Pain / orthodontic courses by Indian dental academy

INTRODUCTIONBy 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.

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

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

BASICS Divisions of Nervous system

– Central Nervous System

– Peripheral Nervous System

– Autonomic Nervous System

Sympathetic

Parasympathetic

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

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

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

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

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 .

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

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.

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 .

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

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 .

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 .

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

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

• 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

– 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

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

• 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 .

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

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 .

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

• Follow up with the criteria mentioned

– Check occlusion

– Remove temporary fillings

• reinstrument to appropriate working length

• Frequent irrigation

• Search for additional canal(s)

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

• 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

CONCLUSIONPain 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”.

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.

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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