This document provides an overview of pain and pain pathways. It defines pain, discusses its history and characteristics. It describes the classification and receptors of pain, as well as the chemical mediators and neural pathways involved in pain transmission and modulation. Specifically, it outlines the three orders of sensory neurons - first order neurons transmit signals from receptors to the spinal cord, second order neurons relay signals within the spinal cord, and third order neurons transmit signals from the spinal cord to the brain. It also briefly discusses theories of pain transmission and modulation.

1. PAIN AND PAIN
PATHWAYS
Presented by:
Dr.Shrawani Chouhan
1st year PG
Department Of Periodontology

2. CONTENTS
• Definition
• History
• Related terms
• Characteristics of pain
• Classification of pain
• Pain receptors
• Chemical mediators involved with pain

3. • Neural pain pathways
• Types of sensory neurons
• Theories of pain
• Pain pathways
• Modulation of pain
• Inhibition of pain
• Pain- dental point of view
• Conclusion
• Reference

4. DEFINITION
• OKESON- “An unpleasant sensation associated with actual or potential
tissue damage and mediated by specific nerve fibers to the brain, where
its conscious appreciation may be modified by various factors.”
• MONHEIM- “An unpleasant emotional experience usually initiated by
noxious stimulus and transmitted over a specialized neural network to
the CNS where it is interpreted as such.”
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45,
Monheim’s local anesthesia and pain control in dental practice; C.Richard Bennett;7th edition ; CBS; Pg no 1-24

5. HISTORY
• Derived from Latin -“Poena” meaning punishment from God.
• Homer thought pain was due to arrows shot by God.
• Aristotle, who probably was the first to distinguish five physical senses
considered pain to the “passion of the soul” that somehow resulted from
the intensification of other sensory experience.
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380

6. RELATED TERMS
• Allodynia
• Hyperalgesia & Hypoalgesia
• Hyperpathia
• Causalgia
• Neuralgia

7. CHARACTERSTICS OF PAIN
1. Threshold and Intensity
• If the intensity of the stimulus is below the threshold (sub-threshold) pain is not felt.
As the intensity increases more and more, pain is felt more and more according to
the Weber-Fechner’s law. This law ensures that while our body can perceive pain due
to low intensity stimulus, a severe crushing injury will not cause death due to pain
sensation, yet as stimulus increases, sense of perception also increases.

8. 2. Adaptation – Pain receptors show no adaptation and so the pain continues as long
as receptors continue to be stimulated.
3. Localization of pain - Pain sensation is somewhat poorly localized. However
superficial pain is comparatively better localized than deep pain.
4. Influence of the rate of damage on intensity of pain
• If the rate of tissue injury (extent of damage per unit time) is high, intensity of
pain is also high.

9. CLASSIFICATION OF PAIN
Based on source/ location/ referral & duration
ACUTE PAIN / TRAUMATIC PAIN CHRONIC PAIN
VISCERAL
/SPLANCNIC PAIN
SOMATIC PAIN MALIGNANT PAIN
OR
CANCER PAIN
NON – MALIGNANT PAIN
OR
BENIGN PAIN
SUPERFICIAL PAIN
OR
CUTANEOUS PAIN
DEEP SOMATIC PAIN MUSCULOSKELETAL PAIN NEUROPATHIC PAIN
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380

10. BASED ON TRANSMISSION
FAST PAIN
 Felt about 0.1 sec after a pain stimulus is applied
 It is described as sharp pain, pricking pain, acute
& electric pain
 Fast sharp pain is not felt in most deeper tissues
of the body
SLOW PAIN
 Usually begins after 1 sec or more and may
range from seconds to minutes
 Described as slow, burning, aching, throbbing,
nauseous pain and chronic pain
 Associated with tissue destruction
Textbook of medical physiology; Guyton & Hall;12th edition; Elseiver; pg no 598-613

11. PAIN RECEPTORS

12. SENSORY RECEPTORS
• At the distal terminals of afferent(sensory) nerves are specialized sensory receptors that
respond to physical or chemical stimuli
• Sensory receptors are specific for certain types of stimuli
• Classified as:- 1)Exteroreceptors
2)Popioreceptors
3)Interoreceptors
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380,

13. EXTEROCEPTORS
• These receptors are stimulated by immediate external environment.
• Located on skin and mucosa
• Examples: Merkle’s corpuscles, Meisser’s corpuscles,
Krause’s corpuscles, free nerve endings
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380

14. PROPIOCEPTORS
• They provide information from the musculoskeletal structures concerning
the presence, position and movement of the body.
• They are chiefly involved with automatic functioning.
• Sensations from these receptors are below conscious levels.
• Examples: Muscle spindles, Golgi tendon organs, Pacinian corpuscles,
Periodontal mechanoreceptors, Free nerve endings.
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-
45, pg no 329-380

15. INTEROCEPTORS
• These are the sensory receptors which are present in and
transmit from the viscera of the body.
• Involuntary function
• Examples: Pacinian corpuscles, Free nerve endings
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380

16. NOCICEPTORS
• A nerve ending that responds to noxious stimuli that can actually or potentially produce tissue damage.
• Free nerve endings i.e., they are not enclosed in a capsule. The receptors for fast pain are sensitive to
mechanical or thermal stimuli of noxious strength. The receptors for slow pain are sensitive not only to
noxious mechanical and thermal stimuli but also to a wide variety of chemicals associated with inflammation.
• These substances include histamine, serotonin, bradykinin, acetylcholine, potassium ions and hydrogen ions.
It is possible that noxious mechanical and thermal stimuli also act through the release of some of these
chemicals.
Patrick Haggard, Lieke de Boer. Oral somatosensory awareness. Neuroscience and Biobehavioral Reviews 2014;47:469-84

17. • Since pain receptors respond to a wide variety of stimuli, they are called polymodal.
• Types of nociceptors :
Aδ Mechanical Nociceptors
C Polymodal Nociceptors
C fibre mechanical nociceptors
High threshold cold nociceptors
Patrick Haggard, Lieke de Boer. Oral somatosensory awareness. Neuroscience and Biobehavioral Reviews 2014;47:469-84

18. Aß - fibres Aδ - fibres C- fibres
Threshold Low Medium High
Axon diameter 6-14μm 1-6μm 0.2-1μm
Myelination Yes Thinly No
Velocity 36-90m/s 5-36m/s 0.2-1m/s
Receptor types Mechanoreceptor Mechano/Nociceptor Nociceptor
Receptive field Small Small Large
Quality Touch Sharp/first pain Dull/second pain
SUMMARY OF RECEPTORS
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380

20. SUBSTANCES
EXITING NCs
HISTAMINE
POTASSIUM
ATP
NEURO
TRANSMITTER
INVOLVED IN
PAIN
STIMULATION
OF
NOCICEPTORS
BRADYKININ
SENSITIZATION
OF NOCICEPTORS
PGE2
PGI2
DISCHARGE OF
PAIN RELEASING
SUBSTANCES BY
NOCICEPTORS
SUBSTANCE – P
GLUTAMATE
ACTIVATION OF
NOCICEPTORS
BY INTERACTING
WITH OTHER
CHEMICAL
MEDIATORS
PGI2
LTs

21. NEURAL PAIN PATHWAYS

22. • Nociception is the neural mechanism by which an individual detects the presence of a potentially tissue
harming stimulus. There is no implication of (or requirement for) awareness of this stimulus.
• The nociceptive mechanism (prior to the perceptive event) consists of a multitude of events as follows:
• Transduction:
• This is the conversion of one form of energy to another. It occurs at a variety of stages along the nociceptive
pathway from:
– Stimulus events to chemical tissue events.
– Chemical tissue and synaptic cleft events to
- Electrical events in neurones.
– Electrical events in neurones to chemical events at synapses.

23. • Transmission:
• Electrical events are transmitted along neuronal pathways, while molecules in the
synaptic cleft transmit information from one cell surface to another.
• Modulation:
• The adjustment of events, by up- or down regulation. This can occur at all levels of
the nociceptive pathway, from tissue, through primary (1°) afferent neurone and
dorsal horn, to higher brain centres.
• Thus, the pain pathway as described by Descartes has had to be adapted with time.

25. SENSORY NEURONS
First Order Second Order Third Order

26. FIRST ORDER NEURON
• Each sensory receptor is attached to a first order primary afferent neuron that carries the impulses to the
CNS.
• The axons of these first-order neurons are found to have varying thickness. It has long been known that a
relationship exists between the diameter of nerve fibers and their conduction velocities. The larger fibers
conduct impulses more rapidly than smaller fibers.
• A general classification of neurons divides the larger fibers from the smaller ones.
• Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45

27. • Type A fibers
• Alpha fibers: size - 13 to 20 µm, velocity - 70 to 120 m/ s.
• Beta fibers: size – 6 to 13 µm, velocity – 40 to 70 m/s.
• Gamma fibers: size – 3 to 8 µm, velocity – 15 to 40 m/s.
• Delta fibers: size – 1 to 5 µm, velocity – 5 to 15 m/s.
• Type C fibers
• Size – 0.5 to 1 µm, velocity – 0.5 to 2 m/s.

28. SECOND ORDER NEURON
• The primary afferent neuron carries impulse into the CNS and synapses with the second-order
neuron.
• “Transmission neuron”
• This second-order neuron is sometimes called a transmission neuron since it transfers the impulse
on to the higher centers.
• The synapse of the primary afferent and the second-order neuron occurs in the dorsal horn of the
spinal cord.
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45

29. THIRD ORDER NEURON
• Cell bodies of third order neurons of the nociception-relaying pathway are housed in: the ventral
posterior lateral, the ventral posterior inferior, and the intralaminar thalamic nuclei.
• Third order neuron fibers from the thalamus relay thermal sensory information to the
somesthetic cortex.
• Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45

30. THEORIES OF PAIN

31. SPECIFICITY THEORY
• Descartes in 1644= pain as a straight through channel
• Muller= information transmission by sensory nerves
• Von frey= specific cutaneous receptors
Monheim’s local anesthesia and pain control in dental practice; C.Richard Bennett;7th edition ; CBS; Pg no 1-24

32. • PATTERN THEORY
• By Golscheider in 1894.
• Stimulus intensity + central summation= critical determinants of pain
• Particular pattern of nerve impulses evoke pain.
Monheim’s local anesthesia and pain control in dental practice; C.Richard Bennett;7th edition ; CBS; Pg no 1-24

33. GATE CONTROL THEORY
• This theory proposed by Melzack and Wall in 1965 and recently re-evaluated is receiving
considerable attention.
• This theory of pain takes into account the relative in put of neural impulses along large and small
fibers, the small nerve fibers reach the dorsal horn of spinal cord and relay impulses to further cells
which transmit them to higher levels.
• The large nerve fibers have collateral branches, which carry impulses to substantia gelatinosa where
they stimulate secondary neurons.
Monheim’s local anesthesia and pain control in dental practice; C.Richard Bennett;7th edition ; CBS; Pg no 1-24

34. • The substantia gelatinosa cells terminate on the smaller nerve fibers just as the latter are
about to synapse, thus reducing activity, the result is, ongoing activity is reduced or stopped
–gate is closed.
• The theory also proposes that large diameter fiber input has ability to modulate synaptic
transmission of small diameter fibers within the dorsal horn.
• Large diameter fibers transmit signals that are initiated by pressure, vibration and
temperature; small diameter fibers transmit painful sensations.
• Activation of large fiber system inhibits small fiber synaptic transmission, which closes the
gate to central progression of impulse carried by small fibers.

35. ROLE OF BRAIN IN GATE CONTROL MECHANISM
Gates in spinal cord are open
Pain signals reach the thalamus through lateral spinothalamic tract
Signals are processed in thalamus
Signal are sent to sensory cortex & perception of pain occurs in cortex
Signals are sent from cortex back to spinal cord and the gate is closed by releasing pain relievers such as opioid
peptides
Minimizing the severity & extent of pain

36. 36

37. PAIN PATHWAYS

39. DUAL PAIN PATHWAYS IN CORD & BRAINSTEM
Neospinothalamic Tract for Fast Pain
• The fast type A(δ) pain fibers transmit mainly mechanical and acute thermal pain.
• They terminate mainly in lamina I at the dorsal horn and these excite second order neurons of
the neospinothalamic tract.
Textbook of medical physiology; Guyton & Hall;12th edition; Elseiver; pg no 598-613

40. Paleospinothalamic tract for Slow Pain
• This pathway transmits pain mainly from peripheral slow chronic Type C pain fibers.
• In this pathway, the peripheral fibers terminate almost entirely in lamina II and III of dorsal
horns of spinal cord, together called as substantia gelatinosa.
Textbook of medical physiology; Guyton & Hall;12th edition; Elseiver; pg no 598-613

41. • Axons of secondary neurons emerge from the spinal nucleus, cross the midline and ascend to
join fibers of mesencephalic nucleus to form trigeminal lemniscus or spinothalamic tract of
5th nerve.
• These tracts continue upward and terminate in the postero ventral nucleus of thalamus.
From here it is transmitted to posterocentral convolutions of cortex.
Textbook of medical physiology; Guyton & Hall;12th edition; Elseiver; pg no 598-613

42. 42
Textbook of medical physiology; Guyton & Hall;12th edition; Elseiver; pg no 598-613

43. PAIN PATHWAY OF MAXILLOFACIAL REGION
• 5th cranial nerve or trigeminal nerve is principal sensory nerve of head region.
• Any stimulus in area of trigeminal nerve is first received by both myelinated and non-
myelinated fibers, and conducted as an impulse along afferent fibers of ophthalmic,
maxillary and mandibular branches into semilunar or gasserian ganglion.
• Pain impulse descends from the pons by spinal tract fibers of trigeminal nerve through the
medulla.

44. MODULATION OF PAIN
• Noxious stimuli of comparable intensity may produce varying degrees of pain in the same
individual under different circumstances.
• For example, an injury acquired by an athlete in the sports field or by a soldier in the
battlefield is less painful than a comparable injury suffered in a road accident.
• In other words, pain can be modulated
Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380

45. INHIBITION OF PAIN

46. NON – PHARMACOLOGICAL MANAGEMENT
 The non – pharmacological management involves the following approaches
 Physiotherapy
 Psychological techniques
 Stimulation therapies – Acupuncture & Transcutaneous Electrical Nerve Stimulation
(TENS)
 Palliative care – involves the alleviation of symptoms but does not cure the disease

47. SURGICAL PROCEDURE FOR THE RELIEF OF PAIN
• CORDOTOMY: In the thoracic region , the spinal cord
opposite to the side of pain is partially cut to interrupt
the anterolateral pathway
• THALAMOTOMY: Involves causter ization of specific
pain areas in the intrathalamic nuclei in the thalamus,
which often relieves suffering type of pain

48. • RHIZOTOMY
• A rhizotomy is a term chiefly referring to
a neurosurgical procedure that selectively
destroys problematic nerve roots in the spinal
cord, most often to relieve the symptoms
of neuromuscular conditions such as spastic
diplegia and other forms of spastic cerebral
palsy

49. OPIOID/ NARCOTIC ANALGESICS
 OPIUM is a raw extract of the poppy plant Papaver somniferum
 During 19th century, MORPHINE was isolated from opium and its pharmacological
effects were characterized
OPIOD RECEPTORS
TYPE CHARACTERIZATION
µ - MU Highly selective for opioids
δ – DELTA Mixed agonist – antagonist response
K - KAPPA Opioid analgesics selective for these
receptors are not identified

50. OPIOID CLASSIFICATION

51. PULPAL PAIN
• It is the most commonly experienced pain in and near the oral cavity.
• Pulpal pain can be diagnosed based on clinical signs and symptoms
• Histological finding.
• Clinically pulp is referred as healthy, reversible pulpitis, irreversible pulpitis.
• Histological as acute, chronic & hyperplastic.
51

52. HYPEREMIA
• The increased pressure against the sensory nerve endings in the pulp might well
produce the sensation of pain. Application of cold produce a sharp hypersensitive
response and heat produce true transient hyperemia and a dull pain.
• An assessment of pain intensity at the time of stimulation, dental history& a thorough
dental examination allow the clinician to differentiate among the normal pulp, dentin
hypersensitivity, and the reversible inflamed pulp.
52

53. • Hyperactive pulpalgia :- It is characterized by a short, sharp, shock pain is felt as a
sensation of sudden shock. It is never spontaneous.
• Dentin Hypersensitivity :- Pain arise in response to thermal, chemical, tactile or osmotic
stimuli and is not caused by any other dental defect or pathology. This pain is explained by,
hydrodynamic theory postulated by Brannstrom.
53

54. • Characteristic features of irreversible pulp condition are :
• Hyperalgesia in the initial stage
• Dull throbbing ache in the later stage
• Lingering pain on application of stimuli
• Pain is spontaneous
• Cause referred pain in other areas
• Relief is provided by cold
54

55. PERIODONTAL PAIN
• Localized, deep throbbing pain
• Involving inflammation of PDL around one or more teeth
• Mobility of tooth.
• Localized bleeding
• Presence of pocket
• Radiographically, bone loss is seen.
• Pain last for hour or day
• Involve tooth is tender on percussion
55

56. Periradicular pain
• Acute apical periodontitis
• The pain has been described as constant, gnawing, throbbing and pounding. Tooth is
tender and slightly elevated in its socket.
• The pain is most persistent, lasting 24 hours a day.
• Acute apical abscess
• Pain is similar to AAP but somewhat lower in intensity. Involved tooth is painful to
movement or mastication
56

57. • Chronic apical periodontitis :
• It is seldom painful.
• Chronic apical abcess/suppurative apical periodontitis :
• It is generally symptoms free. When draining fistula is closed, discomfort ensue.
• Periodontal lesion pain :
• Acute gingival or periodontal abscess
• Tooth is painful to bite on and is not so deep seated or throbbing as that of apical abscess.
• Pain is spontaneous
• Associated localized swelling is there
• Presence of deep PDL pocket is there.
57

58. Pericoronitis
• Severe radiating pain in posterior mouth region and inability to
comfortably close or open mandible.
• Tissue distal to erupting molar is most painful to touch.
58

59. TEMPOROMANDIBULAR JOINT ARTICULAR
DISORDERS
• Capsulitis and Synovitis
• Chief complaint is continuous pain over the joint aggravated by function.
Swelling may be evident and patient may complaint of acute
malocclusion, restricted mouth opening and teeth pain.
59

60. INTERNAL DERANGEMENT
• It includes meniscus displacement, formation of intra articular adhesion and various forms of
arthritis.
• There occur limited jaw opening, deviation on opening, joint clicking, crepitus and pain directly
localized to the joint area in front of the tragus of the ear.
• The pain is dull, boring ache but may be more acute when exacerbated by wide mouth opening.
The symptoms become progressively worse and the degree of pain increase.
• TMJ pain is often referred into temple, cheek and posterior dental area of the maxilla and
mandible.
60

61. CONCLUSION
• Pain is bad, but not feeling pain can be worse.
• Individuals with a congenital absence of pain receptors are extremely rare but not
unknown. Such individuals are very poor at avoiding accidental injuries, and often
inflict mutilating injuries on themselves.
• As a result, their life span is usually short. thus pain, although unpleasant, is a
protective sensation with enormous survival value. Pain is a multidimensional
experience involving both the sensation evolved by noxious stimuli but also the
relation to it.
• The sensation of pain therefore depends in part on the patient past experience,
personality and level of anxiety.
61

62. REFERENCES
• Bells orofacial pain; Jeffrey P. Okeson; sixth edition;quintessence books; pg no 3-45, pg no 329-380
• Textbook of medical physiology; Guyton & Hall;12th edition; Elseiver; pg no 598-613
• Anesthesia for dentistry; Pramod kumar; National books; Pg no 9-18
• Monheim’s local anesthesia and pain control in dental practice; C.Richard Bennett;7th edition ; CBS; Pg no 1-24
• E. H. Ehrmann; The diagnosis of referred orofacial Dental pain; Australian endodontic journal volume no 28 ;2 august
2002
• Leigh A. Lamont,William J. Tranquilli, Kurt A. Grimm; Physiology Of Pain; lamont et al; Volume 30; number 4 ; july
2000
• Patrick Haggard∗, Lieke de Boer; oral somatosensory awareness: volume 47 (2014)