DANYLO HALYTSKY
NATIONAL MEDICAL UNIVERSITY OF LVIV
DEPARTMENT OF THERAPEUTIC DENTISTRY
METHODOLOGICAL GUIDE
for practical classes „Therapeutic dentistry”
(VI semester) for the 3-nd year students
Lviv-2012
The methodological guide worked out by: M. Hysyk, O. Ripetska
Accountable for an issue  first vice-rector of scientific and academicl work, professor,
Corresponding Member of the Academy of Medical Sciences of Ukraine, M.R. Gzhegotskiy.
Reviewers: associate professor of department of Surgical dentistry N. Krupnik,
associate professor of department of Pediatric dentistry N. Chukhraj
Methodological guide for students in Therapeutic dentistry (III semester) was discussed and
approved on the sitting of the department of Therapeutic dentistry (record of proceedings №15,
dated from 11, May, 2010) and approved on the meeting of Methodological committee in dentistry
disciplines on June 22, 2010, protocol № 3.
Computer printing: Oksana Kochegarova
2
CONTENT OF THE COURSE
Page
Plan of the discipline „Therapeutic Dentistry” according to the credit-module
system of the organization of studies (CMSO) .........................................................
Types of self-education work for students.................................................................
Types of individual work for students.......................................................................
The structure of discipline „Preclinical cause of Therapeutic Dentistry” estimation
of grades for current educational activity (converting of traditional marks into
marks, estimation in grates for implementation of individual tasks) ……………….
Introduction …………………………………………………………………………
Practical lesson 20. Medical history report, its contents, getting up
demands.Anatomical-Physiological characteristic of Pulp. Age changes.
Classification of Pulpitis ……………………………………………………………
Practical lesson 21. Acute Pulpitis. Etiology, Pathogenesis, Clinic, Diagnostic,
Differential Diagnostic ……………………………………………………………..
Practical lesson 22. Chronic Pulpitis. Etiology, Pathogenesis, Clinic, Diagnostic,
Differential Diagnostic …………………………………………………………….
Practical lesson 23. Systematization of Treatment methods of Pulpitis. Method of
full and partial Pulp Preservation.Complications.Characteristic of medications ….
Practical lesson 24. Method of vital pulp extirpation, indications. Complications.
Characteristic of medications ………………………………………………………
Practical lesson 25. Method of non-vital pulp extirpation, indications.
Complications. Characteristic of medications. Modern technologies ……………..
Practical lesson 26. Peculierities of Root Canal Preparation and Cleaning in
Treatment of Pulpitis. Obturation of the Root Canal System.Modern materials …..
Practical lesson 27. Module’s control No 3….........................................................
Practical lesson 28. Apical Pericementitis: Etiology and Pathogenesis.
Classification of the Pericementitis ………………………………………………...
Practical lesson 29. Acute Apical Pericementitis: Etiology and Pathogenesis.
Pathological-Morphological changes. Clinic, Differential Diagnosis ……………..
Practical lesson 30. Chronic Apical Pericementitis: Etiology and Pathogenesis.
Pathological-Morphological changes. Clinic, Differential Diagnosis ……………..
Practical lesson 31. Conservative method of treatment of apical pericementitis,
indications. Scheme of treatment of acute apical pericementitis. Modern
technologies, medications ………………………………………………………….
Practical lesson 32. Principles and scheme of treatment of chronic apical
pericementitis. Periapical therapy. Medications ……………………………………
Practical lesson 33. Peculierities of Root Canal Preparation and Cleaning in
Treatment of Apical Pericamentitis. Obturation of the Root Canal System. Modern
materials. Conservative-surgical methods of treatment of Apical Pericementitis ….
Practical lesson 34. Peculierities of restoration of Endodontically Treated Teeth.
Bleaching …………………………………………………………………………...
Practical lesson 35. Physiotherapy methods of treatment of diseases of the
endodontium. Indications and Contraindications …………………………………..
Practical lesson 36. Mistakes and Complications in Pulpitis and Pericementitis
Diagnostic and Treatment. Their correction ………………………………………..
Practical lesson 37. Module’s control 4 …………………………………………..
Practical lesson 38. Summary control № 1……………………………………….
3
PRACTICAL LESSONS
Module 2: „Diseases of the endodontium”– 4,4 credits (133 hours): lectures – 30 hours,
practical lessons – 150 hours, out of class work – 90 hours.
Module № 3
Pulpitis
No
Topic
Pract.
lessons
20
Medical history report, its contents, getting up
demands.Anatomical-Physiological characteristic of Pulp.
Age changes. . Classification of Pulpitis.
Acute Pulpitis. Etiology, Pathogenesis, Clinic, Diagnostic,
Differential Diagnostic
Chronic Pulpitis. Etiology, Pathogenesis, Clinic,
Diagnostic, Differential Diagnostic
Systematization of Treatment methods of Pulpitis.
Method
of
full
and
partial
Pulp
Preservation.Complications.Characteristic of medications.
Method of vital pulp extirpation, indications.
Complications.Characteristic of medications.
Method of non-vital pulp extirpation, indications.
Complications.Characteristic of medications.Modern
technologies.
Peculierities of Root Canal Preparation and Cleaning in
Treatment of Pulpitis. Obturation of the Root Canal
System.Modern materials.
Module’s control No 3.
4
Out of
class
work
2
4
2
21
22
23
24
25
26
27
4
2
4
2
4
2
4
2
4
2
3
2
Out of
class
work
2
Individual
work
Review of
scientific
and
professional
literature,
preparation
of the
written work
and carrying
on scientific
investigation
Module № 4
Diseases of the Pericementum
No
Topic
Pract.
lessons
28
Apical Pericementitis: Etiology and Pathogenesis.
Classification of the Pericementitis.
Acute Apical Pericementitis: Etiology and Pathogenesis.
Pathological-Morphological changes. Clinic, Differential
Diagnosis.
Chronic
Apical
Pericementitis:
Etiology
and
Pathogenesis.
Pathological-Morphological
changes.
Clinic, Differential Diagnosis.
Conservative method of treatment of apical
pericementitis, indications. Scheme of treatment of acute
apical pericementitis. Modern technologies, medications.
Principles and scheme of treatment of chronic apical
pericementitis. Periapical therapy. Medications.
4
29
30
31
32
4
Individual
work
2
4
2
4
2
4
2
Review of
scientific
and
professional
33
34
35
36
37
38
Peculierities of Root Canal Preparation and Cleaning in
Treatment of Apical Pericamentitis. Obturation of the
Root Canal System. Modern materials. Conservativesurgical methods of treatment of Apical Pericementitis.
Peculierities of restoration of Endodontically Treated
Teeth. Bleaching.
Physiotherapy methods of treatment of diseases of the
endodontium. Indications and Contraindications.
Mistakes and Complications in Pulpitis and Pericementitis
Diagnostic and Treatment. Their correction.
Module’s control 4.
Summary control № 1.
4
2
4
2
4
2
4
2
3
4
2
4
OUT OF CLASS WORK
(45 hours)
No
Topic
1.
Preparation for practical lessons  theoretical and practical skills training
2.
Independent work with the topics not including into practical lessons:
- Methods of patients examination with Pulp pathology
- Anatomical-Physiological characteristic of tissues of periodontal split.
Peculiarities of patient examination with periapical pathology.
- Anesthesia in pulpitis treatment.
- Conservative-surgical methods of treatment of apical pericementitis.
3.
Preparation for the module control No 1 – theoretical and practical skills
training
INDIVIDUAL WORK
HISTORY OF DISEASE
(3 points)
No
Topic
1.
Modern irrigation solutions for in endodontics.
2.
Rubber-dam in endodontical treatment.
3.
Modern adhesive filling materials for the obturation of the root canals.
5
literature,
preparation
of the
written work
and carrying
on scientific
investigation
Hours
34
2
3
3
3
Points
1
1
1
THE STRUCTURE OF DISCIPLINE „THERAPEUTIC DENTISTRY”, MARKS FOR CURRENT EDUCATIONAL ACTIVITY (THE
CONVERTATION OF TRADITIONAL ESTIMATIONS IN MARKS, ESTIMATION IN GRADES FOR IMPLEMENTATION OF
INDIVIDUAL TASKS)
ІІІ YEAR (6 SEMESTER)
Module
Module 1.
Diseases of
dental hard
tissues and
endodontium
Number of educational
hours, numder of credits,
ECTS
270
=
9 cr.
Schedule
of
practical
classes
Distribution of
practical classes
Lec.
Convertation of traditional
marks into grades
Grades for the
implementation of the
ISWS
Traditional marks
Traditional marks
„5”
„4”
„3”
„2”
„5”
„4”
„3”
„2”
3
2,5
2
0
9
7
5
0
Number of
grades for
current
educational
activity of
students
Number of
grades for
final module
control
max
114
min
76
max
80
min
50
SWS
Pract.
30
90
Practical
classes
(in all 38)
150
Students who received 76 grades are admitted to final module control. For individual work 6 marks are added.
Introduction
The European Credit Transfer System (ECTS) is being implemented at the Dentistry Faculty
(2009). According to the regulations of the ministry of Health care of Ukraine, the modular credit
transfer system and modular rating assessment system being introduced in Ukraine are congruent
with the ECTS.
The content of the curriculum on the third year ofstudies includes 9 credits (according to
ECTS) or 270 hours, 30 hours are envisaged for lectures, 150 hours for practical classes and 90
hours for independent study.
The content of the curriculum and syllabus is defined by principles and:
- is based on international levels of proficiency;
- matches national qualification levels of achievement;
- has clearly and flexibly formulated objectives and outcomes;
- is based on professional and academic skills;
- covers professional and academic content (areas of subject knowlegde); situational content and
pragmatic content / necessary practical and useful skills;
- takes into account the students backgrounds and their studies and target needs;
- is modular in its organization.
The teaching material of the V semester is divided into 2 thematical modules. The teaching
objectives of the thematical module.
No 1. „Examination of the dental patient” envisage the learning of modern methods of
diagnosis of dental diseases, theory and practical skills in interpreting the obtained data in making
clinical diagnosis. Besides, the dental students gain profocoency in dental anaesthesia, dental
intensive care root canal treatment, tooth extraction, pain medication etc.
The teachinf objectives of the thematical module No 2 „Dental caries and non-caries lesions
of teeth” envisage the learning of causes of occurrence and developmental mechanisms of dental
hard tissie lesions of different origin. The dental students learn to classify dental hard tissue
pathologies, clinical manifestations and course of discase, indications as to applying different
methods of treatment, peculiarities of surgical treatment, cavity preparation, fillings of the dental
hard tissues damaged by dental caries, as well as dental health basics (preventive measures and
remineralization therapy of dental caries).
The Guide for Practical Classes on Therapeutic Dentistry includes: short characteristic of the
theme for each lesson; control questions of the material studied test assignments and situation −
based tasks as well as reference literature. The students are awarded credits for each module and at
the end of the course they are awarded credits for the subjects they learnt.
Practical lesson No 20
Theme: Medical history report, its contents, getting up demands.Anatomical-Physiological
characteristic of Pulp. Age changes. . Classification of Pulpitis.
Short description of a theme
A thorough and precise examination of the orofacial soft tissue, teeth, periodontium, and
occlusion provides adequate information on which diagnosis is based. Only after the abnormalities
of these structures are diagnosed and recorded the treatment planning process should be started. A
treatment plan and subsequent course of treatment will be effective only in case if the information
obtained during the examination prove to be qualitative.
SCHEME OF MEDICAL HISTORY REPORT.
1. Subjective examination.
1. Passport data.
2. Complaints.
3. Anamnesis of the disease /anamnesis morbi/.
4. Anamnesis of the life /anamnesis vitae/.
2. Objective examination.
1. Common condition /status praesens communis/.
2. Local condition /status localis/.
A. Extraoral inspection.
B. Intraoral inspection:
- vestibule of mouth /vestibulum oris/;
- oral cavity /cavum oris propria/.
3. Provisional diagnosis.
4. Additional diagnosis.
5. Differential diagnosis.
6. Final diagnosis.
7. Treatment plan.
8. Diary.
9. Epicrisis.
The patient assessment consists of 2 main parts: subjective and objective.
Subjective part includes:
 Passport data / name, age, address, sex, profession/;
 Complaints /pain, esthetics defects, bleeding, xerostomia, changes of taste,
hypersensivity of dental hard tissues/.
Pain characteristic /types of pain/:
 Boring/terebrant/;
 Colicky;
 Constricting /gripping/;
 Darting /fulgurant/;
 Duii /gnawing, lightning/;
 Food;
 Heterotopic /refered/;
 Homotopic;
 Lancinating;
 Throbbing;
8
 Violent;
 Wandering.
Esthetics defects: changes of color of hard tissues, form and size defects of the tooth,
dentofacial anomaly, anomaly of occlusion and position of the tooth, breakdown of filling.
Anamnesis of the disease (anamnesis morbi). Attention is given to changes in organism from first
manifestations of disease up till the time, of the patient’s visitation. Includes 3 main parts:
Beginning of the disease (we are to ask the patient when and how the disease has begun,
the first symptoms, patient’s opinion as to the causes of disease development).
Dynamics of disease development.
What kind of treatment was carried out and its efficiency.
Anamnesis of life (anamnesis vitae).
This part include:
Living and working conditions.
Communicable diseases that require special precautions, procedures or referral (AIDS,
syphilis, tuberculosis, hepatitis B, herpes simplex).
Allergies or medications that may contraindicate the use of certain drugs.
Systemic diseases and cardiac abnormalities that demand less strenuous procedures or
prophylactic antibiotic coverage.
Physiological changes associated with aging that may demand outer clinical presentation
and influence treatment.
Smoking or drug habit.
Objective part includes:
 Common condition (status praesens communis).
Attention is given to common condition of the patient (constitution, weight) and to
individual organs and systems (absorbent, alimentary, circulatory, cardiovascular, nervous,
urogenital, endocrine). During the medical interview, the dentist must recognize the clinical
manifestation of common diseases. So far as there are many common diseases, like diabetes
mellitus, leucosis, alimentary system pathology, and also a such contagious diseases like a AIDS
(acquired immune deficiency syndrome), syphilis whose the first manifestations become apparent in
oral cavity. That’s why the dentist is sometimes the first health professional to identify a patient
with common disease including the communicable ones.
 Local condition (status localis)
Extraoral inspection.
First, we pay attention to bilateral symmetry of the face, to color of the facial skin. Then, we
examine the ortofacial soft tissues. We start the examination by inspection of the submandibular
glands and cervical nodes for abnormalities in size, texture, mobility, and sensivity to palpation,
then, palpate the masticatory muscles for pain or tenderness and maxillotemporal joint. Next, start
in one area of the mouth and follow a routine pattern of visual examination and palpation of the
cheeks, lips. And also we must check the points of nervus trigeminus exit.
Intraoral inspection.
Vestibule of the mouth (buccal cavity): we examine the vestibule mucosa, lips, facial
alveolar mucosa, frenulums, and occlusion.
Oral cavity: we look at the lingual alveoral mucosa, palate, tonsilar areas, tongue, and
floor of the mouth. A thorough evaluation of all the se structures is necessary before the operative
care is initiated. It is ill-advised inexpendient to plan restorative procedures for a patient while a
life-threatening disease process goes undiagnosed and if a thorough examination was not
preliminary conducted.
Next, we pass to examination of the dentition and teeth. We must pay attention to
compromised or missing dentition, crowded teeth, dichotomy teeth, malformed and migrated teeth,
outstanding teeth, diastema and tremas presence.
9
Examination of the teeth begins from right upper molars to right lower ones. We focus our
attention on the size, color, form, mobility of the teeth, and restorations.
The dental pulp, 75% water and 25% organic, is a viscous connective tissue of collagen
fibers and ground substance supporting the vital cellular, vascular, and nerve structures of the tooth.
It is a unique connective tissue in that its vascularization is essentially channeled through one
opening, the apical foramen at the root apex, and it is completely encased within relatively rigid
dentinal walls. Therefore, it is without the advantage of an unlimited collateral blood supply or an
expansion space for the swelling that accompanies the typical inflammatory response of tissue to
injurious conditions. However, the protected and isolated position of the pulp belies the fact that it
is a sensitive and resilient tissue with a great potential for healing.
The dental pulp occupies the pulp cavity in the tooth. Anatomically the pulp organ is divided
into:
 the coronal pulp located in the pulp chamber in the crown portion of the tooth, including the
pulp horns that are directed toward the incisal ridges and cusp tips;
 the radicular pulp located in the pulp canal(s) in the root portion of the tooth.
The radicular pulp is continuous with the periapical tissues by the connecting through the
apical foramen or foramina of the root. Accessory canals may extend from the pulp canal(s)
laterally through the root dentin to the periodontal tissues. The shape of each pulp conforms
generally to the shape of each of the respective teeth.
The pulp is a unique, specialized organ of the human body serving four functions:
1. Formative or developmental
2. Nutritive
3. Sensory or protective
4. Defensive or reparative.
The formative function is the production of primary and secondary dentin by the
odontoblasts as well as the protective response of reactionary or reparative dentin.
The nutritive function supplies nutriments and moisture to the dentin through the blood
vascular supply to the odontoblasts and their process.
The sensory function provides sensory nerve fibers within the pulp to mediate the sensation
of pain. Dentin receptors are unique because various stimuli elicit only pain as a response. The pulp
usually does not differentiate between heat, touch, pressure, or chemicals. Motor fibers initiate
reflexes to the muscles of the blood vessel walls for the control of circulation in the pulp.
The defensive function of the pulp is related primarily to its response to irritation by
mechanical, thermal, chemical, or bacterial stimuli and removing detrimental substances through its
blood circulation and lymphatic systems. Such irritants can cause the degeneration and death of the
involved odontoblastic processes and corresponding odontoblasts and the formation by the pulp of
replacement odontoblasts (from undifferentiated mesenchymal cells) that lay down irregular or
reparative dentin. The deposition of reparative dentin by the replacement odontoblasts lining the
pulp cavity acts as a protective barrier against caries and various other irritating factors. This is a
continuous but relatively slow process; taking 100 days to form a reparative dentin layer 0.12 mm
thick. In cases of severe irritation the pulp responds by an inflammatory reaction similar to any
other soft tissue injury. However, the inflammation may become irreversible and can result in the
death of the pulp because the confined, rigid structure of the dentin limits the inflammatory
response and the ability of the pulp to recover.
If, however, the irritant is very mild, such as cutting the odontoblastic process more than 1.5
mm peripheral of the pulp at high speed with air-water coolant during cavity preparation, and
although the processes and corresponding odontoblasts then die, no replacement odontoblasts are
formed and thus no reparative dentin. Therefore, there is no barrier (except for the smear layer)
between the dead tracts remaining and the pulp. This may explain why many teeth have pulpal
problems cavity preparation and restoration. Newer dentin bonding agents are promising for sealing
the cut dentinal surfaces.
10
Knowledge of the contour and size of the pulp cavity is essential during cavity preparation.
In general, the pulp cavity is a miniature contour of the external surface of the tooth. The size varies
among the various teeth in the same mouth and among individuals. With advancing age, the pulp
cavity usually decreases in size. Radiographs are an invaluable aid in determining the size of the
pulp cavity and an existing pathological condition. Also with advanced age, the pulp generally
becomes more fibrous because of episodes of irritation and may contain pulp stones or denticles.
The latter are nodular, calcified masses usually appearing in the pulp chamber but also may be in
the pulp canal. These may be attached to the pulp cavity wall or free in the mass of pulp tissue.
Timely root canal therapy is advised before a stone is formed since it can be a significant problem
for the root canal therapist.
Morphology
The pulpal tissue is traditionally described in histologically distinct, concentring zones: the
innermost peripheral pulp core, the cell-rich zone, the cell-free zone, and the peripheral
odontoblastic layer.
The radicular and coronal pulp core is largely ground substance, an amorphous protein
matrix gel surrounding cells, discrete collagen fibers, and the channels of vascular and sensory
supply. The gel serves as a transfer medium, between widely spaced pulp cells and vasculature, for
transport of nutrients and by-products. Terminal neural and vascular components, which divide and
multiply extensively in the subodontoblastic zones, converge into larger vessels and trunks and
together from a main trunk passing through the pulp core to or from the apical foramina. Both
matrix and collagen components are formed and maintained by a dispersed network of
interconnected fibroblastic cells.
Fibrocytes and undifferentiated mesenchymal cells are particularly concentrated in the outer
coronal pulp to form the cell-rich zone subjacent to the peripheral layer of odontoblastic cells.
Functioning like troops in reserve, the mesenchymal cells and/or fibrocytes are capable of
accelerated mitotic differentiation and collagen matrix production to serve as functional
replacements for destroyed odontoblastic cells. They produce reparative dentin when bacteria or
their by-products breach the permeable dentinal wall or a pulpal exposure occurs. A dense and
extensive capillary bed and nerve plexus from the cell-free zone, infiltrate the cell-rich zone, and
separate it from the cellular bodies of the peripheral odontoblastic layer.
Odontoblastic layer
The peripheral cellular layer of the pulp, the odontoblasts, produce primary, secondary, and
reactionary dentin. This layer may also regulate or influence tubular mineralization and sclerosis as
a defense mechanism. Postmitotic and irreplaceable, the columnar cell bodies line the predentin
wall of the pulp chamber in a single layer. From each cell, a single process extends into at least one
third of the tubule and adjacent dental substrate that it formed. Each cell has an indefinite life span,
but crowding from continued deposition of secondary dentin constricts the pulpal chamber to
reduce the initial number of cells by half. The odontoblastic cells are packed closely together, with
both permanent and temporary junctions between the cellular membranes. Just as the peripheral
processes of the odontoblasts are physically interconnected, a third type of intercellular interface, a
communicating junction, mediates transfer of chemical and electronic signals that permit
coordinated response and reaction of the odontoblastic layer. Thus, as an additional protective
response, the integrity and spacing of the odontoblastic layer mediates the passage of tissue fluids
and molecules between the pulp and the dentin. Routine operative procedures, such as cavity
preparation and air-drying of the cut dentinal surface, can temporarily disrupt the odontoblastic
layer and may sometimes inflict permanent cellular damage.
Vascular system
The circulatory system supplies the oxygen and nutrients that dissolve in and diffuse through
the viscous ground substance to reach the cells. In turn, the circulation removes waste products,
11
such as carbon dioxide, by-products of inflammation, or diffusion products that may have
permeated through the dentin before they accumulate to toxic levels. The equilibrium between
diffusion and clearance may be threatened by use of long-acting anesthetics that contain
vasoconstrictors such as epinephrine. An intraligamental injection of a canine tooth with 2%
lidocaine with 1:100.000 epinephrine will cause pulpal blood flow to cease for 20 minutes or more.
Fortunately, the respiratory requirements of mature pulp cells are low so that no permanent cellular
damage ensues.
Inflammation, the normal tissue response to injury and the first stage of repair, is somewhat
modified by the pulp chamber. A stimulus producing cellular damage initiates neural and chemical
reactions that increase capillary permeability so that proteins, plasma fluids, and leukocytes spill
into the confined extracellular space, producing elevated tissue interstitial fluid pressure.
Theoretically, elevated extravascular tissue pressure could collapse the thin venule walls and start a
destructive cycle of restricted circulation and expanding ischemia. However, the pulpal circulation
is unique because it contains numerous arteriole “U-turns”, or reverse flow loops, and arteriolevenule anastomoses, or shunts, to bypass the affected capillary bed. Also, at the periphery of the
affected area, where high tissue pressure is attenuated, capillary recapture and lymphatic adsorption
of edematous fluids are expedited. These processes confine the area of edema and elevated tissue
pressure to the immediate inflamed area. Although tissue pressure at an area of pulpal inflammation
is two to three times higher than normal, it quickly falls to nearly normal levels approximately 1.0
mm from the affected area.
Another protective effect of evaluated but localized pulpal tissue pressure is a vigorous
outward flow of tubular fluid to counteract the pulpal diffusion of noxious solutes through
permeable dentin. However, an inflammatory condition and higher tissue pressure may also induce
hyperalgesia, a lowered threshold of sensitivity of pulpal nerves. Thus, an afflicted tooth exposed to
the added stress of cavity preparation and restoration may become symptomatic or hypersensitive to
cold or other stimuli.
Innervation
Dental nerves are either efferent autonomic C fibers to regulate blood flow or afferent
sensory nerves derived from the second and third divisions of the fifth intracranial (trigeminal)
nerve. Nerves are classified according to purpose, myelin sheathing, diameter, and conduction
velocity. Although a few large and very high-conduction velocity A-(beta) nerves with a
proprioceptive function have been identified, most sensory interdental nerves are either myelinated
A-(delta) nerves or smaller, unmyelinated C fibers. The innervation of the premolar, for example,
consists of about 500 individual A- nerves that gradually lose their myelin coating and Shwann
cell sheathing as they branch and form a sensory plexus of free nerve endings around and below the
odontoblastic layer. The A- nerves have conduction velocities of 13.0 m/s and low sensitization
thresholds to react to hydrodynamic pressure phenomena. Activation of the A- system results in a
sharp, intense “jolt”.
There three to four times more of the smaller, unmyelinated C fibers, which are more
uniformly distributed through the pulp. The conduction velocities of C fibers are slower, 0.5 to 1.0
m/s, and C fibers are only activated by a level of stimuli capable of creating tissue destruction, such
as prolonged high temperatures or pulpitis. The C fibers are also resistant to tissue hypoxia and are
not affected by reduction of blood flow or high tissue pressure. Therefore, pain may persist in
anesthetized, infected, or even nonvital teeth. The sensation resulting from activation of the C fibers
is a diffuse burning or throbbing pain, and the patient may have difficulty locating the affected
tooth.
The afferent transmission of painful sensations, commonly experienced although unreliable
as a warning signal, may not be the primary protective function of pulpodentin innervation.
Experimentally denervated teeth exposed to trauma suffer greater pulpal damage than innervated
controls. The initiation and coordination of the inflammatory cascade; the vascular, tissue, and
12
tubular fluid dynamics; and the immunocompetent response are important protective functions of
the neural components.
Peculiarities of patient assessment with pulp pathology
The patient’s complaint should be recorded in his or her own words. It is wise to listen
carefully to the patient’s description of his problem as it often gives the operator most of the
information he needs to make a diagnosis.
Valuable information may be acquired by asking the patient specific questions about the
symptoms:
 How long have you had the pain?
 When did you first notice the pain or discomfort?
 Can you point to the tooth or area that bothers you?
 Does it hurt to bite on the tooth or to the touch it?
 Describe the pain: sharp or dull, throbbing, mild or severe, localized or radiating, pulsating,
nagging, sudden, off and on, constant, getting better or worsening.
 Does the tooth start hurting by itself or on its own?
 Does it hurt most during the day or at night, and how long does it last?
 What makes it hurt: hot, cold, sweets, chewing/biting, air, other?
 Does the pain linger?
 Have you taking anything to relieve the pain? If so, does it relieve the pain? For how long?
An indication of pulp vitality can be obtained through the results of thermal tests, an electric
pulp test, and a test cavity. In addition, before any tooth is restored with a casting, pulpal evaluation
should be performed. To conduct a thermal test, a cotton applicator tip sprayed with a freezing
agent or hot gutta-percha is applied directly to the tooth. Hot and cold testing should elicit from the
healthy pulp a response that will subside within a few seconds following removal of the stimulus.
Pain lasting 10 to 15 seconds or less after stimulation by heat or cold suggests a hyperemia, an
inflammation that may be reversed by timely removal of the irritant(s). Intense pain of longer
duration from hot or cold usually suggests irreversible pulpitis, which can only be treated by root
canal therapy or extraction. Pain that results from heat but is quickly relieved by cold also suggests
irreversible pulpitis. Lack of response to thermal tests may indicate that the pulp is necrotic.
Adjacent and/or contralateral unaffected teeth should be tested for baseline comparisons as the
duration of pain may differ among individuals.
The electric pulp tester also has value in determining the vitality of the dental pulp. The
electric pulp tester is placed on the tooth and not on a restoration. A small electric current delivered
to the tooth causes a tingling sensation when the pulp is vital and no response when the pulp is
nonvital. It is important to obtain readings on adjacent and contralateral teeth so the tooth in
question can be evaluated relative to the responses of the other teeth. Results of an electric pulp test
should not be the sole basis for a pulpal diagnosis since false positives/negatives can occur. Instead,
electric pulp test results provide additional information that, when combined with other findings,
may lead to a diagnosis. Electric pulp testing is sometimes not possible in teeth with large or fullcoverage restorations.
A test cavity can be performed to help in the evaluation of pulpal vitality when a large
restoration in the tooth may be resulting in false negative responses with other evaluation methods.
This test particularly is an option for diagnosing questionable pulpal vitality of a tooth contemplated
for a replacement casting restoration. By using a round bur and no anesthetic, a test cavity is made
through the existing restoration into the dentin. Lack of sensitivity (response) when the dentin is cut
may indicate a nonvital pulp. However, sclerosed dentin can result in a false negative. Moreover, on
a multiple-rooted tooth, one region of the dentin may respond, whereas there may be no response at
another site, possibly indicating a degeneration of a portion of the pulp. Furthermore, heat generated
by the bur might cause a response, but the pulp may not be healthy. Though there are indications for
the test cavity, its use and diagnostic information attained are limited.
13
Pulpal abnormalities such as pulp stones and internal resorption may be identified in the
anterior periapical radiographs.
Classification of pulp diseases (K 04)
K 04.0 - Pulpitis: acute, chronic (hyperplastic, ulcerous, and purulent).
Pulpal abscess.
Pulpal polyp.
K 04.1 - Necrosis of pulp: pulpal gangrene.
K 04.2 – Regeneration/degeneratioin of the pulp: pulp stones (denticles), pulp calcification.
K 04.3 – Abnormal creation of hard tissues in the pulp.
According to E. Platonov:
Acute: local, diffuse (generalized).
Chronic: fibrous, gangrenous (necrotic), hypertrophic (proliferative).
According to O. Javors’ka:
Acute pulp inflammation:
 Hyperemia of the pulp
 Acute local pulpitis
 Acute diffuse pulpitis
 Acute purulent pulpitis
 Acute traumatic pulpitis: accidentally naked pulp, accidentally wounded pulp, and naked
pulp in cause of fracture of tooth crown.
Chronic pulp inflammation:
 Simple chronic pulpitis
 Chronic hypertrophic pulpitis
 Chronic gangrenous pulpitis
 Concremental pulpitis.
Pulpitis, complicated with focalize pericementitis.
Control questions to practical lesson
Situation tasks and test control
A true cencie in the pulp can be diagnosed by
A. radiographic examinauon
B. histopathologic examinauon
C. pulp tester
D. transiluminauon of pulp
Histologically, the normal dental pulp most closely resembles
A. nervous tissue
B. endothelial tissue
C. granulomatous tissue
D. loose connective tissue
E. dense connective tissue
The tooth pulp is a connective tissue which is composed of:
A. Basal substance, vessels, nerves
B. Vessels, nerves, cellular and fibrous component
14
C. Cellular and fibrous component, basal substance, vessels, nerves
A 51-year-old female patient complains about food sticking in a right inferior tooth. Objectively:
distal masticatory surface of the 45 tooth has a deep carious cavity filled with dense pigmented
dentin that doesn't communicate with the tooth cavity. The patient was diagnosed with chronic
deep caries. What method of examination allowed the dentist to eliminate chronic periodontitis?
A Electro-odontometry
B Probing
C Palpation of projection of root apex
D Percussion
E Cold test
A 35-year-old patient complains about constant dull pain in the 25 tooth that is getting worse when
biting down on food. Objectively: masticatory surface of the 25 tooth has a carious cavity
communicating with the dental cavity. The purulent discharges from the canal followed the probing.
What method of diagnostics should be applied to confirm the diagnosis?
A X-ray examination
B Electric pulp test
C Thermal test
D Bacteriological examination
E Deep probing
Reference literature
1. Nikolyshyn A.K. Therapeutic dentistry /A.K. Nikolyshyn: a textbook is for the students of
dental faculties of higher medical educational establishments of IV level of accreditation in two
volumes, T.I.– Poltava: Divosvit, 2005.– 392 p.
2. Borovskiy E.V. Therapeutic dentistry: a textbook is for the students of dental faculties of higher
medical educational establishments.– M.: Med. Inform. agency, 2006.– 840 p.
3. Nikolyshyn A.K. Therapeutic dentistry /A.K. Nikolyshyn: a textbook is for the students of
dentistry faculties of higher medical educational establishments of IV level of accreditation in
two volumes, T.IІ.–Poltava: Divosvit, 2007.– 280 p.
4. Preclinical course of therapeutic dentistry: course of lectures /L.O. Tsvykh, O.A. Petryshyn,
V.V. Kononenko, M.V. Hysyk.– Lviv, 2002.–159 p.
5. The methodological manual for practical of therapeutic dentistry /L.O.Tsvykh, O.A. Petryshyn,
V.V. Kononenko, M.V. Hysyk.– Lviv, 2003.– 98 p.
Practical lesson No 21
Theme: Acute Pulpitis. Etiology, Pathogenesis, Clinic, Diagnostic, Differential Diagnostic
Short description of a theme
Causes of pulpal inflammation
Like others soft tissues, the pulp reacts to an irritant with in inflammatory response. It was
previously believed that pulpal inflammation was the result of toxic effects of dental materials.
More recent evidence, however, demonstrates that pulpal inflammatory reactions to dental materials
15
are mild and transitory; significant adverse pulpal responses occur more as the result of pulpal
invasion by bacteria or their toxins. Even early enamel caries lesions that extend less than one
fourth of the way to the dentinoenamel junction have been shown to induce a pulpal reaction,
particularly when the caries lesion has advanced rapidly. This is probably due to increase in the
permeability of enamel, allowing the transmission of stimuli along enamel rods.
As a lesion progresses deeper into the tooth, pulpal reaction increases. When actual pulpal
encroachment by bacteria and/or their toxins occurs, severe inflammation or pulpal necrosis
frequently occurs. The outward flow of fluid through dentinal tubules does not prevent bacteria or
their toxins from reaching the pulp and initiating pulpal inflammation. The caries process also
induces the formation of reparative dentin and reactive dentin sclerosis, which increases the
protective effects of the remaining dentin.
When bacterial contamination is prevented, favorable responses in pulpal tissue adjacent to
many restorative materials have been found. Those materials include amalgam, light-activated resin
composite, autocured resin composite, zinc phosphate cement, silicate cement, glass-ionomer
cement, and acrylic resin. Acid etching of dentin has long been considered detrimental to the pulp,
but the pulp can readily tolerate the effects of low pH if bacterial invasion is prevented.
Etiological factors in pulpitis origin.
1. Infection.
2. Thermal irritants.
3. Mechanical trauma.
4. Chemical factors.
5. Concrements.
Acute local pulpitis - (pulpitis acuta focalis)
Complaints: attacks of acute, spontaneous colicky pain, which intensificated after all types
of irritants and in the nighttime. Pain lasts for 10-30 min. with long light periods (without pain).
Patient usually can localize painful tooth.
Objective changes: in the tooth – deep carious cavity filled with soft, pigmented necrotic dentin and
food debris. Pulp chamber is closed.
Exploration of the bottom of the cavity is painful in one or two points (near the pulp horns).
Percussion is not painful.
Thermal test is positive.
EPT – 20-25 mcA (indicates to the decreased pulp reactivity).
Rtg – no changes.
Pathological anatomy: inflammatory edema (tumor) and hyperemia of the pulp tissue.
Differential diagnosis.
 Deep caries – short-lived pain after irritants which passing after their removing. There is no
acute, spontaneous, colicky pain, nighttime pain.
 Acute generalized pulpitis – attacks of colicky or continuous throbbing pain with
irradiation, which last 1-3 hours; light periods are very short or absent.
 Chronic fibrous pulpitis - there is no spontaneous and nighttime pain. In anamnesis – acute
pain in the past. Pulp chamber is perforated, exploration of this place caused acute pain and
bleeding of the pulp.
 Papillitis – inflammation of gingival (interdental) papilla. There is inflammatory blush
(hyperemia) and edema (tumor) of interdental papilla, painful and bleed to touch. Tooth is
intact or with carious lesion, but there is no inflammation in pulp.
After 1-3 days duration, local pulpitis is transferred into the generalized pulpitis.
Acute generalized (diffuse) pulpitis - (pulpitis acuta diffusa)
16
Complaints: acute attacks of spontaneous colicky or throbbing pain, often more intensive in
the nighttime, with irradiation, which last 1-3 hours without light periods. Patient usually cannot
localize the painful tooth.
After 24 hours duration, serous exudate of the inflammatory pulp is transformed into the purulent
exudate. In stage of purulent exudation, when the abscess is formed in the pulp tissue, reaction to
the thermal irritants is changed. In stage of serous exudation could irritants be caused by the pain, in
stage of purulent exudation could irritants be provoked by the pain and hot irritants provoked by the
pain.
Objective changes: deep carious cavity filled with soft, pigmented necrotic dentin and food
debris. Pulp chamber is closed.
Exploration of the all bottom of the cavity is very painful.
Percussion is sometimes a little painful.
Thermal test is positive (provoked very long attack of pain).
EPT – 40-50 mcA.
Rtg – no changes.
Pathological anatomy: inflammatory edema and hyperemia of the pulp tissue; enlargement
of blood vessels, emigration of leucocytes, small hemorrhages, diapedesis of erythrocytes and small
abscesses.
Differential diagnosis.
 Acute local pulpitis - pain last for 10-30 min. with long light periods (without pain), without
irradiation. Patient usually can localize painful tooth. Duration of inflammatory process is 12 days.
 Acute pericementitis - localized gnawing dull pain, violent pain during and after biting;
percussion is very painful; thermal test is negative; EPT100 mcA; palpation of gingiva in
proection of tooth root apex is painful.
 Neuralgia of trifacial (trigeminal) nerve – violent colicky pain during conversation, meal or
after touching the skin of the face. There are no night attacks of pain.
 Maxillary sinusitis – there are several common manifestations: headache, rise of
temperature, weakness. Difficult (rough) breathing through the nose, rhinorrhea.
 Alveolitis – inflammation of alveole after tooth extraction when blood clot was decomposed
or not created at all. Objective changes: alveole is empty, there are many gray coating on
alveole walls, and palpation of gums in this region is very painful.
Control questions to practical lesson
Situation tasks and test control
Person Н., 18-y.o complaints of acute spontaneous paroxysmal pain in tooth that irradiates to right
eye and temporomandibular area. Objectively in 27 tooth deep carious cavity near parapulpar
dentin, dentin is bright and soft. Probing of bottom is sharply painful, positive reaction for cold.
Diagnosis:
A. Acute diffuse pulpitis
B. Acute purulent periodontitis
C. Exacerbation of chronic pulpitis
D. Acute serous periodontitis
E. Acute purulent pulpitis
A patient complains about the temporary pain in the teeth of lower jaw lasting for twenty-four
hours, on the left side. Pain is radiating to ear, back of head, and also increase during eating of cold
17
and hot meal. Objectively: in 36 tooth on a medial surface-deep carious cavity. Probing at the
bottom is sharply painful. What most імовріний possible diagnosis?
A. Acute diffuse pulpitis
B. Acute обмеженний pulpitis.
C. Acute festering pulpitis.
D. Chronic concremental pulpitis.
A woman 40 years old, complains about short lasting, spontaneous(самовільний) pain, also pain
after hot and cold meal in an area 46 tooth. On a occlusal surface of 46tooth, carious cavity filled
with softened dentine. Probing of bottom is painful. A reaction on thermal irritants is sharply
positive and does not disappear after their removal. ЕОD-25 мкА. What is the most correct
diagnosis?
A. Acute localized pulpitis
B. Acute festering pulpitis.
C. Acute diffuse pulpitis.
D. Chronic fibrous pulpitis
E. Exacerbation of chronic pulpitis
The throbbing pain in case of acute pulpitis is caused with:
A. Increasing of hydrostatical pressure inside the pulp chamber
B. Irritation of the nerve terminations by product of anaerobic glycolysis
C. Periodical shunting of blood flow throw arteriolovenular anastomosis
The patient 43 years old complains on spontaneous, paroxysmal night time pain with long painless
period. These complains arise in case of:
A. Acute local pulpitis
B. Acute diffuse pulpitis
C. Chronic fibrous pulpitis
D. Chronic gangrenous pulpitis
E. Chronic hypertrophical pulpitis
Male, 24 years old complains on spontaneous, paroxysmal night time pain with irradiation on the
branches of n.trigeminus with short painless periods. These complains arise in case of:
A. Acute local pulpitis
B. Acute diffuse pulpitis
C. Chronic fibrous pulpitis
D. Chronic gangrenous pulpitis
E. Chronic hypertrophical pulpitis
The patient 23 years old complains on long term pain (10 – 20 min) in tooth 1.1 which arises after
the thermal and chemical irritants, and the retention of food in the interdental spaces of upper
incisors.Periodic acute nighttime pain. The first time he felt the pronounced pain in tooth 1.1- 3
days ago. Objectively: On the medial surface of tooth 1.1 the carious cavity within the circumpulpal
dentin. The dentin of walls and a bottom is softened. The color of dentin is pale yellow. The
probing of the bottom is sharply painful. Percussion of tooth 1.6 is painless. During thermal
diagnostics of tooth 1.1 observed pronounced long-term pain EPT (The pulp electroexcitability test)
– 18 mkA. These complains and the result of objective examination are typical for:
A. Acute local pulpitis
B. Acute diffuse pulpitis
C. Chronic concremental pulpitis
18
D. Acute purulent pulpitis
The patient 43 years old complains on transient pain in upper right premolars which suddenly
occurred twice in the past day. The first time patient felt short term pain in tooth 1.5 which arises
after the thermal irritants, 8 months ago. Objectively: On the medial surface of tooth 1.5 the carious
cavity within the circumpulpal dentin. The dentin of walls and a bottom is softened. The color of
dentin is pale yellow. The probing of bottom is sharply painful. Percussion of tooth 1.5 is painless.
During thermal diagnostics of tooth 1.5 observed pronounced pain which last more than 10 minutes.
EPT (The pulp electroexcitability test) – 17 mkA. These complains and the result of objective
examination are typical for:
A. Acute local pulpitis
B. Acute diffuse pulpitis
C. Chronic concremental pulpitis
D. Acute purulent pulpitis
The patient complains on recurrent pain in the left side of the mandible, which occurs every 5-6
hours without any reason. The pain firstly arises in the area of lower molars and than spreads in the
direction of occiput region. In an hour the pain gradually passes. The patient feels the pain for 2
days. He did not apply for the help. Objectively: On the occlusal surface of the tooth 3.7 the carious
cavity within the circumpulpal dentin with a narrow entrance. The dentin of walls and a bottom is
softened. The color of dentin is pale yellow. The probing of bottom is sharply painful. Percussion of
tooth 3.7 is painless. During thermal diagnostics of tooth 4.7 observed pronounced pain more. EPT
(The pulp electroexcitability test) – 37mkA. These complains and the result of examination are
typical for:
A. Acute local pulpitis
B. Acute diffuse pulpitis
C. Chronic concremental pulpitis
D. Acute purulent pulpitis
The patient complains on spontaneous, paroxysmal pain of upper jaw in the left, which irradiates in
the left temporal area. The first pain attack was 48 hours ago without any reasons and last 30
minutes. The second pain attack was after the 6 hours and last 45 minutes. During the last night the
pain attacks occurs 5-6 times and last for 2-3 hours. One of the attacks was provoked by cold water.
Objectively: On the medial surface of tooth 2.7 the carious cavity within the circumpulpal dentin
with a narrow entrance. The dentin of walls and a bottom is softened. The color of dentin is pale
yellow. The probing of bottom is sharply painful. Percussion of tooth 3.7 is painless. During
thermal diagnostics of tooth 2.7 observed pronounced pain which last continuously. These
complains and the result of examination are typical for:
A. Acute local pulpitis
B. Acute diffuse pulpitis
C. Chronic concremental pulpitis
D. Acute purulent pulpitis
A patient complains of spontaneous, paroxysmal, irradiating pain with short pain-free intervals.
The pain arose 2 days ago and occurs only at night. Make a provisional diagnosis:
A Acute diffuse pulpitis
B Acute deep caries
C Exacerbation of chronic periodontitis
D Acute circumscribed pulpitis
E Acute purulent pulpitis
19
A 29-year-old patient complains about acute attack-like pain in the region of his upper jaw on the
left, as well as in the region of his left maxillary sinus, eye and temple. The pain is long-lasting (2-3
hours), it is getting worse at night. The patient has a history of recent acute respiratory disease.
Objectively: the 26 tooth has a carious cavity, floor probing is painful, thermal stimuli cause longlasting pain, percussion causes slight pain. What is the most likely diagnosis?
A Acute diffuse pulpitis
B Acute focal pulpitis
C Acute apical periodontitis
D Inflammation of maxillary sinus
E Exacerbation of chronic periodontitis
A 38-year-old patient complains of acute paroxysmal pain in the region of his left upper jaw, left
eye and temple. The pain is lasting (2-3 hours), gets worse at night. Objectively: the 26 tooth has a
deep carious cavity, floor probing causes painful response, thermal stimuli provoke long-lasting
pain, percussion provokes minor pain. What is the most likely diagnosis?
A Acute diffuse pulpitis
B Pulpitis complicated by the periodontitis
C Acute limited pulpitis
D Exacerbation of the chronic pulpitis
E Acute purulent pulpitis
A 18-year-old patient complains of acute spontaneous toothache irradiating to the right eye and
temporal region. Objectively: there is a deep carious cavity in the 27 tooth within circumpulpar
dentin. Dentin is light, softened. Probing of the cavity floor and cold test cause acute pain. What is
the most likely diagnosis?
A Acute diffuse pulpitis
B Acute purulent periodontitis
C Exacerbation of chronic pulpitis
D Acute serous periodontitis
E Acute purulent pulpitis
A 32-year-old patient complains of acute spontaneous attacks of pain in the 14 tooth. The pain lasts
for 10-20 minutes and occurs every 2-3 hours. Carious cavity in the 14 tooth is filled with softened
dentin. Probing of the cavity floor is painful at one point. Cold stimulus causes pain. What is the
most likely diagnosis?
A Acute localized pulpitis
B Acute deep caries
C Hyperemia of the pulp
D Exacerbation of chronic pulpitis
E Acute diffuse pulpitis
A patient complains about long-lasting pain attacks in the lower jaw teeth, on the left. The pain
irradiates to the ear, occiput and is getting worse during eating cold and hot food. Objectively: there
is a deep carious cavity on the approximal-medial surface of the 36 tooth. Floor probing is overall
painful and induces a pain attack. What is the most probable diagnosis?
A Acute diffuse pulpitis
B Acute local pulpitis
C Acute purulent pulpitis
D Chronic concrementous pulpitis
E Acute deep caries
20
A patient complains about spontaneous pain in the area of his 15 tooth he has been feeling for 2
days. Thermal stimuli make the pain worse, its attacks last up to 30 minutes. Objectively: there is a
deep carious cavity in the 15 tooth consisting of light softened dentin, floor probing is painful in
one point, reaction to the thermal stimuli is positive, percussion is painless. Make a diagnosis:
A Acute local pulpitis
B Acute diffuse pulpitis
C Pulp hyperemia
D Acute deep caries
E Acute condition of chronic pulpitis
Reference literature
Practical lesson No 22
Theme: Chronic Pulpitis. Etiology, Pathogenesis, Clinic, Diagnostic, Differential Diagnostic
Short description of a theme
Transformation of acute inflammation into the chronic inflammation takes place after
perforation of pulp chamber is arising.
Chronic fibrous pulpitis – (pulpitis chronica fibrosa)
Complaints: often is asymptomatic; sometimes – throbbing pain and discomfort in the tooth,
pain after very strong mechanical and thermal irritants. Some times pain in the tooth occurs after
sharp changes of temperature (from cold to hot temperature), and after suck out from the tooth.
Objective changes: deep carious cavity with soft and dark-brown pigmented walls and
bottom. Pulp chamber is perforated, exploration in this place caused acute pain and bleeding of the
pulp. Some times, when the pulp chamber is closed, exploration of the bottom of the cavity is only
sensitive.
Percussion is not painful.
Thermal test is positive.
EPT – 25-50 mcA
Rtg – no changes.
Pathological anatomy: vascular and exudative reactions are not expressive. Productive
processes are dominated. Transformation of pulp tissue into the fibrous connective tissue, gialinosis
and sclerosis of pulp, decrease of pulp cells takes place. Blood vessels are widening.
Differential diagnosis.
 Profound caries – short-lived pain after all types of irritants which passing after their
removing, there is no acute pain in anamnesis.
 Acute generalized pulpitis - attacks of acute, spontaneous colicky pain, which intensificated
after all types of irritants and in the nighttime. Pain lasts for 10-30 min. with long light
periods, without irradiation. Duration of this type of pulpitis is 2-3 days.
 Chronic necrotic pulpitis – attacks of pain after hot irritant, pulp chamber is open,
exploration of the pulp is painless (deep exploration of the pulp in the root canals is painful).
Chronic proliferative(hypertrophic) pulpitis – (pulpitis chronica hypertrofica)
21
This type of pulpitis is developed after chronic fibrous pulpitis, when the perforation of pulp
chamber is very big and mechanical irritation of pulp taken place. It causes proliferation of pulp
tissue.
Complaints: pain and bleeding occur during mastication and after mechanical irritants.
Objective changes: big carious cavity, pulp chamber is open, and hypertrophic pulp tissue is
coming out from the carious cavity.
Exploration is sensitive on the surface of the pulp, and painful on the deeper layers.
Hypertrophic pulp bleeds during probing.
Percussion is not painful.
Thermal test is negative.
EPT – 40-60 mcA.
Rtg – no changes.
Pathological anatomy – hyperplastic processes and considerable growing of connective
tissue are dominated. There are many young granulation tissue in the pulp. Odontoblasts are only in
the root part of pulp.
Differential diagnosis.
 Hypertrophic papilitis – proliferation of inflamed interdental papilla.
 Granulation tissue, coming from the perforation opening in bi- or trifurcation region (Xray with diagnostic needle is recommended).
Chronic necrotic pulpitis – (pulpitis chronica gangrenosa)
Complaints: throbbing pain after hot irritants, evil smelling, and change of tooth color.
There are no spontaneous attacks of pain.
Objective changes: deep carious cavity with thin walls, pulp chamber is open. Necrotic pulp
is dark colored. Tooth is changed in color (gray colored).
Exploration of the coronal pulp is unpainful, deep exploration is painful.
Percussion is not painful.
Thermal test is positive (hot water).
EPT – 60-80 mcA.
Rtg – some times show deformation and widening of periodontal slit.
Pathological anatomy: structure of coronal pulp is lost. There are no cells and fibers. There
are many colonies of microorganisms, crystals of fat acids, bloody pigments in necrotic pulp tissue.
Differential diagnosis.
Chronic fibrous pulpitis - often is asymptomatic, some times, pain occurs after very strong
mechanical or thermal (as a usual, cold) irritants; there is no pain after hot irritants. Pulp
chamber is perforated, exploration in this place caused acute pain and bleeding of the pulp.
 Chronic apical pericementitis – acute pericementitis in anamnesis. Superficial and deep
exploration is not painful; thermal test is negative; EPT100 mcA; percussion is sensitive or
painful. Some times, on the alveolar gums in projection of root apex can be gingival fistula.

Exacerbation of chronic pulpitis (pulpitis chronica exacerbata)
As a usual chronic fibrous pulpitis is exacerbated. Causes of exacerbation: common
diseases, trauma of pulp through the carious cavity, mistakes during previous tooth filling.
Subjective changes: all signs of acute pulpitis, with anamnesis of previous attacks of acute
pain with/without irradiation. Some times pain is dull, gnawing and constant (continuous).
Objective changes: deep carious cavity, pulp chamber is open; pulp during exploration is
painful; thermal test is positive. Some times there is no pain after irritants.
Differential diagnosis.
 Acute pulpitis
 Acute apical pericementitis
 Exacerbation of chronic apical pericementitis
22
Control questions to practical lesson
Situation tasks and test control
A boy 8 complains about pain in a tooth during a meal. Objectively: in 55 on a proximal surface
deep carious cavity which is reported with the cavity of tooth. Probing of connection is sharply
painful, the bleeding is marked, percussion is painless. Define a diagnosis:
A. Chronic fibrotic pulpitis
B. Chronic hypertrophic pulpitis
C. Chronic gangrenous pulpitis
D. Chronic granulating periodontitis
E. chronic fibrous periodontitis
The pulpexcitability limit in case of chronic pulp gangrene is:
A. 1-2microampere
B. 20-40 microampere
C. 50-90 micmoampere
D. 100-200 microampere
E. 3-8 microampere
Female, 19 years old complains on paroxysmal pain which arises after the various kinds of irritants
and continues after the irritant removal. These complainsare typical for:
A. Acute deep caries
B. Acute diffuse pulpitis
C. Chronic fibrous pulpitis
D. Chronic gangrenous pulpitis
E. Chronic hypertrophical pulpitis
Female, 39 years old complains on ache which arises after the various kinds of irritants
forthemostpart after hot, and continues after the irritant removal.These complains are typical for:
A. Acute deep caries
B. Acute diffuse pulpitis
C. Chronic fibrous pulpitis
D. Chronic gangrenous pulpitis
E. Chronic hypertrophical pulpitis
Male, 32 years old complains on ache which arises after the various kinds of irritants, bleeding
during the ingestion. These complains are typical for:
A. Acute deep caries
B. Acute diffuse pulpitis
C. Chronic fibrous pulpitis
D. Chronic gangrenous pulpitis
E. Chronic hypertrophical pulpitis
The patient 31 years old complains on long- term pain in tooth 4.6 which arises after the thermal
and mechanical irritants, bleeding from the carious cavity, constant discomfort in the tooth.
Objectively: On the distal surface of tooth 4.6 the wide carious cavity with a broken wall, filled
with tumor formation purplish-red color with smooth surface, which is painful in probing. During
thermal diagnostics of tooth 4.6 observed pronouncedlong-term pain. These complains and the
23
result of examination are typical for:
A. Chronicfibrosepulpitis
B. Acute diffuse pulpitis
C. Chronic hyperplastic pulpitis
D. Acute purulent pulpitis
A 26 year old patient complains about a sense of tooth heaviness and pain caused by hot food
stimuli, halitosis. Objectively: crown of the 46 tooth is grey, there is a deep carious cavity
communicating with tooth cavity, superficial probing is painless, deep one is painful, percussion is
painful, mucous membrane has no pathological changes. Make a provisional diagnosis:
A Chronic gangrenous pulpitis
B Chronic fibrous pulpitis
C Acute condition of chronic periodontitis
D Chronic concrementous pulpitis
E Chronic granulating periodontitis
A 38-year-old male patient complains of a carious cavity. He had experienced spontaneous dull
pain in the tooth in question before. Objectively: the distal masticatory surface of the 37 tooth
presents a deep cavity made of soft pigmented dentin. Percussion is painless. After removing the
decay from the cavity, cold water has caused pain lasting for about a minute. X-ray pictur
shows the deformation of the periodontal gap in the region of the 37 root apices. What is the most
likely diagnosis?
A Chronic fibrous pulpitis
B Exacerbation of chronic pulpitis
C Acute deep caries
D Chronic deep caries
E Chronic fibrous periodontitis
A 37-year-old male patient complains about pain of the 46 tooth during food intake, especially hot
food, offensive breath when he sucks his tooth. Objectively: the face is symmetrical, masticatory
surface of the 48 tooth has a deep carious cavity communicating with the dental cavity. X-ray
picture shows widening of periodontal fissure at the root apex of the 46 tooth. What is the most
likely diagnosis?
A Chronic gangrenous pulpitis
B Exacerbation of chronic periodontitis
C Exacerbation of chronic pulpitis
D Chronic fibrous periodontitis
E Chronic fibrous pulpitis
A 30-year-old patient complains of toothache caused by hot and cold stimuli. The pain irradiates to
the ear and temple. Previously there was spontaneous nocturnal toothache. Objectively: on the
occlusal surface of the 37 tooth there is a deep carious cavity communicating at one point with the
tooth cavity. Probing at the communication point, as well as cold stimulus, cause acute pain. The
pain persists for a long time. Electric pulp test result is 5 mA. What is the most likely diagnosis?
A Exacerbation of chronic pulpitis
B Acute diffuse pulpitis
C Exacerbation of chronic periodontitis
D Chronic concrementous pulpitis
E Acute purulent pulpitis
A 32-year-old patient complains of the long-term dull toothache caused by hot food. The toothache
appeared a month ago. Objectively: the 26 tooth has changed in colour, on the masticatory surface
24
there is a deep carious cavity communicating with the tooth cavity. Superficial probing of pulp is
painless, deep probing is painful. Electro-odontodiagnostics results: 85 µA. What is the most likely
diagnosis?
A Chronic gangrenous pulpitis
B Chronic hypertrophic pulpitis
C Chronic fibrous pulpitis
D Chronic fibrous periodontitis
E Chronic concrementous pulpitis
A 34-year-old male patient complains of acute spasmodic pain in the region of his upper jaw on the
left that is getting worse as affected by cold stimuli. Toothache irradiates to the ear and temple. He
had acute toothache of the 37 tooth one year ago, but he didn't consult a dentist. Pain recurred three
days ago. Objectively: the 37 tooth has a carious cavity communicating with the dental cavity.
Probing of the opened carious cavity is extremely painful. X-ray picture shows widening of
periodontal fissure at the root apex of the 37 tooth. What is the most likely diagnosis?
A Exacerbation of chronic pulpitis
B Exacerbation of chronic granulating periodontitis
C Exacerbation of chronic fibrous periodontitis
D Acute diffuse pulpitis
E Acute purulent pulpitis
A 29-year-old patient complains of acute paroxysmal pain in the upper jaw on the left, that gets
worse during having cold food and irradiates into the ear and temple. A year ago she experienced
intense pain in the 27 the tooth but didn't consult a dentist. Three days ago there was the second
attack of pain. Objectively: there is a deep carious cavity in the 27th tooth, interconnecting with the
tooth cavity. Probing the open area causes acute pain. What is the most likely diagnosis?
A Exacerbation of chronic pulpitis
B Acute serous periodontitis
C Acute diffuse pulpitis
D Exacerbation of chronic periodontitis
E Acute limited pulpitis
A 20-year-old patient complains about pain and haemorrhages in the region of the 36 tooth occuring
during eating solid food. Objectively: medial masticatory surface of the 36 tooth has a large carious
cavity occupied by a carneous tumour-like formation, probing induces haemorrhage and pain in the
region of connection of the carious cavity with the pulp chamber. Percussion is painless.
Electroodontodiagnosis is 40 microampere. Roentgenological changes are absent. What is the most
likely diagnosis?
A Chronic hypertrophic pulpitis
B Epulis
C Hypertrophic papillitis
D Chronic gangrenous pulpitis
E Chronic fibrous pulpitis
A 27-year-old male patient complains of aching long-lasting pain in the 15 tooth during having
meals, especially cold food. Sometimes the pain occurs when the temperature changes. Objectively:
on the distal surface of the 15 tooth there is a cavity filled with softened dentin. Probing is painful.
Electroexcitability of the pulp is 35 µA. What is the most likely diagnosis?
A Chronic fibrous pulpitis
B Acute deep caries
C Chronic deep caries
D Hyperemia of the pulp
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E Exacerbation of chronic pulpitis
Reference literature
Practical lesson No 23
Theme: Systematization of Treatment methods of Pulpitis. Method of full and partial Pulp
Preservation.Complications.Characteristic of medications.
Short description of a theme
Methods of pulpitis treatment
A. Methods of pulp preservation (biological)
1. Method of full pulp preservation (conservative)
2. Method of partial pulp preservation (vital pulp amputation, pulpotomy)
B. Methods of pulp removal
1. Vital extirpation (with anesthesia)
2. Non vital extirpation (with devitalizing agents)
3. Combinative method
Choosing of treatment method
Before choosing of treatment method we must take into consideration the type of pulpitis
and some conditions, like a:
 Patient age and common condition
 Prolongation of disease
 Ways of infection entrance into the pulp
 Localization of the carious cavity
 Condition of circumpulpal dentin
 Color, consistence and sensitivity of pulp
 Index of EPT
 Condition of periapical tissues
 Rtg information
Anesthesia of inflammatory pulp
1. Extrapulpal methods:
 General anesthesia (narcosis, analgesia)
 Local anesthesia (injectional: infiltration (subperiosteal, periapical, intraligamentous,
intrapapillar, intraosteal), conduction)
2. Intrapulpal methods:
 Application
 Droock-anesthesia (anesthesia under the pressure)
 Intrapulpal injectional anesthesia
Method of full pulp preservation (conservative)
Indications:
 Reversible pulpitis (hyperemia of the pulp)
26

Traumatic pulpitis (accidentally naked pulp)
Conditions, when we can use this method:
 Young age (under 30 years old)
 Prolongation of disease is no longer than 2 days
 Entrance of the infection was through the carious cavity
 Carious cavity is localized in limits of anatomic tooth crown
 Presence of connected with pulp dentin on the bottom of the cavity
 No changes in periapical tissues
Reversible pulpitis Indirect pulp capping.
This procedure involves the removal of infected dentin except for the deepest, last small
amount, which if removed might expose the pulp. Subsequent placement of restorative materials
must adequately seal the cavity and provide thermal, mechanical, and chemical protection. If the
pulp is healthy, secondary odontoblasts will differentiate and form a layer of reparative dentin for
further protection. The decision on whether to re-enter the cavity at a later time (at least 6 months)
is based on how much infected dentin was left behind during the indirect pulp capping procedure.
This decision must consider the possibility for further injury to the pulp from additional operative
procedures.
The goals of this procedure are to prevent pulp exposure and aid pulpal recovery by
medication. The portion of the remaining softened dentin is covered with calcium hydroxide
liner/base and the excavated area is restored with a temporary material. Calcium hydroxide
promotes reparative dentin bridges over any area of frank pulpal exposure. Such repair usually
occurs in 6 to 8 weeks and may be evident radiographically in 10 to 12 weeks.
Traumatic pulpitisDirect pulp capping.
A direct pulp cap is a technique for treating a pulp exposure with calcium hydroxide to
stimulate dentin bridge (reparative dentin) formation. If the exposure site is the consequence of
infected dentin extending into the pulp, termed a carious pulpal exposure, it is likely that infection
of the pulp has already occurred and removal of the tooth pulp is indicated. If, however, the pulp
exposure occurs in area of normal dentin (usually as a result of operator error or misjudgment),
termed a mechanical pulpal exposure, and bacterial contamination from salivary exposure does not
occur, the potential success of the direct pulp cap procedure is enhanced. With either type of
exposure, a more favorable prognosis for the pulp following direct pulp capping may be expected if:
 The tooth has been asymptomatic (no spontaneous pain, normal response to thermal testing,
and is vital) prior to the operative procedure.
 The exposure is small, less than 0.5 mm in diameter.
 The hemorrhage from the exposure site is easily controlled.
 The exposure occurred in clean, uncontaminated field (such as provided by rubber dam
isolation).
 The exposure was relatively atraumatic and little desiccation of the tooth occurred, with no
evidence of aspiration of blood into the dentin (dentin blushing).
Animal studies have demonstrated that direct pulpal exposures can heal normally, but a
bacteria-free environment is required. The adverse consequences of bacterial contamination of the
pulp have been well documented. Therefore, the only reasonable chance that a direct pulp cap has to
permit formation of a dentin bridge and to maintain pulp vitality is under the most ideal conditions.
If a large number of bacteria from a caries lesion or exposure to the oral flora have contaminated the
pulp, the likelihood of regaining or maintaining a healthy pulp is slight. In addition, aged pulps have
increased fibrosis and a decreased blood supply, and thus a decreased ability to mount an effective
response to invading microorganisms.
27
In one clinical study of direct pulp capping of 38 patients over 3 years, no relationship
between success and factors such as patient age, tooth type, or size of exposure was found.
However, in a larger study of both direct and indirect pulp capping involving 592 patients over a
24-year period, age, tooth type, and extent of exposure did have a bearing on success.
The degree of bleeding affects the success of direct pulp capping; increased bleeding is
associated with increased likelihood of failure.
Direct pulp capping should be attempted only when a small mechanical exposure of an
otherwise healthy pulp occurs. The tooth must be isolated with a rubber dam, and adequate
hemostasis must be achieved. The exposure should be covered with calcium hydroxide because of
its documented ability to provide the highest percentage of success. It must be possible to restore
the tooth with a well-sealed restoration that will prevent subsequent bacterial contamination.
Method of partial pulp preservation (vital pulp amputation)
The main point of the method – operative removing of part of inflammation (coronal pulp)
and medicamental treatment of root pulp.
Indications:
 Traumatic pulpitis (accidentally wounded pulp)
 Acute local pulpitis
 When direct pulp capping method was not effective
Conditions:
 Young age
 Carious cavity is localized on tooth crown
 There is no changes in periapical tissues
Technique stages:
1.
Operative field isolation
2.
Anesthesia
3.
Carious cavity preparation
4.
Opening of pulp chamber
5.
Pulp amputation
6.
Widening of root canals mouth
7.
Hemostasis (diatermocoagulation, haemostatics: sol. of adrenalinum, hemophobinum,
absorbable gelatin sponge, hemocollagene, hemofibrine, alstase…)
8.
Root pulp capping (calcium hydroxide liners: calcipulpe, pulpomixine)
9.
Temporary filling
10. Permanent filling (after 3-4 weeks)
Control questions to practical lesson
Situation tasks and test control
Calcium hydroxide is used as a pulp capping agent because it:
A. Provides a soothing action on pulp
B. Provides an irritant action on pulp
C. Provides good thermal insulation
D. All of the above
A 20 year old patient complains about idiopathic, short-lasting, localized pain in area of 26 tooth,
which last from one day. Objectively: In 26 teeth deep carious cavity of I-class, the dentine on the
walls and bottom is non-pigmented, soft; a carious cavity is not connected with the cavity of tooth.
Probing is strongly painful at the bottom, a reaction to a cold irritants is strongly positive. What is
28
the most rational method of treatment in this case?
A. Biological method
B. Congratulatory amputation
C. Congratulatory extirpation.
D. Devitalized amputation
E. Devitalized extirpation
The principal aim of the pulpal capping is:
A. to preserve the pulp and the odontoblasts in order to allow the reactional dentine
formation
B. to stop the bacterial contamination
C. to avoid pain
D. to avoid inesthetic aspect
E. none of the above
The method of pulpvitality conservation in the root canals calls:
A. Vital amputation
B. Vital extirpation
C. Devital amputation
D. Devital extirpation
For the biological treatment method of acute pulp trauma can be used:
A. MTA (mineral trioxideaggregate)
B. Compomer
C. Zinc -phosphate cement
D. Dual-cured composite
For the biological treatment method of acute pulp trauma can be used:
A. Ca(OH)2 liner
B. Zn-eugenol cement
C. Zinc -phosphate cement
D. Dual-cured composite
A 20-year-old patient complains about feeling spontaneous undurable localised pain in the 26 tooth
for one day. Objectively: the 26 tooth has a deep Black's class I carious cavity. Dentine of its walls
and floor is unpigmented, softened, carious cavity is not communicating with the tooth cavity.
Probing causes acute pain focused at a single point, cold test induces long-lasting pain. What
method of treatment is the most appropriate in this case?
A Biological method
B Vital amputation
C Vital extirpation
D Devital extirpation
E Devital amputation
A 22-year-old patient was undergoing treatment of the 25th tooth for deep acute caries. During
preparation a dentist accidentally opened the horn of pulp. What method of treatment should be
applied?
A Biologic method
B Vital amputation of pulp
C Devital amputation
D Vital extirpation
E Devital extirpation
29
Reference literature
Practical lesson No 24
Theme: Method of vital pulp extirpation, indications. Complications.Characteristic of medications.
Short description of a theme
Method of vital pulp extirpation
Indications: traumatic pulpitis (fracture of tooth crown), acute generalized pulpitis, chronic
fibrous, prolipherative, necrotic pulpitis, concremental pulpitis, exacerbation of chronic pulpitis,
pulpitis complicated with apical pericementitis.
Technique stages:
I visitation:
1. Operative field isolation (rubber dam)
2. Anesthesia
3. Carious cavity preparation
4. Opening of pulp chamber
5. Pulp amputation (excavator, round carbide drill)
6. Widening of root canals orifice (gates-glidden drill, peeso reamer, orifice opener (widener))
7. Pulp extirpation (barbed (nerve) broash)
8. Hemostasis (diatermocoagulation, hemostatics: sol. of adrenalinum, H2O2, hemophobinum,
Alustin…)
9. Widening of root canals (step-back, crown-down techniques; chemical widening: Canal+,
Largal Ultra, Parcan)
10. Cleaning of the root canals with antiseptics (3% sol. of H2O2, sol.NaOCl, 0.2% sol. of
Chlorhexidini bigluconatis, 0.5% sol. of Furacilini, Antiformin, Natrium chloratum…)
11. Hermetization of root canals with cotton with antiseptic (Dicamphen, Cresophene,
Camphocresol, Camphenol, Falicid, Endotine, Grinazole…)
12. Temporary filling
II visitation (after 1-2 days):
1. Removing of the temporary filling
2. Cleaning of root canals with antiseptics
3. Drying of root canals (septopoints(paper), Sikko Tim, Hydrol)
4. Filling of root canals (Sealers: Endomethasone, Endobtur, TubliSeal, Wach’s Cement;
SealApex, Apexit, CRCS (Calcibiotic Root Canal Sealer); Diaket, ThermaSeal, TopSeal, Lee
Endo-Fill; Ketac-Endo. Fillers: Gutta-percha points, silver points)
5. Permanent filling of cavity
One-visit method in treatment of pulpitis
Indications: chronic fibrous pulpitis, chronic proliferative pulpitis, traumatic pulpitis, acute
local pulpitis; orthodontic and prosthetic indications.
Conditions: one-root tooth, no periapical inflammation.
Technique stages:
1. Operative field isolation
30
2. Anesthesia
3. Carious cavity preparation
4. Opening of pulp chamber
5. Pulp amputation
6. Widening of root canals orifice
7. Pulp extirpation
8. Hemostasis
9. Widening of root canals
10. Cleaning of the root canals with antiseptics
11. Drying of root canals
12. Filling of root canals
13. Permanent filling of cavity.
Control questions to practical lesson
The method of pulp vital extirpation is recommended in case of:
A. In patients with acute pulp inflammation types
B. In patients with allergic reactions on anaesthesia
C. In patients with serious somatic pathology
D. In pregnant woman from 1-st to 3-ed month
What is the method of chronic pulp gangrene treatment?
A. Vital amputation
B. Vital extirpation
C. Devital amputation
D. Devital extirpation
E. Biological
F. Theroot apex resection
A patient complains about intensive throbbing toothache in his lower jaw on the left. He can't show
the aching tooth. It hurts all the time, the pain goes down sometimes, but it becomes stronger as
affected by stimuli. Within the last hours the pain provoked by cold stimuli has somewhat reduced.
Objectively: the 17 tooth has a carious cavity, probing causes no pain, the pulp chamber is closed.
What method of treatment is indicated?
A Vital extirpation
B Devital extirpation
C Devital amputation
D Biological method
E Vital amputation
A 46-year-old patient has been diagnosed with chronic concrementous pulpitis of the 27 tooth. Xray picture shows that the concrement is located in the crown part of the tooth cavity and occupies
1/4 of its volume. Select an adequate method of treatment:
A Vital extirpation
B Biologic method
C Devital extirpation
D Vital amputation
E Devital amputation
A 27-year-old patient complains of the long-term pain in the 22 tooth caused by cold and hot food,
31
as well as of spontaneous pain lasting for 30 minutes and occurring 3-4 times per day, getting worse
at night. Pain arose 3 days ago after preparation of the tooth for the acrylic crown.Objectively: the
22 tooth is intact, the thermal test causes acute long-lasting pain, percussion is painless. What is the
optimal treatment tactics?
A Vital pulp extirpation
B Application of fluorine lacquer
C Biological treatment of pulpitis
D Devital pulp extirpation
E Vital pulp amputation
A 46-year-old patient complains about pain and bleeding from the carious cavity of her 27 tooth
during eating. Previously she had spontaneous pain. Examination of the 27 tooth revealed a deep
carious cavity on the masticatory surface consisting of red tissue, probing induced pain and
haemorrhage. What treatment method should be chosen?
A Vital extirpation
B Devital extirpation
C Devital amputation
D Vital amputation
E Biological method
Situation tasks and test control
Reference literature
Practical lesson No 25
Theme: Method of non-vital pulp extirpation, indications. Complications.Characteristic of
medications.Modern technologies.
Short description of a theme
Method of non-vital pulp extirpation
Technique stages:
I visitation
1. Operative field isolation
2. Partial preparation of carious cavity
3. Anesthesia (intrapulpal methods (Anesthopulpe, Pulperyl, Pulpomixine…))
4. Opening of pulp chamber
5. Application of devitalizing paste (Caustinerf arsenical – 7days, Caustinerf rapid – 3days,
Caustinerf Fort sans arsenic – 7-10days, Periodontique sans arsenic – 7days,
Paraformaldegid – 7-10days; Depulpin…)
6. Temporary filling
II visitation
1. Removing of temporary filling
2. Radical preparation of carious cavity
3. Opening of pulp chamber
4. Pulp amputation
32
5. Widening of root canals orifice
6. Pulp extirpation
7. Widening of root canals
8. Cleaning of the root canals with antiseptics
9. Drying of root canals
10. Filling of root canals
11. Permanent filling of cavity.
Control questions to practical lesson
Situation tasks and test control
A dentist was called to a patient being treated in the cardiological department after myocardium
infarction. The patient was diagnosed with acute condition of chronic fibrous pulpitis of the 36
tooth. What method of pulpitis treatment should be chosen taking into account grave condition
of the patient?
A Devital amputation
B Vital extirpation
C Vital amputation
D Devital extirpation
E Conservative method
Reference literature
Practical lesson No 26
Theme: Peculierities of Root Canal Preparation and Cleaning in Treatment of Pulpitis. Obturation
of the Root Canal System.Modern materials.
Short description of a theme
Principles of root canal preparation in pulpitis treatment
Aim: Elimination of microorganisms and their products from the root canal system and to shape it
to receive an inert filling material.
Microorganisms are found to a variable degree up to the
apical foramen in three modes:
1. as a suspension in the root canal
2. colonizing the canal walls and
3. colonizing the dentinal tubules.
It is impossible to completely sterilize the root canal
system due to its complex structure. Luckily for us,
removal of the bulk of the microorganisms and their
products brings about periradicular healing due to an
altered or less pathogenic residual flora.
33
The aim of canal preparation in vital teeth is to remove pulp tissue, which may become necrotic and
infected.
A combined action of mechanical and chemical cleansing is effective in root canal preparation.
Working length determination
From the preoperative radiograph, estimate the average length of
the tooth.
Select a reproducible coronal reference point. It should not be part of a
portion of
tooth or restorative material that is likely to break off. Choose a file that is
large
enough to be visible on the radiograph (at least size 10).
Insert a file into the root canal, 1-2 mm short of the estimated length and
take
a
parallel view radiograph. An average distance of 1 mm short of the
radiographic apex is widely accepted as a reasonable estimate of the
terminal
portion of the canal. Remember, at times, this may be inaccurate by up to
3 mm.(see
fig 1)
Relationship between apical foramen, root tip and apical
constrication. A=Root apex B= Apical constriction
C= Root canal D=Cementum E=Dentin F=Apical foramen
In cases of narrow root tips, and when there is apical root resorption,
working
length should be shortened more than 1 mm. In the former, it is because
perforation
may occur when the root is prepared to a wider diameter(See Fig2) and in
the latter,
the canal exit may be ‘blunderbuss’ shaped that can allow extrusion of
endodontic
materials.
If the tip of the file is short of the radiographic apex by 1 mm, accept it as the working
length. If the file is longer than the radiographic apex, measure the distance between the file tip and
a point 1 mm short of the radiographic apex. Subtract this figure from the length of the diagnostic
file to get the working length.
If the distance between the file tip and the radiographic apex is greater than 1 mm, subtract 1
mm from this distance and add it to the length of the diagnostic file to get the working length.
If you have reasonable number of endodontic cases, it is worth investing in an electronic apex
locator. Many reliable brands are available in the market. I have been using J Morita’s Root ZX to
my fullest satisfaction. Endoseries 5 had covered electronic apex locators.
Once you have determined the working length, it is of utmost importance to restrict instrumentation
to this length. Avoid displacement of the stops.
The width of the taper to which the canal should be prepared should be based on personal
preference and individual clinical experience. If they allow adequate cleaning and obturation,
narrowly tapered preparations are more desirable, as they do not compromise root strength and
avoid strip perforations.
Mechanical preparation refers to controlled removal of dentin by manipulating root canal
instruments. Factors influencing the amount and pattern of dentin removal are,
-design and sharpness of the cutting edge
-the manner in which it is manipulated
-the force applied and
-the operator’s skill.
Operator’s skill is influenced by the ability to discriminate tactile feedback from the
instrument and the ability to manipulate the instruments in a controlled way according to the mental
image of a three dimensional shape of the root canal system.
You can either rotate the root canal instruments (clockwise and withdraw) or used in a pushpull filing motion to remove dentin. Or you can combine the two (ream and file) by 45-90 degree
clockwise movements to engage the dentin and straight pull withdrawal to cut the engaged dentin.
Due to uncontrolled dentin removal, errors in canal preparation viz., ledging, zipping and
transportation of apical foramen may result. A reliable method to reduce uncontrolled forces is to
use flexible files such as Flex-R, Flexo-file, Nickel-Titanium etc.,
34
To avoid procedural errors resulting in loss of working length, use smaller instruments (No. 20 or
smaller) for sufficient time until the larger sizes pass in the canal without force. You can even create
intermediate files as suggested by Weine, by trimming 1 m from the tip of the file and rounding off
sharp edges on a diamond nail file. This way you can convert #10, 15& 20 files to # 12,17 and 22
Step-Back method of root canal widening
The principles of Step - Back technique:
The aim is to remove all the irregularities from the walls of the canals and leave them smooth
and cone-shaped. The working length has been measured before, so we use a file with a small
contra-rotating movement. All instruments inserted into the canal, should be worked at the correct
length with a rubber stop or marking paste. To produce an apical stop you must accumulate filling
and measure.
If you find that size 10 is good, we put it into the canal to fill working length and begin to work.
A size 15 is then used when this feels loose we remove and put 10 again. Sequence of files –
10,15,10,20,15,25,20
Each larger instrument is inserted 1 mm less into the canal, so a size 13 is placed 1mm short of
the working length, size 35 2mm short, 40 is 3mm short and 45 is 4 mm short.
Stage 3: A suitable size Gaize-Gleden bur is used to complete the coronal table. This bur is
inserted into the straight part of the canal and we make a certain action.
Step-back and temp-fillings then pre-root-filling procedures:
1. The patient is questioned about any symptoms since previous visit. If the tooth is painful it
should be repaired and redressed. Local anesthesia if required. Rubber dam is applied
especially in class II.
2. Temporary root filling is removed with bur, cotton wool underneath is removed and reveal
floor of root canal. A paper point is inserted into each canal to check moisture. Canal MUST
be dry.
If any bleeding /pus the canal must be repaired and dressed.
The main techniques
1. Sectional technique (don’t use often because not very good)
2. Single Cone
3. Multiple cone
a. Cold lateral condensation
b. Warm lateral condensation
c. Hot vertical condensation
The object of lateral condensation is to obliterate the canal system with Gutta-Percha and sealer
(the paste)
Instruments required:
1. Gutta-Percha standard, extra fine, fine, non-standard or medium cones
2. Sealer of choice.
3. Endolocking tweezers are for each canal
4. Spreaders more than one size may be necessary.
Pre-Root Filling Procedures:
Spreader is selected and introduced into the canal to insure that it will be reached to within 12mm of the full working length. If not possible we must deepen the canal.
2.
Standardized Gutta-Percha cone is chosen usually one size bigger than the length of the bur
file. If file is 15 then cone is 16.
3.
Master cone is fitted 1 mm short of the working length in each canal then when we put 1st
master core the spreader is pushed gently into the canal displacing the cone to one side.
4.
Spreader is removed take accessory cone, coat with sealer and insert into hole made by the
spreader before this we must put a small amount of paste and put in before master cone.
1.
35
Crown down method of root canal widening
The Crown-Down technique involves the widening of the canal orifices with Gates-Glidden
drills followed by the incremental removal of organic canal contents proceeding from the canal
orifice to the apical portion using manual files. As the process is undergone the files go from longer
and narrower to shorter and wider. Files are used from larger to smaller with no apical pressure.
Nevertheless, the term ''Crown-Down'' does not define the technique in the strictest sense, nor does
it provide a specific sequence for the use of instruments, but rather defines a way to use the
instruments. The preparation of root canals has been revolutionised by the development of Ni-Ti
alloys. The features of this alloy give instruments profound flexibility and allow the manufacture of
more tapered instruments compared with traditional stainless-steel instruments. In the second part
of this review, numerous examples are provided concerning the comparison between different Ni-Ti
systems and their techniques for use. A Crown-Down approach provides certain advantages
including early organic debris removal, the creation of a large reservoir for irrigating solutions, a
straighter access to the apical region of curved canals, and greater precision with regard to the exact
working length and apical size.
Most recently many clinicians have used coronal to apical techniques to clean and shape
root canals. There are several advantages:
 elimination of debris and microorganisms from the more coronal parts of the root canal system
thereby preventing inoculation of apical tissues with contaminated debris;
 elimination of coronally placed interferences that might adversely influence instrumentation;
 early movement of large volumes of irrigant and lubricant to the apical part of the canal;
 facilitation of accurate working length determination as coronal curvature is
 eliminated early in the preparation.
The crowndown and stepback techniques of preparations aim to produce a similar result, i.e.
a flared preparation with small apical enlargement.
The essentials of the coronal to apical approach to root canal cleaning and shaping are as follows:
 development of straight-line access from the occlusal or lingual surface into the pulp chamber;
 removal of all overhanging ledges from the pulp chamber roof;
 removal of lingual ledges or cervical bulges that form due to the deposition of dentine in the
cervical part of the tooth;
 development of divergent walls in the pulp chamber from the cavosurface margin to the
chamber floor;
 cutting of a funnel-shaped preparation, with its narrowest part located in the tooth apically, in a
stepwise manner in the coronal, middle and apical parts of the root canal.
 The benefits of using the crowndown technique are multiple and greatly influence the
achievement of predictable success with root canal treatment.
The clinical benefits of the crowndown technique are:
 ease of removal of pulp stones;
 enhanced tactile feedback with instruments by removal of coronal interferences;
Medicaments for root canal widening
The quality of root canal obturation depends on root canal preparation, root canal filling
material and the filling technique used. The final result will also be influenced by the amount of a
removed smear layer. During root canal preparation, cut debris is smeared over the dentinal surface,
forming a smear layer. The smear layer has been defined as any debris composed of organic and
inorganic particles of calcified tissue, necrotic tissue, odontoblast processes and microorganisms. It
has been described by scanning electron microscopy (SEM) as an amorphous substance with an
irregular surface. Mc Comb and Smith reported that the smear layer was only loosely attached to
the root canal wall whereas other studies demonstrated that the smear layer adhered firmly to
dentine because it was difficult to remove. SEM studies have demonstrated that the smear layer
covers the anatomical structures of the root canal. The smear layer thickness is not constant but
36
ranges from 1 to 5 μm; Goldmann et al. found that it varied between 10–15 μm. There are two
layers The surface layer, i.e., smear debris (SD), covers the orifices of dentinal tubules and is 2 to 5
μm thick. It has higher density
and a higher adhesive potential. The inner layer penetrates into dentinal tubules, occludes them and
provides a natural barrier against fluid movement within the tubules. The smear layer thickness can
be influenced by the type of a root instrument used and by the amount and composition of irrigants
employed.
The smear layer composition has usually been studied in relation to the possibilities of its
removal. It has become apparent that only agents combining both organic and inorganic solvents
can effectively and totally remove smear layers. However, not only the combinations of agents but
also the way of application and their quantity have been found to be important. The syringe
application of irrigants, which is used most frequently, can be replaced by treatment of the root
canal by ultrasound. In endodontics, the ultrasound technique utilizes the mechanical and
cavitations effect and acoustic streaming of ultrasound to remove the surface component of the
smear layer. However, disinfectants and different concentrations of various acids, sodium
hypochlorite and EDTA or their combinations cannot be used in all clinical cases. Their use may be
limited by diagnosis such as a systemic disease, an adverse reaction of the organism, or when tooth
apices are incompletely developed. In these cases, nonirritant mate rials should be preferred and
physiological saline can be the material of choice.
Physiological saline was found to remove the smear layer imperfectly with the use of either
syringe or ultrasound methods. Irrigation with physiological saline should be used only in strictly
indicated cases in which, for instance, the disinfectant may elicit a severe immunological response
or there is a risk of damage to the mesenchymal papilla because the tooth has an incomplete apex.
IRRIGATION
The objectives of this important part of root canal preparation are:
Lubrication of root canal instruments.
Dissolution of organic debris.
Flushing out of inorganic debris.
Elimination of micro-organisms.
The irrigating solutions recommended are:
Sterile water
Saline
Local anaesthetic solution
Sodium hypochlorite
Sodium hypochlorite. The strength of solution recommended varies from 0.3%-5.5% weight
per volume. A suitable source for sodium hypochlorite is a standard household bleach. The exact
concentration should be ascertained and it must be checked that there are no additives. The strength
of household bleaches is usually 5-6% expressed as percentage available chlorine which is
equivalent to approximately 14% weight per volume. The solution may be diluted by adding tap
water.
Irrigation syringe. The Sodium hypochlorite is injected into the pulp chamber using a
disposable syringe and special needle for irrigation. Pic. 38 show a standard hypodermic needle
(top) and below an irrigation needle and syringe (bottom). Note the side of the needle near the tip is
cut away to reduce the risk of forcing the irrigation solution through the apex if the needle became
jammed in the canal. Irrigation should be used copiously throughout canal preparation. After
completion the canal is dried with paper points.
MEDICATION OF THE CANAL
Research in recent years has shown that the prime objective in root canal preparation is to
remove the contents of the canal. In his way the majority of canal debris and micro-organisms is
removed. The introduction of powerful bactericides into the root canal may cause pain and delay
healing by leaching out into the periodontal areas and damaging normal vital tissue.
37
Most authorities do not recommend any intra-canal medication except in the following
circumstances:
Toeliminate the few micro-organisms remaining in the root canal system after preparation.
The importance of using medication for this reason is open to question. If the canal system is
cleaned and obturated any remaining bacteria should be incarcerated and will then die.
To provide a barrier against leakage of the coronal seal which would allow invasion of
micro-organisms into the root canal.
To reduce inflammation of the periapical tissues or remnants of vital pulp if time does not
allow its complete removal.
Calcium hydroxide has a variety of uses but it is thought that the increase in pH encourages
deposition of hard tissue and so promotes healing. It is also useful in the treatment of cases of
chronic wet canals.
There are large numbers of canal medicaments, many of hem offering wild claims of
success. It is suggested the contents on the label are examined and those containing powerful
concentrations of bactericides should be discarded.
Endodontic Obturation
Although periapical healing starts after Root canal cleaning, shaping and disinfection is
done, it is an accepted scientific fact that good obturation is needed for it to stay healed over the
years. An Obturation should:
 Prevent recolonization of the root canal system with microorganisms that can produce
destructive functions by the host tissues
 Prevent Periapical disease in teeth with vital pulps.
 Prevent Periapical Disease in teeth with necrotic pulps and no radiolucency
 Heal Periapical disease in teeth with obvious clinical and radiographic symptoms
Proper root canal filling should achieve three dimensional obturation of the endodontics
space to prevent micro organisms from entering and reinfecting the root canal system and to prevent
tissue fluids from percolating back into the root canal system to provide a culture medium for any
residual bacteria. It should seal all “portals of exit” to impede any sort of communication or exchange between the endodontium and periodontium.
It is clear from the objectives that the most critical area is the apical terminus of the root
canal. While attempting to provide a hermetic seal in this region, we have to keep in mind that when
heated gutta percha cools, always there is contraction. Even though thermo plasticized gutta percha
techniques are fast and good enough for obturating the body of the root canal, it cannot give a
hermetic seal in the apical third.
Another important consideration is that if a post space is to be prepared or in the event of a re- root
canal treatment, we should be able to remove the obturation without jeopardizing the integrity of the
remaining tooth structure. So it is preferable to use a technique that doesn’t leave a ‘difficult to
remove’ carrier in the root canal.
Obturation Techniques:
The most commonly used techniques are lateral condensation and vertical compaction using
gutta percha.
Lateral Condensation Filling Technique
Step 1: Check for Canal Patency
Recall the last file used used at the working length. In this case, the last file used at 24.5 mm
was the 50 K-file. Place this file in the canal and check for canal patency one last time. The
properly placed tip should elicit tugback in the apical region when an attempt to remove the file is
made.
Step 2: Prepare Root Canal Cement
Prepare a mix of root canal cement using the cement powder mixture provided and a few drops of
eugenol. Mix a small amount of eugenol with a small amount of powder using the spatula until the
mixture is loose and tacky. When pulled with a spatula, the cement should stretch about an inch
above the work surface. Continue to add small amounts of powder or eugenol until the desired
38
consistency is attained. When fully mixed, the cement should be smooth and homogenous in
texture, not grainy.
Step 3: Prepare to Fit Master Cone
When fitting the master gutta percha cone you must judge two parameters:
• approximate diameter at the apical constriction, (evidenced by tugback, or resistance at the apex),
and • length at the apex of the root canal that you just cleaned or, working length. Both the tugback
and working length must be correct. When tugback is evident, there will be resistance to removal
and the cone will be engaging in the apical constricture.
• If the taper of the canal is too narrow for the gutta percha cone, the cone will not reach
the apex.
• If the apex is blocked no tugback will be evident.
• If the apex is over-instrumented the gutta percha will extend beyond the apex.
• If the taper of the canal is large enough it will engage at the apical constricture.
Step 4: Select Master Cone
Place the last file to the working length and the last file that you shaped with on the bench top.
Select a gutta percha master cone that reasonably approximates the shape of the prepared canal by
estimating a size that lies between these two files.
Step 5: Measure Cone to Working Length
Using cotton pliers, remove a single gutta percha cone from the package and measure the cone to
the working length. [REMEMBER: Sterile gutta percha cones should be handled with cotton pliers
ONLY to prevent infection.]
Step 6: Place Master Cone in Canal
Place the gutta percha cone in the prepared canal up to the measured working length. If the point
binds before reaching the measured length, select a thinner point.
If the tip goes to measurement but does not elicit tugback, cut away 1 mm from the tip of the cone
and try again. Continue to cut away the tip and try the cone again until tugback is achieved at the
working length. Remember how much you cut away at the tip; you will have to cut this amount
away for each subsequent cone that you use in filling the canal. After cutting away the tip, if
tugback is achieved but the length is too short, the cone must be discarded and a new cone must be
measured and adjusted to fit the canal. When the tip of the cone binds exactly at the working length
and offers resistance to withdrawal or, tugback, check the working length once more to verify that
the measurement is correct. Remember, both the tugback and working length must be correct.
Step 7: Take Radiograph of Master Cone
With the gutta percha cone fitted in the canal, take a radiograph to confirm fit of the master cone.
Develop your radiograph: in the lab, develop your radiograph using the automatic developing unit.
Step 8: Lateral Condensation
Once the master gutta percha cone is fit, the canal is ready to be filled using the lateral
condensation technique. Begin by placing the cement into the canal using the last working length
file. Cover the file with cement and place it into the canal. Use the file to line the walls of the canal
circumferentially, distributing the cement on the walls of the canal evenly, two or three times.
Step 9: Coat Cone with Cement
Using the cotton pliers, remove a gutta percha cone from the package and cover it with an even coat
of cement. Place the cone in the canal it to the working length, until tugback is elicited. Extrusional
cement may be witnessed with the unmounted teeth; this does not cause a problem. While no
cement is irritation-free, once it sets the body accepts it and no long-term irritation persists.
Step 10: Spread Side-to-side
Place a D-11 spreader in the canal along side the cone. Apply pressure apically to push the spreader
in as far as possible, and spread from side to side. This side-to-side or, lateral, spreading motion is
the basis for the technique name, lateral condensation.
The D-11 spreader is available in both titanium and stainless steel. The stainless steel
spreader may be used for straight canals; for curved canals the more flexible titanium spreader
should be used. Stainless steel finger spreaders may also be used.
39
Step 11: Remove Protruding Gutta Percha
Remove the spreader and heat the long end Glick #1 instrument in the Bunsen burner flame. Place
the heated Glick #1 in the canal to the floor of the pulp chamber and move the instrument from side
to side, heating off the protruding gutta percha.
If the instrument is not hot enough, some of the gutta percha may be left behind. The instrument
should be re-heated and the rest of the gutta percha removed.
Step 12: Compress Gutta Percha
Place the spreader into the canal as far as possible apically and spread from side to side,
compressing the gutta percha and cement against the walls.
Step 13: Use Accessory Cones to Fill Canal
Repeat steps 13 through 17 using accessory gutta percha cones, until there is no more room in the
canal for additional gutta percha. Do not place an accessory cone with a diameter larger than the
remaining apical end of the canal. The cone will not fit to the end and this can create gaps in the
filling.
Step 14: Have No Gutta Percha on Floor
When the process is completed there should be no gutta percha on the floor of the chamber. Gutta
percha should be placed in the canal only, and should not extend into the pulp chamber.
Step 15: Remove Remaining Cement
Use cotton to remove any remaining cement from the inside of the chamber.
Step 16: Take Final Radiograph
A final x-ray should be taken when the condensation is completed. In the clinic a final x-ray
is taken without the rubber dam in place and with a final or temporary restoration in place on the
tooth. Clinically it is possible to take a radiograph only in a bucco-lingual direction; however, in the
preclinic, x-rays should be taken in both the bucco-lingual and mesio-distal direction. This will
enable complete visualization of the root canal fill. Develop your radiograph: in the lab, develop
your radiograph using the automatic developing unit
Warm gutta percha techniques:
Thermocompaction technique (McSpadden)
Thermoplasticized injection techniques (Obtura and Ultrafil)
Gutta percha carrier systems (Thermafill and SimpliFill)
1.JSQuick-Fill
Alpha phase gutta -percha, on special design titanium carrier, JS Quick-Fill gives you a
control, smooth obturation all in a single step.
 No heating units or open flame.
 Works with friction heat.
 Fit in your low speed handpiece.
 Chairside efficiency.
Disadvantages:
 The operator cannot control extrusion of obturating material
 If the file is turning in reverse, it can screw itself into the canal and periapical tissues
 The instruments can break
2. Thermoplasticized injection techniques (Obtura and Ultrafil)
 Length control is a disadvantage
 Canal preparation must be sufficient to permit placement of the needle to within 4-6 mm of the
apical preparation
The Obtura II Warm Gutta Percha System. This warm gutta percha-delivery system can
be quickly and efficiently incorp-orated with all down-packing techniques. It is helpful in cases of
internal resorption.
3. System B - The Continuos Wave of Condensation (L. S. Buchanan, 1987) The System B
heat source can monitor the temperature at the tip of its heat carrier device, delivering a precise
amount of heat for an indefinite time without overheating the gutta-percha. These heat carriers are
40
designed to soften the gutta-percha and at the same time condense it. The Continous Wave
Technique requires only one plugger versus four or five when utilizing the Vertical Condensation
Technique as described by Dr. Schilder.
SimpiFill obturation
SimpliFill is the only carrier system where the carrier is not left in the canal. We all know
that removal of carrier is not a pleasant job if we have to go for a post or a retreatment has to be
done. It is the best hermetic seal you can obtain for your well prepared canal. When you push a
5mm of .02 tapered gutta percha into a 4mm of parallel apical preparation, you can understand that
we are providing a cork like tight seal for the apical third.
To me the best advantage of SimpliFill is the opportunity to finish the post cementation in
the same sitting. Because of the tight apical seal, I don’t have to worry that the vibration during the
post space preparation may dislodge the gutta percha or compromise the apical seal. Equally
important are cases with severely curved root canals and canals with curvatures in two planes.
LightSpeed LSX system makes possible cleaning and enlarging the canal and it is only SimpliFill
that can make sure the gutta percha reaches to the apical extent and a hermetic seal is provided. We
can’t push a gutta percha point into such canals because they will buckle and won’t reach till the
full working length
HotShot Cordless Obturation device

Completely cordless

Multiple Uses on Single charge

Easy to Clean

Minimal heat tranmittance

Wide range of temperature settings
GuttaFlow
GuttaFlow® is a completely novel filling system for root canals that combines two products
in one: gutta-percha in powder form with a particle size of less than 30 µm, and sealer. This new
filling system works with cold free-flow gutta-percha, and uses an application system developed to
enable an absolutely simple, safe and hygienic procedure.
Resilon
Resilon is a thermoplastic synthetic polymer based root canal filling material. Based on
polymers of polyester, Resilon Material contains bioactive glass and radiopaque fillers. It performs
like gutta-percha, has the same handling properties, and for retreatment purposes may be softened
with heat, or dissolved with solvents like chloroform. Similar to gutta-percha, there are master
cones in all ISO sizes and accessory cones in different sizes available. It can be bonded with tooth.
There is still not enough evidence that Resilon performs better than Guttapercha. GP with lateral
condensation continues to be GOLD standard for Endo obturation.
The Thermafil System
The Thermafil obturator consists of two parts, the carrier and the gutta-percha. The carrier is
similar to a manual endodontic instrument without the blades, made from a special radio-opaque
plastic. Carrier is coated with GP. Thermafil obturators have a taper of .04 and are available in
various tip sizes starting from size 20 to 140. The chosen size is placed in a special oven and this
warm cone is then pushed into canal giving a 3D filling. However cooling does lead to some
shrinkage.
Disadvantages of Thermafil
This technique leaves a plastic carrier in the canal which poses a problem should you have to
place post or retreat the case. Special oven (therma prep plus oven) is required to heat thermafil
cones. In curved canals carrier usually gets stripped of GP in curvature. You needs special
technique and time to remove nasty carrier in cases which need post core or retreatment.
41
Control questions to practical lesson
Situation tasks and test control
Patients 23 years old was conducted treatment of pulpitis 16 teeth. When endodontic intervention
proved impracticable distal buccal canal was found. Which means you can apply for extension of
chemical root canal?
A. * 10-20 \% solutions of sodium salts of EDTA
B. Resorcinol fluid formalinova
C. 30 \% - solution of silver nitrate
D. Essential Oils
E. Medicines with antibacterial and anti-inflammatory action
The passage of sodium hypochlorite in the periapical region
A. is a cource of a transitory pain that disappears without any sequella
B. needs an immediate surgical therapy
C. is a source of a sharp pain that needs a prescription of anti-inflammatory and
antibiotics
D. needs an injection of a big dose of saline in the preapical region
E. needs an injection of corticosteroids I.M. to stop the inflammatory reaction that follows and
reduce the post operative pain
In the treatment of pulp inflammation the root canal have to be filled up to:
A. Anatomical apex
B. Physiological apex
C. Roentgenological apex
Reference literature
Practical lesson No 27
Theme: Module’s control No 3.
Short description of a theme
Control questions to practical lesson
Situation tasks and test control
42
Practical lesson No 28
Theme: Apical Pericementitis: Etiology and Pathogenesis. Classification of the Pericementitis.
Short description of a theme
Inflammation of the periodontium caused by irritants of endodontic origin may be termed
apical periodontitis.
Pathways of infection
There are several routes through which microorganisms can reach the dental pulp. Openings
in the dental hard tissue wall, resulting from caries, clinical procedures, or trauma-induced fractures
and cracks are the most frequent portals of pulpal infection. However, microbes have also been
isolated from teeth with necrotic pulps and apparently intact crowns. Endodontic infections of such
teeth are preceded by pulp necrosis. It has been suggested that bacteria from the gingival sulci or
periodontal pockets might reach the root canals of these teeth through severed blood vessels of the
periodontium. However, it is very unlikely that microorganisms would survive the immunologic
defenses between the marginal gingival and the apical foramen. The teeth may clinically appear
intact but reveal microcracks in hard tissues. The latter may provide portals of entry for bacteria.
Pulpal infection can also occur through exposed dentinal tubules at the cervical root surface because
of graps in the cemental coating.
It has been proposed that bacteria remaining in infected dentinal tubules can bee a potential
reservoir for endodontic reinfection. Microbial infection has also been claimed to reach and seed in
the necrotic pulp via the general blood circulation by the “anachoresis”. However, bacteria could
not be recovered from the root canals when the blood stream was experimentally infected unless the
root canals were overinstrumented and, presumably, the apical periodontal blood vessels were
injured during the period of bacteremia. Evidence that further discredits anachoresis as a potential
source of necrotic pulpal infection comes from the study of Moller et al in which all experimentally
devitalized pulps (n=26) in monkeys remained sterile for more than 6 months. Therefore exposure
of the dental pulp to the oral cavity is the most important route of endodontic infection.
Microflora of infected and untreated necrotic pulp
The endodontic microbiologic nature of teeth with infected necrotic pulp and apical
periodontitis has been extensively researched. However, the results of most of the earlier
endodontic microbial culture studies have become irrelevant because of the difficulty of avoiding
bacterial contamination from the oral surroundings and the absence of appropriate anaerobic
methods for root canal sampling and cultivation of fastidious organisms.
In principle a sample of the vast oral microbiota can infect the tooth pulp when the integrity
of dental hard tissues is lost. However, the remarkable feature of the endodontic flora is the small
number of species that are consistently isolated from such root canals. Application of advanced
anaerobic techniques helped to establish that the root canal flora of teeth with clinically intact
crowns but having necrotic pulp and diseased periapices is dominated by obligate anaerobes usually
belonging to the genera Fusobacterium, Porphyromonas, Prevotella, Eubacterium ,
Peptostreptococcus. On the other hand, the microbial composition, even in the apical third of the
root canal of periapically affected teeth with pulp canals exposed to the oral cavity by caries, is not
only different but also less dominated by strict anaerobes. In addition, spirochetes have been found
in necrotic root canals using microbiologic methods, dark-field microscopy, and transmission
electron microscopy. Spirochetes are motile, invasive pathogens that are associated with certain
marginal periodontitis and suggested causative agents of acute necrotizing ulcerative gingivitis.
However, their role in apical periodontitis remains to be clarified.
43
Endodontic flora in previously root-filled teeth
The microbiologic nature of root-filled canals is far less understood than that of untreated,
infected, necrotic dental pulps. This is probably a consequence of searching for non-microbial
causes of purely technical nature for the failure of root canal treatments. The taxonomy of the
endodontic flora of root canal-treated teeth depends on the quality of the treatment and obturation of
the canals. As such, teeth with inadequate instrumentation, debridement, root canal medication, and
poor obturation should be expected to harbor a flora that is similar to that found in untreated canals.
On the other hand, only a very restricted number of species has been found in the root canals and
periapices of teeth that have undergone proper, conventional endodontic treatment but that, on
follow up, reveal persisting, asymptomatic periapical radiolucencies.
The bacteria found in these cases are predominantly gram-positive cocci, rods, and
filaments. Using microbiologic techniques, species belonging to the genera Actinomyces,
Enterococcus, Propionibacterium are the most frequently isolated and characterized
microorganisms from such root canals. The repeated recovery of Enterococcus faecalis deserves
particular attention. Although E.faecalis is an insignificant organism in infected but untreated root
canals, it is extremely resistant to most of the intracanal medicaments used, particularly to the
calcium hydroxide-containing dressings. It can also survive in root canals as monoinfection, without
any synergistic support from other bacteria. Thus E.faecalis is a recalcitrant candidate among the
causative agents of failed endodontic treatments.
Earlier microbiologic studies and more recent correlative electron microscopic studies have
shown the presence of yeastlike microorganisms in canals of root-filled teeth with unresolving
apical periodontitis, so as to implicate fungi as potential therapy-resisting endodontic organisms.
Candida albicans is the most frequently isolated fungus from filled teeth with apical periodontitis.
Pathogenicity of endodontic flora
Any microbe that infects the root canals has the potential to initiate a periapical
inflammation. However, the virulence and pathogenicity of individual species vary considerably
and can be affected in the presence of other microbes. Although the individual species in the
endodontic flora are usually of low virulence, collectively they are pathogenic due to a combination
of factors. These factors include (1) interactions with other microorganisms in root canal, so as to
develop synergistically beneficial partners; (2) the release of endotoxins; (3) the synthesis of
enzymes that damage host tissues; (4) the ability to interfere with and evade host defenses.
Apical periodontitis is inflammation of the periodontium caused by infection of the pulp
canal system. It has been the subject of numerous terms and classifications. Periapical lesions,
apical granuloma and cysts, periapical osteitis, and periradicular lesions are frequently used
synonyms. Although periradicular includes inflammation of the furcal and lateral locations, it does
not etymologically distinguish the pulpally derived periodontitis from marginally spreading lesions.
The limitations of the various terms and the arguments for the preferential retention of apical
periodontitis have been discussed recently.
Being an inflammatory disease, apical periodontitis can be classified on the basis of
symptoms, cause, histopathology and so on. The World Health Organization (WHO) classified
apical periodontitis under diseases of periapical tissues into several categories based on clinical
signs.
Code number
WHO (1995)classification of diseases of periapical tissues
Category
K04.4
Acute apical periodontitis
K04.5
Chronic apical periodontitis (Apical granuloma)
K04.6
Periapical abscess with sinus (Dentoalveolar abscess
with sinus, Periodontal abscess of pulpal origin)
K04.60
Periapical abscess with sinus to maxillary antrum
K04.61
Periapical abscess with sinus to nasal cavity
44
K04.62
K04.63
K04.7
K04.8
K04.80
K04.81
K04.82
Periapical abscess with sinus to oral cavity
Periapical abscess with sinus to skin
Periapical abscess without sinus (Dental abscess
without sinus, Dentoalveolar abscess without sinus,
Periodontal abscess of pulpal origin without sinus)
Radicular cyst (Apical periodontal cyst, Periapical
cyst)
Apical and lateral cyst
Residual cyst
Inflammatory paradental cyst
This useful classification, however, does not take into account the structural aspects of the
diseased tissues. As the structural framework forms the basis of understanding of the disease
process, a histopathologic classification is used here. It is based on the distribution of inflammatory
cells within the lesion, the presence or absence of epithelial cells, whether the lesion has been
transformed into a cyst, and the relationship of the cyst-cavity to the root canal of the affected tooth.
Acute apical periodontitis is acute inflammation of the periodontium of endodontic origin
that is characterized by the presence of a distinct focus of neutrophils within the lesion. It is said to
be primary when the inflammation is of short duration and is initiated within a healthy
periodontium in response to irritants. It is called secondary when the acute response occurs in an
already existing chronic apical periodontitis lesion. The latter form is also referred to as periapical
flare-up, exacerbation, or “phoenix abscess”. The lesions may be nonepithelialized or
epithelialized.
Chronic apical periodontitis is a long –standing inflammation of the periodontium of
endodontic origin that is characterized by the presence of a granulomatous tissue, predominantly
infiltrated with lymphocytes, plasma cells, and macrophages. The lesions may be nonepithelialized
or epithelialized.
Periapical true cyst is an apical inflammatory cyst with a distinct pathologic cavity that is
completely enclosed in an epithelial lining so that no communication to the root canal exists.
Periapical pocket cyst is an apical inflammatory cyst containing a saclike, epithelium-lined
cavity that is open to and continuous with the root canal.
Classification of the periapical inflammation (pericementitis)
1. Acute pericementitis
 Serous
 Purulent (suppurative)
2. Chronic pericementitis
 Chronic fibrous pericementitis
 Chronic granulating pericementitis
 Chronic granulomatous pericementitis
3. Exacerbation of chronic pericementitis
Control questions to practical lesson
Situation tasks and test control
Reference literature
45
Practical lesson No 29
Theme: Acute Apical Pericementitis: Etiology and Pathogenesis. Pathological-Morphological
changes. Clinic, Differential Diagnosis.
Short description of a theme
Acute apical periodontitis (primary)
This is usually caused by microorganisms residing in or invading from the apical root canal
into the periapical tissue, but it may also be induced by accidental trauma, injury from
instrumentation, or irritation from chemicals and endodontic materials, each of which can provoke
an intense host response of short duration. It is accompanied by clinical symptoms, such as pain,
tooth elevation, and tenderness to pressure on the tooth.
Histopathologically the tissue changes are generally limited to the apical periodontal
ligament and the neighboring spongiosa. They are characterized by hyperaemia, vascular
congestion, oedema of the periodontal ligament, and extravasation of neutrophils. The latter are
attracted to the area by chemotaxis, induced initially by tissue injury, bacterial products, and
complement factor C5a. As the integrity of the hard tissues (bone, cementum, dentin) has not yet
been disturbed, the periapical changes are radiographically undetectable. If some noninfectious but
irritating agents have induced inflammation, the lesion may subside and the structure of the apical
periodontium will be restored by healing.
When the infection is involved, the neutrophils not only attack and kill the microorganisms
but also release leukotriens and prostaglandins. The former (LTB4) attracts more neutrophils and
macrophages into the area, and the latter activate osteoclasts. In a few days the bone surrounding
the periapex can be resorbed and a radiolucent area may be detectable at the periapex. Neutrophils
die in great numbers at the inflammatory site and release enzymes from their “suicidal bags”,
causing destruction of the extracellular matrices and cells.The self-induced destruction of the tissues
in the “battle zone” is to prevent the spread of infection to other parts of the body and also to
provide space for the deployment of reinforcements arriving in the form of more specialized
defense cells as the battle prolongs to a protracted war.
During the later stages of the acute response, macrophages begin to appear the periapex.
Activated macrophages produce a variety of mediators, among which the proinflammatory (IL-1,
IL-6, TNF-) and chemotactic (IL-8) cytokines are of particular importance.These cytokines
intensify the local vascular response, osteoclastic bone resorption, effector-mediated degradation of
the extracellular matrices, and they can place the body on general alert by endocrine action to
sharply raise the output of acute-phase proteins and other serum factors by hepatocytes. They also
act in concert with IL-6 to up regulate the production of haematopoietic CSF, which rapidly
mobilize the neutrophils and the promacrophages from bone marrow. The acute response can be
intensified (particularly in later stages) by the formation of antigen and antibody complexes. The
acute early lesion may take several possible courses, such as spontaneous healing, further
intensification and spreading into the bone (alveolar abscess), “point” and open to the exterior
(fistulation or sinus tract formation), or the lesion may become chronic.
Clinical features of acute apical periodontitis
Acute, localized, and permanent pain is typical for the acute process in the periapical tissues.
At first the pain is not so acute but according to the changes in quality and quantity of the
exudation, made intensive; throbbing pain occurs.
Acute pericementitis lasts for 2-3 days up to 2 weeks.
The process goes through two stages:
Stage1: intoxication of periapical tissues (the beginning of inflammation). Continuous pain
and sensitiveness during mastication. Percussion of the tooth is painful. There are no changes in the
46
gums near the affected tooth. Regional lymphatic glands can be slightly enlarged and somewhat
painful.
Pathological anatomy: according to the influence of microbial, physical, and other factors
Sign
Acute serous
apical
periodontitis
Acute purulent apical
periodontitis
Exacerbation of chronic apical
periodontitis
cell metabolism in the periapical tissues is changed what leads to the accumulation of altered lactic
acid and acidosis, continued with oedema of connective tissue and increase of blood vessels
permeability and polymorphonuclear migration.
Stage 2: is the stage of (pronounced) marked exudation and continuous pain with growing
intensity. Mastication and even touching to the tooth are painful. Percussion of the affected tooth is
sharply painful mostly in vertical but lately in all directions. Exudation in the apical tissues
provokes the filling of tooth growing and its pathological mobility. Gums at the projection of
periapical process are oedematous and inflamed. Sometimes the percussion becomes less painful
but it leads to the oedema of the vestibule fold. Regional lymphatic glands are increased and
painful. EPT100
Differential diagnosis of acute apical periodontitis
1. Acute pulpitis.
2. Pulpitis, complicated with apical periodontitis:
 spontaneous throbbing pain with irradiation,
 pain increased after all types of irritants, during mastication and at the nighttime.
Light periods is very short or absent at all.
 After perforation of pulp cavity, pulp tissue is painful and bleeds during probing.
3. Acute periostitis:
 Acute pain with irradiation
 Oedema of facial soft tissues
 Palpation is very painful
 Percussion of caused tooth and neighbouring teeth are painful
 Regional lymphatic glands are increased and painful
 Rtg – no changes in the bone tissue
 Asymmetry of the face
4. Acute periosteomyelitis:
 Acute boring, darting pain in the jaw
 Sickness, headache, t=38-40C, fever, sleeplessness, tachycardia, tachypnea
 Asymmetry of the face
 Coated tongue, oedema and inflammation of the gums; fetor ex ore
 Very painful percussion of all teeth on the half of jaw and their mobility
5. Maxillary sinusitis:
 Headache, rhinorrhea, pain in maxillary sinus area, rough breathing; Rtg changes of
maxillary sinus
47
Anamnesis
Kind of
pain
Duration of the
disease - 24
hours
Pain (or
sensitivity)
only during
mastication.
Mobility
of caused
tooth
Changes
of gum’s
mucosa
_
Common
condition
Normal
Duration of the disease - few
days
Continuous dull (gnawing) and
some times throbbing pain, that
increased after touching to the
tooth. Irradiation of the pain
some times occurs. Filling of
“tooth growing”.
+
Inflammation of the gum’s
mucosa; pain during palpation.
_
Continuous dull pain or acute
self-arising pain in the past;
duration – few days.
Continuous dull pain.
+
Oedema and inflammation of
mucosa and, some times, skin.
Pain during palpation.
Presence of gingival fistula.
Sickness, headache, t=38Sickness, headache, t=3840C, leucocytosis.
40C, leucocytosis.
Differential diagnosis of acute serous, purulent and
exacerbation of chronic apical periodontitis
Control questions to practical lesson
Situation tasks and test control
Reference literature
Practical lesson No 30
Theme: Chronic Apical Pericementitis: Etiology and Pathogenesis. Pathological-Morphological
changes. Clinic, Differential Diagnosis.
Short description of a theme
Generally, chronic apical periodontitis is an asymptomatic periapical lesion that is
manifested radiographically. Bacteria and their endotoxins cascading out into the periapical region
from a necrotic pulp cause an inflammatory reaction that produces extensive demineralization of
cancellous and cortical bone. The resulting radiographically evident lesions may be large or small,
diffuse or circumscribed. Occasionally there may be slight tenderness t percussion testing or
palpation testing or both testing methods. Often the patient will say that, although nonpainful, the
tooth feels “different” or “hollow” when percussed. A sinus tract (incorrectly referred to as a
“fistula” or “gum boil”) represents frank suppuration and has been termed a chronic suppurative
48
apical periodontitis or a chronic apical abscess. As pressure from pus is relieved by drainage
through a sinus tract, the sinus tract may close temporarily. When the pressure from pus builds up
again (along with slight tenderness to palpation), the sinus tract returns.
The general absence of symptoms, the presence of a periapiucal radiolucency, and the
confirmation of pulp necrosis confirm the diagnosis of chronic apical periodontitis. A totally
necrotic pulp provides a safe harbor for the primarily anaerobic microorganisms and their noxious
allies: if there is no vascularity, there are no defense cells. For this reason only complete cleansing,
shaping, and obturation of the root canal will eliminate the source of the periapical disease and
create a microenvironment in which this periapical lesions can remineralize.
Pathogenesis of chronic apical periodontitis.
In the continual presence of irritants (e.g., bacteria or their products), the neutrophildominated early lesion gradually shifts to a macrophage, lymphocyte, and plasma cell-rich lesion
that is encapsulated in a collagenous connective tissue. Such asymptomatic, radiolucent lesion can
be visualized as a “lull phase”, after the intense and “high casualty” battle in which neutrophils
“fell” in great numbers but the foreing intrudes into the priapex were temporarily beaten and the
enemy held back in the root canal. The macrophage-derived proinflammatory cytokines (i.e., IL1,6, TNF-) are powerful lymphocyte stimulators. Although the quantitative data on the various
types of cells residing in chronic periapical lesions are probably far from representative,
investigations based on monoclonal antibodies tend to suggest a predominant role for t-lymphocytes
and macrophages.
Activated T-cells produce a variety of cytokines that down regulate the output of
proinflammatory cytokines, leading to the suppression of osteoclastic activity and reduced bone
resorption. On the other hand, the T cell-derived cytokines may concomitantly up-regulate the
production of growth factors (i.e., TGF-), with stimulatory and proliferative effects on fibroblasts
and the microvasculature. Th1 and Th2 cell populations may participate in this process. The option to
down regulate the destructive process explains the absence of (or slowed) bone resorption and
rebuilding of the collagenous connective tissue during the chronic phase of disease. Consequently,
the chronic lesions can remain “dormant” and symptomless for long periods of time without major
changes in the radiographic status. However, at any time the delicate equilibrium prevailing at the
periapex can be disturbed by one or more factors that may favor the microbial enemy stationed
within the root canal. The microbes may advance into the periapex and the lesion spontaneously
becomes acute, with clinical manifestations (i. e., secondary acute apical periodontitis, periapical
exacerbation, phoenix abscess). As a result, microorganisms can be found extraradicularly during
these acute episodes, with possibly rapid enlargement of the radiolucent area. The presence of this
characteristic radiographic feature is because of apical bone resorption occurring rapidly during the
acute phases, with relative inactivity during the chronic periods. The progression of the disease,
therefore, is not continuous, but happens in discrete leaps after periods of “stability”.
Chronic apical periodontitis is commonly referred to as dental or periapical granuloma.
Histopathologically it consists of a granulomatous tissue with infiltrate cells, fibroblasts, and a welldeveloped fibrous capsule. When the epithelial cells begin to proliferate, they may do so in all
directions at random, forming an irregular epithelial mass in which vascular and infiltrated
connective tissue becomes enclosed. In some lesions the epithelium may grow into the entrance of
the root canal, forming a pluglike seal at the apical foramen. The epithelial cells generate an
“epithelial attachment” to the root surface or canal wall, which in TEM reveals a basal lamina and
hemidesmosomal structures. In random histologic sections the epithelium in the lesion
characterically appears as arcades and rings. The extraepithelial tissue predominantly consists of
small blood vessels, lymphocytes, plasma cells, and macrophages. Among the lymphocytes, T-cells
are likely to be more numerous than B-cells and CD4+ cells may outnumber CD8+ cells in certain
phases of the lesions. The connective tissue capsule of the lesion consists of dense collagenous
fibers that are firmly attached to the root surface so that the lesion may be removed in toto with the
extracted tooth.
49
Clinical changes are slightly expressed. The chronic fibrous pericementitis can be outcome
of pulpitis treatment.
Complaints: generally, absent.
Objective changes: deep carious cavity, connected with pulp chamber.
Root canals are with or without filling material.
Exploration is not sensitive.
Percussion is not painful.
Thermal test is negative.
EPT 100
Pathological anatomy: decrease of cells and increase of the mass of the rough (connective) tissue.
Small infiltrates and blood vessels sclerosis occurs. Thickening of the apical part of pericementum
tissues taken place.
Radiographically: widening and deformation of the periodontal split.
Chronic granulating pricementitis characterized by asymptomatic course. Slight pain during
the palpation of mucous opposite to the affected tooth is accompanied by the origin of the sinus
near the projection of the root (it is the main sign of this type of pericementitis).
Objective changes: deep carious cavity, connected with pulp chamber.
Hyperemia of the gingival near the tooth can occur, more often during the exacerbation of
chronic process.
Symptom of vasoparesis – after pressing on the gums by dull end of the instrument turn pale
of mucosa occurs, that replace with stable hyperemia.
Presence of the sinus tract on the gums near the projection of the root of affected tooth is the
main sign of this type of apical periodontitis.
Palpation of the gums is sensible as well as tooth percussion.
Regional lymphatic glands can be enlarged and painful.
Thermal test is negative.
EPT: >100
X-ray: focus of bone resorption (radiolucent area associated with the apex) with not clear
border.
Pathological anatomy: formation of granulating tissue with many capillaries, fibroblasts,
plasmatic cells, leucocytes, osteoclastic bone destruction and the tooth cement resorption.
Toxic products of the local inflammation are absorbed into the blood system leading to the general
intoxication.
Chronic granulomatous pericementitis.
In most cases clinically asymptomatic. Clinical signs are present only during the
exacerbation of the disease. Diagnosis is put according to X-ray examination with the focus of bone
resorption with a clear border and diameter up to 0.5 cm.
Pathological anatomy: this form of inflammation is no so active as chronic granulating
pericementitis, because proliferation prevails over exudation. Pericemental tissues are partially
replaced by granulating tissue. But in this case granulating tissue is limited by fibrous capsule.
Majority of granulomas contain plasmatic cells, blood cells, and sometimes, epithelial cells, which
can form the lining of granuloma. According to the presence of epithelial cells granulomas can be
divided into simple (without epithelial tissue) and complicated, which are more likely to the
periapical cysts (cyst have diameter more than 0.5 cm). Precisely granuloma can be differentiated
from the cyst only according to histological investigations.
Periapical or radicular cyst
Periapical or radicular cysts are generally considered to be a direct sequel to chronic apical
periodontitis, byt not every chronic lesion develops into a cyst. As has been stated before, there are
two distinct categories of radicular cysts: (1) those containing cavities completely enclosed in
50
epithelial lining, and (2) those containing epithelium-lined cavities that are open to the root canals.
The latter was originally described as “bay cysts” but has been newly designated as periapical
pocket cysts. More than half of the cystic lesions are apical true cysts, and the reminders are the
apical pocket cysts. In view of the structural difference between the two categories of cysts, the
pathogenic pathways leading to the formation of them may differ in certain respects.
Periapical true cyst.
There have been several attempts to explain the pathogenesis of apical true cysts. The
process of true cyst formation has been discussed as occurring in three stages. During the first phase
the dormant cell rests of Malassez are believed to proliferate, probably under the influence of
growth factors that are released by various cells residing in the lesion. During the second phase, an
epithelium-lined cavity comes into existence.
There are two long-standing hypotheses regarding the formation of the cyst cavity:
1. The “nutritional deficiency theory” is based on the assumption that the central cells of the
epithelial strands get removed from their source of nutrition and undergo necrosis and
liquefactive degradation. The accumulating products, in turn, attract neutrophilic
granulocytes into the necrotic area. Such microcavities containing degenerating epithelial
cells, infiltrating leukocytes, and tissue exudates coalesce to form the cyst cavity lined by
stratified squamous epithelium.
2. The “abscess theory” postulates that the proliferating epithelium surrounds an abscess
formed by tissue necrosis and lysis because of the inherent nature of epithelial cells to cover
exposed connective tissue surfaces. During the third phase, the cyst grows, the exact
mechanism of which has not yet been adequately clarified.
Histopathologically there are four major components in an apical true cyst: (1) cyst cavity,
(2) epithelial cyst wall, (3) extraepithelial tissue, and (4) collagenous capsule.
The cavity, completely enclosed in epithelial lining, generally reveals necrotic tissue and, on
occasion, cholesterol clefts and erythrocytes (the presence of the latter is probably due to
hemorrhage). The thickness of the stratified squamous epithelium can vary from a few to several
cell layers. The basal cell side of the epithelium is irregular, so as to form ridges. The tissue existing
between the epithelial lining and the fibrous capsule usually consists of numerous blood vessels and
infiltrating cells, predominantly T-lymphocytes, B-lymphocytes, plasma cells, and macrophages.
Neutrophils, which are numerous in the epithelial lining, are rarely found in the extraepithelial area.
Periapical pocket cyst
A periapical pocket cyst is probably initiated by the accumulation of neutrophils around the
apical foramen in response to the bacterial presence in the apical root canal. The microabscess so
formed can become enclosed by the proliferating epithelium that, on coming in contact with the root
tip, forms an epithelial collar with “epithelial attachment”. The latter seals off the infected root
canal and microabscess from the periapical milieu. When the externalized neutrophils die and
disintegrate, the space occupied by them becomes a microcystic sac. The presence of microbes in
the apical root canal, their products, and the necrosed cells in the cyst lumen attract more
neutrophilic granulocytes by a chemotactic gradient. However, the pouchlike lumen, biologically
outside the periapical milieu, acts as a “death trap” to the transmigrating neutrophils. As the
necrotic cells accumulate, the saclike lumen enlarges to accommodate the debris and may form a
voluminous diverticulum of the root canal space extending into the periapical area. Bone resorption
and degradation of the matrices occurring in association with the enlargement of the pocket cyst
may follow a similar molecular pathway, such as in the case of the periapical true cyst. From the
pathogenic, structural, tissue dynamic, and host benefit standpoint, the pouchlike extension of the
root canal space has much in common with a marginal periodontal pocket; hence the name
periapical pocket cyst. Histologically the stratified squamous epithelial lining and the rest of the
cyst wall are similar to those of a true cyst.
51
Differential diagnosis.
1. Chronic middle caries – short-lived pain after chemical and thermal irritants, percussion is
not painful, EPT= 2 – 6 mcA, Rtg: radiolucency beneath the enamel surface.
2. Chronic deep caries - short-lived pain after chemical, thermal, and mechanical irritants
which passing after their removing; percussion not painful, EPT= 2 – 6 – 10 mcA.
3. Chronic apical periodontitis (between each other)
4. Cysts (radicular and follicular)
Control questions to practical lesson
Situation tasks and test control
Patient 40y.o complaints for uncomfortable feeling in 24.. Anamnesis: in area of affected tooth
periodically appeared swelling. Objectively : in 24 widely opened cavity . Probing and percussion
not painful. Positiv symptom of Vasoparesis, on x-ray bone destruction without clear borders. Put a
diagnosis.
A. Chronic granulating periodontitis
B. Chronic fibrous periodontitis
C. Chronic gangrenous pulpitis
D. Chronic granulomatous pulpitis
E. Chronic fibrous pulpitis
Reference literature
Practical lesson No 31
Theme: Conservative method of treatment of apical pericementitis, indications. Scheme of
treatment of acute apical pericementitis. Modern technologies, medications.
Short description of a theme
Aim (purpose) of treatment:
1. Liquidation of periapical inflammation.
2. Prevention of complication origin.
3. Restoration of anatomical structure and function of the tooth.
Methods of apical periodontitis treatment:
1. Conservative
2. Surgical
3. Combinative (conservative-surgical)
Conservative method
Indications:
1. Acute and exacerbation of chronic apical periodontitis
2. Chronic apical periodontitis
52
Contraindications:
1. Increasing of inflammation in spite of periosteotomy and opening of the root apex.
2. Radicular cysts.
The main principle of treatment of acute apical periodontitis – to create a good exudate evacuation.
Ways of exudates evacuation:
1. Through the root canal
2. Through the dentogingival junction
3. Through the incision
4. Through the alveole
Acute toxic pericementitis (produced by the prolonged influence of As-paste or its
overdose). The successful treatment needs quick amputation and extirpation of the pulp remnants.
Root canals should be washed by antiseptics (1-2% chloramin, 3% hydrogen peroxide, furacilinum
1:5). After this procedure medications As-antidotes are left in the root canal (5% solution of unitiol,
1% solution of jodinolum). Electrophoresis with KJ can be recommended when inflammation is not
acute. Temporary filling leaving one of the abovementioned antidotes in the canals can close tooth.
In next visit (after 1-2 days), in the case the signs of inflammation are absent root can be filled. In
the case of acute inflammation (painful percussion, exudation from the canal) the tooth is left open
till next visit.
Acute infectious pericementitis.
In the stage of acute inflammation and exudation the tooth is left open for 2-5 days (it is
important the exudates to go out from the canal). Only in the first stage of acute inflammation,
when there is little exudation tooth can be temporary closed, leaving in the canal antimicrobial and
anti-inflammatory medications.
Trepanation (opening of the tooth) or removing the filling is painful and must be done under
local anesthesia, and with the lowest pressure from the handpiece.
It is very important not only to widen the canal but also to open apical foramen. Only in this case
the exudates will be let out.
When the signs of general intoxication are present (headache, rising of body temperature,
weakness, changes in general blood formula), antibiotics, antimicrobial medications (active to
anaerobic microorganisms) should be administrated.
When the periapical inflammation is complicated by periostitis, periosteotomy must be done
(horizontal incision 2-3 cm long) to achieve exudates and let the pus go out.
In next visit, when the signs of acute inflammation decrease, the canal is mechanically
treated and washed by antiseptic solutions (chloramin, furacilin, chlorhexydin, proteolytic enzymes
or antibiotics) and closed by temporary filling. Root canal is usually filled in the third visit.
Technique stages:
I-st visit
1. Anesthesia
2. Operative field isolation
3. Carious cavity preparation
4. Evacuation of necrotic tissues from the root canal
5. Opening of the root canal apex
6. Cleaning of the root canal with strong antiseptics
7. Hermetization of the root canal with cotton with antiseptic, temporary filling (in the 1-st
stage of periapical inflammation) or leaving the tooth open (in the 2-nd stage of periapical
inflammation)
II-nd visit
53
1. Widening and cleaning of root canal
2. Hermetization of the root canal with cotton with antiseptic
3. Temporary filling
III-rd visit
6. Removing of the temporary filling
7. Cleaning of root canals with antiseptics
8. Drying of root canals
9. Filling of root canals
10. Tooth restoration
Control questions to practical lesson
Situation tasks and test control
Woman А., 20y.o, came with complaints of darkening of crowns of 11 and 21 tooth. 1 year ago she
had a trauma. Objectively: crowns of 11 and 21 are of dark grey color, intact, percussion is not
painful. Mucoalveolar process is not changed. X-ray: in the area of apexes of roots bone
destruction, rounded size of 0,5mm in diameter with clear borders. Propose treatment.
A. Root canal treatment
B. Electrophoresis with antiseptics
C. Extraction of teeth
D. Antibiotics
E. Teeth whitening
Reference literature
Practical lesson No 32
Theme: Principles and scheme of treatment of chronic apical pericementitis. Periapical therapy.
Medications.
Short description of a theme
Treatment of chronic periapical inflammation.
Chronic periapical inflammation belongs to the diseases, which produce the focus of chronic
inflammation in the body. The treatment measures have to be chosen according to the size of the
periapical bone resorption and patient’s general condition (the presence of septic endocarditis,
nephritis, rheumatism).
Treatment methods: conservative, surgical, surgical-conservative.
The aims of the doctor during the treatment are:
 Influence on the microorganisms of root canal (macrocanal).
 Influence on the microorganisms of microcanals
 Stopping the inflammation in the periapical tissues.
 Stimulation the regeneration in the periapical tissues.
 Desensibilization of the body.
54
To achieve goods results root canal must be widely opened at full length allows the influence
on the periapical focus and excludes the canal as the seat (breeding ground, nidus) of bacterial
toxins.
In the front teeth and often in premolars, where root canals are usually single and not obturated,
treatment of chronic periapical inflammation will be less complicated.
Indications to conservative treatment are periapical changes up to 0.5 cm in diameter. The treatment
is conducted in 2-3 visits.
I-st visit : necrectomy, formation of carious cavity, taking into consideration the necessity of
good access to the canals with all endodontic instruments. Portions under the protection of
antiseptic solutions must evacuate necrotic remnants of the pulp very carefully. The dentist mustn’t
allow the debris from the root canal to be pushed beyond the apical foramen. Tooth can be closed
by temporary filling with strong antiseptic (pheresolum, phormakresol) and instrumentation of the
canal will be done in next visit. In the I-st visit instrumentation can also be done but sometimes it
can provoke exacerbation.
II-nd visit: (in 2-3 days) instrumentation of the canals, widening the canals. If the signs of
exudates are finding on the paper point taken out from the canal, medication of the canal with
enzymes, antiseptics has be continued. When the canal is clean the dentist must check up the apical
foramen (it must be open). Reamers or K-files can do the opening of apical foramen. Only in the
case of opened apical foramen we can influence on the periapical focus of inflammation.
III visit: Filling of the root is usually done in the 2 or 3 visit. Before filling the root,
biologically active pastes (with Ca (OH)2, lysozym, metacyl and others) can be put in periapical
focus to stimulate bone regeneration.
Control questions to practical lesson
Situation tasks and test control
Reference literature
Practical lesson No 33
Theme: Peculierities of Root Canal Preparation and Cleaning in Treatment of Apical
Pericamentitis. Obturation of the Root Canal System. Modern materials. Conservativesurgical methods of treatment of Apical Pericementitis.
Short description of a theme
Control questions to the material studied
Situation tasks and test control
Reference literature
Practical lesson No 34
55
Theme: Peculierities of restoration of Endodontically Treated Teeth. Bleaching.
Short description of a theme
Control questions of the material studied
Situation tasks and test control
Reference literature
Practical lesson No 35
Theme: Physiotherapy methods of treatment of diseases of the endodontium. Indications and
Contraindications.
Short description of a theme
Control questions to practical lesson
Situation tasks and test control
A 24-year-old patient complains of aching pain in the 11 tooth that is getting worse during biting
down on food. Two days ago the tooth was filled for pulpitis. Objectively: the 11 tooth is filled. The
thermal test causes no pain, vertical percussion is slightly painful. X-ray picture of the 11 tooth
shows that the endodontic filling is 1 mm above the root apex. Which of the following methods will
be most effective for eliminating this complication?
A Fluctuorization
B Ultrahigh frequency therapy
C Relaxing incision
D Submucous injection of 1% solution of hydrocortisone
E Analgetics
Reference literature
Practical lesson No 36
Theme: Mistakes and Complications in Pulpitis and Pericementitis Diagnostic and Treatment.
56
Their correction.
Short description of a theme
Control questions to practical lesson
Situation tasks and test control
A 45-year-old female patient complains about pain caused by thermal srtimuli and spontaneous pain
in the 26 tooth. A week ago this tooth was treated for pulpitis. Objectively: the 26 tooth is filled,
percussion is painful, thermal stimulus causes slowly intensifying long-lasting pain. X-ray picture
shows that the palatine canal is filled by 2/3, buccal canals contain no filling material. What is the
most probable cause of this complication?
A Incomplete pulp extirpation
B Inadequate canal filling
C Infection
D Inflammation in the periodontium
E Trauma of periodontium tissue
A 24-year-old patient complains of aching pain in the 11 tooth that is getting worse during biting
down on food. Two days ago the tooth was filled for pulpitis. Objectively: the 11 tooth is filled. The
thermal test causes no pain, vertical percussion is slightly painful. X-ray picture of the 11 tooth
shows that the endodontic filling is 1 mm above the root apex. Which of the following methods will
be most effective for eliminating this complication?
A Fluctuorization
B Ultrahigh frequency therapy
C Relaxing incision
D Submucous injection of 1% solution of hydrocortisone
E Analgetics
Reference literature
Practical lesson No 37
Theme: Module’s control 4.
57
Short description of a theme
Control questions to practical lesson
Situation tasks and test control
Reference literature
Practical lesson No 38
Theme: Summary control № 1.
Short description of a theme
Control questions to practical lesson
Situation tasks and test control
Reference literature
58