This document provides an overview of pain, including its definition, classification, transmission pathways, and management. It begins with defining pain and discussing its incidence and epidemiology. Pain is then classified based on its source, duration, and transmission. The pathways of pain transmission from nociceptors to the central nervous system are explained. Finally, the document discusses pain assessment, management guidelines, and concludes with references.
2. • Introduction
• Definition
• Incidence of pain
• Epidemiology
• Classification of pain
• Pain receptors
• Pain transmission
• Theories of pain transmission
• Pathways of pain
• Pathways of pain from oro facial region
• Clinical application
• Pain assessment
• Management of pain
• ADA guidelines for management of dental pain
• Management of post operative pain
• conclusion
• References
3. Pain is a sensory experience of special significance to doctor
and basic scientists.
Pain is an intensely subjective experience.
4. The word pain is derived from the Latin word Peone and the Greek word Poine meaning
penalty or punishment
• “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”
( Monheim's Local Anesthesia And Pain Control In Dental Practice By Leonard M. Monheim 7th edition )
Definition
5. • Pain is “an unpleasant sensory and emotional experience associated with actual or
potential tissue damage, or described in terms of such damage”
(The International Association for the Study of Pain 1994 )
• The subject’s conscious perception of modulated nociceptive impulses that generate an
unpleasant sensory and emotional experiences associated with actual of potential
tissue damage or describe in terms of such damage.
(Bell's orofacial pain 6th edition )
• Pain is defined as an unpleasant and emotional experience associated with or without
actual tissue damage.
(Essentials of medical physiology K Sembulingam 6th edition)
• Pain is an unpleasant sensation as perceived by the patient and in simple terms
described by the patient, as that sensation which hurts.
(Textbook of oral and maxillofacial surgery Neelima Anil Malik 2nd Edition)
6. Orofacial pain is a common complaint affecting the
life of million people around the world.
IT IS THE MOST COMMON REASON WHICH
BRINGS THE PATIENT TO A DENTIST.
Incidence of pain
7. • According to Cohen – it was found that 21.8% of adult experience orofacial pain
symptoms
• The most common pain was toothache, which was estimated to have occurred in
12.3% of the population.
8. EPIDEMIOLOGY
• According to The American Pain Foundation, more than 50 million
people in the US suffer from chronic pain.
• An additional 25%, 20 million experience acute pain from injury or
surgery
• The prevalence of chronic pain ranges from 11% to 40%.
• In 2016, an estimated 20.4% of U.S. adults had chronic pain and 8.0%
of U.S. adults had high-impact chronic pain.
(Prevalence of Chronic Pain and High-Impact Chronic Pain Among Adults — United
States, 2016)
9. CLASSIFICATION OF PAIN
Based on source/ location/ referral & duration
Acute pain/ traumatic pain Chronic pain
Visceral 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
( Pain: Current Understanding of Assessment, Management, and Treatments - NPC
collaborative project with JCAHO 2001)
10. ACUTE PAIN
• Acute has a sudden onset, usually subsides quickly and is characterized by sharp,
localized sensations with an identifiable cause.
• Lasts > 30 days and occurs after muscle strains and tissue injury such as trauma or
surgery.
• A poorly treated pain can cause psychological stress and compromise the immune
system due to the release of endogenous corticosteroids.
(Guyton and hall textbook of medical physiology 12th edition)
11. • Acute pain is usually characterized by increased autonomic nervous system
activity resulting in
• Psychological symptoms such as anxiety
• Tachypnoea
• Tachycardia with hypertension
• Pallor
• Diaphoresis
• Pupil dilation
(Guyton and hall textbook of medical physiology 12th edition)
12. • 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
• It is caused by the activation of pain receptors in the chest, abdomen, or pelvic
areas
• In cancer patients pain is caused by tumour infiltration , radiation & chemotherapy
VISCERAL PAIN
(Essentials of medical physiology K Sembulingam 6th edition)
13. SUPERFICIAL 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
(Textbook of physiology – A.K jain 4th edition)
14. DEEP SOMATIC PAIN
It originates in deep body structures such as periosteum, muscles, tendons,
joints & blood vessels
Strong pressure, ischemia, tissue damage act as stimuli for brain damage
Radiation of pain from original site of injury occur
(Textbook of physiology – A.K jain 4th edition)
15. 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 well being of the patient
• It may be nociceptive, inflammatory, neuropathic or functional in origin
• It varies from extremely severe pain to pain of escalating or non – escalating
nature.
(Essentials of medical physiology K Sembulingam 6th edition)
16. CHRONIC MALIGNANT PAIN
• It occurs in 60-90 % of patients with cancer
• Pain can be related to the tumour or cancer therapy or
may be idiosyncratic
• Pain may also be found at the metastasized regions and
treatment interventions may activate peripheral
nociceptors
• Pain can be somatic/visceral
CHRONIC NONCANCER PAIN
• It is also referred to as chronic non – malignant
pain
• Pain may last for many years and is considered
progressive in nature
• May be nociceptive, neuropathic or mixed in
nature
(Essentials of medical physiology K Sembulingam 6th edition)
17. • Neuropathic pain is a result of an injury or malfunction of the nervous system
• It is described as -
Aching
Throbbing
Burning
Shooting
Stinging
Tenderness/ sensitivity of skin.
NEUROPATHIC PAIN
(Essentials of medical physiology K Sembulingam 6th edition)
18. MECHANISM OF NEUROPATHIC PAIN
Nerve damage / persistent stimulation
Rewiring of pain circuits both anatomically & biochemically
Spontaneous nerve
stimulation
Autonomic neuronal
stimulation
NEUROPATHIC PAIN
Increased discharge of
Dorsal horn neurons
19. This a type of chronic non cancer pain occurring due to musculoskeletal
disorders such as
• Rheumatoid arthritis
• Osteoarthritis
• Fibromyalgia
• Peripheral neuropathies
MUSCULOSKELETAL PAIN
(Essentials of medical physiology K Sembulingam 6th edition)
20. PAIN TYPES - 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
(Guyton and hall textbook of medical physiology 12th edition)
21. OTHER TYPES OF PAIN
REFERRED PAIN
• Pain that is perceived at the site different from its point of origin but
innervated by the same spinal segment
• Usually applies to pain that originates from the viscera
• Eg. The pain associated with MI commonly is referred to the left arm,
neck & chest
BREAKTHROUGH PAIN
• Pain is intermittent, transitory & an increase in pain occurs at a
greater intensity
• Usually lasts from minutes to hours and can interfere with
functioning
• Eg. Neuropathic pain, Lower back pain
(Guyton and hall textbook of medical physiology 12th edition)
23. 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.
• They are distinguished morphologically corpuscular
non corpuscular.
(Essentials of medical physiology K Sembulingam 6th edition)
24. 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.
(Essentials of medical physiology K Sembulingam 6th edition)
25. • 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.
• Since pain receptors respond to wide variety of stimuli, they are called polymodal.
(Essentials of medical physiology K Sembulingam 6th edition)
26. The nociceptive mechanism consists of a multitude of events:
This is the conversion of one form of energy to another.
Stimulus events to chemical tissue events,
Chemical tissue and synaptic cleft events,
Electrical events in neurons to chemical events at synapses.
TRANSDUCTION
(Essentials of medical physiology K Sembulingam 6th edition)
27. • Electrical events are transmitted along neuronal pathways, while molecules in the synaptic
cleft transmit information from one cell surface to another.
• This can occur at all levels of the nociceptive pathway, from tissue, through primary afferent
neuron and dorsal horn, to higher brain centers.
TRANSMISSION
MODULATION
(Essentials of medical physiology K Sembulingam 6th edition)
28. 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 potentials along
specific nerve pathways towards CNS.
(Guyton and hall textbook of medical physiology 12th edition)
30. 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.
• Relationship exists between the diameter of nerve fibers and their conduction
velocities.
(Essentials of medical physiology K Sembulingam 6th edition)
31. CLASSIFICATION OF NEURONS
NERVE
FIBER
DIAMETER
(um)
VELOCITY SENSATIONS
THEY CONDUCT
LOCATION
TYPE A fibers
alpha 13 – 20 70 – 120 m/s
Tactile and
Proprioception
Muscles , golgi
tendon organ and
skin
beta 6 – 13 40 – 70 m/s
gamma 3 – 8 15 – 40 m/s
32. NERVE
FIBER
DIAMETER
(um)
VELOCITY SENSATIONS
THEY
CONDUCT
LOCATION
Delta 1 – 5 5 – 15 m/s Fast sharp pricking
and acute pain,
touch , warmth
,cold
Dentine
,peripheral pulp
and oral mucosa.
TYPE C fibers 0.5 – 1 0.5 – 2 m/s Slow pain & itch ,
warmth , cold
Central pulp &
periodontal
ligament
(Essentials of medical physiology K Sembulingam 6th edition)
33. SECOND ORDER NEURON:
• The primary afferent neuron carries impulse into the CNS and synapses with the
second – order neuron.
• Also 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.
DORSAL HORN
(Essentials of medical physiology K Sembulingam 6th edition)
34. THIRD ORDER NEURON
• Cell bodies of the third order neurons of the nociception – relaying pathway are housed
in:
The ventral posterior lateral,
The ventral posterior inferior,
The intra laminar thalamic nuclei.
• Third order neuron fibers from the thalamus relay thermal sensory information to the
somesthetic cortex.
(Essentials of medical physiology K Sembulingam 6th edition)
36. INTENSITY THEORY
• Pain is produced when any sensory nerve is stimulated
beyond a certain level.
• Pain is supposed to be a non – specific sensation and
depends only on high intensity stimulation.
• Trigeminal system provides an example against this
theory.
• Intensity of stimulation is a factor in causing pain. There
must be some form of summation that occurs for the
subthreshold stimuli to become unbearably painful
(Massieh Moayedi and Karen D. Davis - Theories of pain: from
specificity to gate control J Neurophysiol 109: 5–12, 2013)
37. • Based on this theory there are no
distinct pathways for low- and
high-threshold stimuli.
• Rather, the number of impulses in
neurons determines the intensity
of a stimulus.
• The primary afferent neurons
synpase onto wide-dynamic range
(WDR) 2nd-order neurons in the
dorsal horn of the spinal cord,
where low levels of activity
encode innocuous stimuli, and
higher levels of activity encode
noxious stimuli. (Massieh Moayedi and Karen D. Davis - Theories of pain: from
specificity to gate control J Neurophysiol 109: 5–12, 2013)
38. SPECIFICITY THEORY
(Johannes Muller, 1842):
• Pain is a specific modality equivalent to vision and hearing etc.
• Pain is mediated by free nerve endings.
• Specialization is known to exist in nervous system and there are well known
tracts.
39. • Based on this theory each modality
(touch and pain) is encoded in
separate pathways.
• Touch and pain stimuli are encoded
by specialized sense organs.
• Impulses for each modality are
transmitted along distinct
pathways, which project to touch
and pain centers in the brain,
respectively. DRG, dorsal root
ganglion
(Massieh Moayedi and Karen D. Davis - Theories of pain: from
specificity to gate control J Neurophysiol 109: 5–12, 2013)
40. PATTERN THEORY (Goldscheider, 1894):
• Pain sensation deepens upon spatio – temporal pattern of nerve impulses reaching the
brain.
• According to Woddell (1962) warmth, cold and pain are words used to described
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.
(Massieh Moayedi and Karen D. Davis - Theories of pain: from specificity to gate control J Neurophysiol 109: 5–12, 2013)
41. • The Pattern Theory of Pain
posits that somatic sense
organs respond to a dynamic
range of stimulus intensities.
• Different sense organs have
different levels of responsivity
to stimuli.
• A population code or the
pattern of activity of different
neurons encodes the modality
and location of the stimulus
(Massieh Moayedi and Karen D. Davis - Theories of pain: from
specificity to gate control J Neurophysiol 109: 5–12, 2013)
42. GATE CONTROL THEORY
(Melzack And Wall), 1965
• According to this theory, the pain stimuli transmitted by afferent pain fibres are
blocked by GATE MECHANISM located at the posterior gray horn of the spinal
cord
• If the gate is open pain is felt, and if the gate is closed pain is suppressed
• Impulses in A – δ & C – fibres can be blocked by modulated by A – β activity that
can selectively block impulses from being transmitted to the transmission cells in
the spinal cord and then to CNS resulting in no pain
(Essentials of medical physiology K Sembulingam 6th edition)
43. The Gate Control Theory of Pain proposes that
both large (A-fibers) and small (C-fibers) synpase
onto cells in the substantia gelatinosa (SG) and the
1st central transmission (T) cells.
The inhibitory effect exerted by SG cells onto the
primary afferent fiber terminals at the T cells is
increased by activity in A-fibers and decreased by
activity in C-fibers.
The central control trigger is represented by a line
running from the A-fiber systerm to the central
control mechanisms; these mechanisms, in turn,
project back to the Gate Control system. The T
cells project to the entry cells of the action system.
(Massieh Moayedi and Karen D. Davis - Theories of pain: from
specificity to gate control J Neurophysiol 109: 5–12, 2013)
44. 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
(Essentials of medical physiology K Sembulingam 6th edition)
46. • Nociceptors
• Afferent nerve fibers
• Spinal cord network
Afferent pathways
CNS
Efferent pathways
(Essentials of medical physiology K Sembulingam 6th edition)
47. • Afferent pathways terminate in the dorsal horn of the spinal cord.
• 2nd afferent neuron creates spinal part.
• The portion of CNS involved in the interpretation of the pain signals
are:
Limbic system
Reticular
formation
Thalamus Cortex
(Essentials of medical physiology K Sembulingam 6th edition)
48. • composed of the fibers connecting the reticular formation,
midbrain, and substantia gelatinosa, are responsible for
modulating pain sensation.
The brain first perceives the sensation of pain
(Essentials of medical physiology K Sembulingam 6th edition)
49. • The thalamus, sensitive cortex :
perceiving
describing of pain
localising
• Parts of thalamus, brainstem and reticular formation:
- identify dull longer-lasting, and diffuse pain
• The reticular formation and limbic system:
- control the emotional and affective response to pain
(Essentials of medical physiology K Sembulingam 6th edition)
50. • From the site of pain generation, i.e., from the periphery, the pain senses are
carried by Aδ & C fibers.
• Their cell bodies are situated in the dorsal root ganglion of the spinal nerve.
• Enter the dorsal horn to terminate in the SG (Substantia gelatinosa), situated in the
tip of dorsal horn
• Second order neuron arises, crosses to the opposite side, then moves up through
the white matter of spinal cord to reach the brain.
(Essentials of medical physiology K Sembulingam 6th edition)
51. • Most of these 2nd order neuron travel up as spinothalamic tract (STT),
• Next order neurons arise to terminate on the cerebral cortex, at areas SI & SII
as well as cingulate gyrus.
Thalamus
52. • The neurotransmitter at the synapse between Aδ fiber and 2nd order neuron:
glutamate.
• C fiber & 2nd order neuron: substance P.
• The tip of dorsal horn, particularly the SG plays a key role in modification of pain
perception called gate.
Substance P
(Essentials of medical physiology K Sembulingam 6th edition)
53. PATHWAYS OF PAIN FROM OROFACIAL REGION
(Bell’s orofacial pain 6th edition)
55. DIAGNOSIS BASED ON QUESTIONS??
• Pain to sweetness
• Pain to cold
• Pain on application of cold but relieved by hot
• Pain on chewing
• Pain on swallowing
56. OTHER QUESTIONS
• When did pain start ?
• Where did the pain start ?
• Does anything relieve the pain ?
57. Grossman
Removal of
cause
REVERSIBLE PULPITIS
• It is a mild to moderate inflammatory condition of the pulp caused by
noxious stimuli in which the pulp is capable of returning back to its
un-inflamed state following the removal of the stimuli.
symptom
Patient
complaints of pain
that lasts for
seconds on taking
hot and cold
diagnosis
Can be confirmed
by visual, tactile,
thermal &
radiographic
examination of
the involved tooth
Treatment
Removal of
cause
(Pathways of pulp – cohen 9th edition)
58. • It is a persistent inflammatory condition of the pulp, symptomatic or
asymptomatic, caused by noxious stimuli.
RCT of the affected tooth
Or
Extraction of tooth
• pain that lasts for
several mins to hrs
• spontaneous pain
(Pathways of pulp – cohen 9th edition)
59. PERIODONTAL PAIN
• Localized, deep throbbing pain
• Involving inflammation of PDL
• Mobility
• Localized or generalized bleeding
• Presence of pocket
• Radiographically bone loss
• If pain involve multiple teeth including opposing teeth then occlusal
trauma should be considered.
60.
61. ACUTE GINGIVAL / PERIODONTALABSCESS
• Tooth is painful to bite and not so deep seated
• Throbbing as that of apical abscess
• Spontaneous pain
• Localized swelling
• Presence of deep pocket
(Newman & carranza clinical periodontology 10th edition)
62. PERICORONITIS
• Severe radiating pain in posterior oral region
• Inability to open or close mandible
• Tissue distal to erupting molar is most
painful to touch.
(Newman & carranza clinical periodontology 10th edition)
63. • Odontogenic infection of posterior teeth may refer pain to the ear/TMJ
area.
• In maxillary sinusitis pain may be stabbing, with severe aching
pressure.
• Pain frequently refer to maxillary posterior teeth or upward under the
orbit.
64. TRIGEMINAL NEURALGIA
• Precise cause: unknown
• May be due to vascular compression of gasserian ganglion, viral
infection of neuron.
• Pain: severe, lancinating, shooting into the bone and teeth.
• Electric like quality of pain is unique.
• A trigger zone exists somewhere on the facial skin.
(Burket’s oral medicine 11th edition)
65. ASSESSMENT OF PAIN
METHOD OF PAIN ASSESSMENT
• Comprehensive history intake
Medical history
Physical history
Family history
• Physical exam
• Questioning on characteristic of pain – onset, duration,
location, quality, severity & intensity
• Evaluation of psychological status
(Assessment of pain H. Breivik et al BJA: 101(1), 17–24, 2008)
66. PAIN ASSESSMENT TOOLS
Pain may be accompanied by physiologic signs and symptoms and
there are no reliable objective markers of pain.
The severity of pain can be assessed by –
RATING SCALES
Provide a simple way to
classify the intensity of pain
and should be selected based
on the patients ability to
communicate
MULTIDIMENSIONAL
SCALES
Helpful in obtaining
information about the pain but
are more often time consuming
to complete
(Assessment of pain H. Breivik et al BJA:
101(1), 17–24, 2008)
67. RATING SCALES
SIMPLE DESCRIPTIVE PAIN INTENSITY SCALE
NUMERIC SCALE
(Assessment of pain H. Breivik et al BJA: 101(1), 17–24, 2008)
69. MANAGEMENT OF PAIN
PAIN
Remove or treat
cause
Psychotherapeutic
approaches ( anxiolytics,
biofeedback, relaxation)
Supportive care
( nursing, social )
Inhibition of pain transmission
( electrical stimulation ,
acupuncture)
Neurological
( nerve block)
Palliative radiotherapy
and pharmacotherapy
ANAESTHETICS
( inhalation , local )
.
ANALGESIC
( non-opioid , NSAIDs,
opioids )
70. 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
NON – PHARMACOLOGICAL MANAGEMENT
(Bell’s orofacial pain 6th edition)
71. CORDOTOMY: In the thoracic region , the spinal cord opposite to the side of pain is partially cut to
interrupt the anterolateral pathway
THALAMOTOMY: Involves causterization of specific pain areas in the intra thalamic nuclei in the
thalamus, which often relieves suffering type of pain
SYMPATHECTOMY Excision of the segment of the sympathetic nerve or one or more sympathetic
ganglia
RHIZOTOMY Surgical removal of spinal nerve roots for the relief of pain or spastic paralysis
FRONTAL LOBOTOMY Surgical process involving division of one or more nerve tracts in a lobe
of the cerebrum usually frontal lobe
SURGICAL PROCEDURE FOR THE RELIEF OF PAIN
(Bell’s orofacial pain 6th edition)
72. • Non-opioid analgesics
Non-opioid analgesics include paracetamol and non-steroid anti-
inflammatory drugs (NSAIDs).
• Opioid analgesics
PHARMACOLOGICAL MANAGEMENT
(Essentials of medical pharmacology- K D tripathi 4th edition)
73. ADA guidelines guideline on antibiotic use for the urgent management of pulpal- and periapical-related
dental pain and intraoral swelling
ADA GUIDELINES FOR MANAGEMENT OF
DENTAL PAIN
• The ADA expert panel suggests prescribing antibiotics for immunocompetent adult patients (patients
with an ability to respond to a bacterial challenge) with Pulp necrosis and localized acute apical abscess
in settings in which Definitive, conservative dental treatment is not available.
• This recommendation is specific to situations in which the risk of experiencing systemic involvement is
high and a patient may lack immediate access to care.
• The expert panel suggests not prescribing antibiotics for immunocompetent adult patients with
Symptomatic irreversible pulpitis with or without Symptomatic apical periodontitis, Pulp necrosis and
symptomatic apical periodontitis, or Pulp necrosis and symptomatic apical periodontitis in settings in
which Definitive, conservative dental treatment is available owning to potentially negligible benefits
and likely large harms associated with their use.
(Lockhart P.B , Tampi M.P et al - Evidence-based clinical practice guideline on antibiotic use for the urgent management of pulpal- and periapical-related
dental pain and intraoral swelling A report from the American Dental Association JADA 2019:150(11):906-921)
74. Clinical pathway for treatment of immunocompetent adult patients seeking treatment in a dental setting with a pulpal or
periapical condition, in which definitive conservative dental treatment (DCDT) is not immediately available.
(Lockhart P.B , Tampi M.P et al -
Evidence-based clinical practice
guideline on antibiotic use for the
urgent management of pulpal- and
periapical-related dental pain and
intraoral swelling A report from the
American Dental Association JADA
2019:150(11):906-921)
75. Clinical pathway for treatment of immunocompetent adult patients seeking treatment in a dental setting with a pulpal or
periapical condition, in which definitive conservative dental treatment (DCDT) is immediately available.
(Lockhart P.B , Tampi M.P et al -
Evidence-based clinical practice
guideline on antibiotic use for the urgent
management of pulpal- and periapical-
related dental pain and intraoral
swelling A report from the American
Dental Association JADA
2019:150(11):906-921)
76. MANAGEMENT OF POSTOPERATIVE PAIN
Eighty percent of patients experience acute pain after surgery; of these patients, 86%
experience moderate, severe, or extreme pain. It has also been shown that 77% of
patients believe pain is a necessary part of surgery, and 8% of patients postpone their
procedure because of concerns associated with pain.
Postoperative pain experienced within the first 3 days after surgery is considered
normal and should progressively diminish throughout the healing phase
(Suchetha A, Esha Tanwar et al Post-operative complications after periodontal surgery . IJADS 2018; 4(4): 152-156)
77. Postoperative pain can occur as a result of –
• extensive and long surgical procedures;
• poor tissue handling (including incising with a dull instrument, tissue trauma, and poor local
anaesthesia);
• poor infection control (which increases the risk of postoperative infection);
• poor knowledge of surgical anatomy (which increases the risk of complications, such as nerve injury
and edema) ;
• patients who underwent the procedures that involved mucogingival/ bone or surgeries with large
wounds;
• Patients whose healing process might be delayed (e.g. immunosuppressed people, those with
uncontrolled diabetes, smokers, those taking bisphosphonates, those with a history of radiotherapy in
the head and neck area) ;
• patients with a past history of high analgesic intake after periodontal surgery ;patients experiencing
preoperative anxiety
For relieving pain initially certain medications like nonsteroidal anti-inflammatory drugs (NSAIDs), such
as diclofenac (1 mg/kg) and ibuprofen, paracetamol (15 mg/kg) can be prescribed
(Suchetha A, Esha Tanwar et al Post-operative complications after periodontal surgery . IJADS 2018; 4(4): 152-156)
78. CONCLUSION:
• Pain is bad, but not feeling pain can be worse.
• Pain is multidimensional experience involving the sensation evolved
by noxious stimuli.
• The sensation of pain therefore depends in part on the patients past
experience, personality and level of anxiety.
79. • Everyday patient seeks care for the reduction or elimination of pain.
• The most important part of managing pain is understanding the
problem and cause of pain.
• It is only through proper diagnosis that appropriate therapy can be
selected.
80. REFERENCES…R
1. Burket’s oral medicine (eleventh edition)
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Management of Pain. 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2001:222-240.
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Management of Pain. 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2001:17-25.
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Management of Pain. 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2001:241254.
5. Dunajcik L. Chronic nonmalignant pain. In: McCaffery M, Pasero C, eds. Pain Clinical Manual, 2nd ed. St. Louis, MO:
Mosby Inc; 1999:467-521.
6. Essentials of medical physiology K Sembulingam 6th edition
7. Massieh Moayedi and Karen D. Davis - Theories of pain: from specificity to gate control J Neurophysiol 109: 5–12, 2013
81. REFERENCES…R
8. Pain: Current Understanding of Assessment, Management, and Treatments - NPC collaborative project
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