This document discusses pain control in operative dentistry. It begins with definitions of pain and classifications of pain based on duration (acute, persistent, chronic) and sensory characteristics (fast and slow pain). The neural pathways of pain and various theories of pain are described. Methods of assessing pain and factors that influence pain perception are outlined. Common causes of orofacial pain are listed along with differential diagnosis of pain. Techniques for controlling pain in restorative dentistry are provided, including local anesthesia and gaining patient confidence.

1. 1
PAIN CONTROL IN
OPERATIVE DENTISTRY
Dr.Basavan Gowda
Reader
Dept.Conservative Dentistry
&Endodontics
Navodaya Dental College
Raichur

2. • Probably - most fundamental and primitive sensation
• Distributed more or less all over the body
• Protective in nature and always indicates some serious trouble in the locality, such
as a structural damage or a serious functional or metabolic derangement
INTRODUCTION
2

3. An unpleasant emotional experience associated with actual or potential
tissue damage or described in terms of such damage.
International Association for the Study of Pain (IASP) (WHO)
An unpleasant emotional experience usually initiated by noxious stimulus
and transmitted over a specialized neural network to CNS where it is
interpreted as such.
Monheim
3
DEFINITION

4. • Protective mechanism for the body
• Tissue damage ignites individual’s reaction to pain stimulus
e.g. Skin ischemia - No pain - Desquamation
4
PURPOSE OF PAIN

5. Depending on experience, pain can be classified as :
1. Experimental
2. Acute
3. Chronic
5
CLASSIFICATION OF PAIN

6. • Short duration
• Severe
• Self limiting
Acute
• Associated with postoperative, post
injury
• More duration
• Requires pharmacological
assistance(analgesics)
Persistent
• Long term duration
• Eg.: Cancer & neurogenic pain
• Pharmacological assistance(analgesics) and
cognitive approach
Chronic or Disabling
• Continue beyond expectation for disease
process
• Pain and pain therapy dominate the life
• Depression, anxiety
Depending On Duration
Transient Pain
15

7. Pain is also classified into two types :
FAST PAIN
• Felt within about 0.1 second
• Described as: sharp, pricking, acute, electric pain
• Not felt in most deeper tissue of body
SLOW PAIN
7
• Begins only after 1 second or more & then increases slowly over many
seconds & some times even minutes
• Slow burning, throbbing, nauseous, chronic pain
• Associated with tissue destruction

8. 8

9. 1. Hyperreactive pulpalgia
a. Dentinal hypersensitivity
b. Hyperemia
2. Acute pulpalgia
a. Incipient
b. Moderate
c. Advanced
3. Chronic pulpalgia
a. Barodontalgia
9
PULPAL CAUSES OF PAIN
4. Hyperplastic pulpitis
5. Necrotic pulp
6. Internal resorption
7. Traumatic occlusion
8. Incomplete fracture

10. PAIN OF NON-DENTAL ORIGIN
I) MUSCULAR TOOTHACHE - TEMPORALIS, MASSETER
CLINICAL FEATURES
1. Constant tooth ache which is non pulsatile
2. Not responsive to local provocation of the tooth
3. Pain increases with function of involved muscle
4. LA - not effective
5. LA of involved muscle - reduces toothache
II) NEUROVASCULAR TOOTHACHE - ASSOCIATED WITH MIGRAINE VARIANTS
CLINICAL FEATURES
1. Toothache is characterized by remission
2. Temporal behavior
3. Minor or no dental cause
10

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12. NEURAL PATHWAY OF PAIN
12
Given by Fields -1987 ; modified later by others
Fields divided the processing of pain from the stimulation of primary
afferent nociceptors to the subjective experience of pain into four steps :
•TRANSDUCTION
•TRANSMISSION
•MODULATION
•PERCEPTION

13. III.
13
I. Transduction: process by which noxious stimuli is converted to
electrical activity in the appropriate sensory nerve endings
II. Transmission: refers to neural events that carry nociceptive input
into CNS for proper processing. In this, first and second order
neurons are involved
Modulation: refers to the ability of the CNS to control the pain
transmitting neurons
IV. Perception: if the nociceptive input reaches the cortex, perception
occurs. It is at this point the suffering and pain behavior begins

14. NEUROTRANSMITTERS
SMALL (rapid acting)
Acetylcholine
NOREPINEPHRINE
SEROTONIN
GAMMA
AMINOBUTYRIC ACID
GLYCINE
DOPAMINE
ASPARTATE
LARGE (slow acting)
Substance P
Endorphins
14

15. Referred Pain
58
• The pain is not felt over the area where the viscus is situated but felt
some where else
• Felt in the area where the viscus was situated in the embryonic life
e.g.
• Pain of heart - left arm, neck
• Pain of center of diaphragm - tip of shoulder
• Lower molar to ear

16. FEATURES OF REFERRED PAIN
Wholly spontaneous
Not accentuated by provocation of site
Ceases immediately if primary pain is arrested
Felt in superficial or deep structures
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17. Theories Of Referred Pain
60
• The two most popular theories are
1) Convergence – Projection
2) Convergence - Facilitation
1. Convergence-Projection Theory:
• This is the most popular theory
• Primary afferent nociceptors from both visceral and cutaneous
neurons often converge onto the same second-order pain transmission
neuron in the spinal cord

18. Brain having more awareness of cutaneous than of visceral structure through past
experience, interpret the pain coming from the regions served by cutaneous afferent
fibers
EXAMPLE (Milne et al 1981)
61

19. 2. Convergence – Facilitation Theory:
•Similar to convergence – projection theory
•Believed that the internal organs were insensitive to stimuli and that
they created a irritable focus on the spinal cord leading to R.P.
•Did not hold good

20. 3. Axon-Reflex
Afferent fiber is bifurcated before connecting to the dorsal horn
4. Thalamic Convergence
Referred pain is perceived as such due to the summation of neural
inputs in the brain
63

22. THEORIES OF PAIN
69

23. • Peripheral free nerve endings mediate pain
to the central apparatus
• Direct line from receptor to the brain
• Pulling one end of the rope causes a ring on
the other end of the bell
• No morphological basis
Specificity Theory
Descartes - 1664

24. Intensity Theory :
Mumford & Newton-1971
• Pain is caused when nerve is stimulated beyond certain level
• Pain is non-specific sensation
• Depends on high intensity stimulation
• e.g., application of heat is pleasant ; but more heat causes burning
• Intensity of stimulation is a factor in causing pain

25. Protopathic & Epicritic Theory
72
Head & Rivers 1908
• Two groups of sensory nerves from periphery to CNS
• Protopathic – primitive, yielding diffuse impression of pain & temperature
• Epicritic- concerned with touch & small changes in temperature
• These groups do not exist

26. Pattern Theory
73
Goldscheider 1894
• Pain is produced by intense stimulation of non-specific receptors
• Pain sensation depends on spatiotemporal pattern of nerve impulse
reaching brain
• spatio-temporal:- warmth, cold, pain
(according to Weddel 1955)
• Pattern of nerve impulse entering the brain will be different for different
regions
• Designation of sensation as hot, cold, tingling etc., is somewhat arbitrary
since there are many grades in between

27. 74

28. GATE CONTROL THEORY Melzack & Wall 1965
75

30. • Proposed by Ronald Melzack and Patrick Wall in 1965 & in 1982
• Described psychological mechanism by which psychological factors can
affect the experience of pain
• Neural gate can be open & close - modulate the pain
• Gates are located in spinal cord
• Allow to pass directly to the brain
• Altered prior to being forwarded to the brain (for instance, influenced by
expectations)
• Prevented from reaching the brain (eg: by hypnosis-induced anesthesia)
77

31. CAUSES OF OROFACIAL PAIN
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1. Local Pathosis of Extracranial Structures – can arise from:
a. Tooth pulp, periodontium, periradicular structures, gingiva, mucosa
b. Salivary gland disorders – mumps , acute parotitis (children)
- mucus plug, sialolith (adults)
- Sjogren’s syndrome(inflammation)
c. Ear pain – otitis media, otitis externa, mastoiditis

32. d. Sinus & paranasal pain – maxillary, frontal & ethmoid sinusitis
e. Tongue
f. Eyes
g.Temporomandibular joint articular disorders – polyarthritis, disc derangements,
osteoarthritis, dislocations, fractures
85

33. 2. Intracranial causes –
86
a. Neoplasm
b. Aneurysm
c. Meningitis
d. Hematoma / hemorrhage
e. Edema
f. Abscess
g. Angioma
h. Cerebrovascular accidents
I. Venous thrombosis

34. 3. Referred pain from remote pathologic sites – can be from:
87
a. Heart – angina pectoris , myocardial infarction
b. Thyroid – inflammation
c. Carotid artery – inflammation , other causes
d. cervical spine – inflammation , trauma , dysfunction
e. muscles – myofascial trigger points

35. 4 . Neurovascular causes –
a. Migraine
b. Cluster headaches & chronic paroxysmal hemicrania
c. Headaches with vascular disorders – arteritis, hypertension
d. headaches with substance exposure or withdrawal – nitrates, alcohol, narcotics,
caffeine
e. Headaches with metabolic disorders – hypoxia, hypoglycemia, dialysis
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36. 5. Neuropathic causes –
a. Paroxysmal
- Trigeminal neuralgia
- Glossopharyngeal neuralgia
- Nervus intermedius neuralgia
- Occipital neuralgia
- Neuroma
b. Continuous
- Postherpetic neuralgia
- Post – traumatic neuralgia
- Anesthesia dolorosa
6. Causalgic pain – reflex sympathetic dystrophy - arises from sympathetic nervous system
89

37. 7. Muscular pains –
90
a. Myospasm pain
b. Myositis pain
c. Local myalgia – unclassified
d. Myofascial pain
- tension – type headaches
- coexisting migraine and tension-type headaches
8. Unclassifiable pains / atypical facial pains
a . Atypical odontalgia
b. Burning mouth syndrome

38. HISTORY
1. Chief complaint – a) Location of Pain
b)Onset Of Pain – associated with other factors
- progression
91
c)Characteristics of Pain - Quality
- Behaviour
- Intensity
- Concomitant symptoms
- Flow of the pain
d)Aggravating /Alleviating Factors
e)Past Treatments
2. Past Medical History
3. Psychologic Assessment
DIAGNOSIS OF PAIN

39. CLINICAL EXAMINATION
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1. General examination
• Vital Signs
• Cranial Nerve Evaluation
• Eye / Ear Evaluation
• Cervical Evaluation
• Balance Coordination

40. 2. Muscular examination
• Pain & Tenderness
• Trigger Points & Pain Referral
3. Masticatory Evaluation
• Range Of Mandibular Movements
• Temporomandibular Joint Evaluation
• Oral Structures ( Teeth, Periodontia, Occlusion )
4) Other Diagnostic Tests
• Thermal Test
• Pulp Vitality Test
• Imaging
• Laboratory Tests
MRI
CT
ULTRASOUND
SINGLE PHOTON CT
POSITRON ELECTRON
TOMOGRAPHY
94

41. ASSESSMENT OF PAIN
Numerical Rating Scale 0-10 Scale
Visual Analog Scale Mark point on 10 cm line
McGill Pain Questionnaire
Pt. identifies terms describing pain
from 20 sets of words
West Haven Yale Multidimensional
Pain inventory
Language skills
52 questions assessing various aspects
of pain
Faces Scale
Pictures of Faces ranging from smiling
to crying indicating level of discomfort
96

42. • Biological
• Genetic variations leads differences in amount & type of neurotransmitters.
• Previous pain experience
• Gender
• Cognitive
• Younger –report greater level of pain
• Older children understand the meaning of pain
• Upto 3 months- no understanding of pain but memory is present
• By 6 month respond to pain by anger
• By 20 months anger becomes more dominant
105
Factors That Influence Pain

43. • Psychologial
• Feeling of lack of control - intensify pain perception
• Sociocultural
• Difference in perception exist among different cultural group
• Parents perception & response to their child’s pain strongly influence child’s
perception & his reaction to pain
Are Indians and Females Less Tolerant to Pain? An Observational Study Using a Laboratory Pain Model
Med J Malaysia Vol 6
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44. Differential Diagnosis of Pain
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45. 112

46. SITE OF PAIN REFERRAL INVOLVED TEETH
Frontal region Maxillary incisors
Nasolabial area
Maxillary canine
Maxillary premolars
Temporal region Maxillary 2nd premolar
Below mandibular molar area Maxillary 2nd & 3rd molar
Ear Mandibular molars
114

47. Mental region Mandibular incisor , canine & premolar
Angle of mandible Mandibular first & second molar
Midramal region Mandibular second pre molar
Superior laryngeal area Mandibular 3rd molar
Maxillary premolar Maxillary canine
Maxillary molars
Maxillary canine
Mandibular premolars
Mandibular premolars
Maxillary canine
Maxillary premolars
Mandibular first premolar Mandibular first and second molar
Glick DH 1962
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48. Pulpal And Periapical Pain
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49. Hypothetical Mechanism For Pain In Pulp
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1. Cholinergic neurotransmitters(Ach) – found in pulp
2. ANS :
The neurotransmitters elaborated by autonomic efferent in inflamed pulp
Bradykinin level during inflammation increases significantly
3. Adrenergic neurotransmitters (histamine) released from inflamed pulp
(mast cell)

50. 4. Prostaglandin :
• Present in inflamed tissue
• Create pain by direct irritation of nerve endings
• Alerts the sensors to kinin
• Bradykinin in minute conc. evokes pain
5. Cyclic AMP – cGMP
• Nerve stimulated – increased amount of c AMP – hyperpolarization of
nerve – decreased transmission of nerve impulse
• cGMP – depolarization of neurons – increased neuronal excitability
119

51. 6.Lowered O2 tension
120
• Decreased O2 tension - nerve impulses fired rapidly
• Pulpal ischemia - cell injury
• Outer membranes, subcellular mitochondria, lysosomes damaged
• Accumulation of Ca++ ions and release of enzymes that break down cell
components
• Reduced O2 tension in pulp
• Stimulation of sympathetic and parasympathetic nerves in blood vessels of
pulp, during this period generate pain

52. 7.Increased Intrapulpal pressure –
Inflammation
Increased temperature
Increased intrapulpal pressure
Pain
8.Specific infection of pulp and P.A. tissue
• Responsible for transmitting or modulating nerve impulses
• Therefore may be related to pain or pulpitis.
This theory is still unclear
121

53. METHODS OF PAIN CONTROL
122
1. Removing the cause
2. Blocking the pathway of painful impulses
3. Raising the pain threshold
4. Preventing pain by cortical depression
5. Using psychosomatic methods

54. Method Of Control Of Pain In Restorative Dentistry
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• Gaining confidence of the patient : fear - pain
• Sharp instruments employed with skill and confidence
• Use of cooling devices
• Use of obtundents
• Preventing desiccation of the dentin
• Local anesthesia
• General anesthesia
• Newer methods of pain control