving accurate diagnoses led to insufficient assessment of the pulp
status leading to incorrect treatment selection. Thus, due to this fact, necrotic pulps
were sometimes capped [3].
The first scientific clinical study to compare different capping materials was
made by Dätwyler in 1921, whereupon zinc oxide-eugenol showed the best results.
One year later, Rebel performed the first animal experiments with disastrous results,
so he regarded the exposed pulp as a doomed organ. In 1920, Hermann introduced
calcium hydroxide for root canal fillings. Between 1928 and 1930 he studied the
reaction of vital pulp tissue to calcium hydroxide to prove that it was a biocompat-
ible material. Since then, calcium hydroxide has been recommended by several
authors for direct pulp capping, but it was only in the middle of the twentieth cen-
tury was it regarded as the standard of care [3].

A Shift in the Paradigm of Treating Pulpally Involved Teeth


A change in clinical approach to pulpally involved teeth in pediatric patients will be
proposed in this book and will be described in the different chapters. The change in
approach involves a shift in the traditional paradigm regarding reversibly inflamed
pulp from an “aggressive” approach involving total excavation of the carious dentin
and the danger of exposing the pulp, towards a more “conservative” approach in
which caries may be left in the pulpal wall to prevent pulp exposure. This approach
is being slowly spread in the dental profession, and may become the treatment of
choice for deep caries in modern pediatric dentistry practice.
As long as minimal invasive dentistry is still reluctantly accepted by the profes-
sional community many teeth with reversible pulp inflammation, that could other-
wise be conservatively treated, will become pulpally involved. These teeth will be
treated by the different pulp treatment modalities that will be described in this book.

1.3 The Scope of the Book

The nine chapters of this book will describe in detail the developmental and bio-
medical aspects of the primary pulp and comprehensive clinical diagnosis of the
pulp leading to conservative approaches of pulp therapy, including stepwise excava-
tion, indirect pulp treatment (IPT), and direct pulp capping. In the chapter on step-
wise excavation and IPT, the Hall technique is mentioned. This technique, which
4 A.B. Fuks and B. Peretz

includes cementation of a stainless steel crown on primary teeth without any caries
removal or tooth preparation, has been shown to be successful in several clinical
studies [4]. As this technique contradicts all established accepted principles of good
clinical practice and it is still unknown what is the long-term effect on the develop-
ment of the occlusion, the Hall technique is definitely a proof that after an accurate
diagnosis, caries can be left on a tooth if properly sealed.
Furthermore, even though our message emphasizes the shift toward conservative
approaches, these rely on an accurate diagnosis based on signs and symptoms to
check the appropriateness of the technique for a specific case. Evidently, a thorough
radiographic evaluation is essential for proper diagnosis. Thus, when a conservative
approach is not indicated, the pulpotomy technique, as old as it is (over 40 years),
will be presented, and the various dressing materials will be critically discussed. In
addition, the nature of successful treatment and, more importantly, failures will be
described.
Following the chapter on pulpotomy, an extensive and detailed chapter on pulp-
ectomy and root canal filling (RCT) will be presented, describing in detail the ratio-
nale behind RCT, the techniques to perform RCT, the instruments, and the associated
materials. Again, the success and failure rates of RCT will be described.
A special chapter will be dedicated to the importance of appropriate restorations
of pulpally treated teeth, emphasizing the need of leakage prevention to improve the
final prognosis.
Although this book is mainly dedicated to primary teeth, as previously men-
tioned, children often present pulp pathology in their immature permanent teeth.
These teeth deserve a different treatment approach than the permanent teeth in
adults, and for this reason, a special chapter dealing with this subject is included.
Finally, innovative experimental biological treatment modalities such as using
stem cells, a new and developing area in medicine and in dentistry, will be pre-
sented. This approach will no doubt be one of the most prevailing treatment modali-
ties in the future. It will expand the scope of conservative treatments, giving the
clinician a more versatile arsenal of tools to deal with the damaged pulp.

1.4 The Aim of the Book

This book is aimed to familiarize dental students as well as general practitioners and
pediatric dentists with the different treatment modalities and complications of
uncontrolled caries, offering them the tools to diagnose the degree of pulp inflam-
mation and thus select the most appropriate treatment.
This book is meant to be a tribute to Dr. Sidney B. Finn, one of the pioneers in
pediatric dentistry and mentor of one of the editors (ABF). Dr. Finn’s nice and warm
personality, showing always a humane and empathic attitude toward the patients
and parents, had a tremendous influence on Dr. Fuks’s education and professional
formation.
1 Pediatric Endodontics: Past and Present Perspectives and Future Directions 5

References
1. Finn SB. The children’s dentist, his practice and his community. In: Finn SB, editor. Clinical
Pedodontics. 4th ed. Clinical Pedodontics, Philadelphia: WB Saunders; 1973.
2. Ash M. Wheeler’s dental anatomy, physiology and occlusion. 7th ed. Philadelphia: WB
Saunders; 1992.
3. Dammaschke T. The history of direct pulp capping. J Hist Dent. 2008;56(1):9–23.
4. Innes NP, Stewart M. The hall technique, a simplified method for placing stainless steel crowns
on primary molars, may be as successful as traditionally placed crowns. J Evid Based Dent
Pract. 2015;15(2):70–2.
The Primary Pulp: Developmental
and Biomedical Background 2
Anna B. Fuks, Josimeri Hebling,
and Carlos Alberto de Souza Costa

Contents
2.1 Introduction ...................................................................................................................... 8
2.2 Formation of the Dentin–Pulp Complex .......................................................................... 8
2.3 The Dental Pulp ............................................................................................................... 12
2.3.1 Odontoblasts ......................................................................................................... 13
2.4 Dentin Structure and Composition................................................................................... 14
2.4.1 Types of Dentin .................................................................................................... 14
2.5 Factors Affecting the Dentin–Pulp Complex Response to Stimuli
in Primary Teeth ............................................................................................................... 18
2.6 The Deleterious Effects of Bacterial Infiltration at the Restorative
Material Margins .............................................................................................................. 18
2.7 The Protective Role of the Remaining Dentin Thickness (RDT) .................................... 19
2.8 Clinical Recommendations .............................................................................................. 21
References ................................................................................................................................. 21

A.B. Fuks, DDS (*)


Department of Pediatric Dentistry, The Hebrew University
Hadassah School of Dental Medicine, Jerusalem, 12272, Israel
e-mail: [email protected]
J. Hebling, DDS, MS, PhD
Department of Orthodontics and Pediatric Dentistry, University Estadual
Paulista – UNESP, Araraquara School of Dentistry,
Rua Humaitá, 1.680 – Centro, Araraquara, SP 14.801-903, Brazil
e-mail: [email protected]
C.A. de Souza Costa, DDS, MS, PhD
Department of Physiology and Pathology, University Estadual Paulista – UNESP,
Araraquara School of Dentistry, Rua Humaitá, 1.680 – Centro,
Araraquara, SP 14.801-903, Brazil
e-mail: [email protected]

© Springer International Publishing Switzerland 2016 7


A.B. Fuks, B. Peretz (eds.), Pediatric Endodontics: Current Concepts in Pulp
Therapy for Primary and Young Permanent Teeth,
DOI 10.1007/978-3-319-27553-6_2
8 A.B. Fuks et al.

2.1 Introduction

Maintaining the integrity and health of the oral tissues is the primary objective of
pulp treatment. Premature loss of primary teeth can lead to malocclusion and/or to
esthetic, phonetic, or functional problems. It is important to attempt to preserve pulp
vitality whenever possible; however, when this is not feasible, the pulp can be entirely
extirpated without significantly compromising the function of the tooth [1, 2].
For more than one century, several conservative pulp therapies have been
employed empirically, with no scientific evidence. From the early 1970s, several
clinical and laboratory studies started to appear in the literature, leading to the
development of therapeutic methods based on experimental techniques [3].
Tziafas [4] reported that the current knowledge concerning the molecular and
cellular mechanisms that take place during tooth development stresses the similari-
ties between the developmental and regenerative tissue events. The author suggested
that the most important challenge in dentistry during the last two decades has been
how to integrate the current concepts of biomedical research into the problem of
preservation of tooth structure and function during dental treatment. He also claimed
that the present knowledge of the biological mechanisms of tooth development and
regeneration can provide opportunities to design new strategies or agents for the
preservation of tooth structures and functions.
Since the pulp of a primary tooth is histologically similar to that of a permanent
tooth, the purpose of this chapter is to familiarize the reader with the characteristics
of the development, structure, and function of the dentin–pulp complex. This knowl-
edge will serve as a basis for discussing the diagnosis of pulp pathologies and the
healing potential of the dentin–pulp complex against different noxious stimuli,
which will be discussed in future chapters.

2.2 Formation of the Dentin–Pulp Complex

The dental pulp is a specialized connective tissue of mesenchymal origin surrounded


by tubular dentin walls occupying the pulp chamber and the root canal.
The specific group of pulp cells, known as odontoblasts, is responsible for the
synthesis and deposition of the collagen-rich dentin organic matrix, which is further
mineralized around the pulp tissue. Therefore, dentin and the pulp remain closely
associated during development and throughout life and are commonly referred to as
the dentin–pulp complex (Fig. 2.1a, b).
Events that take place on the dentin reverberate to the pulp and vice versa [5].
The dentin–pulp complex is surrounded on the crown by dental enamel and on
the root by cementum, periodontal ligament, and bone. The harmony of the com-
plex is impaired if the surrounding tissues suffer some kind of injury that can reach
the pulp by the root canal or through the dentinal tubules [5].
Although the tooth is a unique organ, the principles that guide its development
are shared in common with other organs such as lung, kidney, heart, mammary
2 The Primary Pulp: Developmental and Biomedical Background 9

a b

D D

P D

Fig. 2.1 (a) Histological section obtained from sound primary teeth. The tubular dentin (D) was
synthesized and deposited by the odontoblasts (arrows), which are organized in a defined layer of
cells that remains underlying this mineralized tissue. H/E, 32× (P Pulp). (b) High magnification of
the (a). Note the continuous layer of odontoblasts beneath the thin layer of predentin. The subja-
cent pulp tissue (P) exhibits a number of cells, capillaries, and a loose extracellular matrix. H/E,
160× (D dentin)

glands, and hair follicles [6]. The most important developmental events are those
guiding epithelial–mesenchymal interactions, which are characterized by a molecu-
lar cross talk between two tissues of different origins, the ectoderm and the mesen-
chyme [6].
Different stages of tooth development have been recognized at a microscopic
level by their histologic appearance and were classically described as the dental
lamina, bud, cap, and the early and late bell stages. In the modern literature, a func-
tional terminology has been used to describe odontogenesis into four phases: initia-
tion, morphogenesis, cell differentiation (cytodifferentiation), and matrix apposition
[6]. The dental lamina is the first sign of tooth development. At the lamina stage,
cells of the dental epithelium and those of the underlying ectomesenchyme divide at
different rates and continue to grow and thicken to form a bud [6]. At the bud stage,
cells of the ectomesenchyme proliferate and condense to give rise to the dental
papilla. These cells have increased ability to proliferate, mobilize, and
differentiate.
The morphogenetic phase involves the stages of bud, cap, and initial bell phase.
During this period, a number of ectomesenchymal cells adjacent to the epithelium
increase inside the ectomesenchyme, producing the site of origin of the dental
papilla and of the dental follicle. These will develop into the dentin–pulp complex
and into the support tissues of the tooth, respectively [6]. The formation of the
enamel knot, during the transition from bud to cap, marks the beginning of crown
formation. The cells of the enamel knot do not grow and serve as a signal for the
cuspid formation pattern, influencing the form of the crown and the development of
the dental papilla [6].
10 A.B. Fuks et al.

During the initial bell phase, the epithelium cells assume different morphologies,
giving rise to the enamel organ, also called dental organ. This enamel organ is com-
posed of the following four different stratums: internal enamel epithelium, stratum
intermedium, stellate reticulum, and external enamel epithelium.
The internal epithelium of the enamel organ interacts with the undifferentiated
superficial mesenchymal cells (also known as embryonic cells) of the dental papilla
to form enamel, dentin, and pulp. Overall, cells of the internal dental epithelium
elongate and become highly columnar, starting the late bell stage (phase of cytodif-
ferentiation). This modification of the internal dental epithelium cells serves as a
signal for the peripheral mesenchymal cells of the dental papilla, which after lining
the basement membrane differentiate and assume an elongated morphology with
odontoblast phenotype [6]. This phenomenon, characterized as differentiation of
odontoblasts, has been intensely studied, leading to important advances in the
knowledge of pulpal biology, particularly related with the mechanisms of healing of
this specialized connective tissue against injuries and different pathological stimuli.
More details about this issue will be discussed later in this chapter.
It is important to know the basic process of differentiation of the superficial
undifferentiated mesenchymal cells from the dental papilla by stimuli expressed by
cells of the internal dental epithelium. Growth factors, particularly those belonging
to the superfamily TGF-β, are expressed by these epithelial cells. While the mesen-
chymal cells of the most superficial region of the dental papilla become competent,
the last mitosis of the mother cell is positioned adjacent to the basal membrane. The
daughter cells remain in the internal area of the papilla and will be part of the cell-
rich zone that is clearly observed in the mature pulp. At this point both mother and
daughter cells are referred as pre-odontoblasts because they assume the competency
to differentiate into odontoblasts. Between the internal dental epithelium cells and
the pre-odontoblasts is the basal membrane, which is composed of collagen, lam-
inin, heparin sulfate, and other proteoglycans.
This basal membrane has an important role in the reciprocal activation of the
epithelium/mesenchyme, resulting in a variety of epigenetic interactions, determin-
ing the phenotype of the odontoblasts. After the epithelial cells secrete the growth
factors of the TGF-β superfamily, these bioactive proteins remain attached to the
basal membrane. The components of the basal membrane activate these TGFs to
interact with membrane receptors of the pre-odontoblasts. The translation of these
signals results in the activation of the pre-odontoblasts, which start to secrete more
growth factors and express the msxs genes. The final differentiation of the pre-
odontoblasts into odontoblasts occurs only after the interaction of the fibronectin,
which is deposited on the basal membrane and the 165 KDa pre-odontoblasts mem-
brane receptors. The sequence of differentiation of the dental papilla mesenchymal
cells into odontoblasts until the beginning of the synthesis and deposition of
collagen-rich dentinal matrix is presented in Fig. 2.2.
The odontoblasts synthesize the dentinal organic matrix both adjacent to the cel-
lular body and close to the mineralization fronts. During the period of upregulation
of the TGFs, the pre-odontoblasts start to synthesize fibronectin and express the
membrane protein 165 KDa, which is required to interact with the fibronectin.
2 The Primary Pulp: Developmental and Biomedical Background 11

Pre-ameloblast

TGF-β´s
Enamel
Basal membrane
Mantle dentin

165 KDa
Receptors Dentin matrix

Pre-dentin
msx

Pre-odontoblast TGF-β´s

Fibronectin

Fig. 2.2 Mechanism by which the pulpal mesenchymal cells present in the periphery of the dental
papilla are differentiated into odontoblasts (Adapted from [31]) (J. Hebling, 2015)

The msxs homeoproteins are probably involved in the reorganization of the pre-
odontoblast cytoskeleton, which plays an important role in the process of differen-
tiating into elongated cells, referred to as odontoblasts.
The mineralization process is mainly dependent on the odontoblasts’ activities:
they release phospholipids and alkaline phosphatase containing vesicles that pro-
duce the hydroxyapatite crystals. The dentin matrix mineralization is heteroge-
neous, by globular calcification, resulting in fronts of mineralization or calcospherites.
With continuous growth, the crystals tend to fuse (secondary mineralization), form-
ing a mineralized mass around the odontoblastic processes, granting the dentin a
tubular aspect (system of dentinal tubules). The portion of the dental papilla that is
involved with dentin becomes the dental pulp. The odontoblasts form the dentin, but
depend on it to become the pulp. The direction of the odontoblasts is towards the
center, in relation to the dental pulp, and the decrease of the internal space favors a
curved path of these cells. Once the first layer of dentin is formed, the cells of the
internal epithelium (pre-ameloblasts) elongate and differentiate into ameloblasts
starting to produce the enamel organic matrix, which becomes mineralized almost
instantaneously.
As dentin is formed, the most cervical cells of the internal epithelium of the
enamel organ become pre-ameloblasts, an event that occurs from the incisal (or
from the cuspids) to the cervical area. When the dentin formation approximates the
cervical loop, the cells of internal and external epithelium of the enamel organ pro-
liferate from the loop, forming a double layer of cells, also known as Hertwig’s
epithelial root sheath. The expansion of the sheath is followed by the formation of
the radicular dentin. The cells of the dental follicle closer to the external layer of the
12 A.B. Fuks et al.

Fig. 2.3 Histological aspect of the formation of the apex. Hertwig’s sheath, involved by ectomes-
enchymal cells of the papilla, can be seen on the left (Courtesy Prof. Roberto Holland, 2008)

sheath differentiate into cementoblasts and start to produce the cementum organic
matrix; the follicle also produces the periodontal ligament and alveolar bone. There
is a free border on the epithelial sheath, the epithelial diaphragm, which closes
slowly as the root is formed (Fig. 2.3). As long as the apex of the root is not totally
formed, there will be dental papilla, composed of ectomesenchymal cells. This has
clinical relevance, because part of these cells can remain vital even after pulp necro-
sis. In this specific condition, it is possible to have a continuous apexogenesis or the
formation of the radicular apex with dentin. When there is a severe reduction in the
number of ectomesenchymal cells in the dental papillae, the tooth can still have
apexification induced by an intracanal dressing [5]. This issue will be dealt in detail
in Chap. 8.

2.3 The Dental Pulp

The dental pulp is a specialized connective tissue confined between rigid walls of
mineralized tissues (dentin, enamel, and cementum). The dental pulp can commu-
nicate with the external environment of the tooth through the apical foramen, foram-
ina, and/or lateral canals providing the pulp with a low-tolerance environment,
because the nutritional substrate comes from the vascularization that passes through
the small foramens and foramina.
Loose connective tissue forms the stroma (nutritional supportive tissue) and the
parenchyma (functional tissue) of several organs of the human body. In the pulp,
this loose connective tissue forms both the stroma and the parenchyma at the same
time, as it sustains itself and the dentin substrate and produces dentin. With the
2 The Primary Pulp: Developmental and Biomedical Background 13

Fig. 2.4 Sections obtained from human sound teeth showing the radicular (left) and coronal
(right) portions of the pulp tissue. Note the fibrous connective pulp tissue with vascular–nervous
sheath close to the apical foramen (arrows). Conversely, the coronal pulp exhibits loose connective
tissue with a number of blood vessels. H/E, 32×

production of dentin, the pulp remains enclosed within the central part of the tooth,
having a coronal and a radicular portion. In uni-radicular teeth, the coronal and
radicular pulp tissues are contiguous, but in multi-radicular teeth, the floor of the
pulp chamber has a clear distinction: the coronal pulp is rich in cells and extracel-
lular matrix, while the radicular pulp has more fibers, and the vascular–nervous
sheath is more concentrated, with less anastomosis (Fig. 2.4).

2.3.1 Odontoblasts

The odontoblasts have been traditionally described as cells lining the periphery of
the pulpal space and extending their cytoplasmic processes into the dentinal tubules.
These cells have several junctions, which allow for intercellular communication and
help to maintain the relative position of one cell to another. In young permanent
teeth, the pulp tissue exhibits defined zones. The cell-free zone is located just below
the odontoblastic layer and contains an extensive plexus of unmyelinated nerves and
blood capillaries. The cell-rich zone, which presents a number of undifferentiated
mesenchymal cells, is observed adjacent to the cell-free zone. The core of the dental
pulp contains larger blood vessels and nerves, which are surrounded by large area of
extracellular matrix. This pulp morphology is similar to that observed in primary
teeth, but the zones are not so well defined (Fig. 2.5a, b).
Although this description is correct during active dentinogenesis, it is now
accepted that the size of the odontoblasts and the content of their cytoplasmic
organelles vary throughout their life cycle and are closely related to their func-
tional activity. The relationship between the size of the odontoblasts and their
secretory activity can be demonstrated by differences in their size in the crown
and in the root, and different dentinogenic rates may be expressed in these two
areas of the tooth [7].
The odontoblasts are highly specialized cells and are responsible for the forma-
tion of dentin. Due to the extension of their cytoplasmic processes into the dentinal
tubules, these cells compose the main part of the dentin–pulp complex. When this
complex is damaged by disease or attrition, or is affected by operative procedures,
it reacts in an attempt to defend the pulp tissue.
14 A.B. Fuks et al.

a b

Od
D

Fig. 2.5 (a) Sections obtained from human sound primary teeth. Note the presence of tubular
dentin (D), predentin (horizontal arrows), odontoblast layer (Od), cell-free zone (vertical arrows),
cell-rich zone (oblique arrows), and the core of the pulp. H/E, 160×. (b) The core of the pulp tissue
contains a number of blood vessels and nerves, which are surrounded by a large area of extracel-
lular matrix. H/E, 160×

2.4 Dentin Structure and Composition

Dentin is the most abundant mineral component of the teeth. It is composed of 70 %


inorganic crystals (hydroxyapatite), 20 % collagen fibers and other proteins, and
10 % water (all by %volume). Dentin can be classified as primary, secondary, or
tertiary, according to the time of development and the histological characteristics of
the tissue.

2.4.1 Types of Dentin

The primary dentin is composed by the mantle dentin and by the circumpulpal den-
tin, which are physiological structures deposited up to the eruption of the tooth and
its contact with the antagonist. Mantle dentin is the first dentin to be formed. It is
deposited along the enamel–dentin or dentin–cementum junction, parallel to the
tissues coating it. It is almost totally free of developmental defects. The odonto-
blasts, when supported by the basal membrane, have several cytoplasmic projec-
tions. This results in mantle dentin that is highly branched on the periphery
converging into a single prolongation towards the center of the pulp chamber.
Mantle dentin has an approximate thickness of 80–100 μm. The circumpulpal den-
tin is formed after the deposition of the mantle dentin and constitutes the majority
of the dentin. Since the odontoblasts produce the organic dentin matrix centripetally
concerning the pulp, the space available becomes increasingly reduced leading to an
“S”-shaped curvature in the circumpulpal dentin, which is more pronounced at the
crown and more discrete at the root [5].
Secondary dentin is also a physiological structure formed after the radicular den-
tin, maintaining the tubular pattern of the circumpulpal dentin, but its formation is
slower and less regular. It is deposited more on the roof and the floor of the pulp
2 The Primary Pulp: Developmental and Biomedical Background 15

a b c
D D

RD
RD

Fig. 2.6 (a) Section obtained from primary teeth with chronic occlusal caries (slight stimulus). Note
the thick layer of tubular reactionary dentin (RD) deposited in the upper area of the pulp horn (P). (D)
represents dentin. H/E, 32×. (b, c) High magnifications of (a). Note the tubular dentin deposited by
primary odontoblasts (arrows) subjected to a low-intensity stimulus (chronic caries). H/E, 64×

chamber, reducing the pulp horns and the pulpal chamber asymmetrically.
Approximately 1–1.5 μm of dentin matrix is incrementally deposited per day inside
the pulp chamber.
Tertiary dentin is not a physiological structure, since it is produced in response to
stimuli from the external environment, such as caries, attrition, abrasion, restorative
procedures, etc. The formation of tertiary dentin occurs adjacent to the stimuli, modi-
fying the pulpal and dentinal architecture. This dentin can be reactionary, when pro-
duced by preexisting odontoblasts, or reparative, which occurs with the replacement
of dead odontoblasts by new odontoblasts, termed as odontoblast-like cells.
When low-intensity stimuli are applied to the odontoblasts, they respond by
moving rapidly and centripetally in relation to the pulp. These cells then deposit a
matrix that contains irregular and convoluted tubules. The morphology of recently
produced dentinal matrix is characterized by the continuity with the existing dentin
and is known as reactionary dentin (Fig. 2.6a–c).
Conversely, when the injury to the odontoblasts is intense and some of them die,
new odontoblasts are differentiated from pre-odontoblasts (mesenchymal cells that
were formed during dentinogenesis and remained partially in the cell-rich zone of
the adult pulp). These new odontoblasts deposit a matrix of heterogeneous dentin,
which is known as reparative dentin (Fig. 2.7). The process of deposition of repara-
tive dentin is more complex than that of reactionary dentin, because it occurs by
differentiation of the pulpal cells. In this case, undifferentiated reserve mesenchy-
mal cells are used to replace the odontoblasts during the performance of some oper-
ative procedures or even during the fast progression of an acute caries lesion.
Consequently, the number of mesenchymal cells (stem cells) decreases in the pulp
tissue, leading to a reduced potential of healing [8]. Thus, aggression to the dentin–
pulpal complex should be prevented to maintain its functional nature and physio-
logic metabolism, preventing its fast aging.
The predentin is a thin layer of collagen-rich dentin matrix (about 20 μm thick)
recently synthesized by the odontoblasts. As described previously, this non-
mineralized dentin matrix presents fronts of mineralization, also known as
16 A.B. Fuks et al.

CA

Fig. 2.7 Section obtained from primary teeth with acute occlusal caries (CA). Note the layer of
tubular reactionary dentin (horizontal arrows) deposited in the lower part of the picture where the
primary odontoblasts were far from the intense stimulus (pay attention to the dentinal tubule ori-
entation). However, in the upper area of the picture, where the pulp is close to the very deep caries
lesion (CA), a thick layer of reparative dentin with no tubules, termed as reparative dentin (vertical
arrows), can be observed. H/E, 32× (D Dentin, P Pulp)

calcospherites (Fig. 2.8). Failure of the calcospherites to fuse leads to the formation
of hypomineralized areas, known as interglobular dentin. These areas are more vis-
ible in the radicular dentin, where the dentin is produced simultaneously with the
eruptive process, and on the most external portion of the coronal dentin, at the limit
between the mantle and the circumpulpal dentin. Predentin consists mainly of types
I and III collagen, glycoproteins, and proteoglycans.
Another type of hypocalcification is the Tomes’ grainy layer that is formed by
the terminal loops and branches of the odontoblastic membrane. This membrane
configuration is developed during the formation of the radicular dentin, giving to the
peripheral dentin a grainy appearance.
Dentin is composed of tubules. As the odontoblasts secrete the organic matrix,
they emit a projection that is surrounded by liquid, providing the tubular aspect. The
tubules have a lightly conical shape, due to the mineralization process of the peritu-
bular dentin that occurs throughout the life of the tooth. The tubules extend through
the entire thickness of the dentin, following the sinuous track of the odontoblasts.
The number of dentinal tubules varies according to the area when different teeth are
2 The Primary Pulp: Developmental and Biomedical Background 17

Od

Od

Fig. 2.8 Section obtained from sound primary teeth. Between the tubular dentin and the thin layer
of predentin one can see the fronts of mineralization – calcospherites (oblique arrows). Note the
odontoblasts (Od) with their cytoplasmic processes which get inside the dentinal tubules (head
arrow) D dentin. P pulp. H/E, 125×

compared. It has been demonstrated that at the enamel–dentin junction (superficial


dentin), there are approximately 20,000 tubules/mm2, while near the predentin
(deep dentin), this number increases to approximately 75,000 tubules/mm2.
The dentin surrounding the periphery of the dentinal tubules is known as peri-
tubular or intertubular dentin. Intertubular dentin is present between dentinal
tubules. The odontoblast cytoplasmic processes remain within the dentinal
tubules (Fig. 2.8).
Communications among the dentinal tubules, known as dentinal canaliculus, are
frequently observed. The peritubular dentin that constitutes the walls of the dentinal
tubules is four times harder than intertubular dentin, since it consists of approxi-
mately 96 % of hydroxyapatite crystals. Mild stimuli from the external environ-
ment, such as attrition and caries, may cause obliteration of the dentinal tubules,
resulting in dentin sclerosis. Intertubular dentin is partially composed of collagen
fibrils positioned perpendicularly to the long axis of the tubules, surrounding the
tubules (Fig. 2.9a, b). The conditioning of the dentin substrate with acidic agents or
chelating substances decreases or removes the peritubular dentin on the surface,
leaving a mesh of intertubular collagen exposed to the action of bonding agents or
to bacteria from decay [9, 10].
18 A.B. Fuks et al.

a b

ID D

ID
P

ID

ID

ID

Fig. 2.9 (a) Morphology of the dentin structure. Note the dentinal tubules surrounded by peritu-
bular dentin (arrows) as well as a large area of intertubular dentin (ID). MEV, 3.000×. (b) Dentin–
pulp complex. D dentin. P pulp. Cytoplasmic processes from odontoblasts are observed inside the
dentinal tubules. Masson’s trichrome, 125×

2.5 Factors Affecting the Dentin–Pulp Complex Response


to Stimuli in Primary Teeth

Although the life span of primary teeth is shorter and their dentin is thinner when
compared to that of permanent teeth, the dentin–pulp complex response to dental
caries in human primary teeth is similar to that of permanent teeth, including a
reduction in the number of the odontoblasts and an increase in the number of inflam-
matory cells. These are found under very deep lesions and are less numerous in
more distant regions, being almost absent in the radicular apical pulp [11]. The
primary dentition is frequently subjected to stimuli such as trauma or caries with
associated pulpal inflammation [12]. The same factors affect both the dentin–pulp
responses in primary as well as permanent teeth, with respect to external stimuli.

2.6 The Deleterious Effects of Bacterial Infiltration


at the Restorative Material Margins

A significant number of studies have implicated the presence of bacteria and their
products as responsible for induction of the most severe forms of pulp inflammation.
The role of bacteria in the inflammatory reaction was demonstrated by spontaneous
healing of pulp exposures in germ-free animals [13] and subsequently by cavities
restored with different materials and surface sealed with zinc oxide–eugenol cement
to prevent any bacterial contamination originating from microleakage [14].
The presence of bacteria in cavities with a remaining dentin thickness (RDT) of
less than 0.25 mm stimulates a more severe pulpal inflammatory reaction than in simi-
lar cavity preparations in the absence of bacteria [15]. Thus, the presence of bacteria
always increases the mean grade of pulpal inflammation regardless of the RDT [16].
The presence of bacteria in class V cavity was also observed to result in a significant
2 The Primary Pulp: Developmental and Biomedical Background 19

a b

Fig. 2.10 (a) Section obtained from a young sound premolar in which a very deep class V cavity
was prepared and the cavity floor lined with hard-setting calcium hydroxide cement. Note the pulp
tissue with normal histological characteristics. Masson’s trichrome, 64× (D Dentin, P Pulp; verti-
cal arrows odontoblast layer; oblique arrows cell-rich zone). (b) In this human premolar, the cav-
ity floor (dentin) was conditioned and a resin-based material was used as liner. Note the intense
inflammatory response associated with complete pulp tissue disorganization. No microleakage at
the cavity walls was observed after using a specific staining technique (Brown and Brenn) widely
employed for disclosing bacteria. Masson’s trichrome, 64×

decrease in the number of odontoblasts per unit area; this effect was more pronounced
in deep cavities with RDT less than 0.5 mm than in cavities with RDT greater than
0.5 mm [16]. One can conclude that the ability to maintain an effective seal to protect
the pulp from recurrent injury resulting from bacterial microleakage is a decisive fac-
tor in the clinical success of restorative products [17]. However, a number of studies
performed in human teeth have shown pulpal inflammation in the absence of bacteria
[8, 18–22], clearly indicating that other factors, such as the toxicity of dental material
components capable of diffusing through dentinal tubules, are also responsible, at
least in part, for pulp injury after restorative treatment (Fig. 2.10a, b).

2.7 The Protective Role of the Remaining Dentin


Thickness (RDT)

It was found in an in vivo study that the cavity RDT is an important factor mediating
pulpal inflammatory activity, particularly when the RDT is reduced to less than
0.3 mm [8, 22]. With an RDT less than 0.25 mm, a significant decrease in the num-
ber of odontoblasts was observed together with minimal reactionary dentin repair
[23, 24]. It was recently demonstrated that very deep class V cavities prepared in
human premolars (RDT thinner than 0.3 mm) which were subjected to adhesive
restorations resulted in inflammatory pulp reaction associated with inner dentin
resorption [8, 22, 25]. The presence of an RDT of more than 500 mm delays the
diffusion of noxious materials into the dental pulp. In this clinical situation, the
odontoblasts maintain their metabolism, or, in case of a slight stimulus, they may
secrete a reactionary dentin, increasing the total distance between the restorative
material and the pulp [8]. Any additional decrease in the dentin thickness to less
than 500 mm results in a significant reduction in the number of odontoblasts.
20 A.B. Fuks et al.

a b
P

RD

Td
Ad

Fig. 2.11 (a) Deep carious lesion in primary first molar. H/E. 32×. The small image characterizes
the necrotic dentin (oblique arrow) and the presence of microorganisms inside the dentinal tubules
(horizontal arrows). Brown and Brenn technique, 125×. Note the intense inflammatory pulp reac-
tion associated with complete tissue disorganization. (b) Detail of (a). Note the intense deposition
of reparative dentin (RD) adjacent to the primary dentin (D). A heterogeneous and atubular dentin
matrix (Ad) containing parts of dead odontoblasts as well as a tubular dentin (Td) deposited by the
new odontoblast-like cells (arrows) can be observed. H/E, 125× (P Pulp)

This reduction may be compensated for by the differentiation of odontoblast-like


cells from progenitor pulp cells, which migrate to the injury site and secrete repara-
tive dentin. The reparative dentin decreases the dentin permeability and increases
the distance between the restorative material and the pulp, protecting it from nox-
ious products. However, in this specific condition, the number of mesenchymal
stem cells decreases, interfering with the potential of pulpal healing in case of fur-
ther damage to the dentin–pulp complex. Thus, the RDT appears to provide an impor-
tant protective barrier against toxins, bacterial infiltration, or any noxious material
applied to dentin. In this way, it seems adequate to protect the pulp tissue against
irritant stimuli by using biocompatible materials as liners in very deep cavities [8].
Based on the remaining dentin thickness, three situations can be taken into
consideration:

1. Initial carious lesion or shallow cavity preparations (RDT > 500 mm): a localized
reactionary dentin may be secreted facing the restoration site, and intratubular
mineralization (dentin sclerosis) occurs, resulting in a significant decrease in the
dentin permeability and pulp protection. It has been suggested that this stimula-
tion may be due to signaling molecules (i.e., TGF-b1, BMP-2 liberated from the
dentin during demineralization) [26].
2. Carious lesion progression implying a deep cavity preparation (RDT < 500 mm):
these lesions may lead to partial death of odontoblast. Depending on the pulp
inflammatory intensity, progenitor/stem cells can migrate to the injury site and
differentiate to give rise to a new generation of odontoblast-like cells. These cells
are responsible for the deposition of a specific type of tertiary dentin termed as
reparative dentin, as described above [27, 28] (Fig. 2.11a, b).
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