This document discusses dental pain pathways and atypical odontalgia. It defines pain and dental pain, and classifies pain. It discusses theories of pain transmission including the specificity, pattern, and gate control theories. It describes the ascending pain pathway including initiation, transduction, and transmission through the neospinothalamic and paleospinothalamic tracts. It also discusses the descending pain pathway. It then discusses atypical odontalgia including definitions, epidemiology, pathophysiology, clinical features, diagnosis, and treatment. It presents a case study of a 58-year-old female with unexplained pain in her front teeth as an example.

1. DENTAL PAIN
PATHWAY AND
ATYPICAL
ODONTALGIA
DR. AFOLABI B.O (BDS,
Ibadan)

2. DENTAL PAIN PATHWAY
2

3. TABLE OF CONTENTS
• Definitions
• Classification of pain
• Theories of pain
• Ascending pain pathway
• Descending pain pathway

4. DEFINITIONS
• Pain is a subjective unpleasant sensory and emotional experience due to
actual or potential tissue damage, or described in terms of such a damage.
• Dental pain is pain in the teeth or their supporting structures, caused by
dental diseases or pain referred to the teeth by non-dental diseases.

5. CLASSIFICATION OF PAIN
• Somatic/Visceral
• Physiologic/Pathological
• Acute/Chronic
• Fast/Slow

6. THEORIES OF PAIN
1) Specificity Theory by Descartes
2) Pattern Theory by Goldscheider
3) Gate Control Theory by Melzack and Wall

7. Specificity Theory
• Descartes (in 1644) described pain as a 'a specific sensation,
with its own sensory apparatus independent of touch and other
senses'.
• Limitations: Does not explain the inhibition or exaggeration of
pain by emotions or the continued presence of pain after
surgical removal of a body part with its receptors.

8. Pattern Theory
• Goldscheider (in 1894): All skin fiber endings (with the
exception of those innervating hair cells) are identical, and that
pain is produced by intense stimulation of these fibers.

9. Gate Control Theory
• Melzack and Wall (in 1965) proposed the Gate Control Theory which
states that:
• When a pain stimulus is applied on any part of the body, besides
pain receptors, the receptors of other sensations such as touch are
also stimulated which send collaterals to the neurons of the pain
pathway i.e cells of marginal nucleus and substantia gelatinosa.
• These impulses inhibit the release of glutamate and Substance P
from the pain fibres which closes the gate and pain transmission is
blocked.

10. PAIN PATHWAY
• Pathways of pain sensations:
1) Ascending pain pathway
2) Descending pain pathway/analgesic pathway

11. 11

12. ASCENDING
PAIN
PATHWAY

13. ASCENDING
PAIN PATHWAY
• Initiation
• Transduction
• Transmission

14. Initiation
• Pain can be elicited by multiple types of stimuli: mechanical,
thermal and chemical.
• Some chemicals that excite nerves for pain: bradykinin,
serotonin, histamine, potassium ions, acids.
• Prostaglandins and substance P enhance the sensitivity of pain
endings but do not directly excite them.

15. Transduction
• Nociceptors are nerve endings that contain transient receptor
potentials (TRP) channels that detect damage.
• The TRP channels transduce a variety of noxious stimuli into
receptor potentials, which in turn initiate action potential in
the pain nerve fibers.
• The action potential has four main stages: depolarization,
repolarization, hyperpolarization

16. 16

17. Transmission
• There is a dual pathway for transmission of pain signals into the
central nervous system.
• Painful stimuli often gives a 'double pain sensation': a fast-
sharp pain that is transmitted to the brain by the A-delta fiber
pathway, followed by a second or so later by slow pain that is
transmitted by the C fiber pathway.

18. 18

19. Transmission
• On entering the spinal cord from the dorsal spinal roots, the
pain fibers terminate on relay neurons in the dorsal horns.
• The pain signals take two pathways to the brain:
1) The neospinothalamic tract
2) The paleospinothalamic tract

20. Neospinothalamic Tract for Fast Pain
• A-delta pain fibers terminate mainly in lamina I (lamina
marginalis) of the dorsal horns and there, they excite the
second-order neurons of the neospinothalamic tract.
• These give rise to long fibers that cross imediately to the
opposite site of the cord through the anterior commisure and
then turn upward, passing to the brain in the anterolateral
columns.

21. Neospinothalamic Tract for Fast Pain
• A few fibers of the neospinothalamic tract terminate in the
reticular areas of the brain stem, but most pass to the thalamus
terminating in the ventrobasal complex, along with the dorsal
column-medial lemniscal tract for tactile sensations.
• Few fibers terminate in the posterior nuclear group of the
thalamus and from here, thalamic radiations pass to the
somatosensory cortex.
• Glutamate is the neuro transmitter secreted in the spinal cord at
the A-delta pain nerve fiber endings.

22. Neospinothalamic
Tract for Fast Pain

23. Paleospinothalamic Pathway for
Transmitting Slow-Chronic Pain
• This transmits pain mainly from the peripheral slow-chronic type
C pain fibers.
• The peripheral fibers terminate in the spinal cord almost entirely
in laminae II and III of the dorsal horns, which are together
called the substantia gelatinosa.
• Most of the signals then pass through short fiber neurons within
the dorsal horns themselves before entering mainly lamina V,
which is also in the dorsal horn.

24. Paleospinothalamic Pathway for
Transmitting Slow-Chronic Pain
• In lamina V, the last neurons give rise to long axons that mostly join
fibers from the fast pain pathway.
• Only 10-25% of these fibers pass to the thalamus. Most terminate in:
1) The reticular nuclei of the medulla, pons and mesencephalon.
2) The tectal area of the mesencephalon deep to the superior and
inferior colliculi.
3) The periaqueductal gray region surrounding the aqueduct of
Sylvius.

25. Paleospinothalamic Pathway for
Transmitting Slow-Chronic Pain
• Type C pain fibers secrete both glutamate and substance P as
neurotransmitters.
• Glutamate transmitter acts instataneously and lasts for a
few milliseconds.
• Substance P is released much more slowly, building up in
concentration over a period of seconds or minutes.

26. Paleospinothalamic
Pathway for
Transmitting Slow-
Chronic Pain

27. Transmission of Pain in the Oro-facial
Region
• The trigeminal nerve is the largegst and most significant nerve
serving the orofacial structures (oral mucosa, teeth, tongue,
masticatory muscles, facial skin and meningeal linings).
• It is a mixed nerve containing both sensory and motor fibers.

28. Areas Served by Some Specific Cranial
Nerves

29. Transmission of Pain in the Oro-Facial
Region
• The sensory fibers pass from the periphery within opthalmic,
maxillary and mandibular nerves to their cell bodies in the
trigeminal ganglion situated on the floor of the middle cranial
fossa.
• From the ganglion, the sensory nerve fibers pass centrally to
the trigeminal nuclei in the brainstem at the level of the pons.

30. 30

31. Transmission of Pain in the Oro-Facial
Region
• The first neuron carrying information is called the primary
afferent neuron or the first-order neuron and receives stimulus
from the sensory receptor.
• For most regions of the body, this impulse is carried by the
primary afferent neuron into the CNS by way of the dorsal root
to synapse in the dorsal horn of the spinal cord with a second-
order neuron. But, impulses carried by the trigeminal nerve
enter directly into the brain stem in the region of the pons to
synapse with the trigeminal nucleus.

32. 32

33. Transmission of Pain in the Oro-Facial
Region
• Second-order trigeminal neurons (from synaptic junctions with
primary afferents in the subnucleus caudalis) cross to the
contralateral side and ascend to the thalamus by way of the
trigeminothalamic pathways.
• Axons here then synapse with third-relay fibers (third order
neurons) in the thalamus.
• Third-order neurons project to different areas in the
sensory cerebral cortex and to the limbic forebrain

34. 34

35. DESCENDING/ANALGESIC PAIN
PATHWAY
35

36. 36

37. CLINICAL CORRELATES
1) Hyperalgesia
• Pain pathway sometimes becomes excessively excitable, this
gives rise to hyperalgesia.
• Possible causes-
I) Excessive sensitivity of the pain receptors themselves (which is
called primary hyperalgesia).
II) Facilitation of secondary transmission of pain (which is called
secondary hyperalgesia).

38. CLINICAL CORRELATES
2) Allodynia
• Pain response from stimuli which should not normally provoke
pain.
3) Neuralgia
• Severe pain arising from the nerve due to hyperexcitability
which is caused by nerve injury.
• Types- Trigeminal, post-herpetic, glossopharyngeal.

39. CLINICAL CORRELATES
4) Congenital insensitivity to pain
• A condition that inhibits the ability to perceive physical pain.
• It's considered a form of peripheral neuropathy.
• Caused by a genetic mutation leading to a defect in sodium
channel.
• Very rare.

40. CLINICAL CORRELATES
5) Referred pain (also known as reflective pain)
• This is pain at a site different from the place of origin.
• It is usually caused by afferent nerve fibers from tissues
converging onto the same spinal neuron.

41. ATYPICAL ODONTALGIA
41

42. TABLE OF CONTENTS
• Introduction
• Definition
• Epidemiology
• Pathophysiology
• Clinical features
• Diagnosis
• Treatment
• Case presentation
• Conclusion

43. INTRODUCTION
• Atypical odontalgia (AO) represents a clinical challenge for most
dental surgeons.
• Generally, when a patient complains of pain, its origin is
odontogenic, and the professional can identify and treat its cause -
for example, a typical toothache due to pulpitis, caries or periodontal
problem.
• In some situations, pain continues in one or more teeth or in the
socket after extraction without any apparent dental cause, and the
dentist faces the challenge of determining the true non-odontogenic
origin of pain and properly diagnosing it.

44. DEFINITION
• According to the International Association for the Study of Pain,
Atypical Odontalgia (AO) is defined as a “severe throbbing pain
in the tooth without major pathology” and “persistent (chronic)
continuous pain symptom located in the dento-alveolar region
and cannot be explained within the context of other diseases or
disorders” as a subgroup within persistent idiopathic or atypical
facial pain.

45. DEFINITION
• According to the third edition of the International Headache
Classification, it is thought to be a subtype of persistent
idiopathic facial pain and is defined as persistent facial and/or
oral pain, with varying presentations but recurring daily for more
than 2 h per day over more than 3 months, in the absence of a
clinical neurological deficit.
• Definition of AO is still being refined and still remains
ambiguous.

46. EPIDEMIOLOGY
• AO was found in 2.1% of a population of 3000 at the University
of Southern California Orofacial Pain and Oral Medicine Center.
Other studies suggest that AO occurs in 3–6% of patients
undergoing endodontic treatment.(i
• It is generally agreed that AO occurs more frequently in females
than in males; 80–90% of all cases are female.(ii
• Complaints were predominantly reported in the upper jaw (ratio
8 : 2) with the majority in the molar region (ratio 5 : 3)

47. EPIDEMIOLOGY
• List et al. [iii] reported in a study of 46 cases of AO that 56% of
patients complained of pain in the upper jaw, compared with
45% in the lower jaw.
• The condition occurs more commonly in the 4th decade of life.

48. PATHOPHYSIOLOGY
• Current evidence suggests neuropathic mechanisms to explain the
physiopathology of AO.
• Neuropathic physiopathological events may be involved: nerve damage
and ectopic activity due to the formation of neuromas, phenotypic
changes, and increased sympathetic activity in times of stress or anxiety.
• Recent studies do not point to psychiatric comorbidity as a determining
cause for triggering AO, but professionals should be aware of this
condition and cannot disregard it. A high incidence of AO patients presents
these comorbidities, reaching 50% in another study.

49. PATHOPHYSIOLOGY
• Vascular causes presented by Rees and Harris and Kreisberg
have been described as the minor physiopathological
mechanism of AO.

50. CLINICAL
FEATURE
S
Pain is localized to a tooth
that appears clinically and
radiologically sound.
Continous burning/aching
pain in a tooth.
Repeated restorations or
endodontic treatments fail to
resolve the pain.

51. DIAGNOSIS
• There is no gold standard diagnostic protocol for AO and existing ones are
not sufficiently reliable for diagnosis. Since the physiopathology is not well
defined, its diagnosis is often by exclusion.
• Patient assessment should begin with medical history, especially with
regard to pain characteristics.
• The odontogenic causes of toothache must be totally ruled out. For this, a
thorough clinical examination is necessary. One should not forget Rees
and Harris’s observations emphasizing that all possibilities of caries, pulp
disease and crack/fracture of the crown or root should be excluded.

52. DIAGNOSIS
• Despite the limitations of periapical radiographs, they should be
used to assess the periapical region. Volumetric computed
tomography should be performed to rule out any possibility of
periapical endodontic alteration.
• The use of magnetic resonance imaging (MRI), in cases of
suspected non-inflammatory dental pain, can be of great value
as it excludes inflammation processes in the mandibular and
maxillary region. When the diagnosis is uncertain, MRI
reinforces the importance of noninvasive management

53. DIAGNOSIS
• In order to facilitate and assist the diagnostic process, two tools
should be highlighted:
• a) Visual analog scale: diagnostic tool for pain measurement.
• b) QST and QualST: are important allies in the diagnosis of AO. QST
is performed through several stimuli, and only mechanical and
thermal stimuli are related to AO. Of the patients with AO submitted
to these stimuli, 83.7% had some QST abnormality. Performing
bilateral QST (pain side versus pain free side) also helps to detect
neuropathic changes.

54. DIAGNOSIS
• Exclude all hypotheses of non-odontogenic odontalgia.
According to Yatani et al and ICHD-3, after discarding the
hypothesis of dental pain, there are numerous other conditions
of non-odontogenic origin that should be ruled out.
• If a nerve block does not result in pain reduction, then a
diagnosis of AO should be strongly considered.

55. DIAGNOSIS
• Consider psychological aspects: Although psychogenic and
psychiatric factors have no determining relationship in the
development of AO, there was a high incidence of these
patients with psychiatric comorbidities.
• The professional should be aware of these comorbidities, giving
AO a multifactorial etiology. Thus, a biopsychosocial and
interdisciplinary approach are also necessary

56. TREATMENT
• Like diagnosis, AO treatment is challenging. Currently, there is insufficient
evidence to establish a treatment protocol.
• Tricyclic antidepressants are the most cited drugs in case reports and
case-control studies, and for many authors, they are considered the first
choice in treatment. However, these drugs cause adverse effects.
Amitriptyline, for example, causes xerostomia, constipation, urinary
retention, and weight gain and, depending on the dose and the patient,
have varied responses regarding the effectiveness in pain remission.
• Serotonin and norepinephrine reuptake inhibitors, such as and
Duloxetine, have also been used in the management of painful
symptoms.

57. TREATMENT
• More recent studies have assessed the action of botulinum
neurotoxin type A (Onabotulinum toxin A) in pain control.
The good results regarding pain remission point it as a
promising drug in the treatment of AO.

58. CASE PRESENTATION
• A 58-year-old female university teacher who was living with her
husband was referred to a dental clinic after complaining of a heavy,
splitting pain in the four maxillary front post-crown teeth, as if they
were being pressed from the side. Her medical history was
unremarkable except for hypertension and hyperlipidemia. She was
taking candesartan, cilexetil and alprazolam. She had no psychiatric
history and no significant family history.
• No particular psychological factors could be identified; however, she
was anxious about the unexplained pain for a long time.

59. CASE PRESENTATION
• Five months before the first visit, she had undergone root canal treatment
of the left mandibular first molar at a primary dental clinic, and the pain in
the maxillary right and left central incisors and lateral incisor appeared
2 months after dental treatment. Afterwards, she underwent examination
with radiography at a dental college hospital, but no abnormalities were
found, and a CT scan at another dental clinic also revealed no
abnormalities. She was referred to a dental clinic by her primary care
physician.
• Although the patient had anxiety, obvious signs of depression were absent.
Her Zung Self-Rating Depression Scale (SDS) score was 53; however,
she did not have depressive mood, lack of emotion, lack of energy, nor
suicidal idea.

60. CASE PRESENTATION
• She was started on 10 mg of amitriptyline and increased the
dose to 20 mg 1 week later. Her symptoms started to improve
3 weeks after her first visit. She said, “The character of my pain
changed from a feeling of the tooth being broken to a pressure
feeling.” Her symptoms were cured one and a half months after
her first visit. She continued taking 20 mg of amitriptyline for
4 months, and then the dose was gradually tapered and finally
ceased 8 months after the first visit. She experienced a
remission in her symptoms.

61. CONCLUSION
• Recent studies use the 3rd edition of the ICHD classification, in
which AO falls into the “persistent idiopathic facial pain”
category (ICHD-13.12).
• Since the physiopathological process is not defined, the
establishment of a protocol to make its diagnosis is
fundamental.

62. REFERENCES
• https://www.slideshare.net/drshagunagarwal/pain-and-pathways-of-
pain
• https://www.researchgate.net/publication/5661216_Atypical_odontal
gia_-_Pathophysiology_and_clinical_management
• https://www.slideshare.net/DrArsalan/atypical-facial-pain-45639156
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541751/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3400349/
• https://www.scielo.br/j/brjp/a/gyjqMbyZCfrf9BMKHY86JXP/?lang=en