Clinical Endodontics E-Book

Leif Tronstad

• Herausgeber: Thieme
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 562

Veröffentlichungsjahr: 2008

Beschreibung

The third edition of Clinical Endodontics retains the successful format and practical scope of previous editions. The book opens with an overview of the biology of the endodontium and the apical periodontium. It then provides detailed descriptions of the etiology and pathogenesis of endodontic diseases, examination and diagnostic techniques, and treatments. The book also covers instruments, endodontic materials, endodontic retreatment, bleaching, restoration, and prognosis. 

Features:

• Easy-to-reference presentation of dental morphology and treatment guidelines
• Chapter on how to avoid and manage potential complications
• More than 550 high-quality illustrations demonstrating important concepts.

This book is a valuable resource for students that will enable them to fully grasp the fundamental concepts of clinical endodontics. It is also serve as a refresher for general practitioners, postdoctoral students, and endodontists.

Leseprobe

Library of Congress Cataloging-in-Publication Data

Tronstad, Leif.Clinical endodontics: a textbook/Leif Tronstad.—3rd rev. ed.

p.; cm.

Includes bibliographical references and index. ISBN 978-3-13-768103-8 (alk. paper)1. Endodontics-Textbooks. I. Title.[DNLM: 1. Dental Pulp Diseases–therapy.2. Endodontics–methods. WU 230 T854c 2008]RK351.T76 2008617.6’342–dc22

2009 Georg Thieme Verlag,Rüdigerstrasse 14, 70469 Stuttgart, Germanyhttp://www.thieme.deThieme New York, 333 Seventh Avenue,New York, NY 10001, USAhttp://www.thieme.com

Cover design: Thieme Publishing GroupTypesetting by Sommer Druck, FeuchtwangenPrinted in Germany by Graphisches Centrum Cuno GmbH,

Calbe (Saale)

ISBN 978-3-13-768103-8               1 2 3 4 5 6

Important note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book.

Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers’ leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user's own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page.

Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.

This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation, without the publisher's consent, is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing, preparation of microfilms, and electronic data processing and storage.

ToAnne-Gretheand to Nora, Greger, Ulrik, Andrea, Kristin,and Karl-Henrik

Preface to the Third Edition

The scope of the third edition of Clinical Endodontics is as before to be a simple, yet comprehensive textbook in endodontics that serves as an introductory text for dental students and as a suitable refresher source for general practitioners, postdoctoral students, and endodontists. With this concept in mind, Clinical Endodontics summarizes the biology of the endodontiumand theapicalperiodontiumand deals with the etiology and pathogenesis of endodontic diseases. Examination methods, diagnoses, treatment principles, and prognosis of endodontic treatment are discussed, and main endodontic techniques are described. The format of the previous editions has been kept, and new relevant information has been added to the text. The lists of references following each chapter have been updated. I again extend my thanks to friends and colleagues who have contributed illustrational material to the book.

Oslo, Summer 2008                   Leif Tronstad

Table of Contents

1 The Endodontium

Structure

The Dentin

The Dental Pulp

Reaction Patterns

Pulpitis

Pathogenesis of Pulpitis

Systemic Influences

Pulp Necrosis

Repair in the Pulp

Further Reading

2 The Apical Periodontium

Structure

Reaction Patterns

Apical Periodontitis

Etiology of Apical Periodontitis

Pathogenesis of Apical Periodontitis

Radiographic Appearance and Differential Diagnosis

Further Reading

3 Endodontic Symptomatology

Pulpal Pain

Dental Hypersensitivity

Symptomatic Pulpitis

Periapical Pain

Symptomatic Apical Periodontitis

Oral and Perioral Pain of Endodontic Interest

Periodontal Diseases

Infection of Cysts and Salivary Glands

Sinusitis

Temporomandibular Joint Dysfunction Syndrome

Trigeminal Neuritis

Chronic Neurogenic Pain

Referred pain

Further Reading

4 Endodontic Examination and Diagnosis

History

Clinical Examination

Percussion and Palpation Tests

Sensitivity Tests

Provocation Tests

Anesthesia Test

Optical Tests

Radiographic Examination

Tentative Diagnosis

Clinical Diagnosis

Further Reading

5 Treatment of Teeth with Vital Pulp

Endodontic Aspects of Restorative Procedures

Cavity and Crown Preparation

Cavity Cleansing and Drying

Impression Methods

Pulp Protection

Marginal Leakage

Pulp Capping

Indications

Wound Dressing and Tissue Reactions

Pulpal Seal

Follow-up Examination and Prognosis

Capping of the Inflamed Pulp

Pulpotony

Indications

Wound Dressing and Tissue Reactions

Clinical Considerations

Follow-up Examinations and Prognosis

Pulpectomy

Indications

Treatment Principles

Clinical Considerations

Follow-up Examinations and Prognosis

Further Reading

6 Treatment of Nonvital Teeth

Conservative Endodontic Treatment

Indications

Treatment Principles

Clinical Considerations

Follow-up Examinations and Prognosis

Apical Periodontitis Refractory to Endodontic Treatment

Systemic Antibiotic Treatment

Surgical Treatment

Prognosis

Treatment of Immature Nonvital Teeth

Apexification

Follow-up Examinations and Prognosis

Endodontic Treatment of Root-Fractured Teeth

Endodontic Treatment of Endo–Perio Lesions

Surgical–Endodontic Treatment

Indications

Asepsis

Flap Design and Surgical Access

Microbiological and Microscopic Examination

Resorption Lacunae and Perforation Defects

Apicoectomy

Intentional Replantation

Aftercare

Follow-up Examination and Prognosis

Further Reading

7 Endodontic Emergency Treatment

Emergency Treatment of Vital Teeth

Teeth with Symptomatic Pulpitis

Crown Fractures

Dental Hypersensitivity

Traumatic Occlusion

Emergency Treatment of Nonvital Teeth

Symptomatic Apical Periodontitis

Further Reading

8 Endodontic Aspects of Root Resorption

Internal Root Resorption

Cervical Root Resorption

External Inflammatory Root Resorption

Replacement Resorption

Further Reading

9 Endodontic Instruments

Root Canal Instrumentation

Hand Instruments

Engine-Driven Instruments

Root Canal Obturation

Hand Instruments

Gutta-Percha Guns

Surgical Instruments

Further Reading

10 Endodontic Materials

Temporary Filling Materials

Root Canal Filling Materials

Core Materials

Root Canal Sealers

Materials with Assumed Therapeutic Effect

Retrograde Filling Materials

Further Reading

11 Endodontic Techniques

Preparation for Treatment

Access Cavity

Rubber Dam

Root Canal Instrumentation

Step-Back Preparation

Apical Box Preparation

Crown Down Preparation

Instrumentation of Curved Root Canals

Root Canal Obturation with Silver Points

Root Canal Obturation with Gutta-Percha Points

The Dipping Technique

Thermoplasticized Gutta-Percha Techniques

Lateral Condensation Technique

Standardized Endodontic Technique

Two-Step and Other Techniques

Root Canal Obturation with Adhesive Technique

Root Canal Obturation with Pastes

Regenerative Endodontics

Further Reading

12 Dental Morphology and Treatment Guidelines

Maxillary Central Incisor

Treatment Guidelines

Maxillary Lateral Incisor

Treatment Guidelines

Maxillary Canine

Treatment Guidelines

Maxillary First Premolar

Treatment Guidelines

Maxillary Second Premolar

Treatment Guidelines

Maxillary Molars

Maxillary First Molar

Maxillary Second Molar

Mesiobuccal Root of Maxillary Molars

Distobuccal Root of Maxillary Molars

Palatal Root of Maxillary Molars

Treatment Guidelines

Maxillary Third Molar

Mandibular Incisors

Treatment Guidelines

Mandibular Canine

Treatment Guidelines

Mandibular First Premolar

Treatment Guidelines

Mandibular Second Premolars

Treatment Guidelines

Mandibular Molars

Mandibular First Molar

Mandibular Second Molar

Mesial Root of Mandibular Molars

Distal Root of Mandibular Molars

Treatment Guidelines

Mandibular Third Molar

Further Reading

13 Endodontic Complications

Incomplete Analgesia

Access Cavity

Perforations from the Pulp Chamber

Root Perforations

Apical Perforations

Lateral Perforations

Post Perforations

Obliterated Root Canal

Fracture of an Instrument

Adverse Reactions to Medicaments

Local Tissue Irritation

Neurotoxic Reactions

Allergic Reactions

Overfilling of the Root Canal

Vertical Root Fractures

Further Reading

14 Endodontic Retreatment

Indications for Retreatment

Root Filled Teeth with Apical Periodontitis

Root Filled Teeth with Normal Apical Periodontium

Retreatment

Treatment-Resistant Cases

Surgical Retreatment

Further Reading

15 Bleaching of Discolored Teeth

Discoloration of Teeth

Vital Teeth

Nonvital Teeth

Bleaching of Endodontically Treated Teeth

Preparation for Bleaching

Bleaching Agents

Bleaching Procedures

Restoration of the Bleached Tooth

Bleaching of Vital Teeth

Bleaching of Teeth with Enamel Defects

Bleaching of Teeth with Dentin Discolorations

Further Reading

16 Restoration of Endodontically Treated Teeth

Strengthening of Endodontically Treated Teeth

Intracoronal Restorations

Coronal Restorations

Retention of Prosthetic Appliances in Endodontically Treated Teeth

Preparation of Root Canal Post Space

Cementation of Root Canal Posts

Further Reading

17 Prognosis of Endodontic Treatment

Further Reading

Index

1The Endodontium

Structure

The endodontium comprises the dentin and pulp of the tooth. Both tissues develop from the dental papilla, and although the dentin mineralizes and the pulp remains a soft tissue, they maintain an intimate structural and functional relationship throughout the life of the tooth.

All the cells of the endodontium are located in the pulp and only cellular extensions, odontoblast processes, and nerve endings are found in the dentin. Thus, tissue reactions in the dentin are dependent to a great extent on the activity of cells in the pulp. Conversely, pulpal reactions may be significantly modified by tissue changes in the dentin.

The Dentin

Composition and Morphology

The dentin is composed of approximately 70% inorganic material in the form of hydroxyapatite crystals. The organic matrix, about 15–20%, consists of collagen. Noncollagenous proteins constitute 1–2% of the tissue, whereas the remaining 10–12% is water.

The dentin of the fully formed tooth is called primary dentin. It constitutes the bulk of the tooth and is especially characterized by the presence of dentinal tubules (Fig. 1.1). The tubules generally extend from the area of the dentin–enamel and the dentin–cementum junctions to the pulp. The tubules are surrounded by peritubular dentin, which is a dense, highly mineralized tissue with a noncollagenous matrix. Between the tubules we find the intertubular dentin, which consists of mineralized collagen. Unmineralized predentin lines the pulpal aspect of the dentin.

Fig. 1.1 Scanning electron micrographs of fractured coronal dentin from an impacted canine in a 13-year-old.

a Dentin from the middle area of the crown with crosscut dentinal tubules (diameter: 2 μm). Fibers are seen leaving some of the tubules (× 1700).

b Dentin near the enamel–dentin junction (mantle dentin) with crosscut dentinal tubules (arrows). Note small diameter (0.5 μm) of the tubules (× 1700).

c Predentinal surface with intertubular fibrous matrix (× 2600).

Unmineralized matrix may also be seen inside the mineralized primary dentin. Well known is interglobular dentin, which occurs when mineralizing globules fail to coalesce. From a clinical point of view, it is more important that the buccal and lingual portions of the incisal dentin not always unite, but leave an unmineralized central streak or a soft tissue-containing space, sometimes extending all the way to the incisal dentin–enamel junction (Fig. 1.2). Clearly, in such teeth, an apparent uncomplicated crown fracture will cause exposure of the pulp.

Dentinogenesis continues, but at a slower rate, even after the teeth are fully formed. This dentin is called physiologic secondary dentin and it differs from the primary dentin in that its structure and composition may vary within the tooth and from one tooth to the next. As will be discussed later (see p. 26), increased secondary dentin formation in localized areas of the tooth may occur in response to external irritation. The structure of this tissue will depend on the severity of the irritation and the degree of tissue injury in the pulp and appears to be completely unpredictable (Fig. 1.3). As a rule, the secondary dentin formed in response to external irritants is more irregular than the physiologic secondary dentin.

Fig. 1.2 Microradiograph of an incisor from an 11-year-old. Accentuated incremental lines of buccal and lingual dentin (arrows) meet at the radiopaque central streak, but do not join because of a slit in the dentin at this location.

Dentinal Tubules

It is well established that the dentinal tubules may serve as portals of entry for external irritants into the pulp. Thus, from a clinical point of view, the tubules are the most important and interesting component of the dentin.

In the crown of the tooth, the dentinal tubules generally extend from the area of the dentin–enamel junction to the pulp. In the root, the most peripheral dentin is atubular and the tubules thus begin in an area slightly pulpal to the dentin–cementum junction and extend to the pulp. The diameter of the tubules varies from 0.5 μm in the peripheral dentin to 3–4 μm near the pulp. In the bulk of the dentin they have a diameter of about 2 μm. Due to the much larger peripheral than pulpal surface of the dentin, the number of tubules per square millimeter area increases dramatically in a pulpal direction. Thus, at the dentin–enamel junction, the number of tubules is about 8000 per mm2, halfway between the dentin–enamel junction and the pulp it is 20 000–30 000 per mm2, and near the pulp the number may be as high as 50 000–60 000 per mm2. Similarly, the total volume of the dentinal tubules increases in a pulpal direction and may constitute up to 80% of the total volume of the coronal dentin near the pulp.

The dentinal tubules contain tissue fluids (dentin liquor) which is fluid from the pulp tissue filling out the hollows of the dentin. Odontoblastic processes are present in most tubules and they are especially well visualized close to the pulp. Unmyelinated nerve endings may be present as well, usually in intimate contact with the odontoblastic processes (Fig. 1.4). In addition, unmineralized and mineralized collagen fibers are seen in many tubules at all levels of the dentin (Fig. 1.5).

Mineralized deposits of various structure and appearance occur in the dentinal tubules under various clinical conditions. Sometimes these deposits have the appearance of peritubular dentin, and have generally been regarded as resulting from a continuous formation of the peritubular dentin (Fig. 1.6). This is probably a misconception since peritubular dentin is a developmental and not an acquired structure and since it forms in full thickness concomitantly with the intertubular dentin. Toward the lumen of the tubule, the peritubular dentin appears to be lined by an organic sheath which has been termed the lamina limitans (Fig. 1.6). A proper term for tubular deposits inside the lamina limitans would therefore be intratubular dentin.

Fig. 1.3 Localized secondary dentin formation as a result of external irritation (hematoxylin-eosin).

a Secondary dentin (SD) with regular tubular structure indicating mild stimulation of odontoblasts.

b Secondary dentin with an atubular, cell-containing zone at the dentin–secondary dentin interface due to severe disturbance of odontoblast function. The cells have recovered and have continued to lay down tubular dentin.

c Secondary dentin with few tubules due to death of most odontoblastic cells.

Fig. 1.4 Scanning electron micrograph of a tubule from circumpulpal dentin in a 21-year-old. In addition to the odontoblastic process, a slim fiber which divides into two branches and which is interpreted as a nerve fiber is present (× 9000).

Fig. 1.5 Scanning electron micrograph of a tubule from the coronal dentin of a 42-year-old. A fiber consisting of fibrils with the cross-banding typical of collagen visible on their surface is present in the tubule (× 10 000).

Age Changes

Both macroscopic and microscopic changes occur in the dentin with increasing age, and both types of changes are of considerable clinical importance.

The macroscopic age changes are characterized by the lifelong formation of physiologic secondary dentin which continually modifies the size and to some extent the shape of the pulp chamber and the root canal. At first these changes are beneficial in that they give the root canal a size and form that enhances the possibilities for successful endodontic treatment. However, in old age, the root canals may be obliterated to such an extent that necessary endodontic treatment becomes extremely difficult. Physiologic secondary dentin formation also occurs on the walls of lateral and accessory root canals, often causing a complete occlusion of these narrow spaces. This is the reason why accessory canals, for instance, in the furcation area of molar teeth which may be readily demonstrable in young teeth are evident only in rare instances during endodontic treatment of adult patients.

Fig. 1.6

a Electron micrograph of a cross-cut tubule from partly demineralized root dentin. An electron-dense line (lamina limitans) is recognized between the peritubular dentin matrix and the material beginning to occlude the tubule (×20 000).

b Crosscut tubule from undemineralized dentin occluded with material (intratubular dentin) with electron density different from that of peritubular dentin (PD) (×19 000).

The microscopic age changes of the dentin are characterized by the fact that an increasing number of dentinal tubules become obliterated by mineralized tissue. The occluding material is homogenous and consists of a noncollagenous matrix and small hydroxyapatite crystals. Its appearance is similar to that of peritubular dentin, but as a rule it can be distinguished from this tissue by a difference in density or by the presence of the lamina limitans (Fig. 1.6). From a clinical point of view, it is important to know that the formation of the age-related intratubular dentin starts at the apex of the tooth and continues in a coronal direction with increasing age. In the coronal dentin, the intratubular mineralization will not lead to a complete obliteration of the tubules until the patient is in his 70 s. The process is so closely related to age that the coronal extent of the tubular occlusion is used in forensic dentistry for age determination purposes.

Thus, the microscopic dentinal changes that occur as a result of aging render the root of the tooth homogenous with few patent dentinal tubules. Conceivably, this may facilitate endodontic treatment of nonvital teeth where dentinal tubule infection is a definite problem. The tubules of the coronal dentin, on the other hand, will not be significantly affected by the aging process until the patient is old.

The Dental Pulp

Morphology

The dental pulp consists of a richly vascularized and highly innervated connective tissue (Fig. 1.7). It is surrounded by dentin and has a form that mimics the outer contour of the various teeth (Fig. 1.8). The pulp tissue is in communication with the periodontium and the rest of the body through the apical foramen and accessory canals near the apex of the root (Fig. 1.9). Accessory canals are also found laterally in the root and in the furcation area of molar teeth. However, from a practical–clinical point of view, the pulp is an end organ without collateral circulation.

Cells, Fibers, and Ground Substance

The most characteristic element of the dental pulp is the dentin-forming cell, the odontoblast. The odontoblasts are tightly packed, regularly aligned, polarized cells located at the periphery of the pulp with cytoplasmic processes extending into the tubules of the predentin and dentin. This continuous sheet of odontoblasts at the pulp periphery has been termed the odontoblastic layer (Fig. 1.10). Ultrastructurally the odontoblasts are shown to be similar to other connective tissue cells and their identity is mainly determined by their location. The odontoblasts are static post-mitotic cells, apparently incapable of further cell division. Also, the rate of repopulation of the odontoblast layer is extremely slow under physiological conditions. Probably most and possibly all odontoblasts seen in teeth in older individuals are the original cells. The cell bodies of the odontoblasts are united in certain areas by cell-to-cell junctions. This may allow the odontoblasts to function as a syncytium, a continuous layer of cells.

Fig. 1.7 Coronal pulp in the incisor tooth of a monkey. The odontoblast layer bordering the lightly stained predentin as well as cell-free and cell-rich subodontoblastic zones can be recognized (hematoxylin-eosin).

Fig. 1.8 Overview of the tooth with enamel (E), dentin (D), coronal pulp (CP), and root pulp (RP). Note that the pulpal cavity has a shape which mimics the outer contour of the tooth.

Fig. 1.9 Apical part of the root of a human incisor (R) with pulp (P), periodontal ligament (PDL), and alveolar bone (AB). Note that the apical foramen (arrow) is located laterally to the anatomical apex of the tooth (hematoxylin-eosin).

Fig. 1.10 Dentin–pulp interface in a monkey incisor. Adjacent to the dentin (D), the unmineralized (and unstained) predentin, the odontoblast layer, the cell-free zone, and the cell-rich zone can be seen (hematoxylin-eosin).

Another trait of pulp identity is the subodontoblastic region. In the coronal pulp this region is characterized by a cell-free zone and a cell-rich zone beneath the odontoblastic layer (Figs. 1.7, 1.10). The cells of the subodontoblastic region differ from the odontoblasts in that they have a bipolar, sometimes multipolar arrangement. Structurally, the cells resemble fibroblasts of the central pulp, and like the odontoblasts, they are identified by their location. It has been speculated that the subodontoblastic cells have specific functions, for instance, that they are “preodontoblasts” capable of proliferation and differentiation into new odontoblasts. This theory and others have not been substantiated. However, it is known that they are involved in the elaboration of collagen and ground substance like the cells of the rest of the pulp.

In the bulk of the pulp tissue, three main types of cells are seen: inactive mesenchymal cells, fibroblasts, and fibrocytes. The mesenchymal cells are thought to be multipotential in that when they are stimulated and undergo cell division, their daughter cells may develop into any of the mature connective tissue cells, including odontoblasts. The fibroblasts are the most numerous cells in the pulp and are responsible for ground substance and collagen production, collagen degradation, and turnover. The fibrocytes possibly play a role in the maintenance of collagen fibers.

As will be discussed in some detail later, the pulp has cells that under certain circumstances can develop into hard tissue–producing cells. Thus, after pulp capping, the dentin bridge is formed by new odontoblasts (see Fig. 5.11). Cementum- and bone-like tissues as well as more structureless hard tissues may form in the pulp as well. However, it is not quite clear at present which of the cells in the pulp are capable of differentiation into hard tissue-producing cells.

Other stable cellular elements in the pulp either belong to the vascular or the neural system. In addition, inflammatory cells such as lymphocytes, plasma cells, and macrophages are occasionally seen. Mast cells appear to be a rare occurrence in the healthy pulp.

The ground substance of the pulp has a mucoid consistency. It serves as a matrix in which cells, fibers, and blood vessels are embedded. It is organized as a heterogenous colloid with soluble and insoluble components. The main molecular components are proteoglycans which consist of a glycosaminoglycan linked to a protein molecule. Their major functions have been recognized to be the protection of the cellular elements and capillaries of the pulp, their interaction with collagen to form aggregates possibly involved in dentin matrix formation, as well as control or inhibition of mineralization.

The pulp has two main types of fibers, collagen fibers and elastic fibers, the latter always being confined to the walls of larger blood vessels. Thus, the fibers of the intercellular matrix of the pulp are collagenous in nature. The fibers of the young pulp are small and far from numerous. They are distributed diffusely within the tissue and are often covered by a glycosaminoglycan sheath. In the mature pulp, larger fiber bundles can be seen as well, especially along blood vessels in the root pulp. These fibers are usually devoid of a glycosaminoglycan sheath.

Vascular Supply

Blood vessels the size of arterioles branch off the dental artery and enter the pulp through the apical foramen and possibly through accessory canals (Fig. 1.11). Inside the pulp the main arterioles are seen in a central location extending to the coronal pulp. They give off branches that spread in the tissue, diminish in size, and finally become capillaries. An extensive capillary network is formed in the subodontoblast and odontoblast areas of the pulp. The capillaries provide the odontoblasts and other cells of the pulp with an adequate supply of nutrients. The blood then passes from the capillaries to postcapillary venules and to gradually larger venules toward the central region of the pulp where they are seen alongside the arterioles. Two to three venules leave the pulp through the apical foramen and possibly through accessory canals. Outside the tooth the pulp venules join with vessels that drain the periodontal ligament and alveolar bone.

Multiple arteriovenous anastomoses exist in the pulp. These direct connections between arterioles and venules make it possible for the circulating blood to bypass the capillary plexus. They play an important role in the regulation of pulpal blood flow.

Fig. 1.11 Microangiograph showing vasculature in the pulp of a dog incisor. The main vessels are located centrally in the pulp and an extensive capillary network is seen, especially in the subodontoblast and odontoblast regions.

The vascular pattern described above is basically found in all single-rooted teeth and in each root of multirooted teeth. Thus, in multirooted teeth, an alternate blood supply is generally available, resulting in extensive anastomoses in the coronal pulp. However, the main venous drainage sometimes occurs through one root in these teeth. Blood vessels which communicate with the pulp through accessory or lateral canals do not contribute significantly as a source of collateral circulation, except possibly in the apical 1–2mm of the root canal.

The existence of lymphatic vessels in the pulp is a matter of dispute due to limitations in available investigative techniques. Recent ultrastructural studies suggest that lymphatic capillaries arise in the peripheral areas of the pulp and join other lymph vessels to form collecting channels that leave the pulp through the apical foramen. Moreover, there is evidence of anastomoses between lymphatics from the pulp, the periodontal ligament, and the alveolar bone in the periapical area.

Innervation

The innervation of the pulp comprises afferent nerves which conduct sensory impulses (A-fibers) and autonomic nerves (C-fibers) that are mainly involved in neurogenic modulation of the blood flow but also in transmission of pain (see p. 66). The A-fibers are of the trigeminal system. They are myelinated, surrounded by Schwann cells, and enter the pulp in bundles with the blood vessels through the apical foramen. The C-fibers constitute the majority of the pulpal nerves. They are unmyelinated and enclosed singly or in groups by Schwann cells, and enter the pulp with the sensory fibers. Some branching of the nerves occurs in the root pulp and the branching becomes extensive in the coronal pulp. Beneath the cell-rich zone is the plexus of Raschkow, which consists of a large number of both myelinated and unmyelinated nerve axons. From this plexus some sensory nerves without their myelin sheath but still inside their Schwann cells approach the odontoblastic layer. Near the odontoblasts, terminal axons leave their Schwann cells and pass between the odontoblasts to the predentin, and in some instances enter the dentinal tubules, where they end in close proximity of the odontoblastic process (Fig. 1.5). Nerve endings may also be trapped in the mineralized dentin between the tubules. However, most of the sensory nerves end in the odontoblastic layer or they pass between the odontoblasts and return to the area of Raschkow's plexus.

The physiological need for the vast number of nerves in the periphery of the coronal pulp is not immediately understood. In all likelihood they have proprioceptive functions. Thus, it has been shown that patients readily bite three times as hard on pulpless teeth as on teeth with intact pulps.

Age Changes

As discussed above, continued formation of physiologic secondary dentin over the years will lead to a reduction in the size of the pulp chamber and the root canal. Certain changes which occur in the pulp tissue can be related to the aging process as well. A striking observation is a reduced or missing odontoblastic layer in teeth from older individuals (Fig. 1.12). Fibrosis of the pulp is commonly seen and a reduced number of cells is present between the fiber bundles. Arteriosclerotic changes may occur in the pulp vessels, and capillaries and precapillaries commonly calcify. Nerve endings regularly calcify as well. Intrapulpal mineralizations increase with age and especially diffuse calcifications along the vessels of the root pulp are considered to be an age-related phenomenon (Fig. 1.13).

Fig. 1.12

a Coronal pulp (P) from the incisor of a 71-year-old. Large amounts of secondary dentin (SD) have formed. Almost no odontoblasts are present and the pulp is generally poor in cells (hematoxylin-eosin).

b Root pulp poor in cells and rich in fibers (van Gieson stain).

Fig. 1.13

a Diffuse calcifications in root pulp (van Gieson stain).

b Cellular (cementum-like) hard tissue (H) in the root canal near the apical foramen (AF) (hematoxylineosin).

Age reduces the functional capacities of a tissue. It is conceivable, therefore, that the age of a patient may affect unfavorably the outcome of certain endodontic procedures like pulp capping and pulpotomy.

Reaction Patterns

Pulpitis

Like other connective tissues in the body, the pulp reacts to irritants with inflammation (Fig. 1.14). However, the pulp has certain characteristics that make it unique and that may alter this tissue response—sometimes dramatically. Tumor (swelling) is one of the cardinal signs of inflammation. When the pulp becomes inflamed, anatomical limitations, that is, the hard root-canal walls, will preclude an increase in tissue volume. In addition, the pulp almost completely lacks a collateral circulation. These two factors place the pulp at a considerable disadvantage in dealing with edema, necrotic tissue, and foreign material. On the other hand, the pulp is the only connective tissue that has the ability, at least to a certain extent, to protect itself from external irritants by the formation of intratubular and secondary dentin.

In the classic view of pulpal inflammation, immense importance was given to the influence of the anatomical environment on the pulp. It was assumed that with a local inflammation in the pulp there would be an increased blood flow to the inflamed area. The vasodilation and increased capillary pressure and permeability induced by the inflammation would result in an increased filtration from the capillaries into the tissue, which in turn would cause steadily increasing tissue pressure (Fig. 1.15). Gradually, as the pressure outside the vessels rose, the thin-walled vessels were compressed. This would lead to a decrease in blood flow as well as an increase in venous pressure, which in turn would result in increased capillary pressure and a further increase in the filtration from the capillaries to the tissue. Thus, a vicious circle seemed to develop, resulting in a steady increase in tissue pressure. Consequently, since the pulp lacks the possibility of expansion, the final result of the increase in tissue pressure was then thought to be a choking or strangulation of the pulpal vessels at the apical foramen, leading to a stagnation of the blood circulation with resultant ischemia and necrosis.

Fig. 1.14 Local inflammatory responses to external irritation in the pulp of monkey teeth (hematoxylin-eosin).

a Mild inflammation with filled capillaries in the odontoblast layer and few inflammatory cells.

b Moderate inflammation with accumulation of inflammatory cells in the affected area of the pulp.

c Severe inflammation with abscess formation.

However, modern research has not supported the strangulation theory. For example, in experiments where the tissue pressure of the pulp is measured, it has been found that a pressure increase in one area of the pulp does not cause a pressure increase in the rest of the pulp. It has also been shown that when local inflammation is induced in the pulp, the tissue pressure increases only in the inflamed area and not in the entire pulp cavity. Experiments with in vivo microscopy have confirmed that an injury in the coronal pulp results in local circulatory disturbances and, if the injury is severe enough, to complete stasis in the vessels in and near the injured area. The circulation in the root pulp, by contrast, is unaffected in these experiments. Experimental studies on the healing of pulpal inflammation have confirmed these findings (Fig. 1.16), and presently there is convincing evidence that even severe inflammatory changes in a limited area of the pulp do not result in a circulatory stoppage in the entire pulp.

Based on these and other studies, a modern theory on the hemodynamics of pulpitis has developed. The pulp normally has a relatively high blood flow which is not significantly influenced by vasodilator substances. Thus, only minor increases in blood flow occur during pulp inflammation, and only locally in the inflamed area (Fig. 1.17). The increase in capillary permeability, therefore, appears to be considerably more important than the increase in blood flow for the inflammatory response in the pulp. Two possibilities exist for the transport of edematous fluids away from an inflamed area in the pulp: 1) lymphatics, and 2) blood vessels in the adjacent uninflamed tissue. Increased drainage into lymphatic vessels from inflamed areas is known to occur in other tissues. In the pulp the lymphatic flow would be further aided by a positive pressure gradient between the inflamed area and the adjacent uninflamed tissue. Because of the positive pressure gradient, transport of fluids will also occur through the tissue itself to adjacent uninflamed tissue which has normal structural characteristics and where no changes in capillary pressure or permeability have occurred. Here there will be a net absorption of fluids from the tissue into the vessels, thus preventing an increase in tissue pressure in the uninflamed areas of the pulp. A generalized edema of the pulp during inflammation, therefore, is prevented by a localized increase in the tissue pressure in the inflamed area, by an increased lymphatic flow, and by a net absorption into the capillaries of the uninflamed tissue adjacent to the inflamed area of the pulp.

Fig. 1.15 Diagram illustrating the so-called vicious circle of local pulpal inflammation. Broken lines suggest mechanisms which may break the circle.

Thus, the modern view of the reaction pattern of the pulp is as follows: The pulp reacts to irritants with local inflammation in an area of the tissue that is subjected to the irritants. The inflammation may remain as a local inflammation for a long time, sometimes for years, if the irritants are mild. If the irritants are removed, for example, if a carious lesion is excavated and a restoration placed in the tooth, the local inflammation may heal (Figs. 1.18, 1.40, 1.41). The resistance of the pulp to irritants and its ability for repair are considerable. Still, if the irritants are long-lasting and strong enough, the inflammation will spread in the pulp. In most instances the process progresses rather slowly from the periphery where the irritants reach the pulp, toward the central pulp, the root pulp, and the periapical tissues.

Successive necrosis of the tissue in the direction of the apical foramen then takes place (Fig. 1.18).

Pathogenesis of Pulpitis

Inflammation in the pulp develops in the same manner as in other tissues. The cellular phase is dominated at first by neutrophilic leukocytes; lymphocytes, macrophages, and plasma cells appear later. The last cell types, however, dominate the histological picture during sustained pulp inflammation, giving it the character of a chronic inflammation.

Fig. 1.16 Monkey incisor where severe inflammation was induced experimentally in the coronal pulp (van Gieson stain). After 90 days, repair occurred with the formation of fibrous tissue in the coronal pulp.

a No odontoblasts are seen and the root canal walls are covered by a cementum-like tissue.

b The root pulp appears to be unaffected by the extensive tissue reactions further coronally. The odontoblast layer is intact and the tissue remains rich in cells and poor in fibers.

Thus, following the vascular phase of the inflammatory reaction, which in the pulp is characterized by a rather slight increase in blood flow, dilation and increased permeability of the capillaries, and accumulation of fluids in the tissue, the neutrophilic leukocytes are attracted to the area by chemotaxis (Fig. 1.19). They pass through inter-cellular gaps in the vessel walls and accumulate in the tissue, where they function as phagocytes. If at this time the irritants can be removed, there is a considerable potential for repair. If not, probably more neutrophilic leukocytes will arrive on the scene. These cells have a life span of only a few hours and will soon start to break down, releasing toxic cellular components and proteolytic enzymes which may destroy cells, fibers, and ground substance in the inflamed area of the pulp. If the tissue destruction is severe enough, it may be recognized clinically as a drop of pus when the pulp chamber is opened (Fig. 1.20). If the leukocytic breakdown occurs slowly, encapsuled abscesses can form and may be seen microscopically. This encapsulation of the destroyed tissue may for a time delay further tissue destruction. Sometimes even calcification of the abscess membrane is seen (Fig. 1.21). It is not known whether or not pulpal repair may occur at this stage of the inflammatory process.

Fig. 1.17 Diagram showing blood flow in mL/min × g in the coronal pulp (C) and root pulp (R) of healthy (control) and inflamed dogs’ teeth. Experimentally induced pulpitis in the coronal pulp gave only a slight increase in blood flow in the inflamed area, whereas in the root pulp no difference in blood flow was registered between inflamed and healthy teeth.

Gradually, the scene is no longer dominated by neutrophilic leukocytes, but by lymphocytes that have come to the inflamed area, left the capillaries, and aggregated in the tissue. The inflammation is now no longer acute, but chronic, and in addition to the lymphocytes, macrophages and plasma cells will typically be seen in the inflamed area (Fig. 1.22). Both B lymphocytes and T lymphocytes have been recognized in the pulp, representing the humoral- and cell-mediated systems of immunity. Invasion of the pulp tissue by antigenic products may be inhibited by the complexing of these products with antibodies and the formation of antigen–antibody complexes which in turn are phagocytized and digested, especially by macrophages. However, lymphocytes may also have a destructive effect on the pulp tissue, either through direct cytotoxic activity or through biologically active and destructive cytokines. Macrophages can lead to tissue destruction as well through the production of cytokines, collagenase, and other products. Thus, the immune response may inflict further damage to an already injured pulp. This again may result in an increased chemotactic activity and attraction of neutrophilic leukocytes. An acute inflammatory reaction may then be superimposed on the chronic inflammation. This is a rather common occurrence in inflamed pulps, although in many instances an acute episode will be caused by new external irritants reaching the pulp tissue.

Fig. 1.18 Diagram illustrating the possible outcome of reparative treatment of a carious lesion with corresponding local inflammation in subjacent pulp (left). When the irritants are removed and the cavity is restored, the local inflammation will usually heal (top). However, if enough bacteria have reached the pulp, the inflammation will spread in spite of the placement of a restoration, slowly leading to complete pulpal necrosis and the development of an apical periodontitis.

Fig. 1.19 Neutrophilic leukocytes in pulp tissue responding to external irritants reaching the pulp through exposed dentinal tubules (hematoxylin-eosin).

Pulpal inflammation is, therefore, a dynamic process. Various stages of the inflammatory process can often be observed in different areas of the same pulp. A typical observation would be necrosis of the tissue in the area where the inflammation started. The tissue subjacent to this area may be inflamed, dominated by the cells typical of a chronic inflammation. Also, in this area one or more encapsulated microabscesses may be seen. Apical to the inflamed area, noninflamed pulp tissue will be present (Fig. 1.23). Without treatment, the inflammation (and later the necrosis) will gradually spread in an apical direction until the entire pulp becomes necrotic. A total pulpitis in the sense that the entire pulp is infiltrated by inflammatory cells does not seem to occur.

Fig. 1.20 A drop of pus from a pulpal abscess is seen in a carious cavity (hematoxylin-eosin).

A rare variation in the development of pulp inflammation is the formation of a pulp polyp. Under particularly favorable circumstances, the successive breakdown of the pulp can stop temporarily when a carious attack or a traumatic injury has resulted in an opening of the pulp cavity. Instead of becoming necrotic, the pulp tissue may start to proliferate. A proliferating pulpitis or a pulp polyp then develops (Fig. 1.24). On the surface the pulp polyp normally has a necrotic layer, but in some instances it becomes epithelialized. However, the epithelial lining does not give the protection seen in the gingiva. It is infiltrated with inflammatory cells, is ulcerated, and bleeds easily when touched. Occasionally a pulp polyp may reach the gingiva, and a tissue bridge between the gingiva and the pulp is established. A pulp polyp may last for a relatively long time, but the end result will always be total tissue breakdown as described above.

Fig. 1.21 A pulpal abscess subjacent to a carious lesion is “walled off” by calcified tissue (hematoxylin-eosin).

Fig. 1.22 Accumulation of inflammatory cells typical of chronic inflammation is seen in the pulp of a monkey tooth subjacent to secondary dentin (hematoxylin-eosin).

Fig. 1.23 Section from a tooth where pulp has been exposed to the oral cavity for some time. The tissue in the pulp chamber and coronal half of the root canal is necrotic. Subjacent to the necrotic tissue, the pulp is severely inflamed. In the apical area of the root canal the pulp tissue is still uninflamed (hematoxylin-eosin).

Fig. 1.24 Proliferation of tissue from molar root pulp, leading to the formation of a pulp polyp (hematoxylin-eosin).

Etiology of Pulpitis

Inflammation of the pulp can be caused by many etiological factors. For clinical–practical reasons the following division can be made:

1. Infectious pulpitis, due to caries or exposure of the dentin or pulp to the oral cavity;

2. Traumatic pulpitis, due to traumatic injuries of the teeth; and

3. Iatrogenic pulpitis, due to improper and sometimes proper dental treatment.

Dental Caries

When a carious lesion has reached the dentin, the dentinal tubules are portals of entry for bacteria, bacterial products, tissue breakdown products, and irritants from the saliva and the oral cavity. Even in teeth with enamel caries without macroscopic loss of tissue, a few inflammatory cells may be seen in the pulp underneath the lesion, and under dentin caries, inflammatory foci, sometimes with abscesses, may be seen (Fig. 1.25).

It has been assumed that although there are microorganisms in the dentinal tubules of a carious lesion, the pulp will not be infected as long as it is vital. Rather, it is bacterial products that initially cause the inflammation, either through a direct cytotoxic effect or indirectly by their antigenic properties. The classic opinion is that not until the pulp injury is so severe that a localized area of necrosis has developed will it be possible for bacteria to enter the pulp cavity. Bacteria will then establish colonies in the necrotic tissue and the pulp will become infected. However, from recent studies it appears that invasiveness is an important aspect of the virulence of many endodontopathic bacteria. Thus, during the spread of inflammation in the pulp, bacteria may be present both in the part of the pulp that has become necrotic and in the superficial layer of the subjacent vital tissue. The front of infection, in other words, will be at the transition zone between the necrotic and vital (inflamed) pulp tissue.

Fig. 1.25 Section from a tooth with a deep carious lesion. Large amounts of secondary dentin (SD) have formed. The pulp is severely inflamed (hematoxylineosin).

Fig. 1.26 Section from a tooth with a deep carious lesion. Secondary dentin formation is not evident and the pulp is not inflamed (hematoxylin-eosin).

Fig. 1.27 Microradiograph of a tooth with a deep carious lesion. A hypermineralized (sclerotic) zone has formed in the primary dentin between the carious lesion and the pulp.

While marked inflammatory reactions can be observed in the pulp of teeth with only superficial carious lesions, it is also possible to find teeth with much more severe carious attacks without pulpal inflammation (Fig. 1.26). One reason for this seemingly illogical occurrence is that products from the carious lesion may stimulate the pulp to produce intratubular dentin, resulting in a sclerosis of the tubules. A zone of sclerosis is formed in the dentin between the peripheral area of destruction and the pulp (Fig. 1.27). The intratubular deposits in the zone of sclerosis consist of small hydroxyapatite crystals that may obliterate the tubules completely. The deposits are identical with those seen in age-changed dentin (Fig. 1.6). Peripherally to the sclerotic zone, additional intratubular mineralized deposits may be found. These deposits vary considerably in quality and appearance. Usually they consist of large, irregularly arranged, needle-shaped hydroxyapatite crystals, or large, rhomboid-shaped whitlockite crystals (Fig. 1.28). These irregular deposits are in all likelihood not formed by pulpal cells, but result from a passive reprecipitation of minerals that were dissolved in the more peripheral parts of the carious dentin.

The sclerotic zone of the dentin may become an effective barrier which prevents the passage of irritants from the carious lesion to the pulp. The barrier may even be so effective that repair of pulpal inflammation that had developed prior to the formation of the barrier may occur. A permanent repair without treatment is still unthinkable, since an untreated carious process will proceed and gradually break through the sclerotic zone of the dentin so that irritants can reach the pulp once again. Moreover, in most instances the sclerotic zone of the dentin is less than perfect. It may reduce, but usually will not entirely stop, the irritants from the carious lesion reaching the pulp. Also, it should be remembered that the carious process spreads not only in a pulpal direction in the dentin, but in a lateral direction as well, especially in the area near the enamel–dentin junction. This results in irritants reaching the pulp through newly exposed dentinal tubules where intratubular sclerosis has not yet formed. Therefore, from a clinical point of view it must be assumed that the pulp is inflamed to some extent in all teeth with active carious lesions.

It is important to note that the sclerotic zone is formed in the primary dentin (Fig. 1.27). The secondary dentin, which as a rule also forms in the pulp under a carious lesion, will not, however, constitute an effective barrier against the external irritants (Fig. 1.25). On the contrary, when the carious process has broken through to the secondary dentin, the pulp will unquestionably be inflamed. Gradually, the carious process will also break through to the pulp and cause a pulp exposure (Fig. 1.29). At that time the inflammation is usually irreversible with today's treatment methods.

As is evident from the above, the pulp reaction in carious teeth may vary considerably, and it is virtually impossible with clinical means to have an opinion of its severity until the tooth gives a negative sensitivity response which suggests pulp necrosis. The therapeutic implications of this unclear diagnostic situation are discussed in Chapter 5.

Fig. 1.28 Scanning electron micrograph of a dentinal tubule with whitlockite crystals as seen in carious dentin (×17 500).

Fig. 1.29 Section from a tooth with pulp exposure due to caries. The pulp tissue subjacent to the exposure is severely inflamed (hematoxylin-eosin).

Fig. 1.30 Section from a tooth with an enamel–dentin crack filled with bacterial plaque. The crack runs at an angle to the dentinal tubules, and many tubules which are opened up by the crack contain bacteria as well (Brown–Brenn stain).

Dentin Exposed to Oral Cavity

Other etiological factors leading to an infectious pulpitis are conditions that contribute to the exposure of the dentin and dentinal tubules to the oral environment. With the refinement of foodstuffs, severe attrition is not as common as before. On the other hand, abrasion, particularly as a result of tooth-brushing, is becoming a more serious problem. Erosion leading to exposure of dentin was traditionally seen in individuals employed in certain chemical industries. Presently it has become a serious problem in the young generation from excessive intake of sweet and acid soft drinks. Nevertheless, it is periodontal disease and the extensive treatment of this disease that today particularly leads to exposure of dentin. Gingival recession is commonly seen in these patients and the root cementum and peripheral layers of the root dentin are being removed during scaling and root planing. It has also been shown that the so-called enamel cracks that are present in most teeth do not necessarily end at the enamel–dentin junction, but rather extend deep into the dentin (Fig. 1.30). These cracks are filled with plaque and microorganisms, and sometimes defects reminiscent of carious lesions are seen at the bottom of such cracks. Since the cracks usually run at an angle to the dentinal tubules, a large number of tubules may become exposed to the oral environment by a single crack.

Irritants from the plaque and saliva may reach the pulp through the exposed dentinal tubules. This is shown by the fact that mineralized deposits are laid down in the exposed tubules. The intratubular deposits are characterized by the large, needle-like hydroxyapatite crystals and the rhomboidal whitlockite crystals seen peripherially in the tubules of carious lesions (Fig. 1.28). However, only occasionally are exposed tubules fully occluded as seen in age-changed root dentin and in the sclerotic dentin of carious teeth (see Fig. 1.6). Secondary dentin forms as a result of external irritation in all teeth with exposed dentin. The secondary dentin is usually more regular than in carious teeth, but is still characterized by morphological irregularities with a varying number of tubules and with inclusions of functioning blood vessels and strings of soft tissue (Fig. 1.31). Pulp stones may be observed in the coronal pulp of these teeth as well, which have possibly developed as a result of external irritation.

In spite of the mineral deposits in the tubules of the primary dentin and formation of often large amounts of secondary dentin, the exposed dentin remains as a rule partially open to the mouth and does not fully protect the pulp from exogenous irritants. In the pulp of these teeth the odontoblastic layer is reduced or missing (Fig. 1.31). Circulatory disturbances are evidenced by hemorrhages and disintegrating erythrocytes, and the blood vessels are few and prominent. The most conspicuous finding in teeth with long-standing exposed dentin is a fibrosis of the pulp (Fig. 1.32). Large bundles of collagenous fibers are seen in the affected area of the pulp, often in continuity with the secondary dentin. Frequently, fiber bundles may be mineralized.

Connective tissue cells, and sometimes lymphocytes, macrophages, and plasma cells are seen between the fiber bundles. However, a possible inflammatory reaction is mild and will not lead to pulp necrosis. The exception lies in teeth with severe periodontal disease and pocket formation to the foraminal areas of the roots. In such teeth a retrograde pulpitis may develop (Fig. 1.33). In a single-rooted tooth this condition will lead to disturbances in the blood supply to the pulp relatively quickly, resulting in total pulp necrosis. In teeth with multiple roots, a retrograde pulpitis in one root will spread slowly in a coronal direction, and it may take a long time before the entire pulp becomes necrotic.

Fig. 1.31

a Pulp horn from a tooth with exposed dentin. Large amounts of secondary dentin as well as pulp stones (PS) are present. Functioning blood vessels are seen deep inside the secondary dentin (arrow).

b Higher magnification of blood vessels in secondary dentin (hematoxylin-eosin).

Traumatic Injuries

Traumatic injuries to the teeth and jaws will often result in pulpitis and pulp necrosis. A complicated crown fracture with pulp exposure will result in an infectious inflammation of the pulp. The actual crown fracture invariably leads to a hemorrhage in the pulp subjacent to the exposure. The blood clot is an excellent substrate for bacterial growth, and the microorganisms of the plaque accumulating on the fractured surface will readily invade the pulp. A local inflammation is seen in the tissue near the exposure after 2–3 days, and total pulp necrosis in such teeth has been observed as early as 7 days after the injury (Fig. 1.34). However, in some instances it may take weeks before total necrosis is seen.

Fig. 1.32 Pulp horn from a tooth with exposed dentin. Large fiber bundles, few and dilated vessels as well as a calcified area are seen in the pulp tissue (hematoxylin-eosin).

Fig. 1.33 Mandibular molar with severe periodontal disease.

a Section showing bacterial plaque to the apex of the mesial root (Brown–Brenn stain).

b Neighboring section showing retrograde pulpitis reaching the coronal pulp (hematoxylin-eosin).

In root-fractured teeth, the tissue injuries at the fracture line will cause an inflammatory reaction. The pulpal injury is characterized by ruptured vessels and bleeding into the tissue followed by circulatory stasis in the injured area. If the fracture line is in communication with the oral cavity, bacteria will invade the injured tissues (blood clot), and an infectious pulpitis will develop and cause pulp necrosis as described above for teeth with complicated crown fractures. If, on the other hand, a true intra-alveolar fracture is diagnosed, no foreign irritants will be present at the site of injury. Only a mild inflammatory reaction will then follow, clearing up and removing extravasated erythrocytes and tissue breakdown products. Complete pulpal repair will occur in about 80% of such teeth. The remaining 20% are usually teeth with displacement of the coronal fragment during the injury, resulting in severence of the pulpal blood vessels at the fracture site. The pulp tissue of the coronal fragment will then undergo ischemic necrosis (see p. 25). Experience has shown that over time, usually in a few weeks, the ischemic pulp tissue will become infected by way of exposed dentinal tubules and enamel–dentin cracks. Endodontic treatment will then become necessary. However, in the pulp tissue of the apical fragment of the root-fractured teeth, repair usually takes place and the endodontic treatment may be confined to the coronal fragment of the tooth (see p.123).

About 25% of subluxated teeth end up with necrosis of the pulp. The sequence of events leading to this end result is not fully understood. By definition, subluxated teeth are loosened, but not displaced. This means that the pulpal blood vessels are not severed at the apex of the tooth. Rather the injury is characterized by ruptures of intrapulpal blood vessels, bleeding into the tissue, and subsequent infection of blood clots through exposed dentin and cracks as described above.

Luxated teeth by definition are displaced by the injury. Consequently, the pulpal blood vessels of these teeth are severed at the apical foramen and the pulp undergoes ischemic necrosis. Repair is possible in incompletely formed teeth with open apices through recanaliculization and revascularization of the pulp (see p. 27). However, in most instances, the ischemic pulp tissue becomes infected, necessitating endodontic treatment of the teeth.

Iatrogenic Factors

Operative and restorative procedures may lead to pulpal inflammation. The inflammation is mainly caused by dessication or dehydration of the dentin, by toxic influences from materials and cements, and by leakage along the margins of a restoration.

Dehydration of the dentin may result from the heat caused by cavity or crown preparation without water, from the use of thermoplastic impression materials that are too warm, and from a prolonged and continuous blast of air to exposed dentin. As a result of dehydration, tissue fluids from the pulp will flow into the dentinal tubules toward the dentin surface. This fluid flow causes mechanical disturbances in the pulp. The odontoblasts and sometimes other cells may be sucked into the dentinal tubules, and there is an immediate increase in the bloodflow to the area of the pulp subjacent to the dehydrated dentin (Fig. 1.35). There is also an increase in the number of functioning capillaries in the injured area. The injuries result in a mild chemotactic activity and after a few hours, scattered neutrophilic leukocytes are seen in the tissue. The inflammatory reaction to dentin dehydration is generally mild, and it has not been possible to show experimentally that this type of pulpal injury leads to pulp necrosis. However, the inflammation often results in dental hypersensitivity and considerable postoperative discomfort for the patient. There is also some clinical evidence that preparation without water and careless use of thermoplastic impression materials may cause a long-standing chronic inflammation in the pulp with internal root resorption and eventually total pulp necrosis. It is important to understand that it is not the heat itself that causes the pulp reaction, but the dehydration of the dentin. True, it has been shown that a temperature increase of 10 °C in the pulp may cause inflammation. The dentin, however, is an excellent insulator and, for instance, dry cavity preparation gives a temperature increase of only 2–3 °C in the pulp tissue. Thus, cooling of the bur with cold or tempered air will not prevent preparation damage, but rather make it worse. Use of water on the other hand, will prevent dehydration of the dentin and thereby prevent a pulp reaction in an effective and reliable manner.

The placing of a restoration may be harmful to the pulp as well. A good example of this is the insertion of cohesive gold fillings (Fig. 1.36). The “hammering” which is necessary for this technique, the heating of the gold foil, and the prolonged period of dehydration of the dentin in the cavity usually cause a severe pulp reaction characterized by intrapulpal bleeding and inflammation. This pulp reaction may be irreversible.

Cements and filling materials used in dentistry may contain components that are irritating to the pulp (Fig. 1.37). Especially the tooth-colored materials are of interest in this regard; examples of toxic components are fluorides in silicate and glass ionomer cements and chemically active ingredients to influence the setting reaction or improve the color stability of composite resins. Thus, different brands of the same material may have different biological properties depending on the additives the various manufacturers have included in their products. An example of this is seen when the antibacterial effect of commercially available filling materials based on Bowen's resin is studied, in that it varies from no effect to a strong effect. Clinically, the rule should be that a tooth-colored material should be used with a base to protect the pulp (see p. 86).

Fig. 1.34 Pulp horn in a monkey tooth with traumatic pulp exposure (complicated crown fracture). On day 7 after the injury there is evidence of severe hemorrhage in the tissue and the pulp is necrotic (hematoxylin-eosin).

Marginal leakage will occur to a greater or lesser extent with most restorations, and plaque and microorganisms may be found in the gap between the restoration and the cavity wall (Fig. 1.38). Marginal leakage may cause an inflammatory reaction in the pulp. Apparently, the etiological factors are infectious–toxic in nature, but the mechanism is presently not well understood. For example, an amalgam restoration will not seal a cavity any better after 1 week in the mouth than a methyl methacrylate resin filling. Still, under the amalgam restoration no or only a negligible reaction will be observed in the pulp, whereas under the resin restoration usually a severe inflammatory reaction, often with abscess formation, is seen (Fig. 1.37e). It might appear that reactions occur between bacterial and plaque components and components leaking out of the resin restoration, resulting in substances with strong immunogenic properties. This may explain why marginal leakage is more detrimental in conjunction with some filling materials than with others. Finally, it should be remembered that the gap between a restoration and the cavity wall represents a definite risk for the development of secondary caries.

Fig. 1.35 Area of the pulp of a monkey tooth subjacent to a cavity prepared without water. Filled capillaries and a few neutrophilic leukocytes are seen in the odontoblast layer after 1 day (hematoxylin-eosin).

Fig. 1.36 Area of the pulp of a monkey tooth subjacent to a cavity restored with gold foil. A severe inflammatory reaction is seen in the pulp subjacent to the cavity after 30 days (hematoxylin-eosin).

Therapeutic irradiation of the head and neck region may damage the pulp. The odontoblasts are especially sensitive cells, and as a result of irradiation, may elaborate abnormal dentin, sometimes filling large parts of the pulpal cavity. Circulatory disturbances and inflammation may result as well. However, the effect of irradiation on the salivary glands, resulting in a decrease in salivary flow, is of much more profound clinical importance. The teeth become more prone to decay, and especially in the cervical area, caries is rampant, often leading to fracture of the teeth, exposure of the pulp, and gradually to irreversible pulpal inflammation. It is important to note that teeth with pulp involvement in irradiated patients should be treated endodontically rather than by extraction, since extraction may result in radionecrosis of the surrounding bone.

During orthodontic treatment the teeth can be exposed to forces that are strong enough to cause pulp damage. A recent study shows that orthodontic patients 5 years after completion of the treatment have significantly more nonvital incisors than individuals who have not undergone orthodontic treatment. It is not immediately clear how the pulp is injured. Two possibilities appear to exist. Intrapulpal vessels may rupture as a result of the treatment, resulting in internal bleeding. The blood clot may become infected as discussed above, and an infectious pulpitis will lead to pulp necrosis. In some instances the pulpal blood vessels conceivably may be pinched off at the apex of the tooth, resulting in ischemic pulp necrosis.

Fig. 1.37 a–f Examples of pulp reactions observed under tooth-colored filling materials after 8 days: mild in a, b and severe in e, f (hematoxylin-eosin).

Fig. 1.38

a Cavity in a dog tooth filled with glass ionomer cement for 60 days. A bacterial plaque is present between the filling material and the cavity walls (Brown–Brenn stain).

b Higher magnification of bacterial plaque on the cavity floor and bacteria in dentinal tubules (Brown–Brenn stain).