Dr JT (Koos) Marais

 As a service to all referring dentists I will publish the text of my textbook here. Please respect the copyright. The project will be completed over a period of three weeks, starting today, 4 November 2009. The process of editing is never ending and I welcome all criticism, even negative criticism. Printed copies of Part 1, The Essentials of Shaping, Cleaning and Filling Root Canals, can be ordered from the office, at a cost of R200 which includes postage within South Africa.

 ROOT CANAL TREATMENT  

Koos Marais

The essentials of  shaping, cleaning and filling

INTRODUCTION

1.1 What is a root canal treatment?

A root canal treatment is the total removal of all living and dead tissue, healthy or otherwise and micro-organisms from the confines of the root canal system and the total obturation of the space created in the process by means of an insoluble, inert and inactive material.  The removal of material is accomplished by means of irrigation with sodium-hypochlorite and the obturation with a combination of gutta percha and sealer.  Both these processes are greatly facilitated by the process of preparation of the root canals by means of files and burs.

1.2 Why do we do a root canal treatment?

Scientifically, the purpose of a root canal treatment is the removal of diseased, necrotic, gangraneous, decayed or otherwise affected tissue in order to treat current or prevent future, pain, infection, abscesses, immune responses or other pathological conditions of the pulp.  It finds its equivalence in the removal of tonsils or appendices.  Root canal treatment may also be done prophylactically in which case it must be justified by sound clinical judgement, never, never as a matter of routine.  In other words, if the clinician is of the opinion that although the current status of the pulp is good and does not warrant removal, there is a reasonable chance that in the future this will change and that it will be more difficult to perform root canal treatment at that time, or it will lead to destruction and possible remake of expensive restorations, then it might be justified to do a prophylactic root canal treatment.

Practically, a root canal treatment is done in order to alleviate pain, swelling and infection caused by the pulp or to prevent these conditions.

One of the favourite theories is that a root canal treatment is done in order to remove anything that can act as antigen.  This immune response theory justifies the removal of pulpal tissue on the basis of changes in the proteïen structure, caused by pathology, leading to a foreign body response.  In other words, the pulp tissue undergoes changes and acts as an antigen and the body's immune system attacks it.  Literally anything can act as an antigen, i.e. corroded silver points, previously used to fill root canals, necrotic dentine or cementum, medicaments and even gutta percha.  The rationale of a root canal treatment, in terms of the immune response theory then, is to remove anything that can act as an antigen or immunogen from the confines of the root canal system and to prevent the possible future formation of such substances in the root canal system.

Practically, how do we do a root canal treatment?

Root canal treatment is carried out in three phases:

Shaping

Cleaning

Filling

The process of cleaning and shaping may also be referred as the preparation of the root canal.

The process of filling may also be termed the obturation of the root canal.

Probably the most frequent question asked by dental students is “Up to what size must I file?”.  This is a very simple question with a complex answer.  It is the purpose of this entire section on cleaning, shaping and filling of the root canal system to answer that question.

Firstly, no two teeth are identical.  Secondly, there are a multitude of instruments, materials and devices available for root canal treatment.  All these can be used, alone or in conjunction with each other, to do a root canal treatment.  Each of these technologies has its own advantages and disadvantages.

However, there is one central philosophy, which perhaps sums up the answer:

We shape in order to clean and fill

Shaping in itself is not an objective of  root canal treatment.  The true objectives are cleaning and filling.  Therefore, once we have shaped a canal which would allow adequate cleaning and filling, then we have shaped enough.

It is now necessary to carefully study all three sections – shaping, cleaning and filling – in order to understand what constitutes adequate shaping, cleaning and filling.

ANAESTHESIA - A SINE QUA NON FOR ROOT CANAL TREATMENTS

Koos Marais

Primum Non Nocere - First do no harm, this is the very essence of the Hippocratic Oath.  Amongst other things it compels the healer to do everything in his power not to hurt his patient.

There is absolutely no justification for attempting any phase of root canal treatment without proper pain control, i.e. local anaesthesia, even, if it is only for the sake of rubber dam.  For some inexplicable reasons it sometimes happens, even at the obturation stage, that a root canal treatment may cause an unexpected and excruciating, piercing and agonising jolt of acute pain.  It is extremely foolish to risk this, even if the chances of this happening are in the order of twenty percent or less.

Everybody knows, or should know that it is impossible to expose and remove a vital or partly vital pulp without proper anaesthesia.  Any experienced dentist will also know that it is, as a matter of routine, far easier to achieve proper anaesthesia for extraction work than it is for removing pulps.  So every reasonably caring dentist will go to great lengths in order to properly anaesthetise a tooth that he or she is going to start treating endodontically, that is for the first visit.  But in practice it is often found that dentists, including specialists, will rush in at the second or third visits, without taking all the same precautions.  This is what often gives root canal treatments the bad name, amongst patients, that it has.  Proper anaesthesia should be administered for all stages of root canal treatment.  Failure to do so, may lead the caring clinician to hold back or hurriedly finish treatment when in fact he should be carrying on and going forward, figuratively speaking.  Just as the restorative dentist may be tempted to leave soft or discoloured dentine, because the patient is hurting and place an amalgam restoration on top of it, so the endodontist may stop just short of filing, irrigating or obturating to the desired and correct length if the patient is experiencing discomfort or pain.

It is only a subhuman being who fail to be affected himself when confronted on a day to day basis by the suffering of fellow human beings.  This is particularly true in the case of a dentist and his patients.  It is a well-known fact that dentists are prone to several medical and psychological disorders, many of which are stress related.  The proper control of pain is one of the greatest stress reducing factors in a dental practice and therefore it is also in the dentist's own interest to administer effective anaesthesia for all procedures which might elicit pain. 

Sometimes the acutely inflamed pulp will "flatly refuse" to be anaesthetized, even after the administration of several cartridges of anaesthetic solution including attempts at intraligamentary and or intra-osseous injections (Brown, 1981).  If at all possible and practical, these teeth should be left alone for a period of 24 hours, antibiotics, anti-inflammatory drugs and analgesics should be prescribed and a fresh attempt made at a subsequent appointment.  This is obviously not ideal but it is foolish to ignore the fact that some teeth will at some stage prove impossible to anaesthetize.  It is a fact of life.

Most everyday anaesthetic problems are encountered in the lower jaw.  This has been ascribed to various reasons, most of which are very theoretical and speculative  (Roda and Blanton, 1994).

The most important fact of the matter is that it is rather difficult to achieve full anaesthesia of the lower teeth and the dentist should be prepared for it (Walton and Torabinejad, 1992).

Guidelines to painless injections

1. It is a fallacy to believe that cold solutions cause more painful injections.  The nerves surrounding the target area simply do not have cold receptors.

2. Most pain is caused by the sudden explosion of solution into a limited space and not by the penetration of the needle.  (Acupuncturists are no magicians, they are only very aware of the fact that it is not very painful to merely introduce a thin needle into most human tissues).

3. In order to avoid the sudden explosion problem the solution should be very, very slowly introduced into the tissues.  It should take at least 90 seconds to inject 1,8 ml of solution.  In order to get the feel the clinician should take an assembled syringe and press down on it only hard enough for a drop of solution to come out of the needle at a time and observe the flow rate with his own eyes.  In the real situation this first drop must anaesthetize the area surrounding the tip of the needle and the next drop will spread a little further and so on.

4. What little pain is caused by the superficial penetration of the needle can be prevented by the use of topical anaesthetic. However the area onto which the topical anaesthetic is applied should be very dry.  

Absorption from a wet mucosa is impossible.  A combination of suction, cotton wool rolls and dry air should be used to obtain a dry operating field prior to application of the topical anaesthetic solution.

5. The palate is the most difficult area in which to perform a painless injection.  However it is still possible but it requires a good deal of concentration and patience.  The palate from the canine posteriorly can be anaesthetized by a posterior superior palatal nerve block.  This is done roughly 15 mm from the midline just anteriorly to the border of the hard palate. The technique requires again the drying of the injection site and the application of a topical anaesthetic.  Supplement this with the subsequent application of ethyl chloride on a cotton wool pellet to the site.  This will "freeze" the area.  Keeping the cotton wool pellet in position, slowly but in one steady motion introduce the needle.  Express the solution very slowly, a drop at a time.  Keep the cotton wool pellet in position. (Never use ethyl chloride or topical anaesthetic in a rubbing motion.  It will injure the mucosa).  

Anteriorly to the canines the nerve supply of the palatal soft tissues is via the nasopalatine foramen and the mucosa is very dense, tough and fibrous.  As a result there is a lot of resistance and even a drop of anaesthetic solution is experienced as a sudden and relatively large swelling causing much pain.

An alternative method for this and other palatal anaesthesia is to first administer the labial or buccal infiltration, to wait at least two minutes and then to penetrate the needle through the interdental papillae, which will be anaesthetized at this time and then to slowly extrude solution, going a little deeper extruding more solution and so on until the needle almost penetrates the palatal mucosa. At this stage the palatal mucosa adjacent to the tooth can be directly penetrated and properly anaesthetized.

Benefits of a slow injection

1. It is less painful.

2. The solution is delivered and restricted to the area where it is intended and the result is proper anaesthesia.

3. There are far fewer dramatic toxic reactions.

4. If a patient develops an adverse reaction, recognition will often be at a stage when all the solution has not yet been delivered and the administration can then be terminated, limiting the dosage and severity of the reaction.

Helpful hints

1. In the lower jaw, all anaesthesia should consist of the administration of a least two cartridges, i.e. 3,6 or 4 ml, of anaesthetic solution.  One cartridge is very seldom sufficient for root canal work in healthy adults.  

In very young children and debilitated or older patients the dosage may be limited to one cartridge.  

2. It is much more effective to administer the two cartridges one immediately after the other than to only administer one, wait a few minutes, try and fail to enter the pulp chamber or root canals due to inefficient anaesthesia and then to administer a second cartridge.  Once anaesthesia has failed and the patient has become a little anxious it is much more difficult to get anaesthesia (Walton and Torabinejad, 1992).  One "large" dose at the beginning is much more effective.

3. Because of the necessity to deliver two cartridges the clinician should be very careful when using solutions containing adrenaline or non-adrenaline.  Inadvertent intravenous injection of two cartridges can trigger all kinds of cardiovascular problems (Barnard, 1994).  Because of this many clinicians routinely use solutions specifically not containing these drugs.  This is a practice which should be encouraged.

4. Some syringes are designed in such a way that the cartridges can be removed from the side when the plunger is pulled back.  A chairside assistant can remove the first cartridge, while the dentist is keeping the needle in position inside the tissues, and she can then place the second cartridge into the syringe.  This technique eliminates a second penetration of the needle, something which is greatly appreciated by the patient.  

5. When even the described technique for the lower jaw fails, it can be supplemented by retromolar infiltrations - distal to the area of the third or second molars.  The lingual gingival tissue as well as the long buccal nerve should also be anaesthetized.  When this also fails the next step should be intraligamentary or intra-osseous injections around the relevant tooth.  (Brännström, Pashley and Garberoglio, 1985) Several special syringes for this purpose are commercially available but any normal syringe will, perform the same function.  Because these injections are done with great force the cartridges break very easily and the patient should be protected against this.  An easy way of doing this is by taping the entire cartridge with masking tape.  This will prevent glass fragments from entering the eyes or oral cavity in case of a fracture.  An intraligamentary or intra-osseous injection (basically the same thing) is done by pushing the needle from the occlusal side into the ligament.  Much force is needed to extrude the solution because of the resistance of the periodontium.  The solution will tend to spurt backwards not entering the ligament.  The operator has to squeeze hard at the same time pushing down on the needle.  A major problem is bending of the needles. Special short stiff needles, available for some syringes, facilitates this task considerably.  Only about 0,2 ml of solution will give sufficient anaesthesia with an intraligamentary injection.

6. Failure of anaesthesia in the upper jaw can be handled following the same principles as for lower teeth.  

However, in some cases, notably the molars, the problem can be directly ascribed to innervation of the palatal roots by the posterior superior palatal nerve.  Administration of a block of this nerve usually gives a dramatic and profound anaesthesia of the offending tooth.

7. Sometimes, as a very, very last resort it is necessary to inject directly into an exposed pulp.  This is extremely painful.

8. The use of intra-venous sedation, relative analgesia (N₂0) and electronic analgesia are very helpful aids, but no substitute for local anaesthesia.

9. Mainly because of the lack of intra-oral radiograph facilities in day clinics, general anaesthesia is not a good option for root canal treatment.

References

Brännström M, Pashley DH & Garberoglio R (1985). PDL Anaesthesia: Clinical Experience and Review of Recent Research.

Grafica Editriale.  Asti, Italy

Roda RS & Blanton PL (1994). The anatomy of local anaesthesia.  Quintessence International; 25: 27-37

Walton RE & Torabinejad (1992).  Managing local anaesthetic problems in the endodontic patient.  Journal of the American Dental Association; 123, May: 97-102

Brown RD (1981).  The failure of local anaesthesia in acute inflammation.  British Dental Journal; 151: 47

Barnard DP (1994).  Hazards of local anaesthetic injections.  DP Barnard, Pretoria

Pathogenesis of Pulpal Diseases

Etiology

Probably the main course of pulpal disease is caries, a bacterial disease process.  

Without the presence of bacteria, exposed dental pulps can remain healthy, 

theoretically.  This has been proven in bacteria free rats.  The moment bacteria, or 

only some of its products, come into contact with the pulp, the disease process is 

initiated.  It has been proven that this happens as soon as the bacteria have worked its 

way through the enamel to the outer surface of the dentinal tubules.  Once the bacteria 

or their products have come into contact with the dentinal tubules, the homeostasis of 

the dentinal fluid is disturbed and this is transmitted to the pulp.  An inflammatory 

response is initiated and this leads to either regeneration or degeneration.

Ironically, the other main course of pulpal disease is the very process by which the 

primary cause, i.e. caries, is intended to be treated.  That is to say restorative dentistry.  

In other words if the pulp is not killed by the caries, it may well succomb to the 

treatment.  All dental procedures carry with them some risk to the pulp.  These 

include cavity preparation, cavity debridement, placement of bases and liners, etching, 

priming, resuis, light-curing, restorative materials, shrinkage and leakage.  Actually, 

all these procedures have as one of their main objectives the goal of preservation of 

the pulp.  The study of the etiology of pulpal disease is essentially a study of 

preventative endodontics.  To know what the cause of the disease is, is to know how 

to prevent it.  Caries can be prevented by good oral hygiene practices such as regular 

brushing and flossing.  This is supplemented by treatments such as topical and 

systematic fluoride and fissure sealants.  The prevention of caries is also the 

prevention of pulpal disease.  

The prevention of iatrogenic damage to the pulp is essentially, good dentistry.  It 

includes the strict adherence to theoretical and clinical guidelines, to manufacturers 

instructions and to common sense.  Apart from caries, trauma and iatrogenic damage 

to the pulp, there are a number of other causes of pulpal disease.  A comprehensive 

list of the etiology of pulpal disease is shown in Table 1.

Table 1 The Etiology of Pulpal Disease

I. Bacterial

Coronal ingress

Caries

Fracture

Complete

Incomplete

Nonfracture trauma

Anomalous tract

Dens invaginatus 

Dens evaginatus

Radicular lingual groove (a.k.a. palatogingival groove)

Radicular ingress

Caries

Retrogenic infection

Periodontal pocket

Periodontal abscess

Hematogenic

II. Traumatic

Acute

Coronal fracture

Radicular fracture

Vascular stasis

Luxation

Avulsion

Chronic

Adolescent female bruxism

Traumatism

Attrition or abrasion

Erosion

III. Iatral

Cavity

Heat of preparation

Depth of preparation

Dehydration

Pulphorn extensions

Pulp hemorrhage

Pulp exposure

Pin insertion

Impression taking

Restoration

Insertion

Fracture

Complete

Incomplete

3.   Force of cementing

Heat of polishing

Intentional extirpation

Orthodontic movement

Periodontal curettage

Electrosurgery

Laser burn

Periradicular curettage

Rhinoplasty

Osteotomy

Intubation

IV Chemical

Filling materials

Cements

Plastics

Etching agents

Cavity liners

Dentin bonding agents

Tubule blockage agents

Disinfectants

AgNO₃ (silver nitrate)

Phenol

NaFl

Desiccants

Alcohol

Ether

Others

V. Idiopathic

Aging

Internal resorption

External resorption

Hereditary hypophosphatemia

Sickle cell anemia

Herpes zoster infection

HIV and AIDS

The Role of the Etiological Factors

There is no etiological factor which can kill or destroy the pulp in a single stroke.  In fact the pulp is a rather resilient organ.  It exists in a relatively hostile environment being subject to 

tremendous mechanical forces, 

millions of micro-organisms, 

large variations in temperature and a 

wide range of chemical substances in the form of food and drink.  

The pulp is protected from all these influences by its hard shell of enamel and dentine but this protection is by no means absolute.  Somehow the etiological factor finds its way to the pulp, either directly or indirectly.  It is nearly always a slow process and only rarely results in instantaneous necrosis.  The etiological factors, be they bacteria, physical trauma or chemical irritation, only act as a catalyst for the disease process.  It starts the process but does not finish it.  This process is the inflammatory process which is perpetuated as an immunological response.   In the pathogenesis the etiological agent is both the initiator and perpetrator of the inflammatory response (irritant and antigen). After initiating the disease process, the etiological factor, if not eliminated, will continue to stimulate the immune response resulting in disease.

The Role of the Body’s Defense System

Whereas the etiological factor is the original cause of the disease, it is the body’s immune system that is responsible for the most damage.  The cells and tissues of the pulp are slowly destroyed as a result of the interaction of the etiological factors and the body’s defence system.  Most of the cell damage is ascribed to the products of the immune system.  

The intention of the immune system is to defend and does this very effectively.  As the pulp is continuously subjected to the insults of multitude etiological factors, it needs the services of the immune system very much.  As in the rest of the body the process of injury and repair is a continuous and ongoing process.  It is when the etiological factors become overwhelming that the defence process overreacts and so many toxic by-products are created that healing can not take place.  The toxic by-products themselves also act as irritants and the body responds and the vicious cycle continues.  The result is more cell damage and ultimately necrosis.

The Pulpal Defense System

The pulp defends itself against these irritants by means of 

An acute inflammatory response

The immune response and chronic inflammation

The Uniqueness of the Pulp in the Disease Process

The pulp is unique for three reasons

It is totally surrounded by hard tissues that minimizs the possibility of an increase in blood supply.  The apical (and lateral) foramina have a limited capacity .  They won’t allow significantly more blood than normal to enter the pulpal space. 

No true collateral circulation exists.

The pulp protects itself from injury by the deposition of reparative dentine.

The Aging Process of the Pulp 

From eruption and throughout life the pulp continues to produce secondary irritation or reparative dentine.  This results in a progressively smaller pulp space, less nerve tissue, less blood supply, less cells, and more fibrous tissue.  The total volume of pulp tissue decreases and the number of pulp stones and calcifications increase.

Inflammation vs Infection

An inflammatory response is a reaction towards any irritant, microbial or otherwise.  

Infection is the process where a pathogenic micro-organism is introduced to the body resulting in an inflammatory response.

In the case of the pulp an inflammatory response can be elicited by bacteria, bacterial endotoxins, degenerative or breakdown products of pulpal cells, (denaturising or coagulated proteïens) and other mediators of inflammation.  Infection of the pulp by bacteria is the logical conclusion of the caries process.  However, long before the bacteria reach the pulp itself, some of the bacterial products will have elicited an inflammatory response in the pulp through its contact with dentinal fluid in the tubuli.  

An example of a sterile inflammatory response is when a part of a natural tooth is overheated, as happens during drilling.  The odontoblasts in closest proximity to the damaged dentine will undergo lysis, the proteïens will denature, act as antigens and initiate inflammation and an immune response.  Additionally, during cell lysis of the odontoblasts, mediators of inflammation such as histamine, complement, prostaglandins and cytokines are released, enhancing the inflammatory process.

Vascular Changes during Inflammation

The initial response of the micro-circulation to irritation is momentary contraction.  This is immediately followed by vasodilatation.  Because of the wider vessels, blood flow is slowed, and white blood cells migrate through the vessel wall.  There is an increase in local pressure, and extravascular plasma, concentrating platelets outside the micro-circulation and triggering the clotting process.

The pulpal vasculature contains arterio-venous shunts.  These shunts may selectively shut down blood flow to irritated areas allowing normalisation to take place, to promote healing and repair.  Obviously, when the blood supply is cut off to any living tissue for too long, the result is necrosis.  This is what happens when the pulp is overwhelmed by too many etiological agents, in too many sites.

Pathophysiology of the Pulp

The collapse of the micro-circulation, for whatever reason immediately leads to an increase in the hydrostatic pressure.  This in turn leads to an increase in extravascular exudate and an increase in interstitial pressure, further collapsing the venous effluent and arterial supply.  The resulting anoxia or hypoxia leads to local necrosis, breakdown products, an increase in interstitial proteïens and osmotic pressure.  The circle of increased extravasation of fluid and increased tissue pressure is exacerbated.   As soon as pus in the form of micro-abscesses is formed, the disease process is deemed irreversible, ultimately leading to total necrosis of the pulp.

Acute Inflammation

Acute inflammation is the primary mechanism of healing.  This healing will take place as either total regeneration, i.e. replacement of damaged tissues with the same tissues or as scar tissue formation.  When acute inflammation does not result in healing it becomes chronic inflammation, mediated by the immune response.

In acute inflammation several changes take place simultaneously when an irritant is recognised.  Polymorphonuclear cells and monocytes leave the blood vessels and the monocytes are transformed to macrophages.  The polymorphonuclear cells and macrophages then phagocytose the irritant.  This phagocytosing process takes place in 3 distinct stages:

The irritant is coated with antibody and/or complement

It is phagocytosed

It is broken down in the lysosomes

Chemical products are released from the plasma and from the tissue.  From the plasma the kinines, complement and clotting factors are activated and from the tissues histamine and the lymphokines.  The cytotoxic effects of all these products are not limited to the irritants but also affect the bodys own cells.  More cells are killed, more vascular changes take place, more products are released and the vicious cycle continues.  

Alternatively, all toxic products and irritants are phagocytosed and removed and healing takes place.  An acute inflammation of the pulp will usually be in a localized site containing many polymorphonuclear cells and macrophages.  The odontoblasts in this site may appear absent or aspirated into the dentinal tubuli.  Underlying blood vessels will appear dilated.  Healing may eventually appear with normal odontoblasts and normal adjacent pulpal tissue or the odontoblasts may be replaced by transformed mesenchymal cells.  The secondary or reparative dentine may appear normal or it may appear atubular.

Chronic Inflammation

Histologically, chronic inflammation of the pulp is characterised by the presence of large numbers of lymphocytes and plasma cells, throughout the pulp.  This is evidence of the involvement of the immune system in the disease process.  It is also an indication of the failure of the primary defense system, i.e. the acute anti-inflammatory agents (polymorphonuclear cells and macrophages) to clear the irritants.  Once lymphocytes becoming predominant the pulp can be considered to be in an irreversible condition of pulpitis that means that total regeneration will not take place.  The body recognises this and takes other measures to limit the spread of the disease process.  Once chronic inflammation becomes established the disease process will spread to the apical or peri-radicular periodontal tissues.

The Immune System

Whereas the acute inflammatory response is directed non-specifically at all irritating agents, the chronic inflammatory process, is directed at specific agents, called antigens.  An antigen is a foreign body that is a macromolecule composed of a proteïen, a carbohydrate or a glycoproteïen.

Bacteria are obvious examples of antigens.  (Actually bacteria carry specific antigens on their surfaces).  Less obvious examples are breakdown products of pulpal cells and endodontic therapeutic materials such as cements and other materials.  Certain smaller molecules can also act as antigens and are called haptens.  Haptens have to be carried or presented with other proteïens in order to act as antigens.  Gutta percha molecules can act as haptens.

Generally, the chronic inflammatory immune response recruits the lymphocytes and two types are recognized - T lymphocytes and B lymphocytes. T lymphocytes are responsible for cell mediated immunity and B lymphocytes for humoral immunity.  (B lymphocytes produce antibodies which are specific to each antigen).  T lymphocytes can transform to killer T cells that produce lymphokines, products that neutralize foreign matter and mediate inflammation.  T lymphocytes also transform in to helper T cells, activator T cells or suppressor T cells which can influence plasma cells to produce antibodies.  Antibodies are complex molecules and 5 types are recognised:  IgG, IgA, IgM, IgE and IgD.

Overreaction of the immune system causes tissue damage and is known as hypersensitivity.   

A widely used classification of these reactions is the following one proposed by Gell and Coombs.  They classify immunological responses into four main types: 

Type I, anaphylactic reactions; type II, cytotoxic reactions; type III, antigen- antibody complex reactions; and type IV, delayed hypersensitivity reactions.

Type I: Anaphylactic Reaction

The type I immunological reaction deals exclusively with the reactions of one class of immunoglobulin, IgE.  It is constantly formed and has a half-life of 2 to 4 days in blood.  IgE has a special capacity to attach itself for long periods to receptors on basophils or mast cells.  The mast cells for which IgE antibody has a marked affinity play a key role in anaphylactic reactions. The effect of this reaction is the sudden liberation of stored mediators of inflammation mainly histamine.  The primary role of these chemicals released from the mast cells appears to be defence against injury, however pathological changes such as bone resorption may occur as well.

Type II: Cytotoxic Reaction

This class of reaction involves binding of antibodies to antigens on the cell surface.  The reaction may involve the binding of complement and the subsequent inflammatory events or lysis of the cell.   

Type III: Antigen-Antibody Complex Reaction

The formation of complexes between antigen and antibody often causes intense inflammation.  When these complexes form, they activate complement.  Anaphylatoxins and chemotactic factors are generated which cause an influx of fluid and leukocytes into the area of immune complex formation.  The platelets are damaged by the complement activation on their surfaces and they release additional vasoactive amines.  With the influx of fluid and cells more substrates are available for the reaction.  More complement is fixed and more cells invade the area of inflammation.  The PMN leukocytes attempt to ingest the immune complexes, but cannot surround the endothelial cells that are binding the immune complexes and consequently discharge their lysosomal granules against the endothelial cells.  This causes damage to the endothelial cells and the surrounding tissue and intensifies the inflammatory reaction.  The intensified inflammatory reaction imitates the coagulation pathways and fibrin is deposited locally.  If the lesion is due to a single dose of antigen, the inflammation resolves and the tissue damage is repaired with residual scarring.  If the antigen deposition is continued however, chronic inflammation occurs with more severe tissue damage.

Type IV: Delayed Hypersensitivity Reactions

Cell mediated immunity, or type IV immunological reaction does not involve antibody.  Rather it is the sensitised T-lymphocyte which interacts with a specific antigen. This interaction stimulates lymphocyte proliferation and production of a group of substances known as lymphokines.

These lymphokines cause (1) extensive damage to host tissues and destruction of antigens; (2) bone destruction as a result of osteoclast activating factor release, which is produced by the T cells when they encounter an antigen to which they are sensitised; (3) Activation of leukocytes, macrophages and lymphocytes, related to transfer factor, MAF, and lymph-node permeability factor.  T-lymphocytes also help in the destruction of weak antigens by boosting the antibody response of the B- lymphocytes.

Once chronic inflammation has been established there is always periodontal or peri-apical involvement.  Bacterial products, chemical products and breakdown products exit the confines of the root canal through the apical foramen and causes chronic inflammation in the periodontal tissues.  The exact same process is acted out in the periodontal tissues as in the pulp with two major important exceptions.  Firstly, the periodontal tissues have an adequate collateral circulation and secondly the alveolar bone has a physiological capacity for resorbtion and subsequent reformation.  The dentine has no such capacity.  This means that the peri-apical periodontal tissues have an almost unlimited capacity for healing and repair, while the pulp only has a limited capacity.

Acute Pulpitis vs Acute Inflammation of the Pulp

There is considerable confusion surrounding the term acute pulpitis.  It is often used to describe a severe, spontaneous toothache, a condition which would histopathologically almost certainly present as a chronic inflammatory reaction in the pulp.  A true acute inflammation of the pulp, is normally a sub-clinical situation.  The patient may not even be aware of the process.  Sometimes it presents as mild to moderate pain or discomfort, especially when exposing the tooth to cold stimuli.  It is difficult or impossible to localise the exact tooth because the inflammation is limited to the pulpal tissues, which do not contain proprioceptive fibers and receptors.  The pain or discomfort is of a transient and fleeting nature.  This condition resolves spontaneously or it may progress to a chronic pulpitis.

Clinically it is much more important to distinguish between an irreversible and a reversible pulpitis.  Acute inflammation of the pulp may be reversible, but chronic inflammation always is irreversible.

Hyperplastic Pulpitis

This is a dramatic lesion of the pulp, called pulp polyp.  A mushroom of living pulp tissue rises out of the carious crown of the tooth.  The surface is firm and insensitive.  It consists microscopically of capillaries, proliferating fibroblasts and inflammatory cells all covered by a stratified squamous epithelial cover.  The pulp polyp is an extreme macroscopically visible example of chronic inflammation of the pulp.

Pulpal necrosis

As a result of inflammation, centers of liquefaction necrosis develop.  Because of the limited blood supply and insufficient drainage of inflammatory fluids localized increases in tissue pressure develop, leading to unchecked progression until the entire pulp is necrotic.  The localized region of necrosis is bordered by an area of chronic inflammation.  This may be quite narrow and adjacent to it may be a region of histologically normal pulp.  One may expect peri-radicular inflammation not to develop until the entire pulp is necrotic.  However, very often this is not the case.  The coronal pulp may be totally necrotic, bordered by a thin layer of chronic inflammation; the apical pulp is histologically normal but the peri-radicular area is clearly radiographically and histologically chronically inflamed.  It is postulated that the etiological factors had diffused through the “healthy” radicular pulp and elicited a peri-radicular inflammatory response with bone resorption.  This condition is seen in young patients and the conflicting symptoms and signs make an accurate diagnosis very difficult.

Clinical views of chronic pulpal inflammation: The Peri-radicular Lesions

Chronic pulpal inflammation is an irreversible process that ultimately ends in necrosis and eventually manifests as an abscess.  During the course of this process the condition may present clinically in various forms and guises.  Chronic inflammation of the pulp always involves the periodontal i.e. peri-radicular tissues.  Because of the chronic inflammation of the pulp it always requires removal, either by means of a root canal treatment or an extraction.  The periodontal involvement means that the offending tooth is easily localized by tapping the tooth – because the periodontal tissues do contain proprioceptive fibres.  However it is very important to note that many cases do not have this feature and that all cases of teeth sensitive to tapping do not necessarily imply chronic pulpal inflammation.  Also, many cases of chronic inflammation may remain totally symptom free for years. Chronic inflammation of the pulp may also present clinically as an acute toothache requiring urgent treatment.  

The pathogenesis of peri-apical lesions is schematically represented in Figure 1:

Acute Inflammation of the Pulp Healing

Chronic Inflammation of the Pulp

Total Pulpal Necrosis                                                 Acute Apical Periodontitis

             Chronic Apical Periodontitis

Acute Apical Abscess                                                  Chronic Apical Abscess

Figure 1:  The Pathogenesis of Peri-Apical Lesions

Etiology of Peri-radicular or Peri-apical lesions

The same etiological factors that cause pulpal disease may lead to peri-radicular disease.  Additionally, endodontic materials, instruments and procedures may act as irritants.  It is a very simple fact that peri-radicular lesions of pulpal origin are inflammatory responses to irritants from the root canal system.  It is another simple fact that treatment centres solely around the removal or elimination of these irritants.  Remove the irritant and the disease resolves.  It is really that simple.  It is an axiom of endodontics: Remove the antigens and peri-radicular healing will follow.

Terminology:  Acute vs Chronic Periodontitis/Abscess

In the discussion on inflammation of the pulp the terms acute and chronic were used to describe histology conditions.  In the discussion of peri-radicular lesions the terms will be used to describe clinical symptoms.

Apical Periodontitis

Acute Apical Periodontitis (AAP)

Histology: Localized inflammation apically, mainly PMN with some mononuclear cells.

Radiography: Normal to slight thickening of periodontal ligament.  Evidence of coronal disease or treatment.

Symptoms: Slight tenderness to excruciating throbbing pain.  Recent origin.

Signs: Severe tenderness to percussion and apical palpation.

It is thought that the vascular changes, local stasis, release of mediators and dramatic increase in tissue pressure are responsible for the intense pain experienced by the patient.

Chronic Apical Periodontitis (CAP)

This condition differs from AAP in several dramatic aspects.  Firstly it is of a longstanding smouldering nature and secondly, it may present as asymptomatic or mildly symptomatic.  Tests reveal little or no pain upon percussion.  However there always is a clear peri-apical radiolucent area.  Radiographs are the diagnostic key.  Radiographic changes range from thickening of the lamina dura to destruction of apical bone with frank peri-radicular lesions.  

Histologically CAP is classified as either a peri-radicular granuloma or a peri-radicular cyst.  As a third alternative CAP may present with a condition called condensing osteïtitis (Focal Sclerosing Osteomyelitis).

1.  Peri-radicular granuloma

Granulation tissue, small capillaries, fibroblasts, connective tissue fibers, inflammatory infiltrate and usually a connective tissue capsule are present.  Obviously the peri-radicular alveolar bone has been resorbed.

2.  Peri-radicular cyst

Central cavity lined by stratified squamous epithelium.  Lining is incomplete and ulcerated.  Surrounding connective tissue has appearance of peri-radicular granuloma.

Both these conditions (granuloma and cyst) respond favourably to conventional root canal treatment.  Only extremely rarely is surgical enucleation indicated.  Another rare form of CAP is condensing osteïtis or chronic focal sclerosing osteomyelitis.  In contrast to granuloma or cyst, apical bone is not resorbed, it is overproduced.  It’s clinical symptoms are the same and it is successfully treated with root canal treatment.

3.  Condensing osteïtitis

A very low-grade, subclinical inflammatory response may lead to an increase in bone density rather than resorption and lucency.  This response is dependent on the quality, duration, and virulence of the irritants.  This lesion may be clinically asymptomatic or possess the range of pulpal symptomatology.  Radiographically there is increased bone density and opacity at the apex.  Since this is a lesion of endodontic origin, there must be a cause for the pulpal disease.  Microscopically, dense bone with growth lines is prevalent with a mild chronic inflammatory infiltrate in the marrow spaces.  If there is an altered or necrotic pulp, endodontic treatment is indicated.  The opacity may or may not heal.  

Apical Abscesses

An abscess is a localized collection of pus in a cavity formed by the disintegration of tissues.

Acute Apical Abscess (AAA)

AAA can be the end result of a CAP or it can follow directly after pulpal necrosis.  It is usually precipitated by a rapid influx of micro-organisms from the root canal into the peri-radicular tissues.

Radiographically it may appear as a clear distinct radiolucency, but it may also have the appearance of normal tissue.  The patient may or may not have swelling.  Swelling may be localized or it may be diffuse and spread widely (cellulitis).  The involved tooth is insensitive to thermal and electrical stimuli and sensitive to percussion.

In all cases severe pain is present and urgent treatment is necessary.  It is important to note that infection may spread through various facial spaces and may even be life-threatening (Ludwigs Angina and Cavernous Sinus Thrombosis).

Chronic Apical Abscess (CAA)

This condition is associated with a gradual egress of irritants from the root canal into the peri-radicular tissues and formation of an exudate which drains through a sinus tract on the oral mucosa or, rarely, as a fistula on the skin.  The exudates can also drain through the gingival sulcus, mimicking a periodontal pocket.

These teeth are usually without discomfort, until the sinus tract is blocked.  Vitality tests are negative because the pulps are necrotic.  Radiographically, apical bone loss is evident.  Histopathologically, the lesion is similar to CAP with a sinus tract leading away from the suppurative core to the surface.  The sinus tract may or may not be lined with epithelium.  This condition reacts most favourably to root canal treatment.

Non Endodontic Peri-Radicular Lesions

There are a number of diseases that may mimic peri-apical or peri-radicular lesions of endodontic origin.  In some instances a misdiagnosis may even be life threatening.  In most cases lesions of endodontic origin are associated with a non-vital tooth.  Peri-apical lesions of non-endodontic origin are usually but not always associated with vital healthy teeth.  The value of a thorough examination, including vitality testing cannot be over emphasized.

Odontogenic Cysts

Primordial Cysts

Dentigerous cyst

Lateral Periodontal cyst

Odontogenic keratocyst

Residual apical cyst

Fibro-Osseous Lesions

Peri-radicular cemental dysplasia

Osteoblastoma and Cementoblastoma

Cementifying and Ossifying Fibroma

Odontogenic tumors

Ameloblastoma

Non Odontogenic Lesions

Central giant cell granuloma

Nasopalatine Duct cyst

Traumatic bone cyst

Enostosis

Malignancies

Microbiology of the Pulp (From Stock et al)

Peri-radicular disease is caused by bacteria.  Many different species and strains of bacteria have been isolated from root canals. The source of bacteria is almost always the oral cavity, but the unique anaerobic environment of the root canals allow for the development of a population very different from that of the oral cavity.  Certain bacteria will prosper to the detainment of others.  Most often root canal systems are infected by a number of different species.  Only certain bacteria such as Pseudomones and Enterococci may on their own be the cause of a peri-radicular infection.  In these mixed infections one specie produces nutrients for the other and they are interdependent. It is relatively easy to treat these mixed infections also because they are mostly anaerobic in nature and exposure to oxygen, calcium hydroxide and water will kill significant number of bacteria.  On the other hand mono-infections with Enterococci are notoriously difficult to treat.  In fact the most common bacteria found in failed root canal treatment s are the Enterococci.  Bacteria are mostly confined to the root canals.  Only rarely are bacteria found in the peri-radicular area.  Once the bacteria have overwhelmed the peri-radicular immune and defence systems, the result is a full-blown dental abscess.

C:\My Documents\Boek-Wortelkanale\Pathogenesis of Pulpal Diseases.doc

Diagnosis of Pulpal Diseases

Introduction

Every time a dentist plans to place a restoration, a careful diagnosis of the pulpal condition of the tooth should first be made.  Once a dentist has touched a tooth with a rotating instrument, he or she is in one way or another responsible for the future condition of the pulp.  This seems to be a dramatic statement, but there is justification for it.  Often, a patient would receive treatment on an asymptomatic tooth, following which a painful inflammation of the pulp develops.  Before, the patient had no problems, but after treatment, the patient experiences pain and discomfort.  It is common knowledge that after caries, the greatest cause of pulpal disease, is restorative procedures.  In this sense the restorative procedure was therapeutic to the coronal enamel and dentine, but at the same it was time iatrogenic to the pulp.  Or perhaps the pulp had, prior to restorative treatment, been suffering from one of the chronic forms of inflammation, without any symptoms.  The restorative procedure then acted as the final insult, which shifted the balance and resulted in an acute flare-up.  If the chronic inflammation had been pre-diagnosed the patient could have been warned and or a root canal treatment would have preceded restorative treatment.

In time and with experience many practitioners learn to intuitively and automatically  “pre-diagnose” all the pulps of the teeth on which they place simple restorations.  Unfortunately sometimes, this intuitive diagnosis fails and problems arise.  It is best to always follow a system, to make a definitive diagnosis and to forewarn patients of any impending problems such as post-operative sensitivity.  It is better to systematically collect information by taking the history and investigating all the tissues and then to make a definitive diagnosis, before any treatment is prescribed.

Once a patient presents with a main complaint of toothache, the making of a definitive diagnosis is of even greater importance.  The diagnosis of toothache in its many forms dictates the treatment.  Very often toothache requires root canal treatment, but not always.  To treat every tooth that presents itself with symptoms, by means of a root canal treatment, is gross over-treatment.  To do a root canal treatment unnecessarily on any tooth is indefensible.  The nature, cost, sequelae and possible complications of root canal treatment is such that the caring clinician will do everything in his or her power to avoid it.  For this reason he or she should know when there is a chance that the toothache will resolve either spontaneously or with the aid of conservative treatment.  

On the other hand toothache can be so excruciating that the practitioner must know when to intervene.  He or she should know when a pulp has crossed over into a terminal or irreversible state.

In other words when a patient presents with a main complaint of toothache (or sensitivity) the conscientious clinician must be able to make a diagnosis of

1. Reversible pulpitis

or

2. Irreversible pulpitis

Attempting to treat an irreversible pulpitis without root canal treatment will only make matters worse.  Treating a reversible pulpitis with a root canal treatment is over-treatment and maybe even malpractice.  In the case of reversible pulpitis treatment will focus upon removal of the exact etiology (caries, leakage, etc) and subsequent dressing and isolation by means of some form of restoration.  However the patient should also be informed of the unpredictable nature of the condition and that further treatment may be necessary.

The various clinical and histological forms of irreversible pulpitis can all be treated by root canal treatment but there are some subtle differences in approach that necessitates the making of a more descriptive and detailed diagnosis.  For instance, an acute apical periodontitis (AAP) will almost always require the prescription of analgesics, whereas chronic apical inflammation (CAP) in the form of a peri-radicular cyst may require surgical involvement.

There are a number of non-endodontic causes of apparent “toothache”.  Examples are maxillary sinusitis, myocardial infarction, trigeminal neuralgia and atypical facial pain.  Any attempt at dental treatment could have serious or even fatal results.  For this reason it is absolutely imperative that the dentist should know how to make a definitive diagnosis of all the endodontic conditions that present with toothache.  The most common cause of toothache is teeth and therefore all dental causes of toothache should rank highest on the list of differential diagnosis.  BUT, sometimes the toothache is not dental in origin and the practitioner should always be wary of this.  Following a systematic plan during the making of a diagnosis, for each and every patient, protects the practitioner from himself.  It protects from instant or intuitive diagnosis and from jumping to conclusions.

The Diagnostic System

The diagnosis of all medical and dental diseases are made following the same basic system:

1. Personal Details

Find out who the patient is

2. Main Complaint

In one sentence or word, why did the patient decide to consult the doctor – Pain, routine examination, etc.

3. History

In dentistry the medical history precedes the dental history because of the life threatening nature of certain dental procedures interacting with the medical condition.  In endodontics, and in the case of toothache specifically, the taking of the dental history assumes great importance.  

The taking of the history of a patient requires one of the greatest communication skills of the human race – to LISTEN to the patient.

4. Examination

Now, and only now, after listening to the patient, does the doctor (or dentist) begin to examine the patient by looking, probing, feeling and even smelling.

After the clinical examination, the doctor will decide, based upon the information gathered so far, which Special Investigations are required.  

It is debatable and probably ethically wrong to subject a patient to expensive and possibly invasive special investigations if the patient had not yet had an opportunity to present his or her problem to the doctor and the doctor had not at least looked at him or her.  In endodontics the most common special investigation is the radiograph and the same ethical principle is involved.

5. Diagnosis

After gathering all the information, (by listening, looking, feeling and using special technology) the doctor uses his or her brain and common sense.  He or she thinks, weighs all the factors and makes a decision – the diagnosis.  It is not always easy, simple and straightforward.  For instance, many disease conditions are progressive in nature, presenting in various guises along the way.  It is very evident in pulpal disease.  It is difficult to clinically distinguish between an irreversible and reversible pulpitis because certain signs and symptoms overlap and conflict.  .

Notwithstanding all these clinical difficulties, the clinician must make a DIAGNOSIS.  If a diagnosis is not made the fact should be noted, communicated to the patient and all treatment should be considered symptomatic.  It is acceptable to make a PROVISIONAL diagnosis, to be confirmed later.  Based upon the provisional diagnosis, certain diagnostic treatment procedures, such as a temporary dressing or crown may be provided.  The patient is re-examined at a later stage and eventually the diagnosis is confirmed or altered.

The Diagnostic System Expanded for Endodontic Use

1. Personal Details

The reasons for obtaining as much personal and demographic information are obvious.  These include accounting and billing information.  Less obvious reasons may be medico-legal ones, which may only arise several years later.  The minimum information required will be:

Surname

First names

Title

Home address

Home telephone number

Office address

Office telephone and fax number

Name of referring person

Date of birth

Name and address of person responsible for account

It is perhaps appropriate at this stage to mention the importance of communication between doctor and patient about fees.  In one sense, endodontics is a form of elective treatment.  A patient always has an option to have the tooth extracted and the endodontic patient is sovereign in this matter.  A patient must be informed before treatment of all the costs, the nature, risks, advantages, disadvantages and possible complications of endodontic treatment.  If all this has been done and the patient accepts treatment, it is called informed legal consent.  The most appropriate moment to do so is perhaps only after the diagnosis has been made.  It is mentioned here as a subtle reminder that we are dealing with complex people, individual human beings, each with his or her own perceptions, needs and desires.

2. Main Complaint

After meeting a person (patient) during the first stage (personal details) it is common sense, and good manners to enquire for the reason of the visit (consultation).  At this stage, the clinician is looking for one sentence or one word, such as “My teeth are sensitive to cold drinks” or “Terrible toothache”.  This stage serves as the triage system and the purpose is to avoid time wasting and embarrassing incidents, where patients are subjected to detailed examinations and investigations when all they really wanted was to “Have my teeth cleaned” or “Need a crown recemented”.  Once the main complaint refers to anything related to pain, sensitivity, aches, swelling, discomfort or anything similar, it is in order to proceed along the road of endodontic diagnosis.

During the taking of the main complaint, the dentist should resist the temptation to be drawn into a discussion about the detailed dental history.  This comes later.  If the discussion about the main complaint is expanded to include all the symptoms and the nature thereof, it might induce the practitioner to progress into the examination, forgetting to take the medical history.  This could have some serious consequences.

3. Medical History

The medical condition of a patient may influence the diagnosis or the treatment of a patient with dental disease, such as toothache, dramatically.  It may require the prescription of prophylactic antibiotic cover.  In the case of allergic patients it may influence the choice of antibiotics and materials.  For example, some endodontic disinfectants contain iodine and patients may be allergic to iodine.

There are a number of non-dental conditions that mimic toothache or may have the radiographic appearance of peri-apical radiolucencies.  The clinician should always bear these possibilities in mind.  It is easier not to be fooled into a misdiagnosis (and wrong treatment) when a detailed medical history had already revealed the maxillary sinusitis, chronic headaches, cancer, myocardial insufficiency or whatever.  

There is no medical condition that serves as an absolute contra-indication to endodontic treatment.  Certain oncology specialists often demand multiple extractions or even total dentectomy prior to radiotherapy or chemotherapy for cancer patients.  This view can and should be challenged.  With enough care, most teeth can be successfully treated and retained, provided the teeth and periodontal tissues are in a reasonable condition and serve some useful purpose.

The following are a minimum list of questions every patient should be asked:

Have you ever had rheumatic fever?

Have you ever had any disease involving your heart valves?

Do you suffer from any other heart disease?

Do you suffer from

High blood pressure?

Asthma?

Chronic headaches?

Are you allergic to any medication?

Do you take any medication?

Are you under the treatment of a medical doctor?

If yes, please provide his or her name.

Do you suffer from any other serious illness or disease that you would like to bring to our attention?

4. Dental History

“Listen to the Patient, he will tell you the diagnosis.”

The above statement is one of the age-old cornerstones of medicine.  It is quite remarkable how accurate an endodontic diagnosis can be made, just by listening to the patient, asking questions and waiting for the answers.  This information very often swings the balance, or determines the exact nature of the diagnosis.  For instance if a patient presents with a main complaint of a severe toothache and he describes the pain as dull and throbbing, spontaneous and keeping him awake all night, a diagnosis of an irreversible pulpitis indicating root canal treatment, can be made with 99,9% confidence, even before the examination.  This does not mean that the examination is unnecessary.  On the contrary, a very detailed examination will be an absolute requirement, especially to identify the exact offending tooth.

The following questions should be asked

When did the problem start?

Can you associate the advent of the problem with another incident of medical or dental nature?

Can you identify the tooth with the problem?

Has the pain persisted continuously since the start or does it sometimes go away?

Can you identify anything, which causes the problem or the pain, such as eating, or drinking?

Is the tooth sensitive to

Cold

Heat

Eating

Sweets

Chewing

Does the tooth hurt spontaneously without any of the above?

Is the pain sharp and stinging?

Is the pain dull and throbbing?

Does the pain linger for a while after the cold, heat, eating, sweet, chewing or does it go away quickly?

Do you think or know that you grind your teeth?

Have you had recent dental treatment?  If yes, please provide some information.

Have you ever had crowns fitted to your teeth?

Have you ever had a root canal treatment (nerve taken out)?

Do you want to keep all your teeth or would you prefer to have a tooth taken out if it were giving you problems?

Many questions can be added and each case will dictate exactly which questions need to be asked.  It is better to ask more than fewer questions.  One should neither ignore nor attach too much importance to any one single answer.  All the information, including that obtained during the examination, should be weighed together, before a diagnosis is finally made.

It is preferable that the procedure so far – the collecting of personal details, main complaint and the taking of the medical and dental history be conducted in a non-dental environment, such as the dentists office with patient and doctor sitting at a desk, facing each other at eye level.  This will enhance and optimise communication.  A dental surgery contains too many distracting and intimidating sounds, materials and instruments.

5.       The Clinical Examination

The clinical examination is carried out in the dental surgery, with the patient in the dental chair.  The clinical examination will involve the following tissues, in a systematic manner.

The Extra-oral Tissues

The Intra-oral soft tissues

Lip

Tongue

Pharynx

Cheeks

Mouth floor and submandibular lymph glands

Alveolar mucosa

The Occlusion

The Periodontal Tissues

The Status of Oral Hygiene

The Teeth

The Extra-oral Tissues

Observe the patient from the front, sides and also from above (the back of the head).  Note any irregularities or swelling.  Look for signs of inflammation such as redness.  Remember that rare cases of chronic apical abscesses may even present with a draining fistula on the skin.  Palpate the external features of the facial region noting any swelling or tenderness:

The tempero-mandibular joint

Palpate the joint in the static position as well as during movement.  Note any clicking, popping, croaking, tenderness and also note when, i.e. static, opening, closing it occurs.  Repeat the procedure using the fingers to palpate intra-auricularly.

The masticatory muscles

Ask the patient to bite and palpate the anterior border of the massetor.  Note any tenderness.  Palpate the sternocleidomastoid and temporal muscles.

The submandibular lymph nodes

Palpate the submandibular lymph nodes noting any tenderness, swelling, mobility and size.

The Intra-oral soft Tissues

In one sense, the examination of the intra-oral soft tissues is the dentists most important function: It is the duty of the dentist to perform a cancer screening of every patient that he or she ever examines or treats.  Even if a patient merely requests the recementing of a crown or any other “minor” service, the dentist is ethically and morally obliged to do at least a cursory examination of the soft tissues for signs of malignancies.  It is most distressing when oral cancer is discovered and a patient declares that a dentist had recently examined him or her.

Lip

Observe the mucosa for signs of redness, superficial white lesions, swelling, ulcerations or any other abnormalities.

Tongue

Inspect the dorsal and lateral surfaces of the tongue for irregularities, swelling, ulcerations or nodules.

Pharynx

Ask the patient to stick out the tongue and utter “AA”; observe for abnormalities.

Cheeks

Retract the cheeks with a mouth mirror and observe the mucosa.

Mouth floor and Submandibular lymph glands

Visually inspect the floor of the mouth for ulcerations and swelling, redness.  Then palpate the mouth floor with an index finger.  It is also useful to use the index finger of the other hand extra-orally, opposing the exploring finger to feel for any swelling.  In this fashion the presence of any swollen or tender submandibular lymph glands can be discovered.

Masticatory muscles

Palpate the pterygoid muscles for tenderness.  Keeping the fingers in the vestibule, free from the teeth, ask the patient to close the teeth and to bite hard.  Palpate the anterior border of the masseter muscles.

Alveolar mucosa

Observe and palpate the alveolar mucosa in the region of the root apices.  Note any redness, swelling or tenderness.  In the posterior maxilla extend the palpation upwards, away from the root apices to the region of the maxillary antrum.  Note any tenderness in this area.

The Occlusion

A full and detailed examination of the occlusion is a very complex procedure.  Common sense dictates that such a complex procedure should not be carried out on a patient suffering from an acute and severe toothache.  On the other hand if an obvious cause for a toothache is not readily apparent it might well be necessary to perform a more thorough investigation of the occlusion.  Because oral pain does not refer across the midline it is often enough to limit the study of the occlusion to the side of the mouth, left or right, with the pain.

Of particular importance are the following:

Note immediately the strategic importance of all teeth.  In other words are there any superfluous or non-functional teeth.

Note any missing teeth that can be possible causes of lesions such as dentigerous cysts or residual peri-radicular cysts.

Note any RC-IC discrepancies.

Observe, bilaterally, for non-working interferences.

Note open contact areas that might pre-dispose to food impaction – a cause of difficult to diagnose vague toothache.

Observe for signs of fremitus – Ask the patient to bite and keep the index finger against the buccal surface of the maxillary teeth.  Ask the patient to now grind the teeth.  Fremitus can be observed as an abnormal movement of the tooth.

Note any premature contacts, i.e., of teeth that are slightly extruded.  (Teeth with acute apical periodontitis or acute apical abscess sometimes exhibit this feature).

The Periodontal Tissues

As in the case of the occlusion, it defies common sense and logic to subject a patient with acute toothache to a detailed examination of all sulci of all teeth.  The examination must be tailored to the nature of the main complaint and the available information.  In other words if the patient complains of a vague pain in the left of the mouth, then periodontal probing of the teeth of the left side of the mouth might be indicated.  However if the patient is adamant that the problem is located to a specific tooth, then periodontal probing should be limited to that tooth and the two teeth adjacent to it, one mesially and one distally.  The point is that no pulpal condition can be properly diagnosed without consideration of the periodontium.  Note any and all signs of pocketing, bleeding, swelling, loss of attachment, drainage of pus or ulceration.

The Status of Oral Hygiene

Whilst it is not necessary to take a plaque index it is quite in order to make a note of the general status of the oral hygiene.  A very poor standard may be a relative contra-indication for root canal treatment.  A localized collection of plaque may be an indication of a sensitive tooth from which the patient quite naturally tends to shirk away from when brushing.

The Teeth

It is a sound idea to deliberately leave the examination of the individual teeth for last.  It is easy to become engrossed with all the coronal anatomy, pathology and restorations of the teeth and then to forget to examine the soft tissues, occlusion and other structures.  When the teeth are examined, each individual tooth is viewed in isolation (as opposed to when examining the occlusion – i.e. teeth in relation to each other and in function).  Every tooth is observed for signs of disease and every abnormality is noted.  

Again, as in the case of the occlusion and periodontium, it is not fair to the patient to do a detailed examination of teeth distant to a site of excruciating pain.  In other words, limit the examination to the teeth in the area of the pain.  Because of the difficult nature of endodontic diagnosis and specifically the very real possibility of referred pain, it is most often necessary to examine upper and lower teeth on the side of the pain.  Sometimes though, the pain emanates quite clearly from one particular tooth and then it is only necessary to examine that tooth and the two adjacent teeth.

When examining the teeth the following must first be noted

Restorations (Note surfaces and material)

Leakage or deficient margins

Cusp fractures

Decay

Facets. Make a note of all surfaces, which are sensitive to probing.

Decalcification

Discolouration

Developmental disturbances

Following the above visual inspection a series of so-called vitality tests are performed: Cold, Heat, Percussion, Electricity and Bite Force.  These vitality tests are, traditionally, of the utmost importance.

The significance of vitality testing

The ultimate objective of most endodontic diagnostic procedures involving vitality testing is to distinguish between

sound, healthy normal pulps

slightly, reversible inflamed (acute inflammation of the pulp) i.e. reversible pulpitis and

chronically inflamed pulps, i.e. irreversible pulpitis.

To these a fourth category can be added – The totally non-vital, i.e. necrotic pulp.  Indeed L J Baume devised his classification accordingly:  Class I, II, III, IV (See below).

The main problem with measuring nerve response instead of pulpal blood flow lies in the fact that the mechanism of healing is really blood flow.  As long as there is active blood flow pulpal healing is possible and the pulpal condition is in other words reversible in nature. These tests really are a measure of the pulpal nerve’s reaction to external stimuli.  They do not quantify pulpal blood flow or anything else.  The pulpal nerves can and do exist for some time in pulpal tissue which has very little blood flow and which is in fact largely necrotic.  There is also no true correlation between the clinical signs and symptoms of the pulp and its histo-pathological features.  Vitality tests are therefore notorious for all its false positive and false negative results.  Other reasons for the unreliability of vitality testing are: 

Multi-rooted teeth with one necrotic root canal and one or more vital canal.

Variability in conductivity of enamel and dentine of individual teeth.

Influence of restorative materials

Conduction of impulses, especially electrical impulses, to the periodontium giving false positive reactions.

The subjective nature of the patient’s experience of the pain and the dentist’s interpretation of it.

Modern research focus on the development of Doppler Flow Lasers, devices that can to an extent measure pulpal blood flow.

Notwithstanding all the shortcomings of vitality testing, until properly functioning Doppler Flow Lasers become commercially available, the dentist will have to rely on the relatively unreliable results of the vitality test.

Procedures for Vitality Testing

Injudicious use of thermal, electrical and impact (percussion and biting) impulses and forces can cause severe and excruciating pain on a tooth suffering from some form of disease.  Clinicians should exert the greatest care when performing these tests.  Preferably, all tests should be done in a graded fashion, starting with a low intensity, beginning for instance with a blast of air, then cold water and ultimately using ice or something else, when testing with for cold sensitivity. If a patient experiences moderate to severe pain with a low-grade stimulus, it would be foolish to increase the stimulus.  A positive response can be noted.

The clinician will decide empirically on a scale of intensity to record the findings.  An example is:

Negative (No response)

+ (Slight) Within normal limits

++ (Moderate) Beyond normal limits

+++ Severe

Using this scale the reaction to each of the tests must be noted – for instance C++; H+; P-; B-; E20 (Electrical tests are usually recorded with the number on the device)

Procedures for Cold Testing

Using a saliva ejector and cotton wool rolls, dry and isolate the quadrant of teeth to be examined.  Maintain a dry working area throughout the procedure.  Isolate the two adjacent teeth with cotton wool rolls.  Direct the nozzle of the 3 in 1 syringe at the neck of the tooth and blow a short burst of air at it.  If the result is negative, spray a little water at the neck.  If the result is still negative, apply ethyl chloride to a cotton wool pellet, held in tweezers, wait two seconds for the pellet to dry out and apply to the neck of the tooth.  If still no reaction is observed, a negative (-) reaction to cold is noted.  If a positive reaction is observed, at any stage, further testing with colder materials is not done and based upon the patient’s reaction a positive (+) response to cold is noted as described above.  It is up to the clinician’s judgement and common sense to describe a positive response as C+, C++ or C+++.  Also note the duration of the response; fleeting or prolonged.

Procedures for Heat Testing

Again the teeth are isolated and a dry working field obtained.  A small amount of petroleum jelly or other lubricating agent is applied to the necks of the teeth to be tested (Heated gutta percha will stick to dry teeth).  A piece of gutta percha stopping (an old fashioned temporary restorative material) is heated in a flame until soft, kneaded around a flat plastic instrument, re-heated and then applied to the lubricated area.

Exercise caution when working with this material.  It is extremely hot and will cause severe burn wounds to the face, lips or mucosa if accidentally brought into contact with these tissues.  Heat needs to be applied for a few seconds longer than cold, because the reaction is slower.  Therefore, wait also a few seconds before proceeding to the next tooth, otherwise the wrong tooth may be noted as sensitive.  Again note the severity of the response as either 

H-, H+, H++ or H+++ and also note the duration.

Procedures for Percussion Testing

A dry working field is not necessary.  Start using a light tapping action with a fingertip.  If a negative reaction is found increase the intensity.  If it is still negative use the back of a mirror handle.  Finally, if light tapping with the mirror handle gives a negative reaction, increase the force to a moderate tapping.  If at any stage a definite positive response is noted, do not increase the intensity any further.  Note as P-, P+, P++ or P+++.

Procedures for Bite Testing

Any stiff but yielding object, such as wood or plastic may be used.  Special devices such as the Tooth Shooth are also available.  These have sharp pointed edges allowing precise placement on cusps.  Place the object on the tooth and ask the patient to bite.  Indicate as B-, B+, B++ or B+++.

Procedures for Electrical Testing

Several devices are available.  Follow the manufacturer’s instructions.  Usually it is necessary to apply saliva or a lubricant to the neck of the tooth.  It is also necessary, in order to complete the circuit for one part of the device, to be in contact with the patient’s naked skin. Activate the device, asking the patient to indicate as soon as a sensation is felt.  Note the number on the dial as E20, E41 or whatever the case may be.

In order to fully interpret the electrical test it is necessary to have an impression of the general sensitivity of “healthy” teeth.  Test a few teeth especially the contra-lateral tooth, if available.  According to this the tooth in question can be classified as 

EN (within normal limits

E (Hypersensitive to electrical stimulus, i.e. to higher currents)

E (Less sensitive to electrical stimulus, i.e. to lower currents)

A tooth may also test E Neg (Negative to electrical currents)

The L J Baume Classification 

Earlier attempts by Baume to distinguish between a Class 3A and 3B pulp were motivated by the belief that so-called vital pulps (Class 1,2 and 3A) had to be treated differently than Class 3B and Class 4 pulps.  It was believed that the apical extension of the root canal treatment of the vital pulps should be 1mm short of the apex, while the so-called non-vital pulps had to be treated to the apex.  The modern philosophy is to clean, shape and fill to the apical constriction, in all cases.  The Baume classification has made way for the philosophy of reversible pulpitis versus irreversible pulpitis, i.e. To do, or not do, a root canal treatment.

Special Investigations

In the past the taking of microbial cultures from the canal system, to determine the sterility was quite common.  This practice is now more or less limited to research institutions.  Far and away the most common special investigation in endodontics today is the radiograph.  No endodontic diagnosis can be made without at least one, but preferably two peri-apical radiographs, clearly showing the root apex, as well as the crown.  

All diagnostic radiographs should ideally be taken with the cone paralleling technique, properly processed, mounted, dated, documented and stored.   Radiographs should be viewed on an illuminated light box, with the aid of a magnifying glass.  Examine all structures extremely carefully for sites of radio-lucency or radio-opacity or any other signs of abnormality.  

Note the lamina dura.  It should be uninterrupted all the way around the root.  Study the apical areas very carefully for signs of radiolucency.  Observe the crowns for signs of cavities, restorations, especially those in close approximation to the pulp.  Note the horizontal and vertical levels of the alveolar bone for signs of periodontal disease.  Study the number, position and lengths of the roots.  Study the pulp chamber, its relative position, pulp horns, pulp stones and calcifications.  Note the curvatures of the roots.  Also note the proximity of structures such as the maxillary antrum, inferior alveolar canal and mental foramen.  Note impacted teeth and foreign bodies.

Study any existing root canal fillings and note the nature, quality and extent.

6.  The Diagnosis

At this point, all data (main complaint, history and examination) has been collected. It is now necessary to process this data with the aid of education, training, experience, logic, common sense and also …… the sixth sense. 

There is no substitute for clinical experience and common sense.  The subjective nature of history taking and interpretation, the unreliability of vitality testing and the two-dimensional obscurity of radiographs all combine to create a maze of diagnostic uncertainty.  In the end, the endodontist has to take the responsibility and make a diagnosis, based upon all the available evidence, however questionable it may be.

The key to endodontic diagnosis is multiplicity of signs and symptoms.  Ideally all diagnosis should be based on the presence of at least two or more definitive signs and symptoms.  Never condemn a pulp on the evidence of only one sign or symptom.  Always look for more.  When in doubt, wait, treat symptomatically and re-evaluate.

The most common endodontic diagnostic problem is that of the Reversible vs Irreversible pulpitis.  This is covered to some extent by the Baume classification.  A Class I and II pulp can be viewed as Reversible and a Class III and IV as irreversible. 

Obviously an irreversible pulpitis dictates removal, i.e. extraction or root canal treatment.

Diagnosis of Reversible Pulpitis

Main Complaint

The patient may complain of some sensitivity to cold food or drinks.  Alternatively, there may be no main complaint of pain or sensitivity.

Dental History

The patient may report a mild to moderate sensitivity to cold food.  When questioned the patient will confirm that the pain is of a short and sharp nature and that it resolves immediately.  There will be no indication of spontaneous pain or nocturnal episodes of pain.  The pain will be poorly localized.

Clinical examination

There will be no pus, swelling, fistulae or tenderness of the mucosa or periodontium.  The natural crown of the tooth may be sound, with or without a relatively small carious lesion, adequate or leaking restoration and will react to vitality testing as a Baume Class I or II.

Radiograph

There will be no peri-apical radiolucency.  The lamina dura will be intact.  The pulp chamber will not be invaded by carious lesions or violated by restorative procedures.

Diagnosis of Irreversible Pulpitis

Main Complaint

There may be no main complaint, in which ease the condition is discovered during the case of a routine examination.  Alternatively the patient may present with a mild, vague, moderate or severe toothache.

Dental History

A wide range of situations is possible.  The patient may report only vague toothache associated with a tooth, coming and going for years.  Alternatively, the patient may complain of severe and spontaneous toothache of a dull and throbbing nature.  Usually the pain will be localized to a certain tooth.  There may be some history of bite pain.  Sensitivity to warm or hot food or drink may be reported.  The patient may confirm that the pain lingers for a matter of minutes after stimulation.  The patient may also confirm that the pain had woken him or her at night.

Clinical examination

The peri-apical soft tissues may be tender to palpation.  Submandibular lymph glands may be palpable and tender.  There may be signs of fistulae or crevicular pus or a deep pocket may be probed.  The crown of the teeth may exhibit large restorations, with or withouth deficient margins, large carious lesions and will react to vitality testing as a Baume Class III or IV pulp.

Radiograph

Most commonly the apical lamina dura will be interrupted with or without a pronounced peri-apical radiolucency.  In the case of condensing osteïtis the peri-apical area will be a large, diffuse radio-opaque area.  The pulp chamber may be invaded by caries or a large restoration may be closely associated with it.  There may be signs of internal or external resorption.

Following the diagnosis of a reversible pulpitis it is necessary to expand the diagnosis to include the etiology, i.e. caries, leaking restoration.  This will dictate the treatment.

Following the diagnosis of an irreversible pulpitis the diagnosis should be expanded to describe the peri-radicular tissues, i.e. acute or chronic apical periodontitis, acute or chronic apical abscess.  This can only be done with a thorough knowledge of the pathology of these diseases. 

This is also true for all other diseases of the mouth.

THE MANAGEMENT OF ACUTE TOOTHACHE BY MEANS OF AN EMERGENCY ROOT CANAL TREATMENT

Most true dental emergencies, involving toothache, whether it is of a dentinal, pulpal, periodontal, occlusal or whatever nature, will be reported on an unscheduled basis.  The patient will appear on the doorstep of the surgery first thing in the morning or he or she will phone in, asking or demanding to be helped right away.  And quite rightly so.  The dentist is under a moral obligation to alleviate pain when he encounters it and he or she has to do it in a quick, painless and comfortable way for the patient.  In the majority of cases this is quite feasible, but because of the unscheduled nature of these visits the dentist will be under pressure to perform the necessary treatment in the shortest possible time.

It is beyond the scope of this chapter to discuss treatment modalities other than root canal treatments. However, it has to be said that dental pain has many causes and that this pain can be alleviated in ways appropriate to the diagnosis which will not necessarily involve root canal treatment.  This chapter will only deal with the technical procedures involved in relieving pain by doing a so-called emergency root canal treatment. The reader is referred to the chapter on diagnosis for a discussion of the subject of when the removal of the pulp is indicated and when not.

Once the decision has been made to open the pulpal chamber and to remove the pulp in order to alleviate the pain, then it is always preferable to go ahead and carry out the complete preparation and cleaning procedure from start to finish.  Once all the antigens have been removed, all signs and symptoms of endodontic pathology will disappear (Torabinejad and Walton, 1991, Trope, 1990, Tronstad, 1991, 1992).  It might take a few days, but it will disappear.   

So in practical terms all forms of toothache, caused by pulpal pathology, will almost instantaneously be resolved by the cleaning of the root canal (that means total removal of all contents). This also includes abscesses.  There is no scientific basis for the practice of leaving a canal open to "drain" for a day or two.  This is a very doubtful practice which should be strongly discouraged.  The emphasis must always be on the removal of bacteria and other antigens which is accomplished by thorough and efficient cleaning of the canals.  It might indeed be vitally important to supplement this cleaning process by the use of antibiotics - to take care of the extra canal infection, but the ultimate source of this infection will always be the intra canal reservoir of debris and micro-organisms.

In the case of an abscess which keeps on draining pus even after prolonged cleaning, the answer is to keep on cleaning, irrigating and drying the canal until the flow dissipates.  Eventually it just has to.  There will only be so much pus and not more.  It is possible that the canal will keep on draining a clear fluid (serum) or blood, because there is a virtual unlimited supply thereof.  These cases should be treated with a calcium hydroxide dressing and also be closed.  The technique of calcium hydroxide therapy is discussed separately.  No canal should ever be left open.

There is one major constraint, limiting the carrying out of a full and complete preparation and cleaning procedure in the first visit - TIME.  Very often these emergencies have to be treated in a matter of minutes, because that is all the time that is available.  Now, the delicate structure of the apex and the apical constricture can be destroyed forever within a matter of seconds.  Such a damaged apical constricture places severe limitations on the prognosis of a tooth.  A hurried emergency root canal treatment should never be carried out at the expense of the apical anatomy.

Emergency pulpotomy

Fortunately, most acutely inflamed pulps can be calmed without invading the root canals.  All that is necessary is to open the pulp, to excavate with a round bur the contents of the pulp chamber, to dress the exposed pulp stumps with a calcium hydroxide dressing, the placement of a cotton wool pellet and the sealing of the cavity with a temporary restoration.  All pulps which bleed upon instrumentation - a sign of some vitality - can be treated in this way within a matter of minutes.  

There is absolutely no need for any kind of medicated dressing such as Cresophene or Ledermix.  There is no scientific basis for the use of any of these materials other than calcium hydroxide (Watts and Paterson, 1988, Hasselgren and Reit, 1989).

When a pulp chamber is opened and there is very little or no bleeding present chances are excellent for the pulp to be necrotic and possibly infected.  Attempting to treat this kind of situation with pulpotomy therapy is courting disaster.  The only solution is to carry out a thorough and complete instrumentation and cleaning procedure.  The root canal has to be prepared, i.e. shaped and cleaned, completely.  There is no short cut.  The cleaned root canal is then filled with calcium hydroxide dressing.

Adjustment of occlusion

This is another endodontic controversy.  However in practice it is sometimes found that post-operative pain can be controlled by the adjustment of the occlusion, both in centric and eccentric positions.  All root canal treated teeth, especially molars,  should eventually be restored with a cast metal restoration.  Therefore, the removal of some occlusal enamel or restorative material is justified.  When adjusting, the process must be carried out until the tooth is totally free of occlusion.  This can be checked by asking the patient to close on a cellophane strip on the specific tooth and then tugging on the strip.  It should come out easily.  Should the strip be held back the tooth is still in occlusion and further adjustment is necessary.  Very often teeth under root canal treatment will exhibit premature contacts, something which could very possibly have been a contributing factor to the pulpal condition.  Such teeth will prove to be somewhat difficult to adjust occlusally because each adjustment will be only removing some of the premature contact, and the tooth would still be in contact.  Quite a significant amount of adjustment will have to be carried out.

Drugs and antibiotics

Common sense is needed when prescribing medication.  The practitioner should aim to prescribe as little as possible, but in the case of severe swelling, a rise in temperature, or a severe cellulitis, the prescription of an antibiotic is obligatory.

Pain is a physical as well as an emotional issue and patients should be assessed accordingly.  There is no rule.  Some patients will need a combination of centrally acting analgesics and anti-inflammatories while others will need milder medication.  Most often, pain can be controlled by simple aspirin or paracetamol containing medicines.

References

Hasselgren G & Reit C (1989). Emergency pulpotomy: Pain Relieving effect with and without the use of sedative dressings.  Journal of Endodontics; 15: 254-256

Torabinejad M & Walton RE (1991). Managing endodontic emergencies.  Journal of American Dental Association; 122: May 99-103

Tronstad L (1991). Endodontic emergency treatment.  In: Clinical Endodontics.  A Textbook.  Thieme, New York: 134-138

Tronstad L (1992). Recent development in endodontic research.  Scandinavian Journal of Dental Research; 100: 52-59

Trope M (1990). Relationship of intracanal medicaments to endodontic flare-ups.  Endodontology and Dental Traumatology;  6:  226-229

Watts A & Paterson RC (1988). The response of the mechanically exposed pulp to prednisolone and triamcinolone acetonide.  International Endodontic Journal; 21: 9-16

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