Open Journal of Stomatology, 2011, 1, 92-102
doi:10.4236/ojst.2011.13015 Published Online September 2011 (http://www.SciRP.org/journal/OJST/ OJST ).
Published Online September 2011 in SciRes. http://www.scirp.org/journal/OJST
Non-odontogenic toothache revisited
Ramesh Balasubramaniam1*, Lena N. Turner2, Dena Fischer3, Gary D. Klasser4, Jeffrey P. Okeson5
1School of Dentistry, University of Western Australia, Perth, Australia;
2Department of Oral Medicine, School of Dental Medicine, University of Pennsylvania, Philadelphia, America;
3Department of Oral Medicine and Diagnostic Sciences, University of Illinois at Chicago, Chicago, A merica;
4Division of Diagnostic Sciences, Louisiana State University Health Sciences Centre, School of Dentistry, New Orleans, America;
5Department of Oral Health Science, University of Kentuck y, Lexington, America.
Received 17 May 2011; revised 23 June 2011; accepted 5 July 2011.
ABSTRACT
Although pain of dental origin is the most common
orofacial pain, other non-odontogenic pains can af-
fect the orofacial region and occasionally mimic den-
tal pain. These non-odontogenic pains may pose a
diagnostic dilemma for the dental practitioner who
routinely diagnoses and treats dental pain. Knowl-
edge of the various non-odontogenic pains will ulti-
mately prevent misdiagnosis and the delivery of in-
correct and sometimes irreversible and invasive pro-
cedures to patients. The purpose of this article is to
review the clinical presentations of the various types
of non-odontogenic pains which may be mistaken as
dental pain: myofascial, cardiac, sinus, neurovascular,
neuropathic, neoplastic and psychogenic pain.
Keywords: Non-Odontogenic Toothache; Orofacial Pain
1. INTRODUCTION
The orofacial region is the mo st frequent site for patients
seeking medical attention for pain [1,2] with 12.2% of
the population reporting dental p ain as th e most co mmon
orofacial pain [3]. Consequently, it is common for pain
in the orofacial region to be mistaken for a toothache,
and similarly, other pains of the head and neck to mimic
odontogenic pain. Therefore, orofacial pain may pose a
diagnostic dilemma for the dental practitioner. Under-
standing the complex mechanism of odontogenic pain
and the manner in which other orofacial structures may
simulate pain in the tooth is paramount in determining
the correct diagnosis and appropriate treatment.
The purpose of this article is to: a) provide the dental
practitioner with an understanding of pain etiology to
consider when developing differential diagnoses for
orofacial pains, and b) review various types of non-
odontogenic pains which may be mistaken for a tooth-
ache. Ultimately, this article will aid the dental practi-
tioner with preventing misdiagnosis and delivery of in-
correct and sometimes irreversible procedures for non-
odontogenic pains.
2. CLINICAL CHARACTERISTICS OF
ODONTOGENIC PAIN
Odontogenic pain is generally derived from either one of
two structures associated with the tooth: pulpal or pe-
riodontal tissue. Although the mechanisms for both are
of inflammatory origin, their distinct functionality and
embryologic origin [4] results in each pain being per-
ceived differently. Pulpitis is the most common cause of
odontogenic pain [2] and can be divided into two cate-
gories: reversible and irreversible. Reversible pulpitis
indicates that pulpal tissues can repair with the removal
of the local irritant and restoration of the tooth structure.
It is often characterized by a fleeting pain up on provoca-
tion and does not occur spontaneously. Irreversible pul-
pitis has a prolonged duration of pain when stimulated
but may also occur spontaneously.
As a visceral organ, pain of the dental pulp is charac-
terized by deep, dull, aching pain that may be difficult to
localize [5]. It may present as intermittent or continuous,
moderate or severe, sharp or dull, localized or diffuse
and may be affected by the time of day or position of th e
body [6]. After prolonged periods of intense pain, re-
ferred pain may be produced due to central excitatory
effects [7]. The quality of pain may vary based upon the
vitality of the too th as well as the extent of inflammation.
Following prolonged periods of inflammation, pulpal
necrosis may occur. Also, there may be other causes of
pulpal pain that may be difficult to identify such as
“cracked tooth syndrome” whereby a crack or craze may
develop within the tooth [6].
Periodontal pain is more readily localized and identi-
fiable because of proprioceptors located within the pe-

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riodontal ligament. Therefore, periodontal pain will fol-
low the characteristics of p ain of musculoskeletal origin.
The periodontal receptors are able to accurately localize
the pain whether they are lateral or apical to the tooth.
Acute apical periodontitis may be the result of pulpal
necrosis. Similarly, a lateral periodontal abscess may be
a source of odontogenic pain and may be associated with
clinical signs such as edema, erythema and swelling of
the gingival [6]. The diagnosis of pulpal and periodon-
tal pain is often easily established and once diagnosed,
treatment is directed at alleviating the etiology. In rare
cases, odontogenic pain can present as an enigma con-
fusing the clinician. However, the clinician should be
mindful that dental pain is the most common orofacial
pain.
3. CLINICAL CHARACTERISTICS OF
NON-ODONTOGENIC PAIN
The clinical presentation of non-odontogenic pain is
varied and may mimic other pain disorders which may
not originate in the orofacial region. The extent of pain
may vary from very mild and intermittent pain to severe,
sharp, and continuous. Furthermore, pains that are felt in
the tooth do not always originate from dental structures,
so it is important to distinguish between site and source
of pain to provide correct diagnosis and appropriate
treatments. The site of pain is where the pain is felt by
the patient, whereas the source of pain is the structure
from which the pain actually originates. In ‘primary’
pain, the site and source of pain are coincidental and in
the same location. That is, pain occurs where damage to
the structure has occurred. Therapy for primary pain is
obvious and does not pose a diagnostic dilemma for the
clinician.
Pain with different sites and sources of pain, known as
heterotopic pains, can be diagnostically challenging. Once
diagnosed, treatment should be posed at the source of
pain, rather than the site. Neurologic mechanisms of
heterotopic pain is not well understood but it is thought
to be related to central effects of constant nociceptive
input from deep structures such as muscles, joints and
ligament [8].
Although the terms heterotopic pain and referred pain
are often used interchangeably, there are specific distinc-
tions between these terms. Heterotopic pain can be di-
vided more specifically into 3 general types: a) central
pain, b) projected pain, and c) referred pain [4]. Central
pain is simply pain derived from the central nervous
system (CNS) resulting in pain perceived peripherally.
An example of central pain is an intracranial tumor as
this will not usually cause pain in the CNS because of
the brain’s insensitivity to pain but rather it is felt pe-
ri phe rally. Proj ected pain is pain felt in the peripheral dis-
tribution of the same nerve that mediated the primary no-
ciceptive input. An example of projected pain is pain felt
in the dermatomal distribution in post-herpetic neuralgia.
Referred pain is spontaneous heterotopic pain felt at a site
of pain with separate innervation to the primary source of
pain. It is thought to be mediated by sensitization of in-
terneurons located with in the CNS. Pain referred from the
sternocleidomastoid muscle to the temporomandibular
joint is an example of referred pain [4]. The remainder of
this article will focus on non-odontogenic pains of
odontogenic origi n.
3.1. Myofascial Toothache
Skeletal muscle triggers are well recognized in the lit-
erature [9,10] and are illustrated by trigger point map-
ping achieved through palpation of the muscles and de-
scribing the locations of pain referral [11,12]. The trigger
point, a localized hyperexcitable nodule within the mus-
cle, is theorized to be a result of microscopic neuromus-
cular dysfunction at the motor endplate [12]. As it cannot
be identified histologically or by imaging, there is con-
troversy as to the true existence of the trigger point
[12,13]. Clinically, palpating a firm, tender nodule within
a sufficiently irritable muscle may reproduce referred
pain to distant regions upon sustained pressure [12,14].
Hong et al. were able to reproduce referred pain 80% of
the time by palpation of the trigger point with sufficient
pressure for up to 10 seconds [15]. An additional study
was able to reproduce muscle pain with dry needling of
the muscle in 62% of the cases [15].
The theory of convergence supports the mechanism
that is thought to cause pain referral to the trigeminal
sensory complex from other areas of nociceptive input
although it is not well understood. It has been reported
that at least half of the trigeminal nociceptive neurons
are able to be activated by stimulation outside their nor-
mal receptive field [16]. Studies on myofascial pain re-
ferral to other regions of the orofacial region have found
that pain from: a) temporalis muscles referred pain to
the maxillary teeth, b) masseter muscles referred pain
to the maxillary and mandibular posterior teeth, ear and
temporomandibular joint (TMJ), c) lateral pterygoid
muscles referred pain to the maxillary sinus region and
TMJ, d) anterior digastric muscles referred pain to the
mandibular incisors, and e) sternocleidomastoid mus-
cles referred pain to oral structures and the forehead
[11 ,12,17]. Additionally, palpation of the trapezius mus-
cle often refers pain to the mandible or temporalis mus-
cle regions [4,12].
The myofascial toothache is described as non-pulsatile
and aching pain and occurs more continuously than pul-
pal pain [6]. Patients are unable to accurately locate the
source of the pain and often believe pain is originating
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from the tooth. Tooth sensitivity to temperature, percus-
sion or occlusal pressure may be felt as a result of re-
ferred pain from the offending muscle [12]. Pain tends to
be associated with extended muscle use and exacerbated
with emotional stressors, rather than direct provocation of
the affected tooth [6]. Palpation of the trigger point is
able to reproduce the toothache, even modulate the pain
by increasing or eliminating it altogether [6]. In spite of
this, it has been reported that 7% of cases were referred
for endodontic treatment when the primary source of pain
was the muscle of mastication [18]. Linn et al. reported
that 37% of patients diagnosed with muscular orofacial
pain had previously undergone endodontic or exodontic
treatment in an attempt to alleviate their pain [19].
Alleviation of the toothache is often achieved when
local anesthetic is administered to the strained muscle
(source of pain) rather than the tooth (site of pain). Warm
or cold compresses, muscle stretching, massage, and a
restful sleep may alleviate both the muscle and tooth
pain. Elimination of the trigger point and pain of the
muscle should be the aim of the treatment rather than the
tooth itself [1,6].
3.2. Cardiac Toothache
Cardiac pain is an additional source of referred pain to
the jaw mainly due to cardiac ischemia. Angina pectoris
is a symptomatic presentation of ischemic heart disease
that is often used in congruence with cardiac ischemia.
Cardiac ischemia more commonly presents with subster-
nal pain and radiation to the left shoulder and arm [6].
When cardiac pain presents in the orofacial region com-
monly affected areas include pain(s) in the neck, throat,
ear, teeth, mandible and headache [20-24]. In some cases,
orofacial pain is the only complaint in association with
cardiac ischemia. In one study, 6% of patients presenting
with coronary symptoms had pain solely in the orofacial
region while 32% had pain referred elsewhere. Interest-
ingly, bilateral referred craniofacial pain was noted more
commonly than unilateral pain at a ratio of 6:1 [20].
The mechanism of cardiac pain likely involves multi-
ple nociceptive mediators with bradykinin being the
most important, evoking a sympathoexcitatory reflex [25]
and inducing a sympathetic response of the heart [26-28].
Although widely accepted, there is controversy as to
whether the sympathetic response is responsible for the
transmission of pain. Studies on patients who underwent
sympathectomies demonstrated a 50% - 60% complete
relief of angina pectoris, while 40% obtained a partial
relief, and 10% - 20% experienced no relief [29].
Vagal afferent response is thought to also play a role
in the response to cardiac ischemia although its role is
not clearly defined [30,31]. Based on the anatomic dis-
tribution, vagal afferents could be activated when the
infero-posterior surface of the heart is affected, while
sympathetic response is due to stimulation of the anterior
portion [29]. A recent case report suggests an association
between vagal stimulation and toothache in a patient
undergoing experimental treatment with a vagal nerve
stimulator for the treatment of depression [32]. Episodes
of tooth pain were coincidental to duration and fre-
quency of nerve stimulation and once appropriate ad-
justments to the stimulator parameters were made, the
dental pain subsided. Vagal stimulation has been utilized
in other treatments such as drug resistant epilepsy, and
reports of similar painful side effects such as jaw and
tooth pain as well as throat and neck pain have been
noted [33-36]. Consequently, there may be a physiologic
association between vagal stimulation initiated by car-
diac ischemia and odontogenic pain.
Mechanisms of convergence and central sensitization
in the trigeminal nerve complex can also explain pain
referred to orofacial structures [4]. Cardiac nociceptive
input travels to the central nervous system and ascends
to higher centers for processing in regions of conver-
gence, where adjacent nociceptive neurons may become
activated [37]. The stimulation of adjacent neurons that
are not directly involved in the primary source of pain
may be misinterpreted in the cortex, causing an uninten-
tional pain input being referred to other regions and re-
sulting in heterotop ic pain.
Alternate sources of pain should be considered when
local anesthetic and analgesics fail to alleviate dental
symptoms. Appropriate questioning and thorough medi-
cal history are essential in identifying the true source of
pain, especially when a cardiac toothache is suspected.
Clinical characteristics of pain may vary between pa-
tients. Pain may be episodic, lasting from minutes to
hours, and varies in intensity, although almost invariably
is precipitated by exertional activ ities an d alleviated with
rest [37]. Intriguingly, patients experiencing cardiac pain
reported the descriptor of “pressure” more often when
compared to any other disorder [38].
If the pain is associated with cardiac or chest pain, it is
most often relieved by sublingual nitroglycerin and im-
mediate referral to a medical practitioner is imperative.
3.3. Sinus Toothache
Sinusitis is a common aliment in the US, resulting in
about 16 million visits to the ph ysician annually [39,40].
Approximately, 15% of the population reports it as a
chronic problem, [41] with about 10% of maxillary si-
nusitis cases being diagnosed as having an odontogenic
origin [42]. Since the roots of the maxillary dentition are
in intimate contact with, and often protruding into, the
sinus cavity, it is comprehensible that th e dentition cou ld
be a potential source of sinus inflammation and infection.
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As the maxillary sinus grows, its final point o f growth is
coincidental with the growth of the maxillary alveolar
process and eruption of the permanent dentition. This
may result in a protrusion of roots into the sinus cavity
that, in some cases, may be separated only by the
Schneiderian membrane (mucoperiosteum) [43].
Due to the close proximity between maxillary poste-
rior roots and the maxillary sinus, an infectious process
in the dentition or surrounding periodontal tissue may
present as an acute or chronic sinusitis; conversely, in-
flammation and infection originating in the maxillary
sinus may be perceived as odontogenic pain. Patients
may present with facial pain and pressure in the maxil-
lary posterior region. Other symptoms such as headache,
halitosis, fatigue, cough, nasal discharge/drainage or
congestion and ear pain may be more identifiable as be-
ing associated with sinus disease [44]. Sinus pain can
also present as a continuous dull ache or diffuse linger-
ing pain in the maxillary teeth [8,45] with sensitivity to
percussion, mastication, and/or temperature. This hy-
persensitivity is often felt in multiple teeth, making it
more indicative of a pain of sinus origin rather than
odontogenic pain [8,46].
Often a history of respiratory infection, nasal conges-
tion, and sinus disease may precede the onset of the
toothache [8]. Pain may be elicited by palpation of the
infraorbital regions or maneuvering the head to below
the levels of the knees, initiating gravitational shifting of
fluid in the sinus [8,47]. The absence of an offending
tooth or gingival inflammation upon intraoral examina-
tion may further lead to the conclusion that there is sinus
inflammation or infection. Although chronic sinusitis
may erode the wall of the sinus, it is rarely associated
with intraoral soft tissue swelling or pain [48]. Intraoral
or panoramic radiographs may be useful to exclude the
dentition as being the source of the problem. The sinu ses
may appear cloudy, opacified, and congested on the
panoramic radiograph. Increased fluid levels and thick-
ening of the sinus mucosal membrane may be apparent on
CT scan [8].
Once identified, treatment should be directed toward
the maxillary sinus infection. Most cases of acute sinusitis
are of viral origin and require nasal decongesttants, a
therapy targeted at reducing the soft tissue edema to allow
drainage of the sinus through the ostium into the middle
meatus of the nasal cavity [46]. In the cases of bacte-
ria-induced sinusitis, a regimen of antibiotics is addition-
ally prescribed [46]. Management is beyond the scope of a
dental professional and appropriate referral to an otorhi-
nolaryngologist or the general medical practitioner is ap-
propriate once there is a clear understanding that the
source of the odontogenic pain is of sinus origin.
3.4. Neurovascular Toothache
Neurovascular pains or headache is a common complaint.
Typically “headache” is pain localized to the cranium.
However, headache may also present as a variant involv-
ing the orofacial region hence mimicking toothache. Two
primary headache types that may present as toothache are
migraine and trigeminal autonomic cephalalgia (Table
1).
The 1-year period prevalence for migraine is 11.7%
(17.1% in women and 5.6% in men) [49]. Migraines are
typically unilateral, moderate to severe pains of pulsatile
and throbbing quality that are often disabling. Pain usu-
ally lasts between 4 and 72 hours and may b e aggr avated
by routine physical activities. Migraine is often accom-
panied by nausea, vomiting, phonophobia and/or photo-
phobia and may present with (20%) or without aura
(80%). An aura is a reversible focal neurological symp-
tom (visual, sensory and motor phenomena) that devel-
ops between 5 and 20 minutes, subsides within 60 min-
utes and is immediately followed by a headache [50].
Although its prevalence is unknown, Migraine may
present in the midface without involvement of the first
division of the trigeminal nerve [51]. Also there are a
few case reports of patients with oral and dental pain
subsequently diagnosed as migraine [52,53]. Obermann
et al. [54] in a case series involving 7 patients reported
migraine presenting in the face occurred more often in
the maxillary division than the mandibular division of
the trigeminal nerve. Apart from location, the migraine
limited to the orofacial region is similar to “cranial” mi-
graine. Penarrocha et al. [55] reviewed 11 patients with
“lower-half facial migraine” and reported that 45% had
endodontic treatment prior to initially developing pain.
Four of these patients reported a history of migraine
prior to the development of “lower-half facial migraine”.
Of concern, the average time elapsed prior to proper
diagnosis was 101 months (6 to 528 months). Also, 36%
of cases had teeth extracted in an attempt to treat the
pain. Benoliel et al. [56] diagnosed 23 of 328 patients
with “neurovascular orofacial pain” over a 2-year period
and proposed an expansion of the current International
Headache Society classification to include orofacial pain
syndromes.
Trigeminal autonomic cephalalgias (TACs) are a col-
lective term that refers to a group of headaches charac-
terized by unilateral head and/or face pain with accom-
panying autonomic features [50,57]. The International
Classification of Headache Disorders II (ICHD-II) clas-
sifies TACs as: 1) episodic or chronic cluster headache
(CH); 2) episodic or chronic paroxysmal hemicrania (PH)
and 3) Short-lasting Unilateral Neuralgiform headache
attacks with Conjunctiv al injection and Tearing (SUNCT)
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OJST
headache
[50].
Although rare, TACs may present a challenge for the
dentist due to its often overlapping and similar presenta-
tions to true odontogenic pains (Table 1). Individuals
often describe the location of pain due to CH emanating
from the midface region which may be interpreted as
pain originating from the teeth, jaws or the temporo-
mandibular joints [58,59]. Bahra and Goadsby [60] re-
ported that 45% of a group of CH patients were seen by
a dentist prior to receiving the correct diagnosis. They
also found that a misdiagnosis provided by a dentist of-
ten led to unnecessary and inappropriate dental proce-
dure(s). In another study, it was found that 42% of 33
CH patients received some form of invasive and irre-
versible dental procedure as their treatment [61]. It has
been postulated that dental extractions may be a precipi-
tating factor for CH. Penarrocha et al., [62] in a study of
54 CH patients, found that prior tooth extraction or en-
dodontics had been performed in the pain affected quad-
rant in 31 (58%) of the subjects and in the contralateral
quadrant in 18 (33%) subjects. Additionally, they found
that in 24 (44%) cases, tooth extraction was performed
after the onset of pain in an attempt to solve the problem
with only 1 patient repo rting improveme nt.
Due to the short duration of attacks, recurrences, ex-
cruciating intensity and pulsatile pain quality found in
PH, it is possible that this disorder may be mistaken for
dental pulpitis [63]. It is also not uncommon for PH to
manifest in the maxillary region thereby being mistaken
for tooth pain [64]. Benoleil and Sharav [65] reported on
7 PH cases, 4 of which had been confused for pain of
dental origin. Two of these patients received irreversible
dental treatments. Other studies have reported similar
occurrences whereby the spectrum of failed dental
treatment ranged from pharmacological approaches to
full mouth reconst ru ct ion [52,66-68].
Although rare, there are case reports in which SUNCT
patients, in addition to facial pain, complain of pain ra-
diating to adjacent teeth. This has resulted in dentists
delivering therapeutic interventions for tooth pain such
as extraction, occlusal splints and incorrect pharmacol-
ogy [69-71]. In order for dentists to avoid the pitfalls of
providing unnecessary interventions for misdiagnosed
toothaches of neurovascular origin, they must perform a
thorough history and comprehensive clinical examina-
tion. If this process does not yield convincing evidence
of pain from an odontogenic origin then referral to the
appropriate practitioner sho uld be pursued.
3.5. Neuropathic Toothache
Neuropathic pain refers to a pain that originates from
abnormalities in the neural structures and not from the
tissues that are innervated by those neural structures.
These pains pose significant difficulty for the clinician
since the structures the patient reports as painful appear
clinically normal. There are two types of neuropathic
pains that can be felt in teeth: episodic and continuous.
Table 1. Differentiating features of neurovascular pain and dental pain [111,112].
Feature Migraine
Cluster Paroxysmal
hemicrania SUNCT Acute pulpal pain Chronic pulpal pain Periodontal pain
Sex (male:fem ale) 1:3 5:1 1:2 2:1 1:1 1:1 1:1
Age (years) 10 - 50 20 - 40 30 40 - 70 any age any age any age
Pain type pulsating boring boring electric-likethrobbing or
aching tender or aching tender or aching
Pain severity moderate to severe very severevery severe very severemild to severe mild mild
Pain location frontotemporal orbital orbital orbital tooth tooth
tooth/gingival
/bone
Pain duration 4 - 72 hours 15 - 180
minutes 2 - 30 minutes 15 - 240 seconds seconds to daily constant variable
Pain frequency 1/month 1 - 8/day 2 - 40/day 3 - 200/dayvariable Daily Daily
Autonomic
features No; may have with aura Yes Yes Yes No No No
Trigger
stress, foods, vasodilators,
sleep pattern changes,
afferent stimulation,
hormonal changes
alcohol,
nitrates mechanical cutaneous
electric & thermal
stimulation,
tooth percussioninconsistent apical or lateral
tooth pressure

R. Balasubramaniam et al. / Open Journal of Stomatology 1 (2011) 92-102 97
Episodic neuropathic pain is characterized by sudden
volleys of electric-like pain referred to as neuralgia. The
most typical example of this type of pain is trigeminal
neuralgia. When this type of paroxysmal pain is felt in a
tooth it can pose significant diagnostic challenges for the
clinician. The clinical presentation of an episodic neuro-
pathic toothache is a severe, shooting, electric-like pain
that lasts only a few seconds [4,72,73]. The pain is not
always restricted to a tooth but often a broader area. The
pain is not altered by intraoral thermal stimuli [4,6,72]. It
rarely awakes the patient from sleep unlike dental pain.
The most common branch of the trigeminal nerve in-
volved is the mandibular followed by the maxillary and
least involved is the ophthalmic [4,72]. The pain is often
severe with patients reporting the pain as being the most
intense they have ever experienced. Often the patient is
able to trace the pain radiating down the distribution of
the nerve to the tooth [6].
With trigeminal neuralgia there is often a trigger zone
that, when lightly stimulated, provokes the severe par-
oxysmal pain. Anesthetic blocking of the trigger zone
will completely eliminate the toothache and paroxysmal
episodes during the period of anesthesia. On occasion a
tooth can represent the trigger zone, and if this occurs, it
can pose a great diagnostic challenge for the clinician.
Patients with trigeminal neuralgia frequently receive
endodontic treatment for their dental pain [74,75]. Addi-
tional case repor ts also provide examples of the opposite
diagnostic problem: patients with odontogenic dental
pain being diagnosed as having trigeminal neuralgia [76].
In both types of misdiagnosis, the lack of response to
treatment is a key factor in prompting reassessment of
the differential diagnosis.
Continuous neuropathic pains are pain disorders that
have their origin in neural structures and are expressed
as constant, ongoing and unremitting pain. They will
often have high and low intensity but no periods of total
remission. Continuous neuropathic pains that can be felt
in teeth have been referred to as atypical odontalgia
[77,78] or sometimes phantom toothache [79,80]. Con-
tinuous neuropathic pain appears to have its origin asso-
ciated with central plasticity in the trigeminal nuclear
complex of the brain stem [81]. In some instances there
may be a sympathetic component to the pain [82]. Pa-
tients with continuous neuropathic toothache often report
a history of trauma or ineffective dental treatment in the
area [83]. In a study of 42 patients with atypical odon-
talgia, 86% of the patient population was female and
78% reported maxillary pain. Of 119 reported areas of
pain, the most common were the molar (59%), premolar
(27%), and canine (4%) regions [84,85]. The pain may
change in location over time; some studies have reported
pain shifting location in up to 82% of the subjects
[82,86].
It is not unusual for patients with continuous neuro-
pathic toothache to have received multiple endodontic
treatments or extractions for their dental pain [84,86-90].
In many cases, the lack of response to treatment is a key
factor in prompting reassessment of the differential di-
agnosis [91]. Ram et al. [92] in their retrospective study
involving 64 patients reported that 71% had initially
consulted a dentist for their pain complaint, and sub-
sequently 79% of patients received dental treatment that
did not resolve the pain. In one case report, the lack of
an effect of a local anesthetic injection on reducing the
intensity of pain was a significant finding that pro-
mpted consideration of non-odontogenic tooth pain
[90].
The following characteristics of continuous neuro-
pathic toothache can be used to differentiate it from
odontogenic pain: a) diffuse pain, b) pain not always
restricted to a tooth (e.g., the area may be edentulous), c)
pain that is almost always continuous, d) a pain quality
often described as a dull, aching, throbbing, or burning,
e) pain that may or may not be relieved by a diagnostic
intraoral local anesthetic block, f) pain that often lasts
more than 4 months, and g) pain not altered by intraoral
thermal stimuli [4,6,82,85,88,93,94].
3.6. Neoplastic Toothache
Orofacial pain may be the initial symptom of oral cancer
and can motivate patients to seek care from their dental
practitioners. Primary squamous cell carcinoma (SCC)
of the oral mucosa may present with pain and sensory
disturbances that mimic toothache symptoms particu-
larly when located on the gingiva, vestibule or floor of
mouth. One retrospective case series found pain to be the
first clinical sign of oral cancer in 19.2% of cases [95],
while other literature has suggested that two-thirds of
patients with oral cancer have reported localized dis-
comfort within the 6 months preceding a cancer diagno-
sis [96]. Primary intraosseous carcinoma is a SCC that
occurs within the ja ws, has no initial con n ection with the
oral mucosa, and arises from either a previous odonto-
genic cyst or de novo [97]. These malignancies are ex-
tremely rare, but when they do occur, they can be mis-
taken for odontogenic origin since the clinical presenta-
tion of localized bone loss may have the appearance of
localized periodontal disease.
Nasopharyngeal cancers may present with signs and
symptoms that have been confused with, and treated as,
temporomandibular disorders [98,99], parotid gland le-
sions [100], and odontogenic infections with trismus
[101]. While signs and symptoms of nasopharyngeal
carcinomas may mimic temporomandibular disorders,
such as facial pain, limited j aw opening, deviation of the
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R. Balasubramaniam et al. / Open Journal of Stomatology 1 (2011) 92-102 98
jaw on opening, earache, and headache [98,99], some of
these signs may also be found and confused with an
odontogenic et i ology.
Systemic cancers such as lymphoma and leukemia
may have intraoral manifestations that mimic toothache-
like symptoms. Such can cers can infiltrate pain-sensitive
structures such as periosteum and gingiva, thereby caus-
ing localized pain that may be confused with odonto-
genic and/or periodontal conditions [102]. In rare cir-
cumstances, the osseous osteolytic lesions of multiple
myeloma may develop adjacent to teeth. When this oc-
curs, odontogenic pain is common and presents a ra-
diologic diagnostic challenge as the osteolytic lesions
appear to be associated with teeth but are actually related
to the systemic disease [103].
Orofacial pain has also been reported in patients with
distant non-metastasized cancers, most commonly from
the lungs [104-107]. In such circumstances, the facial
pain is almost always unilateral affecting the ear, jaws
and temporal region, frequently described as severe and
aching, and usually continuous and progressive. Such a
presentation may be confused with referred pain of
odontogenic origin.
Orofacial pain may be associated with metastatic ma-
lignancies and when metastatic orofacial tumors occur,
they affect the jaw bones more often than the oral soft
tissues [108]. Metastases most often develop from the
breast in women and the lung and prostate in males, with
the most common sites of occurrence in the jaws being
the posterior mandible, angle of the jaw, and ramus [108,
109]. Pain is a rare complaint in soft tissue metastases
[11 0], whereas in metastatic disease of the jaw bones,
pain has been reported in 39% and paresthesias in 23%
of patients [111]. The pain and clinical presentation can
be misinterpreted as that originating from an odonto-
genic source. In a retrospective case series of metastatic
disease in the jaws, 60% of 114 cases reported the me-
tastatic lesion in th e oral region to be th e first indication
of an undiscovered primary malignancy at a distant site
[109].
Signs and symptoms of orofacial malignancies may
mimic odontogenic etiology. It is important for dental
practitioners to use appropriate judgment when clinical
findings do not correlate with the results of odontogenic
diagnostic testing. Neoplastic toothache must be consid-
ered when localized soft or hard tissue changes develop
in close proximity to odontogenic structures and diag-
nostic findings are equivocal or negative.
3.7. Psychogenic Toothache
Psychogenic pain is pain that is associated with psy-
chologic factors in the absence of any physiologic cause.
The American Psychiatric Association has classified this
condition as a somatoform pain disorder [112], indicat-
ing that clear evidence of a causal relationship between
pain and psychologic factors is not required. While psy-
chologic factors may be implicated, pain conditions clas-
sified under this definition may occur without th e role of
psychologic factors [113].
Pain descriptors are often diffuse, vague, and difficult
to localize [113]. When the somatoform pain disorder is
felt in the teeth, multiple teeth are often involved [6].
Pain may be sharp, stabbing, intense, and sensitive to
temperature changes, all of which are similar to pain
symptoms of odontogenic origin. However, the pain is
inconsistent with normal patterns of physiologic pain
and presents without any identifiable pathologic cause.
When accompanied by other psychiatric features such as
hallucinations or delusions, there is a greater possibility
that the pain is of psychogenic origin [113].
Given that psychogenic toothache is a somatoform
disorder, dental treatment will not resolve symptoms of
pain and may poten tially elicit an unexpected or unusual
response to therapy [6]. Patients should be referred to a
psychiatrist or psychologist for further management.
4. CONCLUSIONS
There are a multitude of non-odontogenic pains that can
present at the site of a tooth and can mimic a toothache.
Dental practitioners should also have an understanding
of the complex mechanism of odontogenic pain and the
manner in which other orofacial structures may simulate
dental pain. In patients who present with toothache pain,
dental practitioners should consider alternate etiologies
of the pain when appropriate diagnostic tests do not lead
to odontogenic etio logy. Failure to establish the etiology
of the pain will result in incorrect diagnosis and inap-
propriate treatment.
REFERENCES
[1] Sarlani, E., Balciunas, B.A., and Grace, E.G. (2005)
Orofacial pain—Part II: Assessment and management of
vascular, neurovascular, idiopathic, secondary, and psy-
chogenic causes. AACN Clinical Issues, 16, 347-358.
doi:10.1097/00044067-200507000-00008
[2] Annino, D.J. and Goguen, L.A. (2003) Pain from the oral
cavity. Otolaryngologic Clinics of North America, 36,
1127-1135. doi:10.1016/S0030-6665(03)00132-4
[3] Lipton, J.A., Ship, J.A. and Larach-Robinson, D. (1993)
Estimated prevalence and distribution of reported orofa-
cial pain in the United States. The Journal of the Ameri-
can Dental Association, 124, 115-121.
[4] Okeson, J.P. (2005) Bell’s orofacial pains: The clinical
management of orofacial pain. Quintessence, Chicago.
[5] Ikeda, H. and Suda, H. (2003) Sensory experiences in
relation to pulpal nerve activation of human teeth in dif-
ferent age groups. Archives of Oral Biology, 48, 835-841.
C
opyright © 2011 SciRes. OJST

R. Balasubramaniam et al. / Open Journal of Stomatology 1 (2011) 92-102 99
doi:10.1016/S0003-9969(03)00176-6
[6] Okeson, J.P. and Falace, D.A. (1997) Nonodontogenic
toothache. Dental Clinics of North America, 41, 367-383.
[7] Falace, D.A., Reid, K. and Rayens, M.K. (1996) The
influence of deep (odontogenic) pain intensity, quality,
and duration on the incidence and characteristics of re-
ferred orofacial pain. Journal of Orofacial Pain, 10,
232-239.
[8] Okeson, J.P. (2000) Non-odontogenic toothache. North-
west Dent, 79, 37-44.
[9] Davidoff, R.A. (1998) Trigger points and myofascial pain:
Toward understanding how they affect headaches.
Cephalalgia, 18, 436-448.
doi:10.1046/j.1468-2982.1998.1807436.x
[10] Mense, S. (2003) The pathogenesis of muscle pain. Cur-
rent Pain and Headache Reports, 7, 419-425.
doi:10.1007/s11916-003-0057-6
[11] Fricton, J.R., Kroening, R., Haley, D. and Siegert, R.
(1985) Myofascial pain syndrome of the head and neck:
A review of clinical characteristics of 164 patients. Oral
Surgery, Oral Medicine, Oral Pathology, 60, 615-623.
doi:10.1016/0030-4220(85)90364-0
[12] Simons, D.G., Travell, J.G. and Simons, L.S. (1999)
Travell and Simons’ myofascial pain and dysfunction:
The trigger point manual. 2nd Edition, Williams & Wil-
kins.
[13] Jerjes, W., Hopper, C., Kumar, M., Upile, T., Madland, G.,
Newman, S., et al. (2007) Psychological intervention in
acute dental pain: Review. British Dental Journal, 202,
337-343. doi:10.1038/bdj.2007.227
[14] Fricton, J.R. (1995) Management of masticat ory myofas-
cial pain. Seminars in Orthodontics, 1, 229-243.
doi:10.1016/S1073-8746(95)80054-9
[15] Hong, C.Z., Kuan, T.S., Chen, J.T. and Chen, S.M. (1997)
Referred pain elicited by palpation and by needling of
myofascial trigger points: A comparison. Archives of
Physical Medicine and Rehabilitation, 78, 957-960.
doi:10.1016/S0003-9993(97)90057-5
[16] Sessle, B.J., Hu, J.W., Amano, N. and Zhong, G. (1986)
Convergence of cutaneous, tooth pulp, visceral, neck and
muscle afferents onto nociceptive and non-nociceptive
neurones in trigeminal subnucleus caudalis (medullary
dorsal horn) and its implications for referred pain. Pain,
27, 219-235. doi:10.1016/0304-3959(86)90213-7
[17] Wright, E.F. (2000) Referred craniofacial pain patterns in
patients with temporomandibular disorder. The Journal
of the American Dental Association, 131, 1307-1315.
[18] Ehrmann, E.H. (2002) The diagnosis of referred orofacial
dental pain. Australian Endodontic Journal, 28, 75-81.
doi:10.1111/j.1747-4477.2002.tb00388.x
[19] Linn, J., Trantor, I., Teo, N., Thanigaivel, R. and Goss,
A.N. (2007) The differential diagnosis of toothache from
other orofacial pains in clinical practice. Australian Dental
Journal, 52, 100-104.
doi:10.1111/j.1834-7819.2007.tb00518.x
[20] Kreiner, M., Okeson, J.P., Michelis, V., Lujambio, M. and
Isberg, A. (2007) Craniofacial pain as the sole symptom
of cardiac ischemia: A prospective multicenter study. The
Journal of the American Dental Association, 138, 74-79.
[21] Tzukert, A., Hasin, Y. and Sharav, Y. (1981) Orofacial
pain of cardiac origin. Oral Surgery, Oral Medicine, Oral
Pathology, 51, 484-486.
doi:10.1016/0030-4220(81)90006-2
[22] Batchelder, B.J., Krutchkoff, D.J. and Amara, J. (1987)
Mandibular pain as the initial and sole clinical manifesta-
tion of coronary insufficiency: Report of case. The Jour-
nal of the American Dental Association, 11 5, 710-712.
[23] Takayanagi, K., Fujito, T., Morooka, S., Takabatake, Y.
and Nakamura, Y. (1990) Headache angina with fatal
outcome. Japanese Heart Journal, 31, 503-507.
doi:10.1536/ihj.31.503
[24] Ishida, A., Sunagawa, O., Touma, T., Shinzato, Y., Ka-
wazoe, N. and Fukiyama, K. (1996) Headache as a mani-
festation of myocardial infarction. Japanese Heart Jour-
nal, 37, 261-263. doi:10.1536/ihj.37.261
[25] Veelken, R., Glabasnia, A., Stetter, A., Hilgers, K.F.,
Mann, J.F. and Schmieder, R.E. (1996) Epicardial bra-
dyki nin B 2 rec ep to rs el ic i t a sympathoexcitatory reflex in
rats. Hypertension, 28, 615-621.
[26] White, J.C. (1957) Cardiac pain: Anatomic pathways and
physiologic mechanisms. Circulation, 16, 644-655.
[27] Staszewska-Barczak, J. and Dusting, G.J. (1977) Sympa-
thetic cardiovascular reflex initiated by bradykinin-in-
duced stimulation of cardiac pain receptors in the dog.
Clinical and Experimental Pharmacology and Physiol-
ogy, 4, 443-452.
doi:10.1111/j.1440-1681.1977.tb02408.x
[28] Pal, P., Koley, J., Bhattacharyya, S., Gupta, J.S. and
Koley, B. (1989) Cardiac nociceptors and ischemia: Role
of sympathetic afferents in cat. The Japanese Journal of
Physiology, 39, 131-144. doi:10.2170/jjphysiol.39.131
[29] Meller, S.T. and Gebhart, G.F. (1992) A critical review of
the afferent pathways and the potential chemical media-
tors involved in cardiac pain. Neuroscience, 48, 501-524.
doi:10.1016/0306-4522(92)90398-L
[30] Meller, S.T., Lewis, S.J., Ness, T.J., Brody, M.J. and
Gebhart, G.F. (1990) Vagal afferent-mediated inhibition
of a nociceptive reflex by intravenous serotonin in the rat.
I. characterization. Brain Research, 524, 90-100.
[31] James, T.N. (1989) A cardiogenic hypertensive chemore-
flex. Anesth Analg, 69, 633-646.
doi:10.1213/00000539-198911000-00016
[32] Myers, D.E. (2008) Vagus nerve pain referred to the cra-
niofacial region. A case report and literature review with
implications for referred cardiac pain. British Dental
Journal, 204, 187-189. doi:10.1038/bdj.2008.101
[33] Liporace, J., Hucko, D., Morrow, R., Barolat, G., Nei, M.,
Schnur, J., et al. (2001) Vagal nerve stimulation: Adjust-
ments to reduce painful side effects. Neurology, 57, 885-
886.
[34] Rush, A.J., Marangell, L.B., Sackeim, H.A., George,
M.S., Brannan, S.K., Davis, S.M., et al. (2005) Vagus
nerve stimulation for treatment-resistant depression: A
randomized, controlled acute phase trial. Biological
Psychiatry, 58, 347-354.
doi:10.1016/j.biopsych.2005.05.025
[35] Carius, A. and Schulze-Bonhage, A. (2005) Trigeminal
pain under vagus nerve stimulation. Pain, 118, 271-273.
doi:10.1016/j.pain.2005.07.022
[36] Shih, J.J., Devier, D. and Behr, A. (2003) Late onset la-
ryngeal and facial pain in previously asymptomatic vagus
nerve stimulation patients. Neurology, 60, 1214.
[37] Kreiner, M. and Okeson, J.P. (1999) Toothache of cardiac
origin. Journal of Orofacial Pain, 13, 201-207.
C
opyright © 2011 SciRes. OJST

R. Balasubramaniam et al. / Open Journal of Stomatology 1 (2011) 92-102 100
[38] Kreiner, M., Falace, D., Michelis, V., Okeson, J.P. and
Isberg, A. (2010) Quality difference in craniofacial pain
of cardiac vs. dental origin. Journal of Dental Research,
89, 965-969. doi:10.1177/0022034510370820
[39] Fagnan, L.J. (1998) Acute sinusitis: A cost-effective ap-
proach to diagnosis and treatment. American Family
Physician, 58, 1795-1802, 1805-1806.
[40] (2000) Antimicrobial treatment guidelines for acute bac-
terial rhinosinusitis. Sinus and Allergy Health Partnership.
Otolaryngology—Head and Neck Surgery, 123, 5-31.
[41] Piccirillo, J.F., Mager, D.E., Frisse, M.E., Brophy, R.H.
and Goggin, A. (2001) Impact of first-line vs second-line
antibiotics for the treatment of acute uncomplicated si-
nusitis. The Journal of the American Medical Association,
286, 1849-1856. doi:10.1001/jama.286.15.1849
[42] Mehra, P. and Murad, H. (2004) Maxillary sinus disease
of odontogenic origin. Otolaryngologic Clinics of North
America, 37, 347-364.
doi:10.1016/S0030-6665(03)00171-3
[43] Brook, I. (2006) Sinusitis of odontogenic origin. Otolar-
yngology—Head and Neck Surgery, 135, 349-355.
doi:10.1016/j.otohns.2005.10.059
[44] Osguthorpe, J.D. and Hadley, J.A. (1999) Rhinosinusitis.
Current concepts in evaluation and management. Medical
Clinics of North America, 83, 27-41.
doi:10.1016/S0025-7125(05)70085-7
[45] Falk, H., Ericson, S. and Hugoson, A. (1986) The effects
of periodontal treatment on mucous membrane thicken-
ing in the maxillary sinus. Journal of Clinical Periodon-
tology, 13, 217-222.
doi:10.1111/j.1600-051X.1986.tb01463.x
[46] Kretzschmar, D.P. and Kretzschmar, J.L. (2003) Rhinos-
inusitis: Review from a dental perspective. Oral Surgery,
Oral Medicine, Oral Pathology, Oral Radiology and
Endodontology, 96, 128-135.
doi:10.1016/S1079-2104(03)00306-8
[47] Murphy, E. and Merrill, R.L. (2001) Non-odontogenic
toothache. Journal of the Irish Dental Association, 47,
46-58.
[48] Rafetto, L. (1999) Clinical examination of the maxillary
sinus. Oral and Maxillofacial Surgery Clinics of North
America, 11 , 35-44.
[49] Lipton, R.B., Bigal, M.E., Diamond, M., Freitag, F.,
Reed, M.L. and Stewart, W.F. (2007) Migraine preva-
lence, disease burden, and the need for preventive ther-
apy. Neurology, 68, 343-349.
doi:10.1212/01.wnl.0000252808.97649.21
[50] Olesen, J. (2004) The international classification of head-
ache disorders. Cephalalgia, 24, 9-160.
doi:10.1111/j.1468-2982.2003.00824.x
[51] Lovshin, L.L. (1977) Carotidynia. Headache, 17, 192-
195. doi:10.1111/j.1526-4610.1977.hed1705192.x
[52] Alonso, A.A. and Nixdorf, D.R. (2006) Case series of
four different headache types presenting as tooth pain.
Journal of Endodontics, 32, 1110-1113.
doi:10.1016/j.joen.2006.02.033
[53] Namazi, M.R. (2001) Presentation of migraine as odon-
talgia. Headache, 41, 420-421.
doi:10.1046/j.1526-4610.2001.111006420.x
[54] Obermann, M., Mueller, D., Yoon, M.S., Pageler, L.,
Diener, H. and Katsarava, Z. (2007) Migraine with iso-
lated facial pain: A diagnostic challenge. Cephalalgia, 27,
1278-1282. doi:10.1111/j.1468-2982.2007.01413.x
[55] Penarrocha, M., Bandres, A. and Bagan, J.V. (2004)
Lower-half facial migraine: A report of 11 cases. Journal
of Oral and Maxillofacial Surgery, 62, 1453-1456.
doi:10.1016/j.joms.2004.01.027
[56] Benoliel, R. and Sharav, Y. (2008) Neurovascular orofa-
cial pain. Cephalalgia, 28, 199-200.
[57] Goadsby, P.J. and Lipton, R.B. (1997) A review of par-
oxysmal hemicranias, SUNCT syndrome and other
short-lasting headaches with autonomic feature, includ-
ing new cases. Brain, 120, 193-209.
doi:10.1093/brain/120.1.193
[58] Brooke, R.I. (1978) Periodic migrainous neuralgia: A
cause of dental pain. Oral Surgery, Oral Medicine, Oral
Pathology, 46, 511-516.
doi:10.1016/0030-4220(78)90381-X
[59] Gross, S.G. (2006) Dental presentations of cluster head-
aches. Current Pain and Headache Reports, 10, 126-129.
doi:10.1007/s11916-006-0023-1
[60] Bahra, A. and Goadsby, P.J. (2004) Diagnostic delays and
mis-management in cluster headache. Acta Neurologica
Scandinavica, 109, 175-179.
doi:10.1046/j.1600-0404.2003.00237.x
[61] Bittar, G. and Graff-Radford, S.B. (1992) A retrospective
study of patients with cluster headaches. Oral Surgery,
Oral Medicine, Oral Pathology, 73, 519-525.
doi:10.1016/0030-4220(92)90088-8
[62] Penarrocha, M., Bandres, A., Penarrocha, M.A. and Ba-
gan, J.V. (2001) Relationship between oral surgical and
endodontic procedures and episodic cluster headache.
Oral Surgery, Oral Medicine, Oral Pathology Oral Ra-
diol Endod, 92, 499-502. doi:10.1067/moe.2001.116153
[63] Sarlani, E., Schwartz, A.H., Greenspan, J.D. and Grace,
E.G. (2003) Chronic paroxysmal hemicrania: A case re-
port and review of the literature. Journal of Orofacial
Pain, 17, 74-78.
[64] Antonaci, F. and Sjaastad, O. (1989) Chronic paroxysmal
hemicrania (CPH): A review of the clinical manifesta-
tions. Headache, 29, 648-656.
doi:10.1111/j.1526-4610.1989.hed2910648.x
[65] Benoliel, R. and Sharav, Y. (1998) Paroxysmal hemicra-
nia. Case studies and review of the literature. Oral Sur-
gery, Oral Medicine, Oral Pathology, Oral Radiology
and Endodontology, 85, 285-292.
doi:10.1016/S1079-2104(98)90010-5
[66] Benoliel, R., Elishoov, H. and Sharav, Y. (1997) Orofa-
cial pain with vascular-type features. Oral Surgery, Oral
Medicine, Oral Pathology, Oral Radiology and Endo-
dontology, 84, 506-512.
doi:10.1016/S1079-2104(97)90267-5
[67] Delcanho, R.E. and Graff-Radford, S.B. (1993) Chronic
paroxysmal hemicrania presenting as toothache. Journal
of Orofacial Pain, 7, 300-306.
[68] Moncada, E. and Graff-Radford, S.B. (1995) Benign
indomethacin-responsive headaches presenting in the
orofacial region: Eight case reports. Journal of Orofacial
Pain, 9, 276-284.
[69] Benoliel, R. and Sharav, Y. (1998) SUNCT syndrome:
Case report and literature review. Oral Surgery, Oral
Medicine, Oral Pathology, Oral Radiology and Endo-
dontology, 85, 158-161.
doi:10.1016/S1079-2104(98)90419-X
C
opyright © 2011 SciRes. OJST

R. Balasubramaniam et al. / Open Journal of Stomatology 1 (2011) 92-102 101
[70] Leone, M., Mea, E., Genco, S. and Bussone, G. (2006)
Coexistence of TACS and trigeminal neuralgia: Patho-
physiological conjectures. Headache, 46, 1565-1570.
doi:10.1111/j.1526-4610.2006.00537.x
[71] de Siqueira, S.R., Nobrega, J.C., Teixeira, M.J. and de
Siqueira, J.T. (2006) SUNCT syndrome associated with
temporomandibular disorders: A case report. Cranio, 24,
300-302.
[72] Loeser, J.D. (2001) Bonica’s management of pain. Lip-
pincott Williams &Wilkins, Philadelphia.
[73] Merrill, R.L. and Graff-Radford, S.B. (1992) Trigeminal
neuralgia: How to rule out the wrong treatment. The
Journal of the American Dental Association, 123, 63-68.
[74] Goddard, G. (1992) Case report of trigeminal neuralgia
presenting as odontalgia. Cranio, 10, 245-247.
[75] Law, A.S. and Lilly, J.P. (1995) Trigeminal neuralgia
mimicking odontogenic pain. A report of two cases. Oral
Surgery, Oral Medicine, Oral Pathology, Oral Radiology
and Endodontology, 80, 96-100.
doi:10.1016/S1079-2104(95)80024-7
[76] Donlon, W.C. (1989) Odontalgia mimicking trigeminal
neuralgia. Anesthesia Progress, 36, 98-100.
[77] Graff-Radford, S.B. and Solberg, W.K. (1993) Is atypical
odontalgia a psychological problem? Oral Surgery, Oral
Medicine, Oral Pathology, 75, 579-582.
doi:10.1016/0030-4220(93)90228-V
[78] Clark, G.T. (2006) Persistent orodental pain, atypical
odontalgia, and phantom tooth pain: When are they neu-
ropathic disorders? Journal of the California Dental As-
sociation, 34, 599-609.
[79] Marbach, J.J. (1978) Phantom tooth pain. Journal of
Endodontics, 4, 362-372.
doi:10.1016/S0099-2399(78)80211-8
[80] Marbach, J.J. (1993) Phantom tooth pain: Differential
diagnosis and treatment. The New York State Dental
Journal, 59, 28-33.
[81] Kwan, C.L., Hu, J.W. and Sessle, B.J. (1993) Effects of
tooth pulp deafferentation on brainstem neurons of the rat
trigeminal subnucleus oralis. Somatosensory and Motor
Research, 10, 115-131. doi:10.3109/08990229309028828
[82] Vickers, E.R., Cousins, M.J., Walker, S. and Chisholm, K.
(1998) Analysis of 50 patients with atypical odontalgia. A
preliminary report on pharmacological procedures for
diagnosis and treatment. Oral Surgery, Oral Medicine,
Oral Pathology, Oral Radiology and Endodontology, 85,
24-32. doi:10.1016/S1079-2104(98)90393-6
[83] Marbach, J.J. (1996) Orofacial phantom pain: Theory and
phenomenology. The Journal of the American Dental As-
sociation, 127, 221-229.
[84] Solberg, W.K. and Graff-Radford, S.B. (1988) Orodental
considerations in facial pain. Seminars in Neurology, 8,
318-323. doi:10.1055/s-2008-1041396
[85] Graff-Radford, S.B. and Solberg, W.K. (1992) Atypical
odontalgia. Journal of Craniomandibular Disorders, 6,
260-265.
[86] Lilly, J.P. and Law, A.S. (1997) Atypical odontalgia mis-
diagnosed as odontogenic pain: A case report and discus-
sion of treatment. Journal of Endodontics, 23, 337-339.
doi:10.1016/S0099-2399(97)80419-0
[87] Truelove, E. (2004) Management issues of neuropathic
trigeminal pain from a dental perspective. Journal of
Orofacial Pain, 18, 374-380.
[88] Battrum, D.E. and Gutmann, J.L. (1996) Phantom tooth
pain: A diagnosis of exclusion. International Endodontic
Journal, 29, 190-194.
doi:10.1111/j.1365-2591.1996.tb01368.x
[89] Reik, L. et al. (1985) Atypical facial pain: A reappraisal.
Headache, 25, 30-32.
doi:10.1111/j.1526-4610.1985.hed2501030.x
[90] Kreisberg, M.K. (1982) Atypical odontalgia: Differential
diagnosis and treatment. The Journal of the American
Dental Association, 104, 852-854.
[91] Klausner, J.J. (1994) Epidemiology of chronic facial pain:
Diagnostic usefulness in patient care. The Journal of the
American Dental Association, 125, 1604-1611.
[92] Ram, S., Teruel, A., Kumar, S.K. and Clark, G. (2009)
Clinical characteristics and diagnosis of atypical odon-
talgia: Implications for dentists. The Journal of the
American Dental Association, 140, 223-228.
[93] Pertes, R.A. and Heir, G.M. (1991) Chronic orofacial
pain. A practical approach to differential diagnosis. Den-
tal Clinics of North America, 35, 123-140.
[94] Rees, R.T. and Harris, M. (1979) Atypical odontalgia.
British Journal of Oral Surgery, 16, 212-218.
doi:10.1016/0007-117X(79)90027-1
[95] Cuffari, L., Tesseroli de Siqueira, J.T., Nemr, K. and
Rapaport, A. (2006) Pain complaint as the first symptom
of oral cancer: A descriptive study. Oral Surgery, Oral
Medicine, Oral Pathology, Oral Radiology and Endo-
dontology, 102, 56-61. doi:10.1016/j.tripleo.2005.10.041
[96] Gorsky, M., Epstein, J.B., Oakley, C., Le, N.D., Hay, J.
and Stevenson-Moore, P. (2004) Carcinoma of the tongue:
A case series analysis of clinical presentation, risk factors,
staging, and outcome. Oral Surgery, Ora l M e di ci ne , Oral
Pathology, Oral Radiology and Endodontology, 98, 546-
552. doi:10.1016/j.tripleo.2003.12.041
[97] Chaisuparat, R., Coletti, D., Kolokythas, A., Ord, R.A.
and Nikitakis, N.G. (2006) Primary intraosseous odonto-
genic carcinoma arising in an odontogenic cyst or de
novo: A clinicopathologic study of six new cases. Oral
Surgery, Oral Medicine, Oral Pathology, Oral Radiology
and Endodontology, 101, 194-200.
doi:10.1016/j.tripleo.2005.03.037
[98] Epstein, J.B. and Jones, C.K. (1993) Presenting signs and
symptoms of nasopharyngeal carcinoma. Oral Surgery,
Oral Medicine, Oral Pathology, 75, 32-36.
doi:10.1016/0030-4220(93)90402-P
[99] Reiter, S., Gavish, A., Winocur, E., Emodi-Perlman, A.
and Eli, I. (2006) Nasopharyngeal carcinoma mimicking
a temporomandibular disorder: A case report. Journal of
Orofacial Pain, 20, 74-81.
[100] Cohen, S.G. and Quinn, P.D. (1988) Facial trismus and
myofascial pain associated with infections and malignant
disease. Report of five cases. Oral Surgery, Oral Medi-
cine, Oral Pathology, 65, 538-544.
doi:10.1016/0030-4220(88)90136-3
[101] Hauser, M.S. and Boraski, J. (1986) Oropharyngeal car-
cinoma presenting as an odontogenic infection with tris-
mus. Oral Surgery, Oral Medicine, Oral Pathology, 61,
330-332. doi:10.1016/0030-4220(86)90411-1
[102] Barrett, A.P. (1984) Gingival lesions in leukemia. A clas-
sification. Journal of Periodontology, 55, 585-588.
[103] Epstein, J.B., Voss, N.J. and Stevenson-Moore, P. (1984)
Maxillofacial manifestations of multiple myeloma. An
C
opyright © 2011 SciRes. OJST

R. Balasubramaniam et al. / Open Journal of Stomatology 1 (2011) 92-102 102
OJST
unusual case and review of the literature. Oral Surgery,
Oral Medicine, Oral Pathology, 57, 267-271.
doi:10.1016/0030-4220(84)90182-8
[104] Abraham, P.J., Capobianco, D.J. and Cheshire, W.P.
(2003) Facial pain as the presenting symptom of lung
carcinoma with normal chest radiograph. Headache, 43,
499-504. doi:10.1046/j.1526-4610.2003.03097.x
[105] Capobianco, D.J. (1995) Facial pain as a symptom of
nonmetastatic lung cancer. Headache, 35, 581-585.
doi:10.1111/j.1526-4610.1995.hed3510581.x
[106] Eross, E.J., Dodick, D.W., Swanson, J.W. and Capobi-
anco, D.J. (2003) A review of intractable facial pain sec-
ondary to underlying lung neoplasms. Cephalalgia, 23,
2-5. doi:10.1046/j.1468-2982.2003.00478.x
[107] Sarlani, E., Schwartz, A.H., Greenspan, J.D. and Grace,
E.G. (2003) Facial pain as first manifestation of lung can-
cer: A case of lung cancer-related cluster headache and a
review of the literature. Journal of Orofacial Pain, 17,
262-267.
[108] Hirshberg, A. and Buchner, A. (1995) Metastatic tumours
to the oral region. An overview. European Journal of
Cancer Part B Oral Oncology, 31, 355-360.
doi:10.1016/0964-1955(95)00031-3
[109] D’Silva, N.J., Summerlin, D.J., Cordell, K.G., Abdelsayed,
R.A., Tomich, C.E., Hanks, C.T., et al. (2006) Metastatic
tumors in the jaws: A retrospective study of 114 cases.
The Journal of the American Dental Association, 137,
1667-1672.
[110] Hirshberg, A., Leibovich, P. and Buchner, A. (1993) Me-
tastases to the oral mucosa: Analysis of 157 cases. Jour-
nal of Oral Pathology and Medicine, 22, 385-390.
doi:10.1111/j.1600-0714.1993.tb00128.x
[111] Hirshberg, A., Leibovich, P. and Buchner, A. (1994) Me-
tastatic tumors to the jawbones: Analysis of 390 cases.
Journal of Oral Pathology and Medicine, 23, 337-341.
doi:10.1111/j.1600-0714.1994.tb00072.x
[112] American Psychiatric Association (1980) Diagnostic and
Statistical Manual (DSM-III). 3rd Edition, Washington
DC.
[113] Dworkin, S.F. and Burgess, J.A. (1987) Orofacial pain of
psychogenic origin: Current concepts and classification.
The Journal of the American Dental Association, 115,
565-571.