The knowledge of pain and pain pathway are essential for a medical professional. Here is my presentation on it from a periodontist's perspective

1. PAIN AND PAIN
PATHWAYS
HARIPRIYA RAJARAM
DEPT OF PERIODONTICS
PANINEEYA DENTAL COLLEGE
HYDERABAD

2. CONTENTS
• DEFINITION
• BENEFITS OF PAIN
SENSATION
• CLASSIFICATION OF PAIN
• TYPES OF PAIN
• NERVE FIBER
• RECEPTORS
• NERVE CONDUCTION
• PAIN PATHWAY
• NEUROTRANSMITTERS
RELEASED IN PAIN
TRANSMISSION
• ANALGESIC PATHWAY
• NEUROTRANSMITTERS
RELEASED IN ANALGESIC
PATHWAY
• THEORIES OF PAIN
TRANSMISSION
• MECHANISM OF PAIN
• PAIN ASSESSMENT
• CLASSIFICATION OF
OROFACIAL PAIN
• PAIN IN PERIODONTIUM
• MANAGEMENT OF PAIN

3. DEFINITION
• An unpleasant sensory and emotional experience associated with actual
or potential tissue damage, or described in terms of such damage.
- Internationl association for the study of pain (IASP)
• An unpleasant emotional experience usually initiated by a noxious
stimulus and transmitted over a specialized neural network to the central
nervous system where it is interpreted as such.
- Monheim’s local anesthesia and pain control in dental
practice
• Unpleasant sensation that occurs from imminent tissue damage
-World health organization

4. BENEFITS OF PAIN SENSATION
• Pain is an important sensory symptom. Though it is an unpleasant sensation.
It has protective or survival benefits such as.
1. It gives warning signal about the existence of a problem or threat. It also
creates awareness of injury.
2. It prevents damage by causing reflex withdrawl of the body from the
source of injury.
3. It forces the person to rest or to minimize the activities thus enabling
the rapid healing of the injured part.
4. It urges the person to take required treatment to prevent major damage.

5. CLASSIFICATION OF PAIN
BASED ON DURATION
PAIN
ACUTE CHRONIC

6. BASED ON LEVEL OF STIMULATION
pain
somatic
Deep
superficial
visceral

7. BASED ON UNDERLYING PATHOLOGY
pain
malignant
Non-
malignant
neuropathic
musculoskel
etal

8. OTHER TYPES OF PAINS:
1.REFERRED PAIN
• Referred pain is the pain that is perceived at a site adjacent
to or away from the site of origin.
• According to dermatomal rule, pain is referred to a structure, which is
developed from the same dermatome from which the pain producing
structure is developed.
• Eg: The pain associated with MI commonly is referred to the left arm,
neck & chest .

9. FAST PAIN SLOW PAIN
Stimulated by either mechanical or
thermal pain stimuli
Mostly by chemical type of pain
stimuli sometimes by mechanical or
thermal.
Transmitted by A𝛿 fibers Transmitted by c type of fibers
Velocity between 6-30 m/sec Velocity is between 2-5 m/sec
Transmission via the
neospinothalamic tract
Transmission via the
paleospinothalamic tract
Glutamate is the neurotransmitter
involved
Substance P is the neurotransmitter
involved
Can be easily located Difficult to locate
It is described as sharp pain, pricking
pain, acute & electric pain
Described as slow, burning, aching,
throbbing, nauseous pain and
chronic pain

10. 4. ACUTE PAIN: Acute has a sudden onset, usually subsides quickly and
is characterized by sharp, localized sensations with an identifiable cause.
5. CHRONIC PAIN:
• Chronic pain is arbitrarily defined as pain lasting longer than 3 to 6
months.
• It begins when pain persists after the initial injury has healed. It is
persistent or episodic pain of duration or intensity that adversely affects
the function and wellbeing of the patient.
• It may be nociceptive, inflammatory, neuropathic or functional in
origin. It varies from unrelenting extremely severe pain to pain of
escalating or non – escalating nature..
.

11. 6. SUB CUTANEOUS PAIN: It is also known as cutaneous pain. It
arises from superficial structures such as skin & subcutaneous tissues.
It is a sharp, bright pain with a burning quality and may be abrupt or
slow in onset.
7. DEEP SOMATIC PAIN: It originates in deep body structures such as
periosteum, muscles, tendons, joints & blood vessels.

12. 8. VISCERAL PAIN Is a type of nociceptive pain that comes from the
internal organs. Unlike somatic pain it is harder to pinpoint. Pain is
described as general aching or squeezing pain
9. NEUROPTHIC PAIN : Neuropathic pain is a result of an injury or
malfunction of the nervous system.

13. NEURON
• Neuron or nerve cell is defined as the structural and functional unit of
nervous system. Neuron is similar to any other cell in the body, having
nucleus and all the organelles in cytoplasm.
• However, it is different from other cells by two ways:
1. Neuron has branches or processes called axon and dendrites
2. Neuron does not have centrosome. So, it cannot undergo division

14. • STRUCTURE OF NEURON
Neuron is made up of three parts:
• 1. Nerve cell body
2. Dendrite
3. Axon.
• Dendrite and axon form the processes of neuron
• Dendrites are short processes and the axons are long processes.
• Dendrites and axons are usually called nerve fibers.
• Nerve cell body is also known as soma or perikaryon. It is irregular in
shape.

15. MYELIN SHEATH
• Myelin sheath is a thick lipoprotein sheath that insulates the myelinated
nerve fiber.
• Myelin sheath is not a continuous sheath.
• It is absent at regular intervals. The area where myelin sheath is absent
is called node of ranvier.
• Segment of the nerve fiber between two nodes is called internode.
• Myelin sheath is responsible for white color of nerve fibers.
• FUNCTIONS OF MYELIN SHEATH
1. Faster conduction
2. Insulating capacity

16. TYPES OF NERVE FIBERS
• There are several types of peripheral nerve fibres in the body.
• Nociceptive stimuli are received by nociceptors and then propagated via
an a or c fibre
• The first are thinly myelinated with a fast conduction of stimuli (1.2–40
m/s), whereas the second are unmyelinated with a slow conduction
(0.13–1.2 m/s).
• The a fibres have different subtypes: α, β, γ and δ.

17. • The C fibres conduct impulses generated by temperature, mechanical
and chemical stimulation.
• The aα fibres conduct motor impulses for the body’s posture and
movement (proprioception)
• The aβ fibres transport impulses generated by touch and signals from
the skin mechanoreceptors.
• The aγ fibres are involved in the regulation of the muscular tone,
• The aδ fibres conduct pain impulses and temperature signals

18. RECEPTORS
• Receptors are sensory (afferent) nerve endings that terminate in
periphery as bare unmyelinated endings or in the form of specialized
capsulated structures.
• Receptors give response to the stimulus.
• When stimulated, receptors produce a series of impulses, which are
transmitted through the afferent nerves .
CLASSIFICATION:
• Generally, receptors are classified into two types:
• Exteroceptors
• Interoceptors.
• Pain can be elicited by mechanical, thermal, and chemical pain stimuli.

19. NERVE CONDUCTION
• The conduction of an impulse by a nerve depends on the electrical
potential that exists across the nerve membrane.
• The nerve cell, being excitable, posseses the ability of transmitting or
conducting impulses along its length.
• The phenomenon is brought about by the flow of current across the
membrane during the transition of the nerve from the resting to active
state.
• Normally, electrolytic solutions containing an equal concentration of
anions and cations are present on both the sides of the cell membrane.

20. • RESTING STATE
• When the nerve is at rest , greater number of anions are present
inside the cell and where as an equal number of cations are present
outside the membrane.
• The difference in respective ion concentrations across the nerve
membrane creates a potential electrical difference between the inside
negative and outside positive.

21. • The electrochemical gradient between outside and inside is -70 to -
90mv.
• The resting potential of nerve is assumed to result from and be
maintained by relative permeability of the cell membrane to
potassium and its relative impermeability to sodium ions.

22. • DEPOLARIZATION
• When a stimulus of sufficient intensity to create an impulse is applied to
the nerve, it results in displacement of calcium ions from
phospholipid binding site.
• This causes alteration in membrane permeability that permits sodium
to increase its rate of diffusion through the membrane into the cell.
• The marked increase in the diffusion of sodium into the cell followed by
passage of postassium out of the cell abolishes the resting potential and
depolarizes the membrane.

23. • As the nerve is stimulated , there is rapid passage of sodium into the cell
and slower passage of potassium out of the cell.
• The stimulation generated is the result of liberation of a transmitter
substance acetylcholine at the site of stimulation.

24. REPOLARIZATION
• Following depolarization, the permeability of nerve membrane again
decreases, while the high permeability to potassium is restored.
• Potassium moves freely out of the cell, thereby restoring the original
electrochemical equilibrium and resting potential.
• Movement of both sodium ions into the cell during depolarization and
potassium out of the cell during repolarization are passive ie., The ions
move along its concentration gradient.

25. • The energy driven ‘sodium pump’ then actively transports sodium out
of the nerve membrane against its concentration gradient while
simultaneously transporting potassium inward to reestablish the resting
state .
• Adenosine triphosphate provides the energy source for the sodium
pump.

26. Absolute refractory period
• The return of the resting potential occurs within 3-4 msec after initial
stimulation.
• During this 3-4 msec interval, the membrane has a reverse potential and
cannot be stimulated .
• The nerve is then in an absolute refractory period.
Relative refractory period
• When the normal iconic distribution pattern begins to return,the nerve
can be stimulated ,but only by a greater than usual stimulus.
• The nerve is then said to be in relative refractory period.

27. All or none phenomenon
• Once an impulse has been initiated within a particular nerve fiber, the
amplitude of electrical change as well as the speed of nerve conduction
remains constant regardless of the quality or intensity of stimulus
applied, which explains the all or none law of nerve action.

29. PAIN PATHWAY
• Pain pathway from the face is carried by the trigeminal nerve. Its also
known as the trigeminal pathway.

30. • Trigeminal nerve carries somatosensory information from
face, teeth, periodontal tissues , oral cavity, nasal cavity,
cranial dura mater and major part of scalp to sensory cortex
• Sensory fibers of trigeminal nerve arise from the trigeminal
ganglion situated near temporal bone.
• Peripheral processes of neurons in this ganglion form three
divisions of trigeminal nerve, namely ophthalmic,
mandibular and maxillary divisions .

31. • Central processes from neurons of trigeminal ganglion enter pons in the
form of sensory root.
• After reaching the pons, fibers of sensory root divide into two groups,
namely descending fibers and ascending fibers.
• Descending fibers terminate on primary sensory nucleus and spinal nucleus
of trigeminal nerve. Primary sensory nucleus is situated in pons. Spinal
nucleus of trigeminal nerve is situated below the primary sensory nucleus
and extends up to the upper segments of spinal cord.
• Ascending fibers of sensory root terminate in the mesencephalic nucleus
of trigeminal nerve, situated in brainstem above the level of primary
sensory nucleus

32. • Majority of fibers from the primary sensory nucleus and spinal nucleus
of trigeminal nerve ascend in the form of trigeminal lemniscus and
terminate in ventral posteromedial nucleus of thalamus in the
opposite side .
• From thalamus, the fibers pass via superior thalamic radiation and reach
the somatosensory areas of cerebral cortex .
• Primary sensory nucleus and spinal nucleus of trigeminal nerve relay
the sensations of touch, pressure, pain and temperature from the
regions mentioned above.
• Fibers from mesencephalic nucleus form the trigeminocerebellar tract
that enters spinocerebellum via the superior cerebellar peduncle of the
same side. This nucleus conveys proprioceptive impulses from facial
muscles, muscles of mastication and ocular muscles.

33. NEUROTRANSMITTERS INVOLVED IN PAIN SENSATION
• Glutamate and substance P are the neurotransmitters secreted by pain
nerve endings.
• Aδ afferent fibers, which transmit impulses of fast pain secrete
glutamate.
• The c type fibers, which transmit impulses of slow pain secrete
substance p.

34. ANALGESIC SYSTEM
• Analgesic pathway that
interferes with pain
transmission is often
considered as descending
pain pathway, the ascending
pain pathway being the
afferent fibers that transmit
pain sensation to the brain .

35. • Fibers of analgesic pathway arise from frontal lobe of
cerebral cortex and hypothalamus
• These fibers terminate in the gray matter surrounding the
third ventricle and aqueduct of sylvius (peri aqueductal
gray matter)
• Fibers from here descend down to brainstem and terminate
on:
• I. Nucleus raphe magnus, situated in reticular formation of
lower pons and upper medulla
• Ii. Nucleus reticularis, paragigantocellularis situated in
medulla

36. • Fibers from these reticular nuclei descend through lateral
white column of spinal cord and reach the synapses of the
neurons in afferent pain pathway situated in anterior gray
horn
• Synapses of the afferent pain pathway are between:
• Aδ type afferent fibers and neurons of marginal nucleus
• C type afferent fibers and neurons of substantia
gelatinosa of rolando.
• At synaptic level, analgesic fibers release neuro
transmitters and inhibit the pain transmission before being
relayed to brain.

37. NEUROTRANSMITTERS OF ANALGESIC PATHWAY
• Neurotransmitters released by the fibers of analgesic
pathway are serotonin and opiate receptor substances
namely enkephalin, dynorphin and endorphin.

38. THEORIES OF PAIN TRANSMISSION
• SPECIFICITY THEORY
• INTENSITY THEORY
• PATTERN THEORY
• GATE CONTROL THEORY

39. 1.SPECIFICITY THEORY
• The classical description was provided by Descartes in 1644 , he said
pain is transmitted through a straight channel from skin to the brain.
• Muller: theory of information transmission only by sensory nerves.
• Von frey: specific cutaneous receptors for mediation of touch, heat ,
pain and cold.
• Free nerve endings were implicated as pain receptors.
• A pain center was was thought to exist within the brain, which was
responsible for all overt manifestations of the unpleasant experience.
• The specificity theory was responsible for the development of several
surgical approaches to the management of chronic pain by cutting
straight through tracts.

40. 2. INTENSITY THEORY OF PAIN
• An intensive (or summation) theory of pain (now referred to
as the intensity theory) has been postulated at several
different times throughout history .
• The theory defines pain, not as a unique sensory experience
but rather, as an emotion that occurs when a stimulus is
stronger than usual.

41. 3. PATTERN THEORY
• The theory suggested that particular patterns of nerve
impulses that evoke pain are produced by summation of
sensory input within the dorsal horn of the spinal column.
• Pain results when the total output of the cells exceeds a
critical level.
• For example, touch plus pressure plus heat might add up in
such a manner that pain was the modality experienced.

42. 4 . GATE CONTROL THEORY
• Psychologist Ronald Melzack and the anatomist Patrick Wall
proposed the gate control theory for pain in 1965 to explain the
pain suppression.
• According to them, the pain stimuli transmitted by afferent pain
fibers are blocked by gate mechanism located at the posterior
gray horn of spinal cord. If the gate is opened, pain is felt. If the
gate is closed, pain is suppressed .

44. Mechanism of gate control at spinal level
• 1. When pain stimulus is applied on any part of body, besides pain
receptors, the receptors of other sensations such as touch are also
stimulated
• When all these impulses reach the spinal cord through posterior nerve
root, the fibers of touch sensation (posterior column bers) send
collaterals to the neurons of pain pathway, i.E. Cells of marginal nucleus
and substantia gelatinosa .
• Impulses of touch sensation passing through these collaterals inhibit the
release of glutamate and substance P from the pain fibers
• This closes the gate and the pain transmission is blocked .

45. Role of brain in gate control mechanism
• According to Melzack and Wall, brain also plays some important role in
the gate control system of the spinal cord as follows:
1. If the gates in spinal cord are not closed , pain signals reach the
sensory cortex .
2. To minimize the severity and extent of pain, the brain sends message
back to spinal cord to close the gate by releasing pain relievers such
as opiate peptides.
3. Now the pain stimulus is blocked and the person feels less pain.

46. SIGNIFICANCE OF GATE CONTROL
• Thus, gating of pain at spinal level is similar to pre synaptic
inhibition.
• It forms the basis for relief of pain through rubbing, massage
techniques, application of ice packs, acupuncture and
electrical analgesia.
• All these techniques relieve pain by stimulating the release of
endogenous pain relievers (opioid peptides), which close the
gate and block the pain signals.

47. • MECHANISMS OF PAIN
• Pain sensation involves a series of complex interactions between
peripheral nerves & CNS
• Pain sensation is modulated by excitatory and inhibitory
neurotransmitters released in response to stimuli
• Sensation of pain is composed of 3 basic processes
• Transduction: this is the first stage where external noxious energy is
converted into electrophysiological activity
• Transmission: in the second stage, transmission, this coded information
is relayed via the spinal cord to the brainstem and thalamus
• Perception:. Finally, connections between the thalamus and higher
cortical centres control perception and integrate the affective response
to pain

49. • PAIN ASSESSMENT
• Pain is considered `the primary symptom that instigates people to seek
medical treatment’ (Turk & Melzack 1992,).
• 1.Verbal communication
• 2.Numeric scale: severity of pain is assessed by asking the patient to
select any number from 1-10 according to the intensity of pain.

50. • 3.Visual analogue scale: pain intensity can be measure by visual
analogue scale. The scale consists of 10 cm lines. On this scale , there is
marking from 0 to 10. 0 means no pain and 10 means very severe pain.
Patient is asked to mark the line which represents pain.

51. 4.Mcgill pain questionnaire: this is useful in the evaluation
of pain. This questionnaire consists of 20 groups with 78
types of pain . in these groups , 1 to 10 is designed for the
assessment of sensory character, group 11 to 15 assess
effective character and from group 16 to 20 to assess
evaluative character of pain.
5. Disability status: this is very important in assessing the
pain. Disability is lack of ability to function normally,
physically and mentally.

52. 6. Multiaxial assessment of pain: this includes 61 item questionnaire
which measure adjustment to pain from cognitive behavioural pattern.
This will help in getting profile of the patient. Patient profile can be
• Disfunctional (low activity with higher degree of
effective distress)
• Distressed( patients think that others are supportive of
their problems)
• Adaptive copers( patients with high level of social
support)
7. Quantitative sensory testing: quantitative testing modalities include
thermal, mechanical and electrical stimuli.

53. • CAUSES FOR OROFACIAL PAIN
1. Intracranial
2. Oral/ salivary
• Pulpal
• Periodontal
• Tongue
• Salivary gland lesions
3. ENT related
4. Musculoskeletal
5. Vascular

54. PAIN IN PERIODONTIUM
• In periodontal structures, pain may be manifested in two different ways:
pain of periapical origin, which is a deep somatic pain; or pain in the
gingival tissue, which is a superficial somatic pain
• Chronic periodontal diseases such as gingivitis and periodontitis are
usually painless, but they may cause mild, episodic or persistent dull
pain due to inflammation or low-grade infection. In contrast, sharp
periodontal pain is often associated with high-grade infection and
inflammation.

55. GINGIVAL AND PERIODONTAL ABSCESSES
• Gingival abscesses, which appear in the gingival sulcus, are
comparatively rare.. Gingival abscesses are usually located in the
marginal interdental tissue.
• Periodontal abscesses usually occur in areas with periodontal pockets,
in which deep spaces are generated around the teeth. They cause a dull,
gnawing, localized pain. The discomfort ranges from low intensity
aches to severe acute pain. Periodontal abscesses may be tender to
lateral periodontal pressure and the pain in the tooth adjacent to the
injury usually worsens with chewing.

56. • DIFFERENTIAL DIAGNOSIS BETWEEN PULPAL AND
PERIODONTAL PAIN

57. • PERICORONITIS
• Pericoronitis is an infection that is associated with an erupting tooth,
especially the third molar. The mucosa covering the tooth becomes
inflamed, with a trauma caused by the opposing teeth and infection
caused by food remnants under the mucosal layer. The pain is intense,
and is usually associated with submandibular adenitis, sore throat,
trismus and fever
•

58. DENTINAL HYPERSENSITIVITY
• It is characterized by short ,sharp pain arising from exposed dentin in
response to stimuli typically thermal, evaporative, tactile, osmotic or
chemical and which cannot be ascribed to any other form of dental
defect or pathology.
THEORIES
• Direct innervation theory
• Odontoblast deformation theory
• Hydrodynamic theory

59. • PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS
• The term “endoperio” describes the relationship between pulpal and
periodontal diseases. Endoperiodontal or pulpoperiodontal lesions are
inflammatory lesions that simultaneously compromise the dental pulp
and structures of the periodontal insertion.
• If the inflammation is confined to the pulp, the patient will describe the
pain as intense and incessant because the neural portion of the pulp
only transmits pain. However, if the inflammation has reached the
periodontal ligament, it will be easier for the patient to determine the
source of the pain, since this structure contains proprioceptive
sensory fibers

60. NECROTIZING PERIODONTAL DISEASES
• Necrotizing periodontal diseases are a group of infectious disorders
comprising necrotizing ulcerative gingivitis, necrotizing ulcerative
periodontitis and necrotizing stomatitis. However, these conditions may
in fact present different stages of the same disease; their etiologies,
clinical characteristics and treatments are similar but they differ in terms
of severity .
• The patient often complains of localized pain in the interdental papilla
• In all these lesions the onset of pain is rapid and its intensity depends on
the extent of the injury. The episodes of pain increase during eating and
tooth brushing, and are usually the reason for patient consultation

61. GINGIAL RECESSION
• Gingival recession reduces the width of keratinized connective tissue
and may cause periodontal discomfort/slight pain, especially during
dental brushing, due to localized inflammation and/or dentin
hypersensitivity.
DESQUAMATIVE GINGIVITIS
• Desquamative gingivitis (DG) is a term that covers epithelial
desquamation, erythema, erosion, and/or vesiculobullous lesions of the
gingival. In DG, the gingivae are deep red in color, shiny, atrophic and
eroded. There is a loss of the characteristic gingival pitting and it peels
easily on minimum contact. Clinically there is a burning sensation or
pain that is intensified by eating hot, acidic or spicy foods.

62. OTHER ENTITIES RELATED TO PERIODONTAL DISCOMFORT
• Gingival enlargement, defined as the abnormal overgrowth of gingival
tissue, is another cause of periodontal discomfort.
• Pyogenic granuloma (pg) is a benign vascular lesion, which some
authors describe simply as a non-infectious inflammatory hyperplasia
characterized by fibrous and granulomatous tissue.
• Clinically, pg usually presents as a smooth or lobulated exophytic
injury, either pedunculated or sessile .The injury may become ulcerated,
and the inflammation may cause pain or discomfort.
• Finally, another situation that can lead to periodontal discomfort include
periodontal ligament strains caused by occlusal trauma, associated
with parafunctional habits.

63. MANAGEMENT OF PAIN
1. ANALGESICS
2. ADJUVANT DRUGS
3. CAUSE RELATED THERAPY
4. RELAXATION
5. COUNSELING
6. PHYSIOTHERAPY
7. SENSORY STIMULATION
8. LOCALANESTHESIA

64. 1.Analgesics
a. Non narcotics : aspirin, acetaminophen and nsaids
b. Narcotic : morphine, buperenorphine, butorphanol, pentazocine.
2. Adjuvant drugs
• Analgesic balms
• Anticonvulsants
• Antidepressants
• Antihistaminic
• Antimicrobials and antiviral agents
• Dietary supplemants
• Neurolytic agents
• Nor epinephrine blockers
• Tranquilizers
• Muscle relaxants

65. 3. RELAXATION
• Autosedation
• Biofeedback
• Occlusal disengagement
o Voluntary disengagement
o Chewing gum
o Interocclusal device
4. COUNSELLING
5. PHYSIOTHERAPY
• Massage
• Exercise
• Deep heat therapy
• Triger point therapy
• Physical activity

66. 6. SENSORY STIMULATION
• Cutaneous stimulation
• Transcutaneous electrical nerve stimulation
• Electro acupuncture
• Percutaneous stimulation
7.LOCALANESTHESIA

67. CONCLUSION
• The most important part of managing pain is understanding the problem
and cause of pain & this is achieved only through proper diagnosis and
appropriate therapy.
• Nothing is more satisfying to the clinician than the successful
elimination of pain.

68. REFERECNCE
• Text book of medical physiology : guyton and hall 5th edition
• Essentials of medical physiology: K sembulingam 5th edition
• Monheim’s local anesthesia and pain control in dental practice
• Carranza’s clinical periodontology 11th edition
• Human physiology : A K jain
• Essentials of medical pharmacology: K D tripathi
• Pain management: A practical guide for clinicians, sixth edition
• Textbook of oral medicine and radiology:ghom 3rd edition