Developing a strategy for managing non-infective acute odontogenic pain in the primary care

setting.

Ian Kerr BDS

StoneRock Dental Care

Abstract

The management of acute dental pain in the primary care setting can be both challenging and highly

rewarding for both patient and dentist but is often completed under stressful time restricted

conditions with little prior warning of the appointment. For this reason the management of the pain

is often suboptimal in outcome which can lead to continued and unnecessary suffering for the

patient and dissatisfaction for the dentist. With a greater understanding of the cause and effect of

dental pain we can a gain insight in to the treatment strategies required to treat acute pain and can

develop ways to incorporate them into our busy daily schedules.

Clinical relevance

This article looks at the causes and effects of acute odontogenic pain and provides evidence based

tips on how to best manage patients presenting with irreversible pulpitis.

Objective statement

The reader should understand the importance of correct treatment of acute odontogenic pain and

gain insight into how to provide this in a busy primary care setting.

Pain; what it means to our patients

The definition of pain given in many articles is as “an unpleasant sensory and emotional experience

associated with actual or potential tissue damage or described in terms of such damage”. As a way

of conveying the full depth and breadth of the suffering that pain, either acute or chronic can bring

in to someone’s life this definition is akin to describing the Pacific Ocean as a “collection of lots of

drops of water”.

Dealing with an unscheduled patient suffering with acute pain can be the most stressful, difficult and

financially least rewarding appointment that we have to contend with in General Practice. It can also

be the professionallymost rewarding treatment we provide and is perhaps the most important thing

that we can ever do for that individual, frequently being the bench mark that we are judged on by

our patients.

With this in mind it is a terrible shame that the emergency visit is often squeezed in to a hopelessly

inadequate space by an exasperated receptionist who has not been given the training or tools to

adequately assess the level of dental emergency. It is this scheduling that is at the heart of what is a

frequently mismanaged dental visit that can so often result in suboptimal outcomes for the patients,

inappropriate prescription of unnecessary antibiotics and a stressed dentist running late for their

next three appointments.

Some of this approach to management of the patient in pain stems from the oft quoted, hopefully,

apocryphal 3 Ps- Penicillin, Paracetamol and Please leave (at least, I think that was what the third

one stood for). This approach, if ever true, was as uncaring as it was pharmacologically inept and has

long been replaced by Prof Hargreaves’s 3Ds approach of Diagnosis, Drugs and Definitive Treatment

which provides us with an excellent frame work within which we can manage our patients. However,

based on the principal that the world can never have too many three letter abbreviations, I would

like to propose the 3 Ts approach; namely Triage, Time and Treatment. In reality the 3Ts is just an

expansion of the 3Ds but by putting the accent on Triage we can empower our reception teams to

gain a far better clinical picture and so understand the appointment scheduling required (Time)

which will allow the patient to receive ideal Treatment (both pharmacological and physical) which

will lead to an optimal outcome.

The key to all successful care is correct diagnosis and for us to have a chance of getting this right it is

important that understand the cause of the pain our patients are suffering. As an addition to this if

we have an understanding of the significance of this pain and the potential long term implications if

it is left untreated we can also see how important getting this diagnosis right is.

Diagnosing Pain: Triage

At the heart of a correct diagnosis is clearly taken clinical history of the presenting complaint. Here is

it possible for the reception team and dentist to work in tandem to triage the case and, if

appropriate, begin treatment with pharmacological approach to offer appropriate relief and

maximise the chances of successful treatment at the time of the appointment. A well-developed

flow chart and in house training will allow the receptionist to gain most of the information needed

for a tentative differential diagnosis. The presenting complaint is best told in the patient’s own

words, remembering the adage “listen to the patient; they are telling you the diagnosis”. These

words can then be summarised into key points, below, that the dentist can review between

appointments to assist in the scheduling and managing of the appointment.

• Site pain

• Character- e.g. sharp, ache, throbbing

• Severity- scale of 1-10

• Does the pain radiate anywhere else

• Timing- was the onset sudden or gradual, how long has it been present, is it continuous or

intermittent, worse at any particular time of the day

• What makes the pain better or worse (including list of pain medication, doses and timings?)

• Is the patient aware of any preceding event, including previous similar episodes?

• Any associated symptoms e.g. bad taste. (1)

This information is very quick and easy to share with the dentist who can gain an idea of how urgent

the visit is and how much time should be allowed. Of particular importance is the list of pain

medication taken to date, as this can offer the dentist an indication of the true level of pain and can

alert the clinical team to any risk of inadvertent overdose. It will also allow the dentist to make a

judgement on what additional pain relief could be taken and can allow him/her to contact the

patient and make recommendations on what dose to take and when to maximise comfort at the

treatment visit. It is so common to hear patients say that they have not taken any pain medication

today as they did not want to mask the symptoms when they knew they were coming in! In reality

that is exactly what we want them to do as we want them with as little central sensitisation and as

few inflammatory markers present as possible if we are to have a chance of getting a “hot pulp”

numb.

Neurophysiology of the pulp and dental pain

The brilliant pain research scientist Clifford Woolfe uses the excellent analogy for pain, as follows: “If

pain were a fire alarm then nociception pain would be sensed only the presence of intense heat,

inflammatory pain would be felt with warm temperatures and pathological pain would be felt if

there was a fault with the fire alarm itself.

Nociceptive pain is an early warning physiological protective system that is concerned with sensing

noxious stimuli- a high threshold pain only activated in the presence of intense stimuli. It presents

itself as something that must be avoided now and overrules all other neural activity.

Inflammatory pain however is an adaptive and protective response. By heightening sensory

sensitivity after unavoidable tissue damage the pain assists in healing of the injured body part by

creating a situation that discourages physical contact and movement. The pain is caused by

activation of the immune system by tissue injury or infection.

Pathological pain is not protective but maladaptive resulting from abnormal functioning of the

nervous system. The symptoms from this pain are a result of a disease state of the nervous system

and is also a result of situations where there is no such damage or inflammation. (2)

In the case of acute odontogenic pain we are dealing primarily with inflammatory pain.

The 2 types of sensory nerve fibres in the pulp are myelinated A fibres (A Delta and A Beta) and

unmyelinated C fibres.90% of the A fibres are A Delta which are mainly located at the pulp dentine

border in the coronal portion of the pulp and concentrated in the pulp horns. The C fibres are

located in the core of the pulp or the pulp proper and extend in to the cell free zone beneath then

odontoblastic layer.

The “A delta fibres are faster than “C” fibres and transmit directly to the thalamus generating a fast

sharp pain that is easily localised. The “C” fibres are influenced by many modulating interneurons

before reaching the thalamus, resulting in a slow pain, which is characterized as dull and aching.

Thus a response to cold that comes and goes almost immediately in relation to the application of

cold is likely to be due to the more superficial “A” delta fibres and can be thought of as being an

indication of “dentine sensitivity” or “reversible pulpitis”. A response to cold that comes slowly and,

crucially, dissipates even more slowly represents “C” fibre or pulpal pain and is much more likely to

indicate an irreversible pulpitis.

Rapid temperature changes cause rapid fluid movement through the dentinal tubules which we feel

as a painful sensation even from a healthy pulp. (This stimulus is brought about by the sudden fluid

movement deforming the cell membranes of the free “A” delta nerve endings). Gradual temperature

changes do not illicit this response. The A delta fibres can be thought of as the ever excited yappy

little dogs of the nerve world, quick to respond to almost any stimulus but rarely causing much harm

whereas the “C” Fibres are the sleepy big dog in the basket that will take more to rouse but once

stimulated is likely to give a far more painful “bite”.

“C” fibre pain is often diffuse pain that can be felt from the chin to the ear and this reflects the fact

that nerve fibres innervate multiple teeth and pulps. “C” fibres exhibit lower excitability than “A”

fibres and so required a higher level of intensity of stimulus to be activated. Interestingly “C” fibres

can survive in the presence of hypoxia which may explain patients experiencing pain the root canal

of a seemingly necrotic pulp is being worked. Patients are not making it up; sometimes what we do

to them really does hurt even when it makes no sense.

When we relate what we know about the nerve fibres involved to the testing we carry out we can

see why pulp “vitality” testing is such a dark art. If we want to have the best idea of what state the

pulp is in we should carry out both thermal and electric pulp testing as this will give us a greater level

of specificity and sensitivity in our testing. Thermal testing relies on the inward and outward

expansion of fluid within the dentinal tubules whereas electric pulp testing relies on ionic transfer.

“A” delta fibres transmit quicker than “C” fibres, have a lower threshold of excitability and are

distributed superficially all of which makes them the nerve fibres that respond to electric pulp

testing. “C” fibre do not respond to EPTs as they require too great a current to overcome their

threshold of excitability.(7) Cold testing again works primarily on “A” delta fibres with the outward

movement of dentinal fluid caused by its contraction gives a greater response than the inward

movement of fluid brought about by heat application. Once there is pulpal inflammation, however,

the resulting lowering of the threshold of excitability of the “C” fibres means heat stimulus will cause

temporary vasodilation within the pulp resulting in increased intrapulpal pressure and intense pain.

The hydrodynamic forces involved in cold testing will often lessen with repeated cold testing making

this type of testing often refractory- the first application of cold gives the most meaningful test result

so don’t waste it. The “A” delta fibres are more susceptible to reduced pulpal blood flow and cannot

survive in anoxic conditions which means we may get negative pulp testing which accurately tells us

that the pulp is irreversibly damaged. As soon as we drill in to the tooth, however, we (the patient

and practitioner) will be quick to discover that the nerve is far from “dead” as the “C” fibres are

surviving the anoxic conditions very well.With this in mind I am always clear in my dialogue with the

patient at this point where we have negative test results and need to enter the tooth. I will tell them

that “the pulp is damaged beyond repair and we must carry out root canal treatment if we are to

restore the tooth but there may still be enough dying tissue left in the tooth to give a response

during treatment; we will still need to make you very numb before we start work”.

Once the injury to the pulp tissues has reached a threshold level the nociceptive fibres of the pulp

relay their message of dental woe up the chain via primary and secondary neurons ultimately

evoking tertiary neuron activation in the cortex and the entire pain matrix. It is worth remembering

that the trigeminal nerve is the largest sensory nerve in the body and accounts for 60% of the

sensory cortex! It protects the brain, breathing, sight, smell, taste and facial function; we are hard

wired to run from any threat to these so no wonder pain, suffering and anxiety in any patient with

toothache can be so high. Once the central nervous system (CNS) is activated there is a downward

neural response that causes nerve induced inflammation at the site of injury; it is this that causes the

bulk of the inflammatory response at the injured site.

Allodynia is defined as a reduction in the pain threshold to the point where non-noxious stimuli are

now perceived as painful. Hyperalgesia is defined as an increase in the magnitude of pain

perception, so that a previously painful stimulus is now perceived as having a larger magnitude of

perceived pain. (If we use sunburn as an analogy then we can see “allodynia” as the pain felt when

wearing a shirt (that is a reduced pain threshold) and hyperalgesia is represented by the increased

pain perception when someone slaps your back (that is an increased pain responsiveness). The

percussive test for a tooth is looking for mechanical allodynia associated with acute apical

periodontitis whilst the increase in response to a hot cup of coffee is an example of thermal

allodynia.

Inflammation in the pulp causes and processes

Bacterial invasion

As ever in dentistry bacteria are at the heart of what we treat and in cases of odontogenic pain it is a

question of bacteria accessing dentine and eventually pulp tissues that can lead to our patients

needing our urgent care. The bacteria can gain access via decay, fracture, leaking margins, deep

periodontal pockets, root surfaces unprotected by cementum, any way they can really but once they

are in the progression of the lesion and eventual pulpal inflammation is inevitable without

intervention. Biologically and developmentally, pulp and dentine function as a complex and may be

regarded as one tissue; both tissues are derived from the dental papilla and development of the two

tissues is closely related. The tissues of the pulpo-dentinal complex are richly endowed with

immunocompetent processes but if left unchecked then the bacteria invasion will defeat the

defences resulting in a progression of pulp disease from reversible pulpitis through to a necrotic pulp

and infected root canals. Once the bacterial metabolites and toxic products arising from the infected

root canal diffuse in to the periapical tissues they will evoke inflammatory disease e.g. apical

periodontitis and eventually apical infection and abscess formation.(3)

Dentine is very porous and once it is breached the tubules provide diffusion channels from the

surface to the pulp. The pulp’s initial response to any invasion by bacteria or their by-products is to

increase the outward flow of dentinal fluid. Dentinal tubule fluid in vital dentine resembles serum

with proteins such as albumin and immunoglobulin G (IgG). The components of this fluid can interact

directly with the bacteria or impede diffusion of noxious products and reduce permeability of

dentine. Bacterial invasion of the tubules acts to impede fluid flow and so promote disease

pathogenesis by allowing for an increased diffusion rate of toxic or noxious products towards the

pulp.

Whilst mutans strep may be the villain of the piece when it comes to early colonisation of the mouth

and erupting teeth and are certainly found in great abundance in primary lesions (along with

lactobacilli) these species are not found in any great significance in deeper, symptomatic cavities. In

superficial cavities it is the gram positive species that dominate but symptomatic pulps are heavily

correlated with the presence of gram negative facultative anaerobes whilst in infected canals the

obligate anaerobes dominate. The association between endotoxins and pulpal pain has been

researched and a strong correlation has been demonstrated (4).

Endotoxins are the lipopolysaccharide complex that constitute the cell wall component of gram

negative bacteria and can either be secreted in vesicles by growing organisms or released into the

environment after cell death. They are capable of initiating various biological responses such as

complement activation, fever induction, macrophage activation, cytotoxicity and bone resorption.

The pain our patients are in is an expression of the pulps inflammatory response to the presence of

endotoxins in the caries affected dentine closest to it. Further research has suggested that high

levels of gram negative bacteria such as the Prevotella and Fusobacterium spp in carious lesions may

be indicative of irreversible pulpal pathology (5)

Dental Pain is an expression of the Inflammatory” soup”

The inflammatory response in the pulp, as a response to the ever approaching bacterial invasion,

reflects the initiation of the tissue’s defence mechanism. The pain our patients feel from irreversible

pulpitis and AAP is induced by pulp tissue damage resulting in cell death and subsequent release of

their intracellular factors which initiate the various pathways (phospholipid and kinin) that

eventually result in mast cells releasing histamine with serotonin release following this. These

factors combined start the depolarisation of the local nociceptive fibres (“A” delta and “C”) giving

rise to the responses for cold (“A” delta) and heat (“C” fibres). As both are stimulated they induce

further pulpal inflammation by producing neuropeptides which when released inside the pulp

initiate dilation of the blood vessels which increases their permeability. This in turn leads to the

release of histamine which results in further neurogenic inflammation. The combination of the

mediators and prostaglandins is sometimes referred to as the “inflammatory soup” and is the start

of the pain cascade. (6)

Pre-treatment Anti-inflammatory medication: does it have a place?

Given that we are dealing with an inflammatory pain it would make sense that anti-inflammatory

pain medication has a place both before and after treatment. It is worth remembering that

numerous studies have shown that inferior dental nerve blocks (IDNB) in patients with pulpitis fail in

anywhere from 30-90% of cases. (Rosenberg 2002, Claffey et al 2004) This high incidence of failureis

most likely due to the highly sensitised nature of the dental pulp due in a large part to the presence

of cyclooxygenase (COX)which, as stated,is a key protagonist in dental inflammation. COX acts on

arachidonic to produce prostaglandins including PgE2 which has been shown to sensitise

transmembrane voltage-gated sodium channels in nociceptive neurons thus facilitating activation of

the pain stimulus, hyperalgesia and, ultimately, decreased anaesthesia. Further possible causes of

failure of IDNB have been suggested including the presence of increased levels of Nav 1.8 and Nav

1.9 subtypes of tetrodotoxin-resistant sodium channels in symptomatic pulps which are poorly

blocked by certain local anaesthetics, lidocaine being one of them. (Hargreaves and Keiser 2002,

Renton et al 2005).

Lidocaine may have one other problem when it comes to inflamed pulps as the acid pH of the

environment can result in a process known as “ion trapping” which reflects the formation of the acid

charged form of the lidocaine molecule which cannot pass through the cell membrane and so is

unable to block the sodium channels of the nociceptors. With this in mind some authors

(Hargreaves and Keiser 2002) have suggested the use of mepivacaine as an alternative to lidocaine

when numbing inflamed pulps because mepivacaine is less susceptible to ion trapping. Preop

ibuprofen and paracetamol may have limited benefit only because sensitization has already taken

place and NSAIDs cannot reduce the amount of Pg already present but may limit further production

One recent study, however, looked at the potential benefit of using preoperative (600mg) ibuprofen

in patients suffering with acute pain associated with irreversible pulpitis (7). In a randomised,

placebo controlled clinical trial the researches compared success rates for IDCBs using 2%

mepivacaine containing 1:100.00 adrenaline in patients given either a placebo or 600mg ibuprofen 1

hour before treatment. Their results showed a success rate of 72% for the test group versus 36% for

the control.

The clinical significance of this approach is clear but for it to have a chance the dentist and

receptionist need to be clear about what they are dealing with they can book an appropriate length

appointment and the patient can be advised (by the dentist after a clear and full review of the

medical history) what to take in terms of pain relief making the upcoming appointment better

planned and more likely to achieve an optimal result.

Scheduling the appointment: Time

It is never possible to know exactly how much time will be required for an unscheduled patient in

pain but if early indicators suggest that this is a patient with a high levels of pain in need of

treatment then a reasonable starting point is 45 minutes of clinical time. With this appointment

there should then be enough time for the clinician to go over medical history, review the presenting

complaint allowing time for the patient to recount it in their own words, take any necessary

radiographs and carry out any appropriate thermal or electric testing of the suspect tooth (along

with necessary control teeth), form a differential diagnosis, discuss this with the patient along with a

suggested treatment plan including all suitable alternatives, gain consent for treatment and then

actually carry out some dentistry.

It is beyond the scope of this article to go in to details of medical history taking but it is worth

remembering, whatever the patient’s medical health, that people who are in severe pain, have had

little or no sleep and who may have skipped most if not all meals over the acute pain episode and

will be far more vulnerable to fainting during treatment. With this in mind it is worth enquiring as to

when they last ate and slept and, if necessary, providing a glucose drink and or a banana before

commencing any treatment, a courtesy that patients are generally hugely appreciative of.

Getting the diagnosis right and doing the right thing: Treatment

If we are seeing someone with an episode of acute orofacial pain then the likelihood is that it will be

of dental origin. It has been reported that up to 85% of cases of pain patients presenting withacute

orofacial pain are suffering with dental pain and this pain will, most likely, be due to inflammation of

either the pulpal or periapical tissues. Working to the principal of “common things occur commonly,

but rare things do happen” we should work methodically through a check list of questions and test

to achieve our diagnosis but we should not be surprised if the diagnosis is that of irreversible pulpitis

or its evil step child acute periapical periodontitis but equally we cannot assume that and miss a

patient suffering with acute myofascial pain or a referred cardiac pain or an onset of neuropathic

pain all of which can easily mimic odontogenic pain.

There is almost certainly a universal law that states that the shorter the appointment time available

the more complex the diagnosis and treatment will be and there is no doubt that a patient clutching

the side of their face, reporting pain from “my back teeth, top and bottom” is a bit of heart sink

moment to even the hardiest of clinicians. That said we can take clues immediately from the fact

that the pain is diffuse as this is a good indicator that any odontogenic pain is likely to be pulpal in

origin as acute apical periodontitis is generally far more clearly defined with the patient able to point

to the offending tooth with great certainty. We can then work through the previous notes and

radiographs looking for large restorations, recent work, recent pain episodes, radiographic change to

pulp chambers anything that will help us narrow our search down. We can then carry out simple

thermal and vitality tests on the teeth (using the equivalent contralateral teeth as controls) to see

which tooth stands out.

The importance of this methodical approach is highlighted by the case below where confusion over

the site of the pain could easily have led to an inappropriate extraction and, no doubt, an irate

patient.

The patient presented in pain to a separate general dentist reporting a diffuse swelling on the lower

left side of the jaw. Reportedly the patient was prescribed a course of antibiotics with the option of

extraction of LL7 there and then, which they declined. Consequentlythey were instructed to return

when the swelling had reduced for extraction of lower left second molar (LL7).

Slide 1 Pre-operative radiograph

Interestingly when the patient returned the pain had localised to the buccal surface of the lower left

first molar (LL6) which the patient reported as being tender to pressure. At this point the author was

able to carry out pulp vitality testing and thermal testing both of which gave a negative response

from LL6 but positive from LL7. A test cavity performed without local anaesthetic in LL6 revealed a

necrotic pulp requiring root canal therapy and restoration. It was suspected at the time that LL6 was

a victim of high pulp horn communicating with the oral environment through an occlusal

wear/erosion facet although there is no way of proving this.

Slide 2 Test Cavity allowing access to necrotic pulp horn

Slide 3: Completed root canal filling with acknowledged cement overfill in distal root.

Shortcomings of testing “vitality”

A false positive response from LL6 could easily have led to a misdiagnosis and potentially

inappropriate care being carried out on LL7. As ever we must always interpret all test results with

caution.

Whenever thermal or electric pulp vitality testing is talked about it is deemed necessary to point out

that the tests are actually sensibility testsas they assess whether there is response to a stimulus

whereas “pulp vitality” implies blood supply, which thermal and electric tests do not confirm.

Although it has been shown that there is no correlation between the results of a pulp test and a

specific histopathological state of the pulp there is a reasonable correlation between a negative

result and a non- vital tooth.

What really matters in this type of testing however is whether one tooth stands out from the others

in its response (either excessive to cold or negative or deranged result to an Electric Pulp tester

(EPT). These tests can also work well as a baseline against which the teeth can be tested again in the

future to see which, if any have changed. Again the odd one out is the tooth of interest. Carefully

recording these results can pay huge dividends a few weeks down the line if a pain is lingering on

and a source has yet to be found

When it comes to cold testing there is often a need to reach for the extreme colds of Endo Ice and I

have heard it said by many speakers at many conferences or lectures that this is all they use when

cold testing. Call me a softy but I think this is rather heavy handed approach when we are potentially

dealing with someone with extreme thermal allodynia. A sensibility test is basically prodding a

suspected corpse with a stick and seeing if it grunts: I prefer to use a not so sharp stick first of all. I

tend to go with the ethyl chloride first suggesting we are at the “tomatoes out of the fridge” level of

cold and if this does not spark a response I reach for the Endo Ice and say we are at the “ice cream

out of the back of the freezer” cold so patients have an idea of what is coming next. If they jumped

with the Ethyl Chloride then my ceiling would have some new dents in it if it had gone in with the

Endo Ice first.

As previously stated a positive test to EPT and cold is suggestive that the “A” delta fibres in the pulp

chamber are responsive. Two key factors in pulp testing are the thickness of the enamel and dentine

and the number of nerve fibres in the underlying pulp. The highest concentration of these neural

elements (the Plexus of Rashcow)is in the pulp horn region with a progressive decrease in the

number of nerve fibres in the cervical and radicular areas being observed. Because it is principally

the fluid in the tubules that conducts electrical impulses from the pulp tester electrode to the pulp,

the shorter the distance between the electrode and the pulp, the lower the resistance to the flow of

current.Consequently EPTs are best positioned on the buccal or palatal surfaces of cusps, just below

the tip for the most prominent cusp. In teeth with calcified canals we may well see a negative result

to thermal testing but the EPT a positive result to EPT which, in the absence of visible apical

pathology can be helpful in making a diagnosis.(8)

The EPT is unreliable for testing immature permanent teeth, however, as full development of the

plexus of Rashkow does not occur until 5 years after tooth eruption (Johnsen 1985). In these teeth

testing with cold is a more reliable test (Fuss et al 1986).

Overall testing with cold and EPT is correct 80% of the time for a positive result and 98% for a

negative one. According to Seltzer 1963 a negative response to EPT was correct (total necrosis) 72%

time and correct for (partial necrosis) 25.7%. Consequently a negative response would indicate a

need for RCT 97.7% time.

Traumatised teeth will also typically give very misleading results to EPTs as will teeth undergoing

orthodontic movement, with the effects of this often being felt several months after the completion

of treatment.

Clearly multi rooted teeth are a law unto themselves as progressive necrosis of the pulp can leave us

with necrotic tissue adjacent to inflamed tissue that can give very varied test results and confusing

symptoms that can leave patients with little idea of what is going on with their tooth and very quick

to correct us if we claim that they have dead or even a dying tooth. My analogy at times like this is

that teeth “do not drop dead of a heart attack but tend to gradually fade more like a gradual loss of

vision or a dimming of a light; the tooth has crossed a threshold that means that the nerve cannot

heal itself but is still alive enough to give you pain and may remain so for some time if we do not

treat it”.

Getting the patient out of pain: The ultimate goal for any emergency appointment

Once we have completed an exhaustive medical and dental/pain history Including an assessment of

the muscles of mastication, temporomandibular joints, taken appropriate radiographs of teeth in the

affected area and completed thermal and electric pulp testing of suspect and control teeth then we

may be closer to a diagnosis, or at least should be able to tell if we have a pain of odontogenic or

non-odontogenic. It is beyond the scope of this article and the intellect of the author to give an

exhaustive list of all causes of non-odontogenic pain but we clearly need to be aware that not all

oro-facial pain is dental in origin.

For the rest of this article we will look primarily at the treatment of irreversible pulpitis as this is so

commonly misdiagnosed or mishandled but will touch upon the deeply unpleasant Acute Apical

Periodontitis (AAP) as well. Again it is beyond the scope of this article to review the management of

Acute Apical Abscess in all but the briefest of detail.

Irreverisble pulpitis (IP) and Acute Apical Periodontitis (AAP); antibiotics are not the answer

Once we have decided that we are dealing with an odontogenic pain we then need to decide which

tooth is to blame and what is wrong with it. As stated before a diffuse, often continuous or

spontaneous pain that can be stimulated by thermal stimulus (usually heat more than cold,

especially in the later stages, although in some cases some patients will feel relief from cold water

applied to the tooth) will represent a tooth with an irreversible pulpitis and the treatment should be

obvious, although finding the offending tooth is often far less so as at this stage no tooth will be

tender. Sadly we see antibiotic use repeatedly in General Dental Practice for patients who have

every one of the signs of irreversible pulpitis.

In cases of moderate to severe pain where no single tooth can be identified as being at fault the

appropriate prescription is one of anti-inflammatory medication and a review every 24 hours or so

depending on pain levels until the guilty culprit reveals itself. The only alternative is a “best guess”

approach that needs to be undertaken with a very clear explanation to the patient that the wrong

tooth may be treated which will result in continued pain and additional future work. In the authors

experience most patients go for the anti-inflammatory medication which is just as well as I am not

sure there are enough trees left on the planet to cover the debate over consent to treatment in

these circumstances. .

Once we have a vital (responsive) tooth that is tender to pressure it is clear which tooth is to blame

but, so it would seem, the treatment becomes less clear as many, many patients suffering with what

is acute apical periodontitis AAP, a non-infective condition, will receive antibiotics as their sole

treatment. Research has shown that 75% of cases presenting with AAP receive antibiotics (9) which

is an inexcusable and damning state of affairs in dentistry. It is as illuminating as it is sad to read

articles form over 30 years ago, quoting literature from almost 50 years ago, that tells us we should

not give antibiotics for these cases.

The use of antibiotics in the management of dental pain remains so wide spread as to remain almost

the norm in general practice despite almost every piece of research and review literature telling us

for decades not to do this. The medical profession is under enormous pressure to curb antibiotic

prescriptions and we, as dentists, must be brought under the same pressure. The advice on when to

prescribe antibiotics for dental patients has been made clear by numerous leading voices, for

example SCDEP and are listed below-

• Pyrexia (oral temperature >37C

• Lymphadenopathy

• Severe local Swelling

• Dysphagia

• Rigors

A spreading cellulitis is of concern and when involving multiple fascial spaces can become a surgical

emergency; referral to a maxillofacial department for management can be considered to be

mandatory for severe cases. (10)

But these are the rare cases; not our everyday normal toothache. We need to be honest as a

profession and particularly as hard working General Dental Practitioners and question how many

times do we see patients meeting the above criteria and then compare this to how many times we,

as a profession, prescribe antibiotics. I am certain that, more than anything, the time (the second of

my 3Ts) available at the emergency dental appointment is the single most important factor in our

prescription pattern for antibiotics.

Acute Apical Periodontitis (AAP) is due to pulpal inflammation spreading in to the apical periodontal

tissues. At its heart it is a ligamentous symptom and can arise from teeth that still respond as being

“vital” or in teeth that contain a necrotic pulp and consequently give a negative response to testing.

It is worth remembering that pulpal necrosis on its own rarely presents as an emergency however

where there is adjacent acute inflammation of adjacent pulp tissue then the tooth can give the

clinical impression of toothache from a vital tooth. The inflammatory process and the build-up of

inflammatory exudate in the periodontal tissues can exude the tooth from its socket giving rise to a

degree of mobility and increased pain on biting (an example of hyperalgesia). The radiographic

picture will reflect the degree of inflammation so may vary from a normal image to a widening of the

periodontal membrane space around the affected root.

No two tooth aches are ever the same; The Central Aspect and Personality of Dental Pain

Central Aspect

Each individual patients’ pain experience is dependent on, amongst other things their age, gender,

ethnicity, culture, personality, stress, depression and anxiety; only they can feel their pain and will

often struggle to accurately articulate it. (11) Sadly even as professionals used to dealing with

patients in pain we are all very poor at gauging other people’s pain as the only way we have of doing

it is through what is known as “pattern matching” which is based on verbal and body language to

match our own experiences which is a very poor system with a high level of bias.

If I have made it through life with no significant pain event, or have been brought up believing that

obvious expressions of pain are just attempts at attention seeking then my bias is going to make me

underplay the extent of my patients pain and make me think that they are making a fuss over

nothing when they tell me that it still hurts after I have given them a cartridge or two of local

anaesthetic. A more useful word than “pain” at times like this is “suffering” which brings in the more

emotional side of pain and allows us to see things not on a purely neuroscience footing but on a

global picture of the patients life journey to this point and their ability to cope with pain and the

severity of pain that this particular episode of tooth ache is giving them right now. It is common for

neuroscientists to refer to the pain matrix as to date no single “pain centre” has been identified to

account for chronic pain, at least.

Once the afferent information has reached the somatosensory cortex and the pain arising from the

affected tooth has been “recognised” then we have crossed from peripheral “nociception (tissue

damage and subsequent neural induced inflammation) in to “sensation”. The somatosensory cortex

regulates our experience of all physical sensations and processes most of the conscious signals that

we are aware of feeling. After “ sensation” will come “behaviour” which will depend on many

factors as listed above and finally will come “suffering” which will also depend on many factors but

will reflect the patient’s life journey with factors such as previous pain episodes, chronic pain,

tendency towards anger, catastrophic thinking, presence of a carer or significant other etc.

It is wrong, therefore to think of the pain pathway from the pulp to the brain being like a telephone

wire simply firing a one way message that elicits a single response. Instead there is a complex

interaction of “up and down” modulation and higher level perception that will determine the state

our pain patient is in and how responsive they are likely to be to our attentions.

Personality of Pain

Our world view, or how we perceive the world around us, is unique to each and every one of us and

alters through life as we build on life experiences. Rather than trying to assimilate every single “bit”

of sensory data that we are hit with we rather see the world through a series of filters- “Delete”,

“Distort” and “Generalise”. The “Delete” filter allows us to skim over masses of background data

that we do not need to know or notice all the time. The more anxious our patients become the more

they will use the “Delete” filter; most of what we are telling them is just not registering. Patients

who are anxious and in pain have one overriding aim- to get out of pain and out of the surgery – long

winded discussions about extensive treatment plans have not part to play in any of this visit. Our

patients at this time need our expertise to diagnose the problem and, if possible, resolve it for them;

they need enough information to be able to consent to care that is appropriate to them and need

and no more.

The “Distort” filter relies upon, amongst other things, memories, previous decisions, attitudes,

values and beliefs. These will build up over a life time and reinforce our world view which we, of

course, believe to be true. If a patient’s perception is that dentistry hurts then it is very likely that it

will hurt for them. A patient’s internal representation which is based on the data they have left after

their filters have removed all the unwanted detail influences their physiological state which in turn

affects their behaviour which gives lead to the patient’s outcome or reaction. As dentists we need to

recognise certain personality types and try and reflect this in our approach.

Highly kinaesthetic individuals are highly sensitive to touch and will be guided by how they feel

internally. Typically they will be hypersensitive to pain and very sensitive to changes in occlusion and

rough restorations and tend not to handle change well in general; they will be all about how it feels.

More Visually powered individuals will often be easily visually distracted and will definitely not want

to see any sight of the needle but will love to see what we have done at the end.

Those patients who favour auditory tonal and auditory digital processes, however, will be much

more interested in the information that they hear and will tend to process the information in steps.

The tonal ones can be very disturbed by the noise of the drill which for a nervous patient in pain can

become the trigger that elicits a whole cascade of behavioural responses. Auditory digital people can

appear aloof or rude as they will tend to have most of their conversations internally. They will tend

to give very poor or limited complaint history and underplay the symptoms. They are very unlikely to

link the pain or suffering (if chronic) with other life events.

Consent: even trickier than usual.

A dental emergency visit to relieve pain, no matter how severe, does not really fulfil the “Webster”

definition of an emergency, even if the patient will certainly see it as one. It is worth remembering

that, on average, patients will have had pain for 3-5 days prior to presenting for treatment for acute

odontogenic pain (12) which means that we could even struggle to refer to them as “urgencies” but

again the patient certainly will. It should go without saying that the standard of care that our

patients expect and deserve and that we are professionally bound to deliver is not in any way

compromised on the basis of “it was just a quick appointment” or “I didn’t have time for….” As the

patients recall of the appointment is likely to be severely compromised it is essential that clear,

extemporaneous notes detailing all tests carried out, radiographs reported on and discussions

conducted are more important than ever. Most of all we must be able to show that we clearly acted

in the patient’s best interest and carried out the least invasive procedure appropriate to the

conditions to relieve the patient of their symptoms.

Treatment

Once we have taken and exhaustive history of the current complaint, previous dental treatment and

medical health; once we have made a tentative diagnosis supported by appropriate tests and

radiographs (at least one confirming, reproducible test that corroborates radiographic or clinical

evidence of pathology is necessary to make a diagnosis of odontogenic pain, rather than non-

odontogenic).; once we have discussed our findings with the patient being mindful of their current

state and underlying psychological type and once we have gained consent to proceed on a basis of

treatment for the pain we should probably do some treatment! (You can see why the second “T” in

our 3Ts is so important).

Irreversible pulpitis

Here with have the famous “hot pulp” presenting with thermally sensitive toothache and

spontaneous often diffuse pain which can be difficult to localise even to one jaw let alone one tooth.

Typically there is no tenderness to palpation or percussion or chewing and little of note will be seen

apically on radiographs. This is the biggest challenge dentally for us as not only do we need to treat

the tooth but we need to identify it first. This information needs to be flagged up at the triage stage

and the appointment scheduled at such a time as to allow for the additional work required in

identifying and anaesthetising a tooth that will be resistant to both! Again the triage stage can assist

by encouraging appropriate use of anti-inflammatory medication before the appointment to

enhance pain relief and potentially assist in anaesthesia. The triage stage will also alert us to the

possibility of an inadvertent overdoes of anti-inflammatory medication and early identification of

this can have significant benefits in patient safety. Paracetamol induced hepatotoxicity remains a

major cause of acute liver failure (ALF) with 18% of cases of ALF in Scotland related to unintentional

paracetamol overdose. (13) The recommended maximum dose of paracetamol for a healthy adult is

4g (8 500mg tablets) but toxicity can be caused with as little as 10g taken in a 24 hour period. When

you consider that there are 45 over the counter medications containing paracetamol it is easy to see

how confusion and desperation can give way to an inadvertent overdose and we as clinicians need

to be able to spot it from a carefully taken pain history. Paracetamol overdose can present with a

range of symptoms from nausea and vomiting to malaise, fulminant liver failure and even death

although it is worth noting that none of the symptoms will present in the first 24 hours. A maximum

dose for ibuprofen for a healthy adult is set at 3.2g within 24 hours with doses in excess of this likely

to present as GI upset and possible somnolence. Patients taking anticoagulant medication as well

will be at increased risk of a bleed given ibuprofens inhibitory effect on thromboxane A2 which

encourages platelet aggregation. That said Ibuprofen 600 mg given four times per day has been

shown to be, statistically significantly, the most preferred analgesic prescribed for patients,

irrespective of their perceived level of pain, endodontic diagnosis, or treatment rendered.(14)

Local anaesthetic solutions and techniques for a “hot pulp” in a lower molar.

If the dental gods are smiling on us then the guilty tooth will be an upper tooth or a lower premolar

or incisor all of which can be managed with buccal and lingual infiltrations of local anaesthetic with a

high degree of efficacy. If the gods are not smiling then the offending tooth with the “hot pulp” will

be a lower molar which, of course, represents the greatest challenge in local anaesthesia. Multiple

studies have shown that failure rates for inferior dental nerve block (IDNB) in patients with

irreversible pulpitis have been reported to be between 44 and 81% (15) although fortunately

multiple studies have shown that a supplemental buccal infiltration of articaine 4% with epinephrine

1:100,000 (Septanest Gold) can significantly lower this. It is probably worth remembering at this

point that soft tissue numbness (which relates to “A” delta fibre anaesthesia) is not well correlated

to pulpal anaesthesia (which is “C” fibre moderated). So, again, patients aren’t making it up when

they say they can still feel it even though their lip is hanging down over their chin.

Interestingly studies by Meechan in 2006 looking at a combined buccal and lingual approach for

infiltration of articaine to assist IDBN found no benefit from the additional lingual infiltration in

molars despite its proven benefit in lower incisors. One study looked at buccal infiltration (BI) with

4% articaine versus an IDNB with 2% lidocaine in a randomized trial looking at efficacy of anaesthesia

for irreversible pulpitis in lower molars and found that although neither technique was 100%

effective BI supplemented with intra-ligamental injection (also of 4% articaine), if necessary, gave

greater anaesthetic benefit than a single IDBN with lidocaine (16) The conclusion from this relatively

small study (50 patients in total) was that our first choice of anaesthetic should be the BI with

additional intraligamental if needed as this technique was more effective, less painful and carried no

risk of nerve damage to the inferior dental nerve. Intra-osseous injections are often mentioned

when discussing a lower molar “hot pulp” and a very simple approach to this can be carried out by

giving a supracrestal injection through the papilla where the cortical plate is very thin allowing easier

infiltration. Often careful probing will allow identification of small bony canaliculus where it is

possible to insert a fine (30/31g) needle directly in to the cancellous bone. It is always worth warning

the patient of possible palpitations when giving adrenaline containing anaesthetics in this manner

(Thayer 2015).

Given the obvious benefits of BI injections and the poor rate of return and increased risks of nerve

damage for a standard IDNB it is surprising that the use of this standard block is as dominant as it is

in dentistry. The alternative of the Gow Gates technique is often suggested as a supplemental

approach if the standard approach has not worked. In the authors opinion, having treated thousands

of lower molars the Gow Gate approach is the injection of choice if at all possible.

The technique was developed by Dr George Gow-Gates in the 1970s and has been extensively

described in the literature (17). It is reported to have lower failure rates and lower incidence of

positive aspiration when compared to conventional IDNBs. When delivered correctly it anesthetizes

the auriculotemporal, inferior alveolar, buccal, mental, incisive, mylohyoid and lingual nerves

meaning that it will anaesthetise the mandibular teeth up to the midline, and associated buccal and

lingual hard and soft tissue. The target site is the neck of the condyle just below the insertion of

lateral pterygoid. As can be seen from the slide (1) this area can be visualised by placing the middle

finger of the supporting hand in to the intertragic notch and aiming the needle just distal to the

maxillary second at the height of its mesio-palatal cusp on a straight line through the tissue straight

at the tip of the middle finger, whilst the patient remains open wide..

Slide 1 external marker for Gow Gate “aiming point”

Slide 2 Intra-oral aiming point for Gow Gates injection

Slide 3 anatomical representation of internal target for deposition of local

anaesthetic solution

The Gow-Gates technique allows the anaesthetic solution to be delivered to an area much less

vascularised than that of the usual injection site for IDNB meaning that not only is the likelihood of

an intra-vascular injection much lower but the anaesthetic is less readily absorbed in to the adjacent

blood vessels ensuring longer periods of anaesthetic without the need for vasoconstrictors. In the

authors experience mepivacaine 3% plain provides ample anaesthesia for not only emergency visits

but for far lengthier root canal treatment visits as well. The positioning of the needle and the

journey to the target site in this technique means that far less muscle tissue is traversed making the

injection far less uncomfortable than conventional IDNBs. Because it anaesthetises the nerve block

before it splits it means we can, in effect deliver three separate injections in one.

The technique does have its draw backs however as it can be used only on patients who can open

wide enough to bring the condylar head out of the glenoid fossa and down the articular eminence so

the target site is exposed. Visualisation of the target site is harder in the absence of upper molar

teeth and patients can find the minute or so it takes to deliver the injection a lengthy time to have

the mouth wide open.

Once we have the tooth numb enough to begin it is often the case that once we hit that hyperaemic

pulp they begin to jump again. At this point the only option left to us is the intrapulpal injection and

here it is all about pressure; we need the needle to be tight in to the pulpal anatomy and we need to

feel resistance as we inject. The choice of anaesthetic solution is largely irrelevant but a cotton wool

pellet soaked in anaesthetic gel and squeezed in to the cavity can sometimes make the injection a

little less unpleasant. Most of all though a calm manner and a reassuring word that the toothache

will be gone at the end of this is what gets patients through this stage.

Anaesthetic stages for a “hot pulp” lower molar

Listed below is my preferred anaesthetic protocol for management of a lower molars with

irreversible pulpitis

• Anaesthetic gel 3 minutes minimum

• Stage 1 BI of articaine 4% with 1:100,000 adrenaline 5 second administration of loading dose

• Second stage 1-2 minutes later full cartridge with final 10% delivered supracrestal through

the papilla, looking for intense blanching of tissues

• Test level of anaesthesia with Endo Ice –if no response proceed with treatment

• If response then use Mepivicaine plain 3% in Gow Gate technique for mandibular nerve

block

• Retest with Endo Ice – if no response proceed with treatment

• If response still then Intraligamental injection using “The Wand” using ½ cartridge at least

• Intrapulpal administered if needed

Total time for full anaesthesia if all stages needed 10-15minutes, on average.

The great news about a hot pulp is, of course, that once we get to it and extirpate it we know that

patient’s pain episode is over and a relatively simple root canal filling appointment can follow to

complete the work with high predictability of success. The same may not be said of the other

common state that we see in emergency dental pain; acute apical periodontitis (AAP). Here the

tooth may be easy to identify and can be relatively simple to anaesthetise the relief of pain is much

less predictable and the risk of after pain much greater.

Acute Apical Periodontitis

The sinking feeling we get when opening a tooth at an emergency visit only to find dry empty canals

with no sign of haemorrhage or suppuration reflects the fact the we know the pain is due to AAP and

is likely to be much less responsive to a simple “open and dress”. Also we know that the biggest

predictor for post-operative pain following endodontics is before pain, when relating to non-vital

teeth (18) which means that the patient may be in for prolonged pain, possibly resulting in chronic

pain if we cannot resolve the acute phase quickly.

The management of AAP poses a degree of controversy with conflicting advice as to whether to

enter the canals or not at an emergency visit.Because AAP is due to pulpal death the recommended

treatment is relief of the inflammatory pressures in the periapical area. This is usually accomplished

via access through the tooth and extirpation of the necrotic pulp (i.e. pulpectomy) (19) Literature

dating from thirty or more years ago certainly favours complete pulp extirpation and root canal

preparation if at all possible whilst the modern message seems to be “if you don’t have time to

prepare the canals thoroughly don’t enter the canals at all”. Interestingly the systematic review

quoted on this subject shows that there is only weak evidence to suggest beneficial pain relief via

the use of cortico-steroid pastes in cases of AAP. Whilst we can hope to decompress the tissues by

the physical act of opening up the coronal canal structure and we can disinfect the coronal tissues

well with sodium hypochlorite, it still seems reasonable that “if chemo-mechanical preparation of

the pulp canal system is of primary importance in the treatment of pulpal disease, then it should be

performed as soon as possible in any emergency”. (Walker 1984)

Pharmacological relief of dental pain following treatment

Whilst a successful pulpectomy in the case of a “hot Pulp” usually spells the end of the patient’s

pain, patients with AAP may still have two or three days more pain before symptoms resolve. In

these cases anti-inflammatory pain killers are the medication of choice. Prof Ken Hargreaves has

written extensively on this topic and has provided perhaps the “instruction manual” on to how best

manage these patients, pharmacologically. His excellent summary article from 2005 (20) details

clearly the prescription pathway to follow but by way of a very brief summary, almost all toothaches

can be managed with ibuprofen and paracetamol so long as the patient can tolerate these drugs. Gel

caps are more rapidly absorbed giving an analgesic affect after 25- 30 minutes. 1000mg paracetamol

+ 600mg ibuprofen has been shown to dramatically improve post op pain above and beyond what is

achieved with 600mg ibuprofen on its own. For patients who cannot tolerate ibuprofen then

1000mg paracetamol combined with 60mg codeine (prescribed as 500/30 tablets) has been shown

to give comparable pain relief to 1000mg paracetamol and 600mg ibuprofen. An additional supply of

information on this topic comes from the Oxford Pain Group League table of analgesic efficacy (EBD

2004:5.1)

Some authors favour the use of corticosteroids for inflammatory pain management but the need to

be used with caution with ulcerative colitis, diverticulitis, diabetes, TB gastric ulceration and acute

psychosis as they can cause mild psychological disturbances such as euphoria, insomnia and

nervousness but can also, rarely cause bipolar and schizophrenic psychosis. Their ability to suppress

the immune system they should be avoided in cases where the considered risk of infection

developing is high. That said dexamethasone is 25 times more potent an anti-inflammatory agent

than cortisol (only glucocorticoids inhibit immune and inflammatory responses) and a single high

dose is virtually without harmful effects and a short course (

As we have alluded to in this article the presence of pain increases the probability of further pain

developing due to complex neural pathways and the release of various neuropeptides. With this in

mind it is easier and better for the patient to prevent pain rather than to allow it to develop and

they try and control it. Thus prescriptions should be written rather with specific times and doses for

the patient to take the medication- “by the clock not by the ache”.

Summary

Dental pain can be excruciating, debilitating and render the patient unable to function properly. Our

swift and skilful intervention can not only end this awful episode for the patient but can reduce the

risk of further, chronic pain developing. As long as we follow the approach of the “3Ds” or the “3Ts”

and never that of the “3Ps” we can provide an invaluable service for our patients, albeit at the

expense of our lunchtimes or early finishes.

References

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carious dentine by culture and real time PCR: association of anaerobes with histopathological

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