The document provides a comprehensive overview of pain, including its definition, history, classification, and characteristics. It details various types of pain, such as nociceptive, neuropathic, and inflammatory pain, and describes the pain pathway and theories explaining pain perception. Additionally, it highlights factors influencing pain and methods for inhibiting pain transmission, emphasizing the protective role of pain despite its unpleasant nature.

1. PAIN PATHWAY
Mohamed Rameez
1

2. CONTENTS
• INTRODUCTION
• HISTORY
• DEFINITION OF PAIN
• CLASSIFICATION OF PAIN
• CHARACTERISTICS OF PAIN
• NEURAL PAIN RECEPTORS
• PAIN PATHWAY
• THEORIES OF PAIN
• FACTORS AFFECTING PAIN
2

3. CONTENTS
• INHIBITION OF PAIN TRANSMISSION
• APPLIED ASPECTS IN ORTHODONTICS
• CONCLUSION
• REFERENCES
3

4. INTRODUCTION
• Pain is a common side effect of orthodontic treatment.
• Pain is a subjective response, which shows large individual
variations.
• It is dependent upon factors such as age, gender, individual
pain threshold, the magnitude of the force applied, present
emotional state and stress, cultural differences, and previous
pain experiences
4

5. • Pain has two features which are nearly universal. First, it is an
unpleasant experience; and secondly, it is evoked by a stimulus
which is actually or potentially damaging to living tissues.
• That is why, although it is unpleasant, pain serves a protective
function by making us aware of actual or impending damage to
the body.
5

6. HISTORY
EARLY THEORIES
• 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.
6

7. MIDDLE AGES
• In the 11th century, Avicenna theorized that there were a number
of feeling senses including touch , pain and titillation.
• In his 1664 Treatise of Man , Rene Descartes theorized that the
body was more similar to a machine, and that pain was a
disturbance that passed down along nerve fibers until the
disturbance reached the brain.
7

8. DEFINITION
The International Association for the Study of Pain
Pain is "an unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such damage“
• Sherrington defined pain as “the psychical adjunct of an imperative
protective reflex” .
8

9. CLASSIFICATION
Pain
nociceptive neuropathic inflammatory
9

10. NOCICEPTIVE PAIN
• Nociceptive pain arises from a stimulation of specific pain
receptors and is a normal response to potential damage or injury
of tissues such as skin, muscles, visceral organs, joints, tendons, or
bones. We all experience this type of pain from time to time it
tends to resolve in a reasonable amount of time. Examples
include:
• •Somatic: muscles, joints, tendons, ligaments bones or skin; this
pain is often localized
• •Visceral: hollow organs and smooth muscle; usually referred
10

11. NEUROPATHIC PAIN
• Its pain initiated or caused by a problem with the signals from the
nerves. The cause can be a number of reasons but it is often
following an injury or disease of the nervous system.
• The nature of neuropathic pain ranges from deficits perceived as
numbness to hypersensitivity (hyperalgesia or allodynia), and to
paresthesia’s such as tingling.
11

12. NATURE OF NEUROPATHIC PAIN
• Allodynia- This means that the pain comes on, or gets worse, with
a touch or stimulus that would not normally cause pain.
• Hyperalgesia- This means that you get severe pain from a
stimulus or touch that would normally cause only slight
discomfort.
• Paraesthesia- This means that you get unpleasant or painful
feelings even when there is nothing touching you, and no
stimulus. For example, you may have painful pins and needles, or
electric shock-like sensations.
12

13. INFLAMMATORY PAIN
• The body responds to damage, injury or any underlying cause by
activating pain pathways to produce inflammation.
• Although long term inflammation can do a lot of damage, initially
its role is protective
• Examples : appendicitis, rheumatoid arthritis, herpes zoster etc..
13

14. CLASSIFICATION
BASED ON PAIN INTENSITY
Pain
Mild Moderate Severe
14

15. 15

16. 16

17. CLASSIFICATION
BASED ON DURATION
17
ACUTE
*SHARP PAIN
*SHORT DURATION
*LOCALIZED IN SMALLER
AREA
CHRONIC
* DULL PAIN
* INTERMITTENT/CONSTANT PAIN
*LONG DURATION

18. CLASSIFICATION
18
PAIN
SOMATIC
SUPERFICIAL DEEP
VICERAL

19. 19

20. REFERRED PAIN
• Referred pain is the painful sensation in a body region distant from the true
source of pain
• Occurs in an area supplied by the same neuro-segment as the involved
organ
• Pain is referred to a structure that is developed from same embryonic
segment or dermatome according to Dermatomal rule
20

21. 21

22. CHARACTERISTICS OF PAIN
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
22

23. PAIN THRESHOLD AND TOLERANCE
23

24. NON ADAPTATION OF PAIN RECEPTORS
• Pain receptors show no adaptation and so the pain continues as long as receptors
continue to be stimulated.
• It serves as a protective function to keep the individual trying to remove the
damaging stimulus or to get rid of it.
24

25. LOCALIZATION OF PAIN
• Pain sensation is somewhat poorly localized. However superficial pain is
comparatively better localized than deep pain.
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.
25

26. PAIN RECEPTORS
26

27. SENSORY RECEPTORS
• Sensory input from various external stimuli is thought to be received by specific
peripheral receptors that act as transducers and transmit by nerve action potential
along specific pathways towards the central nervous system.
• The impulse interpreted is nociceptive ie; causing pain. if it exceeds pain threshold,
that is, the intensity of the stimulus is so great that the receptor is no longer
differentially sensitive.
27

28. SENSORY RECEPTORS
28

29. 29

30. CUTANEOUS RECEPTORS
• The perception of different kinds of sensation has demonstrated
the existence of sensory spots in the skin.
• These sensory spots are thought to contain receptors which are
distinguished by the form of stimulus that excites them and
their location within the skin, and are distinguished
morphologically as corpuscular and non-corpuscular.
30

31. • Although, electron microscopy has defined the presence of many
receptors structurally, functionally three categories of cutaneous
receptors are thought to exist:
31
mechanoreceptors
thermoreceptors .
nociceptors .

32. 32

33. 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.
• They are receptors for fast pain and are
sensitive to mechanical or thermal stimuli
of noxious strength.
33

34. TYPES OF NOCICEPTORS
• Pain receptors which respond to a wide variety of stimuli are
called POLYMODAL
• Sensations mediated by a delta fibers (sharp, intense pain) and c
fibres (persistent ,dull pain)
34
mechanical
• Strong pressure
• Sharp objects
thermal
• Burning heat (>45 c)
• Noxious cold
chemical
• pH extremes
• Environmental irritants
• Internal neuro active
substances

35. 35

36. MECHANORECEPTORS
• Mechanoreceptors respond to tactile non painful stimuli.
• These receptors are divided into two functional groups (rapidly or slowly
adapting) depending on their response during stimuli.
• Rapidly adapting mechanoreceptors respond at the onset and offset of the
stimuli, while slowly adapting mechanoreceptors respond throughout the
stimuli duration.
36

37. NOCICEPTION - STAGES
37

38. TRANSDUCTION
38
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
neurons.
• Electrical events in neurons to chemical events at synapses.

39. 39

40. TRANSMISSION
• Electrical events are transmitted along neuronal pathways, while
molecules in the synaptic cleft transmit information from one cell
surface to another.
40

41. MODULATION
• The adjustment of events,
by up or down regulation.
• This can occur at all levels
of the nociceptive
pathway, from tissue,
through primary afferent
neuron and dorsal horn,
to higher brain centres.
41

42. SENSORY NEURONS
Sensory neurons
First order Second order Third order
42

43. 43

44. 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.
44

45. • A general classification of neurons divides the larger fibers from the smaller
ones.
45

46. 46

47. 47

48. SECOND ORDER NEURON
• The primary afferent neuron carries impulse into the CNS and
synapses with the second-order 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.
48

49. 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 intra-
laminar thalamic nuclei
• Third order neuron fibres from the thalamus relay
thermal sensory information to the somesthetic cortex.
49

50. PAIN PATHWAY
50

51. • From the site of pain generation, i.e.
from the periphery, the pain senses
are carried by Aδ fibres and C fibers.
• Their cell bodies are situated in the
dorsal root ganglion.
• The central processes of the neuron,
lying in the ‘sensory root’ of the
spinal nerve enter the dorsal horn to
terminate in the SGR ( Substantia
Gelatinosa Rolandi), situated in the
tip of dorsal horn.
51

52. • From the SGR, next order ( i.e. 2nd
order) neuron arises, crosses to the
opposite side, then moves up
through the white matter of spinal
cord to reach the brain.
• Most of these 2nd order neurons
travel up as spinothalamic tract (STT),
then ultimately terminate in the
proper area of thalamus.
52

53. • The Neurotransmitter at the synapse
between Aδ fiber & 2nd order
neuron at SGR is glutamate while the
Neurotransmitter between C fiber &
2nd order neuron (slow pain) at SGR
is substance P.
53

54. • From these specific nuclei of
thalamus, next order neurons arise to
terminate on the cerebral cortex, at
areas SI & SII as well as cingulate
gyrus (which is the key area for
production of some emotions).
• At SGR, there is a synapse between
1st order & 2nd order neuron. Also
there is synapse of 2nd & 3rd order
neuron at thalamus.
54

55. Other 2nd order neurons, from SGR also
are known, & they also cross to the
opposite side to reach different areas of
brain.
55

56. • The tip of dorsal horn, particularly the
SGR plays a key role in modification
of pain perception. It is called a gate.
• As a gate can be shut/ partially
opened/ fully opened to control
incoming traffic, so also behaves the
SGR controlling the incoming traffic
of pain.
56

57. SEQUENCES IN PAIN TRANSMISSION
57

58. THEORIES OF PAIN
• INTENSITY THEORY
• SPECIFICITY THEORY
• PROTOPATHIC AND EPICRITIC THEORY
• PATTERN THEORY
• GATE CONTROL THEORY
58

59. INTENSITY THEORY
• According to this view, pain is produced when any sensory nerve
is stimulated beyond a certain level.
• In other words pain is supposed to be a non-specific sensation
and depends only on high intensity stimulation.
• But the trigeminal system provides an example against this
theory.
59

60. • In case of trigeminal neuralgia, the patient can suffer excruciating
pain from a stimulus no greater than a gentle touch, provided it is
applied to a trigger zone.
• Although, the intensity theory is not accepted, it remains true to
say that intensity of stimulation is a factor in causing pain.
60

61. SPECIFICITY THEORY
• It was given by JOHANNES MULLER, 1842.
• According to this view, pain is a specific modality equivalent to
vision and hearing etc.
• Just as there are Meissner corpuscles for the sensation of touch,
Ruffini end organs supposedly for warmth and Krause end organs
supposedly for cold, so also pain is mediated by free nerve
endings.
61

62. • Certain psychophysical studies have been regarded as supporting
specificity theory. Specialization is known to exist in nervous
system and there are well known tracts.
• But concept of specific nerve ending is no long tenable. The
Krause and Ruffini endings are absent from the dermis of about
all hairy skin, so it is certain that these structures cannot be
receptors for cold and warmth.
62

63. PROTOPATHIC AND EPICRITIC THEORY
• HEAD AND RIVERS (1908) postulated the existence of two
cutaneous sensory nerves extending from the periphery to the
CNS.
• The protopathic system is primitive, yielding diffuse impression of
pain, including extremes of temperature and is upgraded.
• The epicritic system is concerned with tough discrimination and
small changes in temperature and is phylogenetically a more
recent acquisition.
63

64. PATTERN THEORY
• It was given by GOLDSCHEIDER, 1894.
• This theory states that pain sensation depends upon spatio – temporal pattern of
nerve impulses reaching the brain.
• According to WODDELL (1962) warmth, cold and pain are words used to describe
reproducible spatio – temporal pattern, or codes of neural activity evoked from skin
by changes in environment.
• The precise pattern of nerve impulse entering the CNS will be different for different
regions and will vary from person to person because of normal anatomical
variations.
64

65. 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 input 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.
65

66. • 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.
66

67. • 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.
67

68. 68

69. 69

70. FACTORS AFFECTING PAIN
• Emotional status:
• The pain threshold depends greatly on
attitude towards the procedure. In case of
emotionally unstable and anxiety patient the
pain threshold is low but reaction is high.
• Fatigue:
• Pain reaction threshold is high in subjects who
has good night sleep and relaxed, than those
persons who are tired.
70

71. • Age :
• Older individuals tend to tolerate pain and thus have higher pain
reaction threshold than young individuals. Perhaps their philosophy
of living or the realization that unpleasant experiences are a part of
life may account for this fact
71

72. • Racial and national characteristics:
• It has been said that racial characteristics
are reflected in the pain. The Caucasian
and Negro races have little or no variation
in the pain reaction threshold.
72

73. • Sex :
• Men have higher pain threshold than
women. This may be a reflection of
man’s desire to maintain his feeling of
superiority and this is exhibited in his
pre determined effort to tolerate pain
73

74. • Fear and apprehension:
• Most cases pain threshold is lowered as
fear and apprehension increases.
Individuals who are extremely fearful tend
to magnify their experiences
74

75. INHIBITION OF PAIN TRANSMISSION
Pain inhibiting mechanism
Endogenous Exogenous
75

76. ENDOGENOUS METHOD
• REMOVING THE CAUSE
• It is a desirable method.
• It is imperative that any removal leave no permanent environmental changes
in tissue, since this condition would then be able to create the impulse, even
though the original causative factor had been eliminated.
76

77. • BLOCKING THE PATHWAYS OF PAINFUL IMPULSES
• This can be done by injecting drug possessing local analgesic property in
proximity to the nerve involved.
• Thus preventing those particular fibers from conducting any impulses
centrally beyond that point. These two method act by altering pain
perception.
77

78. • RAISING THE PAIN THRESHOLD
• Raising pain threshold depends on the pharmacological activity of drugs
possessing analgesic properties.
• These drugs raise pain threshold and therefore alter pain reaction,
conceptually there are two components of pain
(a) Nociceptive
(b) Affective component.
• The path of nociceptive component is Spinothalamic tract to Thalamus. This
component is purely physical component of pain.
78

79. • AFFECTIVE COMPONENT
• It is the psychological component associated with pain.
• The path is that some fibers from Site of injury to thalamus terminate in
some intermediate stations in the reticular formation of brain stem and are
called spino-reticular thalamic system.
• Non-narcotic analgesic like aspirin can inhibit the nociceptive but not the
affective component of pain whereas opioid (Morphine) inhibit affective as
well as nociceptive components of the pain. They act centrally at cortical and
sub cortical centers, to change patient mind and his reaction towards pain
79

80. • PREVENTING PAIN REACTION BY CORTICAL DEPRESSION
• Eliminating pain by cortical depression is by the use of general anesthesia.
• USING PSYCHOSOMATIC METHOD
• This method affects both pain perception and pain reaction. It include audio
analgesia
80

81. ANALGESIC PATHWAY
81
• Analgesic pathway interferes with pain transmission and is often
considered as descending pathway , the ascending pathway being
the afferent fibers that transmit pain sensation to brain.
• Pain sensations may be controlled by interrupting the pain
impulse between receptor and interpretation centers of brain.
• This may be done chemically, surgically or by other means.
• Most pain sensations respond to pain reducing drugs/analgesics
which in general act to inhibit nerve impulse conduction at
synapses.

82. • Fibers of analgesic pathway arises from
frontal lobe of cerebral cortex and
hypothalamus.
• These fibers terminate in the grey
matter surrounding the 3rd ventricle
and periaqueduct grey matter .
• Fibres from here descend down to
brainstem and terminate on:
- Raphae magnus nucleus.
- Nucleus reticularis.
82

83. • These reticular nuclei descend through lateral white column of
spinal cord and reach the synapses of the neuron in afferent pain
pathway situated in the anterior grey horn.
• The synapse between the afferent pain pathway are:
• - Aδ afferent fibers and neurons of marginal nucleus.
• - C type afferent fibers and neurons of Substantia Gelatinosa of
Rolandi.
83

84. • At the synaptic level the analgesia fibers release the
neurotransmitters and inhibit pain transmission before being
relayed to brain.
84

85. PAIN IN ORTHODONTICS
• A common side-effect of orthodontic treatment is pain.
• It is among the top reasons why patients withdraw from orthodontic
procedures.
• Burstone (1962) reported an immediate and delayed painful response
after orthodontic force application
• He attributed the initial response to compression and the delayed
response to hyperalgaesia of the PDL.
Orthodontic pain: from causes to management — a review,Vinod Krishnan European Journal of
Orthodontics 29 (2007) 170–179
85

86. • Burstone (1962) classified a painful response to orthodontic
mechanics in two ways:
• 1. Depends on the relationship of force application with pain
• 2. According to the time of onset.
86

87. • The degree of pain perceived in response to the amount of force application
can be divided into three:
• 1. First degree: the patient is not aware of pain unless the orthodontist
manipulates the teeth to be moved by the appliance, e.g. using instruments
such as a band pusher or force gauge
• 2. Second degree: pain or discomfort caused during clenching or heavy
biting — usually occurs within the first week of appliance placement. The
patient will be able to masticate a normal diet with this type of pain.
• 3. Third degree: if this type of pain appears, the patient might be unable to
masticate food of normal consistency.
87

88. • Based on time of onset, Burstone (1962) further classified pain as follows:
• 1. Immediate: which is associated with sudden placement of heavy forces on
the tooth, e.g. hard figure of eight tie between the central incisors to close a
midline diastema.
• 2. Delayed: produced by variety of force values from light to heavy and
representing hyperalgaesia of the periodontal membrane. This type of pain
response decreases with time i.e. the pain reaction might start as third
degree but become second or a first degree with the passage of time.
88

89. • In orthodontics, a mechanical stimulus is introduced by placing
fixed appliances on the teeth resulting in tooth movement.
• Forces are applied to the dentoalveolar complex resulting in
inflammation or ischemia to the periodontal ligament (PDL) with
subsequent release of histamine , bradykinin, prostaglandins,
substance P, and serotonin
• These mediators stimulate local nerve endings and send pain
signals to the brain.
89

90. • According to Krishnan , the perception of orthodontic pain is due
to change in blood flow caused by appliances, correlated with
release of various substances such as Substance P ,histamine,
serotonin , prostaglandins and cytokines
Orthodontic pain: from causes to management — a review,Vinod Krishnan European Journal of Orthodontics 29 (2007)
170–179
90

91. CAUSE OF PAIN
• Orthodontic separators
• Archwire placement and activation
• Fixed and removable appliance
• Initial tooth positions and force levels
• Orthopedic force and sutural strain
• Debonding
91

92. PAIN CONTROL
• Administration of NSAIDS remain preferred method
• Major concern regarding NSAIDS is interference with inflammatory process
• Low doses administered for two days wont affect tooth movement process as
such
• Current trend is directed towards the use of pre operative analgesics
• Administered one hour before every orthodontic procedure
• Anaesthetic gel ,bite wafers ,transcutaneous electrical nerve stimulation , low-
level laser use and vibratory stimulation
92

93. CONCERNS DURING NSAIDS INTAKE
• Studies have shown that NSAID’s (Indomethacin and imidazole)
decreased the rate of tooth movement when they were injected at
high concentrations, but a statistically significant difference was
not observed between their inhibitory effects.
• Briefly, the increase in PGI2 and TXA2 levels, in periodontal tissues,
enhanced the orthodontic tooth movement
• Whereas the decrease in these arachidonic acid metabolites
reduced the rate of tooth movement.
93

94. MECHANISM OF ACTION OF NSAIDS
94

95. COMMON PAIN RELIEF METHODS
• Nonsteroidal anti-inflammatory drugs (NSAIDS)
• An application of low-level laser therapy
• Chewing gum(aspergum-with aspirn)
• Micro pulse vibration
• Anesthetic Gel ‘oraqix’(lidocaine+prilocaine)
• Transcutaneous electric nerve stimulation(TENS)
95

96. RECENT ADVANCES
• A recent development in this area of pain management is the introduction of
rofecoxib, the cox-2 inhibitor. It has been reported that this drug has no effect on
PGE 1 levels and can be safely used for pain control during orthodontic
mechanotherapy ( Sari et al. ,2004 ).
• Low energy laser irradiation may be useful in reducing the levels of inflammation
and pain , as well decreasing orthodontic treatment time by accelerating the pace of
tooth movement , without causing any side effects.(shimizu et.al 1995, magero et.al
2002
96

97. CONCLUSION
• Pain management and even more important, pain prevention are
given less importance in many orthodontic training programs ’ .
With increased apprehension from patients as well as parents . A
sound knowledge about pain management will help in arriving or
formulating correct methods to measure, evaluate, and manage
pain as well as the distress experienced by orthodontic patients.
The will help in improving not only the living standards of our
patients but also the practice environment of every orthodontic
clinician.
97

98. REFERENCES
• Bell`s ‘Orofacial pain’, 5th edition, Jeffrey P. Okeson.
• Text book of Medical Physiology, 2nd edition, Chaudhari.
• Human physiology , Andrew davies , Asa.H.Blakeley , Cecil Kidd (international
edition).
• Review of medical physiology, William .F. Ganong (20th edition)
• Samson wrights applied physiology, Cyril . A. Keele , Eric Neil and Norman Joels
(thirteenth edition)
• Biological mechanism of tooth movement, Vinod Krishnan
98

99. REFERENCES
• Orthodontic pain: from causes to management — a review,Vinod Krishnan European
Journal of Orthodontics 29 (2007) 170–179
• Pain control in orthodontics using a micropulse vibration device:A randomized
clinical trial, Angle Orthod. 2016;86:625–630.
• Does low level laser therapy relieve the pain caused by the placement of the
orthodontic separators? ——a meta-analysis
• Shi et al. Head & Face Medicine (2015) 11:28 DOI 10.1186/s13005-015-0085-6
99

100. ACKNOWLEDGEMENT
• DR. RAJKUMAR. S.ALLE
• DR. SHWETHA.G.S
• DR. SHASHI KUMAR.H.C
• DR. SUMA.T
• DR. LOKESH.N.K
• DR. KIRAN.H
• DR. SIDHARTH ARYA
• DR. DHARMESH.H.S
• DR.BHARATI
• DR.FAISAL ARSHAD
100

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