This presentation provides an overview of pain and its related aspects in dentistry.

1. PAIN AND PAIN PATHWAYS
B. MRUDULA DEVI
I MDS

2. CONTENTS
1. INTRODUCTION
2. DEFINITION
3. HISTORY
4. THEORIES OF PAIN
5. PAIN RECEPTORS
6. NEUROTRANSMITTERS
7. NERVE CONDUCTION
8. PAIN PATHWAYS
9. TYPES OF PAIN
10. ASSESSMENT OF PAIN
11. MANAGEMENT OF PAIN
12. CONCLUSION
13. REFERENCES

3. INTRODUCTION
• Pain is one of the most commonly experienced
symptoms in Dentistry.
• It is an intensely subjective experience, and is
therefore difficult to describe.
• Often spoken of as a protective mechanism.
• Produced by real or potential injury to the body.

4. DEFINITION
“An unpleasant emotional experience associated
with actual or potential tissue damage or
describe in terms of such damage.”
(International Association for the Study of Pain)
“An unpleasant emotional experience usually
initiated by noxious stimulus and transmitted
over a specialized neural network to the Central
Nervous System where it is interpreted as such.”
(Monheim)

5. HISTORY
• Derived from Greek word, “Poin” meaning
penalty.
• In Latin “Poena” means punishment from
God.
• Aristotle – “Passion of the soul”.
• Plato – Pain is an emotional experience more
than a localized body disturbance.
• John Bonica – Father of Pain

6. Warning
signal
Reflex
withdrawl
Minimizes
the
activities
Urges to
take
treatment
BENEFITS OF PAIN SENSATION

7. THEORIES OF PAIN
• INTENSITY THEORY
• SPECIFICITY THEORY
• PATTERN THEORY
• GATE CONTROL THEORY

8. Descartes (1644) : Straight through channel from skin to brain.
Muller : Information transmission by sensory nerves
Von Frey : Pain receptors – Free nerve endings ; Pain centre - Brain
SPECIFICITY THEORY
INTENSITY THEORY (Mumford & Newton)
“Pain Is A Non Specific Sensation And Depends On High
Intensity Stimulation”

9. PATTERN THEORY (Goldscheider, 1894)
Critical determinants of pain : Stimulus intensity and central
summation
Summation of sensory input Nerve impulses
Source : Massieh Moayedi and Karen;Theories of pain: from specificity to gate control, J Neurophysiol 109: 5–12, 2013.

10. GATE CONTROL THEORY (Melzack and Wall, 1965)
Postulates :
‣ Information is transmitted to CNS by small peripheral
nerves.
‣ Cells in the spinal cord are also facilitated or inhibited by
large peripheral nerves.
‣ Descending control systems modulate the excitability of
cells that transmit information.

11. Source : Massieh Moayedi and Karen;Theories of pain: from specificity to gate control, J Neurophysiol 109: 5–12, 2013.

12. Threshold
and
Intensity
Adaptation
Localization
Rate of
tissue
damage
CHARACTERISTICS OF PAIN

13. PAIN RECEPTORS
Sensory receptors can be classified into :
• Exteroceptors
1. Cutaneous receptors
2. Chemoreceptors
3. Telereceptors
• Interoceptors
1. Visceroceptors
2. Proprioceptors

14. • ALL PAIN RECEPTORS ARE FREE NERVE ENDINGS
(NOCICEPTORS)
‣ They are not enclosed in a capsule.
‣ A nerve ending that responds to noxious stimuli can
actually or potentially produce tissue damage.
• Three types of stimuli excite Pain Receptors
1. Mechanical
2. Thermal
3. Chemical

15. COMPONENTS OF PAIN
• Sensory discriminative component
‣ Processes sensory inputs in the cortex
‣ Assess intensity and duration of pain
• Motivational Affective component
‣ Attention and arousal
‣ Somatic and Autonomic reflexes
‣ Emotional changes associated with pain

16. NEUROTRANSMITTERS
Neurotransmitter is a chemical substance that acts as a
mediator for the transmission of nerve impulse from one
neuron to another neuron through a synapse.
• Excitatory neurotransmitters
Responsible for the conduction of impulse from the
presynaptic neuron to the postsynaptic neuron.
Acetylcholine
Nitric oxide
Histamine
Glutamate
Aspartate.

17. • Inhibitory Neurotransmitters
Inhibit the conduction of impulse from the presynaptic
neuron to the post synaptic neuron.
GABA
Glycine
Dopamine
Serotonin.
• Excitatory and Inhibitory
Noradrenaline
Adrenaline

18. NEUROANATOMY

19. NERVE FIBERS
Based on diameter and rate of conduction of impulses
(Eerlanger and Gasser) :
1. Type A fibres – Aα fibers
Aβ fibers
Aγ fibers
A∂ fibers
2. Type B fibers
3. Type C fibers

21. NERVE CONDUCTION
1. RESTING STATE
2. DEPOLARIZATION
3. REPOLARIZATION

23. PAIN PATHWAYS
Neural Pain Pathways (Field) :
• Transduction: Noxious stimuli leads to electrical activity in
the appropriate sensory nerve ending.
• Transmission: Neural event that carry the nociceptive input
into the central nervous system for proper processing.
• Modulation: Neural impulses (nociceptive) are changed or
altered before reaching the higher centers (Cortex).
• Perception: Interaction of the (cortex, thalamus, and limbic
system) higher centers.

24. SENSORY NEURONS
First Order
Neurons
Second Order
Neurons
Third Order
Neurons

25. First Order Neuron
‣ Carries impulses to the Central nervous System.
‣ Synapses with the second order neuron.
Second Order Neuron
‣ Transfers impulses to higher centers (Transmission
Neuron).
Third Order Neuron
‣ Relay thermal sensory information to the
somesthetic cortex.

26. COMPONENTS OF PAIN PATHWAY

27. Dual Pain Pathways :
The pain signals take two pathways to brain via
1. The Neospinothalamic Tract
2. The Paleospinothalamic Tract

28. Neospinothalamic tract for fast pain
• Neurotransmitter - Glutamate
• A∂ fibres transmit mechanical and thermal pain.
• Termination in the spinal cord : Lamina I (Lamina
Marginalis) of the dorsal horn.
• Excite second-order neurons

29. Termination of neospinothalamic tract
Few fibers terminate in the reticular areas.
Most fibers passes to thalamus and terminate
in the ventrobasal complex.
Few fibers terminate in the posterior nuclear
group of thalamus.
Basal areas of brain and somatosensory
cortex.

30. Paleospinothalamic Pathway for slow pain
• Type C fibres
• Neurotransmitter – Glutamate and
Substance P
• Termination in spinal cord : Lamina II and
Lamina III (Substantia Gelatinosa)

31. Reticular nuclei of medulla, pons and mesencephalon
Tectal area of the mecencephalon deep to the superior and
inferior colliculi
Periductal gray region surrounding the Aqueduct of Sylvius
Intralaminar and ventrolateral nuclei of the thalamus and
certain portions of hypothalamus
Termination of Paleospinothalamic tract

33. DUAL NATURE OF PAIN
• Pain perception
Stimulus Impulse Transmission
• Pain reaction
Inversely proportional to pain threshold

34. TYPES OF PAIN
SOMATIC : Pain arising from skin and deep
structures like muscles , bone , joint and ligament .
‣ Well defined and is generally caused by
inflammatory reactions in the tissues.
i. SUPERFICIAL OR CUTANEOUS
‣ Pain arising from the skin and superficial mucous
membrane
‣ Often felt as pricking type.

35. ii. DEEP PAIN
‣ It has a dull character and is poorly localized.
VISCERAL PAIN :
‣ It is diffuse in nature and is often referred.
‣ Dull aching in character and is accompanied
by sweating, nausea and fall in B.P.
REFERRED PAIN
‣ It is deep pain , whether visceral or somatic which may be felt
in some parts of the body other than the site of stimulation.
Eg. cardiac pain referred to the left arm and
diaphragmatic pain to shoulder.

36. PSYCHOGENIC OR FUNCTIONAL PAIN
‣ No obvious cause is found for the pain.
‣ Vague in nature and does not follow any anatomical
distribution .
NEUROPATHIC PAIN:
‣ Persistent pain that arises from functional changes
occurring in CNS secondary to peripheral nerve
injury.
‣ Damaged nerve elicits sustained activation of
nociceptors, causing neuropathic pain.

37. PERIODONTAL PAIN PULPAL PAIN
Somatic Visceral
More localized Less localized
Related to masticatory
function
Does not respond to
masticatory function
Not a threshold type Threshold type

38. Emotional
States
Fatigue Age
Racial and
Nationality
Characteristics
Gender
Fear and
apprehension
FACTORS AFFECTING PAIN

39. ASSESMENT OF PAIN
Problem Identification
• Self report of pain
• Direct observation of pain-related behaviours
Pain assessment tools
Uni-dimensional measurement tools :
‣ Visual Analogue Scale
‣ Verbal Rating Scale
‣ Numerical Rating Scales

40. Multi-dimensional Pain Measurement Tools
‣ McGill pain questionnaire
‣ Brief pain inventory
‣ Behavioural pain scales
‣ Pain cognition questionnaire
‣ Pain Disability Index

42. MOLECULAR MARKER FOR PAIN
Gene c-fos
‣ Proto-oncogene
It can promote vast intracellular changes.
‣ It is almost certainly involved in the long-term
neurological consequences of noxious
stimulation.

43. Removing the cause
Blocking the pathway
of painful impulses
Raising the pain
threshold
Preventing pain reaction
by cortical depression
Using psychosomatic
methods
MANAGEMENT OF PAIN

44. Elimination of tissue
change
No excitation of free
nerve endings
No initiation of
impulses
REMOVING THE CAUSE
BLOCKING THE PATHWAY OF PAINFUL IMPULSES
• Prevents Depolarization of nerve
fibres
• Prevents conduction of impulses
Use of Local
Anesthetic agent

45. Pharmacological action of drugs
possessing analgesic properties.
Cause of the original stimulus may
not be eliminated.
Pain perception is unaffected,
reaction threshold is raised.
RAISING THE PAIN THRESHOLD

46. ANALGESIC AGENTS
1. NONOPIODS
‣ Action : Peripheral nerve endings
‣ Inhibit Prostaglandin synthesis
‣ Mild to Moderate pain
2. OPIODS
‣ Action : CNS
‣ Depress the central nervous system
‣ Moderate to Severe pain

49. Anticonvulsants:
• Act by blocking sodium channels and
suppressing neuronal discharge
Eg. Carbamazepeine and phenytoin sodium
Antidepressents:
• They act by inhibiting the reuptake and storage
of neurogenic amines
Eg.Serotonin, Norepinephrine, Aminotripyline
Antihistamines:
• They may have analgesic activity by virtue of
inflammation
Eg.Diphenhydramine, Hydroxyzine, Pyrilamine

51. INHIBITION OF PAIN (ANALGESIA)
Two mechanisms :
1. Stimulation produced Analgesia
‣ Segmental inhibition
‣ Supraspinal inhibition
2. Release of endogenous opioid peptide

52. Stimulation produced Analgesia
Electrical stimulation of specific areas of CNS
Pain reduction by inhibiting pain pathways.
Segmental inhibition :
‣ Activation of group A afferent nerve fibres.
‣ Stimulation of dorsal column of spinal cord.

53. Clinical application :
‣ Touching or shaking an injured area
decreases the pain.
‣ Acupuncture
Needles are introduced into specific parts of
the body to stimulate afferent fibres.

54. Transcutaneous Electrical Nerve Stimulation
(TENS) :
‣ Electrodes placed on the surface of skin
stimulate the pain site.

55. Supraspinal inhibition :
Mesencephalic pain inhibitory system
‣ Arises from midbrain ; Descends to dorsal
horn cells.
‣ Contains opiate receptors.
‣ Stimulation of this system causes inhibition
of second order neurons.

56. Release of endogenous opioid peptides :
‣ Substance P
‣ Opiate receptors
‣ Enkephalins and Endorphins
(opioid peptides)

57. Surgical management
Peripheral neurectomy
Electrosurgery
Cryosurgery

58. CONCLUSION
‣ Determining the source and cause of pain is
more important than mere locating the site.
‣ Eliminating the cause of pain is more
important than mere treating the symptom.

59. REFERENCES
1. Arthur C Guyton, John E Hall. Text book of medical
physiology. 10th ed. WB Saunders.
2. K Shambhulingam, Prema Shambhulingam. Essentials
of medical physiology. 5th ed; 2010.
3. C Richard Bennett. Monheim’s local anesthesia and
pain control in dental practice. 10th ed
4. A.K.Jain. Textbook of Human Physiology.3rd ed;2006.

60. 5. Massieh Moayedi and Karen;Theories of pain: from
specificity to gate control, J Neurophysiol 109: 5–12,
2013.
6. Woolf CJ et al. Pain : Moving from symptom control
toward mechanism specific pharmacologic
management. Ann Intern Med. 2004 Mar
16;140(6);441-51.