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Applied
Clinical
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Review
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J Can Dent Assoc 2012;78:c83
l’Association dentaire canadienne

Neuropathic Orofacial Pain Patients

in Need of Dental Care
Gary D. Klasser, DMD, Cert Orofacial Pain; Henry A. Gremillion, DDS

Abstract
fied as nociceptive or inf lamma-
tory. According to the International
Association for the Study of Pain
(IASP), 8 nociceptive pain “arises from
actual or threatened damage to non-
Dental pain is a common complaint among the general population. Most pain is a
neural tissue and is due to the acti-
result of traumatic injury or bacterial infection in pulpal and periapical tissues, and
dental practitioners are successful at diagnosing these conditions and providing vation of nociceptors.” Nociceptive
prompt relief. However, in some cases, patients continue to complain of persistent pain is the term used to describe
pain, which may be categorized as neuropathic. These people may avoid or neglect pain occurring with a normally
routine dental treatment or interventions to prevent precipitation, perpetuation functioning somatosensory nervous
or exacerbation of their pain condition, and practitioners may have to modify their system. It is stimulus dependent and
procedures when managing the dental needs of this unique population. is evoked by high-intensity (noxious)
stimuli. Furthermore, it is biologically
adaptive, as it protects by signaling
potential tissue damage.9
Inf lammatory pain occurs in

D
ental pain is a common response to tissue injury and is sub-
complaint among those seek- sequently followed by an inflamma-
ing dental care. In 1993, an tory response to aid the healing and
estimated 12.2% of the American repair process. It is a spontaneous and
general population had experienced stimulus-dependent pain that involves
toothache in the last 6 months.1 In sensory amplification evoked by both
the United States between 1997 and low- and high-intensity stimuli.
2000, 2.95 million people presented Inf lammatory pain, which creates
to an emergency department with a pain hypersensitivity during healing
chief complaint of toothache or dental and repair, is biologically adaptive and
injury.2 most often reversible.9,10
Most dental pain is a result of Dental practitioners, general prac-
traumatic injury or bacterial infec- titioners and specialists are very suc-
tion originating from pulpal and cessful at recognizing, understanding
periapical tissues 3-7 and is classi- and treating these categories of pains,

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Table 1 Differences between nociceptive, inflammatory and neuropathic pain9

Nociceptive pain Inflammatory pain jadc

Neuropathic (dysfunctional) pain
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Noxious impulses are received and Normal responsiveness of the sensory Noxious impulses originate from an
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transmitted by normal components of the nervous system is altered to address the abnormality in neural structures
Publié par
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sensory nervous system consequences of tissue damage

Normal neural structures Normal neural structures Abnormal neural structures

Abnormal somatic structures Response to tissue injury with active Normal somatic structures
inflammation
Stimulus-dependent pain evoked by high- Spontaneous and stimulus- dependent pain Spontaneous and stimulus-dependent pain
intensity (noxious) stimuli evoked by both low-and high-intensity evoked by both low- and high-intensity
stimuli, which may or may not be noxious stimuli, which may or may not be noxious
Biologically adaptive Biologically adaptive and reversible after Maladaptive and potentially persistent
resolution of the initial tissue injury (unless
a chronic disorder exists, i.e., rheumatoid
arthritis)
Protects by signaling potential tissue Protects by producing pain hypersensitivity Unprotective and unsupportive of healing
damage during healing and repair and repair

bringing prompt relief to their patients. Reported recognized and understood by all dental prac-
success rates (i.e., the treated tooth is still present 5 titioners (Table  1). In addition, a fourth type of
years after initiation of treatment) for endodontic pain, termed mixed pain, has features common to
treatment are in the range of 89.7% to 98.1%.11 all 3 categories.12 In this article, we discuss neuro-
However, in some cases, those who have under- pathic pain in the context of dysfunctional pain
gone dental treatments that have been considered limited to the orofacial region.
both clinically and radiographically successful For clinical purposes, to further categorize
continue to complain of persistent pain. These neuropathic orofacial pain (NOP), a system based
people may be experiencing neuropathic pain. on a temporal assessment may be used. Hence,
Neuropathic pain is defined by the IASP as NOP may be considered continuous or epi-
“pain caused by a lesion or disease of the somato- sodic, each associated with distinct characteris-
sensory nervous system.”8 Furthermore, “neuro- tics. Continuous NOP originates in neural struc-
pathic pain is a clinical description (and not a tures and is manifested as a constant, ongoing
diagnosis) which requires a demonstrable lesion and unremitting pain. Patients usually experience
or a disease that satisfies established neurological varying and fluctuating intensities of pain, often
diagnostic criteria.” However, a patient presenting without total remission. This pain is frequently
with neuropathic pain may not have a “demon- perceived in dental structures and has been
strable lesion or disease.” Costigan and others9 referred to as atypical odontalgia13,14 or sometimes
refer to this as dysfunctional pain. Dysfunctional phantom toothache.15,16 In some cases, this pain
pain is considered to represent a malfunction — may have a sympathetic component.17 Patients
which can be considered a disease in itself — of the experiencing continuous NOP often report a his-
somatosensory apparatus involving spontaneous tory of overt trauma or the pain may have followed
and stimulus-dependent pain (evoked by both dental treatment.18,19
low- and high-intensity stimuli) without known Episodic NOP is characterized by sudden vol-
structural nervous system lesions or active periph- leys of severe, electric-like shooting pain that lasts
eral inflammation. a few seconds to several minutes and is referred
Clearly, the differences between nociceptive, to as neuralgia. 20 The classical example of this
inflammatory and neuropathic pain should be type of pain is trigeminal neuralgia (tic doulou-

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reux). There is often an intraoral or perioral (or fungal) or tumour invasion causes a release of
both) trigger zone that, when lightly stimulated,
provokes severe paroxysmal pain. 20 Anesthetic
neurochemicals and inflammatory mediators from
the peripheral tissues, primary afferent nerve end-
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blocking of the trigger zone may completely elim- ings or both. This can increase membrane excit- Publié par

inate paroxysmal episodes during the duration of ability and decrease the activation threshold of l’Association dentaire canadienne

anesthesia. peripheral nociceptors (a process referred to as

peripheral sensitization) increasing nocicep-
Epidemiology tive input into the central nervous system (CNS).
This bombardment of the CNS induces synaptic
The true prevalence of NOP is unknown, as
plasticity characterized by spontaneous activity,
both continuous and episodic types are relatively
expansion of receptive fields, lowering of activa-
uncommon in general population-based studies.
tion thresholds, hyperexcitability of neurons in the
In one of the few such studies investigating neuro-
CNS, anatomic alterations to inhibitory neurons
pathic pain, the reported prevalence was 0.03% for
and other neural tissues and genetic alterations
persistent idiopathic facial pain and 0.3% for tri-
(a process referred to as central sensitization). 28-32
geminal neuralgia.21 Another study, using a large
Furthermore, non-neural cellular elements, such
US health insurance database containing informa-
as glial cells, have been reported to be intimately
tion on 55 586 people, reported the prevalence of
involved in this process. 33-36
atypical facial pain (0.5%) and trigeminal neur-
algia (1.0%).22 Dental Diagnostic Considerations
The diagnosis of NOP appears to be more
common when patients present to a tertiary care In many cases, people experiencing NOP
orofacial pain centre. In a study carried out at present a dilemma to dental practitioners, as the
a university-based orofacial pain/oral medicine additional nociceptive input to the CNS produced
centre, Suarez and Clark 23 found the prevalence by irreversible or invasive procedures may exacer-
of NOP to be 10.6% (n  = 1049); in a study at the bate the NOP by burdening an already hyper-
same centre, Ram and others24 reported the preva- excitable trigeminal nociceptive system. This often
lence of atypical odontalgia to be 2.1% (n = 3000). leads to misdiagnosis or incomplete diagnosis,
In a study by Israel and others, 25 carried out at a resulting in misdirected or incomplete treatment.
hospital-based oral, facial and head pain centre, It is not uncommon for such patients to return to
the dental practitioner with the complaint of per-
a prevalence of 40% (n  = 120) for atypical facial
sistent pain after receiving treatment deemed suc-
neuralgia was reported. These differences may be
cessful based on clinical and radiographic criteria.
due to inconsistent definitions of NOP and differ-
These people are often submitted to fur-
ences in the inclusion criteria and sample sizes.
ther inconclusive diagnostic testing, including
Pathophysiology unremarkable radiographic evidence of pathology.
In an attempt to resolve the persistent pain, dental
Although the pathophysiology of NOP is yet approaches are frequently implemented, 37 and
to be fully elucidated, studies involving both patients may endure irreversible and sometimes
human and animal models suggest that a number invasive and unnecessary dental treatment of the
of complex peripheral and central mechanisms previously treated areas — soft or hard tissue —
are involved in the initiation and maintenance as well as adjacent and surrounding areas.18,38-42
of this pain. 26,27 Briefly, changes in neural sys- In a retrospective study of 64 patients who had
tems occur as a result of physiologic (peripheral been diagnosed with atypical odontalgia, 71%
and central) events, influenced by neurochemicals, had initially consulted a dentist with their pain
anatomic structures and genetic components. It is complaint and, subsequently, 79% received dental
common for the initiating event(s) to be unknown treatment that did not resolve the pain.24
or unreported, although it is probable that some To avoid this pitfall, diagnosis must begin with
form of mechanical trauma, metabolic disorder, a comprehensive history and clinical and imaging
neurotoxic chemicals, infection (bacterial, viral, examinations. A differential diagnosis must be

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Figure 1: Types of pain that may mimic neuropathic orofacial pain Dental Care Considerations

Pain categories for differential diagnosis

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Patients experiencing NOP are not exempt
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from the need for routine dental treatment, but
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they often neglect maintenancel’Association

and restoration
Publié par
1. Odontogenic pain • Nutritional deficiencies dentaire canadienne

• Pulpal • Connective tissue/ procedures to avoid precipitating, perpetuating

• Periodontal autoimmune diseases, or exacerbating their pain. Unfortunately, this
• Cracked tooth/restoration such as systemic lupus may lead to a progressive decline in their oral
• Osteomyelitis erythamatosus, Sjogren health, which may result in pain amplifica-
• Perimplantitis syndrome, rheumatoid tion from additional nociceptive input into an
• Bacterial, viral, fungal arthritis, systemic sclero-
already dysfunctional nervous system. Therefore,
infection sis, sarcoidosis, mixed
the need for dental practitioners to encourage
connective tissue disease
2. Non-odontogenic • Nerve trauma/neuroma these people to be intimately engaged in appro-
orofacial pain • Polyneuropathy, resulting priate measures to maintain their oral health
• Temporomandibular disor- from alcoholism, chemo- cannot be overstated. Dental practitioners must
der, including myogenous therapy, HIV (human also appreciate and be aware that routine pro-
and arthrogenous pain immunodeficiency virus), cedures may exacerbate these patients’ current
• Sinusitis including nasal etc. pain43,44 and take measures to minimize the risk of
mucosa such occurrences.
• Cervical pain 4. Central pathology
• Neurovascular (migrain- • Central lesions (neoplasm) Appointment Scheduling
ous) toothache • Multiple sclerosis
In NOP, pain often varies and fluctuates in
• Cardiac toothache • Cerebral vascular accident
intensity; therefore, an appreciation of the pain
• Salivary gland disorders/ • Spinal cord injury
cycle is important. If pain is episodic, proced-
disease
5. Psychologic disorders ures should be carried out during periods of
3. Peripheral pathology • Depression lowest pain intensity or remission. Furthermore,
• Eye/ear pain • Anxiety all dental procedures should be performed when
• Temporal arteritis • Obsessive compulsive medication used in the management of NOP is at
• Herpes zoster/post- disorders its peak level of effectiveness. Hence, dental prac-
herpetic neuralgia • Somatoform disorders
titioners should have knowledge of the pharmaco-
• Neoplasm • Cancerphobia
kinetics and pharmacodynamics of their patients’
• Metabolic/endocrine
medication(s) to take advantage of these factors
disorders, such as
and provide maximum comfort with minimal risk
diabetes, hypothyroidism
of pain intensification.

Local Anesthetic
The administration of local anesthetic and
established to rule out pain of dental (soft or hard the use of needles, although routine and rarely
tissue), pathologic (peripheral or central) or psych- resulting in complications, may exacerbate pain in
those with NOP. Despite appropriate and prudent
ologic origin (Fig.  1) Once a diagnosis of NOP is
needle application, peripheral neural trauma may
established, no further dental procedures should
increase pain and there is the potential for hema-
be performed unless specific dental pathosis is toma formation.45,46
clearly identified. In such cases, the dental practi- Furthermore, all local anesthetics have some
tioner must decide whether to treat the patient or degree of neurotoxicity, which may also exacer-
bate pain in the NOP patient.45,47,48 Neurotoxicity
provide a referral to a health care professional who
depends on several factors, including the potency
has an understanding of neuropathic conditions.
of the local anesthetic, its ability to create an
In Canada, an ideal practitioner for such a referral ischemic environment resulting from vasocon-
would be a specialist in oral medicine. striction of alpha receptor-mediated microvessels

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associated with peripheral nerves and the prox- with “booster” doses of anti-neuropathic medica-
imity of the deposition and dispersal of the local
anesthetic to the area of pathology (if such path-
tions before invasive procedures. 53 Administration
of long-acting anesthetic at the end of the pro-
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ology is present).46,49,50 cedure should also be considered to delay post- Publié par

Thus, for a person with NOP induced by per- operative input to the CNS.54,55 l’Association dentaire canadienne

ipheral neural trauma and resulting in a local- Dental procedures may be carried out under
ized neuroma or for someone experiencing neur- general anesthesia, with augmentation from
algia, administration of local anesthetic may have local anesthesia, to avoid potential increased
a direct affect on accessible anatomic structures or enhanced peripheral and central sensi-
and enhance existing pain as peripheral noci- tization. 53,56,57 If adequately trained or with
ceptive input from this routine procedure may assistance, dental practitioners may help patients
augment the centrally based hyperexcitability. achieve greater pain control using behavioural
Alternatively, if the dysfunction or pathology, such approaches, such as self-hypnosis and relaxation
as cerebral vascular compression, were located in techniques. 58
the CNS, there would be minimal concern over a
direct effect on pain exacerbation. Conclusion
Other important factors in the choice of local
It is incumbent on all dental practitioners to
anesthetic are its concentration and the time of
recognize and understand the concept of NOP.
exposure of peripheral neural tissue.49 To mini-
In addition, they must understand that man-
mize the risk of increased pain, dental practi-
agement of these patients often requires a com-
tioners should administer local anesthetic with the
prehensive multidisciplinary team approach
utmost care. They can avoid undue tissue trauma
using multidimensional management strategies.
by using agents that have minimal neurotoxic
The management team must take into account
and ischemic potential, the lowest concentrations
the physiologic, environmental, psychologic and
and the shortest exposure times, maintaining the
genetic dimensions of pain. The dental team
goal of delivering well-controlled and profound
may be called on to provide preventive and
anesthesia.
restorative procedures for patients with NOP.
Preventive and Hygiene Procedures In light of the complexities associated with
Dental practitioners may use several oral NOP, a positive experience can only occur in
hygiene aids and techniques to limit stimulation, the context of open communication among all
avoid an increase in a patient’s NOP and pre- health practitioners and validation, appreciation
vent reluctance to perform normal daily dental and respect for the person experiencing NOP —
hygiene procedures. Soft cleansing aids (a soft understanding their concerns, attention to their
or sponge-like toothbrush), interdental cleaning level of tolerance of procedures and the mutual
devices (various floss textures, dental tape, inter- establishment and agreement on a realistic set
dental cleaners), antibacterial/antiplaque alcohol- of goals. Ultimately, this approach will result in
free mouth rinses, recalcifying and remineralizing the delivery of the best quality of care to these
agents and fluoride supplementation in the form patients. a
of custom trays or pastes, gels or rinses should
be considered. For soft tissue maintenance and The Authors
removal of calcified deposits, dental practitioners
should consider careful and gentle administration Dr. Klasser is associate professor, Louisiana
of local anesthesia to the areas to be treated to pro- State University School of Dentistry, division
duce anesthetic camouflage and, thereby, decrease of diagnostic sciences, New Orleans, LA, USA.

noxious stimuli to the CNS.51,52

Dr. Gremillion is dean and professor, Louisiana
Restorative Procedures State University School of Dentistry, New
Dental practitioners should consider the use Orleans, LA, USA.
of pre-emptive analgesia by providing the patient

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Correspondence to: Dr. Gary D. Klasser, Louisiana State 23. Suarez P, Clark G. Oral conditions of 1,049 patients referred
University School of Dentistry, Division of Diagnostic
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to a university-based oral medicine and orofacial pain center.
Sciences, 1100 Florida Ave., New Orleans, LA 70119, USA. Spec Care Dentist. 2007;27(5):191-5.
Email: gklass@lsuhsc.edu 24. Ram S, Teruel A, Kumar SK, Clark G. Clinical characteristics
DES CONNAISSANCES
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and diagnosis of atypical odontalgia: implications for dentists.
J Am Dent Assoc. 2009;140(2):223-8. Publié par
l’Association dentaire canadienne

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48. Kasaba T, Onizuka S, Takasaki M. Procaine and mepivacaine 54. Gordon SM, Mischenko AV, Dionne RA. Long-acting local

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