Facial/Dental Pain Pathway and Atypical Odontalgia

Clinical presentation focused on Facial and Dental Pain Pathway and Atypical Odontalgia.

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 3

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. 4

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

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

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. 7

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 .  8

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. 9

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

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12. ASCENDING PAIN PATHWAY 12

13. ASCENDING PAIN PATHWAY Initiation Transduction Transmission 13

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. 14

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 15

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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. 17

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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 19

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. 20

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. 21

22. Neospinothalamic Tract for Fast Pain 22

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. 23

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. 24

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. 25

26. Paleospinothalamic Pathway for Transmitting Slow-Chronic Pain 26

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. 27

28. Areas Served by Some Specific Cranial Nerves 28

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. 29

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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. 31

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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 33

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35. DESCENDING/ANALGESIC PAIN PATHWAY 35

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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). 37

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. 38

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. 39

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. 40

41. ATYPICAL ODONTALGIA 41

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

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. 43

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. 44

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. 45

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) 46

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. 47

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. 48

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

50. CLINICAL FEATURES 50

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. 51

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 52

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. 53

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. 54

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 55

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. 56

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. 57

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. 58

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.  59

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. 60

61. CONCLUSION Recent studies use the 3 rd  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. 61

62. REFERENCES https://www.slideshare.net/drshagunagarwal/pain-and-pathways-of-pain https://www.researchgate.net/publication/5661216_Atypical_odontalgia_-_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 62