Mechanism of Odontogenic and Non-Odontogenic Pain CONTENTS: DEFINITION TRIGEMINAL PAIN SYSTEM PERIPHERAL PAIN MECHANISM CENTRAL PAIN MECHANISM NEUROPHYSIOLOGY OF PAIN REFFERED PAIN THEORIES OF PAIN ASSESSMENT OF PAIN PAIN CLASSIFICATION ODONTOGENIC PAIN NON-ODONTOGENIC PAIN HISTORY OF PAIN PHYSICAL EXAMINATION DIAGNOSIS OF PAIN CONCLUSION

1. Mechanism of
Odontogenic and Non-
Odontogenic Pain
Presented by:
Dr Iflah javed
MDS 2ND year
Dept. of Conservative dentistry and
Endodontics

2. CONTENTS:
• DEFINITION
• TRIGEMINAL PAIN SYSTEM
• PERIPHERAL PAIN
MECHANISM
• CENTRAL PAIN MECHANISM
• NEUROPHYSIOLOGY OF PAIN
• REFFERED PAIN
• THEORIES OF PAIN
• ASSESSMENT OF PAIN
• PAIN CLASSIFICATION
• ODONTOGENIC PAIN
• NON-ODONTOGENIC PAIN
• HISTORY OF PAIN
• PHYSICAL EXAMINATION
• DIAGNOSIS OF PAIN
• CONCLUSION

3. DEFINITION:
DORLAND MEDICAL DICTIONARY DEFINED PAIN AS-
A more or less localized discomfort, distress or agony resulting from the
stimulation of specialized nerve endings.
FIELDS DEFINED PAIN AS –
An unpleasant sensation that is perceived as arising from a specific region
of the body and is commonly produced by processes that damage or are
capable of damaging bodily tissues.

4. REVISED INTERNATIONAL ASSOCIATION FOR THE STUDY
OF PAIN (IASP) DEFINITION OF PAIN (2020) AS-
• An unpleasant sensory and emotional experience associated with,
or resembling that associated with, actual or potential tissue
damage.

5. Structure of Orofacial region
Somatic
structures
Neural structures
SUPERFICIAL
STRUCTURES
include skin,
mucosa, gingiva
DEEP
STRUCTURES
include
mucoskeletal and
visceral tissues
PERIPHERAL
NERVOUS
SYSTEM
CENTRAL
NERVOUS
SYSTEM

6. TRIGEMINAL PAIN SYSTEM
ORGANIZATION AND FUNCTION OF PERIPHERAL
TRIGEMINAL PAIN SYSTEM-
The fundamental function is detecting the magnitude, quality,
location and temporal characteristics of innocuous and noxious
sensory input
Mediated by receptors expressed on subclasses of primary
afferent neurons that are activated by various stimuli
Leading to intracellular changes

7. Pain system has 3 main organizational elements-
• Detection
• Processing
• Perception

8. Detection of stimulus
Primary afferent neurons encode this information by
action potential discharge
Information conveyed to the second order neurons by
release of neurotransmitters such as glutamate, SP from
the central and peripheral terminals
Causing vasodilatation and plasma extravasation.

10. Classification of peripheral neurons:

11. • A- delta fibers function in the transmission of first pain that is perceived
as a sharp or bright in quality and can be stimulated by chemical,
mechanical, or thermal stimulus.
• C-fibers transmit second pain that is perceived as dull pain . These fibers
have smallest diameter , slowest conduction velocity, and highest
threshold of activation.

12. ORGANIZATION AND FUNCTION OF CENTRAL
TRIGEMINAL PAIN SYSTEM-
• The second major functional element of pain is processing that takes place
in trigeminal nuclei.
• Peripheral trigeminal neurons enter the medulla forming the trigeminal
spinal tract and terminate in the trigeminal brainstem nuclear
complex(VBSNC)
• PROCESSING TAKES PLACE IN VBSNC.

13. VBSNC PRIMARY SENSORY NUCLEUS OF V
SPINAL TRACT NUCLEUS OF V
Nucleus Caudalis
Nucleus Oralis
Nucleus Interpolaris
(in a retrocaudal direction)
The Nucleus Caudalis is the primary site for integration and
processing of orofacial nociceptive input.

14. • Key components mediating this process include-
Central terminal of primary afferent fiber
Interneurons
Descending neurons
Glia
Projection neurons

15. WDR projection neuron in medullary dorsal
horn

16. Three major classes of projection neuron:
• LOW THRESHOLD MECHANORECEPTOR(LTM) NEURONS- receive
input from non-nociceptive fibers ( i.e. A BETA fibers)
• WIDE DYNAMIC RANGE (WDR) NEURONS - receive input from both
nociceptive and non nociceptive fibers
• NOCICEPTIVE SPECIFIC (NS) NEURONS – Receive input from
nociceptors

17. PERIPHERAL PAIN MECHANISM
• Peripheral sensitization refers to the altered activity and excitability of
peripheral neurons in the presence of inflammatory mediators.

18. G protein coupled receptors
Activation of intracellular signalling pathway
Gs stimulation Gq activation Gi inhibition
of protein kinase A of protein kinase C of PK A
Increase the overall reduced nociceptor
excitability of neurons function

19. Ion channel – voltage gated sodium channels are present .
These are termed as voltage gated as the channels undergo
the conformational change in response to application of
voltage
Leads to sodium influx and membrane depolarization

20. • TRANSIENT RECEPTOR POTENTIAL (TRP) FAMILY of ion
channels are able to respond to temperature changes and are important
for the development of inflammatory pain.
• Channels are- TRPV 1, TRPV 2, TRPM 8, TRPA 1
TRPV 1 is activated by – noxious heat at 43̊C - by inflammatory
mediators such as PGE 2 , bradykinin
Increases the overall excitability of neurons

21. Central pain mechanism

22. • Central Sensitization – increased excitability of central neurons
• Sensitization of central neuron is initiated by barrage of input from C
fibers
When C fiber input is of sufficient intensity
Neuronal changes occur in the central projection neurons
C fibers release neurotransmitter glutamate & SP
Acts on post synaptic NMDA &AMPA receptors or NK 1 receptors
Signal transduction cascade is initiated in the central neuron

23. Neurophysiology of pain
• The body has specialized neurons that respond only to
noxious or potentially noxious stimulation. These neurons are called
Primary afferent nociceptors
• Made up of small-diameter thinly myelinated A delta
and un-myelinated C fibers

24.  Primary afferents with cell bodies in the dorsal root ganglion and sympathetic
postganglionic fibers with cell bodies in the sympathetic ganglion. Primary afferents include
those with large-diameter myelinated (Aα), small diameter myelinated (Ad), and
unmyelinated (C) axons.
All sympathetic postganglionic fibers are unmyelinated.

25. Cross-section of a cutaneous nerve-
illustrating the relative size and degree of myelination of its complement of axons. The
myelin appears as black rings of varying thickness. The unmyelinated axons (C) occur
singly or in clusters.

26. Primary sensory neurons
They synapse in the substantia gelatinosa of the dorsal horn of
the spinal cord with neurons known as second-order pain
transmission neurons.
From here the signals are transmitted along specialized
pathways (spinothalamic and reticulothalamic tracts)
To the medial and lateral regions of the thalamus
To the brain

27. • FIELDS divided the processing of pain from the stimulation of primary
afferent nociceptors to the subjective experience of pain into four steps:
TRANSDUCTION
 TRANSMISSION
MODULATION
PERCEPTION

28. TRANSDUCTION NOXIOUS STIMULUS LEADS TO ELECTRICALACTIVITIES IN
THE SENSORY NERVE ENDINGS.
TRANSMISSION
MODULATION
PERCEPTION
NEURAL EVENTS THAT CARRY THE NOCICEPTIVE INPUT
INTO THE CNS FOR PROCESSING.
ABILITY OF CNS TO CONTROL THE PAIN TRANSMITTING
NEURONS.
NOCICEPTIVE INPUT REACHES THE CORTEX WHERE
PERCEPTION OCCURS WHICH IMMEDIATELY INITIATES A
COMPLEX INTERACTION IN THE NEURONS BETWEEN
HIGHER CENTERS OF THE BRAIN.

29. TRANSDUCTION
Activation of the primary afferent nociceptor.
(thermal and mechanical stimuli, noxious chemicals,
and noxious cold, & Endogenous inflammatory mediators producing
INFLAMMATORY SOUP)
Mediators interact with multiple receptors expressed in nociceptors
Inducing their excitation

30. INFLAMMATORY SOUP:
Arachidonic acid
Prostaglandin Leukotriens Bradykinin
Stimulate primary PMN’s causes sympethetic
afferent nociceptor nerve terminal to
directly release prostaglandin
stimulates nociceptor
(allodynia , hyperalgesia )

32. AXON REFLEX
Activation of cutaneous C fibers causes their cell bodies to
synthesize the neuropeptides, substance P and calcitonin
gene–related peptide (CGRP).
These neuropeptides are then antidromically transported
along axon branches to the periphery by an axon transport
system
where they induce further plasma extravasation and increase
inflammation.
The release of these algogenic substances at the peripheral
axon injury site produces the flare commonly seen around an
injury site and is referred to as Neurogenic inflammation or
the Axon reflex

34. TRANSMISSION
The process by which peripheral nociceptive information is relayed in the
central nervous system.
The primary afferent nociceptor synapses with a second-order pain
transmission neuron in the dorsal horn of the spinal cord
where a new action potential heads toward higher brain structures

36. Central sensitization
• Input from C nociceptors enhances the response of dorsal horn pain-
signalling neurons to subsequent afferent inputs (central sensitization).
• This involves neuropeptides such as substance P (SP) acting at neurokinin
receptors (NKR) and excitatory amino acids (EAA) acting at both the
AMPA/KA and N-methyl-D- aspartate (NMDA) receptors
• Triggering secondary NO (nitric oxide) mechanisms.

38. Large diameter low-threshold mechano receptive primary afferents (A beta
fibres) respond maximally to innocuous tactile stimuli and normally produce
tactile sensation.
When central sensitization is present, A beta fibers become capable of
activating central nervous system pain-signalling neurons
leading to touch-evoked pain (allodynia).

39. MODULATION :-
Modulation refers to mechanisms by which the transmission of
noxious information to the brain is reduced.
Numerous descending inhibitory systems that originate
supraspinally and strongly influence spinal nociceptive
transmission exist.
The ascending nociceptive signal that synapses in the midbrain
area
activates the release of norepinephrine (NE) and serotonin
(two of the main neurotransmitters involved in the descending
inhibitory pathways.)

40. An endogenous opioid system for pain modulation also exists.
Endogenous opioid peptides are naturally occurring pain-dampening
neurotransmitters and neuromodulators that are implicated in pain
suppression and modulation
They reduce nociceptive transmission by preventing the release of
the excitatory neurotransmitter Substance P from the primary
afferent nerve terminal.
The presence of these natural opioid receptors for endogenous
opiates permits morphine-like drugs to exert their analgesic effect.

41. PERCEPTION:-
• Thalamus and Multiple Cortical areas are involved in the
Perception of pain.

42. REFERRED PAIN PATHWAY
• Referred pain from musculoskeletal and visceral sources is usually deep,
dull, aching and more diffuse. The mechanism of referred pain is
enigmatic.
• 2 most popular theories are—

43. Convergence projection theory
• Primary afferent nocciceptors from both visceral and cutaneous
neurons often converge onto the same second order pain transmission
neurons in the spinal cord.

44. Convergence facilitation theory
• Nocciceptive input from the deeper structures causes the resting
activity of second order pain transmission neurons in the spinal
cord to increase or to be facilitated.
• Facilitation from deeper nocciceptive impulses causes the pain to
be perceived in the area that creates the normal, resting
background activity.

45. THEORIES OF PAIN
Specificity theory:
• Refers to a pain system based on a specific set of peripheral nerve fibers
that are nociceptive in function.
• A –delta and C fibers are associated with two qualities of pain, short
latency pricking pain and long latency burning pain respectively .

46. Pattern theory
• Proposes that pain perception is based on stimulus intensity and central
summation.
• Pain is a result of the summation of a spatial and temporal pattern of input.

47. Gate control theory
• Contains elements of both specificity and pattern theories.
• Proposes a dorsal spinal gating mechanism in the substantia gelatinosa
that modulates sensory input by the balance of activity of small diameter
(A-delta C) and large diameter(A-beta) fibres

48. ASSESSMENT OF PAIN:
Visual analog scale
• The most common form used for pain is a 10 cm line, whether
horizontal or vertical, with perpendicular stops at the ends.
• The ends are anchored by “No pain” and “Worst pain imaginable”
• Patients are asked to place a slash mark somewhere along the line to
indicate the intensity of their current pain complaint.
• For scoring purposes, a millimeter ruler is used to measure along the
line and obtain a numeric score for the pain ratings.

49. Visual analog scale

50. McGill Pain Questionnaire
• A verbal pain scale that uses a vast array of words commonly used to describe a
pain experience.
• The words are listed in 20 different categories.
• They are arranged in order of magnitude from least intense to most intense
and are grouped according to distinctly different qualities of pain.
• The patients are asked to circle only one word in each category that applies to
them.

52. McGill Pain Questionnaire
• The first 10 categories represent different sensory descriptors that cover various temporal,
spatial, pressure, and thermal qualities of pain.
• The next five categories are affective or emotional descriptors, category 16 is evaluative
(ie, how intense is the pain experience) the last four categories are grouped as
miscellaneous.
• To score the questionnaire, the words in each category are given a numeric value. The first
word in each category ranks as 1, the second as 2, etc.
• The scores for each category are added up separately for the sensory, affective, evaluative,
and miscellaneous groupings.
• Then the total number of words chosen is also noted.

53. McGill Pain Questionnaire
• Using this questionnaire, it is possible to obtain a sense of the quality of
a patient’s pain complaint (categories 1 through 10),
its intensity (category 16),
 and the amount of emotional or psychological overlay accompanying the
pain (categories 11 through 15).

54. PAIN
According
to intensity According to
temporal
relationship
According
to qualities
According
to onset
According to
localization
localization
a) Mild
b)Moderate
c) Severe
a)Intermittent.
b)Continuous.
c) Protracted.
d) Intractable.
e) Recurrent.
a) Steady pain.
b)Paroxysmal
pain.
c) Bright pain.
d) Dull pain.
e) Itching.
g) Stinging.
h) Burning.
I)Throbbing.
j) Aching.
a)Spontaneous
b) Induced.
c) Triggered
a) Localized.
b) Diffuse.
c) Radiating.
d) Lacinating.
e) Migrating.

55. PAIN
ODONTOGENIC NON-ODONTOGENIC
 PULPAL
 PERIAPICAL/
 PERIODONTAL PAIN
 HETEROTOPIC
 Musculoskeletal
 Neuralgias
 Vascular disorders
 Psychogenic pain
 Generalized pain
 Inflammatory

56. ODONTOGENIC PAIN

57. NORMAL PULP REVERSIBLE
PULPITIS
IRREVERSIBLE
PULPITIS
NECROTIC PULP
SYMPTOMS SHARP PAIN FROM
EXPOSED DENTIN
ON STIMULI
SHARP PAIN ON
THERMAL STIMULI
SPONTANEOUS
SHARP , THROBBING
PAIN
NO THERMAL
SENSTIVITY
RADIOGRAPHIC
FEATURE
NORMAL NO CHANGE NO CHANGE DEPEND ON
PERIAPICAL STATUS
PULP TEST NORMAL RESPONDS- NOT
LINGERING
PAIN - LINGERS NO RESPONSE
PERIAPICAL TEST NORMAL NO RESPONSE NO RESPONSE DEPEND ON
PERIAPICAL STATUS

58. SYMPTOMS RADIOGRAPHIC
FEATURE
PULP TEST PERIAPICAL TEST
NORMAL
PERIAPEX
NONE NO CHANGE RESPONDS
NORMALLY
NO RESPONSE
ACUTE APICAL
PERIODONTITIS
PAIN ON PRESSURE NO CHANGE +/- DEPEND ON PULP
STATUS
TENDER ON
PERCUSSION
CHRONIC APICAL
PERIODONTITIS
PAIN ON PRESSURE PERIAPICAL
RADIOLUCENCY
NO RESPONSE TENDER ON
PERCUSSION
ACUTE APICAL
ABCESS
SWELLING AND
SEVERE PAIN
+/- PERIAPICAL
RADIOLUCENCY
NO RESPONSE TENDER ON
PERCUSSION
CHRONIC APICAL
ABCESS
DRAINING SINUS- NO
PAIN
PERIAPICAL
RADIOLUCANCY
NO RESPONSE NO RESPONSE
CONDENSING
OSTEITIS
VARIABLE INCREASE IN BONE
DENSITY
DEPEND ON PULP
STATUS
+/- TENDER ON
PERCUSSION

59. Fractured tooth
• incomplete fractures through the body of tooth.
• Symptom – pain ranging from mild to excruciating, at the initiation or
release of biting pressure.
• Diagnostic method- tooth may disclose an enamel crack, visualized by dye
or trans-illuminating the tooth with fiber optic light.
• Treatment-a full crown restoration immobilizing the fragments.

60. Pericoronitis
• Pain commonly arises from the supporting gingivae and mucosa when infection arises from
an erupting tooth.
• This is the most common cause for the removal of third molar teeth.
• The pain may be constant or intermittent, but is often evoked when biting down with
opposing maxillary teeth.
• Acute pericoronitis involves bacterial infection around an erupting orr partially erupted
tooth and usually affects the lower third molar.

61. • There may be associated trismus.
• Paracetamol and ibuprofen can be taken together if pain relief with either
alone is insufficient.
• Antibiotics are generally not indicated. Only prescribe an antibiotic for
people who are systemically unwell or if there are signs of severe infection.
• Dental management for dental abscess is either root canal procedure with
removal of the necrotic pulp or tooth extraction.

62. Non- Odontogenic Pain

63. Musculoskeletal Pain:
1. Myofascial pain:
 Myofascial pain (MFP) emanates from small foci of hyperexcitable muscle tissue.
 Clinically these areas feel like taut bands or knots and are termed trigger points.
 Typically the pain is described as a diffuse, constant, dull, aching sensation.

64. • Pathogenesis of MFP is unknown, authors have theorized that muscles
may become disturbed through injury or sustained contraction such as
clenching.
Investigation:
 It should become clear that the pain is triggered by contraction of
masticatory muscles rather than loading of PDLs.
 Palpation of the muscles of mastication should reproduce the pain,
whereas percussion of the teeth should not.

65.  A distinguishing characteristic is the relief of toothache when local
anesthetic is administered to the strained muscle (source of pain) rather
than the tooth (site of pain).
 Therapeutic modalities used to treat MFP include deep massage,
relaxation techniques, “spray and stretch,” muscle relaxants, trigger
point injections and warm or cold compresses, may alleviate both the
muscle and tooth pain.

66. Pain of sinus or nasal mucosal origin:
• Sinus/nasal mucosal pain is another source of pain that can mimic toothache.
• Symptoms of fullness or pressure below the eyes but is generally not particularly painful
unless the nasal mucosa is also affected.
• Pain from the nasal mucosa tends to be dull and aching and can also have a burning
quality typical of visceral mucosal pain.
• Other symptoms consistent with these types of disease e.g.,congestion or nasal drainage

67. • Pains are of viral, bacterial, or allergic etiology.
• When an etiology for pulpal and therefore peri-radicular pathosis is absent,
sinus/nasal mucosal disease should be suspected.
The three cardinal symptoms of Acute Rhinosinusitis are:
(1) Purulent nasal discharge,
(2) Nasal obstruction, and
(3) Facial pain-pressure fullness.

68. • Other symptoms of sinus disease include sensitivity to palpation of
structures overlying sinuses (i.e., paranasal tenderness) and a
throbbing or increased pain sensation when the head is placed lower
than the heart.
• Dental local anesthetic blockade will not abate sinus/nasal mucosal
pain, although topical nasal anesthetic will.
• Physical examination as well as adjunctive tests may be necessary
for a definitive diagnosis.

69. Tests include :
• Nasal cytologic
• Ultrasound studies
• Nasal endoscopes,
• Radiology and
• Computed tomographic imaging.
Treatment of sinus/nasal mucosal pain: is dependent on the etiology (e.g.,
bacterial, viral, allergic, or obstructive).

70. Salivary gland pain:
• Pain referred from one or more of the salivary glands may be perceived as tooth pain.
• Because the primary somatosensory innervation of the major salivary glands comes from
the mandibular branch, it is conceivable that such a presentation will occur most often in
mandibular teeth.

71. Neurovascular pain
• Neurovascular pain or migraine with orofacial symptoms more commonly involves
maxillary division than the mandibular division of trigeminal nerve.
• Primary headache disorders can be grouped into three major subdivisions:
(1) Migraine,
(2) Tension-type headache, and
(3) Cluster headache and other trigeminal autonomic cephalalgias (TACs).

72. • Migraine is a debilitating, inherited, episodic disorder and a form of sensory processing
disturbance in the CNS.
• Migraine has been reported to present as toothache and is likely the most common
neurovascular disorder.
• Symptoms: typically last from several hours to 3 days, with variable pain- free periods.
They tend to be unilateral in presentation and pulsatile in quality, with a moderate to
severe intensity to the pain. Patients may also experience nausea or vomiting, as well as
photophobia or phonophobia, which are different from toothache.

73. • Management:
• Caffeine/ergotamine compounds have been used widely in the past as abortive
agents for migraine headaches, but in contemporary times they have been
replaced with triptans, such as Sumatriptan and Rizatriptan.
• Migraine headaches may partially or fully abate with the use of Nonsteroidal
anti-inflammatory medications in a similar fashion as toothaches.

74. Tension-type headache:
• Tension-type headache is the most frequent headache disorder experienced,
with a wide range of reported prevalence (41% to 96%).
• Tension-type headaches are likely a heterogeneous group of similarly
presenting head pains that have overlapping pathophysiologic mechanisms,
which has led some researchers to consider aspects of tension type
headache to be the same as musculoskeletal orofacial pain, otherwise
known as temporomandibular disorders (TMDs)

75. Cluster headaches
• Unilateral pains defined by the concurrent presentation of at least one ipsilateral
autonomic symptom—such as
• Nasal congestion,
• Rhinorrhea,
• Lacrimation,
• Eyelid edema,
• Periorbital swelling,
• Facial erythema,
• Ptosis, or Miosis—that occurs with the pain.

76. • The major distinguishing features between these headache disorders are the
duration and frequency of the pain episodes, as well as the gender most often
afflicted.
• Cluster headache is the most common of the group, occurring in men three to
four times more often than in women, with pain episodes lasting between 15
minutes and 2 hours that occur at a frequency of eight episodes per day to one
every other day.

77.  Elimination of pain after 10 minutes with inhalation of 100% oxygen is diagnostic for
cluster headache, whereas sublingual ergotamine and sumatriptan are also effective acute
treatments for cluster headache.
Management by the typical clinician is to determine that the pain is not of odontogenic
origin and then to refer the patient to an appropriate care provider.

78. Neuropathic pain:
• Pain originating from any defect in the neural structures is referred to as
Neuropathic pain.
• This type of pain is a diagnostic challenge to the clinician as structures
innervated by these nerves are painful but appears clinically normal.
• Neuropathic pain when experienced is either continuous or episodic in
nature.

79. Neuropathic pain is divided into four subcategories:
Neuralgia,
Neuroma,
Neuritis, and
Neuropathy

80. Neuralgia: Episodic neuropathic pain is referred to as neuralgia and is characterized by severe,
shooting, electric like pain that lasts only a few seconds.
Trigeminal Neuralgia involving the mandibular nerve is the most common type of neuralgia
in the orofacial region.
 This type of paroxysmal pain is felt in the tooth, but is often experienced in a wider area.
Patient reports of pain being felt along the distribution of the nerve involved and is often
experienced following stimulation of the trigger points.
 Trigeminal Neuralgia is characteristically an intense, sharp shooting pain that is most often
unilateral.

81. • Ipsilateral to the perceived location of the symptoms is an area that, on stimulation such as
light touch, elicits sharp shooting pain. The area that elicits the pain is referred to as a trigger
zone.
• Presents in individuals older than 50 years of age.
• Etiology is thought to be irritation/compression of the root of the trigeminal nerve, prior to
the Gasserian ganglion, possibly as a result of carotid artery pressure.
• An important characteristic of trigger zones is that the response to the stimulus is not
proportional to the intensity of the stimulus—that is, slight pressure on a trigger zone results
in severe pain.
• In addition, once triggered, pain typically subsides within a few minutes until triggered
again.

82. • Trigger zones for trigeminal neuralgia tend to be related to areas of dense
somatosensory innervation, such as the lips and teeth. For this reason, triggers
that elicit this type of pain may include chewing and may lead both the patient
and clinician to think of a diagnosis of odontogenic pain.
• In addition, because the trigger involves peripheral input, anesthetizing the
trigger zone may diminish symptoms. This can be very misleading to the
clinician if the assumption is that local anesthetic blocks only odontogenic
pain.

83. Treatment options:
• Several medications, including carbamazepine, baclofen, gabapentin, and more
recently pregabalin and oxcarbazepine, have been used to treat Trigeminal
Neuralgia.
• Clinical trials support carbamazepine as a first-line drug for treating Trigeminal
Neuralgia

84. Neuroma:
• A traumatic Neuroma, also known as an Amputation neuroma, is a
proliferative mass of disorganized neural tissue at the site of a traumatically
or surgically transected nerve.
• Diagnosis, therefore, is confirmation of a significant event that would account
for the damage to the nerve.

85. • Symptoms: will not develop until the neural tissue on the proximal stump has had time
to proliferate, typically about 10 days after the event. Tapping over the area of a
neuroma elicits volleys of sharp electrical pain (i.e., Tinel sign) similar to trigeminal
neuralgia.
• Neuromas most commonly develop in the area of the mental foramen, lower lip, and
tongue, there is some evidence that they can also form in extraction sites and after
pulpal extirpation.
• In contrast to trigeminal neuralgia, there should be a zone of anesthesia peripheral to
the area of the neuroma that can be identified by checking for loss of pin prick
sensibility, such as with the use of an explorer.

86. Treatment:
• May involve surgical coaptation of the nerve with prognosis being variable
and dependent on adequate distal nerve tissue and the time interval between
injury and reconstruction.
• Early recognition and referral are of key importance to prevent significant
distal nerve degeneration

87. Neuritis:
• Neuritis is a condition caused by inflammation of a nerve or nerves secondary to injury or
infection of viral or bacterial etiology.
• Pain from a virally induced neuritis, such as recurrent herpes simplex or herpes zoster, is
associated with skin or mucosal lesions.
• The pain is fairly constant and can be dull, aching, and burning. Also, the pain may be
accompanied by allodynia, a painful response to normally non-noxious stimulation such as
light brushing of the skin.

88. • Oral acyclovir has become the most common treatment for acute herpetic
outbreaks and has been shown to be efficacious in decreasing the duration and
severity of pain after herpes zoster infection.
• The addition of Prednisolone to Acyclovir produces only slight benefits over
acyclovir alone.

89. • The major limitation in the use of
all these terms is that they merely
suggest an area where a pain of
unknown etiology exists and
completely lack any information
regarding the pathophysiology.

90. Neuropathy:
• Neuropathy term preferred as localized, sustained non-episodic pain secondary to an injury
or change in a neural structure.
• Other terms have been used including atypical facial pain.
• Pain of an unknown source that is perceived in a tooth may be labeled atypical odontalgia.
• Pain that persists after the tooth has been extracted is referred to as phantom tooth pain.

91. • A diagnosis of neuropathy is based primarily on history and examination with the use of
selected diagnostic tests to rule out other potential etiologies.
• The history should reveal some inflammation-inducing event.
• The examination is grossly unremarkable with no evidence of local tissue damage,
leaving the clinician to rely mainly on the patient’s report of symptoms.

92. Neuropathies can be classified on the basis of their
clinical presentation:
Peripheral
Neuropathy
Central
Neuropathy

93. • Peripheral neuropathy may develop after sensitization of a peripheral nerve and presents
clinically as described previously.
• Diagnosis of peripheral neuropathy is based on its favorable response to peripheral neural
blockade.
• Treatment is directed at decreasing the sensitization of peripheral nerves and reducing
ectopic neuronal firing.
• Topical as well as systemic medications can be used to treat cutaneous peripheral
neuropathies.
• Topical medications include topical anesthetics, capsaicin-containing compounds, and
anticonvulsants, as well as nonsteroidal anti-inflammatory drugs (NSAIDs),
sympathomimetic agents, and N-methyl-d-aspartate (NMDA) receptor-blocking agents

94. • Central neuropathy: is similar to that of a peripheral neuropathy.
• After sensitization of peripheral nerves and the accompanying nociceptive barrage, the pain
is non-remitting and lacks evidence of tissue insult. Unlike its peripheral counterpart,
allodynia and secondary hyperalgesia are clearly present—that is, the area of pain is
significantly larger than the initial site of injury.
• Local anesthetics are no longer effective.
• Treatment:
• Medications such as NMDA receptor agonists (ketamine), gabapentin, tricyclic
antidepressants, and opioids.
• The prognosis for a central neuropathy is not as good as for a peripheral neuropathy, as
central neuropathic pain tends to become more refractory with time.

95. Toothache referred from a distant organic
source:
• The only common link that can be identified is that branches of cranial nerves
innervate the involved tissues and hence the trigeminal nucleus processes nociceptive
input.
• Once dentoalveolar etiologies for such pain have been ruled out, all possible sources of
non-odontogenic pain, including distant pathology, should be considered in the
differential diagnosis.
• Several of these types of organic pathologies that have been reported to present as
toothache are described as following:

96. Cardiac pain:
• Cardiac pain presents as a crushing substernal pain that most commonly radiates to the
left arm, shoulder, neck, and face.
• Similar to pain of pulpal origin, cardiac pain can be spontaneous and diffuse, with a
cyclic pattern that fluctuates in intensity from mild to severe.
• The pain can also be intermittent and the patient may be completely asymptomatic at
times. The quality of cardiac pain when referred to the mandible is chiefly aching and
sometimes pulsatile.

97. • Cardiac pain may be spontaneous or increased with physical exertion, emotional upset, or
even the ingestion of food.
• Cardiac pain cannot be aggravated by local provocation of teeth.
• Anesthetizing the lower jaw or providing dental treatment will not reduce the pain.
• It can be decreased with rest or a dose of sublingual nitroglycerin.
• Diagnosis of cardiac pain, along with immediate referral, is mandatory

98. Intracranial structures:
• Space-occupying lesions within and around the brain are
known to impinge on structures innervated with
somatosensory fibers, such as the Dural and perivascular
tissues, causing pain.
• These pains are highly variable, with a common complaint
being headache or head pain.
vast differences in clinical
features of such pain,
intracranial lesions have also
been reported to cause
trigeminal neuralgic pain in
response to treatment of what
was first thought to be
toothache.

99. Throat and neck structures:
• Nonodontogenic toothache has been reported to arise from various structures of the neck.
• Squamous cell carcinoma of the lateral pharyngeal surface presenting as ipsilateral
mandibular molar pain has been observed.
• Vascular structures of the neck have also been implicated in the production of toothache
symptoms, with a report of a patient initially presenting for dental care when pain was
from the result of a life-threatening carotid artery dissection.

100. Craniofacial structures:
• Pain from other craniofacial structures has been observed as being the most common reason
for organic pathologies presenting as nonodontogenic toothache.
• Tumors in the maxillary sinus and jaw, as well as metastatic disease, particularly within the
mandible, have been reported.
• The clinical presentation of symptoms is highly variable, but a common feature is sensory
loss along the distribution of the nerve, the result of pain arising from nerve impingement.

101. • Need for regional imaging techniques, such as pantomography or CT (as
opposed to just periapical radiographs).
• One must also not forget that nerve impingement anywhere along the
distribution of the trigeminal nerve, even within the cranial vault itself, can
elicit nonodontogenic tooth pain.

102. • Arteritis being the pain provoking pathology.
• These pains have been described as a continuous dull pain that can sometimes be made
worse with jaw function.
• The stereotypical presentation includes a history of eyesight changes, such as blurred
vision, and the examination feature of pulseless, indurated temporal arteries that are
painful to palpation.
• A laboratory finding of an elevated erythrocyte sedimentation rate (ESR) is suggestive of
the disorder, and diagnosis is confirmed by temporal artery biopsy.
• Treatment includes administration of corticosteroids; therefore, because permanent
blindness is a possible sequela if cranial arteries are left unmanaged, immediate referral to
the appropriate medical colleague is indicated.

103. Psychogenic toothache:
• Psychological stress may lead to development of psychogenic tooth ache.
• Pain may be described as diffused, vague, and non-localized or sharp,
stabbing, intense, with sensitivity to temperature changes.
• Often involves multiple teeth and pain may jump from one tooth to
another.

104. • Psychogenic pain is known to be precipitated by severe psychologic stress.
• The pain may be felt in multiple teeth and may jump around from one tooth to another.
• The intensity of pain reported tends to be more severe than is reflected by the patient’s level
of concern about the condition.
• Patient’s responses to therapy are variable and include a lack of response or an unusual or
unexpected response.
• Early identification of psychogenic pain and referral to a psychologist or psychiatrist is
necessary to avoid irreversible and unnecessary dental treatment.

106. Diagnosing orofacial pain

107. Physical examination
• General examination
• Head and neck inspection
• Stomatognathic system
• Cervical spine examination
• Myofascial examination
• Cranial nerve examination

108. Cranial nerve examination

109. Common diagnostic studies
• PERIODONTAL EXAMINATION
• PERCUSSION TEST
• PALPATION TEST
• PULP VITALITY TESTS-
ELECTRIC PULP TEST
THERMAL PULP TEST
LASER DOPPLER FLOWMETRY
PULSE OXIMETRY
DUAL WAVELENGTH SPECTROPHOTOMETRY
ANAESTHETIC TEST
TEST CAVITY
TRANSILLUMINATION

110. DIAGNOSTIC STUDIES
• RADIOGRAPHIC DIAGNOSIS
• TOMOGRAPHY
• BONE SCAN
• GALLIUM SCAN
• ARTHROGRAPHY
• THERMOGRAPHY

111. Conclusion
• As clinicians who are frequently called on to diagnose and treat complaints of orofacial
pain, it is important to have a thorough knowledge of the odontogenic and nonodontogenic
causes.
• A thorough pain history and an examination of dental and nondental structures are essential
to differentiate between odontogenic and nonodontogenic sources of pain.
• Role of the dental clinician is to diagnose and treat disorders of the oral cavity and
masticatory structures.
• In the event that a nondental pathosis is suspected, a differential diagnosis of probable
disorders is essential as part of a referral to a more appropriate health care provider.

112. REFERENCES:
• ENDODONTICS (6TH EDITION) BY INGLES
• PATHWAYS OF PULP(12TH EDITION) BY STEPHEN COHEN
• Reference article- The revised International Association for the Study of
Pain definition of pain: concepts, challenges, and compromises | 2020
• Reference article- Odontogenic pain of non-odontogenic origin: A review
2017; 3(3): 01-04

113. THANK YOU