Atypical Odontalgia: Unmasking the Phantom

Atypical Odontalgia:

Unmasking the Phantom Peter Foreman DDS Consultant, Pain Management Q E Hospital, Rotorua NZ

Disclosure

Nothing to Disclose

Learning Objectives  Recognize that the apparent site of the pains may not be (or are no longer) the source of the pain, based on an understanding of what we now understand about pain mechanisms  Recognize that sensitization of nociceptors within and around the dental pulp and surrounding areas may lead to CNS changes and the development of central sensitization  Describe how management depends on accurate diagnosis which is critical to avoid treatments which may not only be doomed to failure, but lead to further interventions and increasing pain

Atypical Odontalgia (AO)  Some dental patients develop severe neuropathic pain after endodontia, exodontia, oral surgery and implants  Formerly called “atypical facial pain” (or “phantom tooth pain”) if it occurs in edentulous areas  Both have similarities with phantom limb pain  Both can present difficult diagnostic and treatment challenges

Atypical Odontalgia (AO) [cont’d] History and Symptoms – Mostly pain in teeth, gingiva, or extraction site. Maxillary molar and premolar areas involved more than mandibular.

– Location may change to other teeth or edentulous areas, or face, neck or shoulder (secondary hyperalgesia) – Usually continuous or spontaneous dull ache, but may also be described as burning, sharp, throbbing – May persist for months or years, of varying intensity – Sleep usually undisturbed, worse on awakening

Atypical Odontalgia (AO) [cont’d] History and Symptoms –Other symptoms: headache, hyperesthesia, allodynia.

Sensitive to temperature change, palpation, percussion –History of dental Tx common: endo, extraction, surgery –Numerous clinicians consulted without relief –No clear local, pathological or radiographic signs –If local anesthesia is ineffective it may indicate a central source of pain

Atypical Odontalgia (AO) [cont’d] Predisposing factors –More females than males (2:1) –Age 40 plus - endocrine factors?

–History of similar problems elsewhere?

–Toothache prior to treatment (central sensitization?)

–Is anxiety a factor? (delayed treatment)

Atypical Odontalgia (AO) [cont’d] Other predisposing factors – “There is evidence of a genetic predisposition to deafferentation pain” Devor et al, PAIN, 1990 “Vulnerable people may be at risk every time endodontic treatment is performed. Genetic predisposition could explain the increasing number of patients who undergo extensive, unsuccessful endodontic treatment” Marbach, JADA, 1996

Atypical Odontalgia (AO) [cont’d] “Phantom bite syndrome” –Symptoms include pain, discomfort, paresthesia –Bite “feels wrong” or “lost” –Onset may occur during extensive restorative, prosthetic or surgical treatments –Sometimes wrongly viewed as a psychiatric disorder

Atypical Odontalgia (AO) [cont’d] Effects of AO and “phantom pain” – Patients with unrelenting pain often visit numerous dentists, dental and medical specialists, and others in search of relief – Many undergo multiple extractions and/or irreversible and often harmful procedures, yet they still have pain – There may be a “silent majority” of patients who continue to suffer pain after endodontia, but do not seek further help for fear of more pain and treatment costs Clark, 2006 Turp et al 1998 Wirz et al 2005, 2010

Clinicians Visited Prior To Diagnosis of AO

(of 64 patients with AO seen at USC OFP Clinic) Ram, Antonia, Teruel, Satish, Kumar and Clark. Clinical characteristics and diagnosis of atypical odontalgia: implications for dentists J Am Dent Assoc 2009;140;223-

Atypical Odontalgia (AO)  Patients don’t always return if treatment is unsuccessful – instead, they may decide to have painful teeth extracted – this can worsen the situation in susceptible individuals – their pain often increases when more teeth are extracted

Nicolodi and Sicuteri, 1993.

 Both extraction and endodontia involve deafferentation *  In some, this may lead to changes in the trigeminal system which result in further pain

Aetiology of Atypical Odontalgia (AO) [cont’d]  Some still believe it is not known why patients develop AO  However, neuroplastic changes in the CNS seems a likely cause of persistent neuropathic dental pain, as elsewhere  Complex second order neuron activity may mean the original pain site is no longer

the main pain source

– In other words, has peripheral sensitization led to central sensitization?

Woolff CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature.1983

 Where this occurs, further intervention at the original pain site may be futile, and in fact may create more problems

The Challenge for the Endodontist

Is the pain in the tooth or in the brain?

Staying out of trouble‌

Someone Who Didn’t Stay Out Of Trouble…

Case History Patient History – 42 yrs old female, 5 year Hx. constant, aching orofacial pain.

– diagnosed with “atypical facial pain”

 Past Treatment – repeated root canal treatments (32), plus 3 extractions – still has original pain, and now, severe neuropathic pain

 Pain Clinic Diagnosis

Pain Clinic Diagnosis (cont’d) – significant psychosocial history, parafunctional habits

Management Plan – treat active TrPs (?original source of pain) – medications, psychotherapy, pain management program.

Result: less pain, but remaining neuralgia from

– referred pain from myofascial TrPs in muscles of mastication, sternocleidomastoid, trapezius and multiple RCT’s cervical muscles present.

– neuropathic complications from multiple endodontic Tx?

The Sequel

How could these problems have been avoided?

Richard Kroening MD, PhD, Director, Pain Management Center UCLA School of Medicine

No Diagnosis = No Prognosis

Beware of rushed diagnosis with chronic pain patients “primum non nocere�

first do no harm

Hippocrates

Referred Pain Can Masquerade As Dental Pain If there are no clear signs indicating a dental origin for the pain, why do so many dentists stubbornly continue to search for one, and then carry out multiple and often harmful procedures in a futile attempt to impose a dental solution on a non-dental problem?

David Hay, Head of Oral Health Unit, Green Lane Hospital NZ

Auckland Hospital Pain Clinic Auckland Medical School Dept. Psychiatry and Behav. Sciences (Communication Skills Programme)

U. Washington, Seattle

QE Hospital

Rotorua

AO Frequency and Risk Factors  3-6% incidence of neuropathy after endodontia

Marbach et al 1992, 1993, 1996

 3.4% to 5.5% incidence (confirms Marbach’s results)

Nixdorf et al meta-analysis 2010

 London’s Eastman Institute: much higher 12% prevalence of pain after endodontic treatment  More females, increased incidence after 40+

Polycarpou et al 2005

Nixdorf et al 2010; Riley and Gregg 2001

AO Frequency and Risk Factors (cont’d)  Pain after endodontia affects more than 125,000 individuals in the USA alone Marbach et al 1996

 Non-odontogenic pain is common after root canal therapy. May be over half of all cases Nixdorf et al 2010

 Further treatment of root filled teeth does not always resolve pain, and might exacerbate it  These are worrying statistics

AO Frequency and Risk Factors (cont’d)  Exodontia, third molar surgery, and dental implants can cause injury which can lead to neuropathic pain in susceptible patients  Implant placement in posterior mandible may result in 5-15% of postoperative problems, with permanent neuropathy occurring in approximately 8% of cases  “Nerve lateralization” - greater risk due to perineural damage and ischemic stretching. Neuropathy from implant compression and drill punctures may result in neuroma formation  In some, central pain sensitization may occur

Gregg 2000, Milam 1997

AO Frequency and Risk Factors (cont’d)  Noted few dentists and maxillofacial surgeons consult with colleagues from other disciplines such as pain clinic specialists and neurologists  “Current management of persistent orofacial pain ignores established principles of multimodal and interdisciplinary pain therapy, despite publication in numerous medical guidelines”  “To the contrary, 69.7% rated the efficacy of their procedures highly, despite ongoing patient problems”  Another worrying statistic (or an indictment?)

Wirz et al 2005

AO Frequency and Risk Factors (cont’d) Up to 1/3 of patients attending the Orofacial Pain Clinic at University of Southern California School of Dentistry had seen multiple dentists and undergone multiple irreversible procedures, yet still suffered from pain “Oral surgeons and endodontists are more likely to see persistent pain patients due to referrals. Caution is wise if the pain history is long standing. It is a warning that diagnosis and management may prove difficult�

Clark (2006)

AO Frequency and Risk Factors (cont’d) Numerous patients seen at the Auckland Regional Pain Service had visited many health professionals in search of relief without success. Some ended up much worse Foreman 1985-2002

Accurate diagnosis is the first requirement. It is critical to success.

The warning “No diagnosis, No prognosis” must always be the rule when dealing with persistent pain Kroening, RJ, Director UCLA Pain Management Center, Los Angeles

AO Frequency and Risk Factors (cont’d)  Predisposing factors?

– More females than males (2:1) – Age 40 plus - endocrine factors?

– History of similar problems elsewhere in body?

– Toothache prior to treatment ?

– Is delayed treatment due to fear a factor?

The Physician’s Dilemma: How to Treat Persistent Pain?

Chronic pain is poorly taught in medical schools

The Physician’s Dilemma: How to Treat Persistent Pain?

First stop the prescription pad Next stop

the prescription pad

The Physician’s Dilemma: How to Treat Persistent Pain? (cont’d)

Next stop refer to someone Next stop patient may return, referral unsuccessful

“I think you should see a psychiatrist”

The Dentist’s Dilemma: How Do Dentists Treat Persistent Pain?

Chronic pain is also poorly taught in dental schools

Common Responses To Chronic Orofacial Pain Complaints          

That leaky filling needs replacement It must be a “cracked tooth syndrome” You need a root canal filling I’ll have to do an apicectomy Sorry, I’ll have to extract the tooth Let’s explore that “bone cavity” You’ve got “TMJ syndrome” Your occlusion needs adjustment You need a bite splint I’ll have to refer you to an oral surgeon

Orofacial Pain of Non-Dental Origin The site of the pain is not always its source

Neuropathic + myofascial pain

Myofascial pain (TMD)

 Radiographs show teeth, jaws, and sinuses  They do not show the pain

Orofacial Pain of Non-Dental Origin (cont’d)  Most chronic orofacial pain is myofascial or neuropathic in origin  Myofascial pain – the most common non-odontogenic pain – can mimic dental pain, and co-exist with AO

 Neuropathic pain (AO) – less common, but more difficult to manage

 Both are often misdiagnosed and poorly treated

Orofacial Pain of Non-Dental Origin (cont’d)

Myofascial Pain –deep, dull, aching, intermittent, triggered –variable intensity, pain is commonly referred –relief is achievable with control of causes –myofascial pain is often due to muscle overuse –(bruxism), and other oral habits

Janet Travell MD, 1983 course

“Headache”

“Toothache”

“Sinus pain”

“Toothache” “Sinus pain”

“TMJ syndrome”

“TMJ syndrome”

Myofascial Pain Fortunately, myofascial pain is more common, and easier to diagnose and manage It is often wrongly diagnosed as neuropathic pain Other than dental causes, most persistent orofacial pain is due to myofascial pain and dysfunction, from active myofascial trigger points (TrP’s)

Travell and Simons, 1999

Orofacial Pain of Non-Dental Origin (cont’d)  Neuropathic pain – Sharp, burning, tingling, stabbing, triggered – Constant or intermittent, may refer elsewhere – Relief is often difficult to achieve – Neuropathic pain may follow deafferentation • e.g. from extractions, surgery, endodontia, implants

Orofacial Pain of Non-Dental Origin (cont’d) Neuropathic Pain –if prolonged, pain may lead to development of central sensitization, hyperalgesia, secondary hyperalgesia, and/or allodynia –pain may also be referred, which can confuse the diagnosis and lead to harmful interventions

Involves activity in dorsal horn or trigeminal nucleus

The Dental Pulp

Illustration of the movement of dentinal fluid inside dentinal tubules in response to a hot stimulus (red arrow) and a cold stimulus (blue arrow)

The Dental Pulp (cont’d)  The dental pulp is richly innervated by pain receptors (nociceptors). They are mostly A-delta and C- fibers  A-delta fibers comprise approximately 13%. They are lightly myelinated, medium velocity conductors (5-29 m/sec), and are polymodal responding to thermal, mechanical and chemical stimuli  A-delta fibers are mainly located at the pulp-dentin border in the coronal portion of the pulp and concentrated in the pulp horns  A-delta fibers transmit fast, sharp, pricking, local pain  Examples – pain from exposed dentin or ineffective local anesthesia during cavity preparation

The Dental Pulp (cont’d)  Approximately 87% of pulp fibers are Type C-fibres  Smaller, unmyelinated fibers. Slow conductors (2-3m/sec). Also polymodal, respond with dull, aching, diffuse pain  C-fibers are located in the pulp core, and extend to the cell-free zone under the odontoblastic layer. Activated by factors involving the pulp such as deep untreated caries or injury, resulting in the dull, aching pain of pulpitis  Activity is increased by heat, dental procedures such as extensive, deep restorations, endodontia, and surgery  Particularly responsive if local anesthesia is inadequate

The Dental Pulp (cont’d)  C-fibers also have a more sinister agenda  Involved in the development of temporal summation (or “wind up”), central sensitization, and neuropathic pain.  It is believed they play a key role in the initiation and maintenance of neuropathic pain.  They may also be significant in oral neuropathies like AO

Central Sensitization  Central sensitization was hypothesized by Clifford Woolf, who developed an animal model in 1983 and proved his hypothesis.

Central sensitization is now recognised as a major cause of pain following injury or surgery  It begins with activity in peripheral C-fibers, which can be initiated by mechanical, thermal, or chemical stimuli  Woolf also stated “there is good evidence that central sensitization

also occurs in the trigeminal system”

Woolf CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature. 1983;306:686-688

The spread of pain, allodynia, and hyperalgesia is explained by activated NMDA receptors in the spinal cord dorsal horn. Similar phenomena can occur in the trigeminovascular pain pathways .

Activation of these receptors, which increases calcium conductance, leads to activation of protein kinases, such as 5-HT, bradykinin, and prostaglandins, and to activation of the enzyme nitric oxide synthase.

The Dental Pulp (cont’d)

The home of the bad guys - the C-fibers , who hang out under the odontoblastic layer

The Dental Pulp  In pulpitis, prostaglandins are initially released, which sensitize intradental nerves. This pain can be reduced by NSAID’s  Later, sensitized C-fibers react to heat with increased pain. This is reduced by cold, or cooling from A-fiber vasoconstriction  But if early dental treatment is not sought e.g. anxious patient, relief is temporary, with eventual death of A-fibers from anoxia  Heat levels now increase. The result is intense pain, due to vasodilation and increasing stimulation of C-fibers

Central Sensitization  Prolonged C-fiber activity can now lead to central sensitization due to the release of excitatory substances such as NMDA (nmethyl-d-aspartate)  Once central sensitization has developed, pain is likely to continue despite treatment  This is a trap for the unwary dentist who may carry out more treatments which make matters worse

Central Sensitization  Sensitized WDR second order neurons now interpret all incoming signals as pain (hyperalgesia)  The receptive field also enlarges, leading to spreading pain (secondary hyperalgesia) – e.g. toothbrushing

 Non-painful stimuli, such as light touch, may also be perceived as painful (allodynia)

Central sensitization and neuropathic pain in the orofacial region

NMDA receptor activity increases, “Wind-up” is now under way

Bell’s Orofacial Pains (Okeson)

Central sensitization and neuropathic pain in the orofacial region

Central sensitization prolongs the pain after treatment is completed. e.g. endo or extraction

Bell’s Orofacial Pains (Okeson)

Central Sensitization  Pain originates centrally (trigeminal nucleus)  Pain is often experienced at the original pain site - but it may no longer be its source

Is this a cause of apparent dental pain?

Does this process underly the mystery of AO?

Diagnosis of AO  A thorough history is essential  Duration of pain? What caused it? (caries, injury etc)  Pain – deep, aching? (myofascial) – constant, sharp, burning, stabbing? (neuropathic) – [both may be present]

 Has neuropathic pain present for long?  Is there secondary hyperalgesia?  Suspect central sensitization with AO  Diagnostic test: carefully isolate the area of the pain with local anesthesia. If any pain remains, suspect AO.  Further intervention should be very carefully considered!

Treatment of AO If AO is a central sensitization disorder, invasive procedures which could further exacerbate the situation must be avoided Emphasis should now be on management Medications –prescribe pain medications on a time contingent basis, rather than a pain basis, to maintain optimal drug levels and help prevent breakthrough pain

Botulinum Toxin Sativex Spray(THC)

Prevention Of AO Is Better Than Treatment The Role Of Pre-emptive Analgesia Effective local anesthesia may prevent or at least reduce central sensitization and subsequent pain Foreman PA, Anesthesia Progress 1995 42:36-40

Earlier observations: IV conscious sedation + local anesthesia vs GA alone Recommendation: Always use local anesthesia as an adjunct to GA

Prevention of AO: Pre-emptive Analgesia Dental neuropathies are difficult to diagnose and treat They also consume much time. Prevention may be possible using preemptive local anaesthesia with conscious sedation or GA.

Rules

Foreman PA, Anesthesia Progress 1995 42:36-40

1) Exercise caution when dealing with pains of uncertain origin, particularly if burning, tingling, stabbing, or continuous. They may be of central origin but exhibit peripheral symptoms – Resist demands to intervene if there are no clear indications – Invasive interventions, particularly if repeated, may well exacerbate the pain and lead to further complications

Pre-emptive Analgesia 2) Effective local anesthesia will help block the cascade of events which may lead to the onset of central sensitization. –accurate placement of the local anesthetic is critical, not the quantity injected –perioperative pain control is important in preventing central sensitization (NSAIDs may be as effective as opioids)

Pre-emptive Analgesia 3) If treatment is non-urgent, antibiotics may be useful, with pain and inflammation control from NSAID’s – if local anesthesia is difficult to obtain it may be advisable to delay procedures which add pain and increase sensitization

4) When operating under GA, this will not alone block C-fiber transmission. Adjunctive local anesthesia is now widely used in anesthesia (locally or epidurally), to block nociception and pain transmission, and also assist postoperative pain control

Pre-emptive Analgesia 5) Peripheral nociception may persist or recur beyond the duration of action of local anesthesia, and reactivate central mechanisms – consider use of long acting local anesthetics for major surgery, supported centrally with perioperative NSAID’s or analgesics such as fentanyl with careful monitoring

6) Analgesic drugs should be prescribed on a time contingent, not a pain contingent basis. This helps to maintain optimum concentrations of agents which block central sensitization

AO Conclusions  Neuropathy may follow dental procedures. Once established, management is difficult  Prevention is possible (pre-emptive analgesia)  Be alert when patients have persistent pain and other treatments have failed  Where the diagnosis is in doubt and the patient is insistent, proceed with caution