Терапевтическая стоматология. Клиническая эндодонтия = Therapeutic dentistry. Clinical endodontics

Минск
«Вышэйшая школа»
2022

Утверждено
Министерством образования Республики Беларусь
в качестве учебника для иностранных студентов
учреждений высшего образования
по специальности «Стоматология»

CLINICAL ENDODONTICS
Approved
by the Ministry of Education of the Republic of Belarus
as a manual for foreign students
of higher education institutions
in the speciality “Dentistry”

Л.А. Казеко  Е.Л. Колб  О.С. Городецкая

Терапевтическая стоматология
КЛИНИЧЕСКАЯ ЭНДОДОНТИЯ

L.А. Kazekо  Е.L. Коlb  О.S. Gorodetska
Therapeutic dentistry

УДК 616.314.163-08(075.8)-054.6
ББК 56.6я73
 
К14

Р е ц е н з е н т ы: кафедра терапевтической стоматологии с курсом ФПК и ПК УО «Витебский 
государственный ордена Дружбы народов медицинский университет» (заведующий кафедрой кандидат медицинских наук, доцент Ю.П. Чернявский); заведующий кафедрой общей стоматологии 
ГУО «Белорусская медицинская академия последипломного образования» доктор медицинских наук, 
профессор Н.А. Юдина; доцент кафедры современных технологий перевода УО «Минский государственный лингвистический университет» кандидат филологических наук, доцент Т.И. Голикова

Все права на данное издание защищены. Воспроизведение всей книги или любой ее части не может 
быть осуществлено без разрешения издательства.

ISBN 978-985-06-3410-8 
© Казеко Л. А., Колб Е. Л.,
 
 
Городецкая О.С., 2022
 
© Оформление. УП «Издательство
 
 
“Вышэйшая школа”», 2022

INTRODUCTION

Clinical Endodontics is intended to serve the educational needs of both dental 
students and dental practitioners seeking updates on endodontic theories and techniques. The primary aim has been to provide an understanding of biological processes involved in pulpal and periapical pathologies in an easily accessible form and to 
show how this knowledge affects clinical management. The textbook outlines the 
main issues of clinical endodontics. 
Clinical Endodontics gives a description of diagnostic principles of the pulp and 
apical periodontium state, presents contemporary views on the etiology and pathogenesis of endodontic pathology development. It also provides a description of endodontic instruments as well as modern treatment methods of complicated caries. 
Dental students will be able to learn the classification of pulp and periodontal diseases, their course and clinical manifestations. They will get to know indications and 
contraindications of applying different methods of endodontic treatment, basic principles of mechanical root canal treatment, determination of root canal length and 
medications for intracanal therapy at the endodontic examination, techniques of root 
canal obturation as well as possible mistakes and complications when diagnosing and 
treating pulpitis and apical periodontitis.
Therefore, we have supplemented the core text with numerous figures and photographs. While providing basic information for undergraduate students, the textbook 
might be useful for postgraduates and dental practitioners. This is the first edition of 
the textbook including five chapters. 
The authors hope that the subject of Clinical Endodontics will be useful for foreign students studying dentistry in English.

PULPITIS

GENERAL INFORMATION

The dental pulp is a soft tissue of a mesenchymal origin located in the centre of 
a tooth (Fig. 1.1). It is the principle source of pain in oral cavity and also a major site 
of attention in endodontics and restorative procedures. It consists of specialised cells, 
odontoblasts, arranged peripherally in a direct contact with a dentin matrix. This 
close relationship between odontoblasts and dentin is known as “pulp-dentin complex”. The pulp is a connective tissue system composed of cells, ground substance, 
fibers, interstitial fluid, odontoblasts, fibroblasts and other cellular components. Pulp 
is actually a microcirculatory system consisting of arterioles and venules as the largest 
vascular component. Due to the lack of true collateral circulation, pulp is dependent 
upon few arterioles entering through the foramen. Due to the presence of the specialised cells, i. e. odontoblasts as well as other cells which can differentiate into hard 
tissue secreting cells; the pulp retains its ability to form dentin throughout the life. 
This enables the vital pulp to partially compensate for loss of enamel or dentin occurring with age. The injury to the pulp may cause discomfort and the disease. Consequently, the health of the pulp is important for successful completion of the restorative procedures. 
Thus, the knowledge of the pulp is essential not only for providing dental treatment, but also to know the rationale behind the treatment provided.
The pulp is composed of:
1) cells:


 odontoblasts;


 fibroblasts;


 undifferentiated mesenchymal cells;


 defense cells (macrophages, plasma cells, mast cells);
2) matrix:


 collagen fibers (type I, type II);


 ground substance (glycosaminoglycans, glycoproteins, water);

1

CHAPTER 
CHAPTER 

1

3) blood vessels (arterioles, venules, capillaries);
4) lymphatics (draining to submandibular, submental and deep cervical nodes);
5) nerves:


 subodontoblastic plexus of Raschkow;


 sensory afferent from V nerve and superior cervical ganglion.

When the pulp is examined histologically, it can be distinguished into four distinct zones from the periphery to the centre of the pulp.
Zones of the pulp are:

odontoblastic layer at the pulp periphery;

cell free zone of Weil;

cell rich zone;

pulp core.
Odontoblastic layer consists of odontoblasts that, in their turn. Odontoblasts 
 consist of cell bodies and cytoplasmic processes. The odontoblastic cell bodies form 
the odontoblastic zone whereas the odontoblastic processes are located within predentin matrix. Capillaries, nerve fibers (unmyelinated) and dendritic cells may be 
found around the odontoblasts in this zone.
Cell free zone of Weil is a subodontoblastic layer central to odontoblasts. It contains plexuses of capillaries and small nerve fiber ramifications.
Cell rich zone lies next to the subodontoblastic layer. It contains fibroblasts, undifferentiated cells which maintain a number of odontoblasts by proliferation and 
differentiation.
Pulp core is circumscribed by a cell rich zone. It contains large vessels and nerves 
from which branches extend to peripheral layers. Principal cells are fibroblasts with 
collagen as ground substance.

Crown

Root

Enamel

Dentin

Pulp

Cementum

Periodontal
ligament
Nerve and
blood supply

Figure 1.1. Relation of pulp with its surrounding structures (adapted from medlineplus.gov)

Important features of the pulp. Pulp is located deep within the tooth, so it defies 
visualisation. It gives radiographic appearance as radiolucent line. The normal pulp is 
a coherent soft tissue, dependent on its normal hard dentin shell for protection. Therefore, once exposed, it is extremely sensitive to contact and temperature but the pain 
does not last for more than 1–2 sec after the stimulus is removed. Pulp is totally surrounded by the dentin which limits the area for expansion and restricts the pulp’s ability to tolerate edema. The pulp has almost a total lack of collateral circulation, which 
severely limits its ability to cope with bacteria, necrotic tissue and inflammation. The 
pulp consists of unique cells, the odontoblasts, as well as the cells that can differentiate 
into the hard-tissue secreting cells. These cells form dentin and/or irritation dentin in 
an attempt to protect the pulp from the injury. Pulpal responses are unpredictable.
The innervation of pulp tissue is both simple and complex. Simple in that there 
are only three nerve endings and consequently the pulp lacks proprioception. It is 
complex because of innervation of the odontoblast processes which produces a high 
level of sensitivity to thermal and chemical changes. 
Correlation of clinical signs and symptoms with corresponding specific histological picture is often difficult.

CLINICALLY NORMAL PULP

A clinically normal pulp (healthy pulp) responds normally to the various vitality 
tests and to percussion and palpation. The term “clinically normal pulp” is used to 
classify a pulp that has no signs or symptoms to suggest that any form of the disease 
is occurring. The term “clinically” is used since such a pulp may not be histologically normal and/or may have some degree of fibrosis (scarring) as a result of previous 
injury or stimuli.
A clinically normal pulp is asymptomatic. It produces a mild and transient response to various stimuli but the nature and severity of the response may vary according to the age and state of the tooth. As long as there has been no calcification of the 
coronal pulp space, a clinically normal pulp will react to cold stimuli with a mild pain 
that lasts for no more than 1–2 sec after the stimulus is removed. A clinically normal 
pulp does not respond to heat stimuli. Percussion and palpation tests will not elicit any 
tenderness. A radiographic examination will demonstrate a normal appearance of the 
pulp chamber, root canals and periapical tissues.
Dentine is usually sensitive when exposed to irritants hence dentine sensitivity 
should be distinguished from pulp inflammation. Such a tooth shows no radiographic 
signs of canal obliteration by “asynchronous” calcification as compared to the pulp 
of the adjacent teeth (Fig. 1.2), nor signs of root resorption, but rather an intact lamina dura and a normal periodontal ligament space along its entire radicular length.
The pulp of a tooth with an immature apex, contained within dentin walls that 
are still thin (Fig. 1.3) is healthy, as is the pulp of an elderly patient whose root canal, 
because of the continuous deposition of secondary dentin by the odontoblasts, seems 
to be nearly obliterated (Fig. 1.4).

1

Because of their high frequency and because of the absolute lack of symptoms that accompany them, the calcifications that are frequently observed radiographically within the 
pulp tissue, especially in the crown, can be considered normal 
findings. They may vary in size, from microscopic pulpoliths 
to concretions that occupy almost the entire pulp chamber or 
canal lumen (Fig. 1.5, see the tipped-in colour pages).

Figure 1.3. Tooth appearance:
a – radiographic appearance of a normal pulp in a second molar with an immature apex; b – histologic appearance of a normal pulp in a molar with immature apices (courtesy of Prof. A. Bloom, Boston University)

Figure 1.4. Radiographic appearance of a normal pulp in an elderly patient. Note the sizes of the pulp 
chamber and of the canals of the upper right second molar

Figure 1.2. The canine has sustained trauma years previously. Now 
its pulp appears “precociously aged” with respect to the pulp tissues 
of the adjacent teeth. Note the total radiographic disappearance of 
the pulp chamber and radicular canal

a
b

The etiology of these pulp calcifications is unknown. They can occur around 
nests of cellular degeneration, in the form of dystrophic degeneration, but in the 
absence of such tissue degeneration, their cause remains obscure. They have even 
been described in still-unerupted teeth, which have not been influenced by the same 
functional stresses.
There is undoubtedly a cause-and-effect relationship between calcifications and 
pulp pathology, especially when the tooth has a long history of chronic irritation, 
such as the one caused by dental caries.
These “steal space” calcifications from the cellular component of the pulp can 
also interfere in some way with the vascularisation of the surrounding tissue. It should 
be considered when one is deciding whether to undertake a direct pulp capping.
Even with the passage of years, the odontoblasts do not cease their activity. Thus, it 
is normal to find a gradual diminution of the endodontic space, both coronal and radicular, in an elderly patient, owing to the continued apposition of the secondary dentin.
Furthermore, within the pulp itself the number of cellular components diminishes, while the content of collagen fibers increases. Therefore these are normal findings in the elderly, whose “age” pulps are synchronous in both dental arches.
The situation of the so-called “precocious”, “out of step”, or “asynchronous” 
aging of the pulp of a single tooth is quite different; it is an index of the pulp tissue 
compromise. It may occur, for example, as the consequence of trauma. Such “aging” 
is frequently asymptomatic and most often comes to the attention of the dentist because of the unaesthetic discolouration of the dental crown, as an incidental radiographic finding, or because of the symptoms of periodontitis that can arise after the 
compromised pulp has become necrotic (Fig. 1.6).

Pulpitis is a condition in which the pulp (nerve) of the tooth becomes inflamed, 
causing pain and pressure in the tooth. There are varying degrees of pulpitis, from 
mild to severe (S. Watson, 2014).
When the pulp becomes inflamed, pressure in the pulp chamber affects the nerve 
and connective tissue in the tooth. Extreme cases of pulpitis may result in a phenom
Figure 1.6. An example of the necrotising periodontitis:
a – years following trauma, the pulp of the lower left central incisor, after protracted compromise which has led to 
“asynchronous” restriction of the canal lumen, has finally become necrotic, causing the lesion and the symptoms. 
Note that, although it extends into the lesion, the apex of the right central incisor responds to the vitality tests; b – two 
years later. Note the complete healing of the lesion and the maintenance of the pulp vitality in the right central incisor

a
b

1

enon called referred pain, causing pain from pulpitis to be detected in unrelated areas 
of the face and mouth, ultimately making it difficult for the patient and the dentist to 
pinpoint the exact tooth causing the pain.
Pulpitis is inflammation of a dental pulp tissue. Pulpitis is mainly caused by bacteria infection which itself is a secondary development of caries (tooth decay). It 
manifests itself in the form of a toothache.

PULPITIS ETIOLOGY

The noxious stimuli responsible for pulp inflammation, necrosis, and dystrophy are legion, ranging from bacterial invasion to hereditary dwarfism (Table 1.1). The most frequent 
initial cause of pulp inflammation is a bacterial invasion from a carious lesion. Paradoxically, 
an alarming amount of pulp involvement is induced by the very dental treatment designed to 
repair the carious lesion. An increase in automobile and cycle accidents, as well as accidents 
from body contact sports, has also brought about an increase in pulp death owing to trauma.

Table 1.1. Pulpitis etiology

Bacterial

Coronal ingress
Radicular ingress

1) caries
1) caries
2) fracture
Complete
Incomplete (cracks, infraction)
2) retrogenic
infection
Periodontal pocket
Periodontal abscess

3) nonfracture 
trauma
3) hematogenic

4) anomalous 
tract
Dens invaginatus (aka dens in 
dente)
Dens evaginatus
Radicular lingual groove (aka 
palatogingival groove)

Traumatic
Acute
Chronic
1) coronal fracture
2) radicular fracture
3) vascular stasis
4) luxation
5) avulsion

1) adolescent female bruxism
2) traumatism
3) attrition or abrasion
4) erosion

Iatral

Cavity preparation
1) heat of preparation
2) depth of preparation
3) dehydration
4) pulp horn extensions
5) pulp haemorrhage
6) pulp exposure
7) pin insertion
8) impression taking

Ending of Table 1.1

Restoration
1) insertion

2) fracture
Complete
Incomplete

3) force of cementing
4) heat of polishing

Intentional extirpation and root canal filling 
Periradicular curettage
Orthodontic movement 
Rhinoplasty
Periodontal curettage 
Osteotomy
Electrosurgery 
Intubation for general anesthesia
Lase burn 
Chemical
Restorative materials
1) cements
2) pastics
3) etching agents
4) cavity liners
5) dentin bonding agent
6) dubule blockage agents

Disinfectants 
1) silver nitrate
2) phenol
3) sodium fluoride

Desiccants 
1) alcohol
2) ether
3) others

Idiopathic

Aging
Internal resorption
External resorption
Hereditary hypophosphatemia
Sickle cell anemia
Herpes zoster infection
Human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS)

The causes of pulp inflammation, necrosis, and dystrophy are arranged below in 
logical sequence. 
J. I. Ingle opens the list with the most frequent irritant, microorganisms. Coronal 
caries is by far the most common means of ingress to the dental pulp for infecting 
bacteria and/or their toxins. Long before the bacteria reach the pulp to actually infect 
it, the pulp becomes inflamed from irritation by preceding bacterial toxins. 
K. Langeland observed pulp reactions “with certainty” when superficial enamel 
fissure caries was found clinically. 
M. Brännström and P. Lind observed inflammatory changes in the pulps of 50 of 
74 premolars with initial enamel caries on proximal surfaces but with no radiographic evidence of penetration.