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- Sprache: Englisch
Vital Pulp Treatment A comprehensive reference work covering all aspects of vital pulp treatments in clinical practice Vital Pulp Treatment offers a comprehensive overview of existing and developing vital pulp therapies, the science that underpins them as well as their clinical applications. Preserving dental pulp tissue is critical to oral health and vital pulp treatments are designed to maintain, repair, and regenerate this tissue. With a focus on clinical practice, this book begins with the diagnosis and causes of pulpitis before elaborating on the application of vital pulp treatment after trauma, caries, or dental procedures. Later chapters cover a variety of extent treatment modalities including caries removal, pulpotomy, direct or indirect pulp capping and regenerative endodontic therapies. Vital Pulp Treatment readers will also find: * Clinical photographs to support and highlight key parts of the text * Detailed discussion of topics including pulp diagnostics, deep caries, and pulp exposure management, as well as controversial and clinically relevant discussions * Dedicated treatment of each therapeutic modality with a summary of the state of the art in each case * Outcome measures and follow-up guidelines Rooted in evidence-based dentistry and robust scientific research, Vital Pulp Treatment is ideal for dentists, endodontists, restorative dentists, and dental students looking for information on this critical component of modern minimally-invasive dentistry.
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Veröffentlichungsjahr: 2024
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Table of Contents
Cover
Table of Contents
Title Page
Copyright Page
List of Contributors
Foreword
Preface
1 The Importance of Maintaining Pulp Vitality
Introduction
Dental Pulp Development
Stem Cell Reserve and Healing/Regeneration Potential of the Dental Pulp
Pulp Vascularization and its Clinical Implications
Pulp Innervation and its Contribution to Physiologic Changes
Pulp Response to Restorative Processes
Pulp Vitality and Inflammation
Mechanisms of Pulp Repair
Conclusions
References
2 Biological Basis for Vital Pulp Treatment
Dental Pulp – Structure and Function
Healing Capability of the Dental Pulp
Immunological Response in the Dental Pulp
Diagnostics for Pulpal Disease
Future Vital Pulp Treatments
References
3 Pulpal Diagnosis
Introduction
Diagnoses of Pulpal Status and Their Associated Diagnostic Terminologies
The Diagnostic Process
Preoperative Diagnosis versus Direct Observation
Clinical to Molecular Diagnostic Tests: Possibilities and Challenges
Conclusion
References
4 Vital Pulp Treatment Modalities
Introduction
Vital Pulp Treatment Modalities Aiming Not to Expose the Pulp
Indications – A Pragmatic Subdivision of Extensive Carious Lesions
Understanding Caries Pathology – A Reason to ‘Dare’ Leaving Carious Dentine Behind
Outcomes
Evidence‐based and Consensus Recommendations
Epidemiology of Current Practice
Future
References
5 Vital Pulp Treatment Modalities
Is Exposing the Pulp a Problem? An Introduction
Management of Traumatic and Iatrogenic Pulp Exposures
Indications for Direct Pulp Capping
Factors Affecting the Outcomes of Direct Pulp Capping
Contraindications for Direct Pulp Capping
Evidence‐based Outcomes of Direct Pulp Capping
Future Developments in Direct Pulp Capping
Conclusions
References
6 Vital Pulp Treatment Modalities
Introduction
Definitions
Indications
Contraindications
The Procedure
Clinical Protocol
Achieving Haemostasis
Outcomes of Pulpotomy
Conclusions
References
7 Vital Pulp Treatment – Material Selection
Introduction
Native Pulp Conditions
Pulp Response to Traumatic or Carious Injuries
Decision‐making for Pulp Exposures
Historical Background on VPT Materials and Their Influence on Success
Current Gold Standard and Limitations of VPT Materials
Biology of the Tissue Response and Mechanisms of Repair – Matrix Proteins, Signalling Molecules and Pathways
Opportunities and Next‐generation VPT Materials
Acknowledgements
References
8 Vital Pulp Treatment for Traumatic Dental Injuries
Introduction
Traumatic Dental Injuries
Diagnosing the Pulp Condition
Direct Pulp Capping and Pulpotomies for Managing Traumatised Teeth
What is the Evidence for the Preferred Treatment Choice?
Factors that Affect Outcomes of VPT in TDI
Complications from VPT in Traumatised Teeth
Oral Health‐Related Quality of Life
Differences Between Trauma and Caries Management
Complicated Crown Fracture with Luxation and Complex Injuries
Clinical Protocols for Direct Pulp Capping and Pulpotomy
Future Directions
References
9 Regenerative Endodontics
Introduction
Biological and Mechanical Goals of Pulp Regeneration
Historical Development of Regenerative Endodontics
Revitalization
Endodontic Tissue Engineering
Conclusion
References
10 Outcome of Vital Pulp Treatment and Regenerative Endodontics
Introduction
Outcomes Reporting in VPT
Stakeholder Considerations in Outcome Reporting
Pulp Revitalization as a Regenerative Endodontic Therapy
References
Index
End User License Agreement
List of Tables
Chapter 3
Table 3.1 Current classifications systems of pulpitis.
Table 3.2 Summary findings and evidence certainty for all outcomes using GR...
Chapter 4
Table 4.1 Definitions of the vital pulp treatment modalities presented in t...
Table 4.2 Outcomes that should be checked after treatment of a deep caries ...
Table 4.3 Randomized clinical studies comparing non‐selective (complete) ca...
Table 4.4 Randomized clinical studies comparing selective carious removal o...
Chapter 8
Table 8.1 VPT studies related to CCFs.
Table 8.2 Studies undertaking a pulpotomy on mature teeth.
Table 8.3 Studies that reported concomitant luxation injuries.
Chapter 10
Table 10.1 Clinician‐reported outcomes (CROs) in VPT and PR studies (12, 13...
Table 10.2 Dental patient‐reported outcomes (PROs) in VPT and PR studies (1...
Table 10.3 Outcome consensus for the treatment of pulpitis.
Table 10.4 OHIP‐14 questionnaire.
List of Illustrations
Chapter 1
Figure 1.1 Dental pulp tissue engineering with SHED injected into human root...
Figure 1.2 Sequence of dentine formation – (1) signalling from pre‐ameloblas...
Figure 1.3 Western blotting analysis of pathways affected by BMP‐2 (a known ...
Figure 1.4 Histologic image from the apical papilla, detaching from the root...
Figure 1.5 Histologic image from the pulp tissue encircled by dentine/enamel...
Figure 1.6 Mechanisms of hypoxia‐induced dentinogenesis and angiogenesis. (1...
Figure 1.7 Mechanism of neurogenic inflammation. Dentine stimulation can lea...
Figure 1.8 Molecular responses to activate pulp inflammation. The presence o...
Figure 1.9 Design of a miRNA ‘rich’ scaffold encoding miRNAs to control infl...
Chapter 2
Figure 2.1 Schematic of the two types of tertiary dentine formation processe...
Figure 2.2 A schematic representation of the cellular and molecular immune p...
Figure 2.3 Schematic representation of the interaction between dentine matri...
Chapter 3
Figure 3.1 Illustration of potential next‐generation pulp diagnostic tests a...
Chapter 4
Figure 4.1 Macroscopic view of an extracted tooth with a proximal extensive ...
Figure 4.2 Schematic drawing of a cavitated coronal carious lesion. In Carie...
Figure 4.3 Two teeth, one treated with stepwise excavation and the other wit...
Figure 4.4 The degree of openness is defined as the involvement in the cario...
Figure 4.5 (a) Histological features of a well‐defined deep lesion. (b) Deta...
Figure 4.6 Hard tissue and/or ectopic connective tissue: (a) tertiary dentin...
Figure 4.7 (a) Initial stages of polyps have highly vascular and inflamed ti...
Figure 4.8 Not all treatments with stepwise excavation or selective caries r...
Figure 4.9 Number of registered treatments per 1000 patients. Stepwise excav...
Figure 4.10 First stage of stepwise excavation of a tooth with an approximal...
Chapter 5
Figure 5.1 Tooth 21 with a complicated crown fracture after trauma, resultin...
Figure 5.2 (a) Pronounced bleeding from the pulp tissue exposed over a small...
Figure 5.3 (a) Preoperative radiograph of a 77‐year‐old patient shows caries...
Figure 5.4 The intrapulpal hard tissue formations on the molar teeth may ind...
Figure 5.5 If the pulp tissue is not inflamed, the size of the pulp exposure...
Figure 5.6 (a) A 62‐year‐old patient presents for filling therapy with an ap...
Chapter 6
Figure 6.1 Isolation of several teeth allows better visibility. The rubber d...
Figure 6.2 The tooth, clamp and rubber dam are decontaminated by swabbing a ...
Figure 6.3 Immunofluorescence lamps can be useful in detecting the residual ...
Figure 6.4 Bleeding control is achieved by pressing a cotton pallet soaked i...
Figure 6.5 (a) ProRoot was one of the first HCSCs available, (b) hand mixing...
Figure 6.6 (a). Biodentine is capsulated where a liquid is added before mixi...
Figure 6.7 (a). Well root PT is a premixed putty HCSC that comes ready mixed...
Figure 6.8 Theracal is a light‐cured bioactive material.
Figure 6.9 (a) and (b) It is recommended to assess the tooth for both apical...
Figure 6.10 (a) and (b) Deep lesion. Even though the cavity is deep, a radio...
Figure 6.11 (a) Deep occlusal cavity with ‘sound’ walls. (b) Pulpotomy perfo...
Figure 6.12 (a) Deep mesial cavity with loss of interproximal wall. (b) The ...
Figure 6.13 (a) Extremely deep carious cavity on tooth 1.5. The tooth was vi...
Figure 6.14 (a) After gross carious tissue removal, affected, soft tissue is...
Figure 6.15 (a) In a partial pulpotomy procedures 2–3 mm of pulp tissue are ...
Figure 6.16 (a) Cotton pellets soaked in NaOCl pressed against the pulp tiss...
Figure 6.17 (a) After bleeding control, (b) the entire cavity is filled with...
Figure 6.18 After setting the HCSC the tooth can be selectively etched and s...
Chapter 7
Figure 7.1 (A) Schematic representation of different VPT methods: Indirect p...
Figure 7.2 (A–B) Pulpotomy in Mature Permanent Teeth treated with Biodentine...
Figure 7.3 Schematic representation of the proposed application of functiona...
Figure 7.4 Regenerative strategies for dentine‐pulp complex regeneration. (A...
Chapter 8
Figure 8.1 (a) A clinical photograph of a complicated crown fracture in an e...
Figure 8.2 A seven‐year‐old male patient referred after trauma displaying a ...
Figure 8.4 (a) A clinical photograph of a complicated crown fracture on whic...
Figure 8.5 (a) Clinical photograph of a traumatized maxillary left central i...
Figure 8.6 (a) A periapical radiograph taken 11 days post‐injury when two un...
Figure 8.7 An example of three study cases with crown fractures presenting w...
Figure 8.8 This case features two complicated crown fractures and two compli...
Figure 8.9 (a) The maxillary central incisors sustained complicated crown fr...
Figure 8.10 (a) A periapical radiograph of maxillary right central incisor u...
Figure 8.12 (a) All discoloured WMTA was removed until a hard‐tissue bridge ...
Figure 8.13 A clinical photograph of two complicated crown‐root fractured ma...
Figure 8.14 (a) Trauma to the teeth, lips, soft tissues and a fracture to th...
Chapter 9
Figure 9.1 (a) The apex of a juvenile tooth without completed root growth is...
Figure 9.2 Histological representation of the dentine–pulp complex. (a) An o...
Figure 9.3 (a) Stages 1–5 of root development according to Cvek et al. (3). ...
Figure 9.4 (a) Preoperative radiograph of a lower second premolar with an op...
Figure 9.5 During revitalization, bleeding into the root canal is induced by...
Figure 9.6 (a) The young patient suffered an avulsion of tooth 11, which was...
Figure 9.7 (a) A Hedström file may be bent at the tip to cause bleeding when...
Figure 9.8 (a) Control radiograph after revitalization treatment of teeth 11...
Figure 9.9 (a) Cell‐based endodontic tissue engineering involves the expansi...
Chapter 10
Figure 10.1 Sample visual analogue and numeric rating scales for pain intens...
Figure 10.2 Sample verbal rating scales for pain intensity.
Figure 10.3 Radiographic measurement. l: root length, it was measured from t...
Guide
Cover Page
Table of Contents
Title Page
Copyright Page
List of Contributors
Foreword
Preface
Begin Reading
Index
WILEY END USER LICENSE AGREEMENT
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Vital Pulp Treatment
Edited by
Henry F. Duncan
Professor and Consultant in Endodontics
Division of Restorative Dentistry and Periodontology, Dublin Dental University Hospital Trinity College Dublin, Lincoln Place, Dublin 2, Ireland
Ikhlas A. El‐Karim
Clinical Professor and Consultant in Restorative Dentistry
School of Medicine, Dentistry and Biomedical Sciences, Queen’s University Belfast, Northern Ireland, UK
This edition first published 2024© 2024 John Wiley & Sons Ltd
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The right of Henry F. Duncan and Ikhlas A. El‐Karim to be identified as the authors of the editorial material in this work has been asserted in accordance with law.
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Library of Congress Cataloging‐in‐Publication DataNames: Duncan, Henry, 1971‐ editor. | El‐Karim, Ikhlas A., editor.Title: Vital pulp treatment / edited by Henry F. Duncan, Ikhlas A. El‐Karim.Description: Hoboken, NJ : Wiley‐Blackwell, 2024. | Includes index.Identifiers: LCCN 2023043780 (print) | LCCN 2023043781 (ebook) | ISBN 9781119930389 (hardback) | ISBN 9781119930396 (adobe pdf) | ISBN 9781119930402 (epub)Subjects: MESH: Dental Pulp Diseases–therapyClassification: LCC RK351 (print) | LCC RK351 (ebook) | NLM WU 230 | DDC 617.6/342–dc23/eng/20231107LC record available at https://lccn.loc.gov/2023043780LC ebook record available at https://lccn.loc.gov/2023043781
Cover Design: WileyCover Images: © Henry Duncan
List of Contributors
Isaac J. de Souza AraújoDepartment of Cariology, Restorative Sciences, and EndodonticsUniversity of Michigan School of DentistryAnn Arbor, MI, USA
Department of Bioscience Research, College of DentistryUniversity of Tennessee Health Science CenterMemphis, TN, USA
Lars BjørndalCariology and Endodontics, Section of Clinical Oral Microbiology, Department of Odontology, Faculty of Health and Medical SciencesUniversity of CopenhagenCopenhagen, Denmark
Marco C. BottinoDepartment of Cariology, Restorative Sciences, and EndodonticsUniversity of Michigan School of DentistryAnn Arbor, MI, USA
Department of Biomedical Engineering, College of EngineeringUniversity of MichiganAnn Arbor, MI, USA
Roberto CaredduDivision of Restorative Dentistry and PeriodontologyDublin Dental University Hospital, Trinity College DublinDublin, Ireland
Bruno CavalcantiDepartment of Cariology, Restorative Sciences and EndodonticsUniversity of Michigan School of DentistryAnn Arbor, MI, USA
Daniel Chiego, Jr.Department of Cariology, Restorative Sciences and EndodonticsUniversity of Michigan School of DentistryAnn Arbor, MI, USA
Paul R. CooperFaculty of Dentistry, Sir John Walsh Research InstituteUniversity of OtagoDunedin, New Zealand
Siobhan CushleyCentre for Dentistry, School of Medicine Dentistry and Biomedical SciencesQueen’s University BelfastBelfast, Northern Ireland, UK
Renan Dal‐FabbroDepartment of Cariology, Restorative Sciences, and EndodonticsUniversity of Michigan School of DentistryAnn Arbor, MI, USA
Till DammaschkeDepartment of Periodontology and Operative DentistryUniversity of MünsterMünster, Germany
Henry F. DuncanDivision of Restorative Dentistry and PeriodontologyDublin Dental University Hospital, Trinity College DublinDublin, Ireland
Ikhlas A. El‐KarimDepartment of Restorative Dentistry, School of Medicine, Dentistry and Biomedical SciencesQueen’s University BelfastBelfast, Northern Ireland, UK
Helena FranssonDepartment of Endodontics, Faculty of OdontologyMalmö UniversityMalmö, Sweden
Lara T. FriedlanderFaculty of Dentistry, Sir John Walsh Research InstituteUniversity of OtagoDunedin, New Zealand
Johnah C. GaliciaCollege of Dentistry, Manila Central UniversityEDSA‐MonumentoCaloocan City, Philippines
Kerstin M. GallerDepartment of Operative Dentistry and PeriodontologyFriedrich‐Alexander‐UniversityErlangen, Germany
Bill KahlerFaculty of Medicine and Health, Department of Restorative and Reconstructive Dentistry, Sydney Dental SchoolThe University of SydneySurry Hills, NSW, Australia
Asma A. KhanDepartment of Endodontics, School of DentistryUT Health San AntonioSan Antonio, TX, USA
Yoshifumi KobayashiDepartment of Oral BiologyRutgers School of Dental MedicineNewark, NJ, USA
Mark LappinDepartment of Restorative Dentistry, School of Medicine, Dentistry and Biomedical SciencesQueen’s University BelfastBelfast, Northern Ireland, UK
Fionnuala T. LundyThe Wellcome‐Wolfson Institute for Experimental MedicineSchool of Medicine, Dentistry and Biomedical SciencesQueen’s University BelfastBelfast, Northern Ireland, UK
Venkateshbabu NagendrababuDepartment of Preventive and Restorative DentistryCollege of Dental Medicine, University of SharjahSharjah, UAE
Giampiero Rossi‐FedeleAdelaide Dental School, The University of AdelaideAdelaide, SA, Australia
Emi ShimizuDepartment of Oral Biology, Rutgers School of Dental MedicineNewark, NJ, USA
Matthias WidbillerDepartment of Conservative Dentistry and PeriodontologyUniversity Hospital RegensburgRegensburg, Germany
Foreword
In this era of sustainability, the need for minimally invasive, conservative and biologically based treatment approaches has never been more compelling. The patient‐centred benefits of such strategies have been clearly illustrated in the success of selective removal of deep caries in operative dentistry, and this approach is now attracting significant interest in the field of vital pulp treatment (VPT). VPT offers a suite of minimally invasive therapies that have the potential to make treatment less invasive, simpler and biologically based while replacing more complex and invasive traditional root canal therapies.
Although not a new concept, the last two decades witnessed a remarkable interest in VPT. Advances in pulp biology research and an improved understanding of the nature of the reparative and regenerative processes in dental pulp, coupled with the continued development of biomaterials, have contributed to the trend. Many published clinical studies have recently demonstrated success for VPT over conventional root canal treatment. It is evident that there are advantages in preserving pulp vitality, highlighted by the simplicity of the techniques and potential cost savings and to that end, VPT has now been endorsed by major professional bodies including the European Society of Endodontology and the American Association of Endodontists. However, many dentists point out that they do not feel well‐trained in the area. As the area evolves and the quality of the research supporting VPT continues to improve, it is important that current evidence is summarized and explained systematically in order to improve the understanding of the dental practitioner interested in carrying out VPT. To date, VPT techniques are usually reduced to one chapter in an operative dentistry or endodontic textbook, so we thought it imperative that the breath of VPT, from reasons to keep the pulp, through diagnosis, to management and outcome, were detailed in one user‐friendly text.
Furthermore, at present, controversial practices and lack of consensus among clinicians on the best approach to manage deep caries and exposed pulp remain, and there is a need for more education and training to increase awareness and improve the clinical decision‐making process and appropriate case selection for VPT. The aim of this book is to provide contemporary, evidence‐based and scientific reference to the clinical development and application of VPT in permanent teeth. For this, an international group of experts in pulp biology, cariology, dental trauma, VPT, dental materials and regenerative endodontics contributed chapters highlighting their state‐of‐the‐art skills and knowledge in their respective fields. The result is a book that provides an in‐depth knowledge and understanding of the scientific basis for pulp preservation therapies and the importance of maintaining pulp vitality. Secondly, clear clinical guidance with evidence‐based clinical protocols is provided for all VPT procedures such as direct pulp capping and partial and complete pulpotomy for both the cariously and traumatically exposed pulps. Accurate diagnosis is a prerequisite for successful VPT; therefore, pulpal diagnosis is considered as a standalone chapter, but the subject is covered throughout the book, reflecting the importance and also the limitations of our current practice in this area. The development in applied biomaterials, revitalization and regenerative endodontic treatment as well as expected outcomes and follow‐up, are covered in the later chapters of the book.
The book combines cutting‐edge information with protocols and an array of illustrations, making it suitable for a wide range of clinicians including undergraduate students, postgraduate clinical trainees and researchers, endodontists and general dental practitioners. The book aims to provide a contemporary evidence‐based reference in the first book dedicated to VPT, providing answers to existing controversies and considering future perfectives and development in the field. VPT is no doubt evolving, and the hope is that future editions of this book will keep with the momentum. We hope you enjoy the text.
Ikhlas A. El‐Karim, Belfast, Northern Ireland, UK
Henry F. Duncan, Dublin, Ireland
Preface
Vital pulp treatment in its various forms has been a subject discussed in dentistry courses for decades. However, it is only recently, in the last five years or so, that converging developments in dental material science, pulp biology and dental have made this treatment a valid, predictable and evidence‐based strategy.
It is not even 25 years ago that the long‐term success rate of direct pulp capping was estimated as well below 50%, or a flip of coin; this poor outcome understandably has led many clinicians to view vital pulp treatment as somewhat of a second‐class treatment, more like an attempt rather than as a bone fide definitive treatment. This perception is changing due to clear and compelling evidence from clinical trials supporting vital pulp therapy and it is rather exciting to see a case made for its application made in this book.
Reasons to maintain a functional pulp‐dentine complex are numerous and can be summarized broadly into categories: adding positive features and avoiding potentially negative elements inherent to the main comparator, i.e. root canal treatment (RCT). Vital pulp treatment or VPT retains immunocompetent tissues that effectively provide microbial clearance and protection from apical periodontitis. Moreover, in teeth with incomplete root formation, VPT promotes further dentine apposition and apical maturation. Conversely, RCT is associated with a larger damage to structural integrity, higher cost and specifically for molars with significantly higher clinical complexity.
Indeed, many patients may benefit from VPT in their desire to retain the natural dentition for the long term. It is therefore very fitting and timely that Ikhlas El‐Karim and Henry (Hal) Duncan, two clinicians with a strong biomedical understanding, have edited this book; it offers a compelling and comprehensive update on all aspects of VPT, from the case for the selection of the procedure, over material choices to related biology and outcomes.
A balanced group of international authors has contributed to this volume, providing a broad and well‐reasoned approach. First the case for treating, rather than removing, the pulp is made by Daniel Chiego and Bruno Cavalcanti succinctly from a functional and a biologic approach. The next chapter authored Paul Cooper, Lara Friedlander and Fionnuala Lundy draws from the vast experience of these authors in pulp biology to strengthen the rationale even more.
This book is directed towards clinicians with a scientific mindset and the following chapters provide contemporary viewpoints on practical aspects of vital pulp therapy. First Asma Khan and Johnah Galicia describe various aspects of pulp diagnostics, an essential step in predicable VPT. With the understanding that VPT is often prescribed in treatment of deep caries, Lars Bjørndal and Helena Fransson provide relevant information from the viewpoint of caries removal strategies.
Moving forward to VPT procedures that are more extensive Till Dammaschke in his chapter looks at direct pulp capping, a procedure that has received much attention with the development of silicate‐based biomaterials. Pulpotomy, an approach that aims to physically remove all coronal pulp with little or no capacity to heal is then discussed by the editors themselves, supported by Roberto Careddu and Mark Lapin.
Chapters 7–10 provide important information for other areas that are critical to the current understanding, including materials (Renan Dal Fabbro, Isaac De Souza Araujo and Marco Bottino), treatment of traumatic injuries (Giampiero Rossi Fedele and Bill Kahler) and regenerative procedures (Matthias Widbiller and Kerstin Galler).
The last chapter on epidemiology and outcomes (Siobhan Cushley, Venkatesh Nagendrababu and Emi Shimizu), again written by authorities in the field, completes this volume.
The enthusiasm of the editors and authors for the topic is palpable and fits where the field is moving internationally, that is towards a much broader acceptance of vital pulp therapy. Providing current and directly applicable information that underpins this therapy is a crucial step in this direction. I am convinced that this book will enjoy a wide readership, equally for seasoned clinicians those at the beginning of their careers.
Ove A. Peters, Professor of Endodontics,School of Dentistry, The University of Queensland,Brisbane, QLD, Australia
1The Importance of Maintaining Pulp Vitality
Bruno Cavalcanti and Daniel Chiego, Jr.
Department of Cariology, Restorative Sciences and Endodontics, University of Michigan School of Dentistry, Ann Arbor, MI, USA
Introduction
When the pulp is inflamed, either reversibly or irreversibly, it is important for clinicians to question the success rates, possible outcomes and patient satisfaction associated with each treatment option. This is also true when considering using more conservative options like vital pulp treatment (VPT) or traditional therapies such as root canal treatment. As highlighted elsewhere in this book, both have a good success rate and can be used as reliable options for the management of pulpal disease.
In this context, one question commonly asked by clinicians is ‘what are the real benefits of maintaining the pulp?’ It is well‐known that immature teeth benefit considerably from VPT. However, clinicians may not see the importance of keeping the pulp tissue for other cases, as the only perceived benefit would be the maintenance of tooth sensitivity. While this benefit is correct, the pulp plays other important roles within the tooth, most notably with the molecular mechanisms to defend the body from bacterial challenge. Furthermore, with the fast development of regenerative therapies, the pulp will be essential to rebuild lost tooth structures and improve the tooth’s prognosis. This book chapter will show a number of molecular mechanisms that are involved in this regenerative process, how the pulp physiology contributes to clinical practice and, most important, show the importance of the pulp tissue in the maintenance of tooth homeostasis.
Dental Pulp Development
To appreciate the importance that the pulp plays on tooth homeostasis, it is necessary to appreciate how the dentine‐pulp complex develops. The developmental stages bring a number of insights into the participation of different cell types and the subsequent organization of dental tissues, which can also be recapitulated into the desired repair and regeneration processes after dental procedures.
Tooth development is a process that involves a well‐coordinated effort between cells from different origins, leading to the formation of a complex organ (detailed in Chapter 2). Unfortunately, when analysing pulp repair/regeneration processes, the clinician is not able to mimic whole tooth formation. This is complicated further by the cells present in the pulp tissue that may not have the same potential as the original cells during tooth development. Nonetheless, the translation of the process at the molecular level to the clinical activity can be of great importance to direct future studies and biomaterial development.
In this context, the participation of stem cells in the development process is important. It is now well established that the pulp tissue has its own reserve of multipotent cells, capable of differentiating into the necessary tissues and/or replacing cells that were damaged or simply completed their function and enter into senescence (1). In fact, most dental tissues have their own mesenchymal stem cells; the enamel, for obvious reasons, is deprived of any cells after tooth eruption and, thus, does not have the same regenerative potential as other tissues. The discovery of dental pulp stem cells (DPSCs) brought many possibilities, more specifically in the understanding of the success of VPT and regenerative endodontics. DPSCs are capable of differentiation into a myriad of cells and tissues, including odontoblasts, fibroblasts, endothelial cells and neurons (2–4), being capable of regenerating all cell types necessary to form a new pulp tissue. This potential appears superior to responses observed with other stem cell populations (3). In addition, the literature shows, in animal models, that the neoformed pulp tissue in complete root models is very similar to the original pulp tissue (5, 6) (Figure 1.1). Moreover, these new pulp tissues were induced only in the presence of the host vasculature and DPSCs, suggesting that the potential is there for complete regeneration or at least functional repair.
Cell Signalling and Dental Pulp Development
Most studies using DPSCs have focused on the potential of these cells to differentiate into odontoblasts (7–9). This is understandable as, in the reparative process, clinicians want the neoformed pulp tissue to produce dentine in order for this barrier to serve as protection to the tissue. Understanding odontoblast differentiation is a difficult process: some studies have shown that the reparative dentine, particularly when induced by certain materials, can be tubular (10–12); other studies have shown that, most of the time, the barrier does not have the tubular aspect, meaning that the formed tissue is more akin to ‘osteodentine’ than to actual dentine (13, 14). This brings uncertainty, as there is no specific odontoblast marker(s) to confirm that the differentiated stem cell is a real odontoblast. Studies have looked into dentin‐matrix‐acidic‐phoshoprotein 1 (DMP‐1), dentin‐sialophosphoprotein (DSPP), matrix extracellular phosphoglycoprotein (MEPE), nestin and others, generally trying to observe their presence in combination with each other (2, 7, 15–17). However, it is important to emphasize that some of these genes can be expressed by osteoblasts and other cell types, meaning that the differentiated cells observed in molecular analysis may not be a typical odontoblast cell.
With this, it is possible to separate the two concepts of regeneration and repair: from a clinical standpoint, having an adequate regeneration/repair with a solid dentine (or osteodentine) barrier, pulp vitality and functional tooth is good enough for patient satisfaction. On the other hand, from a research standpoint, it can be frustrating that with all the potential observed from the stem cells, we are still not able to regenerate the tissues as they are, complete with an odontoblast pseudostratified layer, cell junctions and tubular dentine.
Some answers for this dichotomy may be due to a shortage of information on molecular signalling. As discussed above, during tooth development, there is a very well‐coordinated effort and interaction between different cell types and layers to induce tissue formation and even tooth shape (18, 19). For example, it is known that the signalling between the ameloblasts and mesenchymal cells in the dental papilla induces the initial cell differentiation towards odontoblasts, which consequently directs the deposition of an initially ‘disorganized’ layer (the mantle dentine) and then starts the construction of the typical tubular pattern of orthodentine, by a centripetal direction of movement of the odontoblast layer (Figure 1.2). This signalling is comprised principally of DSPP, enamelysin and ameloblastin (20). However, it is evident that the Wnt and Sonic hedgehog (SHH) pathways and the deposition of a baseline collagen matrix are also essential for the correct cell lining (18, 21). With this, attempts were made to use enamel derivative proteins to induce pulp repair. However, there are differences between the differentiation induced by enamel matrix derivatives (EMD) and mineral trioxide aggregate (MTA), for example, even if the gene expression changes are similar (Figure 1.3). Clinically, none of the materials used for pulp capping and/or regenerative procedures is capable of synthesizing and secreting the original signalling molecules layered by ameloblasts. This does not mean that the regeneration process is impossible. The literature has shown examples that the dentine itself is a major reservoir of multiple growth factors that can activate multiple signalling pathways into DPSCs (22). More importantly, these growth factors can be mobilized by current materials used for pulp capping (e.g. calcium hydroxide and MTA), which can be of great importance in chemotaxis prior to inducing cell differentiation and production of the dentine barrier (23–25).
Figure 1.1 Dental pulp tissue engineering with SHED injected into human root canals and transplanted into immunodeficient mice. (a) Low‐magnification and (b) high‐magnification images of tissues formed when SHED mixed with scaffolds (Puramatrix™, rhCollagen type I groups) were injected into full‐length root canals of human premolars. A vascularized connective tissue occupied the full extension of the root canal. Cell densification and many blood vessels were observed along dentin walls. Scaffolds (Puramatrix™) injected into the root canals without cells were used as controls for SHED. Freshly extracted human premolars were used as tissue controls. Black arrows point to blood vessels close to the odontoblastic layer. (c) Graph depicting microvessel density and (d) cellular density of dental pulp tissues engineered with SHED injected into full human root canals. Microvessel density and cellular density were similar in both experimental conditions and the control group (human pulp), as determined by one‐way ANOVA (5). Reproduced with permission from International & American Associations for Dental Research
.
Figure 1.2 Sequence of dentine formation – (1) signalling from pre‐ameloblasts to pre‐odontoblasts (DSPP, enamelysin and ameloblastin) and deposition of a baseline collagen matrix; (2) deposition of pre‐dentine by the immature odontoblasts, leading to signalling to ameloblasts; (3) enamel deposition; (4) dentin (tubular deposition). Both ameloblasts and odontoblasts mature throughout the process.
Figure 1.3 Western blotting analysis of pathways affected by BMP‐2 (a known dentine inducer) and EMD (enamel matrix derivatives) on dental pulp stem cells. Differences can be seen by the increase of expressed Wnt pathway proteins for EMD (a) and the increase of Smad 4 for BMP‐2 in the canonical BMP pathway (b). Unpublished data.
The Role of the Apical Papilla
Last, but not least in tooth development, is the role of the apical papilla. While considered an embryonic tissue, the apical papilla is a mesenchymal tissue that remains active until the complete maturation of the tooth (Figure 1.4). After the deposition of the first layers of dentine at the crown level and subsequent formation of the primitive pulp tissue, the remnants of the dental papilla continue to work with the Hertwig’s epithelial root sheath in order to guide the development of the cementum, alveolar bone, radicular dentine and periodontal ligament (26, 27). As with the crown, the signalling between epithelial and mesenchymal cells is responsible for tissue differentiation of the stem cells present in this tissue and consequent dentinogenesis. Even after the tooth eruption, the root(s) will continue to develop and, until the development is complete, the apical papilla will remain. As the original dental papilla, the apical papilla is rich in undifferentiated cells with multipotent capacity, which makes it a great source of stem cells for revitalization or revascularization procedures (28).
Figure 1.4 Histologic image from the apical papilla, detaching from the root apex of an immature third molar. Observe the high cellularity and vascularization of the tissue, which can be preserved partially and used for endodontic regenerative purposes (HE, 40×).
This understanding of the tooth development process brings insight into the repair process induced by VPTs. The first associated with the presence of undifferentiated cells and its potential to differentiate into odontoblasts and other cell types necessary for repair and regeneration. Second, it is expected that an effective material will closely mimic the interactions between these mesenchymal stem cells and the epithelial cells that formerly underlined the primitive pulp tissue. Third, molecules that participate not only in the differentiation process but also in the cell recruiting events may be of interest for using dental materials. This can happen directly or indirectly as dentine serves as a reservoir for many of these factors, and materials can be affected by extracting them from the tissue and mobilizing them for cell intake.
Stem Cell Reserve and Healing/Regeneration Potential of the Dental Pulp
Current concepts on pulp regeneration rely on stem cells, either by transplantation or by attracting stem cells present in the body to the area, also known as cell homing. The same can be said about the repair process: it is known that the pulp has a reparative potential, and most of this potential comes from the cellularity of the tissue. Notably, previous research has shown that older patients present lower healing potential in the pulp, and that conservative pulp procedures should be mostly reserved for young patients. This comes from the fact that older connective tissues will have their cell turnover and cellularity negatively affected, and the constant production of secondary dentine determines that cells in this ‘older’ pulp tissue may enter senescence (29, 30). The aged pulp tissue will appear radiographically to have smaller pulp chambers and clinically have less profuse bleeding and higher levels of fibrosis. This means that a tooth that has been previously decayed with tertiary dentine production and then restored is pathologically ‘older’ than a completely sound tooth. It is important to differentiate this pulp age from the patient’s age. With this, the literature has shown that the patient’s age has little effect on the success of VPT procedures (31).
Of course, a clinical evaluation of the cellularity of the pulp tissue is not possible currently; in fact, dentistry, despite all the evolution in the last century, still does not have a reliable way to determine an exact pulp diagnosis (see Chapter 3). Thus, the professional opting for a conservative or radical procedure needs to take other factors into account besides the patient’s age. Indeed, the patient’s age still plays a role as the fibre: cell ratio changes over time. But other factors such as clinical diagnosis, dental history and presence of tertiary dentine and/or internal calcifications are also signs that the pulp tissue in question has already been irritated and responded. Having a clinical understanding that an aged tissue can respond less ideally in a young patient and vice versa is essential to explain both success and failure in VPT.
Pulp Vascularization and its Clinical Implications
As with most connective tissues, the dental pulp can be seen as comprised of structural fibres, cells, nerves, blood vessels and lymphatic vessels. However, when looking closely, it is clear that the pulp is more complex; it is made up of different anatomical zones and is encircled by a hard tissue secreted by odontoblasts (Figure 1.5). The impact of these anatomical attributes and other factors on the potential of the pulp to heal and/or on the determination of success in clinical procedures will be discussed further below.
Among these complexities, the internal anatomy of the pulp chamber and canals is one of the factors contributing to the evolution of inflammatory and reparative processes. As stated above, the pulp is surrounded by dentine, which is a hard tissue. This makes it impossible for the pulp tissue to swell and/or expand in case of inflammation. The apical foramen is the main point of entry for the neurovascular bundles, and the more immature the tooth is, meaning that the foramen is increased in size (open‐apex), the better the tissue vascularization is. This happens even in inflammatory events and, thus, can result in better clinical outcomes when performing pulp capping and/or pulpotomy procedures. In addition, due to their small size and inconsistent numbers, lateral canals, for example, do not appear to contribute significantly to the presence of neurovascular bundles.
If clinical outcome and success of VPTs is considered, the presence of vascularization is important, as it is responsible for providing the immune cell response and the nutrients for a successful repair. It is known that angiogenesis can be induced by the presence of hypoxia, which is observed in a connective tissue that achieves 200 μm in size (32). The dental papilla does not have any blood vessels until it achieves this diameter, and cells start to suffer from the lack of oxygen. This lack of oxygen induces the production of hypoxia‐inducible transcription factor 1 – alpha (HIF1‐alpha), which then induces the activation of vascular endothelial growth factor (VEGF), responsible for cell differentiation and formation of new blood vessels (33, 34). This factor is important and explains why the coronal pulp is much richer in microvessels per mm3 than the radicular pulp, as its volume is larger. Moreover, HIF‐1alpha has been connected to increased production of tertiary dentine in inflamed pulps, suggesting these factors can also contribute to the repair process (33, 35). It is essential to understand the role that hypoxia plays, not only in pulp development but also in other aspects of the homeostasis of the tissue. After any sort of damage and/or induced inflammatory process by the presence of bacterial lipopolysaccharides (LPS), it is possible that small areas of the pulp tissue will undergo different levels of hypoxia. The lack of oxygen in this tissue has the primary participation in the angiogenic process, particularly by the expression of HIF1‐alpha and VEGF (Figure 1.6). Other molecules are also related to angiogenesis, more specifically the B‐cell lymphoma 2 (Bcl‐2) (36) and cytokines such as interleukin 1 beta (IL‐1beta) and tumour necrosis factor‐alpha (TNF‐alpha) (37), which all have a clear effect on both the angiogenic and inflammatory processes. Moreover, the presence of hypoxia is known to activate DPSC differentiation and consequent mineralization (35, 38, 39), illustrating the close connection between the pulp damage and the repair process.
Figure 1.5 Histologic image from the pulp tissue encircled by dentine/enamel structure (HE, 40×).
In addition to the simple presence of blood vessels, it is well‐known that a vascularized tissue can also respond more effectively to harm from bacteria and materials in order that the tissue can be repaired or regenerated properly. Many studies on pulp regeneration have been focusing on the importance of vascularization and have specifically shown that, without proper angiogenesis, true regeneration cannot occur. In this context, the use of angiogenic factors such as the above‐cited HIF1‐alpha or the VEGF has been proven as a way to promote angiogenesis by the differentiation of DPSC into endothelial cells and by assisting with anastomosis with the host original blood vessels (2, 33). This process is essential to allow for the complete fill of the pulp space with functional tissue and, in the case of repair, VEGF, for example, could be used as an adjuvant to promote adequate oxygen levels for the pulp tissue during the initial inflammatory process and, consequently, allowing the cells to migrate and differentiate.
Besides blood vessels, lymphatic vessels appear to be of major importance in regulating inflammatory and repair processes. While the literature has opposing views on this subject, with data showing the complete absence of this type of structure (40, 41) and others showing its presence (42–45), it is important to understand how lymphatic drainage can contribute to control inflammation. In this context, lymphatic vessels have the initial function of removing catabolites from the tissues, including inflammatory cells, cytokines and dead bacteria, amongst others, directing them to lymph nodes, which then will work on these drained fluids to eliminate harmful factors (46). When looking at this function in pulp tissue, the controversy regarding the presence or absence of lymphatic vessels continues: in theory, the absence of lymphatic vessels would be a confirmation that pulp does not recover from intense inflammatory processes, as the cytokines and other harmful factors will be chronically acting on the tissue without proper drainage. However, even the studies that show the lack of lymphatic capillaries in the dental pulp state that these studies were done under normal conditions (40, 41), while other studies have specifically shown the presence of these capillaries under inflammation (42, 45). All this conflicting information may, in fact, indicate that the pulp indeed lacks lymphatic circulation, although lymph angiogenesis appears to occur in the presence of pulp damage and inflammation. Additionally, the fact that the pulp tissue is only vascularized from the apical region can also be responsible for the lack of removal of these factors. As the pulp containment within hard tissue walls can contribute to that as blood vessels are dilated, there is an increase in intrapulpal pressure and, consequently, if lymphatic vessels are present, they would be less effective given this pressure. Among the studies that show the presence of lymphatic vessels, there are some observations that are also important, such as the fact that these types of vessels are more prevalent close to the apical region and not in the coronal pulp tissue (47). Clinically, this can also explain why pulpotomies tend to be successful, as the radicular pulp tissue can be more resilient to the inflammatory process because it has higher capability to modulate the inflammatory process due to the presence of lymphatic vessels. Again, these facts can be only observed if pulp vitality is preserved, since true regeneration is not yet achieved clinically, at least in any clinically available technique.
Figure 1.6 Mechanisms of hypoxia‐induced dentinogenesis and angiogenesis. (1) Induction of cell response due to LPS, bacterial products and/or other irritants; (2) promotion of vasodilation by cytokines; (3) increase in inflammatory exudate on the affected tissue; (4) hypoxia; (5) as the hypoxia reaches 200 μm, affected cells release HIF‐1alpha, which directly affects odontoblasts to induce tertiary dentine and/or induces the release of VEGF and Bcl‐2 to form new blood vessels.
Pulp Innervation and its Contribution to Physiologic Changes
Maintaining pulp vitality also results in the presence of functional nerves in the tissue. The pulp is a highly innervated tissue, with many of the nerve bundles close to the odontoblast layer. The pulp possesses sympathetic nerves, which are associated with the blood vessels and their ability to respond with vasodilation or constriction and the ability to participate in the ‘neurogenic inflammation’ process (48, 49). Evidently, the normal physiology (homeostasis) of the tissue is only maintained in case the tissue is preserved properly. This is factually true for the pulp tissue; however, the physiology of the dentine itself is completely dependent on the maintenance of the pulp tissue, with an interrelationship so intertwined that these two tissues together have been called the dentine‐pulp complex. This relationship starts during tooth development stages and goes on through the tooth’s life, and some of the functions discussed here are very important in terms of the long‐term prognosis of the tooth.
Much has been presented about pulp tissue physiology and how its structure affects treatment outcomes. When discussing pulp preservation, the first factor that comes to mind is the ability of the tooth to respond to pain, and it serves as an alert in case something is wrong. Many dentists have had the experience that a devitalized tooth (a root canal‐treated tooth) became decayed, and the carious lesion evolved with no warning underneath a crown, resulting in extensive structure loss and an unrestorable tooth. One can then infer that the pulp tissue, when present, can ‘detect’ this carious lesion, leading the patient to seek dental work before such destruction occurs. Indeed, the pulp has this ability, and it all comes down to the presence of vitality in the tissue.
As stated previously, the pulp tissue is rich in nerves. The most important ones from the point of view of tooth response are the A‐delta and C fibres (50), which include both afferent and post‐ganglionic sympathetic fibres. A‐delta fibres are myelinated which are bundled in a plexus that is mostly located between the core of the pulp tissue and the cell‐free zone. These fibres lose their myelin layer (but not their Schwann cells) when penetrating the cell‐rich and cell‐free zones until reaching the odontoblast layer and, occasionally, the dentine tubules. The literature does not show any evidence of real synapses between these fibres and odontoblasts (51, 52). Independently of the presence or absence of these connections, the close relationship between these A‐delta fibres and the dentine is of major importance in many aspects of pulp physiology, from dentine sensitivity (for example, the hydrodynamic theory) to inflammatory and repair responses (53, 54).
A‐delta fibres conduct the stimuli very quickly, and this translates into a response that is sharp and of short duration. So, when cold is applied on the tooth surface, the dentinal fluid present in the tubules moves towards the pulp, and this movement stimulates the A‐delta fibres present either in the tubules or close to the odontoblast layer. In healthy tissue, this response rapidly subsides as the body temperature stabilizes the fluid movement, eliminating the stimulus to the nerve fibres (53). Sometimes, patients present with hypersensitivity due to exposed dentine. The principle for the painful response is the same. However, the process known as neurogenic inflammation has been proven to happen in the pulp tissue also (55, 56). In this case, the stimulation of a sensory (afferent) nerve fibre can lead to the release of substance P, which is a neuropeptide with major role in the inflammation (55). Substance P has been detected as released from C fibre terminals and is associated with increased pulpal blood flow and, consequently, vasodilation (57). Other neuropeptides such as calcitonin gene‐related peptide (CGRP) also work towards the neural immune response, with a dose‐dependent effect on recruiting T‐cells, for example (58). Understanding this process may bring therapeutic options, as it is clear that the nerves and all neuropeptides detected in the pulp tissue can impact pain control, immune response and inflammation (59) (Figure 1.7). Stimulating the pulp nerves due to tooth damage can lead to hyperalgesia and allodynia at the trigeminal ganglion level (60), so the sensitized tissue will respond to pain more easily. This response, either from a normal pulp or for a pulp with reversible pulpitis, is a good way to raise the patient’s awareness and assist the provider with a pulp diagnosis that does not demand a more radical intervention. In the case of a carious tooth, this inflammatory process can continue to develop. With this and the presence of bacteria, areas of necrosis and anoxia can be observed in the pulp tissue and these fibres, due to the presence of their Schwann cells, start to lose their efficiency as these cells depend on oxygen to survive (54). This helps to explain why tissues with irreversible pulpitis have lingering pain when tissues are stimulated with cold. The speed at which the stimulus is conducted is not the same anymore, and the increase in intrapulpal pressure can lead to a more severe response. This intrapulpal pressure, on the other hand, will not be stimulating the A‐delta fibres but, instead, will be stimulating the C fibres. These fibres, as stated above, are unmyelinated nerve fibres, generally located in the pulp core. In this context, these fibres do not respond to cold stimulus, for example, as they are not connected to the tubular fluid movements. In a normal pulp tissue, these fibres would not be responsible for typical tooth pain; however, given the fact that they respond with a more dull, aching pain, they can assist in diagnosing referred pain, for example (61). In cases of pulpitis, they tend to lead to the most painful episodes, particularly due to their effectiveness in detecting changes in intrapulpal pressure (57). These fibres are also more resistant to hypoxia, meaning that they can be responsive even in cases where the pulp tissue is close to complete necrosis. Again, responses like this can only be used for diagnosis in vital pulps and losing these references can impair the awareness about harmful processes like caries.
Figure 1.7 Mechanism of neurogenic inflammation. Dentine stimulation can lead to C fibres to express and release both substance P and CGRP. Substance P can induce an increase in blood flow and vasodilation, while CGRP can induce the recruitment of T‐cells. CGRP also induces pulp cells to express IL‐8, which can increase the sensitization of neural fibres and make the inflammatory cycle persistent.
Pulp Response to Restorative Processes
Preserving tooth vitality also has an impact on restorative processes. In vitro studies have shown that the presence of pulp tissue alone does not change dentine hydration and, consequently, does not make the tooth more brittle (62). On the other hand, there is evidence showing that the absence of dentinal fluid and consequent maintenance of the collagen structure of the dentine may affect the bonding process (63, 64). The hybridization process with adhesive and the etched dentine can be more effective if a certain level of moisture is present, particularly if the moisture comes from the dentinal tubules. The correlation between the use of dental materials and dentine permeability can also serve as a good reason for keeping pulp vitality, as it is well‐known that the application of chemical, bacterial and thermal stimuli on the dentine surface can have an impact on how the pulp tissue responds (65). When applying dental material against dentine, even without pulpal exposure, one can expect a tissue reaction. Initially, the tissue reaction comes from the simple fact that dentine is being cut by a bur with heat (66). When that happens, some odontoblast extensions will be cut or overheated, leading those cells to their death and consequent release of cytokines that will initiate the inflammatory process. Most of the time, in healthy pulp tissue, this will not result in more damage as the stimulus is of short duration. As we are going to discuss later in this chapter, the inflammatory process is, in fact, necessary for adequate repair and even for regenerative procedures.
With respect to dental material application, studies have shown, for example, that eugenol can have a soothing effect on the pulp, even though it is very cytotoxic (67, 68), indicating that dosage and composition are significant when attempting pulp repair. In addition, when looking for repair, a vital pulp provides an environment where the factors released by the dentine due to the action of dental materials can be effective in promoting cell differentiation, control of inflammation, angiogenesis and other actions (23, 24). In this context, as obvious as it can be, preserving the pulp vitality is essential to promote adequate repair and dentinogenesis, all necessary for adequate healing of the tissue and reestablishment of the homeostasis of the dentine/pulp complex. The same can be said about the presence of bacteria: the vital pulp tissue, besides reporting tissue destruction with pain, can also be responsible for the initial line of defence against microorganisms. There is a lot of information on how bacteria affect odontoblasts and how, even in cases where the pulp is not exposed, bacterial byproducts are known to have an effect on the pulp tissue and, as explained for dental materials, this reaction can start an inflammatory reaction and consequently, the production of tertiary dentine in an attempt to recover tissue homeostasis. Recent studies show that even small amounts of LPS and lipotheicoic acid (LTA) can induce alkaline phosphatase, an indicator of mineralization, in DPSCs (69, 70). This information, associated with dentine permeability, shows the role played by the pulp tissue in the protection of the tooth when faced with microbial and chemical agents. The molecular aspects of this protective effect will be discussed in the next subsection.
Pulp Vitality and Inflammation
Much has been researched and discussed about the effects of inflammation on pulp repair. Currently, it is well established that the reparative process needs some level of inflammation to be effective. While we still cannot control the ‘threshold’ level of inflammation clinically, the knowledge of the participating molecules in both processes is essential to improve the odds of being able to do so in the future.
The molecules involved in the inflammatory process are numerous and have different specific functions. Among these, it is possible to name proinflammatory cytokines, for example. These include some of the already discussed molecules (e.g. HIF‐1alpha) but also interleukin 1 beta (IL‐1beta), interleukin 6 (IL‐6), interleukin 8 (IL‐8) and others. Most of them have been shown to be associated to pulp tissues with irreversible pulpitis, a fact that can also be reproduced with pulp cell cultures under stress (71–76). These studies have proven a direct correlation between levels of cytokines and inflammatory status. However, we have also shown that even a healthy pulp has basal levels of those cytokines, and, as we have demonstrated in previous work, they can be localized in the odontoblast layer of a non‐inflamed tissue (74). This supports that proinflammatory cytokines may also be involved in the regular dentinogenesis process and that this process may be exacerbated in case of higher levels of these cytokines, leading them to induce more tertiary dentine and, consequently, collaborate in the tissue repair (71, 74, 77–80). These papers show that this process can occur on a number of different fronts, such as the activation of the Wnt pathway by the inflammatory cytokines, the activation of substance P by neural stimulus and even the direct release of cytokines by competent cells (e.g. odontoblasts, DPSCs and fibroblasts) when challenged by bacteria and their subproducts (Figure 1.8
