Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.

1. INTRODUCTION
By creation man is a fighter. He has been fighting against all the odds of
nature since the time of creation. That’s what, theory of survival of fittest states.
Pain being always remained the greatest energy of mankind since the time of
evaluation. Pain is always being a driving which made the man to explore the
field of medicine. This fight against pain will be continued till the point of
immortality.
Pain is a malady that crosses almost every medical discipline. In dentistry,
pain is the most common motivation that brings the patients to the dentist and for
those whose are anxious about dental visit, fear of pain is also a primary cause
for avoidance of routine dental care. Pain may be defined as an unpleasant
sensory and emotional experience associated with actual or potential tissue
damage. Various cultural, cognitive, emotional and motivational differences alter
or modulate the intensity of a patient’s response to noxious stimuli.

2. DEFINITION:
An unpleasant sensory and emotional experience associated with actual
or potential tissue damage described in terms of such damage.
- Subcommittee on taxonomy of international association for study of pain

3. HISTORY
 Around 2000 yrs ago the world believed that pain exists outside the body
 2nd
century A.D. Galen noted that pain is recognized in brain
 Aristotle believed in heart as the centre of sensation
 According to Plato pain and pleasure arise within the body
 Leonardo da Vinci pinpointed the sensation of pain to the nerve of touch.
 19th century – with the development of neurology specific pathways
associated with sensations were identified
 Freud gave the concept of psychosomatic nature of pain

4. BASICS
 Divisions of Nervous system
– Central Nervous System
– Peripheral Nervous System
– Autonomic Nervous System
 Sympathetic
 Parasympathetic

5. Central Nervous System
 Includes brain and spinal cord
 Brain
– Cerebral hemisphere
– Cerebellum
– Midbrain
– Pons
– Medulla
Spinal Cord
 Protected by vertebral column
– Cervical – 7
– Thoracic- 12
– Lumbar – 5
– Sacral – 5
– Coccyx -1
Spinal cord architecture
 Gray matter and white matter
Autonomic nervous system
 Synonyms
– Involuntary nervous system
– General visceral efferent system
 Functions
– Haemostasis
– Metabolic activity
 ANS is represented in both PNS and CNS
– somatic and visceral afferent act as input arm
– General visceral efferent as output channel

6. Sympathetic system
 Energy utilization activities ( fright, flight and fight) .
 Thoracic-lumbar system outflow(T1→L2)
 Neurotransmitter – epinephrine and noreinepinephrine
Parasympathetic system
 Conservation and restoration of energy
 Craniosacral system
- Associated cranial nerves 3,7,9 & 10 .
- Spinal nerves S2→S4
 Neurotransmitter → acetylcholine
Peripheral Nervous System
 Includes spinal and cranial nerves and branches
 Peripheral ganglion

7. STRUCTURE OF NEURON
Components
– Cell body : contains spherical nucleus (karyon) giving of one or more
processes .
– An axon is often called nerve fiber
– Cellbody and dendrites form the receptor and the axon is the conducting
zone
protoplasmic processes
Dendrites Axons

8. PHYLOGENIC CONSIDERATIONS
 Phylum – (Greek word means race )
 Primary or main division of the plant or animal kingdom. Grouping organisms
which have common ancestors.
 Components of human brain
– Spinal cord or medulla ( functional in reptiles )
– Mammalian brain / limbic system ( pain and pleasure center ; functional in
humans)
– Cerebral cortex
Pain receptors
 Input to the nervous system provided by sensory reception that detects
sensory stimuli i.e. touch, sound, light, pain etc .
 Detection mechanism – by virtue of different sensitivities.
 All pain receptors are free nerve endings (nociceptors)
 Deep tissues are not supplied by free nerve endings .
 Pain receptors show non adapting nature .
Nerve impulse transmission mechanism
 Cell membrane of body has powerful electrogenic pumps (Na-K pumps)
 More +ve charge on external compared to internal surface ( RMP -90mV).
 Activation stage- potential becomes less –ve i.e. -70mV to -50mV .
 Increased Na permeability
 Inactivation stage (after 10,000th second)
– Na channel closed
– K channel opens

9. SYNAPSES
 Greek word – connection or junction
 They are junctions where the axons or some other portion of presynaptic cell
terminates on dendrites or axons of postsynaptic cell
 Anatomically synapses are knob like structures . Within knobs there are
– Vesicles ( neurotransmitters are stored )
– Mitochondria ( provide ATP )
 Synaptic clefts (200 Å )
 Synapses
– Chemical
– Electrical
 Chemical synapses – by neurotransmitters
 Electrical synapses –acc. to Burnett et al. (1996 ) synapses in which the
synaptic clefts are obliterated behave electrically .
 Acc. to Katz (1974) if electrical impulses cross the gap they can crossover to
adj. fibers which compromises the system .
 Frequency of occurrence of electrical synapses is unknown .

10. Neurotransmitters
 Neurochemicals that transmit impulses across the synaptic cleft
 40 different types of chemicals .
neurotransmitters
Small molecule rapid acting
Class 1 - ach Class 2 – amines Class 3 – amino
acids
Large molecule slow
acting
Hypothalamic Pituitary peptide Peptide of gut

11. NERVE FIBERS
 Each sensory receptor is attached to 1st order neuron .
 1st order neurons have varying thickness
 Velocity of impulse transmission varies with diameter of axon .
– Largest diameter fibers – A fibers (α,β,γ,δ)
– Intermediate diameter – B fibers
– Smallest diameter fibers – C fibers
Aδ vs. C Fiber
 pain , low threshold
– Location – periphery of the pulp
– Produce initial momentary sharp pain
– Stimulation by dentine hypersensitivity .
 C fibers – unmyelinated , small diameter, not specific for pain, high threshold
– Location – core of pulp
– Produce continuous, constant or throbbing pain.
– Stimulation by tissue inflammation and damage.

12. ASCENDING SENSORY TRACTS
 All the sensory information from the sensory segments of the body enter the
spinal cord through the dorsal root of spinal nerves .
 The two major sensory pathways involved are
– Dorsal root column ( medial limeniscal system)
 Touch, vibration, pressure, position sensations
– Anterolateral system
 Pain , thermal, itch , sexual sensations
Dual transmission of pain
 Tracts involved
– Neo-spinothalamic tract
Fast, sharp pain( Aδ fibers )
– Paleo-spinothalamic tract
Slow pain (C fibers )
 Due to double system of pain innervation a sudden onset of painful stimuli
often gives double pain sensation ; fast followed by slow pain .

13. NEO- SPINOTHALAMIC TRACT
 Dorsal root of s.nerve→ 1st order neuron terminate ( lamina 1 ) → 2nd order
neuron crosses to opp. Side of cord → brain through antero-lateral column
 Termination
– Reticular area
– Ventro- basal complex ( thalamus)
– Posterior nuclear group of thalamus
 From here to somatic sensory cortex .
 Neurotransmitter- glutamate
PALEO- SPINOTHALAMIC TRACT
 Dorsal root of spinal nerve → 1st order neuron terminates in laminae 2nd and
3rd → most signals pass through one or more small fibers before entering
lamina 5 through 8 → brain through anterolateral pathway .
Termination
 Widely in brain stem
 Only 1/10 to ¼ to thalamus
 Tectal area of mesencephalon
 Periaqueductal grey region
 From brain stem → intralaminar and central lateral nuclei ( thalamus) →
hypothalamus and basal ganglion
 Neurotransmitter – P substance

14. TRANSMISSION OF TRIGEMINAL NERVE IN CNS
 Sensory root of trigeminal nerve enters the brain , its fibers pass through 3
sensory nuclei
 Mesencephalic nucleus
– Receives fibers carrying proprioceptive impulses of tongue, facial and
orbital muscles , periodontal membrane
 Many fibers form all the three divisions dichotomise to form ascending and
descending branches .
 Principle nucleus receives impulses mediating touch and pressure sensation
from ascending branch .
 Spinal nucleus is divided into three zones
– Descending fibers terminate in spinal nucleus
– The rostrally located par oralis receives tactile input from cutaneous area
of head, mouth, lip and nose .
– Intermedially located par interpolaris receive input from forehead, cheek,
angle of jaw, tooth pulp .
– Cordally located par caudalis receive modalities of touch, pain and
temperature form anterior part of head .
Secondary pathways
 2nd order neuron of trigeminal system form three secondary pathways
– Fibers from principle sensory nucleus form trigeminal limeniscus which
travels with medial limeniscus , together they go to ventro - posterior
nucleus ( thalamus )
 Origin is from spinal trigeminal nucleus analogues with neo–spinothalamic
tract . This neo- trigeminal thalamic tact joins the trigeminal leminiscus and
medial leminiscus and converge into ventro – posterior thalamic nucleus .
 Origin is from spinal trigeminal nucleus analogous to spino-reticulo-thalamic
pathway. This tract receives mechano and thermo receptive information and
convey it to intra-laminar nucleus of the thalamus .

15. REPRESENTATION INTO CORTEX
 Structure of mouth and face , including teeth are represented at cortex for
touch and pressure in post-central gyrus( primary somatic sensory area)
 Spinal nuclei also receive connecting fibers from facio-glossopharyngeal and
vagus nerve .

16. PAIN DUE TO PULPAL DISEASES
• After many investigations it is concluded that there is no correlation between
a patient’s experience of pain , clinical condition and histological appearance
of pulp ( Seltzer et al 1963 ; Mumford 1970 ; Adam et al 1974 )
Pulp exposure
• Pain is frequently experienced
• Pain lasts for 1 second .
• Patient not only feels pain but sees lightening and hears it .
• Reason – numerous nerve endings are subjected to intense stimuli .
Hyperalgasia
• Early state of disturbed pulpal circulation with increased vascularity .
• Reversible
• Pain depends on nature of stimuli
• Initial inflammation → acute condition → chronic condition
Acute pulpitis
• First stage involves dilation of capillaries
• Flow is directly proportional to 4th power of radius ( poiseuille’s law )
• Increased dilation → increased permeability → increased pressure
• Increased pressure inversely affects the walls of veins hence stasis occurs
• Three forms of pain
1. Sharp, lasts for a relatively short time

17. 2. Spontaneous pain( without external stimuli) because of chemical changes
in pulp .
3. paroxysmal pain in short sharp jabs occuring spontaneously
Localization of pain
• Poor localization because of anatomical convergence of pulpal nerves in
trigeminal nuclei and subsequent convergence at higher level .
• Dental pulp does not have individual representation in the human brain .
Sequelae of acute pulpitis
• Periapical disease
• Chronic pulpitis
– Virulence of microorganisms decreases
– Apical foramen has not fully formed – hence better drainage.
Chronic pulpitis
• Types
– Open ( less painful due to increased drainage)
– Closed
• Not sensitive to thermal changes
• Pain is not an important feature of chronic pulpitis unless acute exacerbation
occurs
Pulp gangrene
• Pulp is badly damaged and is associated with gas producing micro organisms

18. • Pain occurs spontaneously
• Dull ache lasts for hours or even days
• Leads to greater thermal expansion of gas which exacerbates pain
• Co-efficient of thermal expansion of gas 0.00367/ºC at constant pressure at
37ºC ( Weast 1972 )
Pulp necrosis
• Death of pulp without micro organisms being necessarily present .
• Pulp dies slowly, losing fluid and becoming dry (in some cases pulp
disappears)
• No pressure so pain is not there
• Symptomless
ENDODONTIC PAIN MANAGEMENT
• Divided into 3 sections
– Pain during treatment
– Pain following instrumentation
– Pain following obturation
Pain management during treatment
• Associated with problem of anesthesia
• Divided into
– anatomic variation

19. – Technical error
Anatomic variation
• Wide flaring mandible
• Long ramus in superior inferior direction
• Bulky musculature or excessive adipose tissue
• Edentulous patient
INFERIOR ALVEOLAR NERVE BLOCK FAILURE
• % failure rate is observed
• The mandible, hard and soft tissues are supplied by plexus of nerves
• This plexus with its many communications may allow sensations even if
primary trunk is blocked .
• Main nerve in this plexus is inferior dental nerve but lingual, buccal, mylohyoid
nerve and sensory fibres from cervical plexus in retromolar area may also
innervate the teeth .
Technical errors
• Technical errors are result of misplacement of needle at the time of injection
• Deep penetration in parotid gland
• Superficial penetration – absence of sign
• Penetration superior to occlusal level – absence of sign
• Sudden agitation or hyperactivity – intravascular injection

20. Solutions
• Gow-gates nerve block
• Introduced by Dr. George Gow-Gates (1973)
• True mandibular nerve block as it provides sensory anesthesia to entire
distribution of 3rd branch of trigeminal nerve .
• Advantage – single injection for anesthesia
– increased success rate (95-99%)
– Fewer post injection complications
• Disadvantage
– Longer time of onset
– Lingual and lower lip discomfort to patient
VAZIRANI – AKINOSI CLOSED MOUTH MANDIBULAR BLOCK
• Introduced by Dr. Joseph Akinosi in 1977
• Closed mouth approach to mandibular anesthesia
Indications
– Limited mandibular opening
– Multiple procedures on mandibular teeth
– Inability to visualize landmarks for IANB
Supplemental Anesthesia
• Supplemental injection approach followed if 1st standard injection is
ineffective

21. • Useful to repeat standard injection only if the patient is not exhibiting classical
signs of soft and hard tissue anesthesia
• For postero-superior maxillary block palatal infiltration provides profound
anesthesia
• For mandibular molars use lingual infiltration and intra-ligamental injection .

22. HOT TOOTH
• Periodontal ligament injection technique of choice if the primary injection is
unsuccessful
• Supplemental injections for the hot tooth are in following order of preference
1. Intra-ligamental injection
2. Intra-septal injection
3. Intra-pulpal injection
Stabident system
• A new intra-bony injection
• Beveled steel wire mounted in slow speed Handpiece used to perforate
cortical plate adjacent to root in question
• Needle of similar diameter and length inserted into tiny opening
• Before perforation 1st inject into attached gingiva

23. MANAGEMENT OF PAIN FOLLOWING INSTRUMENTATION
• Causes – some hypotheses proposed
– Local adaptation syndrome
– Periapical pressure changes
– Microbial flora changes
– Immunological factor
– Psychological factor
Non vital tooth (necrotic pulp)
• Apical radiolucency
• Pain with swelling can sometime arise as result of instrumenting an
asymptomatic, non vital (necrotic) pulp
• Cohen referred to this situation as phoenix abscess
Factors
• Following factors, studied by Torabinajad et al were evaluated
1. Age – 40-45 yrs.
2. Sex – females more
3. Anterior and posterior teeth – no difference
4. Most problematic – mandibular incisor and bicuspids
5. Least problematic – maxillary molars
6. Patient with allergy – increase incidence
7. Presence of systemic disease – no difference
8. Size of radiolucency – inversely proportional
9. Presence of sinus tract – less problematic
10.Systemic medication – analgesics more effective than antibiotics .

24. Vital tooth
• Causes – hyper occlusion
– Overmedication
– Over instrumentation
– Inadequate pulp removal
– Fracture of temporary dressing
Prevention
• Avoid apical extrusion of infected debris
– Crown down instrumentation
– Rotary instrumentation
– Frequent irrigation
• Elimination of all micro organisms
– Complete chemo- mechanical preparation in one visit
– Intracanal medication
• Prophylactic NSAID’s
– Therapeutic blood level of NSAID’s should be attained if possible prior to
initial endo visit .
– Ideally 2 oral doses should be given
Management
• For immediate relief of pain administer local anesthesia

25. • Follow up with the criteria mentioned
– Check occlusion
– Remove temporary fillings
• reinstrument to appropriate working length
• Frequent irrigation
• Search for additional canal(s)

26. MANAGEMENT OF ENDODONTIC PAIN FOLLOWING OBTURATION
• Incidence of acute pain or swelling subsequent to completion of endodontic
treatment is extremely low. Post endodontic pain is usually mild, transient
and managed with an appropriate analgesic.
Causes
• Overfilling or over extension
• Extra short fill
• Hyper occlusion
• Missed canal
• Cracked or split tooth
• Pain full episodes are usually caused by the pressure inherent in the insertion
of root canal filling material.
• Another reason can be chemical irritation from ingredients of root canal
cements or paste. As a rule, these effects are short lived and last only for 24
– 48 hours.
• Another possible cause is fracture of crown or root
Management
• For immediate relief of pain administered local anasthesia
• After that following should be consider
• Check occlusion
• NSAIDS an antibiotics (Swelling)
• Re treatment

27. • Trephination
• Apical surgery
• Extraction
Management
• Attempt to establish drainage through canal (if no drainage- apical
trephination)
• Apply corticosteroids and antibiotics
• Check for swelling (consider antibiotics)
• Prescribe analgesics

28. CONCLUSION
Pain has always challenged mankind by being on undesirable sensation
and man will always find never technique to reduce its agony.
A clinician is always challenged with patient vague description of his
painful condition. Hence adequate knowledge of pain will have his analytic skill
and leading to better understanding of patient conditions and effective treatment
delivery.
As Hilton states “Every pain has its distinct significance and pregnant
if we will but carefully search for it”.

29. Reference:
1. Seltzer Samuel, Pain Control in dentistry diagnosis and management
2. Mumford J.M, Orofacial pain, aetiology, diagnosis and treatment III etd.
3. Guyton C. Arthur. Text book of medical physiology 7th
etd.
4. Bell E. Welden Orofacial pains classification diagnosis and
management 4th
etd.
5. J.M. Mumford, J. Of dent res; 50; p 506.

30. 1.
CONTENTS
 INTRODUCTION
 HISTORY
 DEFINITION
 BASIC TERMINOLOGY
 PHYLOGENIC CONSIDERATION
 PAIN RECEPTORS
 NERVE IMPULSE TRANSMISSION MECHANISM
 BASIC PHYSIOLOGY OF SYNAPSE
 NEUROTRANSMITTERS
 FIBERS AND TRACTS INVOLVED IN PAIN PATHWAY
 THRESHOLD OF PAIN
 CLINICAL CONSIDERATIONS
O PAIN IN ENDODONTICS
O PAIN CONTROL METHODS
 CONCLUSION
 REFERENCES